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and the number of years since cessation. Smoking cessation reduces respiratory symptoms and respiratory infections. Smokers who quit have better pulmonary function than continuing smokers.177 For persons without overt COPD, pulmonary function improves about 5% within a few months of quitting. Cigarette smoking accelerates the age-related decline in lung function; with abstinence, the rate of decline returns to that of never smokers. With sustained abstinence, the risk of developing COPD and the COPD mortality rate are lower than they are in continuing smokers,16 but do not return to the level found in nonsmokers, probably because smoking has resulted in irreversible injury to the airways and parenchyma.1 For example, in the U.S. Veterans Study, the mortality ratio for current smokers was about 12, and was reduced to 10 among ex-smokers 10 years after cessation. After more than 20 years of abstinence, the mortality rate was still twice that of nonsmokers.178 Smokers with destructive lung changes can often stabilize after cessation but do not regain lost lung function.175 Smokers have more respiratory symptoms than do nonsmokers. The frequency of respiratory symptoms in children and adolescents is greater in current smokers than nonsmokers or former smokers.179 The 2004 Surgeon General’s report concluded that smoking was a cause of wheezing in children and adolescents, that there was insufficient evidence to determine whether there was a causal relationship between active smoking and physician-diagnosed asthma in children and adolescents, and that the evidence was suggestive but not sufficient to infer a causal relationship between active smoking and a poorer prognosis for children and adolescents with asthma.1 The 2004 Surgeon General’s report concluded that there is a causal relationship between active smoking and chronic respiratory symptoms (chronic cough, phlegm, wheezing, and dyspnea) among adults.1 These symptoms have a dose-response relationship with the number of cigarettes smoked per day, and they decrease with cessation. Smoking contributes to these symptoms by decreasing tracheal mucous velocity, increasing mucous secretion, causing chronic airway inflammation, increasing epithelial permeability, and damaging parenchymal cells.16 The Surgeon General also concluded that there was inadequate evidence to determine whether there was a causal relationship between active smoking and asthma in adults, that the evidence was suggestive but not sufficient to infer a causal relationship between active smoking and increased nonspecific bronchial hyperresponsiveness, and that active smoking was a cause of poor asthma control.1

Gastrointestinal Disease Cigarette smoking is associated with symptomatic gastroesophageal reflux disease. Compared with nonsmokers, smokers have reduced lower esophageal sphincter pressure and reduced salivary function, which contribute to a longer acid clearance time.180 Up to 100% of duodenal ulcers and 70–90% of gastric ulcers are associated with H. pylori infection.181 The remaining ulcers are linked to the use of nonsteroidal anti-inflammatory drugs.182,183 Smokers of both sexes have a high prevalence of peptic ulcer disease, with a clear dose-response relationship.1,56 The ACS CPS-I found that the relative risk of mortality for peptic ulcer among men was 3.1 for current smokers and 1.5 for former smokers compared with lifetime nonsmokers.12 Duodenal ulcers heal more slowly among smokers than nonsmokers, even with therapy. Both gastric and duodenal ulcers are also more likely to recur among smokers. Smoking cessation is associated with fewer duodenal ulcers, improved short-term healing of gastric ulcers, and reduced recurrence of gastric ulcers.16 Likely mechanisms by which smoking promotes peptic ulcer disease include the potential for tobacco smoke or nicotine to increase maximal gastric acid output and duodenogastric reflux, and to decrease alkaline pancreatic secretion and prostaglandin synthesis.1 Bicarbonate secretion from the pancreas is reduced immediately after smoking, leading to a decrease in duodenal bulb pH.184 The pH level appears to be the most important determinant for the development of gastric metaplasia in the duodenum, which allows colonization by

H. pylori.185 Four studies controlling for H. pylori infection have shown an association between smoking and ulcer.1 The 2004 Surgeon General’s report concluded that smoking causes ulcers in persons who are H. pylori-positive and that the evidence was suggestive but not sufficient to infer a causal relationship between smoking and the risk of peptic ulcer complications.1

Diseases of the Mouth Epidemiological studies from several countries have shown that cigarette smokers have more periodontal disease than do nonsmokers, and the 2004 Surgeon General’s report concluded that smoking causes periodontitis.1,186,187 A recent study concluded that more than 50% of the cases of adult periodontitis in the United States are attributable to cigarette smoking.188 A strong association has been noted between both the duration of smoking and the number of cigarettes smoked per day and the level of periodontal disease.1,188,189 Data from two cohort studies suggest that cigar and pipe smokers also have significantly greater periodontal disease and bone loss than nonsmokers.190,191 Moderate-to-severe periodontal disease occurred in 8% of nonsmokers, 13% of pipe smokers, and 16% of cigar and cigarette smokers.192 Risk decreases with sustained cessation.1 The likely mechanism for smoking-related periodontal disease is reduction in immune response, possibly making the smoker more susceptible to bacterial infection. Smoking also impairs the regeneration and repair of periodontal tissue. The 2004 Surgeon General’s report also concluded that the evidence was not adequate to determine causality between smoking and coronal dental caries, and that the evidence was suggestive but not sufficient to infer a causal relationship between smoking and root-surface caries.1 Chewing tobacco has also been implicated in the development of root-surface caries, and to a lesser extent, coronal caries.193 Leukoplakia or gum recession occurs in 44–79% of smokeless tobacco users133,194 and can occur even among young people.179,195 Gum recession commonly occurs in the area of the mouth adjacent to where the smokeless tobacco is held. Among adult users of smokeless tobacco or snuff, the risk of oral disease has been well documented, and changes in the hard and soft tissues of the mouth, discoloration of teeth, decreased ability to taste and smell, and oral pain have been reported.196–198 One study of smokeless tobacco users in a high school population reported that 49% of these teenaged users (averaging 1.7 years of smokeless tobacco use) had soft tissue lesions, periodontal inflammation, or both, or erosion of dental hard tissues.199

Other Diseases The 2004 Surgeon General’s report reported several other causal relationships between smoking and disease. The report concluded that smoking causes diminished health status that could manifest as increased absenteeism from work and increased use of medical care, adverse surgical outcomes related to wound healing and respiratory complications, low bone density in postmenopausal women (the evidence was suggestive but not sufficient to infer causality in men), and hip fracture.56 It was noted that smoking is one of the major causes of fracture in older persons that can be prevented. The report also concluded that smoking causes nuclear cataracts.1 The 2004 Surgeon General’s report concluded that the following relationships between smoking and disease were suggestive but not sufficient to infer causality: erectile dysfunction, exudative (neovascular) age-related macular degeneration, atrophic age-related macular degeneration, and the opthalmopathy associated with Graves’ disease.1 A recent cohort study reported that smoking is a risk factor for cognitive decline from ages 11 to 64, after adjusting for childhood IQ, level of education, occupational status, and other factors.200 Current smoking is also associated with mental illness. In 2003, among those aged 18 or older who had serious mental illness in the past year, 44% were past month cigarette smokers.201

54

In Utero Effects of Maternal Smoking The effects of maternal smoking on the fetus have been extensively studied. It is well documented that infants born to women who smoke during pregnancy weigh an average of 200–250 g less than those born to nonsmokers.1,16,56 The incidence of low birth weight (less than 2500 g) in infants born to mothers who smoke is twice that of infants born to nonsmokers.16,56 The relationship between maternal smoking and low birth weight is dose dependent and independent of other factors known to influence birth weight, including race, parity, maternal size, socioeconomic status, sex of child, and gestational age.56 Women who stop smoking before becoming pregnant have infants of the same birth weight as never smokers. In addition, pregnant smokers who quit in the first 3–4 months of pregnancy and remain abstinent through the rest of the pregnancy have normal birth weight infants. Pregnant women who stop smoking before the 30th week of gestation have infants with higher birth weight than do continuing smokers.16 Smoking causes both reduced fetal growth and early delivery (often from pregnancy complications).56 However, smoking affects birth weight primarily by retarding fetal growth. The risk of a small-for-gestationage infant is 3.5–4 times higher among women who smoke during pregnancy than among nonsmoking women. Fetal growth restriction could be reduced by an estimated 30% if all women abstained from smoking during pregnancy.1 In 1985, the Centers for Disease Control defined the fetal tobacco syndrome as follows: (a) the mother smoked five cigarettes or more a day throughout the pregnancy; (b) the mother had no evidence of hypertension during pregnancy, specifically no preeclampsia and had documentation of normal blood pressure at least once after the first trimester; (c) the newborn infant had symmetrical growth retardation at term (37 weeks) defined as birth weight less than 2500 g and a ponderal index (weight in grams divided by length) > 2.26; and (d) there was no obvious cause of intrauterine growth retardation, such as congenital malformation or infection.12 Several mechanisms are thought to cause the reduction in fetal growth, including impaired maternal weight gain, increased cyanide exposure (leading to impaired vitamin B12 metabolism), and increased cadmium exposure. The primary mechanism, however, is thought be intrauterine hypoxia, which is caused by increased carboxyhemoglobin production from carbon monoxide (CO) exposure, vasoconstriction of the umbilical arteries, reduced blood flow to the uterus, placenta, and fetus, and direct effectors of nicotine and other toxins in tobacco on the placenta and fetus.1,16 Although fetal growth is diminished among smokers, placenta-to-birth-weight ratios are larger than those of nonsmokers,202 probably because of the larger placental surface necessary to provide adequate fetal oxygenation in smokers. A few studies have shown an association between smokeless tobacco and low birth weight.203,204 The Surgeon General has concluded that maternal smoking causes preterm delivery (RR = 1.5) and shortened gestation. An estimated 7–10% of preterm deliveries could be prevented by eliminating smoking during pregnancy.1 Maternal smoking is also associated with higher fetal, neonatal, and infant mortality, independent of sociodemographic factors for such mortality.16 One large study showed adjusted infant mortality rates of 15.1 per 1000 for white nonsmokers and 23.3 per 1000 for white women who smoked more than one pack per day. Comparable infant mortality rates for black women were 26.0 and 39.9 per 1000, respectively.205 A large retrospective cohort study found that infant mortality was 40% higher if the mother smoked during pregnancy, with a dose-response relationship, and estimated that 5% of infant deaths in the United States were attributable to maternal cigarette smoking. Among American Indians and Alaska Natives, this attributable fraction was 13%. The authors estimated that nearly 1000 infant deaths could be averted if no maternal smoking occurred. 206 Smoking during pregnancy causes placenta previa, abruptio placentae, and premature rupture of membranes.1,16 Up to 10% of placental abruption could be avoided if smoking during pregnancy were eliminated.207 The 2004 Surgeon General’s report concluded that the evidence is suggestive but not sufficient to infer a causal relationship between maternal smoking and ectopic pregnancy and spontaneous abortion. The report also concluded that smoking reduces the risk for

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preeclampsia, but that this decreased risk did not outweigh the many adverse outcomes of maternal smoking.1 The 200156 and 20041 Surgeon General’s reports determined that maternal smoking during and after pregnancy causes sudden infant death syndrome (SIDS). Studies have consistently shown a two- to fourfold increased risk of SIDS among infants whose mothers smoked during pregnancy compared with infants of nonsmoking mothers, even after controlling for other risk factors. Most hypotheses about possible mechanisms center around the effects of maternal smoking on fetal oxygenation and neural development.1,56 One animal study reported that fetal exposure to nicotine led to reduced tolerance of hypoxic episodes and increased mortality.208 Although some studies suggested that smoking during pregnancy might affect physical growth, mental development, and behavior of children, studies are limited by small numbers and the infrequency of events of interest. The 2004 Surgeon General’s report concluded that there is inadequate evidence to determine causality between maternal smoking and congenital malformation, physical growth, and neurocognitive development of children. The report also concluded that the evidence is suggestive but not sufficient to infer a causal relationship between maternal smoking and oral clefts.1 Many studies have shown that smoking results in reduced fertility and fecundity for couples in which one or both partners smoke.1 Animal studies suggest that polycyclic aromatic hydrocarbons have a destructive effect on oocytes and may affect the release of gonadotropins, corpora lutea formation, gamete interaction, and implantation.1 Smoking also increases anovulation and shortens cycles, which may also contribute to reduced fertility and fecundity.209 The 2004 Surgeon General’s report concluded that smoking causes reduced fertility in women, but that evidence was inadequate to determine whether there was a causal relationship between smoking and sperm quality.1

Health Effects on Young People Although many of the adverse health effects from tobacco occur later in life, smoking also has health implications for young people. High school seniors who are regular cigarette smokers are more likely to report shortness of breath when not exercising, cough, productive cough, or wheezing and gasping, even after adjustment for sex, other drug use, and parental education level.210 Cigarette smoking during adolescence also appears to reduce the rate of lung growth and the level of lung function achieved. Young smokers are more likely to be less physically fit than nonsmokers. Smoking by children is also associated with an increased risk for early atheromatous lesions and increased cardiovascular risk factors. Smokeless tobacco use by children is associated with halitosis, periodontal degeneration, and soft tissue lesions.179 Cigarette smoking is also associated with other high risk behaviors among young people, including other drug use, fighting, and high-risk sexual behavior.179 Most young people who smoke regularly are already addicted to nicotine. For example, at least one symptom of nicotine withdrawal was reported by 92% of daily cigarette smokers and 93% of daily smokeless tobacco users aged 12–22 years who had previously tried to quit.211 Among adolescents aged 12–17 years, nearly two-thirds reported at least one indicator of dependence.56 In another study using different measures of nicotine dependence, 91% of daily cigarette users (smoked daily for 2 consecutive weeks or more in the past year), 48% of daily alcohol users, 60% of daily marijuana users, and 79% of daily cocaine users reported one or more indicators of dependence.212 Although it was generally thought that addiction did not occur until after a person started smoking regularly, recent evidence suggests that nicotine addiction may begin to emerge earlier.213

HEALTH RISKS OF SECONDHAND SMOKE Constituents of Secondhand Smoke Secondhand smoke (SHS) is a serious health hazard. In 2006, the Surgeon General concluded that SHS causes premature death and disease

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in children and adults who do not smoke and that there is no riskfree level of exposure to SHS.213a The Society of Actuaries has estimated that SHS costs American society $10 billion annually in health care costs and lost productivity.213b In January of 2006, the California Air Resources Board classified ETS as a Toxic Air Contaminant.213c SHS is a diluted mixture of “mainstream” smoke exhaled by smokers and “sidestream” smoke from the burning end of a cigarette or other tobacco product. It is chemically similar to the smoke inhaled by smokers and contains a complex mix of more than 4000 chemicals, including more than 50 cancer-causing chemicals and other toxic substances such as benzene, cadmium, arsenic, nicotine, carbon monoxide, and nitrogen (Table 54-3).114,213b,214,215 Sidestream smoke is the major component of SHS, providing nearly all of the vaporphase constituents and more than half the particulate matter. Sidestream and mainstream smoke are different in the temperature of combustion of the tobacco, pH, and degree of dilution in air. Five known human carcinogens, nine probable human carcinogens, three animal carcinogens, and several toxic compounds such as ammonia and carbon monoxide are emitted at higher levels in sidestream smoke than in mainstream smoke.114,214,215 Because of their greater mass, cigars generate higher levels of indoor air pollutants than cigarettes. Smoke from one cigar burned in a home can take five hours to dissipate.41 Particulate polycyclic aromatic hydrocarbon (PPAH) levels in restaurants and bars prior to a smoking ban were higher than those at a busy intersection in rush hour or a heavily trafficked city neighborhood.216 Considerable work has been done to develop sensitive and specific markers of exposure to SHS. Vapor-phase nicotine and respirable suspended particulate matter have been identified as markers for the presence and concentration of SHS in the environment, and cotinine (a metabolite of nicotine), and to a lesser degree nicotine, are widely used biomarkers of SHS exposure and uptake in people.114,213a,214,215 Levels of SHS constituents encountered indoors are large enough to be absorbed and result in measurable doses in exposed nonsmokers. However, individual biomarkers of exposure represent only one component of a complex mixture, and measurements of one marker may not wholly reflect exposure to other components of concern.213a Selfreported exposure to SHS underestimates exposure and therefore the risks of such exposure.217 For example, a study of a large nationally representative sample of persons aged 4 years and older indicated that 88% of nontobacco users had detectable levels of serum cotinine, although only 37% of adults and 43% of children were aware they were exposed to SHS.218 The Surgeon General concluded that cotinine is the biomarker of choice for assessing SHS exposure.213a

who have not previously been symptomatic.214 The same conclusions were reached after updated reviews in 1997 and 2004 by the California Environmental Protection Agency (CA EPA).215, 224 The 2006 Surgeon General’s Report also supported these conclusions, determining that SHS causes lower respiratory illnesses in infants and children; middle ear disease (acute and recurrent otitis media and chronic middle ear effusion) in children; cough, phlegm, wheeze, and breathlessness among school-age children; ever having asthma among school-age children; the onset of wheeze illness in early childhood; and lower levels of lung function during childhood. The report concluded that the evidence was suggestive, but not sufficient to infer a causal relationship between SHS exposure and the onset of childhood asthma; and between maternal exposure to SHS during pregnancy and both preterm delivery and a small reduction in birth weight among term infants. Other diseases where the evidence was deemed to be suggestive included prenatal and postnatal exposure to SHS and cancer, leukemia, lymphomas, and brain tumors in children.213a The Surgeon General’s report concluded that the evidence was insufficient to infer a causal relationship between SHS and impaired cognitive development213a; this issues continues to be an active area of research.225 On average, children exposed to SHS have 1.87 more days of restricted activity, 1.06 more days in bed, and 1.45 more days absent from school each year than do nonexposed children. Nationwide, this means 18 million days of restricted activity, 10 million days of bed confinement, and 7 million days of school absence each year attributable to daily SHS exposure.226 A study of 4th grade students reported that exposure to SHS led to 27% more absenteeism due to respiratory illness, and children living in a household with two or more smokers had a 77% increased risk of such absenteeism. Children with asthma were particularly at risk, but those without asthma also had an increased risk of absenteeism if exposed to two or more smokers.227

Secondhand Smoke and Sudden Infant Death Syndrome The California EPA (1997, 2004) and the Surgeon General (2006) have all concluded that there is a causal association between SHS and SIDS, independent of the effect of maternal smoking during pregnancy.213a,215,224 This relationship has been found for SHS exposure from maternal smoking, paternal smoking, and smoking by others in the household. A dose-response relationship was noted with increasing numbers of cigarettes, increasing number of smokers, and increasing duration of exposure to SHS.215,228,229,230

Secondhand Smoke and Adults Secondhand Smoke and Children’s Health Homes are the predominant location for childhood exposure to SHS.213a Exposures are decreasing over time. In 1992/1993, 43% of U.S. households had a smokefree home policy; in 2003, 72% of households had such a policy.219 Similarly, in 2003, 4 million (16%) adolescents aged 12-17 reported being exposed to SHS in the home, a decrease from 26% in 1999. However, among households with a smoker, 40% of adolescents were exposed to SHS daily.220 Urinary cotinine concentrations in infants and young children correlate with the number of smokers in the home 214, 215 and the number of cigarettes smoked by the mother during the prior 24 hours.221 More than 100 epidemiological studies have been published on the health effects of SHS exposure among children. In 1986, the National Academy of Sciences National Research Council (NRC)222 and the Surgeon General223 and concluded that SHS is a major contributor to impaired respiratory health among children, especially young children. In 1993, the U.S. Environmental Protection Agency (EPA) concluded that SHS is causally associated with lower respiratory infections (e.g., bronchitis and pneumonia), increased prevalence of fluid in the middle ear, symptoms of upper respiratory tract irritation, a small but significant reduction in lung function, additional episodes and increased severity of asthma, and new cases of asthma among children

Among adults, exposure to SHS primarily occurs in the workplace and in the home.213a Among healthy adults, the most common complaints after exposure to SHS are irritant effects in the eye conjunctiva and mucous membranes of the nose, throat, and lower respiratory tract.223 The 1997 and 2004 CA EPA reports concluded that SHS causes eye and nasal irritation in adults.215,224 In 2006, the Surgeon General concluded that SHS causes odor annoyance and nasal irritation, but that the evidence was suggestive, but insufficient to infer causality for persons with nasal allergies or a history of respiratory illness to be more susceptible to developing nasal irritation from SHS exposure.213b

Secondhand Smoke and Cancer Lung Cancer In 1986, the U.S. Public Health Service; the NRC; and the Interagency Task Force on Environmental Cancer, Heart, and Lung Disease, each independently concluded that substantial number of lung cancer deaths among nonsmokers could be attributed to involuntary smoking;222,223,231 both the Surgeon General and NRC reports concluded that SHS exposure causes lung cancer in nonsmokers. The EPA reviewed the updated scientific evidence in 1993 and also concluded that exposure to SHS causes lung cancer in nonsmokers. The

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Tobacco: Health Effects and Control

TABLE 54-3. CHEMICAL CONSTITUENTS OF TOBACCO SMOKE THAT HAVE BEEN CLASSIFIED OR IDENTIFIED AS TO THEIR CARCINOGENICITY, REPRODUCTIVE TOXICITY OR OTHER HEALTH HAZARD

CAL/EPA COMPOUND PROP65c//TACd Organic Compounds Acetaldehyde Acetamide Acrolein Acrylonitrile 4-Aminobiphenyl Aniline o-Anisidine Benz[a]anthracene Benzene Benzo[b]fluoranthene Benzo[j]fluoranthene Benzo[k]fluoranthene Benzo[a]pyrene 1,3-Butadiene Captan Carbon disulfide Carbon monoxide Chrysene DDT Dibenz[a,h]acridine Dibenz[a,j]acridine Dibenz[a,h]anthracene 7H-Dibenzo[c,g]carbazole Dibenzo[a,e]pyrene Dibenzo[a,h]pyrene Dibenzo[a,j]pyrene Dibenzo[a,l]pyrene 1,1-Dimethylhydrazine 1-Naphthylamine 2-Naphthylamine Nicotinee 2-Nitropropane N-Nitrosodi-n-butylamine N-Nitrosodiethanolamine N-Nitrosodiethylamine N-Nitroso-n-methylethylamine N’-Nitrosonornicotine N-Nitrosopiperidine N-Nitrosopyrrolidine Styrene Toluene 2-Toluidine Urethane Vinyl chloride Arsenic Cadmium Chromium V1 Leade Nickel

IARC

U.S. EPA

CLASSIFICATION a

CLASSIFICATIONb

2B 2B 3 2A 1 3 2B 2A 1 2B 2B 2B 2A

B2 C B1 B2 B2 A B2 B2 B2 B2

3

3 2B 2B 2B 2A 2B 2B 2B 2B 2B 2B 3 1 2B 2B 2B 2A 2B 2B 2B 2B 2B 2B 2B 1 1 2A 1 2B 1

B2

B2

B2 B2 B2 B2

A B1 A B2 A

yes/yes yes/yes —//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//— yes//yes yes//— yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes yes//— yes//— yes//— yes//yes yes//— yes//— yes//— yes//— yes//— yes//— —//yes —//yes yes//yes yes//yes yes//— yes//yes yes//yes yes//yes yes//yes yes//yes yes//yes

California Environmetnal Protection Agency. Health Effects of Exposure to Environmental Tobacco Smoke. Final Report, 1997. ARB(1993); IARC (1985, 1986, 1987, 1992); California Code of Regulations (1994); U.S. EPA (1994) a International Agency for Research on Cancer (IARC) Classification: 1, carcinogenic to humans, 2A, probably carcinogenic to humans; 2B, possibly carcinogenic to humans; 3, not classified as to its carcinogenicity to humans. b U.S. EPA Classification: A, human carcinogen; B1, probable human carcinogen (primarily on the basis of epidemiological data); B2, probable human carcinogen (primarily on the basis of animal data); C, possible human carcinogen. c Chemicals listed under Proposition 65 are known to the State to cause cancer or reproductive toxicity (California Health and Safety Code Section 25249.5 et seq.) d Substances identified as Toxic Air Contaminants by the Air Responses Board (ARB), pursuant to the provisions of AB 1807 and AB 2728 (includes all Hazardous Air Pollutants listed in the Federal Clean Air Act Amendments of 1990.) e Reproductive toxicant.

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EPA report classified SHS as a “Group A” (known human) carcinogen, a classification that includes asbestos and benzene,214 and estimated that 3000 lung cancer deaths occur among U.S. nonsmokers each year as a result of exposure to SHS. The CA EPA (1997, 2004) also concluded that exposure to SHS causes lung cancer.215,244 In 2002, IARC examined the evidence from 58 studies. Consistent findings of increased risk, a significant dose-response trend with increasing numbers of cigarettes smoked by the spouse, an increased risk in the highest exposure group, and a statistically significant trend for the number of years married to a smoker were noted. IARC also reported that all previously published meta-analyses showed a significant increased risk (relative risks ranging from 1.1-1.6) for exposure to spousal smoking. IARC did its own meta-analysis, which included more recent studies, and found a relative risk of 1.24.114 The 2006 Surgeon General’s report concluded that smoking causes lung cancer among lifetime nonsmokers and that there is a 20-30% increase in the risk of lung cancer from SHS exposure associated with living with a smoker. The risk is lower than that seen with active smoking due to the lower carcinogenic dose received. The report also concluded that the mechanisms by which SHS causes lung cancer are probably similar to those observed in smokers. For example, exposure to SHS causes a significant increase in urinary metabolites of the tobaccospecific lung carcinogen NNK. The report also specifically looked at workplace exposure and noted that indoor air nicotine and/or respirable suspended particulate concentrations levels were comparable between work and residential environments, and that SHS exposures in homes and workplaces were qualitatively similar in chemical composition and concentration. The report examined 25 studies that provided information on workplace SHS exposure and the risk of lung cancer among lifetime non-smokers. The pooled relative risk from a meta-analysis of the studies was 1.22. Studies showed a trend of increased risk with increased duration of exposure, and a threefold increased risk among persons with the highest level of workplace exposure (based on both years and intensity of exposure). As a result, the Surgeon General concluded that the risk of lung cancer applies to all SHS exposure, regardless of location.213a

in adults and estimated that respiratory symptoms are 30 to 60% higher in nonsmokers exposed to SHS than in non-exposed nonsmokers.214 Similarly, exposure to SHS has been estimated to increase the symptoms and severity of existing bronchitis, sinusitis, and emphysema by 44%232 and respiratory work related disability by 80% (from exposure to SHS at work).233 The 2006 Surgeon General’s report concluded that there are multiple mechanisms by which SHS causes injury to the respiratory tract. The report concluded that the evidence was suggestive, but insufficient to infer a causal relationship between SHS exposure and several respiratory diseases: acute respiratory symptoms including cough, wheeze, chest tightness, and difficult breathing among both persons with asthma and healthy persons; chronic respiratory symptoms; adult-onset asthma; worsening of asthma control; and risk for chronic obstructive pulmonary disease.213a Both the 1986 Surgeon General’s report and the 1986 NRC report reviewed the evidence available on SHS and pulmonary function in adults. The Surgeon General’s report concluded that healthy adults exposed to SHS may have small changes in pulmonary function tests, probably because of the irritants in SHS, but are not likely to have significant reduction in pulmonary function as a result of exposure as an adult.223 The NRC concluded that it was difficult to determine how a single factor such as SHS affects lung function, but reported that SHS may add to the burden of environmental insults that can cause chronic lung disease.222 The 1993 EPA report reviewed additional studies of SHS and adult lung function and respiratory symptoms and concluded that SHS exposure may result in small decreases (2.5%) in lung function among adult nonsmokers.214 The 1997 CA EPA report concluded that the small differences in lung function were a basis for concern.224 The 2004 CA EPA report, which identified additional relevant studies, concluded that newer data supported a small but potentially biologically significant effect of SHS on pulmonary function in adults.215 The 2006 Surgeon General’s report concluded that the evidence is suggestive, but not sufficient to infer a causal relationship between short-term SHS exposure and an acute decline in lung function in persons with asthma; and between chronic SHS exposure and an accelerated decline in lung function.213a

Sinus Cancer

Cardiovascular Disease

Both the 1997 and 2004 California EPA report concluded that SHS causes nasal sinus cancer.215,224 IARC noted that there have been four cohort studies and one case-control study that looked at the relationship between exposure to SHS and upper respiratory track cancers. A positive association was found in most of the studies.114 The Surgeon General concluded that the evidence was suggestive, but not sufficient to infer a causal relationship, primarily because of the modest sample sizes of the studies and the need to establish dose-response relationships and to characterize the risk by source and the timing of exposure.213a

More than 20 studies have examined the association between heart disease and exposure to SHS in nonsmokers.213a,215 Although some negative studies have received significant press attention,234 most studies have reported an increased risk of heart disease among persons exposed to SHS. Many of the studies controlled for other cardiovascular risk factors and several demonstrated a positive doseresponse relationship between exposure and disease. A large study that used data from the ACS CPS-II and controlled for other cardiovascular risk factors found about a 20% higher CHD mortality among never smokers exposed to SHS; however, a consistent dose-response trend was not found.235 A review article concluded that exposure to SHS accelerated atherosclerotic lesions.236 A recent cohort study that measured SHS exposure among nonsmokers by cotinine levels rather than self-report and followed participants for 20 years, found that the relative hazards for CHD were 1.45, 1.49, and 1.57 in the 2nd , 3rd, and 4th quartiles of cotinine levels after adjustment for other risk factors.217 A 1999 meta-analytic review of 18 studies concluded that there was a 25% higher CHD risk among never smokers exposed to SHS than in non-exposed never smokers.237 The elevated risk was seen in men, women, those exposed at home, and those exposed at work and a significant dose-response relationship was found.237 In both 1997 and 2004, the CA EPA concluded that there was a causal association between SHS and heart disease mortality and acute and chronic coronary heart disease morbidity.215,224 In 2006, the Surgeon General concluded that SHS causes coronary heart disease morbidity and mortality among both men and women and estimated that there was a 10-30% increased risk.213a Several observational studies have reported that hospital admissions for acute MI declined after a comprehensive local clean indoor air ordinance came into effect.238,238a,238b Various experimental and clinical studies suggest mechanisms for the cardiovascular effects of SHS. The 1997 and 2004 CA EPA reports

Other Cancers The 2004 California EPA report concluded that SHS causes breast cancer, but there is not scientific consensus on this finding.215 IARC noted that there have been five published cohort studies and 10 case-control studies examining this association. Two of the cohort studies were positive (but not statistically significant); three were negative. Seven of the case-control studies showed non-significant increased risk, but no studies showed a dose-response relationship with level of exposure.114 The Surgeon General concluded that the evidence was suggestive, but not sufficient to infer a causal relationship (due to inconsistent findings by age, the lack of an association in large cohort studies, and the lack of causal evidence between active smoking and breast cancer).213a

Secondhand Smoke and Other Diseases Respiratory Disease The effect of SHS on chronic respiratory symptoms or disease in adult nonsmokers is difficult to measure. The EPA concluded that SHS exposure may result in increased frequency of respiratory symptoms

54 concluded that SHS causes altered vascular properties.213c,214 In 2006, the Surgeon General concluded that SHS has a prothrombotic effect, causes endothelial cell dysfunctions, and causes atherosclerosis in animal models. It was also noted that these acute cardiovascular effects occur with short duration of exposure.213a Others have noted that SHS appears to cause decreased oxygen supply and increased oxygen demand—all effects consistent with the mechanisms found for active smoking. Many of the effects are believed to be caused by nicotine and carbon monoxide in SHS, but other toxins may also be important.236 In 2006, the Surgeon General also concluded that the evidence is suggestive, but not sufficient to infer a causal relationship between exposure to SHS and stroke and between exposure to SHS and atherosclerosis in humans.213a

TRENDS IN TOBACCO USE

Prevalence of Cigarette Consumption among Adults and Teenagers Annual per capita consumption of cigarettes reached a peak of 4345 in 1963, a year before the first Surgeon General’s report was published, and, except for an increase from 1971 through 1973, steadily declined (Fig. 54-3). Per capita cigarette consumption was 1691 in 2006, the lowest level since 1935.239,240 Overall the numbers of cigarettes sold in the United States declined from 640 billion in 1981 to 372 billion in 2006. 239,240 From 1964 to the late 1980s, smoking prevalence in the United States decreased an average of 0.5% per year (from 42 % in 1965 to 26% in 1990; in the early 1990s, prevalence was flat,241,242 but then prevalence decreased from 25% in 1997 to 21% in 2005 (Fig. 54-4). 243 In preliminary estimates for the first 9 months of 2006, smoking prevalence was unchanged at 21%.244 In the 2005 National Health Interview Survey (NHIS), smoking prevalence was higher for men (24%) than for women (18%) (Table 54-4). Smoking prevalence was highest in the 18–44 age group (24%) and lowest among Americans aged 65 years and older (8%).243 In 2002, for the first time, there were more former smokers than current smokers.245 Smoking prevalence varies threefold by state, ranging from 12% in Utah to 29% in Kentucky in 2005.246 Among both women and men, the trend in smoking prevalence has been downward. In 1965, smoking prevalence was higher for men

Tobacco: Health Effects and Control

(52%) than for women (34%). From 1965 to 1983, the decline in smoking prevalence was greater for men (17 percentage points) than for women (4 percentage points); however, from 1983 to 2005, the decline in smoking prevalence was comparable for women and men (11 percentage points).241,243 In 2005, the percentage of ever smokers who had quit was marginally for men (51%) than for women (50%).247 The higher proportion for men has sometimes been interpreted to mean that women are less likely to quit smoking than men. However, because men are more likely than women to switch to or continue to use other tobacco products when they stop smoking cigarettes, the sex difference disappears when assessing the cessation of all tobacco use.56 In addition, from 1965 to 2005, the percentage of ever smokers who had quit increased by 31 percentage points for women but by only 23 percentage points for men.241,247 The patterns of cessation among ever smokers are consistent with the historical patterns of smoking among women and men: men began quitting in greater numbers in the 1950s, but women began to quit in the 1960s. Thus, the comparable trend in conjunction with the higher absolute value for men, reflects the fact that early quitters were predominantly male.56,248 Other data show that women are as likely as men to quit for a day and to remain abstinent.249,250 In 1978, the first year data were available from the NHIS for whites, blacks, and Hispanics, smoking prevalence was lower among Hispanics (32%) than among whites (34%) or blacks (37%).241 In 2005, smoking prevalence was 13% among Asians, 16% among Hispanics, 22% and 32% among blacks, and whites, and 32% among American Indians and Alaska Natives.243 Smoking prevalence has declined faster for African Americans that for whites so that prevalence among African American men (formerly higher than for white men) is now comparable to that among white men, and the prevalence in African American women (formerly comparable to white women) is now lower than in white women.251 In 2005, the percentage of ever smokers who have quit was 53% for whites, 45% for Hispanics, 44% for Asians, 39% for blacks, and 38% for American Indians. Unlike the sex differences, which are explained by historical patterns in smoking behavior, the lower proportion among blacks reflects differences in quitting behavior: blacks are more likely than whites to try to quit smoking and are less likely to succeed, even after adjustment for demographic differences.249,252,253 This difference remains even after adjustment for other tobacco use.16 Formal educational attainment exhibits a striking association with smoking prevalence and cessation rates. However, this relationship is

5,000 1st Surgeon general’s report

Broadcast ad ban

4,000 Number of cigarettes

End of WW II

Master settlement agreement

Fairness doctrine messages on TV and radio Nonsmokers’ rights movement 1st Smoking-Cancer begins concern

3,000

2,000

Federal cigarette tax doubles

1,000 Great depression 0 1900

1910

1920

1930

1940

967

1950

1960

1970

1980

1990

2000

Figure 54-3. Adult per capita cigarette consumption and major smoking and health events—United States, 1900–2006. (Source: USDA Tobacco & Situation Outlook report, 2004;1986-2000 Surgeon General's Reports.)

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Behavioral Factors Affecting Health 60

50

Males

Percent

40

30

20

Females

10

19 55 19 57 19 59 19 61 19 63 19 65 19 67 19 69 19 71 19 73 19 75 19 77 19 79 19 81 19 83 19 85 19 87 19 89 19 91 19 93 19 95 19 97 19 99 20 01 20 03

0

Year Figure 54-4. Trends in cigarette smoking among adults (18+) by gender—United States, 1955–2003. Note: Estimates since 1992 include some-day smoking. (Source: 1955 Current Population Survey: 1965-2005, NHIS.)

not linear. The “less than high school graduate” category consists of two groups with distinct smoking patterns: people with 0–8 years and those with 9–11 years of education. Smoking prevalence and cessation rates in the former group are similar to those found among people with 12 years of education, whereas a person in the latter group is

most likely to be a current, ever, or heavy smoker, and the least likely to have quit smoking. After 11 years of education, the likelihood of smoking decreases with each successive year of education. These results persist after adjustment for age, sex, ethnicity, poverty status, employment status, marital status, geographic region, and year of

TABLE 54-4. PREVALENCE OF SMOKING AND PREVALENCE OF QUITTING FOR PERSONS AGED > 18 YEARS, NHIS 2005 Prevalence of Smokinga (%)

RACE/ETHNICITY White, non-Hispanic Black, non-Hispanic Hispanic American Indian/Alaska Native Asian EDUCATION (yr)c <8 9–11d 12 (diploma)e 13–15 >16 AGE GROUP (yrs) 18–24 25–44 45–64 >65 POVERTY STATUS At or above Below Unknown TOTAL

% Ever Smokers Who Have Quitb

MEN

WOMEN

TOTAL

MEN

WOMEN

TOTAL

24.0 26.7 21.1 37.5 20.6

20.0 17.3 11.1 26.8 6.1

21.9 21.5 16.2 32.0 13.3

54.0 37.7 45.2 NA 42.1

52.1 40.8 45.6 NA 47.7

53.1 39.1 45.4 37.7 43.5

21.0 35.3 30.7 26.2 10.1

13.4 27.5 22.3 19.5 8.8

17.1 31.2 26.3 22.5 9.5

60.6 45.5 49.1 51.3 70.8

48.0 41.2 49.1 53.0 68.2

56.3 43.6 49.1 52.1 69.7

28.0 26.8 25.2 8.9

20.7 21.4 18.8 8.3

24.4 24.0 21.9 8.6

19.8 35.7 55.3 85.9

26.4 38.5 55.0 77.4

22.7 37.0 55.1 82.2

23.7 34.3 21.2 23.9

17.6 26.9 16.1 18.1

20.6 29.9 18.4 20.9

51.5 35.4 55.1 51.0

53.4 32.1 49.9 50.4

52.3 33.7 52.8 50.8

CDC, 2006, MMWR; National Interview Survey, 2005. a Persons who reported smoking >100 cigarettes during their lifetime and who reported at the time of interview smoking every day or some days. b Persons who reported smoking >100 cigarettes during their lifetime and who reported at the time of interview that they did not smoke. c Persons aged >25 years d Includes those who attended school for 12 years and did not receive a diploma. e Includes those who received a GED and a high school diploma. NA - Data was not sufficient for reporting, due to small sample sizes.

54 survey.252 In 2005, smoking prevalence was highest among people with 9–11 years of education (31%) and lowest for persons with 16 or more years of education (10%) (Table 54-4).247 Similarly, the percentage of ever-smokers who have quit was lowest among the group with 9–11 years of education (44%) and highest among persons with 16 or more years of education (70%).247 Although the percentage of employees who smoke has decreased, certain subpopulations, including blue-collar and service workers, continue to smoke at higher levels. For the years 1987–1990, roofers (58%) and crane and tower operators (58%) had the highest prevalence of cigarette smoking, and physicians (5%) and clergy (6%) had the lowest prevalence of cigarette smoking.254 The unemployed; the widowed, separated, or divorced; and those below the poverty level are more likely to have ever smoked or to be current smokers and to be heavy smokers (15 or more cigarettes per day). 243,254,255 In 2006, 25% of 8th graders, 36% of 10th graders, and 50% of 12th graders had tried cigarette smoking.256 The prevalence of current smoking (defined as smoking within the past 30 days) among high school seniors decreased from 39% in 1976 to 29% in 1981, and was then relatively stable until 1992, but increased to 36% by 1997 and then decreased to 22% in 2006 (Fig. 54-5). Similarly, prevalence among 10th graders increased from 21% in 1991 to 30% in 1996, then decreased to 14% in 2006. The prevalence of smoking among 8th graders increased from 14% in 1991 to 21% in 1996, then decreased to 9% in 2006. Similar patterns were seen for daily smoking. Among high school seniors, smoking prevalence was higher for girls than for boys until the late 1980s; since 1990, current and daily smoking prevalence has been comparable for girls and boys.256 A larger decline in current smoking prevalence occurred among black high school seniors from 1977 (37%) to 1992 (9%) than among white high school students (38% to 32%).241 Smoking prevalence among black high school students increased from 9% in 1992 to 15% in 1998, but then decreased to 9% in 2004.256 The increase in smoking prevalence from 1992 to 1998 was greater for African American boys than girls, but the subsequent decline was also greater among boys than girls.257,258

The Changing Cigarette Low-Tar Cigarettes Tar is a complex mixture of compounds, including 69 identifiable carcinogens and cocarcinogens.114 Nicotine is the principal constituent responsible for a smoker’s pharmacological response (addiction).3,12 In the early 1950s, when smoking was first associated with lung cancer, a majority of Americans smoked unfiltered (plain) high-tar cigarettes, with a sales-weighted average tar and nicotine content per cigarette of 38 mg and 2.7 mg, respectively, in 1954. By 1998, the sales-weighted average content per cigarette had dropped to 12 mg tar and 0.89 mg nicotine. 1 However, these averages are based on yields from cigarettes as measured by the U.S. Federal Trade Commission (FTC) smoking machine under

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standardized laboratory conditions and do not reflect the actual smoking patterns of persons who smoke filtered cigarettes.101,119 Filtered cigarette use increased from 0.56% in 1955 to 99% in 2003.259 The machine-measured tar and nicotine reductions have come through the use of efficient filters, highly porous cigarette paper, and changing the composition of the tobacco blend. Filters are generally composed of cellulose acetate, although some also have charcoal. Filters reduce the amount of tar inhaled and selectively reduce some of the volatile components of cigarette smoke. Since 1968, filters increasingly have contained perforations (which may or may not be visible) that allow air to dilute the smoke, thus reducing the machine-measured tar and nicotine yield.119,260 Other methods used to reduce the tar and nicotine content yields on the standard smoke assays include the use of porous cigarette paper, which lowers tar, CO, and nitrogen oxides inhaled. Use of reconstituted tobacco (made from tobacco dust, fines, particles from ribs and stems, and additives such as adhesives and cellulose fiber) decreases the tobacco content. Similarly, the use of puffed, expanded, and freeze-dried tobacco decreases the amount of tobacco needed to fill a cigarette. Increasing the length of the cigarette allows more air to enter the paper and for more of the volatile components to diffuse out of the cigarette. Increasing the filter length decreases the amount of tobacco in the cigarette, lengthening filter overwraps reduces the amount of the cigarette smoked under the FTC protocol, decreasing the cigarette circumference reduces the amount of tobacco available for burning, using a more coarsely cut tobacco means the tobacco burns less efficiently, and blending the tobacco with lower nicotineyield strains or different leaf positions can reduce the amount of nicotine available.101,261 However, low tar cigarettes have an elasticity of delivery that allows smokers to get much higher yields of tar and nicotine by altering their pattern of puffing (larger puffs, inhaling more deeply, taking more rapid or more frequent puffs), by blocking the ventilation holes in the filters with their lips or fingers, or by increasing the number of cigarettes smoked per day. These alterations allow smokers to receive much higher deliveries of tar and nicotine from the cigarette, so that most smokers who switch do not substantially alter their exposure to tar and nicotine and therefore do not significantly lower their risk of disease.119 Studies show that low tar cigarettes can deliver the same tar and nicotine as regular cigarettes. Although there appear to be some differences in human nicotine exposure between high- and low-yield cigarettes, these differences are small and do not correspond to the difference in the yields as measured by the FTC smoking machine. Similarly, studies have generally found no relationship between CO levels in the human body and FTC machine yields. In addition, studies suggest that the published tar-to-nicotine ratio based on the FTC machine test does not correspond to actual ratios of tar and nicotine absorbed by smokers. Thus, published tar-to-nicotine ratios cannot be used to estimate the tar exposure of smokers. Studies using biomarkers of exposure to, and doses of, tobacco smoke

45 40 35 30 25 20 15 10 5 0 1975 1977 1979 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 2001 2003 2005 12 th Grade

10 th Grade

8 th Grade

Figure 54-5. Trends in cigarette smoking anytime in the past 30 days* by grade in school— United States, 1975–2006. *Smoking 1 or more cigarettes during the previous 30 days. (Source: Institute for Social Research, University of Michigan, Monitoring the Future Project.)

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Behavioral Factors Affecting Health

components have shown little relationship between biomarkers and tar/nicotine yields as measured by the FTC method.99,119 In general, the FTC method underestimates human exposure to the chemicals in cigarette smoke.101 This machine takes 2-second, 35-mL puffs every 60 seconds until the cigarette is smoked to 3 mm of the filter overwrap, whereas humans, on average, take puffs of greater than 35 mL over 1.8 seconds, every 34 seconds. The FTC method underestimates by a greater degree the amount of smoke drawn from low-yield cigarettes than from high-yield cigarettes.101 In addition, since the FTC machine smokes to within 3 mm of the overwrap, lengthening the overwrap can decrease the apparent yield, even though the remaining tobacco can be smoked.119 Changes in smoking patterns are related to smoker’s self-regulation of their blood nicotine levels and higher yields of nicotine can be obtained by alternating the frequency and depth of inhalation, increasing the number of cigarettes smoked, or mechanically compressing filter tips and blocking air channels with the lips or fingers.12,101,119,260 One study of participants who spontaneously switched to cigarette brands with a lower reported yield compared the smoker’s cotinine levels before and after the switch. Although the FTC-measured nicotine yield was reduced from 1.09 mg to 0.68 mg, the serum cotinine levels were unchanged.262 Another study found that even those smoking ultra-low-yield cigarettes could be exposed to high levels of nicotine and CO.101 Therefore, smokers should be informed that they may not be deriving any health benefit from lowtar products and strongly advised to quit smoking completely. Since their introduction to the U.S. cigarette market in the late 1960s and early 1970s, the so-called low-tar and low-nicotine cigarettes have had rapid increases in market share. The market share of cigarettes yielding 15 mg of tar or less increased from 2% in 1967 to 87% in 1999, and has remained stable at 84% through 2005.259 In addition, since their introduction in the late 1970s, the cigarette brands with 12 mg or less of tar captured 58% of the U.S. market in 2001 and has remained at that level those with less than 7 mg tar, 12%, and less than 4 mg tar, 1%.259 The significant growth of the low-tar cigarette market in the past two decades is attributable to increased public awareness that cigarette smoking, particularly exposure to tar and nicotine, is detrimental to health and to the perception that low-tar cigarettes are safer.119 The progression from unfiltered high-tar, to filtered high-tar, to filtered middle-tar, and to filtered lowtar cigarettes has also been observed in most industrialized countries, although at a slower pace and 5–10 years after the introduction of these changes in the United States.101 Early studies conducted to ascertain the health consequences associated with reduction of cigarette tar and nicotine yields looked promising, with smokers of low-tar or filtered cigarettes appearing to have lower lung cancer risk. Even some later studies have also reported lower risk for lung cancer. However, these studies generally adjusted for the number of cigarettes smoked per day. If increasing the number of cigarettes smoked is a common compensatory mechanism, such adjustment would not be appropriate. In addition, later prospective studies revealed an increase in the risks associated with smoking over the period when tar and nicotine yields were decreasing. For example, lung cancer risk was higher for participants in ACS’s CPS II compared with CPS I, even after adjusting for number of cigarettes smoked per day and duration of smoking.120 Three publications recently reviewed the evidence on cigarette yield and lung cancer risk. The Institute of Medicine (IOM) found the evidence mixed, but concluded that unfiltered cigarettes probably conferred a greater risk than filtered cigarettes.263 National Cancer Institute (NCI) Monograph #13 also reported the evidence on yield and lung cancer risk to be mixed, but noted that lung cancer rates have increased over time and found no convincing evidence that changes in cigarette design have resulted in an important decrease in the disease burden either for smokers as a group or for the whole population. The NCI monograph also noted that adenocarcinoma has replaced squamous cell as the leading cause of lung cancer death in the United States.119 Analyses suggest that the increase in incidence parallels changes in smoking behavior and cigarette design. It has been hypothesized that the smoke from high-tar, unfiltered

cigarettes was too irritating to be inhaled deeply and was deposited in the central bronchi where squamous cell carcinomas occur. Smoke from milder filtered, low-tar cigarettes could be inhaled more deeply, allowing for the development of the more peripheral adenocarcinomas.99,103,104 In addition, low-tar cigarettes have higher levels of tobacco-specific nitrosamines, which have been linked to the development of adenocarcinomas.99,102 The 2002 IARC report concluded that any reduction in lung cancer risk associated with the changing cigarette has been small.114 In addition, the Tobacco Advisory Group of the Royal College of Physicians concluded “there are therefore reasonable grounds for concern that low tar cigarettes offer smokers an apparently healthier option while providing little if any true benefit.”264 With respect to heart disease, studies are mixed. Many of these studies also adjusted for number of cigarettes smoked per day. In addition, CO is thought be a major etiologic agent in CHD, and CO levels do not necessarily correlate with tar or nicotine levels. Differences in cigarette design can influence tar and CO yields in different directions, so studies looking at CHD by tar/nicotine levels may not measure important factors.1,119 The 2004 Surgeon General’s Report concluded that products with lower yields of tar and nicotine have not been found to reduce coronary heart disease risk substantially,1 and the NCI monograph concluded that there is no clear consensus on CHD risks from the use of filtered or low-yield cigarettes.119 Little evidence is available on the relative risks of developing COPD from the smoking of low-tar, low-nicotine cigarettes, but the existing studies generally have not found reduced risk for FEV1 decline or COPD-related mortality from smoking lower yield cigarettes.115,175 The 2004 Surgeon General’s Report concluded that the evidence is suggestive but not sufficient to infer a causal relationship between lower tar cigarettes and lower risk for cough and mucus hypersecretion, that the evidence is inadequate to infer the presence or absence of a causal relationship between lower yield cigarettes and reduction in FEV1 decline rates, and that the evidence is inadequate to infer the presence or absence of a causal relationship between lower tar cigarettes and reductions in COPD mortality. The report concluded that given the strong benefits from smoking cessation on COPD, little public health benefit would be gained by further research on the relationship between cigarette type and COPD.1 The NCI monograph concluded that there was little evidence of a substantial difference in COPD mortality among users of low-tar cigarettes and that there is equivocal evidence for a reduced rate of respiratory symptoms.119 Evidence suggests that the persons most likely to use low-tar cigarettes are those most concerned about smoking and most interested in quitting. Some low tar cigarettes were marketed to smokers who were thinking about quitting with such tags as “All the fuss about smoking got me thinking I’d either quit or smoke True. I smoke True.”119 The data suggest, however, that switchers are not more likely than nonswitchers to become nonsmokers. It has been suggested that the existence of low-tar cigarettes has kept many smokers interested in protecting their health from quitting, and the net effect might have been an increased number of smoking-attributable deaths.101

Potential Reduced Exposure Products (PREPs) Tobacco companies have introduced novel, nontherapeutic nicotinedelivery devices. For example, the Favor Smokeless Cigarette, a nicotine inhaler, was introduced in 1985. The U.S. Food and Drug Administration (FDA) determined that this device delivered a drug, and the inhaler was withdrawn from the market. In 1987, the Pinkerton Tobacco Company introduced Masterpiece Tobacs, a chewing gum containing shreds of tobacco. The FDA determined that chewing gum is a food product and tobacco had not been approved as a food additive and the product was withdrawn from the market. In 1987, the R.J. Reynolds Tobacco Company introduced Premier, a device that heated tobacco rather than burning it. Adverse publicity and consumer complaints about the taste and difficulty lighting the product caused the company to withdraw it before the FDA could determine whether it was a drug delivery device.261 In 1996, the company test marketed Eclipse, which was promoted as a low-smoke cigarette and which, like Premier, heated tobacco.

54 More recently, other tobacco products and devices have been developed and marketed with implied claims for reduced disease risk. For example, Omni cigarettes advertise that they have “Reduced carcinogens. Premium taste.” Advance is marketed as having “a significant reduction in many of the toxins delivered to the smoker.” And Eclipse claims they “may present smokers with less risk of certain smoking-related diseases compared to other cigarettes.”265 The public health community is divided on whether use of PREPs is a viable strategy to reduce tobacco morbidity and mortality. PREPs have the potential to be widely adopted by smokers, much as low-tar cigarettes and filtered cigarettes now dominate the market. A recent JP Morgan survey found that 91% of smokers would be willing to switch brands if a lower risk cigarette became available.266 Recently, the major U.S. tobacco companies have either bought smokeless tobacco companies or developed their own product. These smokeless products are being promoted for “when you can’t smoke,” as a cessation aid, and as a harm reduction strategy.266a However, there are no studies showing smokeless tobacco use increases cessation, and a recent study showed that “switchers” had a higher mortality rate than smokers who quit cigarettes and did not switch to smokeless tobacco.266b In order to conclude that PREPs reduce population risk, several assumptions would need to be met: (a) measurements suggesting reduced exposure to carcinogens and toxins would need to translate into actual reduced exposure (which did not occur with low-tar cigarettes); (b) reduced exposure would need to translate into reduced individual risk; (c) reduced individual risk would need to translate into reduced population risk (e.g., no corresponding increase in initiation or reduction in cessation that negates any reduction in individual risk); and (d) no increase in other diseases or risks (e.g., the increase in adenocarcinoma with low-tar cigarettes). Although promoting the use of purportedly lower risk products seems to make sense at some level, the reality is that none of these assumptions is necessarily true (as was clearly demonstrated by the low-tar experience) and they all need to be tested on a case-by-case basis. Also, the population effects will be determined not only by the characteristics of the products, but also by the way they are marketed and by how consumers respond to that marketing. Several past “harm reduction” strategies have not reduced harm. For example, reducing the amount smoked by 50% may not reduce mortality from tobacco-related disease (probably because of compensation).267,267a Even efforts to eliminate compensation by using nicotine replacement therapies (NRT) so smokers reduce the amount smoked have not reduced their levels of carcinogenic biomarkers as expected.268,269 Similarly, people who switch tobacco products use them differently than those who have always used the other products (e.g., inhalation patterns and number of cigars smoked by former cigarette smokers).1 Finally, the experience with low-tar cigarettes suggests that they may have provided little if any reduction in individual risk and actually increased population harm.119 Cigarettes contain almost 5000 chemical compounds and 60 known carcinogens.114 It is unclear if reducing the levels of a few of these substances will reduce risk. It is also possible that methods used to reduce the level of one toxin or carcinogen could increase the level of others. For example, Eclipse has reduced levels of a few carcinogens, but increased carbon monoxide levels, which increases the risk of CHD.270 Also, there is often not a linear relationship between exposure and disease. For example, the risk of lung cancer is much more strongly related to duration of smoking than to amount smoked per day.271 Also, risk of CHD increases rapidly at very low levels of exposure and then plateaus.272 Any attempt to assess the probable impact of a PREP needs to look at multiple effects and outcomes, since tobacco use affects nearly every organ of the body. Even with modern cigarettes, which have been available for nearly 100 years, new causal risks are still being found.1 Finally, people may use PREPs concurrently with cigarettes, which could expose them to multiple risk factors that may interact in complex and unpredictable ways. Several unintended consequences could actually increase population risk. First, there might be an increase in initiation resulting from the perception that PREPs are safer. Also, some users may later switch

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to cigarettes, potentially resulting in increased disease risk. For example, youth consider low-tar cigarettes to be safer, to have lower tar and nicotine levels than regular cigarettes, believe that these cigarettes take longer to cause addiction, and think that they are easier to quit than regular cigarettes.273 Second, smokers are ambivalent about quitting. The belief that they have taken a positive step to reduce their risk by switching to a PREP allows smokers to rationalize postponing quitting, as was seen with low-tar cigarettes. Thus smokers may not reduce their risk as much as they would have if PREPs had not been on the market. Third, former smokers might relapse. Finally, as was noted earlier, PREPs may introduce unforeseen new disease risks, either from increased exposure to existing toxins, exposure to new toxins, or through the simultaneous use of several products. “Harm reduction” is being pushed as a remedy for smokers who cannot or will not quit. However, this implies that all efforts have been made to help smokers quit and that these efforts have failed. However, effective, low-cost cessation treatments are not yet widely available. This premise also ignores the fact that 70% of smokers want to quit,274 that 42% make a quit attempt of one day or longer each year,243 and that only about 20% use any proven therapies in their quit attempts.275 There is no safe form of tobacco use and there are “clean” forms of nicotine available through NRT. Even long-term use of nicotine would be preferable to the use of a different tobacco product as an alternative to quitting. The Institute of Medicine concluded that an unsuccessful “harm reduction” strategy could lead to long-lasting and broadly distributed adverse consequences, suggesting that these interventions may need to be held to a higher standard of proof and that government should be particularly careful. The fact that it could take decades to be certain about the effects of tobacco PREPs was noted as a reason for particular caution.263 The IOM also recommended that any such strategy should occur only under comprehensive regulation of tobacco products and be implemented within a comprehensive tobacco control program that emphasizes abstinence, prevention, and treatment.263

Cigars and Pipes In the United States, total consumption of cigars decreased yearly from 8108 million in 1970 to 2138 million in 1993, then increased to 5024 million in 2006.240 This increase corresponded with an aggressive marketing campaign, beginning in 1992, that glamorized cigar use.41,114 A 2004 national survey found that 5% of middle school students and 13% of high school students had smoked a cigar in the past 30 day. Prevalence was 2.5 times as high for high school boys as girls.276 Cigar use increases steadily with grade in school, from 12% among 9th graders to 18% among 12th graders.277 Cigar smoking among men decreased from 16% in 1970 to 3% in 1992, then increased to 4% in 2005.241,278 Over the same time period, cigar smoking among women decreased from 0.2% in 1970 to 0.02% in 1992, then increased to 0.3% in 2005. A substantial number of former and never cigarette smokers are cigar smokers. In contrast to cigarettes, the increase in adult cigar use appears to have occurred among those with higher educational and income levels.41 Cigar smoke contains the same toxic and carcinogenic constituents as cigarette smoke,41 but the tar from cigars contains higher concentrations of carcinogenic polycyclic aromatic hydrocarbons (PAH) and tobacco-specific nitrosamine levels are higher in cigar smoke. Carbon monoxide and ammonia are also produced in greater quantities by cigars than cigarettes.279 The 1998 NCI Monograph on cigars concluded that they cause oral, esophageal, laryngeal, and lung cancer.41 Some studies suggest that cigar smoking also increases the risk of pancreatic, bladder, and colon cancer.114,123 The NCI report also concluded that regular cigar smokers have risks of oral and esophageal cancers similar to cigarette smokers, but lower risks of lung and laryngeal cancer, COPD, and CHD.41 However, regular cigar smokers who inhale, particularly those who smoke several cigars a day are at increased risk for COPD and CHD.279,280 The magnitude of risk is proportional to the type and intensity of exposure, so reduced inhalation yields lower risk. However, even those who do not

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Behavioral Factors Affecting Health

inhale are at a higher risk of disease than never-users of tobacco. Mixed smokers (those who use both cigars and cigarettes) and cigarette smokers who switch to cigars are much more likely to inhale and to use cigars regularly, and therefore remain at much higher risk for all major smoking-related diseases.41,43,45 Cigars can deliver nicotine concentrations comparable to or higher than those from cigarettes and smokeless tobacco. Cigar smoke also contains a substantial proportion of its nicotine as freebase nicotine, which is easily absorbed through the oral mucosa. Thus cigar smokers do not need to inhale to ingest substantial quantities of nicotine, although oral absorption produces lower quantities and lower peak blood levels than does inhalation. Because cigars are addictive, their use by young people may potentially lead to switching to other products such as cigarettes.41,279 From 1965 to 2005, the prevalence of pipe smoking among men decreased from 14% to 0.9%.241,247 Pipe smoking has never been common among women (0.2% or less). In 1991, men aged 35–64 years of age (3%) were the primary pipe smokers, with those 18–24 years of age being the least likely to smoke pipes (0.2%). By 2005, use varied from 0.3–0.4% among men aged 25–44 to 1.8% among men aged 45–64.278 Men who smoke pipes are often previous users of another form of tobacco, particularly cigarettes.124 Pipe smoking causes lip cancer1 and is also associated with other diseases, including oropharyngeal, laryngeal, esophageal, and lung cancer and COPD.43–45,61,114,126,281 Some studies have suggested an increased risk of colorectal, pancreatic, and bladder cancer with pipe smoking.114,281 The 1983 Surgeon General’s report concluded that smokers who have used only pipes are not at greater risk for CHD than nonsmokers, but some recent studies suggest an association between pipe smoking and CHD, particularly if the smoke inhalation pattern mimics that for cigarettes.43,44,281 It has been estimated that pipe smoking kills 1100 Americans each year.124

and a cross-sectional study in Sweden found that smokeless tobacco users were more likely to have hypertension.49,283 Some, but not all, studies of the effect of smokeless tobacco on lipids have shown a higher risk of hypercholesterolemia, lower high-density lipoprotein levels, and higher triglyceride levels.48 One study showed an elevated risk of diabetes in smokeless tobacco users.48 A large Swedish cohort study found that smokeless tobacco users were more likely to die of cardiovascular disease than nonusers,49,50 but two case-control studies have not found an increased risk.48 An analysis of both CPS I and CPS II showed increased risk of death from CHD and stroke among smokeless tobacco users.51 Starting in 1986, smokeless tobacco products and advertisements were required by federal law to carry warning labels about the health hazards of their use. Smokeless tobacco is addictive; its use may predispose those who try it to become cigarette smokers.284

Other Tobacco Products Other tobacco products, such as bidis or kreteks (clove cigarettes) are used by 2% of middle school students and 4% of high school students.276 When compared to filter cigarettes, bidis deliver higher amounts of nicotine (1.2 times), tar (2.2 times), and CO (2 times).285 Bidi smoke contains other toxic compounds, including tobacco-specific nitrosamines, phenol, hydrogen cyanide, and benzo[a]pyrene.286,287 Studies have suggested an increase in all-cause mortality among bidi smokers.288 Bidi smokers may have twice the risk of lung cancer as smokers of Western-style cigarettes, and three times the risk of CHD as nonsmokers.289 Some studies also suggest increased risk for oropharyngeal, stomach, esophageal, and laryngeal cancer and adverse reproductive effects.114,290–293 TOBACCO INTERVENTIONS

Smokeless Tobacco Smokeless, “spit,” or oral tobacco (chewing tobacco or snuff) contains tobacco leaves plus sweeteners, flavorings, and scents. Chewing tobacco may be in the form of strands, cakes, or shreds and is either chewed or placed in the mouth. Snuff, which is marketed in a small round can, or tin, is supplied dry or moist and is held (“dipped”) between the gingiva and the lip or cheek. Whereas the smoking of tobacco has declined, the overall prevalence of smokeless tobacco use among U.S. adults has changed little during the last 20 years. The NHIS found that the prevalence of smokeless tobacco use was 5% for men and 2% for women in 1970 and 4.5% for men and less than 1% for women in 2005.241,282 Prevalence tends to be higher in the South and in rural regions, and higher among whites than African Americans.56 Although the overall prevalence of smokeless tobacco use has remained low for the past two decades, the demographics of smokeless tobacco use have changed dramatically. This behavior was formerly found predominantly among older people, particularly older black men and women and older white men. Since the late 1980s, however, smokeless tobacco use, particularly snuff use, has been seen primarily among young white males.241 In 2004, the prevalence of smokeless tobacco use among middle school boys was 4% and among high school boys was 10%. Among high school boys, use was highest among whites (14%), and lower for blacks (3%), Hispanics (8%) and Asians (2%).276,277 Long-term smokeless tobacco use causes periodontal disease and oral leukoplakia, with manifestation occurring even among young people.135,179,195 Among users of smokeless tobacco or snuff, changes in the hard and soft tissues of the mouth, discoloration of teeth, and decreased ability to taste and smell have been reported.197 There is also strong evidence that smokeless tobacco use causes cancer in humans.133 The association for specific cancers is strongest for cancers of the oral cavity,1,133 but increased risks for cancers of the pharynx and stomach have also been reported.139 Smokeless tobacco use causes acute cardiovascular effects, such as increased heart rate and blood pressure levels48 and both a large population-based study

Clinical Treatment for Tobacco Use/Nicotine Dependence The reduced national prevalence of smoking means that many millions of smokers (more than half of ever smokers) have quit smoking.245 In addition, 70% of current smokers want to stop smoking completely,274 and 42% of current daily smokers have stopped smoking for at least 1 day in the previous 12 months because they were trying to quit completely.243 Reasons to quit reported by ex-smokers as contributing to their cessation attempts and continued abstinence include: health problems; strong family pressures, both from spouses and children; peer pressure from friends and coworkers; cost of cigarettes, especially for lower-income individuals; fear of potential adverse effects on personal health or on the health of their children; the likelihood of their children starting to smoke; and concern for cleanliness and social acceptance.12,294 In 2000, the Public Health Service (PHS) published updated clinical guidelines on tobacco dependence treatment that were based on a systematic review of the scientific literature from 1976 to 1998. Meta-analyses of randomized controlled trials that contained at least five months of follow-up served as the basis for the recommendations. The primary findings were that brief advice to quit is effective (30% increase in cessation rates), more intensive counseling is more effective (doubles the quit rate), counseling can be delivered via individual counseling, group programs or telephone counseling, and that FDA-approved medications double quit rates. Patients should also be encouraged to obtain social support for their quit attempt, since this increases cessation rates by 50%.295 Similarly, the U.S. Preventive Services Task Force (USPSTF) strongly recommends that clinicians screen all adults for tobacco use and provide tobacco cessation interventions (brief counseling and pharmacotherapy) to those who use tobacco products. The USPSTF strongly recommends that clinicians screen all pregnant women for tobacco use and provide augmented pregnancy-tailored counseling to those who smoke.296

54 For primary care providers, the recommendations emphasize the importance of (a) systematically asking about tobacco use (so that every patient at every clinic visit has his or her tobacco use documented), (b) strongly advising (in a personalized manner) all tobacco users to quit, (c) assessing the patient’s willingness to quit, (d) assisting the patient in quitting and (e) arranging follow-up (the 5 A’s). The primary care intervention is designed to be brief. Patients not yet willing to quit smoking should receive a motivational intervention to promote later quit attempts. For patients willing to make a quit attempt, the provider should help the patient set a quit date, provide key advice on dealing with problem situations, encourage the use of FDA-approved medications (nicotine patch, gum, lozenge, tablet, inhaler, nasal spray, and the nonnicotine medications bupropion and varenicline) unless contra-indicated, and refer the tobacco user to a telephone quitline or community program. All patients who attempt to quit should have scheduled follow-up in person or by telephone. These recommendations assume that office systems will be developed to assure the assessment of tobacco use and appropriate treatment.295 Evidence of the effectiveness for cessation interventions among youth is lacking.297,298 The PHS guideline gave, a “C” or expert opinion, recommendation that in clinical settings, providers should screen pediatric and adolescent patients and their parents for tobacco use and give a strong message about the importance of abstaining from tobacco use. The guideline also stated that counseling should be considered, but the content modified to be developmentally appropriate, and medications could be considered when there is evidence of nicotine dependence and a desire to quit.295 Similarly, the USPSTF also concluded that there was insufficient evidence to recommend for or against routine screening or interventions to prevent or treat tobacco use and dependence among children and adolescents.296 The Surgeon General concluded that youth smoking cessation programs have low success rates, and it is difficult to attract and keep adolescents in such programs.179 One study determined, however, that in clinical settings where physicians use existing visits to provide cessation counseling, even a very low success rate could still be highly cost effective because of the low cost of such opportunistic interventions and the large potential impact. This conclusion would not extend to youth cessation programs in other settings.299 The PHS guideline gave a “B” recommendation to offering advice and interventions to parents to limit children’s exposure to SHS.295 Administrators, insurers, and purchasers of health care delivery can also promote the treatment for tobacco use/nicotine dependence. Administrators can help ensure that institutional changes to promote cessation interventions are systematically and universally implemented. Insurers should make effective treatments a covered benefit, and purchasers should make tobacco use assessment, counseling, and treatment a contractual obligation. The PHS guidelines recommend that (a) a tobacco use identification system be implemented in every clinic; (b) education, resources, and feedback to promote intervention be provided to clinicians; (c) staff be dedicated to provide effective cessation treatment, and the delivery of this treatment assessed by performance evaluations; (d) hospital policies support the provision of cessation services; (e) effective smoking cessation treatment (both pharmacotherapy and counseling) be included as paid services in health insurance packages; and (f) clinicians be reimbursed for providing effective cessation treatments, and these interventions be among the defined duties of salaried clinicians.295 The PHS guidelines are consistent with other published recommendations.300,301 Tobacco treatment is extremely cost-effective, more so than other commonly covered preventive interventions, such as mammography, treatment for mild-to-moderate hypertension, and treatment for hypercholesterolemia.302–304 An analysis of recommended clinical preventive services that ranked the services based upon disease impact, treatment effectiveness, and cost-effectiveness concluded that treatment of tobacco use among adults ranked first, along with childhood immunizations and aspirin therapy, to prevent cardiovascular events in high risk adults. It also had the lowest delivery rate among the top ranked interventions.304a Some data suggest there are cost savings from

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the treatment of tobacco use, even in the first year, as a result of the rapid decline in risk of acute myocardial infarction and stroke.305 Another study found that the cost of a moderately priced cessation program (brief clinical interventions, free telephone counseling and free NRT) paid for itself within 4 years due to lower hospital costs among successful quitters compared with continuing smokers.306 The managed care plan found that tobacco treatment interventions not only improved quality of care, but also decreased use of medical services: after one year of cessation, ex-smokers’ medical costs dropped progressively and reached levels comparable to those of never-smokers.306 This plan also found that systematic implementation of tobacco treatment interventions accelerated the reduction in smoking prevalence among plan members compared with the general population.307 In addition, provision of preventive services in a health plan is associated with increased patient satisfaction with the plan.308 Telephone quitlines increase cessation rates compared to selfhelp materials.295,309,310 Quitlines have been used within health care systems to provide support for physician advice and brief counseling. When offered a choice of free group programs or free quitline support, more smokers chose quitline support. Group Health Cooperative found that a routine screening system with primary care providers giving cessation advice, medication, and encouragement to get more intensive support; marketing the program; providing quitline services; and covering counseling and medication (with the usual $5 copay) resulted in an annual increase in use of counseling services from 0.5% to 10% of smokers in the plan,307 and a decrease in smoking prevalence from 25% to 15% over 10 years.311 Employers can support employees who want to quit tobacco use by offering (or referral to) a variety of cessation assistance options, including telephone quitlines, self-help programs, formal cessation programs, counseling from a health care provider, and pharmacological aids. Workplace smoking-cessation assistance can be provided on- or off-site, may be run by outside or in-house personnel, and can be an isolated activity or integrated into a comprehensive employee health promotion program. Company incentives to support employee cessation efforts may include full or partial payment of any costs, including pharmacological agents, time released from work for cessation assistance, and lower employee contributions to health benefit costs for nonsmokers.312 Studies have been mixed on the effectiveness of work-site programs. Although one meta-analysis suggested a modest impact, two large trials published subsequently showed either no impact or very small and nonsignificant results.313–315

Performance Measures for the Treatment for Tobacco Use The Institute of Medicine identified cessation help for adult smokers as one of 20 national priority areas for health care quality improvement.316 Treatment of tobacco use is also increasingly a performance measure for accreditation or quality assurance. For example, a majority of plans reported at least some of the measures in the Health Plan Employer Data Information Set (HEDIS).317 A measure of a plan’s smoking cessation activities was first included in December 1996, when HEDIS 3.0 was released. Under this survey measure, managed care plans report the proportion of smokers or recent quitters (within the past year) who had been seen in the plan during the previous year and who had received advice to quit smoking.318 In 2003, the measure was expanded to include the proportions whose health care provider had discussed medications and the proportion whose health care provider had given other assistance in quitting. In 2005, 66–71% (depending on whether Medicare, Medicaid, or commercial plan). Provided advice, 32–39% recommended or discussed medication use, and 34–39% provided other assistance in quitting.319 The Joint Commission on Accreditation of Healthcare Organizations (JCAHO) now requires hospitals to document their provision of smoking cessation treatment for patients admitted for acute MI, heart failure, and community acquired pneumonia.320 In 2005, the Center for Medicare and Medicaid Services (CMS) began a pilot project that provides financial incentives to physicians who deliver targeted interventions.

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Tobacco cessation advice and assistance were among those quality measures.321

Community Interventions to Reduce Tobacco Use Beginning in the 1970s, attention began to focus on community interventions to reduce risk factors. Examples include Finland’s North Karelia Project,322 South Africa’s Coronary Risk Factor Study,323 the Stanford Three Communities Study,324 the Stanford Five Cities Project,325 the Multiple Risk Factor Intervention Trial,326 the Minnesota Heart Health Program,327 and the Pawtucket Heart Health Program.328 Some showed positive results, but in others, unanticipated secular changes in the control group or inappropriate or inadequate interventions led to nonsignificant results. These were followed by the American Stop Smoking Intervention Study for Cancer Prevention (ASSIST) in 1991, a demonstration project in 17 states for community tobacco control activities. ASSIST, funded by the NCI, and conducted in collaboration with the ACS, funded state health departments to form community-based tobacco coalitions that were responsible for developing and implementing comprehensive state plans for tobacco use prevention and control. An evaluation of ASSIST reported that consumption was lower in ASSIST states than in the rest of the country.329 Around the same time, California and Massachusetts had their own statewide initiatives funded by tobacco taxes, providing further data for the evaluation of community-based interventions.

Evidence for Specific Community Interventions As a result of community trials and other controlled studies, enough evidence is available to allow recommendations for effective community interventions. The Guide to Community Preventive Services, an evidence-based guideline, noted that: effective interventions to decrease initiation include raising the price of tobacco products, media campaigns combined with other interventions (such as price increase or community interventions), and community mobilization around minors’ access when combined with other interventions.330 Effective interventions to reduce exposure to secondhand smoke include smoking bans or restrictions. Effective interventions to increase cessation include raising the price of tobacco products, sustained media campaigns (in conjunction with other interventions), telephone quitlines, and reducing the out-of-pocket costs of treatment (i.e., insurance coverage of treatment). Provider reminders alone or in combination with provider training also increased quitting, but provider training alone did not have sufficient evidence of its efficacy to be recommended.309

Preventing Tobacco Use Evidence that knowledge of adverse and long-term health effects did not translate into reduced smoking among youth has led to increased attention on the development of valid theoretical models of smoking initiation and prevention programs. Five stages to smoking initiation among children and adolescents are currently recognized: (a) A preparatory stage in which attitudes and beliefs about the utility of smoking develop. Smoking may be viewed as having positive benefits even though it has yet occurred. (b) The trying stage, which includes the first two or three times an adolescent tries to smoke (usually in a situation involving peers). (c) An experimentation stage with repeated but irregular smoking, in which smoking is usually a response to a particular situation. (d) Regular use; at least weekly smoking across a variety of situations. (e) Nicotine dependence, the physiological need for nicotine.179 Community-based interventions (tobacco price increases, countermarketing campaigns, minors’ access restrictions, and school programs) have been the primary modalities used to prevent initiation.

Increasing Price In 1993, an NCI consensus panel concluded that an increase in cigarette excise taxes may be the single most effective intervention for

reducing tobacco use by youth.331 There is a robust body of evidence on the effectiveness of price increases on youth initiation.179 The Guide to Community Preventive Services identified eight studies that specifically looked at the impact of price on youth and young adults. The Community Guide concluded that a 10% increase in price reduced youth prevalence by 3.7%, decreased initiation by 3.8%, and also decreased the amount smoked by adolescents who continued to smoke.309 One study concluded that youth consumption may be three times more sensitive to price increases than adult consumption.179,331 Another analysis of cigarette excise taxes concluded that an increase in the federal cigarette excise tax would encourage an additional 3.5 million Americans to forgo smoking, including more than 800,000 teenagers and almost two million young adults aged 20–35 years.331,332 Other studies have reported that for every 10% increase in price, total cigarette consumption among youth decreases 7%.309,331–335 Even the tobacco industry has privately acknowledged the effectiveness of price increases on reducing youth smoking: Philip Morris noted that “it is clear the price has a pronounced effect on the smoking prevalence of teenages, and that the goals of reducing teenage cigarette smoking and balancing the budget would both be served by increasing the Federal excise tax on cigarettes.”336 Other tobacco products also respond to price interventions: increases in the price of smokeless tobacco reduce use by adolescent boys, with most of the effect coming from reduced prevalence rather than the amount used by continuing users.333 Studies have also shown that higher cigarette prices increase smokeless tobacco use. Increased cigarette prices also led to more cigar use in New Jersey, and the authors concluded that when excise taxes on other tobacco products do not keep pace with cigarette taxes, substitution occurs.337

Countermarketing Campaigns Media campaigns, when combined with other interventions, are an effective strategy to reduce youth initiation.179 The Community Guide determined that mass media campaigns are effective in reducing youth prevalence. Sustained (at least two years) media countermarketing campaigns reduced self-reported tobacco prevalence by eight percentage points and, for those studies reporting odds ratios, by a median of 74%.309 The 2000 Surgeon General’s Report noted that multicomponent youth-directed programs with a strong media presence have shown long-term success in reducing or postponing youth tobacco use.333 Youth-focused campaigns have been developed and evaluated in several states and nationally. In Massachusetts, adolescents aged 12–13 who had been exposed to the countermarketing campaign as part of a comprehensive program were half as likely to become smokers as those who were not able to recall campaign advertisements.338 In Minnesota, when a youth-focused media campaign was ended, youth awareness of the campaign declined from 85% to 57%, and youth susceptibility to initiate smoking increased from 43% to 53% within 6 months.339 As part of the youth-focused tobacco control program in Florida that was funded by the tobacco industry settlement, the “truth” media campaign was developed. Evaluation results included a 92% brand awareness rate among teens, a 15% increase in agreement with key attitudes about smoking, a 20% decrease in smoking among middle school students and an 8% decrease in smoking among high school students.340 Florida teens exposed to the campaign were also more likely to agree with antitobacco industry attitudes. A longitudinal study reported that Florida teens with strong anti-industry attitudes were four times less likely to start smoking and 13 times less likely to become established smokers than teens with low anti-industry attitudes.341,342 In 2000, the American Legacy Foundation ran a national “truth” campaign. Evaluation results show that exposure to this campaign was associated with an increase in antitobacco attitudes and beliefs.343 Adolescents in tobaccoproducing states were as responsive to the anti-industry ads as adolescents in non-tobacco-producing regions.344 It is estimated that 20% of the decline in youth smoking prevalence in the late 1990s was a result of the “truth” media campaign.345 In contrast, exposure to the

54 Philip Morris’s “Think Don’t Smoke” campaign did not cause an increase in antitobacco attitudes and those exposed to the campaign were more likely to be open to the possibility of smoking.343 Similarly a study of the Phillip Morris parent-targeted campaign “Talk. They’ll Listen” found that each additional viewing of the ad was associated with lower perceived harm of smoking, stronger approval of smoking, stronger intentions to smoke in the future, and greater likelihood of having smoked in past 30 days.345a

School-Based Tobacco Prevention Programs School-based tobacco prevention programs have been shown effective when combined with concurrent, complementary community interventions.179 Current recommendations on quality school-based smoking prevention programs emphasize helping children understand and effectively cope with social influences associated with smoking, highlighting the immediate negative social consequences, and inoculating youth against the effects of pressure to smoke.346,347 Most prevention programs focus on students in grades 6–8, the time of greatest increase in smoking experimentation.348 However, the effects of these programs are not sustained without additional educational interventions, media campaigns, or supportive community programs. Thus, although school-based skills’ training is important for preventing smoking, more sustained and comprehensive interventions may be necessary for long-term success.179

Smoke-Free Policies Another approach to discouraging smoking among youth is the establishment of strong no-smoking policies in schools and on school grounds. Such policies not only directly discourage smoking by youth but increase the likelihood that their teachers, who are role models, will not be seen smoking.

Minors’ Access Restrictions Tobacco products are widely available to minors and commercial outlets are an important source of tobacco for them.333,349 Since 1986, numerous published studies involving purchase attempts by minors confirm that, despite state and local laws banning such sales, they can easily buy tobacco from over-the-counter outlets and vending machines.179,333,349 Active enforcement of tobacco laws increases retailer compliance.179,350 Studies looking at their impact on prevalence, however, are mixed.333,351–353 The Guide to Community Preventive Services reviewed the literature on the effectiveness of minors’ access laws and concluded that they are only effective in conjunction with other community interventions.330 An evaluation in Massachusetts after the defunding of the program showed that communities that had a dramatic reduction in tobacco control funding saw an average increase of 74% in illegal sales to minors, and communities that completely lost their programs had even larger increases.354 It is important to keep in mind that as commercial sales to minors decrease, “social” sources (other adolescents, parents, and older friends) may become more important sources of cigarettes. Thus a comprehensive approach is needed so that smokers of all ages, as well as retailers, do not provide tobacco to minors.333

Eliminating Exposure to Secondhand Smoke Clean Indoor Air Laws Despite substantial progress, 125 million Americans are still exposed to SHS.213a In 2006, the Surgeon General concluded that eliminating smoking in indoor spaces fully protects nonsmokers, but that separating smokers from nonsmokers, cleaning the air, and ventilating buildings cannot eliminate exposure to SHS.213a Homes and workplaces are the primary locations for adult exposure, so interventions include smokefree homes, workplaces, and public places. Although the purpose of smokefree policies is to reduce SHS exposure, these policies also reduce consumption, increase quitting, decrease relapse, and possibly reduce initiation.213a, 309, 330, 333

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The entertainment and hospitality industries have particularly high SHS exposure.213a One study evaluated respirable particle (RSP) air pollution and carcinogenic particulate polycyclic aromatic hydrocarbons (PPAH) in a casino, six bars, and a pool hall. SHS contributed 90–95% of the RSP and 85–95% of the PPAH in these venues. These levels were greater than the levels of these contaminants on major truck highways and polluted city streets. Another study showed that levels of SHS in restaurants are 160–200% higher, and levels in bars are 400-600% higher than in office workplaces.355 Yet, wait staff and bartenders are less likely to have smokefree workplaces.356 Both the Surgeon General’s report and the Guide to Community Preventive Services evaluated the effect of smoking bans and restrictions on exposure to SHS. Both found that smoking bans reduced exposure more than smoking restrictions;213a,309 the Surgeon General also noted that full compliance with smoking bans eliminated exposure. A recent study examined cotinine levels in a nationally representative survey: 12.5% of nonsmoking adults living in counties with extensive smokefree laws were exposed to SHS, compared with 35.1% in counties with limited coverage and 45.9% in counties with no law.356a The health impacts of state-wide smokefree laws have also been studied. Two studies showed dramatic declines in RSP and PPAH after smoking bans were implemented;216,357 other studies have shown improvements in respiratory symptoms, sensory irritation, and lung function in hospitality workers.357a Concerns are often raised about possible adverse economic consequences of smokefree laws on the hospitality industry. A review of the studies on economic effects showed that higher quality studies generally found a positive economic impact of smoking bans. Studies using subjective outcomes (e.g., owner expectations) tended to show a negative impact, while studies using objective outcomes (e.g., revenues, employment, restaurant sale price) usually showed a positive impact. Few of the negative studies were peer reviewed; all were funded by the tobacco industry.358 The Surgeon General concluded that smokefree policies do not have an adverse economic impact on the hospitality industry.213a

Increasing Cessation Increasing the Price of Tobacco Products Price increases are one of the most effective interventions to increase adult cessation, as shown by a substantial body of evidence. The Guide to Community Preventive Services identified 56 studies in the literature. After combining those that used the same data and eliminating weak ones, 17 studies formed the basis of the Guideline conclusion that a 10% price increase decreases consumption by a median of 4.1%. For every 10% increase in price, cessation increased 1.5%.309 Consistent with the larger impact of price on adolescents, one study found that these effects were doubled for persons 20–25 years of age compared with adults aged 26–74.333 Some data suggest that men are more responsive to price than women.333,359 Other data have shown that less educated persons are more responsive to price increases than more educated persons, that blacks are twice as responsive as whites, that Hispanics are even more price sensitive, and that those with family incomes at or below the median were 70% more responsive than those with higher family incomes.333 The 2000 Surgeon General’s Report concluded that the price of tobacco products has an important influence on the demand for tobacco products and that substantial increases in the excise tax on tobacco would have considerable impact on the prevalence of smoking.333 Another study estimated that increasing the federal cigarette tax by $2.00 would reduce total cigarette sales by more than 4 billion packs per year, would decrease adult smoking prevalence rates by 10%, and 4.7 million smokers would quit.360 Even the tobacco industry has privately acknowledged the effect of price on reducing adult cigarette consumption. As Philip Morris noted, “when the tax goes up, industry loses volume and profits as many smokers cut back.”361 “A high cigarette price, more than any other cigarette attribute, has the most dramatic impact on the share of the quitting population . . . price, not tar level, is the main driving

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force for quitting.”362 Smuggling reduces the impact of price increases by making cheaper cigarettes available and it also reduces government revenue from a tax. Large differences in price between states or countries increases the profitability of smuggling. There is also evidence that the cigarette companies themselves have been directly involved with smuggling activities.362a

Countermarketing Evidence for the effectiveness of counteradvertising comes from both national and international data. An econometric analysis of the U.S. Fairness Doctrine (which required one antismoking message for every three to five tobacco advertising messages) concluded that counteradvertising substantially deterred smoking.363 Another study of the Fairness Doctrine concluded that the number of people who successfully quit smoking tripled during the period that the doctrine was in effect.364 An evaluation of a paid media campaign against smoking in Australia found that there was a marked decrease in smoking prevalence attributable to the campaign.365 An evaluation of a Greek media campaign showed that the annual increase in tobacco consumption was reduced to nearly zero as a result of the campaign. When the campaign stopped, consumption again rose at the precampaign rate.366 The Guide to Community Preventive Services found 15 high-quality studies of the effect mass media campaigns on increasing cessation. In all studies, the campaign was concurrent or coordinated with other interventions such as tax increases, community education programs, self-help cessation materials, individual counseling, or other mass media efforts. Various endpoints were measured in the various studies. The campaigns increased cessation by a median of 2.2 percentage points, reduced tobacco consumption by a median 17.5%, and reduced prevalence by a median of 3.4 percentage points.309

Advertising Bans Evidence for the effectiveness of advertising bans is mixed. One study used multiple regression analysis to evaluate the effectiveness of advertising restrictions, price, and income on tobacco consumption in 22 countries from 1960 to 1986. Above threshold levels, both advertising restrictions and higher prices were effective in decreasing tobacco consumption.367 However, an analysis of the 1971 U.S. broadcast media ban did not show an effect.368 This apparent lack of effect may be due in part to these bans being frequently circumvented, such as during the promotions of televised sporting and entertainment events. For example, during a Marlboro Grand Prix telecast, the Marlboro logo was seen or mentioned nearly 6000 times and was visible for 46 minutes of the 94-minute broadcast.369 In addition, after the broadcast ban went into effect in the United States, tobacco advertising merely shifted to other media—newspapers, magazines, outdoor signs, transit, point of sale, and a variety of promotions—at much higher expenditure levels.259 Similarly, other studies have suggested that partial bans are not effective, but that complete bans can decrease consumption.370–372

Quitlines Quitlines have been shown to increase cessation rates. The Guide to Community Preventive Services found 32 high-quality studies of the effectiveness of quitlines. In all studies, telephone support was coordinated with other interventions, such as patient education, providerdelivered counseling, NRT, a cessation clinic, or a televised cessation series. Cessation rates were increased by a median of 2.6 percentage points. Six studies that examined the effect of quitlines plus patient education materials compared with patient education materials alone had a similar magnitude of effect. Five studies examined proactive telephone counseling (quitlines that make follow-up calls). These studies found a median increase in cessation of 41%.309 Quitlines are also offered by states as part of a comprehensive tobacco control program. Some quitline services offer free NRT with the counseling service.373 California was the first state to develop such a quitline. Both randomized clinical trials and real-world evaluation trials of the quitline have shown that it doubled quit rates over self-help materials

alone.374,375 It has been estimated that up to 15% of smokers would use a quitline service, but current quitlines have the capacity to only serve 1–3% of smokers.360

Reducing Out-of-Pocket Costs of Treatment Reducing out-of-pocket costs for cessation treatment increases cessation. The Guide to Community Preventive Services found five high-quality studies assessing the impact of programs that reduced or eliminated costs for nicotine replacement therapy. One study reported that use of treatment increased with reduced payment level. All these studies observed an increase in cessation, with a median increase of 7.8 percentage points. One study reported an increased odds ratio for quitting of 1.63.309

Effectiveness of Comprehensive Tobacco Prevention and Control Programs In the absence of the antismoking campaign, an estimated additional 42 million more Americans would have smoked in 1992. As a result of these campaign-induced decisions not to smoke, an estimated 1.6 million Americans postponed death between 1964 and 1992, gaining 21 years of additional life expectancy on average, and an estimated additional 4.1 million deaths will be avoided or postponed between 1993 and 2015.376 Such analyses must be interpreted cautiously, however, because they rely heavily on assumptions about what would have occurred in the absence of antismoking campaigns. Evaluation of the California tobacco control program has shown that per capita consumption of cigarettes declined significantly in California from January 1989 through December 1993 and the decline was greater than for the United States as a whole.376a From 1989 to 1993, adult smoking prevalence also declined almost twice as rapidly as the rest of the country. One study showed that the increase in youth smoking in the early 1990s was smaller in California than in the rest of the country.333 From 1993 to 1996, in conjunction with program cuts, the rate of decline slowed in California, but still was greater than for the country as a whole.377 From 1988 to 2003, tobacco consumption in California decreased 60%, and California now has the lowest per capita consumption in the United States.378 California has also seen improvements in health outcomes. Lung cancer incidence has declined three times more rapidly in California than in the rest of the country, and has declined among women whereas the rest of the country is still experiencing increasing lung cancer rates among women.379 Six of nine tobacco-related cancers have a lower incidence rate in California than in the rest of the United States (lung/bronchus, esophagus, larynx, bladder, kidney, pancreas).378 Reductions in cardiovascular disease have also been reported. A study of the California program reported that mortality from heart disease declined at a significantly greater rate in California (2.93 deaths per 100,000 population) than in the rest of the country, and estimated that the program was associated with 33,000 fewer deaths from heart disease between 1989 and 1997 than would have been expected without the program.380 Studies have estimated that the California tobacco control program saved $11 million in the first two years and $100 million over seven years by reducing the number of smoking-related low-birthweight babies,381 and another $25 million in the first two years and $390 million over seven years through declines in smoking-related heart attacks and strokes.305 California has reported that for every dollar spent on the program, statewide health care costs are reduced by more then $3.60.382 Massachusetts also experienced a persistent decline in per capita cigarette consumption since the start of its program. From 1992 to 1997, per capita consumption in Massachusetts decreased 31%, compared to an 8% decline in the rest of the country (excluding California). Prevalence declines were also greater (3 percentage points compared to 1 percentage point) than in the rest of the country. And, like California, the increase in youth smoking prevalence in the early 1990s was less in Massachusetts than in the rest of the country. The effect was particularly evident among younger adolescents.333,383

54 Massachusetts reported that its program paid for itself through declines in smoking among pregnant women.384 Arizona also noted greater declines in per capita sales than the rest of the United States after implementation of its program. The state reported that adult prevalence declined at a faster rate than in the rest of the country and that young adult prevalence declined in Arizona at a time when it was increasing nationally.333 The program noted that the decrease in smoking prevalence among low income and low education groups meant a narrowing of disparities in tobacco use.385 In Oregon, trends in per capita consumption were also compared to the rest of the country (excluding California, Massachusetts, and Arizona) preprogram (1993–1996) and postprogram (1997–1998). In 1997–1998, consumption declined 11.3% in Oregon compared to 1% in the rest of the country.333 Oregon also noted an impact from their school program: smoking prevalence decreased faster in schools funded for prevention programs than in nonfunded schools. Even after adjustment for other risk factors, students in funded districts were 20% less likely to smoke than students in nonfunded districts. Changes in prevalence were also greater in school districts with high implementation of the program, whereas smoking prevalence in districts with low implementation stayed nearly the same as in nonfunded districts.386 Florida had focused an effort on youth (“truth” media campaign, youth community activities including youth advocacy groups, school programs, minors’ access enforcement, and youth involvement in the design and implementation of the program). The state documented dramatic declines in current smoking and ever smoking, and large increases in the proportion of “committed never-smokers” among both middle and high school students.387 Evaluations across multiple programs and nationally have also demonstrated the effectiveness of comprehensive tobacco prevention and control programs. An evaluation of the ASSIST demonstration project reported that ASSIST states had a greater reduction in smoking prevalence than non-ASSIST states, and estimated that if all states had implemented ASSIST, there would be 280,000 fewer smokers.329 A national analysis concluded that state tobacco control expenditures reduced cigarette sales over and above any price increases that occurred concurrently (and adjusting for cross-border sales). The study also noted that larger, more established programs may have a larger impact dollar for dollar, and concluded that if states had begun investing at the CDC-recommended minimum funding levels in 1994, the aggregate sales decline would have doubled (i.e., decreased an additional 9%) by 2000.388 A second national analysis reported that increased state tobacco control expenditures reduced youth smoking prevalence and the number of cigarettes smoked per day, and that had states spent the CDC-recommended minimum levels, youth smoking prevalence would have been between 3.3% and 13.5% lower than the observed rate.389 Evidence from well-funded comprehensive state programs (particularly California and Massachusetts) and from controlled studies were analyzed and developed into CDC’s “Best Practices.” In addition, the annual costs to implement comprehensive state tobacco control programs were estimated to range from $7–$20 per capita in smaller states (population less than 3 million), $6–$17 per capita in medium-sized states (population of 3–7 million), and $5–$16 per capita in large states (population greater than 7 million).390

Current Status of Tobacco Control Programs Tobacco Excise Taxes At the end of 2006, the federal cigarette tax was $0.39 per pack.391 By the end of 2006, state excise taxes ranged from $0.07 cents per pack in South Carolina to $2.46 in Rhode Island, with an average state tax of $0.78 per pack (up from $0.381 at the end of 1997). However, federal and state taxes as a percentage of retail price declined from 51.4% in 1965 to 34% in 2006.392 In addition, 44 states and D.C. imposed general sales taxes on cigarettes as of 2006. In 2006, 20 states had a cigarette tax of $1.00 or more and 5 states had a tax of $2.00 or more per pack. New York City increased its local cigarette tax from $0.08 to $1.50 in 2002, and Cook County, Illinois (includes Chicago), increased its cigarette tax from $0.18 to $1.00 in 2004.392

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In 2002, the federal tax on smokeless tobacco was only $0.04 per can of snuff and $0.012 per package of chew tobacco. As of January 2007, 49 states taxed smokeless tobacco.392

Media Campaigns The 1997 Master Settlement Agreement (MSA) imposed restrictions on cigarette marketing in the United States. There could no longer be (a) brand name sponsorship of concerts, team sporting events, or events with a significant youth audience; (b) sponsorship of events in which paid participants were underage; (c) tobacco brand names in stadiums and arenas; (d) cartoon characters in tobacco advertising, packaging, and promotions; (e) payments to promote tobacco products in entertainment settings, such as movies; (f) sale of merchandise with brand name tobacco logos; and (g) transit and outdoor advertising (including billboards).333

Smoke-free Indoor Air Nonsmokers are increasingly able to breathe smoke-free air in indoor environments. Federal agencies have taken action to reduce exposure to SHS. In 1987, the U.S. Department of Health and Human Services instituted a smoke-free buildings policy, and in 1994, the U.S. Department of Defense prohibited smoking in its facilities worldwide. In addition, the Pro-Children Act of 1994 banned smoking in indoor facilities that are regularly or routinely used to provide services to children (e.g., school, library, day care, health care, and early childhood development settings).213a The Occupational Safety and Health Administration proposed standards to restrict exposure to SHS in workplaces, but then withdrew its Indoor Air Quality proposal in 2001, citing the substantial success states and communities, as well as private employers, were having with this issue. In August 1997, the President issued an Executive Order making all federal facilities of the executive branch smoke free, thus banning smoking in all interior space owned, rented, or leased by the executive branch unless there were separately ventilated smoking areas. In November 2004, the Secretary of the Department of Health and Human Services announced a property-wide ban on tobacco use beginning in January 2005, to be implemented as contracts came up for renewal. Policies were also being implemented in the private sector. Effective in 1994, the Joint Commission on the Accreditation of Healthcare Organizations required hospitals to be smoke free. In 1990, smoking was banned on all U.S. domestic flights of less than 6 hours’ duration. Delta Airlines made all its flights smoke free as of January 1, 1995, and other airlines subsequently banned smoking on their trans-Atlantic flights. In 2000, legislation made all flights to and from the United States smoke free. In 1993, Amtrak made most trains smoke free.399 California became a leader in smoke-free environments for its citizens when all workplaces, including restaurants and bars, became smoke free on January 1, 1998. As of January 12, 2007, eight states had comprehensive indoor smoke-free policies that included all workplaces, restaurants, and bars. Five more had state-wide smokefree policies that included workplaces and restaurants, but not bars. As of January, 2007, 2507 localities had passed some form of clean indoor air law, including Lexington, Kentucky. However, as of December 2006, 18 states had legislation that preempted localities from enacting laws to restrict smoking in public places that were more stringent that state laws.355, 402a In addition to reducing the number of and degree of protection afforded by local regulations, preemption prevents the public education that occurs as a result of the debate and community organization around the issue.402 Workplace smoking policies, originally implemented primarily for safety reasons, are now adopted because of health concerns.312 The vast majority of adults recognize the danger of exposure to SHS.213a,403,404 The percentage of Americans who support totally smoke-free indoor workplaces increased from 58% in 1993 to 68% in 1999 405 and 75% in 2002213a Support generally increases after institution of a ban.213a,406 A 1995 survey found that 87% of work sites with 50 or more employees had a smoking policy of some kind.407 A 1994 survey of businesses with up to 25,000 employees found that 54%

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had smoke-free policies and only 7% had no policy on smoking.312 A nationally representative survey of workers conducted in 1992–1993 and again in 1998–1999 found that 46% were covered by a smoke-free workplace policy in 1992–1993 and 70% in 1998–1999. However, significant variation existed by state in 1998–1999, from a high of 80% (Utah, Maryland) to 50% (Nevada).407a Young workers (aged 15 to 19 years), men, blue-collar workers, and service workers were less likely to work in smokefree workplaces, although disparities have narrowed over time.213a,408 In Los Angeles, California, both patron and employee compliance with the smoke-free bar and restaurant laws increased; by 2002, 76% of patrons in freestanding bars and 98% of patrons in bars/restaurants, and 95% of employees in freestanding bars and 96% of employees in bars/restaurants were complying with the law.409 However, in 2000, only 24.5% of states, 45.5% of districts, and 44.6% of schools provided tobacco-free environments in middle, junior, or senior high schools.410 In California, which enacted the first statewide smoke-free workplace law provided sustained media campaigns about the dangers of SHS, the proportion of adults with smoke-free homes increased from 38% in 1992 to 74% in 1999.411 The percentage of households with smoke-free rules increased nationally from 43% in 1992–1993 to 72% in 2003. In 2003, Utah had the highest proportion of homes with such rules (88.8%), and Kentucky had the lowest (53.4%).411a Exposure to SHS has been decreasing in the United States. From 1988–1991, 88% of Americans aged 2 years and older were estimated to be exposed to SHS.218 In the third national report on human exposure to environmental carcinogens, CDC reported that from 1988-1991, the median level (50th percentile) of serum cotinine (a marker for secondhand smoke) among non-smokers was 0.20 ng/mL. From1988–1991 to 1999-2002, the median cotinine level decreased 70% (to 0.059 ng/mL), suggesting a dramatic reduction in exposure. Exposure declined 68% in children, 69% in adolescents, and 75% among adults. Although levels declined in all age, sex, and racial/ethnic categories, exposure was still high among non-Hispanic blacks and in children and adolescents.412 After implementation of the California law creating smoke-free bars, self-reported exposure of bartenders decreased from 28 to 2 hours per week, 59% of those with previous respiratory symptoms reported they no longer had the symptoms, 78% of those with sensory irritation no longer reported those symptoms, and there was an improvement in mean lung function measurements.413

Minors’ Access In 1992, Congress enacted the Synar Amendment. This federal statute and its implementing regulations issued in 1996 require every state to have a law prohibiting tobacco sales to minors under age 18, to enforce the law, to conduct annual statewide inspections of tobacco outlets to assess the rate of illegal tobacco sales to minors, and to develop a strategy and time frame to reduce the statewide illegal sales rate to 20% or less.414,415 Overall, the national retailer violation rate decreased from 41% in 1996 to 12% in 2005.416,417 In 2005, 48 states and DC states met the overall goal of a 20% violation rate.417 Unfortunately, as states have developed minors’ access laws, some have adopted weak laws that include preemptive language preventing stronger local legislation. As of January 1, 2007, 22 states had such preemptive language in their minors’ access legislation.416a,402a In August of 1996, the FDA issued regulations that prohibited the sale of tobacco to persons less than 18 years of age, required retailers to obtain photo identification to verify the age of all persons less than 27 years of age, banned vending machines and self-service displays except in facilities where only adults were allowed, banned sales of single cigarettes and packages with fewer than 20 cigarettes, and banned free samples.418 The FDA rule was challenged in federal court by the tobacco industry, and in 2000, the Supreme Court ruled that Congress had not given the FDA authority to regulate tobacco products.419 Legislation to give FDA such authority has been proposed several times, most recently in early 2007. The MSA of 1998 also contained the following youth access restrictions: restricted free samples except where no underage persons were present, prohibited gifts to youth in exchange for buying tobacco products, prohibited gifts through the mail without proof of

age, and prohibited the sale or distribution of packs smaller than 20 for three years.333 Studies show that internet sales provide easy access by minors to cigarettes because many Internet vendors don’t check ages or have a verification process.420 By the end of 2005, 29 states had passed laws prohibiting delivery of tobacco to individual consumers and/or restricting internet sales in some way.355,420a

Coverage for Tobacco-use Treatment Insurance coverage for tobacco-use treatment has been slowly increasing. In 1996, 18 states had some form of Medicaid coverage for tobacco-use treatment, but none covered all counseling modalities (individual, group, or telephone) and all FDA-approved medications. By 2005, 38 states covered some form of tobacco use treatment for all medicaid recipients, and 1 state offered comprehensive coverage.421 Coverage under managed care also increased from 1997 to 2002. The proportion offering full coverage in 2002 was 5% for OTC NRT gum, 9% for OTC NRT patches, 36% for NRT inhaler and nasal spray, and 41% for Zyban. The proportion offering full coverage for counseling was 16% for group counseling or classes, 19% for individual counseling for pregnant women, 26% for self-help materials, 41% for faceto-face counseling, and 52% for telephone counseling. However, 15% had annual or lifetime limits on coverage for smoking cessation interventions.422 A survey of work sites having at least 10 employees and providing health insurance reported that there was at least some coverage for devices and drugs in 23% of workplaces, for counseling in 22%, but only 5% offered coverage of both drugs/devices and counseling.423 In a survey of state requirements for provision of preventive services, as of June 2001, one state mandated tobacco-use treatment coverage for group health plans only, one for HMOs only, and one for both group plans and HMOs; one required only medication coverage while the others specified cessation counseling coverage.424 An analysis of the extent to which states required insurance coverage for tobacco-use treatment for state employees (5 million workers) at the end of 2002 found that (of 45 reporting) 29 states required coverage for at least one PHS-recommended treatment for at least some employees, but only 17 provided coverage that was fully consistent with the PHS guideline for at least some employees, and only 7 required coverage consistent with the guideline for all state employees.425

Quitlines California was first to have a state quitline (1992). As of August 2006, all states offered quitline services, although historically funding has been erratic, with some states losing and then regaining them. In 2004, the Secretary of DHHS developed a national network of quitlines. This network has a single portal number: 1-800-QUIT NOW. This portal routes callers to their state’s quitline service. As part of the initiative, CDC provided funding to states without these services so that every state had a quitline. CDC also provided funding to states so they could enhance their existing quitline services.425a The Secretary did not provide funding for this initiative, but in 2005, some funding was allocated by Congress for the network. However, for most states, current funding is not high enough to allow widespread promotion and provision of counseling and medication to all tobacco users interested in quitting.

Comprehensive Programs ASSIST, funded from 1991 to 1998 by NCI and conducted in collaboration with ACS, funded 17 states to form community-based tobacco coalitions responsible for developing and implementing comprehensive state plans for tobacco prevention and control. In 1993, CDC began funding, at lower levels, the other 33 states and the District of Columbia through the IMPACT (Initiatives to Mobilize for the Prevention and Control of Tobacco Use) program. In 2000, the ASSIST and IMPACT programs were combined into CDC’s National Tobacco Control Program, with funding averaging $1 million per state. The program had four goal areas (prevent initiation, promote cessation, eliminate exposure to SHS, and eliminate tobacco-related disparities). States are expected to use community and policy interventions and

54 countermarketing campaigns to meet these goals and to evaluate their programs’ success.426 In 1998, the MSA between the states and the major tobacco companies provided $246 billion over 25 years to the states to compensate them for Medicaid costs incurred by tobacco users.427 Although it was expected that states would fund comprehensive tobacco control programs using this settlement, in most cases the funds have been used for other purposes, particularly as states have experienced budget deficits in the first few years of the twenty-first century. Raising the excise tax on tobacco reduces consumption, but the effect is greater if a portion of the tax is used to fund a comprehensive tobacco control program. California was the first state to do so in 1988, when an initiative to increase cigarette taxes by $0.25 per pack dedicated 20% of the increase to tobacco control activities.376a Other states to fund programs using excise taxes included Massachusetts in 1992,383 Arizona in 1995,385 and Oregon in 1997.386 However, all four of these programs have sustained cuts. By 2004, the Massachusetts program had been virtually eliminated (a 92% cut) and the California, Arizona, and Oregon programs severely reduced (45%, 37%, and 69%, respectively).427 Florida’s campaign, funded by its individual settlement with the tobacco industry, was cut 99%, eliminating the effective “truth” marketing campaign.428 Other states dedicated significant cigarette excise tax dollars or MSA funds to tobacco control programs, but from 2002 to 2005, funding for tobacco control programs was cut by 28%. The use of only 8% of excise taxes and the MSA funds dedicated to tobacco control would fund these programs at the CDC-recommended minimum level.390,427 By 2007, only 3 states were funding their tobacco control programs at this level, 28 states and the District of Columbia were funding at less than half the minimum level, and 5 states were not funding these programs at all.428a

Protobacco Influences Advertising and Promotion In 1970, the cigarette industry spent $360 million on advertising and promotion, two-thirds of which was for television and radio advertising. In the United States, broadcast media advertising was banned as of January 1, 1971. In 1975, the cigarette industry spent $490 million on advertising and promotion, two-thirds of that for newspaper, magazine, and outdoor ads. In 1997 (the year of the MSA), the industry spent $5.7 billion in advertising and promotion, with 80% used for promotions, specialty items, and coupons.429 Industry spending on advertising nearly tripled from 1997 to 2001 (to $15.2 billion). Expenditures decreased slightly to 13.1 billion in 2005. The share used for coupons and discounts increased from 27% to 87%. Smokeless tobacco companies spent $251 million on advertising in 2005. Price discounts and free samples accounted for 60% of the advertising budget.429a Tobacco companies maintain that their advertising and promotion are not intended to appeal to teenagers or preteen children. However, on March 20, 1997, the Liggett Group, Inc., as part of the settlement of state lawsuits, acknowledged that the tobacco industry markets to youth under 18 years of age.430 Similarly, documents released in January 1998 showed that in 1975, R.J. Reynolds Tobacco wanted to increase the market share of Camel filter cigarettes among young people 14–24 years of age “who represent tomorrow’s cigarette business.”431 One study found that the MSA had little effect on cigarette advertising in magazines. In 2000, the tobacco industry spent nearly $60 million on advertising in youth-oriented magazines, and advertisements for the three most popular youth brands reached 80% of young people an average of 17 times in 2000.432 A Massachusetts study found that cigarette advertising in magazines with high youth readership increased 33% after the MSA,433 and another study reported that the United States Smokeless Tobacco Company (USST) increased advertising in magazines with high youth readership by 74% from 1998 to 2001 and that nearly half the company’s advertising was in youth-oriented magazines.434 In 2002, a California judge fined R.J. Reynolds Tobacco Company $20 million for advertising in magazines with high youth readership in violation of the state tobacco settlement agreement.435 The promotion of televised sporting and entertainment events heavily expose youth to tobacco

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advertising as well.56,179,436 Moreover, the kinds of activities promoted by tobacco companies (often popular musical and sporting events) and the effort to associate smoking with maturity, glamour, and selfconfidence have a strong appeal to youth. In a 2005 national survey, 81% of youth smokers aged 12–17 preferred Marlboro, Camel, or Newport, the three most heavily advertised brands. Marlboro, the most heavily advertised, was used by 48% of youth, and 40% of smokers over the age of 25.436a Teens have been shown to be three times more sensitive to cigarette advertising than adults.437 One study reported that teens were more likely to be influenced to smoke by tobacco advertising than by peer pressure,438 and another showed that receptivity to advertising was associated with smoking initiation. The biggest impact comes from influencing nonsusceptible youth to become susceptible to smoking.439 After the Joe Camel cartoon character was introduced in 1988, Camel’s share of the adolescent cigarette market increased from 2% in 1978–1980, to 8% in 1989, to more than 13% in 1993.179,440 One study found that the cartoon camel was as familiar to six-year-old children as Mickey Mouse’s silhouette.441 The Joe Camel campaign was one of the tobacco industry’s most heavily criticized advertising campaigns, and there was increased pressure to drop the campaign after the Federal Trade Commission (FTC) filed suit against the company in May of 1997, alleging that the Joe Camel symbol enticed children to smoke. In July of 1997, R.J. Reynolds announced that they were discontinuing Joe Camel in the United States, although they still planned to use the cartoon character for overseas advertising.442 Tobacco company marketing efforts have also targeted women and minorities. The uptake of smoking among women beginning in 1967 was associated with the marketing of cigarette brands specific for women.443 In 1990, after the Secretary of the Department of Health and Human Services, Dr. Louis Sullivan, denounced R.J. Reynolds for “slick and sinister advertising” and for “promoting a culture of cancer,” the company abruptly decided to cancel the launch of Uptown, their new cigarette aimed at blacks.444 Only a month later, the same company was preparing to introduce a new cigarette aimed at young, poorly educated, blue-collar women.445 This cigarette, called Dakota, was also withdrawn after public outcry. Another campaign, called “Find Your Voice” targeted minority women, and brands such as “Rio,” “Dorado,” and “American Spirit” targeted Hispanics and American Indians.355 In 2004, R.J. Reynolds settled a lawsuit with 13 states over Reynolds’ “Kool Mixx” marketing campaign, which the states alleged targeted urban minority youth in violation of the MSA.446 In 2006, R.J. Reynolds settled a lawsuit with 38 states over their candy, fruit, and alcohol flavored cigarettes. The company agreed to a U.S. ban and to restrictions on marketing flavored cigarettes in the future. These examples suggest that new tobacco product introductions aimed at young and minority populations are likely to be aggressively attacked as exploitative. Several studies have looked at the effect of tobacco advertising on smoking, particularly among young people. The 1994 Surgeon General’s Report concluded that “cigarette advertising appears to increase young people’s risk of smoking by affecting their perceptions of the pervasiveness, image, and function of smoking.”179 Similarly, an IOM report concluded that the preponderance of evidence suggests that tobacco marketing encourages young people to smoke.350 The FDA reviewed the evidence when developing the case for regulation of tobacco, and concluded that cigarette advertising is causally related to the prevalence of smoking among young people.418 The U.K. Scientific Committee on Tobacco and Health also concluded that tobacco advertising and promotion influences young people to begin smoking.448 Smoking in the movies has also recently emerged as a tobacco control issue. Several studies have now shown that exposure to smoking in the movies increases youth initiation. For example, one study showed that students in the highest quartile of exposure were 2.72 times more likely to begin smoking compared with students in the lowest quartile of exposure. The effect of exposure was stronger in adolescents with nonsmoking parents. The authors estimated that 52% of smoking initiation could be attributed to exposure to smoking in the movies.449 Another study found that susceptibility to begin smoking increased with higher levels of exposure to smoking in the

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movies.450 In a recent cohort study, one-third of adolescent neversmokers nominated as their favorite film stars those who smoked onscreen. These nominations independently predicted later smoking.451 Although smoking in the United States has declined since the 1950s, and smoking in the movies likewise decreased from 1950 (10.7 incidents per hour) to 1980–1982 (4.9 incidents per hour), it rebounded to 1950 levels in 2002 (10.9 incidents per hour).452 Other studies have shown that smoking is frequent even in G or PG movies.453 Tobacco advertising in magazines can also limit the information provided on the health effects of smoking. For example, many women rely on magazines for information about health. Yet studies have found little coverage of the serious consequences of smoking in these magazines. A recent study examined health and smokingrelated coverage during 2001–2002 in 15 women’s magazines (10 of which were assessed in previous studies), and found that there were only 55 antismoking articles, compared with 726 on nutrition, 424 on ob/gyn issues, 347 on fitness, 340 on diet, and 268 on mental health.454 Only six (out of 4000) articles focused primarily on lung cancer, and two of these did not address the importance of avoiding cigarettes in order to prevent lung cancer. Over the same time period, there were 176 prosmoking mentions (half of which were photographs or illustrations) and three magazines had more prosmoking mentions than antismoking messages. There were 6.4 pages of cigarette advertising for each page of antismoking ads.454 In the United States, the federal Public Health Cigarette Smoking Act of 1969 preempted most state advertising restrictions.455 In addition, as of 1998, 17 states preempted localities from passing their own laws to restrict the marketing of tobacco products.456 As of June 1997, only nine states had laws that restrict the advertising of tobacco products. These laws included restricted advertising on lottery tickets or video games, prohibited advertising within certain distances of schools, and required warning labels on billboards advertising smokeless tobacco products.418,455 In August 1996, the FDA issued a rule that all tobacco advertising must be in black-and-white text only except when it appears in adult publications or in locations inaccessible to young people. Billboards were banned within 1000 feet of schools and playgrounds; events, teams, and entries could be sponsored only in the corporate name, not a brand name; brand name nontobacco items, such as t-shirts, were banned; gifts and items provided in exchange for proof of purchase were banned; and the use of nontobacco names on tobacco items was banned.418 The FDA rule was challenged in federal court and, in 2000, the Supreme Court ruled that the FDA did not have the authority to regulate tobacco.419 In 2004, a bill giving FDA the authority to regulate tobacco failed in conference committee; a similar bill was introduced in early 2007. Some other countries have very broad advertising restrictions.370 For example, Canada passed legislation in 1988 to ban all tobacco advertising in newspapers and magazines published in Canada as well as all point-of-sale tobacco advertising and promotion. In Europe a number of countries have enacted similar restrictions on the use of graphics in tobacco advertising. As of late 2004, at least 12 countries had implemented a total ban on tobacco advertising and marketing.457

Other Interventions Warning Labels Warning labels can have an impact on consumers if they take into account consumers’ previous knowledge of the risks, levels of education, and reading ability. To be effective, labels need to stand out, have a visual impact, be visible, and be content specific (not give just general information).370 There is some evidence that warning labels can have an impact on smoking behavior. In South Africa, tobacco consumption decreased 15% in three years after new warning labels were introduced. Stronger warning labels in Australia appear to have a larger effect on quitting behavior than the old labels, and half of Canadian smokers said that the warning labels had contributed to their desire to quit or to cut back on their consumption.370

individual suits against the tobacco industry.458–462 There have also been successful class action lawsuits against the tobacco industry. One of the earliest successful class action lawsuits involved flight attendants. This lawsuit, brought in 1991, sought damages for diseases in and deaths of flight attendants caused by exposure to SHS in airplanes. The settlement included waivers of all statutes of limitations, thus enabling flight attendants whose exposure happened decades earlier to pursue their claims. It also included the establishment of the Flight Attendant Medical Research Institute as a not-for-profit medical research foundation with funding by the tobacco industry of $300 million.463 Another class action lawsuit that originated in Florida, sought damages against cigarette companies and industry organizations for alleged smoking-related injuries. Initially the class action lawsuit verdict awarded $12.7 million in compensatory damages to three individual plaintiffs, and $145 billion in punitive damages.464 In May of 2003, the Florida appeals court threw out the verdict, concluding that each smoker’s claim was too unique and individualized to be tried collectively in a class action suit. In 2006 this finding was upheld by the Florida Supreme Court, but the court also ruled that the companies are negligent and their products are defective, unreasonably dangerous and addictive. In their individual cases, the plaintiffs must only prove that smoking caused their disease.465 Another class action lawsuit claimed that Philip Morris had defrauded “Lights” smokers by suggesting that light cigarettes were less hazardous than full-flavor cigarettes. In 2003, the Madison County (Illinois) Circuit Court awarded compensatory and punitive damages totaling $10.1 billion. The Illinois Supreme Court overturned this verdict and U.S. Supreme Court let that ruling stand. Lawsuits in other states over “light” cigarettes are still pending.465,466 States have also sued the tobacco companies and some have filed class-action lawsuits over light cigarettes.467 In 1994, Mississippi became the first state to sue the tobacco industry for medical expenses incurred by Medicaid for the treatment of tobacco-related illnesses. In January 1998, the industry had settled with three states (Florida, Mississippi, and Texas) for amounts ranging from $3.4 billion to $15.3 billion. Minnesota also reached a settlement with the tobacco industry. Under the MSA in 1997, the remaining states settled with 11 tobacco companies. Under the MSA, the companies agreed to pay $246 billion over 25 years. Other provisions of the MSA included the significant marketing and minors’ access restrictions mentioned earlier, prohibited the industry from supporting diversion of settlement funds to nonhealth use, restricted the tobacco industry from lobbying against restrictions of advertising on or in school grounds, prohibited new challenges by the industry to state and local tobacco control laws enacted before June 1, 1998. The MSA also required the tobacco industry to contribute $25 million annually for 10 years to support the American Legacy Foundation, to contribute $1.45 billion over five years to support the National Public Education Fund for a national sustained advertising and education program to counter youth tobacco use, and then to contribute $300 million annually to the fund so long as the participating companies hold 99.05% of the market.333 As of early 2007, because of market share losses, there will be no further annual payments to the fund. In 1999, the Department of Justice sued the largest tobacco companies under the Racketeer Influenced Corrupt Organization Act (RICO), charging the tobacco companies with conspiring to conceal the health risks and addictive powers of cigarettes. The government sought the “disgorgement” of $280 billion in “ill gotten gains” that the industry has received by selling cigarettes to people who got addicted before the age of 21 (since the enactment of the act in 1970). The judge found the defendants guilty in late 2006, but said that a district court ruling prevented her from imposing any penalties. As of early 2007, the tobacco industry had announces their intention to appeal the ruling.468,468a TOBACCO ECONOMICS

Industry Lawsuits Historically, individual lawsuits against the tobacco industry have not been successful. However, more recently there have been successful

In 2003, consumers in the United States spent nearly $87 billion on tobacco products, equal to 1.1% of personal disposable income.240,469

54 One recent study estimated that smoking is associated with lower net worth, even after adjusting for a variety of demographic factors. Heavy smokers had a reduction in net worth of more than $8300 and light smokers had a reduction of $2000, compared to nonsmokers. Each adult year of smoking was associated with a 4% reduction in net worth, and the author concluded that smokers appear to pay for tobacco expenditures out of income that is saved by nonsmokers. The author also concluded that a reduction in smoking would boost wealth, especially among the poor.470 The industry directly accounted for about 260,000 jobs in 1993 (tobacco growing, warehousing, manufacturing, and wholesaling.333 In 2005, U.S. tobacco farmers produced an estimated 647 million pounds of tobacco leaf with a value of 1.1 billion, and in 2005 U.S. cigarette manufacturers produced an estimated 496 billion packs of cigarettes, 16% of which were exported.240 In monetary value, domestic tobacco exports (cigarettes, other manufactured tobacco products, and unmanufactured tobacco) accounted for 0.1% of the total export earnings of the United States in 2004.471,471a Cigarette production in the United States is highly concentrated; four major cigarette manufacturers produce nearly all cigarettes in this country.240 In the twentieth century, the importance of tobacco to the overall U.S. economy declined, although its regional and local importance remains high. A 1996 study that looked at the impact of tobacco at the regional level estimated that eliminating spending on tobacco products would have led to 300,000 fewer jobs in the Southeast, but would have increased jobs in all other regions by about the same number. They further estimated that by 2000, the loss of jobs in the tobacco region would fall to about 220,000 while the net impact nationally would be an increase of 133,000 jobs.472 Similarly, a USDA report found that the large declines in tobacco production in the 1980s had a relatively minor impact on the macroeconomy of the major tobacco-growing regions.473 This was attributed to the relatively small share of tobacco (less than 1% of total income) in these regional economies. Until late 2004, a tobacco price support program that was first introduced during the Depression regulated both the number of tobacco producers and the quantity of tobacco produced through a complex system of quotas. This program led to a higher price of tobacco for farmers. In 2003, the estimated gross income per acre for tobacco was $3851, compared with $232 for corn and $242 for soybeans (U.S. Department of Agriculture, unpublished data, 2003). Although the price support program increased prices only marginally (0.52%), it provided a political constituency of quota owners and tobacco farmers who opposed tobacco control interventions. Studies of the impact of the farm support program suggested that the overall impact of the program on tobacco control was probably negative.333,474 In 2004, Congress passed a law that eliminated the price support system and provided a $10.14 billion payout (over 10 years) to tobacco farmers and quota holders; the cost of the buyout will be paid by the tobacco industry.475

Trade Policies In 2003, 70% of tobacco production occurred in six countries: China, India, the United States, Brazil, Indonesia, and Turkey, with most being used to make cigarettes.476 Cigarette production largely occurs in China, the United States, and the European Union. World trade in cigarettes has been continually expanding, and U.S. companies increased exports from 24.3 billion cigarettes per year in the late 1960s to 240 billion in 1996; exports then declined to 111 billion pieces in 2006.240 In the 1990s, 30% of U.S. cigarettes were exported. This amount probably would have been higher except for trade policies that protected domestic tobacco growers and producers. In addition, the laws that apply to domestic cigarettes, such as warning labels and advertising restrictions, do not apply to exported cigarettes. U.S. policies and programs, particularly the Trade Act of 1974, have helped growers and producers expand into foreign markets. The threat of retaliatory trade sanctions under this act successfully opened some foreign markets to U.S. manufacturers. Under the Doggett Amendment of 1998 and guidelines distributed by the Clinton

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administration, the U.S. government stopped promoting the sale or export of tobacco or tobacco products or seeking the removal of nondiscriminatory restrictions on the marketing of tobacco or tobacco products (discriminatory practices could still be challenged). U.S. diplomats were also encouraged to assist and promote tobacco control efforts in host countries.333 However, adherence has varied over time. SMOKING AND THE WORKPLACE

Employee smoking is very costly. Smokers increase absenteeism, health insurance and life insurance costs and claims, worker’s compensation payments and occupational health awards, accidents and fires (and related insurance costs), property damage (and related insurance costs), cleaning and maintenance costs, and illness and discomfort among nonsmokers exposed to SHS. Smokers also take more breaks, averaging 18 days per year on breaks477 and are less productive. One study reported that former smokers are 4.5% more productive than current smokers.478 Former smokers also have less absenteeism than current smokers, but more than never-smokers. Among former smokers, absenteeism decreases with years of cessation.478 Male smokers are absent four days more than male nonsmokers each year (female smokers miss two more days).479 Male smokers incur $15,800 and female smokers incur $17,500 (in 2002 dollars) more in lifetime medical expenses than nonsmokers.480 The economic cost of smoking for the United States, including direct medical costs and loss of productivity from smoking-related deaths, is about $167 billion per year.8 The health-care expenditures attributable to smoking were $75 billion in 1998, or 7.1% of direct medical expenditures for the United States.20 It is estimated that a 1% reduction in health care costs for businesses could increase retained profits by 5%.481 INTERNATIONAL PERSPECTIVE ON TOBACCO

Tobacco use is a major preventable cause of death worldwide. The World Health Organization (WHO) estimates that there are about 1.2 billion smokers in the world.482 Most of these smokers are in developing countries (800 million), and are men (1 billion). Smoking prevalence for men ranges from 29% in the Africa region to 61% in the Western Pacific region. Prevalence for women ranges from 5% in the Southeast Asia region to 21% in the Region of the Americas (Fig. 54-6). Smoking prevalence varies by level of economic development: for men the prevalence is 34% in developed countries, 50% in developing countries, and 54% in transitional countries. For women the respective percentages are 21%, 7%, and 14%.482 For men, prevalence was highest in Kenya (67%), Republic of Korea (65%) and the Russian Federation (63%) and lowest in Sweden (17%). For women, prevalence was highest in Argentina (34%), Norway (32%), Kenya (32%), Denmark and Germany (30%) and lowest in the United Arab Emirates (1%), Thailand (2%), Singapore (3%), China (4%), and Egypt (5%).483 It should be noted, however, that South Asia has high bidi (a type of hand-rolled cigarette) prevalence (21% for men and 4% for women). Low-income and middleincome countries, have four-fifths of the world’s population, and 82% of the world’s smokers.370 Current cigarette smoking among youth aged 13–15 years, according to a survey that assessed 224 sites in 118 countries and 1.7 million students was 9.8% in the Africa region, 18.4% in the Americas region, 4.1% in the Eastern Mediterranean region, 16.2% in the European region, 4.5% in the Southeast Asia region, and 11.8% in the Pacific region.484 Current use of any tobacco product by youth aged 13–15 years, according to a survey conducted in 75 sites in 43 countries and the Gaza Strip/West Bank, ranges from 3% (Goa in India) to 63% (Nagaland in India). Current cigarette smoking in this group ranges from less than 1% (Goa in India) to 40% (Coquimbo in Chile), with nearly 25% of students who smoke having smoked their first cigarette before age 10.485 Other findings included a lack of gender differences in tobacco use among youth and a high rate of use of tobacco products other than cigarettes.486 From

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70

% of smokers among adults Stage 1

% of deaths caused by smoking

Stage 2

Stage 3

40

Stage 4

60 % Male smokers

30

50

% Female smokers

40 Figure 54-6. A model of the cigarette epidemic. (Source: Lopez AD, Collinshaw NE, Piha T. A descriptive model of the cigarette epidemic in developing countries. Tobacco Control. 1994;3:242–7. Reproduced with permission from the BMJ Publishing Group.)

20 30 % Male deaths 20 10 % Female deaths

10

0

0 0

10

20

1970–1972 to 1990–1992, per capita cigarette consumption decreased in the Americas (an average annual decrease of 1.5%), remained unchanged in Europe, and increased in Africa (average annual increase of 1.2%), the eastern Mediterranean (1.4%), Southeast Asia (1.8%), and the Western Pacific (3%). China is a good example of the size and scope of the smoking problem because it is the largest producer and consumer of cigarettes in the world. An estimated 300 million Chinese smoke (53% of men and 3% of women),487 the same number as in all the developed countries combined. By 2025, an estimated 2 million Chinese men will die annually from smoking.488 Before the middle of this century, very few developing countries either produced tobacco or had significant consumption of manufactured cigarettes. In the late 1950s, cigarette manufacturers sought to establish new markets in the developing countries. These countries, with more than half of the world’s population, who may be unaware of the health problems associated with tobacco use, represented a huge, potentially untapped resource for tobacco cultivation, cigarette manufacture, and cigarette marketing. In 1995, 6 low income and 18 lower middle income countries where classified as either net (consumes more tobacco than they produce) or full (does not produce any tobacco but consumes it) importers of tobacco. In these countries reduced expenditures on tobacco imports could have impacts on economic development through improving and increasing trade balance and foreign exchange reserves to fund other essential development projects.370,489,487 Currently, tobacco is grown in more than 100 countries, including 80 that are developing. From 1975–1998, production in developed countries decreased by 31%, and production in developing countries increased 128%. Asia increased its share of world tobacco production from 40% to 60%. The four major tobacco producing countries are China, the United States, India, and Brazil. These four countries account for about two-thirds of world production. The top 20 countries account for 90% of the world’s production. However, in only three countries does the employment as a percentage of the total labor force exceed 1% (Malawi at 2.03%, Turkey at 1.29%, and the Philippines at 1.24%). The average across the 28 highest countries is 0.63%.370 Export earnings from tobacco exceed 1% of total export earnings in nine countries. Two countries are particularly dependent on tobacco exports as a major source of earnings: in 1998, 61% and 23% of export earning came from tobacco for Malawi and Zimbabwe respectively.370 Thus, even very stringent tobacco control policies would likely have minimal negative long-term economic impact, with the largest effect in those few countries that earn a significant share of foreign earnings from tobacco such as Malawi and Zimbabwe.370

30

40

50

60

70

80

90

100

Trade liberalization was estimated to have increased global cigarette consumption by 5%.370 Another study calculated that markets opening in Japan, Taiwan, South Korea, and Thailand increased cigarette consumption by 10%. Two factors are thought to account for this: first, opening the markets decreased the price of both domestic and imported cigarettes, and second, cigarette advertising increased. For example, in Japan, cigarette advertising by U.S. companies doubled, and the domestic companies responded with their own increased advertising.370 Many tobacco-producing countries are poor and lack the resources to grow or import sufficient quantities of food for their populations, yet they divert agricultural land that could be used for growing staple crops such as sorghum and maize to tobacco cultivation. They may perceive tobacco production as (a) a relatively simple mechanism for raising substantial revenue from taxation of tobacco products, (b) an easy way to generate the foreign exchange necessary to buy commodities from abroad and to improve their balance of trade, and (c) a significant source of rural employment and wage production.490 The short-run economic advantages of tobacco growth and consumption come at a high cost. Most obvious are the direct, welldocumented health problems associated with tobacco use. Indirect effects of tobacco production include destruction of agricultural lands and forests and improper use of insecticides by rural farmers. According to United Nations sources, the deforestation problem in many developing countries may soon become a “poor man’s energy crisis.”491 This problem is traceable in large part to the wood burned to flue-cure many varieties of tobacco at high temperatures. Tobacco farmers in developing countries, most of whom depend on wood as their sole source of energy, use the trees from approximately 2 hectares for each ton of tobacco cured, equivalent to two trees for every 300 cigarettes, or 15 packs of cigarettes, produced.492 A direct result of deforestation is soil erosion, which in hilly rural areas may lead to silt-filled rivers and dams during the rainy season and denuded croplands during growing seasons. In addition, because tobacco grows well in sandy soils and many developing countries are located in semiarid lands, tobacco is often grown on agricultural fringe land that borders deserts. As trees in nearby forests are cut down to fuel the curing process, desertification is accelerated and tobacco farmers are forced to move into other, less arid regions. Thus, cultivation of tobacco displaces staple food crops, leading to lost food production.491 Further, the lack of adequate education among rural area tobacco farmers on the proper use of modern insecticides often leads to their indiscriminate dispersal in lakes and rivers. The resultant pollution

54 endangers water sources of rural villagers and surrounding wildlife. Failure to use the gloves and protective garments needed to limit exposure to toxic chemicals in insecticides also increases rural tobacco farmers’ long-term risk of occupationally related diseases such as skin, lung, and bladder cancer.492 The major health consequences associated with smoking (e.g., cancer, heart disease, and COPD), which are well established in developed countries, are becoming increasingly prevalent in the developing world. In 1995, an estimated 1.4 million men in developed countries and 1.6 million men in developing countries (more than half from China) died from smoking-related diseases. Tobacco use also caused an estimated 475,000 deaths among women in developed countries, and an estimated 250,000 deaths among women in developing countries (including 20,000 to 30,000 deaths from smokeless tobacco) in 1995. WHO estimates that smoking caused 3.8 million deaths globally in 1995 (7% of all deaths).489 It is estimated that China will see a dramatic increase in lung cancer deaths, from 30,000 per year in 1975 to 900,000 per year by 2025, and total tobacco deaths will increase to one million before 2010, and to two million by 2025. Similarly, it is estimated that 80 million Indian males currently aged 0–34 will be killed by tobacco. Tobacco is expected to cause 500,000 million deaths among smokers alive today, and before 2020, deaths will average 8–10 million per year or 12% of all deaths. Most of these deaths will be in developing countries.370,489 It has also been estimated that tobacco will kill a billion people in the twenty-first century (10 times more than in the twentieth century).370 There are disturbing parallels between the advertising and promotion techniques used to sell cigarette smoking in the United States and other developed countries in the early twentieth century through the 1920s and the current efforts to promote smoking as a pleasurable status symbol in developing countries. There is also a tragic difference. In the 1920s, producers, consumers, and governments did not know about the adverse health effects of tobacco use. Today, the scientific evidence is incontrovertible. In 1986, the World Health Assembly unanimously adopted a resolution for member states to consider a comprehensive national tobacco control strategy containing nine elements: reducing exposure to SHS; reducing initiation by young people; reducing smoking among health personnel; eliminating those socioeconomic, behavioral, and other incentives that maintain and promote tobacco use; placing health warnings on all tobacco products; establishing educational and cessation programs; monitoring tobacco use and tobacco-related diseases, and the effectiveness of interventions; promoting viable economic alternatives to tobacco production; and establishing a national focal point to coordinate all these activities.489 In 1990, the World Health Assembly passed another resolution urging all member states to implement multisectoral comprehensive tobacco control strategies that contain the nine elements previously listed plus legislative action to protect from SHS in indoor workplaces, enclosed public places, and public transport, with special attention to risk groups such as pregnant women and children; progressive financial measures to discourage the use of tobacco; and progressive restrictions and concerted actions to eventually eliminate all direct and indirect advertising, promotion, and sponsorship concerning tobacco.489 In 1992, the World Bank developed a formal five-part tobacco policy. (a) World Bank activities in the health sector discourage the use of tobacco. (b) The World Bank does not lend directly for, invest in, or guarantee investments or loans for tobacco production, processing, or marketing. For those countries where tobacco constitutes more than 10% of exports, the World Bank is more flexible, but works toward helping these countries diversify. (c) The World Bank does not lend indirectly for tobacco production activities, to the extent practical. (d) Unmanufactured and manufactured tobacco, tobaccoprocessing machinery and equipment, and related services are not included among imports financed with World Bank loans. (e) Tobacco and tobacco-related producer or consumer imports may be exempt from borrowers’ agreements with the World Bank that seek to liberalize trade and reduce tariff levels.493

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In 1996, the World Health Assembly passed a third resolution requesting the director-general to initiate the development of an International Framework Convention for tobacco control (FCTC).494 The FCTC became a top priority for WHO in 1998, due to concern for the growing disease burden from tobacco worldwide. In 1999, the World Health Assembly established an intergovernmental negotiating body to draft and negotiate the FCTC. This negotiating body met six times from October 2000 to March 2003. The World Health Assembly adopted the FCTC in 2003 and within the one-year time frame provided, 167 countries (including the United States) signed the treaty. The treaty came into force for ratifying countries in February 2005, after the required 40 countries had ratified it. As of early 2007, the United States had not yet ratified the treaty. The FCTC calls on countries to: 1. Adopt a nonpreemption clause, making FCTC a floor, not a ceiling for action. 2. Develop and implement a comprehensive, multisectoral national tobacco control strategy and establish focal points for tobacco control; cooperate, as appropriate, with other parties in developing appropriate policies; protect public health policies from commercial and other vested interests of the tobacco industry in accordance with national law. 3. Report on rates of taxation and trends in tobacco consumption. 4. Adopt “in areas of existing national jurisdiction as determined by national law” effective measures to protect from SHS exposure in indoor workplaces, public transport, and indoor public places. Promote adoption of these measures at other jurisdictional levels. 5. Adopt effective measures for the testing of tobacco products and for regulation “where approved by competent national authorities.” 6. In accordance with national law, adopt and implement measures to disclose to government authorities “information about the contents and emissions of tobacco products.” 7. Adopt measures to promote access to educational programs on the health risks of tobacco use and SHS, information about the tobacco industry, training on tobacco control, and involvement of public and private organizations in tobacco control programs. 8. Develop and disseminate guidelines and promote cessation of tobacco use; implement cessation programs in a variety of environments, including national health and education programs and health care facilities; collaborate with other parties to facilitate the accessibility and affordability of treatment, including pharmaceutical products. 9. Adopt and implement measures at the appropriate government level to prohibit sales of tobacco to “persons under the age set by domestic law, national law, or eighteen.” 10. Initiate and coordinate research; promote research that addresses the consequences of tobacco consumption and exposure “as well as research for identification of alternative crops.” 11. Establish, as appropriate, programs for surveillance of tobacco consumption and exposure. 12. Establish a national system for epidemiologic surveillance of tobacco consumption. 13. Subject to national law, “promote and faciliate exchange of publicly available information relevant to the convention; endeavor to establish and maintain an updated database of laws and regulations on tobacco control.”495 In the 1990s, about 13 high-income countries and 30 lowincome countries had laws prohibiting the sale of cigarettes to minors, 11 high-income countries and 6 low-income countries banned vending machines, and 14 high-income and 15 low-income countries had minimum age restrictions for purchase of cigarettes.370 However, few countries effectively enforced these laws. Many jurisdictions also had laws that banned or restricted smoking in public places, workplaces, and transit vehicles. For example, 24 high-income and 74 low-income

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countries required smoke-free public places, 9 high-income and 19 low-income countries required smoke-free restaurants, 9 highincome and 11 low-income countries required smoke-free cafes, 18 high-income and 32 low-income countries had workplace smoking restrictions, and 20 high-income and 23 low-income counties required smoke-free health establishments.370 Enforcement was again the issue. Some 75 countries have at least some type of advertising restriction,487 but the number with comprehensive bans is much lower,489 and such restrictions are frequently circumvented unless they are comprehensive. For example, after a 1976 law in France banned tobacco advertising, it was replaced by advertisements for matches and lighters with the tobacco brand names and logos, until a law was passed banning both direct and indirect advertising. By the end of the 1990s, about 137 countries required health warnings to appear on tobacco product packages. However, in most countries, the warnings were small and ineffective. By the mid1990s, a number of countries had adopted more stringent warnings, including more direct statements of risk, multiple messages, and large and rotating messages. Beginning in 2000, some countries started putting graphic pictures on warning labels (Canada, Brazil, Norway, Thailand, and the European Union).496 In 2002, taxes on cigarettes in the United States ranged from 17% of price (lowest state) to 38% of price (highest state) (Table 54-5). Prices also include $0.46 per pack to cover the MSA. If this cost were also considered a tax, the percentage of price in New York would be 47% and in Kentucky 31%. In comparison, in Europe, New Zealand, Australia, and Hong Kong, tax as a percentage of price ranged from 52% (Hong Kong) to 82% (Denmark).497 A number of countries use part of the revenue generated to operate their comprehensive tobacco control programs.489 Many countries have had difficulty implementing comprehensive tobacco control measures. However, Finland, Iceland, Norway, Portugal, and Singapore have comprehensive tobacco control policies developed since the 1970s. Australia, New Zealand, Sweden, Poland, and Thailand have more recently implemented tobacco control programs. One study used multiple regression analysis to evaluate the effectiveness of advertising restrictions, price, and income on tobacco consumption in 22 countries from 1960 to 1986.498 Above threshold levels, both advertising restrictions and higher prices were effective in decreasing tobacco consumption. Moreover, programs that included high prices, comprehensive bans on advertising, and stringent health warnings decreased tobacco consumption most. This analysis estimated that banning tobacco advertising, requiring strong and varied health warnings on packages, and implementing a 36% increase in real price would decrease tobacco consumption by 13.5%. In 2006, New York City mayor Bloomberg announced a $125M initiative to reduce tobacco use in low and middle income countries with a particular focus on China, India, Indonesia, the Russian Federation and Bangladesh (which have half the world's smokers).498a However, powerful economic forces will continue to militate against a strong tobacco control policy in developing countries. Only a concerted effort by international organizations (i.e., the WHO, the International Monetary Fund, the Food and Agriculture Organization, UNICEF, and NGOs) is likely to be effective in helping developing countries assign a high priority to tobacco prevention and control. CHALLENGES IN TOBACCO USE PREVENTION AND CONTROL

Despite considerable progress, smoking remains the largest cause of preventable death in the United States and most of the industrialized world, and it is rapidly becoming a major cause of death in developing countries as well. Lessons from the considerable progress achieved in tobacco use prevention and control during the past 25 years can help us successfully confront the remaining challenges. The growth of knowledge about the adverse health effects of tobacco has been substantial. Public education campaigns have helped to translate scientific knowledge into improved public awareness

TABLE 54-5. AVERAGE RETAIL CIGARETTE PRICE AND TOTAL TAXES PER PACK (U.S./DOLLARS/PACK OF 20), SELECTED INDUSTRIAL COUNTRIES, JUNE 17, 2002 Country

Price

Tax Incidence

Norway United Kingdom United States (Highest-NY) Canada (Highest-Saskatchewan) Ireland Australia Hong Kong New Zealand Canada (sales-weighted average)c Denmark Sweden Finland Canada (Lowest-Ontario) United States (Lowest-Kentucky) Germany France Belgium Netherlands Austria Luxemberg Italy Greece Spain Portugal

$7.56 $6.33 $5.32 $4.76 $4.46 $4.02 $3.97 $3.88 $3.80 $3.77 $3.64 $3.53 $3.48 $3.27 $2.76 $2.76 $2.63 $2.56 $2.37 $1.94 $1.93 $1.79 $1.66 $1.63

79.2% 79.5% 38.4%a 77.3% 79.0% 68.9% 51.9% 74.5% 71.6% 81.7% 70.5% 79.0% 69.0% 16.9%b 68.9% 75.5% 74.4% 73.0% 73.7% 67.7% 74.7% 72.8% 71.2% 80.7%

Nonsmokers Rights Association Smoking and Health Action Foundation. All figures given in U.S. dollars, for equivalent of 20-cigarette pack in most popular price category. Tax incidence refers to the portion of the total retail price made up of applicable taxes and fees, including excise, sales, VAT Exchange rates as of May 31st, 2002. European Union. “Tax Burden on Tobacco”; U.S., budget/tax documents; Canada, Australia, New Zealand, Hong Kong, Norway, Tobacco Journal international. aNote that U.S. prices include approx. $0.46 per pack to cover the cost of the November 1998 settlement with State Attorneys General. If this amount were considered a tax, tax incidence in New York would be 47%. No municipal taxes are included in this tabulation. bU.S. prices include approx. $0.46 per pack to cover the cost of the November 1998 settlement with State Attorneys General. If this amount were considered a tax, tax incidence in Kentucky would be 31%. cCalculated by provincial proportion of total 2001 cigarette sales. Note that Canadian prices include June 17th, 2002 tax increases.

of some smoking-caused problems, such as lung cancer and cardiovascular disease, but awareness of other smoking-caused cancers, COPD, and reproductive effects is still limited. SHS is increasingly appreciated as a health problem: By 1992, 97% of nonsmokers and 79% of current smokers agreed that exposure to SHS was harmful to healthy adults.499 Smokers are concerned that their addiction is likely to adversely affect their health. In the United States, more than half of all persons who have ever smoked have quit,245 and most continuing smokers have tried.56 Market responses to consumer concerns have included the filter cigarette, substantial reductions in average tar and nicotine content, and new delivery systems. However, because these innovations were perceived as “safer,” it appears that smokers concerned about health issues switched to such products rather than quit tobacco use entirely119 and derived little or none of the purported health benefit due to compensation (e.g., increased number of cigarettes smoked, increased depth of inhalation, smoking more of the cigarette, vent blocking). It is imperative that tobacco users realize there is no safe way to use tobacco and they need to quit. Tobacco companies spend huge sums to advertise and promote cigarettes ($13.1 billion in 2005).259 Although the effect of this

54

Figure 54-7: Influences on the decision to use tobacco. (Source: Tobacco and Situation Outlook Report, 2004;1986–2000 Surgeon General’s Report.)

Antitobacco Health education Economic policy Minors’ access Product regulation Clean indoor air regulation Social advocacy Personal litigation Advertising restrictions Promotional restrictions Widespread social norms Local community norms Behavioral treatment Pharmacologic treatment

activity on overall cigarette consumption is difficult to assess, advertising and promotion likely make smoking more attractive to youth, make continuing smokers less motivated to attempt cessation, and perhaps increase recidivism by providing omnipresent cues that smoking is fun and relaxing and contributes to conviviality (Fig. 54-7). It also appears that advertising was specifically increased to counteract tobacco prevention and control funding of comprehensive tobacco control programs.333 The inverse correlation between the percentage of a magazine’s health articles that discuss smoking and cigarette advertising revenue as a percentage of the magazine’s total advertising revenue suggests that tobacco money also affects editorial decisions.56 Counteradvertising decreases consumption, reduces initiation, and increases cessation, even in the presence of several-fold greater brand-specific, procigarette advertising.309 Some data also suggest that broad bans on tobacco advertising are also effective in reducing tobacco consumption.500 From 1970 to 2002, the percentage of cigarette advertising expenditures allocated to promotions increased from 15% to 87%.259 Promoted cigarette sales have increased since the MSA and are higher in areas with higher cigarette taxes and areas with more comprehensive tobacco control programs.500a Some of these promotional dollars sponsor sports events associated with being healthy, being fit, and being outdoors. The subliminal message is that smoking contributes to health and fitness. Other tobacco company promotional money goes to exhibitions at leading art museums, promoting the association of smoking with culture, sophistication, and artistic achievement. This support may also buy silence, or active opposition to smoking control proposals. In 1994, arts organizations in New York that had been recipients of tobacco philanthropy spoke out against an ordinance to ban smoking in public places.501,502 Continuing the process of changing the social norms of acceptability of tobacco use offers the greatest promise. Nonsmoking is an accepted norm in many socially defined groups in the United States. Rapid growth of community, state, and federal legislation and administrative actions that limit or ban smoking in places of public assembly, coupled with growing and increasingly stringent public and private employer restrictions on workplace smoking, should further limit smoking opportunities and increase the likelihood of quitting. Public health agencies and preventive medicine practitioners can help accelerate social pressure to not smoke by supporting enactment of strict clean indoor air legislation and its enforcement. Economic incentives are one of the most effective strategies to reduce cigarette consumption, prevent initiation, and increase cessation.309,333 Lower-income Americans, overrepresented among current smokers, are especially sensitive to price increases in tobacco products. Health and public health professionals can support initiatives to raise tobacco taxes.

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A young nonsmoker

A current smoker

A former smoker

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Protobacco Psychosocial factors Peer pressure Industry influence Perceived social norms Advertising Promotion Legislation Regulation Economic policy Education

Since 70% of current smokers want to quit smoking,274 and 42% attempt cessation each year,243 both public and private health organizations should be prepared to assist them. Health care professionals should routinely assess tobacco use and advise users to quit. Use of medication and telephone quitlines should be strongly encouraged. Treatment should be fully covered under both public and private insurance. Prevention programs have demonstrated the ability to delay smoking initiation for students in grades 6–10. However, these programs are only effective when they are reinforced by additional educational interventions and supportive community programs. Such programs could include mass media efforts that make smoking appear unattractive, socially unpopular, and sexually unappealing. Communication should also stress that tobacco is an addictive drug. The fact that tobacco use is associated with increased risk of other drug use179 is a potentially powerful message for parents and youth. With the budget deficits of the early twenty-first century, funding for tobacco control programs in states was slashed. If we are to meet the Healthy People 2010 goal of an adult smoking prevalence of 12% and a youth smoking prevalence of 16%, substantially increased funding for comprehensive tobacco control programs that use proven policy, countermarketing, and community interventions will be required. The enactment of an increase in cigarette taxes in California and Massachusetts, with all or part of the revenues used for tobacco control and education, has led to an accelerated decrease in cigarette consumption.333,378 In addition, two national studies have shown that comprehensive tobacco prevention and control programs reduce cigarette consumption overall and smoking prevalence among youth, over and above the effect of any tax increase that funded the program or occurred concurrently. Comprehensive programs are needed that reduce barriers to and involve the widespread use of known effective strategies. Furthermore, new and innovative strategies, particularly that address tobacco use among youth, are also needed. The decrease in cigarette consumption has been termed one of the greatest public health achievements of the twentieth century, but it is only half achieved.503 The challenge of the twenty-first century is to accelerate progress so that the morbity, mortality, and disability caused by tobacco use no longer occurs either in the United States or internationally.

ACKNOWLEDGEMENTS

A special thanks to the following individuals who contributed to this book chapter: Caran Wilbanks, T. Taylor, Lynn Hughley and Brian Judd.

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REFERENCES

1. U.S. Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Office on Smoking and Health; 2004. 2. Jarvis MJ. Why people smoke. BMJ. 2004;328:277–9. 3. U.S. Department of Health and Human Services. The Health Consequences of Smoking: Nicotine Addiction. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, Office on Smoking and Health; 1988. 4. McGinnis JM, Foege WH. Actual causes of death in the United States. JAMA. 1993;270:2207–12. 5. Mokdad AH, Marks JS, Stroup DF, et al. Actual causes of death in the United States, 2000. JAMA. 2004;291:1238–45. 6. Mokdad AH, Marks JS, Stroup DF, et al. Correction: actual causes of death in the United States, 2000 [letter]. JAMA. 2005; 293:293–4. 7. Doll R, Peto R, Boreham J, et al. Mortality in relation to smoking: 50 years’ observations on male British doctors. BMJ. 2004; 328:1519. 8. Centers for Disease Control and Prevention. Annual smokingattributable mortality, years of potential life lost, and productivity losses—United States, 1997–2001. MMWR. 2005;54:625–8. 9. Centers for Disease Control and Prevention. Projected smokingrelated deaths among youth—United States. MMWR. 1996;45:971–4. 10. Centers for Disease Control and Prevention. Addition of prevalence of cigarette smoking as a nationally notifiable condition. MMWR. 1996;45:537. 11. Centers for Disease Control and Prevention. Smoking-Attributable Mortality, Morbidity, and Economic Costs (SAMMEC): Adult SAMMEC and Maternal and Child Health [database online]. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; 2004. Available at: http://www.cdc.gov/ tobacco/sammec. Accessed January 15, 2005. 12. U.S. Department of Health and Human Services. Reducing the Health Consequences of Smoking: 25 years of Progress: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Office on Smoking and Health; 1989. 13. Thun MJ, Day-Lally CA, Calle EE, et al. Excess mortality among cigarette smokers: changes in a 20-year interval. Am J Public Health. 1995;85:1223–30. 14. Centers for Disease Control and Prevention. Cigarette smokingattributable morbidity—United States, 2000. MMWR. 2003;52: 842–4. 15. Nusselder WJ, Looman CWN, Marang-van de Mheen PJ, et al. Smoking and the compression of morbidity. J Epidemiol Community Health. 2000;54:566–74. 16. U.S. Department of Health and Human Services. The Health Benefits of Smoking Cessation: A report of the Surgeon General. Atlanta, GA: Centers for Disease Control and Prevention, Office on Smoking and Health; 1990. DHHS Publication (CDC) 90–8416. 17. Sachs DPL. Cigarette smoking. Health effects and cessation strategies. Clin Geriatr Med. 1986;2:337–62. 18. Omenn GS, Anderson KW, Kronmal RA, et al. The temporal pattern of reduction of mortality risk after smoking cessation. Am J Prev Med. 1990;6:251–7. 19. Taylor DH, Hasselblad V, Henley SJ, et al. Benefits of smoking cessation for longevity. Am J Public Health. 2002;92:990–6. 20. Centers for Disease Control and Prevention. Annual smokingattributable mortality, years of potential life lost, and economic costs—United States, 1995–1999. MMWR. 2002;52:300–3.

21. Centers for Disease Control and Prevention. State estimates of neonatal health-care costs associated with maternal smoking United States, 1996. MMWR. 2004;53:915–7. 22. Sloan FA, Ostermann J, Picone G, et al. The Price of Smoking. Cambridge, MA: Massachusetts Institute of Technology, 2004. 23. Hall JR. The smoking material fire problem. Quincy, MA: National Fire Protection Association; 2006. 24. Kochanek KD, Murphy SL, Anderson RN, et al. Deaths: Final data for 2003: National Vital Statistics Report 54 No. 13. Hyattsville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics, 2006:1–120. 25. Doll R, Peto R, Wheatley K, et al. Mortality in relation to smoking: 40 years’ observations on male British doctors. BMJ. 1994;309: 901–11. 26. Doll R, Gray R, Hafner B, et al. Mortality in relation to smoking: 22 years’ observations on female British doctors. Br Med J. 1980;280:967–71. 27. Kawachi I, Colditz GA, Stampfer MJ, et al. Smoking cessation and time course of decreased risks of coronary heart disease in middleaged women. Arch Intern Med. 1994;154:169–75. 28. Freund KM, Belanger AJ, D’Agostino RB, et al. The health risks of smoking. The Framingham study: 34 years of follow-up. Ann Epidemiol. 1993;3:417–24. 29. Stampfer MJ, Hu FB, Manson JE, et al. Primary prevention of coronary heart disease in women through diet and lifestyle. N Engl J Med. 2000;343:16–22. 30. Rosenberg L, Kaufman DW, Helmrich SP, et al. Myocardial infarction and cigarette smoking in women younger than 50 years of age. JAMA. 1985;253:2965–9. 31. Croft P, Hannaford P. Risk factors for acute myocardial infarction in women: evidence from the Royal College of General Practitioners’ oral contraception study [letter]. BMJ. 1989;298:165–8. 32. Thun MJ, Myers DG, Day–Lally CA, et al. Age and the exposure response relationships between cigarette smoking and premature death in Cancer Prevention Study II. In: Burns DM, Garfinkel L, Samet JM, eds. Changes in Cigarette-Related Disease Risks and their Implication for Prevention and Control. Rockville, MD: U.S. Department of Health and Human Services, National Institutes of Health, National Cancer Institute; 1997. Smoking and Tobacco Control Monograph No. 8. 33. Pooling Project Research Group. Relationship of blood pressure, serum cholesterol, smoking habit, relative weight and ECG abnormalities to incidence of major coronary events: final report of the pooling project. J Chronic Dis. 1978;31:201–306. 34. Watkins LO. Epidemiology and burden of cardiovascular disease. Clin Cardiol. 2004;27(6 Suppl 3):III2–6. 35. Lotufo PA, Gaziano JM, Chae CU, et al. Diabetes and all cause and coronary heart disease mortality among U.S. male physicians. Arch Intern Med. 2001;161:242–7. 36. McBride PE. The health consequences of smoking. Med Clin North Am. 1992;76:333–53. 37. Sidney S, Siscovik DS, Petitti DB, et al. Myocardial infarction and use of low-dose oral contraceptives: a pooled analysis of 2 U.S. studies. Circulation. 1998;8:1058–63. 38. Vessey M, Painter R, Yeates D. Mortality in relation to oral contraceptive use and cigarette smoking. Lancet. 2003;362:185–91. 39. Rosenberg L, Palmer JR, Rao RS, et al. Low-dose oral contraceptive use and the risk of myocardial infarction. Arch Intern Med. 2001;161:1065–70. 40. Doring A, Frohlich M, Lowel H, et al. Third generation oral contraceptive use and cardiovascular risk factors. Atherosclerosis. 2004; 172:281–6. 41. National Cancer Institute. Cigars: Health Effects and Trends. Bethesda, MD: U.S. Department of Health and Human Services,

54

42.

43. 44.

45.

46. 47.

48. 49.

50.

51.

52.

53.

54.

55.

56.

57.

58.

59.

60.

61.

National Institutes of Health, 1998. Smoking and Tobacco Control Monograph No. 9. Iribarren C, Tekawa IS, Sidney S, et al. Effect of cigar smoking on the risk of cardiovascular disease, chronic obstructive pulmonary disease, and cancer in men. N Engl J Med. 1999;340:1773–80. Nyboe J, Jensen G, Appleyard M, et al. Smoking and the risk of first acute myocardial infarction. Am Heart J. 1991;122:438–47. Carstensen JM, Pershagen G, Eklund G. Mortality in relation to cigarette and pipe smoking: 16 years’ observation of 25,000 Swedish men. J Epidemiol Community Health. 1987;41:166–72. Shaper AG, Wannamethee SG, Walker M. Pipe and cigar smoking and major cardiovascular events, cancer incidence and all cause mortality in middle-aged British men. Int J Epidemiol. 2003;32: 802–8. Castleden CM, Cole PV. Inhalation of tobacco smoke by pipe and cigar smokers. Lancet. 1973;2(7819):21–2. Wald NJ, Watt HC. Prospective study of effect of switching from cigarettes to pipes or cigars on mortality from three smoking related disease. BMJ. 1997;314:1860–63. Gupta R, Gurm H, Bartholomew JR. Smokeless tobacco and cardiovascular risk. Arch Intern Med. 2004;164:1845–49. Bolinder GM, Ahlborg BO, Lindell JH. Use of smokeless tobacco: blood pressure elevation and other health hazards found in a largescale population survey. J Intern Med. 1992;232:327–34. Bolinder G, Alfredsson L, Englund A, et al. Smokeless tobacco use and increased cardiovascular mortality among Swedish construction workers. Am J Public Health. 1994;84:399–404. Henley SJ, Thun MJ, Connell C, et al. Two large prospective studies of mortality among men who use snuff or chewing tobacco (United States). Cancer Causes Control. 2005;16:347–58. Critchley JA, Unal B. Is smokeless tobacco a risk factor for coronary heart disease? A systematic review of epidemiological studies. Eur J Cardiovasc Prev Rehab. 2004;11:101–12. Kawachi I, Colditz GA, Stampfer MJ, et al. Smoking cessation in relation to total mortality rates in women: a prospective cohort study. Ann Intern Med. 1993;119:992–1000. Goldenberg I, Jonas M, Tenenbaum A, et al. Current smoking, smoking cessation, and the risk of sudden cardiac death in patients with coronary artery disease. Arch Intern Med. 2003;163:2301–5. Stokes J, Kannel WB, Wolf PA, et al. The relative importance of selected risk factors for various manifestations of cardiovascular disease among men and women from 35 to 64 years old: 30 years of follow-up in the Framingham Study. Circulation. 1987;75[6 Pt 2]: V65–73. U.S. Department of Health and Human Services. Women and Smoking: A Report of the Surgeon General. Rockville, MD: U.S. Public Health Service, Office of the Surgeon General; 2001. Tomatis LA, Fierens EE, Verbrugge GP. Evaluation of surgical risk in peripheral vascular disease by coronary arteriography: A series of 100 cases. Surgery. 1972;71:429–35. Zheng ZJ, Sharrett AR, Chambless LE, et al. Associations of anklebrachial index with clinical coronary heart disease, stroke and preclinical carotid and popliteal atherosclerosis: the Atherosclerosis Risk in Communities (ARIC) Study. Atherosclerosis. 1997;131:115–25. Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med. 1992;326:381–6. Newman AB, Shemanski L, Manolio TA, et al. Ankle-arm index as a predictor of cardiovascular disease and mortality in the Cardiovascular Health Study Group. Arteriolscler Thromb Vasc Biol. 1999;19:538–45. U.S. Public Health Service. The Health Consequences of Smoking: Cardiovascular Disease: A Report of the Surgeon General. Washington, DC: Public Health Service, Office on Smoking and Health; 1983. DHHS Publication (PHS) 84-50204.

Tobacco: Health Effects and Control

987

62. Howard G, Wagenknecht LE, Burke GL, et al. Cigarette smoking and the progression of atherosclerosis. JAMA. 1998;279:119–24. 63. Levey LA. Smoking and peripheral vascular disease. Clin Podiatr Med Surg. 1992;9:165–71. 64. Auerbach O, Garfinkel L. Atherosclerosis and aneurysm of aorta in relation to smoking habits and age. Chest. 1980;78:805–9. 65. Lee AJ, Fowkes FG, Carson MN, et al. Smoking, atherosclerosis and risk of abdominal aortic aneurysm. Eur Heart J. 1997;18:671–76. 66. American Heart Association. Heart disease and stroke statistics— 2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2007;115:69–171. 67. Robbins AS, Manson JE, Lee IM, et al. Cigarette smoking and stroke in a cohort of U.S. male physicians. Ann Intern Med. 1994;120: 458–62. 68. Shaper AG, Phillips AN, Pocock SJ, et al. Risk factors for stroke in middle aged British men. BMJ. 1991;302:1111–5. 69. Shinton R, Beevers G. Meta-analysis of relation between cigarette smoking and stroke. BMJ. 1989;298:789–94. 70. Haheim LL, Holme I, Jermann IH, et al. Smoking habits and risk of fatal stroke: 18 years follow up of the Oslo study. J Epidemiol Community Health. 1996;50:621–4. 71. Wannamethee SG, Shaper AG, Whincup PH, et al. Smoking cessation and the risk of stroke in middle-aged men. JAMA. 1995;274:155–60. 72. Kannel WB. New perspectives on cardiovascular risk factors. Am Heart J. 1987;114(1 pt 2):213–9. 73. Bronner LL, Kanter DS, Manson JE. Primary prevention of stroke. N Engl J Med. 1995;333:1392–1400. 74. Petitti DB, Sidney S, Bernstein A, et al. Stroke in users of low-dose oral contraceptives. N Engl J Med. 1996;335:8–15. 75. Allen DR, Browse NL, Rutt DL, et al. The effect of cigarette smoke, nicotine, and carbon monoxide on the permeability of the arterial wall. J Epidemiol Community Health. 1988;39:286–93. 76. Celermajer DS, Sorensen, KE, Georgakopoulos, et al. Cigarette smoking is associated with dose-related and potentially reversible impariment of endothelium-dependent dilation in healthy young adults. Circulation. 1993;88(5 pt 1):2149–55. 77. Fusegawa Y, Goto S, Handa S, et al. Platelet spontaneous aggregation in platelet-rich plasma is increased in habitual smokers. Thrombosis Research. 1999;93:271–8. 78. Spagnoli LG, Mauriello A, Palmieri G, et al. Relationships between risk factors and morphological patterns of human carotid atherosclerotic plaques: a multivariate discriminate analysis. Atherosclerosis. 1994;108:39–60. 79. Toschi V, Gallo R, Lettino M, et al. Tissue factor modulates the thrombenicity of human atherosclerotic plaques. Circulation. 1997;95:594–9. 80. Burke AP, Farb A, Malcom GT, et al. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med. 1997;36:1276–82. 81. Friedman GD, Siegelaub AB, Seltzer CC, et al. Smoking habits and the leukocyte count. Arch Environ Health. 1973;26:137–43. 82. Kuller LH, Tracy RP, Shaten J, et al. Relation of C-reactive protein and coronary heart disease in the MRFIT nested case-control study. Multiple Risk Factor Intervention Trial. Am J Epidemiol. 1996;144:537–47. 83. Ridker PM, Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med. 1997;336:973–9. 84. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation. 2001;103:1813–8. 85. Di Napoli M, Papa F, Bocola V. C-reactive protein in ischemic stroke: an independent prognostic factor. Stroke. 2001;32:917–24.

988

Behavioral Factors Affecting Health

86. Craig WY, Palomaki GE, Haddow JE. Cigarette smoking and serum lipid and lipoprotein concentrations: an analysis of published data. BMJ. 1989;298:784–8. 87. Krupski WC. The peripheral vascular consequences of smoking. Ann Vasc Surg. 1991;5:291–304. 88. Fortmann SP, Haskell WL, Williams PT. Changes in plasma high density lipoprotein cholesterol after changes in cigarette use. Am J Epidemiol. 1986;124:706–10. 89. Steinberg D, Parthasarathy S, Carew TE, et al. Beyond cholestersol. Modifactions of low-density lipoprotein that increase its atherogenicity. N Engl J Med. 1989;320:915–24. 90. Benowitz NL, Gourlay SG. Cardiovascular toxicity of nicotine: implications for nicotine replacement therapy. J Am Coll Cardiol. 1997;29:1422–31. 91. Cruickshank JM, Neil-Dwyer G, Dorrance DE, et al. Acute effects of smoking on blood pressure and cerebral blood flow. J Hum Hypertens. 1989;3:443–9. 92. Yamashita K, Kobayashi S, Yamaguchi S, et al. Effect of smoking on regional cerebral flow in the normal aged volunteers. Gerontology. 1988;34:199–204. 93. Rogers RL, Meyer JS, Shaw TG, et al. Cigarette smoking decreases cerebral blood flow suggesting increased risk for stroke. JAMA. 1983;250:2796–800. 94. American Cancer Society. Cancer Facts and Figures, 2007. Atlanta, GA: American Cancer Society; 2007:1–52. 95. Vincent RG, Pickren JW, Lane WW, et al. The changing histopathology of lung cancer: a review of 1682 cases. Cancer. 1977;39:1647–55. 96. Churg A. Lung cancer cell type and occupational exposure. In: Samet JM, ed. Epidemiology of Lung Cancer. New York, NY: Marcel Dekker; 1994:413–36. 97. Travis WD, Travis LB, Devesa SS. Lung Cancer. Cancer. 1995;75(1 Suppl):191–202. 98. Wingo PA, Reis LA, Giovino GA, et al. Annual report to the nation on the status of cancer, 1973–1996. With a special section on lung cancer and tobacco smoking. J Natl Cancer Inst. 1999;91:675–90. 99. Hoffmann D, Hoffmann I. The changing cigarette. 1950–1995. J Toxicol Environ Health. 1997;50:307–64. 100. Wynder EL, Muscat JE. The changing epidemiology of smoking and lung cancer histology. Environ Health Perspect. 1995;103(Suppl 8): 143–8. 101. National Cancer Institute. The FTC Cigarette Test Method for Determining Tar, Nicotine, and Carbon Monoxide Yields of U.S. Cigarettes. Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health; 1996. Smoking and Tobacco Control Monograph 7. NIH Publication 96-4028. 102. Hecht SS. Tobacco smoke carcinogens and lung cancer. J Natl Cancer Inst. 1999;91:1194–210. 103. Levi F, Franceschi S, La Vecchia C, et al. Lung carcinoma trends by histologic type in Vaud and Neuchatel, Switzerland, 1974–1994. Cancer. 1997;79:906–14. 104. Thun MJ, Lally CA, Flannery JT, et al. Cigarette smoking and changes in the histopathology of lung cancer. J Natl Cancer Inst. 1997;89:1580–6. 105. Ries LAG, Eisner MP, Kosary CL, et al. SEER Cancer Statistics Review, 1975–2001. Bethesda, MD: National Cancer Institute; 2004. 106. American Cancer Society. Cancer Facts & Figures, 2005. Atlanta, GA: 2005:1–61. 107. U.S. Department of Health, Education, and Welfare. Smoking and Health: Report of the Advisory Committee to the Surgeon General of the Public Health Service. Washington, DC: Public Health Service; 1964. PHS Publication 1103. 108. Ochsner A. My first recognition of the relationship of smoking and lung cancer. Prev Med. 1973;2:611–4.

109. Wynder EL, Mushinski MH, Spivak JC. Tobacco and alcohol consumption in relation to the development of multiple primary cancers. Cancer. 1977;40:1872–8. 110. Doll R, Hill AB. Lung cancer and other causes of death in relation to smoking; a second report on the mortality of British doctors. Br Med J. 1956;2:1071–81. 111. Lange P, Groth S, Nyboe J, et al. Decline of the lung function related to the type of tobacco smoked and inhalation. Thorax. 1990;45, 22–6. 112. Doll R, Peto R. Cigarette smoking and bronchial carcinoma: dose and time relationships among regular smokers and lifelong nonsmokers. J Epidemiol Community Health. 1978;32:303–13. 113. Hammond EC. Smoking in relation to the death rates of one million men and women. In: National Cancer Institute. Epidemiological Approaches to the Study of Cancer and Other Chronic Disease. Washington, DC: National Cancer Institute; 1966. National Cancer Institute monograph, 19. 114. International Agency for Research on Cancer. Tobacco Smoke and Involuntary Smoking. Lyon, France: International Agency for Research on Cancer; 2004. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, 83. 115. Samet JM. The changing cigarette and disease risk: current status of the evidence. In: The FTC Cigarette Method for Determining Tar, Nicotine and Carbon Monoxide Yields of U.S. Cigarettes: Report of the NCI Expert Committee. Bethesda, MD: U.S. Department of Health and Human Services, Public Health Service; 1996. 116. Hammond EC. The long term benefits of reducing tar and nicotine in cigarettes. In: Gori GB, Bock FG, eds. A Safe Cigarette? Banbury Report 3, Proceedings of a Meeting Held at the Banbury Center, Cold Springs Harbor Laboratory, NY, October 14–16, 1979. New York, NY: Cold Spring Harbor Laboratory; 1980:13–8. 117. Tang JL, Morris JK, Wald NJ, et al. Mortality in relation to tar yield of cigarettes: a prospective study of four cohorts. BMJ. 1995;311: 1530–3. 118. Kaufman DW, Palmer JR, Rosenberg L, et al. Tar content of cigarettes in relation to lung cancer. Am J Epidemiol. 1989;129:703–11. 119. National Cancer Institute. Risks Associated with Smoking Cigarettes with Low-Machine Measured Yields of Tar and Nicotine. Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health; 2001. Smoking and Tobacco Control Monograph 13. NIH Publication 02-5074. 120. National Cancer Institute; Changes in Cigarette-Related Disease Risk and Their Implications for Prevention and Control. Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health; 1997. Smoking and Tobacco Control Monograph 8. NIH Publication 97-4213. 121. Chow WH, Schuman LM, McLaughlin JK, et al. A cohort study of tobacco use, diet, occupation and lung cancer mortality. Cancer Causes Control. 1992;3:247–54. 122. Doll R, Peto R. Mortality in relation to smoking: 20 years’ observations on male British doctors. Br Med J. 1976;2:1525–36. 123. Shapiro JA, Jacobs EJ, Thun MJ. Cigar smoking in men and risk of death from tobacco-related cancers. J Natl Cancer Inst. 2000;92:333–7. 124. Nelson DE, Davis RM, Chrismon JH, et al. Pipe smoking in the United States, 1965–1991: prevalence and attributable mortality. Prev Med. 1996;25:91–9. 125. Boffetta P, Pershagen G, Jockel KH, et al. Cigar and pipe smoking and lung cancer risk: A multicenter study from Europe. J Natl Cancer Inst. 1999;91:697–701. 126. Lange P, Nyboe J, Appleyard M, et al. Relationship of the type of tobacco and inhalation pattern to pulmonary and total mortality. Eur Respir J. 1992;5:1111–7. 127. Armitage P, Doll R. The age distribution of cancer and a multistage theory of carcinogenesis. Brit J Cancer. 1954;8:1–12.

54 128. Denissenko MF, Chen JX, Tang MS, et al. Cysotine methylation determines hot spots of DNA damage in the human P53 gene. Proc Natl Acad Sci USA. 1997;94:3893–8. 129. Denissenko MF, Pao A, Moon-shong T, et al. Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hotspots in P53. Science. 1996;274:430–2. 130. Kashiwabara K, Oyama T, Sano T, et al. Correlation between methylation status of the p16/CDKN2 gene and the expression of p16 and Rb proteins in primary non-small cell lung cancers. Int J Cancer. 1998;79:215–20. 131. Franceschi S, Barra S, La Vecchia C, et al. Risk factors for cancer of the tongue and the mouth. a case-control study from northern Italy. Cancer. 1992;70:2227–33. 132. McLaughlin JK, Hrubec Z, Blot WJ, et al. Smoking and cancer mortality among U.S. veterans: a 26-year follow-up. Int J Cancer. 1995;60:190–3. 133. International Agency for Research on Cancer. Smokeless Tobacco and Some Related Nitrosamines. Lyon, France: 2005. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, 89. 134. Council on Scientific Affairs. Health effects of smokeless tobacco. JAMA. 1986;255:1038–44. 135. U.S. Department of Health and Human Services. The Health Consequences of Using Smokeless Tobacco. A Report of the Surgeon General. Bethesda, MD: Public Health Service; 1986. DHHS Publication 86-2874. 136. International Agency for Research on Cancer. Cancer Monodial. Available at http://www-dep.iarc.fr. Accessed August 11, 2005. 137. Winn DM. Tobacco use and oral diseae. J Dental Educ. 2001;65: 306–12. 138. Schlecht NF, Franco EL, Pintos J, et al. Effect of smoking cessation and tobacco type on the risk of cancers of the upper aerodigestive tract in Brazil. Epidemiol. 1999;10:412–8. 139. Boffetta P, Aagnes B, Weiderpass E, et al. Smokeless tobacco use and risk of cancer of the pancreas and other organs. Int J Cancer. 2005;114:992–5. 140. Califano J, van der Reit P, Westra W, et al. Genetic progression model for head and neck cancer: implications for field cancerization. Cancer Research. 1996;56:2488–92. 141. U.S. Department of Health and Human Services. 9th Report on Carcinogens. Research Triangle Park, NC: U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program; 2000. 142. Kuratsune M, Kohchi S, Horie A. Carcinogenesis in the esophagus. I. Penetration of benzo[a]pyrene and other hydrocarbons into the esophageal mucosa. Gann. 1965;56:177–87. 143. Brennan JA, Boyle JO, Koch WM, et al. Association between cigarette smoking and mutation of the p53 gene in squamous-cell carcinoma of the head and neck. N Engl J Med. 1995;332:712–7. 144. La Vecchia C, Franceschi S, Bosetti, F, et al. Time since stopping smoking and the risk of oral and pharyngeal cancers [letter]. J Natl Cancer Inst. 1999;91:726–8. 145. Gammon MD, Schoenberg JB, Ashan H, et al. Tobacco, alcohol, and socioeconomic status and adenocarcinomas of the esophagus and gastric cardia. J Natl Cancer Inst. 1997;89:1277–84. 146. Lagergren J, Bergstrom R, Lindgren A, et al. The role of tobacco, snuff and alcohol use in the aetiology of cancer of the oesophagus and gastric cardia. Int J Cancer. 2000;85:340–6. 147. Kabat GC, Ng SKC, Wynder EL. Tobacco, alcohol intake, and diet in relation to adenocarcinoma of the esophagus and gastric cardia. Cancer Causes Control. 1993;4:123–32. 148. Silverman DT, Morrison AS, Devesa SS. Bladder cancer. In: Schottenfeld D, Fraumeni JF Jr, eds. Cancer Epidemiology and Prevention. New York, NY: Oxford University Press; 1996: 1156–79.

Tobacco: Health Effects and Control

989

149. McLaughlin JK, Blot WJ, Devesa SS, et al. Renal cancer. In: Schottenfeld D, Fraumeni JF Jr, eds. Cancer Epidemiology and Prevention. New York, NY: Oxford University Press; 1996:1142–55. 150. Yamasaki E, Ames BN. Concentration of mutagens from urine by absorption with the nonpolar resin XAD–2: cigarette smokers have mutagenic urine. Proc Natl Acad Sci USA. 1977;74:3555–9. 151. Shiao YH, Rice JM, Anderson LM. von Hippel Lindau gene mutations in N-nitrosodimethylamine-induced rat renal epithelial tumors. J Natl Cancer Inst. 1998;90:1720–3. 152. Public Health Service, Office on Smoking and Health. The Health Consequences of Smoking: Cancer. A Report of the Surgeon General. Rockville, MD: U.S. Department of Health and Human Services; 1982. DHHS Publication (PHS) 82-50179. 153. Muscat JE, Stellman SD, Hoffmann D, et al. Smoking and pancreatic cancer in men and women. Cancer Epidemiol Biomarkers Prevention. 1997;6:15–9. 154. Alguacil J, Silverman DT. Smokeless and other noncigarette tobacco use and pancreatic cancer: a case-control study based on direct interviews. Cancer Epidemiol Biomarkers Prevention. 2004; 13:55–8. 155. Gajalakshmi CK, Shanta V. Lifestyle and risk of stomach cancer: a hospital-based case control study. Int J Epidemiol. 1996;25:1146–53. 156. Chao A, Thun MJ, Henley J, et al. Cigarette smoking, use of other tobacco products and stomach cancer mortality in U.S. adults: The Cancer Prevention Study II. Int J Cancer. 2002;101:380–9. 157. Stryker WS, Kaplan LA, Stein EA, et al. The relationship of diet, cigarette smoking, and alcohol consumption to plasma betacarotene and alpha-tocopherol levels. Am J Epidemiol. 1988; 127:283–96. 158. Bosch FX, Manos MM, Munoz N, et al. Prevalence of human papillomavirus in cervical cancer: a worldwide perspective. J Natl Cancer Inst. 1995;87:796–802. 159. Walboomers JM, Jacobs MV, Manos MM, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol. 1999;189:12–9. 160. Moscicki AB, Hills N, Shiboski S, et al. Risks for incident human papillomavirus infection and low-grade squamous intraepithelial lesion development in young females. JAMA. 2001;285:2995– 3002. 161. Castle PE, Wacholder S, Lorincz AT, et al. A prospective study of high-grade cervical neoplasia risk among human papillomavirusinfected women. J Natl Cancer Inst. 2002;94:1406–14. 162. McCann MF, Irwin DE, Walton LA, et al. Nicotine and cotinine in the cervical mucus of smokers, passive smokers, and nonsmokers. Cancer Epidemiol Biomarkers Prevention. 1992;1:125–9. 163. Prokopczyk B, Cox JE, Hoffmann D, et al. Identification of tobacco-specific carcinogen in the cervical mucus of smokers and nonsmokers. J Natl Cancer Inst. 1997;89:868–73. 164. Holly EA, Petrakis NL, Friend NF, et al. Mutagenic mucus in the cervix of smokers. J Natl Cancer Inst. 1986;76:983–6. 165. Phillips DH, She MN. DNA adducts in cervical tissue of smokers and non-smokers. Mutation Res. 1994;313:277–84. 166. Siegel M. Smoking and leukemia: evaluation of a causal hypothesis. Am J Epidemiol. 1993;138:1–9. 167. Brownson RC, Novotny TE, Perry MC. Cigarette smoking and adult leukemia. A meta-analysis. Arch Intern Medicine. 1993;153: 469–75. 168. Wallace L. Environmental exposure to benzene: an update. Environ Health Perspectives. 1996;104(Suppl 6):1129–36. 169. Winn DM. Epidemiology of cancer and other systemic effects associated with the use of smokeless tobacco. Adv Dent Res. 1997;11: 313–21. 170. Mannino DM, Homa DM, Akinbami LJ, et al. Chronic obstructive pulmonary disease surveillance—United States, 1971–2000. MMWR. 2002;51(SS–6):1–16.

990

Behavioral Factors Affecting Health

171. Troisi RT, Speizer FE, Rosner B, et al. Cigarette smoking and incidence of chronic bronchitis and asthma in women. Chest. 1995;108:1557–61. 172. Dean G, Lee PN, Todd GF, et al. Report on a second retrospective mortality study in North-east England. Part i. Factors related to mortality from lung cancer, bronchitis, heart disease and stroke in Cleveland County, with a particular emphasis on the relative risks associated with smoking filter and plain cigarettes. Research Paper 14. London, England: Tobacco Research Council; 1977. 173. Beck GJ, Doyle CA, Schachter EN. Smoking and lung function. Am Rev Respir Dis. 1981;123:149–55. 174. Walter S, Jeyaseelan L. Impact of cigarette smoking on pulmonary function in non-allergic subjects. Natl Med J India. 1992;5:211–3. 175. U.S. Department of Health and Human Services. The Health Consequences of Smoking: Chronic Obstructive Lung Disease. Washington, DC: Public Health Service, Office on Smoking and Health; 1984. 176. Brown CA, Woodward M, Tunstall-Pedoe H. Prevalence of chronic cough and phlegm among male cigar and pipe smokers. Results of the Scottish Heart Health Study. Thorax. 1993;48: 1163–7. 177. Higgins MW, Enright PL, Kronmal RA, et al. Smoking and lung function in elderly men and women. The Cardiovascular Health Study. JAMA. 1993;269:2741–8. 178. Rogot E, Murray JL. Smoking and causes of death among U.S. veterans: 16 years of observation. Public Health Rep. 1980;95:213–22. 179. U.S. Department of Health and Human Services. Preventing Tobacco Use among Young People: A Report of the Surgeon General. Atlanta, GA: Centers for Disease Control and Prevention, Office on Smoking and Health; 1994. 180. Kahrilas PJ. Cigarette smoking and gastroesophageal reflux disease. Dig Dis. 1992;10:61–71. 181. Kuipers EJ, Thijs JC, Festen HP. The prevalence of Helicobacter pylori in peptic ulcer disease. Aliment Pharmacol Ther. 1995;9(Suppl 2):59–69. 182. Borody TJ, George LL, Brandl S, et al. Helicobacter pylorinegative duodenal ulcer. Am J Gastroenterology. 1991;86:1154–7. 183. Borody TJ, Brandl S, Andrews P, et al. Helicobacter pylorinegative gastric ulcer. Am J Gastroenterol. 1992;87:1403–6. 184. Eastwood GL. Is smoking still important in the pathogenesis of peptic ulcer disease? J Clin Gastroenterol. 1997;25(Suppl 1):S1–7. 185. Tytgat GN, Noach LA, Rauws EA. Helicobacter pylori infection and duodenal ulcer disease. Gastroenterol Clin North Am. 1993;22: 127–39. 186. Mandel I. Smoke signals: an alert for oral disease. J Am Dental Assoc. 1994;125:872–8. 187. Akef J, Weine FS, Weissman DP. The role of smoking in the progression of periodontal disease: a literature review. Compend Contin Educ Dent. 1992;13:526–31. 188. Tomar SL, Asma S. Smoking-attributable periodontitis in the United States: findings from NHANES III. J Periodontol. 2000;71: 743–51. 189. Fox CH. New considerations in the prevalence of periodontal disease. Curr Opin Dent. 1992;2:5–11. 190. Albandar JM, Streckfus CF, Adesanya MR, et al. Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss. J Periodontol. 2000;71:1874–81. 191. Krall EA, Garvey AJ, Garcia RI. Alveolar bone loss and tooth loss in male cigar and pipe smokers. J Am Dent Assoc. 1999;130:57–64. 192. Johnson GK, Slach NA. Impact of tobacco use on periodontal status. J Dent Educ. 2001;65:313–21. 193. Tomar SL, Winn DM. Chewing tobacco use and dental caries among U.S. men. J Am Dent Assoc. 1999;130:1601–10.

194. National Cancer Institute. Tobacco effects in the mouth: a National Cancer Institute and National Institute of Dental Research Guide for Health Professionals. Bethesda, MD: National Institutes of Health; 1993. NIH Publication 93-3330. 195. National Cancer Institute, Smokeless Tobacco or Health: an International Perspective. Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health; 1992: Smoking and Tobacco Control Monograph 2. NIH Publication 92-3461. 196. Christen AG, Swanson BZ, Glover ED, et al. Smokeless tobacco: the folklore and social history of snuffing, sneezing, dipping, and chewing. J Am Dent Assoc. 1982;105:821–9. 197. NIH Consensus Development Panel. National Institutes of Health consensus statement: health implications of smokeless tobacco use. Biomed Pharmacother. 1988;42:93–8. 198. Riley JL, Tomar SL, Gilbert GH. Smoking and smokeless tobacco: Increased risk for oral pain. J Pain. 2004;5:218–25. 199. Greer RO, Poulson TC. Oral tissue alterations associated with the use of smokeless tobacco by teenagers. Oral Surg Oral Med Oral Pathol. 1983;56:275–84. 200. Whalley LJ, Fox HC, Deary IJ, et al. Childhood IQ, smoking, and cognitive change from age 11 to 64 years. Addict Behav. 2005;30: 77–88. 201. Substance Abuse and Mental Health Services Administration. Results from the 2003 National Survey on Drug Use and Health: National Findings. Rockville, MD: Office of Applied Studies; 2004. NSDUH Series H-25, DHHS Publication SMA 04-3964. Available at www.oas.samhsa.gov/nhsda/2k3tabs/Sect7peTabs1to57.htm. Accessed August, 5, 2005. 202. Wingerd J, Christianson R, Lovitt WV, et al. Placental ratio in white and black women: relation to smoking and anemia. Am J Obstet Gynecol. 1976;124:671–5. 203. Gupta PC, Ray CS. Smokeless tobacco and health in India and South Asia. Respirology. 2003;8:419–31. 204. England LJ, Levine RJ, Mills JL, et al. Adverse pregnancy outcomes in snuff users. Am J Obstet Gynecol. 2003;189:939–43. 205. Kleinman JC, Pierre MB Jr, Madans JH, et al. The effects of maternal smoking on fetal and infant mortality. Am J Epidemiol. 1988;127:274–82. 206. Salihu HM, Aliyu MH, Pierre-Louis BJ, et al. Levels of excess infant deaths attributable to maternal smoking during pregnancy in the United States. Matern Child Health J. 2003;7:219–27. 207. Werler MM. Teratogen update: smoking and reproductive outcomes. Teratology. 1997;55:382–8. 208. Slotkin TA, Lappi SE, McCook EC, et al. Loss of neonatal hypoxia tolerance after prenatal nicotine exposure: implications for sudden infant death syndrome. Brain Res Bull. 1995;38:69–75. 209. Windham GC, Elkin EP, Swan SH, et al. Cigarette smoking and effects on menstrual function. Obstet Gynecol. 1999;93:59–65. 210. Arday DR, Giovino GA, Schulman J, et al. Cigarette smoking and self-reported health problems among U.S. high school seniors, 1982–1989. Am J Health Promotion. 1995;10:111–6. 211. Centers for Disease Control and Prevention. Reasons for tobacco use and symptoms of nicotine withdrawal among adolescent and young adult tobacco users—United States, 1993. MMWR. 1994;43:45–50. 212. Centers for Disease Control and Prevention. Symptoms of substance dependence associated with use of cigarettes, alcohol, and illicit drugs—United States, 1991–1992. MMWR. 1995;44:830–1, 837–9. 213. DiFranza JD, Rigotti NA, McNeill AD, et al. Initial symptoms of nicotine dependence in adolescents. Tob Control. 2000;9:313–9. 213a. U.S. Department of Health and Human Services. The Health Consequences of Involuntary Exposure to Tobacco Smoke. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health

54

213b. 213c.

214.

215.

216.

217.

218.

219.

220.

221.

222.

223.

224.

225.

226.

227.

and Human Services, Centers for Disease Control and Prevention, Office on Smoking and Health; 2006. Behan DF, Eriksen MP, Lin Y. Economic Effects of Environmental Tobacco Smoke. Schaumburg, IL: Society of Actuaries; 2005. California Air Resources Board, California Environmental Protection Agency. Final regulation order: Identification of environmental tobacco smoke as a toxic air contaminant. Available at http://www.arb.ca.gov/regact/ets2006/etsfro.pdf. Accessed April 4, 2007. U.S. Environmental Protection Agency. Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders. The Report of the U.S. Environmental Protection Agency. Bethesda, MD: National Institutes of Health; Office of Research and Development, Office of Air and Radiation; 1993. NIH Publication 98–3605. Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. Proposed identification of environmental tobacco smoke as a toxic air contaminant. 2005. Available at http://www.oehha.ca.gov/air/environmental_tobacco/ 2005 etsfinal.html. Accessed April 4, 2007. Available at http:// repositories.cdlib.org/ context/tc/article/1194/type/pdf/viewcontent/. Accessed April 27. 2007. Repace J. Respirable particles and carcinogens in the air of Delaware hospitality venues before and after a smoking ban. J Occup Environ Med. 2004;46:887–905. Whincup PH, Gilg JA, Emberson JR, et al. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ. 2004:329:200–5. Pirkle JL, Flegal KM, Bernert JT, et al. Exposure of the U.S. population to environmental tobacco smoke. JAMA. 1996;275:1233–40. Centers for Disease Control and Prevention. State-specific prevalence of cigarette-smoking adults, and children’s and adolescents’ exposure to environmental tobacco smoke—United States, 1996. MMWR. 1997;46:1038-43. American Legacy Foundation. Second Hand Smoke: Youth Exposure and Adult Attitudes. Washington, DC: American Legacy Foundation, 2005. First Look Report 14. Available at http://www. americanlegacy.org/americanlegacy/skins/alf/display.aspx?Action=d isplay_page&mode=User&ModuleID=8cde2e88-3052-448c-893dd0b4b14b31c4&ObjectID=67f143bf-4dac-400e-a0055f3577160f69. Accessed August 5, 2005. Greenberg RA, Haley NJ, Etzel RA, et al. Measuring the exposure of infants to tobacco smoke: nicotine and cotinine in urine and saliva. N Engl J Med. 1984;310:1075-8. National Research Council, Committee on Passive Smoking. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: National Academy Press; 1986. U.S. Department of Health and Human Services. The Health Consequences of Involuntary Smoking. A Report of the Surgeon General. Rockville, MD: Centers for Disease Control and Prevention, Office on Smoking and Health; 1986. DHHS Publication (CDC) 87-8398. California Environmental Protection Agency. Health Effect of Exposure to Environmental Tobacco Smoke. Sacramento, CA: Office of Environmental Health Hazard Assessment; 1997. Yolton K, Dietrich K, Auinger P, et al. Exposure to environmental tobacco smoke and cognitive abilites among U.S. children and adolescents. Environ Health Perspect. 2005;113:98–103. Mannino DM, Siegel M, Husten C, et al. Environmental tobacco smoke exposure and health effects in children: results from the 1991 National Health Interview Survey. Tob Control. 1986;5:13–8. Gilliland FD, Berhane K, Islam T, et al. Environmental tobacco smoke and absenteeism related to respiratory illness in school children. Am J Epidemiol. 2003;157:861–9.

Tobacco: Health Effects and Control

991

228. Klonoff-Cohen HS, Edelstein SL, Lefkowitz ES, et al. The effect of passive smoking and tobacco exposure through breast milk on sudden infant death syndrome. JAMA. 1995;273:795–8. 229. Schoendorf KC, Kiely JL. Relationship of sudden infant death syndrome to maternal smoking during and after pregnancy. Pediatrics. 1992;90:905–8. 230. Blair PS, Fleming PJ, Bensley D, et al. Smoking and the sudden infant death syndrome: results from 1993–1995 case-control study for confidential inquiry into stillbirths and deaths in infancy. BMJ. 1996;313:195–8. 231. U.S. Environmental Protection Agency. Environmental Cancer and Heart and Lung Disease: Annual Report to Congress (8th). Rockville, MD: Task Force on Environmental Cancer and Heart and Lung Disease; 1985. 232. Mannino DM, Siegel M, Rose D, et al. Environmental tobacco smoke exposure in the home and worksite and health effects in adults: results from the 1991 National Health Interview Survey. Tob Control. 1997;6:296–305. 233. Blanc PD, Ellbjar S, Janson C, et al. Asthma related work disability in Sweden. The impact of workplace exposures. Am J Respir Crit Care Med. 1999;160:2028–33. 234. Enstrom JE, Kabat GC. Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960–1998. BMJ. 2003;326:1057. 235. Steenland K, Thun M, Lally C, et al. Environmental tobacco smoke and coronary heart disease in the American Cancer Society CPS-II cohort. Circulation. 1996;94:622–8. 236. Glantz SA, Parmeley WW. Passive smoking and heart disease: mechanisms and risk. JAMA. 1995;273:1047–53. 237. He J, Vupputuri S, Allen K, et al. Passive smoking and the risk of coronary heart disease: a meta-analysis of epidemiologic studies. N Engl J Med. 1999;340:920–6. 238. Sargent RP, Shepard RM, Glantz SL. Reduced incidence of admissions for myocardial infarction associated with public smoking ban: before and after study. BMJ. 2004;328:977–80. 238a. Bartecchi, C, Alsever, RN, Nevin-Woods, C, et al. Reduction in the incidence of acute myocardial infarction associated with a citywide smoking ordiance. Circulation. 2006;114:1490–96. 238b. Barone-Adesi, F, Vizzini, L, Merletti, F, et al. short-term effects of Italian smoking regulation on rates of hospital admission for acute myocardial infarction. Eur Heart J. 2006; 20:2468–3472. 239. Capehart T. Tobacco Outlook. Washington, DC: U.S. Department of Agriculture; 2006. Publication TBS–261. 240. Capehart T. Tobacco Situation and Outlook Yearbook. Washington, DC: U.S Department of Agriculture; 2006. Publication TBS2006. 241. Giovino GA, Schooley MW, Zhu BP, et al. Surveillance for selected tobacco-use behaviors—United States, 1900–1994. MMWR. 1994:43(SS–3):1–43. 242. Centers for Disease Control and Prevention. Cigarette smoking among adults—United States, 1995. MMWR. 1997;46:1217–20. 243. Centers for Disease Control and Prevention. Cigarette smoking among adults—United States, 2005. MMWR. 2006;55:1145–48. 244. Schiller JS, Coriaty Nelson Z, Hao C, et al. Early Release of Selected Estimates Based on Data from the January–September 2006 National Health Interview Survey. Hyattsville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics; 2007. Available at http://www.cdc.gov/nchs/data/nhis/earlyrelease/ 200703_08.pdf. Accessed April 15, 2007. 245. Centers for Disease Control and Prevention. Cigarette Smoking Among Adults—United States, 2002. MMWR. 2004;53:427–31. 246. Centers for Disease Control and Prevention. State-specific prevalence of current cigarette smoking among adults—United States, 2005. MMWR. 2006;55:1148–51.

992

Behavioral Factors Affecting Health

247. National Center for Health Statistics, National Health Interview Survey, public use data tapes, 2005. 248. Husten CG, Chrismon JH, Reddi MN. Trends and effects of cigarette smoking among girls and women in the United States, 1965–1993. J Am Med Womens Assoc. 1996;51:11–8. 249. Centers for Disease Control and Prevention. Smoking cessation during previous year among adults—United States, 1990 and 1991. MMWR. 1993;42:504–7. 250. Jarvis MJ. Gender differences in smoking cessation: real or myth. Tob Control. 1994;3:324–8. 251. Centers for Disease Control and Prevention. Cigarette smoking among adults—United States, 2001. MMWR. 2003;52:953–6. 252. Zhu BP, Giovino GA, Mowery PD, et al. The relationship between cigarette smoking and education revisited: implications for categorizing persons’ educational status. Am J Public Health. 1996;86: 1582–9. 253. U.S. Department of Health and Human Services. Tobacco Use among U.S. Racial/Ethnic Minority Groups: A Report of the Surgeon General. Atlanta, GA: Centers for Disease Control and Prevention, Office on Smoking and Health; 1998. DHHS Publication (CDC) 87–8398. 254. Nelson DE, Emont SL, Brackbill RM, et al. Cigarette smoking prevalence by occupation in the United States: a comparison between 1978 to 1980 and 1987 to 1990. J Occup Med. 1994;36: 516–25. 255. Novotny TE, Warner KE, Kendrick JS, et al. Smoking by blacks and whites: socioeconomic and demographic differences. Am J Public Health. 1989;78:1187–9. 256. Johnston LD, O'Malley PM, Bachman JG, et al. (December 21, 2006). Decline in daily smoking by younger teens has ended. University of Michigan News and Information Services: Ann Arbor, MI. [On-line]. Available: www.monitoringthefuture.org; accessed 04/15/2007. 257. Centers for Disease Control and Prevention. Cigarette use among high school students—United States, 1991–2003. MMWR. 2004;53: 499–502. 258. University of Michigan, Monitoring the Future Survey, public use data tapes, 1996–2006. 259. Federal Trade Commission. Federal Trade Commission Cigarette Report for 2004 and 2005. Washington, DC: 2007. 260. Centers for Disease Control and Prevention. Filter ventilation levels in selected U.S. cigarettes, 1997. MMWR. 1997;46: 1043–7. 261. Orleans CT, Slade J, eds. Nicotine Addiction: Principles and Management. New York, NY: Oxford University Press; 1993. 262. Lynch CJ, Benowitz NL. Spontaneous cigarette brand switching: consequences for nicotine and carbon monoxide exposure. Am J Public Health. 1978;78:1191–4. 263. Institute of Medicine. Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction. Washington, DC: National Academy Press; 2001. 264. Tobacco Advisory Group of the Royal College of Physicians. Nicotine Addiction in Britain. London, England: Royal College of Physicians of London; 2000. 265. Campaign for Tobacco Free Kids. New tobacco products—lower risk or more of the same? Available at http://www.tobaccofreekids. org/research/factsheets/pdf/0164.pdf. Accessed August 5, 2005. 266. Morgan JP. The path to a safer cigarette. Potentially Reduced Exposure Products (PREPs). Global Equity Research; 2004. 266a. Rodu B, Godshall WT. Tobacco harm reduction: an alternative to cessation strategy for inveterate smokers. Harm Reduction Journal. 2006:3:37–59. 266b. Henley SJ, Connell CJ, Richter P, et al. Tobacco-related disease mortality among men who switched from cigarettes to spit tobacco. Tobacco Control. 2007;16:22–28.

267. Godtfredsen N, Holst C, Prescott E, et al. Smoking reduction, smoking cessation, and mortality: a 16-year follow-up of 19,732 men and women from the Copenhagen Centre for Prospective Population Studies. Am J Epidemiol. 2002;156:994–1001. 267a. Tverdal, A, Bjartveit, K. Health consequences of reduced daily cigarette consumption. Tob Control. 2006;15(6):472–80. 268. Hurt RD, Croghan GA, Wolter TD, et al. Does smoking reduction result in reduction of biomarkers associated with harm? A pilot study using a nicotine inhaler. Nicotine Tob Res. 2000;2:327–36. 269. Hatsukami DK, Henningfield JE, Kotlyar M. Harm reduction approaches to reducing tobacco-related mortality. Annu Rev Public Health. 2004;25:377–95. 270. ECLIPSE Expert Panel. A safer cigarette? A comparative study, a consensus report. Inhal Toxicol. 2000;12[suppl 5]:1–57. 271. Peto R. Influence of dose and duration of smoking on lung cancer rates. In: Zaridze DG, Peto R, eds. Tobacco: A Major International Health Hazard. Lyon, France: International Agency for Research on Cancer; 1986:22–33. 272. Pechacek TF, Babb S. How acute and reversible are the cardiovascular risks of secondhand smoke? BMJ. 2004;328:980–3. 273. Kropp RY, Halpern-Felsher BL. Adolescents’ beliefs about the risks involved in smoking “light” cigarettes. Pediatrics. 2004;114:445–51. 274. Centers for Disease Control and Prevention. Cigarette smoking among adults—United States, 2000. MMWR. 2002;51:642–5. 275. Yankelovich Partners. Smoking Cessation Study. New York, NY: American Lung Association; 1998. 276. Centers for Disease Control and Prevention. Tobacco use, access and exposure to tobacco in media among middle and high school students—United States, 2004. MMWR. 2005;54:297–301. 277. Centers for Disease Control and Prevention. Youth risk behavior surveillance—United States, 2005. Surveillance Summaries. MMWR. 2006;55(SS-5):1–108. 278. Malaracher AM, Thorne SL, Jackson K, et al. Surveillance for selected tobacco use behaviors-United States, 1900–2005. MMWR. (In press) 279. Baker F, Ainsworth SR, Dye JT, et al. Health risks associated with cigar smoking. JAMA. 2000;284:735–40. 280. Jacobs EJ, Thun MJ, Apicella LF. Cigar smoking and death from coronary heart disease in a prospective study. Arch Intern Med. 1999;159:2413–8. 281. Henley SJ, Thun MJ, Chao A, et al. Association between exclusive pipe smoking and mortality from cancer and other disease. J Natl Cancer Inst. 2004;96:853–61. 282. National Center of Health Statistics, National Health Interview Survey, public use data tape, 2005. 283. Bolinder GM, de Faire U. Ambulatory 24-h blood pressure monitoring in health, middle-aged smokeless tobacco users, smokers, and nontobacco users. Am J Hypertension 1998;11:1153–63. 284. Tomar SL. Is use of smokeless tobacco a risk factor for cigarette smoking? The U.S. experience. Nicotine Tob Research. 2003;5: 561–9. 285. Watson CH, Polzin GM, Calafat AM, et al. Determination of tar, nicotine, and carbon monoxide yields in the smoke of bidi cigarettes. Nicotine Tob Research. 2003;5:747–53. 286. Pakhale SS, Jayant K, Bhide SV. Chemical analysis of smoke of Indian cigarettes, bidis and other indigenous forms of smoking— levels of steam-volatile phenol, hydrogen cyanide and benzo(a)pyrene. Indian J Chest Dis Allied Sci. 1990;32:75–81. 287. Nair J, Pakhale SS, Bhide SV. Carcinogenic tobacco specific nitrosamines in Indian tobacco products. Food Chem Toxicol. 1989;27:751–3. 288. Gupta PC, Mehta HC. Cohort study of all-cause mortality among tobacco users in Mumbai, India. Bull WHO. 2000;78:877–83. 289. Rahman M, Fukui T. Bidi smoking and health. Public Health. 2000;114:123–7.

54 290. Gupta PC, Sreevidya S. Smokeless tobacco use, birth weight, and gestational age: population based, prospective cohort study of 1217 women in Mumbai, India. BMJ. 2004;328:1538. 291. Notani NP, Nagaraj Rao D, Sirsat MV, et al. A study of lung cancer in relation to bidi smoking in different religious communities in Bombay. Indian J Cancer. 1977;14:115–21. 292. Sankaranarayanan R, Duffy S, Padmakumary G, et al. Risk factors for cancer of the oesophagus in Kerala, India. Int J Cancer. 1991: 49:485–9. 293. Dikshit RP, Kanhere S. Tobacco habits and risk of lung, oropharyngeal and oral cavity cancer: a population-based casecontrol study in Bhopal, India. Int J Epidemiol. 2000;29: 609–14. 294. Halpern MT, Warner KE. Motivations of smoking cessation: a comparison of successful quitters and failures. J Subst Abuse. 1993;5: 247–56. 295. Fiore MC, Bailey WC, Cohen SJ, et al. Treating Tobacco Use and Dependence: Clinical Practice Guidelines. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service; 2000. 296. U.S. Preventive Services Task Force. Counseling to Prevent Tobacco Use and Tobacco-Caused Disease: Recommendation Statement. Available at http://www.ahrq.gov/clinic/3rduspstf/tobaccoun/tobcounrs.htm. Accessed August 5, 2005. 297. McDonald P, Colwell B, Backinger CL, et al. Better practices for youth tobacco cessation: evidence of review panel. Am J Health Behav. 2003;27(Suppl 2):S144–58. 298. Milton MH, Maule CO, Lee SL, et al. Youth Tobacco Cessation: A Guide for Making Informed Decisions. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; 2004. 299. Coffield AB, Maciosek MV, McGinnis JM, et al. Priorities among recommended clinical preventive services. Am J Prev Med. 2001; 21:1–9. 300. American Medical Association. How to Help Patients Stop Smoking: Guidelines for Diagnosis and Treatment of Nicotine Dependence. Chicago, IL: American Medical Association; 1994. 301. Raw M, McNeill A, West R. Smoking cessation guidelines and their cost effectiveness. Thorax. 1998;53(Suppl 5):S1–38. 302. Tsevat J. Impact and cost-effectiveness of smoking interventions. Am J Med. 1992;93(suppl 1A):S43–7. 303. Cummings SR, Rubin SM, Oster G. The cost-effectiveness of counseling smokers to quit. JAMA. 1989;261:75–9. 304. Cromwell J, Bartosch WJ, Fiore MC, et al. Cost-effectiveness of the clinical practice recommendations in the AHCPR guideline for smoking cessation. JAMA. 1997;278:1759–66. 304a. Maciosek, MV, Coffield, AB, Edwards, NM, et al. Priorities among effective clinical preventive services. Am J Prev Med. 2006;21:52–61. 305. Lightwood JM, Glantz SA. Short-term economic and health benefits of smoking cessation. Myocardial infarction and stroke. Circulation. 1997;96:1089–96. 306. Wagner EH, Curry SJ, Grothaus L, et al. The impact of smoking and quitting on health care use. Arch Intern Med. 1995;155: 1789–95. 307. McAfee T, Wilson J, Dacey S, et al. Awakening the sleeping giant: mainstreaming efforts to decrease tobacco use in an HMO. HMO Pract. 1995;9:138–43. 308. Schauffler HH, Rodriguez T. Availability and utilization of health promotion programs and satisfaction with health plan. Med Care. 1994;32:1182–96. 309. Hopkins DP, Fielding J. Task Force on Community Preventative Services, eds. The guide to community preventive services: tobacco use prevention and control, reviews, recommendations, and expert commentary. Am J Prev Med. 2001;20[2 (Supplemental)]:1–88.

Tobacco: Health Effects and Control

993

310. Stead LF, Perera R, Lancaster T. Telephone counselling for smoking cessation. Cochrane database of Systematic Reviews. 2006. Available at http://www.cochrane.org/reviews/. Accessed April 21, 2007. 311. McAfee T, Sofian NS, Wilson J, et al. The role of tobacco intervention in population–based health care: a case study. Am J Prev Med. 1998;14(3S):46–52. 312. Centers for Disease Control and Prevention. Making your workplace smokefree: a decision maker’s guide. Atlanta, GA: U.S. Department of Health and Human Services, Office on Smoking and Health; 1996. Available at http://www.cdc.gov/tobacco/ secondhand_smoke/00_pdfs/fullguide.pdf. Accessed April 27, 2007. 313. Fisher KJ, Glasgow RE, Terborg JR. Work site smoking cessation: a meta-analysis of long-term quit rates from controlled studies. J Occup Med. 1990;32:429–39. 314. Glasgow RE, Terborg JR, Hollis JF, et al. Take Heart: results from the initial phase of a work-site wellness program. Am J Public Health. 1995;82:209–16. 315. Sorensen G, Thompson B, Glantz K, et al. Work site based cancer prevention: primary results from the Working Well Trial. Am J Public Health. 1996;86:939–47. 316. Institute of Medicine, Adams K, Corrigan JM. Priority Areas for National Action: Transforming Health Care Quality. Washington, DC: 2003. 317. Sennett C. An introduction to HEDIS—The Health Plan Employer Data and Information Set. J Clin Outcomes Management. 1996;3: 59–61. 318. Committee on Performance. HEDIS 3.0. Washington, DC: National Committee for Quality Assurance; 1996. 319. National Committee for Quality Assurance. State of Health Care Quality 2006. Available at http://web.ncqa.org/Default.aspx? tabid=447. Accessed April 15, 2007. 320. Joint Commission on Accreditation of Healthcare Organizations. Specification Manual for National Implementation of Hospital Core Measures Version 2.0. Available at http://www.jcaho.org/pms/ core+ measures/information+on+final+specifications.htm. Accessed August 5, 2005. 321. U.S. Department of Health and Human Services, Centers for Medicare and Medicaid Services. Doctor’s Office Quality Project; 2004. Available at http://www.cms.hhs.gov/quality/doq. Accessed August 5, 2005 322. Puska P, Salonen J, Nissinen A, et al. Change in risk factors for coronary heart disease during 10 years of a community intervention programme (North Karelia project). Br Med J. 1983;287: 1840–4. 323. Roussouw JE, Jooste PL, Chalton DO, et al. Community-based intervention: the coronary risk factor study (CORIS). Int J Epidemiol. 1993;22:428–38. 324. Farquhar JW, Wood PD, Breitrose H, et al. Community education for cardiovascular health. Lancet. 1977;1:1192–5. 325. Farquhar JW, Fortmann AP, Flora JA, et al. Effects of communitywide education on cardiovascular disease risk factors: the Stanford Five-City Project. JAMA. 1990;264:359–65. 326. Multiple Risk Factor Intervention Trial Research Group. Multiple risk factor intervention trial: risk factor changes and mortality results. JAMA. 1982;248:1465–77. 327. Lando HA, Pechacek TF, Pirie PL, et al. Changes in adult cigarette smoking in the Minnesota Heart Health Program. Am J Public Health. 1995;85:201–8. 328. Carleton RA, Lasater TM, Assaf AR, et al. The Pawtucket Heart Health Program: community changes in cardiovascular risk factors and projected disease risk. Am J Public Health. 1995;85: 777–85. 329. Stillman FA, Hartman AM, Graubard BI, et al. Evaluation of the American Stop Smoking Intervention Study (ASSIST): a report of outcomes. J Natl Cancer Inst. 2003;95:1681–91.

994

Behavioral Factors Affecting Health

330. Task Force on Community Preventive Services. Tobacco. In: Zaza S, Briss PA, Harris KW, eds. The Guide to Community Preventive Services: What Works to Promote Health? New York, NY: Oxford University Press; 2005. 331. National Cancer Institute. The Impact of Cigarette Excise Taxes on Smoking Among Children and Adults: Summary Report of a National Cancer Institute Expert Panel. Washington, DC: National Cancer Institute; 1993. 332. Warner KE. Smoking and health implications of a change in the federal cigarette excise tax. JAMA. 1986;225:1028–32. 333. U.S. Department of Health and Human Services. Reducing Tobacco Use: A Report of the Surgeon General. Washington, DC: Centers for Disease Control and Prevention, Office on Smoking and Health; 2000. 334. Tauras JA, O’Malley PM, Johnston LD. Effects of Price and Access Laws on Teenage Smoking Initiation: A National Longitudinal Analysis. 2001. NBER Working Paper No W8331. 335. Ross H, Chaloupka FJ. The effect of cigarette prices on youth smoking. Health Econ. 2003;12:217–30. 336. Johnston M. Teenage Smoking and the Federal Excise Tax on Cigarettes, PM Document No. 2001255224, September 17, 1981. Available at http://www.pmdocs.com/getimg.asp? pgno=0&start= 0&if=avpidx&bool=2001255224&docid=2001255224/5227&doc num=1&summary=0&sel1=. Accessed August 5, 2005. 337. Delnevo CD, Hrywna M, Foulds J, et al. Cigar use before and after a cigarette excise tax increase in New Jersey. Addict Behav. 2004;29:1799–1807. 338. Siegel M, Biener L. The impact of an antismoking media campaign on progression to established smoking: results of a longitudinal youth study. Am J Public Health. 2000;90:380–6. 339. Centers for Disease Control and Prevention. Effect of ending an antitobacco youth campaign on adolescent susceptibility to cigarette smoking—Minnesota, 2002–2003. MMWR 2004;53:301–4. 340. Zucker D, Hopkins RS, Sly DF, et al. Florida’s “truth” campaign: a counter-marketing, anti-tobacco media campaign. J Public Health Manag Pract. 2000;6:1–6. 341. Sly DF, Trapido E, Ray S. Evidence of the dose effects of an antitobacco counteradvertising campaign. Prev Med. 2002;35:511–8. 342. Niederdeppe J, Farrelly MC, Haviland ML. Confirming “truth”: more evidence of a successful tobacco countermarketing campaign in Florida. Am J Public Health. 2004;94:255–7. 343. Farrelly MC, Healton CG, Davis KC, et al. Getting to the truth: evaluating national tobacco countermarketing campaigns. Am J Public Health. 2002;92:901–7. 344. Thrasher JF, Niederdeppe J, Farrelly M, et al. The impact of antitobacco industry prevention messages in tobacco producing regions: evidence from the U.S. truth campaign. Tob Control. 2004;13:283–8. 345. Farrelly M, Davis KC, Haviland ML, et al. Evidence of a doseresponse relationship between “truth” antismoking ads and youth smoking prevalence. Am J Public Health. 2005;95:425–31. 345a. Wakefield M, Terry-McElrath Y, Emery S, et al. Effect of televised, tobacco company-funded smoking prevention advertising on youth smoking-related beliefs, intentions and behavior. Am J Public Health. 2006;96:2154–60. 346. Centers for Disease Cotnrol and Prevention. Guidelines for school health programs to prevent tobacco use and addiction. MMWR. 1994;43(RR–2):1–18. 347. National Institutes of Health. School Programs to Prevent Smoking: The National Cancer Institute Guide to Strategies that Succeed. Bethesda, MD: National Institutes of Health; 1990. NIH Publication 90-500. 348. Flay BR. What we know about the social influences approach to smoking prevention: review and recommendations. In: Bell CS, Battjes R, eds. Prevention Research: Deterring Drug Abuse among

349.

350.

351.

352. 353.

354.

355.

356.

356a.

357.

357a.

358.

359.

360.

361.

362.

362a.

363.

Children and Adolescents. Washington, DC: U.S. Department of Health and Human Services, Alcohol, Drug Abuse and Mental Health Administration, National Institue on Drug Abuse; 1985. NIDA Research Monograph 63. DHHS Publication (ADM) 85–1334. U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration. Fewer Retailers Sell Cigarettes to Youth, 2002. Available at http://prevention.samhsa. gov/tobacco. Accessed August 5, 2005. Lynch BS, Bonnie RJ, eds. Growing Up Tobacco Free: Preventing Nicotine Addiction in Children and Youths. Washington, DC: National Press, 1994. Jason JA, Ji PY, Anes MD, et al. Active enforcement of cigarette control laws in the prevention of cigarette sales to minors. JAMA. 1991;266:3159–61. Di Franza, JR, Carlson RP, Caisse RE. Reducing youth access to tobacco. Tob Control. 1992;1:58. Rigotti NA, DiFranza JR, Chang Y, et al. The effect of enforcing tobacco sales-laws on adolescents’ access to tobacco and smoking behavior. N Engl J Med. 1997;337:1044–51. Tobacco Free Mass. Data reveals 74% increase in illegal cigarette sales to minors. Available at http://www.tobaccofreemass.org/ release31604.php. Accessed August 5, 2005. American Lung Association. State of Tobacco Control: 2004. New York, NY: Available at http://lungaction.org/reports/tobaccocontrol04.html. Accessed August 5, 2005. Shopland D, Anderson CM, Burns DM, et al. Disparities in smokefree workplace policies among food service workers. J Occup Environ Med. 2004;46:347–56. Pickett, MS, Schober, SE, Brody, DJ, et al. Smoke–free laws and secondhand smoke exposure in U.S. non-smoking adult, 1999–2000. Tobacco Control. 2006;15:302–07. Centers for Disease Control and Prevention. Indoor air quality in hospitality venues before and after implementation of a clean indoor air law—Western New York, 2003. MMWR. 2004;53: 1038–41. Farrelly, MC, Nonnemaker, JM, Chou, R, et al. Changes in hospitality workers’ exposure to secondhand smoke following the implementation of New York’s smoke-free law. Tob Control. 2005; 14:236–41. Scollo M, Lal A, Hyland A, et al. Review of the quality of studies on the economic effects of smoke-free policies on the hospitality industry. Tob Control. 2003;12:13–20. Lewit EM, Coate D. Potential for Using Excise Taxes to Reduce Smoking. Cambridge, MA: National Bureau of Economic Research, Inc.; 1981. NBER Working Paper Series 764. Fiore MC, Coyle RT, Curry SJ, et al. Preventing 3 million premature deaths and helping 5 million smokers quit: A national action plan for tobacco cessation. Am J Public Health. 2004;94: 205–10. Merlo E, Senior Vice President of Corporate Affairs, Philip Morris, 1994 draft speech to the Philip Morris USA Trade Council. Available at http://legacy.library.ucsf.edu/tid/oyf35e00. Accessed August 5, 2005. Philip Morris Executive Claude Schwab, “Cigarette attributes and quitting,” PM Doc. 2045447810, March 4, 1993. Available at http://www.pmdocs.com/getimg.asp?pgno=0&start=0&if=avpidx &bool=2045447810&docid=2045447810&docnum=1&summary=0&sel1=. Accessed August 5, 2005. Campaign for Tobacco Free Kids. Tobacco smuggling. 11th world conference on tobacco or health, tobacco fact sheet. Available at http://tobaccofreekids.org/campaign/global/docs/smuggling.pdf. Accessed April 23, 2007. Hamilton JL. The demand for cigarettes: advertising, the health scare, and the cigarette advertising ban. Rev Econ Stat. 1972; 54:401–11.

54 364. Horn D. Who is Quitting and Why. Progress in Smoking Cessation. Proceedings of the International Conference on Smoking Cessation. New York, NY: American Cancer Society; 1978. 365. Pierce JP, Macaskill P, Hill DJ. Long-term effectiveness of mass media anti-smoking campaigns in Australia. Am J Public Health. 1990;80:565–9. 366. Doxiadis SA, Trihopoulos DV, Phylactou HD. Impact of nationwide smoking: why young people do it and ways of preventing it. In: McGrath P, Firestone P, eds. Pediatric and Adolescent Behavioral Medicine. New York, NY: Springer; 1983:132–83. 367. Laugesen M, Meads C. Tobacco advertising restrictions, price, income and tobacco consumption in OECD countries, 1960–1986. Br J Addict. 1991;86:1343–54. 368. Warner KE. Selling health: a media campaign against tobacco. J Public Health Policy. 1986;7:434–9. 369. Blum A. The Marlboro Grand Prix—circumvention of the television ban on tobacco advertising. N Engl J Med. 1991;324:913–7. 370. Jha P, Chaloupka F, eds. Tobacco Control in Developing Countries. New York, NY: Oxford University Press; 2000. 371. Saffer H, Chaloupka F. Tobacco advertising: Economic Theory and International Evidence. Cambridge, MA: National Bureau of Economic Research; 1999. 372. Joossens L. The effectiveness of banning advertsing for tobacco products; 1997. Available at http://www.globalink.org/tobacco/ docs/eu-docs/9710joos.html. Accessed August 5, 2005. 373. North American Quitline Consortium. Mission and Background. Available at http://www.naquitline.org/index.asp?dbid=2&dbsection= about. Accessed April 15, 2007. 374. Zhu S, Stretch V, Balabanis M, et al. Telephone counseling for smoking cessation: effects of single-session and multiple-session interventions. J Counsult Clinical Psychol. 1996;64:202–11. 375. Zhu S, Anderson CM, Johnson CE, et al. Centralised telephone service for tobacco cessation: the California experience. Tob Control. 2000;9(Suppl 2):ii48–55. 376. Office of Disease Prevention and Health Promotion, and Centers for Disease Control and Prevention. For a Healthy Nation: Returns on Investment in Public Health. Washington, DC; 1994. 376a. Hu TW, Bai J, Keeler TE, et al. The impact of California Proposition 99, a major anti-smoking law, on cigarette consumption. J Public Health Policy. 1994;15:26–36. 377. Pierce JP, Gilpin EA, Emery SL, et al. Has the California tobacco control program reduced smoking? JAMA. 1998;280:893–9. 378. California Department of Health Services. California Department of Health Services: Fact sheets. Available at http://www.dhs.ca.gov/ tobacco/html/factsheets.htm. Accessed August 11, 2005. 379. Centers for Disease Control and Prevention. Declines in lung cancer rates—California, 1988–1997. MMWR. 2000;49:1066–70. 380. Fichtenberg CM, Glantz SA. Associations of the California tobacco control program with declines in cigarette consumption and mortality from heart disease. N Engl J Med. 2000;343:1772–7. 381. Lightwood J, Phibbs CS, Glantz SA. Short-term health and economic benefits of smoking cessation: low birth weight. Pediatrics. 1999;104:1312–20. 382. Tobacco Control Section, California Department of Health Services. California Tobacco Control Update, 2000. Available at http://www.dhs.ca.gov/tobacco/documents/pubs/CTCUpdate.pdf. Accessed april 15, 2007. 383. Centers for Disease Control and Prevention. Cigarette smoking before and after an excise tax increase and an antismoking campaign—Massachusetts, 1990–1996. MMWR. 1996;45:966–70. 384. Connolly W, Director, Massachusetts Tobacco Control Program, Joint Hearing of the Pennsylvania House of Representatives Committee on Health and Human Services and the Pennsylvania Senate Committee on Public Health and Welfare, June 22, 1999. Campaign for Tobacco-Free Kids (CFTFK) Fact Sheet, Harm caused

385. 386.

387. 388.

389. 390.

391.

392. 393.

394.

395. 396.

397. 398. 399.

400. 401.

402.

402a.

403.

404. 405.

406.

Tobacco: Health Effects and Control

995

by pregnant women smoking or being exposed to secondhand smoke. Available at http://tobaccofreekids.org/research/factsheets/ pdf/ 0007.pdf. Accessed August 10, 2005. Centers for Disease Control and Prevention. Tobacco use among adults—Arizona, 1996 and 1999. MMWR. 2001;50:402–6. Centers for Disease Control and Prevention. Effectiveness of school-based programs as a component of a statewide tobacco control initiative—Oregon, 1999–2000. MMWR. 2001;50:663–6. Florida Department of Health. Monitoring program outcomes in 2002. Florida Youth Tobacco Survey. 2002;5(1):1–23. Farrelly M, Pechacek T, Chaloupka F. The impact of tobacco control program expenditures on aggregate cigarette sales: 1981–2000. J Health Economics. 2003;22:843–59. Tauras JA, Chaloupka F, Farrelly M, et al. State tobacco control spending and youth smoking. Am J Public Health. 2005;95:338–44. Centers for Disease Control and Prevention. Best Practices for Comprehensive Tobacco Control Programs. Atlanta, GA: U.S. Department of Health and Human Services, Office on Smoking and Health; 1999. Campaign for Tobacco-Free Kids. State cigarette excise tax rates and rankings. Available at http://www.tobaccofreekids.org/research/ factsheets/pdf/0097.pdf. Accessed April 15, 2007. Orzechowski W, Walker RC. The Tax Burden on Tobacco: Historical Compilation—2006. Arlington, VA; 2006. Department of Labor. Indoor air quality. Federal Register. 2001;66:242. Available at http://www.osha.gov/FedReg_osha_pdf/ FED20011217.pdf. Accessed August 5, 2005. Executive Office of the President. Executive Order 13058— Protecting federal employees and the public from exposure to tobacco smoke in the federal workplace. Federal Register. 1997;62: 43449–52. U.S. Department of Health and Human Services. Tobacco-Free HHS; November 10, 2004. Joint Commission on Accreditation of Healthcare Organizations. Smoking standards of the Joint Commission on Accreditation of Healthcare Organizations. Jt Comm Perspect. 1991;Nov/Dec:12–4 Delta Air Lines is the first smokefree U.S. airline worldwide. Wall Street Journal. November 15, 1994:A15. Jones D. Airlines join forces to ban trans—Atlantic smoking. USA Today. January 25, 1995:B1. Americans for Nonsmokers’ Rights. Smokefree transportation chronology. Available at http://www.no-smoke.org/document.php? id=334. Accessed August 5, 2005. Cal Labor Code §6404.5; 1996. Americans for Nonsmokers’ Rights. Overview list—how many smokefree laws? Available at http://www.no-smoke.org/goingsmokefree. php?id=519. Accessed April 15, 2007. Centers for Disease Control and Prevention. Preemptive state smoke-free indoor air laws—United States, 1999–2004. MMWR. 2005;54:250–3. Centers for Disease Control and Prevention. State tobacco activities tracking and evaluation (STATE) System. Available at http://apps. nccd.cdc.gov/statesystem/. Accessed April 15, 2007. McMillen RC, Winickoff JP, Klein JD, et al. U.S. adult attitudes and practices regarding smoking restrictions and child exposure to environmental tobacco smoke: changes in the social climate from 2000 to 2001. Pediatrics. 2003;112:55–60. Blizzard R. Secondhand smoke: harmful or hyperbole. Health & Healthcare. 2004;100–1. U.S. Department of Commerce. National Cancer Institute Sponsored Tobacco Use Supplement to the Current Population Survey, Census Bureau. Public use data tapes, 1993; 1999. Gilpin EA, Pierce JP. Changes in population attitudes about where smoking should not be allowed: California versus the rest of the U.S.A. Tob Control. 2004;13:38–44.

996

Behavioral Factors Affecting Health

407. National Center for Health Statistics. Healthy People 2000 Review, 1997. Hyattsville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 1997. DHHS Publication (PHS) 98–1256. 407a. Shopland DR, Gerlach KK, Burns DM, et al. State-specific trends in smoke-free workplace policy coverage: The current population survey tobacco use supplement, 1993 to 1999. Journal of Occupational Medicine. 2001;43:680–6. 408. Gerlach KK, Shopland DR, Hartman AM, et al. Workplace smoking policies in the United States: results from a national survey of more than 100,000 workers. Tob Control. 1997;6:199–206. 409. Weber MD, Bagwell DAS, Fielding JE, et al. Long term compliance with California’s smokefree workplace law among bars and restaurants in Los Angeles County. Tob Control. 2003;12:269–73. 410. Centers for Disease Control and Prevention. Tobacco Use Prevention from CDC’s School Health Policies and Programs Study (SHPPS)— 2000. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; 2001. 411. Gilpin EA, Farkas AJ, Emery SL, et al. Clean indoor air: advances in California, 1990–1999. Am J Public Health. 2002; 92:785–91. 411a. Centers for Disease Control and Prevention. State-specific prevalence of smoke-free home rules—United States, 1992–2003. MMWR. 2007. In press. 412. Centers for Disease Control and Prevention. Third National Report on Human Exposure to Environmental Chemicals. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Environmental Health; 2005. 413. Eisner MD, Smith AK, Blanc PD. Bartenders’ respiratory health after establishment of smoke-free bars and taverns. JAMA. 1998;280:1909–1914. 414. Substance Abuse and Mental Health Services Administration. Final regulations to implement section 1926 of the Public Health Service Act, regarding the sale and distribution of tobacco products to individuals under the age of 18. Federal Register. 1996;13: 1492–1500. 415. U.S. Department of Health and Human Services. Synar Regulation Guidance Series: Sampling, Inspection, and Change Strategies. Rockville MD: 1996. 416. U.S. Department of Health and Humans Services, Substance Abuse and Mental Health Services Administration. Retailers Cut Cigarette Sales to Youth. Available at http://www.samhsa.gov/SAMHSA_ news/VolumeXIII_5/article11.htm. Accessed April 19, 2007. 416a. American Lung Association. State of Tobacco Control: 2005. New York, NY: American Lung Association; 2005. Available at http:// lungaction.org/reports/tobacco-control06.html. Accessed April 20, 2007. 417. Substance Abuse and Mental Health Services Administration. Tobacco: State Synar non-compliance rate table FFY 1997-FFY 2005. Available at http://prevention.samhsa.gov/tobacco/01synartable. aspx. Accessed April 15, 2007. 418. Food and Drug Administration. Regulations restricting the sale and distribution of cigarettes and smokeless tobacco products to protect children and adolescents—final rule. Federal Register. 1996;61:41, 314–75. 419. Campaign for Tobacco-Free Kids. FDA Authority over tobacco: Legislation will protect kids and save lives. Available at http://www. tobaccofreekids.org/reports/fda. Accessed April 15, 2007. 420. Ribisi KM, Williams RS, Kim AE. Internet sales of cigarettes to minors. JAMA. 2003;290:1356–9. 420a. American Lung Association. State Legislated Actions on Tobacco Issues 2005. Available at http://slati.lungusa.org/ reports/SLATI_05.pdf. Accessed April 20, 2007.

421. Centers for Disease Control and Prevention. State Medicaid Coverage for Tobacco-Dependence Treatments—United States, 2005. MMWR. 2006;55:1194–7. 422. McPhillips-Tangum C, Bocchino C, Carreon R, et al. Addressing tobacco in managed care: results of the 2002 survey. Prev Chronic Dis. 2004;1:1. 423. Partnership for Prevention. Why Invest in Disease Prevention? It’s a Good Business Decision. And It’s Good for American Business. Washington, DC: Partnership for Prevention; 1998. 424. Partnership for Prevention. Preventive services: Helping states improve mandates; 2002. Available at http://prevent.org/images/stories/ Files/publications/Preventive_Services_State_Mandate_Brief_FINAL. pdf. Accessed April 15, 2007. 425. Burns ME, Bosworth TW, Fiore MC. Insurance coverage of smoking cessation treatment for state employees. Am J Public Health. 2004; 94:1338–40. 425a. United States of Department of Health and Human Services. HHS announces national smoking cessation quitline network. Available at http://www.hhs.gov/news/press/2004pres/20040203.html. Accessed April 15, 2007. 426. Centers for Disease Control and Prevention, Office on Smoking and Health. National Tobacco Control Program (NTCP). Available at http://www.cdc.gov/tobacco/ntcp_exchange/index.htm. Accessed August 5, 2005. 427. Campaign for Tobacco-Free Kids. A Broken Promise to Our Children: The 1998 State Tobacco Settlement Six Years Later. Washington, DC; 2004. 427a. Hu, TW, Bai, J, Keeler, TE, et al. The impact of California Proposition 99, a major anti-smoking law, on cigarette consumption. J Public Health Policy. 1994;15:26-36. 428. Schroeder S. Tobacco control in the wake of the 1998 master settlement agreement. N Eng J Med. 2004;350:293–301. 428a. Campaign for Tobacco-Free Kids. A Broken Promise to Our Children: The 1998 State Tobacco Settlement Eight Years Later. Washington, DC: Campaign for Tobacco Free Kids; 2007. 429. Federal Trade Commission. Report to Congress for 1995: Pursuant to the Federal Cigarette Labeling and Advertising Act. Washington, DC; 1997. 429a. Federal Trade Commission. Federal Trade Commission Smokeless Tobacco Report for the Years 2002–2005. Washington, DC: Federal Trade Commission; 2007. 430. Attorneys General Statement Agreement. In: Glob @ Link Resources on Tobacco Control—North American [online database] (cited 20 March 1997). 431. Meier B. Files of R.J. Reynolds tobacco show effort on youths. New York Times, January 15, 1998. 432. King C, Siegel M. The master settlement agreement with the tobacco industry and cigarette advertising in magazines. N Engl J Med. 2001;345:504–11. 433. Bowker D, Hamilton M. Cigarette Advertising Expenditures Before and After the Master Settlement Agreement: Preliminary Findings. Boston, MA: Massachusetts Department of Health; 2000. Available at http://tobaccofreekids.org/reports/addicting/magazines/connolly. pdf. Accessed August 10, 2005. 434. Massachusetts Department of Health. Smokeless Tobacco Advertising Expenditures Before and After the Smokeless Tobacco Master Settlement Agreement. Boston, MA: Massachusetts Department of Health, Massachusetts Tobacco Control Program; 2002. Available at http://tobaccofreekids.org/pressoffice/release503/smokeless.pdf. Accessed August 5, 2005. 435. Girion L, Levin M. R.J. Reynolds fined for ads aimed at teens: tobacco: judgement of $20 million for magazine pitches is first financial penalty for violation of 1998 national settlement. Los Angeles Times. June 7, 2002.

54 436. Siegel M. Counteracting tobacco motor sports sponsorship as a promotional tool: is the tobacco settlement enough? Am J Public Health. 2001;91:1100–6. 436a. Substance Abuse and Mental Health Services Administration. Cigarette Brand Preferences in 2005. The NSDUH Report. 2007. Available at http://oas.samhsa.gov/2k7/cigBrands/cigBrands.htm. Accessed April 24, 2007. 437. Pollay RW, Siddarth S, Siegel M, et al. The last straw? Cigarette advertising and realized market shares among youths and adults, 1979–1993. J Mark. 1996;60:1–16. 438. Evans N, Farkas A, Gilpin E, et al. Influence of tobacco marketing and exposure to smokers on adolescent susceptibility to smoking. J Natl Cancer Inst. 1995;87:1538–45. 439. Kaufman NJ, Castrucci BC, Mowery PD, et al. Predictors of change on the smoking uptake continuum among adolescents. Arch Pediatr Adolesc Med. 2002;156:581–7. 440. Centers for Disease Control and Prevention. Changes in the cigarette brand preferences of adolescent smokers—United States, 1989–1993. MMWR. 1994;43:577–81. 441. Fischer PM, Schwartz MP, Richards JW, et al. Brand logo recognition by children aged 3 to 6 years. JAMA. 1991;266:3145–8. 442. Ono Y, Ingersoll B. RJR retires Joe Camel, adds sexy smokers. Wall Street Journal. July 11, 1997:B1. 443. Pierce JP, Lee L, Gilpin EA. Smoking inititation by adolescent girls, 1944 through 1988: an association with targeted advertising. JAMA. 1994;271:608–11. 444. Ramirez A. Reynolds, after protests, cancels cigarette aimed at black smokers. New York Times. January 20, 1990. 445. Freedman AM, McCarthy MJ. New smoke from RJR under fire. Wall Street Journal. February 20, 1990. 446. Maryland Attorney General. Landmark settlement of “KoolMixx” tobacco lawsuits. Available at http:// www.oag.state.md.us/Press/ 2004/1006c04.htm. Accessed April 19, 2007. 447. Office of the New York State Attorney General. Attorneys general and R.J. Reynolds reach historic settlement to end the sale of flavored cigarettes. Available at http://www.oag.state.ny.us/press/2006/ oct/oct11a_06.html. Accessed April 15, 2007. 448. Scientific Committee on Tobacco and Health. Report of the Scientific Committee on Tobacco and Health. London, England: Her Majesty’s Stationery Office; 1998. 449. Dalton M, Sargent J, Beach M, et al. Effect of viewing smoking in movies on adolescent smoking initiation: a cohort study. Lancet. 2003;362:281–5. 450. Sargent J, Dalton M, Beach M, et al. Viewing tobacco use in movies. Am J Prev Med. 2002;22:137–45. 451. Distefan J, Pierce JP, Gilpin EA. Do favorite movie stars influence adolescent smoking initiation? Am J Public Health. 2004;94: 1239–44. 452. Glantz SA, Kacirk KA, McCulloch C. Back to the future: smoking in movies in 2002 compared with 1950 levels. Am J Public Health. 2004;94:261–3. 453. Polansky JR, Glantz SA. First-run smoking presentations in U.S. movies 1999–2003. Available at http://repositories.cdlib.org/cgi/ viewcontent.cgi?article=1047&context=ctcre. Accessed August 12, 2005. 454. Weiser R. Smoking and Women’s Magazines, 2001–2002. New York, NY: American Council on Science and Health; 2004. Available at http://www.acsh.org/publications/pubID.1004/pub_detail.asp. Accessed April 15, 2007. 455. The Public Health Cigarette Smoking Act of 1969. Public Health Law, 91–222. 456. Centers for Disease Control and Prevention. Preemptive state tobacco control laws—United States, 1982–1998. MMWR. 1999;47:1112–4. 457. Campaign for Tobacco-Free Kids. The United States: no longer a world leader in tobacco control. Available at

458. 459. 460. 461. 462. 463. 464. 465.

466.

467.

468. 468a.

469.

470. 471.

471a.

472.

473.

474.

475. 476. 477. 478.

479.

Tobacco: Health Effects and Control

997

http://www.tobaccofreekids.org/campaign/global/pdf/Straggler. pdf. Accessed August 5, 2005. Keating G. Retrial in L.A. tobacco case set for September. Reuters. August, 15, 2003. Gray M. New York jury awards widow $350,000 in tobacco lawsuit. Associated Press. December 19, 2003. Missouri family awarded $20 million in tobacco suit. Associated Press. February 03, 2005. First individual award against big tobacco in Arkansas is upheld. Associated Press. January 8, 2005. List of large awards in tobacco lawsuits. Associated Press. May 22, 2003. Flight Attendant Medical Research Institute. History. Available at http://www.famri.org/history/index.php. Accessed August 5, 2005. Haggman M, Cunningham L. Tobacco industry lawyers argue against $145B award. Miami Daily Business Review. May 22, 2003. Daynard RA, Sweda EL, Gottlie M. Despite headlines, FL Supreme Court's decision in Engle case will prove to be an enormous blow to cigarette companies. July 6, 2006. Available at http://tobacco.neu.edu/ litigation/cases/pressreleases/ENGLEVFLSUPCT2006.htm. Accessed April 24, 2007. Associated Press. Supreme Court won’t hear ‘light’ cigarette case. MSNBC News. November 27, 2006. Available at http://www.msnbc. msn.com/id/15924872/. Accessed April 24, 2007. Zuckerbrod N. Light cigarette smokers sue tobacco industry in courts nationwide. Detroit News. March 25, 2002. Available at www.detnews.com/2002/health/0204/01/-449181.htm. Accessed August 5, 2005. Harding A. U.S. government opens racketeering case against tobacco industry. BMJ. 2004;329:701. United States of America vs. Philip Morris. Final judgement and remedial order. Available at http://tobaccofreekids.org/reports/doj/ JudgmentOrder.pdf. Accessed April 15, 2007. Capehart T. The Changing Tobacco User’s Dollar. Washington, DC: U.S. Department of Agriculture; 2004:1–8. Publication TBS 257–01. Zagorsky JL. The wealth effects of smoking. Tob Control. 2004;13:370–4. U.S. Department of Agriculture. U.S. Trade Internet System -FAS online. 2007. Available at http://www.fas.usda.gov/ustrade/. Accessed April 27, 2007. Central Intelligence Agency. The world factbook—United States. 2005. Available at https://www. cia.gov/cia/publications/factbook/ geos/us.html Warner KE, Fulton GA, Nicolas P, et al. Employment implications of declining tobacco product sales for the regional economics of the United States. JAMA. 1996;275:1241–6. U.S. Department of Agriculture. Tobacco Situation and Outlook Report. Washington, DC: Economic Research Service; 1997. Publication TBS-239. Zhang P, Husten C. Impact of the tobacco price support program on tobacco control in the United States. Tob Control. 1998;7:176–82. Womach J. Tobacco Quota Buyout. Washington, DC: Congressional Research Service; 2005. Womach J. Tobacco Price Support: an Overview of the Program. Washington, DC: Congressional Research Library; 2004. Weis WL. Can you afford to hire smokers? Pers Adm. 1981;26: 71–3,75–8. Halpern MT, Shikiar R, Rentz AM, et al. Impact of smoking status on workplace absenteeism and productivity. Tob Control 2001;10:233–8. Warner KE, Smith RJ, Smith DG, et al. Health and economic implications of a work-site smoking-cessation program: a simulation analysis. J Occup Environ Med. 1996;38:981–92.

998

Behavioral Factors Affecting Health

480. Hodgson TA. Cigarette smoking and lifetime medical expenditures. Milbank Q. 1992;70:81–115. 481. Center for Prevention and Health Services. Reducing the burden of smoking on employee health and productivity. Issue Brief. National Business Group on Health; 2005;1:1–8. 482. Guindon GE, Boisclair D. Past, Current and Future Trends in Tobacco Use. HNP Discussion Paper No. 6, Economics of Tobacco Control Paper No. 6. Washington, DC: The World Bank; 2003. Available at http://www1.worldbank.org/tobacco/pdf/ Guindon-Past,%20current-%20whole.pdf. Accessed August 10, 2005. 483. Corrao MA, Guindon GE, Sharma N, et al, eds. Tobacco Control: Country Profiles. Atlanta, GA: American Cancer Society; 2000. 484. Global Tobacco Surveillance System Collaborating Group. Global Tobacco Surveillance System (GTSS): purpose, production, and potential. J School Health. 2005;75:15–24. 485. Global Youth Tobacco Survey Collaborating Group. Tobacco use among youth: a cross country comparsion. Tob Control. 2002;11: 252–70. 486. Global Youth Tobacco Survey Collaborating Group. Differences in worldwide tobacco use by gender: findings from the Global Youth Tobacco Survey. J School Health. 2003;73:207–15. 487. Shafy O, Dolwick S, Guindon GE, eds. Tobacco Control: Country Profiles, 2nd ed. Atlanta, GA: American Cancer Society; 2003. 488. Yu JJ, Mattson ME, Boyd GM, et al. A comparison of smoking patterns in the People’s Republic of China with the United States: an impending health catastrophe in the middle kingdom. JAMA. 1990;264:1575–9. 489. Tobacco or Health Programme. Tobacco or Health: First Global Status Report. Geneva, Switzerland: Wor1d Health Organization; 1996. 490. Muller M. Preventing tomorrow’s epidemic: the control of smoking and tobacco production in developing countries. N Y State J Med. 1983;83:1304–9. 491. Whelan EM. A Smoking Gun: How the Tobacco Industry Gets Away with Murder. Philadelphia, PA: George F. Stickley; 1984:166–76.

492. Madeley J. The environmental impact of tobacco production in developing countries. N Y State J Med. 1983;83:1310–1. 493. Barnum H. The economic burden of the global trade in tobacco. Tob Control. 1994;3:358–61. 494. Forty-ninth World Health Assembly. International Framework Convention for Tobacco Control; May 25, 1996. WHA49.17. 495. World Health Organization. WHO Framework Convention on Tobacco Control. Geneva, Switzerland: 2003. 496. Blanke DD. Tools for Advancing Tobacco Control in the XXIst century: Tobacco Control Legislation: An Introductory Guide. Geneva, Switzerland: World Health Organziation, 2003. 497. Smoking and Health Action Foundation. Average retail cigarette price and total taxes per pack (U.S. dollars/pack of 20), selected industrial countries, June 17, 2002. Available at http://www.nsraadnf.ca/cms/index.cfm?group_id=1200. Accessed April 15, 2007. 498. Laugese M, Meads C. Tobacco advertising restrictions, price, income and tobacco consumption in OECD countries, 1960–1986. Br J Addict. 1991;86:1343–54. 498a. Tobacco Free Kids. Michael Bloomberg Announces grantees $125 million to promote freedom from smoking (Press Release). Available at http://tobaccofreekids.org/pressoffice/BloombergRelease.pdf. Accessed April 15, 2007. 499. The Gallup Organziation. Survey of the Public’s Attitudes toward Smoking. Princeton, NJ: The Gallup Organization; 1992. 500. Chaloupka F, Warner KE. The economics of smoking. In: Culyer AJ, Newhouse JP, eds. Handbook of Health Economics. Amsterdam, Netherlands: Elsevier Science Ltd; 2000. 500a. Loomis BR, Farrelly MC, Mann NH. The association of retail promotions for cigarettes with the Master Settlement Agreement, tobacco control programmes and cigarette excise taxes. Tobacco Control. 2006;15:458–63. 501. Qunidlen A. Quid pro quo. New York Times. October 8, 1994. 502. Hicks JP. In council, bill gains to restrict smoking. New York Times. December 8, 1994:B2. 503. Centers for Disease Control and Prevention. Achievements in public health, 1900–1999: Tobacco Use—United States, 1900–1999. MMWR. 1999;48:986–93.

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Brian L. Cook • Jill Liesveld

INTRODUCTION

The abuse of alcohol is more common than any other form of drug abuse throughout the world. The consequences of alcohol use are pervasive in society. From a public health perspective, alcohol use presents a unique dilemma, referred to as the “prevention paradox.”1 This paradox stems from the observation that health and economic consequences resulting from alcohol use are far greater due to hazardous drinking than drinking patterns that constitute a formal diagnosis of alcohol dependence.2 This paradox is further complicated by findings that suggest that low to moderate levels of alcohol use may play a role in reducing mortality for certain disorders, such as cardiovascular disease.3 To better understand this paradox and the risk of alcohol use, it is helpful to stratify alcohol use and risk along a continuum. This continuum stretches from abstinence to alcohol dependence. CATEGORIES OF ALCOHOL USE ALONG THE DRINKING CONTINUUM

week be regarded as harmful because of the biological differences between men and women c. that abstinence be promoted as highly desirable during pregnancy d. that persons who intend to drive, operate machinery, or undertake activities in hazardous or potentially hazardous situations should not drink e. that in any given situation it is difficult to say that there is an absolute safe level of consumption and thus in situations of any doubt people should not drink In this report, a unit or standard drink was equivalent to 8–10 g of alcohol compared with Canada and the United States, where one unit or standard drink contains approximately 13.6 g of alcohol. In essence, no level of alcohol consumption will always be safe for all individuals under all conditions. Rather, increasing levels of consumption hold a progressively increasing risk of causing either acute or chronic damage. Moreover, the level at which risk occurs and its significance are influenced by a combination of personal and environmental factors that render the individual more or less vulnerable to damage from alcohol.

Safe (Low-Risk) Drinking Based on the concept of a continuum of risk, some organizations have proposed guidelines for “safe” (low-risk) drinking, some of which include both the characteristics and circumstances of the drinker as well as levels of consumption. American guidelines for safe drinking generally recommend no more than 2 drinks per day for men, and 1 drink per day for nonpregnant females.4 Slightly higher limits are proposed by U.K. authorities.5 One example of safe drinking guidelines, which also include characteristics of the drinker as well as levels of consumption, is contained in the report of the Australian National Health and Medical Research Council (NHMRC).6 “Is there a safe level of daily consumption of alcohol for men and women?” Recommendations regarding responsible drinking behavior, in which it is recommended that responsible drinking be considered as the consumption of the least amount of alcohol that will meet an individual’s personal and social needs and in any case: a. that men should not exceed 4 units or 40 g of absolute alcohol per day on a regular basis, or 28 units per week; that 4–6 units per day or 28–42 units per week be considered as hazardous and that greater than 6 units per day or 42 units per week be regarded as harmful b. that women should not exceed 2 units or 20 g of absolute alcohol per day on a regular basis, or 14 units per week; that 2–4 units per day or 14–28 units per week be considered as hazardous and that greater than 4 units per day or 28 units per

Hazardous Drinking The term “hazardous drinking” has been used to describe levels of alcohol consumption that expose the drinker to a high risk of physical complications.7 Under certain circumstances, relatively low levels of consumption on isolated occasions may result in damage to the individual drinker. There is evidence as well that levels of consumption far below those found in people diagnosed as alcohol dependent are linked with increased risks of adverse health consequences.8,9 A special case involves the survival and normal development of the fetus of the drinking pregnant woman.10 In this instance, some authorities would assert that there is no safe level of consumption, or that it may be impossible to define such a level.11 As information grows on how alcohol is hazardous to health we find ourselves less secure in defining what is safe.12,13 Rather, alcohol use involves a continuum of risk, defined by host and environmental factors as well as by the levels of alcohol consumption. ALCOHOL ABUSE AND ALCOHOL DEPENDENCY DEFINITIONS

The definitions of alcohol abuse and dependency have evolved over time, and differ somewhat among various organizations (e.g., the World Health Organization (WHO), American Psychiatric Association [APA]). The WHO has recently published its 10th edition of the International Classification of Diseases (ICD-10),14 while The APA recently 999

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published its fourth edition, text revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR).15 The definitions differ primarily in the number and definition of symptoms required before a diagnosis of alcohol abuse or dependency are met. The ICD-10 and DSM-IV were compared in a study by Caetano.16 The one-year prevalence rate of alcohol dependence was higher (5.5% vs. 3.9%) when ICD-10 criteria were applied as compared to the DSM-IV criteria. Predictors of meeting ICD-10 versus DSM-IV criteria were slightly different in the study, thus highlighting differences in these two criteria sets which should be considered in epidemiological research. The DSM-IV definition is most widely used in alcohol use disorder research in the United States at this time. The DSM-IV15 defines alcohol abuse as a “maladaptive pattern of alcohol use leading to clinically significant impairment or distress, as manifested by one or more of the following, occurring within a 12-month period: (a) recurrent alcohol use resulting in failure to fulfill major role obligations at work, school, or home; (b) recurrent alcohol use in situations in which it is physically hazardous; (c) recurrent alcohol-related legal problems; (d) continued alcohol use despite having a persistent or recurrent social or interpersonal problem caused or exacerbated by the effects of alcohol.” The DSM-IV15 defines alcohol dependence as a “maladaptive pattern of alcohol use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following occurring at any time in the same 12-month period: (a) tolerance; (b) withdrawal; (c) alcohol use in greater quantity or for a longer period than intended; (d) persistent desire or unsuccessful efforts to cut down or control alcohol use; (e) a great deal of time is spent acquiring, using, or recovering from alcohol’s effects; (f) important social, occupational, or recreational activities are given up or reduced because of alcohol use; (g) alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused by or exacerbated by alcohol use.” In the DSM-IV15 classification, once an individual meets dependency criteria, the diagnosis of alcohol abuse should no longer be used for that individual. Course specifiers should be used to describe the individual after no criteria for dependence have been met for at least one month. The course specifiers include early full remission, early partial remission, sustained full remission, sustained partial remission, on agonist therapy, or in a controlled environment. Several observations are important regarding the DSM-IV classification system. The DSM-IV classification emphasizes the central role that alcohol comes to play in the life of a dependent individual, not simply the physiological changes associated with heavy alcohol use. Thus, an individual can be classified as alcohol dependent without classical signs or symptoms of physical tolerance and resultant withdrawal upon abrupt discontinuation of alcohol. Also, complete abstinence is not required before the remission course specifiers can be used. If none of the seven dependence criteria symptoms are met during a period of a month or longer, a form of remission is reached which is defined as either partial or full. If continued drinking does not result in full return of three or more dependence criteria symptoms, but does cause at least one dependence symptom, the remission is considered partial. If the full dependence criteria are not met for 12 months or more, the remission category is considered sustained. The utility and predictive validity of these categories remain to be established. EPIDEMIOLOGY OF ALCOHOL ABUSE AND DEPENDENCY

Alcohol is regularly consumed by slightly more than half of the adult United States population. In the 2003 National Survey on Drug Use & Health (formerly called the National Household Survey on Drug Abuse [NHSDA])17 50.1% of all Americans over age 12 reported consuming alcohol. The prevalence of past month alcohol consumption was higher for men (57.3%) than for women (43.2%). 54.4% of nonblacks and 37.9% of blacks admitted to past month use of alcohol. A total of

22 million people in the United States used alcohol in the past month in 2002 compared to 21.6 million in 2003. For those in the over age 18-year group, 62.4% of males and 46.0% of females were current drinkers. While male drinking percentage remained the same as in 2002, for females there was a 2% decrease from the 47.9% identified in 2002. Of interest is that in the age 12–17 age group, 17.1% of males and 18.3% of females were identified as current drinkers, closing the gender gap. In another study by SAMHSA using data from 2002 to 2003, 50.5% of those surveyed had a drink within the past month and 7.6% of those age 12 and over were identified with alcohol abuse or dependence.18,22 Large population-based studies have demonstrated that the lifetime prevalence of alcohol use disorders (abuse and dependence) is even more common. The Epidemiologic Catchment Area study demonstrated that among community-dwelling, nontreatment seeking individuals, that the lifetime prevalence of alcohol dependency was 13.7%.19 Results from the National Comorbidity Survey (NCS) by Kessler et al. demonstrated a lifetime prevalence of alcohol abuse plus dependency of 14.6% in females and 23.5% in males.20 Given these prevalence rates, a conservative estimate of the number of individuals directly affected by alcohol use disorders is at least 20–30 million in the United States at any given time. Additionally, it should be remembered that the number of individuals affected by those with alcohol use disorders through marriage and family, the worksite, and the highways is far greater than the number of individuals with alcohol use disorder. Surveys done in health care settings present a startling example of alcohol-related costs. In a primary care outpatient setting, problem drinking rates of 8–20% are seen, and between 20–40% of patients admitted to general medical hospitals have a history of alcohol use disorders.21 Medical morbidity of this extent obviously translates into significant mortality. United States data from the National Center for Health Statistics indicate 85,000 deaths due to either excessive or risky drinking in the U.S., making alcohol the third leading actual cause of death in 2000.22 This estimate is considered an underestimate, as many deaths which are associated with alcohol use are not coded as such on death certificates. A review of studies across multiple nations examining alcohol-related mortality demonstrated that alcoholics lose on average more than 20 years of potential life.23 In 1998, the estimated economic cost of alcohol abuse exceeded $184 billion in the United States, equivalent to roughly $638 for every man, woman and child living in the United States.24 Economic costs to industry alone in the United States have been estimated at $136 billion for 1990.25 Such costs include absenteeism, sick leave, decreased worker efficiency, and employee replacement costs through workers quitting, being fired, or dying prematurely. These summary statistics can be further broken down into risk indicators, which are more useful for preventive health purposes, such as targeting screening and prevention efforts. Alcohol use disorders are more common in males than females, with the ratio of affected males:females being approximately 2–3:1. While rates of females affected with alcohol use disorders are lower, health-related consequences of alcohol use in females who do not meet diagnostic criteria for alcoholism are more severe than in males. Review of health-related consequences of alcoholism in females later in this chapter will include medical risks associated with alcohol use in nonalcohol dependent drinkers. Age is another factor which can be used to characterize risk. Alcohol use disorders typically are most common in those under 45 years of age. Health-related morbidity is different across the age span, with more unnatural deaths (e.g., accidents, suicides, homicides) observed in younger age groups and more chronic disorders seen in the older age groups. Screening tools and definitions of alcohol use disorders in the elderly are less satisfactory than in middle age, and thus rates of alcohol use disorders in the elderly may be underestimated. A study in the International Journal of Geriatric Psychiatry, focusing on a review of different screening instruments, found that the AUDIT-5 has had promising results over other instruments such as the CAGE and MAST. No studies of alcohol use disorders in

55 elderly people with cognitive impairment were found, indicating a need for research in this area.26 Alcohol use disorders are seen across all socioeconomic groups. Alcohol use disorders cluster weakly in lower socioeconomic groups, but this may simply be secondary to alcohol’s contribution to poor school and job performance. Persons of Asian decent have lower rates of alcohol related disorders, presumably related to decreased levels of alcohol-metabolizing enzymes leading to flush reactions, tachycardia, and headache. Differences between blacks and nonblacks are significant, generally with nonblack rates being lower in both males and females. Drinking is most prevalent in urban America, and geographically in the Northeast. The comorbidity of alcohol use disorders and other psychiatric disorders is very common. The ECA study found that about half of individuals with alcohol use disorders had a concomitant psychiatric disorder.19 In the 2003 NSDUH study, those with a serious mental illness had a 21.3% rate of alcohol dependence and abuse and those without a serious mental illness had a dependence/abuse rate of 7.9%.17 The most commonly observed psychiatric comorbidities include antisocial personality disorder, mood disorders, and anxiety disorders. GENERAL MECHANISMS OF ALCOHOL-RELATED DYSFUNCTION AND DAMAGE

A general schema of the mechanisms involved in alcohol-related tissue injury is provided in Fig. 55-1. Tissue in this context refers to either a single type of cell or a single organ. Besides having direct toxic effects on target tissue, alcohol also may act indirectly through a variety of mechanisms. Other alcohol-associated behaviors involving tobacco, risky sexual behavior, illicit drugs, and other drugs and chemicals as well as nonalcohol-related disease processes, may contribute as cofactors to the development, course, and outcome of alcohol-induced primary damage. In addition, alcohol may act as a factor influencing the development, course, and outcome of coincidental diseases.

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Much of the tissue damage that occurs in association with alcohol use has been attributed, at least in part, to direct toxic effects; for example, alcoholic hepatitis, cardiomyopathy, and neuronal degeneration. New findings however suggest that excitotoxicity mediated through alterations in glutamate neurotransmission may be responsible for many of the central nervous system (CNS) degenerative processes associated with alcoholism (e.g., WernikeKorsakoff syndrome, cerebellar degeneration, dementia associated with alcoholism).27 The effects on the CNS are of also of great importance in the development of various alcohol-related problems associated with acute intoxication and withdrawal from alcohol, as well as alcohol dependence.27,28 Acute effects are particularly important in circumstances under which drinkers may injure themselves or others.29 Alcohol also may act indirectly through the production of metabolic disturbances, endocrine changes,30 immune system changes,31 aggravation of obstructive sleep apnea,32 and displacement of dietary nutrients or impairment of their absorption or use,33 as well as through the effects of diseases caused by alcohol. Obstructive sleep apnea, a complication of alcohol use that occurs as a result of acute intoxication, is potentially important as a direct cause of morbidity and mortality.32 It may contribute also to the course and outcome of other alcohol- as well as nonalcohol-related diseases. This disturbance and its precipitation and aggravation by alcohol have been recognized only recently.34–36 When an alcohol-related health problem does occur, its course and outcome may be influenced by whether or not the affected individual continues to be exposed to alcohol and alcohol-related hazards. Furthermore, course and outcome may be influenced by whether or not he or she seeks, has access to, receives, and adheres to effective treatment, not only for the complications of alcohol use but also for the drinking behavior itself. A summary of the etiological significance of alcohol and associated variables that contribute to the excess mortality of heavy drinkers is provided in Table 55-1.

Ethanol

Tobacco Potential adverse effects

Direct effects

Illicit drugs

Metabolic

Neuroendocrine

Tissue vulnerable or resistant

Other drugs & chemicals

Non-alcoholic diseases

Consumption

Diseases

Response to infection Indirect effects

Adverse effects on target tissue

Adverse environment

Neglect

Sleep apnea Utilization Absorption Nutrient displacenent

Diet

Figure 55-1. Schematic representation of the general mechanisms involved in the development of alcoholrelated tissue injury.

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TABLE 55-1. ETIOLOGICAL SIGNIFICANCE OF ALCOHOL AND ASSOCIATED VARIABLES IN THE EXCESS MORTALITY OF CHRONIC HEAVY DRINKERS Heavy Tobacco Smoking

Effects of Alcohol

Cause of Death Tuberculosis Carcinoma Mouth Larynx Pharynx Esophagus Liver Lung Alcoholic cardiomyopathy Other cardiovascular disease Pneumonia Peptic ulcers Liver cirrhosis Alcoholic Nonalcoholic Suicide Accidents

Emotional Problems

Poor Food Habits

Other Personal Neglect

Increased Environmental Hazards

X

X

X

X XX XX XX XX X X XX XX XX XX

XX XX XX XX XX XX XX XX X

XX X XX XX

X

X XX X

X

XX

X XX XX X

XX

X

X

X, probably indicated; XX, clearly indicated. Where a space is left blank, either the factor is probably of no significance or its role, if any, is unknown. Source: Modified from Popham RE, Schmidt W, Israelstam S. Heavy alcohol consumption and physical health problems. A review of the epidemiologic evidence. In: Smart RG, Cappell HD, Glaser FB, et al (eds). Research Advances in Alcohol and Drug Problems. New York: Plenum Press, 1984, vol 8, pp 149–182.

Morbidity and Mortality The important health problems related to alcohol use were reviewed by the Institute of Medicine.37 The major health problems associated with alcohol use named in this report included alcohol withdrawal syndrome, psychosis, hepatitis, cirrhosis, pancreatitis, thiamine deficiency, neuropathy, dementia, and cardiomyopathy. Alcohol use also plays a key role in injury and accidents, suicide, and homicide. Also

important is a range of adverse pregnancy outcomes and fetal abnormalities caused by the embryotoxic and teratogenic effects of alcohol. The most common medical problems in alcohol-dependent and heavy drinking men, in terms of decreasing lifetime incidence, are trauma, acute alcoholic liver disease, peptic ulceration, chronic obstructive lung disease, pneumonia, hypertension, gastritis, epileptiform disorders, acute brain syndromes, peripheral neuritis, ischemic heart disease and cirrhosis (Table 55-2).38 This pattern of lifetime

TABLE 55-2. RANKING OF LIFETIME INCIDENCE, RATIO OF OBSERVED TO EXPECTED MORTALITY, AND PERCENTAGE OF EXCESS MORTALITY FOR SELECTED CAUSES IN MALE SAMPLES OF ALCOHOL-DEPENDENT AND OTHER HAZARDOUS DRINKERS Lifetime Incidence (%)a Rank 1 2 3 4 5 6 7 8 9 10 11 12

Disease a

Trauma (81.9) Acute alcoholic liver disease (49.9) Peptic ulcer (22.8) Obstructive lung disease (19.0) Pneumonia (16.8) Hypertension (12.4) Gastritis (11.5) Epileptic disorders (10.9) Acute brain syndromes (7.7) Peripheral neuritis (7.1) Ischemic heart disease (8.1) Cirrhosis (6.4)

Mortality Ratiob Rank 1 2 3 4 5 6 7 8 9 10

Cause of Death b

Cirrhosis (7.6) Suicide (4.4) Upper GI and respiratory cancer (4.1) Accidents (3.5) Tuberculosis (2.8) Peptic ulcer (2.8) Pneumonia (2.3) Cardiovascular disease (1.8) All cancer (1.7) Cerebrovascular disease (1.2)

Excess Mortality (%)c Rank

Cause of Death

1 2 3 4 5 6 7

Cardiovascular disease (21.4)c Suicide (14.7) Accidents (11.1) Cirrhosis (11.0) Malignant neoplasms (11.8) Pneumonia (8.8) Cerebrovascular disease (5)

a Based on lifetime incidence of certain diseases and complications in male patients admitted to a Canadian hospital for the treatment of alcoholism. From Ashley MJ, Olin JS, le Riche WH, et al. The physical disease characteristics of inpatient alcoholics. J Stud Alcohol. 42:1–14, 1981. The percentage, in parentheses, is shown after each disease or complication. b Based on analyses of ratios of observed to expected mortality by cause in male samples of alcohol-dependent and other heavy drinkers. From Popham RE, Schmidt W, Israelstam S. Heavy alcohol consumption and physical health problems. A review of the epidemiologic evidence. In: Smart RG, Cappell HD, Glaser FB, et al (eds). Research Advances in Alcohol and Drug Problems. New York: Plenum Press, 1984, vol 8, pp 149–182. The median mortality ratio, in parentheses, is shown after each cause of death. cBased on analyses of percentages of excess mortality in alcohol-dependent and heavy drinking men attributable to selected causes. From Ashley MJ, Rankin JG. Hazardous alcohol consumption and diseases of the circulatory system. J Stud Alcohol. 41:1040–1070, 1980. The median percentage value for excess mortality, in parentheses, is shown after each cause of death.

55 morbidity contrasts greatly with the ranking in terms of excess mortality, namely, cardiovascular disease, suicide, accidents, cirrhosis, malignant neoplasms, pneumonia, and cerebrovascular disease.39 These differences in patterns of morbidity and mortality are related to the lethality of the conditions, the risk of this population dying from these disorders compared with the community-at-large,40 and the frequency of the conditions in the general adult population. The three most common causes of excess mortality, that is, cardiovascular disease, suicide, and accidents, occur as acute problems, associated with sudden and usually unexpected death, whereas cirrhosis of the liver is the main chronic physical health problem in terms of incapacity and excess morbidity. Alcohol use in females results in exposure to all of the risks reviewed for men. Several consequences of drinking are more common in females, often with less quantity of alcohol use than in males. In females, accidents and suicidal mortality predominate in adolescence and young adulthood as health consequences of drinking. In middle age, breast cancer and osteoporosis become issues of concern. Compared to nondrinkers, women who consume an average of one drink per day, increase their risk of breast cancer by approximately 7% while those who consume an average of 2–5 drinks per day increase their risk by 50%.41 Drinking appears to be more detrimental to women than men with respect to liver disease. Higher cirrhosis rates among female alcoholics as compared to male alcoholics, with females having lower consumption rates has been observed in a variety of studies.42–44 Alcohol is also the most widely used substance associated with domestic violence. Females are most commonly the battered party, and both their use of alcohol and their partner’s use of alcohol appear to increase risk. The risk of HIV/AIDS and alcohol use presents similar concerns in females as well as males. Use of alcohol my influence the risk of acquiring HIV infection both through direct effects on the immune system, as well as increased likelihood of unsafe sexual behavior during periods of intoxication. ESTIMATING THE PUBLIC HEALTH IMPORTANCE OF ALCOHOL-RELATED PROBLEMS

In alcohol-consuming nations the public health importance of alcoholrelated health problems usually is considered by each country to be significant.45 There are differences, however, from country to country, concerning the impact of alcohol-related health problems on the total burden of ill health.

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The impact of alcohol-related health problems is felt, both directly and indirectly, by many different groups. This includes those with alcohol-related health problems, their families, other individuals or groups who may suffer injury or loss due to the use of alcohol by others, those who provide services for the prevention and treatment of alcohol-related problems, and the community at large. Many of the effects are tangible but immeasurable, such as the pain and suffering experienced by the alcohol-damaged individual and his or her family. However, other manifestations of alcohol-related problems are suitable for empirical study, for example, the incidence and prevalence of alcohol-related heath problems, the costs of health and social services attributable to these problems, the number of people who are disabled or die from alcohol-related problems, and the economic costs of illness, disability, and death. It may be possible to make reasonably good estimates for specific aspects of mortality and morbidity, for example, the burden of alcoholic psychoses in specialized institutions. Unfortunately, such direct consequences are only a small part of the total problem. This is illustrated in a report on alcohol-related deaths in Canada in 1980 (Table 55-3). Of the almost 18,000 such deaths (10.5% of all deaths), the vast majority (88%) were classified as indirectly related, that is, they were due to accidents, cancers, and circulatory and respiratory diseases in which alcohol was a contributing factor.46 This problem is further exemplified by U.S. studies in which only about 3% of recorded deaths were officially attributable to alcohol, 1.9% were attributable to an alcoholrelated condition, and the remaining 1.2% had an alcohol-related condition listed along with the specified cause of death.47 These figures are small when compared with estimates that alcoholdependence is responsible for 1 in 10 deaths the United States,48 and when follow-up studies demonstrate high alcohol-related mortality.49 Despite such shortcomings in available statistics, there is no doubt about the serious toll of morbidity and mortality that alcohol use exacts from alcohol-consuming societies, such as the United States and Canada. These countries rank as moderate consuming nations, and one can assume that the toll is higher in heavier consuming nations. Selected indicators of the public health impact of alcohol use in Canada (Table 55-3)46,50 illustrate this clearly. In the period of these studies, 1979–1980, of Canadians 15 years and over, at least 12% regularly were consuming enough alcohol to be at increased risk of health consequences, 5% of current drinkers were alcohol-dependent and almost 10% experienced at least one alcohol-related problem. More than one in 10 deaths were alcoholrelated. In an earlier study of premature deaths and potential years of

TABLE 55-3. SELECTED INDICATORS OF THE PUBLIC HEALTH IMPACT OF ALCOHOL USE IN CANADA Indicator Population 15 years and over drinking 14+ drinks per week53

Year 1978–1979

Selected Findings Overall 12% Age group 20–24

Alcohol-dependent persons49 Current drinkers 15 years and older with alcohol-associated problem49

Current drinkers 15 years and over with at least one alcohol-associated problem49 Alcohol-related deaths49

a

1980 1978–1979

1978–1979

1980

Males 19.4% Females 4.8% Males 31.0% Females 8.1%

600,000 persons; 1 in 19 (5.3% of) current drinkers Tension or disagreement with family or friends Problems with health Difficulty with driving Injury to self or other Trouble with the law Trouble with school or work Overall 9.7% Males 12.4% Females 6.1%

6.1% 2.3% 1.5% 1.3% 1.3% 1.2%

17,974 (10.5%) of all deaths Directly related deaths: 2,110a Indirectly related deaths: 15,864b

Deaths due to alcohol-related cirrhosis, alcohol dependency syndrome, the nondependent abuse of alcohol, alcoholic psychoses, and accidental poisoning by alcohol. Deaths due to motor vehicle accidents, falls, fires, drownings, homicides, suicides (5,554 in 1980), as well as circulatory and respiratory diseases and certain types of cancer (e.g., oral, esophageal, and laryngeal) totaling 10,310 in 1980. b

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TABLE 55-4. ESTIMATED COSTS OF ALCOHOL-RELATED PROBLEMS IN THE UNITED STATES IN 1983 $Billion Core Costs Direct

Indirect

Treatment Health support services Subtotal Mortality Reduced productivity Lost employment Subtotal

13.457 1.549 15.006 18.151 65.582 5.323 89.056 104.062

Motor vehicle crashes Crime Social welfare administration Other Subtotal Victims of crime Incarceration Motor vehicle crashes Subtotal

2.697 2.631 0.049 3.673 9.050 0.194 2.979 0.590 3.763 12.813 116.875

Total core costs Other Related Costs Direct

Indirect

Total other related costs Total Costs

%

12.8

76.2 89.0

7.8

3.2 11.0 100.0

Source: Adapted from U.S. Department of Health and Human Services. Sixth Special Report to the U.S. Congress on Alcohol and Health from the Secretary of Health and Human Services. DHHS Publication No. (ADM) 871519. Rockville, MD: U.S. Government Printing Office, 1987 and U.S. Bureau of the Census: Statistical Abstract of the United States, 106th ed. Washington, DC: U.S. Bureau of the Census, 1985. Gross national product (GNP) in 1983: $3305.0 billion; costs of alcohol-related problems: 3.54% of GNP. Total costs of health services in 1983: $355.4 billion; cost of direct services for alcohol-related problems: 4.22% of total costs of health services.

life lost in Canada in 1974, it was concluded that no other risk factor was responsible for more premature mortality than either smoking or hazardous drinking.51 The adverse health consequences of drinking remain a major health problem, despite evidence since this period of study and in association with a plateauing and modest fall in alcohol consumption, that there has been a significant decline in various indicators of alcohol-related health problems in Canada.52,53 Furthermore, tobacco and alcohol continue to rate first and second as risk factors responsible for premature mortality. A different approach to quantifying the effects of alcohol-related health problems is to express them in monetary terms. Such an approach is useful because it provides an estimate of the relative distribution of the costs, for example, across organ systems or various health and social services, as well as a measure of total costs. Thus, these figures can be used to compare the costs of alcohol-related problems with other health problems as a basis for focusing the attention of the community or making policy decisions regarding the funding of prevention, treatment, and research. An example of an economic approach to measuring the magnitude of alcohol-related problems is contained in Table 55-4, which provides an estimate of the costs of alcohol-related problems in the United States in 1983.54,55 First, notice that the total cost is large, $116.875 billion. Of this amount, 89.0% was attributable to core costs, including losses in productivity associated with disability and death (76.2%) and costs incurred in the treatment and care of people with alcohol-related health problems (12.8%). Total alcohol-related health costs ranked a close second to heart and vascular disease, as the prime health cause of economic loss and were well ahead of cancer and respiratory disease. In this analysis, other related costs covered nonhealth alcohol-related costs attributable to motor vehicle crashes and fires, highway safety and the fire protection, and the criminal justice and social welfare systems. The costs of alcohol-related problems were equal to 3.54% of the gross national product, and the direct costs for health services were equal to 4.22% of the total costs of health services. Although these figures are

large, very likely they are underestimates of the true economic costs of alcohol-related problems.

Prevention Strategies The public health approach to disease prevention was first classified in 1957 as proposed by the Commission on Chronic Illness.56 Primary, secondary, and tertiary prevention techniques were defined. In this model, primary prevention is geared towards efforts to decrease new cases of a disorder (incident cases), secondary prevention is designed to lower the rate of established cases (prevalent cases), and tertiary prevention seeks to decrease the amount of disability associated with existing disorder or illness. Gordon57,58 later proposed an alternative classification system which incorporated the concept of the risks and benefits in the evaluation of prevention efforts. His categories of prevention strategies consisted of universal measures, selective measures, and indicated measures. Universal prevention measures are measures of low cost, and low risk for which benefits outweigh costs when they are applied to everyone in an eligible population. Selective measures are desirable only for a select population at above average risk of development of a disorder. Indicated preventive measures are applied to individuals who, upon screening examination, demonstrate high risk of development of a disorder. The Institute of Medicine (IOM) noted that both of these classification systems were designed and worked best for traditional medical disorders59, but that their application to mental disorders was not straightforward. An alternative system was proposed by the IOM, which is referred to as the Mental Health Intervention Spectrum for Mental Illness. This system incorporates the whole spectrum of interventions for mental disorders, from prevention, through treatment, to maintenance. Table 55-5 outlines this spectrum. The term prevention is reserved for those interventions that occur before the initial onset of the disorder, and it incorporates many of Gordon’s concepts such as universal, selective, and indicated measures.

55 TABLE 55-5. MENTAL HEALTH INTERVENTION FOR MENTAL DISORDERS62 1. Prevention Universal Selective Indicated 2. Treatment Case identification Standard treatment for known disorders 3. Maintenance Compliance with long-term treatment After-care

Universal Prevention Efforts A significant amount of evidence suggests that early use of alcohol along with under-achievement, school problems, and aggressive behavior predict future problem drinking. While some of this risk may be due to genetic vulnerability to alcohol use disorders (covered under selective prevention efforts below), clearly genetic-environmental interactions are likely. Broader community context factors external to the individual are also strong predictors of alcohol use and problems. Community use patterns, availability of alcohol (including legal drinking age, cost, and enforcement), and peer group behavior affect the use and abuse of alcohol. Universal prevention efforts have been tried in various forms. Community-based programs for the prevention of alcohol abuse and alcohol-related problems were recently reviewed by Aquirre-Molina and Gorman.60 This review summarized studies concerned with changing the behavior of individuals rather than environmental changes such as altering availability. Data analysis for many such studies is ongoing and hence their ultimate impact is unknown. Community-based studies designed to change behavior of individuals are difficult to design, implement, and complete. A more direct universal prevention strategy involves limiting availability, increasing enforcement of laws pertaining to alcohol use, legislating stricter laws, improving community standards, and increasing the cost of alcoholic beverages through taxation. A substantial body of evidence now supports the view that increases in overall or per capita consumption are associated with higher rates of heavy drinking and, consequently, with increased frequencies of alcohol-related health problems.61–65 Studies of relationships between per capita alcohol consumption and alcohol-related morbidity and mortality have focused on cirrhosis, where a strong positive correlation has been established.66 Per capita consumption also has been correlated positively with total mortality in men,67 international variations in deaths from diabetes mellitus,68 deaths from alcohol-related disease,69 alcoholism death rates,70 and hospital admission for alcohol dependence, alcoholic psychosis, liver cirrhosis, pancreatitis,71 Wernicke’s encephalopathy, and Korsakoff’s psychosis.72 Recognition of the relationships among per capita alcohol consumption, rates of heavy use, and the incidence of alcohol-related health problems has focused attention on universal prevention strategies aimed at the drinking population, generally with the principal objective of reducing per capita alcohol consumption. Critical reviews suggest that measures addressing the economic and physical accessibility of alcohol are among the most effective in this regard.73

Economic Accessibility Numerous studies, reviews, and reports have examined the use of price control via taxation in reducing alcohol consumption and alcoholrelated problems. The accumulated evidence indicates that price control could be effective and, in some instances, powerful, both in relation to other measures and in combination with them.7,54,74–77 According to Cook78,79 and Cook and Tauchen,80 doubling the federal

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tax on liquor in the United States would reduce the cirrhosis mortality rate by at least 20%. An effect on automobile fatalities also was postulated.78 Holder and Blose81 used a system dynamics model to study the effect of four prevention strategies; raising the retail price of all alcoholic beverages by 25% once, indexing the price of alcoholic beverages to the consumer price index (CPI) each year, raising the minimum drinking age to 21 years, and reducing high-risk alcohol consumption through state-of-the-art public education on alcohol-related family disruptions and alcohol-related work problems, against a background of business as usual in three counties of the United States. Although both outcome measures were modestly sensitive to one-time changes in price, the largest effect was obtained by instituting a community education effort concurrently with indexing the prices of alcoholic beverages to the CPI. From an analysis of the price of beer and spirits, other economic and sociodemographic factors, and various regulatory control variables, Ornstein82 concluded that price was the most important policy tool available to regulators in the United States. A similar conclusion arose from a study of the effects of various regulatory measures on the consumption of distilled spirits in the United States over a 25-year period.83 Levy and Sheflin,84 using methods intended to overcome the problem of beverage substitution when price control is not directed at all beverages, estimated that the price elasticity for total alcohol consumption, although less than one (implying that demand is inelastic), was large enough for price policies to be effective in reducing alcohol consumption. Others,85–90 however, have been more guarded in their support for price manipulation as a control measure, pointing out the methodological limitations in econometric analyses, the modest or conflicting implications of some findings, and the possible role of countervailing forces. In a study of individual drinkers, Kendell and colleagues91,92 found that overall consumption and associated adverse effects fell 18% and 16%, respectively, among 463 “regular drinkers” in the Lothian region of Scotland when prices were increased via the excise duty. Heavy and dependent drinkers reduced their consumption at least as much as light and moderate drinkers, with fewer adverse effects as a result. Clinical data also show that alcohol-dependent persons reduce their alcohol consumption as a function of beverage costs.93,94 Further, in an experimental study of price reductions during afternoon happy hours, Babor and associates95 found that such reductions significantly increased alcohol consumption by both casual and heavy drinkers. With the reinstatement of standard prices, drinking in both groups returned to previous levels. These findings and others75,79,80,96 seriously challenge the previously held view that a reduction in overall consumption does not affect consumption by the heaviest drinkers. Further, liver cirrhosis mortality rates, which are considered the most accurate indicator of the prevalence of heavy drinking, respond directly and rather quickly to major restrictions on availability, including economic ones, that produce declines in per capita consumption.7,62,80 It is reported that 4% of deaths worldwide are due to alcohol, putting alcohol deaths on a par with the 4.1% deaths caused by smoking and the 4.4% of deaths caused by high blood pressure. Aldridge reported that if prices for alcohol increase by 10%, deaths in cirrhotic males decrease by 7%, showing that price increase is effective in reducing harm.97 Price elasticities of alcoholic beverages vary by type of beverage, across time, and among countries.7 In the United States, as in Canada and the United Kingdom, beer tends to be relatively price inelastic.62,98,99 However, this general inelasticity does not hold in certain age groups. Grossman and colleagues100–103 estimated the effects on young people of increases in alcoholic beverage prices with regard to alcohol use and motor vehicle mortality. They showed that for beer, the alcoholic beverage of preference in the young, the price elasticity was considerably higher than that usually reported, a 10 cent increase in the price of a package of six 12-once cans resulting in an 11% decrease in the number of youths drinking beer and a 15% decrease in the number of youthful heavy beer drinkers (3–5 drinks per day).100 Further, they predicted that a national policy simultaneously taxing the alcohol in beer and distilled spirits at the same rates and offsetting the erosion in the real beer tax since 1951 would reduce the number of youths 16–21 years old who drink beer frequently (4–7 times a week, about 11% of youths) and fairly

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frequently (1–3 times a week, about 28% of all youths) by 32% and 24%, respectively.104,105 Additional analyses showed dramatic effects of excise tax policies on motor vehicle accidents in youths.101–103 In a multivariate analysis, it was estimated that a policy that fixed the federal beer tax in real terms since 1951 would have reduced the number of motor vehicle fatalities in youths ages 18–20 in the period 1975–1981 by 15%, and a policy that taxed the alcohol in beer at the same rate as the alcohol in liquor would have lowered fatalities by 21%. A combination of the two policies would have caused a 54% decline in the number of youths killed. In contrast, the enactment of a uniform drinking age of 21 years in all states would have reduced such fatalities by 8%, with considerable additional costs in enforcement. Since the principal objective of price control in the public health context is universal prevention, differentially higher price sensitivity among young drinkers for beer is an especially important finding. Price control via taxation has been recommended repeatedly as a strategy for stabilizing or reducing per capita consumption and, thereby, preventing alcohol-related health problems.77,106–108 In the United States, recent public opinion polls indicate clear, majority support for excise tax increases on alcohol for public health purposes.77 However, federal excise taxes on distilled spirits, wine, and beer remained constant in nominal terms (current dollar value) between November 1, 1951, and the end of fiscal year 1985.101 In 1985, the federal excise tax on distilled spirits was raised slightly (as a deficit reduction measure), but federal tax rates on beer and wine were not changed. Thus, the real price of alcoholic beverages has actually declined in recent years, such that between 1960 and 1980 the real price of liquor declined 48%, beer 27%, and wine 20%.78 A similar situation has been documented in Ontario, Canada, where a taxation policy that would maintain a reasonably constant relationship between the price of alcohol and the consumer price index has been a key element in a long proposed, but unimplemented prevention strategy.106 Examples of increased taxation and improved health outcomes can be see in two more recent studies. In 2000, Switzerland imported 2 million bottles of “alcopops” but that jumped to 39 million bottles in 2002. In 2004, Swiss officials quadrupled taxes on alcopops and slowed consumption and decreased sales to young people by half in doing so.109 In the United States on January 1, 1991, the federal excise tax on beer increased for the first time since 1951.109 The rates of STDs, violence, and traffic fatalities decreased when the price of beer increased.110

Similarly, sudden, marked relaxation in the availability of alcohol is associated with increases in overall consumption, heavy drinking, and alcohol-related problems. The Finnish experience, which included a very marked increase in overall consumption in connection with liberalizing legislation that led to an extensive and rapid increase in outlets in previously dry areas, has been detailed115 and summarized105 elsewhere. A number of additional factors play a role in physical accessibility to alcohol. These factors include the times of sale permitted, the types, characteristics, and location of outlets, and the distribution system of alcoholic beverages. Different positive and negative consequences may be seen as a result of even subtle changes. For example, while restricting the number of outlets may lead to decreased consumption, a rise in automobile crashes associated with alcohol use can be seen due to driving after acquiring the beverage of choice, as location of purchase is related to where it is consumed.116 The rapidity with which community changes are made also of importance upon the outcome of the change.45,105,111 If multiple outlets for alcohol sale are added in formerly dry areas, the subsequent marked increase in overall consumption has been previously discussed.111,115 These examples all point to the need for careful consideration and monitoring of changes made in the physical availability of alcohol in society.

Legal Accessibility Age limitations represent a legal barrier to alcohol. Most countries have age restrictions on its purchase or consumption or both.45 Although the data are neither unflawed nor entirely consistent, there is much evidence that the lower the drinking age, the higher the consumption of alcohol45,101,117–120 and the higher the incidence of alcoholrelated problems, particularly among teenagers.45,105,112,117,118,121,122 Lowered blood alcohol content (BAC) limits for legal driving have recently been instituted in most states in the United States. The effect of such measures on automobile crashes and automobile fatalities will be an important outcome measure. The tradeoff of increased costs, potential social stigma, and consequent increased rates of alcohol use disorder diagnoses for individuals caught with the lowered alcohol blood levels has not been factored into decisions to lower the legal driving limits, but obviously some price will be paid.

Selective Intervention Efforts Physical Availability The relationship between the physical availability of alcohol and alcohol consumption and related problems is multifaceted and complex. It is difficult to show the effect of small changes and to untangle the effects of changes in physical availability that take place simultaneously with others, either nonspecific changes (e.g., in the general economy) or specific changes (e.g., in the economic and legal accessibility of alcohol). It is not surprising, therefore, that the evidence concerning the effectiveness of limitations on physical accessibility is mixed.7,45,61,104,105,111–114 Taken together, there is considerable evidence that controls on physical availability can reduce alcohol-related problems and that the consumption of both heavy and moderate drinkers can be reduced. Prohibition is successful in reducing consumption and attendant health risks.7,45,61,105 Such a situation prevails in some countries today.105 With the institution of Prohibition in the United States earlier in this century, cirrhosis mortality rates fell dramatically and remained well below their former levels during the earlier years and to a considerable extent even in the later years, indicative of greatly decreased consumption.61 On repeal of Prohibition and the subsequent increase in the availability of alcohol, consumption rose, and cirrhosis mortality rates gradually increased toward previous levels. Similar trends have been observed in the face of other severe limitations on availability, for example, in Paris during the two World Wars7,65 and during some strikes and periods of rationing.45,104,105,111 Under such conditions, the consumption of both heavy and moderate drinkers is reduced.104,105,111,112

Selective intervention efforts are those efforts geared towards individuals at greater than average risk of development of alcohol use disorders. The strongest predictor of who will develop alcohol dependency comes from the genetic literature. Family studies of alcoholics have clearly demonstrated that alcohol dependency is familial.123 First-degree offspring of an alcohol dependent parent are threefold to fourfold more likely to develop alcohol dependence than those without such a parent. Family studies are not useful in separating environmental factors from genetic factors important to the development of alcohol dependency. Studies of twins124,125 and adoptees126,127 have produced evidence for such genetic factors, although at this time no alcohol dependency gene has been found. While a gene for alcohol dependency awaits discovery, the results of the adoptee studies have demonstrated that heterogeneity in alcohol dependency exists, that is, there exists at least two types of alcohol dependence. The two types of alcoholism have been referred to as milieu-limited alcoholism, which requires the presence of environmental factors for alcoholism to develop (Type I alcoholism), and male-limited alcoholism (Type II alcoholism), which does not.128 These forms of alcohol dependency differ in terms of age of onset and associated symptoms. Type II alcoholism has an early age of onset, and often serious legal manifestations such as driving while intoxicated and fighting. Furthermore, there is evidence of various biological markers that potentially may prove valuable for targeting high-risk populations for intervention trials that have been discovered through various family and genetic studies of alcoholism.129

55 If a strong family history of alcohol dependence is discovered, it is important to educate unaffected individuals in the pedigree of their enhanced risk. This educational component should be added to the other interventions to be described later in this chapter.

Indicated Intervention Efforts Indicated intervention efforts are targeted towards high-risk individuals who are identified through screening to have hazardous drinking or early symptoms of alcohol dependence that have gone undetected. Screening methods are also important to uncover undiagnosed individuals with alcohol dependence, but who are able to mask such symptoms from others.

Screening for Alcohol Dependence Assessing patients for alcohol use disorders in a busy primary care setting is difficult. The importance of screening for alcoholism in primary care settings is essential to public health efforts to reduce the burden of alcohol-related problems. To ascertain a full history of alcohol use, and to assess whether an individual meets DSM-IV criteria for alcohol abuse or dependency, is generally considered too time consuming by many clinicians, and some doubt exists among clinicians of the validity of selfreport regarding use of alcohol. In 2000, only 37% of family physicians felt that their intervention could change an alcoholic’s drinking habits despite 88% of physicians asking new outpatients whether they drank alcohol and 13% using formal screening tools.130 Because of these concerns, a variety of screening tools have been proposed. The most commonly used tools are screening questionnaires and laboratory values. The most common screening questionnaires include the Michigan Alcoholism Screening Test (MAST),131 the abbreviated Brief-MAST,132 and the CAGE instrument.133 Several newer instruments include the Alcohol Use Disorders Identification Test (AUDIT)139 and the TWEAK instrument.140 Laboratory screening tests include blood alcohol levels, liver enzymes elevations, erythrocyte mean corpuscular volume, lipid profiles, and carbohydrate-deficient transferrin.

Screening Questionnaires A number of review articles are available which describe the use of alcohol use screening questionnaires. The U.S. Preventive Services Task Force’s Guide to Clinical Preventive Services, 2nd Edition136 provides a detailed review of the sensitivity and specificity for the MAST (84–100% and 87–95% respectively), Brief-MAST (66–78% and 80% respectively), CAGE (74–89% and 79–95% respectively for alcohol abuse and dependence; but only 49–73% sensitivity for heavy alcohol use), and the AUDIT134 (96% and 96% respectively in an inner city clinic; but only 61% and 90% in a rural setting). These sensitivity and specificity figures are for middle-aged adults. Adolescents and the elderly may not be as adequately screened by these instruments. Other limitations of these screening instruments include the MAST being rather lengthy for routine use (25 questions), the CAGE being most sensitive for alcohol abuse or dependency and not heavy drinking, and both the CAGE and MAST fail to distinguish current from lifetime problems due to alcohol. The AUDIT is very sensitive and specific for “harmful and hazardous drinking,” but uses a one-year timeframe for screening and hence is less sensitive for past drinking problems. Allen et al.137 offer guidelines for selection of screening tests in primary care. Based upon their review of the literature, use of the AUDIT, CAGE, or MAST was recommended. Because of time constraints in primary care, the AUDIT or CAGE were first choice recommendations, and the TWEAK was recommended for pregnant women.135 For adolescents, the adolescent drinking index (ADI)138 was suggested as a good option. In the elderly, two studies139,140 point to deficiencies in the CAGE as a screening tool, and suggest the need for more sensitive and specific tools in this population. Adams et al.140 suggests asking about quantity and frequency of alcohol use in addition to the CAGE to

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increase the detection of elderly hazardous drinking. O’Connell, et al. reported that the AUDIT-5 has had promising results as well in the elderly.26 The National Institute on Alcohol Abuse and Alcoholism (NIAAA) in collaboration with the American Medical Association offers the Helping Patients with Alcohol Problems: A Health Practitioner’s Guide free to help primary care physicians with patients who are risky drinkers. A growing body of research has shown that primary care practitioners can promote significant reductions in drinking levels of problem drinkers who are not alcohol dependent.141

Laboratory Screening Tools Alcohol induces a number of laboratory abnormalities. Unfortunately, to date laboratory tests for screening have not been as sensitive nor as specific for alcohol use disorders when compared to the screening questionnaires reviewed above. Liver enzymes, including gamma glutamyltransferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase have all been used as screening tests. The GGT is the most useful of the liver tests. It demonstrates a sensitivity of between 50–90% for ingestion of 40–60 g of alcohol daily (3–4 standard drinks).142 The GGT rises most rapidly in response to heavy alcohol use, and with abstinence it returns to normal most rapidly. Other liver enzyme tests such as the AST, ALT, and alkaline phosphatase are less specific and sensitive than the GGT. Some have suggested use of the AST:ALT ratio of 1.5–2:1 as being an indicator of liver damage being more likely due to alcohol than other causes. While the AST and ALT are not adequately sensitive or specific to be recommended as screening laboratory tests, they have some utility as supportive tests. The GGT may be most useful as a marker for return to heavy drinking after a period of abstinence in which the GGT has returned to normal. If the GGT rises by 20%, a high likelihood for return to drinking can be assumed. Increase in mean corpuscular volume (MCV) is less sensitive to alcohol use than elevation in the GGT, but it is quite specific to heavy alcohol intake (up to 90%).143 Utility of the MCV is much like that of the AST and ALT, that is, helpful as supporting evidence, but not as a screening tool. The blood alcohol concentration (BAC) is useful, and can even support a diagnosis of alcohol dependence as outlined by the National Council on Alcoholism (NCA).144 A BAC of 100 mg/100 mL is considered a legally intoxicated level in most states, and is conclusive evidence for a driving while intoxicated charge. Individuals nontolerant to alcohol will generally appear intoxicated at such levels. A BAC of 150 mg/100 mL without gross evidence of intoxication suggests significant tolerance to alcohol, and fulfills criteria for alcohol dependence according to the NCA. A BAC of 100 mg/100 mL during a routine physical examination is highly suggestive of alcohol use problems according to the NCA. Thus, screening of BAC in patients who may appear intoxicated or smell of alcohol during a clinic visit can be very useful. A breath analysis of BAC is also a useful tool, and can be used to screen for individuals too impaired to drive home from emergency rooms or clinic visits if intoxication is suspected, and serum BAC cannot be readily performed or if patients refuse blood drawing. Carbohydrate-deficient transferrin (CDT), a protein associated with iron transport, appears to effectively distinguish alcoholics consuming large amounts of alcohol from light social drinkers or abstinent individuals. CDT levels (which elevate due to few conditions other than heavy drinking) decrease the probability of false positives and elevate substantially earlier with heavy drinking than GGT levels. While excellent sensitivity and specificity could be demonstrated, disadvantages include lower sensitivity in women and adolescents, and the high cost of the laboratory analysis.145 Presently, none of the laboratory markers reviewed offer advantages in sensitivity or specificity over the screening questionnaires reviewed. However, in a general medical setting, liver enzymes and

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MCV are often ordered as part of the medical work-up for individuals presenting for care. The laboratory studies in combination with screening questionnaires can be useful in discussions with patients regarding the health consequences of their alcohol use.

Treatment Interventions This chapter is devoted primarily to prevention strategies. While this is the focus of the chapter, unless primary care clinicians become aware of their potential impact on reducing hazardous and problem drinking, it is doubtful that prevention strategies will be emphasized. Similarly, physicians are unlikely to inquire about alcohol use if they feel they lack the skills to intervene or if they feel interventions are unsuccessful. In a survey of Australian medical trainees in internal medicine, psychiatry, and general practice, there was a high level of agreement that alcohol use history should be obtained from all patients, and that problem drinking should be managed, but views on treatment were less positive.146 There was considerable uncertainty regarding treatment modalities most readily available to the primary care physician, that is, brief advice and cognitive-behavioral therapies. In this study, the trainees were most certain that alcoholics anonymous (AA) techniques for treatment were well supported in the literature. While AA has been a well-supported and beneficial treatment for alcohol-dependent individuals since its beginnings in 1935, its fellowship is most appropriate for individuals who are alcohol-dependent and less likely to be an acceptable treatment modality for patients who are nondependent, but who are displaying hazardous drinking styles. This distinction is imperative, as the hazardous drinking population far exceeds the dependent population of drinkers, and as previously noted contributes greatly to the societal burdens of alcohol use problems. The hazardous, but nondependent, population of drinkers is also more likely to respond to brief interventions for alcohol problems. Another reason the primary care physician should be familiar with brief intervention techniques involves the lack of many alcohol-dependent individuals to follow through on recommendations to seek more formal treatment on referral. In a study of 1200 emergency room patients diagnosed as alcohol dependent advised to seek treatment, only 5% did so.147 A similar finding was noted in a study of U.S. veterans screened for at-risk drinking. Of those who were identified as having at-risk drinking, only 5% followed advice to return for a single consultation session regarding their drinking.148 These studies point to the need for the primary care physician to be skilled in office-based techniques to help patients modify and reduce or stop their alcohol use.

Effective Intervention Recent evidence strongly suggests that brief interventions in the early stages of heavy drinking are both feasible and effective.148,149 Edwards and colleagues,150 in a controlled clinical trial of intensive inpatientoutpatient treatment versus brief advice for alcoholism, found the latter to be more effective in nondependent alcohol abusers after two years of follow-up,151 whereas physically dependent patients achieved better results with more intensive treatment. In a randomized controlled trial of general practitioner intervention in patients with excessive alcohol consumption, Wallace and associates152 showed that advice on reducing alcohol consumption was effective. If the results of their study were applied to the United Kingdom, intervention by general practitioners in the first year could reduce to moderate levels the alcohol consumption of some 250,000 men and 67,500 women who currently drink to excess. Other studies have shown the effectiveness of brief intervention in socially stable, healthy, problem drinkers who do not have a high degree of alcohol dependence and whose histories of problem drinking are short.153–157 A careful assessment of alcohol dependence in detected heavy drinkers underpins the determination of the appropriateness of brief intervention.158

To examine whether brief intervention has benefits beyond one year, investigators in Norway159 reassessed 247 adults who in 1986 had been drinking at least 2–3 times per week, had elevated GGT levels and had entered a randomized trial of brief intervention. They received either a 10-minute discussion of possible reasons for elevated GGT or 15 minutes of counseling regarding decreasing drinking and monthly visits until GGT levels normalized or no intervention. Nine years after the original trial (70% follow-up) those who had received brief intervention, had significant decreases in GGT levels. The better outcomes among drinkers with high GGT levels than among those with lower levels suggests that the intervention played a role. This study suggests that brief intervention for risky drinking may be more effective than previously thought. The degree of alcohol dependence also is crucial in determining whether the treatment goal should be moderation (i.e., controlled drinking) or abstinence.149,158,160 Moderation appears to be a realistic alternative in problem drinkers who are not heavily alcohol dependent, as is often the case in the early-stage heavy drinkers.149,154,158,161–163 It may be a more acceptable treatment goal, particularly in environments where alcohol use is especially diffuse163 and among young drinkers, who may perceive the costs of abstinence to outweigh the risks from continued drinking.158,164 A five-step early intervention and treatment strategy for use in clinical practice settings has been developed158, along with self-help manuals149 and procedures for teaching moderate drinking and abstinence.164 Evaluations of brief interventions conducted as part of a general health screening project,165 among problem drinkers in a general hospital,166,167 in community referral centers for referred problem drinkers,161,168 and in a family practice setting169 are promising. This approach may be applicable beyond the clinical setting, for example, in the workplace, with considerable potential for public health impact.153,161 A review of 32 controlled studies of brief interventions demonstrate effectiveness of such techniques across 14 nations.148 Skinner170 has discussed the reasons why early detection and effective intervention strategies deserve major emphasis. To summarize: most heavy drinkers do not seek treatment for their alcohol problems, socially stable persons at early stages of problem drinking have a better prognosis, health professionals in primary care settings are in an excellent position to identify problem drinkers, and brief intervention by health professionals can be effective in reducing heavy alcohol use. Skinner cited reasons why early detection and effective intervention are not occurring, namely, widespread pessimism among health professionals about being able to intervene effectively, confusion regarding responsibility for confronting alcohol problems, uncertainly about the target population, lack of appreciation of what are appropriate interventions, and deficiencies in the practical skills and techniques to carry them out. He suggested that training materials and opportunities be readily available and incorporated into core education programs, and that strenuous efforts be made to convince key people in the health professions to give early detection and effective intervention a high priority.

SUMMARY

Alcohol use problems are not restricted to those with alcohol abuse or dependency. Recognition of hazardous drinking as being linked to many health-related and societal burdens of alcohol is a first step towards a rational public health policy. Primary care providers are asked to screen for and be able to treat many different disorders. Alcohol use problems have, for too long, been viewed as either untreatable, or in all cases needing specialty management. Evidence exists that office screening tools, combined with relatively brief interventions, can be powerful methods to help assist a large population at risk. While the alcohol screening must compete with many disorders for primary care providers’ attention, it is hoped that the data presented in this chapter will raise the priority of alcohol use disorder in the minds of those caregivers.

55 REFERENCES

1. Kreitman N. Alcohol consumption and the prevention paradox. Br J Addict. 1986;81:353–63. 2. Davidson DM. Cardiovascular effects of alcohol. West J Med. 1989;151:430–39. 3. National Institute on Alcohol Abuse and Alcoholism: Moderate drinking. Alcohol Alert No. 16. Bethesda, MD: U.S. Department of Health and Human Services; 1992. 4. Dietary Guidelines Advisory Committee. Report of the Dietary Guidelines Advisory Committee on the Americans, 2005, to the Secretary of Health and Human Services and the Secretary of Agriculture. Washington, DC: U.S. Department of Agriculture; 2005. 5. Secretary of State for Health. The Health of the Nation: A Strategy for Health in England. London: Her Majesty’s Stationery Office; 1992. 6. Pols RG, Hawks DV. Is there a safe level of daily consumption of alcohol for men and women? Recommendations responsible drinking behavior. Technical Report for the National Health and Medical Research Council, Health Care Committee. Canberra: Australian Government Publishing Service; 1987. 7. Bruun K, Edwards G, Lumio M, Makeli K, Pan L, Popham RE, et al. Alcohol Control Policies: Public Health Perspective. Vol 25. The Finnish Foundation for Alcohol Studies. Helsinki: Finnish Foundation for Alcohol Studies; 1975. 8. Kreitman N. Alcohol consumption and the prevention paradox. Br J Addict. 1986;81:353–63. 9. Pequignot G, Tuyns A. Rations d’alcool consommees “declarers” et risques pathologiques. In: INSEAM. Paris; 1975:1–15. 10. Streissguth AP, Clarren SK, Jones KL. Natural history of the fetal alcohol syndrome. Lancet. 1985;2:85–92. 11. Little RE, Streissguth AP. Effects of alcohol on the fetus: impact and prevention. Can Med Assoc J. 1981;125:159–64. 12. Lieber CS: Medical disorders of alcoholism. N Engl J Med. 1995;333(16):1058–65. 13. Popham RE, Schmidt W. The biomedical definition of safe alcohol consumption: a crucial issue for the researcher and the drinker. Br J Addict. 1978;73:233–5. 14. World Health Organization (WHO). The ICD-10 Classification of Mental and Behavioural Disorders. Geneva: World Health Organization, 1992. 15. American Psychiatric Association. DSM-IV-TR: Diagnostic and Statistical Manual of Mental Disorders. 4th ed., Text Revision. Washington, DC: American Psychiatric Association, 2000. 16. Caetano R, Tarn TW. Prevalence and correlates of DSM-IV and ICD-10 alcohol dependence: 1990 U.S. national alcohol survey. Alcohol Alcohol. 1995;30:177–86. 17. Department of Health and Human Services, National Survey on Drug Use and Health, SAMHSA, Office of Applied Studies, Rockville, MD; 2003. 18. Office of Applied Studies. Results from the 2005 National Survey on Drug Use and Health: National Findings. SAMHSA, U.S. Department of Health and Human Services, 2005. Available at www.oas.samhsa.gov. 19. Helzer J. Psychiatric diagnoses and substance abuse in the general population: the ECA data. NIDA Res Monogr. 1988;81:405–15. 20. Kessler RC. McGonagle KA, Shanyang Z, Nelson CB, Hughes M, Eshleman S, et al. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States: results from the national comorbidity survey. Arch Gen Psychiatry. 1994;51:8–19. 21. Allen JP, Maisto SA, Connors GJ. Self-report screening tests for alcohol problems in primary care. Arch Intern Med. 1995;155(16): 1726–30. 22. Mokdad A, Marks J, Stroup D, Gerberding J. Actual cause of death in the United States. JAMA. 2004;291:1238–45.

Alcohol-Related Health Problems

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23. Poldrugo F, Chick JD, Moore N, Walburg JA. Mortality studies in the long-term evaluation of treatment of alcoholics. Alcohol Alcohol Suppl. 1993;2:151–5. 24. National Institute on Alcohol Abuse and Alcoholism, 2000. 10th Special Report to the U.S. Congress, Chapter 6, NIH Publication 001583, Rockville, MD: Department of Health and Human Services; 2000. 25. Burke TR. The economic impact of alcohol abuse and alcoholism. Public Health Rep. 1988;103:564–8. 26. O’Connell H, Chin A, Hamilton F, Cunningham C, Walsh JB, Coakley D, et al. A systematic review of the utility of self-report alcohol screening instruments in the elderly. Int J Geriatr Psychiatry. 2004;19:1074–86. 27. Tsai G, Gastfriend DR, Coyle JT. The glutamatergic basis of human alcoholism. Am J Psychiatry. 1995;152(3):332–40. 28. Gross MM. Psychobiological contributions to the alcohol dependence syndrome: a selective review of recent research. In: Edwards G, Gross MM, Keller M, et al, eds. Alcohol Related Disabilities. Geneva: World Health Organization; 1977:107–31. 29. Borkenstein RF, Crowther RF, Shumate RP, Ziel WB, Zylman R. The Role of the Drinking Driver in Traffic Accidents. Bloomington, IN: Department of Police Administration, Indiana University; 1964. 30. Lieber CS. Medical disorders of alcoholism. Pathogenesis and treatment. In: Smith LH, Jr, ed. Major Problems in Internal Medicine. Vol 22. Philadelphia: WB Saunders; 1982. 31. Kronfol Z, Nair M, Hill E, Kroll P, Brower K, Greden J. Immune function in alcoholism: a controlled study. Alcohol Clin Exp Res. 1993;17:279–83. 32. Remmers JE. Obstructive sleep apnea. A common disorder exacerbated by alcohol. Am Rev Respir Dis. 1984;130:153–5. 33. Rankin JG. Alcohol—a specific toxin or nutrient displacer. In: Hawkens WW, ed. Drug-Nutrient Interrelationships: Nutrition & Pharmacology—An Interphase of Disciplines, Miles Symposium III. Hamilton, Ontario: McMaster University; 1974:71–87. 34. Issa FQ, Sullivan CE. Alcohol, snoring and sleep apnea. J Neurol Neurosurg Psychiatry. 1983;45:353–9. 35. Bonora M, Shields GI, Knuth SL, Bartlett D Jr, St. John WM. Selective depression by ethanol of upper airway respiratory motor activity in cats. Am Rev Respir Dis. 1984;130:156–61. 36. Krol RC, Knuth SL, Bartlett D Jr. Selective reduction of genioglossal muscle activity by alcohol in normal human subjects. Am Rev Respir Dis. 1984;129:247–50. 37. Institute of Medicine. Causes and Consequences of Alcohol Problems: An Agenda for Research. Washington, DC: National Academy Press; 1987. 38. Ashley MJ, Olin JS, le Riche WH, Kornaczewski A, Schmidt W, Corey PN, et al. The physical disease characteristics of inpatient alcoholics. J Stud Alcohol. 1981;42:1–14. 39. Ashley MJ, Rankin JG. Hazardous alcohol consumption and diseases of the circulatory system. J Stud Alcohol. 1980;41:1040–70. 40. Popham RE, Schmidt W, Israelstam S. Heavy alcohol consumption and physical health problems. A review of the epidemiologic evidence. In: Smart RG, Cappell HD, Glaser FB, et al, eds. Research Advances in Alcohol and Drug Problems. Vol 8. New York: Plenum Press; 1984:149–82. 41. American Cancer Society. Detailed Guide: Breast Cancer, 2006. http://documents.cancer.org/104.00/104.00.pdf. 42. Pequignot G, Chabert C, Eydoux H, Courcoul MA. Increased risk of liver cirrhosis with intake of alcohol. Rev Alcohol. 1974;20:191–202. 43. Wilkinson P, Santamaria JN, Rankin JG. Epidemiology of alcoholic cirrhosis. Australas Ann Med. 1969;18:222–6. 44. Loft S, Olesen KL, Dossing M. Increased susceptibility to liver disease in relation to alcohol consumption in women. Scand J Gastroenterol. 1987;22:1251–6.

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Behavioral Factors Affecting Health

45. Moser J. Prevention of Alcohol-Related Problems: An International Review of Preventive Measures, Policies, and Programmes. Published on behalf of the World Health Organization, Toronto: Alcoholism and Drug Addiction Research Foundation; 1980. 46. Health and Welfare Canada. Alcohol in Canada. A National Perspective. 2nd ed. Ottawa: Health and Welfare Canada; 1984 47. Van Natta P, Malin H, Bertolucci D, Kaelber D. The influence of alcohol abuse as a hidden contributor to mortality. Alcohol. 1985;2: 535–9. 48. U.S. Department of Health and Human Services. Fifth Special Report to the U.S. Congress on Alcohol and Health from the Secretary of Health and Human Services. DHHS Publication No. (ADM) 841291. Washington, DC: U.S. Government Printing Office; 1983. 49. Finney JW, Moos RH. The long-term course of treated alcoholism: I. Mortality, relapse, and remission rates and comparisons with community controls. J Stud Alcohol. 1991;52(l):44–54. 50. Ableson J, Paddon P, Strohmenger C. Perspectives on Health. Ottawa, Ontario: Statistics Canada; 1983. 51. Ouellet BL, Romeder JM, Lance JM. Premature mortality attributable to smoking and hazardous drinking in Canada. Am J Epidemiol. 1979;109:451–63. 52. Smart RG. Mann RE. Large decreases in alcohol-related problems following a slight reduction in alcohol consumption in Ontario 1975–83. Br J Addict. 1987;82:285–91. 53. Mann RE, Smart RG, Anglin L. Reductions in liver cirrhosis mortality in Canada: demographic differences and possible explanations. Alcohol Clin Exp Res. 1988;12:1–8. 54. U.S. Department of Health and Human Services. Sixth Special Report to the U.S. Congress on Alcohol and Health from the Secretary of Health and Human Services. DHHS Publication No. (ADM) 871519. Rockville, MD: U.S. Government Printing Office; 1987. 55. U.S. Bureau of the Census. Statistical Abstract of the United States. 106th ed. Washington, DC: 1985. 56. Commission on Chronic Illness. Chronic Illness in the United States. Vol 1. Cambridge, MA: Harvard University Press; 1957. 57. Gordon R. An operational classification of disease prevention. Public Health Rep. 1983;98:107–9. 58. Gordon R. An operational classification of disease prevention. In: Steinberg JA, Silverman MM, eds. Preventing Mental Disorders. Rockville MD: U.S. Department of Health and Human Services; 1987:20–6. 59. Institute of Medicine. Reducing Risks for Mental Disorders. Washington DC: National Academy Press; 1994. 60. Aguirre-Molina M, Gorman DM. Community-based approaches for the prevention of alcohol, tobacco, and other drug use. Annu Rev Public Health. 1996;17:337–58. 61. Popham RE, Schmidt W, de Lint J. The effects of legal restraint on drinking. In: Kissin B, Begleiter H, eds. The Biology of Alcoholism, Vol 4. Social Aspects of Alcoholism. New York: Plenum Press; 1976:579–625. 62. Terris M. Epidemiology of cirrhosis of the liver. Am J Public Health. 1967;57:2076–88. 63. Makela K. Concentration of alcohol consumption. Scand Studies Ciminol. 1971;3:77–88. 64. Schmidt W. Cirrhosis and alcohol consumption: an epidemiologic perspective. In: Edwards G, Grant M, eds. Alcoholism: New Knowledge New Responses. London: Croom Helm; 1977:15–47. 65. Schmidt W, Popham RE. An approach to the control of alcohol consumption. In: Rutledge B, Fulton EK, eds. International Collaboration: Problems and Opportunities. Toronto: Addiction Research Foundation of Ontario; 1977:155–64. 66. Schmidt W. The epidemiology of cirrhosis of the liver: a statistical analysis of mortality data with special reference to Canada. In: Fisher MM, Rankin JG, eds. Alcohol and the Liver. New York: Plenum Press; 1976:1–26.

67. Ledermann S. Alcool, Alcoolisme, Alcoolization: Mortalite, Morbitite. Accidents du Travail Institut National d’Etudes Demographiques, Travaux et Documents, Carrier. No 41. Paris: Presses Universitaires de France; 1964. 68. Keilman PA. Alcohol consumption and diabetes mellitus mortality in different countries. Am J Public Health. 1983;73:1316–7. 69. La Vecchia C, Decarli A, Mezzanotte G, Cislaghi C. Mortality from alcohol-related disease in Italy. J Epidemiol Community Health. 1986;40:257–61. 70. Imaizumi Y. Alcoholism mortality rate in Japan. Alcohol Alcohol. 1986;21:159–62. 71. Poikolainen K. Increasing alcohol consumption correlated with hospital admission rates. Br J Addict. 1983;78:305–9. 72. Truswell AS, Apeagyei F. Incidence of Wernicke’s encephalopathy and Korsakoff s psychosis in Sydney. Paper presented at: Meeting on Alcohol, Nutrition and the Nervous System. Coppleston Postgraduate Medical Institute; March 18, 1981; University of Sydney. 73. Ashley MJ, Rankin JG. A public health approach to the prevention of alcohol-related health problems. Annu Rev Public Health. 1988;9:233–71. 74. Makela K, Room R, Single E, Sulkunen P, Walsh B. Alcohol, Society, and the State I: A Comparative Study of Alcohol Control. Toronto: Addiction Research Foundation; 1981. 75. Popham RE, Schmidt W, de Lint J. The prevention of alcoholism: epidemiological studies of the effects of government control measures. Br J Addict. 1975;70:125–4. 76. Rush B, Steinberg M, Brook R. The relationship among alcohol availability, alcohol consumption and alcohol-related damage in the Province of Ontario and the State of Michigan 1955–1982. Adv Alcohol Subst Abuse. 1986;5:33–4. 77. Wagenaar AC, Farrell S. Alcohol beverage control policies: their role in preventing alcohol-impaired driving. In: Surgeon General’s Workshop on Drunk Driving. Background Papers, Washington, DC, December 14–16. 1988. Rockville, MD: Office of the Surgeon General; 1989. 78. Cook PJ. The effect of liquor taxes on drinking, cirrhosis and auto accidents. In: Moore MH, Gerstein DR, eds. Alcohol and Public Policy: Beyond the Shadow of Prohibition. Washington, DC: National Academy; 1981. 79. Cook PJ. Alcohol taxes as a public health measure. Br J Addict. 1982;77:245–50. 80. Cook PJ, Tauchen G. The effect of liquor taxes on heavy drinking. Bell J Econ. 1982;13:379–90. 81. Holder HD, Blose JO. Reduction of community alcohol problems: computer simulation experiments in three counties. J Stud Alcohol. 1987;48:124–35. 82. Ornstein SI. A survey of findings on the economic and regulatory determinants of the demand for alcoholic beverages. Subst Alcohol Actions Misuse. 1984;5:39–44. 83. Hoadley JF, Fuchs BC, Holder HD. The effect of alcohol beverage restrictions on consumption: a 25-year longitudinal analysis. Am J Drug Alcohol Abuse. 1984;10:375–401. 84. Levy D, Sheflin N. New evidence on controlling alcohol use through price. J Stud Alcohol. 1983;44:929–37. 85. Davies P. The relationship between taxation, price and alcohol consumption in the countries of Europe. In: Grant M, Plant M, Williams A, eds. Economics and Alcohol: Consumption and Controls. London: Croom Helm; 1983. 86. Maynard A. Modeling alcohol consumption and abuse: the powers and pitfalls of economic techniques. In: Grant M, Plant M, Williams A, eds. Economics and Alcohol: Consumption and Controls. London: Croom Helm; 1983. 87. Walsh BM. The economics of alcohol taxation. In: Grant M, Plant M, Williams A, eds. Economics and Alcohol: Consumption and Controls. London and Canberra: Croom Helm; 1983.

55 88. McGuinness T. The demand for beer, spirits and wine in the UK, 1956–1979. In: Grant M, Plant M, Williams A, eds. Economics and Alcohol: Consumption and Control. London: Croom Helm; 1983. 89. Heien D, Pompelli G. Stress, ethnic and distribution factors in a dichotomous response model of alcohol abuse. J Stud Alcohol. 1987;48:450–5. 90. Walsh BM. Do excise taxes save lives? The Irish experience with alcohol taxation. Accid Anal Prev. 1987;19:433–48. 91. Kendell RE, de Roumanie M, Ritson EB. Effect of economic changes on Scottish drinking habits, 1978–1982. Br J Addict. 1983;78:365–79. 92. Kendell RE, de Roumanie M, Ritson EB. Influence of an increase in excise duty on alcohol consumption and its adverse effects. Br Med J. 1983;287:809–11. 93. Bigelow G, Liebson I. Cost factors controlling alcohol drinking. Psychol Record. 1972;22:305–14. 94. Mello NK. Behavioural studies of alcoholism. In: Kissin B, Begleiter H, eds. The Biology of Alcoholism, Vol 3. Physiology and Behaviour. New York: Plenum; 1972. 95. Babor TF, Mendelson JH, Greenberg I, Kuehnle JC. Experimental analysis of the “happy hour.” Effects of purchase price on alcohol consumption. Psychopharmacology. 1978;58:35–44. 96. Moore MH, Gerstein DR. Alcohol and Public Policy: Beyond the Shadow of Prohibition. Washington, DC: National Academy Press; 1981:116. 97. Aldridge S. Alcohol deaths world wide. Lancet. February, 2005. 98. Duffy M. The influence of prices, consumer incomes and advertising upon the demand for alcoholic drink in the United Kingdom. Br J Alcohol Alcohol. 1981;16:200–8. 99. Ornstein SI. Control of alcohol consumption through price increases. J Stud Alcohol. 1980;41:807–18. 100. Grossman M, Coate D, Arluck GM. Price sensitivity of alcoholic beverages in the United States. In: Holder HD, ed. Control Issues in Alcohol Abuse Prevention: Strategies for Communities. Greenwich, CT: JAI Press; 1987. 101. Coate D, Grossman M. Change in alcoholic beverage prices and legal drinking ages: effects on youth alcohol use and motor vehicle mortality. Alcohol Health Res World. 1987;12:22–5, 59. 102. Saffer H, Grossman M. Beer taxes, the legal drinking age, and youth motor vehicle fatalities. J Legal Stud. 1987;16:351–74. 103. Saffer H, Grossman M. Drinking age laws and highway mortality rates: cause and effect. Econ Inquiry. 1987;25:403–18. 104. Room R. Alcohol control and public health. Annu Rev Public Health. 1984;5:293–317. 105. Farrell S. Review of National Policy Measures to Prevent AlcoholRelated Problems. Geneva: World Health Organization; 1985. 106. Schmidt W, Popham RE. Alcohol Problems and Their Prevention. A Public Health Perspective. Toronto: Addiction Research Foundation; 1980. 107. Mosher JF, Beauchamp DE. Justifying alcohol taxes to public officials. J Public Health Policy. 1983;4:422–39. 108. Vernberg WB. American Public Health Association. Alcohol tax reform. Proposed Position Paper, American Public Health Association. Nation’s Health. August, 1986. (Proposed Position Paper.) 109. Huber M. Swiss tax hike causes alcopop sales to fall. Swissinfo. 2005. 110. Chesson H, Harrison P, Kessler WJ. Sex under the influence: the effect of alcohol policy on sexually transmitted disease rates in the United States. J of Law and Econ. 2000;XLII:215–38. 111. Addiction Research Foundation. Alcohol, public education and social policy. Report of the Task Force on Public Education and Social Policy. Toronto: Addiction Research Foundation, 1981. 112. Single E. International perspectives on alcohol as a public health issue. J Public Health Policy. 1984;5:238–56.

Alcohol-Related Health Problems

1011

113. Smith DI. Effectiveness of restrictions on availability as a means of reducing the use and abuse of alcohol. Aust Alcohol Drug Rev. 1983;2:84–90. 114. MacDonald S. Whitehead P. Availability of outlets and consumption of alcoholic beverages. J Drug Issues. 1983;13:477–86. 115. Makela K, Osterberg E, Sulkunen P. Drink in Finland: increasing alcohol availability in a monopoly state. In: Single E, Morgan P, de Lint J, eds. Alcohol, Society and the State. 2. The Social History of Control Policy in Seven Countries. Toronto: Addiction Research Foundation; 1981. 116. Ryan BE, Segars L. Mini-marts and maxi-problems. The relationship between purchase and consumption levels. Alcohol Health Res World. 1987;12:26–9. 117. Smart RG, Goodstadt MS. Effects of reducing the legal alcohol purchasing age on drinking and drinking problems. A review of empirical studies. J Stud Alcohol. 1977;38:1313–23. 118. Vingilis ER, DeGenova K. Youth and the forbidden fruit: Experiences with changes in the legal drinking age in North America. J Criminal Justice. 1984;12:161–72. 119. Williams TP, Lillis RP. Changes in alcohol consumption by 18-year-olds following an increase in New York State’s purchase age to 19. J Stud Alcohol. 1986;47:290–6. 120. Engs RC, Hanson DJ. Age-specific alcohol prohibition and college students drinking problems. Psychol Rep. 1986;59:979–84. 121. Smith DI, Burvill PW. Effect on juvenile crime of lowering the drinking age in three Australian states. Br J Addict. 1986;82: 181–8. 122. Cook PJ, Tauchen G. The effect of minimum drinking age legislation on youthful auto fatalities, 1970–1977. J Legal Stud. 1984;13:169–90. 123. Cotton NS. The familial incidence of alcoholism. J Stud Alcohol. 1979;40:89–116. 124. Hrubec Z, Omenn OS. Evidence of genetic predisposition to alcohol cirrhosis and psychosis: twin concordances for alcoholism and its biological end points by zygosity among male veterans. Alcohol Clin Exp Res. 1981;5:207–12. 125. Schuckit MA. Twin studies on substance abuse: an overview. In: Gedda L, Parisi P, Nance W, eds. Twin Research 3: Epidemiological and Clinical Studies. New York: Alan R Liss; 1981:61–70. 126. Goodwin DW. Alcoholism and genetics. Arch Gen Psychiatry. 1985;42:171–4. 127. Bohman M, Sigvardsson S, Cloninger R. Maternal inheritance of alcohol abuse: cross-fostering analysis of adopted women. Arch Gen Psychiatry. 1981;38:965–9. 128. Cloninger CR, Sigvardsson S, Gilligan SB, et al. Genetic heterogeneity and the classification of alcoholism. In: Gordis E, Tabakoff B, and Linnoila M, eds. Alcohol Research from Bench to Bedside. New York: Haworth Press; 1989:3–16. 129. Tabakoff B, Hoffman P, Lee J, Saito T, Willard B, Leon-Jones F. Differences in platelet enzyme activity between alcoholics and nonalcoholics. N Engl J Med. 1988;318:134–9. 130. Friedmann, PD, McCullough D, Chin MH, Saitz R. Screening and intervention for alcohol problems: a national survey of primary care physicians and psychiatrists. J Intern Med. 2000, 15:4–91. 131. Selzer ML. Michigan Alcoholism Screening Test: the quest for a new diagnostic instrument. Am J Psychiatry. 1971;127:89–94. 132. Pokorny AD, Miller BA, Kaplan HB. The brief MAST: a shortened version of the Michigan Alcoholism Screening Test. Am J Psychiatry. 1972;129:342–5. 133. Mayfield D, McLeod G, Hall P. The CAGE questionnaire: validation of a new alcoholism screening instrument. Am J Psychiatry. 1974;131:1121–3. 134. Babor TF, Grant M. From clinical research to secondary prevention: international collaboration in the development of the Alcohol Use Disorders Identification Test (AUDIT). Alcohol Health Res World. 1989;13:371–4.

1012

Behavioral Factors Affecting Health

135. Russell M, Martier SS, Sokol RJ, Mudar P, Bottoms S, Jacobson S, et al. Screening for pregnancy risk-drinking. Alcohol Clin Exp Res. 1994;18:1156–61. 136. U.S. Preventive Services Task Force. Guide to Clinical Preventive Services. 2nd ed. Baltimore: Williams & Wilkins; 1996. 137. Allen JP. Maisto SA, Connors GJ. Self-report screening tests for alcohol problems in primary care. Arch Intern Med. 1995;155(16): 1726–30. 138. Harrell AV, Wirtz PW. Screening for adolescent problem drinking: validation of a multidimensional instrument for case identification. Psychol Assess. 1989;1:61–3. 139. Fink A, Hays RD, Moore AA, Beck JC. Alcohol-related problems in older persons. Determinants, consequences, and screening. Arch Intern Med. 1996;156(11):1150–6. 140. Adams WL, Barry KL, Fleming MF. Screening for problem drinking in older primary care patients. JAMA. 1996;276(24):1964–7. 141. National Institute on Alcohol Abuse and Alcoholism. The Physician’s Guide to Helping Patients with Alcohol Problems. NIH Publication No. 95-3769, and the ASAM reference guide. 2003. 142. Magruder-Habib K, Durand AM, Frey KA. Alcohol abuse and alcoholism in primary health care settings. J Fam Pract. 1991;32:406. 143. Skinner HA, Holt S, Schuller R, Roy J, Israel Y. Identification of alcohol abuse using laboratory tests and a history of trauma. Ann Intern Med. 1984;101:847–51. 144. Criteria Committee, National Council on Alcoholism: Criteria for the diagnosis and alcoholism. Am J Psychiatry. 1972;129:127–35. 145. Helander A. Biological markers of alcohol use and abuse in theory and practice. In: Agarwal DP, & Seitz HK, (eds.) Alcohol in Health and Disease. New York: Marcel Dekker, 2001. pp. 177–205. 146. Saunders JB. Management and treatment efficacy of drug and alcohol problems: what do doctors believe? Addiction. 1995;90(10): 1357–66. 147. Chafetz ME, Blane HT, Abram HS, Lacy E, McCourt WF, Clark E, et al. Establishing treatment relations with alcoholics. J Nerv Ment Dis. 1962;134:385–409. 148. Bien TH, Miller WR, Tonigan JS. Brief interventions for alcohol problems: a review. Addiction. 1993;88(3):315–35. 149. Babor TF, Ritson EB. Hodgson RJ. Alcohol-related problems in the primary health care setting: a review of early intervention strategies. BrJ Addict. 1986;81:23–46. 150. Edwards G, Orford J, Egert S, Guthrie S, Hawker A, Hensman C, et al. Alcoholism: a controlled trial of “treatment” and “advice.” J Stud Alcohol. 1977;38:1004–31. 151. Orford J, Oppenheimer E, Edwards G. Abstinence or control: the outcome for excessive drinkers two years after consultation. Behav Res Ther. 1976;14:397–416. 152. Wallace P, Cutler S, Haines A. Randomized controlled trial of general practitioner intervention in patients with excessive alcohol consumption. Br Med J. 1988;297:663–8.

153. Sanchez-Craig M, Leigh G, Spivak K, et al. Superior outcome of females over males after brief treatment for the reduction of heavy drinking. Br J Addict. 1989;84:395–404. 154. Sanchez-Craig M, Annis HM, Bornet AR, MacDonald KR. Random assignment to abstinence and controlled drinking: evaluation of a cognitive-behavioural program for problem drinkers. J Consult Clin Psychol. 1984;52:390–403. 155. Skutle A, Berg G. Training in controlled drinking for early-stage problem drinkers. Br J Addict. 1987;82:493–501. 156. Zweben A, Pearlman S, Li S. A comparison of brief advice and conjoint therapy in the treatment of alcohol abuse: the results of the marital systems study. Br J Addict. 1988;83:899–916. 157. Sannibale C. Differential effect of a set of brief interventions on the functioning of a group of “early-stage” problem drinkers. Aust Drug Alcohol Rev. 1988;7:147–55. 158. Skinner HA, Holt S. Early intervention for alcohol problems. J R Coll Gen Pract. 1983;33:787–91. 159. Nilssen O. Long-term effect of brief intervention in at-risk drinkers: a 9-year follow-up study. Alcohol. 2004;39(6):548–51. 160. Stockwell T. Can severely dependent drinkers learn controlled drinking? Summing up the debate. Br J Addict. 1988;83:149–52. 161. Babor TF, Treffardier M, Weill J, Fegueur L, Ferrant JP. Early detection and secondary prevention of alcoholism in France. J Stud Alcohol. 1983;44:600–16. 162. Alden LE. Behavioural self-management controlled-drinking strategies in a context of secondary prevention. J Consult Clin Psychol. 1988;56:280–6. 163. Taylor JR, Heizer JE, Robins LN. Moderate drinking in ex-alcoholics: recent studies. J Stud Alcohol. 1986;47:115–21. 164. Rush BR, Ogborne AC. Acceptibility of nonabstinence treatment goals among alcoholism treatment programs. J Stud Alcohol. 1986;47:146–50. 164. Sanchez-Craig M. A Therapist’s Manual for Secondary Prevention of Alcohol Problems. Procedures for Teaching Moderate Drinking and Abstinence. Toronto: Addiction Research Foundation; 1984. 165. Kristenson H, Hood B. The impact of alcohol on health in the general population: a review with particular reference to experience in Malmo. Br J Addict. 1984;79:139–45. 166. Chick J, Lloyd G, Crombie E. Counselling problem drinkers in medical wards: a controlled study. Br Med J. 1985;290:965–7. 167. Elvy GA, Wells JE, Baird KA. Attempted referral as intervention for problem drinking in the general hospital. Br J Addict. 1988;83:83–9. 168. Chick J. Secondary prevention of alcoholism and the Centres D’Hygiene Alimentaire. Br J Addict. 1984;79:221–5. 169. Mcintosh M, Sanchez-Craig M. Moderate drinking: an alternative treatment goal for early-stage problem drinking. Can Med Assoc J. 1984;131:873–6. 170. Skinner HA. Early detection of alcohol and drug problems—why? Aust Drug Alcohol Rev. 1987;6:293–301.

Prevention of Drug Use and Drug Use Disorders

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Elizabeth B. Robertson • Wilson M. Compton

Drug use and drug use disorders interfere with the normal, healthy functioning across the lifespan but are fundamentally preventable. In considering the opportunities for preventing drug use and drug disorders, it is important to consider that the initiation of drug use, a necessary precursor to drug disorders, is in most cases a voluntary activity. However, the onset of drug disorders (namely abuse and dependence) is much more dependent on genetic variation in combination with specific environmental factors. The onset of drug use is most common during the late childhood and adolescent years. Proximal and distal biological, psychological, social, and environmental precursors originating as early as the prenatal period play a large role in whether experimentation occurs and use persists. On the other hand, for some individuals, the initiation of drug misuse and illicit use of drugs extends well beyond adolescence into adulthood, even in late adulthood. What follows is a review of basic information about drug use and drug use disorders and a review of prevention opportunities. PHARMACOLOGY OF DRUGS OF ABUSE

An understanding of the pharmacological properties of drugs is essential to the understanding of the development of drug abuse and dependence and hence the design of prevention interventions. Four processes are important to the development of drug abuse and dependence: (a) exposure, including timing of exposure and genetic susceptibility; (b) physical dependence, an adaptive state that manifests itself as intense physical disturbance when drug use is suspended; (c) psychological dependence (or “addiction”), a condition under which there is a drive toward periodic or continuous administration of the drug to produce pleasure or avoid discomfit; and (d) tolerance, or the need for increasingly higher doses of a drug to recapture the original effects of the drug. Drug abuse may occur as the result of exposure only, as in the case of binge drinking on the first occasion of alcohol use or driving a vehicle under the influence of an illicit drug. Processes of abuse and dependence reflect characteristics of the drug, the individual user and the context of use. Among the goals of psychopharmacology, epidemiology and etiology research is to gain a better understanding of the processes implicated in the development of dependence based on the drug, the user and their interactions with one another. For example, initial use of a psychoactive drug often results in a pleasurable response. This response is reinforcing or rewarding leading to the desire to use the substance again, thereby maintaining the behavior. The more reinforcing the drug is the more likely the individual will seek the drug and abuse it. This characteristic of the drug is called its abuse liability and has been assessed for

numerous drugs through animal self-administration research. In most cases, this research has shown strong correlations between drugs animals will self administer and those that humans will abuse. In other cases, animals will not self administer drugs humans use, but the value of the animal studies is still great in that it allows for the determination of the general pharmacology and abuse liability of many substances that are then classified according to the Controlled Substance Act (CSA). Classification by the CSA provides one route to prevention as it is intended to curb the distribution of classified substance, thus making them less available to the public. Prevention interventions approach the relaying of information concerning classes of drug in several ways. First, some interventions, especially those for general populations of young children, provide very little or no information on drugs of abuse. Instead they concentrate on skill development and other proven prevention strategies. Other interventions concentrate on targeting a specific group of drugs for a specific population. Drugs to target are typically determined through epidemiologic studies of the population of interest. Finally, some interventions target one specific drug that is a serious problem for a specific population again determined through epidemiologic studies. Some examples of these are steroid abuse among athletes and inhalant abuse among Native Americans.1,2

Cannabinoids Cannabinoids are obtained from the flowering top of the hemp plant. More than 60 cannabinoids have been isolated from the hemp plant, and 1-delta-9-tetrahydrocannabinol (delta-9-THC) has been identified as the constituent responsible for most of the characteristic effects of this category of drug. Cannabis affects cognition, memory, mood, motor coordination, perception, sense of time and, under some conditions, produces feelings of relaxation and well-being. Tolerance is clearly seen after high doses and/or sustained use. Differential tolerance occurs with various effects as well as cross-tolerance to some hallucinogens. Disruption of performance and withdrawal symptoms have been noted after discontinued use of delta-9-THC.3 In particular, withdrawal symptoms characterized by irritability, restlessness, nervousness, decreased appetite, and weight loss have been reported. Cannabis affects the cardiovascular system by increasing heart rate and differentially altering standing and supine blood pressure.

Depressants Depressants generally share sedative and hypnotic properties and are used medically to produce drowsiness, sleep, and muscle relaxation and to prevent convulsions. In addition, barbiturates have anesthetic properties. The effects of these drugs are dose dependent, progressing 1013

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from relaxation to sedation through hypnosis to stupor. In the 1950s, depressants were developed with high anxiolytic and low central nervous system (CNS) depressant properties. These are the benzodiazepine agents, which allow relief of anxiety symptoms with less impairment of respiratory, cognitive, attention, and motor functions than the barbiturates. Depressants have complex effects. For instance, the relative degree of safety, tolerance, and dependence vary from the benzodiazepines, assigned to schedule IV, to those barbiturates, assigned to schedule II, which are associated with toxicity and high abuse liability. Tolerance for and dependence on the various drugs of this class generalize within the class and across classes to some opiates and alcohol. This is termed cross-tolerance and cross-dependence. Since, in our society, alcohol often is not recognized as a depressant drug, its use with sedative-hypnotic drugs results in stupor and death more frequently than might be the case were alcohol’s depressant characteristics more fully appreciated.4

Dissociative Anesthetics Dissociative Anesthetics include drugs such as PCP (phencyclidine), ketamine, and dextromethorphan. PCP was initially developed in the 1950s as an intravenous general anesthetic for surgery. However it has never been approved for use with humans, although it is used in veterinary medicine. Its sedative and anesthetic effects are trance-like and patients experience a feeling of being “out of body”. Other effects are distorted perceptions of sight and sound and feelings of detachment or dissociation from the environment and self. These mind altering effects are not hallucinations. PCP and ketamine are therefore more properly known as dissociative anesthetics. The dissociative drugs act by altering distribution of the neurotransmitter glutamate throughout the brain. Glutamate is involved in perception of pain, responses to the environment, and memory. PCP is considered the typical dissociative drug. Ketamine was developed in 1963 and is currently used as an anesthetic in both humans and animals in an injectable liquid form. For illicit use, the drug is typically evaporated to form a powder that is odorless and tasteless, resulting in some cases of its use as a “date rape” drug.5,6,7

Hallucinogens Hallucinogens, unlike many abused drugs, have no accepted medical use. These drugs share an ability to distort perception and induce delusions, hallucinations, illusions, and profound alteration of mood. Mescaline and psilocin-containing plants have been used ceremonially for centuries, and LSD was synthesized 1925. Under certain conditions, drugs from a variety of classes show hallucinogenic properties. Because of similarities between experiences of persons ingesting hallucinogens and those of mentally ill persons and persons reporting profound religious experiences, these drugs also are called psychotomimetics or psychedelics. Their effects reflect activity at receptors of the serotonergic, cholinergic, and possibly other systems. Tolerance occurs with repeated use of all hallucinogens. As is true for other psychoactive substances, differential tolerance to their various effects can be demonstrated. For example, tolerance to the subjective effects of hallucinogens is greater than that seen for the cardiovascular effects. Considerable cross-tolerance exists among drugs in this category. Symptoms of physical dependence after abrupt withdrawal of phencyclidine have been described, but similar reports for LSD do not exist.7,8

Opioids and Morphine Derivatives Opioids and Morphine Derivatives are drugs that cause analgesia, sedation, and euphoria. Opioids stimulate the higher centers of the brains and slow down the activity of the CNS. The term opioid refers to natural drugs produced from the opium poppy such as opium, morphine, and codeine. Some semisynthetic opiates include heroin and methadone. Many opiate preparations are used in medical practice to manage pain, diarrhea and cough, with therapeutic doses being carefully managed to minimize side effects. Opioids can produce euphoria and are highly addictive, thus there are legal restrictions on their sale and use.9,10

Stimulants Stimulants generally are classified as excitatory in recognition of their main effect on the CNS; specifically the increase in levels of dopamine and inhibitory neurotransmitter. These include cocaine, amphetamines, methylphenidate, and related substances. At low doses, stimulants are associated with feelings of increased alertness, euphoria, vigor, motor activity, and appetite suppression. At high doses, they can cause convulsions and changes in thought characterized on a continuum from hyper-vigilance to suspicion to paranoia. Amphetamine and cocaineinduced psychoses are described in chronic abusers. Paranoid ideation generally is reported in persons with histories of chronic stimulant abuse, but transient psychotic symptoms have been reported with initial use of high doses, and instances of psychoses associated with use of medically prescribed doses also have been reported. With repeated use, tolerance to some drug effects occurs, for example, euphoria and appetite suppression, convulsion, whereas there are increases in other effects such as motor activity, stereotypy, and possibly paranoia. Cocaine has various toxic effects especially upon the cardiovascular system and when cocaine and alcohol are taken together; cocaethylene is produced, which is even more lethal than cocaine.11,12

Inhalants Inhalants are a diverse group of chemicals that easily evaporate, such as solvents, aerosols and gases that cause intoxication when their vapors are inhaled. Vapors of liquid solvents can be sniffed directly from a container, may be poured on a rag and held over the mouth, or may be emptied into a bag that is held over the mouth and nose for inhalation. The rebreathing of exhaled air causes an oxygen deficiency, which can intensify the intoxicating effects. Inhaled vapors enter the bloodstream rapidly and are distributed to the organs with large blood circulation (e.g., liver, brain) and are absorbed quickly into the CNS, depressing many bodily functions. Particularly concerning are the hydrocarbon inhalants, such as solvents, gasoline, paint thinner, etc. These agents are CNS depressants and in moderate doses result in intoxication similar to that caused by alcohol (i.e., giddiness, disinhibition, muscle weakness, lack of coordination, slowed reflexes and slurred speech). High doses can cause severe breathing failure and death. Chronic abuse can lead to irreversible liver damage, brain damage and other health problems.13

Other Compounds Other Compounds that do not fall into the above categories but are abused include anabolic steroids and some over-the-counter (OTC) drugs. Anabolic steroids14,15 are synthetic substances related to the male sex hormones (androgens) that promote the skeletal muscle development (anabolic effect) and the development of male sexual characteristics (androgenic effects). Medical uses of anabolic steroids include treating conditions where the body produces abnormally low amounts of testosterone (e.g., delayed puberty) and treating body wasting (e.g., AIDS and related diseases). These drugs are obtained illegally through diversion from pharmacies; illegal imports from other countries and production in clandestine laboratories. The use of these substances is widespread among athletes motivated, in most cases, by the desire to build muscle and improve sports performance. Anabolic steroids are injected, taken orally or are rubbed into the skin in an ointment form. Most abusers take doses of up to 100 times greater than a therapeutic dose. In addition, many abusers take multiple anabolic steroids together and administer them in multiple ways; sometimes mixing them with other drugs such as stimulants and painkillers. Health consequences associated with abuse of anabolic steroids include: reduced sperm production, shrinking of the testicles, impotence, difficulty and painful urination, baldness, and irreversible breast enlargement in males. In females, health consequences include: development of masculine characteristics such as decreased body fat and breast size, deepening of the voice, excessive body hair, and loss of scalp hair. For adolescents of both genders, abuse can result in termination of the adolescent growth spurt permanently stunting growth. Other severe health, social, and psychological consequences occur for

56 abusers of both genders at all ages and include: liver cysts and cancer, clotting, cholesterol changes, heightened aggression, depressed mood, insomnia, loss of appetite, and muscle/joint pain.1,14

Over-the-counter (OTC) drugs Over-the-counter (OTC) drugs include a variety of preparations with which people self treat for minor ailments from the common cold to pain relief or to improve performance in some way, for example, stimulants, sleep enhancers, and weight control products. Many of these products include a combination of drugs that interact with one another to produce the most positive effect. Taken as directed most OTC drugs are safe, however prolonged use or excessive dosages of some of these drugs can be problematic. For example, long-term or excessive use of analgesics increases the likelihood of gastrointestinal irritation (aspirin) or liver damage (acetaminophen). Excessive dosages of a caffeine product can cause anxiety, increase in general metabolism, elevated heart rate and blood pressure and gastrointestinal irritation. Dextromethorphan, a widely available cough suppressant can, when taken in high doses, produce effects similar to the dissociative anesthetic effects of PCP and ketamine.5

EPIDEMIOLOGY OF DRUG USE

Understanding the nature, extent, and patterns of use and abuse of psychoactive drugs and compounds is a necessary prerequisite to the development of efficacious and effective prevention interventions. Two epidemiological studies, the National Survey on Drug Use and Health (NSDUH)16 and the Monitoring the Future17 survey (MTF), are particularly helpful in tracking drug use over time. Examples from these two data sets are used to demonstrate trends in drug use over time.

Comparison of National Survey on Drug Use and Health (NSDUH) and the Monitoring the Future (MTF) The NSDUH, formerly known as the National Household Survey on Drug Abuse is the primary source of statistical information on the use of illegal drugs by the overall U.S. population and has been conducted by the federal government since 1971. The survey collects data by administering questionnaires to a representative sample of the population 12 years of age and older through face-to-face interviews at their place of residence. Residence is defined as: residents of households, noninstitutional group quarters (e.g., shelters, rooming houses, dormitories), and civilians living on military bases. Homeless persons who do not use shelters, active military personnel, and residents of institutional group quarters, such as jails and hospitals, are excluded. Prior to 1999 the NSDUH’s sensitive data sections were collected using a self-administered answer sheet that the respondent sealed in an envelope, to maximize the sense of privacy, thus facilitating the accuracy of reporting. Nonsensitive sections were administered by the interviewer. Since 1999, the NSDUH interview has been carried out using computer-assisted interviewing (CAI) methodology. The survey uses a combination of computer-assisted personal interviewing (CAPI) conducted by the interviewer and audio computerassisted self-interviewing (ACASI). Sensitive questions previously administered using respondent-completed answer sheets are now administered using ACASI, a procedure designed to be highly private and confidential for sensitive questions thereby increasing the level of honest reporting. The MTF study uses a multistage nationally representative sampling design of secondary schools in the 48 contiguous United States. Data have been collected annually from high school seniors beginning in 1975. From 1991 to the present, data also have been collected yearly from 8th and 10th grade students. The study uses a three stage sampling strategy: (a) geographic region, (b) approximately 420 schools per year, and (c) between 42,000 and 49,000 students per year.

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Weights are assigned to each student to account for school sample sizes and any potential variations in selection throughout the sampling process.17 There are numerous important methodological differences between the NSDUH and the MTF study when it comes to the youth population. Chief among them are differences in setting and method of survey administration. The MTF is conducted in the school setting whereas the NSDUH collects data in homes. Collection in the school setting is thought to provide youth a greater sense of privacy and to promote more accurate reporting; household-based collection is generally thought to yield underreporting of sensitive behaviors such as drug use. Additionally, the NSDUH universe includes school dropouts, who are not represented in the MTF sample. The parental consent procedures are quite different between the two surveys with NSDUH requiring signed parental consent (obtained in person in the household) and MTF using either passive or signed active consent with documents sent from the school to the parents. The second major difference is that MTF uses self-administered paper-pencil questionnaires for data collection while the NSDUH uses interviewer and computer-administered verbal questions. Finally, NSDUH data are collected throughout the year while MTF data are collected primarily in February through May. Figure 56-1 compares data from the NSDUH and MTF on past month use of marijuana by high school seniors.18 Note that the trend lines are very similar in shape over time; however, the MTF data indicate somewhat higher use than the NSDUH. This is thought to be the result of differences in data collection methodology described previously. Figure 56-2 presents comparative data for the same time period for use of cocaine in the past month by 12th grade youth.18 Note that the levels of cocaine use are much lower than those for marijuana and interestingly the trend patterns are quite different. Marijuana use peaked in 1979 and then made a steady decline until the early 1990s whereas cocaine use peaked at about the same time but levels of use remained relatively high until the mid-1980s. Difference in drug use trends are evident for many drugs of abuse and typically relate to factors such as availability and popularity of a particular drug in a particular region or among particular subpopulations.

Etiology Understanding the causal factors that lead to exposure, initiation, progression, and maintenance of drug abuse is fundamental to the development of prevention interventions. Substance use, abuse and dependence result from complex interactions between biological, psychological, and sociologic factors such as the interaction styles of individuals, family members, peers, and other significant others in combination with features of the social context or environment. The life course bio-psycho-social developmental perspective suggests that individual and environmental factors interact to increase or reduce vulnerability to drug use, abuse, dependence, and associated problem behaviors. Vulnerability can occur at many points along the life course but peaks at critical life transitions. Thus, prevention researchers pay particular attention to the significance of timing interventions to coincide with important biological transitions, such as puberty; normative transitions, such as moving from elementary to middle school; social transitions, such as dating; and traumatic transitions, such as the death of a parent. In addition, because vulnerability to drug abuse involves dynamic intrapersonal (e.g., temperament), interpersonal (e.g., family and peer interactions) and environmental (e.g., school environment) influences, prevention intervention research must target interactions between individuals and social systems across the life span. To address this complexity, intervention research needs to test strategies designed to alter specified modifiable mediators to determine which are most related to and effective in reducing drug use initiation and escalation, with what audiences, and under what conditions. An appreciation for the complexity of this work can be gleaned through examining a graphic depiction of spheres of influence on and from the developing human across time (see Fig. 56-3).19

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This meta-theoretical perspective provides a broad view of the complex forces and interactions that inuence developmental, in general, and problem behaviors in particular. In addition, drug abuse and drug-related HIV prevention programs utilized a number of more discrete theoretical perspectives for predicting differential drug use trajectories and elucidating developmentally grounded mediators, or risk and protective factors, malleable to change. Basing an intervention on theory is essential because it guides the development of the intervention content, length of exposure and for whom the intervention should work. It also provides the basis for the development of hypotheses and information critical to the development of a comprehensive evaluation design. Three commonly used theories in prevention are behavioral theory, social learning theory, and social cognitive theory.

Behavioral Theory 20

Social Learning Theory 21 Social learning theory21 emphasizes learning that occurs within social contexts: the family, school, the neighborhood, and community. The basic premise is that people learn from interacting with and observing other people. People who are most salient to the learner (e.g., the parent in early childhood, peers in adolescence) tend to have the most impact on both social knowledge and behaviors. Social learning that translates to changes in behavior occurs through

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Figure 56-2. Trends in past month cocaine use by 12th graders in monitoring the future and national survey on drug use and health surveys (Source: Data from Glantz MG, et al. Personal Communication; 2005).

Percent of 12th graders using cocaine in month prior to survey

Behavioral theory,20 including information processing, places emphasis on learning skills and knowledge and assumes that behavior is based on cognition rather than external forces. Major foci of this

theoretical perspective are that learning occurs through making cognitive connections between stimuli and responses and that when rewarded, especially in close temporal proximity to the response, the connections are reinforced. Additionally, active participation in the learning process is critical. A number of steps in the learning process are delineated that begin with shaping or making successive approximations to the parts of or the whole behavior with increasing accuracy over time. This stresses the importance of repetition, reinforcement, and raising standards to produce successful learning. Behaviors that are not reinforced are not learned.

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Social welfare services Figure 56-3. Bronfenbrenner’s four ecological settings for developmental change.

modeling and imitation, but not all social learning results in behavior change. When behavior is modeled or imitated it is more likely to become integrated into the individual’s repertoire of behaviors if it is positively reinforced by a significant other or a significant other receives strong reinforcement leading to the experience of strong vicarious reinforcement. In other cases the behavior itself can be reinforcing for example through sensory stimulation that is satisfying.

Social Cognitive Theory 21 Social cognitive theory21 is an offshoot of social learning theory emphasizing the cognitive processes that occur during learning. Attention is a critical cognitive feature of this paradigm in that it is associated with expectation of rewards or negative consequences (e.g., when a parent asks “Do you want to do the dishes?” there is no implied consequence for saying no). Individuals develop cognitive expectation about associated behavioral consequences based on verbal and nonverbal reactions they have experienced. Other cognitive strategies related to the development of behaviors, including skills, self-monitoring, self-talk, and self-reinforcement.

Risk and Protective Factors The bio-psycho-social perspective and theories related to prevention implicitly recognize the role of risk and protective factors in shaping developmental trajectories. The concept that risk is associated with increased vulnerability and protection is associated with decreased vulnerability to disease has been a central and longstanding concept in medicine. This paradigm has been adapted for behaviorally-based diseases with one major caveat; for many medical conditions a single source is associated with causation, whereas with behaviorallybased diseases such as substance abuse it is commonly accepted that there are multiple factors associated with disease causation. The bio-psycho-social perspective recognizes that the course of development is affected by multiple factors at multiple contextual levels over time. However it also places the individual at the center because so much of

what occurs during the developmental process is determined by individual characteristics such as temperament, learning and communication styles, and genetic vulnerability to disease.19 The study of behavioral genetics provides a framework for one line of etiologic investigation of risk and protective factors. These studies use standard research designs to look at relationships among individual genetic and environmental factors that appear to influence behavioral outcomes. For example, twin studies compare identical and fraternal twins for similar behavioral endpoints. Adoption studies compare biological and adoptive parents. Heritability, a statistical description of the portion of variability in the behavior that can be ascribed to genetic factors, can be determined by these approaches and can clarify the contribution of genetic and environmental factors to behavioral outcomes that have been demonstrated to be related to familial factors. Intelligence, personality, temperament, psychopathology, alcoholism, and to a lesser extent drug abuse have been shown to be heritable. However, few complex behaviors are under the control of a single gene; rather it appears the multiple genes in combination with environmental influences are responsible for the expression of familial-related characteristics. Over the past two decades other studies have tried to determine constellations of behavioral and environmental risk factors associated with the origins and pathways to drug abuse. Many of these studies have successfully identified factors that help differentiate those more vulnerable to drug abuse from those less vulnerable. Risk and protective factors can affect children through establishing and/or reinforcing a negative developmental trajectory. A trajectory captures how individual children adapt either positively or negatively to their circumstances and is affected by intrapersonal, interpersonal, and environmental factors encountered at different developmental stages over the life course.22,23,24 There are several basic concepts pertaining to risk and protective factors that help to put into perspective their role in development in general and in the development of substance abuse in particular. First, there are many types of risk and protective factors and they occur at all levels of the human ecosystem, but some may be more potent for some individuals than for others or may be more potent at

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one particular developmental stage than another.25,26 Most risk factors have nonspecific effects and a major question is “Do different risk constellations result in particular patterns of negative behaviors and if so what are the mechanisms that account for this?” Many individuals experience multiple risk factors and this places them at greater risk. This is due in part to the fact that after a certain threshold of risk is attained or exceeded there appears to be an accumulation effect. Figure 56-4 illustrates this principle. Note that those individuals with 4–10 protective factors exhibit relatively few risk factors and very low prevalence of 30-day marijuana use. On the other hand, at the 6–7 risk factors threshold there is an absence of protective factors and a steep incline in the prevalence of marijuana use.27 The same principle holds for protective factors, the greater the number of protective factors relative to risk factors the less likely the individual is to experience negative outcomes. In this example (see Fig. 56-5)27 prevalence of academic success, a variable highly associated with low levels of drug use, is highest when there are many protective factors and few risk factors. Note as the number of risk factors increases academic success declines steeply.

A key concept is that some risk and protective factors can not be changed at all (such as genetic vulnerability and gender) and others are not easily changed (such as socioeconomic status). Because these factors are not malleable, they are not good targets for prevention. Rather factors that can be modified, such as specific behaviors and skills are more appropriate intervention targets.25,26 Perhaps the most important consideration about risk for substance abuse is that not all individuals at heightened risk actually use or abuse drugs. For example, a young person with a strong family history of substance abuse and a chaotic home environment who has strong extra-familial support systems such as a positive peer group, a supportive school environment, a community with low tolerance for use, and low availability of drugs may never initiate use. Figure 56-6 provides a framework for characterizing risk and protective factors in five contexts. These contexts often serve as foci for prevention practices. As the second examples suggest, some risk and protective factors may operate on a continuum. That is, in the family domain, lack of parental supervision, a risk factor, indicates the absence of parental monitoring, a key protective factor.26

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However, in most cases risk and protective factors are independent of each other, as demonstrated in the examples in the peer, school, and community contexts. For example, in the school domain, a school with strong “antidrug policies” may still have high availability of drugs if the policies are weakly enforced. An intervention to strengthen enforcement of school policies could create the intended school environment. Because development takes place in context, it is important to consider the ways in which developmental contexts can influence risk and protective factors and life course trajectory. Children’s earliest interactions occur within the family and factors that affect early development are crucial to development. Families foster optimal development when strong bonds are established between parents and the child, parents are involved in the child’s activities, parents meet the child’s material needs (e.g., food, clothing and shelter) and emotional needs (e.g., support and warmth), and firm, clear and consistent limits for behavior are set and enforced in a nonhostile, matter-of-fact manner. On the other hand, children are more likely to experience negative developmental outcomes when there is a lack of mutual attachment and nurturing by parents or caregivers, parenting is inconsistent or harsh, the home environment is chaotic, or the caregiver abuses substances, suffers from mental illness, engages in criminal behavior, or has other severe behavioral or mental health problems. These latter developmental environments, such as households where parents’ abuse of drugs can impede bonding to the family and threaten feelings of security that children need for healthy development.28 For young children already exhibiting serious risk factors, delaying intervention until late childhood or adolescence makes it more difficult to overcome risks because attitudes and behaviors have become well established and not easily changed.29 One of the most well-delineated risk trajectories for subsequent substance abuse is out-of-control aggressive behavior in very young children.30,31,32 If not addressed through positive parental actions, this behavior can lead to additional risks when the child enters school— including heightened aggressive behavior which leads to peer rejection, punishment by teachers, and academic failure. If not successfully addressed through preventive intervention within the home and school contexts, over time these risks can lead to more distal risk behaviors for drug use, such as truancy, delinquency, and associating with drug-abusing peers. This example illustrates several important aspects of successful prevention that will be reiterated later. First, intervening early increases the likelihood of success.28 Second, life transitions, in this case school transitions, are points of vulnerability and provide opportunities for intervention. Finally, interventions that address the problem in multiple contexts are more successful than those confined to a single context.33 Implicit in this example is the idea that later in development, settings outside the family, such as school, with peers and teachers, and in the community, increasingly affect the quality of children’s development. Difficulties in these contexts influence children’s physical, emotional, cognitive, and social development. During the preadolescent and adolescent years, association with drug-using peers is often the most immediate risk for exposure to drug abuse and other delinquent behavior. But other factors such as drug availability, perception that drug abuse is accepted, and inflated misperceptions about the extent to which same-age peers use drugs can influence adolescents to initiate drug use. Even in the adolescent years when youths spend a great deal of time outside the home, parents and caregivers can

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Figure 56-6. Prevalence of academic success by number of risk and protective factors.

provide protection through age-appropriate parental monitoring of social behavior, including establishing curfews, ensuring adult supervision of activities outside the home, knowing the children’s friends, enforcing household rules, facilitating and valuing success in academics, involvement in extracurricular activities, and fostering strong bonds with prosocial institutions, such as the school, recreation activities, and religious institutions. Moreover, research demonstrates that while peers are a major force in determining immediate behaviors, such as choice of clothing styles, activities to participate in and people with whom to associate, parents remain the most important source of information and decision-making around long-term life choices such as school and career.34

Elements of Effective and Ineffective Programs and Strategies Much research has gone into determining what elements of preventive interventions are effective. There is much more to be learned about intervention strategies that do and do not work and about general principles of effective delivery. Thus, an area of research for which there is particular interest is the translation of basic science findings for the development of innovative interventions. To date the program content strategies that have been demonstrated to work typically involve the development of skills. Some of these have been mentioned previously and it was noted that the program or strategy should reflect the needs of the target population. In this section effective and ineffective programs and strategies will be more fully described and related to the pertinent social contexts with some attention to developmental timing. At the intrapersonal level the most important strategies are those that build skills and competencies. Obviously these become more complex over the course of development. For the very young child learning to conform to rules, to behave in prosocial ways, to identify and appropriately express feelings and to control impulses are some of the important skills to learn. During the school years these skills remain important and more skills are added to the repertoire, including academic competence, social resistance, social emotional learning, and normative education.

Family-Based Interventions35 So how does family-based prevention programming aid in building these skills? For the very young the emphasis is on the parent and targets training parents to have developmentally appropriate expectations for their children, adjusting these as the child matures. One universal program teaches the important strategy of reinforcing appropriate behaviors that the child naturally expresses and to the extent possible, ignoring inappropriate behaviors. The program developers call this strategy “catching them being good.”36 Reinforcing weak but existing skills is extremely important because it gives the child a sense of control over her environment while emphasizing that the child has the ability to behave in socially acceptable ways. Of course some children exhibit problem behaviors from a very young age and more targeted approaches are needed. For example, the high pitched cries of prematurely born infants often illicit negative reactions from caregivers, which in turn results in poorer care of these very vulnerable infants. Thus, teaching parents strategies to cope with these and other early problems such as difficult temperamental characteristics can prevent

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the escalation of problem behaviors, help the parents to accept the reality of the problem, and to be patient in training the child in more appropriate reactions, thus providing the parents with the sense of efficacy they need in parenting a difficult child.36,37,38,39 As mentioned, transitions are points of vulnerability and the transition to school and to each additional school level after that are major periods of risk. New expectations for academic and social performance escalate over the school years and these can be very threatening to some children. Parental support and interest is important during these transitions. This generally means becoming familiar with their child’s friends, their friends’ parents and their teachers, monitoring their school work and social opportunities, and taking an active interest in their developing autonomous life.

School-based Interventions At school a number of programs and strategies have also been demonstrated to make for successful transitions and academic careers. One important strategy is appropriate classroom management. Classroom management trains teachers in building strategies for rewarding positive behaviors and over time has the effect of reducing the bulk of negative classroom behaviors.40,41,42 This results in an environment where learning is the primary goal and the primary source of reward. While this may seem self-evident, many beginning teachers are not equipped to manage the types of classroom problem behaviors that take away from the priority of the school—learning. Thus, training teachers to use consistent, easy to learn routines that are fun for the children can enhance learning and bonding to school—two important protective factors. This type of strategy is called an environmental change strategy because it changes the classroom environment from one centered on reducing negative behaviors to one focused on promoting positive behaviors and learning. Another type of classroom management approach, typically used with students in grades K through 3 is called social emotional learning.30–32,43,44 This approach helps children to identify their feelings, such as frustration, anger, and over-stimulation and then provides them tools to manage these feelings. Because this is a classroombased intervention, all of the children know the approach and understand when a particular child is signaling that he or she are having a difficult time and respects his or her efforts to overcome the problem in a prosocial manner. Developing social emotional awareness at a very young age has long term positive effects on both academic and social performance across the school years and into adulthood. The other type of intervention that can take place with young students is promoting academic competence. While this is not restricted to the early grades it can have the most profound effects at that developmental period in fostering a positive attitude toward learning, a sense of accomplishment, and of course, an understanding of the basics necessary for future learning.45 These are all protective factors leading to a greater likelihood of a positive life trajectory. For example, one very potent risk factor for subsequent substance abuse, delinquency, school drop out, and under employment is the inability to read by the end of the second grade.39,40 By ensuring that children get the additional support they may need to achieve reading by this critical period helps to ensure on-going academic success. Of course academic problems can occur throughout an individual’s school career and providing the necessary academic support is an important responsibility of schools. However, parents often need to be the driving force in seeing that this occurs. The transition to middle school or junior high school is typically the transition most proximal to exposure to and/or experimentation with drugs. For this reason several program components have been developed that target this age group in particular. The first is social resistance skills. Resistance skills training is based on the social learning theory and stresses the importance of social factors in the initiation of drug use. Thus, the intervention paradigm focuses on teaching youth skills to handle peer pressure to experiment with drugs. This often includes either role play or video vignettes where an offer

is made and then strategies for rebuffing the offer are taught. Given the developmental status of this age group and their need to conform and maintain peer friendships, resistance strategies that do not alienate peers are taught. Social resistance programs applied in a regular classroom setting are highly successful. For example, in one randomized controlled trial, youths in the intervention groups were 30–40% less likely to initiate tobacco use compared to those in the nonintervention group.46,47 Interestingly, recent findings indicate that six years after this drug abuse prevention intervention was completed, those who received the intervention during junior high school were significantly less likely to have driving violations and points on their Department of Motor Vehicles records than those who did not receive the intervention. This finding illustrates relatively common phenomen in long-term follow-up studies of interventions—cross-over effects—positive effects on behaviors not addressed in the original intervention.48 Normative education is another strategy that has some positive effects but only when used in conjunction with skills development strategies. The goal of normative education is to correct misperceived positive norms about the actual use and acceptance of drug use. One strategy used is to actually survey students in a school about their perceptions of drug use among their peers, their perceptions of their peers’ acceptance of use, and their own drug use. In most cases students’ perceptions of use and acceptance of use are much higher than actual use and acceptance. These data are then reported back to students placing the “real school drug climate” in perspective and allowing students to feel that they are the norm rather than the outliers. It also reinforces the perception of the school as a safe and nurturing environment.46,49,50

Community-based Interventions At the community level and beyond, prevention strategies typically involve policy and media interventions. Policy interventions include activities such as training shopkeepers on how to request identification from purchasers of tobacco and alcohol products and how to refuse sales to those that do not meet the minimum age requirements. Other policy approaches include enforcing college campus rules about the underage use of illicit drugs and any use of illicit drugs.51,52 Media can be a successful tool in reducing the initiation and progression of drug abuse when it is appropriately used. One risk factor for substance abuse is a personality trait called high sensation seeking. For youth with this trait, a media strategy that works is offering alternative activities. In one media intervention study, young adult marijuana users with the high sensation seeking trait were targeted with media messages that offered alternative activities with high sensation value such as rock climbing. Spots were aired in one community; a second community did not receive the media spots. Identified groups of high sensation seekers were followed over time. The intervention community group had a 27% reduction in marijuana use compared to the control community group after 6 months.53,54,55

Ineffective Intervention Strategies Unfortunately, prevention programs and strategies that have been demonstrated to be effective are not always used. The strategy that has been demonstrated to be the least effective is fear arousal.56,57 One way of introducing this strategy is through testimonials from former substance abusers. These types of testimonials can actually have the unintended negative effect of making the drug-dependent life sound romantic. Other fear-inducing strategies include media spots that inaccurately portray the harmfulness of drugs. Youths tend to discount these and substitute the negative information with information that is unrealistically positive. Other ineffective strategies do not have unintended negative effects; however, they are ineffective in the absence of effective strategies. For example, information is an important component of most interventions; however information alone is not effective in altering behaviors. Similarly effective education where children are

56 involved only in activities to build self-esteem, while not harmful, is not effective in developing positive behaviors. Finally, alternate programming only, for example extracurricular activities, is not effective. Thus, these types of strategies should be looked at as “add-ons”.

Program Delivery The state of the knowledge at this point clearly shows that the skills/competency development interventions are the most potent in terms of effectiveness. In addition, there are some general principles of delivery that are often the determining factors in whether an intervention is successful or not. Delivery refers to the way in which the program or strategy is implemented with the target population. Programs that involve interactive activities providing participants with skills practice and then reinforce those skills over time have been found to be the most successful in facilitating the desired behavior change; on the other hand, didactic strategies in which information is delivered in a lecture format have been found to have little effect.56,57,58 Dosage is also critical. That means that a significant amount of the “active ingredients” of the intervention must be delivered and received for it to have the desired effect. In the same vein, providing “booster sessions” in the months and years postintervention to reinforce the important skills that have been developed help to maintain positive behavior change and skills. This implies that the intervention was delivered with fidelity to the program or strategy as originally designed and validated. At this time, little is known about what defines the “active ingredients” of behavioral interventions, thus deviations in the delivery of a program or strategy can inadvertently leave out the most important features of the intervention. Finally, it is critical that prevention efforts be consistent across contexts. That is, efforts at the individual, family, school, and community levels should reinforce one another. Inconsistency across contexts creates confusion and may result in the discounting of all efforts.59 A FINAL MESSAGE TO HEALTH CARE PROVIDERS

This chapter is intended to give an overview of the current state of drug abuse prevention interventions and the knowledge on which they are based. Absent is the role of the physician and other health care providers in reducing the initiation and progression of drug use. Health care personnel have the unique opportunity to interact one-onone with patients about their health behaviors. However, few take the opportunity to screen patients for substance abuse or risks that may subsequently lead to substance abuse. A small but growing body of research is developing and being tested in medical offices, clinics, and hospitals. One approach being investigated is the use of technologybased tools to screen for potential drug-related problem behaviors. For example, one of the most developed research-based tools at this time is for women who have been raped. The intervention is intended to reduce the trauma caused by the rape itself and the postrape forensic evidence collection procedures. Following these experiences substance abuse may begin or be exacerbated. The intervention is provided through a two-part video presentation that addresses the process of the forensic examination to reduce stress and future emotional problems. It also provides information and skills to reduce postrape substance use and abuse. Early findings suggest reductions in alcohol and marijuana use among women who were active users prior to the rape compared to the nonviewers.60,61 Another example of medically-oriented tools being developed and tested is for drug abuse risk and screening among youth. The goals of developing and testing these tools are to involve the primary care physician or physician’s assistant in identifying patients at risk, providing brief interventions, and potentially providing referrals for more intensive intervention. As with all interventions, life transitions may be critical periods for physicians to screen their patients, for example, during school physicals and/or pregnancy examinations.

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REFERENCES

1. Goldberg L, Elliot D, Clarke GN, et al. Effects of a multidimensional anabolic steroid prevention intervention: The Adolescents Training and Learning to Avoid Steroids (ATLAS) program. JAMA. 1996;276(19):1555–62. 2. Kurtzman TL, Otsuka KN, Wahl RA. Inhalant abuse in adolescents. J Adolesc Health. 2001;29(3):170–80. 3. Budney AJ, Moore BA, Vandrey R. Health consequences of marijuana use. In: Brick J, ed. Handbook of Medical Consequences of Alcohol and Drug Abuse. New York: Hawthorn Press, Inc. 2004; 171–217. 4. Yu S, Ho IK. Effects of acute barbiturate administration, tolerance and dependence on brain GABA system: Comparison to alcohol and benzodiazepines. Alcohol. 1990;7(3):261–72. 5. Smith KM, Larive LL, Romanelli F. Club drugs: methylenedioxymethamphetamine, flunitrazepam, ketamine hydrochloride, and gamma-hydroxybutyrate. Am J Health-Syst Pharm. 2002:59(11): 1067–76. 6. Jansen KL. A review of the nonmedical use of ketamine: use, users and consequences. J Psychoactive Drugs. 2000;32(4):419–33. 7. National Institute on Drug Abuse. Hallucinogens and Dissociative Drugs. National Institute on Drug Abuse Research Report Series. Washington, DC: NIH Publication No. 01-4209, 2001. 8. Abraham HD, Aldridge AM, Gogia P. The psychopharmacology of hallucinogens. Neuropsychopharmacology. 1996;14:285–96. 9. Vallejo R, de Leon-Casasola O, Benyamin R. Opioid therapy and immunosuppression: a review. Am J Ther. 2004;11(5):354–65. 10. Zacny JP, Gutierrez S. Characterizing the subjective, psychomotor, and physiological effects of oral oxycodone in non-drug-abusing volunteers. Psychopharmacology. 2003;170(3):242–54. 11. National Institute on Drug Abuse. Methamphetamine Abuse and Addiction. National Institute on Drug Abuse Research Report Series. Washington, DC: NIH Publication No. 02-4210, 2002. 12. National Institute on Drug Abuse. Cocaine Abuse and Addiction. National Institute on Drug Abuse Research Report Series. Washington, DC: NIH Publication No. 99-4342, 2004. 13. National Institute on Drug Abuse. Inhalant Abuse. National Institute on Drug Abuse Research Report Series. Washington, DC: NIH Publication No. 05-3818, 2005. 14. National Institute on Drug Abuse. Community Drug Alert Bulletin: Anabolic Steroids. Washington, DC: NIH Publication Number 004771, 2000. 15. Bahrke MS, Yesalis CE, Wright JE. Psychological and behavioural effects of endogenous testosterone and anabolic-androgenic steroids: An update. Sports Med. 1996;22(6):367–90. 16. Office of Applied Studies, Substance Abuse and Mental Health Services Administration. Results from the 2003 National Survey on Drug Use and Health: National Findings. Rockville, MD: DHHS Publication No. SMA 04-3964, NSDUH Series H-25, 2004. 17. Johnston LD, O’Malley PM, Bachman JG, et al. Monitoring the Future National Results on Adolescent Drug Use: Overview of Key Findings, 2004. Bethesda, MD: NIH Publication No. 05-5726, 2005. 18. Glantz MD, Brodsky MD, Fletcher BW, et al. Twenty years of adolescent drug use: Comparing national survey findings (submitted). 19. Bronfenbrenner U. Ecological Systems Theory. In: Bronfenbrenner U, ed. Making Human Beings Human: Bioecological Perspectives on Human Development. Thousand Oaks, CA: Sage Publication Ltd. 2005. 20. Bijou S. Behavior Analysis. In: Vasta R, ed. Six Theories of Child Development: Revised Formulations and Current Issues. London: Jessica Kingsley Publishers, Ltd. 1992. 21. Bandura A. Social Learning Theory. Englewood Cliffs, New Jersey: Prentice Hall, 1977.

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22. Hawkins JD, Catalano RF, Miller JY. Risk and protective factors for alcohol and other drug problems in adolescence and early adulthood: Implications for substance abuse prevention. Psychol Bull. 1992;112:64–105. 23. Hawkins JD, Catalano RF, Kosterman R, Abbott R, Hill KG. Preventing adolescent health-risk behaviors by strengthening protection during childhood. Arch Pediatr Adolesc Med. 1999;153:226–34. 24. Hawkins JD, Catalano RF, Arthur MW. Promoting Science-Based Prevention in Communities. Addict Behav. 2002;(27):951–76. 25. Durlak JA. Effective prevention and health promotion programming. In: Gullotta TP, Bloom M, eds. The Encyclopedia of Primary Prevention and Health Promotion. New York: Kluwer Academic/ Plenum Publishers, 2003. 26. National Institute on Drug Abuse. Preventing Drug Abuse among Children and Adolescents: A Research-Based Guide. National Institute on Drug Abuse, Washington, DC: NIH Publication No. 04-4212(A);2003. 27. Pollard JA, Hawkins JD, Arthur MW. Risk and protection: Are both necessary to understand diverse behavioral outcomes in adolescence? Soc Work Res. 1999;23(8):145–58. 28. Catalano RF, Haggerty KP, Fleming CB, et al. Children of substance abusing parents: current findings from the Focus on Families project. In: McMahon RJ, Peters RD, eds. The Effects of Parental Dysfunction on Children. New York: Kluwer Academic/Plenum Publishers, 2002;179–204. 29. Ialongo N, Werthamer L, Kellam S, et al. Proximal impact of two first-grade preventive interventions on the early risk behaviors for later substance abuse, depression, and antisocial behavior. Am J Community Psychol. 1999;27:599–641. 30. Bierman KL, Bruschi C, Domitrovich C, et al. Early disruptive behaviors associated with emerging antisocial behavior among girls. In: Putallaz M, Bierman KL, eds. Aggression, Antisocial Behavior and Violence among Girls: A Developmental Perspective. Duke Series in Child Development and Public Policy. New York: Guilford Publications, Inc. 2004;137–61. 31. Farmer AD Jr, Bierman KL. Predictors and consequences of aggressivewithdrawn problem profiles in early grade school. Lawrence Erlbaum. J Clin Child Adolesc Psychol. 2002;31(3):299–311. 32. Miller-Johnson S, Coie JD, Maumary-Germaud A, Bierman K. Peer rejection and early starter models of conduct disorder. J Abnorm Child Psychol. 2002;30(3):217–30. 33. Webster-Stratton C, Reid J, Hammon M. Preventing conduct problems, promoting social competence: a parent and teacher training partnership in Head Start. J Clin Child Psychol. 2001;30:282–302. 34. Hunter FT, Youniss J. Changes in functions of three relations during adolescence. Dev Psychol. 1982;18:806–11. 35. Ashery RS, Robertson EB, Kumpfer KL, eds. Drug Abuse Prevention through Family Interventions. NIDA Research Monograph Number 177. Washington, DC: U.S. Government Printing Office, 1998. 36. Kosterman R, Haggerty KP, Spoth R, et al. Unique influence of mothers and fathers on their children’s antisocial behavior. J Marriage Fam. 2004;66(3):762–78. 37. Madon S, Guyll M, Spoth R. The self-fulfilling prophecy as an intrafamily dynamic. J Fam Psychol. 2004;18(3):459–69. 38. Redmond C, Spoth R, Shin C, et al. Engaging rural parents in familyfocused programs to prevent youth substance abuse. J Prim Prev. 2004;24(3):223–42. 39. Kosterman R, Hawkins JD, Haggerty KP, et al. Preparing for the drug-free years: session-specific effects of a universal parent-training intervention with rural families. J Drug Educ. 2001;31:47–68. 40. Petras H, Schaeffer CM, Ialongo N, et al. When the course of aggressive behavior in childhood does not predict antisocial outcomes in adolescence and young adulthood: an examination of potential explanatory variables. Dev Psychopathol. 2004;16(4):919–41. 41. Schaeffer CM, Petras H, Ialongo N, et al. Modeling growth in boys’ aggressive behavior across elementary school; Links to later criminal involvement, conduct disorder, and antisocial personality disorder. Dev Psychol. 2003;39(6):1020–35.

42. Crijnen AAM, Feehan M, Kellam SG. The course and malleability of reading achievement in elementary school: The application of growth curve modeling in the evaluation of a mastery learning intervention. Learning and Individual Differences. 1998;10(2): 137–57. 43. Elias MJ, Zins JE, Weissberg RP, et al. Promoting Social and Emotional Learning: Guidelines for Educators. Alexandria, VA: Association for Supervision and Curriculum Development; 1997. 44. Greenberg MT, Weissberg RP, O’Brien MU, et al. Enhancing school-based prevention and youth development through coordinated social, emotional, and academic learning. Am Psychol. 2003;58(6–7):466–74. 45. Barrera M, Biglan A, Taylor TK, et al. Early elementary school intervention to reduce conduct problems: a randomized trial with Hispanic and non-Hispanic children. Prev Sci. 2002;3:83–94. 46. Botvin GJ, Griffin KW, Paul E, et al. Preventing tobacco and alcohol use among elementary school students through life skills training. J Res Adolesc. 2004;14(1):73–97. 47. Botvin GJ, Griffin KW. life skills training: Empirical findings and future directions. J Prim Prev. 2004;25(2):211–32. 48. Griffin KW, Botvin GJ, Nichols TR. Long-term follow-up effects of a school-based drug abuse prevention program on adolescent risky driving. Prev Sci. 2004;5:207–12. 49. Dusenbury LA, Hansen WB, Giles SM. Teacher training in norm setting approaches to drug education: A pilot study comparing standard and video-enhanced methods. J Drug Educ. 2003;33(3): 325–36. 50. Donaldson SI, Graham JW, Piccinin AM, et al. Resistance-skills training and onset of alcohol use: evidence for beneficial and potentially harmful effects in public schools and in private Catholic schools. In: Marlatt GA, Vanden Bos GR, eds. Addictive Behaviors: Readings on Etiology, Prevention and Treatment. Washington, DC: American Psychological Association. 1997;215–38. 51. Pentz MA. Institutionalizing community-based prevention through policy change. J Community Psychol. 2000;28(3):257–70. 52. Pentz MA. Comparative effects of community-based drug intervention. In: Baer JS, Marlatt GA, eds. Addictive Behaviors across the Life Span: Prevention Treatment and Policy Issues. Thousand Oaks, CA: Sage Publications, Inc. 1993;69–87. 53. Palmgreen P, Donohew L, Lorch EP, et al. Television campaigns and adolescent marijuana use: tests of sensation seeking targeting. Am J Public Health. 2001;91:292–6. 54. Palmgreen P, Donohew L, Lorch EP, et al. Television campaigns and sensation seeking targeting of adolescent marijuana use: a controlled time series approach. In: Hornik RC, ed. Public Health Communication: Evidence for Behavior Change. Mahway, NJ: Lawrence Erlbaum Associates, Publishers. 2002;35–56. 55. Stephenson MT, Morgan SE, Lorch EP, et al. Predictors of exposure from an antimarijuana media campaign: Outcome research assessing sensations seeking targeting. Health Commun. 2002;14(1):23–43. 56. Tobler NS, Roona MR, Ochshorn P, et al. School-based adolescent drug prevention programs: 1998 meta-analysis. J Prim Prev. 2000;20(4):275–336. 57. Tobler NS. Lessons learned. J Prim Prev. 2000;20(4):261–74. 58. Dusenbury L, Brannigan R, Falco M, et al. A review of research on fidelity of implementations for drug abuse prevention in school settings. Health Educ Res. 2003;18(2)237–56. 59. Ringwalt CL, Ennett S, Johnson R, et al. Factors associated with fidelity to substance use prevention curriculum guides in the nation’s middle schools. Health Educ Behav. 2003;30(3): 375–91. 60. Resnick H, Acierno R, Kilpatrick DG, et al. Description of an early intervention to prevent substance abuse and psychopathology in recent rape victims. Behav Modif. 2005;29:156–88. 61. Acierno R, Resnick HS, Flood A, et al. An acute post-rape intervention to prevent substance use and abuse. Addict Behav. 2003;28: 1701–15.

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Community Health Promotion and Disease Prevention Stephanie Zaza • Peter A. Briss

INTRODUCTION

In 1988, the Institute of Medicine (IOM) released The Future of Public Health,1 a seminal report that found the national public health infrastructure to be in disarray. The IOM committee defined the mission of public health as fulfilling society’s interest in assuring conditions in which people can be healthy. It then developed clear statements about the role of government in three core public health functions: assessing health status, developing policy, and assuring that necessary services are provided. Finally, the committee made specific recommendations for responsibility and action at the national, state, and local levels to achieve the core functions. The 1988 IOM publication was ultimately complemented by the 1994 report of the Department of Health and Human Services (DHHS) Public Health Functions Steering Committee, which described 10 essential public health services that corresponded to the IOM core functions (Table 57-12). The core functions and essential services focused on the roles and responsibilities of governmental public health organizations at the national, state, and local level and were important for refocusing public health organizations and for promoting organized approaches to public health. With the publication in 2003 of The Future of the Public’s Health in the 21st Century,3 the IOM expanded its definition of public health to include all of society’s efforts to achieve improved health. Recommendations addressed health policy at every level of American society and expanded efforts to enlist all sectors in improving health outcomes. For example, in this later report, recommendations for responsibility and action in public health are made not only for governmental entities but also for community representatives and organizations (e.g., congregations, civic groups, and schools), the health care delivery system, employers and business, the media, and academia. In 2005, the Task Force on Community Preventive Services (a nonfederal committee supported by the U.S. Centers for Disease Control and Prevention) released the Guide to Community Preventive Services4 to assist communities in realizing the expanded version of public health suggested by the IOM report. The Community Guide, which provides syntheses of the best available scientific information to support health programs and policies, can help make delivery of the 10 essential health services more effective at the local level.5

Note: The findings and conclusions in this chapter are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.

Taken together, these four reports illustrate the need for a holistic public health approach—one that includes several important emerging themes. First, the reports call for a holistic public health approach that comprehensively and fairly marshals the skills and resources of the entire community to promote health and prevent disease. In addition, they underline the principles of widespread community participation and building of partnerships in public health planning and action. Finally, they highlight the importance of taking an organized and thoughtful approach to the planning and implementation of health programs, which should include using the best available evidence to support decisions and action. This chapter will describe the holistic approach proposed in these seminal reports and provide specific examples of how such an approach is being implemented. In addition, the chapter will provide examples of making the link between different kinds of public health decisions and the best types of evidence to support those decisions. THE HOLISTIC APPROACH

In the holistic approach to public health, communities are the public health agents, and they must concentrate on the needs, preferences, and assets of the entire community. In doing so, they must consider a broad range of health conditions (e.g., chronic diseases such as diabetes and atherosclerosis, viral and bacterial infections, accidental injury), risk factors (such as smoking and inactivity), and protective factors (e.g., education, exercise programs). They must also consider the distribution of life stages within the community, cultural differences, the array of health organizations in the community, and the various assets available in the community to promote health and prevent disease. Organized holistic approaches improve efficiency by allowing programs within the community to leverage each other’s strengths or by allowing programmatic activities to address multiple related outcomes (e.g., reduced levels of smoking, fewer complications of diabetes, improved cardiovascular health). Through broad-based public health activities that involve key stakeholders throughout the community, a richer and more detailed body of information is provided for decision-making. With these relationships and the information they provide, the likelihood that these issues will go unrecognized is reduced, problems can be identified earlier in their natural course, or more proximate solutions might be identified.

Socioecologic Model The socioecologic model is useful for explaining a holistic approach to public health.6 This model describes patterned behavior, such as 1023

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TABLE 57-1. THE CORE FUNCTIONS AND TEN ESSENTIAL SERVICES OF PUBLIC HEALTH Core Functions

Essential Services

Assessment

1. Monitor health status to identify health problems. 2. Diagnose and investigate health problems and health hazards in the community. Policy Development 3. Inform, educate, and empower people about health issues. 4. Mobilize community partnerships to identify and solve health problems. 5. Develop policies and plans that support individual and community health efforts. Assurance 6. Enforce laws and regulations that protect health and ensure safety. 7. Link people to needed personal health services and assure the provision of health care when otherwise unavailable. 8. Assure a competent public health and personal health workforce. 9. Evaluate effectiveness, accessibility, and quality of personal and population-based health services. Serving all 10. Research for new insights and innovative Functions solutions to health problems. Source: Institute of Medicine. The Future of Public Health. Washington, DC; National Academies Press; 1988. Public Health Functions Steering Committee. The Public Health Workforce: An Agenda for the 21st Century. Full Report of the Public Health Functions Project. Washington, DC: U.S. Department of Health and Human Services; 1994.

health risk behaviors (e.g., diet, smoking patterns, drinking), as the outcome of interest; these outcomes are determined by individual, interpersonal, institutional, community, and public policy factors. The model makes explicit the importance of coordinated public health actions at each level to effect change in health behaviors. The focus of the socioecologic model on multiple interacting levels of influence on behavior is consistent with taking broad approaches to public health programming that are not limited to any one agency or sector; indeed, the model allows for and even assumes the need for input and action across the community. A holistic approach that involves all of the stakeholders in an issue is more likely to be accepted by the target population and to identify and avoid unintended consequences. Finally, a holistic approach allows the linking of health promotion activities across different conditions and risk factors to achieve both increased efficiency and greater sustainability.

Infrastructure Realizing the benefits of taking a holistic approach to community health requires a well-organized infrastructure (preferably with predictable and sustainable funding) that can serve as the interface for various community sectors (e.g., schools, work sites, and health care delivery organizations). This infrastructure can serve as the focal point for convening and planning public health activities, securing and distributing funding for these activities, and communicating with staff of other programs and with the public. The infrastructure can consist of both formal and informal networks, paid staff and volunteer experts, leadership teams, and large community coalitions. The infrastructure is only useful, however, insofar as it develops, implements, and supports programs and policies that achieve health goals the community considers important. The inputs to public health activities provided by the infrastructure are important elements in describing those activities and their impacts. Thus, it is also important to document all of the components of the infrastructure as part of the record describing how public health programs were accomplished.

Steps to a HealthierUS A modern example of a federally funded program that follows a holistic approach is Steps to a HealthierUS (www.healthierUS.gov/steps). The program’s purpose is to develop an integrated program of chronic disease prevention and health promotion in each funded community. A range of sectors—public health, education, business, health care delivery, and community and social services—are represented in an infrastructure that is created by Steps to a HealthierUS for each community. The infrastructure provides overall strategic planning and leadership; offers an interface through which sectors can interact; communicates the program to community leaders and residents; and integrates the program with other statewide initiatives, particularly those that are federally funded. Together with sector partners, the program develops, implements, and coordinates programs and activities to accelerate progress toward established Healthy People 20107 objectives for health behavior and health outcomes in six focus areas: diabetes, asthma, obesity, nutrition, physical activity, and tobacco. Clearly, involving multiple sectors and community partners is needed to make progress in the focus areas listed. For example, achieving the public health objectives of improving the quality of care for diabetes, reducing hospitalizations from exacerbations of asthma, or increasing the use of appropriate health care services cannot be achieved without direct improvements to the health care delivery sector. Similarly, complex health risk behaviors, such as smoking, binge drinking, and combining a high-calorie diet with inactivity, will not be addressed in the health care sector alone. There is, therefore, a growing recognition of the importance of school, work-site, and community settings for health promotion activities. For example, activities such as tobacco cessation and nutrition programs as well as organized recreation may require the involvement of the school, business, philanthropic, faith-based, and community-based sectors of the community. Furthermore, these sectors may have less opportunity to meet their objectives if they work independently rather than cooperatively. Ideally, programs should be coordinated across the sectors. For example, some school-based programs have been shown to be more effective if conducted in the context of broader community efforts (such as supporting school smoking bans with community cessation programs for students, faculty, and staff). The Steps to a HealthierUS program adds value by helping to flexibly integrate efforts across the community and across various health challenges. EVIDENCE-BASED DECISION-MAKING IN A HOLISTIC COMMUNITY APPROACH

While local community needs and preferences are driving forces in public health decision-making, other types of evidence are required for long-term sustainability of outcomes, including scientific evidence. Unfortunately, community control may be seen as antagonistic to the recent trend to use the best available science to inform public health decisions, creating tension between public health scientists and on-the-ground practitioners. The tension may be more apparent than real, however. For many public health problems (e.g., type 2 diabetes, smoking, heart disease), we have a good deal of knowledge about their prevalence and causes as well as effective solutions; this information can be learned across communities and then applied in specific contexts. This is similar to the case in clinical medicine, in which a generalizable science tells us about the causes of problems and the solutions that work for most people, but where individual patients and providers must still make decisions about how to proceed. Recent developments in the fields of “evidence-based medicine” and “evidence-based public health” have not only improved the science but have also helped to improve its credibility while speeding its way to the bedside or the community. In communities as well as at the bedside, however, locally appropriate decisions can be informed but not solely determined by this science.

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Evidence

Four Decisions

In common usage, “evidence” is simply “A thing or things helpful in forming a conclusion or judgment.”8 As in the courtroom, some forms of evidence are more persuasive than others, and different types of evidence apply to different types of decisions or questions. In public health we make hundreds of decisions every day, informed by various types of evidence. A call for improving or increasing evidence-based decisionmaking in public health should, therefore, focus on transparently and reliably matching appropriate types of evidence to the various types of decisions.

In establishing programs for promoting health and preventing chronic disease, four primary decisions must commonly be made: (a) Should something be done? (b) What should be done? (c) How should it be done? (d) Is it working or does it need to be modified? As shown in Table 57-2, in each case there are related questions that should be posed9 for each decision. Approaches to making these decisions can be found in a variety of health promotion and planning models and tools, such as Mobilizing for Action through Planning and Partnership (MAPP) and the PRECEDE-PROCEED model.10–11 This section

TABLE 57-2. A FRAMEWORK FOR USING DIFFERENT TYPES OF EVIDENCE TO MAKE DECISIONS IN PUBLIC HEALTH Decision Should something be done? What is the burden of disease?

What is the urgency?

Is it a priority for the community? What is the perceived need?

What should be done? What is the nature of the problem?

What works? What is acceptable to the community?

What can be afforded? What is feasible? How should it be done? What steps are needed to implement this intervention?

What barriers must be overcome to implement this intervention?

Is it working or does it need to be modified? Is it being implemented well?

What does the community think?

Is it improving health risks or outcomes?

Type of Evidence • Surveillance data (measuring morbidity, mortality, years of potential life lost, incidence, prevalence) • Survey data • Vital statistics data • Medical utilization data • Cost data • Basic medical data (e.g., does the condition or risk factor progress rapidly or have serious complications?) • Trend data • Degree to which the problem is understood (e.g., emerging issues such as avian flu or environmental hazards might merit more attention than can be justified based on current burden) • Perceived interest or importance based on surveys, focus groups, political processes, or other information Information gleaned from analysis of conceptual and empirical information on causes, natural course of the problem, and possible points of intervention • Scientific evidence of effectiveness from individual evaluation studies • Systematic reviews of evaluation studies • Information about community members’ understanding and approval of possible intervention strategies from: • Focus groups • Key interviews • Town hall meetings • Anecdote • Political processes Information based on a comparison of typical costs and cost-effectiveness (gleaned from economic analysis) and local assets • Organizational assessment • Experience, interviews, etc. • Documentation from previous implementation of the specific intervention and other related interventions • “Best process” information • Anecdotal experience from others who have implemented the intervention • Documentation from previous implementation • Anecdotal experience from others who have implemented the intervention • Complex systems modeling • Focus groups

• “Process” measures from checklists, interviews, and other data collection tools • Achievement of behavior or health outcomes from evaluation and program monitoring efforts • Focus groups • Interviews • Less formal data collection • Political processes Achievement of behavior or health outcomes from evaluation and program monitoring efforts

Source: Gard B, Zaza S, Thacker SB. Connecting public health law with science. J Law Med Ethics. 2004;32(4 Suppl):100–3.

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focuses on the types of evidence that are used to make decisions and points out the wide variety of information, from scientific to anecdotal, that is applicable. The first decision, “Should something be done?” is the essence of community-based planning for promoting health and preventing disease. Often, the decision about whether to take action relies on surveillance data, surveys, or other studies that indicate the burden of the disease or risk factor in question, frequently expressed as years of potential life lost or costs incurred. Here, communities must also consider the urgency of the issue: Is there an increasing trend? Is the problem particularly severe or disabling? Finally, communities must also consider whether addressing the problem is a priority. In some cases, the level of understanding about the problem will drive priority (e.g., issues that seem more novel may be given higher priority); the perception of risk and the acceptability of potential solutions may also determine priority. In addressing “What should be done?,” communities must first consider the essential nature of the problem. In the PRECEDE portion of the PRECEDE-PROCEED model, Green and Kreuter point out that, “The determinants of health must be diagnosed before the intervention is designed; if they are not, the intervention will be based on guesswork and will run a greater risk of being misdirected and ineffective.”11 For example, a mass media campaign to improve the population’s coverage for a vaccine is unlikely to increase immunization rates if the real problem is that people do not have access to clinics where the vaccine is offered. In brief, a detailed analysis of the local situation is required to understand how the problem should be addressed. Failing to take advantage of the best available generalizable knowledge in addressing local priorities can also result in ineffective or misdirected efforts. The second part of the “what should be done” decision is an understanding of what works. Scientific evidence is the most reliable and generally most appropriate type of evidence for determining what works; scientific evidence consists of individual studies and reviews that synthesize those studies. Ideally, this evidence will show how much change can be expected in the outcomes of interest based on work from other communities or contexts. Individual studies can be an excellent basis for making recommendations; they are relatively easy to find, can provide specific “recipes” for what to do, and are easy to understand. On the other hand, in many cases there will be numerous studies that seem potentially relevant, making it difficult for practitioners to keep up with them, and their results may conflict. In addition, they typically provide little information on which characteristics of the intervention or context contribute most to effectiveness. Literature reviews are helpful for identifying and summarizing the vast scientific literature, but each approach to performing these reviews has disadvantages as well as advantages. Expert or narrative reviews are carried out by experts who gather information based on their own experience and knowledge. These reviews are useful for giving a conceptual overview of a subject but can be subject to conscious or unconscious bias in how information is collected and assembled and how the conclusions relate to that information. In contrast, systematic reviews are based on a priori rules that lay out the study question, a search strategy, criteria for including or excluding studies, parameters that will be applied to judge the quality of each study, and methods for analyzing data. Meta-analyses, a subset of systematic reviews, allow for the calculation of an overall effect size (i.e., the quantifiable effect of the intervention on desired outcomes) for the group of studies included according to specific statistical methods. The advantages of systematic reviews (e.g., reduced bias and improved transparency) come at a cost, however, as they require greater time and technical expertise to conduct, resulting in fewer of these types of reviews being available. Two examples of systematic reviews used to support recommendations for preventive medicine and public health are the Guide to Clinical Preventive Services12 and the Guide to Community Preventive Services.4 The Guide to Clinical Preventive Services, developed by the U.S. Preventive Services Task Force (USPSTF), provides reviews and recommendations about individual clinical services, such as screening tests, counseling on health behavior, and

chemoprophylaxis (www.ahrq.gov12). The Guide to Community Preventive Services,4 in contrast, provides reviews and recommendations about a variety of public health interventions, such as strategies that use education, policy, system change, or environmental approaches to effect change (www.thecommunityguide.org). Together, the two references provide a broad range of interventions that have been shown through extensive scientific study to be effective. Reviewing scientific studies to know what works is necessary for decision-making, but determining “What should be done?” means that additional questions must be asked: (a) What is acceptable to the community? (b) what can our community afford? and (c) what is feasible given our resources and capacity? These questions are answered through focus groups, interviews with key informants, and economic and systems analyses. To address the third major decision, “How should it be done?” communities may be able to consult practice guidelines that provide additional information about how to implement recommended interventions, such as policies to ban smoking, standing orders for routine delivery of vaccinations, or campaigns to enforce laws on safety belt use. With increasing frequency, developers of guidelines and other public health practitioners are developing tool kits and materials to help move recommended interventions into practice. In addition, communities can review “best processes” to obtain information and advice about the ways of implementing programs that have been most successful across studies, as found, for example in the “Community Toolbox” developed by the University of Kansas (http://ctb.ku.edu). Finally, community leaders and members can draw on personal experience and anecdotes as well as documentation from previous implementations to answer the question of how things should be done. The last of the major decisions, “Is it working or does it need to be modified?” is tied to program management, as evaluation of a program is used to determine a program’s effectiveness and, where possible, to improve performance. Ideally, this evaluation process should involve a broad range of stakeholders. The Centers for Disease Control and Prevention (CDC) has outlined a basic framework for evaluating programs that is used widely in public health and consists of just six steps: (a) engage stakeholders; (b) describe the program; (c) focus the evaluation design; (d) gather credible evidence; (e) justify conclusions; and (f) ensure use and share lessons learned.13 The developers of the CDC framework emphasized that the evidence gathered in step 4 must be perceived by stakeholders as relevant in addition to being believable. Thus, a variety of types of evidence might be needed, ranging from systematically collected data obtained through a well-controlled experiment to the results of document review, focus groups, and interviews with key informants. For all of the decisions that have been discussed here, debates are ongoing about what evidence is most appropriate, how to improve the quality of that evidence, and when a body of evidence is sufficiently credible to support action. It is important to report that the need to improve the quality and transparency of the science that supports public health decisions has been recognized and that efforts to make those improvements are ongoing. CONCLUSION

To be successful, initiatives to promote health and prevent disease require a holistic approach, a commitment from the entire community, and a reliance on credible information. The approach described here incorporates all of these elements. REFERENCES

1. Institute of Medicine. The Future of Public Health. Washington, DC; National Academies Press; 1988:19–34. 2. Public Health Functions Steering Committee. The Public Health Workforce: An Agenda for the 21st Century. Full Report of the Public Health Functions Project. Washington, DC: U.S. Department of Health and Human Services; 1994:21.

57 3. Institute of Medicine. The Future of the Public’s Health in the 21st Century. Washington, DC: National Academies Press; 2003:1–18. 4. Task Force on Community Preventive Services. The Guide to Community Preventive Services: What Works to Promote Health? Zaza S, Briss PA, Harris KW, eds. New York: Oxford University Press; 2005:1–506. 5. McGinnis JM. With both eyes open. The Guide to Community Preventive Services. Am J Prev Med. 2005;28(5 Suppl):223–5. 6. McLeroy KR, Bibeau D, Steckler A, et al. An ecological perspective on health promotion programs. Health Educ Q. 1988;15:351–77. 7. U.S. Department of Health and Human Services. Healthy People 2010. 2nd ed. Vols. 1 and 2. Washington, DC: U.S. Department of Health and Human Services, 2000. Vol 1: pp 1–608; Vol 2: pp 1–664. 8. The American Heritage Dictionary of the English Language. 4th ed. Retrieved March 28, 2007, from Dictionary.com website: http:// dictionary.reference.com/browse/evidence.

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9. Gard B, Zaza S, Thacker SB. Connecting public health law with science. J Law Med Ethics. 2004;32(4 Suppl):100–3. 10. National Association of City and County Health Officials. www.naccho.org. Accessed May 16, 2005. 11. Green LW, Kreuter MW. Health Promotion Planning: An Educational and Ecological Approach. 3rd ed. New York: McGraw-Hill; 1999:32–37. 12. Introducing the Third U.S. Preventive Services Task Force. Article originally in Am J Prev Med. 2001;20(3S):3–4. Agency for Healthcare Research and Quality, Rockville, MD. http://www.ahrq.gov/ clinic/ajpmsuppl/berg.htm. Accessed February 2, 2006. 13. Centers for Disease Control and Prevention. Framework for program evaluation in public health. Morb Mortal Wkly Rep. 1999;48(RR-11): 1–35.

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Risk Communication—An Overlooked Tool for Improving Public Health

58

David P. Ropeik

One thousand and eighteen more Americans died in motor vehicle crashes October through December 2001 than in those 3 months the year before, according to researchers at the University of Michigan’s Transportation Research Institute. As those researchers observed “. . . the increased fear of flying following September 11 may have resulted in a modal shift from flying to driving for some of the fearful.”1 One thousand and eighteen people dead, more than one-third the number of people killed in the attacks of September 11, in large part because they perceived flying to be more dangerous and driving less so, despite overwhelming evidence to the contrary. In 1971, President Richard Nixon signed the National Cancer Act and declared “War on Cancer.” In 2004 the National Cancer Institute had a budget of $4.7 billion.2 In 2002, cancer killed 557,271 Americans. That same year, heart disease killed 696,9473. Yet the National Heart, Lung, and Blood Institute spent approximately $1.8 billion on cardiovascular diseases, including heart disease, in 2004.4 And there is no National Heart Disease Act, nor a national “War on Heart Disease”, despite the fact that heart disease kills roughly 25% more Americans each year than cancer, roughly 140,000 more deaths in 2002 alone. Chronically elevated stress is known to weaken the immune system, contribute to cardiovascular and gastrointestinal damage, interfere with fertility, impair the formation of new bone cells, impede the creation of long-term memory, and contribute to a greater likelihood and severity of clinical depression.5 What do these three cases have in common? They demonstrate the threats to public health caused by gaps between risk perception, informed by the intuitive reasoning by which humans gauge the hazards they face, and risk realities based on science. The examples above demonstrate the vital role risk communication can play in advancing public health, by helping narrow those gaps. RISK COMMUNICATION DEFINED

Currently, there are multiple definitions of risk communication; however, most embody the basic idea that by providing people with more information, they will be able to make smarter choices about their health. But that was not always true. The term “risk communication” arose largely as a result of environmental controversies in the 70s, when public concern was high about some relatively lower threats to human and environmental health. Scientists, regulators, and the regulated

community described people as irrational, and their frustration gave rise to efforts to educate the public and defuse those controversies. Early risk communication was viewed as a one-way process in which experts would explain the facts to the ill-informed lay public in ways that would help people behave more rationally, especially about such issues as air and water pollution, nuclear power, industrial chemicals, hazardous waste, and other environmental hazards. Thus, the goal of early risk communication was not always to enlighten people so they might improve their health. Instead, it was frequently a tool to reduce conflict and controversy, and often it was simply an effort by administrators, regulators, or company representatives to diminish opposition to particular product or technology or facilityciting proposal. One researcher defined risk communication as “a code {word} for brainwashing by experts or industry.”6 But risk communication has evolved. This chapter will use the following definition: Risk communication is a combination of actions, words, and other interactions responsive to the concerns and values of the information recipients, intended to help people make more informed decisions about threats to their health and safety.

This definition attempts to embody the ways that risk communication has evolved and matured over the past 15 years or so. Most importantly, the consensus among experts in the field now rejects the one-way “We’ll teach them what they need to know” approach. A National Research Council committee effort to move the field forward produced this definition in 1989. “Risk communication is an interactive process of exchange of information and opinion among individuals, groups, and institutions. It involves multiple messages about the nature of risk and other messages, not strictly about risk, that express concerns, opinions, or reactions to risk messages or to legal and institutional arrangements for risk management.”7 In other words, risk communication should be considered a dynamic two-way interaction. Both sides express their perspectives, and both sides have to listen and respond to information from the other. Perhaps even more fundamental, and intrinsic to the idea of the two-way street, is the growing acceptance among risk communication experts that risk means something inherently different to the lay public than what it means to scientists and regulators. When laypeople are asked to rank hazards in terms of mortality rates, they tend to 1029

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generally agree with the vital statistics. But ask them to rank what is risky and their responses change, with some lesser hazards, such as nuclear power, moving toward the head of the list, and some relatively larger risks, like smoking, moving further down.8 “Risk” is perceived as more than a number by the general public. Other attributes, like trust, dread, control, and uncertainty, also factor into the judgments people make that subsequently influence the nature and magnitude of their fears. As risk communication has evolved, there is increasing (but by no means, universal) acceptance by practitioners that both the science-based view of experts and the intuitive view of risk among the general public are valid, and both must be respected and incorporated if communications about risk is to be effective. This evolution is summed up in Risk Communication and Public Health, edited by Peter Bennett and Kenneth Calman: “. . . there has been a progressive change in the literature on risk: • from an emphasis on ‘public misperceptions’, with a tendency to treat all deviations from expert estimates as products of ignorance or stupidity • via empirical investigation of what actually concerns people and why • to approaches which stress that public reactions to risk often have a rationality of their own, and that ‘expert’ and ‘lay’ perspectives should inform each other as part of a two-way process.”9 People are not being irrational when their fears don’t match the expert view of a potential high-risk situation. While they may not be exclusively relying on evidence from toxicology, epidemiology, statistics, economics, and the other sciences of risk assessment and risk analysis, research from a number of fields has established that the lay public’s perception of risk develops under conditions of “bounded rationality”.10 As it is applied to the perception of risk, bounded rationality essentially describes the process individuals use to make judgments when they have less information, time, or cognitive skills than a fully rational judgment would require. As Reinhard Selten writes “Fully rational man is a mythical hero who knows the solutions to all mathematical problems and can immediately perform all computations, regardless of how difficult they are. Human beings are in reality very different. Their cognitive capabilities are quite limited. For this reason alone, the decision-making behavior of human beings cannot conform to the ideal of full rationality.”11 Gigerenzer and Selten refer to bounded rationality as “the adaptive toolbox,” the set of “fast and frugal rules” or mental processes humans have evolved to apply fact, feelings, instinct, and experience to the choices we face about threats to our survival.12 Neuroscientists have determined that some of the processing of threat information may be determined by aspects of human brain structure. Psychologists have identified a set of affective characteristics that make some risks seem larger and some smaller, the scientific data notwithstanding. Others have described a number of common heuristics and biases, mental shortcuts that turn complicated choices into simple ones, sometimes leading to judgments that seem suboptimal, based solely on “the facts”. These are powerful insights into more effective risk communication. By understanding the biology and psychology of how humans perceive risk, we can understand why and how lay and expert definitions of the very concept of risk vary. Such insights provide critical tools for effective risk communication because they help communicators both understand and respect the validity of the “intuitive reasoning” people use to gauge risk. By understanding and respecting lay perceptions of risk, the risk communicator can choose content, tone, and information delivery processes that increase the likelihood that their audience(s) will be more receptive, and their information will have more utility for the people with whom they are interacting. The Greek Stoic philosopher Epictetus said “People are disturbed, not by things, but by their view of them.” Understanding the roots of what shapes those views allows the true dialogue of modern risk communication to take place.

THE BIOLOGY OF FEAR

Neuroscientist Joseph LeDoux and others have made remarkable discoveries about how the human brain processes raw sensory data into perceptions of threat and hazard. They have found that what we consciously describe as fear begins in the amygdala. External sensory information travels from end organs along neural pathways that send the information to the amygdala and the cortex. But the amygdala, where fear begins, responds before the cortex has a chance to process the information and add its analysis to the risk perception process. This same time lag (LeDoux estimates it at about 20 milliseconds) applies to nonsensory inputs as well, such as thoughts, memories, etc. In very simplified terms, this means that information is processed in the part of the brain where we fear before it is processed in the part of the brain where we think. That alone has profound implications for risk communication since it appears that the hard wiring of the brain, in managing fear, may favor rapid response (i.e., fight-or-flight) over deliberation of the best course of action. Thus, biology may help to explain why risk means one thing to experts and another to the lay public.13 RISK PERCEPTION PSYCHOLOGY

Some of what we are commonly afraid of seems instinctive; snakes, heights, the dark. Indeed, Charles Darwin recognized this and visited the London Zoo’s poisonous snake exhibit, repeatedly tapping on a glass window to provoke a strike by the snake inside, trying to teach himself not to recoil in fear. His effort in self-delivered risk communication failed. The innate fear, and the adaptive “fear first, think second” construction of the brain’s hazard perception systems could not be overcome. But how do people subconsciously decide what to be afraid of, and how afraid to be, when the threat does not trigger an instinctive reaction? When people hear about a new disease, product, or technology; when individuals try to gauge the risk of something against its benefits; when persons learn new information about a potential hazard and try to fit it into what they already know. How does the human mind filter incoming data and translate it into our perceptions of what is risky and what is not? The answers are to be found in two literatures, both of critical relevance to risk communication. The first is the study of how people generally make judgments of any kind, including judgments about risk, under conditions of uncertainty. This work has identified a number of systematic biases that contribute to what seem to be suboptimal irrational choices. The second is the specific study of the psychology of risk perception, which has identified more than a dozen affective attributes of risk that tend to make us more or less afraid, even when our apprehension doesn’t seem consistent with the scientific data.

General Heuristics The discovery of systematic biases that lead to suboptimal choices was championed by, among others, Daniel Kahneman, a social psychologist who was awarded the 2002 Nobel Prize in Economics for his work. Kahneman, Amos Tversky, and others, identified a number of heuristics—mental shortcuts that simplify decision tasks when time, complete information, or both are unavailable. This field has direct relevance to risk communication, as noted in a seminal paper on risk perception: “When laypeople are asked to evaluate risks, they seldom have statistical evidence on hand. In most cases, they must make inferences based on what they remember hearing or observing about the risk in question.” “These judgmental rules, known as heuristics, are employed to reduce difficult mental tasks to simpler ones.”14 Here are some of the heuristics and biases of greatest relevance to risk perception, and therefore to risk communication. Optimism. Many studies have found that people believe their personal risk is lower than the same risk faced by others in similar circumstances. A greater percentage of people think an adverse event might happen than think it will happen to them.15 These biases are often strongest when the risk involves personal choice, such as lifestyle risks including

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smoking, obesity, or wearing safety belts. This underestimate of personal risk poses obvious challenges to achieving effective risk communication about some of the major threats to public health. Availability. Individuals assess probability based on how readily similar instances or occurences can be brought to mind of conceptualization. The risk of terrorism in the United States is statistically quite low. But apprehension is high since September 11, 2001, in part because such an event is more “available” to our consciousness. The availability heuristic explains why, when a risk is in the news, (flu vaccine issues, West Nile virus, child abduction, etc.) it evokes more fear than when the same risk is around, at the same level, but not making headlines. Framing. The way a choice is presented can shape the judgment that results. Imagine you are the mayor of a city of one million people and a fatal disease is spreading through your community. It is occurring mostly, but not exclusively, in one neighborhood of 5000 residents. With a fixed amount of money, you can either (a) save 1000 of the 5000 residents in that neighborhood, 20%, or (b) save 2000 people out of the entire city of 1 million, 0.2%. What do you do? A sizable number of people in risk communication classes choose option A, which produces a greater percentage effectiveness, but condemns 1000 people to death. Reframed, the choice would be: You can spend a fixed amount of money and save 1000 people or 2000. Presented that way, the choice is obvious. But the framing of the question in terms of percentages skews the judgment. Anchoring and Adjustment. People estimate probabilities based on an initial value and adjust from that point. In one experiment, separate groups were asked how many nations there are in Africa. Before giving their answer, each group spun a wheel of chance. The group for which the wheel settled on the number 10 estimated 25 nations. The group whose wheel landed on 65 estimated 45 nations. In another experiment, two groups of high school students estimated the sum of two numerical expressions they were shown for just 5 seconds, not long enough for a complete computation. The median estimate for the first group, shown 9x8x7x6x5x4x3x2x1, was 2250. The median estimate for the second group, shown the same sequence but in ascending order—1x2x3x4x5x6x7x8x9—was 512.16 Representativeness. Kahneman and Tversky describe this as “the tendency to regard a sample as a representation . . .” of the whole, based on what we already know.17 They offer this illustration. Consider a person who is “very shy and withdrawn, invariably helpful, but with little interest in people, or in the world of reality. A meek and tidy soul, he has a need for order and structure, and a passion for detail.” Then consider a list of possible professions for this person; farmer, salesman, airline pilot, librarian, or physician. Without complete data by which to make a fully informed choice, the representativeness heuristic gives you a simple mental process by which to judge, and leads to the choice that the person is probably a librarian. Applied to risk communication, this suggests that if you describe “an industrial chemical used to kill pests,” people are likely to associate it with the universe of industrial chemicals and regard it as a risk, without regard to the details about that specific chemical. Kahneman and Tversy also found that people think a short sequence of events generated by a random process, like coin tossing (or, in the case of risk communication, random natural events like floods, earthquakes, etc.) will represent their understanding of the basic characteristics of the whole process, People think that when tossing a coin, H-T-H-T-T-H is more likely than H-H-H-T-T-T because the second sequence isn’t random, which they expect coin tossing to be. They disregard statistical rationality (both coin toss sequences are equally as likely) because of the heuristic of representativeness.

Risk Perception Characteristics Work in a related field, the specific study of the perception of risk, has gone further and identified a number of attributes that make certain risks seem more worrisome than others.

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These “risk perception factors” are essentially the personality traits of potential threats that help us subconsciously decide what to be afraid of and how afraid to be. They offer powerful insight into why “risk” means different things to the lay public than it does to experts. The following list has been reviewed by Paul Slovic, one of the pioneers in the field of risk perception research. It includes examples to demonstrate each factor, and in some cases, suggestions of how awareness of the factor can be used to guide more effective risk communication. Trust. The more individuals trust, the less they fear, and vice versa. When persons trust the people informing them about a risk, their fears go down. When individuals trust the process deciding whether they will be exposed to a hazard, they will be less afraid. When they trust the agency or company or institution creating the risk, they are less afraid. Most critically, when people trust the agencies that are supposed to protect them, they will be less afraid. If people don’t trust the individuals informing them, the process determining their exposure to a risk, the institution(s) creating the risk in the first place, or the people protecting them, they will be more afraid. Trust comes from openness, honesty, competence, accountability, and respecting the validity of the lay public’s intuitive reasoning about risk. Trust is the central reason why two-way risk communication, in language that validates the feelings and values and heuristic instincts of the audience, is likely to be more effective than one-way communication that only offers the facts. Risk versus Benefit. From taking prescription drugs that have side effects to picking up a cell phone to make that important call while driving, people intuitively measure hazards by comparing risks and benefits. The more they perceive a benefit from any given choice, the less fearful they are of the risk that comes with that choice. This factor explains why, of more than 400,000 “first responders” asked to take the smallpox vaccine in 2002 fewer than 50,000 did. They were being asked to take a risk of about one in a million—the known fatal risk of the vaccine—in exchange for no immediate benefit, since there did not appear to be an actual smallpox threat. Imagine if there was just one confirmed case of smallpox in a U.S hospital. The mortality risk of the vaccine would still be one in a million, but the benefit of the immunization would appear tangible. Control. If a person feels as though he or she can control the outcome of a hazard, that person is less likely to be afraid. This can be either physical control as when a person is driving and controlling the vehicle, or a sense of control of a process, as when an individual feels that he or she is able to participate in policy making about a risk through stakeholder involvement through hearings, voting, etc. This is why shared control, from the one-on-one relationship between doctor and patient, up to community empowerment in the citing of potentially hazardous facilities, is an effective form of risk communication. This is also why, whenever possible, risk communication should include information not just about the risk (“The risk of terrorism has gone from Code Yellow to Code Orange”) but also offer information about what audience members can do to reduce their risk (“Have a family emergency plan in place, just in case”). Imposed versus Voluntary. This is the choice of taking a risk, not the physical control over what happens next. People are much less afraid of a risk when it is voluntary than when it is imposed on them. Consider the driver using his cell phone who looks over at the car in the lane next to him and sees that driver on his phone, speeding up and slowing down and not staying in his lane. Driver A, voluntarily engaged in the same behavior, is angry at Driver B for imposing the risk. Natural versus Human-made. If the risk is natural, people are less afraid. If it’s human-made, such as nuclear radiation, people are more afraid. Radiation from the sun evokes less fear in some people than radiation from a nuclear power plant, or from a cell phone tower. Here is an example of how to use this principle in risk communication. Resmethrin, the chemical used to kill mosquito larvae to

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Behavioral Factors Affecting Health

reduce the risk of West Nile virus, is a pesticide, and its use often evokes community concern. When the minimal risks of resmethrin are described, community resistance is largely unchanged. But when told that resmethrin is essentially a manufactured form of chrysanthemum dust, in essence a natural pesticide, concern (among some people) about the spraying goes down.18 Dread. We are more afraid of risks that might kill us in particularly painful, gruesome ways than risks that might kill us less violently. Ask people which risk sounds worse, dying of a heart attack or dying in a shark attack, and they will say shark attack, despite the probabilities. This principle helps to explain why the United States has a “War on Cancer” but not “War on Heart Disease”, a greater killer. Cancer is perceived as a more dreadful way to die, so it evokes more fear, and therefore more pressure on government to protect us, though heart disease kills far more people each year. Catastrophic versus Chronic. People tend to be more afraid of threats that can kill many in one place at one time (e.g., a plane crash) as opposed to events such as heart disease, stroke, chronic respiratory disease, or influenza, which cause hundreds of thousands more deaths, but spread out over time and distance. This helps to explain the substantial risk communication challenge of getting people to modify behaviors that contribute to these major causes of death. It also suggests how risk communication that frames these killers as cataclysmic might have more impact. An example of such messaging would be, “On September 11, 2001, when catastrophic terror attacks killed roughly 3000 people, 2200 Americans died of heart disease. We don’t see those deaths because they are spread out over the whole country, but heart disease is causing tremendous loss of life in America every day.” Uncertainty. The less people understand a risk, the more afraid they are likely to be. Sometimes uncertainty exists because the product or technology or process is new and has not yet been thoroughly studied, such as nanotechnology. Sometimes uncertainty exists because of unpredictability, as with the sniper in Washington D.C. in 2003, or acts of terrorism. Sometimes scientific answers are available but uncertainty remains because the risk is hard for people to fully comprehend, as with nuclear power or industrial chemicals. Sometimes uncertainty exists because the risk is invisible, as with radon. This is why risk communication should reduce uncertainty by making the risk easier for people to understand. This principle makes clear why risk communication should avoid jargon, and why risk numbers should be conveyed in ways people can relate to (“A one in ten risk is like the risk to one player on a soccer team, excluding the goalie”). When uncertainty exists because all the scientific questions haven’t been answered, the fear that results must be acknowledged and respected. Personal Risk. Understandably, a risk that people think can happen to them evokes more concern than a risk that only threatens others. This is why numbers alone are ineffective as risk communications. One in a million is too high if you think you could be the one. As a demonstration of this, consider how the attacks of September 11th made clear the risk of terrorism not just to Americans anywhere but in America, and the subsequent anthrax attack put the potential threat of bioterrorism into every American mailbox. The idea of “The Homeland” took on a whole new meaning. When the first case of mad cow disease in America was found on a Washington farm in 2003, beef sales barely changed nationwide, but they fell sharply in the Northwest, where people thought the risk was more likely to happen to them. Risk communication that offers only numbers to show that a risk is low is less likely to be trusted, and therefore won’t be as effective as communication that acknowledges that the risk is not zero and accepts that some people might still be concerned. Familiar or New. When people first learn of a risk, and don’t know much about it, they are more afraid than after they have lived with

that risk for awhile and adjusted to it. For example, West Nile virus evokes more fear in communities in which it first appears than in those where its been around for awhile. Using this perception factor in their risk communication, local health officials in one section of Arizona had some success in helping local residents deal with the onset of West Nile virus in 2004 by pointing out that although the risk of West Nile virus was new to them, other communities where the same risk had existed for a few years were far less worried.19 Future Generations. Any risk to children evokes more fear than the same risk to adults. When the Washington D.C. sniper wounded a 13-year-old boy, after having murdered five adults, the local police chief said “He’s getting personal NOW!” The EPA requires all schools in the United States to be tested for asbestos, but not all offices, factories, or other adult workplace locations. This powerful fear must be appreciated in communicating about any risk that involves children. Personification. A risk made real by the identification with of a specific victim particulary when depicted with an image, such as news reports showing someone who has been attacked by a shark or a child who has been kidnapped, becomes more frightening than a risk that may be real, but is not described with an individual to personify it. So, risk communication to encourage healthier lifestyle choices that uses numbers (e.g., “60% of Americans are overweight or obese, representing an important risk factor for heart disease”) may not be as effective as communication that uses those numbers and includes names and faces of actual victims of heart disease, to personify the risk. Fairness/Equity. People are more upset by risks when those who suffer the peril get none of the benefits. Individuals are more upset by risks to the poor, the weak, the vulnerable, the handicapped, than they are about the same risk to the wealthy, or the powerful. An example might be that the developers of a potentially hazardous facility guarantee that local residents get preference in hiring for the jobs at the facility, so that those bearing its risks share in some of its benefits. Risk communication, in actions more than in words, should address this issue. There are a few important general rules about the heuristics and biases mentioned earlier, and the risk perception factors listed immediately above. Several of these factors are often relevant for any given risk. (e.g., cell phones and driving, where issues of risk-benefit, control, optimism bias, and familiarity all play a part.) And, while the research suggests that these tendencies are apparently universal and that people tend to fear similar things for similar reasons, any given individual will perceive a risk uniquely depending on his or her age, gender, health, genetics, lifestyle choices, demographics, education, etc. For example, most people fear cancer, but men fear prostate cancer, and women fear breast cancer. As with population-based risk estimates, risk perception has underlying generalities which are overlaid by individual differences. This means that while it is good risk communication practice to consider the emotional concerns of the audience, not everyone in a large audience shares the same concerns. As the National Research Council report suggests, “For issues that affect large numbers of people, it will nearly always be a mistake to assume that the people involved are homogeneous . . .” It is often useful to craft separate risk communication approaches appropriate for each segment.20 RECOMMENDATIONS

As the National Research Council report noted, “. . . there is no single overriding problem and thus no simple way of making risk communication easy.”21 Therefore, this chapter provides general guidance on the fundamentals of risk communication that need to be applied with good judgment and tailored to each particular situation. The following are widely accepted general recommendations: Include risk communication in risk management. Far more is communicated to people by what you do than what you say. “Risk

58

Risk Communication—An Overlooked Tool for Improving Public Health

communication . . . must be understood in the context of decision making involving hazards and risks, that is, risk management.” (NRC)22 Consider the example cited above of the modest response to federal first responder smallpox vaccination policy. Had the risk perception factor of “risk versus benefit” been considered when the policy was being discussed, officials might have developed a different implementation plan with stronger risk communication strategies. Information that affects how people think and feel about a given risk issue is conveyed in nearly all of the management actions an agency or a company or a health official takes on that issue. All risk management should include consideration of the risk perception and risk communication implications of any policy or action under review. Quite specifically, this means that organizations should include risk communication in the responsibilities of senior managers, not just of the public relations or communications staff. As the NRC report finds, “Risk managers cannot afford to treat risk communication as an afterthought,” that comes at the end of the process after risk assessment has been completed and policy implemented. Recognize that the gaps between public perception and the scientific facts about a risk are real, and lead to behaviors that can threaten public health. These gaps are part of the overall risk that must be managed. Whether people are more afraid of a risk than they need to be or not appropriately concerned, this perception gap is a risk, in and of itself, and must be included in dealing with any specific risk issue and in all risk management and public health efforts, generally. Accepting that these gaps are part of the overall risk is perhaps the key step in recognizing that risk communication is integral to risk management. Consider this example. When the first case of mad cow disease was found in the U.S. in December 2003, the federal government quickly moved to recall from the market all muscle meat that was processed in the region where the sick cow was found. This despite studies in the U.K. that did not find muscle meat to be a vector for spreading bovine spongiform encephalopathy (BSE), the animal version of the disease, into variant Creutzfeld Jacob Disease (vCJD), the human form. Yet even though the science suggested the physical risk from the meat might have been negligible, the government recognized that public apprehension was part of the overall risk and ordered the recall. It was an intelligent action of risk management that had powerful risk communication impact on public judgments about the threat of mad cow disease. Public reaction to that first case of mad cow disease was surprisingly mild. (Wendy’s, the number threehamburger chain in the U.S., reported January 2003 sales up 8.3%. compared to the previous year. Smith & Wollensky’s, which operates 17 steakhouses in the U.S. reported annual January sales up 7.2%.23 The principles of risk communication pertain to all public health issues, not just the environmental issues around which the discipline began. The dichotomy between risk communication, which has generally been thought of as trying to get people to calm down, and health communication, which is often thought of as trying to get people to be more concerned and take action to improve their health, is false. Any action or message that conveys information relevant to someone’s health, ergo his or her survival, triggers risk perception biology and psychology, and the principles of risk communication should be applied. Even an individual doctor describing a treatment or medication or a surgical procedure to a patient in order to get “informed consent” is a form of risk communication. The principles described in this chapter are tools that can make that consent more truly “informed”. Trust is fundamentally important for effective risk communication, and it is on the line with everything you do. “. . . messages are often judged first and foremost not by content but by the source: ‘Who is telling me this, and can I trust them?’ If the answer to the second question is ‘no’, any message from that source will often be disregarded, not matter how well-intentioned and well delivered.”(Bennett and Calman)24 Trust is determined in part by who does the communicating. When the anthrax attacks took place in the fall of 2001, the principal government spokespeople were the Attorney General, the Director of the FBI, and the Secretary of Health and Human Services, and not the director of the CDC or the U.S. Surgeon General— doctors likely to be more trusted than politicians. Indeed, a survey by

1033

Robert Blendon et al. of the Harvard School of Public Health, 10/24-28/2001, found that 48% of Americans would trust the director of the CDC as a source of reliable information in the event of a national outbreak of disease caused by bioterrorism. Only 38%, however, would trust the Secretary of Health and Human Services (HHS), and only 33% would trust the director of the FBI.25 Had risk communication been considered as the anthrax issue was beginning to develop, and incorporated into the deliberations of how to manage the overall anthrax risk, the more trusted officials would have done the majority of the public speaking. This might have helped the public keep its concern about the risk of bioterrorism in perspective. But trust is more than just who does the talking. Trust also depends on competence. If people believe that a public health or safety agency is competent, they will trust that agency to protect them and be less afraid than if they doubt the agency’s ability. When the first mad cow case was found, the U.S. Department of Agriculture and the Food and Drug Administration were able to point out the effective regulatory actions they had taken for years to keep the risk low. Thus, the actions taken by those agencies, years before that first case, established trust, thereby affecting the public’s judgment about the risk. Trust is also heavily dependent on honesty. Honesty is conveyed in many different ways. In some instances, it can even mean apologizing and taking responsibility for mistakes. When leaks developed in underground tunnels that are part of a major transportation project in Boston, press attention and public criticism focused on the contractor responsible for the tunnels until the chairman of the company said at a tense public hearing “We apologize for our mistakes”.26 (Note that the apology was made ‘sincere’ by offering to put money behind it.) Attention thereafter focused less on the company’s culpability. Another example of honesty is avoiding the desire to overreassure. Again, the way the USDA handled mad cow disease illustrates one example. In the years prior to that first sick cow being found, top officials never said there was “zero” risk of mad cow disease, either in animals or in humans, just that the risk was very low. Had they followed the initial inclination of senior USDA officials and promised that the risk was zero, that single case would probably have provoked a more worried public reaction because people might rightly have feared that the government wasn’t being honest and couldn’t be trusted. Obviously, honesty includes not keping secrets, and not lying. In early 2005, Boston University received local and state approval to build a biocontainment level 4 (BL4) laboratory to study highly dangerous pathogens. But news reports surfaced that the university had hidden from local and state approval authorities the fact that workers had mistakenly been contaminated with tularemia in a BL2 lab at BU. Under public pressure, the government approval and review processes had to be reopened. Establish mechanisms to empower real community input. Give people control—a say in their fate. Such mechanisms are a concrete way to follow the widely-accepted recommendation that risk communication is more effective when it is an interaction, not a one-way process. It is even more effective to do this proactively, so shared control and real input into decision-making are well-established should a risk crisis arise. This input must be given more than perfunctory attention. Many government public hearing processes allow people to speak, but prevent officials conducting the meeting from answering the public’s questions and concerns. Such an interaction fails to give the audience a sense of control, and more importantly, can destroy trust since it seems disingenuous to claim an interest in public input but then fail to acknowledge it. Making risk communication an intrinsic component of risk management requires fundamental cultural change. Sharing control, admitting mistakes, acknowledging the validity of intuitive reasoning, accepting that a realistic goal for risk communication is to help people make better judgments for themselves, assuming a nondirective approach, even being open and honest . . . are counter-intuitive and perhaps even counter-cultural to institutions and people who are used to control. These principles may seem foolish in a litigious society. They conflict with the myth of the purely rational decisionmaker. As risk communication researcher and practitioner Peter

1034

Behavioral Factors Affecting Health

Sandman has observed “What is difficult in risk communication isn’t figuring out what to do; it’s overcoming the organizational and psychological barriers to doing it.”27 Nonetheless, countless examples demonstrate how adoption of the principles of risk communication are in the best interests of most organizations, as well as the interest of public health.28 These institutional benefits include: reduced controversy and legal costs, increased support for an agency’s agenda or a company’s brand and products, political support for a candidate or legislation, and more effective governmental risk management that can maximize public health protection by focusing resources on the greatest threats. While these benefits may not be readily quantifiable, and only realized over the long-term, they are supported by numerous case studies, and justify the cultural change necessary for the adoption of risk communication principles. Finally, within constraints of time and budget, any specific risk communication should be systematically designed and executed, and should include iterative evaluation and refinement. “We wouldn’t release a new drug without adequate testing. Considering the potential health (and economic) consequences of misunderstanding risks, we should be equally loath to release a new risk communication without knowing its impact.”29 An empirical process by which to do this has been labeled the “Mental Models” approach. As its developers say “. . . in the absence of evidence, no one can predict confidently how to communicate about a risk. Effective and reliable risk communication requires empirical study. Risk messages must be understood by recipients, and their effectiveness must be understood by communicators.”30 The basic components of the Mental Models approach are: 1. Create an expert model, based on review of the scientific literature and in consultation with experts in the field, that describes in detail the nature of the risk; its hazards, where exposures occur, the range of consequences, and the probabilities. 2. Conduct open-ended interviews to find out what your target audience already knows or doesn’t know about the risk. 3. Based on this smaller interview sample, create a questionnaire to administer to a larger sample to see how well the mental model of the smaller group corresponds to what the larger sample knows and doesn’t know about the risk. 4. Draft risk communication messages that address incorrect beliefs and fill in knowledge gaps between what people don’t know and what the expert model indicates they need to know. Pay attention to the tone and affective qualities of the messages. 5. Evaluate and refine the communication using one-on-one interviews, focus groups, closed-form questionnaires, or problem-solving tasks, trying to develop messages that have the most impact on the greatest number of recipients. Repeat the test-and-refine process until evaluation shows the messages are understood as intended.31 CONCLUSION

Whether terrorism or avian influenza nanotechnology or mad cow disease, risks continually arise. Old ones may fade and our attention to them may wane, but new ones will certainly develop, and our awareness of these new threats will be magnified in an age of unprecedented information immediacy and availability. The human imperative of survival will compel people to use their “adaptive toolbox” to make the best judgments they can about how to stay safe from this evolving world of threat, even though those judgments might sometimes create greater peril. Populations need to understand the risks around them as thoroughly as possible to be able to make sound decisions. It is critical that effective risk communication become an intrinsic part of how government, business, the public health sector, and the medical care system design and execute risk management policy, so that, armed with accurate information, we can make wiser and safer choices for ourselves and for our fellow citizens.

REFERENCES

1. Sivak M, Flanagan M. Consequences for road traffic fatalities of the reduction in flying following September 11, 2001. Transportation Research Part F. July–Sept., 2004; vol. 7, 4–5;301–5. 2. http://cis.nci.nih.gov/fact/1_1.htm 3. http://www.cdc.gov/nchs/fastats/deaths.htm 4. Personal communication, Diane Striar, senior press liaison, NHLBI. 5. Sapolsky R. Why Zebras Don’t Get Ulcers. Owl Books, 2004. 6. Jasanoff S. Differences in national approaches to risk assessment and management. Presented at the Symposium on Managing the Problem of Industrial Hazards. The International Policy Issues, National Academy of Sciences, Feb. 27, 1989. 7. Improving Risk Communication. National Research Council, National Academy Press, 1989;21. 8. Slovic P. Perceptions of Risk. Science. 1987;236,280–5. 9. Bennett P, Calman K. Risk Communication and Public Health, Oxford U. Press, 1999;3. 10. Simon HA. Rational choice and the structure of environments. Psychology Review. 1957;63:129–38. 11. Gigerenzer G, Selten R, eds. Bounded Rationality, the Adaptive Toolbox. MIT Press, 1999;14. 12. ibid, 9. 13. This very simplified synthesis of LeDoux’s work comes from Ledoux J, The Emotional Brain: the Mysterious Underpinnings of Emotional Life. New York: Simon and Schuster, 1998. 14. Slovic P, Fischhoff B, Lichtenstein S. A revised version of their original article appears. In: Kahneman D, Slovic P, Tversky A, eds. Judgment Under Uncertainty: Heuristics and Biases. Cambridge U. Press, 2001;463–89. 15. Weinstein ND. Optimistic biases about personal risks. Science. 1987;246:1232–3. 16. Kahneman D, Slovic P, Tversky A. Judgment and uncertainty...” 1982; 14–15. 17. ibid, 24. 18. Personal observation. Cambridge and Concord, MA, 2002. 19. McNally J. Personal Communication. Mohave Co., AZ: Health Dept., 2004. 20. Improving Risk Communication. National Research Council. Nat. Academy Press, 1989;132. 21. ibid, 3. 22. ibid, 22. 23. Notes obtained from author’s website. 24. Bennett P, Calman K. Risk Communication and Public Health. Oxford U. Press, 1991;4. 25. Blendon B, Benson, J, DesRoches C, et al. Survey Project on American’s Response to Biological Terrorism. http://www.hsph. harvard.edu/press/releases/blendon/report.pdf. 26. Big Dig Firm Apologizes, Considers Fund for Repairs. Boston Globe, Dec. 3, 2004;1. 27. Sandman P. The Nature of Outrage (Part 1). http://www.psandman. com/handouts/sand31.pdf. 28. Powell D, Leiss W. Mad Cows and Mother’s Milk, the Perils of Poor Risk Communication. McGill-Queen’s University Press, 2001. (see also) Bennett and Calman, Part 2, Lessons from Prominent Cases, 81–130. 29. Morgan Granger M, Fischhoff B, Bostrom A, et al. Risk Communication: A Mental Models Approach. Cambridge U. Press, 2002;180. 30. ibid, 182. 31. Morgan, Granger M, Fischhoff B, et al. Risk Communication: A Mental Models Approach. Cambridge U. Press, 2002; Summary of pp 20–1.

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Health Literacy Rima E. Rudd • Jennie E. Anderson • Sarah C. Oppenheimer • Lindsay E. Rosenfeld • Carmen Gomez Mandic

INTRODUCTION AND OVERVIEW

Health literacy has been used as a metaphor as is science literacy or computer literacy, referring to knowledge about and facility with a particular area or process. However, most references to health literacy in scholarly articles move beyond the metaphor and highlight the importance of literacy skills applied in health contexts. Literacy skills encompass a set of related activities that include reading, writing, engaging in oral exchange, and using basic math. Adults apply these skills to numerous health-related activities at home, at work, in the community, and in social service and health care settings. The Institute of Medicine (IOM) report, Health Literacy: A Prescription to End Confusion, proposed that an individual’s health literacy capacity is mediated by education, and its adequacy is affected by culture, language, and the characteristics of health-related settings.1 Health literacy is firmly established as a field of inquiry in medicine and public health. Improved health literacy was included as a communication objective in Healthy People 2010 and the US Department of Health and Human Services (DHHS) articulated an action plan for reaching this objective in its report Communicating Health: Priorities and Strategies for Progress.2 Studies linking health literacy to health outcomes were examined by the Agency for Healthcare Research and Quality (AHRQ) and its report, Literacy and Health Outcomes,3 concluded that the weight of evidence supported a link between literacy and health outcomes. The IOM was asked to examine the scope and rigor of health literacy research. The IOM issued a report offering recommendations for policy makers, researchers, government agencies, and the private sector for needed action and further research.1 Evidence for increased interest in health and literacy links may be found in the published literature. The approximately one dozen published journal articles of the 1970s grew to three dozen in number in the 1980s and burgeoned in the 1990s after the publication of findings from the first National Adult Literacy Survey (NALS). By the end of the century, the published literature addressing health literacy consisted of approximately 300 studies.4 An additional 300 articles have been published between 2000 and 2004.5 Most of the published studies are focused on the reading level of health materials such as patient package inserts, informed consent materials, and patient education pamphlets and booklets. Over time, assessments of materials have included examinations of the match between the reading level of printed health materials and the reading skills of the intended audiences. More recent studies have expanded beyond print materials and are examining health information delivered through various channels of communication including television, websites, and other computer-based technologies. Overall, findings continue to indicate that the demands of health materials and messages exceed the average skills of the public and of the average high school graduate.4,1

A smaller section of the literature has focused on health outcomes. Supported by the development of rapid assessment tools, researchers in the 1990s and beyond were able to explore links between approximations of reading skills and a variety of health outcomes. Most of these outcome studies differentiate between those with high and low scores on rapid assessment tools such as the Rapid Estimate of Adult Literacy in Medicine (REALM)6 and the short form of the Test of Functional Health Literacy in Adults (TOFHLA),7 both of which correlate well with short tests of reading skills. Researchers, in approximately 50 studies, report differences in a wide range of health-related outcomes based on readings skills. Outcome measures included awareness and knowledge of disease and/or medicines, participation in healthful activities (such as screening or breastfeeding), ability to follow a regimen (for a variety of chronic diseases), hospitalization, and indicators of successful disease management (such as glucose measures for diabetes control).

HEALTH LITERACY AS AN INTERACTION

Various definitions of health literacy were put forth in the 1990s when the term health literacy started being used in abstracts, key word listings, and conference titles rather than health and literacy. The following definition used in Healthy People 2010 was most frequently cited: “the degree to which individuals have the capacity to obtain, process, and understand basic health information and services needed to make appropriate health decisions.”8

HHS and the IOM adopted this definition. At the same time, reports issued from both noted that the focus on the “capacity of individuals” needed to be balanced by a concurrent understanding of the communication delivery side as well. Consequently, the IOM committee report states that health literacy is an interaction between social demands and individuals’ skills.1 The IOM report notes that culture, language, and processes used in health care settings were unfamiliar to and often erected barriers for adults seeking advice and care.1 The report also cites findings that the demands of public health and medicine are burdensome and may erect unnecessary barriers to access and care.

Health Demands People engage in a wide range of activities when they take healthrelated action at home, at work, and in the community. In all of these health contexts, adults are provided with materials and tools they are expected to use as they access information and resources and as they 1035

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Behavioral Factors Affecting Health

participate in decisions and actions that influence their health and that of their families.9,10,1 Health information is communicated in a variety of ways. Sometimes it is conveyed via continuous text (prose) such as in the explanatory paragraphs on an informed consent sheet, a discussion of air quality in a newspaper editorial, or a description of the etiology of a particular disease in a patient education brochure or pamphlet. Documents, which include graphic displays, tables, and lists, comprise another type of material used to convey health information. These include weather charts, graphs of health-related trends over time, nutrition labels, as well as tables provided on packages of over-the-counter medicines for determining dose. In addition, documents, such as the open-ended forms ubiquitous in health and social service institutions, serve as the vehicle for information gathering for a wide range of activities including those related to health history, insurance, or research. Critical public and personal health information is also communicated in speech, whether over the airways or in conversation between a care provider and a patient. Social demands in health contexts include the following: • Assumptions made about the public’s background knowledge, culture, and skills; • Reading level of health-related materials designed to provide both background information and tools for action; • Specialized processes used in detection and treatment protocols; • Time limitations on interactions between patients and providers; • Expectations related to priorities and behavior; • A pervasive use of professional jargon and scientific terms in print and oral communication. Researchers have developed and applied several tools for assessing the readability of written materials such as the simplified measure of Gobbledygook (SMOG)11 and other readability formulas, the suitability assessment of materials (SAM)12 and other text assessment approaches, and the PMOSE/IKIRSCH tool which assesses lists and tables.13 However, as of 2005, no studies of health literacy have reported on the development and use of tools to assess and quantify the ease or difficulty of open entry forms, visuals, or oral discourse.

Skills Accessing, comprehending, and acting on health information and services requires individuals to have and use a full range of literacy skills. Individuals’ skills include, but go beyond, word recognition and reading comprehension to encompass a broader range of linked literacy skills such as writing, speaking, listening, and basic math. The 1992 national adult literacy survey (NALS) focused attention on adults’ ability to use print materials for everyday tasks.14 Materials used on the NALS were drawn from six contexts of everyday life including home and family, health and safety, community and citizenship, consumer economics, work, and leisure and recreation. Questions were based on the use of these materials and approximated the tasks adults would undertake in everyday life. Tasks included, for example, determining the price of a food item on sale for a 10 % discount, figuring out the correct dose of medicine to give a child, and filling out a bank deposit slip. Materials included a variety of prose materials (such as narratives, expositions, description, argumentation, and instructions) and documents found in everyday life (such as records, charts, tables, graphs, entry forms, and lists). Both the materials and the tasks associated with the materials were calibrated for level of difficulty. NALS scores were based on adults’ ability to accomplish tasks using printed texts and ranged from 0 to 500. The average NALS score for U.S. adults was 273. Analysts examining both national and international assessments of adult literacy

skills in industrialized nations indicated that scores above 275 reflect an ability to meet the demands within industrialized nations.15 The U.S. findings indicate that about half of U.S. adults have difficulty with complex materials and are limited in their ability to integrate information from complex text.14 A 2004 follow-up analysis of adult literacy skills as applied specifically to health materials and tasks indicates that a majority of adults encounter difficulties with materials such as labels on medicines, health benefit packages, product advertisements, and discussions of health policy issues in newspapers.9 The health activities literacy scale (HALS) yielded scores that are essentially the same as those for NALS, after all, the HALS was based on a sub-set of materials and tasks drawn from the NALS and the international assessments known as the international adult literacy survey (IALS). However, the focus on health materials and tasks grounds the discussion in a health context. New analyses yielded insight into the importance of a number of variables including the importance of access to wealth and its influence on literacy. Scores for the HALS varied by critical factors such as educational attainment, age, wealth, race/ethnicity, and nativity. Educational attainment is the strongest predictor of literacy skills. Overall, those with less than a high school degree or general educational development (GED) certificate have more limited literacy skills than do those with a diploma or education beyond high school. Both the NALS and HALS analyses found that persons over the age of 60 were significantly more likely to have limited functional and health literacy skills than were younger working adults. Older adults’ literacy limitations may be attributed to a number of factors including less schooling than younger adults, visual and cognitive impairments, and lost literacy skills due to diminished use.16,17 Those who are without resources (defined as interest from savings accounts or income from dividends) are also more likely to have limited literacy skills. Table 59-1, drawn from the Education Testing Service (ETS) policy report, Literacy and Health in America, illustrates the interplay among population groups by educational attainment, age, and wealth variables. Overall, the average score for those without a high school diploma or a GED is lower than the scores for others. However, the additional impact of resources may be seen in the difference between the average score of elders who have access to resources and those who do not. Underserved populations such as minorities and immigrants are more likely to have limited literacy skills than are native-born whites.14,9 In addition, one analysis of the NALS offered a portrait of inmates and concluded that prisoners have literacy skills well below those of nonincarcerated persons. However, these skill levels match those of the communities from which they came.18,19 Unfortunately, population groups with limited literacy skills may also have more frequent interactions with social service agencies, legal services, and health care institutions. These environments are saturated with print. Thus the mismatch between the demands of the systems and peoples’ general skills becomes all the more troublesome.

Health Activities and Literacy Challenges A broad notion of health literacy serves to move attention from the clinical encounter to the health-related tasks adults grapple with in the multiple contexts of everyday life. Literacy and Health in America offers a schema for examining health materials, tasks, and skills within five commonly used groupings: health promotion, health protection, disease prevention, health care and maintenance, and navigation. Table 59-2, offers a brief description of each of these groups of activities with examples of a range of materials that adults use and the associated tasks they undertake. While the materials and tasks needed within health care settings and for navigating health and social service systems are arduous, so too are many of the materials and tasks needed for mundane health-related activities at home, at work, and in the community.

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Health Literacy

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TABLE 59-1. AVERAGE HALS PROFICIENCY BY WEALTH STATUS AND LEVEL OF EDUCATION

Wealth Status

Less than High School

High School or GED

Beyond High School

1. Working adults with high likelihood of having savings or dividends, low likelihood of poverty

273

291

321

2. Young adults with low likelihood of both poverty and additional assets

218

267

293

3. Retired adults with high likelihood of additional assets

216

257

285

4. Adults with high likelihood of poverty and receiving food stamps, low likelihood of additional assets

217

264

281

5. Retired adults on social security with high likelihood of poverty, low likelihood of additional assets

188

240

261

Proficiency refers to the average score based on the NALS range of a low of 0 to a high of 500. The mean score for U.S. adults is 273. Education and economic scholars note that literacy scores in the range of 275 and above are needed for participation in the economy of the 21st century. Source: This table is adapted from: Rudd RE, Kirsch I, Yamamoto K. Literacy and Health in America. ETS Policy Report #19. Princeton NJ: Educational Testing Services. 2004.

TABLE 59-2. HEALTH ACTIVITIES, MATERIALS, AND TASKS

Health Activities

Focus

Health Promotion

Enhance and maintain health

Health Protection

Safeguard health of individuals and communities

Disease Prevention

Take preventive measures and engage in screening and early detection

Health Care & Maintenance

Seek care and form a partnership with a health professional such as a doctor or dentist or nurse

Navigation

Access needed services, and get coverage and benefits

Materials Adults are Expected to Use

Tasks Adults are Expected to Accomplish

Label on a can of food or recipes Articles in newspapers and magazines Charts and graphs such as the Body Mass Index Health education materials [such as a well baby booklet] A newspaper chart about air quality A water report in the mail A health and safety posting at work A label on a cleaning product Postings for inoculations & screening Letters re: test results Articles in newspapers and magazines Graphs, charts Health education Health history forms Labels on medicine Develop plan for taking medicine as described Health education booklets Directions for using a tool such as a peak flow meter Schedule and keep appointment Application forms Statements of rights and responsibilities Informed consent forms Benefit packages

Purchase food Prepare a dish from a recipe Plan exercise Maintain healthy habits [re: nutrition, sleep, exercise] Take care of one’s health and that of family members Decide among product options Use products safely Vote on community issues Avoid harmful exposures Take preventive action Determine risk Engage in screening or diagnostic tests Follow up Seek professional care when needed Describe symptoms Follow directions Measure symptoms Maintain health with chronic disease [follow regimen, monitor symptoms, adjust regimen as needed, seek care as appropriate] Locate facilities Apply for benefits Fill out forms Offer informed consent

Source: Rudd RE, Kirsch I, Yamamoto K. Literacy and Health in America. ETS Policy Report #19. Princeton, NJ: Educational Testing Services. 2004.

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Behavioral Factors Affecting Health

IMPLICATIONS

The AHRQ report, Literacy and Health Outcomes, indicates that the new field of health literacy has established links between literacy and health outcomes.3 Approximately 50 such studies are focused on medical settings but have not yet included other health areas such as dentistry, mental health, social work, or pharmacy, for example. Nor have any studies examined outcomes related to activities undertaken at home, at work, or in the community.9 The field of inquiry is broad with a good deal of work yet to be done. Some of this work will contribute to an understanding of health disparities.

Opportunities for Research Health literacy research findings offer important implications for investigators. The very process of research, and the accepted language in and format of documents and questionnaires used for research must be examined through a literacy lens. More rigor must be applied to the development of questionnaires and interview protocols which form the foundation for research. Health researchers have long collected information on income and health as indicators of social status, and the links between income and/or education and health are wellestablished.20 A new focus on education and its component parts will shed light on pathways between education and health outcomes and more clearly establish the role of literacy. Inquiries into socioeconomic and racial/ethnic disparities in health outcomes must include attention to the added barrier of poorly designed materials. For example, parents must grapple with small font and jargon as they attempt to enroll in health insurance programs or to make sense of the handouts and materials they are given for chronic disease management. Furthermore, studies of literacy demands in various contexts such as health care, housing, or employment settings may shed light on how the impact of limited health literacy on health can be modified by access to resources and supports within social environments.21 The differences in health literacy skills by age, race/ethnicity, poverty status, and immigrant status9 may well reflect long-standing discrimination with respect to access to education and other resources for human development especially among older cohorts, racial/ethnic minorities, impoverished communities, and immigrants from underdeveloped countries. Health disparities are also seen between these populations groups and majority population groups in the U.S. The extent to which these differences in health literacy skills are causally related to observed disparities in health outcomes—and thus, the extent to which attention to health literacy in medical and public health interventions can ameliorate such disparities—is a critical area of current and forthcoming health literacy research.

Implications for Practitioners Health literacy is intimately tied to client and practitioner interactions. Studies indicate that many long standing practice recommendations serve to lower literacy demands.22–24 Health educators, for example, have long emphasized the importance of pilot testing materials and programs with members of the intended audiences.24 Public health program developers often engage members of the community as participants in the design and evaluation of programs.25,26 The activated patient model is supported as an important approach for the management of chronic diseases.22 Several approaches hold promise but have not yet been fully evaluated. For example, the American Medical Association suggests that health providers speak with their patients using plain, everyday language.27 Health practitioners are urged to use teach-back approaches, for example, asking patients to describe how they will tell others what they just learned. Effective innovation and progress in this field cannot be made without the ongoing participation and leadership of practitioners and policy makers. The development of all health communications must be appropriately designed with the audience in mind, based on accurate assessments of the public’s knowledge and skills, and be

designed for use. Rigorous formative process and outcome evaluations most be undertaken for health communication efforts whether the focus is on print materials or oral delivery, or interpersonal or mass media channels. Plain language, well designed materials and documents, and educational approaches that go beyond a reliance on the written word will improve health literacy. While the education sector maintains responsibility for building literacy skills, health policy makers and practitioners maintain responsibility for health materials, messages, and procedures. The recommendations for action outlined in the HHS and IOM reports call for the development and testing of programs and materials, and evaluations of new approaches and technologies. This work can be supported through partnerships among and between health professionals, K-12 teachers, adult educators, librarians, and social service agency staff. REFERENCES

1. Institute of Medicine. Health Literacy: A Prescription to End Confusion. Washington, DC: The National Academies Press. 2004. Available at: http://www.nap.edu/books/0309091179/html/. Chapters, 1, 2, & 4. 2. Rudd R. Objective 11-2. Improvement of health literacy. Communicating Health: Priorities and Strategies for Progress. Washington, DC: U.S. Department of Health and Human Services. 2003:35–60. 3. Berkman ND, DeWalt DA, Pignone MP, et al. Literacy and Health Outcomes. Summary, Evidence Report/Technology Assessment: Number 87. AHRQ Publication Number 04-E007-1, January, 2004. Agency for Healthcare Research and Quality, Rockville, MD. http://www.ahrq.gov/clinic/epcsums/litsum.htm 4. Rudd RE, Moeykens BA, Colton TC. Health and literacy: A review of medical and public health literature. In: Comings JP, Garner B, Smith C, eds. The Annual Review of Adult Learning and Literacy. San Francisco: Jossey-Bass Publishers. 2000;158–99. 5. The Harvard School of Public Health: Health Literacy Studies Web Site. Available at: http:www.hsph.harvard.edu/healthliteracy. Accessed February, 2005. 6. Davis TC, Long SW, Jackson RH, et al. Rapid estimate of adult literacy in medicine: A shorthand screening instrument. Family Medicine. 1993;25(6):391–5. 7. Parker RM, Baker DW, Williams MV, et al. The test of functional health literacy in adults: A new instrument for measuring patients’ literacy skills. Journal of General Internal Medicine. 1995;10(10): 537–41. 8. U.S. Department of Health and Human Services. Healthy People 2010: Understanding and Improving Health. 2nd ed. Washington, DC: U.S. Government Printing Office, November, 2000. 9. Rudd RE, Kirsch I, Yamamoto K. Literacy and Health in America. Princeton, NJ: Educational Testing Services. 2004. 10. Rudd RE, Renzulli D, Pereira A, et al. Literacy demands in health care settings: the patient perspective. In: Schwartzberg JG, Van Geest JB, Wang CC, eds. Understanding Health Literacy; Implications for Medicine and Public Health. 2005:69–84. 11. McLaughlin GH. SMOG grading: A new readability formula. Journal of Reading. 1969;12:639–46. 12. Doak L, Doak C, Root J. Teaching Patients with Low Literacy Skills. 2nd ed. Philadelphia, PA: J.B. Lippincott Company. 1996. 13. Mosenthal PB, Kirsch I. A new measure for assessing document complexity: The PMOSE/IKIRSCH Document Readability Formula. Journal of Adolescent and Adult Literacy. 1998;41(8):638–57. 14. Kirsch I, Jungeblut A, Jenkins L, et al. Adult literacy in America: The first look at the results of the National Adult Literacy Survey (NALS). Washington, DC: U.S. Department of Education. 1993. 15. Comings J, Reder S, Sum A. Building a Level Playing Field: The Need to Expand and Improve the National and State Adult Education

59

16.

17.

18.

19.

20.

21. 22. 23.

and Literacy Systems. Cambridge, MA: National Center for the Study of Adult Learning and Literacy (NCSALL); December, 2001. Brown H, Prisuta R, Jacobs B, Campbell A.. Literacy of Older Adults in America: Results from the National Adult Literacy Survey. Washington, DC: National Center for Education Statistics; 1996. Roberts P, Fawcett G. At Risk: A Socio-economic Analysis of Health and Literacy Among Seniors. Ottawa, Ontario: Statistics Canada; 1998. Haigler KO, Harlow C, O’Connor P, et al. Literacy behind Prison Walls: Profiles of the Prison Population from the National Adult Literacy Survey. Washington, DC: National Center for Education Statistics; 1994. Reder S. The State of Illiteracy in America: Estimates at the Local, State, and National Levels. Washington, DC: National Institute for Literacy; 1998. Pamuk E, Makuc D, Heck K., et al. Socioeconomic Status and Health Chartbook. Health, United States. Hyattsville, MD: National Center for Health Statistics; 1998. Lee S, Arozullah A, Cho Y. Health literacy, social support, and health: a research agenda. Social Science and Medicine. 2004;58(7):1309–21. Roter R, Margalit R, Rudd RE. Current perspectives on patient education in the U.S. Patient Education and Counseling. 2001;1472:1–8. Rudd RE, Comings JP. Learner developed materials: an empowering product, Health Education Quarterly. 1994;21(3): 33–44.

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24. National Institutes of Health. Making Health Communication Programs Work. Office of Cancer Communications, National Cancer Institute; 1989. 25. Minkler M, Wallerstein N. Improving health through community organization and community building: a health education perspective. In: Minkler M, ed. Community Organizing and Community Building for Health. 2005;26–50. 26. Centers for Disease Control and Prevention. Principles of Community Engagement. Atlanta, GA: CDC Public Health Practice Program Office; 1997. 27. Weiss B. Health Literacy: A Manual for Clinicians. American Medical Association Foundation and American Medical Association; 2003.

SUGGESTED READINGS

Kirsch I. The International Adult Literacy Survey (IALS): Understanding What Was Measured. Princeton, NJ: Educational Testing Services; 2001. Shire N. Effects of race, ethnicity, gender, culture, literacy, and social marketing on public health. Journal of Gender Specific Medicine. 2002;5(2):48–54.

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V Noncommunicable and Chronic Disabling Conditions

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Screening for Early and Asymptomatic Conditions

60

Robert B. Wallace

DEFINITION OF SCREENING

The typical natural history of diseases and conditions dictates that at some point the biological onset of the disease occurs and progresses at varying rates until they become clinically evident. These rates may be as short as instantaneous, as in acute trauma, or could be life-long, as in a genetic risk factor for Alzheimer’s disease. Primary prevention attempts to intercept the conditions that lead to disease onset, while secondary prevention generally relates to the early and asymptomatic detection of disease; that is, disease screening, in the hope that the trajectory toward clinical illness can be stopped or mitigated in a helpful way. When overt clinical illness is present, tertiary prevention refers to rehabilitative and other factors that deter disease progression and help return the patient to a healthier state. Disease screening usually takes two general forms: (a) screening for proven, biological, or behavioral risk factors for diseases that lead to interventions or treatments in themselves, such as abnormal blood cholesterol or blood pressure levels; or (b) screening directly for evidence of the disease itself, followed by provision of effective treatment to cure or to prevent the progression of pathophysiological processes that will cause overt clinical manifestations. This implies that screening may be done in stages, for instance by screening for general disease susceptibility first, such as for certain demographic or anatomic characteristics, or only if informed consent for the screening procedure is obtained. Disease screening may be applied to general populations irrespective of receipt of medical care (i.e., mass screening), or to clinical populations with various characteristics. In general, disease screening is applied to populations with a relatively low risk of the condition of interest. Because of the great increase in types of screening that have been developed, the general definition of disease screening does not fit all situations. For example, the disease may be overt and the screening is to determine the cause, as in the detection of family violence, or the condition may be overt, but not clinically explored at a primary care visit, as in the case of cognitive impairment or depression.

preventive intervention or therapy must exist and should not encumber a more beneficial outcome when applied to the presymptomatic rather than to the symptomatic stage; (d) The screening test should be acceptable to the population and suitable for general, routine application. Many other criteria for an effective screening test could be added, such as maintenance of test accuracy over time and freedom from screening-related adverse effects. Even with concerted application of these screening criteria, major pitfalls may cause an erroneous assessment of a screening program’s value. An example is lead time bias, the interval between presymptomatic disease detection by a screening test and symptom onset.2 If the natural history of a disease is variable or not thoroughly understood during the presymptomatic and symptomatic stages, a screening test may identify a presymptomatic condition earlier and increase the interval to overt morbidity but not change the ultimate outcome. Length bias occurs when there is a correlation between the duration of disease latency and the natural history of the symptomatic phase.2 If the mild form of a disease has a longer latency and is hence more easily found on screening than are more severe forms of disease, the screening test may appear falsely beneficial. In general, the validity of a screening test depends on the evidence base to justify the screening intervention. Many screening tests may be proven only through one or more randomized clinical trials. Excellent examples of creating the evidence base for screening tests can be found in the work of the U.S. Preventive Services Task Force, part of the Agency for Healthcare Research and Quality.3 Selection and interpretation of screening tests require a combination of subjective and objective criteria. Objective criteria include operating characteristics, predictive value, and cost-effectiveness of the tests, which are tempered by subjective evaluations of individual and public acceptability and financing. The operating characteristics of a screening test are its sensitivity and specificity. These are general test characteristics that can apply to any laboratory or diagnostic test data as well as other information collected from the medical history and physical examination. Sensitivity is the proportional detection of individuals with the disease of interest in the tested population, expressed as follows:

THE ASSESSMENT OF SCREENING TESTS

There are several criteria that aid in selecting and applying an appropriate screening test.1 (a) The disease should be common enough to warrant a search for its risk factors or latent stages because screening for excessively rare diseases may result in unacceptable cost-benefit ratios; (b) The morbidity or mortality (i.e., burden of suffering) of the untreated target condition must be substantial; (c) An effective

Sensitivity (%) =

True positives × 100 True positives + False negatives

True positives are individuals with the disease and whose test result is positive. False negatives are individuals whose test result is negative despite having the disease. Specificity is the proportional detection of individuals without the disease of interest, expressed as follows: 1043

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Noncommunicable and Chronic Disabling Conditions

Specificity (%) =

True negatives × 100 True negatives + False negatives

True negatives are individuals without the disease and whose test result is negative. False positives are those who have a positive test result but do not have the disease. Sensitivity is limited by the proportion of cases missed by the test (false negatives) and specificity is limited by the proportion of noncases found to be positive (false positives). Ideally, a test would have a 100% sensitivity and specificity, but few if any tests have achieved this. Unfortunately, sensitivity and specificity are often inversely related. This relationship has been expressed as the receiver operating characteristic (ROC)4 of a numerically continuous test result. The ROC allows optimal specification of test sensitivity and specificity. The sensitivity, or true-positive ratio, is displayed along the ordinate, and the specificity, or false-positive ratio, is exhibited on the abscissa. As the sensitivity increases, so does the false-positive ratio in most instances. When a ROC has been established for a test, any one of several sensitivity and specificity combinations may be evaluated for suitability in test application and contrasted with potential alternate tests. Further information on the application of ROC curves is available.5 Sensitivity and specificity values from the literature are most applicable to populations and test conditions similar to those under which the values were established. However, it is possible that test properties may differ according to mode of administration (e.g., telephone vs. mail questionnaire) or by any demographic feature of the target population, and thus, further generalization or extrapolation of these values can be misleading. For example, it has been suggested that the increasingly common use of hormone replacement therapy among postmenopausal women may decrease the sensitivity and specificity of mammographic screening.6 Whereas the operating characteristics of a test are of major help in selecting a screening test, the predictive value of a test is a major aid in interpretation of a result. The predictive value of a positive test is the proportion of all individuals with positive tests who have the disease and is expressed as follows: Positive Predictive Value (%) =

True positives × 100 True positives + False positives

The predictive value of a negative test is the proportion of all individuals with negative tests who are nondiseased. This is expressed as follows: Negative Predictive Value (%) =

True negatives × 100 True negatives + False negatives

Predictive values are dependent on both the operating characteristics and the prevalence of the disease in the target population. For any given set of operating characteristics, the positive predictive value is directly related to prevalence, and the negative predictive value is inversely related to prevalence. Therefore, in screening situations where the prevalence is relatively low, the operating characteristics must be very high to avoid low positive predictive values. In most screening situations for serious fatal conditions, such as cancer, the test or test sequence offering the highest sensitivity ordinarily will be preferred. This has the effect of finding as many cases as possible but may correspondingly increase the number of false positives. The effect of sensitivity, specificity, and prevalence on predictive values has been clearly demonstrated.7 Cost-effectiveness is especially important in screening programs because of the number of asymptomatic individuals who must be evaluated for the relatively small number of diseased cases. Formal cost-effectiveness analysis8–10 should be undertaken before program initiation. The program’s value must include an assessment of all costs and a realistic appraisal of effectiveness. Positive predictive values are usually well below 50% for most initial screening situations, so that secondary diagnostic evaluation is nearly always required to eliminate false positives, adding substantially to program cost.

Exhaustive reviews of the efficacy of clinically applicable screening programs have been undertaken by the U.S. Preventive Services Task Force3 and several other disciplinary, specialty and international groups, with recommendations offered in part with consideration of cost-effectiveness. On the other hand, public screening, or mass screening, may have inherent advantages from the standpoint of efficiency. The tests and procedures selected for use are often highly standardized and can be administered more inexpensively than they can in clinical or more specialized settings, and generally they can be applied without the need for direct physician supervision. To enjoy the efficiency of mass screening, such programs must be carefully organized and managed. Recipients of both normal and abnormal test results must be considered. Those with abnormal test results must have a properly organized follow-up evaluation protocol, and those with normal results should be informed of the predictive value of a normal test to avoid false reassurance. Even with the inherent efficiency of mass screening, most such programs must still be focused on populations with sufficient disease or risk factor prevalence to maximize program efficiency. Another application of screening programs is in the clinical context where patients have active clinical problems. Examples include screening on the first evaluative ambulatory clinic visit or at hospital admission. Comprehensive clinical screening with routine physical examinations or laboratory tests, or both, remains controversial, largely because there is very little if any evidence in the scientific literature concerning the efficacy or effectiveness of standard screening tests in the face of existing comorbid illness. For example, is mammography effective in persons with active insulin-dependent diabetes, or cholesterol screening in the face of an active carcinoma? These are questions yet to be adequately addressed in research. In the past, so-called “multiphasic” screening programs had been proposed for persons being admitted to the hospital. It now appears that these procedures have limited utility and high cost primarily because of numerous false-positive tests and irrelevant findings and should be discarded in favor of diagnostic and therapeutic activities directed at the immediate clinical problems.11–13 However, inpatient hospital services have been used as opportunities for categorical screening programs such as undiagnosed human immunodeficiency virus infection,14 alcoholism,15 or nutritional problems among the elderly.16 Multiphasic biochemical screening is still being proposed as a useful inpatient tool.17 Another important issue that has arisen is screening for genetic conditions. This is covered elsewhere in this text.

REFERENCES

1. Wilson JMG, Jungner G. Principles and practice of screening for disease. Public Health Rep. 34, 1968. 2. Pelikan S, Moskowitz M. Effects of lead time, length bias, and false negative assurance on screening for breast cancer. Cancer. 1993;71: 1998–2005. 3. U.S. Preventive Services Task Force. Proceedings available at: http://www.ahrq.gov/clinic/uspstfix.htm. Downloaded Sept. 1, 2006. 4. Swets JA. Measuring the accuracy of diagnostic systems. Science. 1988;240:1285–93. 5. Linden A. Measuring diagnostic and predictive accuracy in disease management: an introduction to receiver operating characteristic (ROC) analysis. J Eval Clin Pract. 2006;12(2):132–9. 6. Laya MB, Larson EB, Taplin SH, et al. Effect of estrogen replacement therapy on the sensitivity and specificity of screening mammography. J Natl Cancer Inst. 1996;88:643–9. 7. Galen RS, Gambino SR. Beyond Normality: The Predictive Value and Efficiency of Medical Diagnosis. New York: John Wiley, 1975. 8. Schneider JE, et al. Clinical practice guidelines and organizational adaptation: a framework for analyzing economic effects. Int J Technol Assess Health Care. 2006;22:58–66.

60 9. Johannesson M. The relationship between cost-effectiveness analysis and cost-benefit analysis. Soc Sci Med. 1995;41:483–9. 10. Gold MR, Siegel JE, Russell LB, Weinstein MC, eds. Cost Effectiveness in Health and Medicine. New York: Oxford University Press, 1996. 11. Whitehead TP, Wotton IDP. Biochemical profiles for hospital patients. Lancet. 1974;2:1439. 12. Korvin CC, Pearce RH, Stanley J. Admissions screening: clinical benefits. Ann Intern Med. 1975;83:197. 13. Burbridge TC, Edwards F, Edwards RG, et al. Evaluation of benefits of screening tests done immediately on admission to hospital. Clin Chem. 1976;22:968.

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14. Trepka MJ, Davidson AJ, Douglas JM, Jr. Extent of undiagnosed HIV infection in hospitalized patients: assessment by linkage of seroprevalence and surveillance methods. Am J Prev Med. 1996;12: 195–202. 15. Bothelho RJ, Richmond R. Secondary prevention of excessive alcohol use: assessing the prospects for implementation. Fam Pract. 1996;13:182–93. 16. Cotton E, Zinober B, Jessop J. A nutritional tool for older patients. Professional Nurse. 1966;11:609–12. 17. Ferguson RP, Kohler FR, Chavez J, et al. Discovering asymptomatic abnormalities on a Baltimore internal medicine service. M Med J. 1996;45:543–6.

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61

Cancer Leslie K. Dennis • Charles F. Lynch • Elaine M. Smith

Neoplasms are diseases characterized by abnormal proliferation of cells. If the proliferating cells invade surrounding tissues, the resultant tumor is malignant; if they do not, it is benign. Some benign neoplasms may be fatal, including histologically benign brain tumors that grow and displace normal brain tissue in the confined space of the skull, and hepatocellular adenomas that rupture and cause bleeding into the peritoneal cavity. Some benign tumors such as intestinal polyps are considered premalignant lesions and confer a high risk of progression to malignancy. The term cancer usually implies a malignant tumor (malignancy), but refers also to brain tumors and some other benign neoplasms. DESCRIPTIVE EPIDEMIOLOGY

Classification Cancers are classified according to their organ or tissue of origin (site or topography code) and histological features (morphology code). A number of classification schemes have been developed, the most recent and widely used of which appears in Chap. 2 of the International Classification of Diseases, 10th revision (ICD-10), which is largely a topography code,1 and the International Classification of Diseases for Oncology, 3rd edition (ICD-O), which contains an expanded version of the topography code in ICD-9 as well as a detailed morphology code.2

Sources of Incidence and Mortality Rates Mortality rates are calculated from death certificate records and population census data. Mortality rates from various countries have been compiled periodically.3 Cancer mortality rates for the United States are published by the United States’ National Cancer Institute (NCI) and Centers for Disease Control and Prevention (CDC).4–6 Population-based cancer registries, which have been established in many countries, provide information on incidence rates. These have been compiled in Cancer in Five Continents, which is jointly published periodically by the International Agency for Research on Cancer (IARC) and the International Association of Cancer Registries (IACR).7 The best source of cancer incidence rates for the United States is the Surveillance, Epidemiology, and End Results (SEER) program of the NCI, which supports a network of 18 population-based cancer registries throughout the country. Results from this program are published annually and more detailed monographs are published periodically.8,9 Both incidence and mortality statistics for the United States are summarized for the lay public and published annually by the American Cancer Society.10 A North American Association of Central Cancer Registries (NAACCR) was established in 1987, and beginning in 1991 the CDC made funds available to individual states for cancer registration. The

cost of collecting high-quality data on a sufficiently large proportion of all cases in a defined population is considerable; however, utilization of these data for research or cancer control purposes justifies cancer registration efforts.

Magnitude of the Cancer Problem In the aggregate, cancer is second only to heart disease as a cause of death in the United States and accounts for about 23% of all deaths.10 Approximately 190 deaths from cancer occur per 100,000 people per year, compared with about 232 per 100,000 from heart disease, 53 per 100,000 from cerebrovascular diseases, 43 per 100,000 for chronic lower respiratory diseases, and 37 per 100,000 from accidents.10 Based on U.S. incidence and mortality rates for 2001–2003, the lifetime probabilities of developing cancer have been estimated to be 45.3% in men and 37.9% in women; the lifetime probabilities of dying of cancer are estimated at 23.4% in men and 19.8% in women.4,10 The National Cancer Institute estimates the direct medical costs of cancer to be $72 billion annually, or about 5% of the total health-care costs in the United States.11

Relative Importance of Specific Neoplasms Age-adjusted incidence and mortality rates, as well as 5-year survival rates, in men and women in the United States are readily available, and Table 61-1 shows such rates for 1998 through 2003.4,10 The most common cancers in men are those of the prostate, lung, and colon and rectum; the cancers causing the most deaths in the United States are lung, colon and rectum, and prostate. In women, breast cancer is by far the most common neoplasm, followed by cancers of the lung, and colon and rectum.10 However, because of the more favorable survival of women with breast than lung cancer, mortality rates of female lung cancer exceed those for female breast cancer in the United States. Another way to judge the importance of a malignancy is by the number of years of life lost due to its occurrence in a population. This measure reflects the incidence of the cancer, the fatality rate in those who develop it, and the age at which the cancer tends to occur. This measure gives more weight to childhood cancers than overall mortality rates, and because of economic implications, it can be of value in setting priorities for research and prevention. In order of estimated years of life lost, the 10 most important cancers in the United States are lung, female breast, colon and rectum, pancreas, leukemia, nonHodgkin’s lymphoma, brain, prostate, ovary, and liver.4 The estimated age-standardized incidence rates of all cancers vary among the various regions of the world, and the cancers of most importance in developing countries are different from those in developed countries such as the United States. In order by numbers of cases, the 10 most common cancers across the globe are those of the 1047

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1048

Noncommunicable and Chronic Disabling Conditions

TABLE 61-1. AVERAGE ANNUAL AGE-ADJUSTED (2000 STANDARD) INCIDENCE AND MORTALITY RATES (1998–2003) AND 5-YEAR RELATIVE SURVIVAL RATES (1998–2002 CASES) BY PRIMARY SITE AND SEX, ALL RACES, SEER 13 AREAS COMBINED Rates (per 100,000) Incidence Site Oral cavity and pharynx Digestive system Colon and rectum Colon Rectum and rectosigmoid Pancreas Stomach Esophagus Respiratory system Lung and bronchus Larynx Bones and joints Soft tissues (including heart) Skin (excluding basal and Squamous cell carcinoma) Melanomas of skin Breast Female genital system Cervix uteri Corpus uteri Ovary Male genital system Prostate gland Testis Urinary system Urinary bladder Kidney and renal pelvis Eye and orbit Brain and nervous system Endocrine system Thyroid Lymphomas Non-Hodgkin’s Hodgkin’s Myeloma Leukemia All sites

5-Year Relative Survival (%)a

Mortality

Male

Female

Male

Female

Male

Female

15.5 110.9 61.4 42.9 18.5 12.6 12.2 7.6 86.6 77.5 6.3 1.0 3.6 25.8

6.3 74.9 45.5 34.2 11.3 9.9 6.1 2.0 51.4 49.1 1.3 0.7 2.4 15.6

4.2 59.9 24.5 20.6 3.9 12.2 6.2 7.7 78.6 75.6 2.5 0.5 1.5 5.3

1.6 36.8 17.1 14.8 2.3 9.2 3.2 1.8 41.7 41.0 0.5 0.3 1.2 2.2

58.1 43.8 66.0 66.0 65.9 5.0b 23.8 16.2 18.2 13.2 65.6 65.9 65.3 88.2

60.6 46.6 63.9 62.8 67.1 5.0b 25.8 17.2b 19.0 17.5 55.0 71.1b 66.0 93.5

22.0 1.2 — — — — 178.9 172.5 5.2 53.8 36.1 16.4 0.9 7.6 4.9 4.1 26.4 23.4 3.0 7.0 16.1 551.8

14.1 132.3 50.3 8.8 23.6 13.8 — — — 17.7 9.0 8.2 0.6 5.3 12.1 11.5 18.4 16.0 2.3 4.5 9.4 411.5

3.9 0.3 — — — — 30.1 29.6 0.3 14.0 7.6 6.1 0.1 5.5 0.8 0.4 10.6 10.0 0.6 4.7 10.1 245.2

1.8 26.2 16.6 2.7 2.0 8.9 — — — 5.2 2.3 2.8 0.1 3.7 0.8 0.5 6.9 6.5 0.4 3.2 5.8 164.7

91.0 88.30b — — — — 99.9c,b 99.9c,b 95.9b 76.7 83.3 65.9 83.7 32.6 90.2b 95.3b 65.2 61.9 82.5 36.6 49.7b 66.6

93.5 89.3 70.5 72.5 84.3 45.8 — — — 71.4b 77.6b 66.5b 83.0 36.2 95.8b 97.4b 69.6 66.2 87.0b 28.8 48.4 65.9

Source: Incidence data from SEER 13 areas (San Francisco, Connecticut, Detroit, Hawaii, Iowa, New Mexico, Seattle, Utah, Atlanta, San Jose-Monterey, Los Angeles, Alaska Native Registry, and Rural Georgia). Mortality data are from the NCHS public use data file for the total United States. aRates are based on follow-up of patients through 2003. bThe relative cumulative rate increased from a prior interval and has been adjusted. cThe relative cumulative rate is over 100% and has been adjusted. Citation: Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*Stat Database: Incidence—SEER 9 Regs Public-Use, Nov 2004 Sub (1973–2003), National Cancer Institute, DCCPS, Surveillance Research Program, Cancer Statistics Branch, released April 2006, based on the November 2005 submission.

lung, stomach, liver, colon and rectum, breast, esophagus, lymphomas and myeloma, mouth and pharynx, prostate, and leukemia.12

Age Cancers most probably arise from DNA-damaged cells that are capable of mitotic division and differentiation. In adults, most cancers are carcinomas that arise from basal epithelial cells of ectodermal or endodermal origin. In children, most cancers are of mesodermal origin and consist largely of leukemias and lymphomas that arise from hematopoietic and lymphoid stem cells and sarcomas that probably develop from undifferentiated cells of embryonal origin.

Incidence rates for the most common childhood cancers in the United States are shown in Table 61-2.4,10 The mortality rates for even the most frequent cancers in children are many times lower than the rates of comparable tumors for all ages (Table 61-1), which largely reflect rates in adults. Cancer is primarily a disease of older adults. With some notable exceptions (e.g., cancers of the female breast and uterine cervix), there is an exponential increase in incidence rates with age. The median age at which cancer was diagnosed from 2000 to 2003 was 68.0 for males and 67.0 for females, and most cancers develop in the sixth, seventh, and eighth decades of life.4

61 TABLE 61-2. ANNUAL INCIDENCE OF SELECTED CANCERS IN CHILDREN UNDER AGE 15, 1998–2003a Ages 0–14 Site All sites Bone and joint Brain and other nervous Hodgkin’s disease Kidney and renal pelvis Leukemia Acute lymphocytic Non-Hodgkin’s lymphomas Soft tissue

Male

Female

15.5 0.6 3.3 0.7 0.7 5.1 4.1 1.2 1.1

13.9 0.6 3.1 0.4 0.9 4.4 3.5 0.6 0.9

Source: Incidence data from SEER 13 areas (San Francisco, Connecticut, Detroit, Hawaii, Iowa, New Mexico, Seattle, Utah, Atlanta, San Jose-Monterey, Los Angeles, Alaska Native Registry, and Rural Georgia). a Rates are per 100,000 and are age-adjusted to the 2000 U.S. standard population (19 age groups—Census P25-1130). Citation: Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*Stat Database: Incidence—SEER 9 Regs Public-Use, Nov 2004 Sub (1973–2003), National Cancer Institute, DCCPS, Surveillance Research Program, Cancer Statistics Branch, released April 2006, based on the November 2005 submission.

Sex Most major cancers occur more frequently in men than in women, exceptions being carcinomas of the breast, thyroid, gallbladder, and other biliary.10 Smoking-related cancers, described in detail subsequently, occur more frequently in men, at least in part because of their earlier and greater exposure to tobacco smoke. Some other cancers, such as carcinomas of the bladder and mesotheliomas, are more frequent in men, at least in part because of their greater occupational exposure to various chemical carcinogens and asbestos, respectively. Other cancers that occur more frequently in men include the lymphomas and leukemias, malignant melanomas, sarcomas of the bone, and carcinomas of the nasopharynx, stomach, kidney, pancreas, colon, rectum, parotid gland, and liver. The reasons for the excess of these cancers in males are uncertain. Women could be either constitutionally less susceptible to these neoplasms or less exposed to whatever environmental factors contribute to their development. Recently, a higher number of new cases of colon cancer were reported among women in the United States.10 It is unclear if this is a change in risk factors, screening activity, or age differential between men and women in the United States.

Cancer

1049

migrants from these countries than in lifelong residents of such areas as North America and Western Europe include cancers of the colon and rectum, which may be related to diets rich in animal products; cancers of the prostate, ovary, corpus uteri, and breast, which have to some extent also been related to high consumption of meats and fats, as well as to endocrinological and reproductive factors; Hodgkin’s disease, which has been hypothesized to be due to a common infectious agent, probably the Epstein-Barr virus that, like polio viruses, may cause clinically overt disease with a frequency directly related to age at initial infection; and non-Hodgkin’s lymphomas and neoplasms of the brain and testis, the causes of which are largely unknown. Other cancers occur more frequently in developing countries and in migrants from these countries. For example, compared to white populations of the United States and Western Europe, migrants from Asian countries have higher rates of stomach cancer, possibly related to intake of preserved foods and infection with Helicobacter pylori; liver cancers, which may, in part, be caused by the production of aflatoxins in contaminated foods and by hepatitis B and C viruses; cancers of the nasopharynx, caused in part by the Epstein-Barr virus (EBV); and cancer of the uterine cervix, which is caused by some types of human papillomaviruses. Cancers that are strongly related to smoking occur with a frequency commensurate with the smoking habits in the population. Thus, cancers of the lung, larynx, bladder, kidney, and pancreas have tended to occur more frequently in developed than developing countries, but rates of these neoplasms are increasing in developing countries where more widespread cigarette smoking has accompanied economic changes. The overall incidence and mortality rates and the ratio of mortality to incidence in various racial and ethnic groups in the United States for 1998–2003 are shown in Table 61-3.4 Compared with data from 1988 to 1992, rates in all racial/ethnic groups have increased with the possible exception of American Indian/Alaska natives, which have the lowest cancer rates. Differences among specific Asian or Pacific Islander groups are available elsewhere for the 1988–1992 rates by racial/ethnic group.14 Similar data from the United States 2000 Census are not available yet. Variations in overall cancer incidence reflect the mix of cancers in the different groups. Variations in mortality are due to differences in both incidence and survival. The differences in the ratio of mortality to incidence rates provide a rough indicator of differences in overall survival from cancer. These are a reflection of both the types of cancer that predominate in the different groups and the level of utilization of screening and treatment services by their members. Less advantaged groups have the highest ratios of mortality to incidence, clearly indicating that improvement of services could have an impact on the cancer burden in these populations.

Time Trends Race and Geography Within individual races, incidence and mortality rates of all cancers vary considerably from one geographic region to another; migrants from one country to another, or their descendants, tend to eventually develop most cancers at rates more similar to those in their country of adoption than to those in their country of origin, suggesting an important role for environmental risk factors in most cancers.13 In the United States, the patterns of cancer occurrence in recent immigrants reflect the cancer patterns in their countries of origin and become less distinct as these groups become more acculturated with the passage of time. The frequency of occurrence of many cancers also varies among racial groups residing in the same country. This variation may be due to factors related to their distinct cultural patterns, social behavior, or economic status, but in some instances may be due to genetic differences among the races. Some cancers appear to be related to a “Western” lifestyle. Cancers that tend to occur at lower rates in developing countries and

Figure 61-1, A and B, shows trends in incidence rates for various cancers in the United States from 1975 to 2002 for men and women, respectively.10 Figure 61-2, A and B, shows trends in mortality rates for the most common cancers in the United States from 1930 to 2002, for men and women.10 The striking increase in rates of lung cancer is largely due to cigarette smoking. The reason for the marked decline in rates of stomach cancer is unknown but may be related to changes in dietary habits, with consumption of less preserved and more fresh and frozen foods. The decline in mortality from uterine cancer is probably due to the decrease in incidence resulting from screening. Breast and prostate cancer incidence increased dramatically in the 1980s and early 1990s as a result of mammography and prostate-specific antigen (PSA) screening, respectively. Recently, there have been declines in mortality rates of these two cancers. Dating back to 1990, mortality rates for all cancer sites have been declining in the United States for the first time in recorded history. Incidence rates have not shown a similar declining pattern, supporting

Noncommunicable and Chronic Disabling Conditions TABLE 61-3. AGE-ADJUSTED INCIDENCE AND MORTALITY RATES OF ALL CANCERS COMBINED IN RACIAL AND ETHNIC GROUPS IN THE UNITED STATES, 1998–2003a Men

Women

1998–2003 Race/Ethnic Group

Incidence*

Mortality*

Ratio

American Indian/Alaska Nativeb Asian or Pacific Islander Black White Hispanicc

275.6 377.9 677.5 555.2 417.4

156.4 146.3 334.5 240.5 168.4

0.57 0.39 0.49 0.43 0.40

Incidence*

Mortality*

231.4 297.4 398.5 427.2 309.0

Ratio

112.5 99.1 193.3 163.7 109.1

0.49 0.33 0.49 0.38 0.35

∗

Incidence data from SEER 13 areas (San Francisco, Connecticut, Detroit, Hawaii, Iowa, New Mexico, Seattle, Utah, Atlanta, San JoseMonterey, Los Angeles, Alaska Native Registry, and Rural Georgia). Mortality data are from the NCHS public use data file for the total U.S. a Rates are per 100,000 and age-adjusted to the 2000 U.S. standard population (19 age groups—Census P25-1103). b Incidence data for American Indians/Alaska Natives include cases from Connecticut, Detroit, Iowa, New Mexico, Seattle, Utah, Atlanta, and the Alaska Native Registry for the time period 1998–2002. Mortality data are from the entire U.S. for the time period 1998–2003. c Hispanic is not mutually exclusive from Whites, Blacks, Asian/Pacific Islanders, and American Indians/Alaska Natives. Incidence data for Hispanics are based on NAACCR Hispanic Identification Algorithm (NHIA) and exclude cases from Hawaii, Seattle, and Alaska Native Registry. Mortality data for Hispanics exclude deaths from Maine, Massachusetts, New Hampshire, and North Dakota. Citation: Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*Stat Database: Incidence— SEER 9 Regs Public-Use, Nov 2004 Sub (1973–2003), National Cancer Institute, DCCPS, Surveillance Research Program, Cancer Statistics Branch, released April 2006, based on the November 2005 submission.

260

260

Male

240

Female

240 Prostate

220

220

200

200

180

180

160

160

140

140

120

120 Lung and bronchus

100 80

Colon and rectum

60

Breast

100 80 Colon and rectum

60 Urinary bladder

40

40

Lung and bronchus Uterine corpus

Non-Hodgkin’s lymphoma 20

Ovary

20 Melanoma of the skin

Non-Hodgkin’s lymphoma

Year of diagnosis

2001 2002

1999

1997

1995

1993

1991

1987

1985

1983

1981

1979

1977

1975

2001 2002

1999

1997

1995

1993

1991

1989

1987

1985

1983

1981

1979

1977

0 1975

0

1989

Rate per 100,000 population

1050

Year of diagnosis

Figure 61-1. Annual age-adjusted cancer incidence rates* among males and females for selected cancers, United States, 1930–2002. ∗ Rates are age-adjusted to the 2000 U.S. standard population and adjusted for delays in reporting with the exception of melanoma.

61 100

Cancer

1051

Lung and bronchus

90

Rate per 100,000 population

80 70 60 50

Stomach

Prostate

40

Colon and rectum

30 20 Pancreas 10 Leukemia

Liver

1930 1932 1934 1936 1938 1940 1942 1944 1946 1948 1950 1952 1954 1956 1958 1960 1962 1964 1966 1968 1970 1972 1974 1976 1978 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002

0

A

Year of death 100 90

Rate per 100,000 population

80 70 60 50 Lung and bronchus 40 Breast 30 20

Stomach

10

Ovary

Colon and rectum

Uterus†

Pancreas 1930 1932 1934 1936 1938 1940 1942 1944 1946 1948 1950 1952 1954 1956 1958 1960 1962 1964 1966 1968 1970 1972 1974 1976 1978 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002

0

B

Year of death

Figure 61-2. A. Annual age-adjusted cancer death rates* among males for selected cancer, U.S., 1930–2002. B. Annual age-adjusted cancer death rates* among females for selected cancer, U.S., 1930–2002. Rates are per 100,000 and are age-adjusted to the 2000 U.S. standard population. *Rates are age-adjusted to the 2000 U.S. standard population. Note: Due to changes in ICD coding, numerator information has changed over time. Rates for cancer of the lung and bronchus, colon and rectum, uterus (uterine cervix and uterine corpus), ovary, and liver are affected by these changes.

the concept that increasing screening and improved therapies are contributing more to the declining mortality. A report evaluating the reduction of breast cancer mortality in the United States from 1975 to 2000 concluded that both screening mammography and treatment primarily contributed to the reduction.15 Comparing 1983–1985 with 1995–2001 newly diagnosed cancer patients, 5-year relative survival

rates have increased from 53% to 65% for all races across all cancer sites in the United States.10 Temporal trends in survival from cancer in children are most encouraging. From 1974 to 2001, five-year survival rates in children under age 15 increased for all sites. From 1995 to 2001, five-year survival rates were 86% for acute lymphocytic leukemia, 52% for acute

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Noncommunicable and Chronic Disabling Conditions

myeloid leukemia, 73% for brain and other nervous system, 86% for non-Hodgkin’s lymphoma, 95% for Hodgkin’s disease, 73% for sarcomas of the bone, 92% for Wilms’ tumor, and 79% for all cancer sites combined.4,10 There has been little change in the incidence of these neoplasms in children, thus reductions in mortality have resulted in prolonged survival due primarily to improved therapy. ETIOLOGY AND PRIMARY PREVENTION

Criteria for Causality Primary cancer prevention is prevention of the initial development of a neoplasm or its precursor. This can be accomplished only if one or more causes of the neoplasm are known, and it is achieved by reducing or preventing exposure to the causative agent or enhancing exposure to the protective agent. A harmful agent is considered causal if reducing or removing a population’s exposure to it results in a decrease in the amount of disease occurring in that population; a protective agent is considered truly beneficial if increasing or expanding a population’s exposure to it results in a decrease in the amount of disease occurring in that population. To determine whether an agent is a cause of a particular disease in humans, information from all relevant studies must be assessed critically. In making such an assessment, evidence for causality is strengthened if the criteria listed in Chap. 2 are met. Additional criteria include evidence that risk is reduced following a reduction in exposure. Attempts to determine whether an agent is carcinogenic in humans must often be made without information on all of these criteria; yet assessment of whatever evidence is available must frequently be made. Investigators must examine existing evidence to identify additional questions that should be addressed by further studies, physicians must assess available evidence to be able to give their patients adequate advice, and public officials must assess the evidence to determine needs for laws and regulations to limit exposure. Each must weigh the evidence for a causal relationship and consider the consequences of falsely implicating a substance as being carcinogenic when it is not and of failing to identify as carcinogenic a substance that is. All must also be willing to alter their opinions as results of additional investigations become available. Errors of judgment can be minimized by a clear understanding of basic epidemiologic principles and by careful examination of available evidence using the above-referenced criteria for assessing causality.

General Etiological Considerations At the level of the cell, cancer is a genetic disease. The development of a cancer appears to involve a multistep accumulation of genetic damage, leading eventually to the development of an abnormal clone of cells with a selective advantage over normal cells, and finally to an incipient tumor that acquires the ability to invade surrounding tissue.16 The molecular epidemiology of cancer involves the use of molecular techniques in epidemiologic studies to provide new insights.17 For each organ site, a tumor is the end result of multiple genetic aberrations that may be caused by multiple agents, and the same endpoint may be reached via different pathways. As a result, multiple risk factors are observed for all cancers, and only a small proportion of individuals who are exposed to most known carcinogens develop cancer. For example, a factor may increase cancer risk if it contributes directly to DNA damage, alters the ability of the cell to recognize or repair damage, inhibits apoptosis, encourages cell proliferation, enhances vascularization of the incipient tumor, or otherwise confers a selective advantage to that clone of cells. Similarly, agents that inhibit tumor development might act by reducing epithelial absorption of carcinogens, inhibiting the enzymatic activation of procarcinogens, enhancing the metabolic destruction of carcinogenic agents, promoting DNA repair, or causing cell differentiation or

apoptosis and thereby reducing the number of stem and intermediate cells susceptible to the effects of carcinogens. Most of the genes in which mutations appear to play a mechanistic role in carcinogenesis are categorized as either oncogenes or tumor suppressor genes, or are involved directly in DNA repair. Most identified oncogenes are mutated forms of genes (proto-oncogenes) that code for proteins involved in signal transduction, the regulation of gene expression, or growth-regulating mechanisms such as growth factors or growth factor receptors; overexpression of these genes results in enhanced cell proliferation. Most known tumor suppressor genes function as negative regulators of cell proliferation. The tumor suppressor gene p53, for example, is mutated in a majority of epithelial tumors. Other contributors to the carcinogenic process probably include genes affecting angiogenesis, metastasis, and other components of the process such as the ability to evade or disable the immune response. The latent period between exposure to some agent and the development of a neoplasm is dependent in part on the mechanism by which the agent operates. For example, mesothelioma follows exposure to asbestos only decades after exposure; the same is true of breast cancers following radiation to the chest, suggesting that these agents act early in the carcinogenic process. On the other hand, endometrial cancers can occur within two years of exposure to exogenous estrogens, suggesting a late-stage effect of these hormones. Reticulum cell sarcomas have developed within just months of exposure to immunosuppressive drugs in persons with renal transplants. A single exposure may act at one or more points in the progression to neoplasia, and its mechanism of action may vary across cancer sites. For example, epidemiologic evidence suggests that tobacco acts early in the carcinogenesis of esophageal and gastric adenocarcinoma, late in pancreatic tumors, and at both early and late stages in lung tumors. It must be emphasized, however, that a risk factor can represent a cause in the public health sense, as defined previously, whether or not its precise mode of action is known. For example, we have only incomplete knowledge of the exact mechanisms by which tobacco smoke increases a smoker’s risk of lung cancer. For the purpose of primary prevention, however, the mechanisms of action are unimportant. Cessation of smoking will significantly reduce the incidence of lung cancer, and that is what we need to know to take preventive action. Some of the known causes of various cancers are described below.

Tobacco Tobacco use is the single largest preventable cause of cancer (and other disease) and premature death in the United States.18 Use of tobacco is responsible for about 21% of all cancer deaths worldwide, which is more than all other known causes of cancer combined.19 Tobacco increases the risk of cancers of the lung, oral and nasal cavities, esophagus, stomach, liver, pancreas, kidney, bladder, cervix, and myeloid leukemia.18–21 Table 61-4 shows the estimated proportion of cases that would be prevented in the absence of tobacco use (the population-attributable risk percent), and the estimated annual number of deaths worldwide and in the United States attributable to tobacco.18,19 Population-attributable risks for tobacco are dependent on the proportion of people in the population who use tobacco, the relative risk of the particular cancer in users of tobacco, and the presence of other causes of the cancers of interest in the population. Estimates of population-attributable risks thus vary among populations, and the values for the United States are different from values for other parts of the world. Overall, these estimates outline the importance of cancer prevention through eliminating smoking in populations. Cigarette smoking is responsible for most cancers of the oral cavity, esophagus, and bladder; and it is a cause of kidney, pancreatic, cervical, and stomach cancers along with acute myeloid leukemia.22,23 In addition to the major cancer sites mentioned above for which the associations with tobacco are well established, a growing body of evidence implicates cigarette smoking as a contributor to the risk of colon and rectal cancers.24 There is little or no evidence of an association with cutaneous melanoma and conflicting evidence for prostate cancer.

61

Cancer

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TABLE 61-4. CANCER DEATHS ATTRIBUTABLE TO SMOKING: WORLDWIDE AND U.S. ESTIMATES∗

Cancer Site Lung and bronchus Oral cavity Esophagus Bladder Pancreas Liver Stomach Leukemia Cervical, uterus All Cancer ∗

Smoking Population Attributable Fraction 70 42 42 28 22 14 13 9 2 21

2001 Deaths Worldwide 856,000 131,000 184,000 48,000 50,000 85,000 111,000 23,000 6,000 1,493,000

Smoking Population Attributable Fraction 86 71 71 41 30 29 25 17 11 29

2006 Deaths in U.S.† 139,716 5,275 9,777 5,355 9,690 4,698 2,858 3,788 407 81,963

Estimated smoking population attributable fraction and worldwide death rates based on Danaei et al., 2005.19 Based on 2006 death rates estimated by the American Cancer Society (Jemal et al., 2006).10

†

Many of these estimates are based on studies of individuals who smoked cigarettes that were popular decades ago. Risks in comparable smokers of filter and low-tar products may be lower but still appreciable. Furthermore, the number of puffs per cigarette and the number of cigarettes smoked per hour are inversely proportional to the amount of nicotine in the tobacco. Low levels of nicotine therefore result in an increased exposure to carcinogens in tobacco smoke. There is no safe cigarette. Risks of a variety of neoplasms are also increased in users of other forms of tobacco. Compared to nonsmokers, risk in pipe and cigar smokers is approximately doubled for lung cancer, increased fourfold for cancer of the larynx, and doubled or tripled for neoplasms of the esophagus, oral cavity, pharynx, and bladder. Pipe smoking approximately triples one’s risk of lip cancer, and chewing tobacco or using snuff results in a fourfold increase in the risk of oral cancer.25 Secondhand smoke and environmental tobacco smoke also significantly increase the risk of lung cancer.26 Secondhand smoke contains more than 50 carcinogens and there is no risk-free level of exposure. Thus, passive smoking may account for the majority of the lung cancer not due to smoking, residential radon, or industrial exposures. The 2006 Surgeon General’s report found that millions of Americans are still exposed to secondhand smoke in their homes and workplaces despite substantial progress in tobacco control.26 Secondhand smoke also causes premature death and disease in children and adults who do not smoke.26 Separating nonsmokers from smokers, ventilating buildings, and cleaning air cannot eliminate exposure to nonsmokers; only eliminating smoking in indoor spaces will do so.

Alcohol The risk of several human neoplasms is clearly associated with alcohol consumption, especially for cancer of the liver, oral cavity, esophagus, and breast.19,27 Risk of hepatocellular carcinomas is increased in heavy drinkers, but the extent to which this is due to the unusually high prevalence of hepatitis B and C in alcoholics is unknown. These tumors tend to develop in alcoholics with macronodular cirrhosis, probably as a result of the rapid regeneration of liver cells in such individuals. If alcohol is a cause of liver cancer, it is an uncommon complication of its use, because these tumors are rare in countries such as the United States where exposure to alcohol is common. Cancer risk is typically increased only in those tissues that come in direct contact with undigested alcohol. Risk is thus increased for squamous cell carcinomas of the mouth (buccal cavity and pharynx), esophagus, and supraglottic larynx, but not, for example, of the lung or bladder. Esophageal, oral, and laryngeal squamous cell cancers are all also related to smoking, and most studies show the effect of smoking on the risk of these tumors to be greater in drinkers than in nondrinkers. Alcohol thus appears to modify the carcinogenic effect of tobacco smoke. It is not known whether alcohol use increases risk of these neoplasms in the absence of tobacco smoke or other carcinogens.28 The

effect of alcohol on these neoplasms may also be greater in individuals with marginal nutritional status than in better nourished individuals. In the United States, alcohol and tobacco account for about 80% of these cancers. Adenocarcinomas of the lower esophagus, gastroesophageal junction, and gastric cardia have also been consistently associated with alcohol use, but the relationship is not as strong as for the squamous cell carcinomas of the upper aerodigestive tract. Risks of cancer of the distal stomach, pancreas, colon, and rectum have not been consistently related to alcohol use, but observed associations between beer and rectal cancers and between heavy drinking and pancreatic cancer warrant further study. An association between alcohol intake and breast cancer has been observed in multiple investigations, even after controlling for known risk factors for breast cancer; while this relationship is not well understood, a recent consensus group suggests that 4–9% of breast cancers may be caused by alcohol consumption.19 Approximately 5% of all cancer deaths worldwide and 4% of cancer deaths in the United States can be attributed to alcohol use.18,19 Most alcohol-related neoplasms develop as a result of smoking as well as drinking, and cessation of smoking would have nearly the same impact on the occurrence of these neoplasms as cessation of drinking.

Industrial Exposures In 1972, the IARC in Lyon, France, initiated a series of monographs on the evaluation of carcinogenic risks to humans. As of 2006, 88 multidisciplinary committees of experts have reviewed the published literature on approximately 900 suspect chemicals, industrial processes, drugs, radiation exposures, and infectious agents and classified them as to their likely carcinogenicity in animals and humans. Of the over 800 chemical and industrial processes evaluated, the available evidence was considered sufficient to clarify 19 agents and groups of agents, 6 mixtures, and 13 industrial processes with exposure circumstances as carcinogenic to humans (Group 1).29–39 These, and the neoplasms most strongly and consistently associated with them, are shown in Table 61-5. Over 50 other chemicals, mixtures, and exposure circumstances were judged to be probably carcinogenic to humans (Group 2A); over 200 others were considered possibly carcinogenic to humans (Group 2B). The remaining chemicals, mixtures, and exposure, circumstances were considered not classifiable as to their carcinogenicity to humans (Group 3). Estimates of the global burden of occupational cancer are in the 2–4% range.40–42

Environmental Pollution The evidence that the agents shown in Table 61-5 are carcinogenic in humans comes from studies of relatively high exposure in the workplace. Exposures outside the workplace to most of these agents are sufficiently rare or at such low levels as to be of little importance. However, there are a few exceptions to this that included indoor exposure

1054

Noncommunicable and Chronic Disabling Conditions

TABLE 61-5. OCCUPATIONAL CAUSES OF CANCER Specific Exposures

Site or Tumor Type

Ionizing Radiation

Agents and Groups of Agents 4-Aminobiphenyl Arsenic and arsenic compounds Asbestos Benzene Benzidine Beryllium and beryllium compounds Bis (chloromethyl) ether and chloromethyl methyl ether Cadmium and cadmium compounds Chromium compounds Erionite Ethylene oxide Formaldehyde Mustard gas (sulphur mustard) 2-Naphthylamine Nickel and nickel compounds Silica, crystalline Talc containing asbestiform fibers 2,3,7,8-Tetrachlorodibenzo-para-dioxin Vinyl chloride

Bladder Lung, skin Lung, mesothelioma Leukemia Bladder Lung Lung Lung Lung, sinonasal Mesothelioma Leukemia, lymphoma Nasopharynx Lung, larynx Bladder Sinonasal, lung Lung Lung All-cancer mortality Liver, lung, brain, leukemia, lymphoma

Mixtures Coal tar pitches Coal tars Mineral oils, untreated and mildly treated Shale oils Soots Wood dust

Skin, lung, bladder Skin Skin Skin Skin, lung Sinonasal

Industrial Processes with Exposure Circumstances Aluminum production

Manufacture of auramine Boot and shoe manufacture and repair Coal gasification Coke production Furniture and cabinetmaking Hematite mining, underground, with exposure to radon Occupational exposure to strong— inorganic—acid mists containing sulfuric acid Iron and steel founding Isopropyl alcohol manufacture, strong acid process Manufacture of magenta Painters

Rubber industry

as a risk factor for lung cancer. A recent report estimates 5% of lung cancers worldwide are attributable to urban air pollution with this risk rising to 7% in low and middle income countries.19

Lung, bladder, lymphosarcomas and reticulosarcomas Bladder Nose, bladder Lung, bladder, skin Lung, bladder, skin Nose Lung Lung, larynx, nasal sinus Lung Nasal sinus Bladder Lung, larynx, esophagus, stomach, bladder, leukemia, lymphoma Bladder, leukemia, lymphoma

to vinyl chloride and asbestos, arsenic in air and drinking water, and point sources of arsenic, chromium, and nickel from industrial pollutants. Numerous efforts have been made to assess the impact of ambient air pollution on lung cancer risk.19,43,44 Although rates of lung cancer are higher in urban than in rural areas, smoking is also more prevalent in urban areas. Primarily from large cohort studies in Europe and the United States, there are now results supporting air pollution

Ionizing radiation can cause a variety of human neoplasms.45 Most of the evidence for this comes from studies that followed individuals exposed to moderate or high doses from nuclear explosions, medical treatments, and occupational sources. Exposures have been both external and internal. IARC has identified radionuclides (plutonium-239, radium-224, radium-226, radium-228, radon-222, and thorium-232) and their decay products as well as phosphorus-32, radioiodines, α-particle-emitting radionuclides, and β-particle-emitting radionuclides, in addition to x- and gamma (γ)-radiation, and neutrons, as carcinogenic to humans.46,47 All humans are exposed to natural radiation. Primary sources of natural radiation include inhalation (mainly radon gas), ingestion, cosmic rays, and terrestrial gamma rays.48 Approximately half of all ionizing radiation received by individuals in the United States comes from natural background sources. Radium is found in soil where it decays to a radioactive gas, radon-222, which can seep into houses and accumulate under conditions of poor ventilation. Overall, radon gas is the greatest contributor to natural radiation exposure, accounting for about 50% of the total average annual effective dose. Radon222 progeny, primarily plutonium-218 and plutonium-214, are the likely cause of lung cancer in uranium miners, and with recent data it is felt that residential radon-222 progeny contribute appreciably to the population’s lung cancer burden.49,50 It has been estimated that 18,600 lung cancer deaths per year are attributable to residential radon progeny in the United States alone.51 Man-made sources of radiation also exist and include medical uses of radiation, atmospheric nuclear testing, nuclear power production, and occupation activities. In developed countries, medical uses of radiation are the largest source of man-made exposure and, on average, amount to about 50% of the 240 mrem global average level of natural exposure.48 Studies of individuals who have received total body radiation from external sources have shown that some organs are more susceptible to the carcinogenic effects of radiation than others. In the atomic bomb survivors in Japan, there were large increases in rates of carcinomas of the anatomically exposed thyroid and mammary glands and of leukemias arising from the highly susceptible cells of the bone marrow; lesser increases in rates of lymphomas and carcinomas of the stomach, esophagus, and bladder were observed; and risks of cancer at other sites were either not altered or the increases were too small to measure with certainty. Risk of leukemia was also increased in early radiologists who took few precautions to reduce their general exposure to radiation and probably also in individuals exposed in utero to x-rays from pelvimetry. Cancer survivorship has been increasing to where cancer survivors now constitute 3.5% of the U.S. population. This is a high-risk group for second cancers, which now account for 16% of all cancer incidence (excluding nonmelanotic skin cancers).52 These second cancers represent a serious side effect of treatment with radiation and chemotherapy. Most types of cancer can be caused by exposure to ionizing radiation.53 External sources of radiation directed at specific sites have resulted in a variety of neoplasms. Breast cancer was induced in women treated with x-rays for a variety of benign breast conditions and in women who received multiple fluoroscopies of the chest in conjunction with pneumothorax treatment of tuberculosis. Individuals treated with x-rays for ankylosing spondylitis have had increased rates of leukemia and lung cancer and, like the atomic bomb survivors, lesser increases in rates of lymphomas and cancers of the stomach and esophagus. An increased risk of lung cancer has been observed in women who received radiation following mastectomy for breast cancer and radiotherapy for Hodgkin’s disease. A strongly elevated risk for breast cancer has been seen after radiotherapy for Hodgkin’s disease. Children treated with x-rays for tinea capitis and enlarged thymus have developed leukemia and neoplasms of the

61 salivary and thyroid glands. Those treated for an enlarged thymus have also had an increased risk of leukemia, and those with tinea capitis developed more brain tumors than expected. Internal exposures to radiation have likewise resulted in increased risks of cancer at specific sites. Inhalation of radioactive dusts contributed to the increased rates of lung cancer in the atomic bomb survivors, and inhalation of radon and its decay products resulted in elevated rates of lung cancer in miners of uranium, iron, and fluorspar. Radium inadvertently swallowed by radium-dial watch painters and administered for treatment of ankylosing spondylitis was concentrated in osseous tissues and caused high rates of bone cancers. Individuals exposed to iodine-131 (I-131) in fallout from a hydrogen bomb test and in emissions from the nuclear power plant accident at Chernobyl subsequently had increased rates of thyroid cancer. The radiopaque contrast material thorotrast that was used to x-ray the liver has resulted in hepatic cancers, as well as leukemias and lung carcinomas. Women receiving cervical radium implants and other forms of pelvic radiation for a variety of gynecological conditions have had increased rates of cancers of the rectum, vagina, vulva, ovary, and bladder, as well as leukemia. The results of most studies show a linear increase in risk of neoplasms with the amount of radiation received over a wide range of observed doses, with a possible decrease in the slope of the doseresponse curve at very high levels of exposure (perhaps due to cell killing). These observations are based primarily on studies of individuals who received from tens to hundreds of rads. Doses commonly received today are orders of magnitude lower, and it is uncertain whether the dose-response curve should be linearly extrapolated to these low levels to provide an estimate of the associated risk. There may be a threshold level below which radiation does not induce neoplasms, perhaps because mechanisms of DNA repair are adequate. If so, linear extrapolation would yield estimates of risk to low levels of radiation that are too high. Conversely, chronic exposure to low levels of radiation might be more carcinogenic, rad for rad, than acute exposure at a higher dose. If so, linear extrapolations would underestimate the risk of low doses. Since there is little evidence for the latter possibility, most authorities believe that it is reasonable, as well as prudent, to assume a linear, nonthreshold dose-response relationship. Recent experimental studies have documented that a single alpha particle can provide permanent damage to a cell.51 This finding supports the biologic plausibility of the linear, nonthreshold relationship. It is difficult to accurately estimate the number of cancers attributable to radiation from all sources experienced by the general population.54 Nevertheless, available knowledge indicates that reducing medical exposures and residential (indoor) radon will have the most impact toward reducing population exposure and radiogenic cancer risk. Political efforts to reduce the likelihood of environmental contamination from nuclear power plants and nuclear weapons will also obviously reduce the risk of radiation-induced neoplasms.

Nonionizing Radiation Nonionizing radiation, in contrast to ionizing radiation, is electromagnetic radiation that does not have sufficient energy to remove electrons to form an ion (charged particle). Nonionizing radiation includes ultraviolet (UV) radiation, visible light, infrared, and microwave and radio frequencies. Among these the major carcinogen is UV radiation which comes from the sun or artificial sources such as tanning beds or booths. UV Radiation. Sunlight is definitely a cause of nonmelanoma skin cancers (squamous and basal cell carcinomas), as evidenced by the observations that these tumors tend to occur on exposed parts of the body, risk increases with the amount of sun exposure, and incidence rates are greater in light-skinned than in dark-skinned individuals. However, these skin cancers are rarely deadly, and routine data on nonmelanoma skin cancer are not collected by cancer registries in the United States. The American Cancer Society estimates over one million cases of basal cell and squamous cell skin cancer in the United States in 2006.18

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The relationship of cutaneous malignant melanomas to sunlight is more complicated.55,56 Various types of sun exposure have been reported to be associated with melanoma, ranging from severe sunburns, occupational activities, vacation sun exposure, beach activities, other recreational activities, cumulative or chronic sun exposure, and early migration to sunny places. Incidence rates for cutaneous melanoma are highest in individuals with little natural skin pigmentation, often with intermittent sun exposure such as sunburns or sunny vacations.55,56 Investigation of migrants to Australia provided evidence that sun exposure at an early age or long-term exposure may be of particular importance.55 Early UV exposure is of concern with the expanding popularity of tanning beds and booths. Current evidence suggests an increase in melanoma risk among tanning bed users. Modern tanning bed units have UV levels comparable to tropical sunlight and irradiate almost 100% of the skin, which is assumed to be 2–10 times more skin surface area than sunlight exposure.57 Incidence rates may increase as younger populations expose more of their bodies to such units. In the white U.S. population, incidence rates of melanomas of the skin have dramatically increased over the last few decades, due in part to changes in diagnostic criteria and enhanced awareness of the importance of early evaluation of melanotic lesions. Melanoma increases with age (the mean age at diagnosis is about 57). While the relationship between cutaneous melanoma and specific types of sun exposure is complex, the American Cancer Society estimates that nearly all skin cancers are related to UV radiation (even familial cancers that are likely related to genetic and UV radiation).18 Because nonmelanotic skin cancers are common and largely attributable to sun exposure, sunlight accounts for approximately 40% of all neoplasms.10,19 Sunlight accounts for less than 2% of cancer deaths, since these neoplasms are infrequently fatal. Since only cutaneous melanoma is routinely collected and reported by cancer registries, less than 2% of reported cancers appear to be due to UV radiation.10 All individuals, but particularly those with light skin who burn easily, should be encouraged to avoid excessive direct exposure to intense sunlight and to use sunshades and sunscreens. Electric and Magnetic Fields. Recent studies have focused public attention on the possible association between exposure to electric and magnetic fields (EMF), particularly from electric power lines and appliances, and risk of cancer. Based on methodological concerns and the lack of experimental evidence, no clear relationships between EMF and chronic disease have been established.58,59 However, an association is observed most consistently in studies of childhood leukemia in relation to postnatal exposures above 0.4 microT.58,59 Study of EMF is made particularly difficult by our inability to identify and accurately measure the relevant exposure. A number of reviews of the subject have been published.58–61

Sex Hormones and Reproductive Factors Sex Hormones. Sex steroid hormones have been associated with an increased risk of most reproductive cancers, including breast, endometrium, ovary, cervix, prostate, and testis. This section will evaluate endogenous and exogenous hormonal risks as well as other reproductive factors, many of which also are linked indirectly to potential hormonal alterations. In evaluating the effects of exogenous female sex hormones on the risk of neoplasms in women, it is important to categorize these substances according to their estrogenic or progestogenic pharmacological effect. At one end of the spectrum are the pure progestational agents, such as depot-medroxyprogesterone acetate (DMPA), which is used as a long-acting injectable contraceptive in many countries and to treat malignant and benign proliferative disorders of the endometrium. Other progestational contraceptives include the “minipill” which is an oral contraceptive (OC), the injectable contraceptive, norethindrone, and subcutaneous implants, such as Norplant. At the other end of the spectrum are the pure estrogen preparations. Between the two ends of the estrogen-progestin spectrum are the sequential OCs which contained only estrogen in pills taken for 2 weeks of a cycle followed by a weak progestin of short duration

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and which had a net estrogenic effect, and the more commonly used combined OCs with an estrogen and a progestin in each pill, and therefore a net pharmacological effect more progestational than the sequential pills. More recent products differ from these older formulations in dosage and in types of estrogens and progestins contained and are referred to as biphasic and triphasic OCs. These products were developed to reduce side effects of the monophasic OCs that administer the same estrogen/progestin dosage throughout the cycle. Because of the breakthrough bleeding side effect of the biphasic formulations, these are not widely used. Although the findings from studies linking these drugs to reproductive cancers that were conducted through the mid-1990s may not be applicable to the newer contraceptive agents, it would seem prudent to assume that they do until results of additional epidemiologic investigations provide evidence to the contrary. The most common are the conjugated “natural” estrogens (e.g., Premarin), used largely to treat or prevent symptoms and conditions associated with menopause, and the nonsteroidal synthetic estrogen, DES (diethylstilbestrol), to prevent early miscarriage. Those used during peri- and postmenopause to reduce menopausal side effects and osteoporosis include estrogen replacement therapy (ERT) and estrogen/progestin hormone replacement therapy (HRT), the most common of which is Prempro. More recent formulations have been marketed with reduced hormonal formulations yet having similar beneficial effects with fewer adverse side effects. Although some studies, including a clinical trial, of breast cancer in women given DES for threatened abortion show no evidence of an increased risk of cancer,62,63 a larger investigation showed a 40% increase risk with a latency period of 20 years after DES exposure.64 The effect of combined OCs on risk of breast cancer has been evaluated in a number of large cohort and case-control studies as well as in meta-analyses65 and the risk is increased by about 25% in current users and declines to that of never users about 10 years after cessation of use. The relative risk estimate (RR) in women who ever used OCs was estimated to be 1.1. Tumors tended to be more localized in users than in nonusers, suggesting enhanced surveillance in recent and current users as an explanation for the increased risk. Even if the findings represent a causal phenomenon, use of OCs would result in few additional cases of breast cancer because most current and recent users of OCs are young women with a low background rate of this disease. However, among those who last used OCs less than 10 years ago, for greater than 5 years, the risk is increased approximately 13%.65 A combined analysis of two studies of DMPA and breast cancer similarly found an increase in risk in recent and current users of this progestational agent but no increase in risk after 5 years since last use, and an overall RR of 1.1 in women who had ever used this agent.66 Studies of breast cancer in relation to ERTs given at menopause have shown an increased risk in women particularly among those who are current users of ERTs for 5 years or longer (RR = 1.2–1.4).67 A small increase in risk with years of use beyond 5 years has been observed in most studies, with a decline in risks to that of nonusers from 2 to 5 years after cessation of use.68 A collaborative reanalysis of 51 studies69 on this issue found that during or shortly after use, there was a RR of 1.02 for each year of use for those with 1–4 years of use, and 1.03 for those with more than five years of use. The addition of a progestin to the regimen increases the risk by an additional 10% over that of ERT users or a 40% greater risk than among never HRT users. Tamoxifen, which has antiestrogenic properties in the breast, and raloxifene, a selective estrogen receptor modulator, have been shown to reduce the risk of breast cancer in the contralateral estrogen receptor positive breast of a woman who receives these adjuvant therapies for primary breast cancer. In regard to risk of breast cancer associated with endogenous sex steroid hormones, several studies have shown that risk is significantly elevated for women in the top quintile of total estradiol (RR = 1.9), or free estradiol (RR = 2.7) after adjustment for BMI and other risk factors.70–73 The risk of endometrial cancer is increased twofold or more in women who took sequential oral contraceptives and who were not monitored for endometrial hyperplasia.67,74,75 In contrast, risk of cancer remains significantly decreased (RR = 0.5) for 20 years or longer in

users of combination OCs76 compared to never users. The reduction in risk is even lower among those who used the progesterone-only OCs and in users of DMPA77 because of their net progestational effect on the endometrium. Those who received estrogens for menopausal conditions, primarily as ERTs, also are at significantly greater risk of endometrial cancer. Tamoxifen, which is used as an adjuvant therapy for breast cancer, has an estrogenic effect on the uterus and has also been shown to increase the risk of endometrial cancer.78 To reduce the risk of endometrial cancer in users of drugs containing estrogens, a progestin is often included, either continuously with the estrogen or cyclically for a specified number of days each month, and this has been shown to markedly reduce the risk of endometrial cancer to that of never users. Several case-control studies have shown an increased total and bioavailable estrogens and decreased plasma levels of sex hormone binding globulin in postmenopausal women who develop endometrial cancer as compared to healthy controls.79,80 In premenopausal women, one epidemiologic study showed a decrease in total and bioavailable estradiol.81 It has further been suggested that in this group of women it is lower progesterone rather than higher estrogen that increases the risk of premenopausal endometrial cancer. Additional evidence of the effects of endogenous hormones on cancer development comes from the increased risk in polycystic ovarian syndrome, a disease that is characterized by low progesterone levels in women who have normal estrogen levels. In both pre- and postmenopausal women, obesity and chronic hyperinsulinemia are associated with changes in total and bioavailable sex steroid levels, especially estrogen. In sum, there are few if any studies that have used a prospective design to directly examine endogenous hormonal levels well in advance of malignancy. Risk of epithelial ovarian cancer in women who have ever used combined OCs is approximately 50% of that of never users, and the risk decreases with duration of use.82 A further reduction in risk is seen in the progesterone-only OCs. The benefit of either type of OC persists 10–20 years after use has been discontinued. The benefit includes women with a family history of ovarian cancer and those with a mutation in the BRCA1 or BRCA2 gene.83,84 Furthermore, the reduced risk is similar in parous and nulliparous women without known infertility. A single study has shown no effect of DMPA on risk of ovarian cancer, thus the association is unclear to date. Several large case-control studies have shown an increased risk of ovarian cancer among either ERT (RR = 1.6) or HRT (RR = 1.2) as well as a significant duration effect (RR = 1.3–1.8).85 In contrast, the Breast Cancer Detection Demonstration Project cohort follow-up study showed no increased risk with either ever or duration in HRT use of four years or more, whereas risk was elevated in ERT users (RR = 1.8–3.2).86 Studies of endogenous hormones associated with ovarian cancer are limited and rely on indirect evidence such as the protective effects of pregnancies and OC use which suppress pituitary gonadotropin secretion and increased risk among women with polycystic ovarian syndrome, who are known to have elevated circulating lutinizing hormones (LH). However, these findings are contradicted by the lack of an increase in risk among those with an early age at menopause and with twin pregnancies, both of which are associated with an increase in gonadotropin levels; in the lack of an increase in ovarian cancer after menopause which is associated with increasing LH and follicle stimulating hormone; and in the increased risk with ERT use and obesity. Research also has shown a lack of association between circulating androgens and ovarian cancer risk in postmenopausal women, but an increased risk is seen with androstendione and dehydroepiandrosterone in premenopausal women. Despite the link between insulin and insulin-like growth hormones (IGF-I) receptor and activation of intracellular signaling pathways and its effects on metabolism of other hormones, studies to date do not support its involvement with ovarian cancer. Likewise, IGF-I, which has been associated with increased risk of other reproductive cancers, breast and prostate, did not show evidence of an association in the only epidemiologic investigation of risk based on prediagnostic data to date.87 In summary, although evidence is accumulating regarding endogenous hormones associated with ovarian cancer, additional investigations particularly among prospective study designs are required.

61 Studies of cervical cancer and menopausal estrogens have not been conducted. Most studies of OCs and invasive cervical cancer have shown an increased risk with greater than 5 years duration of use in the presence of an oncogenic human papillomavirus (HPV) infection. OCs provide hormonal conditions favorable to the persistence of HPV infection88 or transformation of infected cells. Studies of HRTs and risk of cervical cancer are limited but suggest an increased risk in users (RR = 2.3–2.7) and with increasing duration in use.89,90 Combined OCs have clearly been shown to cause benign hepatic cell adenomas and focal nodular hyperplasia. These are highly vascular tumors that can rupture, bleed into the peritoneal cavity, and cause death. Fortunately, they are a rare complication of OC use, occurring at a rate of less than 3 per 100,000 women-years in women under 30 years of age. Case-control studies conducted in developed countries have shown that primary hepatocellular carcinomas are also rare complications of OC use.91 Some of these studies, plus investigations conducted largely in developing countries, provided evidence that this adverse effect is not mediated by enhancing the influence of other factors such as hepatitis B or C on risk. DES was prescribed between 1938 and 1971 to treat up to 5 million women in the United States for threatened abortion. Approximately 80% of the female offspring exposed to DES in utero have been found to have glandular epithelium resembling that of the endometrium, and presumably of Müllerian origin, in the vagina or cervix. This is referred to as adenosis. A small portion of women with this condition have developed clear cell adenocarcinomas of the vagina or (less frequently) the cervix in their teens or twenties especially if their mother took DES early in pregnancy.92 The risk of clear cell carcinoma is between 1.4/1000 and 1/10,000 among exposed women.93 This represents a high proportion of neoplasms in this age group, including virtually all vaginal cancers. Women exposed in utero to DES with vaginal or cervical adenosis should be followed carefully for the development of clear cell carcinoma. Males exposed in utero to DES are at increased risk of cryptorchidism, which is a significant risk factor for testicular cancer. However, only one study has shown a nonsignificant threefold increased risk of testicular cancer among males with prenatal DES exposure. These neoplasms represent the first documented instances of transplacental carcinogenesis in humans. In some countries, DES has been used as a “morning after” pill to prevent pregnancy or to treat menopausal symptoms. These findings suggest that precautions must be exercised not to give DES to women who may be pregnant. Colorectal cancer risk has been shown to be protected among OC ever or new users (RR = 0.4–0.7) compared to never users94–96 as well as in HRT current or ever users (RR = 0.3–0.5).95 Case-control, cohort studies, and a meta-analysis have failed to confirm earlier reports that risk of malignant melanoma is increased by use of OCs.76 Compared to never users, those who used OCs for greater than 1 year showed no excess risk (RR = 0.82–1.15), nor for duration, age first used, recency, or latency effects.97,98 Isolated reports of associations between OCs and pituitary adenomas, choriocarcinomas, gallbladder carcinomas, and thyroid tumors have also appeared, but these observations have not been convincingly confirmed by epidemiological investigations.76 Both prostate and testicular cancers in males have been associated with endogenous sex hormones with the primary hypothesis that androgens are causally related to prostate cancer etiology. Although there have been a number of studies that have investigated the role of androgens, few have had an adequate sample size, serum taken prior to cancer development and diagnosis, or controlled for confounding, especially age-related, known changes in serum hormone levels that may not reflect current cancer risk. In the one prospective study that addressed these issues, the Physicians’ Health Study showed that risk of prostate cancer was greater with increasing testosterone quartile levels (RR = 1.0–2.4), and decreased with increasing sex hormone binding globulin (RR = 1.0–0.4) and estradiol regardless of comparative quartile level (RR = 0.5).99 Testicular cancer has been hypothesized to be associated with initial hormonal exposure levels in utero and in the belief that excess estrogen or insufficient androgens lead

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to testicular cancer. Maternal exogenous estrogen use during pregnancy has been associated with both cryptochordism, a significant risk factor for testicular cancer, and subsequent development of testicular cancer in offspring. Also, risk is greater in male offspring of women having their first child as compared to multiparous women, consistent with plasma estrogen levels which are noted to be higher in primiparous women.100 Although it has been suggested that maternal exposure to DES leads to increased testicular cancer risk, there is insufficient evidence to support this claim.101 Among the testicular cancer risk factors, it appears that late age at puberty is linked to a significant decrease (~50%) in risk of testicular cancer, supporting a hormonal influence in its etiology.102,103 Reproductive Factors. Among women, nulliparity is associated with an increased risk of cancers of the endometrium, ovary, and breast. Risk of ovarian and endometrial cancers decreases with increasing number of pregnancies, whereas pregnancies beyond the first have a lesser protective effect against breast cancer. Risk of breast cancer increases strongly with age at first full-term birth, in contrast to risk of ovarian cancer which actually decreases with increasing age at first birth.104–107 Late age at last birth has been associated with a significant reduction in risk independent of parity for endometrial cancer.108 Earlier age at menarche and late age at menopause are associated with an increased risk of cancers of the breast and endometrium, but not the ovary. Lactation, which suppresses ovarian function, has been inconsistently associated with increasing the risk of breast cancer. The benefit of lactation occurs due to ovulation suppression which is maximal soon after delivery, and short-term lactation appears to have only a small protective effect against ovarian cancer, whereas prolonged lactation seems to confer little additional benefit. Risk of endometrial cancer may be inversely related to duration of lactation, but the effect also is short term, thus there is little or no protection in the postmenopausal years when most endometrial cancers occur. Induced abortion may enhance risk of breast cancer, but studies to date have yielded inconsistent findings. In regard to infertility independent from nulliparity, most studies report an increased risk of epithelial ovarian cancer.82 Although the mechanism is not understood, several studies have shown endometriosis to increase the risk of ovarian cancer, and the risk is further increased among those with ovarian endometriosis.109,110 Although somewhat less clear, most studies have shown that use of fertility agents is not associated with an increased risk of ovarian cancer.111 Tubal ligation confers a 10–80% reduction in ovarian cancer risk regardless of parity and including prospective studies that reduce a potential detection bias of case-control evaluations.112–114 Mechanisms for the associations with parity and lactation are not fully understood, but likely involve endogenous pituitary and ovarian hormones. The development of epithelial ovarian tumors is believed to be promoted by gonadotropin stimulation and reduced by suppression of gonadotropins during pregnancy and lactation. Nulliparous women are on average less fertile than parous women and have more anovulatory menstrual cycles, hence more constant production of estrogens without cyclic progesterone each month. The relative excess of unopposed estrogens is believed to promote endometrial tumor development. Although several mechanisms for the relationship of breast cancer to age at birth of first child have been proposed, none appears adequate. Studies of the endocrinological events associated with childbearing and other endocrinological studies in women at varying risks of cancers of endocrine target organs continue to be conducted to explain the mechanisms by which factors related to childbearing alter risk.

Infectious Agents Significant knowledge has accumulated over the past several decades about the molecular biology of cell transformation by oncogenic DNA and RNA viruses. The evidence is based on the ability of these viruses to modify gene expression in the host cell leading to a better understanding of how these infectious agents are related to the development of cancers. Among the DNA-related cancers in humans are EBV, hepatitis B and C (HBV and HCV), and HPV.

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Among the DNA viruses, EBV, a herpes virus, has been etiologically associated with Burkitt’s lymphoma (BL), nasopharyngeal carcinomas (NPC), and Hodgkin’s disease.115 The EBV genome established a latent infection in B lymphocytes and is transmitted when these lymphocytes replicate. In healthy individuals, cytotoxic T-cell responses against the latent viral proteins prevent uncontrolled replication of the virus in these B cells. This cancer, which is noted as especially aggressive, has the hallmark chromosomal translocation between 8 and 2, 14, or 22.116 Primary EBV is usually asymptomatic in humans and exists as a latent infection which is seroprevalent in over 90% of the adult population worldwide. Almost all individuals with BL or NPC have antibodies against EBV, compared with lower percentages in unaffected persons, and antibody titers are higher in the diseased cases. A cohort study has clearly shown that EBV infection precedes the development of African BL, where it is referred to as endemic BL. In contrast, isolated cases of non-endemic BL occur throughout the world at a much lower incidence and the association with EBV is much weaker, with only 15–30% of cases outside Africa having evidence of prior EBV infection.117 The EBV genome has been demonstrated in tumor cells from most African BL and virtually all NPCs. However, only a small proportion of individuals infected with EBV develop either of these neoplasms and the worldwide distribution of the two malignancies is different. Thus, it is apparent that other factors are essential in conjunction with EBV for these tumors to develop. Chronic malaria and the subsequent immunosuppression or antigenic stimulation may play a role in African BL although the spread of EBV is through saliva not mosquitoes as originally hypothesized. EBV is associated with the undifferentiated NPC type which is detected primarily in men over age 40 years of age, regardless of geographic location. Although the neoplasm is rare, the incidence is very high in Asian and Alaskan native populations with rates between 25–50/100,000 compared to less than 1/100,000 in Caucasian populations.118 In Singapore, where Chinese, Malays, and Indians live in close proximity and share similar dietary and social habits, the incidence of NPC is 18.5, 3.1, and 0.9 per 100,000 in males, respectively, suggesting that genetic rather than environmental exposures are important to the development of this tumor. Although cofactors for NPC are unknown, they may include human leukocyte antigen (HLA) profiles and environmental risks (e.g., chemical exposures, tobacco smoke, or cooking fumes), and dietary factors such as salted fish. An increased risk of NPC has been identified in Chinese populations for HLA types A2, B14, and B46 whereas a reduced risk is found with HLA A11, B13, and B22.118,119 EBV also contributes to the development of Hodgkin’s disease. The virus causes infectious mononucleosis, and those with a history of infectious mononucleosis have a two- to threefold increase in risk of Hodgkin’s disease but not EBV-negative HL. Compared to nondiseased individuals, cases of Hodgkin’s disease have a higher prevalence of antibodies against EBV and higher antibody titers. However, EBV DNA or gene products can be demonstrated in only half of cases, and only 30–40% of cases have anti-EBV antibodies, suggesting either the existence of causal pathways not including EBV or loss of EBV infection after tumor development. In immunodeficient patients such as those receiving transplants or having AIDS, there also is an increased incidence of EBV-associated Hodgkin’s disease.120 There is strong evidence that hepatitis B and C viruses cause hepatocellular carcinoma (HCC), and an IARC working group has judged that both of these viruses are carcinogenic to humans.121 HCC has been increasing worldwide and is now the fifth most prevalent cancer with mortality reaching 500,000 people yearly.122 Although rare in the United States except among Eskimos, HCC is the most common cancer in parts of Africa and China. This cancer can develop in individuals who are chronic carriers of HBV or HCV. In parts of Africa, Asia, and the Pacific, HBV is endemic with most infections occurring during childhood, and 90% of HCC are infected with HBV. Determinants of the chronic carrier states are not fully understood. Transmission of HBV or HCV is through contact with infected bodily fluids. In high-risk areas, perinatal transmission of HBV from mother to child at or soon after birth, before immune competence is fully developed, results in the child becoming a chronic HBV carrier

and at higher risk of subsequently developing HCC. In areas with lower prevalence of HBV, most infections are acquired horizontally in early adulthood through intravenous drug use or unprotected sex. Less commonly, contaminated surgical instruments and donor organs and medical personnel who are in frequent contact with infected blood products are at highest risk if not vaccinated against HBV. Currently there is no vaccine to protect against HCV. Although blood transfusions were once a significant route of transmission, improved diagnostic tests, greater screening, and vaccination against HBV have dramatically reduced the risk of acquisition of HBV. It is uncertain whether either HBV or HCV directly causes hepatomas or whether they cause chronic hepatitis and liver cirrhosis, which lead to repeated periods of cell death and regeneration, and increase the risk of HCC, perhaps in the presence of other carcinogens such as aflatoxins. Kaposi’s sarcoma is caused by another DNA virus, human herpesviridae (HHV-8). Once very rare, in the early 1980s a more aggressive form of Kaposi’s sarcoma associated with immune deficiency began to be seen in AIDS patients and was one of the first indications of the AIDS epidemic. Although the cancer cannot be cured, by treating the immune deficiency, progression of Kaposi’s sarcoma can be slowed or halted. As the mortality rate of AIDS dropped in the 1990s, so also did that of Kaposi’s sarcoma. Blood tests can detect antibodies against Kaposi’s sarcoma and determine whether the individual is at risk of transmitting HHV-8 infection to a sexual partner or whether a donated organ is infected with Kaposi’s sarcoma. It is now well established that oncogenic HPV types are causative in the development of human cancers. HPV is a necessary but not sufficient cause of cervical cancer and also is associated with a high proportion (60–85%) of vulvar, vaginal, penile, and anal sites. Males, most likely due to the characteristics of their genital tissue, have a much lower prevalence of these genital cancers but are the primary source of sexual transmission to the higher-risk females. Recent evidence indicates that 25% of head and neck tumors also are caused by HPV independent of other significant risk factors at these sites, such as tobacco and alcohol. Among the most prevalent and highly oncogenic types are HPV 16 and 18 with a number of other less prevalent oncogenic types that cause genital cancers (HPV 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82). Although the majority of cervical cancers are associated with HPV 16, HPV 18 is most frequently associated with aggressive adenocarcinomas of the cervix in younger aged women. HPV is transmitted primarily through sexual contact and invades the tissues by epithelial microtears. Although well over 50% of adults are thought to have been infected in their genitals with HPV during their lifetime, infections usually are cleared or become latent and undetectable. However, in individuals in whom infection persists for a prolonged period of time, intraepithelial lesions are likely to develop, some of which eventually progress to invasive carcinomas. The factors responsible for progression to anogenital malignancies include hormonal factors (e.g., steroid contraceptives), chemical factors (e.g., cigarette smoking), and immunodeficiency (e.g., human immunodeficiency virus [HIV] infection, immunosuppression for renal transplantation). In contrast, HPV is an independent risk factor for head and neck cancer and does not require the other major risk factors for malignancy to develop. HPV types associated with head and neck cancers have been limited primarily to HPV 16, 18, 31, and 33, and both younger age and male gender are more likely to be infected with the virus in the oral tissues. Recently several HPV vaccines have undergone clinical trials and been approved by the United States Food and Drug Administration. Currently, the HPV vaccine is being targeted only to prepubescent and teenage females prior to their sexual debut, but this focus has raised considerable concern as the source of viral infection to the genitals is primarily from male to female. In addition, this strategy fails to address prevention of HPV-associated head and neck cancers which occur predominantly among males. Among the RNA tumor viruses, the most significant is human immunodeficiency virus (HIV or HTLV-III) which causes acquired immunodeficiency syndrome (AIDS), are at greatly increased risk of Kaposi’s sarcoma and of non-Hodgkin’s lymphomas.123 As of 2006 an estimated 25 million people have died from AIDS alone.124

61 Transmission is through direct contact of a mucous membrane with a bodily fluid containing HIV (e.g., blood, semen, vaginal fluid, breast milk). In addition to destroying CD4+T cells, which are required for functioning of the immune system, and subsequently leading to AIDS, HIV also directly attacks and destroys the kidneys, heart, and brain. Rates of intraepithelial cervical and anal squamous cell carcinomas are also increased in AIDS patients, but increased rates of invasive cancer at these sites have not been observed. Testicular seminomas also occur more frequently in AIDS patients, and there are unconfirmed reports of increased risks of testicular teratocarcinoma, malignant melanoma, leiomyosarcoma, non-small cell lung cancer, multiple myeloma, hepatocellular carcinoma, and Hodgkin’s disease. Another RNA tumor virus, HTLV-I, has been strongly implicated as a cause of adult T-cell leukemias and lymphomas, particularly in some areas of Japan, the South Pacific, the Caribbean, and Africa where the virus is endemic, but this virus is of less significance in the nonendemic United States. The actual population seropositivity level is unclear as most studies have examined selective, high-risk groups. Transmission is believed to occur through cell to cell contact of virusinfected cells during the exchange of bodily fluids (e.g., breast milk, semen, blood transfusions, and contaminated needles of drug users). Four infectious agents other than viruses have been strongly implicated as causes of human cancers. In 1994, an IARC working group125 judged that Shistosoma haematobium was a definite cause of bladder cancer (Group 1), that the liver flukes Opisthorchis viverrini and Clonorchis sinensis were definitely (Group 1) and probably (Group 2) causes of cholangiocarcinomas of the liver, respectively, and that the bacteria H. pylori was a carcinogen for the stomach (Group 1). Schistosomiasis affects more than 200 million people and humans are the host for the blood fluke which infects them through the skin exposed to water containing the infective larvae. The eggs elicit granulomas that cause disease in the urogenital system. O. viverrini infects humans who eat undercooked fresh-water fish and the adult parasite lives within the intrahepatic bile ducts. The highest incidence of cholangiocarcinoma in the world is in Thailand where the parasite is endemic and the vast majority of these cases are caused by this fluke. The relationship of H. pylori to gastric cancer is of potential importance in developed countries. This pathogen has been associated with both intestinal and diffuse histologic types, and most strongly with tumors developing outside the cardia.126 It is estimated that H. pylori infects the gastric mucosa of about half of the world population and 15% of those infected are associated with the development of gastric cancer, the second leading cause of cancer deaths worldwide. In the United States, blacks, Hispanics, and other minorities are more commonly infected with H. pylori and have an incidence and mortality rate 2–3 times that of Caucasians. Over 60% of gastric adenocarcinomas have been attributed to infection with H. pylori. The malignancy can be prevented or produce resolution of premalignant lesions by use of antibiotic therapy.

Nutrition and Physical Activity Reasons for the large international differences in the incidence of most cancers are unknown. Studies of rates in migrants have clearly shown that they are largely due to variation in environmental factors, not in genetic predisposition or susceptibility to carcinogens. Correlational studies have been conducted to identify factors that vary across countries in accordance with variations in the rates of various cancers. These studies have shown a variety of dietary components to be related to a number of different neoplasms. To investigate these associations further, many case-control studies and several large cohort studies have been conducted,127,128 a variety of laboratory investigations have been performed to elucidate possible mechanisms for observed epidemiological findings, and randomized trials of dietary supplements or modifications have been conducted or are under way.129–132 Bias in Dietary Studies. Epidemiological studies of diet and cancer are difficult to perform and evaluate for a variety of reasons. One common problem in all epidemiological approaches is that many individual dietary constituents are highly correlated. For example,

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diets that are poor in animal protein are also likely to be poor in animal fat and high in carbohydrates and fiber. Additionally, food frequency questionnaires (FFQs) vary in the type of nutrients emphasized through kinds of foods listed, methodology for food selection, definitions of food groups, nutrients in databases, instructions given to responders relative to serving size estimations, format for completing the questionnaire (self-administered or clinicianadministered), and methodology for quality control (method of contacting the respondent to resolve items left blank). Under such circumstances, it is difficult to determine which of the interrelated dietary constituents (if any) is responsible for observed variations in risk. Another difficulty is that diet many years prior to the development of a neoplasm may be of the greatest etiological relevance and diets may change over time. Such information is difficult (although not impossible) to obtain in case-control studies. Cohort studies can theoretically overcome this problem, but must include large numbers of subjects and must be continued for decades and hence require large commitments of time and money. Despite these methodological problems, results of recent research strongly suggest that dietary factors contribute to the etiology of a variety of neoplasms. Some of the more likely mechanisms are briefly summarized in the following paragraphs. Overview of Risk. When reviewing preventable lifestyle and environmental factors related to cancer, a recent consensus group examined major dietary issues and physical activity.19 They found evidence that low fruit and vegetable intake are associated with cancer of the colon and rectum, stomach, lung, and esophagus. However, low fruit and vegetable consumption is interrelated to dietary fat intake, obesity, and possibly physical inactivity. Being overweight or obese (high body mass index) have been associated with cancer of the corpus uteri, colon and rectum, breast (postmenopausal), gallbladder, and kidney. Obesity is likely also related to physical inactivity which has been associated with breast, colorectal, and prostate cancers.19 The lack of independence among these factors makes understanding true causal associations difficult. Carcinogenic Mechanisms. Food items may be contaminated by preformed carcinogens. Aflatoxins produced by fungi that can grow in grains and other crops in warm, moist climates have been linked to liver cancers in some parts of the world. In China, mutagens have been detected in fermented pancakes and vegetable gruels, and these have been related to both esophageal cancer in humans and neoplasms of the gullet in chickens; and nasopharyngeal carcinomas have been related to consumption of salted fish and fermented food during infancy. Carcinogens may be formed in the body by bacteria. Nitrites may be ingested in small amounts with preserved meats and fish or formed in larger quantities from dietary nitrates, either spontaneously before being eaten or in the presence of bacteria in the body; and carcinogenic N-nitroso compounds may then be produced from ingested amines and nitrites by bacteria in the stomach of people with chronic gastritis, in the bladder of individuals with urinary tract infection, or in the normal colon and mouth to produce cancers of the stomach, bladder, colon, and esophagus, respectively. Smoked and cured foods, charcoal-broiled meats, and some fruits and vegetables from contaminated areas may contain carcinogenic polycyclic aromatic hydrocarbons. A high-fat diet may increase bile production and produce an environment in the large bowel conducive to the growth of bacteria capable of forming carcinogens, and perhaps steroid hormones, from bile salts. Production of such substances provides one plausible explanation for the observed associations between a high-fat diet and cancers of the colon, breast, and prostate. Obesity. Overnutrition, leading to obesity, has been associated with endometrial and postmenopausal breast cancers. A possible mechanism is tumor promotion by excess endogenous estrogens. In postmenopausal women, estrogens are derived from androgens produced by the adrenal gland. This reaction takes place in adipose tissue and is enhanced in obese women. Also, early menarche is a risk factor for

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breast cancer, late menopause is a risk factor for both breast and endometrial cancers, and both of these factors have been directly or indirectly related to overnutrition. Physical Activity. Although the epidemiologic evidence is not completely consistent, regular exercise appears to reduce the risk of breast cancer, perhaps because of the effects of physical activity on body weight. There is also evidence that exercise exerts an independent effect on the risk of colon cancer, possibly by decreasing stool transit time and therefore the duration of exposure to carcinogens in the gut. Protective Dietary Constituents. Dietary constituents may also protect against cancer. Diets high in fresh fruits and raw vegetables have been associated with decreased risks of carcinomas of virtually all sites within the gastrointestinal and respiratory systems, the uterine cervix, and (less consistently) other tissues. Foods rich in retinol (preformed vitamin A) have also been associated with reduced risks of some epithelial cancers. Levels of many of the potentially protective micronutrients are highly correlated in human diets, making it difficult to determine which micronutrients are most strongly associated with reduced risks, and the specific substances in fruits and vegetables responsible for the apparent protective effects have therefore not been conclusively identified. It is likely that different micronutrients or combinations of micronutrients operate at different sites, and a variety of protective mechanisms have been suggested. For example: the reduced risks of stomach and esophageal carcinomas may be due to inhibition by vitamin C of N-nitroso compound formation; vegetables of the Brassicaceae family have been hypothesized to induce activity of mixed-function oxidases, which may detoxify ingested carcinogens responsible for colon cancer development; and vitamins C, E, and b-carotene quench free radicals that cause oxidative damage to DNA. Dietary fiber may increase the bulk of the bowel contents, dilute intraluminal carcinogens, and enhance transit time through the gut. These mechanisms would reduce contact of the colonic mucosa with carcinogens and explain the inverse association between dietary fiber and the risk of colon cancer. Certain plant foods also contain phytoestrogens. These weak estrogens may reduce the risk of hormonally mediated cancers by binding competitively to estrogen receptors and thereby exerting antiestrogenic effects. Although the evidence that a diet high in fruits and vegetables decreases cancer risk has been used as one rationale for marketing vitamin supplements, there is no evidence that such products are protective against any neoplasm, and some evidence that they may even be harmful. For example, a number of studies have linked high fruit and vegetable intake, as well as high serum b-carotene levels, with a reduced risk of lung cancer, but recent clinical trials of b-carotene supplementation in individuals at high risk of lung cancer found increased lung cancer rates among supplemented patients.133 These findings serve as a reminder that our current understanding of the constituents of fruits and vegetables, and their mechanisms of action, is incomplete. Current knowledge suggests that a prudent diet (rather than the average Western diet) should be lower in meats and animal fats and higher in fresh fruits, vegetables, and fiber. Citrus fruits with high levels of vitamin C, vegetables of the Brassicaceae family, and vegetables rich in b-carotene might be of particular importance. Smoked, charred, or cured meats would be avoided or used in moderation, as would alcoholic beverages. Caloric intake would be optimized to avoid obesity. This diet would do no harm, probably reduce the risk of cancers, and be compatible with diets advocated to reduce risks of cardiovascular and cerebrovascular diseases. There is little evidence that supplementation of a prudent diet with vitamins would have a beneficial effect on cancer risk.

Genetic Factors Initial investigations of the role of genetic factors in cancer etiology limited their focus to determining the prevalence and degree of a specific malignancy in family clusters. Such studies suggested that the

risk of a number of cancers, including breast, ovary, colon, kidney, lung, brain, and prostate, was increased in individuals with a history of the disease in a first-degree relative.134 Segregation analysis suggested that for many of these cancer sites one or more rare autosomal genes was associated with increased cancer susceptibility. Recent work has identified a number of these inherited cancers that result from germline mutations (Table 61-6). However, only a small number of cancers are produced by these single gene mutations and it is likely that most of these have been identified by now. The larger proportion of human cancers is due to multiple gene mutations which are much more difficult to identify. Major genetic causes of cancer involve gene-environmental interactions. Inherited mutations in a cancer susceptibility gene predispose the affected individual to develop cancer, usually at an earlier age than occurs in those with nonfamilial causes. Familial retinoblastoma, the prototype of such a condition, arises because an individual inherits a germline mutation in one allele of the Rb gene, which is then followed by a somatic mutation in the other allele.135 Somatic mutations at both alleles of the gene are required to cause the more rare sporadic cases of retinoblastoma. In the Li-Fraumeni syndrome involving the other major tumor suppressor gene, p53, there is a germline p53 mutation in 50% of these individuals which is associated with a greater incidence of rhabdomyosarcoma, any childhood tumor or sarcoma, brain tumors, breast cancer, leukemia, or adenocortical carcinomas.136 Inherited BRCA1 and BRCA2 mutations affect risk of breast and ovarian cancer.137 The overall portion of breast cancers in the general population or a random selection is significantly lower (~5%) than in studies that usually focus on high-risk familial populations where rates are as high as 80%.138 These genes have received intense public attention because breast cancer is a common disease and because the penetrance of the gene is very high, that is, a large proportion of individuals with the gene mutation will develop cancer. Furthermore, there is significant variability in cancer risk among the BRCA1/2 mutation carriers which will preferentially predispose to ovarian rather than breast cancer or the converse. Other factors can modify the BRCA1/2 breast cancer risk including genes at other loci, such as those involved in hormone or carcinogen metabolism, reproductive history, and exogenous exposures such as OCs and smoking. Nonetheless, the prevalence of these germline mutations among women with breast cancer and in the general population is low and accounts for more than a small percent of all breast or ovarian cancers.

TABLE 61-6. GERMLINE MUTATIONS ASSOCIATED WITH FAMILIAL CANCERS Syndrome

Gene

Cancer

Retinomablastoma

RB

Li-Fraumeni

P53

Familial breast, ovary

BRCA1/ BRCA2 ATM

Retinomablastoma, osteoscarcoma Breast, sarcoma, leukemia, brain Breast, Ovary

Ataxia telangiectasia WAGR Familial adenomatious polyposis/Gardner’s syndrome Hereditary Nonpolyposis Colorectal Cancer (HNPCC) Multiple endocrine neoplasia type 1 Von Hippel-Lindau

WT2/WT1 APC

hMSH2, hMLH1, hPMS1, hPMS2 MEN1 VHL

Breast lymphoma, leukemia, others Wilms’ tumor Colon

Colon

Carcinoids, pancreas, parathyroid, pituitary Renal cell carcinoma, hemangioblastoma

61 Additional genes also have been implicated in breast cancer: CKEK2 and ATM. The CHEK2 gene has a moderate penetrance and is independent of the BRCA1/2 mutations. Those who are carriers of the ATM gene have a rare recessive disorder, ataxia-telangiectasia, which greatly increases the risk of breast cancer.139 Approximately 6% of colorectal cancers can be attributed to known heritable germline mutations. Familial adenomatous polyposis (APC) is an autosomal dominant syndrome presenting with hundreds to thousands of adenomatous colorectal polyps that are caused by mutations in the APC gene. Adenomas typically develop in the mid-teens in these patients, and colorectal cancer is almost certain if this condition is untreated. Lynch syndrome (hereditary nonpolyposis colorectal cancer [HNPCC]) is an autosomal dominant disorder characterized by early onset of colorectal cancer with microsatellite instability. Mutations in mismatch repair genes lead to a lifetime colon cancer risk of 85% in these individuals, and carcinomas of the endometrium, ovary, and other organs also occur with increased frequency in association with HNPCC.140 Other familial genes that have been identified are WT1 and WT2, associated with Wilms’ tumor, nephroblastoma, in children with approximately 2% of those with Wilms’ tumor having a family history and most germline WT1 mutations are de novo mutations.141 The incidence is approximately three times higher in African Americans and Africans than in Asians with rates in United States and European Caucasians intermediate between Africans and Asians.142 Those with bilateral tumors have a germline mutation of the gene and tumors arise only if a second event occurs with loss of function of the remaining normal allele. MEN1 (multiple endocrine neoplasia type 1) syndrome is a hereditary condition characterized by the presence of duodeno-pancreatic endocrine tumors and is an autosomally dominant inherited disorder with a high penetrance. It is characterized by the occurrence of tumors of the parathyroid glands, endocrine pancreas/duodenum, and anterior pituitary gland.143 Individuals with Von Hippel Lindau are at risk for the development of tumors of renal carcinoma, as well as cancers of the pancreas, adrenal glands, brain, spine, eye, and ear.144 Although only a small proportion of cancers appear to be caused by inherited mutations at single loci, it is increasingly clear that genetic factors play an important role in tumors. While some individuals exposed to known carcinogens develop cancer, others with similar exposure do not. These risk modifier genes consist of a number of types. First there are genes involved in the metabolism of environmental carcinogens that can modulate exposure to potentially mutagenic occurrences. One of these groups includes inherited polymorphisms in genes that code for enzymes affecting the ability of the body to metabolize or detoxify carcinogens or potential carcinogens. These include those that code for the glutathione S-transferases (GST), cytochrome P-450 enzymes (CYP), and N-acetyltransferases (NAT). Some of the presumed high-risk genotypes are highly prevalent and may contribute substantially to the overall cancer risk within populations. Growth regulation effects associated with bioavailable steroid hormones can be modified by several of the CYP inherited genotypes which may affect those with BRCA1/2 mutations. Among Caucasians, 40–50% have the glutathione S-transferase M1 (GSTM1) null genotype, which appears to confer a several-fold increased risk of lung and bladder cancer and other tumors.

CANCER CONTROL AND PREVENTION

Overview of Known Causes of Cancer Migrant studies have shown that most unknown causes of cancer are environmental. Such factors are likely related to lifestyle which may include such areas as smoking habits, diet, chemical exposures, and infectious agents. Among worldwide deaths, nine modifiable risk factors are estimated to be responsible for just over one-third of cancer deaths.19 The large task of summarizing such data was undertaken by

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TABLE 61-7. PERCENTAGE OF 2001 WORLDWIDE AND 2006 U.S. CANCER DEATHS MOST PROBABLY ATTRIBUTABLE TO VARIOUS CAUSES OF CANCER*

Cause Smoking Alcohol use Low fruit and vegetable intake Human papilloma virus (HPV) Overweight & obesity Physical inactivity Contaminated injections in health-care settings Urban air pollution Indoor smoke from household use of solid fuels Total joint effect

Worldwide Cancer Deaths in 2001

U.S. Cancer Deaths in 2006†

21% 5% 5%

32% 5% 3%

3%

1%

2% 2% 2%

3% 2% 0.1%

1%

1%

0.2% 35%

0% 41%

∗Estimated risk factor population attributable fractions and worldwide death rates based on Danaei et al., 2005.19 † Based on 2006 death rates estimated by the American Cancer Society (Jemal et al., 2006).10

the Comparative Risk Assessment collaborating groups.19 They examined cancer deaths attributable to smoking (along with indoor smoke from fuel use and urban air pollution), alcohol use, low fruit and vegetable intake, human papillomavirus, overweight and obesity, physical inactivity, and contaminated injections in health-care settings. Their worldwide data and their estimates for high-income countries as applied to U.S. data are summarized in Table 61-7.19,145 The potentially modifiable cancer deaths are largely made up of lung cancer (37%), liver cancer (12%), and esophageal cancer (11%) reflecting cancers with higher proportions of deaths related to potentially modifiable risk factors. While many assumptions were made to create these estimates, the estimates highlight areas in which to focus cancer prevention efforts in order to reduce cancer burden. The largest cancer mortality reduction could be seen if smoking was eliminated. These data also highlight how little is known about preventative factors for cancer in general. We know more about prevention for specific cancer sites. Smoking is estimated to cause 21% of cancer worldwide and 29% in high-income countries. Based on site-specific cancer rates due to smoking in high-income countries and estimated 2006 U.S. cancer rates, smoking may cause as much as 32% of cancer in the United States. Overall, these estimates outline the importance of cancer prevention through eliminating smoking in populations. An additional 10% of worldwide deaths are estimated to be due to alcohol and low fruit and vegetable intake (5% each). Other items are related to specific cancer sites, including human papillomavirus and cervical cancer, contaminated injections in health-care settings and liver cancer, and lung cancer with urban air pollution and indoor smoke from household use of solid fuels.19 The American Cancer Society estimates that while a small percentage of all cancer deaths are due to UV exposure, more than one million cases of basal and squamous cell cancers and all 62,190 new cases of melanoma in 2006 are likely due to UV exposure.18 Use of tanning booths and sunbeds adds to this exposure.

Comprehensive Cancer Control Comprehensive cancer control is an integrated and coordinated approach to reducing cancer incidence, morbidity and mortality

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through prevention, early detection, treatment, rehabilitation, and palliation.146 Cancer researchers and practitioners in federal agencies, public health departments, research centers, medical practices, advocacy groups, and other settings are engaged in an ongoing effort to develop and implement a comprehensive approach to cancer prevention and control in the United States.147 This nationwide effort emphasizes the implementation of evidence-based cancer prevention and cancer strategies at the community level. Such an effort is needed to achieve the ambitious national goals to minimize suffering and death from cancer that have been stated by Healthy People 2010 and the American Cancer Society.

Goals for Cancer Reduction In 1999, the American Cancer Society set bold cancer-reduction goals for 2015 for the United States as a challenge.18 The general goals include a 50% reduction in age-adjusted cancer mortality and a 25% reduction in age-adjusted cancer incidence. Their specific objectives include reducing adult tobacco use (to 12%) and youth tobacco use (to 10%), along with increasing consumption of fruits and vegetables (to 75%), physical activity (to 90% of high school students and 60% of adults), school health education, and sun protection (to 75%). The goals also include increasing detection of breast, colorectal, and prostate cancer through screening.18 The American Cancer Society has focused many goals and prevention efforts on youth related to their belief that starting healthy behaviors in youth is linked to health in adults. The 10 leading health indicators for Healthy People 2010 include several related to cancer, including physical activity, obesity, tobacco use, substance abuse, responsible sexual behavior, and access to health care. The goals related to cancer are to reduce the number of new cancer cases as well as the illness, disability, and death caused by cancer. More information can be found on the Healthy People 2010 website at www.healthypeople.gov.

Strategies for Prevention Efforts The following is a summary of actions that can be taken to reduce cancer burden: 1. Develop effective smoking cessation programs and continue to urge all users of tobacco to stop using this substance in any form, and encourage all nonusers not to start (especially the young). 2. Advise use of alcohol in moderation, especially by smokers. 3. Suggest a diet higher in fresh fruits and vegetables (and fiber), and lower in fats and meats than the average American diet. Avoid blackened, charred, or smoked foods. 4. Urge obese individuals to lose weight and others not to become overweight. 5. Encourage regular exercise. 6. Emphasize the risks of sexually transmitted infections. More specifically, caution women that multiple sexual partners (of both themselves and their partners) enhances their risk of cervical and other anogenital cancers. Caution men that receptive sexual practices are associated with anal cancer and AIDS, which can lead to Kaposi’s sarcoma and other malignancies. Suggest use of barrier contraceptives, especially condoms, to reduce risk of infection. 7. Urge individuals to avoid excess exposure to sunlight and all use of tanning beds or booths, especially if they are light skinned and easily sunburned, and recommend protective clothing and sunscreen use. 8. Support efforts to reduce exposures to known carcinogens in the workplace. 9. Support efforts to identify and reduce exposures outside the workplace to known carcinogens such as arsenic, chromium, nickel, vinyl chloride, and asbestos.

10. Mitigate elevated residential radon levels. Use radiation prudently for medical use. 11. When estrogens are prescribed, use the lowest dose necessary to achieve the therapeutic objective and include a progestin in the regimen.

Screening and Secondary Prevention Screening is often considered a secondary prevention through prevention of the progression of a disease to a fatal outcome by means of early detection followed by definitive treatment. Screening is one component of early detection, but requires effective treatment. The American Cancer Society believes that early detection can help save lives and reduce suffering from cancers of the breast, colon, rectum, cervix, prostate, testis (testicles), oral cavity (mouth), and skin by use of physical examinations and available screening tests. Physical examinations may find cancer early by examination of the breast, colon and rectum, prostate, testicles, oral cavity, and skin. Laboratory tests or x-rays include mammography (for breast cancer), the Pap test (for cervical cancer), and the prostate specific antigen (PSA) blood test (for prostate cancer). In many cases a combination approach is most effective. For colorectal cancer, a combination of fecal occult blood testing, flexible sigmoidoscopy, double-contrast barium enema, and colonoscopy are recommended by the American Cancer Society (www.cancer.org) beginning at age 50. Secondary prevention against a cancer can be achieved only if there is a stage of that cancer that is amenable to cure, and if there is a means of detecting the cancer at that stage.

Planning a Screening Program A number of factors must be considered before initiating a screening program:148,149 1. The sensitivity and specificity of the tests or procedures used for screening: The number of diseased people that will be missed (false negatives) increases as the sensitivity of the test decreases, and the number of well people that will erroneously be considered possibly diseased (false positives) increases as the specificity of the test decreases. 2. The target population: Individuals at highest risk for the disease should be identified, and special efforts should be made to screen such persons. 3. The prevalence of the disease in the target population: For any test of given sensitivity and specificity, numbers of false-positive and false-negative tests are functions of the prevalence of the disease in the target population. More falsenegative tests occur if the disease is common, and more falsepositives if the disease is rare. The latter is of particular importance in screening for cancer. 4. The predictive value of a positive test: This is the proportion of individuals with a positive test who actually have the disease. This proportion declines only slightly as test sensitivity decreases, but declines markedly as test specificity declines. In addition, the predictive value of a positive test declines as the prevalence of the disease diminishes. For example, if we have a test of high sensitivity (e.g., 95%) and high specificity (e.g., 98%), and if the prevalence of the cancer in the target population is 1 per 1000, then only 4.6% of the individuals with a positive test will actually be found to have the disease on further evaluation. The rest will have a false-positive test. 5. The consequences of false-positive tests: A false-positive test is a false alarm. The consequences of this for the individual, the medical care system, and the screening program must be considered. How much inconvenience or psychological trauma will the individual erroneously screened have to bear? Are there sufficient facilities and personnel to provide the necessary diagnostic tests to determine who actually has the disease? What are the costs of these services and who will pay them? Is morbidity associated with further testing

61

6.

7.

8.

9.

10.

11.

(such as biopsies of the breast) acceptable? Do physicians want to have referred to them large numbers of healthy people for diagnostic evaluation? Will possible adverse reactions to the screening program by those falsely screened positive or their physicians have a negative impact on the screening program itself? Consequences of a false-negative test: A false-negative test gives the person screened a false sense of security, and the neoplasm may then progress to a noncurable stage and kill the patient. This could have medical-legal implications, particularly if a more sensitive test could have been used. One missed case can result in unfavorable publicity that can have an adverse impact on the screening program. Applicability of the test: Can the test be administered to the people in the target population? Are special equipment or special resources needed (e.g., electrical power, water, a mobile van, transportation for the potential screenees)? Can the test be administered rapidly? Acceptability of the test: Having made the test available to people in the target population, will the people agree to be screened? What kind of publicity should be given? Are there esthetic or cultural barriers? Is the cost to those being screened acceptably low? Adverse consequences of the test: Is there a possibility that the test will do harm? This issue had originally been a great concern in using mammography to screen for breast cancer. The breast is a radiosensitive organ, high doses of ionizing radiation are known to cause breast cancer, and early mammographic techniques resulted in considerable levels of exposure. This controversy had an adverse impact on breast cancer screening programs, with many women fearing mammography. Similar problems should be anticipated with any future radiographic screening techniques. Life expectancy: Is the individual’s life expectancy longer than the time gained by early screening of asymptomatic individuals? This issue is a concern in screening men over age 75 with PSA for prostate cancer. Older men with no symptoms may die of other causes before a nonsymptomatic prostate cancer grows into a fatal cancer. Thus, it may not be ethical to tell an older man who is more likely to die of other causes that he also has a small prostate cancer. The evaluability of the program: Public and private resources are all too often spent on service programs that are never evaluated, and program evaluators are all too often called upon to assist in program evaluation after a project is fully under way or even completed. The time to begin program evaluation is when the program is being planned.

Evaluation of Methods of Screening and Secondary Prevention The aim of secondary prevention is the prevention of fatal outcome. This implies that a method of secondary prevention of a disease should reduce mortality from that disease, and reduction in mortality should be the measure used to evaluate the method. This is not always done. Two other forms of evaluation have commonly been used, both of which can give misleading results. One of these is the comparison of cases detected at screening with cases detected by other means, with respect to their stage at diagnosis. It is not surprising that those detected at screening tend to be at a less advanced stage. This does not indicate whether the early detection altered the course of the disease, however. This method of evaluation is based on the assumptions that early lesions have the same natural history as symptomatic lesions and that treatment of early lesions alters the course of the disease. Neither assumption is necessarily correct. For example, not all carcinomas in situ of the uterine cervix progress to invasive disease, and individuals with early lung cancer detected at screening with chest x-rays do not have a more favorable prognosis than persons with lung cancer diagnosed later after development of symptoms.

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The other misleading method of evaluating secondary prevention is by comparing survival rates, or time to death, in cases detected at screening and cases detected by other means. There are two problems with this method. One is that the time from diagnosis to death may be longer for individuals who have been screened, not because their death is postponed but only because their disease is diagnosed earlier. This is referred to as lead-time bias. The other problem is known as length-bias sampling and results from the fact that neoplasms grow at varying rates: at any point in time (when screening is performed), there will exist more tumors that are progressing slowly than rapidly. Therefore, compared to tumors in symptomatic cases, a higher proportion of tumors detected at screening will be slow growing, so that survival from time of detection will tend to be longer in screened than symptomatic patients, even if early detection does not result in a prolongation of time to death. Because of the problems of lead-time and length-bias sampling, there is no way of knowing from a comparison of survival rates or survival times whether a secondary prevention program results in a prolonging of life. This can be done only by comparing risks of dying (or risks of advanced disease as a surrogate for mortality) in screened and unscreened individuals. Individuals who volunteer to be screened may differ from those who do not with respect to factors related to risk of death, and these factors must be taken into consideration when comparing mortality rates in screened and unscreened persons. This can be done in two ways: It is preferable to conduct a randomized trial of the secondary prevention method to be evaluated. The other method is to control statistically for differences between the screened and unscreened during data analysis. A classic example of a randomized trial of a procedure for secondary prevention is the study of mammography conducted among members of the Health Insurance Plan (HIP) in New York.150 In 1963, approximately 62,000 women between the ages of 40 and 64 were randomly allocated to one of two groups. Approximately half were offered a series of four annual screenings by mammography and breast palpation (the experimental group). The other half served as a control group and received their usual medical care. Not all women in the experimental group agreed to participate. To eliminate a possible bias due to the remainder being volunteers, the mortality rate due to breast cancer in the entire experimental group was compared to the breast cancer mortality rate in the control group. Inclusion of those not screened in the experimental group gave a conservative estimate of the impact of the program on breast cancer mortality, which represented a combined evaluation of the efficacy and the acceptability of the screening procedures. After 5 years of follow-up, in women in their 50s there was over a 50% reduction in mortality from breast cancer; breast cancer mortality was reduced by one-third in women older than 50. Although there was no beneficial effect on breast cancer mortality in women under 50 after 5 years, follow-up for 18 years showed a small reduction in mortality from breast cancer in these women as well. This observation demonstrates the importance of long-term follow-up in studies of secondary prevention. Once a screening technique is widely believed to be useful, regardless of whether or not it has been rigorously tested, a randomized trial becomes ethically questionable and operationally impossible. Other less satisfactory methods of evaluation must then be used. This is exemplified by the Pap smear for early detection of cervical cancer. When this technique was first introduced, it was greeted with such enthusiasm that suggestions for a randomized trial were not taken. The need to evaluate this procedure subsequently became evident, but by then it was too late for a randomized trial. As a result, a large number of less satisfactory epidemiological studies have been conducted to attempt to measure the effectiveness of the Pap smear.151 Correlational studies have shown that mortality rates from cervical cancer in many populations have declined following the introduction of screening programs, that the magnitude of the decline is correlated with the amount of screening, and that the decline within some of the populations was greatest in those racial and age groups that received the most screening. Case-control studies of women with

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invasive cervical cancer have shown that, compared with normal control subjects, fewer of the cases had prior Pap smears; and a cohort study showed, after controlling for socioeconomic differences between women who enrolled in a screening program and women who did not, that there was a decline in cervical cancer mortality rates in the screened women compared to an increase in rates in those not screened. None of these methods to evaluate the Pap smear are as satisfactory as a randomized trial would have been, although in the aggregate they do provide strong evidence that the procedure reduces mortality.

Current Status of Secondary Prevention of Selected Cancers

Colorectal Cancer Fecal occult blood testing (FOBT) and sigmoidoscopy are both used to screen for colorectal cancer. Randomized trials have suggested that use of FOBT leads to a reduction in colon cancer mortality.160,161 Screening guidelines for colorectal cancer recommend annual FOBT or sigmoidoscopy for individuals age 50 and older, but suggest that evidence is insufficient to determine which test is more effective or whether the use of both tests together would produce additional reductions in mortality.162 However, the level of reduction conferred by FOBT is small, and a large proportion of positive tests are false positives, resulting in many unnecessary clinical follow-up evaluations. The cost-benefit ratio of this procedure is therefore low, as is its acceptability, given the aversion that some people have to fecal testing.

Breast Cancer

Prostate Cancer

Mammographic screening in women over age 50 years has clearly been shown in multiple randomized trials to reduce subsequent mortality from breast cancer by 30–40%,152 and annual mammograms beginning at age 50 are generally recommended. Eight randomized trials of mammography in women 40–49 years of age at entry into the trial have yielded inconsistent results, with none showing a statistically significant reduction in breast cancer mortality after 5–18 years of follow-up. Meta-analyses of data from these trials have yielded different results due to varying lengths of follow-up or methodological concerns about exclusion of some studies. However, meta-analyses with longer follow-up periods show a reduction in risk of dying from breast cancer.153 Mammography may be less efficacious in women under age 50 than in older women because breast tissue of women under age 50 is radiographically more dense than that of older women, and early neoplasms are more difficult to visualize on mammographic films. Also, relatively fewer malignancies and more benign lesions occur in younger women, resulting in more falsepositive screenings. Despite the lack of consistent scientific evidence,154 in 1997 NCI recommended mammographic screening for women in their 40s.155 Nevertheless, there is currently no consensus among experts regarding mammographic screening in women under age 50. Physical examination of the breast by a medical practitioner has been shown to result in the detection of some malignancies missed by mammography and may therefore be of value as a screening modality in conjunction with mammographic screening. Tumors detected by physical examination or by women practicing breast selfexamination have been shown in some studies to be less advanced at diagnosis than symptomatic cancers, but the efficacy of these procedures as primary screening modalities in reducing mortality from breast cancer has not been demonstrated. Randomized trials of breast self-examination have shown no benefit.156,157 Indirect evidence suggests clinical examination of the breast is an important means of averting some breast cancer deaths.156

PSA has been widely incorporated into medical practice as a screening test for prostate cancer and has resulted in an apparent increase in prostate cancer incidence rates in the early 1990s with a suggestion of a reduction in prostate cancer mortality.163 Although PSA testing may prevent deaths by identifying tumors at a treatable stage, there is concern that the test may also identify tumors that would have remained clinically irrelevant during the remainder of a patient’s lifetime and thereby may lead men to undergo invasive and potentially unnecessary treatment. The American Cancer Society recommends annual PSA screening in conjunction with digital rectal examination in men ages 50 and over who are expected to live at least 10 more years, but the screening guidelines from the United States Preventive Health Services Task Force recommend against routine screening by PSA.162,164 This disagreement will not be resolved without substantial further research.

Cervical Cancer Cancer of the cervix has also been clearly shown to be amenable to secondary prevention. Results of a critical review of cytologic screening for cervical cancer were published in 1986.158,159 By combining data from 10 screening programs in eight countries, it was shown that two negative cytologic smears were more effective than one in reducing mortality from cervical cancer (presumably because of a reduction in false-negative diagnoses) and that the protective effect did not decline until 3 years after a second negative smear. Based on these findings, it is recommended that screening for cervical cancer every 3 years is sufficient after a woman has had two normal smears. Some women, however, do develop invasive disease soon after an apparently normal smear, and studies are needed to determine what proportion of such events are a result of prior false-negative smears and how many represent a rapidly progressing form of the disease. This recommendation also does not take into consideration the benefits of an annual appointment, thus it is suspected that women also will not receive an annual pelvic or breast examine or referral for an annual mammogram or assessment for osteoporosis. Furthermore, this recommendation does not consider that many women utilize gynecologists as their routine physician.

Other Cancers A variety of other techniques has been developed for the early detection of cancer. Some have not been rigorously evaluated, and some that have do not show great promise. Studies in industrial settings of urinary cytology for bladder cancer have not yielded encouraging results, and although NCI guidelines recommend oral examination by medical practitioners to screen for oral cancer, the effectiveness of the technique is questionable because of the poor compliance of those individuals at highest risk of the disease.165 The vagueness of clinical symptoms of gastric (stomach) cancer is the major reason patients do not get diagnosed until the cancer has progressed. Current diagnostic modalities consist of endoscopy, which is the most sensitive and specific method for obtaining a definitive diagnosis. It has replaced barium contrast radiographs due to its ability to biopsy and its ability to directly visualize the lesions. Endoscopy has a sensitivity of 98% versus 14% for barium in the early diagnosis of most types of gastric cancer.166,167 Administration of antibiotics against H. pylori have also shown a significant reduction in the incidence of gastric cancer.168 Various screening trials are ongoing in Japan where incidence rates are high.169,170 The disease is sufficiently rare in the United States that large-scale screening is not recommended. Alpha-fetoprotein (AFP) blood levels have been used to screen for primary hepatocellular carcinoma (liver cancer) in individuals serologically positive for hepatitis B surface antigen (HBSAg) in areas where hepatitis B is endemic and liver cancer highly prevalent. A study from China showed improved survival in asymptomatic persons with small tumors detected by this method, but studies to determine whether it reduces mortality from liver cancer have not been completed. Several methods of screening for chronic liver disease include ultrasound, CT scans (computer tomography), MRI (magnetic resonance imaging), angiography, laparoscopy, biopsy, and AFP. Ultrasound is highly specific but not sufficiently sensitive to detect hepatocellular carcinoma or to support its use in an effective surveillance program when a cut-off value of 20 ng/mL is used to differentiate hepatocellular carcinoma from HCV-infected individuals (80–94% specificity and 41–65% sensitivity).171 Use of CT and MRI as an early diagnostic tool in patients with underlying liver cirrhosis who are at high risk of hepatocellular carcinoma is still unclear. It

61 appears that both ultrasound and preferentially MRI would provide greater sensitivity as a screening test.172 Angiography is an x-ray that tends to be uncomfortable, while laparoscopy is a surgical incision of a tube. Thus neither is used for population screening. AFP has limited utility in differentiating hepatocellular carcinoma from benign hepatic disorders because of its high false-positive and falsenegative rates. Serum AFP-3 (one of the three glycoforms of AFP) and DCP (des-gamma-carboxyprothrombin) are other widely used tumor markers for hepatocellular carcinoma and appear to be more sensitive than AFP in differentiating hepatocellular carcinoma from nonmalignant hepatology. Despite considerable interest in the development of ovarian cancer screening using transvaginal ultrasonography or the circulating tumor marker CA-125, neither method is clearly associated with reduced mortality from this disease.173 Improved cancer screening must be a part of any long-term strategy to reduce cancer mortality. These efforts must include both the evaluation of new screening methods and research into the most effective ways to implement the techniques that are of demonstrated benefit. The American Cancer Society believes that early detection is warranted for cancers of the breast, colon, rectum, cervix, prostate, testis, oral cavity, and skin. More information on site-specific recommendations can be found at www.cancer.org.

10. 11.

12.

13.

14.

15.

16.

Cancer Survivorship The National Cancer Institute’s SEER program estimates there are 10.5 million invasive cancer survivors in the United States as of 2003.4 This number is increasing primarily as a result of earlier diagnoses and more effective therapies. This has created a new challenge in comprehensive cancer control that has been recognized in three recent national reports.174–176 Concerns of cancer survivors and their families can include long-term physical, psychosocial, and economic effects of treatment as well as rehabilitation and palliation. Care of these survivors and their families can involve the entire spectrum of comprehensive cancer control from prevention to early detection, treatment, rehabilitation, and palliation.177 To effectively address the needs of this growing population will require a coordinated approach among health-care providers, policymakers, researchers, insurers, advocates, communities, and families. REFERENCES

1. World Health Organization. International Statistical Classification of Diseases and Related Health Problems. 10th revision, ed. Geneva: World Health Organization, 1992. 2. Fritz AG. International Classification of Diseases for Oncology: ICD-O. 3rd ed. Geneva: World Health Organization, 2000. 3. Coleman MP, Esteve J, Damiecki P, et al. Trends in cancer incidence and mortality. IARC Sci Publ. 1993;(121):1–806. 4. Ries L, Harkins D, Krapcho M, et al. SEER Cancer Statistics Review, 1975–2003. Bethesda, MD: National Cancer Institute, 2006. 5. Edwards BK, Brown ML, Wingo PA, et al. Annual report to the nation on the status of cancer, 1975–2002, featuring populationbased trends in cancer treatment. J Natl Cancer Inst. 2005;97(19): 1407–27. 6. U.S. Cancer Statistics Working Group. United States Cancer Statistics: 2002 Incidence and Mortality. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Cancer Institute, 2005. 7. Cancer incidence in five continents. Volume VIII. IARC Sci Publ. 2002;(155):1–781. 8. Bleyer A, O’Leary M, Barr R, Ries LAG, eds. Cancer Epidemiology in Older Adolescents and Young Adults 15 to 29 Years of Age: Including Seer Incidence and Survival, 1975–2000. Bethesda, MD: National Cancer Institute, NIH Pub. No. 06-5767;2006. 9. Singh GK. National Cancer Institute (U.S.). Area Socioeconomic Variations in U.S. Cancer Incidence, Mortality, Stage, Treatment,

17. 18. 19.

20. 21.

22.

23.

24.

25.

26.

27. 28. 29.

Cancer

1065

and Survival, 1975–1999. NIH publication ; no. 03-5417. Bethesda, MD: U.S. Dept. of Health and Human Services, National Institutes of Health, National Cancer Institute, 2003. Jemal A, Siegel R, Ward E, et al. Cancer statistics. CA Cancer J Clin. 2006;56(2):106–30. Cancer trends progress report-2005 update. http://progressreport. cancer.gov. National Cancer Institute, National Institute of Health, Department of Health and Human Services, 2005. Shibuya K, Mathers CD, Boschi-Pinto C, et al. Global and regional estimates of cancer mortality and incidence by site: II. Results for the global burden of disease 2000. BMC Cancer. 2002;2:37. Kolonel L, Wilkens L. Migrant studies. In: Schottenfeld D, Fraumeni J, eds. Cancer Epidemiology and Prevention. 3rd ed. New York: Oxford University Press, 2006. Miller BA, Kolonel LN. National Cancer Institute (U.S.). Cancer Control Research Program. Racial/Ethnic Patterns of Cancer in the United States, 1988–1992. NIH publication; no. 96-4104. [Washington, D.C.]: U.S. Department of Health and Human Services, National Institute of Health, 1996. Berry DA, Cronin KA, Plevritis SK, et al. Effect of screening and adjuvant therapy on mortality from breast cancer. N Engl J Med. 2005;353(17):1784–92. Nowell PC. The clonal evolution of tumor cell populations. Science. 1976;194(4260):23–8. Chen YC, Hunter DJ. Molecular epidemiology of cancer. CA Cancer J Clin. 2005;55(1):45–54; quiz 57. American Cancer Society. Cancer Prevention and Early Detection Facts & Figures 2006. Atlanta: American Cancer Society, 2006. Danaei G, Vander Hoorn S, Lopez AD, et al. Causes of cancer in the world: comparative risk assessment of nine behavioural and environmental risk factors. Lancet. 2005;366(9499):1784–93. Vineis P, Alavanja M, Buffler P, et al. Tobacco and cancer: recent epidemiological evidence. J Natl Cancer Inst. 2004;96(2):99–106. Sasco AJ, Secretan MB, Straif K. Tobacco smoking and cancer: a brief review of recent epidemiological evidence. Lung Cancer. 2004;45 Suppl 2:S3–9. U.S. Department of Health and Human Services. Targeting Tobacco Use: The Nation’s Leading Cause of Death. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 2003. U.S. Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. Rockville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Heineman EF, Zahm SH, McLaughlin JK, et al. Increased risk of colorectal cancer among smokers: results of a 26-year follow-up of U.S. veterans and a review. Int J Cancer. 1995;59(6):728–38. United States Advisory Committee to the Surgeon General, United States. Public Health Service. The Health Consequences of Using Smokeless Tobacco: A Report of the Advisory Committee to the Surgeon General. NIH publication, No. 86-2874. Bethesda, MD.: U.S. Dept. of Health and Human Services, Public Health Service, 1986. U.S. Department of Health and Human Services. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention, Health Promotion, Office on Smoking and Health, 2006. Thomas DB. Alcohol as a cause of cancer. Environ Health Perspect. 1995;103Suppl 8:153–60. Altieri A, Garavello W, Bosetti C, et al. Alcohol consumption and risk of laryngeal cancer. Oral Oncol. 2005;41(10):956–65. Overall evaluations of carcinogenicity: an updating of IARC Monographs volumes 1 to 42. IARC Monogr Eval Carcinog Risks Hum Suppl. 1987;7:1–440.

1066

Noncommunicable and Chronic Disabling Conditions

30. Some organic solvents, resin monomers and related compounds, pigments and occupational exposures in paint manufacture and painting. IARC Monogr Eval Carcinog Risks Hum. 1989;47: 1–442. 31. Chromium, nickel and welding. IARC Monogr Eval Carcinog Risks Hum. 1990;49:1–648. 32. Occupational exposures to mists and vapours from strong inorganic acids and other industrial chemicals. Working Group views and expert opinions, Lyon, 15–22 October, 1991. IARC Monogr Eval Carcinog Risks Hum. 1992;54:1–310. 33. IARC working group on the evaluation of carcinogenic risks to humans: occupational exposures of hairdressers and barbers and personal use of hair colourants; some hair dyes, cosmetic colourants, industrial dyestuffs and aromatic amines. Proceedings. Lyon, France, 6–13 October, 1992. IARC Monogr Eval Carcinog Risks Hum. 1993;57:7–398. 34. Beryllium, cadmium, mercury, and exposures in the glass manufacturing industry. Working Group views and expert opinions, Lyon, 9–16 February, 1993. IARC Monogr Eval Carcinog Risks Hum. 1993;58:1–415. 35. IARC working group on the evaluation of carcinogenic risks to humans: some industrial chemicals. Lyon, 15–22 February, 1994. IARC Monogr Eval Carcinog Risks Hum. 1994;60:1–560. 36. Wood dust. IARC Monogr Eval Carcinog Risks Hum. 1995;62: 35–215. 37. Formaldehyde. IARC Monogr Eval Carcinog Risks Hum. 1995;62: 217–375. 38. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: Polychlorinated Dibenzo-Para-Dioxins and Polychlorinated Dibenzofurans. Lyon, France, 4–11 February, 1997. IARC Monogr Eval Carcinog Risks Hum. 1997;69:1–631. 39. Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxy-2-propanol. IARC Monogr Eval Carcinog Risks Hum. In preparation. 40. Doll R. Epidemiological evidence of the effects of behaviour and the environment on the risk of human cancer. Recent Results Cancer Res. 1998;154:3–21. 41. Doll R, Peto R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst. 1981;66(6):1191–308. 42. Peto J. Cancer epidemiology in the last century and the next decade. Nature. 2001;411(6835):390–5. 43. Vineis P, Forastiere F, Hoek G, et al. Outdoor air pollution and lung cancer: recent epidemiologic evidence. Int J Cancer. 2004;111(5): 647–52. 44. Cohen AJ. Outdoor air pollution and lung cancer. Environ Health Perspect. 2000;108 Suppl 4:743–50. 45. Boice J. Ionizing radiation. In: Schottenfeld D, Fraumeni J, eds. Cancer Epidemiology and Prevention. 3rd ed. New York: Oxford University Press, 2006. 46. Ionizing radiation, part 2: Some internally deposited radionuclides. Views and expert opinions of an IARC working group on the evaluation of carcinogenic risks to humans. Lyon, 14–21 June, 2000. IARC Monogr Eval Carcinog Risks Hum. 2001;78(Pt 2):1–559. 47. IARC Working group on the evaluation of carcinogenic risks to humans: ionizing radiation, Part I, X- and gamma- radiation and neutrons. Lyon, France, 26 May–2 June, 1999. IARC Monogr Eval Carcinog Risks Hum. 2000;75 Pt 1:1–448. 48. UNSCEAR 2000. The United Nations Scientific Committee on the Effects of Atomic Radiation. Health Phys. 2000;79(3):314. 49. Krewski D, Lubin JH, Zielinski JM, et al. A combined analysis of North American case-control studies of residential radon and lung cancer. J Toxicol Environ Health A. 2006;69(7):533–97. 50. Darby S, Hill D, Deo H, et al. Residential radon and lung cancer— detailed results of a collaborative analysis of individual data on 7148 persons with lung cancer and 14,208 persons without lung cancer from 13 epidemiologic studies in Europe. Scand J Work Environ Health. 2006;32 Suppl 1:1–83.

51. National Research Council (U.S.). Committee on Health Risks of Exposure to Radon. Health Effects of Exposure to Radon. Washington, D.C.: National Academy Press, 1999. 52. Travis LB, Rabkin CS, Brown LM, et al. Cancer survivorship— genetic susceptibility and second primary cancers: research strategies and recommendations. J Natl Cancer Inst. 2006;98(1):15–25. 53. Van Leeuwen FE, Travis LB. Second Cancers. In: DeVita VT, Hellman S, Rosenberg SA, eds. Cancer, Principles & Practice of Oncology. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2001;2939–296. 54. Brenner DJ, Doll R, Goodhead DT, et al. Cancer risks attributable to low doses of ionizing radiation: assessing what we really know. Proc Natl Acad Sci U S A. 2003;100(24):13761–6. 55. Armstrong BK. Epidemiology of malignant melanoma: intermittent or total accumulated exposure to the sun? J Dermatol Surg Oncol. 1988;14(8):835–49. 56. Armstrong BK, Kricker A, English DR. Sun exposure and skin cancer. Australas J Dermatol. 1997;38 Suppl 1:S1–6. 57. Wester U, Boldemann C, Jansson B, et al. Population UV-dose and skin area—do sunbeds rival the sun? Health Phys. 1999;77(4):436–40. 58. Feychting M, Ahlbom A, Kheifets L. EMF and health. Annu Rev Public Health. 2005;26:165–89. 59. Ahlbom IC, Cardis E, Green A, et al. Review of the epidemiologic literature on EMF and Health. Environ Health Perspect. 2001;109 Suppl 6:911–33. 60. Heath CW, Jr. Electromagnetic field exposure and cancer: a review of epidemiologic evidence. CA Cancer J Clin. 1996;46(1): 29–44. 61. Washburn EP, Orza MJ, Berlin JA, et al. Residential proximity to electricity transmission and distribution equipment and risk of childhood leukemia, childhood lymphoma, and childhood nervous system tumors: systematic review, evaluation, and meta-analysis. Cancer Causes Control. 1994;5(4):299–309. 62. Colton T, Greenberg ER, Noller K, et al. Breast cancer in mothers prescribed diethylstilbestrol in pregnancy. Further follow-up. JAMA. 1993;269(16):2096–100. 63. Vessey MP, Fairweather DV, Norman-Smith B, et al. A randomized double-blind controlled trial of the value of stilboestrol therapy in pregnancy: long-term follow-up of mothers and their offspring. Br J Obstet Gynaecol. 1983;90(11):1007–17. 64. Greenberg ER, Barnes AB, Resseguie L, et al. Breast cancer in mothers given diethylstilbestrol in pregnancy. N Engl J Med. 1984;311(22):1393–8. 65. Collaborative Group on Hormonal Factors in Breast Cancer, ICRF Cancer Epidemiology Unit, Radcliffe Infirmary, Oxford, UK. Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53,297 women with breast cancer and 100,239 women without breast cancer from 54 epidemiological studies. Lancet. 1996;347(9017):1713–27. 66. Skegg DC, Noonan EA, Paul C, et al. Depot medroxyprogesterone acetate and breast cancer. A pooled analysis of the World Health Organization and New Zealand studies. JAMA. 1995;273(10):799–804. 67. Nelson HD. Assessing benefits and harms of hormone replacement therapy: clinical applications. JAMA. 2002;288(7):882–4. 68. Ewertz M. Hormone therapy in the menopause and breast cancer risk—a review. Maturitas. 1996;23(2):241–6. 69. Breast cancer and hormone replacement therapy: collaborative reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women without breast cancer. Collaborative Group on Hormonal Factors in Breast Cancer. Lancet. 1997;350(9084):1047–59. 70. Colditz GA. Relationship between estrogen levels, use of hormone replacement therapy, and breast cancer. J Natl Cancer Inst. 1998;90(11):814–23. 71. Toniolo PG, Levitz M, Zeleniuch-Jacquotte A, et al. A prospective study of endogenous estrogens and breast cancer in postmenopausal women. J Natl Cancer Inst. 1995;87(3):190–7.

61 72. Key TJ, Appleby PN, Reeves GK, et al. Body mass index, serum sex hormones, and breast cancer risk in postmenopausal women. J Natl Cancer Inst. 2003;95(16):1218–26. 73. Key T, Appleby P, Barnes I, et al. Endogenous sex hormones and breast cancer in postmenopausal women: reanalysis of nine prospective studies. J Natl Cancer Inst. 2002;94(8):606–16. 74. Cook L, Weiss N, Doherty J, et al. Endometrial Cancer. In: Schottenfeld D, Fraumeni J, eds. Cancer Epidemiology and Prevention. 3rd ed. New York: Oxford University Press, 2006. 75. Weiss N. Epidemiology of endometrial cancer. In: Lilienfeld A, ed. Reviews in Epidemiology. Vol. 2. New York: Elsevier, 1983. 76. Prentice RL, Thomas DB. On the epidemiology of oral contraceptives and disease. Adv Cancer Res. 1987;49:285–301. 77. Depot-medroxyprogesterone acetate (DMPA) and risk of endometrial cancer. The WHO Collaborative Study of Neoplasia and Steroid Contraceptives. Int J Cancer. 1991;49(2):186–90. 78. Curtis RE, Boice JD, Jr, Shriner DA, et al. Second cancers after adjuvant tamoxifen therapy for breast cancer. J Natl Cancer Inst. 1996;88(12):832–4. 79. Kaaks R, Lukanova A, Kurzer MS. Obesity, endogenous hormones, and endometrial cancer risk: a synthetic review. Cancer Epidemiol Biomarkers Prev. 2002;11(12):1531–43. 80. Zeleniuch-Jacquotte A, Akhmedkhanov A, Kato I, et al. Postmenopausal endogenous oestrogens and risk of endometrial cancer: results of a prospective study. Br J Cancer. 2001;84(7): 975–81. 81. Potischman N, Hoover RN, Brinton LA, et al. Case-control study of endogenous steroid hormones and endometrial cancer. J Natl Cancer Inst. 1996;88(16):1127–35. 82. Riman T, Nilsson S, Persson IR. Review of epidemiological evidence for reproductive and hormonal factors in relation to the risk of epithelial ovarian malignancies. Acta Obstet Gynecol Scand. 2004;83(9):783–95. 83. Modan B, Hartge P, Hirsh-Yechezkel G, et al. Parity, oral contraceptives, and the risk of ovarian cancer among carriers and noncarriers of a BRCA1 or BRCA2 mutation. N Engl J Med. 2001;345(4): 235–40. 84. Narod SA, Risch H, Moslehi R, et al. Oral contraceptives and the risk of hereditary ovarian cancer. Hereditary Ovarian Cancer Clinical Study Group. N Engl J Med. 1998;339(7):424–8. 85. Garg PP, Kerlikowske K, Subak L, et al. Hormone replacement therapy and the risk of epithelial ovarian carcinoma: a meta-analysis. Obstet Gynecol. 1998;92(3):472–9. 86. Lacey JV, Jr, Mink PJ, Lubin JH, et al. Menopausal hormone replacement therapy and risk of ovarian cancer. JAMA. 2002;288(3):334–41. 87. Lukanova A, Lundin E, Toniolo P, et al. Circulating levels of insulin-like growth factor-I and risk of ovarian cancer. Int J Cancer. 2002;101(6):549–54. 88. Human papillomaviruses. IARC Monogr Eval Carcinog Risks Hum. 1995;64. 89. Smith EM, Ritchie JM, Levy BT, et al. Prevalence and persistence of human papillomavirus in postmenopausal age women. Cancer Detect Prev. 2003;27(6):472–80. 90. Lacey JV, Jr., Brinton LA, Barnes WA, et al. Use of hormone replacement therapy and adenocarcinomas and squamous cell carcinomas of the uterine cervix. Gynecol Oncol. 2000;77(1):149–54. 91. Thomas D. Exogenous steroid hormones and hepatocellular carcinoma. In: Tablr E, DiBiceglie A, Purcell R, eds. Etiology, Pathology, and Treatment of Hepatocellular Carcinoma in North America. Advances in Applied Biotechnology Series. Vol. 13. Houston: Gulf Publishing Company, 1990;77–89. 92. Herbst AL, Ulfelder H, Poskanzer DC. Adenocarcinoma of the vagina. Association of maternal stilbestrol therapy with tumor appearance in young women. N Engl J Med. 1971;284(15):878–81. 93. Melnick S, Cole P, Anderson D, et al. Rates and risks of diethylstilbestrolrelated clear-cell adenocarcinoma of the vagina and cervix. An update. N Engl J Med. 1987;316(9):514–6.

Cancer

1067

94. Fernandez E, La Vecchia C, Franceschi S, et al. Oral contraceptive use and risk of colorectal cancer. Epidemiology. 1998;9(3): 295–300. 95. Hannaford P, Elliott A. Use of exogenous hormones by women and colorectal cancer: evidence from the Royal College of General Practitioners’ Oral Contraception Study. Contraception. 2005;71(2): 95–8. 96. Martinez ME, Grodstein F, Giovannucci E, et al. A prospective study of reproductive factors, oral contraceptive use, and risk of colorectal cancer. Cancer Epidemiol Biomarkers Prev. 1997;6(1):1–5. 97. Pfahlberg A, Hassan K, Wille L, et al. Systematic review of casecontrol studies: oral contraceptives show no effect on melanoma risk. Public Health Rev. 1997;25(3–4):309–15. 98. Karagas MR, Stukel TA, Dykes J, et al. A pooled analysis of 10 case-control studies of melanoma and oral contraceptive use. Br J Cancer. 2002;86(7):1085–92. 99. Gann PH, Hennekens CH, Ma J, et al. Prospective study of sex hormone levels and risk of prostate cancer. J Natl Cancer Inst. 1996;88(16):1118–26. 100. English PB, Goldberg DE, Wolff C, et al. Parental and birth characteristics in relation to testicular cancer risk among males born between 1960 and 1995 in California (United States). Cancer Causes Control. 2003;14(9):815–25. 101. Strohsnitter WC, Noller KL, Hoover RN, et al. Cancer risk in men exposed in utero to diethylstilbestrol. J Natl Cancer Inst. 2001;93(7):545–51. 102. Coupland CA, Chilvers CE, Davey G, et al. Risk factors for testicular germ cell tumours by histological tumour type. United Kingdom Testicular Cancer Study Group. Br J Cancer. 1999;80(11): 1859–63. 103. Weir HK, Kreiger N, Marrett LD. Age at puberty and risk of testicular germ cell cancer (Ontario, Canada). Cancer Causes Control. 1998;9(3):253–8. 104. Titus-Ernstoff L, Perez K, Cramer DW, et al. Menstrual and reproductive factors in relation to ovarian cancer risk. Br J Cancer. 2001;84(5):714–21. 105. Whiteman DC, Siskind V, Purdie DM, et al. Timing of pregnancy and the risk of epithelial ovarian cancer. Cancer Epidemiol Biomarkers Prev. 2003;12(1):42–6. 106. Riman T, Dickman PW, Nilsson S, et al. Risk factors for invasive epithelial ovarian cancer: results from a Swedish case-control study. Am J Epidemiol. 2002;156(4):363–73. 107. Cooper GS, Schildkraut JM, Whittemore AS, et al. Pregnancy recency and risk of ovarian cancer. Cancer Causes Control. 1999;10(5):397–402. 108. Pike MC, Pearce CL, Wu AH. Prevention of cancers of the breast, endometrium and ovary. Oncogene. 2004;23(38):6379–91. 109. Ogawa S, Kaku T, Amada S, et al. Ovarian endometriosis associated with ovarian carcinoma: a clinicopathological and immunohistochemical study. Gynecol Oncol. 2000;77(2):298–304. 110. Brinton LA, Gridley G, Persson I, et al. Cancer risk after a hospital discharge diagnosis of endometriosis. Am J Obstet Gynecol. 1997;176(3):572–9. 111. Ness RB, Cramer DW, Goodman MT, et al. Infertility, fertility drugs, and ovarian cancer: a pooled analysis of case-control studies. Am J Epidemiol. 2002;155(3):217–24. 112. Hankinson SE, Hunter DJ, Colditz GA, et al. Tubal ligation, hysterectomy, and risk of ovarian cancer. A prospective study. JAMA. 1993;270(23):2813–8. 113. Kreiger N, Sloan M, Cotterchio M, et al. Surgical procedures associated with risk of ovarian cancer. Int J Epidemiol. 1997;26(4): 710–5. 114. Miracle-McMahill HL, Calle EE, Kosinski AS, et al. Tubal ligation and fatal ovarian cancer in a large prospective cohort study. Am J Epidemiol. 1997;145(4):349–57. 115. Thompson MP, Kurzrock R. Epstein-Barr virus and cancer. Clin Cancer Res. 2004;10(3):803–21.

1068

Noncommunicable and Chronic Disabling Conditions

116. Manolov G, Manolova Y, Klein G, et al. Alternative involvement of two cytogenetically distinguishable breakpoints on chromosome 8 in Burkitt’s lymphoma associated translocations. Cancer Genet Cytogenet. 1986;20(1–2):95–9. 117. Subar M, Neri A, Inghirami G, et al. Frequent c-myc oncogene activation and infrequent presence of Epstein-Barr virus genome in AIDS-associated lymphoma. Blood. 1988;72(2):667–71. 118. Goldsmith DB, West TM, Morton R. HLA associations with nasopharyngeal carcinoma in Southern Chinese: a meta-analysis. Clin Otolaryngol Allied Sci. 2002;27(1):61–7. 119. Chan SH, Day NE, Kunaratnam N, et al. HLA and nasopharyngeal carcinoma in Chinese—a further study. Int J Cancer. 1983;32(2): 171–6. 120. Dolcetti R, Boiocchi M, Gloghini A, et al. Pathogenetic and histogenetic features of HIV-associated Hodgkin’s disease. Eur J Cancer. 2001;37(10):1276–87. 121. Hepatitis viruses. IARC Monogr Eval Carcinog Risks Hum. 1994;59:1–255. 122. Lavanchy D. Hepatitis B virus epidemiology, disease burden, treatment, and current and emerging prevention and control measures. J Viral Hepat. 2004;11(2):97–107. 123. Schulz TF, Boshoff CH, Weiss RA. HIV infection and neoplasia. Lancet. 1996;348(9027):587–91. 124. Joint United Nations Programs on HIV/AIDS. Overview of the global AIDS epidemic. 2006 report on the global AIDS epidemic, 2006. 125. Schistosomes, liver flukes and Helicobacter pylori. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Lyon, 7–14 June, 1994. IARC Monogr Eval Carcinog Risks Hum. 1994;61:1–241. 126. Munoz N. Is Helicobacter pylori a cause of gastric cancer? An appraisal of the seroepidemiological evidence. Cancer Epidemiol Biomarkers Prev. 1994;3(5):445–51. 127. Hunter DJ, Spiegelman D, Adami HO, et al. Cohort studies of fat intake and the risk of breast cancer—a pooled analysis. N Engl J Med. 1996;334(6):356–61. 128. Dennis LK, Snetselaar LG, Smith BJ, et al. Problems with the assessment of dietary fat in prostate cancer studies. Am J Epidemiol. 2004;160(5):436–44. 129. Christen WG, Gaziano JM, Hennekens CH. Design of Physicians’ Health Study II—a randomized trial of beta-carotene, vitamins E and C, and multivitamins, in prevention of cancer, cardiovascular disease, and eye disease, and review of results of completed trials. Ann Epidemiol. 2000;10(2):125–34. 130. Frieling UM, Schaumberg DA, Kupper TS, et al. A randomized, 12-year primary-prevention trial of beta carotene supplementation for nonmelanoma skin cancer in the physician’s health study. Arch Dermatol. 2000;136(2):179–84. 131. Mayne ST, Cartmel B, Baum M, et al. Randomized trial of supplemental beta-carotene to prevent second head and neck cancer. Cancer Res. 2001;61(4):1457–63. 132. Taylor PR, Greenwald P. Nutritional interventions in cancer prevention. J Clin Oncol. 2005;23(2):333–45. 133. Omenn GS, Goodman GE, Thornquist MD, et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med. 1996;334(18):1150–5. 134. Mueller H, Weber W. Familial Cancer. Basel: Karger, 1985. 135. Knudson AG, Jr. Mutation and cancer: statistical study of retinoblastoma. Proc Natl Acad Sci U S A. 1971;68(4):820–3. 136. Varley J. TP53, hChk2, and the Li-Fraumeni syndrome. Methods Mol Biol. 2003;222:117–29. 137. Rebbeck TR. Inherited predisposition and breast cancer: modifiers of BRCA1/2-associated breast cancer risk. Environ Mol Mutagen. 2002;39(2–3):228–34. 138. Thompson D, Easton D. The genetic epidemiology of breast cancer genes. J Mammary Gland Biol Neoplasia. 2004;9(3):221–36. 139. FitzGerald MG, Bean JM, Hegde SR, et al. Heterozygous ATM mutations do not contribute to early onset of breast cancer. Nat Genet. 1997;15(3):307–10.

140. de la Chapelle A. The incidence of Lynch syndrome. Fam Cancer. 2005;4(3):233–7. 141. Ruteshouser EC, Huff V. Familial Wilms tumor. Am J Med Genet C Semin Med Genet. 2004;129(1):29–34. 142. Green DM. Wilms’ tumour. Eur J Cancer. 1997;33(3):409–18; discussion 19–20. 143. Engelien A, Geerdink R, Lips C. Do patients with multiple endocrine neoplasia syndrome type 1 benefit from periodical screening. Eur J Endocrinol. 2003;149:577–82. 144. Linehan WM, Zbar B. Focus on kidney cancer. Cancer Cell. 2004;6(3):223–8. 145. Jemal A, Thomas A, Murray T, et al. Cancer statistics, 2002. CA Cancer J Clin. 2002;52(1):23–47. 146. Abed J, Reilley B, Butler MO, et al. Comprehensive cancer control initiative of the Centers for Disease Control and Prevention: an example of participatory innovation diffusion. J Public Health Manag Pract. 2000;6(2):79–92. 147. Given LS, Black B, Lowry G, et al. Collaborating to conquer cancer: a comprehensive approach to cancer control. Cancer Causes Control. 2005;16 Suppl 1:3–14. 148. Lilienfeld AM. Some limitations and problems of screening for cancer. Cancer. 1974;33(6):1720–4. 149. Cole P, Morrison AS. Basic issues in population screening for cancer. J Natl Cancer Inst. 1980;64(5):1263–72. 150. Shapiro S. Statistical evidence for mass screening for breast cancer and some remaining issues. Cancer Detect Prev. 1976;1:347–63. 151. Shingleton HM, Patrick RL, Johnston WW, et al. The current status of the Papanicolaou smear. CA Cancer J Clin. 1995;45(5):305–20. 152. Hurley SF, Kaldor JM. The benefits and risks of mammographic screening for breast cancer. Epidemiol Rev. 1992;14:101–30. 153. Lisby MD. Screening mammography in women 40 to 49 years of age. Am Fam Physician. 2004;70(9):1750–2. 154. Eddy DM. Breast cancer screening in women younger than 50 years of age: what’s next? Ann Intern Med. 1997;127(11):1035–6. 155. Kopans DB. The breast cancer screening controversy and the National Institutes of Health Consensus Development Conference on Breast Cancer Screening for Women Ages 40–49. Radiology. 1999;210(1):4–9. 156. Gaskie S, Nashelsky J. Clinical inquiries. Are breast self-exams or clinical exams effective for screening breast cancer? J Fam Pract. 2005;54(9):803–4. 157. McCready T, Littlewood D, Jenkinson J. Breast self-examination and breast awareness: a literature review. J Clin Nurs. 2005;14(5): 570–8. 158. Hakama M, Miller AB, Day NE, et al. Screening for Cancer of the Uterine Cervix: from the IARC Working Group on Cervical Cancer Screening and the UICC Project Group on the Evaluation of Screening Programmes for Cancer. IARC scientific publications, no. 76. Lyon, New York: International Agency for Research on Cancer (Distributed in the USA by Oxford University Press), 1986. 159. Screening for squamous cervical cancer: duration of low risk after negative results of cervical cytology and its implication for screening policies. IARC Working Group on evaluation of cervical cancer screening programmes. Br Med J (Clin Res Ed). 1986;293(6548): 659–64. 160. Kronborg O, Fenger C, Olsen J, et al. Randomised study of screening for colorectal cancer with faecal-occult-blood test. Lancet. 1996;348(9040):1467–71. 161. Hardcastle JD, Chamberlain JO, Robinson MH, et al. Randomised controlled trial of faecal-occult-blood screening for colorectal cancer. Lancet. 1996;348(9040):1472–7. 162. U.S. Preventive Services Task Force. Office of Disease Prevention and Health Promotion. Guide to Clinical Preventive Services: Report of the U.S. Preventive Services Task Force. 2nd ed. [Washington, DC]: U.S. Dept. of Health and Human Services, Office of Public Health and Science, 1996.

61 163. Dennis LK, Resnick MI. Analysis of recent trends in prostate cancer incidence and mortality. Prostate. 2000;42(4):247–52. 164. Harris R, Lohr KN. Screening for prostate cancer: an update of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2002;137(11):917–29. 165. Prorok PC, Chamberlain J, Day NE, et al. UICC Workshop on the evaluation of screening programmes for cancer. Int J Cancer. 1984;34(1):1–4. 166. Longo WE, Zucker KA, Zdon MJ, et al. Detection of early gastric cancer in an aggressive endoscopy unit. Am Surg. 1989;55(2): 100–4. 167. Gallo A, Cha C. Updates on esophageal and gastric cancers. World J Gastroenterol. 2006;12(20):3237–42. 168. Wong BC, Lam SK, Wong WM, et al. Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial. JAMA. 2004;291(2):187–94. 169. Ohata H, Oka M, Yanaoka K, et al. Gastric cancer screening of a high-risk population in Japan using serum pepsinogen and barium digital radiography. Cancer Sci. 2005;96(10):713–20. 170. Lee KJ, Inoue M, Otani T, et al. Gastric cancer screening and subsequent risk of gastric cancer: a large-scale population-based cohort study, with a 13-year follow-up in Japan. Int J Cancer. 2006;118(9): 2315–21. 171. Gupta S, Bent S, Kohlwes J. Test characteristics of alpha-fetoprotein for detecting hepatocellular carcinoma in patients with hepatitis

172.

173.

174.

175.

176.

177.

Cancer

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C. A systematic review and critical analysis. Ann Intern Med. 2003;139(1):46–50. Colli A, Fraquelli M, Casazza G, et al. Accuracy of ultrasonography, spiral CT, magnetic resonance, and alpha-fetoprotein in diagnosing hepatocellular carcinoma: a systematic review. Am J Gastroenterol. 2006;101(3):513–23. NIH consensus conference. Ovarian cancer. Screening, treatment, and follow-up. NIH Consensus Development Panel on Ovarian Cancer. JAMA. 1995;273(6):491–7. Lance Armstrong Foundation, Centers for Disease Control and Prevention. A National Plan for Cancer Survivorship: Advancing Public Health Strategies. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 2004. National Cancer Policy Board (U.S.), Weiner SL, Simone JV. Childhood cancer survivorship: improving care and quality of life. Washington, DC.: National Academies Press, 2003. President’s Cancer Panel. Living Beyond Cancer: Finding a New Balance. Annual Report of the President’s Cancer Panel. National Institutes of Health, National Cancer Institute; 2004. Pollack LA, Greer GE, Rowland JH, et al. Cancer survivorship: a new challenge in comprehensive cancer control. Cancer Causes Control. 2005;16 Suppl 1:51–9.

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62

Heart Disease Russell V. Luepker

INTRODUCTION

Cardioscular diseases (CVDs) are public health concerns around the world, particularly coronary or ischemic heart disease (CHD), hypertensive heart disease, and rheumatic heart disease. CHD remains the leading cause of adult death in industrial societies, although its incidence differs widely and the mortality ascribed to it is changing dramatically (Figs. 62-1 and 62-2). While deaths from CHD are falling in industrialized nations, they are rising dramatically in others particularly in the developing world.1 The decline of age-adjusted U.S. deaths ascribed to CHD continues for men and women, white and nonwhite (Fig. 62-3). The exact causes of the decline are not established, but much is now known about U.S. trends in out-of-hospital deaths, in-hospital case fatality, and longer-term survival after acute myocardial infarction.2 Parallel to the CHD mortality trends are improvements in medical diagnosis and treatment, in population levels of risk factors, and in lifestyle.3 Nevertheless, the critical explanatory data, including incidence trends from representative populations, are few. This deficiency, along with the difficulty of measuring change in diagnostic custom and in severity of CHD, or of its precursor, atherosclerosis, leaves considerable uncertainty about the causes of the mortality trends. Systematic surveillance is now in place in several areas to improve the future detection, prediction, and explanation of trends in CVD rates.2–5 Deaths ascribed to hypertensive heart disease have diminished over recent decades in many industrialized countries.6 In West Africa, Latin America, and the Orient, however, the high prevalence still found in hospitals and clinics indicates the continued worldwide importance of hypertension. Rheumatic fever and rheumatic valvular heart disease remain public health concerns in many developing countries and are still seen among disadvantaged peoples in affluent nations. On the other hand, syphilitic heart disease, a worldwide scourge until the 1940s, is now rare. Cardiomyopathies, often of unknown or infectious origin, constitute a common cause of heart disease in many regions, particularly Africa and Latin America. Finally, congenital heart disease continues to contribute to the heart disease burden among youth and adults of all countries. The worldwide potential for primary prevention of most CVD is established by several salient facts: (a) the large population differences in CVD incidence and death rates; CVD is rare in many countries and common in others; (b) dynamic national trends in CVD deaths, both upward and downward; (c) rapid changes in CVD risk among migrant populations; (d) the identification of modifiable risk characteristics for CVD among and within populations; and (e) the positive results of preventive trials. The following chapter expands on these cardiovascular diseases, their trends and the magnitude of burden on populations. The population-wide factors associated with risk of these diseases are

described. Because the majority of cardiovascular disease is caused by social, cultural, and economic factors, public health approaches are central to prevention and control strategies.

CORONARY HEART DISEASE

CHD remains the leading cause of adult deaths in many industrial societies. Much about its causes and prevention has been learned from diverse research methods, including clinicopathological observations, laboratory-experimental studies, population studies, and clinical trials. The evidence of causation from all these disciplines is largely congruent. As a result, several ubiquitous cultural characteristics described below are now established as powerful influences on population risk of CHD. These influences and risk factors appear to be safely modifiable for individuals and for entire populations.7–10 The sum of evidence suggests that there is widespread human susceptibility to atherosclerosis and, consequently, that CHD is maximally exhibited when the environment is unfavorable. These ubiquitous susceptibilities, exposures, and behaviors lead eventually to the mass precursors of CHD found among so many people in highincidence societies. The rationale and the potential for preventive practice, as well as for public policy in prevention, are based on several well-established relationships: between risk factor levels and CHD, between health behaviors and risk factor levels, and between culture and mass health behaviors.

Epidemiology of CHD Summarized here are the salient observations about CHD: • Population comparisons show large differences in CHD incidence and mortality rates (Fig. 62-2) and in the extent of its underlying vascular disease, atherosclerosis. • Population differences in the mean levels and distributions of CHD risk characteristics (particular lipid levels) are strongly correlated with population differences in CHD rates. • Within populations, several risk characteristics (blood cholesterol, blood pressure levels, diabetes and smoking habits) are strongly and continuously related to future individual risk of a CHD event. • Population differences in average levels of CHD risk characteristics are already apparent in youth. Individual values of children tend to “track” into adult years. • CHD risk characteristics and incidence in migrants rapidly approach levels of the adopted culture. • Trends in CHD mortality rates, both upward and downward, occur over relatively short periods of 5–10 years. These trends 1071

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Figure 62-1. Age-adjusted death rates for coronary heart disease by country and sex, Ages 35–74, 2002. (Source: National Heart, Lung, and Blood Institute. Morbidity and Mortality Chart Book on Cardiovascular, Lung, and Blood Diseases. Bethesda, Maryland, 2004; NIH Publication.)

Figure 62-2. Change in age-adjusted death rates for coronary heart disease in males and females by country, Ages 35–74, 1995–2002. (Source: National Heart, Lung, and Blood Institute. Morbidity and Mortality Chart Book on Cardiovascular, Lung, and Blood Diseases. Bethesda, Maryland, 2004; NIH Publication.)

Figure 62-3. Death and ageadjusted death rates for coronary heart disease, U.S., 1979–2002. (Source: National Heart, Lung, and Blood Institute. Morbidity and Mortality Chart Book on Cardiovascular, Lung, and Blood Diseases. Bethesda, MD, 2004; NIH Publication.)

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Figure 62-4. Average annual percent change in death rates for coronary heart disease by age, race, and sex, U.S., 1999–2002. (Source: National Heart, Lung, and Blood Institute. Morbidity and Mortality Chart Book on Cardiovascular, Lung, and Blood Diseases. Bethesda, MD, 2004; NIH Publication.)

•

•

•

•

tend to be associated with changes in medical care and casefatality rates as well as with trends in incidence and in population distributions of risk characteristics. The recent decrease in age-adjusted CHD mortality rates in the United States is shared by men and women, by whites and nonwhites, and by younger and older age groups (Figs. 62-3, 63-4). The decrease in age-adjusted CHD mortality rates in the United States is associated with an even greater decrease in death rates from stroke. This leads to increases in lifespan. Moreover, in the last decades there has been a lesser decrease in non-CVD deaths and in deaths from all causes (Fig. 62-5). Randomized clinical trials find a direct effect of CHD risk factor lowering on subsequent disease rates. Preventive trials also establish that levels of risk factors, and their associated health behaviors, can be significantly and safely modified. The epidemiological evidence is congruent with clinical animal and laboratory findings about the causes and mechanisms of atherosclerosis, the process that underlies the clinical manifestations of CHD.

Role of Diet Dietary Fats There is considerable evidence that habitual diet in populations, a culturally determined characteristic, has an important influence on the mean levels and distribution of blood lipoproteins and, therefore, on the population risk and potential for prevention of CHD. Several dietary factors influence individual and population levels of lowdensity lipoproteins (LDL) in the blood, a leading pathogenetic factor in atherosclerosis. These include particular fatty acids and dietary cholesterol, the complex carbohydrates of starches, vegetables, fruits and their fibers, alcohol, and caloric excess. Many investigators consider that the cholesterol-raising properties of some habitual diets are essential to the development of mass atherosclerosis, leading in turn to high rates of CHD. Where average total blood cholesterol level in a population is low (less than 200 mg/dL, or 5.2 mmol/L), CHD is uncommon, irrespective of population levels of smoking and hypertension. From this evidence, there is now a consensus about the leading population causes of CHD and general acceptance of policy recommendations that lead toward a gradual, universal change in the

Figure 62-5. Change in ageadjusted death rates since 1950, U.S., 1950–2002. (Source: National Heart, Lung, and Blood Institute. Morbidity and Mortality Chart Book on Cardiovascular, Lung, and Blood Diseases. Bethesda, MD, 2004; NIH Publication.)

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habitual diets of populations in which CHD rates are high. Wherever economically feasible, systematic strategies to detect and manage individuals at excess risk are also recommended. Epidemiological studies comparing stable, rural agricultural societies find a strong relationship between habitual diet, average blood cholesterol levels, and incidence of CHD.11–13 For example, diets of populations with a high incidence of CHD are characterized by relatively high saturated fatty acid (greater than 15% of daily calories) and cholesterol intake and low carbohydrate intake (under 50%). Diets in populations with a low CHD incidence are characterized mainly by low saturated fatty acid intake (less than 10% of calories) and high carbohydrate intake but widely varying total fat intake (varying mainly in the proportion of monounsaturated fatty acid calories).12 Most of the difference in mean population levels of serum total (and LDL) cholesterol can be accounted for by measured differences in fatty acid composition of the habitual diet. Moreover, population CHD rates can be predicted, with increasing precision over time, by average population blood cholesterol levels.14 Cross-cultural comparisons of diet versus postmortem findings of atherosclerosis reveal a strong correlation between habitual dietary fat intake of a population and the frequency and extent of advanced atherosclerotic lesions.15 Studies of migrant populations indicate the predominance of sociocultural influences, including diet, in trends of risk and CHD among migrants. For example, Japanese who migrate to California become taller, heavier, more obese, and more sedentary; their diet changes dramatically; they eat more meat and dairy products, saturated fatty acids and cholesterol, and consume less complex carbohydrate and less alcohol than their counterparts in the Nagasaki-Hiroshima area.16 They develop higher risk profiles and disease rates within a generation. With few exceptions, migrant Hawaiian Japanese have risk factor values intermediate between mainland and California Japanese, and the CHD rate in migrants generally parallels their mean values for risk factor levels. The rapid evolving national trends in CHD deaths are another indication of the predominance of culture in the population causes and prevention of CHD, as disease occurrence changes more rapidly than any genetic characteristics. Nevertheless, systematic explanatory studies of trends in CHD mortality are very recent, and current attempts to estimate the relative contribution of cultural versus medical care contributions are quite tentative.2–4,17,18 In a number of countries on an upward slope of CHD mortality, smoking and calorie and fat consumption are increasing and physical activity is decreasing, while cardiological practice is probably becoming less effective.19 In many other industrial countries, including the United States, decreasing CHD mortality rates parallel improved cardiac care and significant reductions in average risk characteristics.2,3,17,20 Standardized measurements of risk and disease trends are not generally available for comparisons among countries, but the public health implications of these simultaneous trends in behaviors, risk, disease rates, and medical care are immense. Another feature of diet, the relative excess of calorie intake over expenditure, influences health through the metabolic maladaptations of hyperlipidemia, hyperinsulinism, and hypertension.21 This is sometimes called the metabolic syndrome.22 This caloric imbalance occurs in sedentary cultures and results in mass obesity. With or without mass obesity, however, high salt intake and low potassium intake in populations appear to encourage the wide exhibition of hypertensive phenotypes. Other cations (e.g., magnesium, calcium) may also be significant dietary influences on population levels of blood pressure, while alcohol intake is clearly involved (see below). Anthropology and paleontology provide insights into the probable effects of rapid cultural change, including modern diets, from the lifestyle to which humans adapted during earlier periods of evolution. Until 500 or so generations ago, all humans were hunter-gatherers. The habitual eating pattern likely involved alternating scarce and abundant calories and a great variety of foods. It surely included lean wild game and usually a predominance of plant over animal calories, a relatively low sodium and high potassium intake, and of course there was universal breast-feeding of infants. Observations of the eating patterns among extant hunter-gatherer tribes confirm the varied nature and the

TABLE 62-1. A MODEL OF INDIVIDUAL DIET–SERUM CHOLESTEROL (TC) RELATIONS WITH INDIVIDUAL EXAMPLES Mean Diet–TC Effect (mg/dL) Genotypic TC Value(mg/dL) 75 150 300

0

+25

+50

+75

+100

75 150 300

100 175 325

125 200 350

150 225 375

175 250 400

Source: Blackburn H. The concept of risk. In: Pearson TA, Criqui MH, Luepker RV, Oberman A, Winston M, eds. Primer in Preventive Cardiology. Dallas: American Heart Association, 1994, pp 25–41; and Keys A, Grande F, Anderson JT. Bias and misrepresentation revisited—“perspective” on saturated fat. Am J Clin Nutr. 1974;27:188–212. It is assumed that an intrinsic lipid regulatory base exists for each individual and is expressed in the first year of life. On this genotype is superimposed the effect of habitual diet, which is either neutral or cholesterol-raising according to properties determined in controlled Minnesota diet experiments, resulting, in this simple additive model, in the adult phenotypes values.

adequacy (or near adequacy) of such an eating pattern for growth and development, as well as for the potential of longevity and the absence of mass phenomena such as atherosclerosis and hypertension.23–25 Although modern humans can scarcely return to such subsistence economies, the anthropological observations suggest that current metabolic maladaptations derived from affluent eating and exercise patterns imposed rapidly on a very different evolutionary legacy result in the mass precursors of cardiovascular diseases found in modern society.24 Despite the generally strong population (ecological) correlations between diet, blood lipid levels, and CHD rates, these correlations are often absent for individuals within high-risk industrial societies.26 This apparent paradox does not negate the causal importance of diet in mass hypercholesterolemia and atherosclerosis. Consider, for example, the simple additive model of Table 62-1, which suggests the powerful influence, in the individual, of inherent lipid regulation. Different individual lipoprotein genotypes may develop widely different adult risk phenotypes and different serum cholesterol levels, while consuming the same U.S.-type diet. Other individuals may have similar blood cholesterol levels while subsisting on very different diets. In contrast, the population model of Table 62-2 makes the assumption that the multiple genes that influence lipid TABLE 62-2. A MODEL OF POPULATION DIET—SERUM CHOLESTEROL (TC) RELATION WITH POPULATION EXAMPLES Mean Diet–TC Effect (mg/dL)

Population mean TC Lower limit (2.5%) Upper limit (97.5%)

Japan 0

Greece +25

Italy +50

United States +75

Finland +100

75

100

125

150

175

150

175

200

225

250

300

325

350

375

400

Source: Keys A, Grande F, Anderson JT. Bias and misrepresentation revisited—“perspective” on saturated fat. Am J Clin Nutr. 1974;27:188–212; and Keys A, ed. Coronary heart disease in seven countries. Circulation. 1970;41–42 (Suppl I). In this oversimplified model, it is assumed that uncommon single gene effects and widespread polygenic determinants of blood cholesterol levels are randomly and usually distributed among large heterogeneous populations, such that a mean population TC value of 150 mg/dL would prevail (SD ± 37.5 mg/dL) in the presence of a habitual average diet having neutral properties in respect to cholesterol. On this mean and population distribution of intrinsic responsiveness is superimposed the average habitual diet effect for a population, which is either neutral or cholesterol-raising according to the country’s measured diet composition and properties.

62 metabolism are randomly and similarly distributed throughout large heterogeneous populations. Under this condition, population means and distributions of blood lipids are seen to be influenced predominantly by the cholesterol-raising or lowering properties of the habitual diet of the population.27,28 The range and degree of this dietary influence are estimated from short-term controlled diet experiments.29–31 Recently, several well-conducted cohort studies have provided evidence of diet-CHD relationships within societies in which CHD risk is high.32–35 With particular care to reduce variability and increase validity of individual dietary intake assessments, all of these studies were able to demonstrate small but significant and often independent prediction of CHD risk based on entry nutrient intake or other dietary characteristics. In our view, this evidence is less persuasive than the powerful synergism of diet, blood lipid levels, and CHD risk so firmly established over 40 years, but it is clearly confirmatory. With this logic, habitual diet has come to be considered the necessary factor in mass hypercholesterolemia and, thus, in the mass atherosclerosis that leads to high rates of CHD. The population data are, however, equally compatible with another idea, that all three of the major risk factors (i.e., elevated population averages of blood cholesterol, blood pressure, and smoking) are essential for a high population burden of CHD. The relationship of habitual diet to population levels of blood lipids and blood pressure, and to CHD rates, is largely congruent with clinical and experimental observations. First, experimental modification of diet has a predictable effect on group blood lipid levels. When calories and weight are held constant in controlled diet experiments and diet composition is varied, the largest dietary contributions to serum total and LDL cholesterol levels are (a) the proportion of calories consumed as saturated fatty and trans fatty acids, (b) dietary cholesterol, both of which raise cholesterol levels, and (c) polyunsaturated fatty acids, which have a cholesterol lowering effect. The role of monounsaturates is debated, with some suggesting a neutral effect while others a cholesterol-lowering effect.29–31,36 Although this is debated, these clinical experiments confirm the broader relation found between long-term habitual diet and population mean levels of blood lipids.11,12 Animal experiments are not treated here but are relevant to the human diet-CHD relationship in that lesions resembling the human plaque are produced by dietary manipulations of blood lipoprotein levels; the fatty components of these animal plaques are reversible with dietary manipulations to lower blood lipoprotein levels.37,38 Plasma cholesterol-lowering preventive trials, which tend to complete the overall evidence for causation, indicate the feasibility and safety of changing risk factors and demonstrate the actual lag times between such change and its effect on CHD rates.22 The synthesis of results of all these trials and their implications for the public health are central because carrying out the “definitive diet-heart trial” is not considered feasible. Therefore, experimental proof of the role of diet in the primary prevention of CHD is not likely to be established. Lipid-lowering trials demonstrate that substantial lowering of blood lipid levels is feasible, that the progress of arterial lesions is arrested, and that CHD morbidity and mortality are reduced, all in proportion to the cholesterol lowering achieved and its duration. These trials, carried out mainly in middle-aged men with moderately elevated blood lipids, have usually involved cholesterol-lowering medication plus diet. However, because they specifically tested the cholesterol-lowering hypothesis and because their effects are congruent with the observational evidence cited here in support of that hypothesis, these experimental findings have been extrapolated by many authorities to the potential for prevention in the broader population, including older and younger age groups, and those with lower lipid and risk levels.22 Many consider, also, that the results of randomized clinical trials, because of their congruence with the other evidence, may be extrapolated to the larger public health, including the potential for CHD prevention by long-term change in eating patterns of the population as a whole, and, finally, to the prevention of elevated risk in the first place.

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Proteins International vital statistics on deaths correlated with national foodconsumption data indicate that, as with fat consumption, strong ecologic correlations exist between animal protein intake and death rates from CHD, but there is little evidence that this association is causal. Anitschkow39 found originally that it was dietary lipid rather than protein that resulted in hyperlipidemia and atherosclerosis in his experimental rabbits. Controlled metabolic ward studies in men under isocaloric conditions, with fat intake held constant while protein intake was varied between 5 and 20% of daily calories, found no change in blood cholesterol level (University of Minnesota, unpublished data). Neither clinical, experimental, nor epidemiological evidence is now sufficient to attribute a specific effect of dietary protein on either blood lipid levels or CHD risk. The overall importance of the consumption of meats from domesticated animals and of fatty milk products is therefore thought to rest mainly in their fatty acid content rather than their protein content, at least with respect to CHD risk.

Carbohydrates There is generally a positive association between population intake of refined sugars and CHD mortality and a negative relationship between complex carbohydrates and CHD mortality. Although these diet components are seriously confounded with other dietary factors that are strongly associated with carbohydrate intake, the effect of certain fibers, including the pectins in fruit, bran fiber, and the guar gum of numerous vegetables and legumes, on blood sugar and on blood lipid regulation has recently attracted greater interest. This is particularly so now that the fatty acid effects are well delineated; yet they fail to explain all of the observed population differences in blood lipid or all the lipid changes seen during experiments involving different nutrient composition. More important, however, is that plausible mechanisms of atherogenesis are not established for sugars. The broader issue of plant foods (fruits, vegetables, pulses, legumes, and seeds), their complex carbohydrates, protein, other nutrients, and fibers is nevertheless of great public health interest because their consumption may affect the risk of cancers as well as of CVD. The summary view is that the different amounts of sugars consumed in “natural diets” around the world do not account for the important differences found in population levels of blood lipids and their associated CHD risk. High carbohydrate intake is confounded with low fat intake (since protein intake is relatively comparable), and both are associated with low rates of CHD.

Alcohol Positive correlations between alcohol consumption and blood pressure levels found for individuals in population studies appear to be dose-related and independent of body weight and smoking habits.40,41 Evidence is also consistent with respect to the positive relationship of alcohol consumption to blood high density lipoprotein (HDL) cholesterol level and of change in alcohol consumption to change in HDL cholesterol level. Substitution of alcohol for carbohydrates in a mixed U.S. diet results in a rise in HDL, mainly the HDL3 subfraction, one that may not be strongly related to CHD risk.42 Experimentally, myocardial metabolism and ventricular function are affected by relatively small doses of alcohol. In addition, neurohormonal links are established between alcohol-stimulated catecholamine excretion and myocardial oxygen requirements. These effects could act as contributory factors to the clinical manifestations of ischemia. The epidemiological evidence from longitudinal studies about the relation of alcohol to CHD risk is, however, conflicting.43–45 Inverse relationships of alcohol intake and CHD are found in some studies, whereas a U-shaped, linear, or no relationship is found in others. Positive relationships, when found, are usually independent of tobacco, obesity, and blood pressure levels.45 Reasons for these inconsistent findings in the alcohol–coronary disease relationship may involve the poor (self-report) measurement

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for alcohol intake as well as misclassification of the cause of death among heavy drinkers who are known to die of sudden, unexplained causes. Moreover, there are many possible confounding factors, including blood pressure levels, cigarette smoking, and diet. Preventive practice with respect to alcohol is, therefore, based on its social and public health consequences rather than on any possible direct effect, favorable or otherwise, on cardiovascular disease risk. A major concern about regular alcohol use is, however, its enhancement of overeating, underactivity, and smoking, along with its intrinsic caloric density. Given these several relationships, public health recommendations for alcohol are not yet indicated in any quantity, as a “protective measure” for heart diseases.

Salt Salting of food, primarily for preservation, began with civilization and trade. Now salting is based mainly on acquired taste and is likely a “new” phenomenon in an evolutionary sense. Moreover, the mammalian kidney probably evolved in salt-poor regions where the predominantly plant and wild game diet was likely very low in sodium and rich in potassium. Thus survival of humans and other mammals in salt-poor environments may have rested on an evolutionarily acquired and exquisite sodium-retaining mechanism of the kidney. The physiological need for salt under ordinary circumstances is approximately only 1–2 g of sodium chloride per day. It is hypothesized that this mechanism is now overwhelmed by the concentrated salt presented to modern humans in preserved meats and pickled foods, in many processed foods, and in the strong culturally acquired taste for salt.24,46 Clinical, experimental, and epidemiological links between salt intake and hypertension are increasingly well forged.46,47 Marked sodium depletion dramatically reduces blood pressure in persons with severe hypertension. Sodium restriction enables high blood pressure to be controlled with lower doses of antihypertensive drugs. In many patients, salt restriction may result in adequate control of mild to moderate hypertension without drugs.48 Weight reduction and salt restriction appear to be independently important in lowering high blood pressure.48 In summary, a culture with high salt consumption appears to encourage maximal exhibition of an inherent human susceptibility to hypertension. Because potassium tends to reduce the blood pressure–raising effects of sodium, the sodium-potassium ratio of habitual diets also may be important in the public health.49 Surveys consistently find strong relationships between average population blood pressure and salt intake.47,50,51 High blood pressure is usually prevalent in high-salting cultures, irrespective of the prevalence of obesity. In contrast, hypertension is usually absent in low-salting cultures, despite frequent obesity. Moreover, rapid acculturation to greater salt intake among South Pacific islanders who migrate to industrialized countries is associated with an increased frequency of hypertension and elevated mean blood pressure.52 Even within high-salting cultures, when special efforts are made to reduce the measurement error for blood pressure and to characterize individual sodium intake with maximum precision, significant individual salt–blood pressure correlations are usually found.52,53 Despite all this evidence, neither preventive practice nor public health policy on reduction of salting is well advanced. This may be due in part to professional skepticism, based perhaps on the relatively weak individual correlations of salt intake and blood pressure. Admittedly, modification of salt intake by traditional dietary counseling has not been very successful. However, when interventions are attempted in a supportive and systematic way, change in salting behavior is readily achievable.54 In the United States, wider education has significantly and widely influenced food processing and marketing of products with lower salt content, and a great deal of voluntary public health action has been taken by food companies. Current U.S. national dietary goals recommend no more than 4.5–6.0 g of salt daily.55 For individuals, this is achievable by not salting foods at the table, by adding no salt in cooking, and by avoidance of salt-rich foods, particularly canned, processed, and pickled foods. Despite the absence of a strong policy, preventive practice and public health approaches to reduced salt consumption are

increasing. Significant public health effects of such population changes might be expected in high-salting societies, in light of recent trends in blood pressure and stroke observed in Japanese populations.56

Blood Lipoproteins Clinical, experimental, and epidemiological evidence of the relationship between certain blood lipoproteins, atherosclerosis, and incidence of CHD is strong, consistent, and congruent. Because much knowledge is available, we present here only a summary of what we regard as the salient facts in this relationship, along with a few key references. The subject was recently reviewed in detail.22 • Associations are consistently strong between mean population levels of total serum cholesterol and measured CHD incidence.11,12 • Associations are variable between mean population levels of fasting serum triglycerides and coronary disease rates. 57–58 • Total serum cholesterol levels at birth have similar means and ranges in many cultures.59 • Average levels and distributions of total serum cholesterol differ widely for populations of school-age children.59 They tend to parallel the differences found in adult population distributions of blood lipid levels, that is, means and distributions are found to be elevated in youth when they are elevated in adult populations.59 • Means and distributions of total serum cholesterol of migrants rapidly approach those of the adopted country, whether higher or lower than the country of origin.16 • Blood lipids measured in cohorts of healthy adults followed over time show consistently positive relationships, usually with a continuously rising individual risk of CHD according to the entry levels of total serum cholesterol (and LDL), at least until late middle age.8,60,61 • Computation of the population risk attributable to blood cholesterol levels indicates that the majority of excess CHD cases occur in the central segment of the population distribution, that is, 220 to 310 mg/dL, whereas only 10 percent derive from values above 310.7,27 • In healthy cohorts, a strong inverse relationship between individual HDL cholesterol level and its ratio to total cholesterol is found with subsequent CHD risk. It is relatively stronger at older ages and within populations that have a relatively high CHD risk overall.36,58,62 • Large-scale experiments indicate the feasibility and apparent safety of blood cholesterol lowering from moderate changes made in dietary composition, with and without weight loss.10,36,63 • Clinical trials of lipid lowering alone in middle-age, high-risk populations indicates a reduction of CHD risk according to the degree and duration of exposure to the lowered cholesterol level.9,10,64–66 Further, clear evidence has emerged that a class of lipid-lowering agents, the “statins” can reduce the risk of further CHD morbidity and mortality when coronary disease is already clinically apparent.67,68 • There has probably been a significant drop, of approximately 10–15%, in the U.S. mean total serum cholesterol level in the last 20 years, which is partly explained by changes in composition of the habitual diet during this period.69,70 Consensus from these facts has resulted in a vigorous population strategy of reduction in blood lipid level in the United States. Major recommendations are now in place for a change in eating patterns among North Americans.36 Moreover, the U.S. National Cholesterol Education Program has apparently increased both public and professional awareness and has improved the medical practice of lowering blood cholesterol.22,71–75

62

Overweight and Obesity Whatever the physiological or cosmetic disadvantages of obesity and overweight, their relationship to CVD risk and mortality remains interesting, difficult to dissect, and basically unsettled. From a clinical perspective, extreme obesity is associated with manifest physical limitations and a propensity for many disabilities and illnesses. Beyond this, however, associations with cardiovascular diseases are not consistent throughout most of the distribution of relative weight or skin-fold measurements.76 Overweight and weight gain tend to raise risk factor levels, and correction of the many metabolic disorders that accompany obesity is prompt and substantial when weight loss is achieved, with or without an increase in physical activity. When weight loss is carried out primarily through increased physical activity, appetite is generally “selfregulated” and body fat is lost, lean body mass is better maintained, insulin activity is lowered, glucose tolerance is improved, LDL and very low density lipoprotein (VLDL) levels are lowered, HDL level is raised, and cardiovascular efficiency is enhanced. As we shall review here, however, the status of obesity and weight gain and loss as risk factors for CVD is complex. Obesity is arbitrarily considered to be present when the fat content of the body is greater than 25% of body mass in men and 30% in women. Overweight is equally arbitrarily chosen as greater than 130% relative weight, according to life insurance build and mortality tables, or on a body mass index (kg/m2) greater than 26. “Ideal weight” criteria are often based on standards associated with the lowest mortality risk in life insurance experience. The prevalence of overweight (and obesity) in U.S. adults is variously estimated from 20 to 50%, depending on the measurement used and the definition chosen, as well as by age, sex, and race classification. A most salient fact about overweight in the United States is that average weight and relative body weight are increasing, according to national health surveys. Obesity based on a body mass index (wt/ht2) of ≥30 kg/m2 in men (20–74 years of age) rose from 10.7% in 1960–1962 to 28.1% in 1999–2002. In women, similar changes have occurred, with the proportion obese in 1960–1962 being 15.7%, rising to 34.0% in the later survey.77 (Table 62-3) The prevalence of extreme overweight is increasing at a greater rate than is average weight.77 This trend affects all gender and major ethnic groups as shown for overweight. The causes of mass obesity in populations are only partly understood. Widespread abundance, availability, and low cost of calorie-dense foods, along with many environmental cues to appetite, encourage overeating in relation to physiologic need. These environmental “facilitators” act on an apparently widespread genetic susceptibility to obesity. This, in turn, may be an evolutionary legacy from hunter-gatherer lifestyles. Moreover, there are other factors that enhance excess calorie intake relative to need. For example, dietary fat is more efficiently stored as adipose tissue than is carbohydrate under conditions of excess calorie intake.36 Refined sugars have less satiety value than the complex carbohydrates of fruits and vegetables. And alcohol is cheap and available in many societies.

TABLE 62-3. AGE-ADJUSTED PREVALENCE OF OBESITY IN AMERCIANS AGES 20–74 BY SEX AND SURVEY Year

Men

Women

1960–62 1971–74 1976–80 1988–94 1999–2002

10.7 12.2 12.8 20.6 28.1

15.7 16.8 17.1 26.0 34.0

NHES 1960–62; NHANES: 1971–74, 1976–80, 1988–94, and 1999–2002. Note: Obesity is defined as BMI of 30.0 or higher. Source: CDC/NCHS. Health, United States, 2004.

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One major cause of mass obesity in Western populations appears to be the increase of relative sedentariness. Americans are, on average, heavier now than they were earlier in this century when, in fact, they consumed significantly more calories per day.36 The stable, rural, laboring populations that consume (and expend) more energy are, in turn, the leaner populations.11 Unfortunately, however, sedentariness in populations is largely confounded with calorie density and other differences in eating patterns. Comparisons among and within populations in the Seven Countries Study illustrate the complexity of the relationship of overweight and obesity to CHD and to death from all causes.11,12 Among populations, CHD incidence is not correlated with any measure of obesity or overweight. The population distributions of skin-fold obesity are, however, strikingly different. They almost fail to overlap, for example, between the highest skin-fold values found among Serbian farmers and the lowest values among sedentary U.S. rail clerks.11 Obesity is, therefore, a mass phenomenon and is apparently strongly determined by (a) the average energy expenditure of the population and (b) the composition (caloric density) of the diet. Within populations the picture is highly variable. In East Finns, with high CHD rates, incident CHD cases are evenly distributed across the entry distribution of skin-fold fatness and overweight. In another population with a high CHD incidence—U.S. railroad workers—the relationship between skin-fold obesity and CHD death is weakly positive, in contrast to an insignificant and opposite relationship for relative body weight. In another population with a high CHD incidence, consisting of rural Dutch men, there is a strongly positive linear relationship between CHD incidence and overweight and obesity throughout the wide range of values found there. Among men from the southern Mediterranean regions of Italy, Greece, and Yugoslavia, there is a U-shaped relationship between overweight or obesity and CHD risk, as well as with deaths from all causes. There the thinnest individuals as well as the heaviest and fattest have the higher disease rates; lowest disease risk is found for those with intermediate weight values.11,12 Multivariate analysis in the Seven Countries Study, used to adjust for the many confounding variables related alike to body mass and to CHD, shows no consistent relationship of 10-year CHD incidence with either relative weight or fatness.12 In most of these populations there is a tendency for CHD incidence to be slightly higher in the upper than in the lower half of the fatness distributions, but this tendency disappears when other variables are simultaneously considered. Similarly, except for men at the extremes of the distribution, within generally high-incidence and overweight U.S. populations, there is little relationship between obesity or overweight and risk of CHD or death in men. Within populations, several other longitudinal studies, including the Framingham Heart Study,78 the Evans County Study,79 and the Manitoba Study,80 suggest that an independent contribution of relative weight to risk in a society with high CHD incidence may be reflected only in very long-term CHD risk. In Framingham, in addition, weight gain since youth is a risk predictor for CHD.78 Finally, in the Evans County Study, initial overweight and weight gain over time are also strongly related to the seven-year incidence of new hypertension.79 The ability to distinguish CVD risk according to the body distribution of obesity, usually measured as the ratio of waist to hip circumference (WHR), is relatively recent.81 WHR is positively related to risk of CHD, premature death, non-insulin–dependent diabetes mellitus, and cancers in women, as well as to established CVD risk factor levels. The finding that several diseases correlate better with fat distribution than with general measures of overweight or obesity has raised major new hypotheses about possible separate metabolic entities and about the pathogenesis, risk, and treatment of obesity.82,83 Results of autopsy studies are inconclusive. The International Atherosclerosis Project concluded that the degree and severity of atherosclerosis were not consistently associated with overweight and obesity.84 Finally, a major gap exists in our knowledge of the effect of weight reduction on disease risk in a relatively overweight society

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at high risk from combined CHD risk factors. This hugely confounded question, as well as the effects of weight cycling, remains to be clarified.85 In summary, obesity and overweight are centrally involved with the many metabolic maladaptations related to diabetes mellitus, hypertension, blood lipids, and probably atherogenesis. It is central to the metabolic syndrome.22 These maladaptations are particularly amenable to correction by weight loss, with or without increased physical activity. The epidemiological evidence indicates, however, that relative body weight and obesity have a different disease-related significance in different populations and cultures. This may be due in part to different composition of the diets by which individuals and populations become obese, as well as to coexisting elevated distributions of other CVD risk characteristics. In most societies with high CHD incidence in which the issue has been systematically studied, the independent relationship between overweight, obesity, and CHD risk is seen mainly at the extremes of relative weight and over the longer term. Inconsistent disease associations and the obvious and dramatic declines in CVD deaths in the United States over the last 40 years, despite the clearly increased average U.S. body mass, indicate the primary importance for population CVD risk of factors other than overweight and obesity.

Physical Inactivity Two primal human activities are the obtaining and consuming of food. Only since the advent of agriculture, and more recently of urbanization and industrialization, has the sustained subsistence activity of humans changed dramatically. In affluent industrial societies with automated occupations, motorized transport, and sedentary leisure, reduced energy expenditure is one of the more profound changes in human behavior. Aside from its likely importance as a fundamental departure from evolutionary adaptations and its apparently determining effect on mass obesity, the evidence specifically linking physical activity to chronic and CVD disease risk is difficult to obtain and interpret. A definitive, long-term controlled experiment on habitual activity with respect to CVD risk is not considered feasible.86 Here is a brief synthesis of the evidence relating habitual activity to CHD risk. The caliber of the coronary arteries at autopsy is larger in very active people, but limitations of design, method, feasibility, and cost have prevented a satisfactory study of the effect of exercise training on changes in coronary angiograms or functional measures of ischemia. Clinical trials of cardiac rehabilitation after myocardial infarction, including the effects of exercise training, are difficult. Nevertheless, Oldridge and colleagues87 carried out a meta-analysis on the “better-designed” studies, noting first that many of the trials demonstrated an effect of exercise on levels of risk factors and exercise tolerance. They used rigorous criteria for inclusion of 10 trials in their statistical summary, which estimated a 24% reduction in deaths from all causes in patients undergoing cardiac rehabilitation and a 25% reduction in CVD mortality. Both estimates were statistically significant and clinically important. The incidence of nonfatal myocardial infarction, however, was 15% higher (not statistically significant) in all the treatment groups combined and 32% higher (P = 0.058) in the groups in which cardiac rehabilitation was begun early (i.e., within eight weeks after infarction). Thus, cardiac rehabilitation with exercise apparently had no overall effect on risk of nonfatal infarction and, when initiated early, may even have increased the incidence of nonfatal infarction. In addition to fatal and morbid outcomes, there is a growing consensus on the benefits of physical activity among patients with clinically significant cardiovascular diseases including myocardial infarction, angina pectoris, peripheral vascular disease, and congestive heart failure. Symptom reduction, improved exercise tolerance and functional capacity, and improvement in psychological wellbeing and quality of life are among the benefits.88 Exercise also improves lipids and blood pressure and helps control obesity.89 The major source of information about the role of physical activity in the primary prevention of CHD is indirect, from observational

studies. These usually involve attempts to identify the confounding effects of lifestyle characteristics other than physical activity.89 A review by Powell and colleagues90 concluded that the majority of observational studies meeting their criteria found a significant and graded relationship between physical inactivity and the risk of first CHD event and that studies with a stronger design were more likely to show an effect. These authors calculated a median risk ratio of 1.9, that is, a 90% excess risk of CHD among physically inactive persons. We analyzed the subset of 16 studies from the review of Powell et al that measured individual levels of physical activity, and we added recent studies from the Multiple Risk Factor Intervention Trial (MRFIT) and U.S. railroad workers.89,91,92 All 18 studies showed that habitual physical activity was inversely related to death from CHD or death from all causes. The more recent studies adjusted for confounding risks and this adjustment usually diminished, but did not abolish, the risk associated with physical inactivity. Several studies found that the relation was largely explained by the level of physical fitness, in that the gradient of risk with the level of physical activity largely disappeared when measures of fitness were controlled. In a cohort study, fitness measured by a maximal exercise treadmill test predicted all-cause mortality for men and women, independently of other risk characteristics.93 The duration, frequency, and intensity of physical activity that may be protective against CHD remain, nevertheless, at issue. Recent studies suggest that an energy expenditure of 150–300 kcal daily, in activity of moderate intensity such as walking and working around the house, is associated with lower risk, as is a moderate amount of vigorous physical activity.89,91,92,94 Anthropologic observations suggest that healthy farmers and herdsmen rarely work at a pace that leads to shortness of breath or exhaustion. Systematic observations in the Seven Countries Study indicate that even a substantial amount of regular, vigorous physical activity does not necessarily protect an individual or a population from CVD risk, particularly if other risk factors such as mass hypercholesterolemia are prevalent. In that study, farmers and loggers in eastern Finland were found to be the most physically active of men, and yet they had the highest rates of CHD; there was little less risk among the more physically active within that population.11,12 The interpretation of these many observations is that habitual, current physical activity very likely protects against coronary death.89 A basic uncertainty that remains is whether the apparent benefit is due to physical activity itself or to its effect on other risk factors. People tend to exercise if they are able to and if they feel good when they exercise. Fitness, a component strongly determined by constitution, may be a major contributor to an apparently protective effect of physical activity. It is possible that fitness determines both who will be active and who will be protected from CHD. At least two other pieces of evidence suggest that constitution is not the major operant. Any protective effect of having once been a college athlete, and thus presumably genetically superior, disappears with time after graduation, whereas current physical activity is associated with lower risk.95 Moreover, it seems that genetic factors are likely to be less important to participation in moderate exercise than to participation in vigorous exercise, but both carry a lower risk of CHD. Finally, safety should be the foremost consideration both in prescribing exercise for individuals and in making recommendations for the public health. Several studies have found an excess risk of primary cardiac arrest during and shortly after strenuous exercise in all subjects, regardless of their level of habitual physical inactivity, despite a much lower overall risk of sudden coronary death in habitually active subjects.96,97 They concluded that the reduced risk of sudden death due to regular physical activity was greater than the excess risk of sudden death during vigorous activity. This view, important for the public health, would be small comfort, however, to the families of those stricken while running. The evidence suggests that brisk walking or other moderately vigorous activity is the more reasonable exercise prescription, at least for sedentary and middle-aged people who have not maintained their fitness from youth.89

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Diabetes and Hyperglycemia

Elevated Blood Pressure: Hypertension

Since the insulin era began, enabling persons with diabetes to survive, a strong relationship between diabetes and atherosclerosis risk has emerged. Most who die with diabetes succumb to advanced atherosclerosis. In addition, there are important mechanistic interrelations between insulin-glucose regulation, lipoprotein and uric acid metabolism, obesity and hypertension, on the one hand, and atherosclerosis on the other. Unfortunately, the prevalence of diabetes in the U.S. population is rising associated with increasing obesity.98 The longterm effects of this trend are unknown. The association of clinical diabetes mellitus with CHD and atherosclerotic manifestations is documented clinically, pathologically, and epidemiologically.99,100 It is thought that hyperinsulinemia, hypoglycemic episodes, or both in treated diabetics, coupled (formerly) with the common prescription of a high-fat, low-carbohydrate lowfiber diet, increases vascular complications. Cross-cultural comparisons suggest that the risk of atherosclerosis and CVD in diabetic patients is indeed related to factors other than the glucose-insulin disorder itself. For example, apparently low rates of atherosclerosis exist in diabetic eastern Jews, Chinese, and Southwest American Indians.99,100 The Pima Indians of Arizona are thought to be an example of the theoretical “thrifty genotype,” that is, a population only recently (in evolutionary terms) exposed to calorie abundance, that frequently (50% of adults) develops an obese, diabetic phenotype but nevertheless manifests little CVD.101 In longitudinal studies among cohorts, clinical diabetes mellitus is associated with excess CHD risk and severity of CHD, and many studies confirm the excess of fatal myocardial infarction in women with diabetes.102 The excess risk among diabetics is not always differentiated by the degree of hyperglycemia or the degree of control. Much of the excess CHD risk in diabetics is, in fact, accounted for by associated risk variables.99,100 More severe atherosclerosis, diabetic cardiomyopathy, and a hypercoagulable state are also thought to contribute to the excess risk of diabetes.100 Finally, in most autopsy studies, coronary artery disease and the frequency and severity of myocardial infarction are greater in diabetics than in control subjects.99,100 Diabetic treatment by the control of blood glucose levels is the mainstay of therapy. However, the role of glucose control in the reduction of cardiovascular and other complications has been controversial. The University Group Diabetes Program (UGDP) reported an increased rate of myocardial infarction with the use of first-generation sulfonyl ureas despite effective blood glucose control.103 These effects are not seen with later agents.104 The Diabetes Control and Complications Trial (DCCT) studied “tight” glucose control in insulin-dependent diabetics. Findings included significant reduction in retinopathy, microalbuminuria, and clinical neuropathy. Elevated LDL cholesterol levels were also reduced with tight control.105 Cardiovascular and peripheral vascular disease was also reduced, but did not reach significance.106 Recently, a meta-analysis of clinical trials of the hypoglycemic drug rosiglitazone found increases in myocardial infarction and cardiovascular death.108 The implications of these observations are still unclear. In healthy persons glucose intolerance alone is weakly and inconsistently associated with CVD risk.100,107 However, high insulin activity was found to be a significant independent predictor of coronary events in cohorts studied in Australia, France, and Finland,100 and it has also been proposed as a cause of excess atherosclerosis in Asian migrants.108 In summary, the relationship between diabetes, atherosclerosis, and coronary disease is well established among persons with clinical diabetes living under the conditions of affluent Western culture. Data from other cultures suggest, however, that other factors, such as physical activity, body weight, blood pressure, blood lipid levels, dietary composition, and smoking habits, greatly affect the risk of CHD among diabetics. This, plus evidence that the metabolic disorders of middle-age persons with diabetes can be significantly improved through exercise and modified by diet and weight loss, provide a sound rationale for preventive practice. More study of these complex issues is needed to develop an effective preventive approach to noninsulin-dependent diabetes mellitus itself.

The epidemiology, control, and prevention of hypertension and its complications are summarized here. It is estimated that hypertension contributes to more than onehalf of adult deaths in the United States. It is a strong and independent risk factor for CHD and stroke, and there are plausible mechanisms for its effects on atherosclerosis and vascular disease. Patients with CHD have higher average blood pressure than control subjects. Experimental atherosclerosis induced in animals is directly related to pressure levels within the arterial system. In cohort studies, elevated blood pressure is positively, continuously, and independently related to CHD risk, according to increasing levels of systolic or diastolic blood pressures. The relationship of elevated blood pressure to risk of cerebrovascular hemorrhage and congestive heart failure is even stronger than the relationship to risk of CHD and thrombotic stroke. The preventive potential for hypertension control is illustrated by drug trials that have demonstrated a significant decrease in rate of stroke and heart failure. The Systolic Hypertension in the Elderly Project (SHEP) demonstrated the importance of systolic blood pressure control in this group.109 Results of other trials suggest that CHD risk is lowered by control of hypertension, but most have had insufficient power to study this question.110 The recent ALLHAT study treated hypertension with diuretics and more recent antihypertensive drugs with CHD as an endpoint. There was no placebo group. They found thiazide-type diuretics to be superior to more modern agents for combined CVD, stroke and heart failure.111 Blood pressure control has greatly improved in the United States in the last 20–25 years, according to surveys showing a substantial decrease in the proportion of hypertensive persons unidentified or not under control.55,112,113 These trends have occurred in parallel with downward trends for both CHD and stroke mortality, although a direct relationship cannot be established. In fact, the mortality rate from stroke was diminishing long before safe and effective antihypertensive therapy was widely used. Moreover, stroke death rates in the United States fell during the 1950s and 1960s, when CHD death rates were rising sharply.2 Estimated changes in death rates for CHD and stroke, based on models of hypertension control, suggest a large potential for the prevention of CVD. Primary prevention of hypertension would likely have even more impressive effects on the public health. Present challenges to preventive practice lie mainly in more effective control of elevated blood pressure in the elderly and in finding the ideal combination of drug and hygienic management for correction of mild or borderline levels of high blood pressure. The larger public health challenge lies in improvement of population wide correlates of hypertension, such as physical inactivity, overweight, and high salt and alcohol intake. Such primary preventive and public health approaches promise to minimize the exhibition of high blood pressure, since human populations are apparently widely susceptible.

Tobacco Smoking The broader relationship of tobacco to disease and health is detailed in Chap. 54. Much of the clinical evidence of a direct relationship between cigarette smoking and coronary disease was, until recently, anecdotal. Experimentally, ischemic pain, angiographic coronary spasm, and electrocardiographic findings are now demonstrated during smoking in patients with compromised coronary circulation.114 For individuals living within societies with a high CHD incidence, smoking is consistently found to be a strong and independent risk factor for myocardial infarction and sudden death.93–95 The risk is continuous from persons who have never smoked, to ex-smokers, to those who smoke even in small amounts and is also related to duration of the habit.115,116 Interactions with other risk factors are also important, as indicated by the weak association of smoking with CHD risk in low-risk societies.11,12 For example, the observed incidence of CHD in populations that do not have a base of relative mass hypercholesterolemia is much lower than the risk predicted with multiple

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regression equations derived from U.S. or northern Europe data.115 The Japanese, for example, with a heavy prevalence of smoking and substantial amounts of hypertension, but without hypercholesterolemia, show much less coronary heart disease than would be predicted.11,12 As is the case with serum cholesterol level, most of the CHD cases attributable to smoking derive from the central part of the distribution, that is, light and moderate smokers; the prevalence of heavy smokers is low. A 17% population-attributable risk fraction for smoking and CHD deaths in the United States was estimated (conservatively) in the Carter Report.117 Smoking is particularly significant in CHD risk among women.118 Smoking cessation is associated with lower CHD rates according to years of cessation.119 While those who have never smoked have the best disease experience, long-term quitters approximate their rates, and even temporary quitters have a better risk experience than persistent smokers.120 Improvement in the prognosis of survivors of myocardial infarction who quit smoking also tend to confirm the harmful cardiovascular effects of cigarettes and supports the potential for CHD prevention by reduction of tobacco use.116,121 Synthesis of this evidence, therefore, suggests that cigarette smoking is neither a primary nor a necessary factor in determining population rates of CHD. It is, rather, a strong and independent risk factor for CHD and vascular disease among individuals living in high-incidence populations where there is a significant background of coronary and peripheral atherosclerosis. Mechanisms presumed to be important in CHD include the physicochemical effects of tobacco, that is, increased heart rate and myocardial contractility and greater myocardial oxygen demand due to raised catecholamine levels, decreased oxygen-carrying capacity of the blood, elevated fibrinogen levels, and platelet-aggregating effects. Other possible mechanisms include elevated fasting blood glucose levels and white blood cell counts and lower HDL levels, all found among smokers.114 A public health policy to foster so-called safer cigarettes, at least with respect to lowering CVD risk, is not supported by the evidence of persistent high exposure to gas-phase toxins in “low-yield” cigarette users.114 Moreover, the promotion and adoption of Western-type cigarettes and smoking patterns in developing countries augurs ill for the future CVD risk in those populations. In contrast, smoking prevalence has decreased substantially in the United States, where large numbers of educated adults in particular have stopped smoking. This is attributed to increased community awareness of the health need to stop smoking, to social pressure and legislation for “clean air” and “smoke-free” environments, and to a greater access to the support and skills needed for quitting. The downward U.S. trend in smoking is not as evident, however, among lower socioeconomic groups and heavy smokers.122 Under “ideal” supportive circumstances, such as that given highrisk participants in the MRFIT, smoking cessation success rates approximate 40% in the first year, with maintenance of this rate for up to four years among volunteer participants. Thus a long-standing medical pessimism about helping patients stop smoking might be replaced by optimism for cessation programs that are systematically applied. Moreover, communitywide educational and legislative efforts are increasingly effective.123,124 The results of all these efforts and the population trends downward in smoking frequency provide a rational basis for more public programs and for a more focused national policy to reduce cigarette smoking and tobacco production. It is equally possible that the currently declining rate of cigarette smoking will level off, unless educational programs and wider social support for nonsmoking behavior reach the lower socioeconomic classes, heavy smokers, women, and youth.

diabetes and insulin levels to atherosclerosis and to thrombosis. The interaction between chronic arterial wall disease and the blood properties leading to coagulation continues to be a major subject for research as it becomes clear that a critical fixed obstructive lesion is not necessary for myocardial infarction. In fact, thrombi forming on so-called “soft plaques” which rupture account for a significant proportion.125 The components of the coagulation system found so far to be of major interest are platelets and fibrin and they aggregate when cell walls are damaged and develop fibrin platelet masses, and platelet aggregation.126,127 Of the several hemostatic variables measured with respect to subsequent CHD risk, fibrinogen has received the most attention. Several investigators conclude that an elevated fibrinogen level is likely to be causally associated with CHD but that its elevation overall may be due primarily to smoking.126 As for primary prevention of CHD events with low-level anticoagulation, such as with small doses of aspirin, this appears now to be established for nonfatal myocardial infarction in men.128

Physical Environment It is increasingly apparent that modern industrialized society developed an environment which is not conducive to good health.129 Communities are built without parks, playgrounds, libraries, nearby stores, sidewalks, or public transit. The result is dependence on personal automobiles and social isolation. These environments may actually promote chronic diseases such as CHD. There is increasing understanding of the effects of these practices and attempts to promote healthier community designs. The weather, particularly the influx of cold fronts and rapid falls in barometric pressure, has been correlated with new hospital admissions for coronary events and sudden death.130 Reasonable preventive practice includes advice to avoid exposure, in particular the combination of isometric work and cold, and to use light face masks to maintain a favorable personal air temperature and humidity. Similarly, atmospheric inversions and air pollution are related to hospitalization and death rates from pulmonary and cardiovascular diseases, particularly in the elderly. These observations are increasingly linked to specific environmental pollution agents including nitrogen, sulfur dioxide, ozone, lead, and particulate matter.131 Most recently fire particles (PM2.5) < 2.5 µm have received attention. The result of combustion, they easily reach the alveoli. Experimental data suggests they may play a role in the etiology and onset of cardiovascular diseases.

Social Support Several prospective population-based studies have established social support or “social connectedness” as a factor associated with reduced risk of death. Two large studies—one from Finland132 and one from Sweden133—examined CVD disease risk. The pattern of results suggests a relationship between social support and mortality, at least in men. Whether this is a causal relationship or is attributable to a confounding variable such as baseline health or to personality characteristics such as hostility is unclear, and this line of investigation might well be continued. Attempts have been made to change psychosocial characteristics experimentally and to measure CHD risk factors and disease changes. Recently, the enhancing recovery in coronary heart disease patients (ENRICH) trial tested cognitive behavioral therapy and antidepression medications post myocardial infarction to increase social support and decrease depression. The trial showed no difference in the endpoint of recurrent myocardial infarction and death.134

Hemostatic Factors For decades, arguments have existed about the relative predominance of the role of classical risk factors versus thrombosis in the pathogenesis of atherosclerosis and CHD. A more unified theory now joins the effects of diet and blood lipids, physical activity and smoking, and

Gender and Estrogens The excess risk of CHD and atherosclerosis in men at earlier ages is documented throughout affluent Western society. The sex differential is much less prominent, however, in nonwhite populations and in

62 areas where the overall incidence is relatively low.135 The particular susceptibility of men is only partly explained by their higher risk factor configurations between the ages of 25 and 60. On the other hand, the relative protection from CHD among premenopausal women is assumed to be related to hormones, although the effect of early oophorectomy, menopause, or estrogen replacement therapy on known risk factor distributions in women fails to completely explain these differences. In countries with a high incidence of CHD, where there is relative mass hyperlipidemia much more of the plasma cholesterol is carried in the HDL fraction in women. Recent experimental evidence concerning mechanisms of LDL and HDL function, related to cell receptors and lipid transport in and out of the arterial wall, confirm this particular biological difference as a likely cause for some of the sex difference in CHD risk. In contrast, women have a proportionately greater risk of angina pectoris than of myocardial infarction or sudden death. While they have less severe atherosclerosis in the coronary arteries, the sex difference is not as apparent in cerebral, aortic, and peripheral vessels. Survival of women after myocardial infarction is poorer in-hospital, although this is balanced by greater outof-hospital death for men. Finally, trends in CHD deaths in the United States indicate that the age-specific decline in mortality is proportionately greater in women than in men.2 Similarly, the rise in CHD death rates among women in eastern Europe, where CVD deaths overall are increasing rapidly, is proportionately greater in women and in young women.136 The excess risk of thromboembolism, stroke, and myocardial infarction in women taking oral contraceptives (OCs), and the interaction of OCs with age and smoking, are well established. Young women taking OCs have systematically higher serum lipid levels, higher blood pressure, and impaired glucose tolerance compared with control subjects.137 Numerous epidemiologic studies evaluated the use of postmenopausal estrogen in the primary prevention of cardiovascular disease.138 Meta-analysis suggested a relative risk of 0.50–0.65 for coronary artery disease in estrogen users.139 These data exemplify the danger of extrapolating observational studies to therapeutic lesions. When randomized studies of hormone replacement therapy were performed the Heart and Estrogen/Progestin Replacement Study (HERS) and the Women’s Health Initiative (WHI) trial, no benefit and potential harm was observed.140,141 In summary, the sex differential for atherosclerosis and cardiovascular disease events and their time trends is not completely explained on the basis of known effects of hormones on the level of risk factors. More study of gender difference is needed.

Genetic Factors Much current work is opening up the understanding of hostenvironmental relationships. The relative contribution of genes to disease risk of populations can be exaggerated, however, by studies of gene effects when limited to homogeneous, high-risk cultures where exposure is great and universal. Most of the lack of understanding, and much of the difficulty in identification of susceptible persons, lies in the unavailability of specific genetic markers for CVD and the incapacity of family studies to discriminate intrinsic components without such markers. Recent findings of the gene loci for apolipoprotein regulation hold great promise of an improved understanding of individual differences in blood lipoproteins and their response to diet. There is, for example, evidence of the genetic inheritance of LDL subclasses HDL, apo-B and apo-E.142 A substantial proportion of the variation in apo-B levels (43%) may be explained by a major locus.143 A major gene controlling LDL subclasses may account for much of the familial aggregation of blood lipids and CHD risk.144 Most intrinsic blood lipoprotein regulation, however, is clearly polygenic and strongly interactive with the environment, especially with composition of the habitual diet. Controlled experiments in metabolically normal people suggest that there is a normal distribution of individual blood lipid responses to a known dietary change.145

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The rare major gene effects that cause extreme manifestations of the hyperlipidemias are increasingly well characterized, but they account for only a small fraction of the mass phenomenon of hypercholesterolemia found in affluent cultures. Thus most atherosclerotic complications and most of the excess CHD events in the general population cannot be attributed to major gene effects. Nevertheless, gene-culture interactions remain important to preventive practice for better detection and individualized therapy of patients who have elevated blood lipid values. A potentially important aspect of genetically determined diet responses now under investigation is the response of individual lipoprotein fractions to specific dietary factors, mainly fatty acids and cholesterol. A wider issue, however, is the relative magnitude of the contribution of intrinsic regulation to the large population differences found for average blood lipid values and their distributions. For the time being, this contribution remains speculative. Genetic control of CVD risk factors other than blood lipids is even less well-known.146 For example, not yet identified are genetic traits that might affect individual sensitivity to salt intake, to the atherogenic effect of cigarette smoking, or to the regulation of blood insulin and glucose levels, arterial wall enzymes, or personality type. There has been growing research on the genetics of hypertension. Markers have been discovered in a disease which is most likely polygenic for the proportion heritable.147 The public health view that a favorable environment assures minimal expression of phenotypic risk provides the rationale for a population approach to prevention. This rationale has not been effectively challenged, but neither has it been universally accepted.

Combined Risk Factors Clinical, laboratory, and epidemiological studies of CVD risk factors have been oriented mainly toward determining individual causal roles for each factor. Cardiovascular diseases are clearly related, however, in both individuals and communities, to multiple factors operating together over time. Multiple-factor risk is firmly established and actually is quantified for both CHD and stroke. Based mainly on Framingham and Pooling Project analysis, a consistent, independent, and at least additive contribution is found for each of the major risk factors: cigarette smoking, arterial blood pressure, and total serum cholesterol level.60 The risk ratio between highest and lowest categories for combined risk within populations is approximately eight- to tenfold, in contrast to the risk ratio for single risk factors, which is approximately two- to fourfold. Prediction regressions derived from follow-up experience in European men, with the use of four major risk factors at baseline, when applied to men in the United States, show the multiple-risk concept to be “universal.” That is, the regressions define a continuum of CHD risk among individual U.S. men in a society that has quite different CHD rates overall.148 The slope of the relationship (regression) between the combined risk factors and disease, however, is much steeper in the United States than in the European population. At any given level of multiple risk, U.S. rates are twice those in Europe. This cultural difference in the “force” of risk factors indicates that a sizable influence on population differences in CHD risk remains unknown, although lifelong exposure to CHD risk is not captured in a single measure. Another indication of the combined force of risk factors comes from studies of low risk groups within industrialized populations. Those with low lipids, normal blood pressure, nonsmokers, nonobese, and without diabetes have very low CHD and stroke rates.149,150,151 Nevertheless, since these few risk factors operate universally and explain a substantial part of individual and population risk differences, public health action on that part of the difference now explained is both promising and indicated. Still another interpretation of the evidence of combined risk of CHD is that the synergism between risk characteristics leads to a major potential for preventive effects in the population by achieving relatively small shifts in the means and distributions of the multiple risk factors. This does not exclude the possibility of a population threshold for risk factors, below which population risk is remote. That

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is indicated by the relative scarcity of mass atherosclerosis and CHD in societies in which average serum total cholesterol levels are less than 200 mg/dL. Nor does it exclude the concept of necessary versus contributory causes. In the absence of the presumed necessary factor (i.e., mass hypercholesterolemia), population risk is negligible. It may be that the departures from perfect prediction, found with the use of multiple regression analysis, are due in part to their failure to include the duration of exposure to, or the directionality of, a particular risk level. RHEUMATIC HEART DISEASE

Rheumatic fever and rheumatic heart disease remain important public health problems in the world.152 It is a particular problem where poverty, overcrowding, malnutrition, and inadequate medical care are found.153–158 Even in industrialized societies, a relatively high prevalence of rheumatic fever persists in pockets of poverty, and outbreaks have been reported recently in affluent areas.159–164 Despite that rheumatic fever is demonstrably preventable and rheumatic heart disease has declined dramatically in most industrialized nations, this condition remains a major public health problem internationally. For more than 40 years it has been known that group A streptococcus infection underlies initial and recurrent attacks of rheumatic fever (see Chap. 9). The immunologic mechanisms and circumstances by which infection with this organism produces rheumatic fever and rheumatic heart disease and acute and chronic glomerulonephritis are well understood.165 In some surveys, as many as 3% of patients develop rheumatic fever after known streptococcal infections.166 As many as 50% of those who have once had rheumatic fever will, if untreated, experience attacks after a subsequent streptococcal infection. This suggests that host factors significantly determine susceptibility. Age is also an obvious factor, for example, infants do not develop rheumatic fever even though they are susceptible to streptococcal infection and glomerulonephritis. Such differences in susceptibility are clearly developmental, such as the variation with age, but others may have a genetic basis. The tendency of rheumatic fever to cluster in families, however, may be explained by shared environment as well as genes. During the 1960s, the incidence of acute rheumatic fever per 100,000 urban children 2–14 years of age in the United States ranged from 23 to 28 for whites and 27 to 55 for blacks. The incidence was still higher in Puerto Ricans. Currently it is closer to 2 per 100,000 with most cases among the underprivileged. In other parts of the world, the lowest rates of rheumatic fever have been observed in Scandinavia, with 1.3 cases per 100,000. In underdeveloped nations, the rates are much higher. Prevalence among school-age children in South America ranges from 1 to 10%.167 Mortality from rheumatic fever and rheumatic heart disease has fallen significantly in the United States in this century. It was 14.8 per 100,000 in 1950, 7.3 in 1970, and 2.7 in 1986, a decline of 82%. The diagnosis of acute rheumatic fever is made principally from clinical findings with the revised Jones criteria (see Chap. 9).168 These may be insufficiently sensitive, however, to detect mild cases, particularly in Western countries where clinical patterns have changed so that arthritis is often the only presenting manifestation; chorea, subcutaneous nodules, and erythema marginatum are now rarely seen. Diagnosis may be complicated by the lack of a preceding sore throat or an apparent infection.169 Current recommendations for the primary prevention of acute rheumatic fever and rheumatic heart disease and prophylaxis for bacterial endocarditis in those with known rheumatic valve disease are found on the American Heart Association website: www.heart.org. CONGENITAL HEART DISEASE

Malformations of the cardiovascular system are among the more frequently occurring congenital defects. They result from developmental errors caused by inherent defects in the genetic material of the embryo, environmental factors, or both.170–175

Family studies suggest that the offspring of parents with congenital heart disease have malformation rates ranging from 1.4 to 16.1%.176 Identical twins are both affected 25–30% of the time. While these and other findings of familial aggregation suggest genetic factors, common environment may also play a role.175 Chromosomal aberrations or mutations account for less than 10% of all congenital cardiovascular anomalies. In addition, noncardiac disorders also produce cardiovascular defects; these include Marfan’s syndrome, Friedreich’s ataxia, glycogen storage disease, and Down’s and Turner’s syndromes. Maternal viral infections during pregnancy are estimated to cause up to 10% of all congenital cardiac malformations. Rubella in the first 2 months of pregnancy is associated with congenital malformations in about 80% of live births and is thought to account for 2–4% of all congenital heart disease. Subclinical Coxsackievirus infections may be related to congenital heart disease. Acute hypoxia, residence at high altitudes, high carboxyhemoglobin levels, and uterine vascular changes from cigarette smoking are other potential causes.174 Maternal x-ray exposure results in an increased incidence of Down’s syndrome and possibly other congenital defects.173 Maternal metabolic defects, such as diabetes mellitus and phenylketonuria, are associated with increased incidence of congenital heart defects. Animal investigations, which have not been substantiated in humans, indicate that dietary deficiencies in the mother may result in congenital malformations. Obstetric problems are associated with congenital heart disease, including association of advanced maternal age with Down’s syndrome and a history of vaginal bleeding (threatened abortion) during the first 11 weeks of gestation with prematurity. The teratogenic potential of drugs, such as thalidomide and folic acid antagonists, is well documented. In addition, dextroamphetamines, anticonvulsants, lithium chloride, alcohol, and progesterone/estrogen are highly suspected teratogens acting in the first trimester of pregnancy, as are certain pesticides and herbicides (see Chap. 33).177 Data on the true incidence of congenital heart disease are limited. The chief sources of information are birth certificate and hospital birth data.171,172 Birth certificate data usually underestimate the true rate as the defect may not be discovered until later. It is estimated that there are 32,000 live- births with congenital heart disease in the U.S. and 1.5 million worldwide annually.178,179 A U.S. multicenter collaborative study in 1970 yielded the following incidence rates for congenital heart disease: 8.1 per 1000 total births, 7.6 per 1000 live births, and 16.5 per 1000 twin births.180 Most are correctable by modern medical and surgical methods, including cardiac transplantation; it is estimated that only one child per 1000 cannot be helped by such approaches.181 As a result, infant mortality from congenital cardiovascular disease has fallen steadily (Fig. 62-6). As with other conditions, mortality among black youth has fallen less than for whites. The correction of congenital defects by surgical and other interventions is an important factor in increasing survival. Patients who have been repaired live into adulthood presenting new challenges in their care.178,182 Although the overall incidence of congenital heart disease has apparently remained stable, the distribution of types of defects may be shifting. This includes unexplained increases in ventricular septal defects and patent ductus arteriosus. A decline in the number of infants born with rubella-caused defects may be explained by vaccination programs.180 Primary prevention of congenital heart disease includes the following established measures:171 1. Genetic counseling of potential parents and families with congenital heart disease 2. Rubella immunization programs a. Identification of susceptible women of childbearing age by serologic examination b. Immunization of susceptible women c. Avoidance of pregnancy for 2 months after rubella vaccination 3. Avoidance of exposure to viral diseases during pregnancy

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Figure 62-6. Infant mortality from congenital malformations of the circulatory system by race, U.S., 1970–2001. (Source: National Heart, Lung, and Blood Institute. Morbidity and Mortality Chart Book on Cardiovascular, Lung, and Blood Diseases. Bethesda, MD, 2004; NIH Publication.)

4. Administration of all usual vaccines to all children to eliminate reservoirs of infection 5. Avoidance of radiation during pregnancy 6. Avoidance of exposure to gas fumes, air pollution, cigarettes, alcohol, pesticides, herbicides, and high altitude during the first trimester of pregnancy 7. Avoidance of drugs of any kind during the first trimester of pregnancy, especially drugs of known or suspected teratogenic potential. CARDIOMYOPATHIES AND MYOCARDITIS

Cardiomyopathies are a broad group of cardiac diseases that involve the heart muscle. Although less common in industrialized nations, they account for 30% or more of heart disease deaths in some developing countries.183 They are of diverse etiology and are usually classified by the functional results of their effects on the myocardium: dilated or congestive, hypertrophic and restrictive. Some recommendations suggest that the term “cardiomyopathy” be reserved for disease of unknown origin involving heart muscle.183 However, the common use of the term still associates it with specific causal syndromes when these are known. Some cardiomyopathies are diagnosed in their acute phase, where inflammation of the myocardium is common (myocarditis). While myocarditis is particularly difficult to categorize, diagnosis has been facilitated by the widespread use of endomyocardial biopsy.184 These techniques have suggested that an inflammatory reaction is more common than was previously suspected. Identified causes include infectious, metabolic, toxic, allergic, and genetic factors.185 Myocarditis and cardiomyopathy may be mild and undetected but also can be rapidly fatal with progressive heart failure. In industrialized nations, cardiomyopathies appear to be increasing in prevalence, although it is unclear whether there is an actual increase or an increase in professional awareness and improved diagnostic techniques.186 The latter include use of the echocardiogram, Doppler flow studies, and catheter-based endomyocardial biopsy. Surveillance of Olmsted County, Minnesota, found an incidence of idiopathic dilated cardiomyopathy of 6 per 100,000 person years. Overall prevalence was 35.3 per 100,000 population.187 Mortality from cardiomyopathy in the United States varies by age, race and sex (Table 62-4). Mortality is higher in blacks than whites and greater in men than women. Mortality increases with age, suggesting the pattern of a chronic condition. Alcohol abuse is an important cause of cardiomyopathy, accounting for approximately 8% of all cases in the United States.186,188

Alcohol causes myocardial damage by several mechanisms.189,190 These include (a) a direct toxic effect, (b) effects of thiamine deficiencies, and (c) effects of additives such as cobalt in alcoholic beverages. Abstinence from alcohol may halt or even reverse the cardiomyopathy.191 Another major cause of cardiomyopathy in industrialized countries is viral infection, particularly Coxsackie B virus, echovirus, influenza, and polio,192 often beginning as a viral myocarditis. Subclinical viral disease is thought to be more common than was previously suspected, with most patients recovering without sequelae. More severe forms, however, result in dilated cardiomyopathy and death due to congestive heart failure or arrhythmias. Recent research has suggested an autoimmune component and indicated that immunosuppressive therapy may be helpful in modifying the disease.193 However, early clinical trials have shown no benefit for corticosteroids.194 Hypertrophic cardiomyopathy (HCM) is another cause of death.195 Largely undetected until the advent of echocardiographic techniques, it is becoming increasingly clear that this condition can be fatal and be managed with pharmacologic therapy.195 An Italian registry for HCM found a majority of patients were male (62%) and 89% were New York Heart Association class I–II. Most were in their fourth to sixth decade of life. Cardiovascular mortality was 1% per year, mainly due to heart failure.196 The genetic origins of this condition are increasingly apparent.197 In South and Central America, trypanosomiasis (Chagas’ disease) is endemic; an estimated 20 million people are afflicted.198 Extensive chronic myocarditis with heart failure may be observed years after the initial infection with the trypanosome. An acute infectious phase, characterized by fulminant

TABLE 62-4. DEATH RATES FOR CARDIOMYOPATHY BY AGE, RACE, AND SEX, U.S., 2001 Deaths/100,000 Population Ages 35–44 45–54 55–64 65–74 75–84

Black Male White Male 13.09 23.75 43.33 67.19 127.71

3.71 7.22 14.95 35.24 83.03

Black Female

White Female

6.14 11.98 19.72 36.27 69.07

1.28 2.82 6.37 17.22 42.41

In 2001, within sex groups, cardiomyopathy mortality was higher in blacks than in whites at each age; within race groups, it was higher in males than in females.

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and fatal myocarditis, occurs mainly in children. In most cases, however, an average of 20 years passes before Chagas’ cardiomyopathy becomes clinically apparent. An autoimmune process may play some role in the disease.199 Diagnosis is made by means of serologic study or a xenodiagnostic test. Although antiparasitic agents, such as nitroimidazole derivatives, can alter the acute infestation, there is little evidence that they are effective for the cardiomyopathy.183 Schistosomiasis is a major public health problem in the Nile and Yangtze basins where the parasitic infection is endemic, involving 85% of the population in certain areas. Chronic pulmonary embolization leads to pulmonary hypertension and right heart failure, but direct involvement of the myocardium is rare. New antiparasitic agents can limit the infection, but the main preventive strategy is a public health approach to controlling the vectors. There is increasing awareness of cardiomyopathy in Africa where it is suspected to be higher than reported based on autopsy studies.200 Unfortunately, there are few data on etiology and prevalence. SYPHILITIC HEART DISEASE

Although the prevalence and patterns of syphilis worldwide have been altered significantly in the antibiotic era, it remains an important public health problem in many nations. Recent reports indicate a rise in reported cases of primary and secondary syphilis in the United States, and surveys in developing nations indicate continued high incidence and prevalence rates.201 An increase in reported cases and a general decline in medical alertness to this condition encourage a continuing reservoir for late complications. Life-threatening tertiary syphilis is found in approximately 25–30% of untreated cases.202 Approximately 10% of those are cardiovascular syphilis, manifest predominantly as uncomplicated syphilitic aortitis, aortic aneurysm, aortic valvulitis with regurgitation, and coronary ostial stenosis.203 Although a course of antibiotic therapy is indicated when cardiovascular syphilis is diagnosed, there is little evidence that it alters the course of the cardiovascular disease. Because syphilis remains preventable, detectable, and treatable in the early stages, public health approaches should lead to eradication of the late effects of syphilis, including those in the cardiovascular system.204

PREVENTIVE STRATEGIES

A population approach to CVD prevention has been formally outlined by the World Health Organization and articulated in the Vancouver Declaration.7,205 It embraces both the systematic practice of screening and education for high risk, where national priorities can afford such practices, and broad public health policy and programs in health promotion for communities. Strategies for preventive practice are now widely available. Community-based strategies, programs, and materials are becoming available. National programs are under way in blood pressure control, diet and blood lipids, and smoking. Finally, healthpromotion resource centers are now established for training in the design and dissemination of preventive programs. The student and the health worker are referred to these sources: the Centers for Disease Control and Prevention, Atlanta, GA (www.cdc.gov/heartdisease/prevention/htm); and the Office of Prevention, Education and Control, National Heart Lung and Blood Institute, Bethesda, MD (www.nhlbi.nih.gov/about/opec/).

REFERENCES

1. Yusuf S, Reddy S, Ounpuu S, et al. Global burden of cardiovascular diseases: part I: general considerations, the epidemiologic transition, risk factors, and impact of urbanization. Circulation. 2001;104:2746–53.

2. Higgens M, Luepker R, eds. Report of a conference on trends and determinants of coronary heart disease mortality: international comparisons. Int J Epidemiol. 1989;18(Suppl 1). 3. McGovern PG, Jacobs DR, Jr, Shahar, et al. Trends in acute coronary heart disease mortality, morbidity, and medical care from 1985 through 1997: the Minnesota Heart Survey. Circulation. 2001;104: 19–24. 4. Tunstall-Pedoe H (ed), Kuulasmaa K, Tolonen H, et al., with 64 other contributors for the WHO MONICA Project. In: TunstallPedoe H, ed. MONICA Monograph and Multimedia Sourcebook. Geneva: World Health Organization, 2003. 5. Evans A, Tolonen H, Hense HW, et al. Trends in coronary risk factors in the WHO MONICA Project. Int J Epidemiol. 2001; 30(Suppl 1):S35–S40. 6. World Health Organization. World Health Statistics 2005. Geneva; 2005. 7. World Health Organization. Prevention of Coronary Heart Disease: Report of a WHO Expert Committee. WHO Technical Report Series, No. 678. Geneva; 1982. 8. Inter-Society Commission for Heart Disease Resources. Optimal resources for primary prevention of atherosclerotic diseases. Circulation. 1984;70:153A–205A. 9. Gotto AM, Jr. Lipid management in patients at moderate risk for coronary heart disease: insights from the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS). Am J Med. 1999;107:36S–39S. 10. The Multiple Risk Factor Intervention Trial Research Group. Mortality after 16 years for participants randomized to the Multiple Risk Factor Intervention Trial. Circulation. 1996;94:946–51. 11. Keys A, ed. Coronary heart disease in seven countries. Circulation. 1970;41–2 (Suppl I). 12. Keys A. Seven Countries: Death and Coronary Heart Disease in Ten Years. Cambridge, MA: Harvard University Press, 1979. 13. Gordon T, Garcia-Palmieri MR, Kagan A, et al. Differences in coronary heart disease mortality in Framingham, Honolulu and Puerto Rico. J Chronic Dis. 1974;27:329–44. 14. Rose G. Incubation period of coronary heart disease. Br Med J. 1982;284:1600–1. 15. McGill HC, Jr, ed. Geographic Pathology of Atherosclerosis. Baltimore: Williams & Wilkins, 1968. 16. Marmot MG, Syme SL, Kagan A, et al. Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: prevalence of coronary and hypertensive heart disease and associated risk factors. Am J Epidemiol. 1975;102:514–25. 17. Blackburn H. Trends and determinants of CHD mortality: changes in risk factors and their effects. Int J Epidemiol. 1989;18 (Suppl 1): S210–S215. 18. Stern MP. The recent decline in ischemic heart disease mortality. Ann Intern Med. 1979;91:630–40. 19. Cooper R. Rising death rates in the Soviet Union: the impact of coronary heart disease. N Engl J Med. 1981;304:1259–65. 20. Luepker RV. Epidemiology of atherosclerotic disease in population groups. In: Pearson TA, Criqui MH, Luepker RV, Oberman A, Winston M, eds. Primer in Preventive Cardiology. Dallas: American Heart Association, 1994;1–10. 21. Elmer PJ. Obesity and cardiovascular disease: practical approaches for weight loss in clinical practice. In: Pearson TA, Criqui MH, Luepker RV, Oberman A, Winston M, eds. Primer in Preventive Cardiology. Dallas: American Heart Association, 1994;189–204. 22. Grundy SM, Cleeman JI, Merz CN, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. Circulation. 2004;110:227–39. 23. Truswell AS. Diet and nutrition of hunter-gatherers. In: Elliott K, Whelan J, eds. Health and Disease in Tribal Societies. Ciba Found Symp. 1977;49: 213–22.

62 24. Blackburn H, Prineas RJ. Diet and hypertension: anthropology, epidemiology, and public health implications. Prog Biochem Pharmacol. 1983;19:31–79. 25. Eaton SB, Konner M. Paleolithic nutrition: a consideration of its nature and current implications. N Engl J Med. 1985;312:283–9. 26. Jacobs DR, Anderson J, Blackburn H. Diet and serum cholesterol: do zero correlations negate the relationships? Am J Epidemiol. 1979;10:77–88. 27. Blackburn H. The concept of risk. In: Pearson TA, Criqui MH, Luepker RV, Oberman A, Winston M, eds. Primer in Preventive Cardiology. Dallas: American Heart Association, 1994;25–41. 28. Blackburn H, Jacobs DR. Sources of the diet-heart controversy: confusion over population versus individual correlations. Circulation. 1984;70:775–80. 29. Keys A, Grande F, Anderson JT. Bias and misrepresentation revisited— “perspective” on saturated fat. Am J Clin Nutr. 1974;27:188–212. 30. Hegsted DM, McGandy RB, Myers ML, et al. Quantitative effects of dietary fat on serum cholesterol in man. Am J Clin Nutr. 1965;17:281–95. 31. Ascherio A, Hennekens CH, Buring JE, et al. Trans-fatty acids intake and risk of myocardial infarction. Circulation. 1994; 89:94–101. 32. Shekelle RB, Shryock AM, Paul O, et al. Diet, serum cholesterol, and death from coronary heart disease: the Western Electric Study. N Engl J Med. 1981;304:65–70. 33. Kromhout D, de Lezenne Coulander C. Diet, prevalence and 10-year mortality from coronary heart disease in 871 middle-aged men: the Zutphen study. Am J Epidemiol. 1984;119:733–41. 34. McGee DL, Reed DM, Yano K, et al. Ten-year incidence of coronary heart disease in the Honolulu Heart Program: relationship to nutrient intake. Am J Epidemiol. 1984;119:667–76. 35. Kushi LH, Lew RA, Stare FJ, et al. Diet and 20-year mortality from coronary heart disease: the Ireland-Boston Diet-Heart Study. N Engl J Med. 1985;312:811–8. 36. Mattson FH, Grundy SM. Comparison of effects of dietary saturated, monounsaturated, and polyunsaturated fatty acids on plasma lipids and lipoproteins in man. J Lipid Res. 1985;26:194–202. 37. St. Clair RW. Atherosclerosis regression in animal models: current concepts of cellular and biochemical mechanisms. Prog Cardiovasc Dis. 1983;26:109–32. 38. Clarkson TB, Bond MG, Bullock BC, et al. A study of atherosclerosis regression in Macaca mulatta: V. Changes in abdominal aorta and carotid and coronary arteries from animals with atherosclerosis induced for 38 months and then regressed for 24 or 48 months at plasma cholesterol concentrations of 300 or 200 mg/dL. Exp Mol Pathol. 1984;41:96–118. 39. Anitschkow N. Experimental atherosclerosis in animals. In: Cowdry EV, ed. Arteriosclerosis. New York: Macmillan, 1983;271. 40. Wallace RB, Lynch CF, Pomrehn PR, et al. Alcohol and hypertension: epidemiologic and experimental considerations. Circulation. 1981;64:41–7. 41. Dyer AR, Stamler J, Paul O, et al. Alcohol, cardiovascular risk factors and mortality: the Chicago experience. Circulation. 1981;64: 20–7. 42. Haskell WL, Comargo C, Williams PT, et al. The effect of cessation and resumption of moderate alcohol intake on serum high density lipoprotein subfractions. N Engl J Med. 1984;310:805–10. 43. Ellison RC. Balancing the risks and benefits of moderate drinking. Ann NY Acad Sci. 2002;957:1–6. 44. Djoussé L, Ellison RC, Beiser A, et al. Alcohol consumption and risk of ischemic stroke: The Framingham Study. Stroke. 2002;33: 907–12. 45. Li JM, Mukamal KJ. An update on alcohol and atherosclerosis. Curr Opin Lipidology. 2004;15:673–80. 46. Kare MR, Fregly MJ, Bernard RA, eds. Biological and Behavioral Aspects of Salt Intake. New York: Academic Press, 1980.

Heart Disease

1085

47. Freis ED. Salt, volume and the prevention of hypertension. Circulation. 1976;53:589–95. 48. Writing Group of the PREMIER Collaborative Research Group. Effects of comprehensive lifestyle modification on blood pressure control. JAMA. 2003;289:2083–93. 49. Meneely GR, Battarbee HD. High sodium–low potassium environment and hypertension. Am J Cardiol. 1976;38:768–85. 50. Gleibermann L. Blood pressure and dietary salt in human populations. Ecol Food Nutr. 1973;2:143–56. 51. INTERSALT Cooperative Research Group. INTERSALT: an international study of electrolyte excretion and blood pressure: results for 24 hour urinary sodium and potassium excretion. Br Med J. 1988;297:319–28. 52. Joseph JG, Prior IAM, Salmond CE, et al. Elevation of systolic and diastolic blood pressure associated with migration: the Tokelau Island Migrant Study. J Chronic Dis. 1983;36(7):507–16. 53. Kesteloot H, Vuylsteks M, Costenoble A. Relationship between blood pressure and sodium and potassium intake in a Belgian male population group. In: Kesteloot K, Joossens J, eds. Epidemiology of Arterial Blood Pressure. The Hague: Nijhoff, 1980;345–51. 54. Appel LJ, Brands MW, Daniels SR, et al. Dietary approaches to prevent and treat hypertension: a scientific statement from the American Heart Association. Hypertension. 2006;47:296–308. 55. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC VII Report. JAMA. 2003;289:2560–72. 56. Shimamoto T, Komachi Y, Inada H, et al. Trends for coronary heart disease and stroke and their risk factors in Japan. Circulation. 1989;79:503–15. 57. Hulley SB, Rosenman RH, Banol RD, et al. Epidemiology as a guide to clinical decisions: the associations between triglycerides and coronary heart disease. N Engl J Med. 1980;302:1383–9. 58. NIH Consensus Development Panel: Triglyceride, high density lipoprotein, and coronary heart disease. JAMA. 1993;269: 505–10. 59. Conference on Blood Lipids in Children: Optimal levels for early prevention of coronary artery disease. Prev Med. 1983;12:725–905. 60. The Pooling Project Research Group. Relationship of blood pressure, serum cholesterol, smoking habits, relative weight and ECG abnormalities to incidence of major coronary events: final report of the Pooling Project. J Chronic Dis. 1978;31:201–306. 61. Stamler J, Wentworth D, Neaton JD. Is the relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA. 1986;256:2823–8. 62. Gordon T, Castelli W, Hjortland MC, et al. High density lipoprotein as a protective factor against coronary heart disease. Am J Med. 1977;62:707–14. 63. National Diet-Heart Study Research Group. The National DietHeart Study: final report. Circulation. 1968;37:1–428. 64. Frick MH, Elo O, Haapa K, et al. Helsinki Heart Study: primary prevention trial with gemfibrozil in middle-aged men with dyslipidemia. N Engl J Med. 1987;317:1237–45. 65. Shepherd J, Cobbe SM, Ford I, et al. For the West of Scotland Coronary Prevention Study Group: Prevention of coronary heart disease with provastatin in men with hypercholesterolemia. N Engl J Med. 1995;333:1301–7. 66. Scandinavian Simvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344: 1383–9. 67. Kiekshus H, Pedersen TR. Reducing the risk of coronary events: evidence from the Scandinavian Simvastatin Survival Study. Am J Cardiol. 1995;76:64C–68C.

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68. Pfeffer MA, Sacks FM, Move LA, et al. Cholesterol and recurrent events: a secondary prevention trial for normolipidemic patients. CARE Investigators. Am J Cardiol. 1995;76:98C–106C. 69. Johnson CL, Rifkind BM, Sempos CT, et al. Declining serum total cholesterol levels among U.S. adults. JAMA. 1993;269:3002–8. 70. Arnett DK, Jacobs DR, Luepker RV, et al. Twenty-year trends in serum cholesterol, hypercholesterolemia, and cholesterol medication use: The Minnesota Heart Survey, 1980-1982 to 2000-2002. Circulation. 2005;112:3884–91. 71. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). JAMA. 2001;285: 2486–97. 72. The Expert Panel. Report of the National Cholesterol Education Program Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults. Arch Intern Med. 1988;148: 36–69. 73. National Cholesterol Education Program. Second report of the Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel II). Circulation. 1994;89:1329–1445. 74. National Cholesterol Education Program. Report of the Expert Panel on population strategies for blood cholesterol reduction. Arch Intern Med. 1991;151:1071–84. 75. National Cholesterol Education Program: Report of the Expert Panel on blood cholesterol levels in children and adolescents. Pediatrics. 1992;89:525–84. 76. Barrett-Connor EL. Obesity, atherosclerosis and coronary heart disease. Ann Intern Med. 1985;103:1010–9. 77. Flegal KM, Carroll MD, Ogden CL, et al. Prevalence and trends in obesity among U.S. adults, 1999–2000. JAMA. 2002;288:1723–7. 78. Hubert HB, Feinlieb M, McNamara PM, et al. Obesity as an independent risk factor for cardiovascular disease: a 26-year followup of participants in the Framingham Heart Study. Circulation. 1983;67: 968–77. 79. Tyroler HA, Heyden S, Hames CG. Weight and hypertension: Evans County studies of blacks and whites. In: Paul O, ed. Epidemiology and Control of Hypertension. New York: Grune & Stratton, 1975. 80. Rabkin SW, Mathewson FAC, Hsu PH. Relation of body weight to the development of ischemic heart disease in a cohort of young North American men after a 26-year observation period: the Manitoba study. Am J Cardiol. 1977;39:452–8. 81. Larsson B, Svardsudd K, Welin L, et al. Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13-year follow-up of participants in the study of men born in 1913. Br Med J. 1984;288:1401–4. 82. Donahue RP, Abbott RD, Bloom E, et al. Central obesity and coronary heart disease in men. Lancet. 1987;1:821–4. 83. Bjorntorp P. The associations between obesity, adipose tissue distribution and disease. Acta Med Scand. 1988;723:121–34. 84. Montenegro MR, Solberg LA. Obesity, body weight, body length, and atherosclerosis. Lab Invest. 1968;18:594–603. 85. Lissner L, Bengtsson C, Lapidus L, et al. Body weight variability and mortality in the Goteborg prospective studies of men and women. In: Bjorntorp P, Rossner S, eds. Proceedings of the European Congress of Obesity. London: John Libbey, 1989;55–60. 86. Taylor HL, Buskirk ER, Remington RD. Exercise in controlled trials of the prevention of coronary heart disease. Fed Proc. 1973;32: 1623–7. 87. Oldridge NB, Guyatt GH, Fischer ME, et al. Cardiac rehabilitation after myocardial infarction: combined experience of randomized clinical trials. JAMA. 1988;260:945–50.

88. Blackburn H, Jacobs DR. Physical activity and the risk of coronary heart disease [Editorial]. N Engl J Med. 1988;319:1217–9. 89. NIH Consensus Development Panel on Physical Activity and Cardiovascular Health. Physical activity and cardiovascular health. JAMA. 1996;276:241–6. 90. Powell KE, Thompson PD, Caspersen CJ, et al. Physical activity and the incidence of coronary heart disease. Annu Rev Public Health. 1987;8:253–87. 91. Leon AS, Connett J, Jacobs DR, Jr, et al. Leisure-time physical activity levels and risk of coronary heart disease and death: the Multiple Risk Factor Intervention Trial. JAMA. 1987;258:2388–95. 92. Slattery ML, Jacobs DR, Jr., Nichaman MZ. Leisure time physical activity and coronary heart disease death: the U.S. Railroad Study. Circulation. 1989;79:304–11. 93. Blair SN, Kohl HW, Paffenbarger RS, Jr, et al. Physical fitness and all-cause mortality: a prospective study of healthy men and women. JAMA. 1989;262:2395–2401. 94. Paffenbarger RS, Jr, Wing AL, Hyde RT. Physical activity as an index of heart attack risk in college alumni. Am J Epidemiol. 1978;108:161–75. 95. Paffenbarger RS, Jr, Hyde RT, Wing AL, et al. A natural history of athleticism and cardiovascular health. JAMA. 1984;252:491–5. 96. Siscovick DS, Weiss NS, Fletcher RH, et al. The incidence of primary cardiac arrest during vigorous exercise. N Engl J Med. 1984;311:874–7. 97. Mittleman MA, Maclure M, Tofler GH, et al. Triggering of acute myocardial infarction by heavy physical exertion: protection against triggering of regular exertion. N Engl J Med. 1993;329:1677–83. 98. American Heart Association. Heart Disease and Stroke Statistics— 2005 Update. Dallas, TX: American Heart Association; 2005. 99. West KM. Epidemiology of Diabetes and Its Vascular Lesions. New York: Elsevier,1978;375–402. 100. Pyorala K, Laakso M, Uusitupa M. Diabetes and atherosclerosis: an epidemiologic view. Diabetes Metab Rev. 1987;3:463–524. 101. Knowler WC, Bennett PH, Hammon RF, et al. Diabetes incidence and prevalence in Pima Indians: a 19-fold greater incidence than in Rochester, MN. Am J Epidemiol. 1978;108:497–505. 102. Barrett-Connor E, Wingard DL. Sex differential in ischemic heart disease mortality in diabetics: a prospective population-based study. Am J Epidemiol. 1983;118:489–96. 103. University Group Diabetes Program. A study of the effects of hypoglycemic agents on vascular complications in patients with adult onset diabetes. V. Evaluation of phenoformin therapy. Diabetes. 1975;24:65–184. 104. United Kingdom Prospective Diabetes Study Group. United Kingdom prospective diabetes study (UKPDS) 13: relative efficacy of randomly allocated diet, sulphonylurea, insulin, or metformin in patients with newly diagnosed non-insulin dependent diabetes followed for three years. Br Med J. 1995;310:83–8. 105. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993;329:977–86. 106. Nissen SE, Wolski. Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. N Engl J Med. 2007;356:2457–71. 107. Stamler R, Stamler J, Lindberg HA, et al. Asymptomatic hyperglycemia and coronary heart disease in middle-aged men in two employed populations in Chicago. J Chronic Dis. 1979;32: 805–15. 108. Hughes LO. Insulin, Indian origin and ischemic heart disease [Editorial]. Int J Cardiol. 1990;26:1–4. 109. SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. JAMA. 1991;265:3255–64.

62 110. Hypertension Detection and Follow-Up Group. The effect of treatment on mortality in “mild” hypertension. N Engl J Med. 1982;307:976–80. 111. The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic. JAMA. 2002;288:2981–2997. 112. Luepker RV, Arnett DK, Jacobs DR, Jr., et al. Trends in blood pressure, hypertension control, and stroke mortality, 1980 to 2002: the Minnesota Heart Survey. Am J Med. 2006;119:42–49. 113. U.S. Department of Health and Human Services. Morbidity and Mortality: 2004 Chart Book on Cardiovascular, Lung and Blood Diseases. Washington, DC: National Institutes of Health, 2004. 114. McGill HC, Jr. Potential mechanisms for the augmentation of atherosclerosis and atherosclerotic disease by cigarette smoking. Prev Med. 1979;8:390–403. 115. Kannel WB, McGee DL, Castelli WP. Latest perspectives on cigarette smoking and cardiovascular disease: the Framingham Study. J Cardiovasc Rehab. 1984;4:267–77. 116. Wilhelmsen L. Coronary heart disease: epidemiology of smoking and intervention studies of smoking. Am Heart J. 1988;115:242–9. 117. Amler RW, Dull HB, eds. Closing the Gap: The Burden of Unnecessary Illness. New York: Oxford University Press, 1987. 118. Willett WC, Green A, Stampfer MJ, et al. Relative and absolute excess risks of coronary heart disease among women who smoke cigarettes. N Engl J Med. 1987;317:1303–9. 119. Doll R, Hill AB. Mortality in relation to smoking: ten years’ observations of British doctors. Br Med J. 1964;1:1399–1410. 120. Freidman GD, Petitti DB, Bawol RD, et al. Mortality in cigarette smokers and quitters: effect of base-line differences. N Engl J Med. 1981;304:1407–10. 121. Aberg A, Bergstrand J, Johansson S, et al. Cessation of smoking after myocardial infarction: effects on mortality after ten years. Br Heart J. 1983;49:416–22. 122. Luepker RV, Rosamond WD, Murphy R, et al. Socioeconomic status and coronary heart disease risk factor trends: the Minnesota Heart Survey. Circulation. 1993;88:2172–9. 123. Luepker RV, Murray DM, Jacobs DR, Jr, et al. Community education for cardiovascular disease prevention: risk factor changes in the Minnesota Heart Health Program. Am J Prev Med. 1994;84:1383–93. 124. Public Health Service, Office on Smoking and Health: Report of the Surgeon General. Reducing the Health Consequences of Smoking: Twenty-Five Years of Progress. Rockville, MD: U.S. Department of Health and Human Services, 1989. 125. Farb A, Tang AL, Burke AP, et al. Frequency of active coronary lesions, inactive coronary lesions and myocardial infarction. Circulation. 1995;92:1701–9. 126. Meade TW. Clotting factors and ischemic heart disease. In: Meade TW, ed. The Epidemiological Evidence from Anti-coagulants in Myocardial Infarction: A Reappraisal. New York: John Wiley & Sons, 1984. 127. Libby P, Simon DI. Inflammation and thrombosis: The clot thickens. Circulation. 2001;103:1718–20. 128. Ridker PM, Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. NEJM. 1997;336:973–9. 129. Jackson RJ. The impact of the built environment on health: an emerging field. Am J Public Health. 2003;93:1382–4. 130. Beard CM, Fuster V, Elveback LR. Daily and seasonal variation in sudden cardiac death, Rochester, Minnesota, 1950–1975. Mayo Clin Proc. 1982;57:704–6. 131. Brook RD, Franklin B, Cascio W, et al. Air pollution and cardiovascular disease: a statement for healthcare professionals from the expert panel on population and prevention science of the American Heart Association. Circulation. 2004;109:2655–71.

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132. Kaplan GA, Salonen JT, Cohen RD, et al. Social connections and mortality from all causes and from cardiovascular disease: prospective evidence from Eastern Finland. Am J Epidemiol. 1988;128:370–80. 133. Orth-Gomer K, Johnson JV. Social network interaction and mortality: a six year follow-up study of a random sample of the Swedish population. J Chronic Dis. 1987;40:949–57. 134. Writing Committee for the ENRICHD Investigators. Effects of treating depression and low perceived social support on clinical events after myocardial infarction. JAMA. 2003;289:3106–16. 135. McGill HC Jr, Stern MP. Sex and atherosclerosis. In: Paoletti R, Gotto AM, Jr, eds. Atherosclerosis Reviews. New York: Raven Press, 1979; vol 4:157–242. 136. Demirovic J. Recent trends in coronary heart disease mortality among women in Yugoslavia. CVD Epidemiology Newsletter. 1988;44:96–7. 137. Wahl P, Walden C, Knopp R, et al. Effect of estrogen/progestin potency on lipid/lipoprotein metabolism. N Engl J Med. 1983;308: 862–7. 138. Grady D, Rubin SM, Petitti DB, et al. Hormone therapy to prevent disease and prolong life in postmenopausal women. Ann Intern Med. 1992;117:1016–37. 139. Stampfer MJ, Colditz GA. Estrogen replacement therapy and coronary heart disease: a quantitative assessment of the epidemiologic evidence. Prev Med. 1991;20:47–63. 140. Hulley S, Grady D, Bush T, et al. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. JAMA. 1998;280:605–13. 141. Writing Group for the Women’s Health Initiative Investigators: Risks and benefits of estrogen plus progestin in healthy postmenopausal women. JAMA. 2002;288:321–33. 142. Austin MA, King MC, Bawol RD, et al. Risk factors for coronary heart disease in adult female twins: genetic heritability and shared environmental influences. Am J Epidemiol. 1987;125:308–18. 143. Hasstedt SJ, Wu L, Williams RR. Major locus inheritance of apolipoprotein B in Utah pedigrees. Genet Epidemiol. 1987;4:67–76. 144. Austin MA, King MC, Vranizan KM, et al. Inheritance of lowdensity lipoprotein subclass patterns: results of complex segregation analysis. Am J Hum Genet. 1988;43:838–46. 145. Jacobs DR, Anderson JT, Hannan P, et al. Variability in individual serum cholesterol response to change in diet. Arteriosclerosis. 1983;3:349–56. 146. Hunt SC, Hasstedt SJ, Kuida H, et al. Genetic heritability and common environmental components of resting and stressed blood pressures, lipids, and body mass index in Utah pedigrees and twins. Am J Epidemiol. 1989;129:625–38. 147. Dominiczak AF, Brain N, Charchar F, et al. Genetics of hypertension: Lessons learnt from mendelian and polygenic syndromes. Clin Experiment Hypertens. 2004;26:611–20. 148. Keys A, Aravanis C, Blackburn H, et al. Probability of middle-aged men developing coronary heart disease in five years. Circulation. 1972;45:815–28. 149. Stamler J, Stamler R, Neaton JD, et al. Low risk-factor profile and long-term cardiovascular and noncardiovascular mortality and life expectancy: findings of the 5 large cohorts of young adults and middle-aged men and women. JAMA. 1999;282:2012–8. 150. Daviglus ML, Stamler J, Pirzada A, et al. Favorable cardiovascular risk profile in young women and long-term risk of cardiovascular and all-cause mortality. JAMA. 2004;292:1588–92. 151. Daviglus ML, Liu K, Pirzada A, et al. Favorable cardiovascular risk profile in middle age and health-related quality of life in older age. Arch Intern Med. 2003;163:2460–8. 152. Carapetis JR, Steer AC, Mulholland EK, et al. The global burden of group A streptococcal diseases. Lancet Infect Dis. 2005;5:685–94. 153. Strasser T: Rheumatic fever and rheumatic heart disease in the 1970s. Public Health Rev. 1976;5:207–34.

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Noncommunicable and Chronic Disabling Conditions

154. World Health Organization. Intensified Program: Action to Prevent Rheumatic Fever/Rheumatic Heart Disease. WHO Document WHO/CVD/84.3. Geneva: World Health Organization, 1984. 155. Wang ZM, Zou YB, Lei S, et al. Prevalence of chronic rheumatic heart disease in Chinese adults. Int J Cardiol. 2006;107:356–9. 156. Bar-Dayan Y, Elishkevits K, Goldstein L, et al. The prevalence of common cardiovascular diseases among 17-year-old Israeli conscripts. Cardiology. 2005;104:6–9. 157. Hanna JN, Heazlewood RJ. The epidemiology of acute rheumatic fever in Indigenous people in north Queenland. Aust N Z J Public Health. 2005;29:313–7. 158. Ahmed J, Zaman MM, Hassan MMM. Prevalence of rheumatic fever and rheumatic heart disease in rural Bangladesh. Trop Doct. 2005;35:160–1. 159. Veasy LG, Tani LY, Hill HR. Persistence of acute rheumatic fever in the intermountain area of the United States. J Pediatr. 1994;124:9–16. 160. Hoffman JIE. Congenital heart disease. Pediatr Clin North Am. 1990;37:25–43. 161. Zangwill KM, Wald ER, Londino AV. Acute rheumatic fever in western Pennsylvania: a persistent problem into the 1990s. J Pediatr. 1991;118:561–3. 162. Carapetis JR, Currie BJ. Rheumatic fever in a high incidence population: the importance of monoarthritis and low grade fever. Arch Dis Child. 2001;85:223–7. 163. Giannoulia-Karantana A, Anagnostopoulos G, Kostaridou S, et al. Childhood acute rheumatic fever in Greece: experience of the past 18 years. Acta Paediatr. 2001;90:809–12. 164. Kurahara DK, Grandinetti A, Galario J, et al. Ethnic differences for developing rheumatic fever in a low-income group living in Hawaii. Ethn Dis. 2006;16:357–61. 165. Wannamaker LW, Matsen JM, eds. Streptococci and Streptococcal Diseases: Recognition, Understanding, and Management. New York: Academic Press, 1972. 166. Gordis L, Lilienfeld A, Rodriguez R. Studies in the epidemiology and preventability of rheumatic fever. II. Socio-economic factors and the incidence of acute attacks. J Chronic Dis. 1969;21:655–66. 167. Pan American Health Organization. Fourth Meeting of the Working Group on Prevention of Rheumatic Fever. Quito, Ecuador, 1970. 168. Dajani AS, Ayoub EM, Bierman FZ, et al. Guidelines for the diagnosis of rheumatic fever: Jones criteria, updated 1992. JAMA. 1992;268:2069–73. 169. Wannamaker LW. The chain that links the heart to the throat. Circulation. 1973;48:9–18. 170. Elliot RS, Edwards JE. Pathology of congenital heart disease. In: Hurst JW, ed. The Heart. New York: McGraw-Hill, 1978. 171. Congenital Heart Disease Study Group. Primary prevention of congenital heart disease. In: Wright IS, Fredrickson DT, eds. Cardiovascular Diseases, Guidelines for Prevention and Care. Reports of the Inter-Society Commission for Heart Disease Resources. Washington, DC: Government Printing Office, 1972;116. 172. Higgins ITT. The epidemiology of congenital heart disease. J Chronic Dis. 1965;18:699. 173. Nora JJ. Etiologic factors in congenital heart diseases. Pediatr Clin North Am. 1971;18:1059–74. 174. Fredrich J, Alberman ED, Goldsteen H. Possible teratogenic effect of cigarette smoking. Nature. 1971;231:529. 175. Rose V, Gold RJM, Lindsay G, et al. A possible increase in the incidence of congenital heart defects among the offspring of affected parents. J Am Coll Cardiol. 1985;6:376–82. 176. Ferencz C. Offspring of fathers with cardiovascular malformations. Am Heart J. 1986;111:1212–3. 177. Zierler S. Maternal drugs and congenital heart disease. Obstet Gynecol. 1985;65:155–65. 178. Perloff JK, Warnes CA. Challenges posed by adults with repaired congenital heart disease. Circulation. 2001;103:2637–43.

179. Boneva RS, Botto LD, Moore CA, et al. Mortality associated with congenital heart defects in the United States—trends and racial disparities, 1979–1997. Circulation. 2001;103:2376–81. 180. NHLBI Working Group on Heart Disease Epidemiology: Report. NIH Report 79-1667. Washington, DC: Government Printing Office, 1979. 181. Bailey NA, Lay P. New horizons: infant cardiac transplantation. Heart Lung. 1989;18:172–8. 182. Williams RG, Pearson GD, Barst RJ, et al. Report of the National Heart, Lung, and Blood Institute Working Group on research in adult congenital heart disease. J Am Coll Cardiol. 2006;47:701–7. 183. World Health Organization. Cardiomyopathies: Report of a WHO Expert Committee. WHO Technical Report Series, No. 697. Geneva: World Health Organization, 1984. 184. Fowles RE. Progress of research in cardiomyopathy and myocarditis in the USA. International Symposium on Cardiomyopathy and Myocarditis. Heart Vessels Suppl. 1985;1:5–7. 185. Olsen EGJ. What is myocarditis? International Symposium on Cardiomyopathy and Myocarditis. Heart Vessels Suppl. 1985;1:1–3. 186. Shabeter R. Cardiomyopathy: how far have we come in 25 years? How far yet to go? J Am Coll Cardiol. 1983;1:252–63. 187. Gillum RF. Idiopathic cardiomyopathy in the United States, 1970–1982. Am Heart J. 1986;111:752–5. 188. Okada R. Wakafuji S. Myocarditis in autopsy. International Symposium on Cardiomyopathy and Myocarditis. Heart Vessels Suppl. 1985;1:23–9. 189. Rubin E. Alcoholic myopathy in heart and skeletal muscle. N Engl J Med. 1979;301:28–33. 190. Alexander CS. Cobalt-beer cardiomyopathy: a clinical and pathological study of twenty-eight cases. Am J Med. 1972;53:395–417. 191. Regan TJ, Haider B, Ahmed SS, et al. Whisky and the heart. Cardiovasc Med. 1977;2:165. 192. Levine HD. Virus myocarditis: a critique of the literature from clinical, electrocardiographic and pathologic standpoints. Am J Med Sci. 1979;277:132–43. 193. McAllister HA, Jr. Myocarditis: some current perspectives and future directions. Tex Heart Inst J. 1987;14:331–4. 194. Parrillo JE, Cunnion RE, Epstein SE, et al. A prospective, randomized, controlled trial of prednisone for dilated cardiomyopathy. N Engl J Med. 1989;321:1061–8. 195. Wigle ED. Hypertrophic cardiomyopathy 1988. AHA-Mod Concepts Cardiovasc Dis. 1988;57:1–6. 196. Cecchi F, Olivotto I, Betocchi S, et al. The Italian registry for hypertrophic cardiomyopathy: A nationwide survey. Am Heart J. 2005;150:947–54. 197. Ahmad F, Seldman JG, Seldman CE. The genetic basis for cardiac remodeling. Ann Rev Genomics & Human Genetics. 2005;6: 185–216. 198. Hagar JM, Rahimtoola SH. Chagas’ heart disease. Curr Probl Cardiol. 1995;20:825–924. 199. World Health Organization. Report of the WHO Consultation on Cardiomyopathies: Approaches to Prevention and Early Detection. WHO Document, WHO/CVD/85.6. Geneva; World Health Organization, 1985. 200. Sliwa K, Damasceno A, Mayosi BM. Epidemiology and etiology of cardiomyopathy in Africa. Circulation. 2005;112:3577–83. 201. Centers for Disease Control. Summary of notifiable diseases— United States. MMWR. 1988;36:54–8. 202. Clark EG, Danbolt N. The Oslo study of the natural course of untreated syphilis: an epidemiologic investigation based on a re-study of the Boeck-Bruusgaard material. Med Clin North Am. 1964;48:613. 203. Musher DM. Syphilis. Infect Dis Clin North Am. 1987;1:83–95. 204. Jackman JD, Jr, Radolf JD. Cardiovascular syphilis. Am J Med. 1989;87:425–433. 205. Farquhar JW. The place of hypertension control in total cardiovascular health: perspectives outlined by the Victoria Declaration. Clin Exp Hypertens. 1995;17:1107–11.

Renal and Urinary Tract Disease

63

Rebecca L. Hegeman

INTRODUCTION

With over 50 million individuals worldwide having chronic kidney disease (CKD), a well recognized risk factor for cardiovascular disease, CKD is emerging as a worldwide public health problem.1 As countries develop and industrialize, diseases related to infections, crowding, and poor nutrition recede, and chronic disease associated with affluence, aging, overnutrition, medical interventions, drugs, addictions, and other exposures becomes prominent. While diseases of westernized societies are the main focus of this chapter, globalization has contributed to an increasing rate of noncommunicable chronic disease worldwide. In 2003 it was estimated that 60% of deaths worldwide would be due to noncommunicable diseases, with 16 million deaths resulting from cardiovascular disease and 1 million deaths from diabetes.2 Thus, the information in this chapter pertains to an ever widening circle of communities. With ischemic heart disease and cerebrovascular disease now listed as the number one and two causes of death worldwide, it is very probable that renal disease related to vascular disease will become more prevalent. In addition the increase in the prevalence of diabetes virtually assures that chronic kidney disease will continue to be a major cause of morbidity and mortality. Rates of most renal diseases and of end-stage renal disease (ESRD) in westernized societies rise with age, and increased longevity enhances the expression of both. More males than females are affected by many renal diseases, and more males enter ESRD treatment programs. Some groups recently absorbed into industrialized societies, such as U.S. blacks, North American Indians, Hispanics and Mexican Americans, urban South African blacks, Australian aborigines, Pacific Islanders, and New Zealand Maoris, have especially high rates of renal disease, in part from conditions such as hypertension and diabetes that were rare in their forebears. ESRD treatment programs themselves have produced a whole new set of clinical, economic, and sociological perspectives and concerns. Renal and urinary tract diseases are frequently asymptomatic for most of their course, and diagnosis is frequently dependent on laboratory and radiologic studies. Clinical renal disease may be manifested by blood, protein, or white blood cells in the urine, often with hypertension. Heavy protein excretion, decreased levels of serum albumin, hyperlipidemia, and edema characterize the “nephrotic syndrome.” Excretory renal function can be normal or impaired and can remain stable or progress to renal failure. Renal impairment generates, and is exacerbated by, hypertension. ESRD defines a situation of chronic irreversible renal failure in which prolonged survival is not possible without dialysis or renal transplantation. Specific diseases are diagnosed by history and clinical findings, biochemical, serological, imaging, and urodynamic studies, and sometimes by biopsy of the kidneys, bladder, or prostate. Kidney biopsy specimens are examined by light, immunofluorescent, and electron microscopy to aid in diagnosis and prognosis. The serum creatinine

level provides an approximate measure of renal insufficiency, although it varies with muscle mass and diet, underestimates renal insufficiency in the elderly, is relatively insensitive to loss of the first 50% of renal function, and is less sensitive to progressive loss of function in severe renal failure. Glomerular filtration rate (GFR), precisely measured by iothalamate and inulin clearances, can be estimated by creatinine clearance. More recently the MDRD GFR equation has been validated and made readily available. This was developed from data on large numbers of patients screened for a clinical trial in whom iothalamate GFR was measured and takes into account serum creatinine, age, race, and gender.3 Estimating GFR is very important in assessing patients with kidney disease and continues to be a subject of intense interest. The National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF K/DOQI) guidelines were first officially put forth in February 2002 and have been largely adopted in research and practice communities. In these guidelines chronic kidney disease has been divided into stages 1 through 5 based on an estimation of GFR with treatment recommendations determined by stage. This classification system was recently endorsed by the Kidney Disease: Improving Global Outcomes (KDIGO) group, an independent group dedicated to the improvement of care of kidney disease patients worldwide.4 This classification relies heavily on the level of GFR but is independent of the methods by which GFR is measured thus providing a powerful stimulus to ensure that serum creatinine measurements become uniform across laboratories, more generalizable estimating equations are developed and alternative filtration markers, such as cystatin C, are evaluated more extensively.5 Although specific interventions for many diseases are not yet available, progressive renal damage may be slowed by a few standard maneuvers, thereby avoiding or postponing the development of ESRD. Control of coexisting or secondary hypertension, moderate dietary protein restriction, blockade of the renin/angiotensin/ aldosterone system in patients with proteinuria and in diabetics, and strict control of blood glucose levels are of proven value.6–8 Other strategies recommended include control of hyperlipidemia, control of obesity, reduction of left ventricular hypertrophy, cessation of tobacco use, and improved nutritional status including a low-sodium diet.9

SPECIFIC RENAL DISEASES

Diabetic Renal Disease Diabetic nephropathy is the leading cause of ESRD in the United States, accounting for approximately 40% of all patients on dialysis.10 While the overall incidence of ESRD due to diabetes has leveled off in recent years, over the last decade the number of new patients with diabetes as their primary cause of ESRD has doubled. With the increasing prevalence of diabetes in the general population it is predicted that 58% 1089

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of all prevalent ESRD patients in 2030 will have diabetes mellitus as their primary diagnosis. Of the estimated 18.2 million diabetic individuals in the United States, 5–10% have insulin-dependent diabetes mellitus (IDDM) and 90–95% have noninsulin-dependent diabetes mellitus (NIDDM). The lifetime risk of developing nephropathy in IDDM is approximately 30–40%, peaking after approximately 18–20 years. The lifetime risk in NIDDM is less well defined but probably is around 33%. Because most patients with diabetes have NIDDM, the majority of patients in dialysis units have NIDDM. The incidence of ESRD caused by diabetic nephropathy is increased in certain racial and ethnic groups including Hispanics, African-Americans, and Native Americans. Most of the increase in these groups seems to be caused by NIDDM. Familial clustering of diabetic nephropathy has also been noted and may be due to genetic inheritance, shared environment or both.11,12 The National Institute of Diabetes, Digestive and Kidney Diseases (NIDDKD) has established a multicenter consortium to identify the gene(s) responsible for diabetic nephropathy.13 It should also be noted that up to 30% of patients with NIDDM and chronic kidney disease do not have diabetic nephropathy, but some other pathology, most commonly vascular disease.14 The pathogenesis of diabetic nephropathy is not yet fully understood. Early on the glomerular and tubular basement membranes thicken, and there is accumulation of extracellular matrix in the glomerular mesangium. Over time the glomerular capillary lumina are obliterated and the glomerular filtration rate eventually declines. Functionally, there may be an initial increase in the glomerular filtration rate, but this is followed by the development of proteinuria and systemic hypertension with an eventual decline in renal function. Hyperglycemia is a necessary factor initiating the above events, and tight glucose control reduces the onset of diabetic kidney disease. Current studies are focusing on the role of advanced glycosylation end-products (AGEs), the polyol pathway, transforming growth factor-β, and endothelins (as well as several others) in the accumulation of the extracellular matrix and other histochemical abnormalities which eventually lead to the decline of renal function in diabetics.15 The most important early clinical marker of diabetic nephropathy is microalbuminuria, or “dipstick-negative” urinary albumin excretion. This corresponds to a urinary albumin excretion rate of 30–300 mg/day or 20–200 mcg/min.16 Unfortunately it is not as early a marker for diabetic nephropathy as might have been hoped in that irreversible kidney damage may have already occurred by the time it is detected. It is also a risk factor for increased overall mortality. Identification of diabetics with microalbuminuria is important because patients with microalbuminuria progress to develop overt diabetic nephropathy (excretion of > 300 mg. protein per 24 hours) and eventually ESRD, and treatment appears to delay this progression.17 Several major clinical trials have provided guidance for therapy in diabetics to prevent diabetic nephropathy and the complications associated with it. Treatment of overt diabetic nephropathy with an angiotensin-converting enzyme (ACE) inhibitor in patients with IDDM and NIDDM has been shown to delay (but not totally halt) the rate of deterioration of renal function. This effect is independent of the effect of ACE inhibition on the treatment of blood pressure.18 This effect has also been shown for angiotensin receptor blockers (ARBs), and there is now evidence that the combination of an ACE inhibitor and an ARB may have additional benefit.19 The Diabetes Control and Complications Trial (DCCT) has demonstrated the beneficial effects of intensive insulin therapy on the development of type I diabetic nephropathy. Since then several other trials have supported this finding, including the United Kingdom Prospective Diabetic Study which demonstrated the benefit of intensive insulin therapy in type II diabetics.20,21 In the DCCT the mean adjusted risk of microalbuminuria ( 28 mcg/min) was reduced by 34% in the group of patients on intensive insulin therapy with no baseline retinopathy. Unfortunately intensive insulin therapy did not show a significant benefit in preventing the development of overt diabetic nephropathy in patients who already had microalbuminuria. More recently pancreatic transplantation has been shown to stabilize the progression of diabetic kidney disease at several stages.22

Hypertension is more common in diabetics with microalbuminuria, especially in patients with NIDDM, and is both a predictor and a consequence of nephropathy in NIDDM. Hypertension has been shown to increase the rate at which diabetic nephropathy progresses and antihypertensive therapy has been shown to slow its course.23 Although the incidence of diabetic nephropathy among patients who have had IDDM for 25 years or more is falling, the increasing population of elderly patients with NIDDM marks diabetic nephropathy as a continued major cause of morbidity and mortality.24 For this reason annual screening for microalbuminuria is recommended for all diabetics older than 12 years. If microalbuminuria is present and persists, ACE inhibitor or ARB therapy is appropriate in both normotensive and hypertensive patients. Serum potassium and creatinine will need to be monitored, and females of child-bearing age will need to be cautioned about becoming pregnant due to the known adverse effects of ACE inhibition and ARBs on the fetus. Glycemic control should be monitored on a regular basis as well as blood pressure control. In addition, microalbuminuria is frequently associated with elevated levels of cholesterol and triglycerides, so dietary restriction of cholesterol and weight reduction should be emphasized. Cigarette smoking has also been associated with the development and progression of microalbuminuria and should be discouraged.25 While significant advances have been made in the approach to patients with diabetic nephropathy, we await the results of ongoing basic science research studies and clinical trials, which will increase the knowledge and improve the management of diabetic nephropathy, hopefully eliminating or at least significantly reducing the requirement for renal replacement therapy with its attendant comorbidity in this population.

Hypertensive Renal Disease Hypertension can both produce and complicate renal disease, and its contribution to renal insufficiency is probably underestimated. Hypertensive renal disease accounts for 30% of the prevalent ESRD cases in the United States and is particularly common in AfricanAmericans receiving ESRD treatment.26 While most patients with ESRD have hypertension, the majority of patients with hypertension do not go on to develop ESRD. It seems that elevated blood pressure is permissive to renal disease, especially glomerulosclerosis, in only certain individuals. Among hypertensive patients in the Multiple Risk Factor Intervention Trial (MRFIT), the incidence of all-cause ESRD per 100,000 person-years of hypertension was 16.38 for AfricanAmericans compared with 3.00 for white Americans.27,28 Primary hypertensive renal disease can be of two kinds. The more common, sometimes called “nephrosclerosis,” is a form of chronic renal insufficiency associated with long-standing blood pressure elevation. The second, a form of accelerated renal failure associated with malignant hypertension, is now rare where treatment of hypertension is widespread. Additional risk factors for nephropathy in hypertensive persons include the degree of systolic hypertension, the presence of diabetes, male sex, increasing age, and high normal serum creatinine levels. Although widespread treatment of hypertension has reduced other hypertensive morbidities, its effect on hypertensive renal disease is still not clear. Two regional studies in the United States showed that renal damage can progress in some treated hypertensive persons despite adequate blood pressure control,29,30 and the communitybased Hypertension Detection and Follow-up Program (HDFP) confirmed this phenomenon.31 More recently the African-American Study of Kidney Disease and Hypertension (AASK) looked at 1094 African-Americans with long-standing hypertension, proteinuria, and unexplained progressive renal disease. Again there was no significant difference in rate of progression of kidney disease between blood pressure groups, although it should be noted that blood pressure was controlled to at least 140/90 or less in both groups. An ACE inhibitor was shown to be more effective in slowing progression of renal disease.32 The inability to show an effect of lower target blood pressures may be related to the length of follow-up in these studies. Long-term follow-up of the participants in the MDRD study suggest that a lower

63 target blood pressure may slow the progression of nondiabetic kidney disease in patients with moderately to severely decreased kidney function and proteinuria.33 Regardless of study results, most seasoned practitioners feel that blood pressure control is mitigating much hypertensive renal disease, and the HDFP suggests the superiority of aggressive control over a more relaxed treatment approach. The definition of adequate blood pressure control continues to evolve. Fear of the J-curve phenomenon (increased mortality with lower BPs) in the general hypertensive population has been tempered by the results of several studies including the Hypertension Optimal Treatment (HOT) study where lowering of the diastolic BP to the low 80s in hypertensive individuals was associated with lower cardiovascular morbidity and mortality in diabetics.34 In the context of proteinuric renal disease, lowering blood pressure beyond conventional recommendations has been shown to be beneficial in delaying progression of renal disease, but a more recent study did not support this.7,35 It has also become clear that over 50% of hypertensive individuals will require several antihypertensive agents to control blood pressure to the levels obtained in these studies. Retrospective and prospective analyses of large cohorts of hypertensive subjects and comparisons of therapeutic regimens are ongoing and will continue to help clarify some of these issues.

Glomerulonephritis Glomerulonephritis (GN) encompasses several syndromes with a variety of pathological changes in the renal glomerulus. Injury to the glomeruli is manifest by variable degrees of hematuria and/or proteinuria, red blood cell casts, hypertension, edema, oliguria/anuria, and renal insufficiency. This injury is categorized by morphological or clinical features, precipitating events, or associated conditions. Most forms of GN are probably immunologically mediated, and genetic predispositions to some are suggested by family clusters and by associations with certain HLA types. Associations with specific infections are well established, especially in the developing world, but few precursors or etiologic factors are recognized in the common forms of GN that persist in westernized countries. With the accumulation of series of cases from different parts of the world, there is evidence for geographic, climatic and ethnic differences in the incidence and prevalence of various lesions that may lead to further discoveries about the underlying pathogenesis of various GNs. GN is a common cause of renal failure and renal death in the developing world, and it is the third most common cause of treated ESRD in the United States, behind diabetes and hypertension.10 Pathological diagnosis relies on renal biopsy, which does have risks and is done with variable frequency in different parts of the world. Little is known about the distribution or natural history of mild GN or the extent to which subclinical GN might be eroding renal function in the broader community. This could change as more attention is being paid to individuals with GFRs in the 15–60 mL/min range. Chronic Idiopathic GN. The major morphological categories of idiopathic GN are minimal change disease (MCD), focal segmental glomerular sclerosis (FSGS), mesangial proliferative GN, membranous GN (MGN), and membranoproliferative GN (MPGN). There are probably interfaces among these categories. Each can afflict subjects of all ages, but the distributions are dependent on age. MCD is the most common lesion in children, whereas adults have a broader distribution of all these forms of GN. Idiopathic GN may be associated with infections such as hepatitis B or C or malignancies. MCD has the best prognosis, with remission usual before adulthood. MGN remains the most common cause of idiopathic nephritic syndrome worldwide. It may remit but remains a common cause of renal failure from GN. The incidence of FSGS has increased significantly in the last two decades and is frequently secondary to or associated with other diseases, including infections. It is now the most common primary glomerulopathy underlying ESRD in the United States.36 MPGN, type I, is frequently associated with hepatitis C but other infections and/or tumors may cause a lesion of MPGN. MCD has typically responded

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to therapy more reliably than other forms of GN although FSGS with nonnephrotic range proteinuria may have a better prognosis. Immunosuppressive therapy continues to be used for treatment of various forms of idiopathic GN, but ACE inhibition and/or angiotensin receptor blockers to reduce proteinuria are now a mainstay of treatment for all proteinuric renal diseases.35,37 Risk factors for progression of idiopathic MGN, and probably other forms of GN, include elevated serum creatinine, hypertension, male gender, age 50, renal biopsy evidence of glomerular sclerosis and/or interstitial fibrosis, and the persistence of heavy proteinuria. Progression is rare if protein excretion remains mild or falls toward normal, whether spontaneously or with treatment. With progressive proteinuria, it is highly probable that patients will progress to ESRD. IgA Nephropathy. IgA nephropathy and thin basement membrane nephropathy continue to be the most common findings underlying a clinical presentation of asymptomatic hematuria and IgA nephropathy is considered to be the most common form of glomerulonephritis in the world.38 It is more common in the western Pacific rim where incidence in older patients is reported to be increasing,39 while in Europe and the United States, lower prevalence rates have been reported. Again local variability in health screening practices and indications for kidney biopsy will influence these statistics. Investigators in Japan found previously unknown IgA mesangial nephropathy in 16% of living kidney donors.40 Males predominate by at least 2:1, and, unlike other glomerular diseases, the prevalence is lower in African-Americans. There have been reports of familial clustering. The pathogenesis of IgA nephropathy remains unknown but it is associated with abnormal deposition of IgA in the glomerular mesangium.39 A number of genetic polymorphisms have been described that may be associated with susceptibility or progression of disease, but it is too early to tell which ones play the largest role. It is thought that multiple viral and bacterial infections can trigger a clinical exacerbation with gross hematuria and sometimes acute renal insufficiency, but again a specific agent has not been clearly identified. The clinical presentation may be quite variable and includes several syndromes. Most patients present with microscopic or macroscopic hematuria. In 30–40% of patients there may be proteinuria usually associated with microscopic hematuria, and in 10% of patients there is acute renal insufficiency, edema and hypertension on presentation. Skin lesions (Henoch-Schonlein purpura) develop more often in children, and these patients may have skin, joint, and intestinal involvement. Glomerular IgA deposition is associated with several disorders including hepatic cirrhosis, gluten enteropathy, HIV infection, Wegener’s granulomatosis, systemic lupus erythematosus, minimal change disease and membranous nephropathy. IgA nephropathy usually has an indolent course with about 25–30% of patients reaching ESRD within 20–25 years.39 Patients who present with hypertension, heavy proteinuria or an elevated creatinine are at higher risk for progression to ESRD. There is currently no definitive cure for IgA Nephropathy, but there is now more emphasis on treatment with immunosuppressive therapy for those with proteinuria ( 0.5–1.0 g/day) and/or rising serum creatinine despite angiotensin inhibition. Randomized clinical trials have demonstrated the benefit of angiotensin converting enzyme inhibitors and/or angiotensin II receptor antagonists.19,41 Efforts should be also be directed at controlling hypertension, goal BP 125/75, and hyperlipidemia if present. A recent multi-centered trial did not demonstrate a benefit of fish oil on progression of disease.42 Allograft survival in patients who receive a kidney transplant is good although recurrence of IgAN after renal transplantation is common and becoming a more important cause of graft failure as control of rejection improves.39 Poststreptococcal Glomerulonephritis. The epidemiology and pathogenesis of poststreptococcal glomerulonephritis (PSGN) are well defined.43 It is characterized by the onset of hematuria, proteinuria, hypertension, and sometimes oliguria and renal insufficiency 7–15 days after a streptococcal upper respiratory infection and 21–40 days after a streptococcal skin infection. Although most common in children, it can

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occur at all ages. Epidemic disease occurs in crowded and unhygienic living conditions and is common in tropical countries and Third World populations, especially in association with anemia, malnutrition, and intestinal parasites. It may occur in seasonal patterns and sometimes in cycles separated by several years. Epidemic disease is now uncommon in most westernized countries, although sporadic cases continue. Asymptomatic disease is more common than clinical disease in most studies. Males predominate among patients with clinical but not subclinical disease. Only certain strains of streptococci have nephritogenic potential: nontypeable group A streptococci may also have that potential. It has been estimated than an average of 15% of infections with nephritogenic strains result in PSGN, with fully 90% of cases being subclinical, but the proportion varies with site of infection, the epidemic (if any), and the strain. Recurrence is uncommon. PSGN is due to glomerular immune complex deposition, although the constituent streptococcal antigens are still being identified. A genetic predisposition is evidenced by attack rates in siblings of index cases of up to 37.8% after throat infections and 4.5% after skin infections. A streptococcal origin of acute GN is suggested if cultures or antigen tests have been positive for streptococci, or serum levels of antistreptolysin O (ASO) antibodies are elevated after throat infections (60–80% of cases), or if antihyaluronidase and antideoxyribonuclease antibodies are elevated after skin infections. A transient depression of serum complement helps differentiate PSGN from some other forms of GN. Renal biopsy is rarely indicated. Prevention of PSGN involves improved nutrition, hygiene, and living conditions. Antibiotic treatment of streptococcal infections does not prevent PSGN, although it can confound the diagnosis by reducing ASO antibody production. Treatment does, however, reduce spread of streptococci to contacts and lessen their risk of getting PSGN. Prophylactic treatment for subjects at risk is recommended during epidemics and for siblings or families of patients with PSGN. When active disease is clinically severe, control of volume status and blood pressure is critical. Urine abnormalities may persist for months after the acute attack. However, with follow-up limited to 10–15 years, studies of broad populations rather than of subjects initially hospitalized show complete recovery for most children, with rapidly progressive acute disease in less than 0.1% and chronic renal failure in less than 1%. More recently an epidemic episode due to group C Streptococcus zooepidemicus was described in Brazil.44 Of the original group of 134 patients, three patients died in the acute phase and five patients required chronic dialysis. Of 69 patients examined after a mean of two years, 42% had hypertension, 34% had microalbuminuria and 30% had reduced renal function.44 Adults have about twice the rate of long-term urine abnormalities as children, and chronic renal failure is more common, although still exceptional. Superimposed hypertension, renal changes with aging, and the hyperperfusion phenomenon might contribute to such a course.

Autosomal Dominant Polycystic Kidney Disease Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic renal disorder and the fourth most common single cause of ESRD in the United States.10 It is characterized by fluid-filled cysts in the kidney, which can compress surrounding tissue leading to renal insufficiency and eventually ESRD. It occurs in every one of 400–2000 live births, and an estimated 500,000 people have the disease in the United States.45 Approximately 86% of patients with ADPKD have an abnormality in a gene on chromosome 16 (PKD1 gene locus), and most of the remaining patients have an abnormal gene on chromosome 4 (PKD2 gene locus)46 The phenotype associated with PKD2 is usually less severe although penetrance can be variable for both. Approximately 10% of patients have a new mutation with no family history of ADPKD. Abnormalities in the regulation of cell growth, epithelial fluid secretion and extracellular matrix metabolism contribute to the clinical problems associated with ADPKD. Renal manifestations of ADPKD include hematuria, urinary tract infections, flank pain, nephrolithiasis,

hypertension, and the most serious, renal failure. Approximately 45% of patients will have end-stage renal disease by 60 years of age. Currently there is no curative treatment for ADPKD. Cyst un-roofing, dietary protein restriction and inhibition of the renin-angiotensin-aldosterone axis have not been shown to clearly delay progression of disease. Control of hypertension to 140/90 is beneficial and should be aggressively pursued although it does not change the rate of progression of disease. Urinary tract infections should be treated immediately. Extrarenal manifestations include hepatic cysts, cardiac valve abnormalities, colonic diverticula, hernias, and intracranial saccular aneurysms. Rupture of the intracranial aneurysms is associated with high morbidity and mortality, and screening is recommended for highrisk patients, such as those with a positive family history of intracerebral bleed, warning symptoms, a previous rupture, or a high-risk occupation where loss of consciousness would place the patient or others at risk. The diagnosis of ADPKD has traditionally been done by ultrasound or CT evaluation of the kidneys. The sensitivity of these tests is not very high when used in patients under 20–25 years of age although ultrasound has been shown to be fairly sensitive and well standardized for patients 30 years. Genetic testing can now establish the genotype in approximately 60% of individuals with ADPKD. If a mutation can be identified within a single family member, then testing can be used to determine if relatives carry that mutation and have ADPKD. Genetic counseling is very important for patients with this disorder.47

Analgesic Nephropathy Analgesic nephropathy (AAN) is a slowly progressive renal disease caused by the long-term ingestion of analgesics, classically a combination of agents including aspirin, phenacetin, acetaminophen, caffeine, and/or codeine. It was estimated to be the cause of ESRD in ~ 1–3% of patients in the United States with a higher prevalence in Australia and Europe. While the prevalence of AAN has decreased secondary to the removal of phenacetin from the market, the disease has not been completely eliminated. The prevalence of AAN has been studied more extensively in Australia and Europe where it has been more prevalent.48,49 The pathogenesis of AAN is not well understood.50 Examination of the kidneys reveals chronic interstitial inflammation and papillary necrosis. In more advanced cases, cortical scarring occurs, most pronounced over the necrotic papillae, and gross examination of the kidneys reveal them to be small and nodular. Involvement of the medulla and papillae is felt to be secondary to increased concentration of the drugs in these areas with the generation of oxygen radicals and reduction of medullary blood flow due to inhibition of prostaglandins. AAN is more common in women. Individuals who have chronic pain for which analgesics may be consumed regularly and those with a history of peptic ulcer disease or gastric complaints are more likely to have a history of analgesic consumption. The patients may not be taking the medications at the time of presentation, but it is estimated that at least 1–2 kg of an offending agent need to have been ingested at some time to cause significant renal disease. The urinalysis may be normal or show pyuria, bacteriuria, and proteinuria, which is usually mild. Reduced ability to concentrate urine and renal tubular acidosis may occur, and there may be evidence for papillary necrosis when the kidneys are imaged as well as the reduced size and nodularity previously noted. In addition to being the sole cause of ESRD in some cases, analgesic use contributes to more minor degrees of renal dysfunction in many other cases, and it is very probable that it contributes to the decline in renal function in patients with other underlying causes of renal insufficiency. The nephrotoxicity of nonsteroidal anti-inflammatory agents (NSAIDs) has been recognized for some time now and is characterized by one of several presentations: acute renal failure secondary to renal vasoconstriction; interstitial nephritis with or without nephrotic syndrome and minimal change disease; hyperkalemia; sodium and water retention; and papillary necrosis. People with underlying volume depletion and/or those with chronic renal insufficiency have a higher risk of developing problems. Most of these conditions

63 are reversible. NSAIDs are nonselective inhibitors of cyclooxygenase. Of the two related isoforms, COX-2 is constitutively expressed and is the predominant form in the kidneys. Selective COX-2 inhibitors, introduced more recently for their favorable GI side-effect profile, have also been shown, not surprisingly, to cause nephrotoxicity.51 AAN is preventable, and renal disease has been shown to decrease with decreased availability of agents such as phenacetin. The United States National Kidney Foundation published a position paper regarding analgesic use. It has been recommended that overthe-counter combination analgesics be eliminated and all prescription combination analgesics have a warning on them regarding the risk of renal damage.52 Aspirin as a single agent does not appear to impair renal function when used in therapeutic doses, especially the small doses recommended for prevention of cardiovascular events. There is an increased risk of larger doses leading to reversible deterioration of renal function in patients with underlying renal disease, and renal function should be monitored. For patients without liver disease, acetaminophen remains the nonnarcotic analgesic of choice, particularly for patients with underlying renal disease. Habitual consumption should be discouraged as a case-control study done in Maryland, Virginia, West Virginia, and Washington, DC suggests that there may be an increased risk of renal insufficiency in patients who have taken large amounts over a lifetime.53 Prolonged regular use of NSAIDs and COX-2 inhibitors have recently been suspected of having adverse cardiac as well as renal effects and prolonged use should be discouraged.54 Renal function should be monitored if regular use is necessary. NSAIDs should be avoided altogether in pregnancy. Use of NSAIDs in combination with other analgesics needs to be prospectively evaluated and should be avoided at this time.

Acute Renal Failure Acute renal failure (ARF) is characterized by a relatively acute deterioration in renal function. Because defining the exact rate and nature of the deterioration is difficult to do, ARF is not well defined and therefore, it is difficult to compare rates and outcomes. Most cases of community-acquired ARF have a single, treatable cause of renal failure that is either prerenal (secondary to vomiting, poor intake, diarrhea, glycosuria, gastrointestinal bleeding and diuretics) or postrenal (secondary to prostate enlargement from hyperplasia or carcinoma).55 It is not very common and the prognosis is usually good. The incidence of hospital-acquired ARF is increasing with one study showing an incidence of 4.9% in the 1970s and another 7.2% in the mid-1990s.56,57 It is more common in patients with underlying chronic kidney disease, 15.7% versus 5.3% in patients with normal renal function.57 Greater than 60% of patients with hospital-acquired ARF have had more than one renal insult. It is frequently caused by decreased renal perfusion usually secondary to volume contraction, poor cardiac output or sepsis. In one study postoperative patients accounted for 18% of all ARF, and contrast media and aminoglycosides combined accounted for another 19%. Prognosis appears to correlate with the severity of renal insufficiency and degree of oliguria/anuria.56 The frequency of ARF in intensive care units ranges from 6 to 23%. Nearly all of these patients have had multiple renal insults, and it is frequently seen in the context of multiorgan failure. Survival is significantly reduced in these patients, especially in the presence of multiorgan failure. ARF caused by blood loss and crush injuries is common during war and natural disasters. ARF secondary to general trauma has declined, as has pregnancy-related ARF. Abortion contributed to much of ARF in the past, and now preeclampsia/eclampsia and uterine hemorrhage cause the majority of pregnancy-related ARF. ARF is being seen more commonly now in patients with AIDS, malignancy, and sepsis. The use of NSAIDs and angiotensin converting enzyme inhibitors may also contribute to the development of ARF in patients with underlying renal hypoperfusion. ARF rates secondary to contrast and antibiotics appears to be stable. Despite increasing awareness of the etiology of ARF and advancing technology, the mortality of ARF has not decreased significantly

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over the last several decades. It appears that ARF is not just a marker for severe comorbid conditions, and even mild episodes are associated with increases in morbidity and mortality. A multicenter observational study of 17,126 ICU patients in Austria showed a mortality of 62.8% in patients requiring renal replacement therapy compared to 38.5% in matched controls without ARF.58 The exact reason for the above is not clear, and may be related to distant biochemical and histologic effects of renal ischemia on cardiac function and other organ systems yet to be elucidated. While short-term survival is not good for patients with ARF in the ICU, the long-term outcomes in patients who survive to hospital discharge are much better. Of the patients who survived to hospital discharge among 979 critically ill patients with ARF requiring renal replacement therapy (RRT), six month survival was 69% and five year survival 50%.59 Preventive options are limited for most causes of ARF and consist of blood pressure support, optimization of cardiac function, treatment of underlying conditions including sepsis and limiting nephrotoxic agents. Volume expansion with normal saline and use of nonionic radiocontrast agents have been shown to reduce the incidence of radiocontrast nephropathy while the role of Nacetylcysteine (NAC) remains less clear. Lack of significant toxicity and low cost have contributed to an increase in its use prior to radiographic procedures which is probably appropriate.60 The Program to Improve Care in Acute Renal Disease (PICARD) is an observational registry of critically ill patients with acute renal failure maintained at five geographically diverse academic medical centers in the United States.61 The PICARD investigators have used their registry to examine the epidemiology of ARF or acute kidney injury (AKI) as it now being called as well as the pathobiology of ARF. Timing and modality of RRT in treatment of ARF remain controversial. There is no clear indication that continuous forms of RRT are superior, but they are frequently used in patients with hemodynamic instability.

Renal Disease and Illicit Drugs Renal disease related to drug abuse is being recognized more frequently as a cause of renal disease and has great social and economic impact. According to the 2001 National Survey on Drug Abuse, an estimated 15.9 million Americans currently use illicit drugs, and a significant positive and independent association between illicit drug use and risk for mild kidney function decline has been demonstrated.62 Several syndromes are recognized. Focal segmental glomerulosclerosis (FSGS) occurs in intravenous heroin addicts, with heavy proteinuria and progression to renal failure in a few months to years. There is no effective treatment. An immunologic mechanism is postulated, mediated through a response to heroin itself, to adulterants, or to infectious agents. FSGS associated with drug abuse occurs in all ethnic groups, but rates are especially high in young black males, leading to the hypothesis that parental drug abuse unmasks a genetic predisposition to FSGS in blacks similar to that seen for hypertension. It has been suggested that heroin nephropathy is on the decline with an increase in HIV nephropathy. Renal deposition of amyloid, associated with chronic inflammation and infection, occurs in skin poppers.63 Proteinuria and sometimes renal failure is diagnosed at an average age of 41 years, 10 years older than FSGS patients. In a New York City autopsy series, 5% of addicts and 26% of addicts with suppurative skin infections had unsuspected renal amyloidosis.64 Other renal diseases related to drug abuse include immunecomplex GN associated with infectious endocarditis or hepatitis B antigenemia, membranoproliferative GN and cryoglobulinemia associated with hepatitis C, necrotizing vasculitis related most strongly to amphetamine abuse, tubular dysfunction and occasionally acute renal failure in solvent sniffers, acute renal failure due to muscle breakdown, and the renal syndromes of human immunodeficiency virus infection. Treatment of addicts with ESRD is often complicated by noncompliance, communicable diseases like hepatitis B, hepatitis C, and AIDS, and, with continued drug abuse, infection and clotting of vascular access and recurrence of disease in kidney transplants. Because

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of the interfaces of drug addiction with crime, some of these subjects are incarcerated. Such problems accentuate dilemmas about responsibility for personal health and allocation of limited resources.

Renal Disease and the Human Immunodeficiency Virus The understanding of renal disease associated with human immunodeficiency virus (HIV) infection continues to evolve. Renal disease may occur at all stages of HIV illness including the asymptomatic stage, but many complications are associated with acute illness. Patients may develop fluid and electrolyte disorders, acid–base disturbances, and/or acute renal failure secondary to volume depletion, infections, drugs and/or abnormal adrenal steroid synthesis and secretion. There is also a histologically unique nephropathy associated with HIV called HIV nephropathy. Patients with this disorder usually have nephrotic range proteinuria accompanied by renal insufficiency which progresses fairly rapidly to ESRD (within three to six months).65 On exam there is frequently no significant peripheral edema or hypertension, and the kidneys are normal to increased in size despite being highly echogenic. This may be contrasted to heroin-associated nephropathy in which hypertension is frequently present, the kidneys are small, and progression to ESRD is a slower process. Although it is not always possible to distinguish HIV-associated disease from other forms of glomerulosclerosis, the following pathological findings are felt to be very suggestive of HIV nephropathy and include focal to global glomerulosclerosis, collapse of the glomerular tuft, severe tubulointerstitial fibrosis with some inflammation, microcyst formation, tubular degeneration, and characteristic tubuloreticular inclusions.65 While HIV nephropathy was initially noted to be more prevalent in young black males who were IV drug users; it is now known that it can occur in most risk groups. It has even been reported in children of HIV-infected mothers, where vertical transmission accounts for infection. Development of HIV nephropathy also appears to be more likely in blacks and males. Patients who are HIV positive and develop acute renal failure due to acute tubular necrosis (ATN) tend to be younger than the non-HIV positive patient with ATN, and frequently the ATN is associated with sepsis. Treatment consists of conservative, supportive care, and hemodialysis may be used until kidney function returns. Much of the ATN associated with HIV disease is preventable if patients receive adequate volume support prior to use of nephrotoxic agents or during episodes of hypovolemia and if attention is paid to medication/ antibiotic dosing.66 There is no proven cure for HIV nephropathy. There has been a decrease in overall morbidity and mortality due to HIV disease with the introduction of highly active antiretroviral therapy (HAART) in the mid 1990s.67 The use of protease inhibitors may be helping to reduce the likelihood of progression of HIV nephropathy to ESRD. Except for a peak in 1998, the number of new ESRD patients with HIV nephropathy has remained stable since 1995; 836 patients were reported in 2002.26 This coincides with the advent of HARRT therapy. Symptom-free HIV-positive subjects with chronic renal failure can do quite well on dialysis, but chronic dialysis of subjects with clinical AIDS is complicated by concomitant illness, cachexia, infectious hazards, and prolonged hospitalizations, and survival is usually short.

Hemolytic Uremic Syndrome (HUS) HUS is one of several clinical syndromes that affect the vasculature of the kidney producing a thrombotic microangiopathy. It is discussed here in relationship to a bacterium, Escherichia coli O157:H7, which has emerged as a major cause of diarrhea, particularly bloody diarrhea, in North America. Several studies68 have now shown that this E. coli is responsible for most cases of HUS in children, which is a major cause of acute renal failure. While it has been isolated in many parts of the world, its prevalence is unknown. Infections are more common in

warmer months, and transmission may occur via undercooked beef, fecally contaminated water, and person-to-person. Infection has also been associated with unpasteurized commercial apple juice.69 Patients typically present with abdominal cramping, diarrhea (nonbloody or bloody), nausea, and vomiting. HUS has been reported to occur in about 6% of patients with infection and is diagnosed anywhere from 2 to 14 days after the onset of the diarrhea. It is more likely to affect young children and the elderly. It is characterized by microangiopathic hemolytic anemia, thrombocytopenia and renal failure. Central nervous system manifestations may be present. The renal pathologic lesions include edematous intimal expansion of arteries, fibrinoid necrosis of arterioles, and edematous subendothelial expansion in glomerular capillaries.70 There is no specific therapy which has proven to be effective for HUS secondary to E. coli infection. Treatment involves supportive therapy with red blood cell transfusions, control of hypertension and dialysis if necessary. Apheresis may be helpful in more severe cases with central nervous system involvement. The prognosis for typical childhood HUS is usually good. Neurological involvement, prolonged oliguria, elevated white blood cell count, age under two years, and atypical presentations have been associated with a poorer prognosis. The mortality rate is 3–5%, and about 5% of patients who survive have severe sequelae, including ESRD. To prevent E.coli infection, patients should be counseled about the risk of eating undercooked ground beef. A thorough history should be taken in suspected cases, and cases should be reported early to prevent spread. Hand washing is essential in institutions such as day-care centers and nursing homes, and children with a known infection should be kept at home. Use of antidiarrheals for acute infectious diarrhea is potentially dangerous. URINARY TRACT DISEASES

Urinary Tract Infections Urinary tract infections (UTIs) are one of the most common types of infection encountered in clinical medicine. They account for more than 7 million physician visits and necessitate or complicate over 1 million hospital admissions annually in the United States.71 The estimated annual cost of UTIs is $1.6 billion for evaluation and treatment.72,73 Uncomplicated UTIs are most frequent in young, healthy, sexually active women with normal urinary tracts, and it is estimated that 40–50% of women will have a UTI in their lifetime. UTIs are also common in preschool girls, in postmenopausal women, and in elderly men and women, especially those who are institutionalized and those with indwelling urinary catheters. UTIs in older men are often associated with urinary retention due to benign prostatic hypertrophy (BPH), urethral strictures, calculi, and debilitating illness and are thus designated as complicated and more difficult to treat. Boys and men with normal urinary tracts are not often affected, but men can acquire bacterial UTIs through heterosexual or homosexual intercourse, and recurrent UTI is the hallmark of chronic prostatitis. Use of immunosuppressive drugs and recent antibiotic use also place individuals at risk for complicated UTIs. Most infections are localized to the bladder and urethra, but some involve the kidneys and renal pelves (pyelonephritis), or the prostate. UTIs rarely lead to renal damage or failure unless they are associated with diabetes, pregnancy, reflux, obstruction, or neurogenic bladder. Diabetic persons with UTIs risk papillary necrosis and sepsis; abortion and other complications can result from UTIs in pregnancy; and morbidity and mortality of UTIs increase greatly in the elderly and in those with complicating conditions, such as spinal cord injury. Most UTIs in young women are new events, are uncomplicated, and caused by E. coli and other bowel organisms that enter the bladder through the short female urethra. Subjects with recurrent UTIs have increased density of bacterial receptors on epithelial cell surfaces in the vagina and bladder. Women with blood groups A and AB who are nonsecretors of blood group substance are at greater risk.

63 Intercourse, diaphragm use, and failure to void after intercourse all increase risk. Women who have closely spaced recurrent infections with the same organisms or who have pyelonephritis should be evaluated for urinary tract abnormality, as should men with persistent infection. Complicated UTIs are frequently caused by non-E. coli pathogens such as Enterococcus and Klebsiella species. In the presence of symptoms, white cells and bacteria in a cleanvoid midstream specimen of urine usually indicate a UTI. The usual bacterial count considered diagnostic on urine culture is 100,000/mL, but many patients have lower counts, including half of those with cystitis and most patients with urethral syndromes. Enterobacteriaceae colony counts as low as 100/mL, have a sensitivity and specificity for UTI of 94% and 85%. Subjects with recurrent UTIs can perform an easy and relatively inexpensive dip slide urine culture technique, and self-treatment under medical guidance can be initiated. Many uncomplicated UTIs are treated based on symptoms and pyuria alone. Screening for bacteriuria in symptom-free persons is not costeffective and may lead to inappropriate treatment, drug reactions, and selection of resistant organisms. Treatment of asymptomatic bacteriuria is not generally recommended, except in pregnant women, diabetics, and children with vesicoureteral reflux. Symptomatic infections are treated by antimicrobials, and infections associated with sexual intercourse can usually be prevented by single-dose prophylactic therapy. Repeated or prolonged antibiotic treatment can select antibiotic-resistant organisms. Some broad-spectrum antimicrobial agents may not pose this threat and are sometimes used for prophylaxis in subjects with chronic infections. UTIs are the leading form of nosocomial infection and are especially common in nursing homes. Spread can be reduced by separation of catheterized patients from others who are debilitated or catheterized, and by washing the hands after patient contact. For subjects who require temporary catheterization, risks of infection can be reduced by aseptic insertion, curtailed duration of catheterization, and meticulous care of the patient and the drainage system. However, infection remains very common in persons with chronic indwelling catheters. The bacterial flora in the urine of catheterized subjects is in flux, colonization is often asymptomatic, and repeated courses of treatment are not advised. Interstitial cystitis is a syndrome of unknown etiology and pathogenesis with symptoms similar to UTIs. It is characterized by nocturia, urgency, and suprapubic pressure and pain with filling of the bladder. It is more common in women and may be the cause of multiple outpatient physician visits. Therapy is frequently not completely effective, and it can occasionally lead to a significant decrease in quality of life.

Urinary Stone Disease Urinary stone disease has been recognized since antiquity and continues to be a major cause of morbidity. The incidence is increasing not only in the United States, but Sweden and Japan, and is felt to be related to increased dietary animal protein intake.74 It is estimated that 10–12% of individuals will have a kidney stone during their lifetime. Risk factors for development of a stone include male sex, Caucasian race, obesity, hypertension, diet high in animal protein and salt but low in calcium and fluid, hot climate or occupation, and family history of kidney stones.75 Drugs such as triamterene and indinavir may precipitate as crystals in the urinary tract. The initial stone usually presents in the third to fifth decade and up to 50% will have a recurrent stone within five years. Geographic variations in incidence may be attributable to temperature and sunlight exposure as well as access to beverages. Urinary stone disease is relatively uncommon in underdeveloped countries where bladder stones predominate. Most kidney stones (75–85%) contain calcium, primarily in the form of calcium oxalate. The remaining stones contain uric acid, struvite, cystine, and/or small amounts of other compounds. The content of the stone may give clues to the underlying physiological problem, especially in the case of stones without calcium. Disorders associated with stone disease include primary hyperparathyroidism, renal tubular

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acidosis, enteric hyperoxaluria, sarcoidosis, cystinuria, and urinary tract infection or obstruction. Risk factors associated with calcium stone formation include low urinary volume, hypercalciuria, hyperoxaluria, hypocitraturia, and hyperuricosuria.76 Most patients present with flank pain radiating into the groin which is abrupt in onset and frequently severe. Gross or microscopic hematuria, dysuria, frequency, nausea, and vomiting can be present. Occasionally, patients will have an ileus. Diagnosis is confirmed by abdominal plain film, ultrasound, IVP, or CT. Most kidney stones pass spontaneously, and the patient can be supported with analgesics. Urological intervention may be required including endoscopic “basket” removal, extracorporeal shock-wave lithotripsy (ESWL), endoscopic lithotripsy with ultrasonic, electrohydraulic, or laser probes, open pyelolithotomy, and percutaneous nephrolithotomy. These procedures have reduced the costs, morbidity, and hospitalization rates compared with open surgery which is rarely used anymore. The primary objective of therapy is to prevent the formation of recurrent stones. Patients are asked to strain their urine for stone collection and composition analysis. Conservative management includes analgesics, adequate fluid intake (≥ 2 L/day), dietary sodium restriction, and moderate calcium intake. Maintaining calcium intake helps prevent absorption of oxalate and outweighs the risk associated with high calcium intake. Oxalate restriction, reduction of animal protein intake, thiazide diuretics, and other agents may also be recommended depending on the patient’s underlying medical condition and the cause of stone formation.

Prostate Cancer Prostate cancer is a disease of aging men and is an important public health problem in the United States as well as throughout the world. It is the most commonly diagnosed cancer in men except for nonmelanoma skin cancer in the United States and is the second leading cause of male cancer deaths.77 It is the sixth most common cancer in the world and the most common cancer in men in Europe, North America, and some parts of Africa. It accounts for 15.3% of all cancers in men in developed countries and 4.3% in developing countries.78 The incidence, prevalence, and mortality rates from prostate cancer increase with age, particularly after 50 years of age. In the National Cancer Institute’s Surveillance Epidemiology and End Results (SEER) program, the incidence of new cases in white U.S. men in 1995 was approximately 200, 600, and 900 per 100,000 in men aged 50–59, 60–69, and 70 or over.79 The incidence of prostate cancer peaked in the early 1990s, in part, but not entirely, related to use of the prostate specific antigen (PSA) as a screening tool. There was a subsequent decline during the mid 1990s perhaps related to the screening effect. The incidence is steadily rising again in almost all countries.78 While the presence of histologic cancer appears to be related to age, both genetic and environmental risk factors appear to increase the development of clinical prostate cancer. Asian men have a lower incidence of and mortality due to clinical prostate cancer while Scandinavian men have a higher incidence. Men tend to take on the risk of their host country, but race is also a factor. AfricanAmerican men have a higher incidence than do black men in Africa or Asia and a higher incidence than white men or Hispanics. AfricanAmerican men are also diagnosed with later-stage disease, and their survival rates are shorter. In general, socioeconomic status is not felt to explain the incidence differences between African-Americans and whites. There is an increased risk of prostate cancer for men with a family history. While both prostate cancer and BPH appear to be androgen dependent, it has been difficult to determine whether or not BPH is a risk factor for prostate cancer because both are common in men as they age. The risk attributable to prostatitis has similar issues. Associations with venereal disease, sexual activity, and smoking have been proposed but not proven. Studies have been conflicting regarding vasectomy, but more recent studies have not found evidence for an association. Additional possible risk factors include elevated testosterone levels, a high intake of dietary fat, and other dietary habits. Several genetic mutations/ deletions and polymorphisms may be associated with an increased risk for prostate cancer but no single prostate cancer gene has been

Noncommunicable and Chronic Disabling Conditions

Bars: Rate per million population

identified. These findings may support increased attention to screening in certain populations such as African-Americans. Patients typically present with symptoms of urinary tract obstruction (urgency, nocturia, frequency, and hesitancy) from an enlarged prostate gland causing bladder-neck obstruction. These symptoms are essentially the same as those seen with BPH. Other less common signs and symptoms include back pain from vertebral metastases and new onset of impotence. A few patients have symptoms related to urinary retention caused by bladder-neck obstruction, bilateral hydronephrosis from periaortic lymph node enlargement, or spinal cord compression from epidural extension. Rarely, patients present with an enlarged supraclavicular node or elevation of liver tests. Prior to the increased use of the PSA for screening, diagnosis was made by assessing symptoms, performing a digital rectal exam of the prostate, and transrectal ultrasonography. Today an increasing number of patients present with elevated PSA levels obtained during screening exams. PSA is a glycoprotein produced almost exclusively by prostate epithelial cells. While PSA is elevated in men with prostate cancer and has been shown to correlate with tumor burden in men with established cancer, it is not specific for prostate cancer and may be elevated in cases of prostatitis and BPH. Concerns have been raised about its use as a screening tool leading to increased detection of insignificant cancers with an increase in expense and side effects. Survival studies have yet to show a reduction in mortality because of screening. Currently there is no consensus on the use of the PSA and digital rectal examination for the detection of prostate cancer, but experts do agree that providing education to patients on the risks and benefits of screening is important and some groups recommend annual screening for males 50 years with a life expectancy of at least 10 years. Many of the small, well differentiated carcinomas remain confined to the prostate and are only detected at autopsy (latent or autopsy cancers). The majority of tumors never become active, but how to predict which will become so has not been determined. It is estimated that the average lifetime risk of developing prostate cancer in an American male is 17% while the risk of dying from prostate cancer is only 3%.77 Management of prostate cancer may include watchful waiting, hormonal therapy, prostatectomy, and radiation therapy depending on the stage of the cancer. Treatment considerations should include age, life expectancy, comorbid conditions, side effects, and costs. Urinary incontinence, impotence, and radiation morbidity comprise the treatment related adverse effects. The Prostate Cancer Prevention Trial looked at the use of finasteride, a 5-alpha reductase inhibitor which prevents conversion of testosterone to dihydrotestosterone, as a chemo preventive agent. While it prevented or delayed the number of cancers and reduced urinary tract symptoms, it also was associated with an increased risk for high-grade prostate cancer.80 Currently there are ongoing trials looking at similar agents as well as chemotherapy for various stages of diagnosed prostate cancer. Multiple clinical trials are currently underway which should help identify the best method of screening, as well as chemo preventive therapies and therapies for the various stages of prostate cancer.

Prostatic Hyperplasia BPH is extremely common in older men. It has been reported that BPH can be found in 88% of autopsies in men ≥ 80 years of age, and that nearly 50% of men ≥ 50 years of age have symptoms compatible with BPH.81 Three men in ten may ultimately require surgery. While it frequently causes morbidity, it is rarely responsible for death. The cause of BPH is not known. Necessary conditions are the presence of androgens and aging. No associations with sociocultural factors, sexual behavior, use of tobacco or alcohol, or other diseases have been consistently demonstrated, and there is no firm evidence that BPH is a precursor of prostate cancer. In BPH subjects, a period of rapid prostate enlargement occurs, usually after the age of 50, followed by stabilization. Clinical symptoms result from variable compression of the bladder outlet, with difficulties in urinating, and the potential for infection, complete obstruction, and bleeding. Age, urinary flow rate and prostate volume are risk factors for acute urinary retention. Serum PSA is a strong predictor of growth and may be a predictor of risk for urinary retention. The natural history of symptoms can vary greatly. Many subjects have mild symptoms for years, with no change, and many do not require surgical intervention. Evaluation consists of rectal examination, blood chemistry studies, urinalysis and culture, measurement of residual urine volume after voiding, cystourethroscopy, urodynamic evaluation, and imaging or contrast studies of the kidneys and ureters.82 Many patients can be observed while monitoring for progression. Alpha-adrenergic blocking agents and 5-alpha reductase inhibitors have been shown to delay progression of the symptoms and when used in combination may have a greater effect. Alpha reductase inhibitors may reduce the size of the prostate and when used alone or in combination with alpha-adrenergic blocking agents in some studies have been shown to reduce the incidence of acute urinary retention.83 For more severe symptoms, prostatectomy is the standard of care. Indications for surgery vary, need better definition, and should be weighed against the comorbidities, complications, outcomes, and costs. Firm indications are acute urinary retention, hydronephrosis, recurrent urinary infections, severe hematuria, severe outflow obstruction, and urgency incontinence. Persistence of symptoms and impotence can result from surgery in a significant minority of subjects. Newer procedures are being developed including the use of prostatic stents, balloon dilatation of the prostate, laser prostatectomy, and microwave hyperthermia.

END-STAGE RENAL DISEASE (ESRD)

Overall, it is estimated that there are more than 19 million adult Americans affected by chronic kidney disease. ESRD or stage 5, the most advanced stage, affects more than 500,000 people in the United States.26 Although the prevalent ESRD rate has risen each year since 1980, the rate of increase has been falling steadily since the early 1990s. (Fig. 63-1) ESRD can be caused by many renal diseases and by some

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Figure 63-1. End-stage renal disease (ESRD). Adjusted prevalence rates and annual percentage change. (Source: USRDS, 2004.)

63 urinary tract diseases when they are complicated by chronic obstruction or infection. In the United States, diabetic nephropathy is the primary diagnosis in 45% of the prevalent ESRD population, up from 20% of the prevalent population in 1980.26 Hypertension is the primary diagnosis in 30% of the prevalent ESRD population and glomerulonephritis causes 20 % of ESRD compared with 40% in 1980. There appears to be a slowing of the number of patients whose ESRD is caused by more rare diseases such as Wegener’s granulomatosis and lupus, but the number of patients with a primary diagnosis of multiple myeloma/light chain nephropathy continues to increase, perhaps partially related to the aging of the population plus other unknown factors.26 At the end of 2002, approximately 309,000 ESRD patients were being treated in the United States and its territories. Another 122, 375 patients had renal transplants. Both the incidence rate and the prevalence rate of ESRD increase with age until 65–74 years at which point the rates decline. The median age of incident ESRD patients has increased 21% from 54 in 1978 to 65 years in 2002. The greatest increase has occurred among Asian patients, from 44 in 1978 to 65 in 2002, a 47% increase. Patients age 45–64 accounted for 35% of the incident population. Only 13% of the incident population is age 20–44, compared to 27% in 1980. Patients age 75 and older now make up 25% of the population, up from only 8% in 1980. Definite gender and racial differences do exist and they have remained consistent in the United States over the past two decades. While blacks constitute 12–13% of the general population in the United States, they constitute 29–33% of the ESRD population, a rate fourfold higher than that of whites. The ESRD incidence and prevalence rates for Asian/Pacific Islanders and Native Americans are between those of whites and blacks. Prevalent rates of ESRD among males are 1.4 times higher than among females, a rate that has been very consistent over the years.26 The first patient with chronic renal disease was dialyzed in 1960 by Belding Scribner. During the 1960s the development of vascular access, chronic peritoneal dialysis catheters, and improved immunosuppressive therapies allowed patients to choose between some form of hemodialysis, peritoneal dialysis or renal transplantation. With the enactment of the Social Security Amendments of 1972 (effective in July 1973), treatment became available for all patients with ESRD. Currently patients choose one of the above therapeutic modalities based on a combination of medical and social factors. Transplantation is regulated by national and local policies, physician and patient preference, and availability of donor organs. Relatively recent advances in the treatment of ESRD patients include high flux, bicarbonate hemodialysis using biocompatible membranes, automation of peritoneal dialysis, use of vitamin D derivatives for treatment of renal osteodystrophy, and genetically engineered erythropoietin for treatment of anemia reducing the need for blood transfusions. Continued advancements in the development of immunosuppressive agents have improved the one-year first-time cadaveric transplant survival from 70% in 1984 to 90% in 2002. Despite improvements in dialysis technology, mortality remains high. For example, at age 45 the expected remaining lifetime of a white male with ESRD on dialysis is 7.1 years compared with 32.8 years for a white male from the general population. Survival for patients receiving a transplant cannot be directly compared to that for dialysis patients due to selection factors; however, in the example above survival extends to 18.7 years when including all patients with ESRD including those who received a renal transplant. Gross mortality rates of dialysis patients in the United States have been the highest in any surveyed country in the past and continue to be high. An increase in dialysis dose above the currently recommended dose did not improve survival as demonstrated in the HEMO study.84 Age, primary diagnosis, acceptance of patients with multiple comorbid conditions, transplantation rates, dose of dialysis delivered, patient compliance, nutrition, and predialysis therapy all may contribute to this phenomenon. The total Medicare payment per patient year (average for all ESRD patients of all ages) is estimated to be $46,490 for the years 1998–2002. Transplantation costs are less than those for dialysis patients, at $18,394 per patient year. This does not include the cost of organ procurement for transplantation patients. Annual costs for all ESRD patients rise with

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age, primarily due to the decline in transplantation rate for elderly patients. Diabetic patients with ESRD are more costly to treat than nondiabetics.26 Current efforts are being directed at determining if short daily dialysis or prolonged nocturnal dialysis will decrease the mortality rates of ESRD patients. In addition, the Health Care Financing Agency is sponsoring a national study to determine whether more effective and cost efficient ESRD care can be provided using a capitated system. It should be noted that in many low-income countries, such as India, dialysis is currently not available to 95% of the population.1 THE FUTURE

Progress has clearly been made in several areas of renal and urinary tract diseases. In addition to the decrease in the death rate from hypertensive renal disease, renal infections, and renal congenital abnormalities, the incident rate for ESRD caused by diabetes has begun to stabilize, and that for ESRD caused by glomerulonephritis has begun to decline.26 As a specific example, since 1992 the incident rates for white patients with diabetic ESRD have declined 46% in those age 20–29 and 9% in those age 30–39. While rates for blacks remain the highest, the rate of increase appears to be slowing as does the rate of rise for Hispanics. The incident and prevalent rates for Native Americans has slowed but this is due to a change in census methods and will need to be reevaluated.26 While progress has been made, the number of patients age 45–64 reaching ESRD continues to increase in a linear fashion and, with the exception of pediatric patients, waiting times for transplantation continue to increase. Thus, the cost of providing care has not decreased. In 2002, total Medicare costs for the ESRD program were $17 billion. There also continues to be a discrepancy in incidence of ESRD among racial groups, with the rates among black patients having actually increased 27% for those age 20–29 and 62% for those age 30–39. This may reflect the fact that blacks are more likely to have type II diabetes which is becoming more prevalent as obesity becomes a major public health problem. This, along with the increased incidence of hypertension in blacks, makes it more difficult to treat. While development of strategies such as the Kidney Early Evaluation Program (KEEP) to provide early detection and prevent progression of CKD is clearly important, society will need to address how best to support these programs both in terms of manpower and monetary funds. For westernized societies who have already made a large commitment to life support for subjects with irreversible renal failure, supporting the funding for these programs will continue to be a challenge. For all societies, the challenge remains to better understand the factors that contribute to ESRD. The public health perspectives of many of these diseases remain poorly defined and the distributions and natural histories of many remain obscure. While progress has been made in identifying specific prevention and treatment strategies, many diseases continue to lack specific strategies, and the prevalence of ESRD will continue to increase. Epidemiological and health services research in renal and urinary tract diseases continues to expand. In the United States the NIDDKD have collated existing data on rates, morbidities, mortalities, resource utilization, and costs. They are supporting studies on diabetic renal disease, hypertension, progressive glomerular sclerosis, progression of renal failure, urinary tract obstruction, prostatic hyperplasia, prostatic cancer screening, and urinary incontinence. They have also established research initiatives in interstitial cystitis, HIV-associated renal disease, the genetic basis of polycystic kidney disease, and renal disease and hypertension in minorities. The CDC’s National Health and Nutrition Examination Survey (1988–1994 & 1999–2000) collected information that will yield estimates of rates of kidney stones, UTIs, interstitial cystitis, prostate disease, bladder dysfunction, microalbuminuria, and elevated serum creatinine levels and will give us a better understanding of the risk factors for the various stages of chronic kidney disease. To prevent or delay kidney damage, the National Kidney Foundation has established a free screening program (KEEP) for individuals at increased risk for developing kidney

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disease with the goals of raising awareness about kidney disease, providing free testing and encouraging people “at risk” to visit a doctor and follow the recommended treatment plan. Educational information and support is also being provided. The well established United States Renal Data System continues to provide valuable longitudinal data on patients with ESRD. Results of the NIH sponsored Frequent Hemodialysis Nocturnal Trial evaluating the effect of daily and nocturnal dialysis on morbidity and mortality in ESRD patients should be available within the next two to three years.84 The results of these initiatives should invigorate the practice of nephrology, guide judicious apportionment of limited resources, support formulation of rational health policy, and improve the overall outcomes for patients with renal and urinary tract disease.

REFERENCES

1. Dirks JH, de Zeeum D. Prevention of chronic kidney and vascular disease: Toward global health equity—The Bellagio 2004 Declaration. Kidney Int. 2005;68(S98):S1–S6. 2. Beaglehole R, Yach D. Globalization and the prevention and control of non-communicable disease: the neglected chronic diseases of adults. Lancet. 2003;362:903–8. 3. Levey AS, Bosch JP, Lewis JB, et al. a more accurate method to estimate glomerular filtration rate from serum creatinine: A new prediction equation. Ann Intern Med. 1999;130:461. 4. Levey AS, Eckardt KU, et al. KDIGO. KI. 2005;67:2089–100. 5. Lamb EJ, Tomson CR, Roderick PJ. Estimating kidney function in adults using formulae. Ann Clin Biochem. 2005;42:321–45. 6. Pedrini MT, Levey AS, et al. The effect of dietary protein restriction on the progression of diabetic and nondiabetic renal diseases: A metaanalysis. Ann Intern Med. 1996;124:627–32. 7. Klahr S, Levey AS, et al. The effects of dietary protein restriction and blood pressure control on the progression of chronic renal disease. N Eng J Med. 1994;330(13):877–84. 8. The Diabetes Control and Complications (DCCT) Research Group. Effect of intensive therapy on the development and progression of diabetic nephropathy in the Diabetes Control and Complications Trial. Kidney Int. 1995;47:1703–20. 9. Striker G. Report on a workshop to develop management recommendations for the prevention of progression in chronic renal disease. JASN. 1995;5(7):1537–40. 10. Collins AJ, Kasiske B, et al. Excerpts from the United States Renal Data System 2004 Annual Data Report: Atlas of End-Stage Renal Disease in the United States. AJKD. 2005;45(1), Suppl 1 (January):S61. 11. Borch-Johnsen K, Norgaard K, et al: Is diabetic nephropathy an inherited complication? Kidney Int. 1992;41:719–22. 12. Selby JV, FitzSimmons SC, et al. The natural history and epidemiology of diabetic nephropathy. JAMA. 1990;263(14):1954–60. 13. Genetic Determinants of Diabetic Nephropathy. The Family Investigation of Nephropathy and Diabetes (FIND). JASN. 2003;14: S202–S204. 14. Kramer HJ, Nguyen QD, Curhan G, et al. Renal insufficiency in the absence of albuminuria and retinopathy among adults with type 2 diabetes mellitus. JAMA. 2003;289(24):3273–7. 15. Mogyorosi A, and Ziyadeh FN. Update on pathogenesis, markers and management of diabetic nephropathy. Curr Opin Nephrol Hypertens. 1996;5:243–53. 16. Messent JWC, Elliott TG, Hill RD, et al. Prognostic significance of microalbuminuria in insulin-dependent diabetes mellitus: A twentythree year follow-up study. Kidney Int. 1992;41:836–9. 17. Parving HH, Lehnert H, Brochner-Mortensen J, et al. Irbesartan in patients with type 2 diabetes. N Eng J Med. 2001;345(12):870–8. 18. Lewis EJ, Hunsicker LG, et al. The effect of angiotensin-convertingenzyme inhibition on diabetic nephropathy. N Eng J Med. 1993;329:1456–62.

19. Nakao N, Yoshimura A, Morita H, et al. Combination treatment of angiotensin—II receptor blocker and angiotensin-convertingenzyme inhibitor in non-diabetic renal disease (COOPERATE): a randomised controlled trial. Lancet. 2003;361(9352):117–24. 20. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Eng J Med. 1993;329(14):977–86. 21. UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. BMJ. 1998;317:703–13. 22. Fioretto P, Steffes MW, Sutherland DE, et al. Reversal of lesions of diabetic nephropathy after pancreas transplantation. N Eng J Med. 1998;339(2):69–75. 23. Clark CM, Jr, Lee DA. Prevention and treatment of the complications of diabetes mellitus. N Eng J Med. 1995;332(18):1210–7. 24. Bojestig M, Arnqvist HJ, et al. Declining incidence of nephropathy in insulin-dependent diabetes mellitus. N Eng J Med. 1994;330:15–8. 25. Bennet PH, Haffner S, et al. Screening and management of microalbuminuria in patients with diabetes mellitus: Recommendations to the Scientific Advisory Board of the National Kidney Foundation from an ad hoc committee on the Council on Diabetes Mellitus of the National Kidney Foundation. Am J Kid Dis. 1995;25(1):107–12. 26. Collins AJ, Kasiske B, et al. Exerpts from the United States Renal Data System 2004 Annual Data Report: Atlas of End-Stage Renal Disease in the United States. AJKD. 2005;45(1):Suppl 1:S61. 27. Klag MJ, Whelton PK, Randall BL, et al. End-stage renal disease in African-American and white men. 16-year MRFIT findings. JAMA. 1997;277:1293–8. 28. Norris KC, Agodoa LY. Unraveling the racial disparities associated with kidney disease. Kidney Int. 2005;68:914–24. 29. Tierney WM, McDonald CJ, Luft FC. Renal disease in hypertensive adults: effect of race and type 2 diabetes mellitus. Am J Kidney Dis. 1989;13:485–93. 30. Rostand SG, Brown G, Kirk KA, et al. Renal insufficiency in treated essential hypertension. N Eng J Med. 1989;320:684–8. 31. Schulman NB, Ford CE, Hall WD, et al. Prognostic value of serum creatinine and effect of treatment of hypertension on renal function: results from the Hypertension Detection and Follow-up Program. Hypertension. 1989;13(suppl):S180–S193. 32. Agodoa LY, Appel L. African american study of kidney disease and hypertension. JAMA. 2001;285(21):2719–28. 33. Sarnak MJ, Greene T, Wang X, et al. The effect of a lower target blood pressure on the progression of kidney disease: long-term follow-up of the modification of diet in renal disease study. Annals Internal Med. 2005;142(5):342–51. 34. Hansson L, Zanchetti A, Curruthers SG, et al. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomized trial. Lancet. 1998;351(9118):1755–62. 35. Kramer B, Schweda F. Rami in non-diabetic renal failure (REIN study). Lancet. Vol 350, Issue 9079, p. 736. 36. Kitiyakara C, Eggers P, Kopp JB. Twenty-one-year trend in ESRD due to focal segmental glomerulosclerosis in the United States. Am J Kid Dis. 2004;44(5):815–25. 37. Cattran D. Management of membranous nephropathy: When and what for treatment. J Am Soc Nephrol. 2005;16:1188–94. 38. Van Paassen P, van Rie H, Tervaert JW, et al. Signs and symptoms of thin basement membrane nephropathy: A prospective regional study on primary glomerular disease—The Limburg Renal Registry. Kidney Int. 2004;66(3):909–13. 39. Feehally J, Barratt J. IgA Nephropathy. J Am Soc Nephrol. 2005;16:2088–97. 40. Suzuki K, Honda K, Tanabe K, et al. Incidence of latent mesangial IgA deposition in renal allograft donors in Japan. Kidney Int. 2003;63(6):2286–94.

63 41. Praga M, Gutierrez E, Gonzalez E, et al. Treatment of IgA nephropathy with ACE inhibitors: A randomized and controlled trial. JASN. 2003;14:1578–83. 42. Hogg RJ, Lee J, Nardelli NA, et al. Multicenter, placebo-controlled trial of alternate-day prednisone (QOD-PRED) or daily omega-3 fatty acids (OM-3 FA) in children and young adults with IgA nephropathy (IgAN). Report of the Southwest Pediatric Nephrology Study Group. Abstract SU-PO 979. JASN. 2003;14:751A. 43. Rodriguez-Iturbe B. Acute poststreptococcal glomerulonephritis. In: Schrier RW, Gottschalk CW, eds. Diseases of the Kidney. 4th ed. Chap. 63. Boston: Little, Brown & Co; 1986. 44. Pinto SW, Sesso R, Vasconceles E, et al. Follow-up of patients with epidemic poststreptococcal glomerulonephritis. Am J Kid Dis. 2001;38(2):249–55. 45. Gabow PA. Autosomal dominant polycystic kidney disease. N Eng J Med. 1993;329(5):322–42. 46. Peters DJ, et al. Chromosome 4 localization of a second gene for autosomal dominant polycystic disease. Nat Genet. 1993;5(4): 359–62. 47. Grantham J. Editorial: “Dangerfield’s disorders”: rise to the forefront. NephSAP. 2005;4:161–5. 48. Sandler DP, Weinberg CR. Analgesic use and chronic renal disease. N Engl J Med. 1989;321:1126–7. 49. Pommer W, Glaeske G, Molzahn M. The analgesic problem in the Federal Republic of Germany: Analgesic consumption, frequency of analgesic nephropathy and regional differences. Clin Nephrol. 1986;26:273–8. 50. Gault MH, Barrett BJ. Analgesic nephropathy. AJKD; Vol 332, no 3. 1998; p. 351–60. 51. Braden GL, O’Shea MH, Mulhern JG, et al. Acute renal failure and hyperkalemia associated with cyclooxygenase-2 inhibitors. Nephrol Dial Transplant. 2004;19:1149. 52. Eknoyan G. Current status of chronic analgesic and nonsteroidal antiinflammatory nephropathy. Curr Opin Nephrol Hypertens. 1994;3: 182–8. 53. Perneger TV, Whelton PK, Klag MJ. Risk of kidney failure associated with the use of acetaminophen, aspirin, and nonsteroidal antiinflammatory drugs. N Eng J Med. 1994;331(25):1675–9. 54. Bresalier RS, Sandler RS, Quan H, et al. Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. N Eng J Med. 2005;352:1092. 55. Kaufman J, Dhakal M, et al. Community-acquired acute renal failure. Am J Kidney Dis. 1991;17:191–8. 56. Hou SH, Bushinsky DA, Wish JB, et al. Hospital-acquired renal insufficiency: a prospective study. Am J Med. 1983;74:243–8. 57. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Disease. 2002;39(5):930–6. 58. Metnitz PG, et al. Effect of acute renal failure requiring renal replacement therapy on outcome in critically ill patients. Crit Care Med. 2002;30(9):2051–8. 59. Morgera S, Kraft AK, Siebert G, et al. Long-term outcomes in acute renal failure patients treated with continuous renal replacement therapies. Am J Kid Dis. 2002;40(2):275–9. 60. Birtch R, Krzossok S, et al. Acetylcysteine for prevention of contrast nephropathy: meta-analysis. Lancet. 2003;362:598–603. 61. Mehta RL, et al. Program to Improve Care in Acute Renal Disease: spectrum of acute renal failure in the intensive care unit: the PICARD experience. IK. 2004;66:1613–21.

Renal and Urinary Tract Disease

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62. Vupputuri S, Batuman V, Muntner P, et al. The risk for mild kidney function decline associated with illicit drug use among hypertensive men. Am J Kid Dis. 2004;43(4):629–35. 63. Neugarten J, Gallo GR, et al. Amyloidosis in subcutaneous heroin abusers (“skin poppers’amyloidosis”). Am J Med. 1986;81:635–40. 64. Menchel S, Cohen D, Gross E, et al. A protein-related renal amyloidosis in drug addicts. Am J Pathol. 1983;112:195–9. 65. Humphreys, MH. Human immunodeficiency virus-associated glomerulosclerosis. Kidney Int. 1995;48:311–20. 66. Rao TKS, Friedman EA. Outcome of severe acute renal failure in patients with acquired immunodeficiency syndrome. Am J Kidney Dis. 1995;25(3):390–8. 67. Mocroft A, et al. Decline in AIDS and death rates in the EuroSIDA study: an observational study. Lancet. 5 July, 2003;362(9377):22–9. 68. Boyce TG, Swerdlow DL, Griffin PM. Escherichia Coli 0157:H7 and the hemolytic-uremic syndrome. NEJM. 1995;333(6):364–8. 69. Morbidity and Mortality Weekly Report: Outbreak of Escherichia coli O157:H7 infections associated with drinking unpasteurized commercial apple juice. JAMA. 1996;276(23):1865. 70. Remuzzi G, and Ruggenenti P. The hemolytic uremic syndrome. Kidney Int. 1995;47:2–19. 71. Stamm WE, Hooton TM. Management of urinary tract infections in adults. N Eng J Med. 1993;329(18):1328–34. 72. Foxman B. Epidemiology of urinary tract infections: incidence, morbidity, and economic costs. Am J Med. 2002;113(Suppl 1A):5S–13S. 73. Foxman B. Epidemiology of urinary tract infections: incidence, morbidity, and economic costs. Disease-A-Month. 2003;49(2):53–70. 74. Stamatelou KK, Francis ME, Jones CA, et al. Time trends in reported prevalence of kidney stones in the United States: 1976–1994. Kidney Int. 2003;63:1817. 75. Curhan GC, Willett WC, Rimm EB, et al. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med. 1993;328:833. 76. Pak CYC. Etiology and treatment of urolithiasis. Am J Kidney Dis. 1991;18(6):624–37. 77. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2006. CA Cancer J Clin. 2006;56:106. 78. Gronbery H. Prostate cancer epidemiology. Lancet. 2003;361: 859–64. 79. Hankey BF, Feuer EJ, Clegg LX, et al. Cancer Surveillance Series: Interpreting trends in prostate cancer—Part I: Evidence of the screening in recent prostate center incidence, mortality, and survival rates. J Natl Cancer Inst. 1999;91(12):1017–24. 80. Thompson IM, Goodman PJ, Tangen CM, et al. The influence of finasteride on the development of prostate cancer. N Engl J Med. 2003;349(3):215–24. 81. Napalkov P, Maisonneuve P, Boyle P. Worldwide patterns of prevalence and mortality from benign prostatic hyperplasia. Urology. 1995;46(3 Suppl A):41–6. 82. Boyle P. New insights into the epidemiology and natural history of benign prostatic hyperplasia. Progress in Clinical & Biological Research. 1994;386:3–18. 83. McConnell JD, Roehrborn CG, Bautista OM, et al. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Eng J Med. 2003;18:349(25):2387–93. 84. Website: www.clinicaltrials.gov

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64

Diabetes Janice C. Zgibor • Janice S. Dorman • Trevor J. Orchard

INTRODUCTION

Diabetes is an important chronic disease both in terms of the number of persons affected and the considerable associated morbidity and early mortality. In this review we will focus on the epidemiology and public health implications of diabetes. Diabetes is a chronic disease in which there is a deficiency in the action of the hormone insulin. This may result from a quantitative deficiency of insulin, an abnormal insulin level, resistance to its action, or a combination of deficits. Two major forms of the disease are recognized: type 1 diabetes (formerly referred to as insulin-dependent diabetes) which comprises about 10% of all cases, and type 2 diabetes (formerly referred to as non-insulin-dependent diabetes), which accounts for about 90% of the cases. Type 2 diabetes may occasionally occur as a result of other diseases such as acromegaly and Cushing’s syndrome. Metabolic disorders such as hemochromatosis, can also cause the disease. Diabetes can also be drug induced, for example, by steroids and possibly by the thiazide diuretics and oral contraceptives. Finally, diabetes may occur secondary to disease processes directly affecting the pancreas, such as cancer or chronic pancreatitis, which destroy the insulin-producing beta cells in the pancreatic islets (of Langerhans). However, these are relatively rare causes of diabetes. In addition to these primary and secondary types of diabetes, two further classifications of abnormalities of glucose tolerance are of note. Gestational diabetes occurs during pregnancy but typically remits shortly after delivery. Impaired glucose tolerance (IGT) or impaired fasting glucose (IFG), now termed “prediabetes,” are conditions in which blood glucose is elevated but not high enough to be classified as diabetes. Nonetheless these conditions may carry some increased risk of large vessel (e.g., coronary heart) disease.1 Both gestational diabetes2 and prediabetes3 carry an increased risk for the subsequent development of type 2 diabetes. The types of diabetes and clinical stages are outlined in Fig. 64-1. The other potential precursor to type 2 diabetes is the metabolic syndrome. The metabolic syndrome represents a set of risk factors that predispose individuals to both cardiovascular disease and diabetes. Metabolic syndrome factors include abdominal obesity, atherogenic dyslipidemia (elevated triglyceride levels, smaller LDL particle size, and low HDL cholesterol), raised blood pressure, insulin resistance (with or without glucose intolerance) and prothrombotic and proinflammatory states. The metabolic syndrome is associated with the prediction of both diabetes and cardiovascular disease independent of other factors.4 It is hypothesized that clinical improvement in these factors may prevent or delay the onset of diabetes and cardiovascular disease. DIAGNOSIS

The diagnosis of type 1 diabetes is fairly straightforward. Type 1 diabetes often, though by no means always, has its onset in childhood. Classically the child will have symptoms of excessive thirst

(polydipsia), excessive urination (polyuria), and weight loss. In a child with high blood sugar, these symptoms almost invariably point to type 1 diabetes. Patients lose virtually all capacity to produce insulin and without treatment they develop severe metabolic disturbances, including ketoacidosis and dehydration, which can lead to death. As death from ketoacidosis is largely preventable, the continuing though small number of deaths from this cause represents a challenge to our preventive health services.5,6 In an international study, wide variations in mortality from acute diabetes complications were noted, with high rates in Japan and low rates in Finland.7 This variation was thought to reflect disease incidence (low in Japan and high in Finland) and resulting availability of skilled health care.7 Type 2 diabetes usually presents in adulthood. In the past, the terms non-insulin-dependent, maturity-onset, and mild diabetes have been used. These terms are somewhat misleading, since type 2 diabetes may present in youth and the complications may be far from mild. Patients with type 2 diabetes, however, produce some insulin, although its secretion is often delayed, and there is usually some resistance to its action in the peripheral tissues. This resistance is often associated with elevated concentrations of insulin, particularly in newly recognized cases. However, concentrations are now recognized to be low in many type 2 diabetes subjects, especially after accounting for obesity and using more specific assays.8 In type 2 diabetes, often the diagnosis is not made on the basis of classic symptoms of diabetes but rather on the presentation of one of the complications. Such complications can be macrovascular (accelerated atherosclerosis with coronary artery, peripheral vascular or cerebrovascular manifestations), microvascular (with disease of the small vessels in the kidneys or the eyes), or neuropathic (which may take the form of a variety of neurological syndromes). In addition, the disease may also be recognized as a result of routine screening for elevated blood glucose or by the presence of glucose in the urine. Some cases, however, may be diagnosed because of classic symptoms. (Table 64-1) Over the years, both the diagnostic criteria and dose of glucose in the standard test for type 2 diabetes (i.e., the oral glucose tolerance test (OGTT)) have varied. Current diagnostic criteria from the American Diabetes Association (ADA) and the World Health Organization (WHO) are presented in Table 64-2. The WHO and ADA criteria differ in that the ADA relies on IFG while the WHO relies on both fasting and post challenge (2 hour) glucose levels. The preference for using a fasting test only, rather than a full OGTT is largely based on the concept that diagnostic testing would be easier and therefore more frequent. The controversy surrounding these tests is based on the fact that these diagnostic tests may identify somewhat different populations.9 Further, data from the Cardiovascular Health Study (CHS) in older Americans suggests that IGT is more predictive of CVD than its fasting corollary IFG.10 The impact of these different criteria on the prevalence of diabetes has been studied by many investigators. 1101

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Noncommunicable and Chronic Disabling Conditions

Stages

Normogloycaemia Normal glucose tolerance

Types

Hyperglycaemia Diabetes mellitus Impaired glucose regulation Not insulin Insulin IGT and/or IFG requiring requiring for control

Insulin requiring for survival

Type 1 • Autoimmune • Idiopathic Type 2∗ • Predominantly insulin resistance • Predominantly insulin secretory defects

Other specific types∗ Gestational diabetes

Because of changes in the criteria for the diagnosis of type 2 diabetes, estimates of the prevalence and temporal trends of type 2 diabetes are difficult, if not impossible, to evaluate. Furthermore, the different criteria for type 2 diabetes used by different research groups and countries make geographical comparisons difficult. As major efforts are made to identify the specific genetic abnormalities in diabetes and to define the disease on the basis of genotypic rather than phenotypic expression, such as hyperglycemia and insulin levels, there may soon be yet another way of classifying diabetes. Furthermore the development of the glycosylated hemoglobin (GHB) test,11 which provides an integrated measure of hyperglycemia over the prior two to three months, represents another dimension that may add to the ability to define diabetes. Currently, clinicians use hemoglobin A1c for this test, although it is not accepted for diagnostic purposes due to methodological variation and other considerations.

Heterogeneity in Primary Diabetes Although the two different primary types of diabetes have been described, the classification of diabetes into these groups is not simple. For example, children classified with type 1 diabetes may actually have Maturity-Onset Diabetes (MODY),12,13 which is characterized by an autosomal dominant pattern of inheritance and a low frequency ketoacidosis. Children in such families, however, are often treated with insulin, although they do not depend on insulin for their survival and actually have type 2 diabetes. Since MODY is uncommon, accounting for <5% of all type 2 diabetes cases, this section will focus on type 1 diabetes and type 2 diabetes. Similarly 5–10% of adults with presumed type 2 diabetes, have evidence of autoantibodies seen in type 1 diabetes, and may have an incomplete form of type 1 diabetes, sometimes called LADA (latent autoimmune diabetes of adulthood).14

Type 1 Diabetes Descriptive Epidemiology. Type 1 diabetes is caused by the autoimmune destruction of the beta cells of the pancreas, and represents approximately 10% of all cases with diabetes. At present, lifelong insulin therapy is the only treatment for the disease. Without exogenous insulin injections, individuals with type 1 diabetes will not survive. Although the prevalence of type 1 diabetes is <1% in most populations, the geographic variation in incidence is

Figure 64-1. Disorders of glycemia: etiological types and clinical stages. ∗In rare instances patients in these categories (e.g., Vacor Toxicity, Type 1 presenting in pregnancy, etc.) may require insulin for survival. (Source: Adapted from the World Health Organization.50)

enormous, ranging from <1/100,000 per year in China to approximately 40/100,000 per year in Finland (Fig. 64-2).15 The only chronic childhood disorder more prevalent than type 1 diabetes is asthma. It has been estimated that approximately 20 million people worldwide, mostly children and young adults, have type 1 diabetes.16 The incidence of type 1 diabetes is increasing worldwide at a rate of about 3% per year.17 This trend appears to be most dramatic in the youngest age groups, and is completely unrelated to the current increase in type 2 diabetes in children. More children with beta cell autoantibodies, a hallmark of type 1 diabetes, are being diagnosed with the type 1 diabetes around the world each year. Although the peak age at onset is at puberty, type 1 diabetes can also develop in adults. Epidemiologic studies have revealed no significant gender differences in incidence among individuals diagnosed before age 15.18 However, after age 25, the male-to-female incidence ratio is approximately 1:5. Significant differences have also been reported depending on socioeconomic status, however results have been conflicting.19 Incidence of type 1 diabetes in Lithuanians aged 0–39 years varies by the urban-rural setting, and the time change differs for men and women during 1991–2000. There is also a notable seasonal variation in the incidence of type 1 diabetes in many countries, with lower rates in the warm summer months, and higher rates during the cold winter.20 Genetic Susceptibility. First degree relatives have a higher risk of developing type 1 diabetes than unrelated individuals from the general population (approximately 6% vs. <1%, respectively).21 These data suggest that genetic factors are involved with the development of the disease. At present, there is evidence that more than 20 regions of the genome may be involved in genetic susceptibility to type 1 diabetes. However, none of the candidates identified have a greater influence on type 1 diabetes risk than that conferred by genes in the HLA (Human Leukocyte Antigens) region of chromosome 6. This region contains several hundred genes known to be involved in immune response. Those most strongly associated with the disease are the HLA class II genes (i.e., HLA-DR, DQ, DP). These molecules are involved in the processing of antigens from inside the cell to its surface in order to stimulate an immune response. However, it has become apparent that neither genetic nor environmental risk factors alone contribute to the development of type 1 diabetes. Rather, it is clear that gene-environmental interactions are involved.

64 TABLE 64-1. PERCENT OF POPULATION WITH PHYSICIAN DIAGNOSED AND UNDIAGNOSED DIABETES AND IMPAIRED GLUCOSE TOLERANCE IN THE U.S. POPULATION AGE ≥ 20 YEARS (NHANES III) FROM 1988 TO 1994167

≥ 20

20–39

40–49

50–59

60–74

≥ 75

Classification

aDiagnosed Diabetes All Races Both Sexes Male Female White Both Sexes Male Female Black Both Sexes Male Female

5.1 4.9 5.4

1.1 1.1 1.1

3.9 3.3 4.4

8.0 9.6 6.6

12.6 11.8 13.3

13.2 13.8 12.8

5.0 5.0 5.0

1.0 1.2 0.9

3.3 3.0 3.5

7.5 9.9 5.3

11.3 10.9 11.7

12.6 13.2 12.3

6.9 5.9 7.8

1.6 1.6 1.6

6.2 5.5 6.7

13.8 13.0 14.5

20.9 16.8 23.9

17.5 14.7 19.0

Prediabetes†

bUndiagnosed Diabetes FPG ≥ 126mg/dL All Races Both Sexes Male Female White Both Sexes Male Female Black Both Sexes Male Female

2.7 3.0 2.4

0.6 0.5 0.6

2.5 3.6 1.6

4.6 3.3 5.8

6.2 8.4 4.5

5.7 7.3 4.7

2.5 2.9 2.1

0.4 0.4 0.4

2.1 2.9 1.3

4.0 3.5 4.4

6.0 8.2 4.3

4.9 6.0 4.3

3.4 2.6 4.0

1.4 1.1 1.7

3.9 4.3 3.7

6.1 3.0 8.5

7.7 6.6 8.5

4.9 0.0 7.6

bImpaired Fasting Glucose (110–125 mg/dL) All Races Both Sexes Male Female White Both Sexes Male Female Black Both Sexes Male Female

6.9 8.7 5.2

2.8 4.5 1.2

7.1 10.1 4.3

8.0 9.2 6.8

14.0 16.2 12.3

14.1 17.9 11.9

6.9 9.0 5.0

2.7 4.8 0.8

6.7 10.2 3.2

7.7 9.1 6.4

13.9 15.6 12.5

13.7 18.4 11.0

6.2 6.7 5.8

2.8 3.3 2.5

7.0 6.7 7.2

10.0 9.3 10.5

12.1 15.4 9.8

15.7 18.7 14.1

aBased on self-report that the persons had been told by a doctor that they had diabetes, plus current or past use of diabetic therapy. bBased on the results of 75-g oral glucose tolerance test conducted in the morning after an overnight 10- to 16-hour fast in persons with no medical history of diabetes.

Figure 64-2. Type 1 diabetes incidence rates worldwide. FIN = Finland, SAR = Sardinia, SWE = Sweden, NOR = Norway, US-WI = US-Wisconsin, US-PA = US-Pennsylvania, ITA = Italy, ISR = Israel, JAP = Japan, CHI = China

1103

TABLE 64-2. CRITERIA FOR THE CLASSIFICATION OF DIABETES

Diabetes*

Age

Diabetes

Gestational diabetes¶

ADA168

WHO

A. Symptoms (polyurea, polydipsia, unexplained weight loss) of diabetes and casual (anytime of day without regard to meals) plasma glucose ≥ 200mg/dL or B. a,§ Fasting plasma glucose ≥ 126 mg/dL or C. 2 hour plasma glucose ≥ 200 mg/dL during an OGTT‡ Impaired fasting glucose Fasting glucose 100mg/ dL to 125 mg/dL

A. Confirmatory symptoms or B. a,§ Fasting plasma glucose ≥ 126 mg/dL and 2 hour plasma mg/dL glucose ≥ 200 during an OGTT‡

Fasting ≥ 95 mg/dL (plasma) 1 h ≥ 180 mg/dL (plasma) 2 h ≥ 155 mg/dL (plasma) 3 h ≥ 140 mg/dL (plasma)

Women meeting the WHO criteria for diabetes or IGT are classified as having gestational diabetes mellitus

Impaired glucose tolerance 2 h plasma glucose§ 140 mg/dL to 199 mg/dL Two or more of the following values after a 100-g oral glucose load after an overnight fast (8–14 h)

∗Diabetes is subclassified as: Gestational: Diabetes or impaired glucose tolerance is first recognized during pregnancy. Usually remits postpartum a criteria need to be present on at least two occasions in the absence of unequivocal hyperglycemia. †Prediabetes = impaired fasting glucose or impaired glucose tolerance. ‡Following 75 g or oral glucose load. §Fast = no caloric intake for ≥ 8 hours. ¶ Risk factor assessment should be done at first prenatal visit.

A. IDDM1. The HLA class II genes, also referred to as insulindependent diabetes mellitus 1(IDDM1), contribute approximately 40–50% of the heritable risk for type 1 diabetes.22 When evaluated as haplotypes, DQA1*0501-DQB1*0201 and DQA1*0301-DQB1*0302 are most strongly associated type 1 diabetes in Caucasian populations. They are in linkage disequilibrium with DRB1*03 and DRB1*04, respectively. Specific DRB1*04 alleles also modify the risk associated with the DQA1*0301-DQB1*0302 haplotype. Other reported high risk haplotypes for type 1 diabetes include DRB1*07-DQA1*0301-DQB1*0201 among AfricanAmericans, DRB1*09-DQA1*0301-DQB1*0303 among Japanese, and DRB1*04-DQA1*0401-DQB1*0302 among Chinese. DRB1*15-DQA1*0602-DQB1*0102 is protective and associated with a reduced risk of type 1 diabetes in most populations. Recent reports suggest that other genes in the central, class I, and extended class I regions may also increase type 1 diabetes risk independent of HLA class II genes.23,24 Individuals with two high risk DRB1-DQA1-DQB1 haplotypes have a significantly higher type 1 diabetes risk than individuals with no high risk haplotype. The type 1 diabetes risk among those with only one susceptibility haplotype is also increased, but the effect is more modest. As shown in Table 64-3, relative risk estimates range from 10 to 45 and 3 to 7, respectively, for these groups, depending on race.21

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Noncommunicable and Chronic Disabling Conditions

TABLE 64-3. SEVERAL TYPE 1 DIABETES SUSCEPTIBILITY GENES Gene HLA-DQB1 INS CTLA4

Locus 6p21.3 11p15. 5 2q31–35

Variant *0201 & *0302 Class I Thr17Ala

Estimated RR† 3–45 1–2 1–2

RR relative risk

†

In terms of absolute risk, Caucasian individuals with two susceptibility haplotypes have an approximately 6% chance of developing type 1 diabetes through age 35 years. However, this figure is substantially lower in populations where type 1 diabetes is rare (i.e., < 1% among Asians). In addition to IDDM1, two other genes are now known to influence type 1 diabetes risk.25 These include insulin (INS) and cytotoxic T lymphocyte-associated 4 (CTLA-4). B. INS. The INS gene, located on chromosome 11p15.5, has been designated as IDDM2. Positive associations have been observed with a nontranscribed variable number of tandem repeat (VNTR) in the 5’ flanking region.26,27 There are two common variants. The shorter class I variant predisposes to type 1 diabetes (approximate relative increase: 1–2), whereas the longer class III variant appears to be dominantly protective. The biological plausibility of these associations may relate to the expression of insulin mRNA in the thymus. Class III variants appear to generate higher levels of insulin mRNA than class I variants. Such differences could contribute to a better immune tolerance for class III-positive individuals by increasing the likelihood of negative selection for autoreactive T-cell clones. The effect of INS appears to vary by ethnicity, with lesser effects in non-Caucasian populations.28 C. CTLA-4. The CTLA-4 gene is located on chromosome 2q31–35,25 where multiple type 1 diabetes genes may be located. CTLA-4 variants have been associated with type 1 diabetes, as well as other autoimmune disease. CTLA-4 negatively regulates T-cell function. However, impaired activity, which has been associated with the Thr17Ala variant, may increase type 1 diabetes risk. Overall, the relative increase in risk for the CTLA4Ala17 variant has been estimated as approximately 1.5. Environmental Risk Factors. The epidemiological patterns described above suggest that environmental factors contribute to the etiology of the type 1 diabetes. In particular, the recent temporal increase in type 1 diabetes incidence points to a changing global environment rather than variation in the gene pool, which require the passage of multiple generations. Twin studies also provide evidence for the importance of environmental risk factors for type 1 diabetes. Type 1 diabetes concordance rates for monozygous twins are higher than those for dizygous twins (approximately 30% vs. 10%, respectively).22 However, most monozygous twin pairs remain discordant. Thus, type 1 diabetes cannot be completely genetically determined. Environmental risk factors are thought to act as either “initiators” or “accelerators” of beta cell autoimmunity, or “precipitators” of overt symptoms in individuals who already have evidence of beta cell destruction.29 They also may function by mechanisms that are directly harmful to the pancreas, or by indirect methods that produce an abnormal immune response to proteins normally present in cells. The type 1 diabetes environmental risk factors that have received most attention are viruses, infant nutrition, and hygiene. A. Viruses. Enteroviruses, especially Coxsackie virus B (CVB), have been the focus of numerous ecologic and case-control studies.30 CVB infections are frequent during childhood and are known to have systemic effects on the pancreas. Recent

prospective studies are helping to elucidate the role of viruses to the etiology of type 1 diabetes. For example, enteroviral infections occurring as early as in utero appear to increase a child’s subsequent risk of developing the disease.31,32 Other viruses, including mumps,33 cytomegalovirus,34 rotavirus,35 and rubella,36 have also been associated with the disease. B. Nutrition. Another hypothesis that has been the subject of considerable interest relates to early exposure to cow’s milk protein and the subsequent development of type 1 diabetes. The first epidemiologic observation of such a relationship was by Borch-Johnsen et al., who found that type 1 diabetes children were breast-fed for shorter periods of time than their non-diabetic siblings or children from the general population.37 The authors postulated that the lack of immunologic protection from insufficient breast-feeding may increase risk for type 1 diabetes later during childhood. It was also postulated that shorter duration of breastfeeding may indirectly reflect early exposure to dietary proteins that stimulate an abnormal immune response in newborns. Most recently it has been hypothesized that the protective effect of breast-feeding may be due, in part, to its role in gut maturation.38–40 Breast milk contains growth factors, cytokines, and other substances necessary for the maturation of the intestinal mucosa. Breast-feeding also protects against enteric infections during infancy, and promotes proper colonization of the gut. Interestingly, enteroviral infections can also interfere with gut immunoregulation, which may explain the epidemiologic associations between viral infections and type 1 diabetes. C. Hygiene. The role of hygiene in the etiology of type 1 diabetes is also currently being explored.41,42 It has been hypothesized that delayed exposure to microorganisms due to improvements in standard of living hinders the development of the immune system, such that it is more likely to respond inappropriately when introduced to such agents at older (compared to younger) ages. This explanation is consistent with recent reports indicating that factors such as day care attendance,41 sharing a bedroom with a sibling, and contact with pets are protective against type 1 diabetes.42 Further studies are needed to determine if improved hygiene can explain the temporal increase in the incidence of type 1 diabetes worldwide. Treatment and Prevention of Type 1 Diabetes. At the present time, there is no way to prevent type 1 diabetes. Lifelong insulin injections are the only available treatment for the disease. Although a cure for type 1 diabetes is currently unavailable, several large multinational investigations have been designed to evaluate a variety of primary and secondary disease interventions. The tested interventions have included prophylactic nasal insulin (Diabetes Prediction and Prevention Project [DIPP] in Finland),43 oral and injected insulin (Diabetes Prevention Trial-1 [DPT-1] in the U.S.),44 as well as high doses of nicotinamide (European Nicotinamide Diabetes Intervention Trial [ENDIT]),45 and the avoidance of cow’s milk exposure during the first six months of life (trial to reduce in genetically at-risk [TRIGR] in Finland, U.S. and other countries).46 These investigations focus on “prediabetic” individuals identified from families with at least one child with type 1 diabetes. DIPP and TRIGR use HLA-DQB1 screening and recruit only individuals at increased genetic risk. The remaining trials recruit relatives with evidence of beta cell autoimmunity as a pre-clinical marker for disease. To date, none of these interventions have prevented or delayed the onset of type 1 diabetes.44–46 However, with the formation of Type 1 Diabetes TrialNet47 a collaborative network of clinical centers and experts in diabetes and immunology, new intervention strategies are currently being planned. It is ultimately hoped that through genetic testing, individuals at high risk for type 1 diabetes could be identified prior to the onset of the disease—at a time when primary prevention strategies could be safely administered. It is most likely that such predictive genetic testing would be offered to families with an affected individual before it was made available to the general population.

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Type 2 diabetes Epidemiology. Type 2 diabetes is more difficult to define than type 1 diabetes. The rates among and within countries vary dramatically, partially depending on the specific classification criteria used for type 2 diabetes. Worldwide, it is estimated that in 2000, 171 million people had diabetes. The prevalence is expected to increase to 366 million by 2030 according to estimates from the WHO.48 Type 2 diabetes occurs in all races, but the prevalence tends to be higher among American Indians, Micronesians, Polynesians, African-Americans, and Mexican Americans.49 The prevalence of diabetes is higher in developed countries compared to developing countries, however a considerable increase in prevalence is already being observed in developing nations due to urbanization and westernization.50 For example, in communities where there has been rapid economic development, such as in Korea51 and among the Pima Indians52 there appears to be a marked and rapid increase in the incidence and prevalence of type 2 diabetes.51 In 2005, 14.6 million persons in the United States were estimated to have diagnosed diabetes according to the National Health Interview Survey. This represents an increase from 5.8 million in 1980. It is also estimated that almost one-third as many cases (6.2 million) of type 2 diabetes are undiagnosed. This is made clear by data from the National Health and Examination Survey where the overall prevalence of diagnosed and detected diabetes in the adult U.S. population (> 20 years ) is estimated to be about 7% (~20.8 million), with 1.4 million newly diagnosed cases each year.53 Risk Factors. A pattern of increasing mean weight of the population parallels the increasing prevalence of type 2 diabetes.54 Similarly, within a population there is a strong correlation between degree of obesity and risk of type 2 diabetes.52,55,56 The prevalence of obesity in the United States, defined as a Body Mass Index (BMI) of greater than 30 kg/m2, has increased from 12% in 1991 to 19.8% in 2000,57 for a total of 44.3 million obese adults. The highest prevalence for obesity was reported in Mississippi at 25.9% in 2001. A corresponding increase is reported in diabetes prevalence from 4.9% in 1990 to 7.3% and 7.9% in 2000 and 2001 respectively.57 Interestingly, within a country such as the United States, one generally finds an inverse relationship between obesity and socioeconomic class,58 with higher rates of type 2 diabetes in lower socioeconomic groups.59 However, a risk factor associated with higher socioeconomic status is decreased physical activity. As socioeconomic status increases, the overall level of physical activity generally declines, especially that related to work. Further, lower rates of physical activity are found in ethnic minorities.60 Thus, at the same time that caloric intake is increasing, physical activity is decreasing, most likely leading to an increased prevalence of obesity within the population. Data from the South Pacific suggest that physical activity itself may be an independent risk factor for type 2 diabetes, separate from obesity,61 while a recent prospective study in the U.S. also suggests reduced physical activity predicts type 2 diabetes.62 According to national data from 2003, approximately one-half of U.S. adults age 18–44 achieved recommended levels of physical activity (at least 30 min/day at least 5 days per week).60 Nutrition plays a role in both diabetes risk and prevention, while no clear evidence exists supporting a low fat diet for diabetes risk or prevention, the type and quality of fat may be more important than total fat intake. Substituting unsaturated fat for saturated and trans fat are important, however, for prevention strategies. Also, substituting complex carbohydrates such as whole grains for refined grain foods will help individuals achieve a healthy body weight and thus prevention of diabetes and/or cardiovascular disease.63

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developing type 1 diabetes, they may also play a role in type 2 diabetes.65 Several candidate genes have been found to contribute to type 2 diabetes susceptibility, including mutations in the insulin gene,66 the glucokinase gene,67 and mitochondrial gene.68 However, it is unlikely that any of these alterations explain the genetic susceptibility to type 2 diabetes on a population basis. Thus family and pedigree studies are still needed to determine the contribution of these genetic markers to the development of type 2 diabetes. Diabetes Prevention. The development of type 2 diabetes is a twostage process, with the first stage being resistance to insulin’s action (likely exacerbated by obesity and physical inactivity) and the second stage being failure of the pancreas to increase insulin secretion enough to overcome this resistance. This theory receives support from a number of reports including one from the Pima Indians, which showed differing predictive values of fasting and post challenge insulin values for developing type 2 diabetes consistent with a hyperinsulinemic phase followed by eventual insulinopenia.69 The interaction between obesity and physical inactivity in relation to the prevention of type 2 diabetes has been studied recently through well-conducted randomized controlled trials. These trials applied sound methods for implementing diabetes prevention strategies, and will be briefly reviewed. The focus of these trials was lifestyle modification including weight loss and increased physical activity. The Da Qing study70 followed 577 subjects with IGT from local clinics. Subjects were randomized at the clinic level to diet, exercise, diet and exercise, or a control group and followed for six years. Intervention groups experienced a significantly lower incidence of type 2 diabetes compared to controls (31%, 46%, 42%, and 67.7% respectively). A lower incidence of diabetes was also seen in those with lower BMIs. Similar to the Da Qing trial, the Finnish Diabetes Prevention Study71 examined whether the onset of type 2 diabetes could be prevented through lifestyle modification in subjects with IGT. Five hundred twenty-two subjects were randomized to an intervention group that received individualized counseling aimed at weight reduction, dietary fat reduction, saturated fat reduction, increased dietary fiber, and increased physical activity. The trial demonstrated that lifestyle changes significantly reduced the risk of diabetes in middle-aged, overweight subjects. After a modest (4.7%) weight loss, those in the intervention group experienced a 58% reduction in incidence of diabetes over a mean follow-up of 3.2 years. Moreover, blood pressure, triglycerides, and high-density lipoprotein cholesterol levels also improved significantly. The study to prevent noninsulin-dependent diabetes mellitus (STOP-NIDDM) trial72 randomized 714 (IGT) subjects to acarbose and 715 subjects to a control group. After a mean follow-up of 3.3 years, compared to controls, there was a 25% relative risk reduction in the incidence of diabetes. Finally, in the Diabetes Prevention Program (DPP)73 3234 subjects with IGT were randomized to placebo, metformin (850 mg twice daily) or intensive lifestyle modification. The lifestyle modification consisted of weekly one-on-one counseling for a 16-week curriculum during the first 24 weeks of the study. Subsequent visits were held about once per month. The goal of the lifestyle arm was 7% weight loss and 150 minutes per week of physical activity. Intensive lifestyle modification reduced the incidence of type 2 diabetes in persons at high risk by 58% in comparison to the metformin study group in which incidence was reduced by 31%. The DPP has also shown that these interventions reduce the incidence of new metabolic syndrome by 41% (lifestyle) and 17% (metformin) compared with placebo.74

Screening Genetic Factors. Genetic factors play an extremely important role in the development of type 2 diabetes. In a large study of twins Pyke found that the concordance rates for type 2 diabetes among monozygotic twins was over 90% compared to 50% for type 1 diabetes.64 Twin studies, however, do not provide the complete story. In recent years there have been numerous studies of the relationship of genetic markers to the development of type 2 diabetes as well as of type 1 diabetes. Although HLA genes are related primarily to the risk of

The recent emphasis on diabetes prevention has prompted a growing number of blood glucose screenings. The purpose of screening is to identify asymptomatic individuals who may have diabetes, however, screening is not the same as diagnosis, as diagnostic tests are performed in individuals with signs and symptoms of the disease.75 Further, the effectiveness of diagnosing an asymptomatic individual is still speculative.76 Screening in the community setting outside a health care setting may not be completely effective because of the

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possibility of inadequate follow-up after a positive test, or repeat testing in those who are negative. Therefore this type of screening is currently not recommended.75 Screening by a health care professional or within the health care setting for pre-diabetes and diabetes should be considered in those ≥ 45 years of age, particularly in those with a BMI ≥ 25 kg/m2. In those < 45 years of age, screening should be considered if they have another risk factor for diabetes (e.g., physically inactive, first-degree relative with diabetes, member of a high-risk ethnic population, delivered a baby weighing > 9 pounds or diagnosed with gestational diabetes, are hypertensive (≥ 140/90 mmHg), high-density lipoprotein cholesterol (HDLc) level <35 mg/dL and/or a triglyceride level >250 mg/dL, have polycystic ovarian syndrome (PCOS), previously tested and had IGT or IFG, other clinical conditions associated with insulin resistance, or a history of vascular disease).75 Any screening should be followed by education about results and risk for future disease. A policy ensuring adequate follow-up should also be in place.

MORBIDITY AND COMPLICATIONS OF DIABETES

Prior to the introduction of insulin in 1922 by Banting and Best, life expectancy of patients with type 1 diabetes was about 1–2 years. After the development and widespread use of insulin, there was a dramatic increase in life expectancy for patients with type 1 diabetes. Suddenly those with type 1 diabetes could lead relatively normal lives. However, 20–30 years later the long-term sequelae of type 1 diabetes began to become evident. Both type 1 diabetes and type 2 diabetes patients are at risk for these long-term complications. Complications come mainly from disorders of the circulation, either macrovascular, including accelerated atherosclerosis resulting in stroke, heart and peripheral vascular disease, or microvascular disorders of the kidney and retina, as well as neuropathy. The complications appear to be similar for both type 1 diabetes and type 2 diabetes, although the prevalence may be somewhat higher in type 1 diabetes mainly due to longer diabetes duration in those with type 1. The relationships with age and duration also vary between the two types of diabetes, partly because of the younger age of onset of type 1 diabetes (which leads to complications at a younger age) and the difficulty of determining the onset of type 2 diabetes (which means complications are often present at the onset of known disease). However, careful analysis controlling for these time-dependent variables suggests that the incidence of the microvascular complications is remarkably similar by true duration.77 The following discussion will mainly focus on type 1 diabetes, since these data are more complete.

Mortality Mortality rates for people with diabetes are two- to threefold higher than those without diabetes, with cardiovascular disease as the leading cause of death.78 In an international study, Diabetes Epidemiology Research International (DERI), mortality in young cohorts of type 1 diabetes cases from four different countries (the United States, Israel, Japan, and Finland) was investigated. The study showed tremendous variation in diabetes-related mortality. In addition to the high mortality from acute complications, the Japanese cohort also had a high mortality from renal disease (276/100,000/y) compared to Finland (16/100,000/y, p <0.05).79 Data from the Children’s Hospital of Pittsburgh diabetes registry as of 1982, demonstrated a sevenfold increased risk of death overall, and a 20-fold increased risk in those over the age of 20 compared to the general population.80 While over half of the deaths were due to renal disease, there was an 11-fold increased risk of death from CVD compared to the general population of the same age. These findings were particularly significant in the 30 age group. The Steno group further demonstrated the strong effect of renal disease with those developing proteinuria, having an eightfold greater risk of coronary heart disease (CHD) than a matched group who did not develop proteinuria.81 These results were supported by Krolewski et al.,82 where in type 1 diabetes subjects seen at

the Joslin Clinic,81 CHD deaths occurred early after the third decade of age, and over the next 25 years. One-half died of or had CHD. The Allegheny County registry has more recently shown an improvement in 20-year survival by diagnosis cohort (1965–69, 1970–74, 1975–79).83 When cause-specific mortality was examined, the County cohort combined with mortality from the Epidemiology of Diabetes Complications Study cohort, a significant decline in renal84 and acute complications85 was noted. There were, however, differential results by race where African-Americans experienced a fivefold excess mortality due to acute complications.85 This decline in mortality may be explained by only a decline in acute complications, but microvascular complications as well. Data from the Steno Clinic in Denmark showed declining trends in microvascular complications by diagnosis cohort at 20 year duration.86 Similar results were also shown in the EDC cohort in those who had reached 20 years of diabetes duration; however there was not a corresponding decline in CHD,87 although the number of events was relatively small. Longer follow-up is necessary to determine any definitive trends in macrovascular disease.

Diabetic Retinopathy Epidemiology. The prevalence of diabetic retinopathy is highly related to diabetes duration for both type 1 and type 2 diabetes.75 After 20 years of type 1 diabetes, virtually 100% of patients show some evidence of damage to the retina called background retinopathy. Similar prevalence rates are seen in type 2 diabetes for patients treated with insulin, although rates are lower (around 55%) for those not on insulin.88 In addition, as many as 70% of patients who have type 1 diabetes89 and 30% of patients who have type 2 diabetes88 on insulin may develop proliferative changes in the eyes that may lead to blindness. In 2002, three million adults age 18 or greater reported some type of visual disturbance. In the 20–74 age group, diabetes is the leading cause of blindness in the United States, and is responsible for approximately 12,000–24,000 new cases of blindness year. The crude prevalence of retinopathy in people over the age of 40 is 40.3% in people with diabetes compared to 3.4% in the general population.90 Prevention. Retinopathy was the primary outcome of a major U.S. study called Diabetes Control and Complications Trial (DCCT).91 This landmark study clearly demonstrated the value of intensive therapy (with normal blood sugars as a goal) for type 1 diabetes subjects in preventing or delaying the microvascular complications. Progression of retinopathy was reduced by 54% in the intensive therapy group compared to conventional therapy over a mean follow-up period of 6.5 years.92 In type 2 diabetes, the United Kingdom Prospective Diabetes Study (UKPDS) demonstrated that achieving near normal glycemic control, reduced the risk of two-step progression of diabetic retinopathy by 21%,93 while reducing blood pressures resulted in a 34% risk reduction for deterioration of retinopathy by two or more steps over 7.2 years of follow-up.94 As diabetic retinopathy can be detected before it threatens vision, blindness due to diabetic retinopathy can be prevented in many cases. Detecting and treating diabetic eye disease can reduce vision loss by 50–60%.94 The Diabetic Retinopathy Study has demonstrated that individuals with severe diabetic retinopathy can be treated successfully and their vision preserved with laser photocoagulation therapy.95 It is thus important that patients and physicians be educated about the need for frequent eye examinations and that adequate clinical treatment for diabetic retinopathy be available in the community.

Renal Disease Epidemiology. Diabetic renal disease is a major cause of morbidity and mortality among those with diabetes.5,79,96,97 Diabetes is currently the leading cause of treatment for end stage renal disease (ESRD), accounting for 44% of the 42,813 new ESRD cases during 2001. According to the 2001 data, 142,963 people with diabetes have ESRD and are living on chronic dialysis or with a kidney transplant. Diabetes increases the risk of renal failure 17- to 20-fold. Approximately 40% of people with type 1 diabetes97,98 eventually develop significant

64 clinical proteinuria and renal disease. Studies from Pittsburgh89 suggest that around 70% of type 1 diabetes subjects will eventually have some degree of renal damage (i.e., including those with microalbuminuria—a more modest degree of abnormal urinary albumin excretion that is predictive of more advanced disease). The relative risk of mortality from renal disease for persons with diabetes compared to the general population is highest for those in the 15- to 44-year age group, consistent with a higher prevalence and severity in type 1 diabetes.96 Prevalence rates are somewhat lower in type 2 diabetes overall, partly because the later age of onset means many patients may have died from heart disease before there has been sufficient duration to develop renal disease. Despite recent advances in the diagnosis and treatment of renal failure in diabetes, the problem has not been resolved. Prevention. The presence of microalbuminuria appears to predict the subsequent development of diabetic nephropathy and end stage renal failure.99 Of particular note is the value of ACE inhibitors and angiotensin receptor blockers (ARB) in slowing the progression of renal disease.75 The effect of ACE inhibitors appears to be independent of any blood pressure lowering effect. Hypertension, which may be primary or secondary to the renal disease, accelerates the development of renal failure. Lipid disturbances may also predict the development of microalbuminuria.100 The major predictor, however, of the development of early diabetic renal disease is poor glycemic control.101 The value of an intensive therapy regimen was also clearly demonstrated in the DCCT (54% reduction).91 Interestingly, in type 1 diabetes, insulin resistance is emerging as a powerful predictor of nephropathy102 as well as coronary artery disease (CAD), which may explain their association. Further, much attention is being paid to the genetic susceptibility to nephropathy, as there is clearly a major genetic component.103

Neuropathy Epidemiology. Another major complication of diabetes is neuropathy. Clinically significant neurological disability usually does not occur until at least five years after the diagnosis of diabetes. The major consequences of diabetic neuropathy are pain, weakness, and loss of sensation. Parallel disorders of the autonomic nervous system may lead to problems of sexual function and urinary and gastrointestinal abnormalities. Research has focused on the metabolic causes of the nerve damage and the specific biochemical lesions that lead to neurological changes.104 One recent epidemiological study has demonstrated both a high prevalence of distal symmetrical neuropathy in type 1 diabetes, 70% after 30 years,89 and a strong relationship with cardiovascular risk factors, for example, lipid disturbances, cigarette smoking and especially hypertension.105 A major problem in diabetic neuropathy is how to measure it. Multiple techniques are currently advocated.105–107 However, this further complicates determining the actual prevalence of this complication. Prevention. It has long been recognized that strict control of blood sugar may improve neural function, for example, peripheral nerve conduction.108 The DCCT and UKPDS results also confirm the value of lower blood sugar levels in preventing/delaying clinical neuropathy.91,93 The above findings concerning blood pressure and lipids suggest that studies to evaluate the benefits of controlling these factors may also be worthwhile. Another area that has been investigated recently is the role of a new group of drugs called aldose reductase inhibitors. Although the results have been variable, most trials to date have involved late-stage neuropathy.109 A greater benefit might be seen if these metabolically active drugs were used earlier.

Macrovascular Disease and Atherosclerosis The most convincing epidemiological evidence for increased cardiovascular disease in diabetes comes from large-scale prospective studies, many of which were primarily designed to study cardiovascular disease in the general population. Studies like Framingham110 have demonstrated that the diabetic individual (uniquely defined in Framingham as “glucose intolerant”) has a greatly enhanced risk and that

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cardiovascular disease is the leading cause of death in those with diabetes.111,112 Diabetes leads to a greater than normal risk for all manifestations of atherosclerosis, including coronary, cerebrovascular, and peripheral vascular disease.110,113 The latter is so common in diabetes that half of all lower extremity amputations in the United States occur in persons with diabetes.59 In the general population women have a lower risk of CHD than men, but this advantage is lost in women with diabetes, who have rates approaching those of men.78,114–117 A meta-analysis suggests that a reduction in the gender differential for CHD in diabetes is true for CHD mortality but not for morbidity.118 The survival of diabetic patients, especially women, after a cardiac event also appears to be less than that seen in the general population.119,120 Although when it occurs, atherosclerosis is often more extensive in diabetic121,122 than in nondiabetic subjects, although not all studies show a clear relationship between blood sugar and CVD. For example in the UKPDS, HbA1c was a borderline predictor of myocardial infarction (MI) and intensive therapy had only a borderline (p 0.052) 16% reduction in CHD events.93 Divergent opinions also are apparent in terms of the role of blood sugar in the nondiabetic range. Some studies have shown the group with IGT to have a greater than normal risk of CVD.1,123 Early studies failed to show a relationship between blood glucose levels in the nondiabetic range and CVD,124 however recent meta regression analysis and pooled analyses show a relationship in the normal glucose range.125,126 Recently, investigators from the Epidemiology of Diabetes Interventions and Complications Study (follow-up of the DCCT) reported on the long-term benefit of early intensive glycemic control on the incidence of CVD. Among 1375 patients, the number of incident CVD events in those intensively treated during the DCCT compared to those on conventional therapy (46 compared to 98 events).127 The IGT stage is often characterized by hyperinsulinemia and insulin resistance. In the Paris study, in multivariate analyses, insulin concentration rather than diabetic IGT status was the stronger predictor of CHD.128 A further factor linked with hyperinsulinemia is central adiposity, which was discussed earlier as a risk factor for the development of diabetes.129,130 Central adiposity is also a risk factor for CVD independent of obesity,131 a finding most clearly shown in women. Consequently a male type of fat deposition (if found in women) may be associated with hyperinsulinemia132 and thus may provide a marker for a metabolic derangement predisposing to both diabetes and CVD generally, and the relatively poorer cardiovascular prognosis of diabetic women. This association of central adiposity with insulin resistance and the metabolic syndrome is thought to be the prime basis of the excess CVD in type 2 diabetes and glucose intolerance and also has been proposed as a leading feature of CVD in type 1 diabetes.133,134 As lipoproteins are altered in diabetes, it is tempting to hypothesize that these changes account for the increased CVD risk seen in diabetes. Many studies,110,111,116,129,130 have shown that serum cholesterol levels relate to CVD risk in those with diabetes in a way similar to that seen in the general population. However, total and LDL cholesterol levels are not greatly elevated in many diabetics, so the role of cholesterol in explaining the increased risk in diabetes is limited.135 Data from the Multiple Risk Factor Intervention Study (MRFIT),136 which screened over 360,000 men for CVD risk factors and subsequently followed them for mortality, suggests diabetic men had rates three times higher than nondiabetics all along the cholesterol curve. The MRFIT data is exclusively type 2 diabetes. In type 1 diabetes, as indicated earlier, it appears that the major determinant of CVD risk is proteinuria98 although recent data suggest that hypertension, white blood cell count, HDLc, non-HDLc, diabetes duration and smoking are associated with incident CAD events.134 If cholesterol concentration has a limited role, other lipid measures may be of greater importance to diabetes. Reports suggest that triglyceride level is an independent risk factor for CVD in diabetes.137,138 Furthermore, alterations in HDL concentration and lipoprotein composition occur in diabetes, which may further increase cardiovascular risk.139 Insulin itself, beyond its effect on the lipids, can have direct effects on the arterial wall that promote

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atherogenicity.140–142 Hyperinsulinemia has also been related to blood pressure elevation.143–146 The importance of insulin is also shown by its demonstration as an independent risk factor for CVD in some,147–150 but not all,151–153 prospective studies of men in the general population, however distinguishing insulin effects per se from hyperinsulinemia representing insulin resistance is difficult. Many studies have demonstrated altered hemostatic factors including platelets and fibrinogen which may provide yet another mechanism for the enhanced CVD risk in diabetes.154,155 Thus it is abundantly clear that those with diabetes have severe handicaps to face in terms of cardiovascular risk above and beyond the lipoprotein disturbances.

SUMMARY AND FUTURE

The DCCT and UKPDS have put beyond question the value of intensive therapy to lower blood sugar levels in terms of the so called triopathy of type 1 and type 2 diabetes complications (retinopathy, nephropathy, and neuropathy).156 As intensive therapy with insulin also increases the risk of severe hypoglycemia91 and is difficult to translate into general practice, it would seem prudent to also focus on other CVD risk factors (e.g., hypertension and hyperlipidemia) to prevent these complications in type 2 diabetes. Studies examining cardiovascular events among people with type 2 diabetes demonstrate that controlling these risk factors can directly impact the occurrence of both new157–161 and repeat events.162–164 Two major trials165,166 are underway testing the value of intensive glycemic therapy in terms of CHD prevention and another trial (BARI2D) addresses the best means of treating patients with diabetes and heart disease. While the evidence for the prevention of diabetes and its complications is clear, translation into the community of diabetes care providers and patients is difficult. The goal of prevention is to improve short and long term outcomes as well as the economic consequences of a disease. Models of chronic illness care that focus on a multilevel approach to primary and secondary prevention are necessary in order to prevent the morbidity and mortality associated with diabetes.

REFERENCES

1. Fuller JH, Shipley MJ, Rose G, et al. Coronary-heart-disease risk and impaired glucose tolerance: the Whitehall Study. Lancet. 1980;1373–6. 2. O’Sullivan J. Quarter century study of glucose intolerance: incidence of diabetes mellitus by USPHS, NIH, and WHO criteria. In: Eschwege E, ed. Advances in Diabetes Epidemiology. Amsterdam, Elsevier Biomedical Press, 1982:123–31. 3. Jarrett RJ, Keen H, McCartney P. Worsening of diabetes with impaired glucose tolerance: ten-year experience in the Bedford and Whitehall Studies. In: Eschwege E, Ed. Advances in Diabetes Epidemiology. Amsterdam, Elsevier Biomedical Press, 1982:95–102. 4. Lorenzo C, Okoloise M, Williams K, et al. The metabolic syndrome as predictor of type 2 diabetes. The San Antonio Heart Study. Diabetes Care. 2003;26:3153–9. 5. Orchard TJ. From diagnosis and classification to complications and therapy. Diabetes Care. 1994;17:326–38. 6. Holman RC, Herron CA, Sinnock P. Epidemiologic characteristics of mortality from diabetes with acidosis or coma, United States, 1970–78. Am J Pub Health. 1983;73:1169–73. 7. LaPorte RE. Diabetes Epidemiology Research International Mortality Study Group. Major cross-country differences in risk of dying for people with IDDM. Diabetes Care. 1991;14:49–54. 8. Temple RC, Luzio SD, Schneider AE, et al. Insulin deficiency in non-insulin-dependent diabetes. Lancet. 1989;293–5. 9. Unwin N, Shaw J, Zimmet P, et al. Impaired glucose tolerance and impaired fasting glycaemia: the current status on definition and intervention. Diabet Med. 2002;19:708–23.

10. Smith NL, Barzilay JI, Shaffer D, et al. Fasting and 2-hour postchallenge serum glucose measures and risk of incident cardiovascular events in the elderly: the Cardiovascular Health Study. Arch Intern Med. 2002;162:209–19. 11. Duncan BB, Heiss G. Nonenzymatic glycosylation of proteins-a new tool for assessment of cumulative hyperglycemia in epidemiologic studies, past and future. Am J Epidemiol. 1984;120:169–89. 12. Moller AM, Dalgaard LT, Pociot F, et al. Mutations in the hepatocyte nuclear factor-1a gene in Caucasian families originally classified as having type 1 diabetes. Diabetologia. 1998;41:1528–31. 13. Lehto M, Wipemo C, Ivarsson SA, et al. High frequency of mutations in MODY and mitochondrial genes in Scandinavian patients with familial early-onset diabetes. Diabetologia. 1999;42:1131–7. 14. Zimmet PZ, Tuomi T, Mackay IR, et al. Latent autoimmune diabetes in adults (LADA): the role of antibodies to glutamic acid decarboxylase in diagnosis and prediction of insulin dependency. Diabet Med. 1994;11:299–303. 15. Karvonen M, Tuomilehto J, Libman I, et al. World Health Organization DIAMOND Project Group: Review of the recent epidemiological data on the world wide incidence of Type 1 (insulin-dependent) diabetes mellitus. Diabetologia. 1993;36:883–92. 16. Holt RIG. Diagnosis, epidemiology and pathogenesis of diabetes mellitus: an update for psychiatrists. Br J Psychiatry. 2004;184:S55–S63. 17. Onkamo P, Vaanenen S, Karvonen M, et al. Worldwide increase in incidence of type 1 diabetes—the analysis of the data on published incidence trends. Diabetologia. 1999;42:1395–1403. 18. Kyvik KO, Hystrom L, Gorus F, et al. the epidemiology of type 1 diabetes mellitus is not the same in young adults as in children. Diabetologia. 2004;47:377–84. 19. Pundziute-Lycka A, Zaliinkevicus R, Urbonaite B, et al. Incidence of type 1 diabetes in Lithuanians aged 0–39 years varies by the urban-rural setting, and the time change differs for men and women during 1991–2000. Diabetes Care. 2003;26:671–6. 20. Dorman JS, LaPorte RE, Songer TJ. Epidemiology of Type 1 Diabetes. In: Sperling MA, ed. Type 1 Diabetes: Etiology and Treatment. Totowa, NJ, Humana Press, 2003:3–22. 21. Dorman JS, Bunker CH. HLA-DQ locus of the human leukocyte antigen complex and type 1 diabetes mellitus: a HuGE review. Epidemiol Rev. 2000;22. 22. Hirschhorn JN. Genetic epidemiology of type 1 diabetes. Pediatr Diabetes. 2003;4:87–100. 23. Nejentsev S, Reijonen H, Adojaan B, et al. The effect of HLA-B allele on the IDDM risk defined by DRB1*04 subtypes and DQB1*0302. Diabetes. 1997;46:1888–92. 24. Lie BA, Todd JA, Pociot F, et al. The predisposition to type 1 diabetes linked to the human leukocyte antigen complex includes at least one non-class II gene. Am J Hum Genet. 1999;64:793–800. 25. Anjos S, Polychronakos C. Mechanisms of genetic susceptibility to type 1 diabetes: beyond HLA. Mol Genet Metab. 2004;81:187–95. 26. Bennett ST, Wilson AJ, Esposito L. Insulin VNTR allele-specific effect in type 1 diabetes depends on identity of untransmitted paternal allele. Nat Genet. 1997;17:350–2. 27. Pugliese A, Zeller M, Ferndandez JA. The insulin gene is transcribed in human thymus and transcription levels correlated with allelic variation at the INS VNTR-IDDM 2 susceptibility locus for type 1 diabetes. Nat Genet. 1997;15:293–7. 28. Undlien DE, Hamaguchi K, Kimura A. Type 1 diabetes susceptibility associated with polymorphism in the insulin gene region: a study of Blacks, Caucasians, and Orientals. Diabetologia. 1994;37: 745–9. 29. Rewers M, Norris J, Dabelea D. Epidemiology of Type 1 diabetes mellitus. Adv Exp Med Biol. 2004;552:219–46. 30. Dahlquist G. The aetiology of type 1 diabetes: an epidemiological perspective. Acta Paediatr Suppl. 1998;425:5–10. 31. Dahlquist G, Frisk G, Ivarsson SA, et al. Indications that maternal coxsackie B virus infection during pregnancy is a risk factor for childhood-onset IDDM. Diabetologia. 1995;38:1371–3.

64 32. Hyoty H, Hiltunen M, Knip M, et al. A prospective study of the role of coxsackie B and other enterovirus infections in the pathogenesis of IDDM. Childhood diabetes in Finland (DiMe) Study Group. Diabetes. 1995;44:652–7. 33. Hyoty H, Hiltunen M, Reuranen A. Decline of mumps antibodies in type 1 (insulin-dependent) diabetic children with a plateau in the risking incidence of type 1 diabetes after introduction of the mumpsmeasles-rubella vaccine in Finland. Diabetologia. 1993;41:40–6. 34. Pak CY, McArthur RG, Eun HM. Association of cytomegalovirus infection with autoimmune type 1 diabetes. Lancet. 1988;2:1–4. 35. Honeyman MC, Coulson BS, Stone NL. Association between rotavirus infection and pancreatic islet autoimmunity in children at risk of developing type 1 diabetes. Diabetes. 2000;49. 36. McIntosh EDG, Menser M. A fifty-year follow-up of congenital rubella. Lancet. 1992;340:414–5. 37. Borch-Johnsen K, Joner G, Mandrup-Poulsen T, et al. Relation between breast-feeding and incidence rates of insulin-dependent diabetes mellitus. A hypothesis. Lancet. 1984;2:1083–6. 38. Kolb H, Pozzilli P. Cow’s milk and type 1 diabetes: the gut immune system deserves attention. Immunol Today. 1999;20:108–10. 39. Harrison LC, Honeyman MC. Cow’s milk and type 1 diabetes. Diabetes. 1999;48:1501–7. 40. Vaarala O. Gut and the induction of immune tolerance in type 1 diabetes. Diabetes Metab Res Rev. 1999;15:353–61. 41. McKinney PA, Okasha M, Parslow R, et al. Ante-natal risk factors for childhood diabetes mellitus, a case-control study of medical record data in Yorkshire, UK. Diabetologia. 1997;40:933–9. 42. Marshall AL, Chetwynd A, Morris J, et al. Type 1 diabetes mellitus in childhood: a matched case control study in Lancashire and Cumbria, UK. Diabet Med. 2004;21:1035–40. 43. Kupila JS, Keskinen P, Simell T. Intranasally administered insulin intended for prevention of type 1 diabetes—a safety study in healthy adults. Diabetes Metab Res Rev. 2003;19:415–20. 44. Diabetes Prevention Trial-Type 1 Study Group: Effects of insulin in relatives of patients with type 2 diabetes mellitus. N Engl J Med. 2002;346:1685–91. 45. The European Nicotinamide Diabetes InterventionTrial (ENDIT) Group: Intervening before the onset of type 1 diabetes: baseline data from the European Nicotinamide Diabetes Group. Diabetologia. 2003;46:339–46. 46. Paronen J, Knip M, Savilahti E, et al. Effect of cow’s milk exposure and maternal type 1 diabetes on cellular and humoral immunization to dietary insulin in infants at genetic risk for type 1 diabetes. Diabetes. 2000;49:1657–65. 47. Type 1 Diabetes Trial Net. Available at: www.diabetestrialnet org. 48. World Health Organization: Diabetes. World Health Organization, 2005. 49. Zimmet P. Epidemiology of diabetes and its macrovascular manifestations in Pacific populations: the medical effects of social progress. Diabetes Care. 1979;2:85–90. 50. World Health Organization. Definition, Diagnosis, and Classification of Diabetes Mellitus and its Complications. Geneva, Department of Noncommunicable Disease Surveillance, 1999;2–7. 51. Min HK, Yoo HJ, Lee HK, et al. Clinico-genetic genesis of diabetes mellitus. In: Minuira A, Baba S, Goyo Y, Kobberling J, eds. Changing Patterns of the Prevalence of Diabetes Mellitus in Korea. Amsterdam, Excerpta Medica, 1982. 52. Bennett PH, Rushforth NB, Miller M, et al. Epidemiologic studies of diabetes in the Pima Indians. Recent Prog Horm Res. 1976;32: 333–76. 53. Centers for Disease Control and Prevention: National diabetes fact sheet: general information and national estimates on diabetes in the United States. Atlanta, GA: Department of Health and Human Services; 2005. 54. Medalie JH. Risk factors other than hyperglycemia in diabetic macrovascular disease. Diabetes Care. 1979;2:77–84.

Diabetes

1109

55. Keen H. The incomplete story of obesity and diabetes. In: Howard A, ed. 1st International Congress on Obesity. London, Newman Publishing, 1975. 56. VanItallie TB. Obesity: adverse effects on health and longevity. Am J Clin Nutr. 1979;32:2723–33. 57. Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA. 2003;289:76–9. 58. Rimm IJ, Rimm AA. Association between socioeconomic status and obesity in 59,556 women. Prev Med. 1974;3. 59. Palumbo PJ, Melton JL. Peripheral vascular disease and diabetes. In: Harris MI, Cowie CC, Stern MP, Boyko EJ, Reiber GE, Bennett PH, eds. Diabetes in America. Washington DC, NIH, NIDDK, 1995:401–8. 60. Centers for Disease Control and Prevention: Division of Nutrition and Physical Activity. Department of Health and Human Services, 2005. 61. Taylor RJ, Bennett PH, Legonidec G, et al. The prevalence of diabetes mellitus in a traditional-living Polynesian population: the Wallis Island survey. Diabetes Care. 1983;6:334–40. 62. Manson JE, Nathan DM, Krolewski AS, et al. A prospective study of exercise and incidence of diabetes among U.S. male physicians. JAMA. 1992;268:63–7. 63. Schulze MB, Hu FB. Primary prevention of diabetes: what can be done and how much can be prevented? Annu Rev Public Health. 2005;26:445–67. 64. Barnett AH, Eff C, Leslie RDG, et al. Diabetes in identical twins: a study of 200 pairs. Diabetologia. 1981;20:87–93. 65. Tuomilehto-Wolf E, Tuoilehto J, Cepaitis Z, Lounamaa R, DIME Study Group. New susceptibility haplotype type 1 diabetes. Lancet. 1989;11:299–302. (abstract) 66. Bell GI, Karem JH, Rutter WJ. Polymorphic c DNA region adjacent to the 5’ end of the human insulin gene. Proc Natl Acad Sci USA. 1981;78:5759–63. 67. Vionnet N, Stoffel M, Takeda J, et al. Nonsense mutation in the glucokinase gene causes early-onset non-insulin-dependent diabetes mellitus. Nature. 1992;356:721–2. 68. Reardon W, Ross R, Sweeney MG, et al. Diabetes mellitus associated with a pathogenic point mutation in mitochondrial DNA. Lancet. 1992;340:1376–9. 69. Saad MF, Knowler W, Pettitt DJ, et al. The natural history of impaired glucose tolerance in the Pima Indians. N Engl J Med. 1988;319:1500–6. 70. Pan X-R, Li G-W, Hu Y-H, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance: The Da Qing IGT and Diabetes Study. Diabetes Care. 1997;20:537–44. 71. Tuomilehto J, Lindstrom J, Eriksson JG, et al. Finnish Diabetes Prevention Study Group: Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 2001;344:1390–2. 72. Chiasson JL, Josse RG, Gomis R, et al. Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM Trial Research Group. Lancet. 2002;359:2072–7. 73. Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346:393–403. 74. Orchard TJ, Temprosa M, Goldberg R, et al. Diabetes Prevention Program Research Group: The effect of metformin and intensive lifestyle intervention on the metabolic syndrome: the Diabetes Prevention Program randomized trial. Ann Intern Med. 2005;142:611–9. 75. American Diabetes Association. Standards of Medical Care in Diabetes. Diabetes Care. 2005;28:S4–S36. 76. Engelgau MM, Narayan KMV, Herman WH. Screening for Type 2 diabetes. Diabetes Care. 2000;23:1563–80. 77. Knuiman MW, Welborn TA, McCann VJ, et al. Prevalence of diabetic complications in relation to risk factors. Diabetes. 1986;35: 1332–9.

1110

Noncommunicable and Chronic Disabling Conditions

78. Wingard DL, Barrett-Connor E. Heart disease and diabetes. In: National Diabetes Data Group, ed. Diabetes in America. Bethesda, National Institutes of Health;1995, 429–48. 79. Orchard TJ. Diabetes Epidemiology Research International Mortality Study Group. International evaluation of cause-specific mortality and IDDM. Diabetes Care. 1991;294:1651–4. 80. Dorman JS, LaPorte RE, Kuller LH, et al. The Pittsburgh insulindependent diabetes mellitus (IDDM) morbidity and mortality study. Mortality results. Diabetes. 1984;33:271–6. 81. Jensen T, Borch-Johnsen K, Kofoed-Enevoldsen A, et al. Coronary heart disease in young type 1 (insulin-dependent)diabetic patients with and without diabetic nephropathy: incidence and risk factors. Diabetologia. 1987;30:144–8. 82. Krolewski AS, Kosinski EJ, Warram JH, et al. Magnitude and determinants of coronary artery disease in juvenile-onset, insulin-dependent diabetes mellitus. Am J Cardiol. 1987;59. 83. Nishmura R, LaPorte RE, Dorman JS, et al. Mortality trends in type 1 diabetes. The Allegheny County (Pennsylvania) Registry 1965–1999. Diabetes Care. 2001;24:823–7. 84. Nishmura R, Bosnyak Z, Orchard TJ. Incidence, treatment and prognosis of end stage renal disease of type 1 diabetes diagnosed between 1965–79 in Allegheny County. Diabetes. 2001;50:A179. 85. Bosnyak Z, Nishimura R, Orchard TJ. Excess mortality in African Americans with type 1 diabetes largely due to acute complications: a population based perspective in the Pittsburgh metropolitan area. Diabetes. 2002;51:A63. 86. Hovind P, Tarnow L, Rossing K, et al. Decreasing incidence of severe diabetic microangiopathy in type 1 diabetes. Diabetes Care. 2003;26:1258–64. 87. Pambianco G, Zgibor J, Orchard T. Temporal trends in type 1 diabetes: coronary artery disease, proliferative retinopathy, and overt nephropathy. Diabetes. 2003;52:A40. 88. Klein R, Davis MD, Moss S, et al. The Wisconsin Epidemiologic Study of Diabetic Retinopathy: A Comparison of Retinopathy in Younger and Older Onset Diabetic Persons. Plenum Press; 1985. 89. Orchard TJ, Dorman JS, Maser RE, et al. Prevalence of complications in IDDM by sex and duration. Pittsburgh Epidemiology of Diabetes Complications Study II. Diabetes. 1990;39:1116–24. 90. Eye Diseases Prevalence Research Group. The prevalence of diabetic retinopathy among adults in the United States. Arch Ophthalmol. 2004;122:552–63. 91. DCCT Research Group. The Diabetes Control and Complications Trial. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993;329:977–86. 92. DCCT Research Group. The Diabetes Control and Complications Trial. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993;329:977–86. 93. UK Prospective Diabetes Study (UKPDS) Group. Intensive bloodglucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998;352:837–53. 94. UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. BMJ. 1998;317:703–13. 95. Diabetic Retinopathy Study Group. Photocoagulation treatment of proliferative diabetic retinopathy. Clinical application of Diabetic Retinopathy Study (DRS) Findings. Ophthalmology. 1981;88:583. 96. Geiss LS, Herman WH, Teutsch S. Diabetes and renal mortality in the United States. Am J Pub Health. 1985;75:1325–6. 97. Knowles HC. Magnitude of the renal failure problem in diabetic patients. Kidney Int. 1974;6:52–7. 98. Borch-Johnsen K, Kreiner S: Proteinuria: value as predictor of cardiovascular mortality in insulin dependent diabetes mellitus. BMJ. 1987;294:1651–4.

99. Viberti G. Etiology and prognostic significance of albuminuria in diabetes. Diabetes Care. 1988;11:840–5. 100. Coonrod BA, Ellis D, Becker DJ, et al. Predictors of microalbuminuria in individuals with IDDM. Diabetes Care. 1993;16:1376–83. 101. Lloyd CE, Becker D, Ellis D, et al. Incidence of complications in insulin-dependent diabetes mellitus: a survival analysis. Am J Epidemiol. 1996;143:431–41. 102. Orchard TJ, Chang Y-F, Ferrell RE, et al. Nephropathy in type 1 diabetes: a manifestation of insulin resistance and multiple genetic susceptibilities? Kidney Int. 2002;62:963–70. 103. Boright AP, Paterson AD, Mirea L, et al. Genetic Variation at the ACE gene is associated with persistent microalbuminuria and severe nephropathy in type 1 diabetes: the DCCT/EDIC Genetics Study. Diabetes. 2005;54:1238–44. 104. Winegrad AI, Morrison AD, Greene DA. Late Complication of Diabetes. New York: Grune & Stratton;1979. 105. Forrest KY, Maser RE, Pambianco G, et al. Hypertension as a risk factor for diabetic neuropathy. Diabetes. 1997;46:665–70. 106. Maser RE, Nielsen VK, Bass EB, et al. Measuring diabetic neuropathy: assessment and comparison of clinical examination and quantitative sensory testing. Diabetes Care. 1989;12:270–5. 107. American Diabetes Association, American Academy of Neurology. Report and recommendations of the San Antonio conference on diabetic neuropathy. Diabetes Care. 1988;11:592–7. 108. Ward J, Fisher DJ, Barnes CG, et al. Improvement in nerve conduction following treatment of newly diagnosed diabetics. Lancet. 1971;1:428. 109. Boel E, Selmer J, Flodgaard HJ, et al. Diabetic late complications: will aldose reductase inhibitors or inhibitors of advanced glycosylation endproduct formation hold promise? J Diabetes Complications. 1995;9. 110. Kannel WB, McGee DL. Diabetes and glucose tolerance as risk factors for cardiovascular disease: The Framingham Study. Diabetes Care. 1979;2. 111. Barrett-Connor E, Wingard DL. Sex differential in ischemic heart disease mortality in diabetics: A prospective population-based study. Am J Epidemiol. 1983;118:489–96. 112. Panzram G. Mortality and survival in type 2 (non-insulin-dependent) diabetes mellitus. Diabetologia. 1987;30:123–31. 113. Donahue RP, Orchard TJ. Diabetes mellitus and macrovascular complications. An epidemiological perspective. Diabetes Care. 1992;15:1141–55. 114. Decourten M, Hodge AM, Zimmett P. Epidemiology of diabetes–– lessons for the endocrinologist. Endocrinologist. 1998;8:6–70. 115. American Diabetes Association. Standards of medical care for patients with diabetes mellitus. Diabetes Care. 1998;21:S23–S34. 116. Jarrett RJ, McCartney P, Keen H. The Bedford Survey: Ten year mortality rates in newly diagnosed diabetics, borderline diabetics and normoglycaemic controls and risk indices for coronary heart disease in borderline diabetics. Diabetologia. 1982;22: 79–84. 117. Barrett-Connor E, Cohn BA, Wingard DL, et al. Why is diabetes mellitus a stronger risk factor for fatal ischemic heart disease in women than in men? J Am Med Assoc. 1991;265:627–31. 118. Orchard TJ. The impact of gender and general risk factors on the occurrence of atherosclerotic vascular disease in NIDDM. Ann Med. 1995. 119. Abbott RD, Donahue RP, Kannel WB, et al. The impact of diabetes on survival following myocardial infraction in men vs. women. J Am Med Assoc. 1988;260. 120. Donahue RP, Goldberg RJ, Chen Z, et al. The influence of sex and diabetes mellitus on survival following acute myocardial infarction: A community-wide perspective. J Clin Epidemiol. 1993;46. 121. Waller BF, Palumbo PJ, Lie JT. The Heart in Diabetes Mellitus as Viewed from a Morphologic Perspective. Mount Kisco, NY, Futura Publishing Company, Inc., 1981. 122. Dortimer AC, Shenoy PN, Shiroff RA. Diffuse coronary artery disease in diabetic patients. Circulation. 1978;57.

64 123. Eschwege E, Ducimetiere P, Papoz L, et al. Blood glucose and coronary heart disease. Lancet. 1980;472–3. 124. The International Collaborative Group. Joint discussion. J Chron Dis. 1979;32:829–37. 125. Gao W, Qiao Q, Tuomilehto J. Post-challenge hyperglycaemia rather than fasting hyperglycaemia is an independent risk factor of cardiovascular disease events. Clin Lab. 2004;50:609–15. 126. Levitan EB, Song Y, Ford ES, et al. Is nondiabetic hyperglycemia a risk factor for cardiovascular disease? A meta-analysis of prospective studies. Arch Intern Med. 2004;164:2147–55. 127. National Institutes of Health. Tight glucose control lowers CVD by about 50 percent in diabetes. NIH News. 2005;1980. 128. Eschwege E, Richard JL, Thibult N. Coronary heart disease mortality in relation with diabetes, blood glucose, and plasma insulin levels: the Paris Prospective Study, ten years later. Horm Metab Res Suppl. 1985;15:41–6. 129. Ohlson LO, Larsson B, Svardsudd K. The influence of body fat distribution on the incidence of diabetes mellitus: 13.5 years of followup of the participants in the study of men born in 1913. Diabetes. 1985;34:1055–8. 130. Haffner SM, Stern MP, Hazuda HP, et al. Role of obesity and fat distribution in non-insulin-dependent diabetes mellitus in Mexican Americans and non-Hispanic Whites. Diabetes Care. 1986;9: 153–61. 131. Lapidus L, Bengtsson C, Larsson B. Distribution of adipose tissue and risk of cardiovascular disease and death: a 12 year follow-up of participants in the population study of women in Gothenburg, Sweden. BMJ. 1984;289:1257–61. 132. Peiris AN, Mueller RA, Struve MF. Splanchnic insulin metabolism in obesity: influence of body fat distribution. J Clin Invest. 1986;78:1648–58. 133. Soedamah-Muthu SS, Chaturvedi N, Toeller M, et al. EURODIAB Prospective Complications Study Group: Risk factors for coronary heart disease in type 1 diabetes patients in Europe. Diabetes Care. 2004;27:530–7. 134. Orchard TJ, Olson JC, Erbey JR, et al. Insulin resistance-related factors, but not glycemia, predict coronary artery disease in type 1 diabetes. Diabetes Care. 2003;26:1374–9. 135. Orchard TJ. Dyslipoproteinemia and diabetes. Endocrinol Metab Clin North Am. 1990;19:361–80. 136. Stamler J, Vaccaro O, Neaton JD, et al. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. Diabetes Care. 1993;16:434–44. 137. Janka HU. Five-year incidence of major macrovascular complications in diabetes mellitus. Horm Metab Res Suppl. 1985;15:15–19. 138. West KM, Ahuja MMS, Bennett PH, et al. The role of circulating glucose and triglyceride concentrations and their interactions with other “risk factors” as determinants of arterial disease in nine diabetic population samples from the WHO multinational study. Diabetes Care. 1983;6:361–9. 139. Howard BV. Lipoprotein metabolism in diabetes mellitus. J Lipid Res. 1987;28:613–28. 140. Stout RW, Bierman EL, Ross R. Effect of insulin on the proliferation of cultured primate arterial smooth muscle cells. Cir Res. 1975;36:319–27. 141. Stout RW. The effect of insulin and glucose on sterol synthesis in cultured rat arterial smooth muscle cells. Atherosclerosis. 1977;27:271–8. 142. Porta M, LaSelva M, Molinatti P, et al. Endothelial cell function in diabetic microangiopathy. Diabetologia. 1987;30:601–9. 143. Modan M, Halkin H, Almog S, et al. Hyperinsulinemia: a link between hypertension obesity and glucose intolerance. J Clin Invest. 1985;75:809–17. 144. Christlieb AR, Krolewski AS, Warram JH. Insulin and diastolic hypertension. Circulation. 1984;70:61. 145. Donahue RP, Orchard TJ, Becker DJ, et al. Sex differences in the coronary heart disease risk profile. A possible role for insulin. The Beaver County Study. Am J Epidemiol. 1987;125:650–7.

Diabetes

1111

146. Ferrannini E, Buzzigoli G, Bonadonna R, et al. Insulin resistance in essential hypertension. N Engl J Med. 1987;317:350–7. 147. Ducimetiere P, Eschwege E, Papoz L, et al. Relationship of plasma insulin levels to the incidence of myocardial infarction and coronary heart disease mortality in a middle-aged population. Diabetologia. 1980;19:205–10. 148. Pyorala K. Relationship of glucose tolerance and plasma insulin to the incidence of coronary heart disease: results from two population studies in Finland. Diabetes Care. 1979;2:131–41. 149. Welborn TA, Wearne K. Coronary heart disease incidence and cardiovascular mortality in Busselton with reference to glucose and insulin concentrations. Diabetes Care. 1979;2:154–9. 150. Despres J, Lamarche B, Mauriege P, et al. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med. 1996;334:952–7. 151. Ferrara A, Barrett-Connor EL, Edelstein SL. Hyperinsulinemia does not increase the risk of fatal cardiovascular disease in elderly men or women without diabetes: The Rancho Bernardo Study, 1984–1991. Am J Epidemiol. 1994;140:857–69. 152. Orchard TJ, Eichner JE, Kuller LH, et al. Insulin as a predictor of coronary heart disease: Interaction with Apo E phenotype. A report from MRFIT. Ann Epidemiol. 1994;4:40–5. 153. Welin L, Eriksson H, Larsson B, et al. Hyperinsulinemia is not a major coronary risk factor in elderly men. Diabetologia. 1992;35: 766–70. 154. Colwell JA, Winocour PD, Halushka PV. Do platelets have anything to do with diabetic microvascular disease? Diabetes. 1983;32:14–9. 155. Jensen T, Stender S, Deckert T. Abnormalities in plasma concentrations of lipoproteins and fibrinogen in type 1 (insulin-dependent) diabetic patients with increased urinary albumin excretion. Diabetologia. 1988;31:142–5. 156. Steinberg D, Parthasarathy S, Carew TE, et al. Beyond cholesterol: modifications of low-density lipoprotein that increase its atherogenicity. N Engl J Med. 1989;320:615–24. 157. Downs JR, Clearfield M, Weis S, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels. JAMA. 1998;279. 158. Elkeles RS, Diamond JR, Poulter C, et al. Cardiovascular outcomes in type 2 diabetes. A double-blind placebo-controlled study of bezafibrate: the St Mary’s Ealing, Northwick Park Diabetes Cardiovascular Disease Prevention (SENDCAP) Study. Diabetes Care. 1998;21:641–8. 159. Koskinen P, Manttari M, Manninen V, et al. Coronary heart disease incidence in NIDDM patients in the Helsinki Heart Study. Diabetes Care. 1992;15:820–5. 160. UK Prospective Diabetes Study Group. Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39. BMJ. 1998;7160: 713–20. 161. Hansson L, Zanchetti A, HOT Study Group, et al. Effects of intensive blood-pressure lowering and low dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. Lancet. 1998;351:1755–62. 162. Goldberg RB, Mellies MJ, Sacks FM, et al. Cardiovascular events and their reduction with pravastatin in diabetic and glucose-intolerant myocardial infarction survivors with average cholesterol levels. Subgroup analyses in the Cholesterol and Recurrent Events (CARE) Trial. Circulation. 1998;98:2513–9. 163. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group: Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med. 1998;339. 164. Pyorala K, Pedersen TR, Kjekshus J, et al. Cholesterol lowering with simvastatin improves prognosis of diabetic patients with

1112

Noncommunicable and Chronic Disabling Conditions

coronary heart disease. A subgroup analysis of the Scandinavian Simvastatin Survival Study (4S). Diabetes Care. 1997;20:614–20. 165. www.accord.cardio.on.ca/index-e.htm. 166. Veterans Administration: Kirkman MS, McCarren M, Shah J, Duckworth W, Abraira C, VADT Study Group. Journal of Diabetes and its Complications. 2006;20(2):75–80.

167. Harris MI, Flegal KM, Cowie CC, et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The third National Health and Nutrition Examination Survey, 1988–1994. Diabetes Care. 1998;21:518–24. 168. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2006;29:S43–8.

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David B. Coultas • Jonathan M. Samet

Diseases of the respiratory system are an important public health problem in all countries. The respiratory system, which includes the lungs and the upper airway that joins the trachea to the larynx, is exposed to a wide range of potentially injurious agents (Table 65-1). On average, an adult inhales about 5 L of air per minute; with exercise, the amount may increase 20-fold or more. With 10,000–20,000 L of air inhaled daily, agents present even in low concentrations may be toxic. The respiratory system is equipped with a remarkably effective system of defense mechanisms against inhaled particles and gases. Disease may result, however, if an acute exposure overwhelms the defenses (e.g., toxic gas inhalation), if an agent is particularly toxic even at low concentrations (e.g., toluene diisocyanate), if exposure is sustained (e.g., cigarette smoking), or if the exposed person is particularly susceptible (e.g., asthmatics). Respiratory diseases are major causes of disability and death worldwide,1,2 with over 11 million deaths or about 20% of all deaths due to perinatal respiratory conditions, lower respiratory tract infections, chronic respiratory diseases, and lung cancer (Table 65-2). The distributions of causes-of-death from respiratory diseases varies between countries and regions with lower respiratory tract infections predominating in the developing countries of Africa, Eastern Mediterranean, and Southeast Asia; and chronic respiratory diseases such as chronic obstructive pulmonary disease (COPD) and asthma, and lung cancer deaths occurring more frequently in more developed regions including the Americas, Europe, and Western Pacific. Among children under 5 years of age, about 21% of all deaths, or 2.27 million deaths in 2000, were due to pneumonia;3 and about 90% of these deaths were among children from 42 developing countries. The markedly higher childhood mortality from acute respiratory tract infections in developing countries as compared with those in developed countries probably reflects poorer nutrition and immunization practices and more frequent low birth weight, crowding, and indoor and outdoor air pollution.4 Emerging infections (e.g., SARS) and increasing international travel are a growing public health concern for children and adults.5 Chronic diseases of the respiratory system and respiratory tract cancer are major causes of morbidity and mortality among adults. Internationally, the rates of occurrence of respiratory tract cancer and of nonmalignant chronic diseases of the respiratory system can be directly related to patterns of cigarette smoking.6 However, inconsistencies in the association between mortality from COPD and patterns of cigarette smoking have been found.7 These inconsistencies may be partly explained by differences among countries in reporting of COPD mortality and smoking prevalence. Despite the limitations of available data, mortality from all tobacco-related diseases is estimated to increase dramatically over the next two decades. For example, in 1990, approximately 3 million total deaths were attributed to tobacco and the number is estimated to grow to 8.4 million in 2020, with the largest increases of tobacco-related deaths coming in India, China, and other parts of Asia.1 Other environmental

and occupational respiratory exposures cause potentially preventable chronic respiratory diseases. Indoor air pollution from domestic wood burning for cooking has been associated with an increased risk of chronic bronchitis and chronic airflow obstruction.8 In many countries, environmental and occupational agents that cause disease have become subject to regulation to ensure that workplaces are healthful and that neither outdoor nor indoor air causes adverse effects. Such regulations are not in place throughout the world, however, and where they do exist, enforcement and compliance are variable.

PEDIATRIC RESPIRATORY DISEASES

Respiratory Distress Syndrome Respiratory distress syndrome (RDS) in the newborn results primarily from surfactant deficiency associated with lung immaturity.9 Because of surfactant deficiency, the lung does not effectively exchange oxygen and carbon dioxide after birth, and positive pressure ventilation is frequently required to maintain life. Bronchopulmonary dysplasia or chronic lung disease of infancy is a frequent sequela of RDS and is characterized by persistent pulmonary dysfunction usually defined as need for ventilatory support or supplemental oxygen at 36 weeks after conception.9 The prognosis of BPD is variable and it may be a risk factor for chronic lung disease in childhood and adulthood.10 In the late 1980s, between 60 and 70 thousand cases of RDS were reported annually in the United States and about 5000 children died per year from RDS, accounting for 20% of all neonatal deaths.11 With changes in obstetric and neonatal care mortality of very low birth weight infants (501–1500 g)12 RDS-related mortality has declined.13 However, among black infants RDS-related mortality declined less rapidly compared to white infants.13 Of infants who survive RDS, estimates of the proportion in whom BPD develops vary from 10 to 45%.14 Several risk factors have been established for RDS, including prematurity, male sex, white race, cesarean section, and perinatal asphyxia.15 The incidence of RDS is inversely related to gestational age and birth weight, both measures of fetal prematurity. Among infants less than 28 weeks gestation, the incidence of RDS is approximately 80%, declining to about 60% after 29 weeks gestation, and is less than 1% 39 weeks gestation.15 Overall, about 70% of very low birth weight infants develop RDS.12 Prevention of premature birth represents the most effective method for reducing morbidity and mortality associated with RDS.16 However, because prematurity is frequently a result of poor socioeconomic conditions, and therefore not directly amenable to medical intervention, prematurity and RDS will remain public health problems until underlying causes can be remedied. Medical interventions discussed below offer the best available methods for lessening morbidity and mortality from RDS. 1113

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Noncommunicable and Chronic Disabling Conditions TABLE 65-1. MECHANISMS OF LUNG INJURY AND EXAMPLES OF INJURIOUS AGENTS AND ASSOCIATED DISEASES Example Mechanism of Injury Infection Carcinogenesis Immunologic Inflammation Fibrogenesis Other

Agent

Disease

Respiratory syncytial virus Streptococcus pneumonia Cigarette smoke Asbestos Thermophilic actinomycetes Cigarette smoke Oxides of nitrogen Asbestos Coal dust Plicatic acid Cotton dust

Bronchiolitis Pneumonia Lung cancer Mesothelioma Hypersensitive pneumonitis COPD Silo-fillers’ lung Asbestosis Coal workers’ pneumoconiosis Western red cedar workers’ asthma Byssinosis

Prenatal identification of fetuses at high risk for RDS can be accomplished by analysis of amniotic fluid phospholipids.15 As the fetus matures, amniotic fluid lecithin concentration increases while sphingomyelin concentration remains constant. Ratios of lecithin to sphingomyelin (L/S) of 2:1 or greater are associated with low risk for RDS. The probability of RDS is 40% with a L/S ratio less than 1.5, 33% with a ratio of 1.5:2, and 10% with a ratio of 2 or greater.15 However, the L/S ratio may not predict lung maturity in diabetic mothers.15 Medical interventions including antenatal corticosteroids and surfactant replacement provide partial solutions for the prevention of RDS and its complications.9 The administration of corticosteroids to the mother within seven days of delivery has been shown to decrease the frequency of RDS and mortality among infants delivered before 32–34 weeks gestation, but there is insufficient evidence that repeated doses beyond seven days are beneficial and may in fact be harmful.9 Moreover, while post-natal corticosteroids have been used to treat BPD, the available evidence suggests that the long-term complications outweigh the short-term benefits.17 Surfactant replacement with either natural extracts or synthetic forms has proven effective for decreasing complications associated with RDS with an overall 40% reduction in mortality.9 Prophylactic treatment is most effective when delivered at the time of delivery compared to waiting until the development of symptoms in infants at risk for RDS, and natural extracts are more effective than synthetic forms.9

CYSTIC FIBROSIS

In the United States, cystic fibrosis is the most common lethal genetic disease in whites of Northern European descent, estimated to occur in about 1 in 3500 live births in 1990.18 The disease occurs less frequently in other racial and ethnic groups in the United States with estimates of 1 in 14,000 black births; 1 in 11,500 Hispanic births; 1 in 10,500 American Indian and Alaska Native births; and 1 in 25,500 Asian births.18 Cystic fibrosis is transmitted as an autosomal recessive trait, and the heterozygote frequency in persons of Northern European descent is about 1 in 25.19 More than 1000 mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene on chromosome 7 have been characterized since the gene was identified in 1989, and one mutation (delta F508) accounts for about two-thirds of all CF alleles worldwide.20 The CFTR gene mutations result in an inability of epithelial cells to secrete chloride ions and the production of an abnormally thick mucus, and impaired binding and killing of bacteria.21 This defect affects the lungs, intestines, and exocrine glands and may result in diverse clinical manifestations, but patients invariably develop chronic obstructive pulmonary disease from repeated infections that destroy lung tissue.21 Pulmonary involvement has been reported in over 90% of all patients with cystic fibrosis and accounts for the majority of hospital admissions and deaths.22 The prognosis for patients with cystic fibrosis has improved markedly over the last 35 years. Based on data from the National

TABLE 65-2. WORLDWIDE AND REGIONAL NUMBERS OF DEATHS (×1000) FROM RESPIRATORY DISEASES, 2002 Western Pacific

Eastern Mediterranean

Condition

Americas

Europe

Perinatal conditions LRI Chronic respiratory disease Asthma COPD Cancer trachea/bronchus/lung All deaths

175 (3.2∗) 223 (3.0)

65 (0.7) 280 (2.9)

349 (2.9) 471 (3.9)

303 (7.3) 348 (8.4)

554 (5.2) 1104 (14.4)

1012 (6.9) 1453 (9.9)

2462 (4.3) 3884 (6.8)

398 (7.3) 18 (0.3) 241 (4.5)

404 (4.2) 43 (0.5) 261 (2.7)

1609 (13.5) 42 (0.4) 1375 (11.5)

155 (3.7) 16 (0.4) 95 (2.3)

257(2.4) 26 (0.2) 117 (1.1)

874 (6.0) 99 (0.7) 656 (4.5)

3702 (6.5) 240 (0.4) 2748 (4.8)

231 (4.3) 5421

266 (3.8) 9564

427 (3.6) 11,940

27 (0.7) 4152

17 (0.2) 10,664

174 (1.2) 14,657

1243 (2.2) 57,029

∗% of all deaths for region. Source: www.who.int./whr/2004/annex/en/ (Annex Table 2)

Africa

SE Asia

Total

65

Respiratory Disease Prevention

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Cystic Fibrosis Patient Registry, the median survival in the United States has increased from 14 years in 1969 to 33 years in 2001.20 The improving prognosis of cystic fibrosis probably reflects the beneficial effects of early recognition, nutritional support, and antibiotic therapy.20,22 While associated with ethical and logistical challenges, screening for cystic fibrosis during the pre- and postnatal periods has received growing attention as a method for prevention of cystic fibrosis.20 However, because there are over 1000 mutations that may cause cystic fibrosis it is not feasible to conduct population-wide screening of all parents for these mutations. Therefore, prenatal screening programs have often focused on affected families and screening for the most common mutations. Since 80% of children with the disease are born into families without a history of cystic fibrosis,23 using this method of prenatal screening will have little impact on the incidence of the disease. Moreover, the sensitivity for detecting the 25 most common genetic mutations among affected couples varies widely between ethnic groups, and the predictive value for detecting affected fetuses is low.24 Because of the limitations of prenatal screening, most screening programs for cystic fibrosis have focused on early detection through screening of newborns. In 2003, the Centers for Disease Control and the Cystic Fibrosis Foundation conducted a workshop to review benefits and risks of newborn screening for cystic fibrosis,20 and concluded that “the magnitude of the health benefits from screening for cystic fibrosis is sufficient that states should consider including routine newborn screening for cystic fibrosis in conjunction with systems to ensure access to high-quality care.” An estimated 800,000 newborns will be screened in the United States by the end of 2004 through 11 statewide programs.20 The improving survival among persons with cystic fibrosis has been attributed to better medical care through comprehensive centers that provide a multidisciplinary approach to management.25 However, the relative contributions of the various components of care to the improvement cannot be readily established. The details of management of cystic fibrosis are beyond the scope of this review and have been discussed extensively elsewhere.25

respiratory tract infections is low in the United States and other more developed countries, about 0.1 deaths annually per 1000 children from birth through the age of five years. However, mortality rates for this same age group vary widely between developed and developing countries and are more than 1000 times greater in some developing countries.27 Moreover, under-five mortality rates within developing countries vary substantially.27 Many risk factors for respiratory tract infection have been identified. In developing countries, overcrowded dwellings, poor nutrition, low birth weight, and possibly intense smoke pollution underlie the high rates.4,36,37 Studies in developed countries have shown that males have higher rates of infection, as do younger siblings of schoolage children who introduce infections into households. Children from homes of lower socioeconomic status also tend to have more respiratory infections. Maternal cigarette smoking has also been causally linked to increased occurrence of respiratory tract infections during the first years of life.38 Attendance at day care centers also increases the occurrence of respiratory tract infections among preschool children.4 Some studies indicate that breast-feeding decreases risk and that use of a gas-fueled stove increases risk, but the evidence on these associations is conflicting.39–41 Present understanding of risk factors for respiratory tract infection in childhood indicates several approaches for primary prevention. In developing countries, improved living conditions, better nutrition, breast feeding, and reduction of smoke pollution indoors should reduce the burden of morbidity and mortality associated with respiratory tract infections.42,43 In developed countries, mothers should be encouraged to stop smoking or to avoid smoking in the presence of their children. Effective vaccines are available for a limited number of bacteria (e.g., Streptococcus pneumoniae, Haemophilus influenzae)44 and viruses (e.g., influenza)45 that cause respiratory tract infections. However, the use of these vaccines as a public health intervention remains an active area of investigation and recommendations of expert groups are evolving. For example, the Advisory Committee on Immunization Practices now recommends influenza vaccination for children 6–23 months of age.45

Respiratory Tract Infection

Asthma

Respiratory tract infections are the main cause of morbidity and mortality among children living in developing countries and, although a much less frequent cause of death, the predominant source of morbidity including hospitalizations among children living in developed countries.4,26–28 Respiratory viruses are responsible for most childhood respiratory tract infections, although bacteria, Mycoplasma and Chlamydia cause some infections at particular ages. Respiratory tract infections in childhood may plausibly have long-term sequelae, including loss of lung function after severe episodes of lower respiratory tract infection, the development of asthma, the development of bronchiectasis, and an increased risk of developing COPD in adulthood.29–31 In developed countries the predominant clinical syndromes associated with childhood respiratory tract infection include colds (infections of the upper respiratory tract), epiglottitis (infection of the epiglottis), croup or laryngeotracheobronchitis (infection of the larynx and large airways), bronchiolitis (infection of the small airways), and pneumonia (infection of the lung tissues). Rhinoviruses are most closely associated with colds, parainfluenza viruses with croup, respiratory syncytial virus with bronchiolitis, and various viruses, including respiratory syncytial virus and the parainfluenza viruses with pneumonia.32,33 Bacteria cause epiglottitis. Epiglottitis, croup, bronchiolitis, and pneumonia may be severe and cause death through respiratory failure. In less developed countries, measles and whooping cough may be important causes of severe respiratory tract infection.34 Childhood respiratory tract infections are extremely common. Surveillance data for general population samples worldwide show that children experience five to nine respiratory illnesses during the first year of life;4 by the teenage years children still have about two or three respiratory illnesses annually.35 Mortality from childhood

Asthma is a chronic condition characterized by airway inflammation and hyperresponsiveness; reversible airflow obstruction; and episodic wheezing, cough, and dyspnea.46 Asthma results from a number of genetic variations and environmental exposures in early childhood, and the phenotypic expression of the disorder is heterogeneous.47 Various methods are used to measure the occurrence of asthma making comparisons between studies difficult.48 Numerous investigations of the occurrence of asthma in children have been conducted worldwide, and data from cross-sectional and longitudinal investigations indicate a wide range in the prevalence and incidence of childhood asthma.46,49,50 The International Study of Asthma and Allergies in Childhood (ISAAC) used standardized questionnaires to determine the prevalence of asthma-related symptoms among children 6–7, and 13–14 years of age from 156 centers in 56 countries.51 More than 750,000 children were surveyed and the prevalence of self-reported wheezing in the previous 12 months ranged from 1.6 to 36.7%.49 In the United States, data from nationwide samples and survey populations using different measures of asthma (“during the past 12 months, have you had asthma?” or “episode of asthma or asthma attack during the preceding 12 months”) compared to the ISAAC study also indicates that asthma is a common disease in children and has increased over the period from 1980 through 1995 (Fig. 65-1).52 While explanations for these wide variations in the occurrence of asthma between countries and over time remain an active area of investigation, the lower prevalence of asthma in developing countries and variation in prevalence within populations with similar genetic backgrounds suggest a major role for environmental factors in the variation in the occurrence of asthma. In cross-sectional and prospective investigations many personal, lifestyle, and environmental risk factors have been identified for asthma (Table 65-3).47,50 Among the personal factors, genetic

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Noncommunicable and Chronic Disabling Conditions

90 80 70

Per 1000

60

0–4 5–15 15–34 35–64 ≥ 65

50 40 30 20 10 0 1980

1985

1990

1995

Figure 65-1. Estimated annual prevalence of self-reported asthma by age group in the United States, 1980–1995. (Source: Adapted from Mannino et al. 2002.52)

susceptibility likely plays a major role determined by a number of genetic variations, which control multiple biological mechanisms involved in asthma including allergic sensitization, inflammation, and bronchial hyperreactivity.47 Studies of familial aggregation of asthma and twins show a strong familial influence on the prevalence and incidence of asthma,50 but these studies do not separate genetic from common environmental effects.47 While genetic susceptibility has a major role in the development of asthma and is an active area of investigation, many other personal characteristics have been associated with asthma (Table 65-3). Data from Tucson, Arizona,53 and Rochester, Minnesota,54 show a sharp decline in the incidence of asthma from early childhood to adolescence (Fig. 65-2) with a corresponding shift from a higher occurrence in males during early childhood to a higher occurrence in females in adolescence and young adulthood,50 which may be explained by differences in airway geometry.55 The occurrence may vary widely between racial and ethnic groups56 and is higher in blacks compared with whites.52 Atopy, defined by positive skin tests to common aeroallergens, predicts increased risk of asthma if present in the parents or child.50 Similarly, in prospective investigations of persons without asthma at baseline, bronchial hyperresponsiveness is associated with development of recurrent wheezing or asthma.50

TABLE 65-3. RISK FACTORS FOR CHILDHOOD ASTHMA

Personal and Genetic Factors Age Male gender Race/ethnicity Family history Atopy Obesity Bronchial hyperreactivity

Environmental and Lifestyle Factors Maternal smoking Environmental tobacco smoke Personal smoking Respiratory tract infections Allergen exposures Breastfeeding Ambient air pollution

Figure 65-2. Annual incidence rates per 100,000 person-years by sex and age for definite and probable asthma cases among Rochester residents, 1964 through 1983. Hatched bars = females; shaded bars = males. (Source: Yunginger JW, Reed CE, O’Connell EJ, et al. A community-based study of the epidemiology of asthma. Incidence rates, 1964–1983. Am Rev Respir Dis. 1992;146:888–94.)

In addition to personal characteristics a number of pre- and postnatal factors have been associated with the development of asthma (Table 65-3).47,50 Prenatal factors associated with an increased risk of asthma include younger maternal age (e.g., < 26 years) and maternal smoking during pregnancy.57 While the fetus may be sensitized to allergens in utero the risk of allergen exposures during pregnancy is uncertain.47 Low birth weight (< 2500 g) is associated with an increased risk of asthma. The role of breastfeeding as a risk factor for asthma is controversial; the mixed findings may be explained by methodological differences between studies.47 In several cohort studies, breastfeeding through the first four months of life is associated with a decreased risk of incident asthma.50 Childhood obesity has consistently been associated with an increased risk for development of asthma.50 A wide range of environmental risk factors for asthma has been investigated including viral lower respiratory tract infections, and indoor and outdoor exposures.50 More severe episodes of lower respiratory tract infection are associated with subsequent asthma and increased airway reactivity.50 Involuntary exposure to tobacco smoke, particularly maternal smoking, is independently associated with asthma.58–60 Exposure to aeroallergens such as house dust mite, cockroach, and fungi during infancy is associated with a marked excess risk of asthma.50,61 While a number of infectious and environmental agents have been linked to the development of asthma, patterns of exposure to other infectious agents (e.g., bacteria) and bacterial components (e.g., endotoxin) during infancy may partly explain the rising occurrence of asthma in developed countries with decreased exposure and the lower occurrence in developing countries where exposures are higher. This potential explanation for variations in the occurrence of asthma has been termed the “hygiene hypothesis.”62 Few investigations of the primary prevention of asthma through control of modifiable risk factors have been conducted.63,64 At least four randomized primary prevention trials are in progress, and results from one randomized trial in Canada of high risk infants enrolled before birth (n = 545) compared a multifaceted intervention (i.e., avoidance of house dust mite, pets, environmental tobacco smoke, day care until after the first year of life; delay of solid foods; and encouragement of breast feeding) to a control group has demonstrated a lower occurrence of asthma in the intervention group (16.3%) compared to the control group (23.0%) at two-years of age (odds ratio 0.60 [95 confidence interval 0.37–0.95]).64 In a similar study of 251 infants from the UK, investigators found a lower risk of asthmarelated symptoms at three years of age, but the difference was not statistically significant.65 Moreover, there was no difference in the prevalence of physician-diagnosed asthma.

65 The natural history of wheezing illnesses and childhood asthma have been described in a number of longitudinal studies in developed countries.66 Asthma symptoms usually begin in infancy and early childhood, and remit over time. In a longitudinal study of 826 newborns, Martinez et al.67 found that about 30% of children develop a wheezing illness during the first 3 years of life, and of these children about 60 percent are symptom-free at age six and overall only about 15% develop persistent wheeze and asthma.66 In a study of more than 11,000 children from the UK, only 50% of children who had a diagnosis of asthma at age five years continued to have the diagnosis at age 10 years.68 Involuntary exposure to tobacco smoke, ambient air pollution, and infections have been shown to exacerbate asthma.38,69,70 Most preventive strategies for asthma have been directed at secondary prevention with pharmacologic and other interventions to lessen morbidity.66 The use of bronchodilators, corticosteroids, and disodium cromoglycate greatly reduces morbidity from asthma. Many nonpharmacological interventions have been examined, including environmental control, prevention of sensitization in infancy and childhood, immunizations, allergen immunotherapy, physical training, chest physiotherapy, and education.71–73 In the United States74 and internationally,46 strategies for asthma education have been developed to prevent morbidity and mortality from asthma. Death from childhood asthma, although infrequent, is well documented and potentially preventable. Childhood mortality rates from asthma vary from country to country and by age, sex, and race in the United States. In the United States, annual mortality rates for asthma among children 5–14 years of age increased 89% during the period 1980 through 1999, from 1.9 per million to 3.6 per million, respectively.52 There was little change in the mortality rate from asthma for children four years of age and less. During this period the mortality rates were consistently higher among blacks compared with whites. Findings from retrospective studies suggest that clinical severity of asthma predicts risk of death.75 Factors that are suspected to affect mortality include failure on the part of patients and physicians to recognize severity, behavioral patterns, underuse of inhaled or oral corticosteroids, overuse and overdependence on nebulizers, and additive toxicity from combined use of theophylline and beta-agonists. For individual children, however, the predictive value of these factors is limited. ADULT RESPIRATORY TRACT DISEASES

Asthma As in children, the occurrence of asthma varies widely worldwide and regionally.76,77 In the early 1990s, a standardized cross-sectional survey, the European Community Respiratory Health Survey, was conducted at 48 centers in 22 countries and 137,619 adults 20–44 years of age were enrolled.76 Overall, the median prevalence of reported current asthma was 4.5% with a range of 2.0–11.9%. This variation in the prevalence of asthma was further supported by measurement of bronchial hyperresponsiveness with overall prevalence of 13.0% and range of 3.4–27.8%. In the United States, the overall prevalence of self-reported current, health-professional-diagnosed asthma among adults 18 years of age and older was 7.5% in 2002, and ranged from 4.7% in the U.S. Virgin Islands to 11.5% in Puerto Rico. Moreover, during the period 1980 through 1996, the prevalence of asthma in the United States increased with the greatest increase (124%) among persons 15–34 years of age.52 In addition to childhood asthma extending into adulthood, other risk factors for asthma in adults include personal characteristics, lifestyle, and environmental exposures. Among adolescents and adults, asthma is more common among females compared to children, where asthma is more common among males. This difference may be explained by differences in airway geometry and increased bronchial hyperresponsiveness among adult females compared to males.76 However, the higher incidence in older women may partly be explained by physician bias in labeling obstructive lung disease in women as asthma rather than COPD.53

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A number of lifestyle characteristics and environmental exposures have been investigated as potential factors contributing to the rising occurrence of asthma in adults including nutritional factors,78–80 smoking,81 and occupational exposures.82–84 Overall, results from longitudinal studies and randomized trials of dietary intake of various nutrients have been inconsistent.78 In contrast, a consistent finding in children and adults has been the association between increasing weight and increased risk for asthma. Among 135,000 Norwegians, 14–60 years of age, Nystad et al.79 found that among men and women, overweight and obesity were associated with an increased risk for asthma. For obesity (BMI > 30 kg/m2) the relative risks (95% CI) for asthma among men and women were 1.78 (1.35–2.34) and 1.99 (1.67–2.37), respectively, adjusted for smoking, education, and physical activity. Evidence on the association between active smoking and development of asthma has been inconsistent,81,85 and the inconsistency may be partly attributed to methodological differences between studies. Longitudinal studies provide the strongest evidence for making causal inferences. In a recent prospective case-control study of incident asthma in Finland,86 the adjusted risk of asthma was increased among current (OR = 1.3, 95% CI = 1.0–1.8) and former smokers (OR = 1.5, 95% CI = 1.1–2.0) compared to never-smokers. Occupational asthma is of special concern, with approximately 250 causative agents identified.82 The population attributable risk for occupational exposures has ranged from 5 to 30% depending on the methods used to define asthma and exposure.83,84 The economic impact of asthma is greatest among persons 18 years of age and older.87 In 1985, the overall costs for asthma in the United States were estimated at $4.5 billion with approximately 66% of the costs associated with persons 18 years of age and older. Emergency room use, hospitalizations, and death accounted for 43% of the total economic impact of asthma, suggesting that asthma costs could be reduced by interventions targeting these three areas. Overall, strategies for asthma management and prevention in adults differ little from those in children and incorporate pharmacological and other interventions. However, many asthmatics do not receive optimal medical management.88,89 Control of exposure to house dust mite allergen has not been effective in adult asthmatics.90 Early recognition of the relationship between an occupational exposure and asthma is important since prompt removal from exposure correlates best with full resolution of asthma.82 Certain occupations may be associated with an increased risk of death from asthma.91 While death from asthma is uncommon, the majority of asthma deaths occur in adults and asthma mortality rates among adults have increased worldwide;92,93 however, since 1996 mortality rates among adults in the United States have started to decline.52 Mortality rates are highest among females and blacks.52 Among asthmatics fewer than 5% die from asthma.92–95 Population-based investigations have provided conflicting results on survival among adults with asthma that may be partly explained by methodological differences.92–95 Impaired lung function is associated with increased mortality.95

Chronic Obstructive Pulmonary Disease COPD is a clinically applied term for persistent and generally symptomatic obstruction to airflow within the lungs. The lungs of most persons with COPD display a mixture of emphysema, enlargement and destruction of the air spaces, and inflammation and narrowing of the smaller airways, although in some persons emphysema or airway abnormalities may predominate.96,97 Emphysema reduces the driving pressure for airflow, and the airway abnormalities increase the resistance to airflow. A small number of cases of COPD, distinguished by severe emphysema, occur in smokers and nonsmokers with deficiency of alpha-1-antitrypsin, a substance that defends against injury by proteolytic enzymes,97 however, most cases result from cigarette smoking.85 Occupational agents can also contribute to the development of COPD.98 Other postulated risk factors for COPD include childhood respiratory tract infection29,30 and hyperresponsiveness of the airways of the lung.99,100

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Noncommunicable and Chronic Disabling Conditions

The natural history of COPD generally follows a slow but progressive course that offers a lengthy time window for intervention. The results of epidemiological studies suggest that impaired lung growth from smoking during childhood and adolescence101 and sustained loss of ventilatory function beyond that expected from aging alone causes clinically evident COPD (Fig. 65-3).85,96 The rate of decline in smokers tends to increase with the amount smoked, and smoking cessation results in a slower rate of decline compared with that in smokers unable to quit.85 Among smokers with mild airflow obstruction, moderate to marked airways hyperreactivity is more common in women (48%) compared with men (25%)102 and is associated with accelerated decline in lung function.100 Clinicians make the diagnosis of COPD in patients with sufficient chronic airflow obstruction to result in shortness of breath and limitation of exercise capacity. In epidemiological studies COPD is considered to be present if lung function tests demonstrate a specified degree of impairment or if a physician’s diagnosis is reported. Although prevalence can be readily assessed with the use of these criteria, a physician’s diagnosis may result in substantial diagnostic misclassification.103 Moreover, incidence cannot be described over short periods because of the slow evolution of impairment in persons developing COPD. Epidemiological data from throughout the world show that COPD is common among adults, with wide variation in prevalence estimates.96,104,105 While differences in the definition of COPD partly contribute to the variation in prevalence, population differences in the distribution of risk factors also explain differences in prevalence.104 The prevalence is greater among men than among women, and increases with age and the extent of smoking.106 Mortality rates for COPD, although subject to well-described limitations,107 provide another measure of occurrence.104 Unfortunately, procedures and codes for classifying COPD as the underlying cause of death have not been consistent across this century. Consequently, mortality trends must be interpreted cautiously. Moreover, attribution of a death to COPD ordinarily requires contact

with a clinician and diagnosis of the disease. In spite of the limitations of death certificates in investigating COPD, mortality data for the United States document a dramatic increase in deaths from COPD.104 In 1980, 52,193 deaths were attributed to categories related to COPD; by 2000 the number of deaths from COPD was 119,054.104 Mortality rates have been consistently higher among whites compared to blacks, and while men have had higher mortality rates than women, during the period from 1980 through 2000, women experienced a greater increase in mortality rates and in 2000, the number of deaths from COPD was higher among women (n = 59,636) compared to men (n = 59,118).104 Worldwide, mortality rates among countries are highly variable, but overall, mortality from COPD has been increasing. In 1990 COPD was ranked as the sixth leading cause of death in the world and by 2020 it is estimated to be the third leading cause of death.1 The 1984 Report of the Surgeon General concluded that 80–90% of COPD in the United States is attributable to cigarette smoking.96 The slow evolution of COPD provides an opportunity to identify and to target for intervention the smokers in whom the disease is developing. With sustained smoking, lung function in smokers, declining at a more rapid rate (Fig. 65-3), tends to drop below normal levels. Lung function testing of chronic smokers can identify individuals whose function has dropped below the range of normal values but not yet reached the degree of impairment associated with frank COPD.108 These at-risk persons could then be targeted for intensive smoking cessation interventions.109

Acute Respiratory Distress Syndrome The clinical syndrome of acute respiratory distress syndrome (ARDS) was originally described in the late 1960s; it represents a diffuse response of the lung to a wide variety of causative factors including pneumonia, aspiration and other inhalational injuries, sepsis, trauma, pancreatitis, multiple transfusions, and drug overdose.110 The clinical picture comprises pulmonary edema that does not have a cardiac basis and respiratory failure.

5

4

A Normal

2

B Normal

FEV,(liters)

3

Figure 65-3. Decline of FEV1 at normal rate (solid line) and at an accelerated rate (dashed line). A, Person who has attained a “normal” maximal FEV1 during lung growth and development; B, Person whose maximal FEV1 has been reduced by childhood respiratory infection, CAO = chronic airflow obstruction (Source: From U.S. Department of Health and Human Services: The Health Consequences of Smoking. Chronic Obstructive Pulmonary Disease. DHHS Publication No. (PHS) 84-50205, Rockville, MD: Office on Smoking and Health, 1984.)

1 CAO

0 25

35

45

55 Years

65

75

65 Because of the multiple causes of ARDS and the lack of a consistent definition, the incidence of ARDS has been difficult to determine.110,111 Estimates of the incidence of ARDS in the United States from an ARDS research network range from 17.3 to 64.2 per 100,000 inhabitants per year.112 Overall, about 25% of patients with any one of the risk factors will develop ARDS, ranging from 13% among patients with drug overdose to 43% among patients with sepsis.113 Increasing age and active smoking have been associated with increased risk for development of ARDS.113,114 Mortality from ARDS is high, with 40–60% of patients dying from complications including sepsis and multi-organ failure.110 In summary, acute respiratory distress syndrome occurs as a consequence of severe lung injury by diverse and distinct agents. Preventive strategies must be directed toward the causative factors (e.g., pneumonia, sepsis, and motor vehicle accidents).

Pulmonary Thromboembolism The diagnosis of pulmonary thromboembolism presents a number of diagnostic challenges and thus frequently goes undetected. Therefore, available estimates of incidence, which range from 1.2 to 1.8 per 1000 persons/year underestimate the true occurrence of the condition.115 While pulmonary thromboembolism is associated with high mortality, differences between study populations and follow-up contribute to wide variations in reported case fatality (2.3–28%).115 Overall, mortality rates for pulmonary thromboembolism in the United States have declined during the period 1979 through 1998, from 191 per million to 94 per million, respectively.116 A number of patient characteristics have been associated with increased mortality including increasing age, being male and black, and associated comorbid conditions (e.g., trauma, cancer).116 Identification of risk factors for pulmonary thromboembolism (Table 65-4)115 is key for making a correct diagnosis. Several recent reports have highlighted the importance of long-distance air travel as a cause of thromboembolic disease.117,118 However, about 50% of patients with pulmonary embolism do not have clinically evident risk factors (i.e., trauma, surgery, marked immobility, or active cancer).119 Therefore, a high index of suspicion is necessary for making the diagnosis of pulmonary thromboembolism.

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Because of the high frequency of pulmonary thromboembolism and the difficulties of diagnosis, prevention has been a major area of investigation, and the evidence and recommendations for prevention have been extensively reviewed elsewhere.120 Both pharmacological and mechanical methods are available for prevention of thromboembolism, and the selection of specific preventive interventions is determined based on the patient’s risk for thromboembolism and for bleeding complications from the pharmacological agents used for prevention.

Diffuse Parenchymal Lung Diseases The diffuse parenchymal lung diseases, also referred to as interstitial lung diseases, are a heterogeneous group of disorders comprising more than 200 entities, many of which are rare with no known cause, and result from injury to the pulmonary interstitium (Table 65-5).121 However, in the general population only five major diagnostic categories of these diseases are usually seen, including occupational and environmental, drug- and radiation-induced, connective tissue diseases, idiopathic interstitial pneumonias, and granulomatous disorders.122 In a population-based investigation of the occurrence of interstitial lung diseases the overall prevalence was higher in men compared with that in women, 81 per 100,000 and 67 per 100,000, respectively.122 The overall incidence was 32 per 100,000/year among men and 26 per 100,000/year among women.122 Idiopathic pulmonary fibrosis is the single-largest category, accounting for 51% of all incident cases. Interstitial lung diseases of known cause (e.g., asbestosis, coal workers’ pneumoconiosis, silicosis, hypersensitivity pneumonitis, drug induced) compose only about 15% of incident cases in the general population. While few etiological studies have been conducted, both endogenous and environmental factors have been proposed as determinants of interstitial lung diseases of unknown causes. With regard to endogenous factors, rare familial forms of diffuse parenchymal lung diseases provide evidence for genetic factors in the development

TABLE 65-5. DIFFUSE PARENCHYMAL LUNG DISEASES

Known Causes Inhaled agents Inorganic dusts, gases or fumes Organic dusts Drugs Poisons Radiation Infectious agents Medical Conditions Chronic pulmonary edema Chronic uremia Hepatitis, cirrhosis Transplantation rejection Metastatic cancer

TABLE 65-4. RISK FACTORS FOR VENOUS THROMBOEMBOLISM

Personal and Genetic Factors Increasing age Obesity Inherited thrombophilias (e.g., Factor V Leiden mutation)

Lifestyle and Environmental Cigarette smoking Long-haul air travel Immobility

Women’s Health Pregnancy Oral contraceptives Hormone replacement therapy

Unknown Causes Idiopathic Interstitial Pneumonias (IPF, NSIP, DIP, RBILD, COP, AIP)∗ Sarcoidosis Collagen-vascular disorders Angiitis and granulomatosis Eosinophilic pneumonias Histiocytosis X Hereditary and familial disorders (e.g., tuberous sclerosis) Storage disorders (e.g., amyloidosis, alveolar proteinosis)

Medical Illness Previous venous thromboembolism Cancer Hypertension Congestive heart failure Stroke

Surgical Trauma Orthopedic surgery Other major surgeries, especially for cancer Source: Data from Goldhaber SZ. Pulmonary embolism. Lancet. 2004;363: 1295–1305.

∗

IPF = idiopathic pulmonary fibrosis, NSIP = nonspecific interstitial pneumonia, DIP = desquamative interstitial pneumonia, RBILD = respiratory bronchiolitis interstitial lung disease, COP = cryrptogenic organizing pneumonia, AIP = acute interstitial pneumonia. Source: Adapted from Demedts M, Wells AU, Anto JM, et al. Interstitial lung diseases: an epidemiological overview. Eur Respir J. 2001;18(Suppl 32):2S–16S.

1120

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of these disorders, however, the genetic determinants of these diseases remain an active area of investigation.123,124 Inhalation of environmental agents and exposure to drugs account for most interstitial lung diseases of known cause, and a growing number of recent investigations have found associations between environmental exposures and idiopathic pulmonary fibrosis.123–131 Examples of environmental factors that have been associated with idiopathic pulmonary fibrosis include cigarette smoking, working with livestock, wood dust, and metal dust. Infectious agents, viruses,127 and Mycoplasma132 have been implicated as causes of pulmonary fibrosis, indistinguishable from idiopathic pulmonary fibrosis, but the importance of these agents as causes of interstitial lung disease in the general population is not known. The risk of sarcoidosis is increased with agricultural employment and work environments with mold/mildew exposure.131 Exposure to environmental agents may also alter risk of development of interstitial lung diseases of known or unknown cause; cigarette smoking decreases the risk of sarcoidosis131 and hypersensitivity pneumonitis,133 and increases the risk of other interstitial lung diseases.134 Because most interstitial lung diseases are of unknown cause, little can be offered for prevention now. However, growing evidence suggests that exposure to environmental agents is associated with idiopathic pulmonary fibrosis, the most common interstitial lung disease. As evidence accumulates to fulfill the criteria for causation for specific exposures and determinants of individual susceptibility are identified, specific recommendations for prevention may be possible.

Sleep Apnea The sleep apnea syndrome is characterized by excessive daytime sleepiness, snoring, and many episodes of cessation of breathing during sleep.135 In the majority of cases, the syndrome results from recurrent collapse of the pharynx with blockage of the passage of air.135 Because of recurrent apneas, significant lack of oxygen may develop and cause fragmented sleep and secondary complications. The excessive daytime sleepiness may result in a number of psychosocial problems and substantially increases the risk of automobile accidents.136 If untreated, moderate to severe sleep apnea syndrome results in excess mortality.136 Based on a number of surveys that have been conducted worldwide, the prevalence of the sleep apnea syndrome in the general population is estimated to be less than 5%.136 The prevalence is higher among men, habitual snoring, and obese persons and increases with age. Because of the increasing occurrence of obesity and high prevalence of the syndrome in the general population, with the associated morbidity and mortality, the sleep apnea syndrome presents a major public health problem. Little information is available on the prevention of morbidity and mortality from the sleep apnea syndrome, and the long-term benefits of treatment remain to be established.135 For moderate to severe sleep apnea, continuous positive airway pressure through a nasal mask is the main treatment modality. Because obesity is often associated with the syndrome, weight reduction is frequently recommended but offers limited improvement unless body weight is substantially reduced. Alcohol avoidance is recommended because it can cause sleep apnea in persons who simply snore and can worsen the severity of apnea among patients with the sleep apnea syndrome. CONCLUSIONS

Respiratory diseases are common causes of morbidity and mortality worldwide, and many of these diseases can be prevented. Because the occurrence of the various respiratory diseases may vary widely in different geographic locations, epidemiological data are important for development of prevention strategies. Of particular public health concern is tobacco smoking, a major cause of avoidable respiratory disease from the prenatal period through adulthood.

REFERENCES

1. Murray CJL, Lopez AD. Alternative projections of mortality and disability by cause 1990–2020: global burden of disease study. Lancet. 1997;349:1498–1504. 2. World Health Organization: www.who.int/whr/2004/annex/en/ 3. Black RE, Morris SS, Bryce J. Where and why are 10 million children dying every year? Lancet. 2003;361:2226–34. 4. Graham NMH. The epidemiology of acute respiratory infections in children and adults: a global perspective [Review]. Epidemiol Rev. 1990;12:149–78. 5. Morens DM, Folkers GK, Fauci AS. The challenge of emerging and re-emerging infectious diseases. Nature. 2004;430:242–9. 6. Stanley K, Stjernsward J. Lung cancer—a worldwide health problem [Review]. Chest. 1989;96(Suppl 1):1S–5S. 7. Brown CA, Crombie IK, Tunstall-Pedoe H. Failure of cigarette smoking to explain international differences in mortality from chronic obstructive pulmonary disease. J Epidemiol Commun Health. 1994;48:134–9. 8. Perez-Padilla R, Regalado J, Vedal S, et al. Exposure to biomass smoke and chronic airway disease in Mexican women: a case-control study. Am J Respir Crit Care Med. 1996;154:701–6. 9. Fraser J, Walls M, McGuire W. Respiratory complications of preterm birth. BMJ. 2004;329:962–5. 10. Eber E, Zach MS. Long term sequelae of bronchopulmonary dysplasia (chronic lung disease of infancy). Thorax. 2001;56:317–23. 11. Wegman ME. Annual summary of vital statistics—1989. Pediatrics. 1990;86(6):835–47. 12. Horbar JD, Dadger GJ, Carpenter JH, et al. Trends in mortality and morbidity for very low birth weight infants, 1991–1999. Pediatrics. 2002;110:143–51. 13. Malloy MH, Freeman DH: Respiratory distress syndrome mortality in the United States, 1987 to 1995. J Perinatol. 2000;20(7):414–20. 14. Horbar JD, Soil RF, Sutherland JM, et al. A multicenter randomized, placebo-controlled trial of surfactant therapy for respiratory distress syndrome. N Engl J Med. 1989;320(15):959–65. 15. Verma RP. Respiratory distress syndrome of the newborn infant [Review]. Obstet Gynecol Surv. 1995;50(7):542–55. 16. Stahlman MT. Medical complications in premature infants: is treatment enough? [Editorial]. N Engl J Med. 1989;320(23):1551–3. 17. Yeh TF, Lin YJ, Lin HC, et al. Outcomes at school age after postnatal dexamethasone therapy for lung disease of prematurity. NEJM. 2004;350:1304–13. 18. FitzSimmons SC. The changing epidemiology of cystic fibrosis [Review]. Pediatrics. 1993;122(1):1–9. 19. Collins FS. Cystic fibrosis: molecular biology and therapeutic implications [Review]. Science. 1992;256:774–9. 20. Grosse SD, Boyle CA, Botkin JR, et al. Newborn screening for cystic fibrosis. Evaluation of benefits and risks and recommendations for state newborn screening programs. MMWR. October 15, 2004;53(RR-13):1–36. 21. Ratjen F, Doring G. Cystic fibrosis. Lancet. 2003;361:681–9. 22. Ramsey BW. Management of pulmonary disease in patients with cystic fibrosis [Review]. N Engl J Med. 1996;335(2):179–88. 23. Ryley HC, Goodchild MC, Dodge JA. Screening for cystic fibrosis [Review]. Br Med Bull. 1992;48(4):805–22. 24. Palomaki GE, FitzSimmons SC, Haddow JE. Clinical sensitivity of prenatal screening for cystic fibrosis via CFTR carrier testing in a United States panethnic population. Genet Med. 2004;6(5):405–14. 25. Yankaskas JR, Marshall BC, Sufian B, et al. Cystic fibrosis adult care consensus conference report. Chest. 2004;125:1S–39S. 26. Williams BG, Gouws E, Boschi-Pinto C, et al. Estimates of worldwide distribution of child deaths from acute respiratory infections. Lancet Infect Dis. 2002;2:25–32. 27. Mullholland K. Global burden of acute respiratory infections in children: implications for interventions. Pediatr Pulmonol. 2003;36: 469–74.

65 28. Thompson WW, Shay DK, Weintraub E, et al. Influenza-associated hospitalizations in the United States. JAMA. 2004;292:1333–40. 29. Samet JM, Tager IB, Speizer FE. The relationship between respiratory illness in childhood and chronic airflow obstruction in adulthood [Review]. Am Rev Respir Dis. 1983;127(4):508–23. 30. Barker DJ, Godfrey KM, Fall C, et al. Relation of birth weight and childhood respiratory infection to adult lung function and death from chronic obstructive airways disease. Br Med J. 1991;303(6804): 671–5. 31. Singleton RJ, Redding GJ, Lewis TC, et al. Sequelae of severe respiratory syncytial virus infection in infancy and early childhood among Alaska native children. Pediatr. 2003;112:285–90. 32. Wright AL, Taussig LM, Ray CO, et al. The Tucson children’s respiratory study. II. Lower respiratory tract illness in the first year of life. Am J Epidemiol. 1989;129(6):1232–46. 33. Glezen P, Denny FW. Epidemiology of acute lower respiratory disease in children. N Engl J Med. 1973;288(10):498–505. 34. Chretien J, Holland W, Macklem P, et al. Acute respiratory infections in children. A global public health problem. N Engl J Med. 1984;310(15):982–4. 35. Monto AS, Ullman BM. Acute respiratory illness in an American community. The Tecumseh study. JAMA. 1974;227(2):164–9. 36. Smith KR, Samet JM, Romieu I, et al. Indoor air pollution in developing countries and acute lower respiratory infections in children. Thorax. 2000;55:518–32. 37. Mahalanabis D, Gupta S, Paul D, et al. Risk factors for pneumonia in infants and young children and the role of solid fuel for cooking: a case-control study. Epidemiol Infect. 2002;129:65–71. 38. U.S. Environmental Protection Agency. Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders. EPA/600/ 6-90/006F. Washington, DC: Government Printing Office, 1992. 39. Bauchner H, Leventhal JM, Shapiro ED. Studies of breast-feeding and infections. How good is the evidence? [Review]. JAMA. 1986;256(7):887–92. 40. Samet JM, Marbury MC, Spengler JD. Health effects and sources of indoor air pollution. Part I [Review]. Am Rev Respir Dis. 1987;136(6):1486–1508. 41. Samet JM, Lambert WE, Skipper BJ, et al. Nitrogen dioxide and respiratory illnesses in infants. Am Rev Respir Dis. 1993;148:1258–65. 42. Victora CG, Kirkwood BR, Ashworth A, et al. Potential interventions for the prevention of childhood pneumonia in developing countries: improving function. Am J Clin Nutr. 1999;70:309–20. 43. Jones G, Steketee RW, Black RE, et al. How many child deaths can we prevent this year? Lancet. 2003;362:65–71. 44. Russell FM, Buttery J. Vaccine development for capsulate bacteria causing pneumonia. Curr Opin Pulm Med. 2003;9:227–32. 45. Greenberg, Piedra PA. Immunization against viral respiratory disease. A review. Pediatr Infect Dis J. 2004;23:S254–S261. 46. Global Initiative for Asthma. Available at: www.ginaasthma.com. Last accessed March 8, 2005. 47. Bracken MB, Belanger K, Cookson WO, et al. Genetic and perinatal factors for asthma onset and severity: a review and theoretical analysis. Epidemiol Rev. 2002;24(2):176–89. 48. Peat JK, Toelle BG, Marks GB, et al. Continuing the debate about measuring asthma in population studies. Thorax. 2001;56:406–11. 49. Beasely R, Ellwod P, Asher I. International patterns of the prevalence of pediatric asthma. The ISAAC program. Pediatr Clin N Am. 2003;50:539–53. 50. King ME, Mannino DM, Holguin F. Risk factors for asthma incidence. Panminerva Med. 2004;46:97–111. 51. Weiland SK, Bjorksten B, Brunekreef B, et al. Phase II of the international study of asthma and allergies in childhood (ISAAC II): rationale and methods. Eur Respir J. 2004;24:406–12. 52. Mannino DM, Homa DM, Akinbami LJ, et al. Surveillance for asthma—United States, 1980–1999. MMWR Surveillance Summaries. 2002;51(SS-1):1–13.

Respiratory Disease Prevention

1121

53. Dodge R, Cline MG, Burrows B. Comparisons of asthma, emphysema, and chronic bronchitis diagnoses in a general population sample. Am Rev Respir Dis. 1986;133(6):981–6. 54. Yunginger JW, Reed CE, O’Connell EJ, et al. A community-based study of the epidemiology of asthma. Am Rev Respir Dis. 1992;146:888–94. 55. Taussig LM. Maximal expiratory flows at functional residual capacity: a test of lung function for young children. Am Rev Respir Dis. 1977;ll6(6):1031–8. 56. Coultas DB, Gong H Jr, Grad R, et al. Respiratory diseases in minorities of the United States [published erratum appears in Am J Respir Crit Care Med. 1994 Jul; 150(1):290] [Review]. Am J Respir Crit Care Med. 1994;149(3 Pt 2):S93–S131. 57. Jaakkola JJK, Gissler M. Maternal smoking in pregnancy, fetal development, and childhood asthma. Am J Public Health. 2004;94:136–40. 58. Martinez FD, Cline M, Burrows B. Increased incidence of asthma in children of smoking mothers. Pediatrics. 1992;89(l):21–6. 59. Infante-Rivard C. Childhood asthma and indoor environmental risk factors. Am J Epidemiol. 1993;137(8):834–44. 60. Stoddard JJ, Miller T. Impact of parental smoking on the prevalence of wheezing respiratory illness in children. Am J Epidemiol. 1995;141(2):96–102. 61. Sporik R, Holgate ST, Platts-Mills TA, et al. Exposure to house-dust mite allergen (Der p I) and the development of asthma in childhood. A prospective study. N Engl J Med. 1990;323(8):502–7. 62. Ramsey CD, Celedon JC. The hygiene hypothesis and asthma. Curr Opin Pulm Med. 2004;11:14–20. 63. Becker AB, Chan-Yeung M. Primary prevention of asthma. Curr Opin Pulm Med. 2002;8:16–24. 64. Becker A, Watson W, Ferguson A, et al. The Canadian asthma primary prevention study: outcomes at 2 years of age. J Allergy Clin Immunol. 2004;113:650–6. 65. Woodcock A, Lowe LA, Murray CS, et al. Early life environmental control. Effect of symptoms, sensitization, and lung function at age 3 years. Am J Respir Crit Care Med. 2004;170:433–9. 66. Guilbert T, Krawiec M. Natural history of asthma. Pediatr Clin N Am. 2003;50:523–38. 67. Martinez FD, Wright AL, Taussig LM, et al. Asthma and wheezing in the first six years of life. N Engl J Med. 1995;332:133–8. 68. Park ES, Golding J, Carswell F, et al. Preschool wheezing and prognosis at 10. Arch Dis Child. 1986;61:642–6. 69. American Thoracic Society. Health effects of outdoor air pollution. Part 1 [Review]. Am J Respir Crit Care Med. 1996;153:3–50. 70. American Thoracic Society. Health effects of outdoor air pollution. Part 2. Am J Respir Crit Care Med. 1996;153: 477–98. 71. Abramson MJ, Puy RM, Weiner JM. Is allergen immunotherapy effective in asthma? A meta-analysis of randomized controlled trials. Am J Respir Crit Care Med. 1995;151:969–74. 72. Blessing-Moore J. Does asthma education change behavior? To know is not to do. Chest. 1996;109:9–11. 73. Morgan WJ, Crain E, Gruchalla RS, et al. Results of a home-based environmental intervention among urban children with asthma. NEJM. 2004;351:1068–80. 74. National Asthma Education Program. Guidelines for the Diagnosis and Management of Asthma. Publication No. 91-3042. Bethesda, MD: National Heart, Lung, and Blood Institute, 1991. 75. Strunk RC. Death due to asthma. New insights into sudden unexpected deaths, but the focus remains on prevention [Editorial]. Am Rev Respir Dis. 1993;148:550–2. 76. Janson C, Anto J, Burney P, et al. The European Community Respiratory Health Survey: what are the main results so far? Eur Respir J. 2001;18:598–611. 77. Centers for Disease Control and Prevention. Asthma prevalence and control characteristics by race/ethnicity—United States, 2002. MMWR. 2004;53:145–8.

1122

Noncommunicable and Chronic Disabling Conditions

78. McKeever TM, Britton J. Diet and asthma. Am J Respir Crit Care Med. 2004;170:725–9. 79. Nystad W, Meyer HE, Nafstad P, et al. Body mass index in relation to adult asthma among 135,000 Norwegian men and women. Am J Epidemiol. 2004;160:969–76. 80. Ford ES, Mannino DM, Redd SC, et al. Body mass index and asthma incidence among USA adults. Eur Respir J. 2004;24:740–4. 81. Thomson NC, Chaudhuri R, Livingston E. Asthma and cigarette smoking. Eur Respir J. 2004;24:822–33. 82. Chan-Yeung M, Malo JL. Occupational asthma. N Engl J Med. 1995;333(2):107–12. 83. LeMoual N, Kennedy SM, Kauffmann F. Occupational exposures and asthma in 14,000 adults from the general population. Am J Epidemiol. 2004;160:1108–16. 84. Arif A, Delclos GL, Whitehead LW, et al. Occupational exposures associated with work-related asthma and work-related wheezing among U.S. workers. Am J Ind Med. 2003;44:368–76. 85. U.S. Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. 86. Piipari R, Jaakkola JJK, Jaakkola N, et al. Smoking and asthma in adults. Eur Respir J. 2004;24:734–9. 87. Weiss KB, Gergen PJ, Hodgson TA. An economic evaluation of asthma in the United States. N Engl J Med. 1992;326:862–6. 88. O’Dowd LC, Fife D, Tenhave T, et al. Attitudes of physicians toward objective measures of airway function in asthma. Am J Med. 2003;114:391–6. 89. Ford ES, Mannino DM, Williams SG. Asthma and influenza vaccination. Findings from the 1999–2001 National Health Interview Survey. Chest. 2003;124:783–9. 90. Woodcock A, Forster L, Matthews E, et al. Control of exposure to mite allergen and allergen-impermeable bed covers for adults with asthma. N Engl J Med. 2003;349:225–36. 91. Schenker MB, Gold EB, Lopez RL, et al. Asthma mortality in California, 1960–1989. Demographic patterns and occupational associations. Am Rev Respir Dis. 1993;147:1454–60. 92. Nakamura Y, Labarthe DR. Secular trends in mortality from asthma in Japan, 1979–1988: Comparison with the United States. Int J Epidemiol. 1994;23(1):143–7. 93. Lang DM, Polansky M. Patterns of asthma mortality in Philadelphia from 1969 to 1991. N Engl J Med. 1994;331(23):1542–6. 94. Silverstein MD, Reed CE, O’Connell EJ, et al. Long-term survival of a cohort of community residents with asthma. N Engl J Med. 1994;331(23):1537–41. 95. Lange P, Ulrik CS, Vestbo J. Mortality in adults with self-reported asthma. Copenhagen City Heart Study Group. Lancet. 1996;347(9011): 1285–9. 96. U.S. Department of Health and Human Services. The Health Consequences of Smoking. Chronic Obstructive Pulmonary Disease. DHHS Publication No. PHS184-50205. Rockville, MD: Office on Smoking and Health, 1984. 97. Pauwels RA, Buist AS, Calverley PMA, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO global initiative for chronic obstructive lung disease (GOLD) workshop summary. Am J Respir Crit Care Med. 2001;163:1256–76. 98. Trupin L, Earnest G, San Pedro M, et al. The occupational burden of chronic obstructive pulmonary disease. Eur Respir J. 2003;22:462–9. 99. O’Connor GT, Sparrow D, Weiss ST. The role of allergy and nonspecific airway hyperresponsiveness in the pathogenesis of chronic obstructive pulmonary disease [Review]. Am Rev Respir Dis. 1989;140(l):225–52.

100. Tashkin DP, Altose MD, Connett JE, et al. Methacholine reactivity predicts changes in lung function over time in smokers with early chronic obstructive pulmonary disease. The Lung Health Study Research Group. Am J Respir Crit Care Med. 1996;153:1802–11. 101. Gold DR, Wang X, Wypij D, et al. Effects of cigarette smoking on lung function in adolescent boys and girls. N Engl J Med. 1996;335:931–7. 102. Kanner RE, Connett JE. Altose MD, et al. Gender difference in airway hyperresponsiveness in smokers with mild COPD. The Lung Health Study. Am J Respir Crit Care Med. 1994;150(4):956–61. 103. Coultas DB, Mapel DW. Undiagnosed airflow obstruction: prevalence and implications. Curr Opin Pul Med. 2003;9:96–103. 104. Mannino DM, Homa DM, Akinbami LJ. Chronic obstructive pulmonary disease surveillance—United States, 1971–2000. MMWR Surveillance Summaries. 2002;51/SS-6:1–16. 105. Lundback B, Lindberg A, Lindstrom M, et al. Not 15 but 50% of smokers develop COPD?—report from the obstructive lung disease in northern Sweden studies. Respir Med. 2003;97:115–22. 106. Pauwels RA, Rabe KF. Burden and clinical features of chronic obstructive pulmonary disease (COPD). Lancet. 2004;364:613–20. 107. Feinleib M, Rosenberg HM, Collins JG, et al. Trends in COPD morbidity and mortality in the United States. Am Rev Respir Dis. 1989;140:S9–S18. 108. Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J. 1977;1(6077):1645–8. 109. Anthonisen NR, Connett JE, Kiley JP, et al. Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA. 1994;272(19):1497–1505. 110. Ware LB, Matthay MA. The acute respiratory distress syndrome. NEJM. 2000;342:1334–49. 111. Frutos-Vivar F, Nin N, Esteban A. Epidemiology of acute lung injury and acute respiratory distress syndrome. Curr Opin Crit Care. 2004;10:1–6. 112. Goss CH, Brower RG, Hudson LD, et al. Incidence of acute lung injury in the United States. Crit Care Med. 2003;31:1607–11. 113. Hudson LD, Milberg JA, Anardi D, et al. Clinical risks for development of the acute respiratory distress syndrome. Am J Respir Crit Care Med. 1995;151:293–301. 114. Iribarren C, Jacobs DR, Sidney S, et al. Cigarette smoking, alcohol consumption, and risk of ARDS. Chest. 2000;117:163–8. 115. Goldhaber SZ. Pulmonary embolism. Lancet. 2004;363:1295–1305. 116. Horlander KT, Mannino DM, Leeper KV. Pulmonary embolism mortality in the United States, 1979–1998. An analysis using multiplecause mortality data. Arch Intern Med. 2003;163:1711–7. 117. Lapostolle F, Surget V, Borron SW, et al. Severe pulmonary embolism associated with air travel. N Engl J Med. 2001;345:779–83. 118. Hughes RJ, Hopkins RJ, Hills S, et al. Frequency of venous thromboembolism in low to moderate risk long distance air travellers: the New Zealand Air Traveller’s Thrombosis (NZATT) study. Lancet. 2003;362:2039–44. 119. Cushman M, Tsai AW, White RH, et al. Deep vein thrombosis and pulmonary embolism in two cohorts: the longitudinal investigation of thromboembolism etiology. Am J Med. 2004;117:19–25. 120. Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism. The seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest. 2004;126:338S–400S. 121. Demedts M, Wells AU, Anto JM, et al. Interstitial lung diseases: an epidemiological overview. Eur Respir. 2001;18(Suppl 32):2S–16S. 122. Coultas DB, Zumwalt RE, Black WC, et al. The epidemiology of interstitial lung diseases. Am J Respir Crit Care Med. 1994;150(4): 967–72. 123. Crystal RG, Bitterman PB, Mossman B, et al. Future research directions in idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2002;166:236–46.

65 124. du Bois RM. The genetic predisposition to interstitial lung disease. Functional relevance. Chest. 2002;121:14S–20S. 125. Scott J, Johnston I, Britton J. What causes cryptogenic fibrosing alveolitis? A case-control study of environmental exposure to dust. Br Med. 1990;1301:1015–7. 126. Iwai K, Mori T, Yamada N, et al. Idiopathic pulmonary fibrosis. Epidemiologic approaches to occupational exposure. Am J Respir Crit Care Med. 1994;150:670–5. 127. Egan JJ, Stewart JP, Hasleton PS, et al. Epstein-Barr virus replication within pulmonary epithelial cells in cryptogenic flbrosing alveolitis. Thorax. 1995;50:1234–9. 128. Hubbard R, Lewis S, Richards K, et al. Occupational exposure to metal or wood dust and aetiology of cryptogenic fibrosing alveolitis. Lancet. 1996;347:284–9. 129. Baumgartner KB, Samet JM, Stidley CA, et al. Cigarette smoking: a risk factor for idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 1997;155:242–8. 130. Baumgartner KB, Samet JM, Coultas DB, et al. Occupational and environmental risk factors for idiopathic pulmonary fibrosis: a

131.

132.

133.

134.

135. 136.

Respiratory Disease Prevention

1123

multicenter case-control study. Am J Epidemiol. 2000;152: 307–15. Newman LS, Rose CS, Bresnitz EA, et al. A case control etiologic study of sarcoidosis. Environmental and occupational risk factors. Am J Respir Crit Care Med. 2004;170:1324–30. Tablau OC, Reyes MP. Chronic interstitial pulmonary fibrosis following Mycoplasma pneumonias pneumonia. Am J Med. 1985;79(2):268–70. Morgan DC, Smyth JT, Lister RW, et al. Chest symptoms in farming communities with special reference to farmer’s lung. Br J Ind Med. 1975;32(3):228–34. Desai SR, Ryan SM, Colby TV. Smoking-related interstitial lung diseases: histopathological and imaging perspectives. Clin Radiol. 2003;58:259–68. Caples SM, Gami AS, Somers VK. Obstructive sleep apnea. Ann Intern Med. 2005;142:187–97. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea. A population health perspective. Am J Respir Crit Care Med. 2002;165:1217–39.

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Jennifer L. Kelsey • MaryFran Sowers

Musculoskeletal disorders are common, affect all age groups, and are associated with a great deal of disability, impairment, and handicap. More than 12 million people in the United States have their activity limited by musculoskeletal disorders, a figure greater than for any other disease category (Fig. 66-1).1 Musculoskeletal impairments affect about 14% of the population, with the spine most commonly involved, followed by the lower extremity or hip and the upper extremity or shoulder (Table 66-1).2 Each year about 11% of the population in the United States experience a musculoskeletal injury severe enough that medical care is sought or activity is restricted for at least half a day.2 The total economic cost to the United States of musculoskeletal conditions was estimated to be $284 billion in 2000,3 second only to diseases of the circulatory system. Indirect costs from lost earnings and services represent a particularly high proportion of this cost, since many people are affected during their most productive years.

DISORDERS PRIMARILY OF ADULTS

Low Back and Neck Pain From 75 to 85% of people experience low back pain at some time during their lives.4 Most episodes of low back pain improve within a few weeks, but recurrences are common, and low back pain often becomes a chronic problem with intermittent, usually mild, exacerbations.5 In a study of English patients seen by general practitioners for low back pain, after one year only 25% had no pain or disability, even though the majority were no longer seeking care from their practitioner for their problem.6 In a small proportion of cases the pain becomes constant and severe, and such cases account for a high proportion of the cost; one study found that 25% of the cases accounted for 90% of the costs.7 The specific lesion responsible for low back pain usually is not known. It is likely that the different conditions comprising the category “low back pain” (e.g., sprains and strains, disc herniations, spinal stenosis, spondylosis and spondylolisthesis, facet abnormalities) have in part different etiologies. However, until these specific conditions are identified and differentiated in epidemiologic investigations, the category “low back pain” as a whole must generally be considered as a single category. Techniques such as magnetic resonance imaging and computerized tomography are not particularly helpful in most instances because of the low correlation between symptomatology and the abnormalities seen on imaging.5 Low back pain is more common in people who do heavy manual work than in those whose work is sedentary. Jobs that involve heavy lifting (e.g., of objects weighing 25 lb or more) are associated with an increase in risk for back pain. Components of lifting that appear to increase the risk for both herniated disc and low back pain in general include frequent lifting of heavy objects while bending and

twisting the body, holding heavy objects away from the body while lifting, and failing to bend the knees while lifting.8–10 Several studies have found a modest association between cigarette smoking and low back pain and between smoking and herniated disc, probably because of the pressure exerted by frequent coughing or the decreased diffusion of nutrients into the intervertebral disc.11 Motor vehicle driving and exposure to other forms of whole body vibration are detrimental to the spine.9,12–15 Some evidence suggests that tallness is a risk factor for low back pain, that heavy body weight has little or no effect, and that a narrow spinal canal increases the risk, at least for lumbar disc herniation.16,17 Although psychological factors are often said to play a role in the etiology of low back pain, there is little firm evidence to support or refute this belief. Among possible psychological risk factors, the strongest evidence is for low social support in the workplace and low job satisfaction.18 One useful approach to the prevention of low back pain is modification of factors in the work place.7 Although low back x-rays and medical examinations have not proved useful as routine screening tests for selection of workers, selection on the basis of strength testing for jobs involving heavy manual work appears to reduce the likelihood of back injury. Training workers to bend the knees while lifting does not seem to have reduced the number of back injuries, partly because of poor compliance. Educational programs implemented among postal workers19 and nurses20 have also not reduced the frequency of low back problems. Rather, redesigning jobs to minimize bending and twisting motions and to reduce the amount of weight lifted may be more likely to decrease the number of back injuries and also may allow an injured worker to return to work sooner. Wearing lumbar supports in some high-risk occupations is sometimes used for primary prevention, but the limited available evidence suggests that it is probably not effective.21 Exercises to strengthen back and abdominal muscles and to improve overall fitness can somewhat decrease the incidence and duration of low back pain.22 Other possible methods of primary prevention include cessation of smoking, moving around from time to time in situations requiring prolonged exposure to one position, and vibration dampening. Use of motor vehicles with adjustable seat positioning and good lumbar support, reducing the amount of time professional drivers must drive, and improving the ergonomic properties of their driving situation may also be beneficial.15,23 Most back pain improves without any specific therapy. Predictors of disability from low back pain include long duration of the pain; a history of previous low back pain, disability, and hospitalizations; low educational level and employment grade; psychosocial factors such as dissatisfaction with the job and low social support on the job; heavy physical demands on the job; heavy smoking; whether insurance payments are being received; the perception of fault; and whether a lawyer has been retained.24–26 Of considerable importance in tertiary prevention for many people with acute low back pain is a continuation of normal activities to the extent tolerated, and a prompt 1125

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1126

Noncommunicable and Chronic Disabling Conditions 15,000

2

6,000 3

4

3,000

5

6

7

8

m ste sy

11

12

Cir

cu

lat

ory

ele tal sk ulo

10

Ne sys tem sen rvous se sys org tem Re a an spi ns d rat ory sys Me tem nta l di sor Dig de rs est En ive d o sys an c r d m ine tem eta , Nu Ge bolic tritio na nito d uri isord l, na ry ers sys tem N eo Ac pla cid an sm d v ents, s i Sk olenc poiso in a nin e tiss gs, ue nd su dis bc u e ase tan Inf eo e s us dis ctive ea ses and pa ras itic

9

sc

Figure 66-1. Estimated number of persons in the United States in 1984 with limitation of activity attributable to specific disease categories. (Source: Holbrook TL, Grazier L, Kelsey JL, Stauffer RN. The Frequency, Occurrence, Impact, and Cost of Musculoskeletal Conditions in the United States. Chicago: American Academy of Othopaedic Surgeons; 1984.)

9,000

Mu

Persons with limitation of activity (Thousands)

1 12,000

Disease categories

return to work (Table 66-2).26,27 On first returning to work, however, the worker should avoid lifting heavy objects, bending, twisting, sitting in a low chair, and remaining in the same position for long periods of time. Ergonomic redesign of physically demanding jobs may facilitate return to work.28 Because surgical treatment is often unsatisfactory, conservative approaches such as strengthening exercises, physical therapy, and back schools are frequently used for tertiary prevention. Evidence from randomized trials indicates that exercises that include aerobic conditioning and strengthening of the back and legs can reduce the likelihood of recurrences.22 Although back schools have different emphases, most (a) teach patients enough about spinal mechanics so that they can use their backs effectively

and avoid pain and damage, (b) try to effect attitude changes through psychological approaches, and (c) offer exercise and physical fitness programs.29 There have been no definitive evaluations of the efficacy of back schools, and their effectiveness remains controversial.30 The percentage of the population having neck pain at some time during their lives is around 60–70%.31 As with low back pain, neck pain can be caused by a variety of different lesions, and recurrences are

TABLE 66-2. SELECTED OUTCOMES AT 12 WEEKS IN A RANDOMIZED TRIAL OF BED-REST FOR 2 DAYS, BACK MOBILIZING EXERCISES, AND CONTINUATION OF NORMAL ACTIVITIES AS TOLERATED, IN PATIENTS WITH ACUTE LOW BACK PAIN

TABLE 66-1. PREVALENCE OF MUSCULOSKELETAL IMPAIRMENTS IN THE UNITED STATES IN 1995 Outcome Measure Type of Impairment

Estimated No. of Affected Individuals

% of Population

All musculoskeletal impairments Back or spine Lower extremity or hip Upper extremity or shoulder

36,438,000 18,454.000 13,421,000 4,563,000

13.7 7.0 5.1 1.7

Source: Data from Praemer, Furner A, Rice DP. Musculoskeletal Conditions in the United States, 2nd Edition. Rosemont IL: American Academy of Orthopaedic Surgeons; 1999.

Number of sick days Intensity of pain (11-point scale) Ability to work (11-point scale) Lumbar flexion (modified Schober method) Oswestry back-disability index (range 0–100)

Normal Activities (N = 62)

Bed Rest (N = 59)

Exercises (N = 41)

9.2 2.1 7.7

7.2 1.8 7.8

4.7 1.3 8.5

6.3

6.0

6.6

11.8

10.8

7.4

Source: Modified from Malmivaara A, Häkkinen U, Aro T, et al. The treatment of acute low back pain—bed rest, exercises, or ordinary activity? New Engl J Med. 1995;332:351–5.

66 common. The number of people with neck pain appears to have been increasing. This increase is thought to be attributable to the lower percentage of the work force participating in heavy manual work and the greater number of people sitting for long periods in front of video display terminals. Knowledge of risk factors for neck pain is scanty. Previous neck pain and low back pain are strong predictors.32,33 Prolonged exposure to awkward postures, especially in poorly designed workspaces, appears to be associated with mild neck pain. For instance, frequent use of video display terminal with a fixed keyboard height that requires a bent neck can cause neck pain.34,35 Some evidence indicates that heavy lifting, cigarette smoking, frequent aquatic diving from a board, motor vehicle driving, and exposure to other sources of wholebody vibration increase the risk for neck pain in general or prolapsed cervical intervertebral disc in particular.36–38 There have been a few reports that repetitive motions, forceful exertions, prolonged neck flexion, handling tasks that involve reaching, pushing, and pulling, constrained positions, arm force, arm posture, and twisting and bending of the trunk may also be related to risk for neck or neck/shoulder pain.32,35,39 Several psychological factors have been associated with the development of neck pain, but results are inconclusive as to which are most important.35,40,41 Little research has been undertaken on the primary prevention of neck pain or on ways to reduce the likelihood of disability among those with neck pain. However, it would be expected that reductions in the amount of heavy lifting, reaching, pushing, and pulling, cigarette smoking, prolonged time spent in awkward positions such as a video display terminals, motor vehicle driving, and exposure to other forms of wholebody vibration would result in decreased risks. Encouraging workers using video display terminals to take frequent breaks appears to enhance recovery from neck and upper-limb disorders,42 and might reduce the likelihood of developing neck pain in the first place.43

Osteoporosis Osteoporosis is characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increased risk of fracture.44 Fractures of the hip, vertebrae, and distal radius are particularly common. Although osteoporosis may occur secondarily to such conditions as hormonal defects, connective tissue disorders, or certain drug therapies, most cases are idiopathic. Males have higher bone mass than females, and American Blacks have higher bone mass than non-Hispanic whites, Hispanic whites, and Asian-Americans.45 After about age 40–50 years, bone mass is lost in both men and women of all racial and ethnic groups, but a particularly rapid decrease occurs in women in the years around and following menopause. Most research on osteoporosis has been undertaken in women, and unless specifically indicated, the material presented in this section pertains mainly to women. It has been estimated that a white woman of age 50 has a 17% chance of fracturing a hip, a 16% chance of fracturing a distal forearm, and a 16% chance of having a clinically diagnosed vertebral fracture during the remainder of her lifetime.46 Bone mass in later adulthood, when osteoporotic fractures are most common, depends on bone mass in young adulthood, when bone mass is at its peak, and on the extent of bone loss after the peak is reached. Heredity is an important determinant of bone mass in childhood, adolescence, and early adulthood, but the role of genetics on rates of bone loss with aging or in association with menopause is less clear. Most osteoporosis is considered to be polygenic, resulting from the interaction of common polymorphic alleles with multiple environmental factors.47 Although evidence is not definitive, it appears that weight, physical activity, calcium intake, and possibly other nutrients also affect bone mass in childhood, adolescence, and early adulthood, but to a lesser extent than heredity.48,49 In some adolescents and young adults, disruptions of the reproductive hormone axis from anorexia, intense athletic activity, and use of progestin-only injectable contraceptives can lead to lower than normal bone mass.50 The relatively rapid rate of bone loss in middle-aged and older women has been related to a decrease in estrogen production. Women

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who have had an oophorectomy have earlier loss of bone mass than other women. On the average, the lower the endogenous estrogen concentration around the time of menopause, the higher the rate of bone loss.51 Thin women are at higher risk than obese women, partly because of their lower estrogen production, their lower concentration of circulating estrogens, and the decreased mechanical stress on their bone. In the adult years a low level of dietary calcium consumption is modestly associated with lower bone mass, and calcium supplementation affords some protection against loss of bone mass.52,53 The role of other dietary constituents is less clear. It is known that prolonged immobilization may result in loss of bone mass. The effect of light physical activities like walking is uncertain, but more vigorous impact and nonimpact exercise programs have been shown to have a modest protective effect against loss of bone mass in the lumbar spine and probably the hip as well.54 Whether exercise reduces the risk for fractures is unclear.55 Cigarette smoking after menopause increases the risk for osteoporosis and hip fracture.56 Heavy, but not moderate, alcohol consumption57 and corticosteroid use58 are associated with lower bone mass and an increased risk for fracture at all ages, while use of thiazide diuretics is associated with increased bone mass and decreased risk of hip fracture.51 Recommended prevention strategies start with measures that will promote adequate bone mass at an early age, such as a diet adequate in calcium accompanied by adequate vitamin D acquired through diet or sunlight exposure, sufficient physical activity, and not smoking. In adulthood, randomized trials indicate that supplemental calcium affords a small amount of protection against loss of bone mass.52 Vitamin D formulations have a positive effect on bone mass, and probably reduce the frequency of vertebral fractures, but whether they also reduce the incidence of nonvertebral fractures is less certain.59 Randomized trials have shown that exercise programs involving aerobic activity, weight bearing activity, resistance exercises, and endurance and strength training result in less loss of bone mass.54,60,61 Additional research is needed to determine the intensity and types of exercise that are most beneficial.54 Because dietary calcium, calcium supplements, vitamin D and physical activity have only modest beneficial effects on the preservation of bone mass in perimenopaual and postmenopausal women, pharmaceutical agents may be recommended to prevent or retard loss of bone mass. Although menopausal hormone therapy with estrogen alone or estrogen with progestin protects against loss of bone mass and the occurrence of fractures while it is taken, it is no longer recommended for prevention because of the conclusion by the Women’s Health Initiative62 that its long-term risks outweigh its long-term benefits. Bisphosphonates such as alendronate (Fosamax) prevent or retard loss of bone mass, but alendronate has been shown to protect against fractures only in women who already have very low bone mass.63 Trials with newer bisphosphonates, including etidronate and risedronate, show similar results.64 Some users experience gastrointestinal side effects, and, in addition, the long-term effects of the bisphosphonates are not known. The selective estrogen receptor modulator raloxifene (Evista) has been shown to retard loss of bone mass and to reduce the occurrence of vertebral fractures, but not to reduce the risk for nonvertebral fractures, including hip fracture.65 Calcitonin in both intranasal and injectable forms has been shown to reduce somewhat the likelihood of new vertebral fractures, and is sometimes recommended for women who cannot take the other agents.66 Teriparatide, a recombinant human parathyroid hormone that acts through increasing bone formation, reduces the risk for both vertebral and nonvertebral fractures. Its long-term effects are not known, however, and it is approved for use for a maximum of two years in patients at high risk for fracture.66 In summary, the usefulness of pharmaceutical agents in the prevention of osteoporosis and osteoporotic fractures in women without very low bone mass has not been clearly demonstrated, as each of these drugs has limitations. In recent years, screening apparently healthy perimenopausal and postmenopausal women for high fracture risk by measuring their bone mineral density has been undertaken, most commonly by dual energy x-ray absorptiometry. However, many questions remain about the

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appropriateness of screening, such as who should be screened, what skeletal sites should be screened, whether multiple measurements over time are needed, what other information on risk should be obtained along with the measurement of bone mass, and what therapy should be recommended for those with various degrees of low bone mass.67 Because of the uncertainties associated with available therapies, it is not clear what should be done as a result of findings on screening, unless bone mass is found to be very low. Ultrasonography, which is usually applied to the heel bone and which may provide information about the architecture and elasticity of bone as well as about bone mineral density, has been found to predict hip fracture.68 Since ultrasound is less expensive, faster, and radiation-free compared to other methods commonly used to measure bone density, it may be increasingly used as a screening tool. Because ultrasound and bone densitometry predict fractures, in part independently, it has been suggested that using both measures would likely predict fracture occurrence better than either one alone.69 However, questions remain about the utility of screening by any means. Reducing the likelihood of falls among both women and men with osteoporosis may be an important way to prevent fractures. Risk factors for falls include increasing age, female sex, functional limitations (including problems with balance and gait and poor muscle strength), arthritis, symptoms of depression, orthostatic hypotension, cognitive impairment, visual impairment, various other chronic illnesses, and use of multiple prescription medications.70,71 The greater the number of these risk factors, the higher the risk of falling. Table 66-3 shows strategies demonstrated in randomized controlled trials to reduce the likelihood of falling among elderly women and men living in the community. Nonspecific advice about modification of home hazards has not proved effective,70,72 but standardized assessment by an occupational therapist coupled with specific recommendations and follow-up after hospital discharge has been associated with a 20% reduction in risk of falls both inside and outside the home among persons who have a history of falling in the previous year.72 Whether a fracture results from a fall and the site of the fracture will depend on such factors as the orientation of the fall, a person’s ability to initiate protective responses, the presence of shock absorbers such as a person’s fat, and bone strength.71,73,74 Falling sideways or straight down greatly increases the risk for a hip fracture, while breaking the fall with an outstretched hand decreases the risk of fractures of several sites including the hip, but increases the risk for distal forearm fracture.74 Falls from heights or on to hard surfaces increase the risk for fractures.74 A history of falls, a recent increase in the number of falls, and previous fractures are predictive of hip fracture.75 Architectural and geometrical properties of bone also affect the likelihood of a fracture.76,77 Randomized trials in nursing homes and in certain other populations at high risk for hip fracture have shown that institutions with programs in which hip protectors are provided have reduced risks for hip fracture, although compliance is a problem.78

Osteoarthritis Osteoarthritis, a heterogeneous condition of poorly understood etiology, is characterized by focal loss of articular cartilage with proliferation and remodeling of subchondral bone. Manifestations include pain TABLE 66-3. STRATEGIES DEMONSTRATED IN RANDOMIZED TRIALS TO BE EFFECTIVE IN REDUCING THE OCCURRENCE OF FALLS AMONG ELDERLY PEOPLE LIVING IN THE COMMUNITY

Health Care-Based Strategies Balance and gait training and strengthening exercises Reduction in home hazards after hospitalization Discontinuation of psychotropic medications Multifactorial risk assessment with targeted management Community-Based Strategy Specific balance and strength exercise programs Source: Modified from Tinetti ME. Preventing falls in elderly persons. New Engl J Med. 2003;348:42–9.

and stiffness accompanied by loss of function. The presence and severity of osteoarthritis in most population studies has been classified using radiographic criteria defined in the Atlas of Standard Radiographs of Arthritis.79 These criteria include osteophytes, bony spurs, joint space narrowing, subchondral cysts, and bony remodeling. Newer imaging technologies characterize other important attributes of the disease processes, including bone marrow edema and irregularities of articular cartilage.80,81 Idiopathic osteoarthritis may affect single joint groups (most commonly the knees, hands, feet, hips, and spine) or may present as generalized osteoarthritis, characterized by involvement of three or more joint groups and typically affecting perimenopausal and postmenopausal women.82 Secondary osteoarthritis follows the occurrence of traumatic, congenital, developmental, or systemic disorders involving the joints. The etiology of osteoarthritis is multifactorial and associated with systemic factors, including obesity, aging, gender, and heritability. Obesity is known to increase the risk for osteoarthritis of several joints.83,84 Even in middle-age, obesity is associated with more than a twofold increase in knee osteoarthritis.85 The prevalence of osteoarthritis and the proportion of cases that are moderate or severe increase with age. 86 Under age 45, the age-specific prevalence is higher in men than women, while over age 55, the age specific prevalence is greater in women than men. Women have a greater number of joints involved and more frequently report morning stiffness, joint swelling, and nocturnal pain.87 The more common occurrence of Heberden’s nodes in women is believed to be related to a single autosomal gene that is dominant in women and recessive in men.88 Heritability estimates from twin studies range from 0.39 to 0.65, and are independent of known risk factors including obesity.89 Studies using techniques of recombinant DNA analysis have demonstrated linkage of a polymorphism of the type II collagen gene (Col2A1) with generalized osteoarthritis.90 Repetitive joint trauma associated with occupational activity predisposes to osteoarthritis. For instance, high prevalence is found in the elbows and knees of miners,91 in the fingers of cotton pickers,92 in the hips of farmers,93 and in the fingers, elbows, and knees of dock workers.94 Jobs requiring a great deal of knee bending, squatting, kneeling, stair climbing, heavy lifting, and mechanical loading increase the risk for knee osteoarthritis.95 The knee is among the commonly affected joints. Radiographic evidence of knee osteoarthritis, defined as grade two or greater, is estimated to be present in about 30% of people over the age of 65 years, and of those with radiographic evidence, one-third are symptomatic.96 The frequency of radiographic knee osteoarthritis is rarely evaluated in persons younger than age 55, but one study reported that in women aged 40–55, the prevalence is 15%.97 Disabling symptoms in the knee occur in about 10% of persons older than age 55, and of these, about one quarter are severely disabled.98 On a population basis, the magnitude of the disability from knee osteoarthritis is considered to be as great as the disability associated with heart disease, and is greater than the disability from any other medical condition among the elderly.99 A World Health Organization report predicts that in the next 15 years knee osteoarthritis will become the fourth most important global cause of disability in women and eighth most important cause in men.96 Studies in persons with radiologic evidence of knee osteoarthritis have identified the following factors to be predictive of knee pain: severity of radiographic changes, presence of morning stiffness, crepitus on passive range of motion, and a feeling of low spirits.100 In addition to obesity, other nonoccupational risk factors for osteoarthritis of the knee include knee injury, meniscectomy, and also the presence of Heberden’s nodes.101 Several studies have noted an inverse association between osteoporosis and osteoarthritis of the knee and hip.102 A history of unilateral knee injury has been strongly associated with ipsilateral but not contralateral osteoarthritis of the knee.95 Recreational, low-impact physical activity, including running, does not appear to be associated with knee osteoarthritis in most people, but elite athletes and recreational runners who already have abnormal or injured joints are at increased risk for osteoarthritis.103

66 Osteoarthritis of the hip is more weakly associated than the knee with obesity, hip injury, and Heberden’s nodes, but is rather strongly associated with developmental disorders that may affect the shape of the hip joint, including developmental dislocation of the hip and slipped capital femoral epiphysis.102 Osteoarthritis of the knee is associated with decreased survival in persons aged 55 and older.104 Likely explanations for this observation include the association of obesity with both osteoarthritis and mortality and possibly the adverse effects of treatment with nonsteroidal anti-inflammatory drugs (NSAIDs). One study noted excess proportionate mortality from gastrointestinal diseases in persons with osteoarthritis,104 while another demonstrated an increased incidence of gastroduodenal ulcers in subjects with osteoarthritis and knee pain.105 Finally, osteoarthritis of the knee, especially with concomitant pain, often results in long-term activity and mobility limitation.105 Regarding primary prevention, several potentially modifiable risk factors have been identified, including obesity and repetitive joint usage and trauma. Weight loss can lower risk for the development of osteoarthritis and probably also slows disease progression.106 Reduction in the number of injuries and reduction of exposure to repetitive mechanical stress on the joints in the work place should be beneficial. While early treatment of conditions such as developmental dislocation of the hip, slipped epiphysis, and various other developmental and acquired bone and joint disorders may curtail the development of, or limit the extent of, osteoarthritis, studies suggest the importance of prevention of these disorders in the first place rather than relying on treatment alone. For example, Pinczewski and colleagues107 reported that 70% of persons with anterior cruciate ligament injuries treated surgically with a patellar tendon graft developed radiological evidence of osteoarthritis within seven years. Screening tests for osteoarthritis are not presently available. However, two biomarkers may emerge as candidates for screening. Elevated levels of cartilage oligomeric matrix protein (COMP), a glycoprotein found in cartilage as well as in ligaments, tendons, menisci, and synovial tissue, have been identified in persons with knee osteoarthritis compared with those unaffected, as well as persons with osteoarthritis-related collagen gene mutations, synovitis, and inflammatory arthropathy due to rheumatoid arthritis.108,109 Sowers and colleagues110 reported that baseline hsC-reactive protein (hsC-RP)

Musculoskeletal Disorders

concentrations increased in a progressive manner with each interval of the Kellgren-Lawrence scale for prevalent knee osteoarthritis or incident osteoarthritis and in women with bilateral knee osteoarthritis compared with unilateral osteoarthritis of the knee. Unfortunately, neither COMP nor hsC-RP is specific for osteoarthritis. Intervention strategies aimed at controlling the symptoms of pain, stiffness, and the functional limitations associated with knee osteoarthritis have been organized into a set of clinical recommendations (Table 66-4).111 The first recommendation indicates that optimal management incorporates a combination of nonpharmacological and pharmacological modality. Recommended nonpharmacological modalities include exercise programs and physical therapy, weight loss, and wedged insoles, frequently accompanied by a pharmacological intervention. Educational activities include learning appropriate methods of lifting and bending to maintain and improve muscle strength, flexibility, and range of motion.112–115 Whether acupuncture is effective as a treatment for osteoarthritis remains an open question.116 If medication is used, acetaminophen (paracetamol) is generally the first choice rather than NSAIDs because of its better overall gastrointestinal system safety profile.117 Recently, the use of therapeutic agents for osteoarthritis has become more complex in regard to weighing the benefits from relief of pain and disability versus the possibility of adverse events. There is support for the use of NSAIDs, although the addition of a gastroprotective agent, such as a histamine2 receptor antagonist, may be required to reduce the risk of duodenal and gastric ulcers.111 Until recently, alternative recommendations to NSAIDs would have included COX 2 selective inhibitors,118 but recent reports of adverse cardiovascular events have led to a worldwide withdrawal of some products.119 Slow-acting agents for osteoarthritis, including glucosamine sulfate, chondroitin sulfate, diacerein, and hyaluronic acid, have been evaluated largely in terms of their effect on pain rather than structure.120,121 This has led to the conclusion that these agents have efficacy in the treatment of pain, but at this time there is minimal knowledge of their effect on structure.111 Joint replacement has become the intervention of choice for individuals with severe pain and disability refractory to nonsurgical treatment.111,122 The success of total hip replacement has been recognized for many years, while more recently it has been concluded that total knee replacement is also safe and effective in reducing pain and improving function and quality of life.122

TABLE 66-4. RECOMMENDATIONS FOR MANAGEMENT OF OSTEOARTHRITIS OF THE KNEE BASED ON BOTH EVIDENCE AND EXPERT OPINION 1 2

3 4 5 6 7 8 9

1129

Optimal management of knee osteoarthritis requires a combination of nonpharmacological and pharmacological treatment modalities. The treatment of knee osteoarthritis should be individually tailored, taking into account: (a) Knee risk factors (obesity, adverse mechanical factors, physical activity) (b) General risk factors (age, comorbidity, polypharmacy) (c) Level of pain intensity and disability (d) Signs of inflammation (e) Location and degree of structural damage. Nonpharmacological treatment of knee osteoarthritis may include education, exercise, appliances (sticks, insoles, knee bracing), and weight reduction Paracetamol is the oral analgesic to try first and, if successful, the preferred long-term oral analgesic. Topical applications (NSAID, capsaicin) have clinical efficacy and are safe. NSAIDs should be considered in patients unresponsive to paracetamol. In patients with an increased gastrointestinal risk, nonselective NSAIDs and effective gastroprotective agents should be considered. Opioid analgesics, with or without paracetamol, are useful alternatives in patients in whom NSAIDs, are contraindicated, ineffective, and/or poorly tolerated. Symptomatic slow-acting drugs (glucosamine sulfate, chondroitin sulfate, avocado-soybean-unsaponifiable [ASU], diacerein, and hyaluronic acid) reduce symptoms and may modify structure. Intra-articular injection of long acting corticosteroid is indicated for flare of knee pain, especially if accompanied by effusion.

Source: Data from Jordan KM, Arden NK, Doherty M, et al. EULAR Recommendations 2003: an evidence based approach to the management of knee osteoarthritis: Report of a Task Force of the Standing Committee for International Clinical Studies Including Therapeutic Trials (ESCISIT). Ann Rheum Dis. 2003;62:1145–55.

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Noncommunicable and Chronic Disabling Conditions

Rheumatoid Arthritis Rheumatoid arthritis is a chronic inflammatory disease thought to be of autoimmune etiology, characterized by proliferative synovitis that results in bony erosion and destruction of articular cartilage; these processes give rise to typical articular deformities. The clinical symptoms include stiffness, pain, and swelling of multiple joints, most commonly the small joints of the hands and wrists. Rheumatoid arthritis usually develops over time in a symmetric fashion. It also may be associated with a variety of extra-articular manifestations that incorporate many characteristics of a systemic disease including vascular, renal, and eye disease complications. The clinical course is highly variable. Persistent rheumatoid arthritis is associated with progressive disability123,124 and earlier mortality.125 Although some studies suggest that, overall, the disease course may be more benign than previously thought,126 other studies indicate that the impact of inflammation on the vasculature is substantial, and that the use of treatments to control inflammation may improve quality of life and functioning but not vascular integrity.125 The lifetime incidence of rheumatoid arthritis is between 0.5% and 1.0%, with an annual incidence of 25–50/100,000.127 Prevalence and incidence estimates of rheumatoid arthritis have been limited by the absence of a gold standard against which classification systems can be evaluated. Current classification systems have evolved over time from the 1958 American Rheumatism Association (ARA) criteria128 and the New York criteria129 to the current 1987 criteria of the American College of Rheumatology (ACR).130 A recent study used data from the Third National Health and Nutrition Examination Study (NHANES III) to compare rheumatoid arthritis prevalence estimates in persons over the age of 60 using three different rheumatoid arthritis classifications.131 The prevalence was about 2% using each set of criteria. In NHANES III, the prevalence of rheumatoid arthritis was approximately 1.5 times greater in older women than older men.131 Prevalence increased with age, with 1.6–1.9% affected in the 60–70 year age range compared to 2.5–2.8% in persons 70–80, suggesting there is more rheumatoid arthritis in older birth cohorts.127 In the Olmsted County, Minnesota, catchment area, the incidence of severe extra-articular manifestations was 1 per 100 person-years of follow-up; approximately 15% of rheumatoid arthritis patients had these manifestations at any given time.132 Several American Indian tribes have particularly high prevalences of rheumatoid arthritis, including the Yakima of central Washington State and the Mille-Lac Band of Chippewa in Minnesota. Asians, including Japanese and Chinese, appear to have lower prevalences than Whites.133 Genetic factors have an important etiologic role in rheumatoid arthritis.134 The disease exhibits familial aggregation and a higher concordance rate in monozygotic than in dizygotic twins. Studies have demonstrated a strong association between the class II major histocompatibility antigen HLA-DR4 and rheumatoid arthritis; in whites, the relative risk for this association exceeds 4.0.135,136 This association occurs across race/ethnic groups, with the exceptions of the Yakima Indians of Washington State, Asian Indians, Greeks, and Israeli Jews. Further, the HLA-DR4 subtype has been associated with the extra-articular manifestations.134 In those who lack HLA-DR4, there is frequently an association between rheumatoid arthritis and HLA-DR1. HLA-DR10 and HLA-DR14 may also be associated with rheumatoid arthritis.137 Other genetic markers of immunologic status are being investigated.134 The role of infectious agents as etiologic factors in rheumatoid arthritis has been extensively explored, but no specific agent has been implicated.138 Declining incidence among women, but not men, was noted between the periods 1960 through 2000; these findings were consistent with a protective effect of oral contraceptives first reported by the Royal College of General Practitioners Oral Contraceptive Study.139 A meta-analysis confirmed a protective effect of oral contraceptive use on the development of rheumatoid arthritis, with a pooled relative risk of 0.70.140 It is thought that oral contraceptives, and possibly noncontraceptive hormone replacement therapy, modifies the course of rheumatoid arthritis by preventing the progression of mild to severe disease, rather than preventing the development of disease. Rheumatoid arthritis is associated with excess mortality, with a standardized mortality ratio of about 170.133,141 Causes of death that

are more frequent in persons with rheumatoid arthritis include respiratory and infectious diseases and gastrointestinal disorders. It is likely that some of the excess mortality is related to complications of therapy. Persistent synovitis, the presence of rheumatoid factor, extraarticular involvement, functional losses, low levels of education, and the HLA-DR4 epitope have been associated with increased mortality and excess disability.142,143 Disability is a major concern among persons with persistent rheumatoid arthritis. A meta-analysis found that physical demands of the job, older age, low functional capacity, and lower educational attainment are factors that predict work disability. There was little evidence that biomedical factors, personal factors (i.e., coping strategies) and adaptive programs at work are important in contributing to or ameliorating work disability.144 Methods of primary prevention or screening for rheumatoid arthritis are not currently available. First-line medical therapy incorporates salicylates or NSAIDs. These drugs are anti-inflammatory, analgesic, and antipyretic, and lead to improvement in pain and swelling. However, there is no evidence that they affect the underlying disease process. It is now recommended that second-line therapies that may modify the course of the disease be initiated early in persons with persistent synovitis.145 Such therapies include antimalarial drugs, sulfasalazine, methotrexate, intramuscular gold, D-penicillamine, azathioprine, and cyclosporin A. Oral corticosteroids probably have a role in management of the rheumatoid arthritis patient as an adjunct to remittive therapy.145

Foot Disorders in Older Adults About three-fourths of fully active older adults complain of painful feet.146,147 Among institutionalized adults, foot problems are one-fifth as common, indicating an important etiologic role for stress on the feet from ordinary physical activity. In a survey in which feet were professionally examined in a sample of community-dwelling older adults in Massachusetts,148 the prevalence of foot disorders was higher still, including 75% for toenail disorders, 60% for lesser toe deformities, 58% for corns and calluses, 37% for bunions, and 36% for signs of fungal infection, cracks/fissures, or maceration between toes. Toenail conditions, fungal symptoms, and ulcers or lacerations were more common in men, while bunions and corns and calluses were more frequent in women. Foot pain, especially if chronic and severe, can be a significant cause of disability.149,150 In addition, even slight deformities of the foot can lead to impaired proprioception, skeletal problems, changes in gait and balance, and pain, resulting in increased risks for falls151 and foot fracture.152 The prevalence and severity of foot conditions increase with age, as the aging process can result in neuropathy, ischemia, and atrophy of the planter fat pad.153 With age, the skin of the foot may become dry, scaly, thin, and less elastic, the dermis may atrophy, and the nail plate tends to become thin. These changes predispose to a variety of conditions, such as callus formation, plantar keratosis, heel pain, susceptibility to infection, and other skin and nail problems. Chronic conditions such as diabetes, peripheral vascular disease, and arthritis often involve the feet,153 and obesity has been reported to be a risk factor for foot pain.150 A variety of static and functional deformities of the feet, such as hallus valgus, digiti flexus, and trophic changes, are related to degenerative disease. The majority of painful conditions of the foot seen by orthopedists originate in soft tissues such as muscles, ligaments, tendons, nerves, and blood vessels. Articular and skeletal disorders of the feet may result from congenital abnormalities, infections, neoplasms, and trauma,154 as well as from osteoarthritis, rheumatoid arthritis, and, less commonly, gout. Improperly fitting shoes and other stresses on the foot can lead to bunions, hammer toes, and claw toes. Prevention at all levels includes appropriate treatment of diseases that can involve the feet, the wearing of proper shoes, wearing socks or stockings, bathing the feet frequently, avoidance of obesity, protection against infection and trauma to the feet, and proper care of toenails.155 Once foot problems occur, soft, well-padded shoes should

66 be worn to relieve pressure in sore areas. Pads, moleskin, lamb’s wool, and hammer-toe pads applied to localized areas of soreness may be helpful. In most instances, these simple methods can reduce much of the discomfort associated with foot problems. In some cases, rest, application of heat and cold, specific exercises, and use of special corrective shoes may be needed.154 Almost half of all people with foot disorders are not receiving care for the problem.155

Paraplegia and Quadriplegia The most common cause of paraplegia and quadriplegia in Western countries is vertebral fractures and dislocation from trauma. Complete transection of the spinal cord results in paralysis of all muscles supplied by motor neurons below the level of the lesion and in the loss of skin sensation in all areas supplied by sensory neurons below the lesion. Because neurons in the central nervous system do not regenerate, both motor and sensory paralysis is permanent. The effect on the patient, family, and friends is immediate and enormous. Most affected individuals were previously independent and must learn to cope with partial or complete paralysis, loss of sensation in major parts of the body, and loss of voluntary control over body functions, frequently including bowel and bladder dysfunction and loss of sexual function. The patient’s work, marriage, family, and social relationships are likely to be substantially altered.156 In the United States, nearly 200,000 people are disabled with spinal cord injuries, with 11,000 new cases occurring each year157 Spinal cord injuries occur most frequently in persons ages 15–40 years, are 3–4 times more common in males than females, and are more frequent in blacks than whites.157–159 In developed countries, motor vehicle accidents, especially those involving motorcycles, are by far the leading cause of these injuries. One study in the United States160 found that among those whose spinal cord injury occurred as a result of being in a motor vehicle, 70% were involved in a vehicle rollover, and 39% were ejected from the vehicle. Only 25% reported using seatbelts. In another study161 drugs and alcohol had been used before the injury in at least 25% of cases. Other major causes are falls (especially in the elderly); sports and recreational activities such as diving in shallow water, injuries sustained during gymnastics and hard contact sports; violence-related injuries; and self-inflicted injuries.158,159,161,162 In developed countries the proportion of spinal cord injuries attributable to sports and recreational activities has increased in recent years, while the proportion of work-related accidents has decreased in many countries as safer work practices have been implemented. In developing countries, other common causes include falling from trees, carts, and bicycles, and carrying heavy loads on the head; violence has become a more common cause in recent years.158 The most important primary prevention measures in developed countries are those that reduce the likelihood of motor vehicle accidents and lessen the risk of injury if accidents do occur. These measures include not driving after drinking alcoholic beverages; reduced speed limits; use of seat belts, headrests and airbags; and wearing of helmets by motorcyclists. Prevention of falls in the elderly and safety measures in occupational and recreational settings are also important. For instance, in high school and collegiate football, rules banning “spearing” or initial contact with the top of the helmet when making a tackle have markedly reduced the frequency of permanent cervical quadriplegia resulting from participation in that sport.163 In Canada, a decline in the number of major spinal cord injuries has been noted in ice hockey following the implementation of educational programs and rules changes; injuries from being checked or pushed from behind into boards were especially affected.164 In developing countries, education on safe tree climbing and on carrying heavy objects is needed.158 The number of survivors with paraplegia and quadriplegia has greatly increased because of medical and surgical advances. Since most of those injured are in their late teens and early adult years, enormous costs and very long-term severe disability ensue. Lifetime costs per patient generally range from about $500,000 to over $2 million.162 In addition to psychological problems, the greatest difficulties are in self-care, locomotion, obtaining employment, and medical

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complications. Common medical complications include urinary tract infections, pressure sores, cardiac and vascular problems, and autonomic dysreflexia.165 Patient education and good nursing care can reduce the likelihood of many of these complications, especially pressure sores and urinary tract infections.158 The main object of tertiary prevention is to return the affected person to maximum physical and social functioning. Both physical and psychological adjustments are needed. Accordingly, in addition to specialists in orthopedic and neurological surgery, other specialists that should be involved in therapy of these patients include occupational and physical therapists, psychiatrists, orthotics specialists, urologists, and vocational counselors. Long leg braces, crutches, and gait training may help highly motivated paraplegics with low-level lesions return to walking and may even enable them to become selfsupporting. Because many paraplegics drive cars, wheelchair accessibility of public buildings is becoming increasingly important.166 Sexual counseling also may be helpful for many.

DISORDERS PRIMARILY OF CHILDREN

Scoliosis Scoliosis, or abnormal lateral curvature of the spine associated with rotation of the vertebrae, is the most common cause of spinal deformity in North American children.167 Of the various forms of scoliosis, the most common and serious is adolescent idiopathic scoliosis. About 2–3% of children develop curves of 10° or more before growth ceases, and about 2–3 per 1000 children develop curves of 30° or more.168,169 Persons left with significant curvature frequently develop spinal osteoarthritis in adulthood; lung and heart complications may occur. Also, further curve progression sometimes takes place in adults. Scoliosis is most frequently diagnosed around the ages of 11–14 years in girls and 14–16 years in boys. The ratio of female to male cases seen at surgery is as high as 5–1, but mild curves of less than 15° are found with almost equal frequency in both sexes. Once girls have reached menarche, their risk for developing scoliosis is reduced.170 Although surgical series have indicated that scoliotic curves are most common at the thoracic level, screening programs identifying children who do not necessarily seek medical care have found that the peak frequency is at the thoracolumbar level.171 The risk for scoliosis in first-degree relatives of cases is about 3–4 times higher than in other children.172 Twin studies indicate a genetic etiology for both the development and progression of scoliosis,173 but the mode of inheritance is uncertain. Little is known of other risk factors for development of the disease. Some evidence suggests that prepubertal standing height, sitting height, recent increase in sitting height, and early age at gain in sitting height are predictive,174 and that children who are skeletally more mature, taller, and leaner at the onset but not at the end of puberty are most likely to be affected.170,176 These observations suggest that the scoliotic spine grows faster and earlier than the normal spine.170,176,177 Impaired visual and vestibular functioning, defects in proprioceptive postural control, asymmetric muscle activity, unequal leg length, high concentrations of calcium in paraspinal muscles, collagen disorders, and defects of the elastic fiber system may be etiologically involved, but evidence is not conclusive.176,178,179 Most curves do not progress. The main risk factors for progression of existing curves are double curves as opposed to single curves, thoracic curves as opposed to curves at lower levels, curves of greater magnitude, absence of a sacral tilt, limb length inequality, early chronological age, skeletal immaturity, and female sex.180,181 Because so little is known of the etiology of adolescent idiopathic scoliosis, primary prevention is not feasible. However, detection of early disease by screening is being undertaken in many places and screening for scoliosis is required by law in some states in the United States. It is assumed that with early detection, affected children can be treated by conservative means and thereby avoid surgery. The traditional screening test for scoliosis has been the forward-bend test, in which the child’s back is examined while he

Noncommunicable and Chronic Disabling Conditions

Slipped Capital Femoral Epiphysis Slipped epiphysis of the head of the femur, in which epiphysis of the head of the femur is displaced backward and downward off the diaphysis, is primarily a disease of adolescents. It is closely related to the adolescent growth spurt and does not occur once the epiphysis is fused to the shaft of the femur. In the northeastern United States about 1 in 800 males and 1 in 2000 females will be diagnosed as having a slipped epiphysis before they reach 25 years of age.189 The magnitude of the male excess varies from one geographical area to another and appears to have decreased over time. The median age at diagnosis is 13 years for males and 11–12 years for females; the earlier age in females corresponding to their earlier onset of puberty. Blacks are affected more frequently than whites. In most studies in northern latitudes, symptoms begin more frequently in spring and summer than in fall and winter.190,191 A large proportion of children with slipped epiphysis are markedly overweight;192,193 about half are at or above the 95th percentile for their age (Fig. 66-2). Children with slipped epiphysis tend to have undergone slower-than-average skeletal maturation and to be tall for their age at the time of diagnosis.194 Familial aggregation of cases has been reported,195 but it is not clear whether this aggregation is primarily attributable to inherited characteristics or to common environmental factors. Many of these risk factors are related either to a weakening of the epiphyseal plate, such as occurs during periods of rapid growth, or to increased shearing stress on the plate.196 Animal experiments indicate that a deficit of sex hormones relative to growth hormone brings about a widening of the epiphyseal plate and a reduction in the shearing force necessary to displace the epiphysis.197 Higher body weight increases the shearing stress on the epiphyseal plate, and also

Males (49.1)

Females (49.2)

50 40 30 20 10

(5.1)

(5.0) Ex pe c te d

Ob se rv e d

Ex pe c te d

0 Ob se rv e d

or she bends forward from the waist. The rotation that accompanies the lateral curvature in scoliosis results in posterior prominence of the ribs on the concave side of the curvature, so that a “rib hump” is often apparent on forward bending. The forward-bend test has good specificity but fairly low sensitivity. Moiré topography, in which a photograph of the back is used to measure the degree of topographic asymmetry, and the humpometer, which measures back contour and shape, are not recommended as screening procedures; despite their high sensitivity, their relatively low specificity results in excessive numbers of false postitives.177,182 The inclinometer (scoliometer), which measures trunk asymmetry as an indicator of trunk rotation, has been reported to have high sensitivity and fairly good specificity, but it has not been used much and only limited evaluation has been undertaken.183,184 Most school screening programs use the forward-bend test. In the United States, school screening programs are identifying large numbers of children with possible spinal curvatures. Positive screening tests are followed up with x-ray examination for more definitive diagnosis. Curves of over 5° are monitored by further x-ray examination every few months. Should a curve progress to 20°–25°, treatment is generally indicated to try to prevent further progression. Braces are most commonly used for curves of 25°–40°, while surgery to correct at least part of the deformity and to halt further progression is often indicated for curves of 40° or greater, particularly in children who are likely to continue growing. Many questions have arisen about the desirability of widespread screening for scoliosis.185–187 First, it is uncertain that school screening programs have brought about a reduction in the prevalence of severe deformities and thereby the number of operations needed. In particular, the efficacy of conservative treatment in preventing progression is uncertain. Also, many children screened as positive are not subsequently seen for definitive diagnosis. On the other hand, many false positives occur, resulting in referral for far too many x-ray examinations as well as a great deal of medical expense and anxiety. Better training and evaluation of the staff who do the screening may be needed.169,185 The optimal ages for screening and whether males should be screened at all have not been determined. Because of these uncertainties about the effectiveness of screening for scoliosis, the U.S. Preventive Services Task Force was unable to recommend for or against routine screening of adolescents for scoliosis.188

Percentage

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Figure 66-2. Percentage of children with slipped epiphysis with weights at or above 95th percentile for their age. (Source: Adapted from Kelsey JL, Acheson RM, Keggi KJ. The body builds of patients with slipped capital femoral epiphysis. Am J Dis Child. 1972;124:276–81.)

is associated with an increased tilting backwards of the femur, further increasing the sheering stress.198 Children with the unusual combination of being overweight and undergoing slow maturation would appear to be at high risk, and these children should be carefully watched for slipped epiphysis. The only known means of primary prevention is avoidance of obesity in adolescents. No screening tests for slipped epiphysis exist, but the diagnosis should be suspected in adolescents who have a limp and hip or knee discomfort, especially if there is restriction of internal rotation of the hip. X-ray examination should be performed immediately to confirm the diagnosis. The condition is bilateral in 20–25% of cases. Decision analysis has indicated that prophylactic pinning of the asymptomatic contralateral hip should be considered in children with a slipped epiphysis in one hip.199 At a minimum, the contralateral hip should be carefully monitored, especially for those whose first slipped epiphysis occurred at an early age.193,200 Slippage that is stable, meaning that weight bearing is possible with or without crutches, and slight degrees of slippage that are treated early by hip pinning have a favorable prognosis, whereas cases diagnosed late and that involve severe displacement are more likely to result in early onset of osteoarthritis of the hip and permanent disability despite treatment.

Fractures in Children Each year about 1 in 20–25 children fracture or dislocate a bone.201,202 One-third of children fracture at least one bone before 17 years of age.203 In childhood, fracture incidence rates increase until about ages 11 years in females and 14 years in males,203 with males at higher risk throughout childhood and adolescence.203–205 In one series204 over one-half of childhood fractures occurred while the child was at play, participating in a sport, or in a traffic accident. In another series,205 36 % of childhood fractures occurred during sports and leisure-time activities, and 3.5 % were the result of assaults. The U.S. Health Interview Survey indicates that the bones most frequently fractured in children are the hand, radius and ulna, carpals, skull and face, clavicle, foot and ankle, and humerus.1 Fractures of the phalanges of the hands often occur during contact sports, skating, playing and fighting, while fractures of the distal forearm tend to result from a fall on an outstretched hand, particularly during ball games, and bicycle, playground, and skateboard accidents. Carpal and metacarpal fractures most often result from fighting, falls, bicycle accidents, ball games, skiing, and skating. Fractures of the clavicle frequently occur during falls, ball games, and contact sports. Ankle fractures most often result from the foot being caught in a bicycle wheel and from falls, and also from ball games, skateboards, roller skates, mopeds, motorcycles, skiing, skating, cycling, and playing.204 Tall and heavy children as well as those who smoke may be at elevated risk for childhood fractures.206

66 The primary prevention of fractures in children depends mainly upon reducing the number of sports and recreational injuries, automobile and bicycle accidents, falls, child-battering injuries, and other traumas. The use of impact absorbing surfaces in playgrounds could reduce the frequency of fractures at many sites, and wearing wrist guards during certain sports could reduce the risk of fractures of the radius and ulna.205 Fractures usually heal rapidly in children; the younger the age, the more rapid the healing. However, if the growth plate is involved in the fracture, growth in that bone may be adversely affected, particularly if a crushing injury has occurred. Other complications are rare but may include infection, delayed union, nonunion, avascular necrosis, and malunion. Prevention of these complications involves thorough cleansing and removal of all dead and contaminated tissue from an open (compound) fracture and competent initial treatment of the fracture.

Developmental Dysplasia/Dislocation of the Hip In developmental dysplasia/dislocation of the hip the head of the femur is displaced completely or partially out of the acetabulum. Partial displacement is sometimes referred to as subluxation of the hip. Because many dislocations tend to occur immediately after birth or occasionally later during the first year of life, the term “developmental dislocation/dysplasia of the hip” is now frequently used instead of the older term “congenital dislocation of the hip.”207 In about 80% of cases the diagnosis is made shortly after birth, and in the remaining cases the diagnosis is made later, especially when the child starts to walk. Although it is possible that some of these late-diagnosed cases represent dislocations missed around the time of birth, there is good evidence that some dislocations do develop after birth.207 Developmental dislocation/dysplasia of the hip includes the following categories: (a) dislocated hips, which are hips dislocated in a resting position, with the dislocation present at birth; (b) located but unstable or dislocatable hips, which are hips that rest in a located position but are unstable or dislocatable on clinical examination and provocative maneuvers; (c) dysplastic hips, in which the acetabulum is shallow or dysplastic.207 The prevalence of developmental dysplasia/dislocation of the hip varies considerably from one geographic area to another. Frequencies ranging from 1 per 1000 to 10 per 1000 births have been reported in most North American and Western European populations and in Israel, Australia, and New Zealand. Higher rates of from 10 per 1000 to 100 per 1000 have been observed in the Navajo, Apache, and CreeOjibwa Indians of North America, in the Lapps, and in the populations of Hungary, northern Italy, Brittany, and the Faroe Islands. Developmental dysplasia/dislocation of the hip is rare among blacks in South Africa, the West Indies, and Uganda, as well as among Chinese living in Hong Kong.176 Although the frequency of developmental dysplasia/ dislocation of the hip has been reported to be rising in certain areas, much of the apparent rise may be attributable to more extensive screening after birth and to increased awareness by physicians. In North America, girls are affected more frequently than boys in the ratio of about 6 to 1. Rates are also higher in whites than blacks. In most areas, a greater than expected number of cases are encountered in children born in late fall and winter than in summer.208 Familial aggregation of cases occurs; both hereditary and environmental factors contribute to the familial excess.209,210 On the average, infants with developmental dysplasia/dislocation of the hip have had longer gestation periods than other infants and are considerably more likely to have been born by breech delivery than other infants.208,210 Position in utero may be involved in the etiology, since breech position in utero elongates the ligament of the hip joint capsule by persistent upward pressure of the greater trochanter.211 Ligamentous and capsular laxity are also probably predisposing factors.212 No feasible methods of primary prevention are known. In regard to secondary prevention, it is now routine to examine newborn infants for developmental dysplasia/dislocation of the hip. Without prompt treatment the affected leg may be shorter, the child may limp, gait abnormalities may develop, surgery may be required, and osteoarthritis of the hip is likely to occur in young adulthood. Two screening tests

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have generally been used: the Ortolani and the Barlow. The Ortolani test involves placing the hip in flexion and gently adducting and then abducting the hip. The test is considered positive if a palpable jerk and audible clunk are heard as the head of the femur returns to the acetabulum. Some practitioners also consider an audible click to constitute a positive test. In the Barlow test, gentle downward pressure is exerted over the lesser trochanter with the hip in flexion and adduction; the unstable hip shifts from the acetabulum, and a sensation similar to the Ortolani sign is produced. When the leg is allowed to abduct, the hip is reduced. About half of the hips noted to be unstable or dislocatable immediately after birth become stable within a few days;213 thus, these tests are often repeated at around three weeks. Infants showing positive results then are treated with braces, splints, or harnesses for 2–4 months. X-ray examination of the hip is of limited value in the newborn, but is an important diagnostic tool in children past the age of 3 months. Routine checks on hips of these infants should be done until they are walking well. If the disease is diagnosed after the neonatal period, surgery is generally required, and the prognosis is poorer.214 Despite the routine use in many locales of screening tests for developmental dysplasia/dislocation of the hip, many questions have arisen regarding the effectiveness of screening by the Ortolani and Barlow tests.215–217 For instance, it appears that incidence rates of developmental dysplasia/dislocation of the hip requiring prolonged treatment are no lower now than they were before screening became widespread. Both the sensitivity and specificity of the screening tests are poor. In one study,215 only one-third of genuine cases were detected, and the ratio of false positives to true positives was 10 to 1. Thus, for every one infant who benefits from splinting as a result of a positive test, 10 infants undergo unnecessary splinting. Furthermore, there is no consensus on indications for treatment, the timing of treatment, and the type of splint to be used. The question has arisen as to whether the screening procedures may themselves induce hip dislocation. Although these screening tests require experienced examiners for proper performance and interpretation, inexperienced examiners are often used, thus increasing both false-positive and false-negative rates. Better knowledge of which hips will spontaneously stabilize would allow better decisions about the cases who should receive immediate treatment. Disagreement exists about the significance of a soft audible or palpable click without evidence of abnormal movement between the femoral head and acetabulum.218 More data are needed to resolve these issues, but in the meantime, routine screening with these tests is recommended by most professional groups.219,220 In recent years, ultrasound, which provides a defined image of the bony and cartilaginous neonatal hip, has become widely available for screening for developmental dysplasia/dislocation of the hip. Although it was initially believed that it might alleviate some of the problems with the Barlow and Ortolani tests,221,222 its use as a routine screening test in all infants has not been found to be cost-effective. Even its use as a screening test in high-risk infants is controversial. Among its limitations are its high cost, the large proportion of hips testing positive on screening that develop normally, and the tendency of some cases to occur after the neonatal period.219,220,223,224 In addition, while adequate inter-observer agreement in reading ultrasound scans may be obtained with proper training, producing the scans is subject to even more variability. Thorough training and more attention to detail are needed to improve this situation.225 Although ultrasound may be of some value in following up infants who show instability on the Ortolani or Barlow test,217,226 professional groups do not recommend routine screening with ultrasound for either all infants or those at high risk.219,220

CONCLUSION

The extent to which musculoskeletal disorders may be prevented varies considerably from one disorder to another. Some methods of primary prevention are possible for back disorders, osteoporosis,

1134

Noncommunicable and Chronic Disabling Conditions

osteoarthritis, foot disorders, paraplegia and quadriplegia, slipped epiphysis, and fractures. However, these preventive measures frequently involve changes in individual behavior that are difficult to achieve. Screening tests for scoliosis, congenital dislocation of the hip, and osteoporosis are available. Although the tests for scoliosis and congenital dislocation of the hip are widely used at present, many questions regarding their efficacy remain unresolved. Secondary and tertiary prevention are the levels more frequently used for the major musculoskeletal disorders of adults. However, with the exception of reconstructive joint surgery, secondary and tertiary prevention for such common problems as back pain and the arthritic disorders often have met with only limited success. Because of the chronicity of most of the common musculoskeletal conditions and the frequent reliance on only partially successful secondary and tertiary prevention measures, it is not surprising that musculoskeletal disorders have such a major effect on the quality of life and are associated with such high individual and societal costs. Improving the quality of life of affected individuals and further development and evaluation of screening tests will remain important in the management of musculoskeletal disorders, but it is also hoped that more emphasis will be placed on identification of feasible ways of preventing these disorders from occurring in the first place. Since the elderly are most frequently affected by musculoskeletal disorders and since the numbers of elderly will be increasing greatly over the next several decades, development of better methods of prevention at all levels is an urgent public health concern.

REFERENCES

1. Holbrook TL, Grazier K, Kelsey JL, et al. The Frequency of Occurrence, Impact, and Cost of Musculoskeletal Conditions in the United States. Chicago: American Academy of Orthopaedic Surgeons; 1984. 2. Praemer A, Furner A, Rice DP. Musculoskeletal Conditions in the United States, 2nd Edition. Rosemont IL: American Academy of Orthopaedic Surgeons; 1999. 3. The Bone and Joint Decade: www.usbjd.org/about/index.cfm? pg=fast.cfm, 2005. 4. Andersson GBJ. Epidemiology of low back pain. Acta Orthop Scand Suppl. 1998;281:28–31. 5. Deyo RA, Weinstein JN. Low back pain. New Engl J Med. 2001;344:363–70. 6. Croft PR, Macfarlane GJ, Papageorgiou AC, et al. Outcome of low back pain in general practice: a prospective study. BMJ. 1998;316: 1356–9. 7. Snook SH. Low back pain in industry. In: White AA III, Gordon SL, eds. Symposium on Idiopathic Low Back Pain. St. Louis: CV Mosby; 1982. 8. Kelsey JL, Githens PB, White AA III, et al. An epidemiologic study of lifting and twisting on the job and risk for acute prolapsed lumbar intervertebral disc. J Orthop Res. 1984;2:61–6. 9. Lüra JP, Shannon HS, Chambers LW, et al. Long-term back problems and physical work exposures in the 1990 Ontario Health Survey. Am J Public Health. 1996;86:382–7. 10. Hoogendoorn WE, Bongers PM, de Vet HC, et al. Flexion and rotation of the trunk and lifting at work are risk factors for back pain: results of a prospective cohort study. Spine. 2000;25:3087–92. 11. Leboeuf-Yde C. Smoking and low back pain. A systematic literature review of 41 journal articles reporting 47 epidemiologic studies. Spine. 1999;15:1463–70. 12. Kelsey JL, Githens PB, O’Connor T, et al. Acute prolapsed lumbar intervertebral disc: An epidemiologic study with special reference to driving automobiles and cigarette smoking. Spine. 1984;9: 608–13. 13. Pope MH, Magnusson M, Wilder DG. Kappa Delta Award. Low back pain and whole body vibration. Clin Orthop Relat Res. 1998;354: 241–8.

14. Lings S, Leboeuf-Yde C. Whole-body vibration and low back pain: a systematic, critical review of the epidemiological literature 1992–1999. Int Arch Occup Environ Health. 2000;73:290–7. 15. Krause N, Rugulies R, Ragland DR, et al. Physical workload, ergonomic problems, and incidence of low back injury: a 7.5-year prospective study of San Francisco transit operators. Am J Ind Med. 2004;46:570–85. 16. Heliovaara M. Epidemiology of Sciatica and Herniated Lumbar Intervertebral Disc. Helsinki: Publications of the Social Insurance Institution, Finland, 1988. 17. Leboeuf-Yde C. Body weight and low back pain. A systematic literature review of 56 journal articles reporting on 65 epidemiologic studies. Spine. 2000;15:226–37. 18. Hoogendoorn WE, van Poppel MN, Bongers PM, et al. Systematic review of psychosocial factors at work and private life as risk factors for back pain. Spine. 2000;25:2114–25. 19. Daltroy LH, Iversen MD, Larson MG, et al. A controlled trial of an educational program to prevent low back injuries. New Engl J Med. 1997;337:322–8. 20. Lagerström M, Hansson T, Hagberg M. Work-related low-back problems in nursing. Scand J Work Environ Health. 1998;24: 449–64. 21. Jellema P, van Tulder MW, van Poppel MN, et al. Lumbar supports for prevention and treatment of low back pain: a systematic review within the framework of the Cochrane Back Review Group. Spine. 2001;26: 377–86. 22. Lahad A, Malter AD, Berg AO, et al. The effectiveness of four interventions for the prevention of low back pain. JAMA. 1994;272: 1286–91. 23. Porter JM, Gyi DE. The prevalence of musculoskeletal troubles among car drivers. Occup Med. 2002;52:4–12. 24. Tubach F, Leclerc A, Landre MF, et al. Risk factors for sick leave due to low back pain: a prospective study. J Occup Environ Med. 2002;44:451–8. 25. Deyo RA, Diehl AK. Psychosocial predictors of disability in patients with low back pain. J Rheumatol. 1988;15:1557–64. 26. Cats-Baril WL, Frymoyer JW. Identifying patients at risk of becoming disabled because of low-back pain. The Vermont Rehabilitation Engineering Center predictive model. Spine. 1991;16:605–7. 27. Malmivaara A, Häkkinen U, Aro T, et al. The treatment of acute low back pain—bed rest, exercises, or ordinary activity? New Engl J Med. 1995;332:351–5. 28. Loisel P, Abenhaim L, Durand P, et al. A population-based, randomized clinical trial on back pain management. Spine. 1997;22: 2911–8. 29. Hall H, Iceton JA. Back school: An overview with specific reference to the Canadian back education units. Clin Orthop Rel Res. 1983;179: 10–7. 30. Lønn JH, Glomsrod B, Soukup MG, et al. Active back school: prophylactic management for low back pain. A randomized, controlled, 1-year follow-up study. Spine. 1999;24:865–71. 31. Côté P, Cassidy JD, Carroll L. The Saskatchewan Health and Back Pain Survey. The prevalence of neck pain and related disability in Saskatchewan adults. Spine. 1998;23:1689–98. 32. Smedley J, Inskip H, Trevelyan F, et al. Risk factors for incident neck and shoulder pain in hospital nurses. Occup Environ Med. 2003;60:864–9. 33. Croft PR, Lewis M, Papageorgiou AC, et al. Risk factors for neck pain: a longitudinal study in the general population. Pain. 2001;93: 317–25. 34. Yu ITS, Wong TW. Musculoskeletal problems among VDU workers in a Hong Kong bank. Occup Med. 1996;46:275–80. 35. Korhonen T, Ketola R, Toivonen R, et al. Work related and individual predictors for incident neck pain among office employees working with video display units. Occup Environ Med. 2003;60: 475–82.

66 36. Kelsey JL, Githens PB, Walter SD, et al. An epidemiologic study of acute prolapsed cervical intervertebral disc. J Bone Joint Surg. 1984;66A:907–14. 37. Magnusson ML, Pope MH, Wilder DG, et al. Are occupational drivers at an increased risk for developing musculoskeletal disorders? Spine. 1996;21:710–7. 38. Krause N, Ragland DR, Greiner BA, et al. Physical workload and ergonomic factors associated with prevalence of back and neck pain in urban transit operators. Spine. 1997;22:2117–26. 39. Ariens GA, van Mechelen W, Bongers PM, et al. Physical risk factors for neck pain. Scand J Work Environ Health. 2000;26:7–19. 40. Leclerc A, Niedhammer L, Landre MF, et al. One-year predictive factors for various aspects of neck disorders. Spine. 1999;24: 1455–62. 41. Ariens GA, van Mechelen W, Bongers PM, et al. Psychosocial risk factors for neck pain: a systematic review. Am J Ind Med. 2001;39: 180–93. 42. van den Heuvel SC, de Looze MP, et al. Effects of software programs stimulating regular breaks and exercises on work-related neck and upper-limb disorders. Sand J Work Environ Health. 2003;29:106–16. 43. Mclean L, Tingley M, Scott RN, et al. Computer terminal work and the benefit of micrbreaks. Appl Ergon. 2001;32:225–37. 44. Anonymous. Who are candidates for prevention and treatment for osteoporosis? Osteoporos Int. 1997;7:1–6. 45. Villa ML, Nelson L. Race, ethnicity and osteoporosis. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego, Academic Press; 2001. 46. Melton LJ III, Chrischilles EA, Cooper C, et al. How many women have osteoporosis? J Bone Miner Res. 1992;7:1005–10. 47. Peacock M, Turner CH, Econs MJ, et al. Genetics of osteoporosis. Endocr Rev. 2002;23:303–26. 48. Bonjour JP, Rizzoli R. Bone acquisition in adolescence. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego: Academic Press; 2001. 49. Specker BL, Namgung R, Tsang RC. Bone mineral acquisition in utero, during infancy, and throughout childhood. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego: Academic Press; 2001. 50. Sowers M. Premenopausal reproductive and hormonal characteristics and the risk for osteoporosis. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego: Academic Press; 2001. 51. Cauley JA, Salamone LM. Postmenopausal endogenous and exogenous hormones, degree of obesity, thiazide diuretics, and risk of osteoporosis. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego: Academic Press; 2001. 52. Shea B, Wells G, Cranney A, et al. Meta-analysis of calcium supplementation for the prevention of postmenopausal osteoporosis. Endocr Rev. 2002;23:552–9. 53. Cumming RG. Calcium intake and bone mass: a quantitative review of the evidence. Calcif Tissue Int. 1990;47:194–201. 54. Wallace BA, Cumming RG. Systematic review of randomized trials of the effect of exercise on bone mass in pre- and postmenopausal women. Calcif Tissue Int. 2000;67:10–8. 55. Karlsson M. Does exercise reduce the burden of fractures? Acta Orthop Scand. 2002;73:691–705. 56. Law MR, Hackshaw AK. A meta-analysis of cigarette smoking, bone mineral density and risk of hip fracture: recognition of a major effect. BMJ. 1997;315:841–6. 57. Kanis JA, Johansson H, Johnell O, et al. Alcohol intake as a risk factor for fracture. Osteoporosis Int. 2005;16:737–42. 58. Kanis JA, Johansson H, Oden A, et al. A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res. 2004;19:893–9. 59. Papadimitropoulos E, Wells G, Shea B, et al. Meta-analysis of the efficacy of Vitamin D treatment in preventing osteoporosis in postmenopausal women. Endocr Rev. 2002;23:560–9.

Musculoskeletal Disorders

1135

60. Bonaiuti D, Shea B, Iovine R, et al. Exercise for preventing and treating osteoporosis in postmenopausal women. Cochrane Database Syst Rev. 2002;3:CD000333. 61. Wolff I, van Croonenborg HC, Kemper CG, et al. The effect of exercise training programs on bone mass: a meta-analysis of published controlled trials in pre- and postmenopausal women. Osteoporos Int. 1999;9:1–12. 62. Writing Group for the Women’s Health Initiative Investigators. Risks and benefits of estrogen plus progestin in healthy postmenopausal women. Principal results from the Women’s Health Initiative randomized controlled trial. JAMA. 2002;288:321–33. 63. Cummings SR, Black DM, Thompson DE, et al. Effect of alendronate on risk of fracture in women with low bone density but without vertebral fractures: results from the Fracture Intervention Trial. JAMA. 1998;280:2077–82. 64. Cranney A, Guyatt G, Griffith L, et al. Summary of meta-analyses of therapies for postmenopausal osteoporosis. Endocr Rev. 2002;223: 570–8. 65. Ettinger B, Black DM, Mitlak BH, et al. Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxofene. Results from a 3-year randomized clinical trial. JAMA. 1999;282:637–45. 66. Zizic TM. Pharmacologic prevention of osteoporotic fractures. Am Fam Physician. 2004;70:1293–1300. 67. Nelson HD, Helfand M, Woolf SH, et al. Screening for postmenopausal osteoporosis: a review of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2002;137:529–43. 68. Hans D, Dargent-Molina P, Schott AM, et al. Ultrasonographic heel measurements to predict hip fracture in elderly women: the EPIDOS prospective. Lancet. 1996;348:511–4. 69. Nguyen TV, Center JR, Eisman JA. Bone mineral density-independent association of quantitative ultrasound measurements and fracture risk in women. Osteoporos Int. 2004;15:942–7. 70. Tinetti ME. Preventing falls in elderly persons. New Engl J Med. 2003;348:42–9. 71. Schwartz AV, Capezuti E, Grisso JA. Falls as risk factors for fractures. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego: Academic Press; 2001. 72. Cumming RG, Thomas M, Szonyi G, et al. Home visits by an occupational therapist for assessment and modification of environmental hazards: a randomized trial of falls prevention. J Am Geriatr Soc. 1999;47:1397–1402. 73. Cummings SR, Nevitt MC. A hypothesis: the causes of fracture. J Gerontol. 1989;44:M107–M111. 74. Keegan THM, Kelsey JL, King AC, et al. Characteristics of fallers who fracture at the distal forearm, foot, proximal humerus, pelvis, and shaft of the tibia/fibula compared to fallers who do not fracture. Am J Epidemiol. 2004;159:192–203. 75. Schwartz AV, Nevitt MC, Brown BW, Jr., et al. Increased falling as a risk factor for fracture among older women: The Study of Osteoporotic Fractures. Am J Epidemiol. 2005;161:180–5. 76. Faulkner KG, Cummings SR, Black D, et al. Simple measurement of femoral geometry predicts hip fracture: The Study of Osteoporotic fractures. J Bone Miner Res. 1993;8:1211–7. 77. Singh YM, Nagrath AR, Maini PS. Changes in trabecular pattern of the upper end of the femur as an index of osteoporosis. J Bone Jt Surg. 1970;52A:457–67. 78. Parker MJ, Gillespie LD, Gillespie WJ. Hip protectors for preventing hip fractures in the elderly. Cochrane Database Syst Rev. 2004;3:CD001255. 79. Council for International Organizations of Medical Sciences. The Epidemiology of Chronic Rheumatism. Atlas of Standard Radiographs of Arthritis. Vol. 2. Oxford: Blackwell; 1963. 80. Sowers MF, Hayes C, Jamadar D, et al. Magnetic resonancedetected subchondral bone marrow and cartilage defect characteristics associated with pain and x-ray-defined knee osteoarthritis. Osteoarthritis Cartilage. 2003;11:387–93.

1136

Noncommunicable and Chronic Disabling Conditions

81. Myers SL, Dines K, Brandt DA, et al. Experimental assessment by high frequency ultrasound of articular cartilage thickness and osteoarthritic changes. J Rheumatol. 1995;22:109–16. 82. Altman RD, Asch E, Bloch DA, et al. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Arthritis Rheum. 1986;29:1039–49. 83. Carman WJ, Sowers M, Hawthorne VM, et al. Obesity is a risk factor of osteoarthritis of the hand and wrist: a prospective study. Am J Epidemiol. 1994;139:119–29. 84. Davis MA, Ettinger WH, Neuhaus JM. The role of metabolic factors and blood pressure in the association of obesity with osteoarthritis of the knee. J Rheumatol. 1988;15:1827–32. 85. Lachance L, Sowers MF, Jamadar D, et al. The experience of pain and emergent osteoarthritis of the knee. Osteoarthritis Cartilage. 2001;9:527–32. 86. Lawrence RC, Hochberg MC, Kelsey JL, et al. Estimates of the prevalence of selected arthritic and musculoskeletal diseases in the United States. J Rheumatol. 1989;16:427–41. 87. Acheson RM, Chan Y-K, Clemett AR. New Haven Survey of Joint Diseases. XII. Distribution and symptoms of osteoarthrosis in the hands with reference to handedness. Ann Rheum Dis. 1970;29:275–86. 88. Stecher RM. Heberden’s nodes: A clinical description of osteoarthritis of the finger joints. Ann Rheum Dis. 1955;14:1–10. 89. Spector TD, Cicuttini F, Baker J, et al: Genetic influences on osteoarthritis in women: a twin study. BMJ. 1996;312:940–3. 90. Palotie A, Vaisanen P, Ott J, et al. Predisposition to familial osteoarthrosis linked to Type II collagen gene. Lancet. 1989;1:924–7. 91. Lawrence JS. Rheumatism in coal miners. Part 3. Occupational factors. Br J Ind Med. 1955;12:249–61. 92. Lawrence JS. Rheumatism in cotton operatives. Br J Ind Med. 1961;18:270–6. 93. Croft P, Coggon D, Cruddas M, et al. Osteoarthritis of the hip: An occupational disease in farmers. BMJ. 1992;304:1269–72. 94. Partridge REH, Duthie JJR. Rheumatism in dockers and civil servants: A comparison of heavy manual and sedentary workers. Ann Rheum Dis. 1968;27:559–68. 95. Davis MA, Ettinger WH, Neuhaus JM, et al. The association of knee injury and obesity with unilateral and bilateral osteoarthritis of the knee. Am J Epidemiol. 1989;130:278–88. 96. Murray CJ, Lopez AD. The Global Burden of Disease. Global Burden of Disease and Injury Series, Vol I. Harvard School of Public Health, World Bank, and World Health Organization, Geneva; 1996. 97. Sowers MF, Lachance L, Hochberg M, et al. Prevalence of radiographically defined osteoarthritis of the hand and knee in a population of pre- and perimenopausal women. Osteoarthritis Cartilage. 2000;8:69–77. 98. Peat G, McCarney R, Croft P. Knee pain and osteoarthritis in older adults: a review of community burden and current use of health care. Ann Rheum Dis. 2001;60:91–7. 99. Guccione AA, Felson DT, Anderson JJ, et al. The effects of specific medical conditions on the functional limitations of elders in the Framingham study. Am J Public Health. 1994;84:351–8. 100. Hochberg MC, Lawrence RC, Everett DF, et al. Epidemiologic associations of pain in osteoarthritis of the knee: data from the National Health and Nutrition Examination Survey and the National Health and Nutrition Examination-I Epidemiologic Follow-up Survey. Arthritis Rheum. 1989;18:4–9. 101. Cooper C, McAlindon T, Snow S, et al. Mechanical and constitutional risk factors for symptomatic knee osteoarthritis: differences between tibiofemoral and patellofemoral disease. J Rheumatol. 1994;21: 307–13. 102. Felson DT. Epidemiology of hip and knee osteoarthritis. Epidemiol Rev. 1988;10:1–28. 103. Lane NE. Exercise: a cause of osteoarthritis. J Rheumatol Supp. 1995;43:3–6.

104. Monson RR, Hall AP. Mortality among arthritics. J Chron Dis. 1976;29:459–67. 105. Hochberg MC, Lawrence RC, Everett DF, et al. Epidemiologic associations of pain in osteoarthritis of the knee. Semin Arthritis Rheum. 1989;18 (Suppl 2):4–9. 106. Felson DT, Ahange Y, Anthony JM, et al. Weight loss reduces the risk for symptomatic knee osteoarthritis in women. The Framingham Study. Ann Intern Med. 1992;116:535–9. 107. Pinczewski LA, Deehan DJ, Salman LJ, et al. A five-year comparison of patellar tendon versus four-strand hamstring tendon autograft for arthroscopic reconstruction of the anterior cruciate ligament. Am J Sports Med. 2002;30:523–36. 108. Vilim V, Vytasek R, Olejarova M, et al. Serum cartilage oligomeric matrix protein reflects the presence of clinically diagnosed synovitis in patients with knee osteoarthritis. Osteoarthritis Cartilage. 2001;9: 612–8. 109. Forslind K, Eberhardt K, Jonsson A, et al. Increased serum concentrations of cartilage oligomeric matrix protein. A prognostic marker in early rheumatoid arthritis. Br J Rheumatol. 1992;31:593–8. 110. Sowers MF, Jannausch M, Stein E, et al. C-reactive protein as a biomarker for emergent osteoarthritis. Osteoarthritis Cartilage. 2002;10:595–601. 111. Jordan KM, Arden NK, Doherty M, et al. EULAR Recommendations 2003: an evidence based approach to the management of knee osteoarthritis: Report of a Task Force of the Standing Committee for International Clinical Studies Including Therapeutic Trials (ESCISIT). Ann Rheum Dis. 2003;62:1145–55. 112. Petrella RJ, Bartha C. Home based exercise therapy for older patients with knee osteoarthritis: a randomised clinical trial. J Rheumatol. 2000;27:2215–21. 113. Deyle GD, Henderson NE, Matekel RL, et al. Effectiveness of manual physical therapy and exercise in osteoarthritis of the knee: a randomised controlled trial. Ann Intern Med. 2000;132:173–81. 114. Mazzuca SA, Brandt KD, Katz BP, et al. Effects of self-care education on the health status of inner-city patients with osteoarthritis of the knee. Arthritis Rheum. 1997;40:1466–74. 115. Griffin MR, Brandt KD, Liang MH, et al. Practical management of osteoarthritis. Integration of pharmacologic and nonpharmacologic measures. Arch Fam Med. 1995;4:1049–55. 116. Ezzo J, Hadhazy V, Birch S, et al. Acupuncture for osteoarthritis of the knee: A systematic review. Arthritis Rheum. 2001;44:819–25. 117. Abramson SA. Et tu, acetaminophen? Arthritis Rheum. 2002;46:2831–5. 118. Bjordal JM, Ljunggren AE, Klovning A, et al. Non-steroidal antiinflammatory drugs, including cyclo-oxygenase-2 inhibitors, in osteoarthritic knee pain: meta-analysis of randomised placebo controlled trials. BMJ. 2004;329:1317. 119. Singh D. Merck withdraws arthritis drug worldwide. BMJ. 2004;329:816. 120. Das A, Jr, Hammad TA. Efficacy of a combination of FCHG49 glucosamine hydrochloride, TRH122 low molecular weight sodium chondroitin sulfate and manganese ascorbate in the management of knee osteoarthritis. Osteoarthritis Cartilage. 2000;8:343–50. 121. Pelletier JP, Yaron M, Haraoui B, et al. Efficacy and safety of diacerein in osteoarthritis of the knee: a double-blind, placebo-controlled trial. The Diacerein Study Group. Arthritis Rheum. 2000;43:2339 –48. 122. Chard J, Lohmander S, Smith C, et al. Osteoarthritis. In: Godlee F, ed. Clinical Evidence. A Compendium of the Best Evidence for Effective Health Care. London: BMJ Publishing Group. 2002; 212–1237. 123. Westhoff G, Listing J, Zink A. Loss of physical independence in rheumatoid arthritis: interview data from a representative sample of patients in rheumatologic care. Arthritis Care Res. 2000;13:11–22. 124. Barrett EM, Scott DG, Wiles NJ, et al. The impact of rheumatoid arthritis on employment status in the early years of disease: a UK community-based study. Rheumatology (Oxford). 2000;39: 1403–9.

66 125. Boers M, Dijkmans B, Gabriel S, et al. Making an impact on mortality in rheumatoid arthritis: targeting cardiovascular comorbidity. Arthritis Rheum. 2004;50:1734–9. 126. Gabriel SE. Update on the epidemiology of the rheumatic diseases. Curr Opin Rheumatol. 1996;8:96–100. 127. Uhlig T, Kvien TK. Is rheumatoid arthritis disappearing? Ann Rheum Dis. 2005;64:7–10. 128. Ropes MW, Bennett GA, Cobb S, et al. Revision of diagnostic criteria for rheumatoid arthritis. Bull Rheum Dis. 1958;9:175–7. 129. Bennett PH, Burch TA. New York symposium on population studies in the rheumatic disease: New diagnostic criteria. Bull Rheum Dis. 1967;17:453–8. 130. Arnett FC, Edworthy SM, Bloch DA, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 1988;31:315–24. 131. Rasch EK, Hirsch R, Paulose-Ram R, et al. Prevalence of rheumatoid arthritis in persons 60 years of age and older in the United States: effect of different methods of case classification. Arthritis Rheum. 2003;48:917–26. 132. Turesson C, O’Fallon WM, Crowson CS, et al. Occurrence of extraarticular disease manifestations is associated with excess mortality in a community based cohort of patients with rheumatoid arthritis. J Rheumatol. 2002;29:62–7. 133. Kelsey JL, Hochberg MC. Epidemiology of chronic musculoskeletal disorders. Ann Rev Public Health. 1988;9:379–401. 134. Turesson C, Weyand CM, Matteson EL. Genetics of rheumatoid arthritis: Is there a pattern predicting extraarticular manifestations? Arthritis Rheum. 2004;51:853–63. 135. del Junco DJ, Luthra HS, Annegers JF, et al. The familial aggregation of rheumatoid arthritis and its relationship to the HLA-DR4 association. Am J Epidemiol. 1984;119:813–29. 136. Goldstein R, Arnett FC. The genetics of rheumatic disease in man. Rheum Dis Clin North Am. 1987;13:487–510. 137. Weyand CM, Goronzy JJ. Inherited and non-inherited risk factors in rheumatoid arthritis. Curr Opin Rheumatol. 1995;7:206–13. 138. Albani S, Carson DA. Etiology and pathogenesis of rheumatoid arthritis. In: Koopman WJ, ed. Arthritis and Allied Conditions. A Textbook of Rheumatology. 13th ed. Baltimore: Williams & Wilkins; 1997: 979–92. 139. Kay CR. The Royal College of General Practitioners’ Oral Contraception Study: some recent observations. Clin Obstet Gynaecol. 1984;11:759–86. 140. Spector TD, Hochberg MC. The protective effect of the oral contraceptive pill on rheumatoid arthritis: an overview of the analytic epidemiological studies using meta-analysis. J Clin Epidemiol. 1990;43: 1221–30. 141. Kirwan JR, Silman AJ. Epidemiologic, sociological, and environmental aspects of rheumatoid arthritis and osteoarthritis. Bailliere’s Clin Rheumatol. 1987;1:467–89. 142. Alarcón GS. Epidemiology of rheumatoid arthritis. Rheum Dis Clin North Am. 1995;21:589–604. 143. Pincus T, Callahan LF. Formal education as a marker for increased mortality and morbidity in rheumatoid arthritis. J Chronic Dis. 1985;38:973–84. 144. de Croon EM, Sluiter JK, Nijssen TF, et al. Predictive factors of work disability in rheumatoid arthritis: a systematic literature review. Ann Rheum Dis. 2004;63:1362–7. 145. Weinblatt ME. Treatment of rheumatoid arthritis. In: Koopman WJ, ed. Arthritis and Allied Conditions. A Textbook of Rheumatology. Baltimore: Williams & Wilkins. 1997;1131–41. 146. Evanski PM. The geriatric foot. In: Jahss MH, ed. Disorders of the Foot. Philadelphia: W.B. Saunders; 1982. 147. Elton PJ, Sanderson SP. A chiropodial survey of elderly persons over 65 years in the community. Public Health. 1986;100:219–22. 148. Dunn JE, Link CL, Felson DT, et al. Prevalence of foot and ankle conditions in a multiethnic community sample of older adults. Am J Epidemiol. 2004;159:491–8.

Musculoskeletal Disorders

1137

149. Benvenuti F, Ferrucci L, Guralnik JM, et al. Foot pain and disability in older persons: An epidemiologic survey. J Am Geriatr Soc. 1995;43:479–84. 150. Leveille SG, Guralnik JM, Ferrucci L, et al. Foot pain and disability in older women. Am J Epidemiol. 1998;148:657–65. 151. Tinetti ME, Speechley M, Ginter SF. Risk factors for falls among elderly persons living in the community. N Engl J Med. 1988;319: 1701–7. 152. Keegan THM, Kelsey JL, Sidney S, et al. Foot problems as risk factors of fractures. Am J Epidemiol. 2002;155:926–31. 153. Robbins JM. Recognizing, treating, and preventing common foot problems. Cleve Clin J Med. 2000;67:45–57. 154. Helfand AE. At the foot of South Mountain. A 5-year longitudinal study of foot problems and screening in an elderly population. J Am Podiatr Assoc. 1973;63:512–21. 155. Edelstein JE. Foot care for the aging. Physical Ther. 1988;68:1882–6. 156. Smart CN, Sanders CR. The Costs of Motor Vehicle Related Spinal Cord Injuries. Washington, D.C.: Insurance Institute for Highway Safety; 1976. 157. Centers for Disease Control and Prevention: www.cdc.gov/ncipc/ fact_book/25_Spinal_Cord_Injury.htm, 2003 158. Ackery A, Tator C, Krassioukov A. A global perspective on spinal cord injury epidemiology. J Neurotrauma. 2004;21:1355–70. 159. Stover SL, Fine PR. The epidemiology and economics of spinal cord injury. Paraplegia. 1987;25:225–8. 160. Thurman DJ, Burnett CL, Beaudoin DE, et al. Risk factors and mechanisms of occurrence in motor vehicle-related spinal cord injuries: Utah. Accid Anal Prev. 1995;27:411–5. 161. Woodruff BA, Baron RC. A description of nonfatal spinal cord injury using a hospital-based registry. Am J Preventive Med. 1994;10:10–4. 162. Sekhon LH, Fehlings MG. Epidemiology, demographics, and pathophysiology of acute spinal cord injury. Spine. 2001;26 (24 Suppl):S2–S12. 163. Torg JS, Vesgo JJ, Sennett B, et al. The National Football Head and Neck Injury Registry: 14-year report on cervical quadriplegia, 1971 through 1984. JAMA. 1985;254:3439–43. 164. Tator CH, Provvidenza CF, Lapczak L, et al. Spinal injuries in Canadian ice hockey: documentation of injuries sustained from 1943–1999. Can J Neurol Sci. 2004;460–6. 165. Krassionkov AV, Furlan JC, Fehlings MG. Medical co-morbidities, secondary complications, and mortality in elderly with acute spinal cord injury. J Neurotrauma. 2003;20:391–9. 166. Sutton RA, Bentley M, Castree B, et al. Review of the social situation of paraplegic and tetraplegic patients rehabilitated in the Hexham Regional Spinal Injury Unit in the north of England over the past four years. Paraplegia. 1982;20:71–9. 167. Winter RB. Spinal problems in pediatric orthopaedics. In: Morrissey RT, ed. Lovell and Winter’s Pediatric Orthopaedics, Vol. 2. Philadelphia: Lippincott; 1990. 168. Shands AR, Eisberg HB. The incidence of scoliosis in the state of Delaware. J Bone Joint Surg. 1955;37A:1243–9. 169. Morais T, Bernier M, Turcotte F. Age- and sex-specific prevalence of scoliosis and the value of school screening programs. Am J Public Health. 1985;75:1377–80. 170. Hazebroek-Kampschreur AAJM, Hofman A, Van Dijk AP, et al. Determinants of trunk abnormalities in adolescence. Int J Epidemiol. 1994;23:1242–7. 171. Brooks HL, Azen SD, Gerberg E, et al. Scoliosis: A prospective epidemiological study. J Bone Joint Surg. 1975;57A:968–72. 172. Wynne-Davies R. Familial (idiopathic) scoliosis. A family survey. J Bone Joint Surg. 1968;50B:24–30. 173. Kesling KL, Reinker KA. Scoliosis in twins. A meta-analysis of the literature and report of six cases. Spine. 1997;22:2009–14. 174. Nissinen M, Heliövaara M, Seitsamo J, et al. Trunk asymmetry, posture, growth, and risk of scoliosis. A three-year follow-up of Finnish prepubertal school children. Spine. 1993;18:8–13. 175. Willner S. A Study of height, weight, and menarche in girls with idiopathic structural scoliosis. Acta Orthop Scand. 1975;46:71–83.

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176. Kelsey JL. Epidemiology of Musculoskeletal Disorders. New York: Oxford University Press; 1982. 177. Nissinen M, Heliövaara M, Ylikoski M, et al. Trunk asymmetry and screening for scoliosis: a longitudinal cohort study of prepubertal school children. Acta Paediatr Scand. 1993;82:77–82. 178. Keessen W, Crowe A, Hearn M. Proprioceptive accuracy in idiopathic scoliosis. Spine. 1992;17:149–55. 179. Miller NH. Cause and natural history of adolescent idiopathic scoliosis. Orthop Clin North Am. 1999;30:343–52. 180. Dickson RA, Stamper P, Sharp AM, et al. School screening for scoliosis: Cohort study of clinical course. BMJ. 1980;2:265–7. 181. Lonstein JR. Natural history and school screening for scoliosis. Orthop Clin North Am. 1988;19:227–37. 182. Laulund T, Sojbjerg JO, Horlyck E. Moiré topography in school screening for structural scoliosis. Acta Orthop Scand. 1982;53: 765–8. 183. Grossman TW, Mazur JM, Cummings RJ. An evaluation of the Adams forward bend test and the scoliometer in a scoliosis school screening setting. J Pediatr Orthop. 1995;15:535–8. 184. Côté P, Kreitz BG, Cassidy JD, et al. A study of the diagnostic accuracy and reliability of the scoliometer and Adam’s forward bend test. Spine. 1998;23:796–803. 185. Williams JI. Criteria for screening: Are the effects predictable? Spine. 1988;13:1178–86. 186. U.S. Preventive Services Task Force. Screening for adolescent idiopathic scoliosis. Review article. JAMA. 1993;269:2667–72. 187. Goldberg CJ, Dowling FE, Fogarty EE, et al. School scoliosis screening and the United States Preventive Services Task Force. Spine. 1995;20:1368–74. 188. U.S. Preventive Services Task Force. Screening for adolescent idiopathic scoliosis. Policy statement. JAMA. 1993;269:2664–6. 189. Kelsey JL. Incidence and distribution of slipped capital femoral epiphysis in Connecticut. J Chronic Dis. 1971;23:567–87. 190. Loder RT. A worldwide study on the seasonal variation of slipped capital femoral epiphysis. Clin Orthop Relat Res. 1996;322:28–36. 191. Brown D. Seasonal variation of slipped capital femoral epiphysis in the United States. J Pediatr Orthop. 2004;24:139–43. 192. Kelsey JL, Acheson RM, Keggi KJ. The body builds of patients with slipped capital femoral epiphysis. Am J Dis Child. 1972;124: 276–81. 193. Loder RT. The demographics of slipped capital femoral epiphysis. An international multicenter study. Clin Orthop Relat Res. 1996;332:8–27. 194. Sørenson KH. Slipped upper femoral epiphysis. Acta Orthop Scand. 1968;39:499–517. 195. Rennie AM. Familial slipped upper femoral epiphysis. J Bone Joint Surg. 1967;49B:535–9. 196. Weiner D. Pathogenesis of slipped capital femoral epiphysis: current concepts. J Pediatr Orthop. 1996;B5:67–73. 197. Morscher E. Strength and morphology of growth cartilage under hormonal influence of puberty. Reconstr Surg Traumatol. 1968;10: 3–104. 198. Loder RT, Aronsson DD, Dobbs MB, et al. Slipped capital femoral epiphysis. AAOS Instructional Course Lectures. 2001;50:555–70. 199. Schultz WR, Weinstein JN, Weinstein SL, et al. Prophylactic pinning of the contralateral hip in slipped capital femoral epiphysis: evaluation of long-term outcome for the contralateral hip with use of decision analysis. J Bone Joint Surg. 2002;84A:1305–14. 200. Hurley JM, Betz RR, Loder RT, et al. Slipped capital femoral epiphysis. The prevalence of late contralateral slip. J Bone Joint Surg. 1996;78A:226–30. 201. National Center for Health Statistics. Current Estimates from the National Health Interview Survey, United States, 1987. Vital and Health Statistics, Series 10, No. 166; 1988. 202. Rivara FD, Calonge N, Thompson RS. Population-based study of unintentional injury incidence and impact during childhood. Am J Public Health. 1989;79:990–4.

203. Cooper C, Dennison EM, Leufkens HG, et al. Epidemiology of childhood fractures in Britain: a study using the general practice research database. J Bone Miner Res. 2004;19:1976–81. 204. Landin LA. Fracture patterns in children. Analysis of 8,682 fractures with special reference to incidence, etiology and secular changes in a Swedish urban population 1950–1979. Acta Orthop Scand. 1983;202 (Suppl):1–109. 205. Lyons RA, Delahunty AM, Kraus D, et al. Children’s fractures: a population based study. Injury Prev. 1999;5:129–32. 206. Jones IE, Williams SM, Goulding A. Associations of birth weight and length, childhood size, and smoking with bone fractures during growth: evidence from a birth cohort study. Am J Epidemiol. 2004;159:343–50. 207. Mooney JF, Emans JB. Developmental dislocation of the hip: a clinical overview. Pediatr Rev. 1995;16:299–303. 208. Robinson GW. Birth characteristics of children with congenital dislocation of the hip. Am J Epidemiol. 1968;87:275–84. 209. Record RC, Edwards JH. Environmental influences related to the etiology of congenital dislocation of the hip. Br J Prev Soc Med. 1958;12:8–22. 210. Gunther A, Smith SJ, Maynard PV, et al. A case-control study of congenital hip dislocation. Public Health. 1993;107:9–18. 211. Jones DH. The early diagnosis of congenital dislocation of the hip joint. Br J Clin Pract. 1965;19:443–9. 212. Carter CO, Wilkinson J. Persistent joint laxity and congenital dislocation of the hip. J Bone Joint Surg. 1964;46B:40–5. 213. Sharrard WJW. Pediatric Orthopaedics and Fractures, Vol 1, Oxford: Blackwell Scientific; 1993. 214. Cunningham KT, Beningfield SA, Moulton A, et al. A clicking hip in a newborn baby should never be ignored. Lancet. 1984;1:668–70. 215. Knox EG, Armstrong EH, Lancashire RJ. Effectiveness of screening for congenital dislocation of the hip. J Epidemiol Community Health. 1987;41:283–9. 216. Leck I. An epidemiological assessment of neonatal screening for dislocation of the hip. J R Coll Physicians Lond. 1986;20:56–62. 217. Holen KJ, Tegnander A, Bredland T. Universal or selective screening of the neonatal hip using ultrasound? J Bone Joint Surg. 2002;84B:886–90. 218. Fulton MJ, Barer ML. Screening for congenital dislocation of the hip: An economic appraisal. Can Med Assoc J. 1984;130:1149–56. 219. American Academy of Pediatrics Committee on Quality Improvement, Subcommittee on Developmental Dysplasia of the Hip. Clinical practice guidelines: early detection of developmental dysplasia of the hip. Pediatrics. 2000;105:896–905. 220. Patel H, with the Canadian Task Force on Preventive Health Care. Preventive health care, 2001 update: screening and management of developmental dysplasia of the hip in newborns. CMAJ. 2001;164: 1669–77. 221. MacFarlane A. Screening for congenital dislocation of the hip. BMJ. 1987;294:1047. 222. Berman L, Klenerman L. Ultrasound screening for hip abnormalities. Preliminary findings in 1001 neonates. BMJ. 1986;293:719–22. 223. Hernandez RJ, Cornell RG, Hensinger RN. Ultrasound diagnosis of neonatal congenital dislocation of the hip. A decision analysis assessment. J Bone Joint Surg. 1994;76B:539–43. 224. Rosendahl K, Markestad T, Lie RT. Ultrasound screening for developmental dysplasia of the hip in the neonate: the effect on treatment rate and prevalence of late cases. Pediatrics. 1994; 94:47–52. 225. Rosendahl K, Aslaksen A, Lie RT, et al. Reliability of ultrasound in the early diagnosis of developmental dysplasia of the hip. Ped Radiol. 1995;25:219–24. 226. Elbourne D, Dezateux C, Arthur R, et al. On behalf of the UK Collaborative Hip Trial Group: Ultrasonography in the diagnosis and management of developmental hip dysplasia (UK Hip Trial): clinical and economic results of a multicentre randomized controlled trial. Lancet. 2002;360:2009–17.

Neurological Disorders

67

James C. Torner • Robert B. Wallace

INTRODUCTION

Neurological disorders include many diseases and conditions of acute and chronic development. The etiology of these disorders can be infectious, toxic, genetic, traumatic, and ischemic, and related to other chronic pathophysiologies. The occurrence may be at birth, which may confer a lifelong disability, or may occur in middle or late life, which may result in progressive disability and death. Neurological disorders may have an insidious onset or have symptoms that are nonspecific, making classification difficult. Early stages of some disorders are characterized by a variable presentation or by subtle signs and symptoms that are difficult to detect or that go unrecognized. Individuals often ignore symptoms until function is impaired. Some disorders in children may be developmental and may go undetected until the children reach the age at which deficits could be assessed. Hence, recognition, diagnosis, and progression of neurological symptoms may affect the true magnitude and onset of neurological disorders. Diagnoses of neurological disorders requires not only recognition of symptoms but confirmation with a neurological examination. The neurological examination may be specific to symptoms and to onset. Diagnostic tests have changed with advances in imaging and electrophysiological testing. The use of computerized tomography (CT) scanning, magnetic resonance imaging (MRI), cerebral blood flow measurement and positron emission tomography (PET) have increased the certainty of diagnoses. Additional cognitive tests developed by neuropsychologists have aided in the diagnosis of cognitive decline. Hence the evaluation of incidence and prevalence over time is difficult due to changing diagnostic criteria and the likelihood of changing classifications and inclusion of milder or early-onset disease. The burden of neurological disease is increasingly important as a determinant of health policy in costs and services. The Global Burden of Disease Study utilized the Disability Adjusted Life Years (DALYs) as an estimate of magnitude or burden of diseases.1–3 Brain diseases encompass a broad spectrum including neurological, neurosurgical, and psychiatric conditions. Thirty-three percent of the years lived with disability and 13% of the DALYs are from neurological and psychiatric disorders. The major impact of the aging related disorders of Parkinson’s disease, Alzheimer’s disease, and other dementias and cerebrovascular disease on the global burden is evident world-wide and also in North America (Table 67-1).

U.S. MORTALITY, INCIDENCE AND PREVALENCE OF NEUROLOGICAL DISORDERS

The International Classification of Diseases Version 10 was implemented in 1999. Comparability of the classification depends on the condition.4 Table 67-2 includes mortality data for the United States for 2002 for neurological conditions identified by the new ICD10

classification. Since 1999, crude mortality rates of neurological disorders have been increasing mainly due to the increasing number of older persons. Most are low with exception of cerebrovascular conditions, dementia and Alzheimer’s disease and Parkinson’s disease. Cerebrovascular disease remains a major cause of death with a rate of 56.4 per 100,000 persons. The mortality rate for cerebrovascular disease has been declining across both genders and all races groups. Rates of death from progressive neurological disorders such as Parkinson’s disease and Alzheimer’s disease have increased as the population becomes older. Using discharge diagnoses as measures of the magnitude of neurological disorders on the health care system; from the National Hospital Discharge Survey of 2004 shows that discharge rates for epileptic seizures, migraine, multiple sclerosis (MS) and malignant brain neoplasms were highest when the first-listed diagnoses were used5 (Table 67-3) (Fig. 67-1). Increases in admissions from 1990 were observed in 2004 in HIV, brain neoplasm, Alzheimer’s disease, Parkinson’s disease, carpal runnel syndrome, and cerebrovascular disease. These reflect the increasing incidence with aging and an increase in prevalence due to the chronic nature and successful treatment of some of these conditions. The use of CT and MRI has improved diagnosis and changes in classification are reflective of this. The last national assessment of clinic use was the National Ambulatory Medical Care Survey (NAMCS) of 1991–1992. The NAMCS examined the 7,253,000 visits to neurologists that were reported by respondents.6 The rate of visits was 2.9 per 100 persons per year. Only 6% of the visits were referred, and 15.5% were new patients. Most of the visits (81%) were due to symptoms with 43% of those from nervous system problems and 23% from musculoskeletal complaints. The main reasons for the visits were headaches (18%), seizures (9%), and sensory disturbances (5.5%). Only 36% of the visits resulted in a diagnosis of nervous system disorders; 21% were symptoms and signs, 15% were musculoskeletal conditions, 8% were mental disorders, and 7% were injuries or poisonings. In the NAMCS of 1993, visits to neurologists increased to 8,393,000 (1.2% of total visits) but there were 22,556,000 (3.1%) total visits for symptoms from the nervous system, and 77,737,000 (10.8%) visits with a principal diagnosis of nervous system or sense organ disorders. Headaches accounted for 10,736,000 visits (1.5%).7 The 2004 National Health Interview Survey asked respondents about conditions causing the highest percentage of limitation of activity.8 Stroke was reported in 2.6%. Prevalence varied by gender, age, race, education, and income. Pain disorders reported were migraine headaches, 15.3% of adults in the last three months. Low back pain was prevalent in 27.1% and neck pain in 14.6%. Migraine was more common in younger women. Back and neck pain were also more in women. The magnitude of neurological disorders worldwide and in the United States is wide ranging in incidence, prevalence, and mortality 1139

Copyright © 2008 by The McGraw-Hill Companies, Inc. Click here for terms of use.

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Noncommunicable and Chronic Disabling Conditions

TABLE 67-1. GLOBAL ESTIMATES OF DEATHS AND DALYS FROM GLOBAL BURDEN OF DISEASE STUDY, 2000 Global Cause

Deaths∗

Japanese encephalitis Parkinson’s disease Multiple sclerosis Meningitis Epilepsy Migraine Alzheimer’s disease Cerebrovascular disease

4 90 17 156 98 0 276 5101

% Deaths 0.01 0.16 0.03 0.28 0.18 0.00 0.50 9.16

U.S., Canada

DALYs∗

%

Deaths∗

426 1473 1475 5751 7067 7539 12464 45677

0.03 0.10 0.10 0.39 0.48 0.51 0.85 3.10

0 16 3 1 2 0 61 197

Cuba % Deaths 0.00 0.58 0.11 0.04 0.07 0.00 2.20 7.09

U.S., Canada DALYs∗ 0 227 110 47 262 490 1415 1594

Cuba % 0.00 0.49 0.24 0.10 0.57 1.07 3.08 3.47

∗

In thousands. Source: Murray CJL, Lopez AD, Mathers CD, et al. The Global Burden of Disease 2000 project: aims, methods, and data sources. November, 2001 Research Paper No 01.1 Harvard Burden of Disease Unit.

as well as across ages and etiologies. The remainder of the chapter describes several neurological disorders that are an increasing public health problem and with some the etiology is yet to be identified. CEREBRAL PALSY

Cerebral palsy (CP) is a group of nonprogressive motor impairment syndromes that arise during brain development and is recognized early in life as the child develops.9 CP is classified based on the extremities involved and the neurological dysfunction (spastic, athetotic, hypotonic, dystonic, or combined). The most common form is spastic CP which is present in about 80% of prevalent cases. The presence of other neurological disabilities, such as mental TABLE 67-2. NUMBER OF DEATHS AND DEATH RATE IN U.S. POPULATION OF NEUROLOGICAL DISORDERS, 2002

ICD10

Disorder

G00–G03 G04–05 G10 G12.2 G20 G30 G35 G40–G41 G47 G61–G63

Meningitis Encephalitis Huntington’s disease Motor neuron disease Parkinson’s disease Alzheimer’s disease Multiple sclerosis Epilepsy Sleep disorders Guillain-Barre syndrome and other Neuropathies Myasthenia gravis Muscular dystrophy and other myopathies Cerebral palsy Plegias and paralysis Hydrocephalus Neurological disorders Brain pathology Spinal disorders Congenital malformations HIV with encephalopathy Dementia Cerebrovascular disease CNS slow Infections

G70 G71

G80 G81–G83 G91 G00–G99 C70–C72 M46–M51 Q04 B22 F00–F03 I60–I69 A81

Number

Rate per 100,000

700 365 741 5723 16857 58866 3124 1380 480 513

0.24 0.13 0.26 1.98 5.85 20.41 1.08 0.48 0.17 0.18

752 1212

0.26 0.42

1200 1139 692 103064 12830 500 375 160 41794 162672 220

0.42 0.39 0.24 35.74 4.45 0.17 0.13 0.06 14.49 56.41 0.08

Source: http://wonder.cdc.gov/wonder/data/mortSQL.html

retardation, seizure disorders, and sensory problems, are more common in persons with CP. The Metropolitan Atlanta Developmental Disabilities Surveillance Program in 1991 found that 48% of 599 CP children in their study had vision impairment, 8% had hearing impairment, and 17% had mental retardation.10 CP occurs between 1.5–3.0 of every 1000 live births. However this rate depends on definition and inclusion based on impairment.9–11 Because CP is developmental, it may present in a variety of forms and severities and may disappear with growth. Case ascertainment may require surveillance using multiple sources. The Disabilities Education Act allows surveillance through special education programs in school systems. In Atlanta over 90% of children with developmental disabilities could be identified through education sources.12 Prevalence then may be a better measure than incidence. CP has been identified by early school age in 1.4–5.1 per 1000 children. In Atlanta the prevalence rate was 2.4 per 1000 in ages 3–10 years and the rate was lowest in the younger ages (2.0/1000) for both disabling and nondisabling CP. There is a slight excess of males and blacks among affected persons in Atlanta. Ethnicity is not consistently related, however to CP. Prematurity is the most important risk factor with weight at birth the surrogate measure. Nearly one-fourth of children with CP are less that 1500 grams at birth and one-half are less than 2500 grams. Innate genetic factors may play role in CP occurrence. Several studies have reported positive familial history and genetic risk in CP children. Twins are at higher risk but they share a common pregnancy and birthing process.13 Other risk factors include maternal factors prior to pregnancy such as long menstrual cycles and a history of spontaneous abortions and stillbirths. Low socioeconomic status increases the risk of CP. During pregnancy, factors that may increase risk include hyperthyroidism, thyroid hormone drugs, and exogenous estrogen. There is an association with occurrence of other congenital malformations which has also been observed.9,10,15 At birth, low birth weight and immaturity are among the most consistent risk factors for CP. Several factors may contribute to early delivery or low birth weight. These include intrauterine infection and congenital malformations. A number of markers of maternal infection have been linked to CP, including chorioamnionitis, maternal fever, antibiotic use, uterine tenderness, and neonatal sepsis.18,19 Intracranial hemorrhage in premature infants is associated with CP. The increase in survival of infants with very low birth weight, has increased the causal distribution of CP. A study by Pharoah et al showed that low birth weight infants account for nearly 50% of cases of CP.14 Physical injury during the perinatal and postnatal periods such as intrauterine exposure to heavy metals, neonatal hyperbilirubinemia, and exposure to benzyl alcohol may be related to CP occurrence.20 Severe asphyxia at birth may account for about 10% of all CP.21–23 Difficult birth is associated with increased risk of CP only among children who have neurological symptoms in the neonatal period. Postnatal causes of CP include neonatal encephalopathy, trauma, or occlusion of a cerebral artery or vein. These may account for 12–21% of cases.

67 TABLE 67-3. NATIONAL HOSPITAL DISCHARGE SURVEY, 2004 ICD9 42 191 225 225.2 320 322 323 331 332 333 340 342 343 344 345 346 349 351 353 354 354.2 355 356 357 358 359 430 431 432 433 434 435 436 437 438 721 722 723 724 742 756 800 801 803 805 806 847 850 851 852 853 854

DESCRIPTION HIV Malignant neoplasm of brain Benign neoplasm of brain to other parts of nervous system Benign neoplasm of cerebral meninges Bacterial meningitis Meningitis of unspecified cause Encephalitis, myelitis, and encephalomyelitis Alzheimer’s disease Parkinson’s disease Other extrapyramidal disease and abnormal movement disorders Multiple sclerosis Hemiplegia Infantile cerebral palsy Other paralytic syndromes Epilepsy Migraine Other and unspecified disorders of the nervous system Facial nerve disorders Nerve root and plexus disorders Carpal tunnel syndrome Lesion of ulnar nerve Mononeuritis of lower limb Hereditary and idiopathic peripheral neuropathy Inflammatory and toxic neuropathy Myoneural disorders Muscular dystrophies and other myopathies Subarachnoid hemorrhage Intracerebral hemorrhage Other and unspecified intracranial hemorrhage Occlusion and stenosis of precerebral arteries Occlusion of cerebral arteries Transient cerebral ischemia Acute but ill-defined cerebrovascular disease Other and ill-defined cerebrovascular disease Late effects of cerebrovascular disease Spondylosis and allied disorders Intervertebral disc disorders Other disorders of cervical region Other and unspecified disorders of back Other and congenital anomalies of nervous system Other congenital musculoskeletal anomalies Fracture of vault of skull Fracture of base of skull Other and unqualified skull fractures Fracture of vertebral column without spinal cord injury Fracture of vertebral column with spinal cord injury Sprains and stains of joints and adjacent muscles Concussion Cerebral laceration and contusion Subarachnoid subdural, and extradural hemorrhage, following injury Other and unspecified intracranial hemorrhage following injury Intracranial injury of other and unspecified nature

2004 65 84 23 6 7 4 85 22 11 28 4 6 7 60 59 12 6 4 49 9 4 10 8 5 25 65 26 144 318 180 82 35 31 98 37 27 155 7 16 16 29 4 83 9 8 57 24 50 11 5

Source: Centers for Disease Control and Prevention http://www.cdc.gov/nchs/ about/major/hdasd/nhds.htm#Publications

Neurological Disorders

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Most of the risk factors for CP are in the prenatal period. The decreased use of isoimmunization for Rh factors has been associated with a decrease of CP of the athetoid type. Improvements in obstetric and neonatal care and an increasing frequency of obstetric interventions have not been associated with a decrease in incidence of CP.8,24,25 Abnormalities of coagulation such as factor V Leiden and antiphospholipid antibodies have been associated with CP in fullterm infants.26,27 Studies have shown a possible protective effect of administration preceding delivery of magnesium sulfate for protection from cerebral hemorrhage and development of CP.28 The paucity of information about and the variety of causal factors for the majority of CP that is not attributable to birth events severely limits the development of strategies for prevention. HIV INFECTION

Since 1981 when the human immunodeficiency virus (HIV) type 1and the acquired immunodeficiency syndrome (AIDS) first appeared in the United States the epidemic has increased to nearly a half million people.29 Almost half have died from this devastating infection. HIV has manifestations in neurological disorders also. Neurological manifestations include HIV dementia, myelopathies, neuromuscular disorders, and CNS infections of cryptococcal meningitis, toxoplasmosis, progressive multifocal leukoencephalopathy, cytomegalovirus, myocabacterium tuberculosis, neurosyphilis, and primary CNS lymphoma. Meningitis, neuropathy, and myopathy can occur before the AIDS-related complex is present. Dementia, myelopathies, and opportunistic infections are present as the disease progresses into AIDS.30,31 Estimates of incidence and prevalence of the neurological manifestation of HIV are problematic. Many of the studies are retrospective based on autopsy or clinical populations.30 The estimates vary widely depending on the population and the definition used. Most often the diagnosis is based on clinical findings without verification. Some estimates are based on HIV-AIDS cohorts but generalizations between locations and severity of illness is problematic. With the introduction of highly active antiretroviral therapy (HAART) in the 1990s, there has been a significant decline in opportunistic infections. HAART has increased survival for individuals with HIV/AIDS.32,33 HIV-associated dementia (HIV-D) has decreased by 40–50%.34 The prevalence of sensory neuropathies however is in excess of 20%.35 Prolonged HAART may further increase this rate. HIV-D and HIVrelated sensory neuropathies (HIV-SN) have a combined prevalence of between 30–50% in advanced HIV disease, suggesting that HAART does not provide complete protection against neurological damage.36 HIV dementia is characterized by cognitive and memory impairment. It is associated with the onset of AIDS and it is estimated that approximately 3% of AIDS patients present with dementia as their first symptom. The prevalence varies by type of study from 7 to 66%.37–39 An estimate derived from CDC data is that 2.8% of AIDS cases have dementia.37 The Multicenter AIDS Cohort Study found a 3.3% figure. They also found that after AIDS has developed there was a 7% incidence per year of dementia.38 Factors associated with HIV dementia include lower CD4+ cell counts, anemia, low body mass index, older age, and other systemic AIDS symptoms.38 The proportion of AIDS cases with dementia has not changed but there is some indication of improvement with zivovudine treatment.40,41 Inflammatory demyelinating polyneuropathies may occur either in acute or chronic form. The estimates are from 0.5 to 3.0% of patients have these conditions.30,42 Other neuropathies may occur. Sensory neuropathy occurs in the later stages of HIV infection.43 Toxic neuropathy associated with antiretroviral agents also occurs.44,45 The manifestation of these disorders is severe pain and impaired walking ability. It is estimated from a clinical population that 13% of the patients may be affected.46,47 Opportunistic infections are a hallmark of AIDS progression. Infections can affect the central nervous system. Cryptoccocal meningitis is present in about 10% of AIDS cases and is associated

1142

Noncommunicable and Chronic Disabling Conditions National hospital discharges1990 and 2004 1990

Discharges, thousands

2004

0

50

100

150

200

250

300

350

HIV Brain neoplasms Alzheimer’s disease Parkinson’s disease Multiple sclerosis Epilepsy Migraine Carpal tunnel syndrome Spondylosis Cerebrovascular disease Subarachnoid hemorrhage Intracerebral hemorrhage Other intracranial hemorrhage Occlusion of precerebral arteries Occlusion of cerebral arteries Transient cerebral ischemia Figure 67-1. United States Hospital Discharge Rates 1990 versus 2002 for selected neurological diseases; first diagnosis.

with a drop in CD4+ count below 200 cells/mm3.48,49 A common cause of mass lesion abscesses is toxoplasmosis. The prevalence varies between locations. CNS infection is a result of latent reactivation and may be inhibited by prophylactic treatment of pneumonia. CMV infection can lead to retinitis and encephalitis in patients with HIV.50,51,55 CMV retinitis is common in patients with CMV infection causing visual loss or blindness in 15–28% of AIDS patients. Encephalitis presents with confusion, disorientation, and memory loss and may occur in approximately 2% of AIDS patients. Primary CNS lymphoma is rare but has been increasing due to immunosupression frequency.53 Up to 3% of AIDS patients develop CNS lymphoma. Many of these patients are diagnosed at autopsy. Prior AIDS-related illness and low CD4+ counts are linked to lymphoma occurrence.54 The public health burden of HIV and AIDS remains a challenge. With increasing survival, the prevalence of HIV or AIDS neurological conditions will increase. HIV-associated dementia (HIV-D) remains a common problem of dementia worldwide and with the magnitude of HIV in Africa, the rates of dementia may be a pending epidemic. HIV-related sensory neuropathies (HIV-SN) represent the most common neurological disorders associated with AIDS and may also increase. CREUTZFELDT-JAKOB DISEASE

Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, invariably fatal brain disorder. There are three major types of CJD: sporadic CJD, hereditary CJD, and acquired CJD. In the United States the incidence is from 250 to 300 new cases per year.55,56

Acute but ill-defined

There is no treatment that can cure or control CJD. Current treatment is aimed at alleviating symptoms and making the patient as comfortable as possible. About 90% of patients die within one year. Patients progress through failing memory, behavioral changes, lack of coordination and visual disturbances toward mental deterioration, involuntary movements, blindness, weakness of extremities, and coma. The cause of CJD is a type of protein called a prion. Prions exist as harmless proteins but can take the infectious form which has a different folded shape than the normal protein. In the mid 1980s bovine spongiform encephalopathy (BSE) emerged in the United Kingdom in cattle. Infected animals may have consumed contaminated cattle feed, perhaps with scrapie leading to the silent spread of the BSE epidemic. Acquired CJD called variant (vCJD) has been identified in young people.57,58 This form of CJD is different than sporadic CJD in age of onset and symptomatology. The clinical manifestations in vCJD patients include psychiatric symptoms such as anxiety, depression, and withdrawal. The development of neurological signs, such as myoclonus and extrapyramidal dysfunction, is often delayed for several months after illness onset. The most striking early neurological sign in some vCJD patients is persistent dysesthesia or paresthesia. vCJD has been linked to ingestion of beef tainted with BSE; most cases have occurred in the United Kingdom and Europe. Cases may still occur because of the long latency of the abnormal prion in the manifestation of symptoms. An interesting finding is the susceptibility for vCJD. All vCJD patients to date have been homozygous for methionine at the polymorphic codon 129 of the human prion protein gene.57,58 Although the scientific basis is unknown, researchers have suggested that methionine homozygosity may be associated

67 with a shorter incubation period, younger age distribution, and specific clinicopathologic profile. The possibility exists that vCJD could potentially occur in persons who are heterozygous or homozygous for valine at codon 129 after a longer incubation period. While the possibility of vCJD exists in the United States, only one human case has been reported in a person who spent time in the United Kingdom. The United States Department of Agriculture (USDA) has conducted a large, nationwide survey of cattle for slaughter and there is a very low probability of bovine or human CJD in the United States. The bloodborne transmission of vCJD has long been possible.59 A probable bloodborne, person-to-person transmission of vCJD was reported in the United Kingdom in a 69-year-old man who had vCJD onset in late 2002. Both the donor and recipient died of pathologically confirmed vCJD. The patient was the first ever with methionine and valine heterozygosity at the polymorphic codon 129 of the prion protein gene, which indicates that persons who are not homozygous for methionine can be susceptible to infection by the BSE agent. The FDA has recommended a blood donor deferral policy to exclude donors who have spent specific periods of time in the United Kingdom and other European countries.59 This policy was implemented in 1999. Further surveillance for vCJD in Europe is warranted due to the long incubation period and the possibility of a delay in codon 129 heterozygote persons. In the United States little risk is estimated from cattle due to the limited number of infected cattle. WEST NILE VIRUS

West Nile Virus (WNV)was first discovered in the West Nile District of Uganda in 1937. WNV spread across areas of Africa, Eastern Europe, West Asia, and the Middle East. It eventually began appearing in the Eastern United States in 1999. In 2005, WNV spread into areas of the western United States. Over 2700 human cases were observed, representing 19% of the counties of the United States. However the largest number of cases occurred in California. Cases occurred from June to November with the peak period in August and September.60–62 WNV is transmitted by a mosquito vector and can result in encephalitis in infected humans and equine. WNV can also result in wild and domestic bird mortality. Certain birds (e.g., corvids, common grackles, house finches, and house sparrows) develop high-titer WNV viremia, making them highly infectious to feeding mosquitoes. Many of these species also have high (>40%) mortality from WNV infection.1,6 The Culex species of mosquito is the most prevalent in case pools.63 Neurological symptoms of meningitis, encephalitis, or acute flaccid paralysis occurred in 42.5% of the symptomatic cases. West Nile fever was present in 52.2% of the cases and 5.3% had unspecified illnesses. It is estimated that 80% of cases are asymptomatic.61,64 The severe symptoms can include high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, vision loss, numbness, and paralysis. These symptoms may last several weeks, and neurological effects may be permanent. Ongoing WNV surveillance monitors the spread of the virus and helps target prevention and control strategies. Increased arboviral diagnosis, testing, and reporting, through the ArboNET surveillance system detects increased transmission of all endemic and foreign arboviruses.65 No effective vaccine exists for humans; hence prevention of WNV disease is dependant upon community mosquito control and personal protection against mosquito bites by use of repellents and minimization of outdoor exposure. SEIZURE DISORDERS

Seizures are alterations in consciousness associated with an abovenormal discharge of neurons of the brain. Seizures can be classified based on etiology as acute symptomatic (provoked) seizures and unprovoked seizures. Unprovoked, recurrent seizures are considered epilepsy. Seizures are classified by onset as simple or complex partial

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seizures, or generalized major motor, absence, or myoclonic seizures. EEGs are used to verify the diagnosis and to determine the electrical activity pattern.66–68 Epilepsy occurs mostly in the young and the old. The overall incidence in the Rochester, Minnesota population studies for 50 years was 44 per 100,000 persons.69 All convulsive disorders had an incidence of 130 per 100,000 persons. The incidence of partial seizures cases was observed to be 25 per 100,000 and generalized onset to be 19 per 100,000. Generalized seizures are highest during the first year of life, decrease throughout childhood and increase again in the elderly. Partial seizures have a relatively constant rate up to age 65 and then increase sharply. For generalized seizures with onset in early life, females are at higher risk, and for later life seizures, males are at higher risk. For partial seizures, the rates are similar until age 65 when men are at higher risk. There has been a slight decrease in incidence of epilepsy over time, but an increase in incidence in the elderly. The prevalence of epilepsy varies widely among populations, from 27 to 40 per 1000. In Rochester, the prevalence in 1980 was 6.8 per 1000. Sixty percent were partial seizures and 75% were of unknown etiology. The prevalence in several studies is higher in blacks in the 20–66 year age range.70 A number of factors have been associated with epilepsy and are related to development of definable brain lesions. These include severe head injury, stroke, CNS infection, brain tumors, and CNS degenerative diseases.71,72 Factors that have a causal pathway are associated at birth with brain development, such as mental retardation and cerebral palsy. Febrile seizures are related to increased seizure risk. These may occur in 2.3–4.7% of children. Other factors that have shown a relationship, but without a direct causal pathway, are drug abuse—for example, heroin—and medical conditions such as asthma, hypertension, and depression. Suggested but unproven risk factors include pre- or perinatal adverse events and immunizations. Positive family history has also been associated with development of epilepsy. Familial aggregation is strongest for febrile seizures.73 Twin studies have shown a higher concordance for monozygotic compared to dizygotic twins.74 The role of genetics in partial epilepsy is being explored but will require further studies of gene-environment interaction. Seizure control can be obtained in a majority of patients. Recurrence rates show that 25% will suffer a recurrence in the two years following the first seizure but this rate varies by the presence of risk factors. HEADACHES

Headache is the most common neurological disorder. Based on a telephone interview in a population-based study, 90% of men and 95% of women reported a headache in the last year. From 65 to 71% of women and 48–50% of men report one headache per month. Headache is one of the most common symptoms prompting people to seek medical care.75,76 It is estimated that 5.5 million days of activity restriction can be attributed to headache each year by adults in the United States.77,78 From the National Health Interview Survey in 2003, 15.1% of adults reported a severe headache or migraine in the previous three months. Headaches may be primary or secondary to another disorder such as brain tumor, stroke, or vasculitis. Primary headaches can be classified into tension-type, migraine, and cluster. Diagnosis is based on clinical presentation. Classification criteria were established by the International Headache Society.79,80 Distinguishing aspects of migraine include unilateral onset with associated anorexia and sometimes nausea and vomiting. The presence of a warning (aura) has also been described as a prodromal change in mood and is used as part of the diagnosis. The incidence of migraine depends on gender, age and type. The lifetime prevalence of migraine has been estimated to be 8% with women having a prevalence of 25%. A one year prevalence is 6% for men and 15% for women. In general, women have more migraines than men do, particularly with auras occurring most frequently in young adult life. The incidence of migraines from the Rochester, Minnesota population was 294 per 100,000 for women and 137 per 100,000 for men using data from 1979 to 1981. Between age five and puberty the incidence probably approximates 10% per year.81

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The incidence increases in females with the onset of menses. The peak age for women is between 20 and 24 years of age. The incidence returns to the male level at about the age of 40. In both women and men, incidence appears to decrease, beginning in the early 40s. Prevalence of migraine headache may vary in populations and may be increasing. This could be due to varying definitions. Using the International Headache Society criteria, the prevalence of migraine in four population-based studies was from 13 to 15% in women and 4–6% in men.82 Data from Rochester, Minnesota showed an increased from 25.8 per 1000 to 41 per 1000 from 1981 to 1989 in both sexes combined. While migraine was thought to occur more often in high socioeconomic groups, data from the American Migraine Society shows the opposite. Data from the National Health Interview Survey also showed the low socioeconomic and middle economic groups may have similar rates. Rates of clinically diagnosed migraine may be higher due to higher rates of physician diagnoses in the high socioeconomic population.78,83 The risk of migraine may be familial but may be overestimated due to biases in ascertainment.84 The strongest evidence of a genetic association is from the higher concordance in monozygotic than in dizygotic twins. If genetic factors contribute to a person’s propensity for migraine, then other factors, usually exogenous, are likely to play an important role in determining the occurrence and frequency. Risk factors for headache onset in women are related to menstrual flow or the use of oral contraceptives. Other factors include ingestion of some foods (those with tyramine, including chocolate and aged cheeses) or alcoholic beverages (red wines, particularly). Psychosocial characteristics also appear to be associated with headache occurrence. These include characteristics of perfectionism, inflexibility, and hypochondriasis, as well as propensity to anxiety and depression. Stress and psychosocial events may be important. The consequences of migraine are not viewed as life-threatening but migraine may be associated with hypertension, atherosclerotic heart disease, and stroke.85 In contrast to migraine are cluster headaches which occur in groups most often in the spring and fall. These occur more in men than women. Onset is also in midlife but later than migraine. The incidence is 15.6 per 100,000 for men and 4.0 per 100,000 for women.86 Smoking may be associated with cluster headaches but personality characteristics may also play a role. Cluster headache occurrence appears to be related to peptic ulcer occurrence as well as cancer-related deaths. The cost of headaches is enormous. The restricted activity and disability, the use of medications, and the number of physician visits for diagnosis and treatment is large. Annual productivity lost due to migraine alone is estimated at $1 billion per year.87 NEUROTOXIC DISORDERS

Classic heavy metal exposures and solvents have led to neurological disorders. Occupational exposures have also been reported for acute neurological disease following exposure to industrial chemicals.88,89 Neurotoxic effects of organophosphorus insecticides include paralysis.90 Implications of chemicals for chronic diseases are being evaluated. For Parkinson’s disease the relationship of 1-methyl-4-phenyl tetrahydropyridine (MPTP) to parkinsonism symptoms demonstrated the influence of acute ingestion. Similar compounds such as paraquat and rotenone have caused parkinsonism in animals. Pesticides have been observed in several human studies to be related to neurological symptoms. A meta-analysis found a combined odds ratio of 1.94 (CI = 1.49–2.53).91 Chemicals in herbicides, insecticides, alkylated phosphates, organochlorines, and wood preservatives have also demonstrated increased risk.92–95 Alzheimer’s disease has been speculated to be potentially of neurotoxic origin but studies have not been conclusive. Chemicals implicated include aluminum, and solvents and electromagnetic fields. Further research is needed to provide evidence.

Amyotrophic lateral sclerosis (ALS) has been investigated particularly in the geographical cluster of the Western Pacific. Considerable research into the role of cycad derivatives and ALS has been done. Other studies have examined the association of heavy metals and ALS. Occupations with heavy metal exposure may be of higher risk. The role of agricultural chemicals has also been postulated because of a higher risk observed in farmers. Recently Persian Gulf War veterans were observed to have a higher rate of ALS. The source of the exposure is unknown.96 MULTIPLE SCLEROSIS

Multiple sclerosis (MS) is one of the demyelinating diseases and is characterized by white matter lesions.97 Classification of MS is dependent on clinical criteria that feature multiple lesions in the CNS separated in multiple locations and symptomatic attacks. Clinical presentation occurs in midlife and is highly variable. The spectrum of MS ranges from benign disease to rapidly fatal cerebral demyelination. Symptoms include sensory, visual, and motor dysfunction. The disease is generally progressive and is characterized by clinical remissions and exacerbations.98 Diagnosis of MS has been aided by the use of MRI which may detect early lesions.99 Onset of MS occurs between ages 15 and 65 years. The median ages at onset for cases identified in Rochester, Minnesota were 34 years for men and 32 years for women.100 Women had an incidence of 7.7 per 100,000, and 3.4 per 100,000 for men. MS shows a north-south geographical distribution. Another disease, which had a differential geographic pattern, was poliomyelitis. However with MS the northern hemisphere has distinct high risk zones. Prevalence increases as latitude increases. This has been observed in the United States and Europe. High-risk areas have prevalence rates of MS of greater than 50 per 100,000; low-risk areas have less than 5 per 100,000. Studies among migrants suggest that persons who move from an area of high prevalence to one of low prevalence take on the risk level of their new environment. The country (latitude) and the age of migration appear to an important determinant in MS risk.101,102 Migration before early adolescence (before age of 15) shifts the risk to the new country. With migration after 15 years, the individual has the risk of the former country. Kurtzke in studies of the Faroe Islands, felt that a minimum exposure time of two years was necessary to confer susceptibility.103–105 After 50 years of studying MS the causes are still unknown. The hypothesis is that gene and environmental factors are necessary for MS occurrence. Ethnic background may play a role since the highest rates are in areas populated by those with a northern European/Scandinavian background. Clusters and epidemics of MS have been reported. Clusters have been reported in Canada, Norway, and Florida. Epidemics have occurred in the Faroe lslands and in Iceland.103–105 No cases of MS were apparent before 1945. Since then cases have been reported with peaks in 1945, 1955, and 1965. Infectious agents have been studied extensively, but no single agent has yet been identified. Measles virus and canine distemper virus has received the most attention. Case-control studies have demonstrated a relationship with dog ownership. Infection may also be related to immunologic changed to increase susceptibility. Ecological studies have shown associations with low temperature, plants, soil, industrialization, meat consumption, type of meats, and dairy foods. Other factors that have been investigated with conflicting results include trauma, and exposure to trace elements and heavy metals, such as zinc and lead. Cigarette smoking may exacerbate the MS symptoms. Studies have demonstrated an increased risk in long-term smokers.106 A possible role for genetic factors in the etiology of MS has also been investigated. Caucasians of European descent are at highest risk. There has been familial aggregation of MS reported in several studies.107 Familial aggregation may be due to shared environment or genetic susceptibility. Twin studies have generally found a greater concordance for MS among monozygotic twins than among dizygotic twins. The risk to family members is low with 4% for siblings and

67 2–4% for children depending on gender. Since northern Europeans have a higher frequency of HLA-DR2, haplotype studies of HLA in MS have been the most consistent.108 Further candidate genes are peptide transporter genes and genes encoding tumor necrosis factor. The incidence of MS may be increasing as reported in Rochester, Minnesota.100 Changes in diagnostic studies may lead to improved ascertainment but few longitudinal, population-based databases exist. Survival is longer for women than men. Approximately 75% of MS patients will survive 25 years or more.109 The rate of progression and disability is variable. Many patients, even with progression, remain ambulatory for many years. There is currently no definitive therapy for MS that affects the ultimate course of the disease but steroid or ACTH therapy is used for acute exacerbations. Beta-interferon and azathioprine may be helpful in preventing relapses but data on rate of progression are inconclusive. STROKE

Stroke is as the third leading cause of death and a major a cause of long-term disability in the United States. It is estimated from population studies that strokes occur in 500,000 new cases and 200,000 recurrent cases each year.110 The total prevalence of stroke is estimated to be 4.7 million people in the United States. Stroke costs approximately $51.2 billion every year for acute care and long-term consequences. Stroke has declined over the past 30 years and has slowed in the most recent decade. Blood pressure control has been responsible for most of the major decline. Hence, stroke incidence and mortality reduction still remain as one of the health targets for the U.S. population. There has been a major recognition of stroke subtypes in classification, epidemiology and treatment. In the International Classification of Diseases, etiology, and pathology divides stroke into nine major groupings. Hemorrhagic stroke includes subarachnoid and intracerebral hemorrhage and well as other or unspecified intracranial hemorrhage. Ischemic stroke classification is based upon the location and duration of the occlusion. In addition, nonspecific categories of acute but ill-defined, and late effects of cerebrovascular disease are also used. New codes in ICD-10 were developed but the classification is similar.4 The comparability of ICD-9 and ICD-10 for cerebrovascular disease showed an increase by 6% for ICD-10 due to the inclusion of deaths from pneumonia secondary to stroke.4 The further classification is based upon stroke etiology, that is, occlusive disease and embolic origin. Large vessel occlusive disease and small vessel disease have differential causation and prognosis. Nearly one-third of strokes are of embolic origin, small-vessel thrombotic comprise 20%, and large vessel at 31%. Hemorrhagic stroke accounts for the remainder at 17%.110,111 Stroke mortality differentially affects individuals by race and gender. The highest risk group is black males. In 2000, the rate for black males was 87.1, for black females it was 78.1, with white males at 58.6 and white females at 57.6. Hispanics and Asian/Pacific Islanders and American Indian/Alaskan Native groups have lower rates of stroke mortality. From 1990 to 2000, the stroke mortality rate fell 12.3%. However, the actual number of strokes rose by 9.9%. With the increasing number of persons 65 years and older, the number of stroke deaths will continue to increase. There is a geographic variation in stroke. Mortality rates for stroke are higher in the southeast part of the United States.112 This is known as the stroke belt. Lowest rates are found in the mountain states. Differences may be due to risk factors such as hypertension and diabetes and suggested differences in access and type of care for stroke.113 Stroke risk factors can be classified in terms of nonmodifiable risk factors and modifiable risk factors. Those not modifiable include age, gender, race, and family history. Nonmodifiable risk factors alert us to those populations that we can target for modifiable risk factors. Those modifiable risk factors include hypertension, smoking, diabetes, cardiac disease, hyperlipidemia, physical activity, obesity, nutrition, drug abuse, hormone therapy, inflammatory disease, and biomarkers of risk.

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High blood pressure remains as the major modifiable risk factor for heart disease and stroke.114,115 The Multiple Risk Factor Intervention Trial (MRFIT) examined 350,000 men from 1973 to 1975 and followed for major fatal outcomes. An eightfold increased risk across systolic blood pressure (SBP) deciles and a fourfold risk for diastolic blood pressure (DBP) were observed. A comprehensive analysis of risk by blood pressure by MacMahon et al, showed that the associations of DBP with stroke demonstrated a “positive, continuous, and apparently independent association” which was consistent across all studies.116 Within the range of DBP (70–110 mm Hg), there was no evidence of any threshold. Approximately 50 million adults in the United States have high blood pressure. There has been an increase in the awareness of high blood pressure. The National High Blood Pressure Education Program began in 1972 and it has increased awareness of the importance of detection and control of blood pressure which has resulted in not only more hypertension control but also in the reduction of heart disease and stroke.117 Stroke risk increases with cigarette smoking independent of hypertension or age.118 The general increase is nearly 40% for men and 60% for women. The risk for smokers of two packs per day is approximately twice that of smokers who smoke less than half a pack per day.31 Evidence suggests that smokers decrease their risk when then quit and is back at the risk of nonsmokers 5 years after quitting.119 The risk for stroke is greater with the presence of diabetes. Studies have demonstrated a 1.5- to 3.0-fold increase in risk. Diabetes has been shown to be a consistent factor for atherothrombotic stroke. For hemorrhagic stroke the risk is reversed. Diabetics have age-adjusted stroke mortality and morbidity rates higher than nondiabetics.120 As evidence of the progression of atherosclerosis and increased risk for stroke, carotid stenosis is an important indicator. The risk of carotid disease was clearly demonstrated in the prospective followup of the North American Symptomatic Carotid Endarterectomy Trial (NASCET).121 The follow-up of patients with 70–99% stenosis demonstrated the risk of any ipsilateral stroke at three years was 28.3% for medically randomized arm and the combined disabling or fatal ipsilateral stroke risk was 14.0%. Over 80% of the first strokes were of large-artery origin. Clearly, the debate is what the magic cutoff for risk is and should patients be screened. Cardiac disease and abnormalities including coronary artery disease, congestive heart failure, left ventricular hypertrophy, valvular heart disease, atrial fibrillation, and cardiac thrombosis increase the risk of stroke. In Rochester, Minnesota the relative risk estimate for stroke was 2.2 and in Framingham the magnitude was similar with 1.9 for men and 2.2 for women.122 Atrial fibrillation affects close to 2 million individuals in the United States. Fifteen percent of the strokes occur in patients with atrial fibrillation. Data from Rochester, Minnesota indicated that atrial fibrillation has been increasing as a cause of ischemic stroke for both men and women and is independent of age.40 Cerebral infarction from sickle cell disease may be preventable according to a randomized clinical trial (stroke prevention in sickle cell anemia) to evaluate the prevention of a first stroke in children with sickle cell disease.123 Regular red cell transfusions sufficient to reduce the percentage of Hb S gene product from over 90 to less than 30 of total hemoglobin was associated with a marked reduction in stroke. High plasma levels of lipids are an important modifiable risk factor for coronary heart disease.124 In the Atherosclerosis Risk in Communities (ARIC) study cohort in 305 subjects with clinical ischemic stroke, the analyses demonstrated weak and inconsistent associations with each of the five lipid factors.125 Only among women was high HDL cholesterol associated with decreased risk of stroke. Overweight adults are a major epidemic and these adults are at an increased risk of developing numerous chronic diseases. In the women of the Nurses’ Health Study, and the men in the Health Professionals Follow-up Study, the risk of developing stroke increased with levels of overweight among both women and men.126 In a study of stroke subtype, the incidence of ischemic stroke, hemorrhagic stroke (subarachnoid or intraparenchymal hemorrhage), and total stroke was examined in the Nurses Health Study.127 During

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16 years of follow-up, 866 total strokes (including 403 ischemic strokes and 269 hemorrhagic strokes) occurred. Women with increased BMI (> or = 27 kg/m2) had significantly increased risk of ischemic stroke, with relative risks of 1.75, for BMI of 27–28.9 kg/m2; 1.90 for BMI of 29–31.9 kg/m2; and 2.37 for BMI of 32 kg/m2 or more. For hemorrhagic stroke there was a nonsignificant inverse relation between obesity and hemorrhagic stroke. Weight gain from age 18 years until 1976 was associated with an RR for ischemic stroke of 1.69 for a gain of 11–19.9 kg and 2.52 for a gain of 20 kg or more. Also weight change was not related to risk of hemorrhagic stroke. Physical inactivity has been demonstrated to increase the risk of stroke two- to threefold. Recently, in a cohort study in Finland of 2011 men the risk of low cardiorespiratory fitness was evaluated with the maximum oxygen consumption. The relative risk was 3.2 for all strokes and 3.5 for ischemic stroke.128 Another controversial risk factor has been the use of exogenous estrogens. Use of oral contraceptives has increased, and there is uncertainty about the stroke risk associated with their use. In casecontrol study techniques of women with ischemic stroke from four Melbourne hospitals, the current use of the oral contraceptives, in doses of < or = 50 µg estrogen, was not associated with an increased risk of ischemic stroke.129 In female members of the California Kaiser Permanente Medical Care Program, the odds ratio for ischemic stroke among current users of oral contraceptives, as compared with former users and women who had never used such drugs, was 1.18.130 The adjusted odds ratio for hemorrhagic stroke was 1.14. However with respect to the risk of hemorrhagic stroke, there was a positive interaction between the current use of oral contraceptives and smoking. For postmenopausal estrogens the observational studies warranted prospective trials. The Women’s Health Initiative (WHI) trial of estrogen plus progestin was stopped early because of adverse effects, including an increased risk of stroke in the estrogen plus progestin group.131 For combined ischemic and hemorrhagic strokes, the intention-to-treat hazard ratio (HR) for estrogen plus progestin versus placebo was 1.31. The HR for ischemic strokes was 1.44 and for hemorrhagic stroke, 0.82. Excess risk of all stroke was apparent in all age groups, in all categories of baseline stroke risk, and in women with and without hypertension, prior history of cardiovascular disease (CVD), use of hormones, statins, or aspirin. Another randomized, double-blind, placebo-controlled trial of estrogen therapy was done in postmenopausal women who had recently had an ischemic stroke or transient ischemic attack.132 With a mean follow-up period of 2.8 years, the women in the estrogen group compared to placebo group showed no benefit (relative risk in the estradiol group, 1.1). The women who were randomly assigned to receive estrogen therapy had a higher risk of fatal stroke (relative risk, 2.9). This therapy was shown not to be effective for the primary or secondary prevention of cerebrovascular disease. Epidemiologic evidence, animal studies, angiographic and ultrasound studies in humans, and a limited number of clinical trials suggest that vitamins C and E may be protective and that folate, B6 and B12, by lowering homocysteine levels, may reduce stroke incidences. Few population-based studies have examined the relationship between dietary intake of folate and risk of stroke. In the National Health and Nutrition Examination Survey I Epidemiologic Followup Study (NHEFS), dietary intake of folate was assessed at baseline using a 24-hour dietary recall.133 Incidence data for stroke over an average of 19 years of follow-up showed a relative risk of 0.79. Although hypercoagulable states are most often associated with venous thrombosis, arterial thromboses are reported in protein S, protein C, and antithrombin III deficiencies, factor V Leiden and prothrombin gene mutations, hyperhomocysteinemia, dysfibrinogenemia, plasminogen deficiency, sickle cell disease, and antiphospholipid antibody syndrome. Antiphospholipid antibodies have been associated with increased stroke risk. In the Stroke Prevention in Young Women Study, a positive anticardiolipin antibody and/or lupus anticoagulant was found in a greater proportion of cases. The findings support the importance of more research to determine the

role of antiphospholipid antibodies as an independent risk factor for stroke.134 The role of C-reactive protein (CRP) in stroke was observed in several studies to predict incident stroke independent of LDL cholesterol. Statins have also been shown to reduce CRP independent of lipid changes. In the Physicians’ Health Study of healthy middle-aged men and in the Women’s Health Study of healthy postmenopausal women, total cholesterol and CRP both predict incident myocardial infarction and only CRP predicts incident stroke.135,136 Similar findings have been found in the National Health and Nutrition Examination Survey (NHANES), the Leiden 85-Plus Study and the Framingham Heart Study. In the Framingham Heart Study, CRP was found to be a strong predictor of stroke even after adjustment for other risk factors. The plaque stabilization concept through anti-inflammatory mechanisms provides a working hypothesis as to why statins might reduce cerebrovascular risk.137–139 Primary prevention includes modifying risk factors of lifestyle and behavior such as not smoking; diet such as fish, fruits, and vegetables; adequate physical exercise; limiting alcohol; and adhering to physician recommendations for screening, monitoring, and treating blood pressure, cholesterol, and diabetes (blood glucose). Secondary prevention requires intervention by the health care provider, which includes hypertension treatment, cholesterol treatment, for example, statins, TIA treatment, antiplatelets, anticoagulation for atrial fibrillation and other cardiac sources, ACS treatment, and carotid endarterectomy. Recently the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) completed double-blind, active-controlled trials. The study enrolled 42,448 patients, >55 years old, with hypertension (systolic BP >140 mmHg and/or diastolic BP >90 mmHg) and at least one other coronary heart disease (CHD) risk factor. Treatment comparison was with the diuretic chlorthalidone and three other agents.140–142 The doxazosin treatment arm of the blood pressure-lowering component of the trial had a higher incidence of major CVD events compared to chlorthalidone. The doxazosin arm, compared with the chlorthalidone arm, had a higher risk of stroke (RR, 1.19). For lisinopril versus chlorthalidone, lisinopril had higher six-year rates of combined stroke (6.3% vs. 5.6%; RR, 1.15). Thiazide-type diuretics were found to be superior. In a meta-analysis the odd ratios for differences in systolic pressure between group in 62,605 hypertensive patients.143 Compared with old drugs (diuretics and beta-blockers), calcium-channel blockers and angiotensin converting-enzyme inhibitors offered similar overall cardiovascular protection, but calcium-channel blockers provided more reduction in the risk of stroke (13.5%). All of the antihypertensive drugs had similar long-term efficacy and safety but calciumchannel blockers were more effective in stroke prevention. The Scandinavian Simvastatin Survival Study demonstrated with 5.4 years of follow-up a significant change in stroke risk by lowering cholesterol of 3.4% versus 4.6%(p = 0.03).144 The study showed that a 28% risk reduction in stroke and TIA could be achieved. It was noted in the study that 55% of the subjects also were on aspirin. Another study, the Long-term Intervention with Pravastatin in Ischemic Disease (LIPID), demonstrated a similar result of 3.4% compared to 4.4%; a p-value of 0.02.145 The risk reduction of 24% was found in nonhemorrhagic strokes; 84% of the patients were also on aspirin. A meta-analysis of 12 trials comprising 182 strokes in the statin group and 248 in the placebo group demonstrated that stroke was reduced in all trials or secondary prevention trials. However, subgroup analysis indicated that no difference in primary prevention was evident. Aspirin has been studied in a number of trials with differing dosages. A meta-analysis of 16 trials with a dosage ranging from 75 to 1500 mg/day was done.146 The hemorrhagic stroke rate was .26% or an increased risk of 12% was found. However the ischemic stroke rate of 1.7% was associated with a 39% risk reduction. Hence there was greater benefit than risk with aspirin use. Anticoagulants have been evaluated in stroke prevention. For patients with atrial fibrillation, Warfarin reduces stroke by 68%. The

67 annual stroke rate reduced from 4.5 to 1.4% per year. However, there is a tendency for cardioembolic stroke to undergo hemorrhagic transformation. Also, patients under 60 years old with lone atrial fibrillation without other stroke risk factor were observed to not need warfarin.148 Surgical prevention of stroke was shown to be efficacious through the North American Symptomatic Carotid Endarterectomy Trial (NASCET).149,150 Patients less than 80 years old with a recent hemispheric TIA or nondisabling stroke and atherosclerotic lesion were included in the trial. Patients with a stroke from a cardioembolic source or uncontrollable hypertension or diabetes were not included. The average age was 66 years (range 35–80 years) and one-third of the subjects were women. Thirty-two percent had a prior stroke. Most risk for surgery was early with a 5.8% incidence of stroke or death. However, at two years the risk of ipsilateral stroke was reduced by 65% in patients with a >70% carotid stenosis. The European Carotid Surgery Trial (ECST), and the VA Cooperative Study (VACS) also demonstrated that carotid endarterectomy decreases stroke in symptomatic patients with high-grade extracranial carotid artery stenosis.150 The combined risk ratio estimate was 0.67 and found a similar benefit for men and women. Carotid endarterectomy to reduce the incidence of cerebral infarction in patients with asymptomatic carotid artery stenosis was studied in a prospective, randomized, multicenter trial. Patients with asymptomatic carotid artery stenosis of 60% or greater reduction in diameter were randomized—and after a median follow-up of 2.7 years the aggregate risk over five years for ipsilateral stroke and any perioperative stroke or death was estimated to be 5.1% for surgical patients and 11.0% for patients treated medically. Stroke prevention requires then a combination or continuum risk factor assessment, modification and interventions. Modifiable risk factors such as blood pressure, cholesterol, blood sugar, body mass index, homocysteine, and smoking habits can be routinely done. Prescription and adherence of blood pressure medications, statins, and antiplatelets agents have been shown to be effective as secondary prevention methods. Surgical prevention by carotid endarterectomy has also proven to be effective but should be reserved for those with highgrade stenosis. The role of angioplasty in secondary or tertiary prevention of ischemic strokes still needs evidential proof. With increasing age of the population there will be an increase in the number of strokes. Prevention is the key in the next decade to provide a decrease in disability and death. PARKINSON’S DISEASE

Parkinson’s disease is a progressive neurologic disorder with bradykinesia, resting tremor, rigidity, and postural reflex. The disorder is due to progressive loss of pigmented neurons associated with loss of dopamine. The onset is insidious, progression tends to be gradual, and the course of the disease is usually prolonged. Diagnosis is based on clinical criteria which have changed over time due to changes in clinical practice. Misdiagnosis with depression and multiple system involvement leads to variable case determinations. Parkinson’s disease may occur with dementia in 10–25 % of cases.151 Incidence rates for Parkinson’s disease are varied and reported to range from 4 to 20 per 100,000. In Rochester, Minnesota the incidence was 20.5 per 100,000 and in a study in northern Manhattan the rate was 13 per 100,000.152,153 The incidence rates increase with age with the highest rates in 70 to 79-year-olds. Prevalence of Parkinson’s disease has varied widely with the range from 31.4 to 347 per 100,000.154 Differences in case ascertainment using clinical, drug usage, and survey data may account for this variation. There has been little change in the age-adjusted incidence in Parkinson’s disease over time but with increasing age and survival the number of affected individuals is likely to increase. Parkinsonism may be a direct result from exposure to toxins (e.g., carbon monoxide or manganese), drugs (e.g., phenothiazides), traumatic or vascular lesions of the brain, or tumors.155

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Arteriosclerosis, when present, is most likely a concurrent disease rather than a subtype of parkinsonism. Postencephalitic parkinsonism is well recognized but accounts for a relatively small and decreasing proportion of all prevalent cases. However, the cause of most cases of Parkinson’s disease remains obscure. Age is a known risk factor because the occurrence is dependent upon the loss of neurons, which indicates a chronic onset. Whether or not men or women are at greater risk is difficult to establish. Population studies have suggested men are at higher risk but the prevalence may be higher in women due to their longer survival. The debate of genetic predisposition versus environmental exposure is unresolved. Several studies of familial aggregation suggest that a positive family history of Parkinson’s disease is present in 16 to 41% of idiopathic cases. Pure genetic forms may account for only 10–15% cases. Twin studies do not show a relationship with clinical Parkinson’s disease or f-dopa uptake analysis.156 Environmental exposures are suggested through variations in the geographic distribution of the disease and by associations from analytical studies.155 Parkinson’s disease incidence is higher in Europe and North America.155 With population studies, the rates are higher for whites and Hispanics than blacks; however, the door-to-door survey in Copiah County, Mississippi found no difference in rates.155 A difference in clinical diagnosis of Parkinson’s disease may play a role in this relationship. Etiological studies using a variety of case ascertainment methods have suggested that rural residence, farming, well-water drinking, and herbicide/pesticide exposure are related to Parkinson’s disease.155 Infectious agents have been evaluated, particularly focusing on the epidemic of 1918. However no agents or relationships have been found. Coronavirus titers have been found to be elevated in Parkinson’s patients which may indicate an animal exposure. Other factors that have been suggested but unproven include head trauma and emotional stress.157,158 Recent studies suggest that diet may be important. Animal fat and protein intake may increase risk. Antioxidants have demonstrated inconsistent results as a protective factor.159,160 Numerous studies have reported a lower risk of Parkinson’s disease among cigarette smokers. Various explanations for this observation have been proposed, but whether the inverse association between cigarette smoking and risk of Parkinson’s disease has biological significance or behavioral relationship remains controversial.155,161 Caffeine consumption may also be protective.162 The observation that drug abusers exposed to the meperidine derivative MPTP sometimes have a syndrome clinically indistinguishable from advanced Parkinson’s disease, as well as subsequent studies using animal models of MPTP toxicity, support the hypothesis that environmental exposures may be important in causing Parkinson’s disease.163–165 Parkinson’s disease remains an increasing problem with the advancing age of the population. The disease leads to progressive disability. Agents have demonstrated efficacy in limiting the symptoms and disability. The etiology has yet to be determined. DEMENTIAS

Dementia is a relatively heterogeneous clinical syndrome characterized by a decline in intellectual functioning such as memory, reasoning, judgment, calculation, abstraction, and language. In addition to the decline in cognitive abilities, there are clear decrements in everyday functioning such as activities of daily living and social activities. The diagnosis of dementia requires that there be no coexisting disturbances of consciousness166 or any other acute conditions or situations that preclude clinical or psychological evaluation of cognitive performance. There is no universal agreement on the criteria for the dementia syndrome, but several useful published criteria exist in the International Classification of Diseases and elsewhere.166–168 The dementia syndrome has many known causes, including a variety of concurrent nonneurologic diseases, medications, and toxic environmental exposures;166 some dementia patients with defined environmental or anatomic causes may have their syndromes at least partially

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reversible. However, it is generally felt that over half of clinical dementia cases are due to Alzheimer’s disease (AD), with the next most common causes being related to cerebrovascular disease and Parkinson’s disease.169 Human immunodeficiency virus is neurotropic, and an AIDS-related dementia syndrome has been identified as the most common neurologic complication of this disease. However, AIDS is associated with increased risk of other important central nervous system conditions, some of which may have dementialike clinical features, and the differential diagnostic possibilities must be kept in mind.170 The epidemiology of the dementias and AD suggests that they are an important and growing public health problem, particularly among older persons. While community surveys of the prevalence and incidence of dementia and AD can be methodologically challenging, it appears that the prevalence of dementia in persons 85 years and older and residing in the community may be as high as 40–50%.171,172 The prevalence of dementia has been found to double every five years of age from age 3–70.173 Accurate geographicallybased prevalence and incidence of dementia are sometimes hampered by several factors, including frequent supervening of substantial clinical morbidity, the refusal or inability of demented patients to participate in surveys and the increased likelihood that dementia patients will be institutionalized. However, there is considerable geographic variation with low incidence rates reported in developing countries.174–176 Because it is the most common form of dementia, AD has received substantial attention in terms of etiology, pathogenesis, and prevention. As dementia in general, AD increases in incidence with increasing age among older persons.177,178 The geographical variation may be due to variation in diet, education, life expectancy, socialcultural factors and environmental factors. Several putative risk factors for AD have been identified, such as prior head trauma and aluminum exposure, but few have received consensual agreement as to being true causes, and no known risk factors as yet form a specific prevention strategy.179–181 Possible preventive effects of exogenous estrogen use are still unproven.181 Other possible protective factors include education, gene APO E2, antioxidant consumption, and use of some anti-inflammatory medications. The discovery of genetic factors with three genes (APP, PS1, and PS2) in familial and APO E4 in nonfamilial AD is an important advance but not yet confirmed in large studies.173,182,184 Interventions are still focused on the caregivers and behavioral management.185,186 Focusing on risk factors for cardiovascular and cerebrovascular disease may lessen the risk for multi-infarct dementia. CONCLUSION

The changing incidence of neurological conditions is in part changing diagnosis and classification. The increasing prevalence of chronic neurological conditions is due to the aging of the population, effective treatments, and longer survival. New problems such as the spread of WNV or the zoonotic spread of CJD have increased the need for surveillance, prevention, and health care. This has profound impacts on the magnitude of disability and impairment in the population and will have more as the number of people with chronic conditions increase. There are still many neurological conditions that public health screening or prevention await further research. The exciting findings of genetic predisposition aided with environment interaction studies are important for future research in determining causation and risk. The need for public health and clinical services will continue to grow as the neurological disease burden increases. REFERENCES

1. Murray CJL, Lopez AD, Mathers CD, et al. The Global Burden of Disease 2000 Project: aims, methods, and data sources. Harvard Burden of Disease Unit; November, 2001. Research Paper No. 01.1.

2. Mathers CD, Lopez AD, Murray CJL. The burden of disease and mortality by condition: data, methods, and results for 2001. In: AD Lopez, CD Mathers, M Ezzati, DT Jamison, CJL Murray, eds. Global Burden of Disease and Risk Factors. New York, Oxford University Press; 2006. 3. Mathers CD, Bernard C, Moesgaard Iburg K, et al. Global Burden of Disease in 2002: data sources, methods and results. Global Programme on Evidence for Health Policy Discussion, Paper No. 54. World Health Organization; December, 2003. 4. Anderson RN, Minino AM, Hoyert DL, et al. Comparability of cause of death between ICD-9 and ICD-10: preliminary estimates. Natl Vital Stat Rep. May 18, 2001;49(2):1–32. 5. Centers for Disease Control and Prevention http://www.cdc.gov/ nchs/about/major/hdasd/nhds.htm#Publications 6. Schappert SM. Office visits to neurologists: United States, 1991–1992. Advance Data from Vital and Health Statistics, No. 267. National Center for Health Statistics; 1995. 7. Wodwell DA, Schappert SM. National Ambulatory Medical Care Survey: 1993 summary. Advance Data from Vital and Health Statistics, No. 270. National Center for Health Statistics, 1995 8. Summary Health Statistics for U.S. Adults National Health Interview Survey, 2004. Vital and Health Statistics, Series 10, Number 228, U.S. Dept. of Health and Human Services; May 2006, DHHS Publication No. (PHS) 2006–1556. 9. Kubak KCK, Leviton A. Cerebral palsy. N Eng J Med. 1994;330: 188–95. 10. Stanley F, Blair E, Alberman E. Cerebral Palsies: Epidemiology and Causal Pathways. London: Mac Keith Press; 2000. 11. Nelson KB, Grether JK. Causes of cerebral palsy. Curr Opin Pediatr. 1999;11:487–91. 12. Boyle CA, Yeargin-Allsopp M, Doernberg NS, et al. Prevalence of selected developmental disabilities in children 3-10 years of age: the Metropolitan Atlanta Developmental Disabilities Surveillance Program, 1991. MMWR. 1996;45:SS–2;1–14. 13. Nelson KB, Ellenberg JH. Childhood neurological disorders in twins. Paediatr Perinat Epidemiol. 1995;9:135–45. 14. Pharoah POD, Cooke T, Rosenblood I, et al. Trends in the birth prevalence of cerebral palsy. Arch Dis Child. 1987;62:379–89. 15. Pharoah PO, Platt MJ, Cooke T. The changing epidemiology of cerebral palsy. Arch Dis Child Fetal and Neonatal Ed. 1996;75(3): F169–73. 16. Meberg A, Broch H. A changing pattern of cerebral palsy. Declining trend for incidence of cerebral palsy in the 20-year period 1970–1979. J Perinat Med. 1995;23(5):395–402. 17. Grether JK, Cummins SK, Nelson KB. The California cerebral palsy project. Paediatr Perinat Epidemiol. 1992;6:339–51. 18. Murphy CC, Yeargin-Allsopp M, Decoufle P, et al. The administrative prevalence of mental retardation in 10-year-old children in metropolitan Atlanta, 1985 through 1987. Am J Public Health. 1995;85:319–23. 19. O’Shea TM, Preisser JS, Klinepeter KL, et al. Trends in mortality and cerebral palsy in a geographically based cohort of very low birth weight neonates born between 1982 and 1994. Pediatrics. 1998;101:624–7. 20. Benda GI, Hiller JL, Reynolds JW. Benzyl alcohol toxicity: impact on neurologic handicaps among surviving very low birth weight infants. Pediatrics. 1986;77:507–12. 21. Nelson KB, Ellenberg JH. Antecedents of cerebral palsy: multivariate analysis of risk. N Engl J Med. 1986;315:81–6. 22. Blair E, Stanley FJ. Intrapartum asphyxia: a rare cause of cerebral palsy. J Pediatr. 1988;122:575–9. 23. Nelson KB, Ellenberg JH. Antecedents of cerebral palsy: univariate analysis of risks. Am J Dis Child. 1985;139:1031–8. 24. Stanley JK, Watson L. The cerebral palsies in Western Australia: trends, 1968 to 1981. Am J Obstet Gynecol. 1988;158:89–93. 25. Emond A, Golding J, Peckham C. Cerebral palsy in two national cohort studies. Arch Dis Child. 1989;64:848–52.

67 26. Nelson KB, Grether JK. Potentially asphyxiation conditions and spastics cerebral palsy in infants of normal birthweight. Am J Obstet Gynecol. 1998;179:507–13. 27. Harum KH, Hoon AH, Kato GJ, et al. Homozygous factor V mutation at a genetic cause of perinatal thrombosis and cerebral palsy. Dev Med Child Neurol. 1999;41:777–80. 28. Nelson KB, Grether JK. Can magnesium sulfate reduce the risk of cerebral palsy in very low birth weight infants? Pediatrics. 1995;95: 263–9. 29. Centers for Disease Control and Prevention. U.S. HIV and AIDS reported through December 1994. HIV/AIDS Surveillance Report. 1994;6:1–9. 30. Dal Pan GJ, McArthur JC. Neuroepidemiology of HIV Infection. Neurol Clin. 1996;14:359–81. 31. McArthur JC. HIV dementia: an evolving disease. J Neuroimmunol. Dec 2004;157(1–2):3–10. 32. Sacktor N. The epidemiology of human immunodeficiency virusassociated neurological disease in the era of highly active antiretroviral therapy. J Neurovirol. Dec 2002;8 (2):115–21. 33. Gray F, Chretien F, Vallat-Decouvelaere AV, et al. The changing pattern of HIV neuropathology in the HAART era. J Neuropathol Exp Neurol. May 2003;62(5):429–40. 34. Brodt HR, Kamps BS, Gute P, et al. Changing incidence of AIDSdefining illnesses in the era of antiretroviral combination therapy. AIDS. 1997;11:1731–8. 35. Schifitto G, McDermott MP, McArthur JC, et al. Incidence of and risk factors for HIV-associated distal sensory polyneuropathy. Neurology. 2002;58:1764–8. 36. Bouwman FH, Skolasky R, Hes D, et al. Variable progression of HIV-associated dementia. Neurology. 1998;50:1814–20. 37. Johnson RT, McArthur JC, Narayan O. The neurobiology of human immunodeficiency virus infection. FASEB J. 1988;2:290–2981. 38. McArthur JC. Neurologic Manifestations of AIDS. Medicine (Baltimore). 1987;66:407–37. 39. Janssen RS, Nwanyanwu, Selik RM, et al. Epidemiology of human immunodeficiency virus encephalopathy in the United States. Neurology. 1992;42:1742–6. 40. McArthur JC, Hoover DR, Bacellar H, et al. Dementia in AIDS patients: Incidence and risk factors. Neurology. 1993;43:2245–53. 41. Navia BA, Jordon BD, Price RW. The AIDS dementia complex. I. Clinical features. Ann Neurol. 1986;19:517–24. 42. Arendt G, Hefter, Buescher L, et al. Improvement of motor performance of HIV-positive patients under AZT therapy. Neurology. 1992;42:891–5. 43. Cornbalth DR, McArthur JC. Predominantly sensory neuropathy in patients with AIDS and AIDS-related complex. Neurology. 1988;38:794–6. 44. Pizzo PA, Eddy J, Falloon J, et al. Effect on continuous intravenous infusion of zidovudine (AZT) in children with symptomatic HIV infection. N Eng J Med. 1988;319:889–96. 45. Fuller GN, Jacobs JM, Guilloff RJ. Nature and incidence of peripheral nerve syndromes in HIV infection. J Neurol Neurosurg Psychiatry. 1993;56:372–81. 46. Blum A, Dal Pan G, Raines C, et al. ddC-related toxic neuropathy: Risk factors and natural history. Neurology. 1993;4(2):A190. 47. Lambert JS, Seidlin M, Reichman RC, et al. 2’,3’-dideoxyinosine (dI) in patients with the acquired immunodeficiency syndrome or AIDSrelated complex: A phase I trial. N Engl J Med. 1990;322:1333–40. 48. Chuck SL, Sande MA. Infections from cryptococcus neoformans in acquired immunodeficiency syndrome. N Eng J Med. 1989;321: 794–9. 49. Larsen RA, Leal MA, Chan LS. Fluconazole compared with amphotericin B plus flucytosine for cryptococcal meningitis in AIDS: A randomized trial. Ann Intern Med. 1990;113:183–97. 50. Jabs DA, Green WR, Fox R, et al. Ocular manifestations of acquired immunodeficiency syndrome. Ophthalmology. 1989;96:1092–9.

Neurological Disorders

1149

51. Degans J, Portegies P. Neurological complications of infection with human immunodeficiency virus type 1: A review of literature and 241 cases. Clin Neurol Neurosurg. 1989;91:199–219. 52. Guiloff RJ, Fuller GN, Roberts A, et al. Nature, incidence and prognosis of neurological involvement in the acquired immunodeficiency syndrome in central London. Postgrad Med J. 1988;64: 919–25. 53. Eby NL, Grufferman S, Flannelly CM, et al. Increasing incidence of primary brain lymphoma in the U.S. Cancer. 1988;62:2461–5. 54. Rosenbloom ML, Levy RM, Bredesen DE, et al. Primary central nervous system lymphomas in patients with AIDS. Ann Neurol. 1988;23:S13–S16. 55. Johnson RT. Prion diseases. Lancet Neurol. Oct 2005;4(10): 635–42. 56. Belay ED, Schonberger LB. The public health impact of prion diseases. Annu Rev Public Health. 2005;26:191–212. 57. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol. 1999;53:283–314. 58. Centers for Disease Control and Prevention. Bovine spongiform encephalopathy in a dairy cow—Washington state, 2003. MMWR. 2004;52:1280–85. Will RG. Acquired prion disease: iatrogenic CJD, variant CJD, kuru. Br Med Bull. 2003;66:255–65. 59. Turner ML. vCJD screening and its implications for transfusion— strategies for the future? Blood Coagul Fibrinolysis. Jun 2003;14 (1):S65–8. 60. Hayes EB, Komar N, Nasci RS, et al. Epidemiology and transmission dynamics of West Nile virus disease. Emerg Infect Dis. 2005;11:1167–73. 61. Watson JT, Pertel PE, Jones RC, et al. Clinical characteristics and functional outcomes of West Nile fever. Ann Intern Med. 2004;141:360–5. 62. O’Leary DR, Marfin AA, Montgomery SP, et al. The epidemic of West Nile virus in the United States, 2002. Vector Borne Zoonotic Dis. 2004;4:61–70. 63. Komar N. West Nile virus: epidemiology and ecology in North America. Adv Virus Res. 2003;61:185–234. 64. Davidson AH, Traub-Dargatz JL, Rodeheaver RM, et al. Immunologic responses to West Nile virus in vaccinated and clinically affected horses. J Am Vet Med Assoc. 2005;226:240–5. 65. CDC. West Nile Virus Activity—United States, January 1–December 1, 2005. MMWR. 2005;54:1253–6. 66. Commission on Classification and Terminology of the International League against Epilepsy. A revised proposal for the classification of epilepsy and epileptic syndromes. Epilepsia. 1989;30:268–78. 67. Commission on Epidemiology and Prognosis, International League against Epilepsy. Guidelines for epidemiologic studies on epilepsy. Epilepsia. 1993;34:592–6. 68. Commission on Classification and Terminology of the International League against Epilepsy. A proposal for revised clinical and electroencephalographic classification of epileptic seizures. Epilepsia. 1981;22:489–501. 69. Hauser WA, Annegers JF, Rocca WA. Descriptive epidemiology of epilepsy: Contributions of population-based studies from Rochester, Minnesota. Mayo Clin Proc. 1996;71:576–86. 70. Haerer AF, Anderson DW, Schoenberg BS. Prevalence and clinical features of epilepsy in a biracial United States population. Epilepsia. 1986;27:66–75. 71. Hauser WA. Epidemiology of epilepsy. In: Gorelick PB, Alter M, eds. Handbook of Neuroepidemiology. Marcel Dekker, Inc., New York; 1994:315–56. 72. Annegers JF, Rocca WA, Hauser WA. Causes of epilepsy: contributions of the Rochester Epidemiology Project. Mayo Clin Proc. 1996;71:570–5. 73. Hauser WA, Annegers JF, Anderson VE, et al. The risk of seizure disorders among relatives of children with febrile convulsions. Neurology. 1985;35:1268–73.

1150

Noncommunicable and Chronic Disabling Conditions

74. Kaneko S Okada M, Iwasa H, et al. Genetics of epilepsy: current status and perspectives. Neurosci Res. 2002;44:11–30. 75. Silberstein SD, Lipton RB. Headache epidemiology. Emphasis on migraine. Neuroepidemiology. 1996;14:421–34. 76. Leviton A. Epidemiology of headache. Adv Neurol. 1978;19: 341–353. 77. National Center for Health Statistics. Advance Data. Vital and Health Statistics of the Unit PHS. Pub 53, Hyattsville; 1979. 78. Stang PE, Osterhaus JT. Impact of migraine in the United States: data from the National Health Interview Survey. Headache. 1993;33:29–35. 79. Centers for Disease Control. Health, United States, 2005. Library of Congress Catalog Number 76–641496. 80. International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias, and facial pain. Cephalalgia. 1988;8:1. 81. Olesen J, Lipton RB. Migraine classification and diagnosis: International Headache Society criteria. Neurology. 1994;44(4): S6–S10. 82. Stang PE, Yanagihara T, Swanson JW, et al. Incidence of migraine headache: A population-based study in Olmsted County, Minnesota. Neurology. 1992;42:1657–62. 83. Stewart WF, Shechter A, Rasmussen BK. Migraine prevalence. A review of population-based studies. Neurology. 1994;44(4): S17–S23. 84. Lipton RB, Stewart WF. Migraine in the United States: a review of use. Neurology. 1993;43(3):6–10. 85. Couch JR, Hassanein RS. Headache as a risk factor in atherosclerosis-related diseases. Headache. 1989;29:49–54. 86. Swanson JW, Yanagihara T, Stang PE, et al. Incidence of cluster headaches: A population-based study in Olmsted County, Minnesota. Neurology. 1994;44:433–7. 87. Osterhaus JT, Gutterrnan DL, Plachetka JR. Healthcare resources and lost labor costs of migraine headaches in the U.S. Pharmacoeconomics. 1992;2:67. 88. White RF, Proctor SP. Solvents and neurotoxicity. Lancet. 1997;349:1239–43. 89. Landrigan PJ, Kreiss K, Xintaras C, et al. Clinical epidemiology of occupational neurotoxic disease. Neurobehav Toxicol. 1980;2:43–8. 90. Senanayake N, Karalliedde L. Neurotoxic effects of organophosphorus insecticides. NEJM. 1987;316:761–3. 91. Priyadarshi A, Khuder SA, Schaub EA, et al. A meta-analysis of Parkinson’s disease and exposure to pesticides. Neurotoxicology. 2000;21:435–40. 92. Semchuck KM, Love EJ, Lee RG. Parkinson’s disease and exposure to agricultural work and pesticide chemicals. Neurology. 1992;42: 1328–35. 93. Butterfield PG, Valanis BG, Spencer PS, et al. Environmental antecedents of young-onset Parkinson’s disease. Neurology. 43:1150-1158, 1993. 94. Seidler A, Hellenbrand W, Robra BP, et al. Possible environmental, occupational and other etiologic factors for Parkinson’s disease: a case-control study in Germany. Neurology. 1996;46:1275–84. 95. Gorell JM, Johnson CC, Rybicki BA, et al. The risk of Parkinson’s disease with exposure to pesticides, farming, well water, and rural living. Neurology. 1998;50:1346–50. 96. Horner RD, Kamins KG, Feussner JR, et al. Related articles, occurrence of amyotrophic lateral sclerosis among Gulf War veterans. Neurology. 2003;61(6):742–9. Review. Erratum in: Neurology. 2003;61(9):1320. 97. McFarlin DE, McFarland HF. Multiple sclerosis. Parts 1 and 2. N Engl J Med. 1982;307:1183–8, 1246–51. 98. Thompson AJ, Hutchinson A, Brazil J, et al. A clinical and laboratory study of benign multiple sclerosis. QJ Med. 1986;58: 69–80.

99. McDonald I. Diagnostic methods and investigation in multiple sclerosis. In: Compston A, ed. McAlpine’s Multiple Sclerosis. 3rd ed. New York, Churchill Livingstone; 1998:251–79. 100. Wynn DR, Rodriguez M, O’Fallon WM, et al. A reappraisal of the epidemiology of multiple sclerosis in Olmsted County, Minnesota. Neurology. 1990;40:780–6. 101. Alter M, Leibowitz U, Speer J. Risk of multiple sclerosis related to age of immigration to Israel. Arch Neurol. 1966;15:234–7. 102. Dean G. Annual incidence, prevalence and mortality of multiple sclerosis in white South African-born and in white immigrants to South Africa. BMJ. 1967;2:724–30. 103. Kurtzke JF, Hyllested K. Multiple sclerosis in the Faroe Islands I. Clinical and epidemiological features. Ann Neurol. 1979;5:6–21. 104. Kurtzke JF, Hyllested K. Multiple sclerosis in the Faroe Islands II. Clinical update, transmission, and the nature of MS. Neurology. 1985;36:307–28. 105. Kurtzke JF, Hyllested K. Multiple sclerosis in the Faroe Islands III. An alternative assessment of the three epidemics. Acta Neurol Scand. 1987;76:317–39. 106. Hernan M, Olek M, Ascherio A. Cigarette smoking and incidence of multiple sclerosis. Am J Epidemiol. 2001;154:69–74. 107. Weinshenker BG. Epidemiology of multiple sclerosis. Neurol Clin. 1996;14:291–308. 108. Compston A. Genetic suspectibility to multiple scelerosis. In: Compston A, ed. McAlpine’s Multiple Sclerosis. 3rd ed. Churchill Livingstone, New York; 1998:101–42. 109. Poser CM. The epidemiology of multiple sclerosis: A general overview. Ann Neurol. 1994;36(S2):S180–S193. 110. Broderick J, Brott T, Kothari R, et al. The Greater Cincinnati/ Northern Kentucky Stroke Study: preliminary first-ever and total incidence rates of stroke among blacks. Stroke. Feb 1998;29(2): 415–21. 111. Keir SL, Wardlaw JM, Warlow CP. Stroke epidemiology studies have underestimated the frequency of intracerebral hemorrhage. A systematic review of imaging in epidemiological studies. J Neurol. Sep 2002;249(9):1226–31. 112. Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtypes of acute ischemic stroke: definitions for use in a multicenter clinical trial. Stroke. 1993;23:35. 113. Lanska DJ. Geographic distribution of stroke mortality in the United States, 1939-1941 to 1979-1981. Neurology. 1993;43:1839. 114. Krishner HS. Medical prevention of stroke. South Med J. Apr 2003;96(4)354–8. 115. He J, Whelton PK. Elevated systolic blood pressure and risk of cardiovascular and renal disease: overview of evidence from observational epidemiologic studies and randomized controlled trials. Am Heart J. 1999;138(3 Pt 2):211–9. 116. Stamler J, Stamler R, Neaton JD. Blood pressure, systolic and diastolic, and cardiovascular risks. U.S. population data. Arch Intern Med. 1993;153(5):598–615. 117. MacMahon S, Peto R, Cutler J, et al. Blood pressure, stroke, and coronary heart disease. Part 1, Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet. Mar 31, 1990;335(8692):765–74. 118. SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. Final results of the Systolic Hypertension in the Elderly Program (SHEP). JAMA. 1991;265:3255–64. Sinton R, Beevers G. Meta-analysis of the relation between cigarette smoking and stroke. BMJ. 1989;25:298:784–94. 119. Wolf PA, D’Agostino RB, Kannel WB, et al. Cigarette smoking as a risk factor for stroke. The Framingham Study. JAMA. Feb 19, 1988;259(7):1025–9. 120. Barrett-Connor E, Khaw KT. Diabetes mellitus: an independent risk factor for stroke? Am J Epidemiol. Jul 1988;128(1):116–23.

67 121. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325(7):445–53. 122. Tsang TS, Petty GW, Barnes ME, et al. The prevalence of atrial fibrillation in incident stroke cases and matched population controls in Rochester, Minnesota: changes over three decades. J Am Coll Cardiol. 2003;42(1):93–100. 123. Styles LA, Hoppe C, Klitz W, et al. Trachtenberg E. Evidence for HLA-related susceptibility for stroke in children with sickle cell disease. Blood. Jun 1, 2000;95(11):3562–7. 124. Gorelick PB, Mazzone T. Plasma lipids and stroke. J Cardiovasc Risk. Aug 1999;6(4):217–21. 125. Shahar E, Chambless LE, Rosamond WD, et al. Atherosclerosis Risk in Communities Study. Plasma lipid profile and incident ischemic stroke: the Atherosclerosis Risk in Communities (ARIC) study. Stroke. 2003;34(3):623–31. 126. Field AE, Coakley EH, Must A, et al. Impact of overweight on the risk of developing common chronic diseases during a 10-year period. Arch Intern Med. 2001;161(13):1581–6. 127. Rexrode KM, Hennekens CH, Willett WC, et al. A prospective study of body mass index, weight change, and risk of stroke in women. JAMA. 1997;277(19):1539–45. 128. Kurl S, Laukkanen JA, Rauramaa R, et al. Cardiorespiratory fitness and the risk for stroke in men. Arch Intern Med. 2003;163(14): 1682–8. 129. Siritho S, Thrift AG, McNeil JJ, et al. Risk of ischemic stroke among users of the oral contraceptive pill: The Melbourne Risk Factor Study (MERFS) Group. Stroke. 2003;34(7):1575–80. 130. Petitti DB, Sidney S, Bernstein A, et al. Stroke in users of low-dose oral contraceptives. N Engl J Med. 1996;335(1):8–15. 131. Wassertheil-Smoller S, Hendrix SL, Limacher M, et al. WHI Investigators. Effect of estrogen plus progestin on stroke in postmenopausal women: the Women’s Health Initiative: a randomized trial. JAMA. 2003;289(20):2673–84. 132. Viscoli CM, Brass LM, Kernan WN, et al. A clinical trial of estrogen-replacement therapy after ischemic stroke. N Engl J Med. Oct 25, 2001;345(17):1243–9. 133. Bazzano LA, He J, Ogden LG, et al. Dietary intake of folate and risk of stroke in U.S. men and women: NHANES I Epidemiologic Follow-up Study. National Health and Nutrition Examination Survey. Stroke. 2002;33(5):1183–8. 134. Moster ML. Coagulopathies and arterial stroke. J Neuroophthalmol. 2003;23(1):63–71. 135. Ridker PM, Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med. 1997;336:973–9. 136. Ridker PM, Hennekens CH, Buring JE, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular events in women. N Engl J Med. 2000;342:836–43. 137. Gussekloo J, Schaap MC, Frolich M, et al. C-reactive protein is a strong but nonspecific risk factor of fatal stroke in elderly persons. Arterioscler Thromb Vasc Biol. 2000;20:1047–51. 138. Ford ES, Giles WH. Serum C-reactive protein and self-reported stroke: findings from the Third National Health and Nutrition Examination Survey. Arterioscler Thromb Vasc Biol. 2000;20: 1052–6. 139. Ridker PM, Rifai N, Pfeffer M, et al. Long-term effects of pravastatin on plasma concentration of C-reactive protein. Circulation. 1999;100:230–5. 140. Ridker PM, Rifai N, Lowenthal SP. Rapid reduction in C-reactive protein with cerivastatin among 785 patients with primary hypercholesterolemia. Circulation. 2001;103:1191–3. 141. ALLHAT Collaborative Research Group. Major cardiovascular

events in hypertensive patients randomized to doxazosin vs

Neurological Disorders

1151

chlorthalidone: the Antihypertensive and Lipid-lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. 2000;283(15):1967–75. 142. Davis BR, Cutler JA, Gordon DJ, et al. Rationale and design for the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). ALLHAT Research Group. Am J Hypertens. 1996;9(4 Pt 1):342–60. 143. The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. 2002;288(23):2981–97. 144. Staessen JA, Wang JG, Thijs L. Cardiovascular protection and blood pressure reduction: a meta-analysis. Lancet. 2001;358(9290): 1305–15. 145. Anonymous. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) Lancet. 1994;344(8934):1383–9. 146. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med. 1998;339(19): 1349–57. 147. He J, Whelton PK, Vu B, et al. Aspirin and risk of hemorrhagic stroke: a meta-analysis of randomized controlled trials. JAMA. 1998; 280(22):1930–5. 148. Morley J, Marinchak R, Rials SJ, et al. Atrial fibrillation, anticoagulation, and stroke. Am J Cardiol. Jan 25, 1996;77(3):38A–44A. 149. Goldstein LB, Hasselblad V, Matchar DB, et al. Comparison and meta-analysis of randomized trials of endarterectomy for symptomatic carotid artery stenosis. Neurology. 1995;45(11): 1965–70. 150. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273(18):1421–8. 151. Aarsland D, Tandberg E, Larsen JP, et al. Frequency of dementia in Parkinson’s disease. Arch Neurol. 1996;53:538–42. 152. Mayeux R, Marder K, Cote L, et al. The frequency of idiopathic Parkinson’s disesae by age, ethnic group and sex in northern Manhattan, 1988-1993. Am J Epidemiol. 1995;142:820–7. 153. Rajput AH, Offord KP, Beard CM, et al. A case-control study of smoking habits, dementia, and other illnesses in idiopathic Parkinson’s disease. Neurology. 1987;37:226–32. 154. Tanner CM, Goldman SM. Epidemiology of Parkinson’s disease. Neurol Clin. 1996;14:317–35. 155. Tanner CM, Chen B, Wang WZ, et al: Environmental factors in the etiology of Parkinson’s disease. Can J Neurol Sci. 1987;14:419–23. 156. Bharucha NE, Stokes L, Schoenberg BS, et al. A case-control study of twin pairs discordant for Parkinson’s disease: A search for environmental risk factors. Neurology. 1986;36:284–8. 157. Piccini P, Burn D, Sawle G, et al. Dopaminergic function in relatives of Parkinson’s disease patients: a clinical and PET study. Neurology. 1995;45(suppl 4):A203. 158. Goetz CG, Stebbins GT. Effects of head trauma from motor vehicle accidents on Parkinson’s disease. Ann Neurol. 1991;29:191–3. 159. Logroscino G, Marder K, Cote L, et al. Dietary lipids and antioxidants in Parkinson’s disease: a popluation-based, case-control study. Neurology. 1996;39:89–94. 160. Fahn S, Cohen G. The oxidant stress hypothesis in Parkinson’s disease: Evidence supporting it. Ann Neurol. 1992;32:804–12. 161. Mayeux R, Tang MX, Marder K, et al. Smoking and Parkinson’s disease. Mov Disord. 1994;9:207–12. 162. Ascherio A, Zhange SM, Hernan MA, et al. Prospective study of caffeine consumption and risk of Parkinson’s disease in men and women. Ann Neurol. 2001;50:56–63.

1152

Noncommunicable and Chronic Disabling Conditions

163. Marras C, Tanner CM. The epidemiology of Parkinson’s disease. In: RL Watts, WC Koller, eds. Movement Disorders Neurologic Principles and Practice. New York, McGraw Hill, 2004:177–195. 164. Le Witt PA. Clinical trials of neuroprotection in Parkinson’s disease: Long-term selegiline and alpha-tocopherol treatment. J Neural Transm Suppl. 1994;43:171–81. 165. Kopin IJ, Markey SP. MPTP toxicity: implications for research in Parkinson’s disease. Ann Rev Neurosci. 1988;11:81–96. 166. McKhann G, Drachman D, Folstein M, et al. Clinical diagnosis of Alzheimer’s disease: report of the NINCDS-ADRDA Work Group. Neurology. 1984;34:939–44. 167. National Institutes of Health Consensus Development Conference. Differential diagnoses of dementing diseases. JAMA. 1987;258: 3411–9. 168. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC; 1994. 169. Larson EB, Kukull WA, Katzman RA. Cognitive impairment: dementia and Alzheimer’s disease. Ann Rev Pub Health. 1992; 13:431–449. 170. Oster S, Christoffersen P, Gundersen HJ, et al. Six billion neurons lost in AIDS. A stereologic study of the neocortex. APMIS. 1995;103:525–9. 171. Simpson DM, Tagliati M. Neurologic manifestations of HIV infection. Ann Int Med. 1994;121:769–85. 172. Jorm AF, Korten AE, Henderson AS. The prevalence of dementia, a quantitative integration of the literature. Acta Psychiatr Scand. 1987;76:456–79. 173. Henderson AS, Jorm AF. Definition of epidemiology of dementia: a review. In: Mario M, Sartorius N, eds. Dementia. John Wiley, West Sussex, UK; 2000:1–34. 174. Jorm AF, Jolley D. The incidence of dementia: a meta-analysis. Neurology. 1998;51:728–33. 175. Chandra V, Pandav H, Dodge H, et al. Incidence of Alzheimer’s disease in rural community in India: The Indo-U.S. Study. Neurology. 2001;57:985–9.

176. Hendrie HC, Osuntokun BO, Hall KS, et al. Prevalence of Alzheimer’s disease and dementia in two communities: Nigerian Africans and African Americans. Am J Psychiatr. 1995;152: 1485–92. 177. Colsher P, Wallace RB. Epidemiologic in studies of cognitive function in the elderly: methodology and non-dementing acquired dysfunction. Epidemiologic Rev. 1991;13:1–27. 178. Evans DA, Funkenstein HH, Alberts, M, et al. Prevalence of Alzheimer’s disease in community population of older persons. JAMA. 1989;262:2551–6. 179. Evans DA. Estimated prevalence of Alzheimer’s disease in the United States. Milbank Q. 1990;68:267–79. 180. Larson EB, Kukull WA. Prevention of Alzheimer’s disease—a perspective based on successes in the prevention of other chronic diseases. Alzheimer Dis Associated Disorders. 1996;10(suppl):9–12. 181. Tang MX, Jacobs D, Stern Y, et al. Effect of oestrogen during menopause on risk and age at onset of Alzheimer’s disease. Lancet. 1996;348:429–32. 182. Rao VS, Cupples LA, Vanduijn CM, et al. Evidence for major gene inheritance of Alzheimer disease in families with and without apolipoprotein E Epsilon-4. Am J Human Genetics. 1996;59: 664–75. 183. Report of the U.S. Preventive Services Task Force. Guide to Clinical Preventive Services. 2nd ed. Alxandria, VA: International Medical Publishing, Chapter 48. 184. Shumaker SA, Legault C, Rapp SC, et al. Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in postmenopausal women: the Women’s Health Initiative Memory Study—A randomized control trial. JAMA. 2003;289:2651–62. 185. Brodaty H, Gresham M. Effect of a Training Programme to Reduce Stress in Carers of Patients with Dementia. Br Med J. 1989; 299:1375–9. 186. Haupt M, Karger A, Janner M. Improvement in agitation and anxiety in demented patients after psychoeducative group intervention with their caregivers. Int J Geriatr Psychiatr. 2000;15(12): 1125–9.

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Dawn M. Oh • Kean T. Oh

Although the prevalence of blindness worldwide is not precisely known, new global estimates from 2002 World Health Organization (WHO) show at least 37 million people are blind and another 124 million people have low vision. This figure is based on the standard international definition of blindness: a visual acuity (VA) of less than 3/60 or corresponding visual field loss in the better eye with best possible correction, and a VA of <6/18 (but greater than 3/60 or a field loss of less than 20%) constituting “low vision.” Because of the essential nature of vision for most endeavors, the frequency of blindness also reflects a global loss in disability-adjusted life years, and is considered by WHO to be a key barrier to development worldwide. The causes of blindness and visual loss, most preventable through primary intervention or secondary therapy, include a small core of major diseases including: cataract (47.8%), glaucoma (12.3%), diabetic retinopathy (4.8%), macular degeneration (8.7%), trachoma (3.6%), onchocerciasis (0.8%), and corneal opacities (5.1%) (Fig. 68-1). However the fraction of the blindness burden for each disease differs substantially from region to region (Fig. 68-2). The total disease burden of blindness varies along a variety of demographic factors. First, blindness rates vary geographically (Fig. 68-3) with the largest impact occurring in regions least able to afford the loss in human resources or address economic costs of treatment. More than 90% of the world’s visually impaired are found in developing countries. Furthermore, WHO estimates that some 75% of all worldwide blindness is avoidable through prevention or treatment. Age also remains the primary risk factor associated with most blinding disorders, regardless of etiology (Fig. 68-3) with more than 82% of all blindness occurring in the 50+ age group (though they constitute only 19% of the world population). This age-related distribution has been further deepened by an aging world where populations over 50 years of age increased by 30% (versus an overall population increase of 18.5%) from the last global blindness estimates of 1990. Indeed, that the blindness rate remained stable despite the aging effect over this time (38 million estimated blind in 1990) signifies a lower than projected blindness rate (With age increases the projection was 52 million blind in 2002.). This decrease has been attributed to a variety of factors, including increase in public awareness and accessibility of services, to successful elimination efforts for blindness in Gambia, India, Morocco, Nepal, Sri Lanka, Thailand, and other nations with previously high endemic blindness rates. Finally, blindness and visual impairment are unequally distributed between men and women, with females having a significantly higher risk of visual impairment (a female:male ratio ranging from 1.5 to 2.2 worldwide).1 Some visual disorders, while not major causes of blindness worldwide, represent significant medical cost, and, without treatment, significant loss of daily life functions, as in the case of uncorrected refractive error. Another area of public health interest among the lessblinding disorders is international emphasis on screening children for amblyopia, treatable only in childhood. Minor visual complications

may also characterize populations at increased risk for developing blinding visual diseases; for example, myopics are at increased risk for retinal detachments and glaucoma. Major recent research has provided new insights into causes, risk factors, and treatments of most visual disorders. This research reinforces the need for multidisciplinary, and often developmentoriented, consideration and intervention in the area of visual health. The need for sufficient and appropriate data to make such policy decisions has generated new methodologies for measurement, such as WHO programs that use a standardized method of low-cost, smallscale field surveys to provide more reliable blindness data than were previously available. These new research approaches are even more crucial as more diseases are found to have multifactoral causes, and the traditional areas of public health interest, such as health behavior patterns (smoking and cataracts or age-related macular degeneration [AMD]), nutrition (vitamin A and xerophthalmia, antioxidants and AMD), and education (trachoma and public health education), are drawn into the circle of causation for blinding disorders. This chapter emphasizes and reviews the major causes of blindness worldwide as well as other important visual disorders, notes risk factors where information is available, and suggests the most important clinical and public health interventions to control these conditions. CATARACT

Unoperated cataract is the main cause of visual loss globally, with 20 million people currently estimated to have severely reduced vision (3/60 or worse) as a result of cataracts. With current global aging rates, and the prevalence of cataract doubling with each decade of age after 40 years, this number is expected to reach 40 million by 2020. Primarily a disease of aging, cataract describes the opacification of the lens of the eye. This gradually blinding process is associated in its most common form (“senile cataracts”) with an increase in the weight and thickness of the lens and a decrease in accommodation as new layers of cortical fibers are laid down, hardening the lens nucleus. While not subject to primary prevention in most cases, effective surgery for the removal of the lens and its replacement have been developed and dramatically refined. The most desirable treatment is now phacoemulsification, removal of cataract tissue, of the lens. The international lack of access to trained ophthalmologists and issues of surgical cost, however, leave the statistics of blindness from cataract high, despite this effective treatment. Issues of education and cultural acceptance have complicated efforts to increase access to care, with studies in Nepal and Kenya reporting that even with free surgery and transport use rates from 70% to below 60% occurred.2 In wealthier nations, with greater access to both surgery and information, the demand for cataract surgery has now extended to portions of the population who would not even be considered visually reduced elsewhere. 1153

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1154

Noncommunicable and Chronic Disabling Conditions studies have not found a definitive relationship. While studies of vitamin therapy are not yet complete, the main preventive measures remain decreasing UV-B exposure and smoking cessation. Current international focus is on the development of low-cost intraocular lenses, sutures, and other equipment used in cataract surgery, as well as the training of human resources for surgery in many of the world’s least developed countries, which carry high disease burdens. The importance of this human resource increase is exemplified in Africa where there is only about 1 ophthalmologist per 1 million people. Regular ophthalmologic examinations are necessary for proper identification of cataracts and eventual surgery.

13 0.8 3.6 3.9 4.8 47.8

5.1

GLAUCOMA

8.7

12.3 Cataract

Childhood blindness

Glaucoma

Trachoma

AMD∗

Onchocerciasis

Comeal opacities

Others

Diabetic retinopathy ∗AMD–Age-related

Macular Degeneration.

Figure 68-1. Causes of blindness. (Source: Resnikoff S, Pascolini D, Etya’ale D, et al. Global data on visual impairment in the year 2002. Bull World Health Organization; November 2004:82 (11).)

Although cataract development is predominantly associated with age, in developing nations it often occurs earlier in life: India reports average age of development for visually significant cataracts to occur some 14 years earlier than in the United States with 82% of Indians ages 75–83 with visually significant cataract or aphakia versus 46% in the United States at the same age. Outside of the primary risk factor of age, some environmental, physical, and nutritional risks have also been associated with earlier onset or progression of cataracts. These include exposure to UV-B light, diabetes, high blood pressure, corticosteroid therapy, smoking, alcohol, protein energy malnutrition, and dehydration.3 These last two risk factors may indicate an antioxidant relationship with cataracts and suggest that studies in antioxidants may implicate dietary protective factors, but

While glaucoma is considered with some certainty to be the second leading cause of blindness worldwide behind cataracts, the estimated disease burden of 6.7 million cases expected worldwide by 2000 proved an underestimate, and current estimates are subject to controversy. This is due in no small part to the persistent lack of an accessible inexpensive consistent screening test and system. Demographybased models however, suggest a rate of around 9.3 million people having some type of bilateral glaucoma blindness. Eighty-five percent of patients affected by glaucoma are in the developing world.4 The total numbers affected by glaucoma are split between primary angle closure glaucoma (PACG) and primary open angle glaucoma (POAG). The overwhelming majority of cases of PACG are in Asia and Asian-descent populations, while POAG is distributed throughout the world, with high rates in populations of African-descent. The rate of occult glaucoma is roughly equal to that of detected disease even in developed nations, making it a further public health challenge. Like cataract and AMD, glaucoma is predominantly a disease of aging, with prevalence rates increasing dramatically over the age of 65, making it another of the visual disorders being affected by the graying of the world’s population. Although in the past elevated intraocular pressure (IOP) was considered the cause and part of the definitive diagnosis of the disease, it is now accepted that elevated IOP may be associated with as little as 10% of POAG. The characteristic visual field loss that describes glaucoma has remained constant, however, for over a century, with progressive damage of optic nerve fibers causing a loss of vision from peripheral to central vision in a spiraling pattern. This damage is related to changes in vascular perfusion of the optic nerve head and is worsened by elevated IOP. Progression of the disease can be prevented in many cases by trabeculectomy or topical drug treatments, which lower IOP. However, patients often, especially in the developing world, do not present for treatment until substantial permanent visual loss has already occurred. Clearly glaucoma is a prime target for early intervention measures; unfortunately, making an early diagnosis is problematic, especially when characteristic field loss, often not noticeable until 80% or more of the optic nerve is permanently damaged, is now

Global estimate of visual impairment, by WHO region (millions), 2002:

Figure 68-2. Visual impairment by region. (Source: WHO Fact Sheet N°282, November 2004.)

Population # of blind people % of total blind # with low vision # with visual impairment

African region

Region of the Americas

672.2

852.6

Eastern Mediterranean region 502.8

877.9

SouthEast Asia region 1590.8

6.8

2.4

4

2.7

11.6

18%

7%

11%

7%

20

13.1

12.4

26.8

15.5

16.5

Western Pacific region

Total

1717.5

6213.9

9.3

36.9

32%

25%

100%

12.8

33.5

32.5

124.3

15.5

45.1

41.8

161.2

European region

68

Disabling Visual Disorders

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Prevalence of blindness

Blindness prevalence (%) <0.3 >0.3 <0.4 >0.5 <1 >1

World Health Organization

The boundaries and names shown and the designations used on this map do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement.

Figure 68-3. Geography of blindness (Source: Available at http://www.who.int/blindness/data_maps/blindness.jpg. WHO maps and information website.)

considered the definitive diagnostic tool. Other measurements of optic nerve head signs, such as cup-to-disc ratios, cup asymmetry, and splinter hemorrhages, although useful supplemental information, lack both sensitivity and specificity. These complications in addressing glaucoma have led to it being left off of the systematic goals for the VISION 2020 plans of WHO for the time being. While epidemiologic studies of POAG are limited by their differing disease definitions, small sample sizes, and questionable sampling methods, they suggest a number of risk factors for the development of POAG, with or without elevated IOP (sometimes called “normal or low-tension glaucoma”). Age is the most constant risk factor, with the incidence over 60 years being seven times that of the under 40 age group. Race is another factor, with the risk for blacks shown to be four times greater than that for whites in both the United States and United Kingdom, and with most glaucoma in blacks occurring at a younger age. Family history of glaucoma is also a risk factor, with approximately 13–26% of cases having a genetic component. Other putative risk factors include diabetes (via increased IOP); myopia; hypertension; inconsistent associations with modifiable risk factors including smoking and an atherosclerotic diet; and protective effects from vitamin B12, ω-3 fatty acid, magnesium, and exercise.5 Glaucoma is a serious public health challenge, as efforts center on identifying causes that may help prevent the disease as well as developing more useful screening techniques, especially for international field work. MACULAR DEGENERATIONS AND DYSTROPHIES

A wide spectrum of macular disease contributes significantly to blindness in the United States and worldwide, encompassing known hereditary dystrophies and multifactorial degenerations such as age related macular degeneration. Without accurate understanding of the disease process, primary intervention may be misguided and ineffective. Recent progress in molecular genetics has allowed many hereditary macular dystrophies to be mapped, and in many instances, the specific gene causing the disease has been defined. While no definitive treatments for macular dystrophies exist, identification of the underlying gene and its function has provided insight into specific disease processes. For instance, Stargardt macular dystrophy is the

most common macular dystrophy with a prevalence of about 1 in 10,000, and known to be caused by the ABCA4 gene. Animal models raise the possibility of deleterious effects of high dose vitamin A supplements and the potential role of excess sunlight exposure.6 Thus, while no clinical trials yet exist, patient counseling includes avoidance of ubiquitous “eye health” supplements with vitamin A, and recommendation of good UV light eye protection. Then, patients with all forms of macular dystrophies respond well to low vision rehabilitation. Most individuals have small, well-defined central scotomas with healthy paracentral and peripheral vision facilitating their rehabilitation with low vision devices. Finally, genetic counseling for families with inherited retinal diseases is necessary to educate them regarding the risk of disease in further children.

Age-Related Macular Degeneration AMD is the leading cause of blindness for people older than 65 years in the United States, Western Europe, and Australia (representing roughly 50% of all blindness by cause in these regions). AMD is defined by diffuse morphologic changes at the level of the retinal pigment epithelium (RPE).7 Patients experience central vision loss through atrophy of the RPE and retina or due to the development of choroidal neovascularization (CNV). Although no incidence rates are available for AMD, studies in the U.S. population have reported prevalences ranging from 6.4 to 16% in the elderly and rates of nearly 20% in the most old.7,8 It is believed that the number of advanced AMD cases in the United States will be 7.5 million by the year 2030, up from 2.7 million in 1973.8 The Age Related Eye Disease Study (AREDS) estimated that there are 8 million people at risk for progressing to advanced AMD.9 The pathophysiology of macular degeneration is poorly understood and likely multifactorial. Proposed mechanisms have included oxidant stress and atherosclerosis10,11 with reported risk factors including age, sex, family history, iris color, cardiovascular disease, body mass index,12 smoking, light exposure, and nutritional deficiency in antioxidants and zinc.13 Many of these risk factors are defined by population-based studies and, depending on the study, have variable validity. For instance, sun exposure and iris color were not found to be risk factors by the genetics factors in AMD study group.14

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However, other factors, specifically smoking, continue to be validated by follow-up studies. Thornton et al. reviewed the smoking association and found that 17 studies of various designs showed a strong association while five studies found no correlation. Subsequent to that study, the Genetics Factors in AMD study showed an increasing risk with rising pack years of smoking so that by 40-pack years, risk for both geographic atrophy and CNV formation was significantly increased. Cessation of smoking reduced risk of AMD and required more than 20 years to approximate the risk of nonsmokers.15–17 Cardiovascular risk factors such as C-reactive protein, IL-6 and homocysteine also continue to be validated by multiple centers.18–20 Recent advances have also implicated inflammation and the immune system in the pathogenesis of AMD. A single polymorphism in the complement factor H gene, Tyr402His has been associated with as much as 43–50% AMD cases. This single nucleotide polymorphism may confer susceptibility to AMD both for geographic atrophy and CNV development. Patients homozygous for this polymorphism were found to be 6.3 times more at risk than patients with the “wild type” sequence and the risk was highest for homozygous smokers.21–23 The AREDS demonstrated clear preventative benefit to the use of antioxidants and zinc in AMD. This study showed a 19% reduction in progression of patients with intermediate AMD to advanced AMD that was defined by clear vision affecting changes.24 While previous studies examining the role of micronutrient supplementation were equivocal, the AREDS shifted patient counseling to actively promoting vitamin supplementation to patients at risk.25 When considering the population at risk of 8 million Americans, over 300,000 people taking these antioxidants would be prevented from progressing to advanced AMD and associated vision loss in the next five years. The economic public health effect is illustrated by a similar model demonstrating a savings of 5.6 billion Canadian dollars when considering just photodynamic therapy as a treatment, let alone the current and future pharmacologic agents such as pegaptanib and ranibizumab. The authors suggest that these savings could be magnified tenfold in the United States due to currency and population.26 Lutein supplementation has also been suggested as a means of slowing the progression of geographic atrophy as well.27 Other dietary risk factors associated with atherosclerosis and high body mass index, such as dietary fat, also appear to carry increased risk for AMD. Thus, dietary modification is a strategy for primary prevention of AMD.28 Finally, smoking cessation is strongly recommended from the standpoint of AMD risk reduction as well. Treatment of AMD currently focuses on neovascularization associated with AMD. Initially, treatment only involved thermal photocoagulation of CNV. The efficacy of laser was demonstrated to prevent further vision loss through the multicenter macular photocoagulation studies (MPS). Photodynamic therapy (PDT) and intravitreal pharmacologic agents such as pegaptanib (Macugen) now also are used to treat CNV from AMD.29 The pharmacologic agents target vascular endothelial growth factor (VEGF) and its role in AMD. At best, however, current treatment strategies tend only to stabilize vision with only a small fraction of patients experiencing substantial improvement in their central vision. Future medications include the use of ranibizumab (Lucentis) and bevacizumab (Avastin). Early case series as well as a double blinded multicenter trial raise the possibility of vision, improvement for patients with choroidal neovascularization.30,31 The comparison of ranibizumab and bevacizumab raises economic and ethical issues given the initial use of bevacizumab for AMD as an “off label” approach and the significant difference in cost between it and both ranibizumab and pegaptanib. Currently, however, low vision management plays a key role in the care of patients with AMD. It will likely continue to maintain its place in the care of AMD patients despite recent pharmacologic advances.

Other Macular Conditions associated with Central Vision Loss Other conditions known to be associated with CNV in the macular include presumed ocular histoplasmosis, pathologic myopia, angioid

streaks, and idiopathic causes. AREDS recommended supplementation has not been examined regarding risk reduction in these conditions. Treatment of CNV in these conditions tends to parallel AMD and includes thermal ablation, once again evaluated in the MPS series of studies, PDT, anti-VEGF medications and thermal photocoagulation. Another clinical trial known as the subfoveal surgical trials (SST), also evaluated the efficacy of subfoveal surgery for conditions with CNV. The SST showed no benefit comparing surgical removal of CNV due to histoplasmosis or idiopathic causes to observation. There was a marginal benefit shown evaluating quality of life factors between surgical patients and those randomized to observation.32,33 RETINAL VASCULAR DISEASE

Diabetic retinopathy is the leading cause of blindness in the United States among individuals 20–64 years old, accounting for 12% of all new cases of blindness each year. This retinal vascular disease causes visual morbidity through the proliferation of neovascular fronds and the development of macular edema. There are roughly 700,000 Americans with proliferative retinopathy and more than 500,000 with macular edema.34 Primary prevention of diabetic retinopathy is based on good diabetic and hypertensive control. The Diabetes Control and Complication Trial (DCCT) demonstrated a 60% reduction in the risk of retinopathy with intensive control (versus standard treatment) of insulin-dependent diabetes mellitus (IDDM). After 3.5 years, the risk of progression was more than 5 times lower with intensive control.35 The results of the DCCT indicate that careful control of blood sugars in all diabetics will retard the onset of diabetic retinopathy. The UKPDS, further demonstrated that lowering the glycosylated hemoglobin just one point resulted in a significant reduction of intervention. Screening for the presence of diabetic retinopathy is a very important first step to secondary management, and guidelines have been established for both IDDM and non-insulin–dependent diabetes mellitus (NIDDM) patients. One study showed that only 40–45% patients with diabetes mellitus were appropriately screened and of those patients, 11% required treatment for diabetic retinopathy. Treatment of diabetic retinopathy has been guided by a series of well-designed multicenter trials. Initial studies demonstrated that panretinal photocoagulation reduced the risk of severe visual loss by greater than 50% over no treatment.36 Later multicenter trials established firm definitions and guidelines for the treatment of clinically significant diabetic macular edema. Focal photocoagulation reduced visual loss from diabetic macular edema by about 50% as well.37 The second most common retinal vascular disease involves retinal vein occlusion. Risk factors for retinal vein occlusion include hypertension, cardiovascular disease, diabetes mellitus, increasing age, and glaucoma.38 Patients with a 677 C-T mutation in the methylenetetrahydrofolate reductase gene (MTHFR) were thought to have an increased risk of thromboembolic events. However, more recent studies show that this relationship is more related to total serum homocysteine and low folate levels. Regardless, patients with multiple thromboembolic events, including BRVOs and CRVOs should be screened for low folate levels and high serum homocysteine.39 Folate supplementation in these instances may reduce the risk for further events. Branch retinal vein occlusion (BRVO) causes decreased vision primarily by cystoid macular edema, neovascularization, and ischemia. Focal photocoagulation for macular edema resulted in 65% gains in visual acuity among treated patients. Scatter laser photocoagulation was found to lower the risk of vitreous hemorrhage following the development of neovascularization.40,41 Central retinal vein occlusion, however, did not demonstrate benefit for macular edema following focal photocoagulation, though panretinal photocoagulation was an effective means of treatment for iris and angle neovascularization following an ischemic CRVO. Treatment at this stage prevents further progression to neovascular glaucoma and potentially, the loss of the eye.42 Retinal vascular disease is a common cause of visual morbidity in the United States and worldwide. Because risk factors involve systemic

68 disease, prevention of major retinal vascular disease involves control of these systemic diseases. Large multicenter trials have studied and established the management of these diseases following their development.

TRACHOMA

Responsible for 5.9–8 million cases blindness worldwide, trachoma, unlike the above visual disorders, is an infectious disease, concentrated in poor and rural areas of the world, with the highest burden among women and children.43 While no longer a leading cause of blindness worldwide (Trachoma represented some 15% of global blindness as recently as 1990), it remains the leading infectious cause. Its cost, given its early effects in children, is estimated at US$ 2.9 billion a year in productivity loss.44 Chlamydia trachomatis, the causative microorganism, and eyeseeking flies, the vector of transmission, are endemic in Central America, Brazil, Africa, the Eastern Mediterranean, and several Asian nations. C. trachomatis causes an inflammation in the eye, resulting in the formation of follicles in the conjunctiva which scar the eyelid until it turns inwards with the lashes rubbing the eye, gradually leading to blindness. This process can be halted at the primary level by the improvement of living standards and hygiene in endemic areas, as proper face-washing with clean water is protective. This control may be supplemented by the new availability of the longacting azithromycin as an effective but extremely expensive treatment and by surgery on underturned lids to prevent progression to blindness. This combination of strategies has been labeled “SAFE” (surgery, antibiotics, face-washing, and environmental improvement) and implementation of control efforts in the last decade have reduced rates in such counties as Morocco by 90%, giving encouragement to other regions in the possibilities for eradication of a disease which is considered one of the world’s oldest known infectious diseases, having been described by the ancient Egyptians.45 Nevertheless, 50 years of global public health efforts to eradicate trachoma has emphasized that, without improvement in the sanitation, water, population densities, economies, and attention to literacy and cultural appropriateness in public education programs, secondary interventions will not be successful in completely controlling the disease.

ONCHOCERCIASIS

In endemic regions of Africa, the Arabian Peninsula, and the Americas, onchocerciasis, or “river blindness,” is the second leading infectious cause of blindness. Of those currently infected, approximately 99% are in Africa. While the dermatologic effects of onchocerciasis are more common among the infected (6 million people), the blindness is nevertheless an important issue in visual health.1 The disease, caused by the parasite Onchocerca volvulus, is spread by the black fly population in endemic areas, and the intensity of infection is the best indicator of risk for developing blindness. Unfortunately, onchocerciasis is a public health example where development projects have assisted in the proliferation of the disease by increasing vector breeding sites (near fast-flowing rivers or streams). Current international efforts at eradication are focused on both controlling the vector and the use of a recently developed suppressive drug, ivermectin, which is being distributed with WHO efforts. Based on past experience with problems of access, understanding of the disease, and cultural appropriateness of development projects, these efforts are now targeted at developing local initiatives and community-based prevention plans. XEROPHTHALMIA

The leading cause of blindness in children worldwide is now cornea scarring primarily from blinding malnutrition, also known as xerophthalmia, resulting from vitamin A deficiency. A difficulty in estimating

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consistent rates and impact comes from a high rate of mortality from malnutrition and measles within this category of children.46 Other children show primarily signs of clinical xerophthalmia, from eye dryness to ulceration. In this case, the micronutrient deficiency leads to irreversible blindness in the young. Current recommendations include exclusive breast-feeding for the first 4–6 months of life and complementing diets with food items high in vitamin A. Preventive interventions include programs to distribute high doses of vitamin A to infants and children in areas with high rates of micronutrient deficiency. In the case of xerophthalmia, the nutritional deficiency leading to blindness also represents an increased risk for other childhood illnesses and mortality. AIDS AND THE EYE

AIDS is an increasing world health problem, and more than 200,000 individuals are affected by it in the United States. Because of its overall increasing prevalence, it has also become a significant cause of visual morbidity. Between 40 and 70% of all AIDS patients exhibit ocular disease, and postmortem examinations have found evidence of ocular disease in greater than 95% of cases.47,48 AIDS may involve the eye directly by causing a microangiopathy, characterized by the presence of cotton wool spots, or by opportunistic infection, or neoplastic and neuro-ophthalmologic manifestations. Anterior segment manifestations include common diseases, such as molluscum contagiosum, as well as rare diseases, such as microsporidial keratitis and Kaposi’s sarcoma. The most common posterior segment opportunistic infection is cytomegalovirus (CMV) retinitis. It affects between 5 and 40% of AIDS patients. CMV rarely causes retinal disease unless the CD4 count falls below 50 cells/mm3. CMV viral load also has been found to play a key role in predicting CMV retinitis. Initially, CMV retinitis may be asymptomatic or present with trivial symptoms. Hence, screening this population is important to identify patients requiring initiation of therapy. Antivirals for CMV have been shown in the studies for ocular complications of AIDS (SOCA) to prolong the life of AIDS patients. Finally, CMV retinitis predisposes patients to retinal detachments, even as the retinitis itself goes into remission. The incidence of CMV retinitis—associated retinal detachment is 24% at one year. Highly active antiretroviral therapy (HAART) strategies have allowed recovery of patients CD4 counts. For patients with CMV retinitis in remission, maintenance therapy is continued to prevent reactivation of CMV retinitis. Once the CD4 count of a patient recovers, however, maintenance therapy can safely be discontinued. However, the HAART strategy has introduced a new condition to these patients as their immune system recovers known as immune recovery uveitis.49 In the era of HAART, CMV viral load has become more predictive of mortality and quality of life.60 Thus, shifting efficacy in therapy for AIDS patients has resulted in improved mortality and new conditions related to immune system recovery. RETINOPATHY OF PREMATURITY

Retinopathy of prematurity (ROP) is a multifactorial disorder of premature infants that affects 1300 children each year.50,51 Between 85 and 90% of low-birth weight children exposed to oxygen will demonstrate some evidence of ROP, though relatively few infants suffer severe visual impairment.52 It is estimated that only 6% of infants reach a stage of ROP requiring treatment.53 Time of oxygen exposure and to a lesser degree oxygen concentration, low birth weight, and short gestation are key risk factors for the development of ROP. Exposure to high concentrations of oxygen interferes with the process of retinal vascularization in premature infants. Consequently, neovascularization, vitreous hemorrhage, and tractional retinal detachment by fibrovascular proliferation results in visual morbidity.54,55 It was previously felt that careful management of arterial oxygen could prevent the onset of ROP, but increased ability of neonatologists to keep

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smaller, more premature infants alive has resulted in a resurgence of ROP in spite of careful oxygen control. It is now evident that ROP is driven by multiple factors in addition to oxygen exposure.56 Because of the high incidence of ROP in low birth-weight infants, careful screening is an important step in the management of this disease. Current recommendations call for infants below 1500 g birth weight to be carefully screened at specific intervals. Cryotherapy for patients who reach a well-described threshold stage has reduced the risk for retinal detachment in these infants by 50%. Laser photocoagulation has recently supplanted cryotherapy as the primary means of treatment of threshold ROP.57 The Early Treatment for ROP (ETROP) study has addressed guidelines for earlier treatment of ROP than threshold level using laser photocoagulation to improve outcomes.58 For patients who develop subtotal retinal detachments, scleral buckling surgery has a high rate of success. Without this surgery, 85% of patients will progress slowly. Once total retinal detachments develop, they are often complicated and require extensive surgical intervention. Thus, advances in neonatology have resulted in an increased incidence of ROP in spite of careful oxygen management. Primary prevention of ROP must address means of reducing premature and low-birth weight infants. Studies have examined vitamin E as a prevention strategy for ROP, but this supplementation has been shown to only possibly reduce the severity of disease. Once ROP is identified, however, management guidelines allow prevention of visual morbidity in the majority of infants. Long term risk for adults with ROP includes high myopia, macular dragging and retinal detachment. The final report from the cryotherapy for ROP study showed the rate of retinal detachment after 10 years was still 4.4% in treated patients.59 These patients will need lifetime ophthalmologic monitoring and care.

OTHER VISUAL PROBLEMS

Although we have considered the most common blinding disorders, the most common ocular complaint is loss of sight due to refractive error. In the case of myopia, this means that distant objects are focused anterior to the retina because of a longer eye and cannot be seen clearly. In, hyperopia there is a shorter eye where the focus falls behind the retina, making closer objects difficult to view. Finally, with presbyopia there is a loss of accommodative functioning, where the eye cannot adjust to bring near objects into focus; this accommodative loss is primarily associated with aging. The majority of cases of refractive error can be corrected through glasses; however, severely myopic patients are also at increased risk (regardless of refractive correction) for retinal detachments and glaucoma, both potentially blinding. Another common visual disorder that has been subject to extensive public health intervention at the screening level is amblyopia. Amblyopia describes the preferential use of one eye. This imbalance in use occurs from different refractive errors or muscle balance in each eye during the first six years of life. The most effective treatment remains early patching of the dominant eye, with cases being identified as early as possible. To reach these cases, vision-screening is recommended worldwide at the preschool and elementary levels. Visual disorders span a large range of effects, from the inconvenience of refractive error, to infectious diseases, to blinding degenerative disorders. In each case, however, appropriate screening identification and intervention remains the international challenge of the public health community.

REFERENCES

1. Resnikoff, Pascolini D, Etya’ale D, et al. Global data on visual impairment in the year 2002. Bull World Health Organization. November 2004;82 (11). 2. Brian, Garry, Hugh Taylor. Cataract blindness—challenges for the 21st century. Bull World Health Organization. 2001;79:249–56.

3. Krumpaszky HG, Klaus V. Epidemiology of the causes of blindness. Opthalmologica. 1996;210:1–84. 4. Goldberg, Ivan. Conference Report: Glaucoma in the 21st Century Conference, Hong Kong, China, 1999. Asian J Ophthalomol. 2000;3:2. 5. Tielsch JM. The epidemiology and control of open angle glaucoma: a population-based perspective. Annu Rev Public Health. 1996;17: 121–36. 6. Weng J, Mata NL, Azarian SM, et al. Insights into the function of Rim protein in photoreceptors and etiology of Stargardt’s disease from the phenotype in abcr knockout mice. Cell. 1999;98:13–23. 7. Sarks SH, Sarks JP. Age related macular degeneration: atrophic form. In: Ryan SJ, ed. Retina. 2nd ed. St. Louis: CV Mosby. 1994;1071–1102. 8. Hyman LG, Lilienfeld AM, Ferris FL, et al. Senile macular degeneration: a case control study. Am J Epidemiol. 1983;118:213–27. 9. Bressler NM, Bressler SB, Congdon NG, et al. Potential Public Health Impact of Age-Related Eye Disease Study Results: AREDS report No. 11. 10. Katz ML, Parker KR, Handelman GJ, et al. Effects of antioxidant nutrient deficiency on the retina and retinal pigment epithelium of albino rats: a light and electron microscopy study. Exp Eye Res. 1982;34:339–69. 11. Gass JDM. Pathogeness of disciform detachment of the neuroepithelium. I: General concepts and classification. Am J Ophthalmol. 1967;63:573–85. 12. Johnson EJ. Obesity, lutein metabolism, and age-related macular degeneration: a web of connections. Nutr Rev. 2005;63(1):9–15. 13. Mares-Perlman JA, Fisher AI, Klein R, Palta M, et al. Lutein and zeaxanthin in the diet and serum and their relation to age-related maculopathy in the third national health and nutrition examination survey. Am J Epi. 2001;153:424–32. 14. Khan JC, Shahid H, Thurlby DA, et al. Age related macular degeneration and sun exposure, iris colour and skin sensitivity to sunlight. Br J Ophthalmol. 2006;90:29–32. 15. Khan JC, Thurlby DA, Shahid H, et al. Smoking and age related macular degeneration: the number of pack years of cigarette smoking is a major determinant of risk for both geographic atrophy and choroidal neovascularization. Br J Ophthalmol. 2006;90:75–80. 16. Thornton J, Edwards R, Mitchell P, et al. Smoking and age-related macular degeneration: a review of association. Eye. 2005;19:935–44. 17. Clemons TE, Milton RC, Klein R, et al. Age-Related Eye Disease Study Research Group. Risk factors for the incidence of advanced agerelated macular degeneration in the Age-Related Eye Disease Study (AREDS). AREDS report No. 19. Ophthalmology. 2005;112:533–9. 18. Vine AK, Stader J, Branham K, et al. Biomarkers of cardiovascular disease as risk factors for age-related macular degeneration. Ophthalmology. 2005;112:2076–80. 19. Seddon JM, George S, Rosner B, et al. Progression of age-related macular degeneration: prospective assessment of C-reative protein, interleukin 6, and other cardiovascular biomarkers. Arch Ophthalmol. 2005;123:774–82. 20. Seddon JM, Gensler G, Milton RC, et al. Association between C-reative protein and age-related macular degeneration. JAMA. 2004;291: 704–10. 21. Haines JL, Hauser MA, Schmidt S, et al. Complement factor H variant increases the risk of age-related macular degeneration. Science. 2005;308:362–4. 22. Donoso L, Kim D, Frost A, et al. The role of inflammation in the pathogenesis of age related macular degeneration. Surv Ophthalmol. 2006;51:137–52. 23. Sepp T, Khan JC, Thurlby DA, et al. Complement factor H variant Y402H is a major risk determinant for geographic atrophy and choroidal neovascularization in smokers and nonsmokers. Invest Ophthalmol Vis Sci. 2006;47:536–40. 24. Age-Related Eye Disease Study Research Group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with

68

25. 26.

27.

28.

29.

30.

31.

32.

33.

34. 35.

36.

37.

38. 39.

vitamins C and E, beta carotene and zinc for age-related macular degeneration and vision loss: AREDS report No. 8. Arch Ophthalmol. 2001;119:1417–36. Hogg R, Chakravarthy U. AMD and micronutrient antioxidants. Curr Eye Res. 2004;29:387–401. Trevithick J, Massel D, Robertson JM, et al. Model study of AREDS antioxidant supplementation of AMD compared to Visudyne: a dominant strategy? AREDS report No. 11. Ophthalmic Epidemiol. 2004;11: 337–46. Johnson EJ. Obesity, lutein metabolism and age-related macular degeneration: a web of connections. Nutr Rev. 2005;63:9–15. Richer S, Stiles W, Statkute L, et al. Double-masked, placebo-controlled, randomized trial of lutein and antioxidant supplementation in the intervention of atrophic age-related macular degeneration: the Veterans LAST study. Optometry. 2004;75:216–20. Mozaffarieh M, Sacu S, Wedrich A. The role of carotenoids lutein and zeaxanthin in protecting against age related macular degeneration: a review based on controversial evidence. Nutr J. 2003; 2:20. Gragoudas ES, Adamis AP, Cunningham ET Jr, et al. Pegaptanib for neovascular age-related macular degeneration. NEJM. 2004;351: 2805–16. Avery RL, Pieramici DJ, Rabena MD, et al. Intravitreal bevacizumab (Avastin) for neovascular age-related macular degeneration. Ophthalmology. 2006;113:363–72. Heier JS, Antoszyk AN, Pavan PR, et al. Ranibizumab for treatment of neovascular age-related macular degeneration. A phase I/II multicenter, controlled multidose study. Ophthalmology. 2006. Hawkins BS, Bressler NM, Bressler SB, et al. Surgical removal vs observation for subfoveal choroidal neovascularization, either associated with the ocular histoplasmosis syndrome or idiopathic: I. Ophthalmic findings from a randomized clinical trial: Submacular Surgery Trials (SST) Group H Trial: SST Report No. 9. Arch Ophthalmol. 2005;122:1597–611. Hawkins BS, Miskala PH, Bass EB, et al. Surgical removal vs observation for subfoveal choroidal neovascularization, either associated with the ocular histoplasmosis syndrome or idiopathic: II. Qualityof-life findings from a randomized clinical trial: SST Group H Trial: SST Report No. 10. Arch Ophthalmol. 2004;122:1616–28. Patz A, Smith RE. The ETDRS and Diabetes 2000 [Editorial]. Ophthalmology. 1991;98:739–40. Diabetes Control and Complications Trial. The effects of intensive diabetes treatment on the progression of diabetic retinopathy in insulin dependent diabetes mellitus. Arch Ophthalmol. 1995;113:36. Diabetic Retinopathy Study Research Group. Photocoagulation treatment of proliferative diabetic retinopathy: clinical application of Diabetic Retinopathy Study (DRS) findings. DRS Report 8. Ophthalmology. 1981;88:583–600. Early Treatment Diabetic Retinopathy Study Research Group. Photocoagulation for retinal macular edema. ETDRS Report No. 4. Int Ophthalmol Clin. 1987;27:265–72. Gutman FA. Evaluation of a patient with central retinal vein occlusion. Ophthalmology. 1983;90:481–3. Cahill MT, Stinnett SS, Fekrat S. Meta-analysis of plasma homocysteine, serum folate, serum vitamin B (12) and thermolabile MTHFR genotype as risk factors for retinal vascular occlusive disease. Am J Ophthalmol. 2003;136:1136–50.

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40. Branch Retinal Vein Occlusion Study Group. Argon laser photocoagulation for macular edema in branch retinal vein occlusion. Am J Ophthalmol. 1984;98:271–82. 41. Branch Retinal Vein Occlusion Study Group. Argon laser scatter photocoagulation for prevention of neovascularization and vitreous hemorrhage in branch retinal vein occlusion. Arch Ophthalmol. 1986;104:34–41. 42. The Central Vein Occlusion Study Group. A randomized clinical trial of early pan retinal photocoagulation for ischemic central vein occlusion. The Central Vein Occlusion Study Group N report. Ophthalmology. 1995;102:1434–44. 43. World Health Organization. WHO Press Release (WHO/45); Jun 17, 1996. 44. Trachoma: at a glance. International Trachoma Initiative: www.worldbank. org/hnp. 45. West SK. Trachoma: new assault on an ancient disease. Prog Retin Eye Res. Jun 2004;23(4):381–401. 46. Gilbert C, Foster A. Childhood blindness in the context of VISION 2020—The Right to Sight. Bull World Health Organ. 2001;79: 227–32. 47. Jabs DA, Green WR, Fox R, et al. Ocular manifestations of acquired immune deficiency syndrome. Ophthalmology. 1989;96:1092–9. 48. Pepose JS. Ophthalmic manifestations of HIV infection. Curr Topics in AIDS. 1989;2:191–206. 49. Wohl. HIV Clin Trials; 2005. 50. Patz A, Payne JW. Retinopathy of Prematurity. In: Duane TD, ed. Clinical Ophthalmology. Philadelphia: Harper & Row. 1983;3(20):1–19. 51. Patz A. Symposium on retrolental fibroplasia. Summary. Ophthalmology. 1979;86:1761–3. 52. Flynn JT, O’Grady GE, Herrera J, et al. Retrolental fibroplasia: I. Clinical Observations. Arch Ophthalmol. 1977;95:217–23. 53. Cryotherapy for Retinopathy of Prematurity Cooperative Group. Multicenter trial of cryotherapy for retinopathy of prematurity: preliminary results. Arch Ophthalmol. 1988;106:471–9. 54. Palmer EA. Retinopathy of Prematurity. Focal Points: Clinical Modules for Ophthalmologists. San Francisco: American Academy of Ophthalmology. 1993; vol 11, module 3. 55. James S, Lanman JT. History of oxygen therapy and retrolental fibroplasia. Prepared by the American Academy of Pediatrics Committee on Fetus and Newborn, with collaboration of special consultants. Pediatrics. 1976;57:591–642. 56. Tasman W, Patz A, McNamara JA, et al. Retinopathy of prematurity: a life of a lifetime disease, Am J Ophthalmology. 2006;141:167–74. 57. Rezai KA, Eliot D, Ferrone PJ, et al. Near confluent laser photocoagulation for treatment of threshold retinopathy of prematurity. Arch Ophthalmol. 2005;123:621–6. 58. Good WV. Early Treatment for Retinopathy of Prematurity Cooperative Group. Final results of the Early Treatment for Retinopathy of Prematurity (ETROP) randomized trial. Trans Am Ophthalm Soc 2004;102:233–48. 59. Palmer EA, Hardy RJ, Dobson V, et al. 15-year outcomes following threshold retinopathy of prematurity: final results from the multicenter trial of cryotherapy for retinopathy of prematurity. Arch Ophthalmol 2005;123:311–8. 60. Jabs DA, Holbrook JT, Van Natta ML, et al. Risk factors for mortality in patients with AIDS in the era of highly active antiretroviral therapy. Ophthalmology 2005;112:771–9.

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Psychiatric Disorders

69

Evelyn J. Bromet

Psychiatric disorders occur in every socioeconomic, racial, and cultural group in the world and are among the top 10 contributors to the global burden of disease.1 In the United States, 8–18% of children and adolescents and 26% of adults recently experienced a psychiatric or substance use disorder.2,3 Alzheimer’s disease is found in 8–15% of people over age 65.4 In the last several decades, a great deal has been learned about the distribution of psychiatric and substance use disorders in the population, their familial, biologic, social, and psychologic risk factors, illness course and prognosis, and the socioeconomic costs of these disorders. Psychiatric disorders account for a large proportion of all chronic health problems. Moreover, an individual’s mental state greatly influences general health status and ability to access needed health care services. Four issues underscore the importance of mental health issues for public health and preventive medicine: (a) quality of life is largely determined by a person’s mental state; (b) a large proportion of people in primary care have undetected psychiatric or substance disorders; (c) many physical disorders have an important mental component; and (d) as the risk of premature death recedes, the risk of chronic impairment rises. Given the significance of mental health problems, the search for causes is urgent.5 As modifiable risk factors are identified, primary prevention becomes increasingly appropriate and cost-beneficial. Progress in our understanding of the public health significance of mental disorders follows on the heels of the advances in classification and diagnosis. Current concepts of mental illness are rooted in the diagnostic characterizations of Kraepelin and Bleuler.6 The current classification system used in the United States is the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, now in its fourth edition (DSM-IV).7 This document reflects a consensus about the types of mental disorders present throughout the life cycle and the constellation of signs and symptoms characterizing each disorder. In making a diagnosis, a clinician depends mainly on the results of a comprehensive mental examination, which focuses on the patient’s (a) cognition; (b) current state of consciousness, confusion, or contact; (c) mood or affect; (d) connectedness of thought patterns, hallucinations, delusions, or distortion of thoughts and ideas; (e) personality (e.g., passivity, aggression, helplessness, rebelliousness); (f) behavior patterns, and (g) the complaint bringing the patient into treatment. In epidemiologic research, these domains are systematically evaluated using structured or semistructured diagnostic instruments. Epidemiologic research designed to estimate the incidence and prevalence of mental disorders evolved over the past 100 years. Three generations can be identified: (a) the period before World War II, in which information about mental illness typically was provided by key informants and agency records (the median prevalence rate in these reports was 3.6%); (b) World War II to the 1970s, in which representative samples of the population were interviewed with

extensive psychological and psychosomatic symptom inventories from which psychiatrists made ratings of levels of impairment (the median rate was 20%); and (c) 1970s to the present, in which representative population samples are interviewed with structured diagnostic interview schedules.8 The lifetime prevalence of psychiatric disorders ranges from 30% in the Epidemiologic Catchment Area (ECA) studies9 conducted in the early 1980s to almost 50% in the National Comorbidity Survey Replication (NCS-R)10 conducted in 2001–2003. This chapter focuses on findings from recent epidemiologic studies, although important earlier results and classic studies are also described. For a more detailed historical account of the epidemiology of mental disorders, see recent reviews.5,8,11 To ground the research reviewed in this chapter, it is important first to describe the basic tools that are used for case ascertainment in psychiatric research. One set of tools was developed for clinical research in patient populations. The need for these was first articulated in the early 1960s, when it was recognized that hospital admissions in England were more often diagnosed with depression while similar patients in the United States were given the diagnosis of schizophrenia.12 This observation led to the first international study of diagnosis (the U.S.-U.K. project) which trained psychiatrists in both countries to use systematic interviewing techniques and explicit diagnostic criteria. Under these conditions, the diagnostic distributions in England and the United States proved to be remarkably similar.13 The WHO program of research on schizophrenia also demonstrated the value of using uniform, structured assessment with patients within and outside the formal treatment network.14,15 In the United States, the need to define homogeneous patient populations for clinical drug trials and multicenter collaborative research propelled the development of pivotal semistructured assessment procedures for use by psychiatrists.16 One of the most influential measures came about as an offshoot of the multisite NIMH Collaborative Program on the Psychobiology of Depression. In order to insure that patients from different centers would be reliably classified, the investigators developed the Schedule for Affective Disorders and Schizophrenia17 (SADS), a semistructured diagnostic interview schedule designed for experienced clinicians, and the Research Diagnostic Criteria18 (RDC), which provided operational criteria for the classifying the most prevalent disorders found in patient populations. The Structured Clinical Interview for Diagnosis (SCID) was subsequently created for clinically experienced raters to match the DSMIII-R and DSM-IV criteria.19 As important as these tools are for classifying patients, a tool was also needed to reliably diagnose respondents in large-scale population-based research. For such studies, nonclinical, or lay, interviewers are more cost-effective than clinicians. In the late 1970s, the National Institute of Mental Health (NIMH) developed the Diagnostic Interview Schedule (DIS),20 a fully structured instrument designed specifically for lay interviewers. The ECA was the first large-scale 1161

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study to administer the DIS. Nearly 20,000 individuals from catchment areas in New Haven, St. Louis, Baltimore, Los Angeles, and Durham, North Carolina were interviewed.21 The DIS has been translated into many languages. A subsequent instrument, the Composite International Diagnostic Interview (CIDI), was developed by the WHO to permit diagnoses to be coded according to the DSM and the ICD systems. An expanded version of CIDI was recently administered to more than 10,000 respondents in the National Comorbidity Survey Replication3,10 and has been translated for use in countries in Asia, South America, Africa, and Europe. This chapter is organized around Morris’ framework on the uses of epidemiology.23 In providing an overview of public health psychiatry, this chapter reviews information on the epidemiology, treatment, and prevention of mental disorders.

COMMUNITY DIAGNOSIS

General Prevalence Studies The first U.S. prevalence study of mental illness (or insanity as it was then called) was conducted in Massachusetts in 1854 by a physician, Edward Jarvis, who undertook a census of the “insane” by gathering information from general practitioners, other key informants such as clergymen, and records of mental hospitals and other official agencies.24 Jarvis identified 2632 lunatics and 1087 idiots needing “the care and protection of their friends or of the public for their support, restoration, or custody.” This method of using key informants to identify cases of mental illness was the method of choice for psychiatric epidemiology until after World War II. After World War II, several studies of mental health in the general population were conducted using symptom inventories to determine rates of psychological impairment. The most well known was the Midtown Manhattan study.25 Symptom data were collected by social workers, and psychiatrists then used this information to rate the level of impairment. More than 20% of the population was judged as being severely impaired. The first national morbidity study was conducted in the 1950s by investigators at the University of Michigan.26 Consistent with the Midtown Manhattan finding, 20% of the population said yes when asked whether they ever felt that they were going to have a nervous breakdown. National studies have also been conducted on drinking patterns and alcohol-related problems, and about 12% of respondents were classified as “heavy drinkers.”27 The high rates of impairment from these symptom-based studies were regarded with skepticism. Surely the rate of diagnosable disorders would be lower than 20%. In fact, the findings from subsequent studies of diagnosis also produced unexpectedly high rates of psychopathology. The first large-scale study was the ECA which was designed as a longitudinal study.28 Specifically, the DSM-III version of the DIS was administered in face-to-face interviews conducted initially and at one-year follow-up. The resulting incidence,29 6-month,30 and lifetime31 prevalence rates are presented in Table 69-1. Overall, 25% of the population had a lifetime disorder, and 12% had a disorder in the past year. The most common disorders were alcohol abuse/dependence, phobias, major depression, and drug abuse. The least common disorders were schizophrenia, mania, and somatization. Three important observations resulted from this study. First, most disorders had their onset in adolescence or young adulthood. Second, only a minority of respondents with a diagnosable mental disorder received care, and most of that was obtained from general practitioners, not mental health specialists. Third, the rate of comorbidity was high. For example, almost one-third of respondents with a mental disorder had a comorbid substance use disorder. The ECA findings on the prevalence of schizophrenia merits separate comment. The differential diagnosis of schizophrenia versus other psychotic conditions is difficult to formulate even for experienced psychiatrists. Thus the reliability of this diagnosis in the ECA was low, and prevalence estimates are better determined from more reliable sources of information, such as case registries and psychiatrist

TABLE 69-1. AVERAGE RATES OF PSYCHIATRIC DISORDER IN THE EPIDEMIOLOGIC CATCHMENT AREA STUDY (N = 18,571), CONDUCTED IN SELECTED CATCHMENT AREAS OF NEW HAVEN, CT; DURHAM NC; ST. LOUIS, MO; BALTIMORE, MD; AND LOS ANGELES, CA

Disorder Alcohol abuse/ dependence Phobia Drug abuse/ dependence Major depressive episode Obsessive-compulsive Antisocial personality Panic Cognitive impairment Schizophrenia Mania Somatization

Lifetime Prevalence

6-mo. Prevalence

1-yr. Incidence

13.3 12.5

4.7 7.7

1.8 4.0

5.9

2.0

1.1

5.8 2.5 2.5 1.6 1.3 1.3 0.8 0.1

3.0 1.5 0.8 0.8 1.3 0.8 0.5 0.1

1.6 0.7 — 0.6 1.2 — — —

Prevalence rates adapted from Kessler RC, Chiu WT, Demler O, et al. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62:617–27; and incidence rates from Eaton WW Jr, Kramer M, Anthony JC, et al. The incidence of specific DIS/DSM-III mental disorders: Data from the NIMH Epidemiologic Catchment Area Program. Acta Psychiatr Scand. 1989;79:163–78. Incidence rates do not include data from the New Haven site. Rates of cognitive impairment reflect current impairment at the time of interview only. Clinical data are based on the Diagnostic Interview Schedule and DSM III. Rates are expressed as percentages.

interviews. A recent review of such studies found that the median point prevalence of schizophrenia is 4.5 per 1000.33 Ten years after the ECA was conducted, Kessler and colleagues undertook the first national probability sample study of the distribution of DSM-III-R disorders.33 In this study, known as the National Comorbidity Survey (NCS), a modified version of the CIDI was administered from 1990 to 1992 to 8098 individuals aged 15–54 from the 48 contiguous states. Special efforts were made to recruit initial nonrespondents, and the final response rate was 82.6%. To assess psychotic disorder, respondents endorsing psychotic symptoms were reinterviewed by telephone by a psychiatrist with the SCID. Overall, almost 50% of the sample met criteria for a psychiatric or substance use disorder in their lifetime, and about one-quarter had a diagnosable condition in the year prior to interview. Consistent with the ECA results, the most prevalent conditions were depression, anxiety, and substance use disorders. Among respondents with a disorder in the prior 12 months, 17.4% had a single disorder, 23.1% had two disorders, and 58.9% had three or more disorders. Consistent with the ECA, the age of onset of most disorders was adolescence or young adulthood. A replication of the NCS was conducted from 2001 to 2003 with close to 10,000 individuals selected from throughout the United States.3,10 Table 69-2 provides the lifetime and 12-month prevalence rates from this recent survey. The overall rates of disorder were similar to those found a decade earlier. The most prevalent disorders were major depression, alcohol abuse, social phobia, and specific phobia. One-quarter of respondents met criteria for two or more disorders in their lifetime, and the age of onset continued to be adolescence and young adulthood.

Comparative Studies Research comparing the rates of mental illness across geographic areas dates back to the pioneering work of Faris and Dunham,34 who showed that hospitalization rates for schizophrenia in Illinois state institutions decreased progressively with distance away from the center of

69 TABLE 69-2. LIFETIME AND 12-MONTH PREVALENCE RATES OF DSM-IV PSYCHIATRIC DISORDERS IN THE NATIONAL COMORBIDITY SURVEY REPLICATION (N = 8098) CONDUCTED IN 2001–2003

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systematic efforts, such as the World Mental Health Survey Consortium, appears to outweigh the limitations. INDIVIDUAL RISKS AND CHANCES

DSM-III-R Disorder Mood disorders Major depressive disorder Dysthymia Bipolar disorders Anxiety disorders Panic disorder Agoraphobia without panic disorder Social phobia Specific phobia Generalized anxiety disorder Post-traumatic stress disorder Substance use disorders Alcohol abuse Alcohol abuse with dependence Drug abuse Drug abuse with dependence Any disorder 2+ disorders 3+ disorder

Lifetime (%)

12-month (%)

Several individual risk factors are associated with the occurrence of psychiatric disorders, including gender, age, social class, marital status, ethnicity, physical health, family history of mental disorder, and season of birth.

16.6 2.5 3.9

6.7 1.5 2.6

4.7

2.7

Gender

1.4 12.1 12.5 5.7 6.8

0.8 6.8 8.7 3.1 3.5

13.2

3.1

5.4 7.9 3.0

1.3 1.4 0.4

46.4 27.7 17.3

26.2 5.8 6.0

Gender differences in rates of substance abuse, anxiety disorders, and depression have been confirmed in community samples, primary care patients, and treatment samples in psychiatric and substance abuse clinics. The male:female ratios are approximately 6:1 for alcoholism, 1:2 for depression, and 1:2 to 1:3 for phobias. Many social and biological factors have been hypothesized to underlie these differences, including recurrence risk,46 drinking habits, expressing emotion, social roles, role performance and role-related strains, as well as professional biases in diagnosis.47 In contrast, there is no overall gender difference in the prevalence of schizophrenia although the age at first hospitalization occurs earlier in males (late teen to early 20s) than females (late 20s). Psychopathology is twice as common in prepubertal boys than girls, but the sex ratio reverses itself during adolescence. At the other end of the life spectrum, a recent study found that the eight-year incidence rate of dementia was somewhat lower in men (14.4 per 1000) than women (19.0 per 1000).48

Chicago. Forty-six percent of the cases were from the inner city area compared with 13% from the outermost districts. Faris and Dunham hypothesized that the inner city environment elicited mental illness, rejecting the alternative explanation that social selection or drift was responsible for these higher rates (see later on). Since then, studies conducted in other urban areas have consistently shown the same pattern. Urban-rural differences in rates of treated mental illness have been studied extensively. Dohrenwend and Dohrenwend’s classic review35 concluded that neuroses and personality disorder were more prevalent in urban areas, but schizophrenia rates did not differ according to urbanicity. While some subsequent evidence has supported their conclusions for adults36–38 and children,39–40 recent findings are somewhat at odds with these conclusions. For example, Van Os and colleagues41 found that the prevalence of psychosis in a community sample increased progressively with level of urbanization. A populationbased study in France found no significant urban-rural differences in general psychopathology.42 Urban-rural differences in the prevalence of dementia have also been evaluated, with three Scandinavian studies reporting significantly lower rates in rural compared to urban areas.43 Such studies are important both for understanding underlying risk factors and for determining where to locate mental health intervention programs. International variations in rates of mental disorders and substance use disorders have also been the focus of research.44 Using an expanded version of the CIDI, a recent international study, the World Mental Health Survey Consortium, found that the prevalence of recent episodes of DSM-IV disorders ranged from 4.3% in Shanghai to 26.4% in the US (interquartile range = 9.1–16.9%).22 In studies based on the DIS, the rates of alcoholism in 10 regions around the world ranged from 5% in Taiwan to 22% in Korea.45 In spite of differences in prevalence, the clinical profiles were similar, with the mean age of onset in the early 20s, the mean number of symptoms about four, and males having significantly higher rates than females. International studies that use the same protocol are criticized for lacking cultural sensitivity regarding how psychiatric and substance disorders are manifested. On the other hand, studies that use unique tools provide prevalence estimates that cannot be compared. Thus in the absence of biological markers of disease, the value of current

Age Some psychiatric disorders, such as attention deficit-hyperactivity disorder, first appear in childhood. As noted earlier, other diagnoses, such as mood and anxiety disorders, also have their onset early in life and decrease progressively with age.10,33 For alcohol-related problems, the peak period of heavy drinking is early 20s,49 but the rate of diagnosable alcohol abuse/dependence who appear for treatment peaks in the early 40s. Finally, dementia is rare in people under age 60, but after that, the rate doubles every five years.43

Social Class Numerous studies have been undertaken to understand the relationship between social class and mental illness, also encompassed by the term, health disparities. As noted above, the ecological studies, starting with that of Faris and Dunham, emphasized the importance of social class in relation to schizophrenia and argued that features of the physical or social environment of poor neighborhoods caused the higher than expected numbers of patients from those areas. Other nonecological studies also support an environmental explanation. For example, in their classic study, Hollingshead and Redlich found that among psychiatric patients, schizophrenia was associated with being born and raised in lower social class neighborhoods.50 Their findings suggest that downward social mobility does not explain the social class pattern. More recent studies, however, indicate that social selection is the more plausible explanation for schizophrenia. In a classic study of occupational attainment, patients with schizophrenia had jobs with lower status than those of their fathers and than what had been predicted by their school careers.51 Currently in schizophrenia research, the potential genetics findings have tipped the balance in favor of the social selection rather than the social causation hypothesis.52 Lower social class status is also associated with higher rates of depressive symptoms, alcohol abuse or dependence, drug abuse or dependence, and antisocial personality disorder.10,52 In addition, lower social class status is a risk factor for many psychiatric disorders of both childhood53 and old age.54 Social causation, rather than social

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selection, is the primary explanation for the social class findings for these conditions.

Ethnicity The NCS33 found no differences in rates of anxiety disorders according to ethnicity. However, compared to blacks, whites had higher rates of mood and substance use disorders and lifetime comorbidity. Except for enuresis, Costello and colleagues also found similar rates of psychopathology in black and white children.53 Consistent with the NCS finding for mood disorder, research on suicide has consistently found that whites have significantly higher rates of suicide than nonwhites, particularly white males. Later in this chapter we discuss the temporal changes in the suicide rate of young white males. Here it is important to note that the age-adjusted suicide rates for Native Americans and Chinese-Americans are substantially higher than those for whites. In fact, the rate for native American youth is more than double that of same-age peers.55 Research on psychosis has shown that some ethnic groups have higher than expected rates of schizophrenia, especially indigenous populations of certain regions of Croatia56,57 and western Ireland.58 In older studies of psychiatric patients in the United States, African-American patients were disproportionately diagnosed with schizophrenia and were hospitalized at a younger age and for longer periods of time than whites. However, these findings are generally attributed to clinical bias and racism. Indeed the NCS found no race differences in the rates of clinician-derived diagnoses of psychosis.59

Marital Status Being single and being separated or divorced are associated with an increased risk of several psychiatric disorders, although whether this reflects cause or consequence is unknown. Community studies have also found that married men are less depressed than unmarried men, but married women are more distressed than unmarried women.25 This suggests that being married is a protective factor for men but not for women. In schizophrenia, several studies have found that being single at the time of first hospitalization confers a poorer prognosis. However, this finding may be an artifact of gender, age, and/or poor premorbid functioning.

Physical Health Status Several sources of evidence point to strong links between physical and mental health.5 First, psychiatrically ill populations have higher than expected mortality than their nonpsychiatrically ill counterparts. In one study, the adjusted mortality rate of psychiatric patients was elevated two- to threefold.60 Another study reported that 6% of patients reporting to a psychiatric emergency service died within two years of the visit, whereas the expected rate was 1.6%.61 In a community sample aged 55 and older, the odds of dying over a 15month period was four times higher for people with a mood disorder than for persons who did not have a mood disorder.62 A second source of evidence is that hospitalized patients have an elevated rate of psychiatric disorders compared to nonhospitalized controls. It has long been known that infectious diseases can produce serious mental disorders.5 In addition, high rates of major depression and depressive symptoms are found in patients hospitalized with chronic conditions, such as multiple sclerosis, cancer, diabetes mellitus, cardiovascular disease, thyroid disease, and chronic pain.63 One study reported that 61% of severely ill hospital patients were depressed compared with 21% of less ill patients.64 Whether depression and related disorders are a risk factor for disease onset or disease severity, a consequence of disease, or a consequence of hospital-induced disability is difficult to determine.

Third, outpatient primary care patients have high rates of psychiatric symptoms.63 In the ECA, 22% of respondents who recently attended a medical care facility met criteria for a DSM-III disorder compared with 17% of nonattenders.65 A review of British studies of psychiatric morbidity in general practice patients concluded that 20–25% suffered from psychiatric disturbances, primarily mood disorders.66 In a large international study of ambulatory patients, the WHO assessed more than 5000 patients in 15 primary care centers around the globe and found that 24% were diagnosed with a psychiatric or substance use disorder.67 Despite the high prevalence of psychiatric disorders, especially depression, psychiatric problems in primary care patients are often undetected or are misdiagnosed, in part because both physicians and patients focus on somatic symptoms and possible physical diagnoses.

Familial Aggregation Considerable research on familial aggregation of psychopathology has been conducted. In schizophrenia, monozygotic twins have a concordance rate for schizophrenia between 33% and 78% compared with 8–28% for dizygotic twins. The risk for developing schizophrenia, given the presence of an affected first-degree relative, is approximately 10% (compared with an overall prevalence of less than 1%).68 Weissman69 reviewed findings from family studies of depression and reported a two- to threefold increase in major depression in adult firstdegree relatives of patients with depression. Weissman’s study of the offspring of depressed parents also found a threefold increase in risk for psychiatric disorder (24% compared with 8% among controls).70 The preponderance of evidence regarding alcoholism deriving from family, twin, and adoption studies also points to a genetic vulnerability for developing this disease.71 Modern studies of genetic causes of mental disorders, and the interaction of genetic and environmental factors, hold great promise for clarifying these familial associations observed over the past 50 years.5

Season of Birth Seasonal variation in rates of stillbirths, neonatal deaths, and congenital rubella is amply documented, although the impact of seasonal variation appears to have diminished over time.72 In England, Scandinavia, and the United States, patients with schizophrenia are disproportionately likely to be born during the winter or spring months. Possible explanations for this phenomenon include nutritional factors during pregnancy, genetic factors, and exposure to infectious or viral agents.73 CAUSES

New understandings of the origins and course of mental disorder emerge when clinical research, laboratory studies, sociological inquiries, and epidemiology interact. A dramatic illustration occurred early in the twentieth century, when pellagra psychosis accounted for almost 10% of the admissions to mental hospitals. In South Carolina during the early 1920s, Goldberger et al.74 showed that pellagra was associated with a nutritional deficiency, although the specific items missing from the diet were only later identified. As a result of dietary changes, pellagra psychosis became rare in the United States, although it remains endemic in parts of Africa and India. This section is limited to a discussion of social and physical environmental causes of mental disorders. Because psychiatric disorders often develop insidiously, it is often difficult to separate risk from consequence. Thus here we use the terms risk factor and correlate interchangeably. Genetic causes, and gene-environment interactions, have also been found for rare conditions, such as early-onset Alzheimer’s disease, and candidate genes are being studied for other psychiatric disorders. To date, the findings are regarded as very preliminary and thus are not included below.

69

Social Environment Stress in the social environment has been linked to a variety of common mental disorders. As mentioned earlier, ecological studies hypothesized that environmental stress was a cause of mental disorders. Here we conceptualize stress as a set of disruptive environmental presses or stimuli and review findings on personal rather than ecologically determined stressors. Communitywide Traumas. Communitywide stressors expose large numbers of people to uncontrollable events and thus provide a unique opportunity to understand both short-term and long-term psychological sequelae. Recent examples include the nuclear power plant accidents at Three Mile Island (TMI) in 1979 and at Chornobyl in 1986, the terrorist attack on 9/11, and the 2005 tsunami. Like many disasters, the TMI and Chornobyl accidents were not acute, timelimited events but involved a sequence of interrelated stressful occurrences that unfolded over a long period of time, including the initial crisis, intermittent radiation leaks, difficulties surrounding the cleanup operations, and in the case of Chornobyl, permanent evacuation and elevated rates of thyroid cancer in children. The 9/11 and tsunami catastrophes occurred abruptly, but they too created a number of other crises in their wake. These events have all been shown to elevate the rate of psychopathology. For example, the TMI study of mothers of preschool children living within 10 miles of the plant found that the rate of depression and anxiety doubled during the year after the accident75 and remained high over the subsequent 10 years.76 Similarly, populations residing near Chornobyl had significantly poorer mental health than controls 6–11 years after the disaster.77 Research on 9/11 victims and the tsunami survivors also demonstrate the psychological toll of these kinds of events. In general, the psychiatric sequelae of human-made and natural disasters have consistently found that in the short term, survivors experience anxiety and mood problems. The greater the magnitude of the disaster, the greater and the longer is the effect. The disorder that has mostly frequently been studied after disasters is posttraumatic stress disorder (PTSD). This disorder is defined as a response to an unusual stressor in which an individual reexperiences the traumatic event through recurrent thoughts or dreams, experiences psychic numbing, and has symptoms such as sleep disturbance, survivor guilt, difficulty concentrating, hyperarousal, avoidance of activities associated with the event, and an intensification of symptoms if reexposed to a similar event. PTSD is often comorbid with mood, anxiety, and substance disorders. Thus, in disaster studies, the most consistent risk factors for PTSD are similar to those for other adverse mental health outcomes. These include being female, having a prior history of psychiatric disturbance, and having greater involvement in the disaster in terms of loss of life or property or fear of adverse health consequences.78 Studies of combat veterans show that such trauma is a particularly potent trigger of short-term and long-term adverse mental health consequences. Since the Vietnam war, there has been considerable interest in the emotional well-being of combat veterans, especially the onset and persistence of PTSD. A national study of Vietnam veterans conducted in the late 1980s reported a point prevalence rate of 15.2% and a lifetime rate of 31% among combat veterans.79 These high rates led the Department of Veterans Affairs to increase research and treatment programs for this vulnerable group. Recent studies of Gulf War veterans also show elevated rates of mood and anxiety disorders, especially PTSD.80 Personal Adversities and Strains. Another common method for studying stress is to administer a checklist of positive and negative life events. Studies employing these checklists typically find that these events play a relatively minor and transient role in evoking psychiatric symptoms in general population samples. In vulnerable populations, these events sometimes have more important consequences. For example, in schizophrenia, life events were shown to trigger psychotic episodes, particularly in patients having inadequate social support.81 Personal vulnerability factors can also increase the impact of life events,

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especially in depressed populations.82 For example, a seminal study by Brown and colleagues found that working class women were at particular risk when they lacked a confiding relationship with their husbands, were not employed outside the home, had three or more children under the age of six years, or endured the loss of their own parents in childhood.83 Two specific events, unemployment84 and bereavement85 have been studied extensively. Both were shown to produce short-term deleterious effects in more than 50% of exposed individuals. The vulnerability factors that magnified the impact of these stressors included inadequate social support, poor physical health, and preexisting financial difficulties. Chronic strains at work or at home are also associated with impairments in mental health. With regard to the work environment, employees in jobs characterized by high levels of demand, little autonomy over decision making, conflicting requirements, and taskrelated ambiguity experience higher levels of psychological symptoms and alcohol abuse than employees with less occupational strain.86 The combination of high demands and low decision latitude is particularly stressful.87,88 Marital stress is associated with depression and substance abuse; moreover stress in the family environment is a well-documented risk factor for behavioral problems in children. Indeed, children reared in families with high levels of conflict, abuse, or neglect are at risk for a range of health problems, including depression, sleep disorders, developmental delay, generalized anxiety, school behavior problems, phobias, and antisocial behavior.89

Physical Environment Three aspects of the physical environment are described in this section: toxic exposures in the work place, lead exposure among children, and homelessness. Occupational Exposures. Exposure to lead, mercury, carbon monoxide, carbon disulfide, and the like may cause serious central nervous system (CNS) disturbances. In Alice in Wonderland, Lewis Carroll immortalized the well-known hallucinations, delusions, and mania produced by high-level mercury exposure in the character of the Mad Hatter. Since the nineteenth century, dramatic case reports have described cognitive and neurasthenic symptoms and even suicide in workers exposed to a variety of solvents. An issue of ongoing public health concern is the potential health effects of low-level neurotoxic exposures. Lead and solvents are two such exposures that have been investigated extensively. Recent epidemiologic studies suggest that even at accepted levels, occupational lead exposure can have an adverse effect on neurocognitive functioning.90 Several Scandinavian studies of male workers chronically exposed at threshold or subthreshold levels to solvents reported significantly more CNS symptoms (headaches, fatigue, depression dizziness, memory disturbances), nonspecific somatic complaints (nausea, abdominal pain, skin problems, and aches and pains), and impaired performance on cognitive tasks compared with unexposed controls.91–94 A study of female workers also found that low-level solvent exposure was significantly associated with increased depression, CNS disturbance, and an array of nonspecific somatic complaints.95 However, these studies contain some serious methodological flaws,96 and further confirmation from epidemiologic research is needed. One difficulty with occupational studies of this sort is sample bias because workers who are sensitive to the exposure find employment elsewhere, and the sample is then subject to the “healthy worker” effect. It has also been hypothesized that the combination of low-level exposure and high occupational stress is especially deleterious, but empirical findings have so far been mixed.97–99 In this regard, it is interesting to note that mass psychogenic illness has been found in workplaces containing both high stress and low-level solvent exposures.100 Lead Exposure in Children. Environmental exposure to lead was shown to have a significant effect on the cognitive performance of children. In their classic study, Needleman et al. took tooth samples from elementary school children and showed that lead exposure was

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significantly related to lower intelligence test scores, even after adjusting for 39 risk factors, including social class and parental IQ.101 In an 11-year follow-up study of these children, higher dentin lead levels continued to be predictive of both school performance and school dropout.102 Although this study was the object of considerable controversy, the central findings have been confirmed in many subsequent studies. Homelessness. Rates of mental illness among homeless adults and children are alarmingly high. In one study, more than one-quarter of homeless individuals were found to have a major chronic mental illness, such as schizophrenia or substance abuse.103 Compared with socioeconomically matched controls, homeless children have more overt health problems and more psychiatric risk factors, such as abuse, neglect, and elevated blood lead levels.104 In some cities, deinstitutionalization of the mentally ill from state mental hospitals contributed significantly to the problem of homelessness. The risk of homelessness among discharged state hospital patients was as high as 28% in New York City.105 New interventions have been designed to address the mental health and substance abuse problems in homeless populations, but this is particularly difficult population to engage and maintain. For a review of this research, see reference.106 HISTORICAL TRENDS

Although in psychiatry, historical trends are difficult to study because the diagnostic nomenclature and availability of services have shifted over time, important research has been conducted on the temporal stability of psychosis, depression, adolescent suicide, and suicidal behavior.

Psychosis A major debate centers on whether the prevalence of schizophrenia increased as a function of industrialization. A pioneering analysis by Goldhamer and Marshall focused on mental hospital admission rates for psychosis from 1840 to 1940.107 They concluded that a progressive increase in hospital admissions occurred among the elderly, but the rates of psychosis (primarily schizophrenia) among young and middle-aged groups changed very little. Eaton, however, extended the time period to 1970 and reported that the prevalence of psychosis did indeed increase.108 Potential explanatory factors include changes in environmental exposures, infant mortality and longevity, lifestyle changes associated with industrialization, and/or artifactual variables such who enters the treatment system and availability of services.109 As intriguing as these hypothese are, however, a subsequent study found no temporal changes, and the issue remains unsettled.110

Depression Evidence has also accumulated regarding an increase in depression since World War II. In Lundby, Sweden, a longitudinal study was initiated in 1947111 in which direct interviews by psychiatrists, information from key informants, and medical records were used to determine psychiatric diagnoses of the entire population. Based on follow-up interviews by psychiatrists in 1957 and 1972 with 97% of the original cohort, a significant increase in the incidence of nonpsychotic depression was detected. Although the Lundby study remains the only direct source of evidence regarding an increase in depression, other indirect sources of evidence, such as the suicide patterns discussed below, also suggest that depression has increased.112 As with psychosis, temporal changes, if present, could be due to either environmental factors or artifactual variables, such differential mortality, changes in diagnostic criteria, reporting biases, and changing attitudes about depression in society.

Suicide in Adolescents and Young Adults Between 1955 and 1980, the rate of suicide in people 15–24 years of age tripled, increasing from 2.6 per 100,000 population to 8.5 per

100,000 population, making suicide the second leading cause of death in this age group.113 The group at highest risk was white males. In addition to sex, the chief risk factors were prior suicide attempts, substance abuse, mental illness, and family history of mood disorder and suicide. The presence of firearms in the home is perhaps the most important risk factor.114 Thus public health programs aimed at reducing adolescent suicide must focus not just on personal risk factors but also on lethal agents in the home environment.

Suicide Behaviors Suicide ideation and attempts are precursors to completed suicide. A recent report by the NCS investigators compared the rates of suicide behaviors (i.e., ideation, plans, gestures, and attempts) in the 1990–1992 NCS cohort with those of the 2001–2003 NCS-R cohort.115 Overall, the rates proved to be remarkably stable. For example, 2.8% of the earlier and 3.3% of the more recent cohort reported suicidal ideation (having serious thoughts of suicide). The one important difference, however, was the extent to which respondents with ideation and attempts received treatment. In the 1990–1992 cohort, 40% of ideators who made a suicide gesture and 50% who made a serious attempt received treatment. However, in the later cohort, the proportions receiving treatment doubled. COMPLETING THE CLINICAL PICTURE

Since the majority of individuals with common mental disorders do not receive treatment from mental health specialists, community studies are needed to improve our understanding of their clinical signs and prognosis. Thus, recent studies applying formal diagnostic criteria to community populations have helped complete the clinical picture by pointing out that the syndromes of depression and alcoholism, for example, may be different in treated and untreated groups. A study of white collar employees found that 10% of managers and professions met lifetime criteria for alcoholism, but the vast majority of these cases became social drinkers with no serious legal, social, occupational, or clinical consequences.116 Thus unlike impressions from clinical samples, or individuals who attend Alcoholics Anonymous, these findings suggest that community respondents meeting diagnostic criteria for alcoholism may not have significant social and occupational impairment in the long-term. Thus, the poor prognosis ascribed to conditions such as alcoholism derives in part from the clinician’s illusion, that is, from treating chronic cases who stay in the service system.117 Another important aspect of the clinical picture is comorbidity. Psychiatric patients in treatment often meet criteria for more than one psychiatric disorder, sometimes labeled primary and secondary disorders. For example, patients with primary alcoholism often develop secondary depression during the course of the alcoholism. Schizophrenic patients discharged after their first lifetime admission often develop depression during the subsequent year. Patients with major depression often suffer from an accompanying anxiety disorder such as phobia or panic disorder. However, people often enter treatment precisely because they have more than one disorder. Community studies thus are able to complete the clinical picture regarding comorbidity. In this case, recent epidemiological findings confirm that multiple psychiatric disorders also co-occur in the general population.3,118 Examples of highly comorbid conditions include alcoholism and drug abuse, alcoholism and antisocial personality, obsessivecompulsive personality and panic disorder, depression and anxiety disorder, and depression and somatization. IDENTIFYING NEW SYNDROMES

By systematizing clinical observations, epidemiologists can potentially identify new syndromes. For example, until the early 1980s, depression was considered an adult disorder that rarely occurred during childhood. Several factors converged to increase the awareness

69 that children can become clinically depressed, including the increasing rate of adolescent suicide and suicide attempts, the increased frequency with which depression was observed in pediatric settings, and the high rates of depression reported in research on the offspring of clinically depressed parents. Recent epidemiologic findings suggest about 2% of preadolescents and 5–10% of adolescents suffer from clinical depression.119 Epidemiological studies of occupational exposures identified syndromes associated with specific toxic chemicals such as lead, cyanide, carbon monoxide, carbon disulfide, and mercury.120 For example, the constellation of symptoms resulting from carbon monoxide (an exposure occurring in blast furnace workers, fire fighters, fork-lift truck operators, and others) includes disturbances in concentration, memory, impulsivity, and lack of insight into one’s behavior. As noted, the phrase “mad as a hatter” stemmed from observations of specific types of tremors among workers in the hatting industry who were exposed to high levels of mercuric nitrate in Europe during the nineteenth century. EVALUATING MENTAL HEALTH SERVICES

This section provides a brief historical overview of American psychiatric service delivery, a discussion of factors associated with entry into treatment, and approaches to preventing mental disorders. It is not intended as an exhaustive review but rather as an overview of key issues.

Historical Overview of American Psychiatric Care In 1841, when Dorothea Lynde Dix began her crusade on behalf of the mentally ill, there were only 18 hospitals in the United States devoted exclusively to the care of the mentally ill. The vast majority of psychiatrically ill individuals were in jails and poorhouses, kept at home, boarded out, or auctioned off to the highest bidder. Echoing Horace Mann’s 1828 plea that the mentally ill be declared “wards of the state,” Dix convinced the Massachusetts legislature that local communities had shown themselves incapable of caring for the mentally ill. Like other reformers, she did not hesitate to reinforce her arguments with the economic lure that decent treatment in small and geographically isolated state hospitals would cure psychiatrically disturbed individuals quickly, making them productive members of society instead of drains on the public purse. In 1843, the Commonwealth of Massachusetts voted to make all of the indigent mentally ill wards of the state and to enlarge Worcester State Hospital, a mental hospital established as a result of Horace Mann’s efforts a decade before. The Dix-Mann doctrine that the mentally ill should be wards of the state reached its most explicit expression with the passage of the New York State Care Act of 1890. This legislation provided for removal of the mentally ill from local poorhouses and jails to state hospitals, where they were to be supported and treated at state expense. The law further required each state hospital to admit all cases of mental illness from its district, regardless of prognosis. Following its initiation in New York, other states adopted the Dix-Mann principle of complete state care for the seriously mentally ill. A major consequence of this action was the isolation of mental patients and of psychiatry from the mainstream of medicine. Although some state hospitals in the United States were established explicitly as custodial institutions, most attempted to apply moral treatment, and some closely approached that ideal. Even the best-managed hospitals, however, did not long continue to function as the small rural, therapeutic retreats envisioned by Dix and Mann. New asylums were built as older ones overflowed, and the demand for accommodation always seemed to exceed capacity. As chronic cases accumulated and new admissions rose, overcrowding led to deterioration in the standards of care. At the start of the 1900s, the “cult of curability” yielded to the notion, “once insane, always insane.” Moral treatment precepts were forgotten, and behavior was controlled with physical restraints and seclusion.

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The National Association for Mental Hygiene was founded in 1909, with the aim of improving the care and treatment of patients in mental hospitals. After World War I, the mental hygiene movement turned its attention to prevention by early detection and treatment of mental disorders, a strategy exemplified by its active support for the development of child guidance clinics and parental education. The rapid growth of child guidance clinics and other outpatient psychiatric services marked the beginning of organized community-based psychiatry in the United States, which had begun in the late nineteenth century in Europe. By the mid-1930s, nearly all state mental hospitals had at least one outpatient clinic. In 1946, Congress passed the National Mental Health Act (Public Law 79-487), thereby creating the National Institute of Mental Health. For the first time, the federal government took responsibility for research, training of personnel, and assisting the states in prevention, diagnosis, and treatment of serious psychiatric disorders. Having grown at a steady rate for over a century, the resident patient population reached an all-time high of 560,000 in 1955. The decline of resident mental patients began due to three factors: the introduction of neuroleptic drugs, which accelerated management and sometimes even recovery and enabled some patients to be treated at home; the introduction of the therapeutic community, or communityoriented treatment within the hospital, which reduced the demoralization of custodial care; and the geographic decentralization of large state mental hospitals, which led to closer relationships between state hospitals and local communities. Starting in 1960, a systematic policy of releasing patients was initiated, based on successful reforms in England, where a reduction of the patient census had preceded the use of neuroleptic drugs. Length of stay was also shortened for acute admissions. As the number of acute admissions increased, custodial hospitals were somewhat transformed into short-term intensive treatment centers. This “revolving door” situation highlighted the need for expanded community treatment. In the short period of about 25 years, mental hospital censuses decreased from 560,000 in 1955 to 214,065 in 1981.121 In 1955, Congress enacted the Mental Health Study Act (Public Law 84-182) to evaluate the “human and economic problems of mental illness.” This act led to the establishment of the Joint Commission on Mental Illness and Health. The Commission’s final report, Action for Mental Health, recommended that services for the mentally ill be expanded. The Commission recommended establishing (a) outpatient mental health facilities in communities to provide immediate care for acutely disturbed patients, (b) one clinic per 50,000 population, (c) inpatient psychiatric units in every general hospital with 100 or more beds, (d) maximum occupancy in state mental hospitals of 1000 beds, and (e) expanded mental health education to reduce the stigma associated with mental illness. In 1963, President Kennedy delivered a message to Congress on mental illness and mental retardation in which he proposed a national federally funded program for setting up comprehensive community mental health centers and for improving care in state hospitals. This set the stage for the passage of the Community Mental Health Centers Act of October 1963. The newly mandated community mental health centers had to provide five essential services: inpatient care, outpatient care, emergency services, partial hospitalization, and consultation and education. Over time, five additional services were to be added: diagnostic services, rehabilitation services, precare and aftercare services, training, and research and evaluation. The centers were to serve geographically defined catchment areas of 75,000–200,000 people. By 1980, 717 community mental health centers had been funded across the country (2000 had been envisaged), with the federal government investing more than 1.5 billion dollars. In 1977, President Carter signed an executive order establishing The President’s Commission on Mental Health to review and make new recommendations on the mental health needs of the nation. Among its 100 recommendations were the following: improving linkages between community support networks and mental health facilities; expanding services to children, minorities, the elderly, and the chronically mentally ill; the continued phasing down of large state mental hospitals; and the development of a case management system

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by the states. In 1980, President Carter signed the resulting Mental Health Systems Act (Public Law 96-398) into law. However, the subsequent Omnibus Budget and Reconciliation Act of 1981 (Public Law 97-35) rescinded continued federal management and turned responsibility for provision of community mental health services to the states through the block grant. At present, in New York and other states, treatment of the chronically mentally ill, both young and old, is the primary focus of community mental health centers. In the mid-1990s, the financial burden associated with mental disorders was estimated to be $99 billion in direct and $79 billion in indirect costs, calculated based on absenteeism, unemployment, social service utilization, related accidents, and crime. Together the direct and indirect costs comprised more than 10% of all health care costs in the United States.122 Indeed, the negative economic consequences exceeded the direct costs of treatment.123 Treatment studies have been funded to improve patients outcomes and reduce this cost. As we enter the twenty-first century, several issues raised by nineteenth and twentieth century reformers remain remarkably pertinent for public mental health. The first is the goal of keeping mentally ill people out of jails. In fact, correctional facility placement has become so pervasive that the rate of mental illness in prisons is 2–4 times greater in jails and prisons than in the general population. Meanwhile, correctional facilities do not have sufficient staff to provide adequate or appropriate treatment for the severely mentally ill in their midst.121 Second, nonprofit advocacy organizations have become more numerous, and with internet access, their mission and educational materials are readily accessible to families, patients, and physicians. Readers interested in finding specific organizations can check the website for the National Institute of Health’s Substance Abuse and Mental Health Services Administration. Yet in spite of the ease of obtaining information, mental illness remains stigmatized in the general population and underdetected in primary care settings. Third, the Surgeon General’s report on mental health122 emphasized that not only is evidence-based treatment important, but also age, sex, race, and culture must be taken into account. Yet, tailoring treatment to the needs of patients and their families is rarely accomplished. Fourth, most individuals with mental illness and even suicidal behaviors continue to be treated in the general medical or primary care sector. Yet medical students and general medicine residents receive even fewer hours of training on the diagnosis and treatment of mental illness and substance use disorders than was true of their predecessors.

Preventive Interventions Two psychiatric disorders were eradicated through primary prevention efforts: pellagra psychoses and brain damage from measles and rubella.5 In the workplace, reductions in exposures to heavy metals have led to marked decreases in the occurrence of neuropathy or encephalopathy. Similarly, the passage of laws to reduce lead in paint in the United States has aimed at improving cognitive performance in children. The increase in suicide in adolescents and young adults led to the creation of school-based programs aimed at preventing teen suicide.124 The goals of these programs are to heighten awareness of the problem, to promote the identification of students at risk, and to provide information about mental health resources. Shaffer et al. studied 1000 13- to 18-year-old students from six high schools who were exposed to one of three programs. Although the three programs used significantly different techniques, the authors felt that they were not differentially effective, concluding that the true value of the programs was their screening function, in which 3% of the students reported that they were suicidal and in need of professional help. Early detection is the cornerstone of secondary prevention. The most famous example in psychiatry is the elimination of general paresis (syphilitic psychoses) through antibiotic therapy. Secondary prevention programs have been implemented in the early phases of a variety of high-risk situations. Examples of such programs include ones aimed at reducing (a) psychosis in high risk adolescents, (b) substance abuse and delinquency in young adolescents with a history of poor

academic performance and disruptive behaviors; and (c) depression in high-risk groups, such as low-income mothers and adults undergoing major life changes.125 In this regard, Kessler and colleagues have strongly advocated for developing interventions for secondary disorders given the high rate of comorbidity in the population.126 The well-documented delays in initial treatment seeking127 and continued unmet need for treatment, especially in underserved populations,128 also support the importance of early detection and accessibility to care. Delays in treatment can lead to greater severity, and failure to treat conditions when they first arise, that is, in adolescence and young adulthood, can lead to social and economic consequences, such as school failure, teenage pregnancy, and unstable employment. The workplace is a focal point of many secondary intervention programs. Many companies established Employee Assistance Programs and the like to assist troubled employees. The goal of these programs is to detect mental health problems at an early stage and offer interventions that might avert a full-blown psychiatric episode.129,130 Similarly, exercise and health programs aimed at reducing physical symptoms (e.g., smoking, obesity, high blood pressure) also are expanding in occupational settings. In light of the significant relationship between physical and mental health, it is believed that these programs will have a positive effect on the psychological well-being of employees. Clinical trials focused on psychotherapeutic medications or other forms of therapy are examples of tertiary prevention efforts focused on treating symptoms and hence minimizing the disabilities and impairments in quality of life among patients with severe mental illness, particularly schizophrenia and mood disorders. For example, the NIMH developed a depression awareness program to educate psychiatrists, general practitioners, and the lay public about the symptoms and new treatments for mood disorders. A review of the vast psychiatric treatment literature is beyond the scope of this chapter; however, clinical drug trials are being conducted for an array of new medications targeted to symptoms of psychosis, depression, obsessive-compulsive symptoms, panic attacks, cognitive decline, and other disabling symptom complexes. CONCLUSION

Considerable progress has occurred in research on the epidemiology and prevention of mental disorders.131,132 Although most of the achievements have occurred at the level of descriptive epidemiology, analytic findings on variables associated with onset and course, including genetic factors, and an array of treatment intervention studies are also expanding.5 Recent advances in molecular genetics, brain imaging techniques, statistical methods, and measurement are having a major impact on the scope and focus of current research. Ultimately, the goal is to identify modifiable risk factors that can be translated into preventive interventions. REFERENCES

1. World Health Organization. The World Health Report: 2001; Mental Health: New Understanding. New Hope. Geneva: WHO; 2001. 2. Costello EJ, Egger H, Angold A. 10-year research update review: the epidemiology of child and adolescent psychiatric disorders: I. Methods and public health burden. J Am Acad Child Adolesc Psychiatry. 2005;44:972–86. 3. Kessler RC, Chiu WT, Demler O, et al. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62:617–27. 4. Ritchie K, Kildea D. Is senile demential “age-related” or “ageingrelated”?—evidence from meta-analysis of dementia prevalence in the oldest-old. Lancet. 1995;346:931–40. 5. Susser E, Schwartz S, Morabia A, et al. Psychiatric Epidemiology: Searching for the Causes of Mental Disorders. New York: Oxford; 2006.

69 6. Kendall RE. The Role of Diagnosis in Psychiatry. Blackwell Scientific Publications: Oxford; 1975. 7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: American Psychiatric Association; 1994. 8. Dohrenwend BP, Dohrenwend BS. Perspectives on the past and future of psychiatric epidemiology: The 1981 Rema Lapouse Lecture. Am J Public Health. 1982;72(11):1271–9. 9. Regier D, Burke J. Psychiatric disorders in the community: The Epidemiologic Catchment Area study. In: Hales R, Frances A, eds. American Psychiatric Association Annual Review. Vol. 6, Chap. 27. Washington, DC: American Psychiatric Press; 1987. 10. Kessler RC, Berglund P, Demler O, et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62: 593–601. 11. Grob GN. The origins of American psychiatric epidemiology. Am J Public Health. 1985;75(3):229–36. 12. Kramer M. Cross-national study of diagnosis of the mental disorders: origin of the problem. Am J Psychiatry. 1969;125(10S):1–11. 13. Cooper JE, Kendell RE, Gurland BJ, et al. Psychiatric Diagnosis in New York and London: A Comparative Study of Mental Hospital Admissions. London: Oxford University Press, Institute of Psychiatry, Maudsley Monographs, No. 20; 1972. 14. World Health Organization. Schizophrenia: A Multinational Study. Geneva: World Health Organization; 1975. 15. Sartorius N, Jablensky A, Korten A, et al. Early manifestations and first-contact incidence of schizophrenia in different cultures: A preliminary report on the initial evaluation phase of the WHO Collaborative Study on Determinants of Outcome of Severe Mental Disorders. Psychol Med. 1986;16:909–28. 16. Feighner JP, Robins E, Guze SB, et al. Diagnostic criteria for use in diagnostic research. Arch Gen Psychiatry. 1972;26:57–63. 17. Endicott J, Spitzer R. A diagnostic interview: The schedule for affective disorders and schizophrenia. Arch Gen Psychiatry. 1978; 35:837–44. 18. Spitzer R, Endicott J, Robins E. Research diagnostic criteria: Rationale and reliability. Arch Gen Psychiatry. 1978;35:773–82. 19. Spitzer R, Williams B, Gibbon M, et al. The Structured Clinical Interview for DSM-111-R (SCID): I. History, rationale, and description. Arch Gen Psychiatry. 1992;49:624–9. 20. Robins LN, Helzer JE, Croughan J, et al. National Institute of Mental Health Diagnostic Interview Schedule. Arch Gen Psychiatry. 1977;34:129–33. 21. Eaton WW, Kessler LG, eds. Epidemiologic Field Methods in Psychiatry: The NIMH Epidemiologic Catchment Area Program. Orlando, Florida: Academic Press, Inc.; 1985. 22. WHO World Mental Health Survey Consortium. Prevalence, severity, and unmet need for treatment of mental disorders in the World Health Organization World Mental Health surveys. JAMA. 2004; 291:2581–90. 23. Morris JN. Uses of Epidemiology. 2 ed. London: Livingstone; 1964. 24. Jarvis E. Insanity and Idiocy in Massachusetts: Report of the Commission on Lunacy, 1855. Cambridge, MA: Harvard University Press; 1971. 25. Srole L, Langner TS, Michael ST, et al. Mental Health in the Metropolis: The Midtown Manhattan Study. New York: Harper & Row: 1962. 26. Gurin G, Veroff J, Feld J. Americans View Their Mental Health. New York: Basic Books; 1960. 27. Cahalan D. Understanding America’s Drinking Problem: How to Combat the Hazards of Alcohol. San Francisco: Jossey-Bass Publishers; 1987. 28. Eaton WW Jr, Regier DA, Locke BZ, et al. The Epidemiologic Catchment Area Program of the National Institute of Mental Health. Public Health Rep. 1981;96(4):319–25.

Psychiatric Disorders

1169

29. Eaton WW Jr, Kramer M, Anthony JC, et al. The incidence of specific DIS/DSM-III mental disorders: Data from the NIMH Epidemiologic Catchment Area Program. Acta Psychiatr Scand. 1989;79:163–78. 30. Myers JK, Weissman MM, Tischler GL, et al. Six-month prevalence of psychiatric disorders in three communities. Arch Gen Psychiatry. 1984;41:959–67. 31. Robins LN, Heizer JE, Weissman MM, et al. Lifetime prevalence of specific psychiatric disorders in three sites. Arch Gen Psychiatry. 1984;41:949–58. 32. Saha S, Chant D, Welham J, et al. A systematic review of the prevalence of schizophrenia. PLOS Medicine. 2005;2:413–33. 33. Kessler RC, McGonagle KA, Shao S, et al. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Arch Gen Psychiatry. 1994;51:8–19. 34. Faris R. Dunham H. Mental Disorders in Urban Areas: An Ecological Study of Schizophrenia and Other Psychoses. New York: Hafner Publishing Co.; 1939. 35. Dohrenwend BP, Dohrenwend BS. Psychiatric disorders in urban settings. In: Arieti S, ed. American Handbook of Psychiatry, Vol. 2: Child and Adolescent Psychiatry, Sociocultural and Community Psychiatry. New York: Basic Books; 1974. 36. Mueller DP. The current status of urban-rural differences in psychiatric disorder: An emerging trend for depression. J Nerv Ment Dis. 1981;169(1):18–27. 37. Brown GW, Davidson S, Harris T, et al. Psychiatric disorder in London and North Uist. Soc Sci Med. 1977;11:367–77. 38. Blazer W, Oeorge LK, Landerman R, et al. Psychiatric disorders: A rural/urban comparison. Arch Gen Psychiatry. 1985;42:651–6. 39. Rutter M, Yule B, Quinton D, et al. Attainment and adjustment in two geographical areas: III. Some factors accounting for area differences. Br J Psychiatry. 1974;125:520–33. 40. Offord D, Boyle M, Szatmari P, et al. Six-month prevalence of disorder and rates of service utilization. Arch Gen Psychiatry. 1987;44:832–6. 41. Van Os J, Hanssen M, Bijl RV, et al. Prevalence of psychotic disorder and community level of psychotic symptoms: an urban-rural comparison. Arch Gen Psychaitry. 2001;58:663–8. 42. Kovess-Masfety V, Lecoutour X, Delavelle S. Mood disorders in urban/rural settings: Comparisons between two French regions. Soc Psychiatry Psychiatr Epidemiol. 2005;40:613–8. 43. Jorm AF, Korten A, Henderson AS. The prevalence of dementia: A quantitative integration of the literature. Acta Psychiatr Scand. 1987;76:465–79. 44. Weissman MM, Bland R, Canino G, et al. Cross-national epidemiology of major depression and bipolar disorder. JAMA. 1996;276: 293–9. 45. Helzer JE, Canino GJ, eds. Alcoholism in North America, Europe, and Asia. NY: Oxford University Press; 1992. 46. Kessler RC, McGonagle KA, Nelson CB, et al. Sex and depression in the National Comorbidity Survey. II: Cohort effects. J Affec Dis. 1994;30:15–26. 47. Bebbington P. The origins of sex differences in depression: Bridging the gap. Int Rev Psychiatry. 1996;8:295–332. 48. Fuhrer R, Dufouil C, Dartigues JF, et al. Exploring sex differences in the relationship between depressive symptoms and dementia incidence: prospective results from the PAQUID study. J Am Geriatr Soc. 2003;51:1178–80. 49. Cahalan D, Cisin IH. American drinking practices: Summary of findings from a national probability sample. 1. Extent of drinking by population subgroups. In: Ward DA, ed. Alcoholism, Introduction to Theory and Treatment. Chap. 8. Dubuque, Lowa: Kendall Hunt Publishing Co.; 1980. 50. Hollingshead AB, Redlich FC. Social Class and Mental Illness: A Community Study. New York: John Wiley & Sons; 1958. 51. Goldberg E, Morrison S. Schizophrenia and social class. Br J Psychiatry. 1963;109:785–802.

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Noncommunicable and Chronic Disabling Conditions

52. Dohrenwend BP, Levav I, Shrout PE, et al. Socio-economic status and psychiatric disorders: the causation-selection issue. Science. 1992;255:946–52. 53. Costello EJ, Angold A, Burns BJ, et al. The Great Smoky Mountains Study of youth: goals, design, methods, and the prevalence of DSMIII-R disorders. Arch Gen Psychiatry. 1996;53:1129–36. 54. Berkman LF, Berkman CS, Kasl S, et al. Depressive symptoms in relation to physical health and functioning in the elderly. Am J Epidemiol. 1986;124:372–87. 55. May P. Suicide and self-destruction among American Indian youths. American Indian and Alaska Native Mental Health Research. 1987;1:52–69. 56. Kulcar Z, Crocetti GM, Lemkau PV, et al. Selected aspects of the epidemiology of psychoses in Croatia, Yugoslavia: II. Pilot studies of communities. Am J Epidemiol. 1971;94:118–25. 57. Crocetti GM, Lemkau PV, Kulcar Z. Selected aspects of the epidemiology of psychoses in Croatia, Yugoslavia: III. The cluster sample and the results of the pilot survey. Am J Epidemiol. 1971;94: 126–34. 58. Walsh D, O’Hare A, Blake B, et al. The treated prevalence of mental illness in the Republic of Ireland. The three county case register study. Psychol Med. 1980;10:465–70. 59. Kendler KS, Gallagher TJ, Abelson JM, et al. Lifetime prevalence, demographic risk factors, and diagnsostic validity of nonaffective psychosis as assessed in a U.S. community sample. Arch Gen Psychiatry. 1996;53:1022–30. 60. Babigian HM, Odoroff CL. The mortality experience of a population with psychiatric illness. Am J Psychiatry. 1969;126:470–480. 61. Munoz RA, Marten S, Gentry KA, et al. Mortality following a psychiatric emergency room visit: An 18-month follow-up study. Am J Psychiatry. 1971;128:220–4. 62. Bruce ML, Leaf PJ. Psychiatric disorders and 15-month mortality in a community sample of older adults. Am J Public Health. 1989;79: 727–30. 63. Katon W. The epidemiology of depression in medical care. Int J Psychiatry Med. 1987;17:93–112. 64. Moffic H, Paykel E. Depression in medical inpatients. Br J Psychiatry. 1975;126:346–53. 65. Kessler LG, Burns BJ, Shapiro S, et al. Psychiatric diagnoses of medical service users: Evidence from the Epidemiologic Catchment Area Program. Am J Public Health. 1987;77:18–24. 66. Blacker CVR, Clare AW. Depressive disorder in primary care. Br J Psychiatry. 1987;150:737–51. 67. Üstün TB, Sartorius N. Mental Illness in General Health Care: An International Study. NY: John Wiley & Sons; 1995. 68. Kendler KS. The genetics of schizophrenia: An overview. In: Tsuang MT, Simpson JC, eds. Nosology, Epidemiology and Genetics of Schizophrenia. Chap. 18. New York: Elsevier; 1988. 69. Weissman MM. Advances in psychiatric epidemiology: Rates and risks for major depression. Am J Public Health. 1987;77:445–51. 70. Weissman MM, Prusoff BA, Gammon GD, et al. Psychopathology in the children (ages 6–18) of depressed and normal parents. J Am Acad Child Psychiatry. 1984;23(1):78–84. 71. Merikangas KR. The genetic epidemiology of alcoholism. Psychol Med. 1990;20:11–22. 72. Hare E. Aspects of the epidemiology of schizophrenia. Br J Psychiatry. 1986;149:554–61. 73. Bromet EJ, Dew MA, Eaton W. Epidemiology of psychosis with special reference to schizophrenia. In: Tsuang M, Tohen M, Zahner G, eds. Textbook in Psychiatric Epidemiology. Chap. 14. NY: Wiley; 1995. 74. Goldberger J, Waring CH, Tanner WF. Pellagra prevention by diet in institution inmates. Public Health Rep. 1925;38:2361–8. 75. Bromet EJ, Parkinson D, Schulberg HC, et al. Mental health of residents near the TMI reactor: A comparative study of selected groups. J Prevent Psychiatry. 1982;1:225–75.

76. Dew MA. Bromet Predictors of temporal patterns of psychiatric distress 10 years following the nuclear accident at Three Mile Island. Soc Psychiatry Psychiatr Epidemiol. 1993;28:49–55. 77. Havenaar JM, Bromet EJ. The experience of the Chornobyl nuclear disaster. In: Lopez-Ibor JJ, Christodoulou G, Maj M, et al. eds. Disasters and Mental Health. London, John Wiley; 2005. 78. Norris FH, Friedman MJ, Watson PJ, et al. 60,000 disaster victims speak: an empirical review of the empirical literature, 1981–2001. Psychiatry. 2002;65:207–39. 79. Kulka RA, Schlenger WE, Fairbank JA, et al. Trauma and the Vietnam War Generation: Report of Findings from the National Vietnam Veterans Readjustment Study. NY: Brunner/Mazel; 1990. 80. Black DW, Carney PC, Peloso PM, et al. Gulf war veterans and anxiety: prevalence, comorbidity, and risk factors. Epidemiol. 2004; 15:135–42. 81. Zubin J, Steinhauer R, Day R, et al. Schizophrenia at the crossroads: A blueprint for the 80s. Compr Psychiatry. 1985;26:217–40. 82. Paykel E. Contribution of life events to causation of psychiatric illness. Psychol Med. 1978;8:245–53. 83. Brown G, Harris T. Social Origins of Depression: A Study of Psychiatric-Disorder in Women. New York: The Free Press; 1978. 84. Kates N, Greiff BS, Hagen DQ. The Psychosocial Impact of Job Loss. Washington, DC: American Psychiatric Press; 1990. 85. Jacobs S, Hansen F, Berkman L, et al. Depressions of bereavement. Compr Psychiatry. 1989;30:218–24. 86. Kasl S. Epidemiological contributions to the study of work stress. In: Cooper C, Payne R, eds. Stress at Work. Chap. 1. New York: John Wiley & Sons; 1978. 87. Karasek R. Job demands, job decision latitude, and mental strain: Implications for job redesign. Adm Sci Q. 1979;24:285–306. 88. Phelan J, Schwartz JE, Bromet EJ, et al. Work stress, family stress and depression in professional and managerial employees. Psychol Med. 1991;21:999–1012. 89. Garfinkel B, Carlson G, Weller E, eds. Psychiatric Disorders in Children and Adolescents. Philadelphia: WB Saunders Co.; 1990. 90. Barth A, Schaffer AW, Osterode W, et al. Reduced cognitive abilities in lead-exposed men. Arch Occup Environ Health. 2002;75: 394–8. 91. Elofsson S, Gamberale F, Hindmarsh T, et al. Exposure to organic solvents. Scand J Work Environ Health. 1980;6:239–73. 92. Husman K. Symptoms of car painters with long-term exposure to a mixture of organic solvents. Scand J Work Environ Health. 1980; 6:19–2. 93. Larsen F, Leira H. Organic brain syndrome and long-term exposure to toluene: A clinical, psychiatric study of vocationally active printing workers. J Occup Med. 1988;30:875–8. 94. Orbaek P, Risberg J, Rosen 1, et al. Effects of long-term exposure to solvents in the paint industry. Scand J Work Environ Health. 1985;11(2):1–28. 95. Parkinson DK, Bromet EJ, Cohen S, et al. Health effects of longterm solvent exposure among women in blue collar occupations. Am J Indus Med. 1990;17:661–75. 96. Errebo-Knudsen E, Olsen F. Organic solvents and presenile dementia (the painter’s syndrome): A critical review of the Danish literature. The Sci Total Environ. 1986;48:45–67. 97. House J, McMichael A, Wells J, et al. Occupational stress and health among factory workers. J Health Soc Behav. 1979;20:139–60. 98. Bromet EJ, Ryan CM, Parkinson DK. Psychosocial correlates of occupational lead exposure. In: Lebovits AH, Baum A, Singer JE, eds. Advances in Environmental Psychology, Vol. 6: Exposure to Hazardous Substances: Psychological Parameters. Chap. 2. Hillsdale, New Jersey: Lawrence Erlbaum Associates; 1986. 99. Bromet EJ, Dew MA, Parkinson DK, et al. Effects of occupational stress on the physical and psychological health of women in a microelectronics plant. Soc Sci Med. 1992;34:1377–83. 100. Colligan M, Murphy L. Mass psychogenic illness in organizations: An overview. J Occup Psychol. 1979;52:77–90.

69 101. Needleman HL, Gunnoe C, Leviton A, et al. Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N Engl J Med. 1979;300(13):689–95. 102. Needleman HL, Schell A, Bellinger D, et al. The long-term effects of exposure to low doses of lead in childhood: A l-year follow-up report. N Engl J Med. 1990;322(2):83–8. 103. Koegel P, Burnam A, Farr RK. The prevalence of specific psychiatric disorders among homeless individuals in the inner city of Los Angeles. Arch Gen Psychiatry. 1988;45:1085–92. 104. Alperstein G, Rappaport C, Flanigan JM. Health problems of homeless children in New York City. Am J Public Health. 1988;78: 1232–3. 105. Susser E, Lin S, Conover S, et al. Childhood antecedents of homelessness in psychiatric patients. Am J Psychiatry. 1991;148: 1026–30. 106. Martens WH. A review of physical and mental health in homeless persons. Public Health Rev. 2001;29:13–33. 107. Goldhamer H, Marshall A. Psychosis and Civilization. Glencoe, Illinois: Free Press; 1955. 108. Eaton WW Jr. The Sociology of Mental Disorders. New York: Praeger; 1980. 109. Hafner H. Are mental disorders increasing over time? Psychopathology. 1985;18:66–81. 110. Krupinski J, Alexander L. Patterns of psychiatric morbidity in Victoria, Australia in relation to changes in diagnostic criteria 1848–1978. Soc Psychiatry. 1983;18:61–7. 111. Hagnell O, Lanke J, Rorsman B, et al. Are we entering an age of melancholy? Depressive illnesses in a prospective epidemiological study over 25 years: the Lundby Study, Sweden. Psychol Med. 1982;12:279–89. 112. Klerman GL, Weissman MM. Increasing rates of depression. JAMA. 1989;261:2229–35. 113. Rosenberg ML, Smith JC, Davidson LE, et al. The emergence of youth suicide: An epidemiologic analysis and public health perspective. Am Rev Public Health. 1987;8:417–40. 114. Brent DA, Perper JA, Allman CJ. Alcohol, firearms, and suicide among youth: Temporal trends in Allegheny County, Pennsylvania, 1960 to 1983. JAMA. 1987;257:3369–72. 115. Kessler RC, Berglund P, Borges G, et al. Trends in suicide ideation, plans, gestures, and attempts in the United States, 1990–1992 to 2001–2003. JAMA. 2005;293:2487–95. 116. Bromet EJ, Parkinson D, Curtis EC, et al. Epidemiology of depression and alcohol abuse/dependence in a managerial and professional workforce. J Occup Med. 1990;32:989–95. 117. Cohen P, Cohen J. The clinician’s illusion. Arch Gen Psychiatry. 1984;41:1178–82.

Psychiatric Disorders

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118. Robins LN, Regier DA, eds. Psychiatric Disorders in America. NY: Free Press; 1991. 119. Weller E, Weller R. Depressive disorders in children and adolescents. In: Garfinkel B, Carlson G, Weller E, eds. Psychiatric Disorders in Children and Adolescents. Chap. 1. Philadelphia: WB Saunders; 1990. 120. Collier HE. The mental manifestations of some industrial illnesses. Occup Psychol. 1939;113:89–97. 121. Human Rights Watch (2003) Ill-Equipped: U.S. Prisons and Offenders with Mental Illness, New York: Internet: http://www. hrw.org/press/2003/10/us102203.htm. 122. Mental Health: A Report of the Surgeon General. 1999. http://www. surgeongeneral.gov/library/mentalhealth/home.html. 123. Hu TW. Perspectives: an international review of the national cost estimates of mental illness, 1990–2003. J Ment Health Policy Econ. 2006;9:3–13. 124. Shaffer D, Garland A, Gould M, et al. Preventing teenage suicide: A critical review. J Am Acad Child Adolesc Psychiatry. 1988;27: 675–87. 125. Price RH, Smith SS. A Guide to Evaluating Prevention Programs in Mental Health. Washington, DC: U.S. Government Printing Office; 1984. 126. Kessler RC. Epidemiology of psychiatric comorbidity. In: Tsuang M, Tohen M, Zahner G, eds. Textbook in Psychiatric Epidemiology. Chap. 7. NY: Wiley; 1995. 127. Christiana JM, Gilman SE, Guardino M, et al. Duration between onset and time of obtaining initial treatment among people with anxiety and mood disorders: an international survey of members of mental health patient advocate groups. Psychol Med. 2000;30: 693–703. 128. Wang PS, Lane M, Olfson M, et al. Twelve-month use of mental health services in the United States. Arch Gen Psychiatry. 2005;62:629–40. 129. Kessler RC, Ames M, Hymel PA, et al. Using the World Health Organization Health and Work Performance Questionnaire (HPQ) to evaluate the indirect workplace costs of illness. J Occup Environ Med. 2004;46:S23–537. 130. Simon GE, Barber C, Birnbaum HG, et al. Depression and work productivity: the comparative costs of treatment versus nontreatment. J Occup Environ Med. 2001;43:2–9. 131. Tsuang M, Tohen M, eds. Textbook in Psychiatric Epidemiology. 2nd ed. NY: Wiley; 2002. 132. Kessler RC. Psychiatric epidemiology: selected recent advances and future directions. Bull World Health Organ. 2000;78:464–74.

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Childhood Cognitive Disability

70

Maureen S. Durkin • Nicole Schupf • Zena A. Stein • Mervyn W. Susser

Mental retardation or cognitive disability occurring in childhood is a condition with enormous public health implications for at least four reasons. One is its relative frequency; with prevalence as high as 1% or greater in most populations, mental retardation is among the most common childhood disability.1–3 Another is its early onset and frequent life-long duration. A third is its socioeconomic impacts, which include adverse impacts on productivity and quality of life of affected individuals and caregivers as well as increased expenditures for medical care and residential services. A fourth reason is that prevention, whether primary, secondary, or tertiary, is attainable via public health interventions for nearly all forms of mental retardation. Examples of primary prevention include nutritional interventions such as iodine and folic acid supplementation and food fortification, immunization programs, and removal of environmental sources of lead exposure. Early identification followed by therapeutic interventions, for conditions such as Down syndrome and phenylketonuria (PKU), are examples of secondary prevention of mental retardation. Examples of tertiary prevention include early cognitive stimulation, special education, and habilitation to enhance functioning. One of the challenges mental retardation poses to public health is that certain prevention strategies, highly effective in one respect, have had the paradoxical side effect of increasing the occurrence of mental retardation in the population in terms of either incidence (new cases) or prevalence (by means of improved survival). Examples of this paradox include mental retardation associated with inborn errors of metabolism, Down syndrome, and premature birth. These and other specific topics in mental retardation are discussed below, following an overview of definitions and prevalence.

example, in people with mental retardation, identifiable neuropathological lesions often correlate weakly or not at all with specific causes and/or clinical/functional attributes.7,8 The dominant approach to defining and classifying mental retardation is by severity of disability rather than by cause. The International Classification of Diseases (ICD-9, ICD-10)9,10 as well as the Diagnostic and Statistical Manual (DSM-IV-TR)11 and former versions of the American Association on Mental Retardation classification4 distinguish four grades of severity defined in terms of IQ (Table 70-1). The most recent version of the American Association on Mental Retardation’s classification system has moved away from distinguishing grades of intellectual deficit and toward defining severity in terms of the level of support required for optimal functioning (e.g., intermittent, limited, extensive, and pervasive levels of support).12 Classification based on etiology is increasingly used, as advances in cytogenetics, molecular and biochemical genetics, and brain imaging improve our ability to determine specific causes. Etiologic classifications have clear advantages for epidemiologic research and for primary prevention. They may also be preferable to functional classifications for assessing specific needs for appropriate medical care, rehabilitation, and other services.13 However, even with recent advances in knowledge and diagnostic capabilities, most cases of mental retardation cannot be attributed with certainty to a specific cause. Table 70-2 provides an outline of the categories of known causes of mental retardation.

DEFINITION AND CLASSIFICATION

Studies of the true incidence of mental retardation are not possible because only a minority of cases survive long enough to be identified and because the onset and recognition of disability are often insidious during the course of a child’s development.14,15 The descriptive epidemiology of mental retardation is based largely on prevalence (the number of existing cases in a population at a given time) rather than incidence (the number of newly occurring cases during a given time period). In describing the prevalence of childhood cognitive disability, it is useful to combine moderate, severe, and profound grades of intellectual disability into a single category of severe mental retardation (IQ below 50 or 55) and distinguish this from mild mental retardation (IQ between 50 or 55 and 70 or 75). Table 70-3 contrasts the major epidemiologic characteristics of these two classes. In developed countries, the prevalence of severe childhood mental retardation consistently ranges from 3 to 5 per 1000 (Table 70-4) and more than 50% of cases are attributed to genetic causes. Mild mental retardation in developed countries varies widely in prevalence, is generally more frequent than severe forms, is strongly associated with low socioeconomic status, and is rarely associated with known causes or with other neurologic disorders. A male excess is observed in both severe and

Mental retardation implies significant deficits, with onset early in life, in intelligence (as measured by standardized intelligence tests) and in adaptive behavior (e.g., communication, self-care, social interaction, school, and/or work).4 The deficits are recognized in the performance of social roles and age-appropriate tasks. The infant and preschool child may fail to achieve developmental milestones of sitting, responding to familiar faces, walking, talking, and sphincter control at expected ages. The schoolchild falls short of social expectations for classroom behavior and for reading, writing, and arithmetic. The adult may have difficulty in performing work within and outside the home, communicating, or understanding money, transport, and locality. Functional limitations in mental retardation can potentially be identified at three levels: impairment (altered brain structure and/or function), disability (deficits in intellectual function and adaptive behavior), and social participation (limitations in social roles and opportunities experienced by persons with disabilities due to environmental conditions).5,6 One-to-one correlations between currently understood causes, identifiable impairments, and levels of disability and participation appear to be the exception rather than the rule. For

INCIDENCE AND PREVALENCE

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TABLE 70-1. CLASSIFICATION OF MENTAL RETARDATION BY GRADE OF SEVERITY OF INTELLECTUAL DEFICIT

Severity

ICD-9a Code

Mild Moderate Severe Profound Unspecified

317.00 318.00 318.10 318.20 319.00

ICD-10b Code F70.0-F70.9 F71.0-F71.9 F72.0-F72.9 F73.0-F73.9 F79.0-F79.9

Approximate IQ Rangec 50–55 to 70–75 30–35 to 50–55 20–25 to 35–40 <20–25

a World Health Organization. International Classification of Diseases. 9th ed. Geneva: World Health Organization; 1980.9 bWorld Health Organization. International Classification of Diseases—10th, 2nd ed. Geneva: World Health Organization; 2006.10 cPrecise IQ cut-points may vary to allow for differences between tests. Guidelines of the American Association on Mental Deficiency4 and the Diagnostic and Statistical Manual (DSM-IV-TR) of the American Psychiatric Association11 recommend the use of these or similar cut-points as well as clinical judgment and assessment of adaptive skills in the diagnosis and classification of severity of mental retardation.

Several cross-sectional studies of age-specific prevalence rates conducted in different decades and populations consistently show, for both severe and mild mental retardation, increasing prevalence with age during childhood followed by declining rates with advancing age throughout adulthood.1 Severe mental retardation is much more likely than mild to be diagnosed during infancy. The increasing prevalence with age during childhood could be due to increases with age in the use of specialty services and in the probability of being included in agency records1 as well as the likelihood of exposure to postnatal causes (infections, trauma). For severe mental retardation, excess mortality is responsible for the decline in prevalence with age after childhood. For mild mental retardation, the decline in prevalence may be partly due to mortality, but could alternatively be due to the fact that societies do not universally require of adults the cognitive skills they require of school children; a degree of recovery is also probable. Thus, many persons categorized as mildly retarded in school become indistinguishable from the general population during adulthood. SELECTED CAUSES

Chromosomal Anomalies mild mental retardation, due in part to the contribution of X-linked forms of mental retardation (discussed below). The few estimates available from less developed countries point to elevated prevalence rates of severe mental retardation (Table 70-4). This may be due to the higher frequency in those settings of nutritional, traumatic, and infectious causes of brain damage and, in some populations, to factors such as consanguinity and advanced maternal age.16 Low socioeconomic status is the strongest and most consistent predictor of mild mental retardation but is usually found to have little or no association with the prevalence of severe mental retardation (Table 70-3).17,18 This pattern points to the role of poverty and social disadvantage in the etiology of mild mental retardation. Preschool programs providing social and intellectual stimulation may boost IQ and reduce the risk of mild mental retardation in vulnerable groups.19–22

TABLE 70-2. MAJOR CATEGORIES OF KNOWN CAUSES OF MENTAL RETARDATION WITH SPECIFIC EXAMPLES OF EACH Causal Category

Specific Examples

Chromosomal

Down syndrome Cri-du-chat Phenylketonuria (PKU) Fragile X syndrome Hypothyroidism Iodine Folate Maternal PKU

Single gene Hormonal Specific nutritional Deficiency/dietary factor (prenatal) Infection Prenatal Perinatal Postnatal Toxic exposure Prenatal

Postnatal Traumatic brain injury, anoxia Perinatal Postnatal

Rubella Toxoplasmosis Syphilis Human immunodeficiency virus Measles encephalitis Ionizing radiation Fetal alcohol syndrome Lead Lead Prolonged, obstructed labor Premature birth Motor vehicle collision Fall Near drowning

Chromosomal anomalies, including structural and numerical anomalies, are a major cause of severe mental retardation. Structural changes result from chromosome breakage and rearrangement and can be induced by a variety of exposures, including ionizing radiation, viral infections, and toxic substances. Numerical anomalies arise through nondisjunction during meiosis or mitosis or through lagging of chromosomes at anaphase of cell division. Among several types of abnormalities of chromosome number that occur, trisomies play the largest role in the etiology of mental retardation. As a whole, chromosomal anomalies contribute more to fetal loss than to live births and mental retardation. About 40% of miscarriages, 6% of stillbirths, and less than 1% of live births have been estimated to be chromosomally aberrant.23 After 8 weeks gestational age, the proportion of chromosomal aberrations lost by miscarriage exceeds 90% for all but trisomy 21 (Down syndrome), XXX, XXY (Klinefelter’s syndrome), and XYY.23 In Sweden, chromosomal anomalies, primarily Down syndrome, were reported to cause more than 30% of prevalent cases of severe mental retardation.24,25

Down Syndrome Down syndrome is the most common genetic cause of mental retardation and the leading known cause of severe mental retardation in developed countries.26,27 All cases of Down syndrome result from partial or complete duplication of chromosome 21 in the genome.28 The most common form (95% of cases at birth) is standard trisomy, involving duplication of chromosome 21. In over 90% of these cases, the extra chromosome is of maternal origin, due to nondisjunction during meiosis.29–31 Translocation of chromosome 21 material to another chromosome (usually 13 or 18) and mosaicism (transmission of a cryptic trisomy 21 cell line from an unaffected parent) are rare causes of Down syndrome.32,33 The most striking epidemiologic characteristic of Down syndrome is the marked increase in risk with increasing maternal age, from approximately 1 per 1500 live births at ages 20–24 to 1 per 600–700 live births at ages 30–34 to 1 per 50 live births at ages 41–45.34 Increased availability of effective birth control in the 1960s was followed by reductions in the number and proportion of births to older women and corresponding reductions in the prevalence of Down syndrome at birth.33 Also contributing to reductions in the frequency of Down syndrome births is the availability of prenatal diagnosis followed by therapeutic abortion.26 Studies in multiple populations found this to reduce the number of infants born with Down syndrome by 6–8%.35,36 However, the era of decreased prevalence at birth has also been an era of increased longevity of persons with Down syndrome. The net effect of these two trends has been a rise in the prevalence of Down syndrome in adolescents and adults. It was estimated that even

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TABLE 70-3. EPIDEMIOLOGIC CHARACTERISTICS OF SEVERE AND MILD MENTAL RETARDATION Severe Prevalence range in childhood (/1000): Populations with advanced medical care Less developed countries Life expectancy % with other neurodevelopmental or sensory disorders % with other psychiatric disorders % with known genetic cause % with unknown cause Usual age at recognition Duration Male-Female ratio Major demographic risk factors

Association with social class

Mild

2.5–5.0 5.0–25.0 Considerably shorter than general population About 85%

2.5–40.0 (Estimates not available) Somewhat shorter than general population

Higher frequency than general population About 50% Minority Infancy or preschool years Lifelong Male excess (1.1 to 1.4:1) Maternal age is a strong predictor of trisomies, which cause about 30% of severe mental retardation Prevalence is relatively even across the social classes

Higher frequency than general population

About one-third

Small percentage Majority School age May be restricted to school age Male excess (1.1 to 1.8:1) Low socioeconomic status

Occurs predominantly in children of low social class

Sources: Alberman E. Main causes of major mental handicap: prevalence and epidemiology. Ciba Found Symp. 1978;59:3–16; Eyman RK, Grossman HJ, Chaney RH, et al. The life expectancy of profoundly handicapped persons with mental retardation. N Engl J Med. 1990;323:584–9; Kaveggia EG, Durkin MV, Pendleton E, et al. Genetic studies on 1,224 patients with severe mental retardation. In: Proceedings of the Third Congress of the International Association for the Scientific Study of Mental Deficiency. Warsaw: Polish Medical Publishers; 1975, pp 82–93; Kiely M. The prevalence of mental retardation. Epidemiol Rev. 1987;9:194–218; Murphy CC, Yeargin-Allsopp M, Decoufle P, et al. The administrative prevalence of mental retardation in 10-year-old children in metropolitan Atlanta, 1985 through 1987. Am J Public Health. 1995;85(3):319–23.

with improved screening and assuming increased use of selective abortion to prevent Down syndrome births, prevalence rates may be higher in the twenty-first century than ever before.27 Despite the strong association between Down syndrome risk and maternal age, most Down syndrome births are to women under 35 because these women contribute the great majority of births. Thus, prenatal screening for Down syndrome is optimally provided for all pregnancies, regardless of maternal age. The discovery of safer and more practical screening methods for this anomaly during the first trimester of pregnancy, therefore, has been an important public health goal.37–39 The patented “integrated test” as a method of screening for Down syndrome (based on the integration of maternal age, first trimester measures of ultrasound fetal nuchal translucency and maternal serum pregnancy associated plasma protein A, and early second trimester measures of four maternal serum markers: α-fetoprotein, human chorionic gonadotropin, unconjugated estriol, and inhibin-A) has a sensitivity of 85% or higher and a false-positive rate as low as 1%.38,40,41 A disadvantage of this approach is that the final screening result is not available until the second trimester of pregnancy, when therapeutic abortions are less safe and acceptable than during the first trimester.39 Positive prenatal screening results for Down syndrome are followed by diagnostic testing based on analysis of amniotic fluid or chorionic villus sampling, which also can detect fetuses with other chromosomal abnormalities, including other autosomal trisomies, sex chromosome abnormalities, and structural rearrangements.42 Prenatal screening for Down syndrome was shown to be a highly cost-effective method for preventing mental retardation worldwide.43 Two factors inhibiting its widespread application, however, are that the required systems for providing prenatal care are not available in many populations, and it is not universally acceptable to therapeutically abort affected fetuses.43 About one-third of children with Down syndrome have congenital heart defects and 2–5% have duodenal obstruction. Other conditions that occur with increased frequency in Down syndrome are childhood leukemia, recurrent infections, hypothyroidism, and seizure disorders. Mental retardation is virtually always present though with early intervention and inclusive education, impressive gains are seen in cognitive and social functioning of persons with

Down syndrome. Adults with Down syndrome show a variety of agerelated changes in physical and functional capacities suggestive of premature or accelerated aging,44 including changes in skin tone, hypogonadism, increased frequency of cataracts, increased frequency of vision and hearing loss, hypothyroidism, seizures, degenerative vascular disease, and early and severe Alzheimer’s disease.44–46 The increased life span of individuals with Down syndrome and accompanying age-associated morbidity have important consequences for medical care and community services as well as sustained support from family members who are facing new concerns about the need for prolonged care of offspring with Down syndrome.

X-Linked Mental Retardation Sex-linked disorders arise from differences, between males and females, in gene expression from the sex chromosomes. Only males fully express genes located on the X chromosome. Early in embryonic development of females, each cell randomly inactivates either the maternal or paternal X chromosome. Thus, if a female is heterozygous for an X-linked mutant gene, on the average approximately half of her cells have the normal and half the abnormal allele as the functional member. This averaging of the effects of the two X chromosomes protects females from certain disorders transmitted on the X chromosome, such as hemophilia. Genes on the X chromosome are associated with a number of neurologic and cognitive disorders, including Lesch-Nyhan syndrome, Duchenne’s muscular dystrophy, X-linked hydrocephalus, Menkes’ syndrome (kinky hair disease), and fragile X syndrome; of these, fragile X syndrome is the most common known form of inherited mental retardation.

Fragile X Syndrome A fragile site on the X chromosome, fra(X), was first identified in males from families with X-linked mental retardation. In cytogenetic studies, Lubs48 described a constriction on the long arm of the X chromosome. Sutherland49 showed that the fragile X site could be routinely observed as a gap or break in the X chromosome when culture media deficient in folate or thymidine were used, and the site has been

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TABLE 70-4. SEVERE MENTAL RETARDATION IN CHILDHOOD: SELECTED ESTIMATES OF PREVALENCE Location

Reference

Data Source

Age

Prevalencea

8–10 5–14 10 19 7 11 16 11–16 5–15 5–9 11–15 7–12 0–14 7–10

3.70 3.40 3.84 3.73 2.40 3.30 3.40 2.88 4.50 12.40 24.30 4.90 2.94 4.61 2.82 2.71 4.08 17.00 5.28 3.60 19.00 4.3 (year 1996) 3.3 (year 2000)

Aberdeen, Scotland Isle of Wight, England Quebec, Canada Netherlands United Kingdom

Birch, et al. 1970b Rutter, et al. 1970c McDonald, 1973d Stein, et al. 1976e Peckham and Pearson, 1976f

Follow-up of births Population screening, evaluations Agency records Birth cohort, military records Birth cohort, examinations, interviews

Uppsala County, Sweden Salford, England Karnataka, India Karachi, Pakistan Kuruma City, Japan Beijing, China New Brunswick, Nova Scotia, Canada North West Spain

Gustavson, et al. 1977g Fryers and Mackay, 1979h Narayanan, 1981i Hasan and Hasan, 1981j Shiotsuki, et al. 1984k Zuo, et al. 1986l McQueen, et al. 1987m

Registry, agency, vital records Agency records Household survey, evaluations Household survey, evaluations

Diaz-Fernandez, 1988n

Registry

May Pen, Jamaica Bangladesh Atlanta, Georgia, United States Karachi, Pakistan Atlanta, Georgia, United States

Thorburn, et al. 1992o Zaman, et al. 1992p Murphy, et al. 1995q Durkin, et al. 1998r Bashin, et al. 2006 s

Household survey, evaluations Household survey, evaluations School and other record review Household survey, evaluations School and other record review

Household survey, evaluations Agency records

5–9 10–14 2–9 2–9 10 2–9 8

a

Prevalence per 1000. Birch HG, Richardson SA, Baird D, et al. Mental Subnormality in the Community: A Clinical and Epidemiologic Study. Baltimore: Williams & Wilkins; 1970. cRutter M, Tizard J, Whitmore K, eds. Education, Health and Behaviour. London: Longman; 1970. dMcDonald AD. Severely retarded children in Quebec: prevalence, causes and care. Am J Mental Defic Res. 1973;78:205–15. eStein ZA, Susser MW, Saenger G, et al. Mental retardation in a national population of young men in The Netherlands: 1. Prevalence of severe mental retardation. Am J Epidemiol. 1976;103:477–89. fPeckham C, Pearson R. The prevalence and nature of ascertained handicap in the National Child Development Study (1958 cohort). Public Health. 1976;90:111–21. gGustavson KH, Hagberg B, Hagberg G, et al. Severe mental retardation in a Swedish county. I. Epidemiology, gestational age, birth weight and associated CNS handicaps in children born 1959–1970. Acta Paediatr Scand. 1977;66:373–9. hFryers T, MacKay RI. The epidemiology of severe mental handicap. Early Hum Dev. 1979;3:277–94. iNarayanan HS. A study of the prevalence of mental retardation in southern India. Int J Ment Health. 1981;10:28–36. jHasan Z, Hasan A. Report on a population survey of mental retardation in Pakistan. Int J Ment Health. 1981;10:23–7. kShiotsuki Y, Matsuishi T, Toshimura K, et al. The prevalence of mental retardation in Kurume City. Brain Dev. 1984;6:487–90. lZuo QH, Zhang ZX, Li Z, et al. An epidemiological study on mental retardation among children in Chang-Qiao area of Beijing. Chin Med J. 99(1):9–14. m McQueen PC, Spence MW, Garner JB, et al. Prevalence of major mental retardation and associated disabilities in the Canadian maritime provinces. Am J Ment Defic. 1987;91(5):460–6. n Diaz-Fernandez F. Descriptive epidemiology of registered mentally retarded persons in Galicia (Northwest Spain). Am J Ment Retard. 1988;92(4):385–92. o Thorburn M, Desai P, Paul TJ, et al. Identification of childhood disability in Jamaica: the ten question screen. Int J Rehabil Res. 1992;15:115–27. p Zaman SS, Khan NZ, Durkin MS, et al. Childhood Disabilities in Bangladesh. Dhaka: Protibondhi Foundation, 1992. q Murphy CC, Yeargin-Allsopp M, Decoufle P, et al. The administrative prevalence of mental retardation in 10-year-old children in metropolitan Atlanta, 1985 through 1987. Am J Public Health. 1995;85(3):319–23. r Durkin MS, Hasan ZM, Hasan Z. Prevalence and correlates of mental retardation among children in Karachi, Pakistan. Am J Epidemiol. 1998;147(3):1–8. S Bashin TK, Brocksen S, Avchen RN, et al. Prevalence of four Developmental Disabilities Among Children Aged 8 years—Metropolitan Atlanta Developmental Disabilities Surveillance Program, 1996 and 2000. MMWR. 2006;55(SS01):1–9. b

localized to Xq27.3. In 1991, the isolation of the fra(X) locus (FRAXA) located at the beginning of the FMR-1 gene permitted direct diagnosis at the DNA level.50–52 Understanding of the inheritance of this condition has changed accordingly and affords a unique opportunity to examine the influence of a genetic factor on development. Segregation analysis that followed the intergenerational passage of the FRAXA gene in affected families revealed an unusual pattern of inheritance.53 Some males who carry the FRAXA genotype appear to be clinically unaffected and do not express the fragile site on cytogenetic testing. These nonpenetrant normal transmitting males (NTMs) transmit the mutation to daughters who, although unaffected themselves, may have affected children. Thus, grandsons of NTMs are often mentally retarded and granddaughters may show some cognitive impairment.53 A risk of mental retardation depending upon the generation position within the family is known as the Sherman paradox: mothers and

daughters of nonpenetrant males, both obligate carriers of the gene and phenotypically similar, have differing penetrance in their offspring. Brothers of NTMs have low penetrance (approximately 9%) while grandsons and great grandsons have high penetrance (approximately 40–50%).53 The molecular basis of the Sherman paradox has now been elucidated. The FRAXA site contains an exon of the FMR-1 gene responsible for the fragile X mental retardation. This exon includes a repetitive CGG sequence that demonstrates length variation in normal and in fra(X) individuals, and a cytidine phosphate guanosine (CpG) island that can be preferentially methylated in fra(X) cases.54,55 The length of the CGG repeat in genomic DNA correlates with risk for the fragile X syndrome. Normal individuals have fewer than 55 CGG repeats. NTMs and carrier females have “premutations,” in which the number of CGG repeats ranges from 55 to 200. Individuals with the fragile X phenotype show amplification to more than

70 200 CGG repeats and hypermethylation of the adjacent “CpG island” region; this is associated with lack of expression of FMR-1 mRNA.56,57 Thus DNA methylation is a critical feature of the fragile X phenotype. Expansion of the premutation to the full mutation occurs only in female meiotic transmission;50,58,59 during oogenesis, risk for expansion to the full mutation increases with the number of repeats, in a dose-response manner.58,61 Hence women who have inherited the premutation are generally not cognitively impaired,49,61,62 yet they may transmit an expanded allele to their offspring, increasing the risk of fra(X). As CGG repeat is amplified, it becomes more unstable, leading to both mitotic and meiotic instability.50,55,60 In addition, several cases were found with atypical mutations at the FRAXA site, two involving a deletion and one a point mutation in the FMR-1 gene.61,63 Other fragile sites (FRAXD, FRAXE, FRAXF) are found close to the FRAXA site. FRAXE is associated with learning disabilities, but is caused by a different expanding trinucleotide repeat.64 The full mutation is almost always associated with mental retardation in males. The level of cognitive disability can range from mild to severe. Other features of the fragile X syndrome phenotype include distinctive facial characteristics (elongated face, large ears, prominent forehead and jaw, and macrocephaly), macroorchidism in postpubescent males, hyperflexible joints, attention deficits, and autistic-like behaviors. A high proportion of females with the full mutation, though not necessarily mentally retarded, do exhibit selective cognitive deficits.65 In addition, there is increasing evidence of a continuum or spectrum of effects in both females and males with premutations. For example, female carriers of the premutation have an increased risk for premature ovarian failure, and male carriers are at especially high risk for a recently identified neurodegenerative disorder known as the fragile X-associated tremor/ataxia syndrome or FXTAS.66,67 Hagerman and colleagues hypothesized that FXTAS results from a “toxic gain of function” because in persons with premutations characterized by an excessive number of CGG repeats, FMR1 mRNA is expressed at elevated levels, while those with full mutations lack FMR1 mRNA expression.68 Prevalence of the Fragile X Syndrome. As mentioned, the fragile X syndrome is the most common known cause of inherited mental retardation. Recent population-based studies incorporating molecular diagnostic methods found that the prevalence of the full mutation ranges from approximately 1 per 2500 to 1 per 6000 males,69–71 and the prevalence of premutations is as high as 1 per 70 to 1 per 259 females and 1 per 810 males.72–76 The high prevalence and health implications of FMR-1 mutations point to the potential public health benefits of population screening for these mutations. Population screening (prenatal or preconception) could lead to accurate identification of fetuses affected by the full mutation and could provide a cost-effective means of preventing mental retardation.76–78 However, this would require more genetic counseling resources than are currently available, to educate and help families to interpret results that indicate premutation or full mutation carrier status. In addition, arguments for newborn screening for fragile X syndrome have been made on the grounds that early identification will allow earlier access to therapies to improve cognitive and behavioral outcomes.79 However, further research and consensus is needed regarding the ethical and economic aspects of broad populationbased screening for fragile X mutations. In contrast to population screening, considerable consensus has been achieved regarding the benefits of screening or testing for fragile X mutations in targeted patient populations: those with a family history of fragile X syndrome or mental retardation of unknown etiology; offspring of known carriers of a premutation; children with developmental delays of unknown etiology including autism spectrum disorders; women with premature ovarian failure of unknown etiology; and adults ages 50 and older with onset of intention tremor and ataxia of unknown etiology.67,80 The full spectrum of X-linked mental retardation may involve many distinct pathogenic mechanisms. Studies suggest that over 100 different X-linked learning disorders may exist,81 although most are

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rare and have been observed only in studies of single families. Because many X-linked learning disorders are not associated with additional phenotypic features (i.e., are nonsyndromic) and can only be identified by genetic mapping, the full extent and diversity of X-linked mental retardation will be determined only with genetic screening of all affected individuals.

Autosomal Genetic Causes Autosomally inherited disorders are rare but important causes of mental retardation. Autosomal dominant disorders causing cognitive disability in childhood include tuberous sclerosis and neurofibromatosis. The more common mode of transmission is through autosomal recessives. A number of metabolic disorders transmitted in this fashion, including phenylketonuria, are marked by progressive mental retardation with systemic manifestations.

Phenylketonuria This rare defect of amino acid metabolism occurs in 1 in 12,000 to 15,000 Caucasian live births, with somewhat lower rates in other races. Deficient metabolism of phenylalanine causes it to accumulate, which when untreated leads to hyperphenylalaninemia that damages the developing brain, and in most cases results in severe mental retardation.82 Newborn screening based on analysis of newborn blood permits early treatment by a special diet that diminishes phenylalanine levels. The diet must be continued at least through puberty to protect brain development in persons with PKU. In countries with routine neonatal screening programs and effective follow-up of affected children, primary PKU mental retardation is now rarely seen. A problem resulting from the success of neonatal screening programs for PKU is the emergence of “maternal PKU” affecting offspring of women successfully treated in childhood.83 Themselves of normal or near normal intelligence, at childbearing age these women will often have high blood levels of phenylalanine unless their dietary intake of phenylalanine is strictly controlled. Their surviving offspring are at increased risk of mental retardation, microcephaly, congenital heart disease, intrauterine growth retardation, and behavioral problems.84–86 Mental retardation is observed in as many as 50% of children of mothers with uncontrolled PKU (defined as blood phenylalanine level of more than 600 µmol/L) throughout most or all of their pregnancies.87 The most favorable outcomes are observed in women whose dietary restrictions to reduce maternal blood phenylalanine levels and prevent phenylalanine metabolite accumulation are started before conception and maintained throughout pregnancy.88 Routine umbilical cord blood screening, while it cannot prevent cases, can detect women with hyperphenylalaninemia and thus prevent recurrence in future pregnancies. From a public health perspective, the problem is to identify and locate the population of women at risk prior to their first pregnancies.89 The experience of the New England Maternal PKU Project suggests that the majority of women with classic PKU can be found, but a much lower proportion of those with atypical hyperphenylalaninemia are likely to be identified in time to permit primary prevention in their first-born children.89 Because newborn screening for PKU succeeded in preventing one cause of mental retardation, newborn screening programs in developed countries expanded late in the twentieth century to include other conditions for which identifying and intervening during the newborn period can prevent neurologic damage, such as congenital hypothyroidism, galactosemia, and maple sugar urine disease. In contrast, developing countries for the most part have not yet implemented newborn screening programs, though studies showed that newborn screening and intervention as a strategy for preventing learning and developmental disabilities in low income countries would be highly cost effective.43 Recent advances in the technology for newborn screening, specifically the development of tandem mass spectrometry, make it possible to screen newborns for more than 30 metabolic conditions using a single blood spot. However, most of these conditions are extremely rare and the benefits of early identification and treatment are not yet established.90

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Nutritional Causes Iodine Deficiency Cretinism is a form of mental retardation resulting from hypothyroidism and typically is complicated by hearing loss, motor impairment, and abnormal growth and physical development. Sporadic congenital hypothyroidism occurs in about 1 in 3500 births. Newborn screening programs currently in operation throughout the developed world permit early detection and treatment of this condition, which in turn, prevent the brain damage that causes sporadic cretinism. A far more common cause of cretinism in some populations occurs prenatally due to maternal hypothyroidism associated with dietary deficiency of iodine. Iodine deficiency, defined for adults as an average daily iodine intake of less than 100 µg, is endemic in large populations throughout the world, particularly in mountainous areas and interior regions where iodine has been leached from the soil.91 Some estimates suggest that nearly 1 billion people worldwide are at risk for iodine deficiency disorders.92 In addition to endemic cretinism, which affects an estimated 3.2 million people and is a leading cause of mental retardation worldwide, the spectrum of iodine disorders includes spontaneous abortion, stillbirth, infant mortality, goiter, and impaired cognitive functioning (apart from that associated with frank cretinism).93 Prevention of iodine deficiency and endemic cretinism is achieved in many developed countries by fortifying dietary salt at a level of 1 part of iodide per 10,000–50,000 parts salt, and is being promoted worldwide by the World Health Organization as a costeffective method for preventing mental retardation.93,94 In nonindustrialized communities, where the distribution of iodinized salt often proves infeasible, endemic cretinism can be prevented by annually giving women of childbearing age high doses of iodine in an oil solution, taken either orally or by intramuscular injection.93 Effective prevention of prenatally acquired cretinism requires that maternal iodine deficiency and hypothyroidism be corrected very early in pregnancy or preferably before conception. Considerable international pressure is now being exerted against the problem of iodine deficiency; and ongoing efforts will be needed to bring about full prevention of this important cause of mental retardation.

Folate Deficiency Neural tube defects including spina bifida are one of the most common and most disabling birth defects worldwide. Prevalence at birth varies geographically and over time, from less than 1 to more than 6 per 1000 live births, with peaks among the poorest classes and during times of famine and economic strife. Among children born with spina bifida in the developed world, approximately 75% survive past infancy. Hydrocephalus is a regular accompaniment, usually treated with an intracranial shunt to preserve brain tissue and prevent mental retardation. A wide range of intellectual function is found among survivors; fewer than half have severe intellectual disability and many have normal levels of intelligence. Physical accompaniments, including limitations in mobility and in sphincter control, create major nursing problems. The pathogenesis of spina bifida, as in neural tube defects for which survival is rare (anencephalus, encephalocele, iniencephaly), apparently involves failure of the embryonic neural tube to fuse completely, a process that should be completed by the 20th postconceptional day. Epidemiologic studies demonstrated conclusively that preconceptional and periconceptional maternal folate consumption influences the incidence and prevalence of neural tube defects, an observation with enormous potential for primary prevention.95 It remains likely that there still is a genetic influence, such that genetically predisposed mothers or offspring are sensitive to relatively mild deficiency, while a much larger percentage of the population are sensitive to severe deficiency. Current knowledge suggests that primary prevention of approximately 70% of neural tube defects in live births can be achieved if mothers take 4 mg of folic acid, a synthetic form of folate, preconception and periconception. Prevention of neural

tube defects therefore currently hinges on how, and no longer on whether, to deliver the necessary supplement. An unavoidable problem is that the folate or folic acid should be taken at a time that the woman will not usually know she is pregnant. One cost-effective strategy, similar to that used to prevent iodine deficiency, is to supply it to the whole population, for example in the bread flour.96,43 Folates are present in the normal diet, in leafy vegetables, but whether dietary advice alone would result in consumption of sufficient amounts by those who need it is doubtful. Not all neural tube defects will disappear given preventive policies based on current knowledge, even though we can be confident that the incidence will decrease by at least half. Future research should clarify residual causes. Prenatal screening for neural tube defects is now done routinely and with increasing accuracy in settings with advanced levels of prenatal care. Effective prenatal diagnosis involves screening maternal serum at 16 weeks gestation for elevated levels of α-fetoprotein (AFP) and following positive screening results with ultrasound anomaly scans to detect spinal abnormalities and/or amniocentesis to detect elevated AFP levels in amniotic fluid.97 Some difficulties persist with the procedure, apart from the hazards associated with amniocentesis. Even in the most experienced laboratories, the procedure is not entirely specific: other conditions raise AFP levels, and sometimes even with very high levels the fetus is apparently normal. Testing of AFP is also not entirely sensitive; affected fetuses, especially those with closed spina bifida but occasionally other types too, may not be detected. When a positive diagnosis is made, prevention involves therapeutic abortion. This course may be less acceptable than in Down’s syndrome because the risk of a false-positive result (and the consequent termination of a normal pregnancy) is much higher (up to 3% or more depending on cutoff levels and gestational age).97 Both prenatal detection of neural tube defects and folic acid fortification of the food supply have contributed to steady reductions in the prevalence of neural tube defects in live births in populations where they are provided, but their availability on a global scale remains very limited.98–100,43

Premature Birth Infants born prematurely and at very low birth weight (less than 1500 g) are surviving with increased frequency due to advances in perinatology and neonatal medicine. Survivors of very low birth weight carry a high risk of mental retardation as well as cerebral palsy (especially spastic diplegia), epilepsy, and vision and hearing impairments. Increases in the prevalence of cerebral palsy have been observed in several developed countries since the 1970s and may be attributable to concomitant improvements in the survival of very preterm infants.101 The impact of this trend on the prevalence of mental retardation per se is not clear, though follow-up studies of very low birth weight infants are consistent in showing an inverse association between gestational age at birth and the risk of cognitive disability in childhood.102,103 Although prematurity is an important risk factor for mental retardation, up to 75% of survivors of even very preterm birth (e.g., less than 33 weeks gestation) exhibit a normal course of development and functioning in childhood.104 One factor that is strongly predictive of which premature infants will have poor developmental outcomes is the occurrence of white matter lesions observable neonatally on cranial ultrasound scans.105–108 Further study is needed to determine the etiology of brain lesions associated with preterm birth and specific mechanisms for the variability in neurodevelopmental outcomes, as well as the potential for interventions to prevent neurologic damage and improve outcomes.

Infections At least 20 different infectious agents can cause brain damage and mental deficiency in children. Congenital syphilis, the first congenital disorder to be linked to an infectious cause, is now a rare and preventable cause of mental retardation. Rubella, like syphilis, is a fetal infection. It affects the fetus only if the mother contracts the disease

70 between the 8th and 13th weeks of pregnancy. It has been virtually eliminated as a cause of mental retardation in vaccinated populations. Brain damage from other intrauterine infections (toxoplasmosis, cytomegalovirus, varicella) may follow either prenatal or perinatal transmission. When exposure occurs during the first or second trimester of pregnancy, several impairments are recognizable at birth and may include microcephaly, hydrocephaly, growth retardation, cataracts, seizures, rashes, jaundice, and hepatosplenomegaly.109 Exposure late in pregnancy or during delivery may result in inapparent infection at birth and onset of developmental delay during infancy or childhood. Inapparent toxoplasmosis infection at birth, for example, is reported to cause neurodevelopmental disabilities in 80–90% of cases by age 20 years.110–113 Evidence has also been reported that untreated maternal urinary track infections, a common medical complication affecting 4–7% of pregnancies, is a risk factor for mental retardation in offspring.114 Postnatally acquired meningitis and encephalitis associated with a variety of infectious agents also leave a proportion of children with permanent cognitive disability, particularly in less developed countries where access to vaccination and treatment is more limited and often delayed.115 Adverse reactions to the pertussis vaccine causes encephalitis and residual mental retardation in children, but the risk is likely to be lower than the risk of death from pertussis infection in unvaccinated populations.116,117 The effects of mother-to-child transmitted HIV infection on the neurodevelopment of the child are devastating and can result in acquired microcephaly and cognitive and movement disabilities.118 Fortunately, antiretroviral treatment, especially when combined with Caesarian delivery, can prevent most cases of vertical HIV transmission and thus can potentially prevent HIV from causing cognitive disability in children.119

Environmental Toxins Lead Lead, absorbed from a variety of sources, has long been known to cause the serious and often fatal condition of lead encephalopathy in children. Survivors were regularly severely mentally retarded and could be found in populations and institutions housing retarded persons. In recent decades, neuropsychologic impairments of various kinds have been recognized even in children with moderately raised lead levels, well below levels that cause acute lead encephalopathy. Current evidence suggests a dose-response relation of lead exposure in early childhood to mental performance and perhaps also to hyperactivity. The United States government now considers levels higher than 10 µg/dL to be potentially neurotoxic and estimates that more than 17% of young children have levels in this range.120 In many populations, socioeconomic status and iron deficiency are confounded with and may interact with lead poisoning in its effect on IQ. In the United States the effects are more marked on urban children living in poverty. Prevention is not simple but is certainly feasible and, in the long run, is likely to be cost-effective when balanced against reduced health costs and improved school performance and quality of work.121–123 What is required is control of industrial processes, removal of lead from gasoline and paint, maintaining low lead levels in soil, monitoring residences (many houses still have the remains of lead paint, within and without), screening young children, and possibly, environmental lead abatement. For those with raised lead levels, removal from the source of exposure and possibly chelation treatment to increase the level of excretion are indicated.

Alcohol Heavy alcohol abuse during pregnancy is associated with fetal alcohol syndrome in offspring. This syndrome includes mild to moderate cognitive disability, low birth weight, microcephaly, stunting, flattened nasolabial facies, and narrow palpebral tissues. Studies in the United States have found the prevalence of fetal alcohol syndrome to range from 2.8 to 4.6 per 1000 live births.124 A frequency at birth of

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1.7 per 1000 was observed in Gothenburg, Sweden,125 a population in which nearly 10% of the cases of mild mental retardation in school children was attributed to this cause.126 Recently, studies have reported the prevalence of fetal alcohol syndrome to be as high as 2–7% in selected populations.127,128 Prevention is easier to prescribe than to execute. In view of evidence that alcohol consumption during pregnancy is associated with a variety of adverse fetal outcomes other than mental retardation, abstinence or restricted drinking during pregnancy has become a worthwhile public health objective. However, surveillance data from the United States in 2002 indicated that 10% of pregnant women had consumed alcohol during pregnancy and approximately 2% had engaged in binge drinking or frequent alcohol use.129

Trauma Traumatic brain injury is an important preventable cause of intellectual deficiency.130 The annual incidence of head injury (with loss of consciousness) in the United States is about 2.3 per 1000 in children under 15 years and increases to 60 per 1000 among 15- to 19-yearold boys.131 The major causes are motor vehicle collisions, falls, and assaults. Throughout childhood, boys have a twofold higher risk of severe head injury relative to girls. It has been estimated that 5–10% of all cases are fatal and that another 5–10% result in a wide range of neuropsychologic sequelae.132 Permanent declines in IQ and adaptive function are observed in a proportion of cases,133 but further longitudinal and intervention studies are needed to understand the predictors and prevention of these outcomes. PREVENTION

Clearly, mental retardation has many causes. Preventive strategies must focus on each in turn. Sometimes, as with prenatal screening, there are exemplary preventive programs, which can be applied wherever the administrative and economic structure can support them. Programs involving prenatal diagnosis followed by selective abortion or gene therapies call for a high level of organization; for some, they will also involve a conflict of values. Programs that require intensifying education for many children over a prolonged period call for a major allocation of funds and human resources. Twelve recommendations for prevention have been compiled by the Joint Commission of the International Association for the Scientific Study of Mental Deficiency and the International League of Parents of Retarded Children and accepted by the World Health Organization: 1. Genetic counseling, prenatal diagnosis, early identification, and proper treatment are important in preventing mental retardation of genetic origin. 2. Prevention of infections and parasitic diseases contributes significantly to the prevention of mental retardation. 3. Monitoring the environment to protect against pollutants and other chemical and physical hazards is an important part of prevention programs. 4. Safe environments for young children and the prompt treatment of injuries should reduce accidental causes of mental retardation. 5. The nutrition of mothers and children is important, especially in developing countries. 6. Good obstetrics and good care of the newborn reduce the incidence of mental and physical handicap. Good care includes adequate treatment of maternal illness, such as diabetes or toxemia; prompt recognition of obstetrical abnormalities; adequate monitoring of the fetus; immediate resuscitation of the infant; and prediction, prevention, and treatment of biochemical disorders, such as respiratory distress syndrome, hypoglycemia, anoxia, and all causes of cerebral damage. 7. Social and educational stimulation is essential for proper mental growth and development. It is an important element in preventing mental retardation, especially mild mental

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retardation. Suitable interventions are needed for children whose families do not provide this stimulation. 8. In more severely retarded persons, proper stimulation, modern principles of rehabilitation, and good remedial service can also reduce disability and prevent the development of secondary handicaps. 9. Improving living standards and the general health of the population constitutes an important element of nonspecific prevention of mental retardation. Preventive programs for mental retardation should be an integral part of all general health planning and programs. 10. The patterns of preventive programs and the speed with which they are implemented will vary according to resources, but high priority should be given to the problem in all countries. 11. International cooperation on many levels is necessary to speed up the development of effective preventive measures. 12. Research into the causes of mental retardation should be encouraged and facilitated. The effectiveness of preventive measures should be tested and monitored continuously. Special attention should be given to evaluative research in the biomedical and psychosocial spheres.

CARE: COMMUNITY SERVICES FOR MENTAL RETARDATION

Many mentally retarded persons achieve considerable self-reliance with maturity and training, so that the deficit even when severe is seen as relative rather than absolute. The early years are often those for which the family of birth provides basic care and support, while for the later years the community does this increasingly. A family with a mentally retarded child experiences major impacts. There is shock and pain, when the diagnosis is imparted, and a time of emotional turbulence and readjustment to a new kind of parental role often follows. The turbulence is often compounded by concern about effects on other family members, especially siblings; painful embarrassment before friends, neighbors, and strangers; and economic strain. The strain is not limited to the early years. A mentally retarded person may remain emotionally and physically dependent on parents long after the departure of other children. With improved medical care and increasing longevity of persons with severe mental retardation, dependence may continue into a phase when parents lack the physical, psychological, and economic resources to provide adequate care. For some families, residential placement of the child at an early age is the most suitable arrangement. For many others, the family home is preferred. Whichever course is followed, cooperative arrangements between a family and appropriate community services work best. The types of services needed change over the course of the individual’s life. In adulthood, there is often a continued need for sheltered living, work, and recreational services. Families play an important role in planning transitions in services, recognizing that the rights of retarded people, who may be limited in arguing their own case, need special protection. Increasingly, persons with mental retardation themselves are being consulted.

CONCLUSION

Today, the field of mental retardation involves public health in some of the most critical issues facing society. The selected issues touched on here are intended to serve as an introduction to the potential role of public health. Societal forces will shape future public health views and actions, as they have in the past. Scientific and technologic advances bring new opportunities for prevention and change in the balance between incidence and prevalence. In these emerging circumstances, the choices societies make among the forms of prevention and care can have profound effects.

REFERENCES

1. Kiely M. The prevalence of mental retardation. Epidemiol Rev. 1987;9:194–218. 2. Power C. A review of child health in the 1958 birth cohort: National Child Development Study. Paediatr Perinat Epidemiol. 1992;6: 81–110. 3. Halfon N, Newacheck PW. Prevalence and impact of parentreported disabling mental health conditions among U.S. children. J Am Acad Child Adolesc Psychiatry. 1999;38(5):600–9. 4. Grossman HJ, ed. Classification in Mental Retardation. Washington, DC: American Association on Mental Deficiency; 1983. 5. Susser MW, Watson W. Sociology in Medicine. Oxford, England: Oxford University Press; 1971. 6. World Health Organization. International Classification of Functioning, Disability and Health. Geneva: World Health Organization, 2001. 7. Epstein CJ. The Consequences of Chromosome Imbalance. Cambridge, England: Cambridge University Press; 1986. 8. Shaw CM. Correlates of mental retardation and structural changes of the brain. Development. 1987;9:1–8. 9. World Health Organization. International Classification of Diseases, 9th ed. Geneva: World Health Organization; 1980. 10. World Health Organization. International Classification of Diseases10, 2nd ed. Geneva: World Health Organization; 2006. 11. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IVTR). Washington, DC: American Psychiatric Association; 2000. 12. Luckasson R, Coulter DL, Polloway EA, et al. Mental Retardation: Definition, Classification, and Systems of Supports, 9th ed. Washington, DC: American Association on Mental Retardation; 1992. 13. Burack JA, Hodapp RM, Zigler E. Issues in the classification of mental retardation: differentiating among organic etiologies. J Child Psychol Psychiatry. 1988;29(6):765–79. 14. Hook EB. Incidence and prevalence as measures of the frequency of birth defects. Am J Epidemiol. 1982;116:743–7. 15. Stein ZA, Susser MW. The epidemiology of mental retardation. In: Butler NR, Connor BD, eds. Stress and Disability in Childhood. Bristol, England: Wright; 1984, pp 21–46. 16. Durkin MS. Epidemiology of developmental disabilities in lowincome countries. Ment Retard Dev Disabil Res Rev. 2002;8(3): 206–11. 17. Stein ZA, Susser MW, Saenger G. Mental retardation in a national population of young men in the Netherlands: 2. prevalence of mild mental retardation. Am J Epidemiol. 1976;104:159–69. 18. Stein ZA, Susser MW, Saenger G, et al. Mental retardation in a national population of young men in the Netherlands: I. prevalence of severe mental retardation. Am J Epidemiol. 1976;103:477–89. 19. Stein ZA, Susser MW. The mutability of intelligence and the epidemiology of mild mental retardation. Rev Educ Res. 1970;40: 29–67. 20. Garber H, Heber R. The Milwaukee Project: Early Intervention as A Technique to Prevent Mental Retardation. The University of Connecticut Technical Papers. Storrs, CT: University of Connecticut; 1973. 21. Love JM, Kisker EE, Ross C, et al. The effectiveness of early head start for 3-year-old children and their parents: lessons for policy and programs. Dev Psychol. 2005;41(6):885–901. 22. Ramey CT, Bryant DM, Wasik BH, et al. The Infant Health and Development Program for low birth weight, premature infants: program elements, family participation and child intelligence. Pediatrics. 1992;89:454–66. 23. Kline J, Stein Z, Susser M. Conception to Birth: Epidemiology of Prenatal Development. New York: Oxford University Press; 1989. 24. Gustavson KH, Hagberg B, Hagberg G, et al. Severe mental retardation in a Swedish county. I. Epidemiology, gestational age, birth

70

25.

26.

27.

28. 29. 30.

31.

32.

33.

34.

35.

36.

37.

38. 39. 40.

41.

42.

43.

44. 45.

weight and associated CNS handicaps in children born 1959–1970. Acta Paediatr Scand. 1977;66:373–9. Gustavson KH, Hagberg B, Hagberg G, et al. Severe mental retardation in a Swedish county: etiological and pathogenic aspects of children born 1959–1970. Neuropadiatrie. 1977;8:293–304. Siffel C, Correa A, Cragan J, et al. Prenatal diagnosis, pregnancy terminations and prevalence of Down syndrome in Atlanta. Birth Defects Res (Part A). 2004;70:565–71. Nicholson A, Alberman E. Prediction of the number of Down’s syndrome infants to be born in England and Wales up to the year 2000 and their likely survival rates. J Intellect Disabil Res. 1992;36: 505–17. Holtzman DM, Epstein CJ. The molecular genetics of Down syndrome. Molec Genet Med. 1992;2:105–20. Hassold T, Chiu D, Yamane JA. Parental origin of autosomal trisomies. Ann Hum Genet. 1984;48:129–44. Stewart GD, Hassold TJ, Berg A, et al. Trisomy 21 (Down syndrome): studying nondisjunction and meiotic recombination by using cytogenetic and molecular polymorphisms that span chromosome 21. Am J Hum Genet. 1988;42:227–36. Sherman SL, Takaesu N, Freeman SB, et al. Trisomy 21: association between reduced recombination and nondisjunction. Am J Hum Genet. 1991;49:608–20. Hook EB. Epidemiology of Down syndrome. In: Pueschel SM, Rynders JE, eds. Down Syndrome: Advances in Biomedicine and the Behavioral Sciences. Cambridge, MA: Ware Press; 1982, pp 11–88. Staples AJ, Sutherland G, Haan EA, et al. Epidemiology of Down syndrome in South Australia, 1960–89. Am J Hum Genet. 1991;49:1014–24. Huether CA, Ivanovich J, Goodwin BS, et al. Maternal age specific risk rate estimates for Down syndrome among live births in whites and other races from Ohio and Metropolitan Atlanta, 1970–1989. J Med Genet. 1998;35:482–90. Kallen B, Knudsen LB. Effect of maternal age distribution and prenatal diagnosis on the population rates of Down syndrome—a comparative study of nineteen populations. Hereditas. 1989;110:55–60. Egan JF, Benn PA, Zelop CM, et al. Down syndrome births in the United States from 1989 to 2001. Am J Obstet Gynecol. 2004;191: 1044–8. Nicolaides KH, Azar G, Byrne D, et al. Fetal nuchal transluscency: ultrasound screening for chromosomal defects in first trimester of pregnancy. BMJ. 1992;304:867–9. Wald NJ, Rodeck C, Hackshaw AK, et al. SURUSS in perspective. BJOG. 2004;111:521–31. Simpson JL. Choosing the best prenatal screening protocol. New Engl J Med. 2005;353(19):2068–70. Reddy UM, Mennuti MT. Incorporating first-trimester down syndrome studies into prenatal screening: executive summary of the National Institutes of Child Health and Human Development Workshop. Obstet Gynecol. 2006;107(1):167–73. Mallone FD, Canick JA, Ball RH, et al. First-trimester or secondtrimester screening, or both, for Down’s syndrome. New Engl J Med. 2005;353(19):2001–10. Benn PA, Horne D, Birganti S, et al. Prenatal diagnosis of chromosome abnormalities in a population of patients identified by triplemarker testing as screen positive for Down syndrome. Am J Obstet Gynecol. 1995;173:496–501. Durkin MS, Schneider H, Pathania VS, et al. Learning and developmental disabilities. In: Jamison DT, Breman JG, Measham AR, et al, eds. Disease Control Priorities in Developing Countries, 2nd ed. New York: Oxford University Press; 2006, pp. 933–51. Martin GM. Genetic syndromes in man with potential relevance to pathobiology of aging. Birth Defects Orig Artic Ser. 1978;14:5–39. Wisniewski KE, Wisniewski HM, Wen GY. Occurrence of Alzheimer neuropathology and dementia in Down syndrome. Ann Neurol. 1985;17:278–82.

Childhood Cognitive Disability

1181

46. Schupf N, Silverman WP, Sterling RC, et al. Down syndrome, terminal illness and risk for dementia of the Alzheimer type. Brain Dysfunction. 1989;2:181–8. 47. Zigman WB, Schupf N, Lubin RA, et al. Premature regression of adults with Down syndrome. Am J Ment Defic. 1987;92:161–8. 48. Lubs HA. A marker-X chromosome. Am J Hum Genet. 1969;21: 231–44. 49. Sutherland GR. Fragile sites on human chromosomes. Demonstration of their dependence on the type of tissue culture medium. Science. 1977;197:265–6. 50. Oberle I, Rousseau F, Heitz D, et al. Instability of a 550-base pair DNA segment and abnormal methylation in fragile X syndrome. Science. 1991;252:1097–1102. 51. Kremer EJ, Pritchard M, Lynch M, et al. Mapping of DNA instability at the fragile X to a trinucleotide repeat sequence p(CCG)n. Science. 1991;252:1711–4. 52. Verkerk AJMH, Pieretti M, Sutcliffe JS, et al. Identification of a gene (FMR-1) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome. Cell. 1991;65:905–14. 53. Sherman SL, Jacobs P, Morton NE, et al. Further segregation analysis of the fragile-X syndrome with special reference to transmitting males. Hum Genet. 69:289–299, 1985. 54. Bell MV, Hirst MC, Nakahori Y, et al. Physical mapping across the fragile X: hypermethylation and clinical expression of the fragile X syndrome. Cell. 1991;64:861–6. 55. Vincent A, Heitz D, Petit C, et al. Abnormal pattern detected in fragile X patients by pulsed field gel electrophoresis. Nature. 1991;349: 624–6. 56. Pieretti M, Zhang F, Fu YH, et al. Absence of expression of the FMR-1 gene in fragile X syndrome. Cell. 1991;66:817–22. 57. Nolin SL, Brown WT, Glicksman A, et al. Expansion of the fragile X CGG repeat in females with premutation or intermediate alleles. Am J Hum Genet. 2003;21:709–17. 58. Yu S, Pritchard M, Kremer E, et al. Fragile X genotype characterized by an unstable region of DNA. Science. 1991;252:1179–81. 59. Smits A, Smeets D, Dreesen J, et al. Parental origin of the Fra(X) gene is a major determinant of the cytogenetic expression and the CGG repeat length in female carriers. Am J Med Genet. 1992;43:261–7. 60. Fu YH, Kuhl DPA, Pizzuti A, et al. Variation of the CGG repeat at the fragile X site results in genetic stability: resolution of the Sherman Paradox. Cell. 1991;67:1047–58. 61. Gedeon AK, Baker E, Robinson H, et al. Fragile X syndrome without CCG amplification has an FMR1 deletion. Nat Genet. 1992;1:341–4. 62. Bennetto A, Tassone F, Schwartz PH, et al. Profile of cognitive functioning in women with fragile X mutation. Neuropsychol. 2001;15:290–9. 63. Wohrle D, Kotzot D, Hirst MC, et al. A microdeletion of less than 250 kb, including the proximal part of the FMR-1 gene and the fragile site, in a male with the clinical phenotype of fragile X syndrome. Am J Hum Genet. 1992;51:299–306. 64. Feldman EJ. The recognition and investigation of X-linked learning disability syndromes. J Intellect Disabil Res. 1996;40:400–11. 65. Hinton VJ, Halperin JM, Dobkin CS, et al. Cognitive and molecular aspects of fragile X. J Clin Exp Neuropsychol. 1995;17: 518–28. 66. Hagerman RJ, Leehey M, Heinrichs W, et al. Intention tremor, parkinsonism, and generalized brain atrophy in male carriers of fragile X. Neurology. 2001;57:127–30. 67. Jacquemont S, Hagerman RJ, Leehey MA, et al. Penetrance of the fragile X-associated tremor/ataxia syndrome (FXTAS) in a premutation carrier population: initial results from a California familybased study. JAMA. 2004;291:460–9. 68. Hagerman PJ, Hagerman RJ. The fragile-X premutation: a maturing perspective. Am J Hum Genet. 2004;74:805–16.

1182

Noncommunicable and Chronic Disabling Conditions

69. Morton JE, Bundey S, Webb TP, et al. Fragile X syndrome is less common than previously estimated. J Med Genet. 1997;34:1–5. 70. Turner G, Webb T, Wake S, et al. Prevalence of fragile X syndrome. Am J Med Genet. 1996;64:196–7. 71. Crawford DC, Meadows KL, Newman JL, et al. Prevalence of the fragile X syndrome in African-Americans. Am J Med Genet. 2002;110:226–33. 72. Rousseau F, Rouillard P, Morel ML, et al. Prevalence of carriers of premutation-size alleles of the FMR1 gene—implications for the population genetics of the fragile X syndrome. Am J Hum Genet. 1995;57:1006–18. 73. Dombrowksi C, Levesque S, Morel ML, et al. Premutation and intermediate-size FMR1 alleles in 10,572 males from a general population: loss of an AGG interruption is a late event in the generation of fragile X syndrome alleles. Hum Mol Genet. 2002;11:371–8. 74. Toledano-Alhadef H, Basel-Vanagaite L, et al. Fragile X carrier screening and the prevalence of premutation and full-mutation carriers in Isreal. Am J Hum Genet. 2001;69:351–60. 75. Crawford DC, Acuna JM, Sherman SL. FMR1 and the fragile X syndrome: human genome epidemiology review. Genet Med. 2001;3:359–71. 76. Pesso R, Berkenstadt M, Cuckle H, et al. Screening for fragile X syndrome in women of reproductive age. Prenat Diagn. 2000;20: 611–4. 77. Murray J, Cuckle H, Taylor G, et al. Screening for fragile X syndrome. Health Technol Assess. 1997;1(4):1–71. 78. Musci J, Caughey AB. Cost-effectiveness of prenatal populationbased fragile X carrier screening. Am J Obstet Gynecol. 2003;189(Suppl), A197:S117. 79. Bailey DB. Newborn screening for fragile X syndrome. Ment Retard Dev Disabil Res Rev. 2004;10:3–10. 80. Committee on Genetics, American College of Obstetrics and Gynecology. Screening for fragile X syndrome, ACOG Committee Opinion. Obstet Gynecol. 2006;107:1483–5. 81. Stevenson RE, Schwartz CE. Clinical and molecular contributions to the understanding of X-linked mental retardation. Cytogenet Genome Res. 2002;99(1–4):265–75. 82. Waisman HA, Harlow HF. Experimental phenylketonuria in infant monkeys. Science. 1965;147(3659):385–95. 83. Lenke RR, Levy HL. Maternal phenylketonuria and hyperphenylalanemia: an international survey of the outcome of treated and untreated pregnancies. N Engl J Med. 1980;303:1202. 84. Levy HL, Waisbren SE. Effects of untreated maternal phenylketonuria and hyperphenylalaninemia on the fetus. N Engl J Med. 1983;309(21):1269–74. 85. Waisbren SE, Hanley W, Levy HL, et al. Outcomes at age 4 years in offspring of women with maternal phenylketonuria: the Maternal PKU Collaborative Study. JAMA. 2000;283:756–62. 86. Rouse B, Azen C. Effect of high maternal blood phenylalanine on offspring congenital anomalies and developmental outcome at ages 4 and 6 years: the importance of strict dietary control preconception and throughout pregnancy. J Pediatr. 2004;144:235–9. 87. Waisbren SE, Azen C. Cognitive and behavioral development in maternal phenylketonuria offspring. Pediatrics. 2003;112:1544–7. 88. Lee PJ, Ridout D, Walter JH, et al. Maternal phenylketonuria: report from the United Kingdom Registry 1978–1997. Arch Dis Child. 2005;90:143–6. 89. Waisbren SE, Doherty LB, Bailey IV, et al. The New England Maternal PKU Project: identification of at-risk women. Am J Public Health. 1988;78(7):789–91. 90. Botkin JR, Clayton EW, Fost NC, et al. Newborn screening technology: proceed with caution. Pediatrics. 2006;117(5):1793–9. 91. Delange F. The disorders induced by iodine deficiency. Thyroid. 1994;4:107–28. 92. Delange F, Dunn JT, Glinoer D. Iodine Deficiency in Europe: A Continuing Concern. New York: Plenum Press; 1993.

93. Hetzel BS. The Story of Iodine Deficiency: An International Challenge in Nutrition. Oxford: Oxford University Press; 1989. 94. WHO, UNICEF and ICCIDD (International Council for the Control of Iodine Deficiency Disorders), Assessment of the Iodine Deficiency Disorders and Monitoring Their Elimination. WHO/NHD/ 01.1, Geneva:WHO; 2001. 95. Medical Research Council. Vitamin prevention of neural tube defects: results of the Medical Research Council Vitamin Study, MRC Vitamin Study Research Group. Lancet. 1991;338:131–7. 96. Romano PS, Waitzman NJ, Scheffler RM, et al. Folic acid fortification of grain: an economic analysis. Am J Public Health. 1995;85: 667–76. 97. Cuckle HS, Thornton JG. Antenatal diagnosis and management of neural tube defects. In: Levene MI, Lilford RJ, eds. Fetal and Neonatal Neurology and Neurosurgery. Edinburgh: Churchill Livingstone; 1995, pp 295–309. 98. Roberts HE, Moore CA, Cragan JD, et al. Impact of prenatal diagnosis on the birth prevalence of neural tube defects, Atlanta, 1990–1991. Pediatrics. 1995;96:880–3. 99. Eichholzer M, Tonz O, Zimmermann R. Folic acid: a public health challenge. Lancet. 2006;367:1352–61. 100. Feldkamp M, Friedrichs M, Carey JC. Decreasing prevalence of neural tube defects in Utah, 1985–2000. Teratology. 2002;66: S23–S28. 101. Bhushan VG, Paneth N, Kiely JL. Impact of improved survival of very low birth weight infants on recent secular trends in the prevalence of cerebral palsy. Pediatrics. 1993;91:1094–1100. 102. Escobar GJ, Littenberg B, Petitti DB. Outcome among surviving very low birthweight infants: a meta analysis. Arch Dis Child. 1991;66:204–11. 103. Hack M, Fanaroff AA. Outcomes of children of extremely low birthweight and gestational age in the 1990s. Early Hum Dev. 1999;53:193–218. 104. Paneth N, Rudelli R, Kazam E, et al. Brain Damage in the Preterm Infant. Clinics in Developmental Medicine No. 131, London: Mac Keith Press; 1994. 105. DeVries LS, Eken P, Groenendaal F, et al. Correlation between degree of periventricular leukomalacia diagnosed using cranial ultrasound and MRI later in infancy with cerebral palsy. Neuropediatrics. 1993;24:263–8. 106. Paneth N, Rudelli R, Kazam E, et al. Brain damage in the preterm infant. In: Clinics in Developmental Medicine, No. 131. London: Mac Keith Press; 1994. 107. Dammann O, Leviton A. Neuroimaging and the prediction of outcomes in preterm infants. New Engl J Med. 2006;355:727–9. 108. Whitaker AH, Feldman JF, VanRossem R, e al. Neonatal cranial ultrasound abnormalities in low birth weight infants: relation to cognitive outcomes at age six. Pediatrics. 1996;98:719–29. 109. Ramer JC, Miller G. Overview of mental retardation. In: Miller G, Ramer JC, eds. Static Encephalopathies of Infancy and Childhood. New York: Raven Press; 1992, pp 1–10. 110. Koppe J, Loewer-Sieger D, de Roever-Bonnet H. Results of 20 year follow-up of congenital toxoplasmosis. Lancet. 1986;1:254–6. 111. Wilson C, Remington J. Development of adverse sequelae in children born with subclinical congenital Toxoplasmosis infection. Pediatrics. 1980;66:767–74. 112. Koskiniemi M, Lappalainen M, Hedman K. Toxoplasmosis needs evaluation: an overview and proposals. Am J Dis Child. 1989;143: 724–8. 113. Ross DS, Dollard SC, Victor M, et al. The epidemiology and prevention of congenital cytomegalovirus infection and disease: activities of the Centers for Disease Control and Prevention Workgroup. J Women’s Health. 2006;3:224–9. 114. McDermott S, Callaghan W, Szwejbka L, et al. Urinary tract infections during pregnancy and mental retardation and developmental delay. Obstet Gynecol. 2000;96:113–9.

70 115. Durkin MS, Khan NZ, Davidson LL, et al. Prenatal and postnatal risk factors for mental retardation among children in Bangladesh. Am J Epidem. 2000;152:1024–32. 116. Hinman AR, Koplan JP. Pertussis and pertusis vaccine: reanalysis of benefits, risks and costs. JAMA. 1984;251:3109–13. 117. Cody CL, Baraff LJ, Cherry JD, et al. Nature and rates of adverse reactions associated with DPT and DT immunizations in infants and children. Pediatrics. 1981;68(5):650–60. 118. Belman AL. AIDS and pediatric neurology. Neurol Clin. 1992;8(3): 571–602. 119. Jackson JB, Musoke P, Fleming T, et al. Intrapartum and neonatal single-dose nevirapine compared with zidovudine for prevention of mother-to-child transmission of HIV-1 in Kampala, Uganda: 18 months follow-up of the HIVNET 012 randomized trial. Lancet. 2003;362:859–68. 120. Weitzman M, Aschengrau A, Bellinger D, et al. Lead-contaminated soil abatement and urban children’s blood lead levels. JAMA. 1993;269(13):1647–54. 121. Needleman HL. Childhood lead poisoning: a disease for the history texts. Am J Public Health. 1991;81(6):685–7. 122. Ruff HA, Bijur PE, Markowitz M, et al. Declining blood levels and cognitive changes in moderately lead-poisoned children. JAMA. 1993;269(13):1641–6. 123. Khan NZ, Khan AH. Lead poisoning and psychomotor delay in Bangladeshi children. Lancet. 1999;353(9154):754. 124. Sampson PD, Streissguth AP, Bookstein FL, et al. Incidence of fetal alcohol syndrome and prevalence of alcohol-related neurodevelopmental disorder. Teratology. 1997;56(5):317–26.

Childhood Cognitive Disability

1183

125. Hagberg B. Pre- and perinatal environmental origin in mild mental retardation. Ups J Med Sci Suppl. 1987;44:178–82. 126. Hagberg B, Hagberg G, Lewerth A, et al. Mild mental retardation in Swedish school children: prevalence. Acta Paediatr Scand. 1981;70:441–4. 127. May PA, Fiorentino D, Phillip GJ, et al. Epidemiology of FASD in a province in Italy: prevalence and characteristics of children in a random sample of schools. Alcohol Clin Exp Res. 2006;9:1562–75. 128. Viljoen DL, Gossage JP, Brooke L, et al. Fetal alcohol syndrome epidemiology in a South African community: a second study of a very high prevalence area. J Stud Alcohol. 2005;66:593–605. 129. Centers for Disease Control and Prevention. Alcohol consumption among women who are pregnant or who might become pregnant— United States, 2002. MMWR. 2004;53(50):1178–81. 130. Chadwick O, Rutter M, Brown G, et al. A prospective study of children with head injuries: II. cognitive sequelae. Psychol Med. 1981;11:49–61. 131. Annegers JF, Grabow JD, Kurland LT, et al. The incidence, causes, and secular trends of head trauma in Olmsted County, Minnesota, 1935–1974. Neurology. 1980;30:912–9. 132. Frankowski RF, Annegers JF, Whitman S. Epidemiologic and descriptive studies part I: the descriptive epidemiology of head trauma in the United States. In: Becker DP, Povlishock JT, eds. Central Nervous System Trauma Status Report. Bethesda, MD: National Institute of Neurological Diseases and Stroke; 1985, pp 33–43. 133. Taylor HG, Yeates KO, Wade SL. A prospective study of short- and long-term outcomes after traumatic brain injury in children: behavior and achievement. Neuropsychology. 2002;16(1):15–27.

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Prevention of Disability in Older Persons

71

William H. Barker

Increased risk of disease, disability, and death are well-known accompaniments of old age. While disease incidence and death are the conventional indices of a society’s health status, functional disability is perhaps the most consequential index when dealing with health in old age. This chapter defines the character and magnitude of disability in old age, reviews preventive and restorative approaches to specific and general causes of disability among the elderly, and examines the role of health-care organizations in facilitating the delivery of such services. DIMENSIONS OF THE PROBLEM

Concept and Measurement of Disability Conceptually disability has been classified by the World Health Organization as part of a continuum of stages of disease impact that include:l Impairment. The loss or abnormality of psychological, physiological, or anatomical integrity at the level of specific organ systems. Disability. The inability to perform an activity within the range considered normal for a human being, hence a functional limitation experienced at the level of the person as a whole. Handicap. A disadvantage resulting from an impairment or disability which if not addressed, limits an individual’s ability to fulfill certain desired social roles. Collectively this continuum has been referred to as the “disablement model.” Figure 71-l depicts the conditions, which characterize dysfunction at each of the three stages of the model, and the types of functional assessment and medical, restorative, and social intervention appropriate to maintaining and improving function and limiting disability at each stage. A wide variety of systems have been developed for measuring functional ability/disability.2 The best-known of these are the Activities of Daily Living (ADL) and the Instrumental Activities of Daily Living (IADL) indices. The ADL index, first introduced by Katz and colleagues, classifies limitations in six fundamental, sociobiological functions of daily living: bathing, dressing, toileting, transferring from bed or chair, continence, and feeding.3 Lawton and others broadened the scope with the IADL concept which incorporates measures of more complex adaptive or self-maintaining functions such as housekeeping, money management, and grocery shopping.4 In addition to screening and care planning for individual patients, these measurement systems have been very useful for describing the disability status of the elderly population, estimating community and

institutional service needs, and evaluating outcomes of interventions designed to limit disability. The emerging concept of “preclinical disability” focuses on identifying stages in the natural history of functional loss, which precede the onset of overt ADL or IADL dependencies. This phenomenon was originally measured in terms of adaptive modifications in the performance of common tasks such as doing housework or getting out of bed.5 Physiologic and performance measures of lower extremity function have also been shown to be powerful predictors of future onset of frank disability.6 More recently investigators have focused on a complex of physiologic deteriorations characterized as “frailty” which identifies older persons at high risk of decline in functional status. “Frailty” has been defined operationally as having at least three of the following attributes: unexplained weight loss, poor grip strength, self-reported exhaustion, slow walking speed, low physical activity.7

Magnitude of Aging and Disability The aging or graying of populations is occurring in all parts of the world, most profoundly in developed areas, as illustrated in estimates compiled by the United Nations (Fig. 71-2). Driven by a combination of increasing average life expectancy and decreasing birthrates, this “longevity revolution” will result in ever-increasing numbers of persons over 80 years of age among whom functional disability is most prevalent. The proportion of elderly Americans with disability living both in the community and in nursing homes at the end of the twentieth century has been estimated at approximately 20%. Among community dwelling disabled elderly, the most common ADL dependencies include bathing and transferring, while dependence on assistance with eating is least common. Shopping and meal preparation are the most common IADL dependencies. All domains of ADL and IADL limitation increase dramatically with age and are generally more prevalent in women than men. There is a strong association between ADL limitation and the presence of chronic medical conditions. With few exceptions such as stroke and hip fracture, it has been difficult to establish direct cause and effect relationships between specific morbidities (diseases) or combinations of morbidities and the onset of disability. Nonetheless, it is reasonable to presume that a substantial amount of disability is attributable to physical and physiological impairments resulting from specific chronic diseases.8,9 In turn, the prevention of such impairments and consequent disability would be largely dependent on the success with which major chronic diseases are prevented or controlled using techniques reviewed in other chapters in this volume. A substantial amount of disability in old age may also be explained and 1185

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1186

Noncommunicable and Chronic Disabling Conditions Organ level

Person level

Societal level

Pathology

Behavioral

Role assignment

Anatomical, physiological, mental and psychological deficits

Performance deficits within the physical and social environments

Environmental and societal deficits influenced by social norms and social policy

Determine

Contribute to

Create

Conditions:

Key terms: Impairment (Organic dysfunction)

Disability (Difficulty with tasks)

Handicap (Social disadvantage)

Limitations in using skills, performing activities, and fulfilling social roles Analysis: Selected diagnostic descriptors

Selected performance (behavioral) descriptors

Selected role descriptors

Functional assessment of abilities and activities Interventions: Medical and restorative therapy

Figure 71-1. The functional approach to medical care and the disablement model.

potentially prevented by attention to lifestyle, physical, psychological, environmental, and social support factors, which increase the risk of functional decline among older persons.10 Comprehensive strategies of health promotion, multidisciplinary assessment and rehabilitation, and environmental adaptation constitute the armamentarium of preventive approaches to such factors. A further dimension of the societal impact of disability in old age is the strong relationship between functional impairment and use of health services. A study from the Medicare Current Beneficiary Survey documented dramatic increase in the aggregate annual physician, pharmaceutical, hospital, and long-term care expenditures incurred by older persons making the transition to greater levels of functional dependency in a given year (Table 71-1).

Secular Trends The phenomenon of increasing life expectancy in old age has given rise to a number of forecasts with respect to the burden of disability to be anticipated. At one extreme is Fries’s “compression of morbidity” thesis, which, with reference to Fig. 71-3, argues that age of onset of disabling chronic disease among the elderly is being postponed to a greater degree than life expectancy is expanding.11 Under these

Adaptive equipment and reduction of physical and attitudinal barriers

Supportive services and social policy changes

All needing long-range coordination to improve and maintain functioning

circumstances, age-specific prevalence and aggregate years of disability before death would be expected to diminish. At the other extreme is the “failure of success” thesis promulgated by Gruenberg12 and others, which argues that increase in life expectancy among the elderly is largely the result of advances in life-sparing medical treatments of existing disease, which, with reference to Fig. 71-3, results in increase in the average duration of certain chronic disabling diseases. This phenomenon would result in expanded future need for chronic care services. Others have suggested that increased life expectancy reflects a combination of both of these phenomena, resulting in delayed age of onset of chronic disease and disability but not substantially reducing the overall health service burden.13 Various longitudinal population studies to empirically assess trends in the burden of disability among older persons are ongoing in the United States and elsewhere.14 Common to such studies is a quest to identify and quantify determinants of disability free aging, variably referred to as “active life expectancy”15 or “successful aging.”16 Among these, the National Long-Term Care Survey (NLTCS), a longitudinal study involving very large sequential cohorts of older Americans, first documented a decline of one to two percentage points in the prevalence of chronic disability between l982 and l989, translating into an estimated 540,000 fewer older persons with chronic disabilities

71

Europe

Impairments and Losses

More developed regions

Old age is associated with increased occurrence of a wide array of physiological, physical, mental, and social impairments or losses, which may contribute independently or collectively to disabilities. These include elevated blood pressure, decreased immune response, reduced visual, auditory, and olfactory acuity, loss of muscle and bone mass, fragility of the skin, slowing of mental response, decreased cognitive ability, loss of spouses and companions, reduced income, and loss of social roles and of autonomy. Some of these changes and their consequences, referred to as “senescence,” are intrinsic to the biology of aging. Examples include age-related decline in the individual’s maximum oxygen consumption (V02 max), a fundamental index of capacity for physical activity; decrease in muscle mass (sarcopenia); modifications of lens protein leading to cataract formation and loss of vision; decrease in bone density with resultant osteoporosis and heightened risk of fracture; and stiffening of arterial walls causing increased systolic blood pressure and risk of disabling cerebrovascular accident. A growing body of evidence indicates that many physiological, physical, and mental changes as well as virtually all social changes associated with old age are not intrinsic to the aging process but are due to potentially modifiable extrinsic or self-induced factors.

Northern America

15 %

World

Less developed regions

10

5

Africa

0 1950

1970 1960

1990 1980

2010 2000

1187

or deconditioning. Also important are the contributions to the prevention or reversal of disability attributable to health promotion, and therapeutic, rehabilitative, and environmental interventions.

25

20

Prevention of Disability in Older Persons

Disuse/Deconditioning

2025 2020

Year

Figure 71-2. Percentage of population 80 years and over in different regions of the world. UN data and predictions 1950 to 2025. (Source: Davies AM. Epidemiology and the challenge of aging. In: Brody JA, Maddox GL, eds. Epidemiology and Aging:An International Perspective, New York; Springer; 1988.)

than would have been expected.17 Surveys conducted in 1994 and 1999 have documented further declining prevalence of disability, involving both the black and non-black population, for a net change from 26.2% in 1982 to 19.7% in 1999 (Table 71-2). HEALTH PROMOTION AND PREVENTION

In considering approaches to prevention of disability in the aging population, and indeed in the aging individual, it is useful to bear in mind several phenomena that are involved in the occurrence of disability. These include the contributions to disability attributable to biologic changes of aging, pathologic disease processes, and disuse

The first level of preventable extrinsic factors in functional decline is discontinuation of usual activity referred to as “disuse” or “deconditioning.”18 This may occur insidiously as older persons withdraw from usual activities either voluntarily in response to a sense of “growing old” or involuntarily as a consequence of intercurrent acute illness, retirement from work, etc. The best studied model of global disuse/ deconditioning, and one to which older persons are particularly prone on their own volition or their physician’s or family’s bidding, is extended bed rest. Going to bed for a prolonged period of time may lead to a litany of physiologic adaptations and potentially disabling consequences as listed in Table 71-3. Of particular concern because of their potential contribution to limitation of mobility and risk of falls and fractures are physiological and structural changes in muscle, bone, and joint tissues. Rate of decrease in muscle strength may be as high as 5% per day in the bedfast individual, with leg muscles tending to lose strength faster than arm muscles. Disuse osteoporosis results from both cessation of bone synthesis and increased resorption and tends to predominantly affect weight-bearing bones. Immobility and loss of weightbearing forces on joints contribute to changes in both periarticular and articular tissue structure, which may lead to joint contractures. Also contributing directly or indirectly to bed rest–induced disability are atelectasis and other pulmonary changes that predispose

TABLE 71-1. TOTAL HEALTH-CARE SPENDING (MEDICAL CARE AND FORMAL LONG-TERM CARE COSTS) ACCORDING TO LEVEL OF DEPENDENCY OVER 1 YEAR AND ESTIMATED ADDITIONAL COSTS OF CARE FOR PERSONS MAKING THE TRANSITION TO MORE DEPENDENT STATES: U.S. PERSONS AGED 66 YEARS AND OLDER, 1995 Annual Per Persons Cost, $, by Status After 1 Year Baseline Status No ADLs No ADLs ≥ 1 ADL in community Totals

No ADLs 4771 4771

≥1 ADL, No NH Use

NH Use

18,025 19,408

36,596 40,877

Difference 13,254 31,825 21,469

U.S. Estimates No. Making Transition 939,520 302,042 188,087 1,429,649

Total Additional Cost, $ Billions 12.45 9.61 4.04 26.1

Note: ADLs = activities of daily living; ≥ 1 ADL = help received in 1 or more ADLs (eating, dressing, bathing, using the toilet, getting into and out of a chair); NH = nursing home. Source: Guralnik J, et al. Medical and long-term care costs when older persons become more dependent. Am J Public Health. 2002;92:1244–5.

1188

Noncommunicable and Chronic Disabling Conditions TABLE 71-3. COMPLICATIONS OF BEDREST Cardiovascular

Respiratory

Musculoskeletal

Gastrointestinal Genitourinary

Figure 71-3. Cenceptual relationship between age and percentage of the population remaining free of the respective stages in the natural history of chronic disabling disease.

Skin Functional Psychological

Decreased cardiac output, contributing to decreased aerobic capacity Orthostatic intolerance Venous thrombophlebitis Atelectasis Relative hypoxemia Pneumonia Muscle atrophy and loss of strength Decreased muscle oxidative capacity, contributing to decreased aerobic capacity Bone loss (osteoporosis) Constipation Incontinence Renal calculi Pressure sores Impaired ambulation Sensory deprivation

Source: Harper CM, Lyles YM: Physiology and complications of bed rest. J Am Geriatr Soc. 1988;36:1047–54.

to pneumonia, slowing of peristalsis with resulting constipation, bladder emptying difficulties leading to urinary incontinence, sustained pressure on fragile skin predisposing to pressure sores, and sensory deprivation leading to an array of negative affective and cognitive effects. Clearly an essential principle is to avoid taking to bed in old age, except as truly necessitated by medical problems. Instances of the latter should be minimized, with emphasis on progressive mobilization of bed-bound patients, first from bed to chair, then to ambulation with or without assistance. This should include purposeful activity such as ambulating to meals and dressing in normal clothing as opposed to institutional bed clothing.

Physical Activity Regular physical exercise is perhaps the single most important health promotional activity for preventing many of the dysfunctional consequences of aging. Numerous studies have demonstrated that older persons, like their younger counterparts, can significantly increase physical fitness, as reflected in V02 max, by engaging in regular aerobic exercise. Furthermore there is clear experimental evidence involving older subjects that progressive resistance training can both retard and reverse losses of muscle mass and strength as well as bone density.19,20 Several controlled trials have demonstrated improvements in gait speed, stair climbing, rising from a chair, and other significant physical tasks following participation in exercise programs conducted among frail nursing home residents.21,22 TABLE 71-2. POPULATION DISTRIBUTION (AGE-STANDARDIZED TO 1999 OVER-65 POPULATION) OF DISABILITIES 1982–1999 1982

1984

1989

1994

1999

Nondisabled IADL only 1 or 2 ADLs 3 or 4 ADLs 5 or 6 ADLs Institutional

73.8 5.7 6.9 3.0 3.7 6.8

73.8 6.2 7.0 3.1 3.4 6.6

75.6 4.8 6.7 3.7 3.0 6.1

77.5 4.4 6.1 3.4 3.0 5.7

80.3 3.2 6.0 3.5 2.9 4.2

Total Disabled, %

26.2

26.2

24.4

22.5

19.7

Distribution by disability %

Source: Manten KG, Gu X. Changes in the prevalence of chronic disability in the United States black and nonblack population above age 65 from 1982 to 1999. Proc Natl Acad Sci USA. 2001;98:6554–9.

The application of such experimental observations to preventing disability is captured in the concept of “threshold levels” as follows: Strength, aerobic power and other indices of physical ability change on continuous scales whereas functional and quality of life changes are quantal. Thus a very small strength gain may be accompanied by a considerable functional improvement if it takes the patient from being just unable to transfer independently to being just able to do so. This also applies in reverse: A gradual loss of strength may not be apparent until the patient is suddenly unable to perform a crucial function.23

In spite of the demonstrated benefits of regular physical activity, the majority of older Americans live essentially sedentary lives, which prompted the Public Health Service in the late 1990s to set a national goal of reducing to less than 25% the proportion of persons over age 65 who engage in no leisure time physical activity. The Surgeon General’s recommendations call for 30 minutes a day of moderate activity which may consist of walking, gardening, cycling, swimming, and other and which must be sustained for benefits to accrue. There are a number of proven approaches that individuals, physicians, and communities may take to promote physical activity among older persons.24 EARLY INTERVENTIONS AND REHABILITATION

Despite the best efforts of primary and secondary prevention and health promotion, the majority of older persons will develop one or more potentially disabling medical conditions. Under these circumstances the goals of health care, where possible, will be early medical or surgical intervention, rehabilitation, or continuing supportive or palliative care to limit disability and provide for highest level of independence of individuals and their caregivers. Components of such tertiary prevention include both specific interventions for individual disabling conditions and provision of comprehensive geriatric medicine services. SELECTED DISABLING CONDITIONS

Falls and Fractures Falls occur among some 20–30% of community dwelling elderly persons per year and an even greater percent of nursing home residents, with attendant risks of fracture, soft tissue injury, and psychological

71 compromise to independence. Risk of falling increases with the number and type of chronic disabling conditions present and medications being taken. Visual and proprioceptive abnormalities, musculoskeletal and neurological diseases, depression and dementia, and hypotensioninducing conditions (biologic and iatrogenic) are particularly important. A fall risk index has been successfully used to guide preventive interventions.25 A variety of exercise and balance training programs have also been found to reduce incidence of falling.26 To avoid certain secondary consequences of falls such as hypothermia or pressure sores from prolonged immobility, recurrent fallers should be provided with portable alarm systems as well as instructions for effectively maneuvering to right themselves following a fall. Wearing an external protective device over the hip has been shown to reduce frequency of fracture among fall-prone frail elderly persons.27 More than a million fractures occur in older persons in the United States each year, the three most common sites being vertebrae, proximal hip, and distal forearm (Colles’ fracture). The principle contributing factor is osteoporosis or loss of bone mass, a progressive natural process that begins in the fourth or fifth decade of life and renders aging individuals increasingly susceptible to fracture associated with relatively minor trauma. Osteoporosis is accentuated in women following menopause, and age-specific risks of osteoporotic fractures are markedly higher among older women versus men (Fig. 71-4). Osteoporosis is significantly retarded by postmenopausal estrogen replacement therapy, by oral bisphosphonates, and probably by regular exercise and supplemental calcium intake throughout adulthood.28 Hip fractures are associated with more deaths, disability, and medical costs than all other osteoporotic fractures combined. Over 300,000 occur annually in the United States, and there is evidence that the age-specific incidence of hip fracture has been increasing in some industrialized societies.29 Between l0% and 20% of older patients who have fractured their hips die within 6 months, and a substantial percentage of survivors are destined for long-term nursing home placement. There is, however, considerable potential for reducing mortality and institutional placement and restoring mobility, with or without assistive devices, if patients receive timely surgical, medical, and particularly rehabilitative care (see under “Geriatric Strategies”).

Incontinence

Incidence per 100,000 person-years

Urinary incontinence is defined as “the involuntary loss of urine so severe to have social and/or hygienic consequences.” A symptom with multiple causes, rather than a discrete disease process, incontinence affects l5–30% of community-dwelling elderly and at least half of all nursing home residents. In addition to its immense psychosocial

4000

Men

Women

3000

1189

burden on afflicted individuals and their caretakers, the costs of managing urinary incontinence in the United States are estimated at over $l0 billion annually. This disabling condition of old age can in many instances be cured or effectively controlled through appropriate medical and nursing assessment and intervention.30 There are several subtypes of incontinence each representing a distinctive pathophysiological mechanism. Stress incontinence, a particularly common form in women, results from dysfunction at the bladder outlet allowing urine leakage during times of increase in intra-abdominal pressure, such as coughing or sneezing. Pelvic muscle exercises are often effective in controlling this condition. Urge incontinence consists of loss of urine as a consequence of uninhibited bladder muscle contractions, usually resulting from a neurologic condition such as stroke or local bladder irritation. If not cured through treating a local cause such as urinary tract infection, urge incontinence may be controlled with anticholinergic agents, which inhibit bladder contraction. Overflow incontinence occurs when the bladder does not empty normally and becomes overdistended due to one of a variety of neurologic impairments or local obstructions. This may be correctable through surgery where indicated (e.g., prostatectomy) or managed through a program of intermittent catheter drainage. Functional incontinence occurs when the lower urinary tract is functionally intact, but impaired mobility or cognition prevents the individual from getting to toilet facilities. This variant is controllable through regular, assisted access to toilet facilities.

Sensory Impairment—Hearing and Vision The l995 U.S. National Health Survey Supplement on Aging established prevalence rates of hearing impairment of 35% at age 70–74, rising to 58% at 85+ years of age among community-dwelling men and 22% and 49% among women at the same ages. Prevalence of significantly impaired vision, including blindness, among men and women ranged from 12% to 15% at 70–74 years of age to 26–34% over age 85; 92% of persons over age 70 reported using glasses, most of which were prescribed. In addition to potentially profound limitations in an individual’s ability to communicate with others, impairments in both of these sensory systems are associated with significant limitations in performing traditional ADL and IADL functions as well as with depression and cognitive difficulty.31 Early detection and therapeutic intervention may reverse or delay sensory impairments attributable to certain specific degenerative disease processes, such as visual loss due to diabetic retinopathy or glaucoma. In large measure, the task of reducing disability due to sensory loss in old age focuses upon restoring the lost sense as in surgical treatment of senile cataract or prosthetic treatment in presbycusis. Cataract surgery with lens implantation has been shown to improve physical function as well as vision.32 Hearing aides, voice amplifying devices, and lip reading represent the mainstays of hearing rehabilitation, which, if used effectively, can reverse physical and particularly psychosocial disability associated with hearing loss.

Depression and Dementia

2000

Vertebral

Hip

1000 Hip Colles’ 35–39

Prevention of Disability in Older Persons

85– Age group, years

Colles’ 85–

Figure 71-4. Incidence rates for the three common osteoporotic fractures (Colles’, hip, and vertebral) in men and women, plotted as a function of age at the time of the fracture. (Source: Riggs BL, Melton LJ. Involutional osteoporosis. N Engl J Med. 1986;314:1676–86.)

Mental and psychological disability among the elderly are major societal concerns, particularly in long-term care institutions. Depression and dementia constitute the most prominent forms of affective and cognitive disorders encountered in old age. Both conditions may result from multiple causes, and while generally not preventable, the impact of depression and dementia on affected individuals or their caregivers may be alleviated through judicious intervention. Major depression, found in some 5% of older persons in the community, and minor depression, found in some 10–20%, are associated with increased risk of physical disability.33 A variety of antidepressant drugs as well as electroconvulsive therapy are effective in treating late-life depression and its disabling effects.34 Best results appear to be achieved through collaborative care management involving mental health and primary care practitioners working together.35

1190

Noncommunicable and Chronic Disabling Conditions

Broadly defined by the DSM-III-R as “a loss of intellectual abilities sufficient to interfere with social or occupational functioning,” dementia is a disabling mental condition, well known to aging societies, which increases dramatically in prevalence from 2% to 3% at age 65% to 25% or above at age 85 (Fig. 71-5). The most common pathologic subtypes of dementia are Alzheimer’s disease and multi-infarct dementia. A small percent of cases of potentially reversible dementia occur secondary to treatable causes including hypothyroidism, subdural hematoma, drug toxicity, and others. A number of drugs, largely cholinesterase inhibitors, show modest effects in alleviating if not reversing the dysfunctional behaviors of dementia,36 and a number of epidemiologic studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDS) may protect against development of Alzheimer’s disease.37 A variety of intervention strategies have been developed with the twin goals of maintaining independence and dignity for dementia patients and providing social and psychological support for their caregivers.38 These invariably involve a multidisciplinary approach. Patient care includes continuing attention to basic medical and nursing needs, with particular emphasis on adequate nutrition, assistance with toileting and grooming, and prevention or early treatment of minor infections and skin breakdown. Regularly scheduled occupational and recreational therapy help to maintain patient morale. Support for caregivers in the community includes counseling and education about the natural course and management of dementia, particularly the highly stressful memory loss and aberrant behavior; assistance with obtaining legal, financial, and safety advice; and provision of temporary relief through day care or short-term residential respite care. To ensure appropriate and effective care for patients with advanced disease, often accompanied by wandering and abusive behavior, special care dementia units have been quite widely and successfully introduced in nursing homes in the United States and elsewhere.39 In addition to the burden suffered directly by patients and their caregivers, Alzheimer’s and related disorders pose an immense

40

monetary cost, estimated by the Alzheimer’s Association in 2000 at some $100 billion annually in the United States.

Stroke and Parkinson’s Disease Stroke and Parkinson’s disease (PD) represent two of the most common disabling neurologic conditions of old age, both of which are candidates for early preventive or rehabilitative intervention. Stroke or cerebrovascular disease comprises a heterogeneous group of pathological entities all of which carry a high risk of residual disability. While age-specific stroke mortality rates have declined dramatically, and levels of disability among survivors of incident stroke have improved in recent decades,40 stroke remains the third leading cause of death and the most severely disabling condition of old age. Among acute stroke survivors, 30–40% become dependent in self-care, with most functional recovery occurring within 3–6 months poststroke; over 50% experience significant depression and social isolation, and 20–30% are institutionalized for continuing care.41 Randomized trials have found that hospital-based special stroke units, which combine acute medical-nursing expertise and multidisciplinary rehabilitation, yield decreased mortality and in some instances decreased long-term disability and institutional placement when compared to stroke management on general medical units.42 Among a number of recent trials of thrombolytic therapy in acute ischemic stroke, significantly lower rates of poststroke disability have been observed in patients treated within 3 hours of onset of stroke.43 PD is a degenerative condition resulting largely from deficiency of the neurotransmitter substance dopamine in the midbrain and causing generalized movement and postural abnormalities. Disabling manifestations include tremulous hands, shuffling gait with tendency to fall, plus some dulling of the intellect. Increasingly common with aging, the prevalence is estimated at 500–l000 per l00,000 over age 60, with more than half of prevalent cases being over 70 years of age. Some Parkinsonism among older persons is drug-induced by neuroleptic agents and may resolve when the offending drug is discontinued. Conventional treatment to ameliorate manifest disability in PD consists of one of a variety of dopamine replacement regimens plus physical therapy. Deep brain stimulation, neurotransplantation with human transformed cell lines, as well as pallidotomy represent evolving surgical interventions with potential for controlling the disabling effects of PD.44

35 United States (1978)

Prevalence (%)

30 Denmark (1963)

England (1970)

25

New Zealand (1983)

20

Finland (1985)

15

10

5

65

70

75 80 Age (yrs)

85

90

Figure 71-5. Age-specific prevalence rates from moderate or severe dementia in five studies: England (1970), United States (1978), Denmark (1963), Finland (1985), and New Zealand (1983).

Heart Failure and Chronic Obstructive Pulmonary Disease Heart failure (HF) and chronic obstructive pulmonary disease (COPD) constitute the two most common disabling chronic cardiopulmonary conditions of old age. From a public health perspective, the impact of both conditions on society at large in the United States and elsewhere is manifest by increasing mortality and morbidity rates for both conditions among older persons since the l980s. From a clinical perspective, impact of these conditions on patient functional status and quality of life has been shown to be partially controllable through use of selected medical and rehabilitative interventions. HF is the most common reason for hospitalization among persons over age 65 in the United States, with rates rising steeply between the seventh and ninth decades of life. Increasing incidence and prevalence of HF is attributed to increased numbers of surviving patients with ischemic heart disease who are at high risk of developing HF.45 Randomized clinical trials in the past decade have shown significant improvement in survival and in functional capacity among patients treated with angiotensin-converting enzyme inhibitors or beta blockers.46 Additionally, physician-nurse practitioner coordinated care has been shown to reduce hospitalizations and improve quality of life among community-dwelling older patients with chronic HF.47 COPD, the end stage of prolonged insult to the bronchi, bronchioles, and lung parenchyma from tobacco smoke and other atmospheric

71 pollutants, is the fifth common cause of death in the United States, with prevalence rates and death rates rising among persons over 70 years of age in recent decades. Loss of capacity for physical activity and psychological distress due to oxygen deprivation are the main functional impacts of COPD on the individual. A meta-analysis of l4 randomized trials of rehabilitation programs offered to patients with activity limitation attributable to COPD found clinically significant improvement in health-related quality-of-life measures and functional capacity when compared with conventional care.48 While physical exercise is considered the central pillar of these programs, it is likely that attention to nutrition and psychosocial status and other programmatic activities also contribute to the positive results.

Arthritis and Spinal Disorders Arthritis and back pain caused principally by degenerative osteoarthritis are the two most common causes of activity limitation among persons over age 65. The disabling effects of both conditions may be alleviated by nonpharmacologic, pharmacologic, or operative interventions. Self-reported arthritis with activity limitation occurs among some 12% of persons 65–74 years of age and 20% of those over 85 years old.49 Exercise to relieve stiffness and pain and strengthen muscles, accompanied by analgesic medication as needed, is the first line of treatment for symptomatic arthritis.50 When joints have been anatomically severely damaged and symptoms are unresponsive to these nonoperative strategies, surgical joint replacement, accompanied by aggressive physical therapy, may provide dramatic improvement. Degenerative disease of the cervical or lumbar spine, with pain and/or resulting gait disability, affects many older persons in the United States in any given year. Use of analgesic medication and well-directed physical therapy, supplemented by lidocaine or steroid injection therapy, constitute the preferred strategy of interventions proven effective in these conditions. Surgical decompression (laminectomy) should be reserved for those patients with unrelieved pain and/or significant neurological impairments secondary to encroachment on the spinal cord or cauda equina. Compression fractures, typically involving the thoracic or thoracolumbar spine are painful and may lead to secondary kyphotic deformity. Treatment comprises pain relief and judicious restoration of mobility. Percutaneous vertebroplasty and kyphoplasty are emerging surgical approaches which may hasten and improve recovery.51

Transitions: Retirement, Bereavement, Relocation Certain discrete transitions in social circumstances place older persons at increased risk of onset or worsening of disabling physical and mental health problems. Most prominent among these transitions are retirement, loss of spouse, and residential relocation. These events are commonly associated with loss of autonomy and control over one’s life, as well as loss of the social and psychological support, which contribute to physical and mental well-being. The major impacts of retirement on well-being relate to reduction in income and attendant increase in various mental health problems. Loss of spouse and the accompanying experience of loneliness and bereavement are associated with increased likelihood of a variety of nonspecific mental and physical symptoms as well as excess mortality. The excess mortality is more common in men than women and peaks during the first 6 months of bereavement. Residential relocation, particularly placement in an assisted living facility or a nursing home, represents an unusually stressful event, depriving the old person of a familiar social and physical environment as well as much of her sense of autonomy. The nursing home experience may be aggravated further by the use of physical and chemical restraints which diminish or distort mental performance and increase the risk of iatrogenic illness or injury. Such untoward effects as well as increased risk of death tend to be concentrated in the early months following residential relocation.16 Reduction in the health risks and increased mortality associated with social transitions may be achieved through various supportive

Prevention of Disability in Older Persons

1191

and autonomy-enhancing interventions. Providing material assistance, medical attention as needed, and companionship are fundamental supportive approaches. Teaching, encouraging, and enabling are important autonomy-enhancing approaches, in contrast to excessive cautioning and “doing for” which may induce a sense of helplessness. A number of observations in nursing homes have demonstrated improvement in mental health and other health status indices among residents maintained free of unnecessary restraints and encouraged to exercise initiative and choice in pursuit of daily activities. The “Eden Alternative,” a forward-looking strategy for humanizing the entire milieu of nursing homes, has begun to be implemented in homes in the United States and elsewhere since its introduction in the late 1990s.52 At the level of primary prevention directed to social transitions of aging, a society’s or community’s existing policies and practices may be altered with respect to both retirement and nursing home placement.53 Normative, if not legally mandated, retirement age can and has been increased in some settings. Rehabilitative and communitybased services can and have been successfully implemented as alternatives to custodial placement in nursing homes. Such continuing care alternatives have been most fully developed in societies with comprehensive health-care systems.54 HEALTH-CARE DELIVERY

The Geriatric Medicine Movement The breadth of threats to health and independent functioning in old age and the attendant potentials for preventive interventions, as reviewed above, constitute a major challenge to develop suitable prevention-oriented health-care delivery systems. In recognition of this challenge, the World Health Organization convened an expert panel in l974 on “Planning and Organization of Geriatric Services.” This body recommended that countries develop integrated health services for older persons, including “elements of medical and social prevention, multidisciplinary assessment, home and institutional curative treatment, rehabilitation, long-term care and supportive social welfare.”55 This spectrum of services, with dedicated professionals and resources, constitutes the essence of the modern geriatric medicine movement, which was pioneered in Great Britain and has now developed in many other parts of the world.56 The principle focus of this field of medicine, captured in the motto, “adding life to years,” is the provision of timely interventions to treat and prevent unnecessary disease, disability, and dependency at all stages. Translating this concept into practical terms, comprehensive health services for older persons include an array of community, hospital, and institutional continuing care elements and academic commitments such as developed in Great Britain and summarized in Table 71-4.

Geriatric Strategies Comprehensive geriatric assessment (CGA) represents the core clinical activity of geriatric medicine. Practiced in inpatient and outpatient settings on the part of geriatricians, nurses, social workers, rehabilitation therapists, and others working in collaboration, geriatric assessment identifies the vulnerable elderly patient’s medical, psychosocial, and functional capabilities and problems, and leads to appropriate preventive, curative, rehabilitative, and long-term care.57 A metaanalysis of 28 controlled trials reported the odds of surviving and living in the community as well as showing improvement in physical or mental status at 6–l2 month follow-up are generally more favorable for patients managed by CGA programs. Programs which include control over implementing medical recommendations and provide extended ambulatory follow-up are more likely to be successful.58 The need for progressive geriatric care is particularly evident in the acute hospital sector where older patients not only constitute the largest constituency of admissions, but are at particularly high risk of experiencing decline in physical and mental function.59 Such strategies have been incorporated into hospitals in various ways in Great

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TABLE 71-4. SOME SPECIFIC ELEMENTS OF COMPREHENSIVE HEALTH SERVICES FOR THE ELDERLY IN GREAT BRITAIN Community Enrollment in primary care practice General practitioner Attached community nurses Home visiting by general practitioners Social service liaisons Home help Meals on wheels Domiciliary occupational therapy General Hospital Acute geriatric services Defined catchment population Geriatric medicine specialists, house officers Multidisciplinary teams Rehabilitation emphasis Home visiting Day hospital Respite admissions Liaison consultation with other hospital services Medicine Orthopedics Psychiatry Institutional Continuing Care Medical surveillance, avoid frequent transfer to hospital Multidisciplinary rehabilitation, maintenance of function Social and recreational activities Education Academic departments of geriatric medicine Required curriculum in medical schools Formal postgraduate specialty training Source: Modified from Barker WH. Adding Life to Years: Organized Geriatrics Services in Great Britain and Implications for the United States. Baltimore: Johns Hopkins University Press, 1987, p 170.

Britain, the United States, and elsewhere, as shown in Fig. 71-6. The simplest approach (C in the figure) involves referral for consultation by a multidisciplinary geriatrics team. The modality labeled (T) in the figure consists of a special hospital-based or affiliated unit to which patients are transferred for geriatric rehabilitation following acute care on a medical or surgical service. The third modality (A in the figure), involves designating part of an inpatient medical service as an acute geriatric admitting unit. Among the documented successes of hospital-based geriatric programs, three prototypic experiences are illustrative. The first of these, based at the Sepulveda Veterans Administration Medical Center in Los Angeles, comprised a 15-bed geriatric unit operated by a full-time medical, nursing, and social work team, with part-time participation by rehabilitation therapists and others. In a randomized trial, older hospitalized patients transferred to the geriatric unit, when compared with controls managed on a general medical unit, over a 1 year follow-up, experienced significantly lower mortality, a reduced likelihood of nursing home admission, fewer overall acute hospital and nursing home days, significantly greater improvement in functional status and morale, and lower average cost of care.60 The second experience involved a collaborative geriatric orthopedic rehabilitation unit (GORU) developed in Sterling, Scotland, in which elderly female patients with hip fracture were transferred postoperatively to the care of a multidisciplinary service headed by a geriatrician. In a randomized trial comparing patients managed by the GORU with those managed by the orthopedic service, median combined length of acute hospital and postacute rehabilitation stay was

Figure 71-6. Potential intervention by special geriatrics services in the course of acute hospital admission in the United States. A, admit to acute geriatrics service; C, geriatric consultation on acute medical and surgical services; T, postacute transfer to special geriatric rehabilitation unit. (Source: Barker WH. Adding Life to Years: Organized Geriatrics Services in Great Britain and Implications for the United States. Baltimore: Johns Hopkins University Press; 1987, p 131.)

shorter, fewer patients were discharged to long-term institutional care, and more patients attained high levels of independence in activities of daily living which persisted over 12 months follow-up.61 The third experience is the Acute Care for the Elderly (ACE) unit developed at the Case Western Reserve Medical Center in Cleveland, Ohio. Designed to avoid the cascade of “hazards of hospitalization” for older patient,59 the ACE unit incorporates a set of explicit geriatric care principles into routine acute care beginning at the time of admission to hospital. These include patient-centered care protocols to maintain or restore continence, mobility, skin integrity, mental health, etc., and daily rounds by a multidisciplinary team. A randomized trial showed significantly better functional status at discharge and lower rate of posthospital nursing home placement for the ACE unit patients, with comparable lengths of stay and hospital bills for these patients and control patients admitted to acute general medicine units.62

Comprehensive Health Services Successful provision of geriatric assessment, rehabilitation, and continuing care with a preventive orientation is most likely to occur in a comprehensive health-care program in which the various elements listed in Table 71-4 are linked together under one system of financing. Such systems have been developed in Great Britain, Scandinavian countries, and a number of other societies with national health programs. In the United States, fragmentation among health-care payors and an excessive reliance on costly institutional services (acute hospitals and nursing homes) has left many gaps in the provision of services which could prevent or alleviate disability and dependency in old age. A limited number of demonstration projects, including the PACE/On Lok Program for All-Inclusive Care of the Elderly and the Social Health Maintenance Organization (SHMO), as well as the Veteran’s Administration health services, have developed model comprehensive programs for older persons in the United States.63 Furthermore, many innovative care delivery strategies for maintaining maximal functional well-being among older persons living

71

Community Resources and policies Self-management supprt

Informed, activated patient

Health system Organization of health care Decision support

Delivery system design

Productive interactions

Clinical information systems

Prepared, proactive practice team

Functional and clinical outcomes Figure 71-7. The Chronic Care Improvement Model. (Source: Wagner EH. Chronic disease management: What will it take to improve care for chronic illness? Eff Clin Pract. 1998;1:2–4.)

in the community with chronic conditions have been introduced in recent years. A promising example being widely implemented in the United States and elsewhere is the “Chronic Care Model” developed by Wagner and colleagues, which, as illustrated in Fig. 71-7, incorporates key elements as follows: proactive efforts to involve patients in self-management; delivery system (practice) design to include team care; decision support to bring to bear best current evidencebased interventions; and efficient information systems to track patient progress. At such time that a national health program should evolve, policy makers will be well provided with these model experiences to draw upon in ensuring financing for progressive comprehensive services for society’s oldest and most vulnerable members. RECOMMENDED GENERAL READINGS

Albert SM. Public Health and Aging. An Introduction to Maximizing Function and Well-Being. New York: Springer; 2004. Lorig K, Holman H, Sobel D, et al. Living a Healthy Life with Chronic Conditions. Palo Alto: Bull Publishing Company; 1994. REFERENCES

1. International Classification of Impairments, Disabilities and Handicaps (ICIDH). Geneva, World Health Organization; l980. 2. Andresen EM, Rothenberg BM, Zimmer JG. Assessing Health Status among Older Adults. New York: Springer; l997. 3. Katz S, Ford AB, Moskowitz RW, et al. Studies of illness in the aged. The index of ADL. JAMA 1963;l85:9l4–9. 4. Lawton MP, Brody EM. Assessment of older people: self-maintaining and instrumental activities of daily living. The Gerontologist 1969;9: l79–86. 5. Fried LP, Herdman SJ, Kuhn KE, et al. Preclinical disability: hypotheses about the bottom of the iceberg. J Aging Health. 1991;3:285–300. 6. Guralnik J, Ferrucci L, Simonsick E, et al. Lower-extremity function in persons over the age of 70 years as a predictor of subsequent disability. N Engl J Med. 1995;332:556–61. 7. Ferrucci L, Guralnik J, Studenski S, et al. Designing randomized trials aimed at preventing or delaying functional decline and disability in frail older persons: A consensus report. J Am Geriatr Soc. 2004;52:1–10. 8. Boult C, Kane RL, Louis TA, et al. Chronic conditions that lead to functional limitation in the elderly. J Gerontol 1994;49:M28–M36.

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9. Ettinger WH, Fried LP, Harris T, et al. Self-reported causes of physical disability in older people: the Cardiovascular Health Study. J Am Geriatr Soc. 1994;42:l035–44. 10. Stuck A, Walthert J, Nikolaus T, et al. Risk factors for functional status decline in community-living elderly people: a systematic review of the literature. Soc Sci Med. 1999;48:445–9. 11. Fries JF. Aging, natural death, and the compression of morbidity. N Engl J Med. 1980;303:l30–5. 12. Gruenberg EM. The failures of success. Milbank Mem Fund Q. 1977;55:3–24. 13. Manton KG. Changing concepts of morbidity and mortality in the elderly population. Milbank Mem Fund Q. 1982;60:l83–244. 14. Freedman V, Martin L, Schoeni R. Recent trends in disability and functioning among older adults in the United States: a systematic review. JAMA. 2002;288:3137–46. 15. Katz S, Branch LG, Branson MH, et al. Active life expectancy. N Engl J Med. 1983;309:l2l8–24. 16. Rowe JW, Kahn RL. Human aging: usual and successful. Science. 1987;237:l43–9. 17. Manton KG, Corder LS, Stallard E. Estimates of change in chronic disability and institutional incidence and prevalence rates in the U.S. elderly population from the l982, l984, and l989 national long-term care survey. J Gerontol. 1993;48:Sl53–Sl66. 18. Bortz WM. Disuse and aging. JAMA. 1982;248:l203–8. 19. Fiatarone MA, Evans WJ. The etiology and reversibility of muscle dysfunction in the aged. J Gerontol. 1993;47:77–83. 20. Evans WJ. Effects of exercise on body composition and functional capacity of the elderly. J Gerontol. 1995;50A:l47–50. 21. McMurdo ME, Rennie L. A controlled trial of exercise by residents of old people’s homes. Age and Ageing. 1993;22:ll–5. 22. Fiatarone MA, O’Neill EF, Ryan ND, et al. Exercise training and nutritional supplementation for physical frailty in very elderly people. N Engl J Med. 1994;330:l769–75. 23. Young A. Exercise and physiology in geriatric practice. Acta Med Scan Suppl. 1986;7ll:227–32. 24. Physical Activity and Older Americans. Benefits and Strategies. June 2002. Agency for Healthcare Research and Quality and the Centers for Disease Control and Prevention. http://www.ahrq.gov/ppip/activity.htm. 25. Tinetti ME, Baker DI, McAvay G, et al. A multifactorial intervention to reduce the risk of falling among elderly people living in the community. N Engl J Med. 1994;33l:82l–7. 26. Province MA, Hadley EC, Hornbrook MC, et al. The effects of exercise on falls in the elderly. A preplanned meta-analysis of the FICSIT trials. JAMA. 1995;273:l34l–7. 27. Lauritzen JB, Peterson MM, Lund B. Effect of external protectors on hip fractures. Lancet. 1993;34l:ll–3. 28. Cranney A, Guyatt G, Griffith L, et al. Meta-analysis of therapies for postmenopausal osteoporosis. Summary of meta-analyses of therapies for post menopausal osteoporosis. Endocr Rev. 2002;23: 570–8. 29. Melton JL, O’Fallon WM, Riggs L. Secular trends in the incidence of hip fractures. Calcif Tissue Int. 1987;4l:57–64. 30. Ouslander J, Johnson T. Incontinence. In: Hazzard W, Blass JP, Ettinger WH, et al, eds. Principles of Geriatric Medicine and Gerontology. New York: McGraw-Hill; 2003. 31. Campbell VA, Crews JE, Moriarity DG, et al. Surveillance for sensory impairment, activity limitation, and health-related quality of life among older adults. Surveillance for selected public health indicators affecting older adults—United States, 1993–1997. MMWR CDC Surveill Summ. 1999;48(8):131–56. 32. Applegate WB, Miller ST, Elam JT, et al. Impact of cataract surgery with lens implantation on vision and physical function in elderly patients. JAMA. 1987;257:l064–6. 33. Lenze E, Rogers J, Martire L, et al. The association of late-life depression and anxiety with physical disability. A review of the literature. Am J Geriatr Psychiatry. 2001;9:113–35.

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34. Katz I, Alexopoulos GS, eds. Consensus Update Conference: Diagnosis and Treatment of Late-Life Depression. Am J Geriatr Psychiatry. 1996;4(l)Sl–S95. 35. Unutzer J, Katon W, Callahan C, et al. Collaborative care management of late-life depression in the primary care setting. JAMA. 2002;288:2836–45. 36. Trinr N, Hoblyn J, Mohanty S, et al. Efficacy of cholinesterase inhibiters in the treatment of neuropsychiatric symptoms and functional impairment in Alzheimer disease. A meta-analysis. JAMA. 2003;289:210–6. 37. Etminan M, Gill S, Samii A. Effect of non-steroidal anti-inflammatory drugs on risk of Alzheimer’s disease. Systematic review. BMJ. 2003; 327:128–31. 38. Mace NL, Rabins PV. The 36-Hour Day: A Family Guide to Caring for Persons with Alzheimer Disease. Baltimore: Johns Hopkins University Press; l999. 39. Maslow K. Current knowledge about special care units: Findings of a study by the U.S. Office of Technology Assessment. Alzheimer’s Disease and Associated Disorders. 1999;8(l):Sl4–S40. 40. Barker WH, Mullooly JP. Stroke in a defined elderly population, l967–l985. A less lethal and disabling but no less common disease. Stroke. 1997;28:284–90. 41. Dombovy ML. Rehabilitation and the course of recovery after stroke. In: Whisnant JP, ed. Stroke: Populations, Cohorts, and Clinical Trials. Butterworth Heinemann: Oxford; l993:2l8–37. 42. Stroke Unit Trialists’ Collaboration. Organised inpatient (stroke unit) care after stroke (Cochrane Review). In: The Cochrane Library. Oxford: Update Software; 2003, Issue 3. 43. Lindsberg P, Kaste M. Thrombolysis for acute stroke. Curr Opin Neurology. 2003;16:73–80. 44. Meara J. Parkinsonism and Other Movement Disorders. In: Tallis R and Fillet H, eds. Brocklehurst’s Textbook of Geriatric Medicine and Gerontology, 6th ed. London: Churchill Livingstone; 2003. 45. Garg R, Packer M, Pitt B, et al. Heart failure in the l990s: Evolution of a major public health problem in cardiovascular medicine. J Am Coll Cardiol. 1993;22(A):3A–5A. 46. Yan A, Yan R, Liu P. Narrative review: Pharmacotherapy for chronic heart failure: Evidence from recent clinical trials. Ann Intern Med. 2005;142:132–45. 47. Phillips CO, Wright SM, Kern DE, et al. Comprehensive discharge planning with postdischarge support for older patients with congestive heart failure: a meta-analysis. JAMA. 2004;291:1358–67. 48. Lacasse Y, Wong E, Guyatt GH, et al. Meta-analysis of respiratory rehabilitation in chronic obstructive pulmonary disease. Lancet. 1996;348:lll5–9.

49. Lawrence RC, Helmick CG, Arnett FC et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arth. Rheum. 1998;41:778–99. 50. American Geriatrics Society Panel. Exercise prescription for older adults with osteoarthritis pain: Consensus practice recommendations. J Am Geriatr Soc. 2001;49:808–23. 51. Jeong G, Bendo J. Spinal disorders in the elderly. Clin Orthop. 2004;425:110–25. 52. Thomas W. Life Worth Living. How Someone You Love Can Still Enjoy Life in a Nursing Home. The Eden Alternative. Acton, Massachusetts: Vander Wyk and Brunham; 1996. 53. Townsend P. The structured dependency of the elderly: A creation of social policy in the twentieth century. Ageing and Society. 1981;l:5–28. 54. Barker WH. Adding Life to Years: Organized Geriatrics Services in Great Britain and Implications for the United States. Chapters 9–ll. Baltimore: Johns Hopkins University Press; l987. 55. Planning and Organization of Geriatric Services. World Health Organizational Technical Report Series No. 548. Geneva, World Health Organization; l974. 56. Barker WH. Geriatrics internationally. In: Fox R, Horan M, Puxity J, eds. Medicine in the Elderly: A Problem Solving Approach. London: Edward Arnold; l990. 57. Rubenstein L, Wieland D, Bernaki R. Geriatric Assessment Technology. The State of the Art. Milan, Italy: Editrice Kurtis; 1995. 58. Stuck AE, Siu AL, Wieland D, et al. Comprehensive geriatric assessment a meta-analysis of controlled trials. Lancet. 1993;342: l032–6. 59. Creditor MC. Hazards of hospitalization of the elderly. Annal Int Med. 1993;ll8:2l9–23. 60. Rubenstein LZ, Josephson KR, Wieland GD, et al. Effectiveness of a geriatric evaluation unit: A randomized clinical trial. N Engl J Med. 1984;3ll:l664–70. 61. Kennie DC, Reid J, Richardson IR, et al. Effectiveness of geriatric rehabilitative care after fracture of the proximal femur in elderly women: A randomized clinical trial. BMJ. 1988;297: l083–6. 62. Landefield SC, Palmer RM, Kresevic DM, et al. A randomized trial of care in a hospital medical unit especially designed to improve the functional outcomes of acutely ill older patients. N Engl J Med. 1995;332:l338–44. 63. Calkins E, Boult C, Wagner E, et al. New Ways to Care for Older People. Building Systems on Evidence. New York, NY: Springer Publishing Company; 1998.

Nutrition in Public Health and Preventive Medicine

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Marion Nestle

The role of nutrition in public health and preventive medicine is selfevident: people must eat to live. Both inadequate and excessive food intake can adversely affect health, and both contribute to the leading causes of morbidity and mortality in every nation, developing as well as industrialized. Because all people consume food, all have an interest in the effects of diet on health. Nutrition, therefore, becomes an unusually accessible entry point into public health education and intervention programs. Because food intake is determined not only by individual choice but also by cultural and social norms, economic status, and agricultural and food policies, public health approaches to dietary intervention are not only appropriate, but necessary. This chapter discusses diet and nutrition within the broad context of public health. It describes the health impact of dietary intake below and above recommended levels of energy and essential nutrients. It reviews current standards and guidelines for patterns of food intake that best meet nutritional requirements, improve nutritional status, and promote health. Finally, it suggests public health strategies to address behavioral and environmental barriers to consumption of healthful diets by individuals and populations. DIETARY REQUIREMENTS AND ALLOWANCES

People require a continuous supply of external food sources of energy and essential nutrients to maintain life, grow, and reproduce.1,2 By definition, essential nutrients are those that cannot be synthesized in adequate amounts by the body; their dietary or metabolically induced deficiency causes recognizable symptoms that disappear when they are replaced. The list of nutrients essential or otherwise useful to human physiology is long, complex, and almost certainly incomplete. It includes the more than 40 distinct substances listed in Table 72-1: sources of energy, amino acids, fatty acids, vitamins, minerals and trace elements, fiber, and water. As indicated in Table 72-1, other nutrients also may be required under certain conditions. Malnutrition refers to excessive and unbalanced—as well as deficient—intake of essential nutrients. Fat-soluble vitamins and virtually all of the mineral elements cause disease symptoms when consumed or absorbed in excess. The adverse effects of overconsumption of energy, saturated fat, cholesterol, salt, sugars, and alcohol are important public health concerns. For each nutrient, a certain range of intake meets physiologic requirements but does not induce harmful symptoms.3 Optimal levels of intake of specific nutrients for individuals, however, can only be estimated. Individuals vary in nutrient requirements, and research on human nutritional requirements is incomplete.

Many countries have developed standards of nutrient adequacy for their populations for purposes such as nutrition education, nutrition counseling, food labeling, and dietary intervention programs. Because standards are based on interpretation of the existing research, they differ from one country to another.4 Until the late 1980s in the United States, the National Academy of Sciences’ Food and Nutrition Board (now in the Institute of Medicine) estimated levels of nutrient intake “adequate to meet the known nutritional needs of practically all healthy persons,” and published them every decade or so as recommended dietary allowances (RDAs).5 The RDAs were (and continue to be) set at levels that prevent overt signs of nutritional deficiency in 97–98% of the population—two standard deviations above mean requirements. Although lower levels of intake meet the nutritional needs of most individuals, RDAs were widely misinterpreted to be minimal requirements. For this reason, and because the RDAs addressed nutrient deficiencies but not excesses that might raise risks for chronic diseases, the Food and Nutrition Board (FNB) replaced them beginning in 1997 with new standards—Dietary Reference Intakes (DRIs)—developed jointly with Canada (Fig. 72-1). The FNB developed the DRIs in line with the current direction of nutrition science toward increasing complexity and individualization of dietary standards and recommendations, a trend much at odds with public health approaches. Although the 1989 RDAs appeared in a slim volume of under 300 pages easily summarized in two tables, the DRIs comprise six volumes of 400–800 printed pages each.6–11 The DRIs include the former RDAs, but also introduce three new components: adequate intake (AI), tolerable upper intake level (UL), and estimated average requirement (EAR). Table 72-2 defines these standards and summarizes how they are meant to be used for diet assessment and planning. The DRIs are individualized into values for 10 age categories (among infants, children, males, and females) and for pregnant and lactating women. They are based on biochemical, epidemiological, and clinical research, but such data are limited and many values have had to be estimated or extrapolated, especially for younger and older age groups. Thus, the DRIs are subject to many of the same criticisms that had been applied to the former RDAs. As Table 72-2 shows, the RDA (or the AI) continues to be used as a goal for individual intake even though it greatly exceeds average requirements. The DRIs are meant to apply to nutrient intake from food, but some RDAs or AIs are set so high that it would be difficult, if not impossible, to meet them through normal dietary intake. For example, on the basis of levels required for maximum retention, the AI for calcium is set at 1200 mg per day for older adults, an amount obtainable only by consuming large amounts of dairy foods, supplements, 1195

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TABLE 72-1. DIETARY COMPONENTS CONSIDERED ESSENTIAL FOR HUMAN HEALTH∗

TABLE 72-2. DIETARY REFERENCE INTAKES: DEFINITIONS AND USE

Category

Definitions

Examples Carbohydrate, fat, protein, alcohol† Isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine, histidine Linoleic acid, linolenic acid‡

Energy sources Essential amino acids

Essential fatty acids Vitamins Water-soluble

Biotin,§ choline,¶folate, niacin, pantothenic acid, riboflavin, thiamin, vitamin B6 (pyridoxine), vitamin B12 (cobalamins), vitamin C (ascorbates) Vitamins Aa, Db, E, K§ Calcium, chloride, magnesium, phosphate, potassium, sodium Chromium, cobalt,ccopper, fluoride, iodine, iron, manganese, molybdenum, selenium, zinc

Fat-soluble Minerals Trace elements

Recommended Dietary Allowance (RDA): Average daily dietary intake level sufficient to meet the nutrient requirement of nearly all (97–98%) healthy individuals in a group Adequate Intake (AI): An estimate of the RDA based on observed or experimentally determined approximations of nutrient intake by a group (or groups) of healthy people Tolerable Upper Intake Level (UL): Highest level of daily nutrient intake likely to pose no risks of adverse health effects to almost all individuals in the general population Estimated Average Requirement (EAR): Nutrient intake value estimated to meet the requirement of half the healthy individuals in a group Use in Assessment and Planning Type of Use

See references 6-11. Carbohydrates (starches and sugars), proteins, fat, and alcohol contribute about 4, 4, 9, and 7 kcal/g, respectively. ‡ Other fatty acids in the omega-3 series may have essential functions. § Synthesized by intestinal bacteria in uncertain amounts. ¶ Synthesized in the body, but not always in adequate amounts. aIncludes beta-carotene, alpha-carotene, and beta-cryptoxanthin precursors. bSynthesized through the action of sunlight on skin, but required in the diet if sun exposure is limited. cConsumed as part of vitamin B . 12

EAR

RDA

†

1.0

1.0 UL

EAR RDA

0.5

0.5

0

Risk of adverse effects

Risk of inadequacy

or fortified foods. Ideally, the DRI would relate calcium intake to prevention of osteoporosis, but data are inadequate to do so (hence: AI, not RDA). It is uncertain whether a level this high is reasonable, or instead is needed to compensate for the effects of consuming diets high in protein, sodium, and phosphorus, all of which promote calcium excretion. In contrast, international standards relate calcium to animal protein intake and, as a result, range widely; the lower the amount of animal protein (and the phosphorus that goes with it) in the diet of a population, the less calcium is recommended.4 Because DRI levels so depend on the criteria and assumptions used in establishing them, careful interpretation is essential.6,7 The UL component has two purposes. For vitamins and minerals, which rarely are consumed in excess from food (a rare exception is vitamin A toxicity from eating polar bear liver), the UL sets limits

0 Observed level of intake

Figure 72-1. Dietary reference intakes. The risk of inadequate intake increases as it approaches the EAR. The AI is not pictured because it does not bear a consistent relationship to the EAR or RDA. The RDA meets the requirements of most people in a population. At levels of intake above the UL, risks of excess intake increase. See Table 72-2 for an explanation of abbreviations.

For Groups

Assessment

Fiber Water ∗

For Individuals

AI

UL

Probability of inadequate intake (intake at EAR means 50% probability of inadequacy) Low probability of inadequacy at RDA level Low probability of inadequacy at AI level Intake above UL increases risk of adverse effects

Prevalence of inadequate intake (defined as < EAR) Do not use Intake at AI implies low prevalence of inadequacy Prevalence of population at risk of excess intake

Planning EAR

Do not use

RDA AI UL

Aim for this intake Aim for this intake Guide for limiting intake

Intake distribution with low prevalence of inadequacy Do not use Mean intakes Intake distributions with low prevalence of adverse effects

on intake of dietary supplements. The UL also addresses dietary risks for chronic disease from overconsumption of such nutrients as energy, sugars, and sodium. For example, more than 95% of men and 75% of women in the United States consume sodium at levels that exceed the UL; not coincidentally, nearly one-fourth of the population has hypertension. Because practically all dietary sodium comes from salt added to processed foods, the UL has implications for the food industry. The lower the UL, the more pressure on food companies to reduce salt in their products.8 Upper limits on sources of energy such as saturated fat, trans fat, cholesterol, and sugars are especially controversial because avoiding them means consuming less of their main food sources.9 NUTRITIONAL DEFICIENCIES: CAUSES AND CONSEQUENCES

Inadequate dietary intake is only one cause of nutrient deficiency. Symptoms also result from conditions that interfere with appetite; impair nutrient digestion, absorption, or metabolism; or substantially increase nutrient requirements or losses. Deficiencies may appear clinically as starvation, protein-energy malnutrition, syndromes of deficiency of single nutrients (e.g., pellagra, scurvy, iron-deficiency anemia), or as a wide range of less-specific symptoms.1,2 The number of people throughout the world who suffer from nutritional deficiencies can only be estimated. About 900 million

72 people, most of them in low-income countries, are considered to be chronically undernourished and food insecure, based on a food supply cut point of 2300 kcal per day or uncertain ability to obtain food due to lack of money or other resources.10,11 Widespread nutritional deficiencies occur most often when income, education, and housing are inadequate, where water supplies are contaminated with infectious organisms that induce diarrheal diseases, or where populations are at war or under siege.12 In countries where such conditions predominate, more than one-third of children under the age of 5 years suffer from some degree of malnutrition.13,14 Malnutrition is usually a direct consequence of poverty. Except in the very poorest or most conflicted countries, food production is adequate to meet energy requirements, but the segments of the population most in need are unable to purchase or use foods appropriately. In industrialized countries, dietary deficiencies are less prevalent. Food insecurity, defined as an inability to acquire adequate food in socially acceptable ways, affects an estimated 11.0% of the U.S. population; food insecurity with involuntary hunger affects an estimated 3.9%.15 Such findings, however, are only rarely accompanied by clinical signs of nutrient deficiencies. When clinical signs do occur, they are usually associated with the additional nutritional requirements of pregnancy, infancy, early childhood, or aging, the toxic effects of alcohol or drug abuse, or illness, injury, or hospitalization.1,2 Regardless of cause, inadequate dietary intake profoundly affects human function. It induces rapid and severe losses of body weight and electrolytes, decreases in blood pressure and metabolic rate, electrocardiogram abnormalities, losses in muscle strength and stamina, and gastrointestinal and behavioral changes.1 The result is a generalized lack of vigor, alertness, and vitality that reduces productivity and impairs the ability of people to escape the consequences of poverty. Of special concern is the loss of immune function that accompanies starvation. Malnourished individuals lose cellular immune competence and demonstrate poor resistance to infectious disease. Infections, in turn, increase nutrient losses and requirements, and, in the absence of adequate nutrient intake, induce further malnutrition. This cycle is the principal cause of death among young children in developing countries and is an important cause of morbidity in malnourished children and adults everywhere.16,17 Protein-energy malnutrition is the collective term for the clinical effects of this cycle on young children. Survivors display typical effects of starvation: depression, apathy, irritability, and growth retardation. Protein-energy malnutrition usually is classified into two entities— kwashiorkor and marasmus—on the basis of clinical signs and on the relative intake of protein to energy. Kwashiorkor is characterized by edema and fatty infiltration of the liver and is associated with a relative deficit of protein to energy. Marasmus is manifested as generalized wasting due to overall nutritional deprivation. In practice, such distinctions blur. Undernourished children exhibit symptoms that fall between the two extremes, and similar diets contribute to either form.1 Numerous methods to prevent poverty-associated malnutrition in adults and children by improving household food security have been demonstrated to be effective in developing countries. Among them are programs that redistribute income, subsidize food prices, promote agricultural production, provide food supplements, and educate.18,19 Improvements in sanitation and in primary health care are also essential components of programs to reduce nutritional deficiencies.20 Addressing the factors that raise risks for malnutrition would improve health and life expectancy for large segments of low-income populations.21 DIET AND CHRONIC DISEASE

As nutritional deficiencies decline in prevalence in industrialized as well as developing countries, they are replaced rapidly by chronic conditions of dietary excess and imbalance. In the late 1980s, three comprehensive reports reviewed the entire spectrum of evidence linking diet to chronic diseases, and estimated the incidence and prevalence, cost to society, and overall public health impact of these conditions in

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the United States and Europe.28–30 More recent reports document the increasing burden of disease from chronic, noncommunicable diseases due in part to excessive intake of food and energy.22,23 In today’s era of rapid globalization, populations in developing countries move quickly from classic patterns of malnutrition to rising rates of chronic diseases.24 This “nutrition transition” means that as in industrialized countries, overweight and obesity now predominate as diet-related health problems in countries where undernutrition still exists among large segments of their populations.34–36 In the United States, four of the ten leading causes of death— coronary heart disease, cancer, stroke, and diabetes—are chronic diseases related in part to diets containing excessive energy, fat, saturated fat, cholesterol, salt, or alcohol, and too little fiber, along with too sedentary a lifestyle. These conditions account for more than 60% of annual deaths, but because they have multiple causes, the proportion attributable to diet alone is difficult to determine. One estimate attributes 18.1% of annual deaths to tobacco abuse, 16.6% to poor diet and physical activity (later corrected to 15.2%25), and 3.5% to alcohol abuse.26 Imprecision in such estimates is inevitable given the difficulties inherent in design, conduct, and evaluation of research on diet and disease. Nutrition research is complicated by individual variations in dietary requirements, limitations in the ability of investigators to obtain accurate information about the dietary intake of individuals or populations, and by other endlessly debated methodologic issues. Dietary changes over time are especially difficult to estimate. Firm proof of dietary causality is virtually impossible to demonstrate for diseases affected by so many other risk factors—genetic, environmental, and behavioral. Instead, investigators identify associations between diet and disease from studies of laboratory animals and from biochemical, epidemiologic, and clinical investigations in humans.27 Because each of these methods has limitations, diet-disease associations are usually inferred from the totality of available evidence and are considered most compelling when data from all sources are consistent, strongly correlated, highly specific, dose-related, and biologically plausible.28 Despite the difficulties, health authorities repeatedly reach the same conclusion about diet and disease risk: the preponderance of evidence supports the health benefits of diets that balance energy intake with physical activity, emphasize consumption of foods from plant sources, and minimize consumption of foods high in saturated and trans fats, carbohydrates, and alcohol.

DIETARY RECOMMENDATIONS

An ideal diet provides energy and essential nutrients within optimal ranges from foods that are available, affordable, and palatable. Until the mid-1970s, government and health agencies in the United States advised the public to select diets from specific groups of foods (e.g., dairy, meat, fruits and vegetables, grains) in order to ensure adequate intake of nutrients most likely to be consumed at below-standard levels.9 As chronic diseases replaced nutrient deficiencies as public health problems, dietary recommendations shifted to address prevention of these increasingly prevalent conditions.

Dietary Goals and Guidelines The first U.S. report to reflect this new focus established numerical targets for dietary changes to reduce chronic disease risk: reduce intake of fat (to 30% or less of total energy), saturated fat (10%), sugar (10%), cholesterol (300 mg/day or less), and salt (5 g/day); increase intake of foods containing naturally occurring sugars and starches (48%); consume alcoholic beverages in moderation; and balance energy intake against expenditure to maintain appropriate body weight. To achieve these targets, the report advised the public to consume more fruits, vegetables, and grains, and to select meat and dairy foods low in fat.29 This advice proved so controversial that subsequent federal nutrition policies have tended to omit explicit percentage goals.9

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U.S. dietary guidance policy is expressed in the Dietary Guidelines for Americans, a joint publication of the U.S. Department of Agriculture (USDA) and the Department of Health and Human Services (HHS), issued at 5-year intervals since 1980.30 Like the development of Dietary Reference Intakes (DRIs) from RDAs, the guidelines have evolved toward the increasingly complex and individualized. The first four editions contained just seven precepts; the fifth edition added three more. The sixth edition in 2005 contained 41 recommendations—23 for the general population and 18 for specific population groups such as overweight children, pregnant women, or older adults.31 The increasing complexity is best illustrated by the sugar guideline. In 1980, it was “Avoid too much sugar”; in 2005, it was “Choose and prepare foods and beverages with little added sugars or caloric sweeteners, such as amounts suggested by the USDA Food Guide and the DASH Eating Plan.” As for increasing individualization: the USDA Food Guide lists serving numbers and sizes for foods in 11 groups at 12 levels of energy intake; the DASH (Dietary Approaches to Stop Hypertension) diet lists food servings in 8 groups at 4 levels of energy intake. The movement away from public health approaches to dietary advice is due to two factors: science and politics. Nutrition science is increasingly focused on identification of genetic profiles that can be used as a basis for individualized dietary intervention. This approach is known variously as nutrigenomics,32 nutrigenetics,33 or, when it involves identification of metabolic components of body fluids or tissues, metabolomics34 (hence the drive to produce nutraceutical foods and supplements).35 Politics is involved when food companies exert political pressure to prevent governments from issuing dietary advice that might result in reduced sales of their products. In 2004, for example, sugar lobbying groups pressed HHS to threaten withdrawal of funding from the World Health Organization (WHO), which was considering advising member countries to restrict intake of added sugars to 10% of daily energy intake.36 Lobbying groups successfully pressured WHO member states to reject inclusion of that recommendation in a resolution to institute measures to prevent mortality, morbidity, and disabilities resulting from noncommunicable diseases.37,38

The Current Consensus: Food Guides Despite the scientific and political controversy, dietary recommendations for chronic disease prevention have remained much the same for decades. Virtually all say: vary food intake; balance food energy with physical activity to maintain weight; favor fruits, vegetables, and whole grains; choose lean meats and low-fat dairy foods; avoid foods high in fats, sugars, and salt; and drink alcohol in moderation, if at all.39,40 The 2005 U.S. Dietary Guidelines do contain some quantitative recommendations: at least 30 minutes of daily physical activity, 20–35% of energy from total fat, less than 10% from saturated fatty acids, less than 300 mg per day of cholesterol, and less than 2300 mg sodium per day. They also advise minimal intake of trans fatty acids.31 Similar recommendations have been issued by U.S. health organizations and agencies concerned with coronary heart disease and stroke,41 cancer,42 diabetes,43 and hypertension.44 Many countries have attempted to translate such recommendations into public health advice presented in graphic forms such as plates, shopping carts, or pagodas.45 The most common format is that exemplified by the USDA’s now obsolete Food Guide Pyramid, a visual representation of recommendations to consume more foods from its base (grains, fruits, vegetables), and fewer from its upper sectors (meat, dairy, and foods high in fats and sugars).46 This design generated controversy from the outset, first because of its implied restrictions on meat, dairy, and processed foods,9 and later for its failure to distinguish healthful from less healthful fats and carbohydrates.47 Translating the new 41 dietary guidelines into a consumer guide to food choices presented even more difficult challenges when the USDA replaced the pyramid in 2005. The USDA dealt with those challenges by stating that “One size does not fit all” and creating 12 separate pyramids for individuals of differing energy needs.48 The

Figure 72-2. The pyramid design featured as part of the USDA’s 2005 Food Guidance System emphasizes exercise and provides dietary advice for individuals through its website, www.MyPyramid. gov.

basic pyramid design, which emphasizes exercise, self-education through use of a website, and individual prescriptions for food choices based on age, sex, and activity level, is shown in Fig. 72-2. Despite ongoing debates about dietary advice, its consistency for so many chronic diseases has encouraged collaboration on common recommendations for primary prevention. These constitute a consensus,49 now worldwide.22 The obvious next step is to develop public policies to promote their implementation.50 The recent increase in worldwide obesity, for example, calls for interventions that reduce barriers to following advice about healthful diets and activity patterns.51,52 BARRIERS TO IMPLEMENTATION

Although the ultimate decisions targeted by dietary recommendations are personal food choices, individuals make such choices within the context of the social, economic, and cultural environments in which they live. Adults prefer foods that taste, look, and smell good, are familiar, and provide variety, but such preferences are strongly influenced by family and ethnic background, levels of education and income, age, and gender.53 Food production, marketing, and the demand for convenience at low cost are strong determinants of food choices and create barriers to dietary change.9

Food Production Food production, distribution, and marketing in the United States have undergone significant changes that affect food availability and, therefore, consumption patterns. In 2000, the U.S. food system accounted for nearly 8% of the Gross Domestic Product (GDP), employed 12% of the labor force, and generated nearly $800 billion in expenditures. The proportion of that amount going to the farm sector has declined steadily since the early 1970s and is now less than 20%54 (the remaining 80% goes for marketing costs such as labor, packaging, transportation, other business expenses, profit, and advertising55). Since 1935, the number of U.S. farms fell from 7 million to under 2 million, but production became increasingly centralized and efficient; the largest 8% of farms account for 68% of production.56 This trend has been accompanied by an increase in consumption of processed foods. In 1980, the average number of items in a supermarket was about 14,000; in 1999 it was more than 40,000.54 In 2004, manufacturers introduced nearly 18,000 new food and beverage products, among them more than 2700 candies, 2600 snack foods, 1300 ice cream novelties, 700 soft drinks and waters, 600 fruit drinks, and 460 jams and sweet toppings.57 Many such products are misleadingly advertised as “healthy” because they are reduced in fat or sugars or have vitamins added.58

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Food Marketing Advertising promotes consumption of entire categories of foods, stimulates food production, processing, and marketing, and builds brand loyalty among adults and children.59,60 Direct (measurable) advertising costs are estimated at nearly $12 billion annually, much of it for television commercials for food and beverages purchased outside the home; for every “measured” dollar, companies spend an additional $2 on supermarket fees, coupon campaigns, trade shows, Internet marketing, and other such indirect methods, bringing the total to about $36 billion.54 In 2003, for example, McDonald’s spent $619 million in measured dollars on U.S. advertising, PepsiCo spent $208 million on soft drinks alone, M&M Mars spent $77 million for its candies, and Altria spent $25 million just to advertise Kool-Aid.61 Some marketing methods are more subtle and involve changes in societal norms favoring larger portions and more frequent eating occasions.62 The influence of food marketing on consumption patterns, particularly of children, is of great concern as the advertisements rarely display foods consistent with dietary guidelines, and evidence increasingly links consumption of fast food and soft drinks to higher energy consumption, overweight, and poor diet quality, especially among children.63,64

Demand for Convenience and Low Cost More than half of U.S. women with children under 1 year of age work outside the home, a trend sufficient to explain why convenience is so prominent a motive for food selection.65 Higher disposable incomes in two-income families, and less leisure time, also contribute to demands for convenience. Thus, the share of food expenditures for foods prepared outside the home increased from about 26% in 1960 to 47% in 2000.54 Although the fastest growth in sales occurred among fast-food or quick-service restaurants, future growth is expected to occur in full-service restaurants.66 In 2003, McDonald’s alone generated $17 billion in annual sales from more than 31,000 outlets serving nearly 50 million people in more than 119 countries each day.67 Low prices are an incentive for consumption, and energydense fast-foods cost less per kcal than do fruits and vegetables.68 Advice to consume more healthful diets confronts such barriers.

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availability of total energy in the food supply increased from 3300 to 3900 kcal per day from 1970 to 2000,74 and dietary intake surveys report an increase of 200 kcal per day, nearly all derived from carbohydrates.75 Such observations reflect the environment of food intake in the United States. Consumers who are well informed about nutrition— and make choices based on this information—tend to be older, better educated, and wealthier, demonstrating that diet is an indicator of social class. For many people, convenience and low cost take precedence over nutritional quality. Markets selling healthful foods are rarely located in low-income communities.76 Because meals are increasingly purchased at restaurants and at fast-food and takeout places, and because foods high in processed oils and sugars are inexpensive to produce and profitable to market, the food industry has an increasing influence over dietary choices. In this situation, public health strategies to improve dietary intake are especially desirable. ASSESSMENT OF NUTRITIONAL STATUS

As with any other public health campaign, the first step in dietary intervention is to identify the nutritional problems and, therefore, the needs of the population at risk.50 Evaluation of nutritional status is complicated by the many genetic, medical, behavioral, and environmental factors that influence development of diet-related conditions, by the multiplicity of signs and symptoms of malnutrition, by the lack of suitable biochemical or clinical markers for these signs and symptoms,1,2 and by the lack of precision in available assessment methods.27 Assessment is also complicated by the variety of personal, cultural, and economic factors that influence food choice as well as the many social factors that lead to health inequalities.77,78

Assessment Methods: Individuals and Populations To date, no single, independent measurement of dietary, biochemical, or clinical status has been found adequate to confirm the nutritional status of individuals or populations. Instead, nutritional risk is defined by a combination of methods: nutritional history, medical history and physical examination, body measurements, and laboratory tests.79,80 Table 72-3 lists examples of elements of these

THE ENVIRONMENT OF FOOD CHOICE

Americans perceive that they are well informed about the effects of diet on health and want to eat healthfully, but say they are confused by the variety of nutrition messages given by government, industry, health authorities, and the media, especially since most come from food companies and media. Qualitative research reveals considerable consumer skepticism about dietary advice and tendencies to ignore recommendations seen as inconsistent or difficult to follow.69 This research confirms the well-established principle that education alone is insufficient to change behavior; environmental changes are needed to facilitate more healthful food choices.70 If nutrition messages are perceived as confusing, they also are perceived as requiring unacceptable changes in eating patterns, preparation effort, or cost. For example, the major sources of saturated fat in the U.S. diet in 1999 were dairy foods (24%), meat (21%), shortenings (15%), and salad and cooking oils (12%).71 Cheese alone provided 11% of the saturated fat. To reduce saturated fat to 10% of energy or less, it is necessary to eat less of those foods or to replace them with fruits, vegetables, and grains. In 2000, the leading sources of energy in U.S. diets were soft drinks, cakes and pastries, hamburgers, pizza, and potato and corn chips; these five food groups accounted for 20% of cumulative energy intake.72 Advice to eat less of them confronts the economic interests of their producers. Food supply data (an indirect measure of dietary intake) do indicate some favorable shifts since the 1970s: a slight decline in the availability of red meat, replacement of whole with low-fat and skim milk, replacement of animal fats with vegetable oils, and increases in availability of fruits and vegetables.73 However, the per capita

TABLE 72-3. SURVEY ELEMENTS FOR NUTRITIONAL STATUS EVALUATION Nutritional History

Medical History & Physical

Dietary Intake • Food record • 24-hour recall • Food frequency • Diet history • Use of supplements • Eating habits

Signs of Undernutrition

Related Social Factors • Income • Educational level • Ethnicity • Use of food assistance • Medications • Activity levels

Chronic Disease Risk Factors

Body Measures

Laboratory Tests

• Height • Weight • Skinfolds • Waist circumference • Hip circumference

• Hemoglobin, hematocrit • Iron and iron-binding • Serum vitamins and minerals • Blood glucose • Blood cholesterol • Lipoproteins • C-reactive protein

• Low weight for height • Recent weight loss • Clinical signs of malnutrition • Chronic or acute conditions • Medication use • Substance abuse • Overweight • Elevated blood glucose • High blood pressure • High blood cholesterol • Waist-hip ratio

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methods used in population surveys. In practice, surveys rarely use the full range of nutritional assessment methods; many of them are too imprecise, inconvenient, or expensive for frequent use. Instead, professional judgment is needed to evaluate the severity of selected nutritional risk factors. Short of duplicate meal analysis (and even this method has limitations), techniques to determine the usual dietary intake of individuals are imprecise; standard methods yield estimates that cannot be interpreted too literally. These include a record of foods consumed during a specified time period (Food Record), retrospective recall of foods consumed within a recent time period (24-Hour Recall, or longer), and measures of the frequency of consumption of specific index foods (Food Frequencies).27 The nutrient content of foods identified by these methods is obtained from tables of food composition, which also are imprecise estimates.81 The diets are compared to standards of nutrient intake such as the DRIs82 or to recommended patterns of food consumption described by dietary guidelines or food guides. Each of these methods, used singly or in combination, has strengths and weaknesses. All yield useful, if imprecise, information.28 Demographic and socioeconomic data are especially useful as indirect indicators of nutritional risk in community surveys where detailed diet histories, physical examinations, and laboratory tests would be impractical. The simplest and most useful indicator of undernutrition is low weight for height. Other clinical signs listed in Table 72-3 are useful for assessing the nutritional status of hospital patients.1 Evaluation of chronic disease risk is accomplished through measurements of blood glucose, blood pressure, blood cholesterol, and body weight. The high prevalence of these risk factors is the basis of large-scale public health campaigns such as the U.S. National Cholesterol Education Program.83 Because no simple screening measure is available for evaluation of diet-related cancer risk, promotion of healthier diets to the entire population is a reasonable public health strategy.

National Nutrition Monitoring The prevalence of diet-related risk factors and conditions in the United States is determined by remnants of the 1990 National Nutrition Monitoring and Related Research Program, now expired. The program coordinated the monitoring activities of 40 surveys conducted by 22 federal agencies that measured health and nutritional status, food and nutrient consumption, food composition, dietary knowledge and attitudes, foods available for purchase, and socioeconomic indicators related to dietary intake.84 Early concerns about the limited ability of the program to provide data on trends in dietary intake patterns, hunger prevalence, and dietary patterns of minority groups85 were eventually addressed. Its principal surveys were the National Center for Health Statistics’ National Health and Nutrition Examination Survey (NHANES) and USDA’s Continuing Survey of Food Intake of Individuals (CSFII). NHANES collected data from dietary interviews, physical examinations, and biochemical and hematological tests from a probability sample of the U.S. population from 1971 to 1974 (NHANES I), 1976 to 1980 (NHANES II), 1988 to 1994 (NHANES III), and later. It surveyed the Hispanic population from 1982 to 1984 (HHANES).86 The CSFII collected information about household food consumption along with measures of knowledge and attitudes about nutrition and health.87 In 2002, the surveys were merged into one continuous survey called “What We Eat in America.”88 Without reenactment of the legislation mandating and funding these surveys, their future is uncertain.89

Community Nutrition Assessment Methods for assessment of the nutritional needs of communities vary only slightly from conventional means of community health assessment. Table 72-4 lists the principal data elements used to evaluate

TABLE 72-4. DATA ELEMENTS FOR COMMUNITY NUTRITION ASSESSMENT

Community Descriptors • Geographical position, boundaries • Population within boundaries, density • Community agencies, services • Community health-care services • Hospitals, clinics • Educational institutions

Population Descriptors • Age, gender, racial, and ethnic distribution • Income • Education • Employment • Length of time in location • Primary language

Health Status Indicators • Infant mortality • Low birth weight

• Life expectancy • Chronic disease rates • Leading causes of death

Nutritional Status Indicators • See Table 72-3

Food and Nutrition Resources • Use of federal food assistance • Nonparticipation rates for eligible persons • Soup kitchens, food pantries, food banks • Food markets: number, kind, location • Nutrition education and training programs • Food and nutrition advocacy groups • Weight control programs • Worksite wellness programs

the level of nutritional risk in communities. These elements include geographic, demographic, socioeconomic, and health descriptors. They also include descriptors of food and nutrition resources in the community, utilization rates for such resources, and indicators of food availability, intake, and nutritional status obtained from nutrition monitoring surveys. In developing countries with high rates of clinically apparent conditions of undernutrition, investigators have selected elements from this list to develop rapid, convenient, and relatively inexpensive screening instruments to evaluate nutritional risk under field conditions. These methods, which range from a graded series of bracelets to measure arm circumference to comprehensive surveys, have been used successfully to identify children and adults at high nutritional risk who can be targeted for intervention.90 In the United States, advocates for the poor in more than 250 communities since 1980 have developed methods to document the need for federal food assistance; these typically include data on poverty levels, the severity of individual and family food insecurity, nonparticipation of eligible persons in food assistance programs, and increasing demands for private-sector soup kitchens and food pantries.91 POLICY RECOMMENDATIONS AND IMPLEMENTATION STRATEGIES

The quantity, strength, and consistency of evidence that relates dietary factors to chronic diseases, and the substantial impact of these conditions on health, are reasons enough to promote policies to make it easier for people to consume more healthful diets (and be more active). Current policies could be altered to address environmental as well as behavioral barriers to dietary change. Table 72-5 outlines some suggestions for policy changes aimed at reducing dietary risks for chronic diseases. Public health strategies begin with public education. Although education may not be sufficient to improve dietary behavior, it can facilitate change, especially when education interventions involve the target audience in the design, conduct, and evaluation of their own dietary plans, employ multiple educational strategies, and use a team approach.70 Currently, most public information about nutrition derives from food industry marketing, and no government agency can compete with that level of funding. The success of the National Cholesterol Education Program is evidence that well-funded campaigns can be

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TABLE 72-5. PUBLIC HEALTH POLICIES TO REDUCE DIETARY RISKS FOR CHRONIC DISEASE

REFERENCES

Educate the Public

1. Shils ME, Olson JA, Shike M, et al, eds. Modern Nutrition in Health and Disease, 9th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1998. 2. Bowman BA, Russell RM. Present Knowledge in Nutrition, 9th ed. Washington, DC: ILSI Press; 2006. 3. Mertz W. The essential trace elements. Science. 1981;213: 1332–8. 4. FAO/WHO Joint Expert Consultation: Human Vitamin and Mineral Requirements. March 12, 2002. Available at ftp://ftp.fao.org/es/esn/ nutrition/Vitrni/vitrni.html. 5. National Research Council, Food and Nutrition Board. Recommended Dietary Allowances, 10th ed. Washington, DC: National Academy Press: 1989. 6. Beaton GH. Uses and limits of the use of the recommended dietary allowances for evaluating dietary intake. Am J Clin Nutr. 1985;41: 155–64. 7. Beaton GH. Statistical approaches to establish mineral element recommendations. J Nutr. 1996;126:2320S–8S. 8. Center for Science in the Public Interest. Salt, The Forgotten Killer. February 2005. Available at www.cspinet.org. 9. Nestle M. Food Politics: How the Food Industry Influences Nutrition and Health. Berkeley: University of California Press; rev. ed., 2007. 10. FAO. The State of Food Insecurity in the World. 2004. Available at www.fao.org. 11. Shapouri S, Rosen S. Food Security Assessment. USDA/ERSGFA-15. May 2004. Available at www.ers.usda.gov/publications/gfa15. 12. Action Against Hunger. The Geopolitics of Hunger, 2000–2001. Boulder, CO: Lynne Rienner; 2001. 13. UNICEF. The State of the World’s Children. 2005. Available at www.unicef.org/sowc05. 14. Grandesso F, Sanderson F, Kruijt J, et al. Mortality and malnutrition among populations living in South Darfur, Sudan. JAMA. 2005;293: 1490–4. 15. Nord M. Briefing room: food security in the United States. November 15, 2006. Available at www.ers.usda.gov/Briefing/FoodSecurity. 16. Ezzati M, Lopez AD, Rodgers A, et al. Selected major risk factors and global and regional burden of disease. Lancet. 2002;360: 1347–60. 17. Black RE, Morris SS, Bryce J. Where and why are 10 million children dying every year? Lancet. 2003;361:2226–34. 18. Leathers HD, Foster P. The World Food Problem: Tackling the Causes of Undernutrition in the Third World, 3rd ed. Boulder, CO: Lynne Rienner; 2004. 19. Ismail S, Immink M, Mazar I, et al. Community-based Food and Nutrition Programmes: What Makes Them Successful? Rome: FAO; 2003. 20. Bartram J, Lewis K, Lenton R, et al. Focusing on improved water and sanitation for health. Lancet. 2005;365:810–2. 21. Ezzatti M, Vander Hoorn S, Rodgers A, et al. Estimates of global and regional potential health gains from reducing multiple major risk factors. Lancet. 2003;362:271–80. 22. WHO/FAO. Diet, Nutrition and the Prevention of Chronic Diseases. Geneva: WHO Technical Report No. 916: 2003. 23. Robertson A, Tirado C, Lobstein T, et al. Food and Health in Europe: A New Basis for Action. WHO Regional Publications, European Series, No. 96: 2004. 24. Caballero B, Popkin BM, eds. The Nutrition Transition: Diet and Disease in the Developing World. Academic Press; 2002. 25. Mokdad AH, Marks JS, Stroup DF, et al. Correction: actual causes of death in the United States, 2000. JAMA. 2005;293:293–4. 26. Mokdad AH, Marks JSA, Stroup DF, et al. Actual causes of death in the United States, 2000. JAMA. 2004;291:1238–45. 27. Lee RD, Nieman DC. Nutritional Assessment, 3rd ed. McGraw-Hill, 2002.

• Replace energy-dense foods of minimal nutritional value (“junk” foods) with fruits and vegetables • Eat smaller portions, fewer snacks • Recognize misleading advertising and health claims

Educate Children • Integrate nutrition education into school curricula • Provide school meals consistent with Dietary Guidelines • Recognize food marketing strategies • Distinguish commercial from educational messages

Health Professionals: Counseling and Practice • Use nutrition in health promotion and disease prevention • Counsel patients about diet, nutrition, and health • Counsel patients to address environmental as well as behavioral determinants of dietary choices • Obtain reimbursement for nutrition counseling and services

Federal Agencies: Regulations and Guidance • Nutrition information readily available at fast-food restaurants • Energy (calorie) labeling on takeout containers • Total energy content labeled on single-serve packages • Enforceable guidelines for health claims on food package labels • Enforceable guidelines for television advertising of foods during children’s viewing hours • More fruits and vegetables for recipients of food assistance • Unambiguous dietary recommendations focused on food choices

Congress: Legislative Actions • Farm subsidies for fruit and vegetable production • Campaign contribution reforms (so legislators can make decisions independent of corporations) • Restrict vending of “junk” foods in schools • Restrict food marketing to children • More comprehensive nutrition monitoring • Mandate and fund research on the nutrient composition of food, dietary intake methods, environmental determinants of food choice, and effective interventions in dietary behavior

effective,83 and similar levels of funding for nutrition education could prove equally successful.92 Public education campaigns that transmit culturally sensitive messages designed to address the needs and attitudes of specific target groups have been applied successfully to promote breastfeeding and other dietary improvements in developing countries, and use of these techniques has shown promise in improving the nutritional status of low-income homemakers, increasing the prevalence of breastfeeding, and improving health and function among the elderly and minority groups.52 As always, education methods that empower community members to determine their own dietary needs and interventions are most likely to be effective. Beyond education, public health strategies must address the environment of food choice. The current environment promotes food overconsumption, especially by young children. Educating the public about personal responsibility in dietary choice is necessary but not sufficient; it also is necessary to provide information to permit informed choices and to make the food environment more conducive to making such choices. The suggestions in Table 72-5, remote from personal choice as they may seem, address such approaches. They point to the need for further research as a basis for program development. More comprehensive information about the nutrient composition of food, dietary intake, the environmental determinants of food choice, and the effects of those determinants on health would establish a more rigorous basis for policies and programs to improve the nutritional health of the population.

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28. Willett W. Nutritional Epidemiology, 2nd ed. Oxford Press, 1998. 29. Select Committee on Nutrition and Human Needs, United States Senate. Dietary Goals for the United States, 2nd ed. 1977. 30. Anderson GH, Black R, Harris S, eds. Dietary guidelines: past experience and new approaches. J Am Diet Assoc. 2003;103 (12, Suppl 2): S1–S59. 31. DHHS and USDA. Dietary Guidelines for Americans, 6th ed. 2005. Available at www.healthierus.gov/dietaryguidelines. 32. Kaput J, Rodriguez RL. Nutritional genomics: the next frontier in the postgenomic era. Physiol Genomics. 2004;16:166–77. 33. Ordovas JM, Mooser V. Nutrigenomics and nutrigenetics. Curr Opinion Lipidol. 2004;15:101–8. 34. Whitfield PD, German AJ, Noble P-JM. Metabolomics: an emerging post-genomic tool for nutrition. Brit J Nutr. 2004;92:549–55. 35. Chadwick R. Nutrigenomics, individualism and public health. Proc Nutr Soc. 2004;63:161–6. 36. Waxman A. The WHO global strategy on diet, physical activity and health: the controversy on sugar. Development. 2004;47(2): 75–82. 37. World Health Assembly. Global strategy on diet, physical activity and health. May 22, 2004. 38. Zarocostas J. WHO waters down draft strategy on diet and health. Lancet. 2004;363:1373. 39. Keys A, Keys M. Eat Well and Stay Well. New york, NY: Doubleday; 1959. 40. Cannon G. Food and Health: The Experts Agree. London: Consumers’ Association; 1992. 41. Consensus Panel. AHA guidelines for primary prevention of cardiovascular disease and stroke. Circulation. 2002;106:388–91. 42. American Cancer Society. Nutrition and physical activities: ACS recommendations for nutrition and physical activity for cancer prevention. Available at www.cancer.org. 43. American Diabetes Association position statement: evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications. J Am Diet Assoc. 2002;102:109–18. 44. National Heart Lung and Blood Institute. Your guide to lowering high blood pressure. Available at www.nhlbi.nih.gov. 45. Painter J, Rah J-H, Lee Y-K. Comparison of international food guide pictorial representations. J Am Diet Assoc. 2002;102:483–9. 46. USDA. Food Guide Pyramid, 1992 (updated 1996). Available at www. cnpp.usda.gov/Publications/MyPyramid/OriginalFoodGuidePyramids/ FGP/FGPPamphlet.pdf. 47. Willett WC, Skerrett PJ. Eat, Drink and Be Healthy: The Harvard Medical School Guide to Healthy Eating. Free Press; 2002. 48. USDA. Steps to a healthier you, 2005. Available at www. mypyramid.gov. 49. Eyre H, Kahn R, Robertson RM, et al. Preventing cancer, cardiovascular disease and diabetes: a common agenda for the American Cancer Society, the American Diabetes Association, and the American Heart Association. CA. 2004;54(4):190–207. 50. Gibney MJ, Margetts BM, Kearney JM, et al. Public Health Nutrition. Blackwell Science; 2004. 51. Nestle M, Jacobson MF. Halting the obesity epidemic. A public health policy approach. Public Health Rep. 2000;115:12–24. 52. WHO and World Bank. Food Policy Options: Preventing and Controlling Nutrition Related Non-Communicable Diseases. Report of a World Health Organization and World Bank Consultation, November 20–21, 2002. 53. Nestle M, Wing R, Birch L, et al. Behavioral and social influences on food choice. Nutr Rev. 1998;56:s50–s64. 54. Harris JM, Kaufman P, Martinez S, et al. The U.S. food marketing system, 2002. USDA Agric Econ Rep No. AER811; August 2002. 55. USDA Economic Research Service. Briefing room: food marketing and price spreads: USDA marketing bill, 2002. Available at www. ers.usda.gov/Briefing/FoodPriceSpreads/bill.

56. USDA. Agriculture Fact Book, 2001–2002. Available at www.usda. gov/factbook. 57. Productscan. Stagnito’s New Products Magazine. December 2004. 58. Turcsik R. Smart cookies. Prog Grocer. May 1, 2004. 59. Linn S. Consuming Kids: The Hostile Takeover of Childhood. New Press; 2004. 60. Schor JB. Born to Buy: The Commercialized Child and the New Consumer Culture. Scribner; 2004. 61. Brown K, Endicott RC, McDonald S, et al. 100 leading advertisers. Ad Age. June 28, 2004. 62. Wansink B. Environmental factors that increase the food intake and consumption volume of unknowing consumers. Annu Rev Nutr. 2004;24:455–79. 63. Institute of Medicine. Preventing Childhood Obesity. National Academies Press; 2005. 64. Pereira MA, Kartashov AI, Ebbeling CB, et al. Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis. Lancet. 2005;365:36–42. 65. Harris J M, Kaufman P, Martinez S, et al. The U.S. Food Marketing System, 2002: Competition, Coordination, and Technological Innovations into the 21st Century. USDA. June 2002. 66. Stewart H, Blisard N, Bhuyan S, et al. The demand for food away from home: full-service or fast food? USDA Ag Econ Rep No. 829; January 2004. 67. McDonald’s. Investor fact sheet. Available at www.mcdonalds.com. 68. Drewnowski A, Barratt-Fornell A. Do healthier diets cost more? Nutr Today. 2004;39(4):161–8. 69. International Food Information Council. How consumers feel about food and nutrition messages, February 2002. Available at http:// ific.org. 70. Glanz K, Rimer BK, Lewis FM, eds. Health Behavior and Health Education: Theory, Practice, and Research, 3rd ed. Jossey-Bass; 2002. 71. Gerrior S, Bente L. Nutrient content of the U.S. food supply, 1909–99: a summary report. USDA Home Econ Res Rep No. 55. USDA; June 2002. 72. Block G. Foods contributing to energy intake in the U.S.: data from NHANES III and NHANES 1999–2000. J Food Comp Anal. 2004;17:439–47. 73. Putman JJ, Allshouse JE. Food Consumption, Prices, and Expenditures, 1970–97. USDA. Stat Bull No. 965; April 1999. 74. Gerrior S, Bente L. Nutrient Content of the U.S. Food Supply, 1909–1997. USDA Home Econ Res Rep No. 54. March 2001. 75. Centers for Disease Control and Prevention. Trends in intake of energy and macronutrients—United States, 1971–2000. MMWR. 2004;53(04):80–82. 76. Leibtag ES, Kaufman PR. Exploring food purchase behavior of lowincome households: how do they economize? USDA/ERS Ag Inform. Bull No. 747-07: June 2003. 77. Marmot M. The Status Syndrome: How Social Standing Affects our Health and Longevity. Times Books; 2004. 78. Marmot M. Social determinants of health inequalities. Lancet. 2005;365:1099–1104. 79. Patterson RE, Pietinen P. Assessment of nutritional status in individuals and populations. In: Gibney M, et al, eds. Public Health Nutrition. Blackwell; 2004:66–82. 80. Thompson FE, Subar AF. Dietary assessment methodology. In: Coulston AM, Rock CL, Monsen ER, eds. Nutrition in the Prevention and Treatment of Disease. San Diego, CA: Academic Press; 2001. 81. USDA: Nutrient Data Laboratory Available at www.nal.usda.gov/ fnic/foodcomp. 82. Institute of Medicine. Dietary Reference Intakes: Applications in Dietary Assessment. National Academies Press; 2000. 83. National Heart, Lung and Blood Institute. National Cholesterol Education Program home page. Available at www.nhlbi.nih.gov/about/ncep.

72 84. Kuczmarski MF, Moshfegh A, Briefel R. Update on nutrition monitoring activities in the United States. J Am Diet Assoc. 1994;94:753–760. 85. Nestle M. National nutrition monitoring policy: the continuing need for legislative intervention. J Nutr Educ. 1990;22:141–4. 86. National Center for Health Statistics. National Health and Nutrition Examination Survey home page. Available at www.cdc.gov/nchs/ about/major/nhanes/datalink.htm#NHANESI. 87. Tippett KS, Enns CW, Moshfegh AJ. Food consumption surveys in the U.S. Department of Agriculture. Nutr Today. 1999;34(1):33–40. 88. Food Surveys Research Group: What we Eat in America. Available at www.barc.usda.gov/bhnrc/foodsurvey/home.htm.

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89. Wotecki CE, Briefel RR, Klein CJ, et al. Nutrition monitoring: summary of a statement from an American Society for Nutritional Sciences Working Group. J Nutr. 2002;132:3782–3. 90. Jelliffe DB, Jelliffe EFP. Community Nutritional Assessment. Oxford; 1989. 91. Poppendieck J. Sweet Charity: Emergency Food and the End of Entitlement. Viking; 1998. 92. Reger B, Wootan MG, Booth-Butterfield S. A comparison of different approaches to promote community-wide dietary change. Am J Prev Med. 2000;18(4):271–5.

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Postmarketing Medication Safety Surveillance: A Current Public Health Issue

73

Mirza I. Rahman • Omar H. Dabbous

With more than 3.6 billion prescriptions being dispensed annually in the United States, it is clear that Americans are using more prescribed medication than at any other time in history.1 In addition, the use of nonprescription medication, including alternative medicines, is growing rapidly. While this increased medication use is due to a variety of reasons, including an aging population, the availability of many more effective drugs for myriad chronic diseases, and the desire to prevent disease, it can lead to unwanted adverse events (AEs), even as they provide great benefit. It has been estimated that AEs cost the health-care system several billion dollars due to excess morbidity and mortality. However, the benefits of pharmaceutical products should not be minimized, as they can save the health-care system billions of dollars by changing the course of disease and disease management (e.g., decreased disability, less surgery, etc.). Medication-related AEs occur frequently and while all of these AEs cannot be prevented, improving processes is the only way to improve quality.2 Unfortunately, health care lags behind other highrisk industries in its attention to ensuring basic safety. There is a need to identify and learn from errors through mandatory reporting efforts. The Institute of Medicine has called for a nationwide mandatory reporting system to be established, and the data received should be analyzed to identify safety issues that require a broad-based response.2 From 2000–2005, there were 11 drug withdrawals for safety reasons in the United States.3 The regulatory agency that is responsible for postmarketing safety surveillance (PMSS) in America is the Food and Drug Administration (FDA). As such, the FDA reviews reports of adverse drug reactions from studies and from PMSS reports. While the FDA has the authority to withdraw the approval of a drug, in all of these cases, the drug’s sponsor voluntarily withdrew the drug from the market. However, the FDA has been criticized for not acting quickly enough on evidence it obtained, and informing physicians and patients about safety issues concerning some of these drugs that were subsequently withdrawn from the market.4 Because no drug is absolutely safe—there is always some risk of an adverse reaction— the FDA’s approval of a drug for marketing is contingent on its continued assessment of that drug’s risks and benefits.4 This chapter will review the current U.S. PMSS process, describe the MedWatch program, and discuss the types of AEs that exist along with their reporting requirements. It will also show how AE reporting, along with analysis of those case reports, utilizing

techniques such as data mining, can lead to signal detection and drug withdrawals as necessary, to protect the public health.

Safety Surveillance PMSS is the process for monitoring all marketed pharmaceuticals and medical devices to ensure timely identification, evaluation, and communication of any new or unexpected adverse reactions or safety concerns.5 It is done to promote and protect the public health, to identify early signs of safety problems, to supplement data from premarketing trials, and to ensure regulatory compliance. It is required as soon as a drug is marketed and for as long as it is being marketed. Moreover, special PMSS studies may be required as a condition of marketing approval.5 When discussing PMSS, some definitions of the terms used might be helpful. An AE is defined as an untoward medical occurrence, though not necessarily causal. An adverse drug reaction (ADR) is defined as an untoward medical occurrence caused by a drug. A signal highlights a possible causal relationship between an AE and a drug and requires further investigation.5 The regulations that govern PMSS in America are: • 21 CFR 314.80: Postmarketing reporting of adverse experiences for drugs. • 21 CFR 600.80: Postmarketing reporting of adverse experiences for biologics. While there is clearly regulatory interest and more focus on serious AEs (see Fig. 73-1) and those that occur with greater frequency (see Fig. 73-2), all AEs that may pose a risk to patients are of concern.6,7 However, the current Adverse Event Reporting System (AERS) is a passive, spontaneous, postmarketing safety surveillance system. It is voluntary, except for pharmaceutical manufacturers, which are mandated to report to the FDA any AE that is reported to them. This factor, combined with reluctance of health-care professionals to report AEs due to concerns regarding malpractice litigation or follow-up paperwork, too often leads to AEs not being reported. Regulatory agencies, pharmaceutical manufacturers, health-care professionals, and consumers all participate in the PMSS process. The PMSS mission is to implement the systematic review of spontaneous postmarketing data for proactive risk identification, assessment, and quantification, to help ensure safe use of a drug. 1205

Copyright © 2008 by The McGraw-Hill Companies, Inc. Click here for terms of use.

1206

Noncommunicable and Chronic Disabling Conditions

Any adverse experience occurring at any dose that results in any of the following outcomes: 1. Death 2. Life-threatening adverse experience 3. Inpatient hospitalization or prolongation of existing hospitalization 4. A persistent or significant disability/incapacity 5. A congenital anomaly/birth defect 6. An important other medical event (that may not result in death, be life-threatening, or require hospitalization may be considered a serious adverse experience when, based upon appropriate medical judgment, may jeopardize the patient or subject and may require medical or surgical intervention to prevent one of the outcomes listed in this definition) Figure 73-1. Serious adverse events.6

In general, signal generation is done using clinical trials data, the medical literature, knowledge of class effects, and spontaneous reports. There are numerous challenges with spontaneous reports databases, including the fact that they are numerator based, that they are subject to many reporting biases, that they can be hard to place in population context, that they are clearly dependent on coding practices, and given the extensiveness and complexity of the coding dictionary, there can be a dilution of the signal. Additionally, spontaneous PMSS databases were developed for regulatory reporting, and as such, differences that exist with national reporting requirements can alter the type, frequency, and number of PMSS reports that get entered into a database. Also, different companies may interpret the regulations differently, resulting in differential reporting of AEs. Furthermore, changes take place over time with respect to dictionary coding versions, with reporting standards, and with product labeling. Data migration may cause sufficient changes to take place so that data conversion and legacy data can be lost. Moreover, causality assessment is rarely consistent. There are several factors that affect both the quality and quantity of postmarketing reports. This is sometimes referred to as the “Weber effect,” where a newly introduced drug results in a peak in postmarketing reports during the second year of being marketed.8 Additionally, if a drug is the first in its class, as opposed to being the second or third drug in a class to be marketed, there can be higher reporting rates of postmarketing safety surveillance reports. Furthermore, items such as publicity, whether it is from a regulatory action such as a “Dear Doctor Letter,” litigation, or coverage in the media, can all result in increased postmarketing reports. In addition, some countries, including the United States, allow for consumers to report AEs, whereas other countries only allow health-care professionals to make such AE reports. This can result in higher numbers of reports, though the information that is received may not be completely valuable or beneficial when searching for safety signals. Consumer reports can also be increased as a result of direct consumer advertising, especially when consumer hotlines are published. There are two key approaches to safety surveillance within spontaneous-report databases. Intra-product signaling seeks to identify changes in the overall AE pattern for specific products over time. This monitors selected AEs for a specific product over time to determine changes in the frequency and severity of AE reports. The other type of approach is the inter-product signaling which compares a specific product with all products in the database. This inter-product signaling is called data mining and essentially it determines

Very common Common (frequent) Uncommon (infrequent) Rare Very rare

≥1/10 (≥10%) ≥1/100 and <1/10 (≥1% and <10%) ≥1/1,000 and <1/100 (≥0.1% and <1%) ≥1/10,000 and <1/1,000 (≥0.01% and <0.1%) <1/10,000(<0.01%)

Figure 73-2. Frequency of adverse events.7

a disproportionality score to detect drug-event combinations that are distinct or stand out from the background rate. Both approaches should be used to systematically screen large data sets to identify and analyze drug-event associations. These are, however, hypothesis-generating approaches, to search for new, preventable, serious AEs with potential public health importance. In addition, the surveillance program should be set up to evaluate new and emerging safety signals. Thus, it is clear that the safety surveillance process is an iterative one, which the FDA issued Guidance documents about in 2005.9,10,11 PMSS should evaluate multiple data sources, whether screening large regulatory databases, looking at company databases, or looking at drug-lot-related AEs for manufacturing problems. The surveillance process screens the data using both the intra-product and the interproduct methods. The object is to identify safety signals for further review, to develop a case definition, to compile a case series, and then to characterize that case series. Subsequently, to help further characterize identified safety signals, data mining (see below) can be used to evaluate reporting rates with statistical measures of disproportionality. Additionally, targeted pharmacoepidemiologic studies, whether cohort, case-control, or other study designs, can be used to assess the risk attributed to a drug exposure. Some pharmacoepidemiologic studies can allow for the estimation of the relative risk of an outcome associated with a product and may also allow estimates of an AE incidence rate. Furthermore, surveys of health-care professionals along with the creation of patient registries can help in the evaluation of safety signals. A registry is “an organized system for the collection, storage, retrieval, analysis, and dissemination of information on individual persons exposed to a specific medical intervention who have either a particular disease, a condition (e.g., a risk factor) that predisposes [them] to the occurrence of a health-related event, or prior exposure to substances (or circumstances) known or suspected to cause adverse health effects.”10 Finally, in some circumstances, additional controlled clinical trials may be required to establish whether or not an identified safety signal is a true safety risk.

MedWatch MedWatch is the FDA’s safety information and adverse event reporting program that has been operational since 1993. Its primary risk communication tool is its website: http://www.fda.gov/medwatch/ index.html. MedWatch serves both health-care professionals and the medical product-using public. Medical product safety alerts, recalls, withdrawals, and important labeling changes that may affect the health of all Americans can be quickly disseminated to the medical community and the general public via the MedWatch website, thereby improving patient care. In part, MedWatch was designed to educate health professionals about the critical importance of (1) being aware of, (2) monitoring for, and (3) reporting AEs and problems to the FDA and/or the manufacturer. MedWatch allows health-care professionals and consumers to report serious problems that they suspect are associated with the drugs and medical devices they prescribe, dispense, or use. Reporting can be done online, by phone, or by submitting a MedWatch 3500 form by mail or fax. The main purpose of the MedWatch program is to enhance the effectiveness of postmarketing surveillance of medical products as they are used in clinical practice and to rapidly identify significant health hazards associated with these products. Its four goals are to (a) make it easier for health-care providers to report serious events, (b) make it clearer to health- care providers what types of AEs the FDA is interested in receiving, (c) more widely disseminate information on the FDA’s actions that have resulted from AE and product problem reporting, and (d) increase health-care providers’ understanding and awareness of drug- and device-induced disease. Thus, despite AERS being a passive, spontaneous, postmarketing safety surveillance system, health-care professionals should report AEs associated with pharmaceutical products (and are required to do so for AEs associated with biologics), as this can lead to the discovery of new safety signals. The voluntary reporting form (3500) is shown in Fig. 73-3.

73

Postmarketing Medication Safety Surveillance: A Current Public Health Issue

1207

Figure 73-3. U.S. Food and Drug Administration. MedWatch, the FDA Safety Information and Adverse Event Reporting Program. For voluntary reporting of adverse events, product problems, and product use errors. http://www.fda.gov/medwatch/index.html

1208

Noncommunicable and Chronic Disabling Conditions

Known side effects Unavoidable

Avoidable

Medication errors

Product quality defects

Preventable adverse events

Remaining uncertainties Injury or death

• Unexpected side effects • Unstudied uses • Unstudied populations

Figure 73-4. Sources of risk from drug products. (Source: CDER 2005 Report to the Nation.)

Adverse Events As stated above, an AE is considered to be associated with the use of a drug in humans, whether or not it is drug-related. There are two types of AEs, Type A and Type B. While usually less serious, Type A reactions are more common, can usually be predicted, frequently are a consequence of an exaggerated pharmacologically mediated reaction, and they are dose dependent. The more serious, less frequent, Type B reactions are unpredictable and thus are often referred to as idiosyncratic or bizarre reactions. PMSS is designed to discover new Type B reactions, as the Type A reactions are usually well described from clinical trial experience. In Fig. 73-4, which describes the various sources of risk from drug products, PMSS is used to try and discern new safety signals that are described as unexpected side effects, meaning that they are not described on the label. The FDA prides itself on protecting consumers and promoting public health. It is one of the nation’s oldest and most respected consumer protection agencies. In 1906, Congress passed the Food and Drugs Act, which was the first nationwide consumer protection law.12 This act made it illegal to distribute misbranded or adulterated foods, drinks, and drugs across state lines. Over the past century, the FDA’s mission has been to promote and protect the public health by helping safe and effective products reach the market in a timely way, while monitoring products for continued safety after they are in use, and helping to get the public accurate, science-based information needed to improve health.12 Central to the FDA’s regulatory activities is deciding, based on available scientific evidence, whether a new product’s benefits to users will outweigh its risks. Since no regulated product is totally risk-free, these judgments are important. The FDA will allow a product to present more of a risk when its potential benefit is great—especially for products used to treat serious, life-threatening conditions. However, medical products need to be proven safe and effective before patients can use them. As the initial testing of products is based on a relatively small number of users, and because variations in quality can occur in manufacturing, the FDA keeps careful watch on reports of AEs with products after they are marketed. The agency currently receives more than 460,000 AE reports a year, including more than 25,000 submitted directly from individuals through the MedWatch program.3 As shown in Table 73-1 and Fig. 73-5 below, the number of AE reports to the TABLE 73-1. ADVERSE EVENTS REPORTED IN 2005 Number 25,325 213,537 84,770 140,436 464,068

Type MedWatch 15-day reports— serious unlabeled Serious labeled Nonserious labeled All

Reporter

%

Directly from individuals Manufacturer

5 47

Manufacturer Manufacturer All

18 30 100

FDA has nearly tripled in the last decade.3 Additionally, about 95% of all AE reports come from pharmaceutical manufacturers, with nearly half of all AE reports being serious, unlabeled reports, which must be sent to the FDA within 15 days of a manufacturer learning of the AE.3 If this monitoring turns up a problem that needs to be corrected, the FDA can ask the manufacturer to recall the product, withdraw approval (of a drug, for example), require labeling changes, or send warning letters to physicians and other health practitioners. It is this PMSS that enhances the FDA’s ability to identify and correct risks from medical products that emerge after they are marketed. All health-care professionals (HCPs) need to be confident about the positive benefit-risk assessment of the products they prescribe. As such, they need to be cognizant of the benefits of those products as well as be made aware as soon as possible about the various safety issues that are discovered with more widespread use of such products. It is only following regulatory approval and widespread marketing that rare AEs associated with a product will be recognized. This can lead to a situation where a safety issue is not discovered or there is a delay in uncovering a new safety signal. As shown in Table 73-2, 11 drugs have been withdrawn from the U.S. market since 2000 due to safety concerns generated in part by a review of cumulative PMSS data.3 Thus, it is incumbent upon all HCPs to report AEs, either to the manufacturers or to the appropriate regulatory authority in their countries. Within the medical environment related to the prescription of pharmaceutical products, risk management is a process of reducing the risks of a product and increasing its benefits in order to optimize that product’s benefit-risk ratio. The FDA views risk management as an iterative process encompassing the assessment of risks and benefits, the minimization of risks, and the maximization of benefits.9 Specifically, risk management is an iterative process of (a) assessing a product’s benefit-risk balance, (b) developing and implementing tools to minimize its risks while preserving its benefits, (c) evaluating tool effectiveness and reassessing the benefit-risk balance, and (d) making adjustments, as appropriate, to the risk-minimization tools to further improve the benefit-risk balance.9 This four-part process should be continuous throughout a product’s lifecycle, with the results of risk assessment informing the sponsor’s decisions regarding risk minimization.9 Regulatory agencies and pharmaceutical companies practice risk management globally; an example is the following case study.

Case Study 1. Rotavirus Vaccines and Intussusception In August 1998, RotaShield vaccine was licensed for the prevention of rotavirus gastroenteritis in the United States.13 However, clinical trials had demonstrated an increased risk (though not statistically significant) of intussusception in patients receiving the vaccine. Subsequently, as part of the postmarketing surveillance program, the Centers for Disease Control and Prevention (CDC) instituted a special watch for reports of intussusception to the Vaccine Adverse Experience Reporting System (VAERS) database. By June 1999, with cases of intussusception increasingly being associated with use of the vaccine, the CDC recommended suspending the use of RotaShield. An analysis of the cases demonstrated that there was a more than 20-fold increase in the incidence of intussusception shortly after administration of the first dose of the vaccine compared to unvaccinated infants.13 Based on a risk-benefit analysis regarding the use of this vaccine in the United States, the recommendation for universal vaccination in the United States with RotaShield was rescinded. One consequence of this decision was that, owing to local concerns about using a vaccine withdrawn from the U.S. market, even if the risk-benefit equation in the developing world substantially favored its use, this vaccine was removed from the market.14 The manufacturer later ceased production of RotaShield. In February 2006, the RotaTeq vaccine was licensed for the prevention of rotavirus gastroenteritis in the United States.15 This approval was only garnered after the completion of clinical trials

73

Postmarketing Medication Safety Surveillance: A Current Public Health Issue

500,000

1209

464,068 423,031 370,898

Number

322,691 278,266 285,107 266,978 247,607

250,000

212,978 191,865 156,477

0 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 Calendar year Direct (MedWatch)

15-day

Periodic

Nonserious periodic

involving >70,000 infants looking at a primary safety outcome of cases of intussusception occurring. Within 42 days of any dose, there were six cases among RotaTeq recipients and five cases among placebo recipients. The data did not suggest an increased risk of intussusception relative to placebo.16,17 However, the manufacturer of RotaTeq has committed to conducting another study after licensure of approximately 44,000 children, and the CDC will also conduct a large study in its Vaccine Safety Datalink Project (VSD), which evaluates vaccine safety among approximately 80,000 U.S. infants every year.16,17 In addition, for the first three years of licensure, the manufacturer will report cases of intussusception to FDA within 15 days of receiving them, and all other serious side effects on a monthly basis. The FDA and CDC will be closely monitoring the VAERS for any reports of intussusception. Although there is no evidence to date that RotaTeq causes intussusception, this aggressive post-licensure monitoring should enhance the FDA’s ability to detect this risk.16,17

Data Mining Data mining has been defined as “The nontrivial extraction of implicit, previously unknown, and potentially useful information from data.”18 However, an easier way to grasp the concept of data mining is to think

Figure 73-5. Post-Marketing Adverse Event Reports. (Source: CDER 2005 Report to the Nation.)

of it as a process that uses automated, analytic tools to search large databases, in order to discern useful information. The goal of data mining is to simplify the process for sorting through vast amounts of data to generate valuable and actionable information in support of a business proposition. Given the large volume of data that is collected in a variety of industries and the speed with which it is being accumulated, digging through those databases to get to the kernels of knowledge may be impossible if done manually. The development of powerful computers, along with software that contains data-mining algorithms, provide individuals with an additional tool to better do their job. Before any data-mining algorithms or models are used on a database, it is important to first make sure that the data have been collected appropriately and that they have been organized and checked for accuracy. Subsequently, there is a choice from among multiple data-mining methods that can be used. Among these are the MultiItem Gamma Poisson Shrinker (MGPS) algorithm, which generates an Empirical Bayesian Geometric Mean (EBGM) score (see Table 73-3), the Proportional Reporting Ratio (PRR) method, and the Bayesian Neural Network approach.19, 20, 21 Both the MGPS and PRR methods will generate similar drug-event combinations for further investigation when the observed number of cases with the drug-event combination is >20 or the expected number of cases with the drug-event combination is <1.22

TABLE 73-2. RECENT SAFETY-BASED NEW MOLECULAR ENTITY WITHDRAWALS3

Drug Name Cisapride Troglitazone Alosetron

Year Approved & Withdrawn

Cerivastatin

1993/2000 1997/2000 2000/2000 (Remarketed in 2002 with restricted distribution) 1997/2001

Rapacuronium

1999/2001

Etretinate Levomethadyl Rofecoxib Valdecoxib Natalizumab

1986/2002 1993/2003 1999/2004 2001/2005 2004/2005 (Remarketed in 2006 with restricted distribution) 1975/2005

Pemoline

Approved Use

Reason Withdrawn

Heartburn Diabetes Irritable bowel syndrome

Fatal arrhythmia Liver toxicity Ischemic colitis/ severe constipation

Cholesterol reduction Anesthetic Psoriasis Opiate dependence Pain relief Pain relief Multiple sclerosis

Muscle damage and kidney failure Severe breathing difficulty Birth defects Fatal arrhythmia Heart attack/stroke Skin disease Brain infection

ADHD

Liver failure

1210

Noncommunicable and Chronic Disabling Conditions TABLE 73-3. EMPIRICAL BAYESIAN GEOMETRIC MEAN (EBGM) TERMS • “N” is the observed number of cases with the combination of items. • “E” is the expected number of cases with the combination. Calculated as: E

Observed # cases with DRUG —————————————— Total # cases RR

EBGM EB05 EB95 90% CI

×

Observed # cases with EVENT ——————————————— × Total # cases

Total # cases

Relative Reporting Ratio. (The same as N/E.) Observed number of cases with the combination divided by the expected number of cases with the combination. This may be viewed as a sampling estimate of the true value of observed/expected for the particular combination of drug and event. Empirical Bayesian Geometric Mean. A more stable estimate than RR; the so-called “shrinkage” estimate. A value such that there is less than a 5% probability that the true value of observed/expected lies below it. A value such that there is less than a 5% probability that the true value of observed/expected lies above it. The interval from EB05 to EB95 may be considered to be the “90% confidence interval.”

Data from the WebVDME User Guide.23

EBGM is a statistical measure of disproportionality, comparing the observed and expected reporting frequency within a database. The determination of the expected reporting frequency assumes complete independence of cases associated with either a drug or an event.23 Thus, in a hypothetical database of 100 cases, if Drug Z represented 20 cases in the database and there were 10 cases of hepatic failure, the expected reporting frequency would be 20/100 (probability of Drug Z) × 10/100 (probability of hepatic failure) × 100 cases (total database size) 2 expected cases. If the observed number of drug-event cases was 8, then the relative reporting ratio (RR) would be 8/2 (N/E) 4 and the EBGM would be about 4, depending on the amount of “shrinkage” that occurs based on the model. The larger the number of AE reports for a particular drug (for a drug that has been on the market for a long time and may have a lot of AE reports in the database) and/or the larger the number of cases of a particular AE (a common AE), the larger the expected “E” will be. The larger the “E,” the smaller the EBGM. A new drug or a very rare AE would represent lower proportions of the total database and thus the expected “E” would be lower. Data mining is used in the review of safety surveillance data to detect strong, consistent associations that occur at higher than expected frequencies. Data mining usually uses AE safety databases that lack denominator data. It detects frequency of drug-event combinations in postmarketing reports. It also determines the relative frequency of drug-event combinations for drug X relative to any other drug. Data mining attempts to quantify the strength of a potential drug-event association, whereas signal scores are calculated and represent the relative reporting rate for AEs.10,22 It is important to stress that an elevated-signal score is a measure of statistical association and not a causal association between an AE and a drug. Data mining does not equal “data dredging.” It is a systematic screening for drug-event combinations that are being reported disproportionately. It is essentially a quantitative signal detection method. The data-mining method that is currently being used widely in the United States, by both the FDA and the pharmaceutical industry, is the MGPS, which adjusts for the multiplicity of drugs and events per record.22 The MGPS generates an EBGM, which is an estimate of the relative reporting ratio. It is the ratio of the observed over the expected counts. A 90% confidence interval is calculated around the EBGM. Both of the FDA’s postmarketing safety surveillance databases, the AERS and the VAERS, are used in safety signaling and data mining, along with the World Health Organization’s AE database. The FDA’s databases contain all U.S. reports along with serious, unlabeled reports from outside the United States. The WHO database contains reports from more than 65 national authorities, including the FDA’s database.

The FDA’s Spontaneous Reporting System (SRS) was in operation from 1968 to October 1997. The reports were transitioned to the AERS, which has been used from October 1997 to the present. A publicly released version can be purchased on a quarterly basis. It is a passive surveillance system wherein direct volunteer reporting accounts for about 5% of reports received. Ninety-five percent of reports in the FDA’s postmarketing safety surveillance database come from pharmaceutical companies, as they are mandated by regulations to report AEs that they receive. The combined SRS AERS database currently contains more than 2.7 million reports and is growing rapidly, adding 460,000 reports annually. The number of reports has nearly tripled in the last 10 years, and because the FDA is interested in serious, unlabeled reports, these have grown as a percentage of the total number of reports submitted to the FDA. Some of the limitations of the FDA’s AERS database are a substantial lag time, substantial underreporting, and increased reports as a result of stimulated reporting. Additionally, there can be biased reporting due to a number of factors, such as publicity and regulatory letters, and because of the differential interpretation of the reporting regulations, reports may differ by country and company. Additionally, duplication, quoting errors, variable historical data, poor quality of information, and changes over time are all limitations to information recorded in the AERS database. The data-mining output is similar to the safety surveillance output in that hypotheses are generated and these may need to be evaluated with additional quantitative analyses as appropriate using industrial databases, stimulated reporting, enhanced surveillance, or the conduct of new epidemiological studies. An example of data mining is given in Case Study 2.

Case Study 2. Hepatic Failure and Thiazolidinediones INTRODUCTION

In this case example, the FDA’s SRS AERS database, through the end of the third quarter 2005, was data mined to determine the lower 95% confidence interval limit of the Empirical Bayesian Geometric Mean scores (denoted as EB05), a measure of disproportionality, for hepatic failure associated with the use of thiazolidinediones. The drugs of interest were pioglitazone, rosiglitazone, and troglitazone. The event of interest was hepatic failure.

EB05 Guideline A guideline that has been used for identifying a signal score for pair-wise combinations as higher-than-expected is an EB05 ≥2.

73

Postmarketing Medication Safety Surveillance: A Current Public Health Issue

Hepatic failure

0

100

200

300

400

500

N

5

38

0 ≤ EB05 ≤ 1 < EB05 ≤ 2 < EB05 ≤ 4 < EB05 ≤ 8 < EB05 < ∞

[1968–85]–[2005]

63

[1968–85]–[2004]

Pioglitazone

[1968–85]–[2003]

Troglitazone

102

195

285 427

430 433 434

Pioglitazone

13

24

38

49

56

63

Rosiglitazone

11

36

47

88

122

135

434 135

[1968–85]–[2002]

Troglitazone

[1968–85]–[2001]

[1968–85]–[2000]

[1968–85]–[1998]

[1968–85]–[1999]

Association

[1968–85]–[1997]

Hepatic failure

Item

Rosiglitazone

1211

0 ≤ EB05 ≤ 1 < EB05 ≤ 2 < EB05 ≤ 4 < EB05 ≤ 8 < EB05 < ∞

Figure 73-6. The number of cases of hepatic failure in the AERS database associated with the thiazolidinediones.

Figure 73-8. The cumulative annual number of cases of hepatic failure in the AERS database associated with the thiazolidinediones.

This criterion ensures with a high degree of confidence that, regardless of count size, the particular drug-event combination is being reported at least twice as often as it would be if there were no association between the drug and the event.22

Data Source This report contains the most currently available, cumulative data from the FDA’s SRS AERS database, through the end of the third quarter of 2005. This database contains approximately 2.7 million patient records. It includes branded and generic prescription products that are marketed in the United States. The database contains both U.S. reports (including consumer reports) and a subset of non-U.S. reports (AEs that are both serious and unexpected, that is, not contained in the U.S. package insert). All data were retrieved utilizing Lincoln Technologies WebVDME 5.2, which is a data-mining application used in PMSS to support product risk management. Unless specified, individual case reports were not specifically checked for duplicate reporting. However, the vendor does implement an algorithm to screen the database for duplicates as part of standard data cleansing. Searches were conducted based on “drug mentions within a report.” This means that all case reports where the selected drug is classified as either a concomitant or suspect drug are included.

Data Output Figures 73-6 through 74-9 show the frequency and EB05 scores, both total and cumulative by year, of hepatic failure associated with the use of the thiazolidinediones. AEs in the FDA database are codified using

Hepatic failure Item 13.093

Troglitazone Rosiglitazone

1.877

the MedDRA dictionary. It is important to note that a single case report may contain more than one preferred term. The color of the bar represents a measure of disproportionality, that is, “how disproportionate” the observed report frequency of the AE-drug combination is compared to what might be expected, if all AE-drug combinations in the database were independent. The color scale ranges from a light grey, which represents low disproportionality (that is, the observed frequency is not substantially different from the expected) while the darker grey represents AE-drug combinations with higher measures of disproportionality.

Interpretation These figures demonstrate the increased frequency and EB05 scores, both total and cumulative by year, of hepatic failure associated with the use of the troglitazone. While all the thiazolidinediones are associated with reports of hepatic failure, and this is a well-recognized AE associated with the use of thiazolidinediones, both the frequency (434) and the EB05 (13.09) noted with troglitazone were significantly higher than those of the other thiazolidinediones. This suggested an association between troglitazone and hepatic failure that required further investigation, with possible regulatory action.

Withdrawal An evaluation of the FDA’s SRS AERS database, through the end of the third quarter of 2005, showed that the frequency of reports and EB05 scores were significantly higher for hepatic failure associated with the use of troglitazone, compared to the other thiazolidinediones. However, even based on the information available back in March 2000, the FDA announced that troglitazone, which was approved in January 1997, was being voluntarily withdrawn from the U.S. market by its manufacturer because of reports of hepatotoxicity.

1.219

Pioglitazone 0

5

10

15

EB05 0 ≤ EB05 ≤ 1 < EB05 ≤ 2 < EB05 ≤ 4 < EB05 ≤ 8 < EB05 < ∞

Figure 73-7. The disproportionality score (EB05) of cases of hepatic failure in the AERS database associated with the thiazolidinediones.

SUMMARY

PMSS uses both intraproduct and inter-product signaling to detect and evaluate new safety signals. The object is to identify safety signals for further review, to develop a case definition, to compile a case series, and then to characterize that case series. Inter-product signaling, also called data mining, does not supplant traditional safety surveillance methods. Instead, it supplements these methods and allows a systematic identification and evaluation of potential safety signals.

1212

Noncommunicable and Chronic Disabling Conditions

2.602

4.91

7.82

9.782

13.035

Pioglitazone

0.829

0.969

1.126

Rosiglitazone

0.73

1.125

1.038

[1968–85]–[2005]

[1968–85]–[2002]

0.737

[1968–85]–[2004]

[1968–85]–[2001]

Troglitazone

[1968–85]–[2003]

[1968–85]–[2000]

[1968–85]–[1998]

[1968–85]–[1999]

Association

[1968–85]–[1997]

Hepatic failure

13.023

13.086

13.086

1.21

1.217

1.935

1.872

1.233 1.684

0 ≤ EB05 ≤ 1 < EB05 ≤ 2 < EB05 ≤ 4 < EB05 ≤ 8 < EB05 < ∞

Figure 73-9. The cumulative annual disproportionality score (EB05) of cases of hepatic failure in the AERS database associated with the thiazolidinediones.

The interpretation of data-mining results needs the expertise of safety reviewers and medical officers to analyze and interpret the data appropriately. Data-mining signals by themselves are not indicators of problems, but are indicators of possible problems. Moreover, caution must be exercised with any comparison of disproportionality ratios across different products, for example, comparison with competitor drugs, because of the various limitations that exist when making these kinds of comparisons. Additionally, pharmacoepidemiologic studies, whether cohort, case-control, or other study designs, can be used to assess the risk attributed to a drug exposure. Furthermore, the creation of registries along with surveys of health-care professionals can help in the evaluation of safety signals. In some circumstances, additional controlled clinical trials may be required to establish whether or not an identified safety signal is a true safety risk. Finally, all safety signals should be evaluated recognizing the possibility of false positives. In addition, the absence of a signal does not mean that a problem does not exist.

REFERENCES

1. IMS Health. U.S. Prescription Activity by Channel, 2005. National Prescription Audit Plus, 1/2006 . Available at http://www.imshealth. com/ims/portal/front/articleC/0,2777,6599_73914140_77266142,00. html. Accessed on Sept 15, 2006. 2. Kohn LT, Corrigan JM, Donaldson MS. To Err is Human. Washington DC: National Academy Press; 2000. 3. FDA. CDER 2005 Report to the Nation: Improving Public Health Through Human Drugs. Rockville, MD. 2006. Available at http://www.fda.gov/cder/reports/rtn/2005/rtn2005.pdf. Accessed on Sept 15, 2006. 4. GAO. Drug Safety: Improvement Needed in FDA’s Postmarket Decision-making and Oversight Process. Washington, DC: U.S. GAO; 2006. 5. Talbot J, Waller P. Stephens’ Detection of New Adverse Drug Reactions. West Sussex: John Wiley & Sons; 2004. 6. 21 CFR, § 314.80. http://www.access.gpo.gov/nara/cfr/ waisidx_00/ 21cfr314_ 00.html. Accessed on Sept 15, 2006. 7. CIOMS Working Group V. Current Challenges in Pharmacovigilance: Pragmatic Approaches. Geneva: CIOMS; 2001. 8. Weber, JCP. Epidemiology of adverse reactions to nonsteroidal antiinflammatory drugs. Adv Inflam Res. 1984;6:1–7

9. FDA. Guidance for Industry: Development and Use of Risk Minimization Action Plans. 2005. Available at: http://www.fda.gov/ cder/guidance/6358fnl.pdf. Accessed on Sept 15, 2006. 10. FDA. Guidance for Industry: Good Pharmacovigilance Practices and Pharmacoepidemiologic Assessment. 2005. Available at: http:// www.fda.gov/ cder/guidance/6359OCC.pdf. Accessed on Sept 15, 2006. 11. FDA. Guidance for Industry: E2E Pharmacovigilance Planning. 2005. http://www.fda.gov/cder/guidance/6355fnl.pdf. Accessed on Sept 15, 2006. 12. FDA. Office of Public Affairs: An FDA Overview: Protecting Consumers, Protecting Public Health. 2004. Available at http://www. fda.gov/oc/opacom/fda101/fda101text.html. Accessed on Sept 15, 2006. 13. CDC. Intussusception among recipients of rotavirus vaccine— United States, 1998–1999. MMWR. 1999;48:577–81. 14. Melton L. Lifesaving vaccine caught in an ethical minefield. Lancet. 2000;356:318. 15. Merck & Co., Inc. (2006) RotaTeq Prescribing Information. http:// www.merck.com/product/usa/pi_circulars/r/rotateq/rotateq_pi.pdf 16. Shaw AR. The Rotavirus Vaccine Saga. Annu Rev Med. 2006;57: 167–80. 17. FDA. CBER Product Approval Information-Licensing Action RotaTeq Questions and Answers. 2006. Available at http://www. fda.gov/Cber/products/rotamer020306qa.htm. Accessed on Sept 15, 2006. 18. Frawley W, Piatetsky-Shapiro G, Matheus C. Knowledge discovery in databases: an overview. AI Magazine. 1992;13:57–70. 19. DuMouchel W. Bayesian data mining in large frequency tables, with an application to the FDA Spontaneous Reporting system. Am Stat. 1999;53:177–90. 20. Evans SJ, Waller PC, Davis S. Use of proportional reporting ratios (PRRs) for signal generation from spontaneous adverse drug reaction reports. Pharmacoepidemio Drug Saf. 2001;10:483–6. 21. Bate A, Lindquist M, Edwards IR, et al. Bayesian neural network method for adverse drug reaction signal generation. Eur J Clin Pharmacol. 1998;54:315–21. 22. Szarfman A, Machado SG, O’Neill RT. Use of screening algorithms and computer systems to efficiently signal higher-than-expected combinations of drugs and events in the U.S. FDA’s spontaneous reports database. Drug Saf. 2002;25:381–92. 23. Phase Forward Lincoln Technologies. WebVDME 5.1 User Guide. Waltham, MA: Phase Forward Incorporated; 2006.

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Postmarketing Medication Safety Surveillance: A Current Public Health Issue

SUGGESTED READINGS

Clark JC, Klincewicz SL, Stang PG. Spontaneous adverse event signaling methods: classification and use with health care treatment products. Epidemiologic Rev. 2001;23(2):191–207. Fletcher AJ, Edwards LD, Fox AW, et al. Principles and Practice of Pharmaceutical Medicine. West Sussex: John Wiley & Sons; 2002. Hauben M. A brief primer on automated signal detection. Ann Pharmacother. 2003;37:1117–23. Mann R, Andrews E. Pharmacovigilance. West Sussex: John Wiley & Sons; 2002.

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Meyboom RHB, Lindquist M, Egberts ACG, et al. Signal selection and follow-up in pharmacovigilance. Drug Safety. 2002;25: 459–65. Strom B. Pharmacoepidemiology. West Sussex: John Wiley & Sons; 2002. Yee CL, Klincewicz SL, Knight JF, et al. Practical considerations in developing an automated signaling program within a pharmacovigilance department. Drug Inf J. 2004; 38:293–300 Zanardi LR, Haber P, Mootrey GT, et al. Intussusception among recipients of rotavirus vaccine: reports to the vaccine adverse event reporting system. Pediatrics. 2001;107:E97.

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VI Health-Care Planning, Organization, and Evaluation

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74

The American Health-Care System: Structure and Function Glen P. Mays • F. Douglas Scuthfield

This chapter examines the mechanisms through which health services are organized, financed, and delivered in the United States. Collectively, these mechanisms function as a complex and adaptive system in which purchasers, providers, consumers, and regulators of health services interact in ways that are not always coordinated or expected. These actors and their actions evolve over time in response to each other and to changes in their external environment, including changes in medical knowledge and technology, changes in the political and economic climate, changes in social norms and values, and changes in population health and disease processes. Understanding the major actors within the nation’s health system and the ways in which they interact provides a basis for managing and improving the performance of the system in terms of the accessibility, quality, and cost of health services. HEALTH CARE AS A COMPLEX AND ADAPTIVE SYSTEM

A universal, national system of health insurance and health care does not exist in the United States as it does in many other industrialized countries. This fact often leads observers to conclude that the United States lacks an organized and coordinated health system. Nevertheless, a functioning health system does exist in the United States, one that relies on a combination of governmental action, market forces, and voluntary charitable initiatives to deliver health services to populations in need. Consequently, the U.S. health system operates through the complex and changing interactions of multiple public sector and private sector actors.1 Concepts from general systems theory are useful in understanding the structure and operation of the nation’s complex health system. These concepts stress the importance of identifying the major actors within a system, the resources on which these actors depend, the mechanisms through which these actors interact, and the principal external forces that affect these actors.2 The actors within the nation’s health system can be classified generally as health-care purchasers, providers and other suppliers, consumers, and policy-makers/regulators. The resources used by these actors include funding, personnel, facilities, technology, and information. These resources are organized by providers and suppliers through their interaction with purchasers and policy makers to produce services for consumers. The health system, like all systems, is dynamic with many feedback loops among purchasers, providers, consumers, and policy makers. This allows for continual change within the system and therefore continual change in the system’s performance. Because of the interdependencies among different actors, efforts to modify one component of the system are likely to affect other components. As a consequence, health interventions

and reform efforts may have both direct and indirect effects on the health system, leading to both intended and unintended outcomes. For example, efforts to expand the array of health services covered by private health insurers may have indirect and unintended effects on the number of consumers without health insurance coverage, which in turn may affect the volume of care delivered through hospital emergency departments. The nation’s health system is highly sensitive to the economic, political, social, demographic, and technological environments in which it operates. This external environment heavily influences the structure and operation of the system and its evolution over time. For example, the changing demographic composition of the United States, with an aging population and the growing size of racial and ethnic minority groups, influences the types of services provided by the health system and the geographic location of these services. Changes in the economy also dramatically impact the system, with economic growth and job creation leading to heightened demand for private health insurance and health care while economic decline and job loss leading to shrinkage of the private health insurance market and increased demand for publicly provided insurance and health care. The changing nature of disease and health risk also shapes the health-care system. In the early 1900s the leading causes of death were infectious diseases, many of which were linked to environmental concerns such as water quality, waste disposal, vector control, and food safety. A century later, the major causes of death are largely chronic diseases such as cardiovascular disease, cancer, stroke, and respiratory diseases that affect older populations and are linked to lifestyle issues including nutrition, physical activity, and tobacco use. As a consequence, today’s decision makers in health policy and administration must emphasize interventions that support health behavior change and chronic disease management to address contemporary health issues, unlike the decision makers of previous generations who focused on environmental interventions such as water purification and sewage disposal. Even since the 1950s dramatic changes have occurred in the patterns of disease and illness to which the health system must respond.3 Death rates from cardiovascular disease and stroke have declined while those from many cancers have increased. Overall, reductions in death rates have resulted in increasing longevity, which in itself has generated greater economic and political stress on the health system in programmatic areas such as Medicare, retiree health insurance coverage, and long-term care. The nation’s health system contains a multitude of subsystems that govern different types of health services for different population groups within society. These subsystems include safety-net healthcare systems that serve the uninsured and others who lack access to mainstream medical care providers, the mental health and substance abuse care systems that deliver specialized services to treat populations 1217

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Health-Care Planning, Organization, and Evaluation

with these conditions, and long-term care systems that deliver a variety of health and support services to population groups who are limited in their ability to perform activities of daily living. While these different subsystems are highly interactive and interdependent, the degree of formal coordination across these subsystems varies and is often quite limited. HEALTH SYSTEM PERFORMANCE AND OUTCOMES

From a societal perspective, the universal goal of any health system is to ensure access to high quality health services to all members of society for as little cost as possible. Three key areas of health system performance therefore involve the accessibility, quality, and cost and efficiency of health services produced by the system. A fourth area of performance involves equity within the system, as indicated by the extent to which different population groups within society experience the different levels of accessibility, quality, and cost/efficiency within the system. In practice, these four dimensions of health system performance are highly interdependent. Efforts to increase access to care within the health system may lead to higher costs, while efforts to constrain health-care costs may have adverse effects on access and quality. Efforts to optimize health system performance in all four areas simultaneously have proven exceedingly difficult due to the complex nature of the health system. Historically, actors within the U.S. health system have focused on different elements of health system performance at different points in time. During the 1960s, public concerns about access to care led to the development of new public programs such as Medicare and Medicaid to provide health care for population groups that faced particularly difficult barriers to care, including the elderly, disabled, and poor. The rapid escalation in national health-care spending during the 1970s and 1980s led both policy makers and private purchasers to focus on cost containment during this period, resulting in the increasing use of managed care strategies in both public sector and private sector health insurance programs. Health-care spending slowed during the 1990s, but growing public dissatisfaction with managed care strategies and the limits they place on consumer choice and provider autonomy led to a reduction in the use of these strategies, at least in the private sector. Since the beginning of the twenty-first century, growing public awareness about gaps in the quality of health care has led to an increasing focus on quality improvement strategies in the public and private sectors, with both public programs and private insurers and providers experimenting with new ways of measuring the quality and safety of

health care and creating incentives for providers to improve their adherence to evidence-based standards of care.4 A return to large annual increases in health-care spending has also caused both public and private purchasers to focus again on cost-containment efforts, leading to experimentation with new “consumer-driven” health insurance designs that require consumers to assume more responsibility for balancing issues of cost, choice, and quality when selecting health insurance coverage and health-care providers. Some actors within the health system also have begun to give increased attention to issues of equity and to disparities in health-care accessibility, quality, and cost across racial, ethnic, and socioeconomic subgroups within society.5 While modest progress has been made in some areas, the United States continues to face difficult challenges in improving access, quality, efficiency, and equity within the health system. COMPONENTS OF THE SYSTEM

The next few sections examine the major components of the U.S. health system as defined by the major actors within the system and the resources used by these actors. The major actors profiled here include health-care providers such as hospitals and physician organizations, health-care purchasers including private health insurance arrangements as well as public insurance programs, and major health policy and regulatory bodies that govern various components of the system. In examining the resources used by these different actors, we focus on financial resources as well as the human resources represented within the health profession’s workforce. Although not every component of the system is addressed in detail, we examine the major determinants of health system performance and the key drivers of health system change.

Health-Care Providers Hospitals Hospitals remain the predominant institutional health-care provider in the U.S. health system despite significant changes over time in the organization of care within the hospital and the types of care delivered by these institutions. Hospital-provided health care continues to account for the largest single share of national health-care spending, representing approximately 31% of the nation’s total health-care expenditures in 2003 (Fig. 74-1).6 However, the continued growth of health care delivered in physician offices and other outpatient settings, along with the growing importance of outpatient prescription drugs, has chipped away at the historical pre-eminence of hospitalbased care in recent years.

Other spending 23%

Hospital care 31%

Program administration and net cost 7%

Figure 74-1. National healthcare spending by type of care, 2003. (Source: Centers for Medicare & Medicaid Services, Office of the Actuary, National Health Statistics Group.)

Prescription drugs 11%

Nursing home care 7%

Physician and clinical services 22%

74 Historical Origins. The hospital has not always been a highly regarded component of the health-care system. The hospital had its origins in the religious orders of medieval times that provided care for the poor. In the United States, the earliest hospitals were the almshouses and poor houses, a legacy of the British tradition. These institutions were dark and often unsanitary facilities, unappealing and to be avoided if at all possible. Only people without homes and families received health care in these facilities; anyone of means was cared for in their home by their family. The first modern U.S. hospital was the Pennsylvania Hospital, founded in Philadelphia in 1751. Slowly throughout the 1800s, other large facilities were built, such as the Massachusetts General Hospital in Boston. It was not until the middle 1900s, however, that the modern hospital became a central component of the health-care system. The rise of the contemporary hospital resulted from a number of significant changes in the way medicine was practiced. Advances in surgical technology and practice during the mid- and late 1800s allowed the hospital to become a locus for surgical procedures. The discovery of anesthesia in the 1850s made possible more complicated and lengthy procedures that previously could not be performed because of the pain associated with them. Moreover, the discovery of sepsis and antiseptic techniques during the late 1800s allowed clinicians to understand and reduce the risk of postoperative infection. During this same period, the new science of microbiology ushered in a new understanding of disease and its causes. New technologies to assist in the diagnosis and treatment of patients developed rapidly during this period, including the discovery of the electrocardiograph and the x-ray. The early clinical technologies and laboratories were primitive by today’s standards and were both large and expensive. It made sense to provide a central place, the hospital, where all physicians could have access to these facilities. To this day, the hospital continues to serve as a central repository of advanced technology for the medical community, although increasingly, medical technologies are being distributed to physicians’ offices and other outpatient settings. The development of the nursing profession was critical to the emergence of the modern hospital. Prison inmates often provided what nursing care was available in the hospitals of the early 1800s. During the Crimean War of the 1850s in Europe, Florence Nightingale demonstrated the advantages of professional nursing services on mortality among wounded soldiers. She later developed nurse training programs in Britain, and hospitals in the United States followed suit. The availability of well-trained nursing personnel made hospitals much safer and more effective health-care facilities. Improvements in physician training also facilitated the development of the modern hospital. Before 1900, medical education in the United States was seriously deficient, with most physicians being trained in proprietary apprenticeships that emphasized lectures but little exposure to patient care. The development of professional licensure helped to transform American medical education by requiring licensed physicians to graduate from an approved medical school and pass a standardized examination. American medical schools significantly improved their educational programs in response to Abraham Flexner’s 1910 review of medical education in the United States and Canada. The Flexner Report, which was funded by the Carnegie Foundation at the urging of the American Medical Association, identified features of the most effective medical schools, including (a) requiring students to have college degrees before admittance; (b) using a 4-year curriculum with 2 years devoted to basic sciences and 2 years devoted to full-time clinical instruction; (c) using faculty that are actively engaged in medical research; and (d) educating medical students and medical residents in a teaching hospital that is owned and operated by the university. The Flexner Report and the educational standards it triggered helped to establish academic and teaching hospitals as leading institutions within the nation’s health-care system, while promoting tighter relationships between physicians and hospitals. The proliferation of health insurance during the latter half of the twentieth century also fueled the development of the modern hospital. Advances in hospital-based technology and professional nursing care made hospital stays increasingly costly for patients. Private health

The American Health-Care System: Structure and Function

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insurance emerged during the Great Depression to assist individuals with limited incomes in paying for this care, and it grew rapidly after World War II as an employee benefit. The advent of public insurance programs during the 1960s, especially Medicare and Medicaid, provided additional financial support for hospital services for some populations not covered by employment-based insurance. These public programs also pressed for the development of quality review processes and accreditation programs that could offer the government as well as private purchasers assurance that the facilities receiving their payments were delivering care consistent with accepted standards of care. Accreditation by a recognized body such as the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) soon became a requirement for hospital participation in Medicare. Types of Hospitals. Modern hospitals can be classified by a variety of characteristics including length of stay, type of service, ownership, number of beds, and involvement in medical education and research (Table 74-1). There are short-term and long-term hospitals with the dividing point being an average length of stay of 30 days. Hospitals can also be characterized by type of service, with the most common type of facility being the general hospital that provides a broad array of acute-care services for a broad array of population groups. In contrast to the general hospital, specialty hospitals focus on providing a narrower scope of services for more tightly defined population groups. Children’s hospitals, for example, specialize in delivering care to address the health conditions affecting infants, children, and adolescents, while women’s hospitals focus on providing obstetrical and gynecological care and other services tailored to women’s healthcare needs. Psychiatric hospitals, which specialize in delivering inpatient mental health care, represent one of the oldest forms of specialty hospitals in the United States, although their numbers have declined since the 1960s due to improvements in prescription drug therapies and the efforts of federal and state governments to shift more mental health patients to community-based settings. Specialty hospitals for respiratory diseases and eye diseases also have existed in the United States for many decades. More recently, a variety of other types of specialty hospitals has emerged in the United States in response to the growing demand for specialty care and the lucrative payments that public and private health insurance programs offer for these services. These specialty facilities include heart hospitals that specialize in cardiac services and procedures, orthopedic hospitals that specialize in joint repair and replacement services, and cancer hospitals that specialize in advanced cancer care. Many of these specialty facilities have been developed at least in part by groups of specialty physicians seeking more control over their practice environments and more revenue in the form of facility payments for inpatient care. General hospitals have raised objections to the proliferation of these specialty hospitals, arguing that they skim off only the most profitable patients and hospital services, thereby compromising the ability of general hospitals to deliver equally important but less profitable services such as trauma and burn care and to provide uncompensated care to the uninsured. Specialty hospitals, in turn, argue that they are able to improve quality of care and health outcomes by focusing on the delivery of a narrow scope of services to high volumes of patients with similar conditions. In response to this debate, the U.S. Congress in 2003 placed a moratorium on the approval of new specialty hospitals for participation in the federal Medicare program until the effects of these new facilities on the health-care system can be determined. Nearly a third of the nation’s short-stay hospitals are public facilities owned by federal, state, or local governments. These facilities typically serve population groups that lack access to private hospital care. Federal hospitals serve designated groups of people who are eligible for care based on some type of federal entitlement program. For example, Indian Health Service hospitals serve members of federally recognized tribes, Veterans Affairs hospitals serve defined categories of eligible veterans, and Department of Defense hospitals serve active duty military personnel. By contrast, most state-owned hospitals historically have focused on providing care for

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Health-Care Planning, Organization, and Evaluation TABLE 74-1. U.S. SHORT-STAY HOSPITALS, BEDS, AND OCCUPANCY RATES 1980–2002 Hospital Characteristics

1980

1990

Number of Hospitals All hospitals

6965

6649

Federal hospitals Nonfederal hospitals

359 6606

337 6312

5830 3322 730 1778

Community Nonprofit For profit State-local government 6–24 beds 25–49 beds 50–99 beds 100–199 beds 200–299 beds 300–399 beds 400–499 beds 500 beds or more

Number of Hospital Beds All hospitals Federal Nonfederal Community Nonprofit For profit State-local government 6–24 beds 25–49 beds 50–99 beds 100–199 beds 200–299 beds 300–399 beds 400–499 beds 500 beds or more

Hospital Occupancy Rate* All hospitals Federal Nonfederal Community Nonprofit For profit State-local government 6–24 beds 25–49 beds 50–99 beds 100–199 beds 200–299 beds 300–399 beds 400–499 beds 500 beds or more

2000

2001

2002

5810

5801

5794

245 5565

243 5558

240 5554

5384 3191 749 1444

4915 3003 749 1163

4908 2998 754 1156

4927 3025 766 1136

259 1029 1462 1370 715 412 266 317

226 935 1263 1306 739 408 222 285

288 910 1055 1236 656 341 182 247

281 916 1070 1218 635 348 191 249

321 931 1072 1190 625 358 174 256

1,364,516

1,213,327

983,628

987,440

975,962

117,328 1,247,188

98,255 1,115,072

53,067 930,561

51,900 935,540

49,838 926,124

988,387 692,459 87,033 208,895 4932 37,478 105,278 192,892 172,390 139,434 117,724 218,259

927,360 656,755 101,377 169,228 4427 35,420 90,394 183,867 179,670 138,938 98,833 195,811

823,560 582,988 109,883 130,689 5156 33,333 75,865 175,778 159,807 117,220 80,763 175,638

825,966 585,070 108,718 132,178 4964 33,263 76,924 174,024 154,420 119,753 84,745 177,873

820,653 582,179 108,422 130,052 5629 33,200 76,882 171,625 152,682 123,399 77,145 180,091

77.7

69.5

66.1

66.7

67.8

80.1 77.4

72.9 69.2

68.2 65.9

69.8 66.5

66.0 67.9

75.6 78.2 65.2 71.1

66.8 69.3 52.8 65.3

63.9 65.5 55.9 63.2

64.5 65.8 57.8 64.1

65.8 67.2 59.0 64.9

46.8 52.8 64.2 71.4 77.4 79.7 81.2 82.1

32.3 41.3 53.8 61.5 67.1 70.0 73.5 77.3

31.7 41.3 54.8 60.0 65.0 65.7 69.1 72.2

31.3 42.5 55.5 60.7 65.5 66.4 68.9 72.8

32.4 44.0 56.7 61.7 66.7 68.2 70.5 74.0

∗

Estimated percent of staffed beds that are occupied. Sources: American Hospital Association Annual Survey of Hospitals. Hospital Statistics, 1976, 1981, 1991–2004 Editions. Chicago. (Copyrights 1976, 1981, 1991–2004) as published in National Center for Health Statistics, Health United States, 2004. Hyattsville, MD: U.S. Public Health Service, 2005.

the mentally ill. In recent decades many of these state facilities have been closed or scaled back as the care for many mental health disorders has shifted to outpatient settings. Many states continue to own and operate university hospitals that provide advanced medical care and support the medical education and research that is conducted by state-sponsored medical schools and academic health centers.

Local government hospitals are the predominant type of public hospital in the United States, and include facilities owned by cities, counties, and special governmental districts. These facilities typically serve as key safety net providers in their communities by caring for disproportionate numbers of uninsured and publicly insured patients who lack access to private hospitals and physicians. Steady growth in the

74 number of Americans without health insurance coverage in the United States has created heightened financial difficulties for public hospitals in recent decades. In many cases these hospitals are less able to upgrade their facilities, purchase new medical technologies, and expand clinical capacity than their privately owned counterparts. As a consequence, these public hospitals face mounting difficulties in attracting patients with private health insurance or Medicare coverage, which further limits their sources of revenue. In recent decades, financial and operational difficulties have caused public hospitals in some communities to close, thereby forcing the surviving private hospitals to assume responsibility for serving the uninsured and publicly insured patients. Another type of local hospital, the public authority hospital, is financed in part by local tax dollars but operates more like a private organization than a governmental agency. These hospitals are financed by a special hospital assessment district similar to a water or fire district, and are governed by a board that may include local elected officials or their appointees. These hospitals are often exempted from administrative rules that govern local government agencies such as hiring and purchasing requirements, thereby giving the hospitals additional flexibility in their operations. Private not-for-profit hospitals are the most common type of short-stay hospital in the United States, accounting for more than half of all hospital beds in the nation. These hospitals are organized by community, religious, or philanthropic organizations and receive exemptions from federal, state, and/or local taxes in exchange for the community benefits they generate. Any financial earnings generated by a not-for-profit hospital are reinvested in the institution rather than paid out to owners or investors. Some of these hospitals function as safety-net hospitals by pursuing a religious or charitable mission to serve the uninsured and other disadvantaged populations who lack access to mainstream medical care providers. Other not-for-profit hospitals serve a broad cross-section of the population residing in their service area but position their services and facilities to be especially attractive to those populations with insurance, thereby ensuring the institutions’ financial viability. In several states, these facilities are now required to justify their tax exempt status by reporting the amount of charity care and other community benefits they produce each year. Proprietary hospitals have been a part of the nation’s health-care system since the early 1900s but they account for only a small percentage of all hospital beds. During the early 1900s, prominent physicians developed proprietary hospitals for their own use, but in recent decades, physician-owned general hospitals have declined in prevalence. More recently, investor-owned hospital corporations emerged beginning in the 1960s and steadily increased the number of hospitals they own and operate. Like other investor-owned corporations, these hospitals are owned by stockholders. Proprietary hospital corporations grew rapidly in the 1980s and 1990s through a combination of building new hospitals, buying existing hospitals, and securing contracts to manage independently owned hospitals. Proprietary hospital corporations have faced obstacles to growth in recent years due to the Federal Trade Commission’s increased scrutiny of hospital acquisitions for their potential anticompetitive effects. Additionally, several of the largest corporations have faced federal and state lawsuits concerning their billing practices and physician compensation arrangements, resulting in large fines. Physician-owned specialty hospitals represent another type of proprietary hospital that has emerged in recent years, but their impact on the health-care system remains unclear at this point. Partly in response to the growth of proprietary hospital corporations, not-for-profit multihospital systems have developed and grown rapidly in recent decades. These systems bring multiple not-for-profit hospitals together under common ownership and/or management in order to improve the competitive position of the hospitals, realize economies of scale in purchasing and operations, strengthen negotiating leverage with health insurers, and improve coordination of services across multiple facilities and care settings. Many of these hospital systems are local in their reach and include multiple hospitals operating within a single geographic region or state. Other systems include hospitals in multiple regions across the country. In addition to

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hospitals, these systems often include other types of health-care institutions such as home health agencies, nursing facilities, outpatient centers, and physician practices. Over the past two decades, large numbers of independent hospitals have consolidated into these multihospital systems, at least partly in response to the growth of managed care and the desire to strengthen their negotiating leverage with health insurers. Hospital Structure. There are three primary sources of authority in the hospital: the governing board, the administration, and the medical staff. The governing board has the ultimate responsibility for the hospital by establishing policy, hiring the chief administrator, and appointing members of the medical staff leadership. By virtue of these responsibilities, the board is ultimately accountable for quality of care within the hospital. As a result, many hospitals have added members of the medical staff to the board and most have increased their investments in quality assurance activities. In some hospital systems and corporations, hospital governance is the responsibility of the governing board for the parent company. The mutual dependence between the governing board and the medical staff is formalized by the governing bylaws for the medical staff. These bylaws, which are typically established by the hospital board, define the rules and regulations governing physician interaction with the hospital. Election and duties of the medical staff officers and committees and processes for awarding and maintaining admitting privileges are defined by these bylaws. Challenges Facing the Hospital. The key pressures facing hospitals have evolved considerably over the past decade. Hospitals in many communities enjoy a stronger negotiating position relative to health insurers today than they did a decade ago, due in part to consolidation in the hospital industry and continued growth in demand for hospital services. This has allowed many hospitals to secure higher payments from private health insurers, thereby helping them to accommodate the rising costs of serving uninsured patients and those covered by public programs such as Medicaid and Medicare. These same developments—hospital consolidation and growth in demand for care—have helped to reduce or eliminate problems of excess hospital capacity and overbedding that were present in many communities during the 1980s and 1990s. The closure of underutilized hospitals has helped to eliminate excess capacity in some communities, as have the efforts of hospitals to convert unused bed capacity into new and upgraded facilities such as private rooms and outpatient clinics. After more than a decade of stagnant or declining hospital admissions and bed capacity, many hospitals serving urban and suburban communities are now confronting growing demand for care and bed shortages (Table 74-2). These problems are attributable to a combination of factors including population growth, the aging of the American population, and a reduction in insurers’ use of aggressive managed-care techniques to limit hospital admissions and reduce lengths of stay. An ongoing shortage of nurses and other hospital personnel has exacerbated these constraints by limiting the ability of hospitals to staff all of their licensed beds. As a result, many hospitals are experiencing periodic overcrowding in their emergency departments as patients wait for inpatient beds to become available, leading these facilities to divert ambulances to other available hospitals.7 Hospitals continue to be challenged by technological developments and competitive dynamics that lead services formerly delivered in hospital settings to be delivered in alternative, outpatient settings. These developments have led to expanded hospital roles in outpatient service delivery (Table 74-2). However, these developments also have brought physicians into competition with hospitals for the delivery of an expanding array of services. Physicians are developing the capacity to deliver a variety of diagnostic and surgical procedures in their offices, including sophisticated imaging and laboratory testing, rather than referring patients to hospital-based facilities for these services. Physicians are also continuing to develop ambulatory surgery and diagnostic centers that serve as lower-cost alternatives to hospitalbased facilities for performing a variety of outpatient procedures.

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Health-Care Planning, Organization, and Evaluation TABLE 74-2. U.S. HOSPITAL ADMISSIONS, LENGTHS OF STAY, AND OUTPATIENT VISITS BY SELECTED CHARACTERISTICS, 1980–2002 Hospital Characteristics

1980

1990

2000

2001

2002

Admissions All hospitals

38,892

Number in Thousands 33,774 34,891 35,644

36,326

Federal Nonfederal

2044 36,848

1759 32,015

1034 33,946

1001 34,644

1027 35,299

36,143 25,566 3,165 7,413

31,181 22,878 3,066 5,236

33,089 24,453 4,141 4,496

33,814 27,983 4,197 4,634

34,478 25,425 4,365 4,688

159 1,254 3,700 7,162 6,596 5,358 4,401 7,513

95 870 2,474 5,833 6,333 5,091 3,644 6,840

141 995 2,355 6,735 6,702 5,135 3,617 7,410

140 1,030 2,422 6,778 6,630 5,328 3,779 7,706

162 1,062 2,471 6,826 6,800 5,607 3,593 7,958

9.9

9.1

6.7

6.6

16.8

14.9

12.8

13.2

11.7

9.6

8.8

6.6

6.6

6.5

7.6 7.7 6.5 7.3

7.2 7.3 6.4 7.7

5.8 5.7 5.4 6.7

5.7 5.6 5.4 6.7

5.7 5.6 5.3 6.6

5.3 5.8 6.7 7.0 7.4 7.6 7.9 8.7

5.4 6.1 7.2 7.1 6.9 7.0 7.3 8.1

4.2 5.1 6.4 5.7 5.7 5.5 5.6 6.2

4.0 5.0 6.4 5.7 5.6 5.4 5.6 6.1

4.1 5.0 6.4 5.7 5.5 5.5 5.5 6.1

262,951

Number in Thousands 368,184 592,673 612,276

640,515

50,566 212,385

58,527 309,657

63,402 531,972

64,035 548,242

75,781 564,734

202,310 142,156 9,696 50,459

301,329 221,073 20,110 60,146

521,405 393,168 43,378 84,858

538,480 404,901 44,706 88,873

556,404 416,910 45,215 94,280

1,155 6,227 17,976 36,453 36,073 30,495 25,501 48,430

1,471 10,812 27,582 58,940 60,561 43,699 33,394 64,870

4,555 27,007 49,385 114,183 99,248 73,444 52,205 101,378

4,556 27,941 51,331 114,921 99,596 75,242 59,580 105,314

5,930 29,726 53,342 117,573 102,424 79,092 57,841 110,475

Community Nonprofit For profit State-local government 6–24 beds 25–49 beds 50–99 beds 100–199 beds 200–299 beds 300–399 beds 400–499 beds 500 beds or more

Average Length of Stay All hospitals Federal Nonfederal Community Nonprofit For profit State-local government 6–24 beds 25–49 beds 50–99 beds 100–199 beds 200–299 beds 300–399 beds 400–499 beds 500 beds or more

Hospital Outpatient Visits All hospitals Federal Nonfederal Community Nonprofit For profit State-local government 6–24 beds 25–49 beds 50–99 beds 100–199 beds 200–299 beds 300–399 beds 400–499 beds 500 beds or more

Number of Days 6.8

Note: Data for additional years are available. Sources: American Hospital Association Annual Survey of Hospitals. Hospital Statistics, 1976, 1981,1991–2004 Editions. Chicago. (Copyrights 1976, 1981, 1991–2004: Used with the permission of Health Forum LLC, an affiliate of the American Hospital Association.) Health, United States, 2004.

Some physicians have developed specialty hospitals that compete directly with general hospitals in the delivery of specialized inpatient services. These developments threaten to redirect important sources of revenue from hospitals to physician practices and change the historically symbiotic relationships that have existed between hospitals and physicians.8 In some cases, hospitals have created joint ventures with

physicians for the development of these new facilities in order to retain some ownership and control over the activities. In other cases, hospitals have revoked the admitting privileges of physicians who invest in these types of facilities in order to discourage their development and growth. In still other cases, hospitals have pressured health insurers to exclude physician-owned facilities from their provider networks.

74

Ambulatory Care Providers Ambulatory care includes a wide range of health professionals, settings, and services for the “walking” or noninstitutionalized patient. Ambulatory care providers play a central role as the initial and continuing point of contact with the health-care system for most people. Collectively these providers offer preventive, screening, and diagnostic services as well as ongoing treatment services and follow-up care for patients that do not require inpatient or residential care. These providers also serve as brokers by referring patients to more specialized medical services available in hospitals and other institutional settings. Ambulatory health care includes the following major types of personal health-care services: • Preventive care is designed to avoid the onset and/or progression of disease and injury. Examples of these services include vaccinations that prevent the occurrence of infectious diseases, as well as screening tests for cancer or high blood pressure that enable the early detection and treatment of diseases or risk factors in order to forestall disease progression and complications. Services designed to prevent the occurrence of disease altogether are defined as primary prevention activities, whereas services aimed at early detection to limit and/or reverse the progression of disease are defined as secondary prevention activities. The preventive services delivered in ambulatory care settings are typically referred to as clinical preventive services and may be performed in many different settings including physician offices, community health centers, worksite health clinics, hospital outpatient clinics, pharmacies, mobile health clinics, and even health fairs. These services may be performed by physicians or by a variety of other health professionals including nurse practitioners, physician assistants, clinical pharmacists, and nurses. • Primary care focuses on the diagnosis, treatment, and management of routine, nonemergent health conditions. Primary care physicians assume primary responsibility for the delivery of these services, although physician extenders such as nurse practitioners and physician assistants also play major roles in the delivery of these services in many settings. Primary care physicians are commonly defined to include those physicians specializing in general practice, family medicine, general internal medicine, pediatrics, and obstetrics/gynecology. Physicians practicing in other specialty areas, particularly internal medicine subspecialties such as cardiology and rheumatology, may also deliver primary care services to patients under their care. Individuals with some form of health insurance typically receive most of their primary care in physician office settings, while uninsured individuals and those who face other barriers in accessing mainstream physician practices often receive primary care from alternative settings such as community health centers, hospital outpatient clinics, urgent care centers, and hospital emergency departments. • Secondary care focuses on the diagnosis, treatment, and management of complex health conditions that require specialized clinical knowledge and skills. Most secondary care is provided by specialty physicians in physician office settings or in more specialized ambulatory facilities such as imaging and surgery centers or hospital outpatient clinics. Primary care physicians play key roles in identifying the need for secondary care and referring patients to specialty physicians for consultation, diagnosis, and treatment. The secondary care provided by physician specialists also serves as an entry point for tertiary care and quaternary care services—the most complex types of medical services that are often provided on an inpatient basis at advanced medical centers. • Rehabilitative care is designed to restore and preserve function in patients affected by disease and injury. These services may be delivered in both inpatient and ambulatory care settings. Patients who are hospitalized for care may receive rehabilitation services in inpatient settings such as rehabilitation units and skilled nursing facilities immediately following their

The American Health-Care System: Structure and Function

1223

hospital admissions. Patients may also receive rehabilitative services in ambulatory settings such as hospital outpatient clinics, outpatient therapy centers specializing in physical, occupational, and/or speech therapy, and in the home through home healthcare providers. Rehabilitative care is commonly delivered by a variety of ancillary therapists and therapy assistants with more complex and advanced care being managed by physicians specializing in physical medicine and rehabilitation. • Long-term care is designed to provide assistance to patients with health-related impairments in their ability to perform routine activities of daily living such as bathing, dressing, transferring, walking, preparing meals, and taking medications. These services may be delivered in both institutional and ambulatory care settings. Institutional settings for longterm care include nursing homes, assisted living centers, and board and care facilities. Ambulatory providers of long-term care include home-care providers, visiting nurses associations, adult day care centers, and respite care programs. These ambulatory services are designed to enable patients to remain living at home as an alternative to more costly institutional care settings. In addition to these personal health services, public health services are also provided to both institutionalized and noninstitutionalized populations with the goal of reducing the incidence of disease and injury. These population-based services include activities to protect the safety of water and food supplies, identify and assess community health needs, investigate health threats, and educate the public about health issues. These services, which are discussed in more detail in the following chapter, generally do not involve the direct provision of services to individuals and therefore are not typically considered part of the ambulatory health-care system. Office-Based Ambulatory Care. Most of the ambulatory care delivered in the United States is provided in office-based practice settings (Table 74-3). Although hospital-based settings deliver significant amounts of ambulatory care, the predominant source of this care is the physician’s office, including solo physician practices, partnerships, and group practices. Physicians provide a broad array of services in their offices, including routine examinations, evaluation and management services, diagnostic services that include imaging and laboratory tests, counseling, and surgical procedures. The scope of services provided in physicians’ offices has been expanding over time, particularly in the areas of diagnostic testing and surgical procedures where advances in medical technology have allowed these services to move from inpatient to outpatient settings. A solo practice consists of a single physician practicing alone in an office-based setting, whereas a partnership practice includes two physicians practicing together. A group practice is typically defined as the combination of three or more physicians practicing together in an office-based setting. True group practice involves the sharing of revenue and expenses, staff, medical records, and other resources and may involve sharing responsibilities for night and weekend on-call duties and hospital rounding. Some physicians share only physical space or staff, but this arrangement does not constitute a formal group practice. Most ambulatory care services historically have been provided by physicians in solo office-based practice. This arrangement offers the physician the greatest degree of professional and organizational independence and the ability to be self-employed. Although solo practitioners still account for a large share of ambulatory care, group practice and hospital-based practices are expanding dramatically. A variety of factors have led physicians to seek alternatives to solo practice in recent years, including rising practice expenses and the cost of purchasing new office-based medical technologies, the growth of managed care and the desire to develop practice arrangements that enhance physician negotiating leverage with health insurers, and changing physician lifestyles and the desire to practice in settings that offer less demanding work schedules. Some of the earliest group practices in the United States were started by industries that needed to provide care to employees in rural

1224

Health-Care Planning, Organization, and Evaluation TABLE 74-3. U.S. OUTPATIENT PHYSICIAN VISIT CHARACTERISTICS, 1995–2002 Physician Visit Characteristics

1995

1997

1998

1999

2000

2001

2002

Total

697,082

787,372

829,280

756,734

823,542

880,487

889,980

Under 18 years 18–44 years 45–64 years 45–54 years 55–64 years 65 years and over 65–74 years 75 years and over

150,351 219,065 159,531 88,266 71,264 168,135 90,544 77,591

158,423 245,127 192,753 105,511 87,243 191,069 99,714 91,355

168,520 260,379 203,296 112,316 90,979 197,085 102,306 94,779

135,627 227,005 201,911 108,597 93,315 192,190 92,642 99,548

163,459 243,011 216,783 119,474 97,309 200,289 102,447 97,842

168,663 244,288 239,106 130,795 108,310 228,430 112,978 115,452

183,027 240,432 242,142 131,806 110,336 224,380 109,331 115,049

Number of Visits in Thousands

Physician Visits as a Percentage of all Outpatient Visits (Hospitals, Emergency Departments, and Offices) Total Under 18 years 18–44 years 45–64 years 45–54 years 55–64 years 65 years and over 65–74 years 75 years and over

81.0 77.2 76.8 84.7 84.2 85.4 87.2 88.2 86.1

82.1 77.7 78.6 85.3 84.8 85.8 87.8 88.6 87.1

82.5 78.9 79.3 85.5 85.0 86.2 87.4 88.6 86.2

80.2 74.1 75.7 83.9 83.0 84.9 87.2 87.3 87.1

81.1 77.0 77.0 84.7 84.0 85.6 86.7 87.9 85.4

82.2 78.0 76.9 85.4 84.6 86.3 88.6 89.1 88.2

82.1 78.7 76.5 85.4 84.5 86.5 88.7 89.3 88.2

Number of Visits per 100,000 Population Total, age adjusted Total, crude Under 18 years 18–44 years 45–64 years 45–54 years 55–64 years 65 years and over 65–74 years 75 years and over

271 266 213 203 309 286 343 534 494 588

300 295 222 226 351 316 406 596 552 653

312 308 235 240 358 327 407 609 569 659

283 279 188 209 344 305 405 592 521 679

304 300 226 224 358 323 412 612 577 654

316 314 233 222 373 336 431 678 625 739

316 314 252 218 366 332 417 661 606 722

Male, age adjusted Male, crude Under 18 years 18–44 years 45–54 years 55–64 years 65–74 years 75 years and over

232 220 209 139 229 300 445 616

255 243 225 145 251 370 516 653

261 251 239 149 251 379 538 640

246 235 189 150 247 361 510 663

261 251 231 148 260 367 539 670

275 264 235 152 273 371 598 758

270 261 254 145 270 359 580 685

Female, age adjusted Female, crude Under 18 years 18–44 years 45–54 years 55–64 years 65–74 years 75 years and over

309 310 217 265 339 382 534 571

344 345 219 306 377 439 581 652

360 362 231 328 399 433 595 671

317 320 187 267 361 445 530 689

345 348 221 298 384 453 609 645

356 362 231 291 397 485 648 726

359 365 250 290 390 471 628 746

White, age adjusted White, crude Under 18 years 18–44 years 45–54 years 55–64 years 65–74 years 75 years and over

282 281 237 211 286 345 496 598

310 310 243 234 324 410 547 653

316 317 235 248 328 406 572 669

292 293 197 222 312 410 526 687

315 316 243 239 330 416 568 658

338 343 260 242 354 451 651 764

330 335 272 234 346 431 611 720

African American, age adjusted African American, crude Under 18 years 18–44 years 45–54 years

204 178 100 158 281

260 228 145 186 294

281 259 217 207 310

239 211 144 155 277

239 214 167 149 269

212 189 102 154 286

283 253 196 173 281

(Continued)

74

The American Health-Care System: Structure and Function

1225

TABLE 74-3. U.S. OUTPATIENT PHYSICIAN VISIT CHARACTERISTICS, 1995–2002 (Continued) Physician Visit Characteristics

1995

1997

1998

1999

2000

2001

55–64 years 65–74 years 75 years and over

294 429 395

396 582 607

411 511 537

404 485 608

373 512 568

341 426 473

2002 386 659 ∗ 812 ∗

Sources: Centers for Disease Control and Prevention, National Center for Health Statistics, National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey. Health, United States, 2004.

areas where medical care was unavailable. The Mayo Clinic in Rochester, Minnesota, was the first successful nonindustrial group practice. Mayo, which was originally organized as a single-specialty group in 1887 and later expanded to a multispecialty group, became a reputable model for other physician practices in the United States. In 1931, the Committee on the Costs of Medical Care issued a report suggesting a major role for group practice, especially those associated with hospitals, in providing comprehensive care. Unfortunately the far-sighted recommendations contained in that report were never implemented, in large measure due to the vigorous opposition of organized medicine such as the American Medical Association. Developments in medical practice, especially increasing specialization and advances in medical technology, have also spurred the movement to group practice. Group practices have provided a structure for sharing the costs associated with increasingly complex and expensive office facilities, equipment, and personnel. Group practice is viewed as a strategy for improving quality of care by facilitating referral arrangements and coordination of care across different physicians and specialties, and by enhancing opportunities for informal consultations and information-sharing among physicians. Group practice is also viewed as a strategy for improving the efficiency of medical practice by pooling resources to support nonphysician staff such as nurse practitioners, physician assistants, and general office staff to perform activities that do not require specialized medical knowledge. Group practices can also offer physicians more appealing work environments by sharing responsibilities for after-hours coverage and rounding with hospitalized patients, and providing more flexible work hours. There are currently over 16,000 group practices in the United States according to the American Medical Association’s periodic surveys of physicians.9 Most of these groups are relatively small with an average size of less than 10 physicians, but the prevalence of larger groups has grown over time. Recent evidence indicates an increasing preference for group practice among physicians, particularly among younger physicians, women, and physicians practicing in areas that are more heavily penetrated by managed care plans. Furthermore, physicians are increasingly practicing in more corporate-oriented environments as employees of a practice rather than as owners. Recent trends in the ownership and management of physician practices have raised questions about the future role of these practices within the nation’s health-care system. During the 1990s, many hospital systems were aggressively seeking relationships with physician practices in order to improve their ability to compete for contracts with health insurers and operate successfully under capitated payment systems with health maintenance organizations (HMOs). Some hospital systems were directly purchasing physician practices and employing their physicians, especially primary care physicians, while other systems were forming alliances with these physicians through physicianhospital organizations (PHOs) and related arrangements. Since that time, however, HMO enrollment failed to grow as expected in many communities, and many health insurers have scaled back the use of managed care techniques such as selective contracting with hospital systems.16 As a result, physician-hospital relationships have become less important for contracting, and hospital systems in many communities have divested their owned primary care practices and PHOs. Most recently, hospital systems in some communities have begun to pursue tighter relationships with specialty physician practices in order to compete more effectively for patients in profitable specialty service areas such as cardiac care and orthopedics. Some hospital systems have established joint ventures with single-specialty

groups to develop ambulatory surgery centers, thereby avoiding direct competition with these groups in the delivery of ambulatory services. Hospital systems in some communities have purchased specialty physician practices and directly employed specialist physicians in order to strengthen these relationships. Hospital-Based Ambulatory Care. Although hospitals historically have focused on the provision of inpatient care, they also serve as major sources of ambulatory care services. Hospitals traditionally have delivered a great deal of ambulatory care through their emergency departments, which provide care not only for patients with emergent conditions but also for patients who need routine primary care but lack access to mainstream providers. Some hospitals have created primary care outpatient clinics to reduce crowding in their emergency departments and redirect primary care patients to more appropriate and less costly care settings. Many hospitals also operate specialty outpatient clinics and ambulatory surgery centers that serve as important sources of specialty care. These ambulatory services have become increasingly important sources of revenue for hospitals as services historically provided on an inpatient basis continue to shift to outpatient settings. Some hospitals directly employ specialist physicians and other personnel to provide these outpatient services, while others contract with specialty group practices for this purpose. Freestanding Ambulatory Centers. While hospitals and physicians’ offices account for the vast majority of ambulatory care delivered in the United States, a small but growing amount of care is provided by private, freestanding ambulatory centers that are not based in hospitals or physician practices. Many of these freestanding centers provide outpatient surgical services, while others provide diagnostic tests and imaging services, emergency and urgent care services, and rehabilitation services. Some of these centers are owned and operated by proprietary corporations that directly employ physicians and other clinical personnel to staff the centers, while other centers are developed as joint ventures with physician groups and/or hospitals. Ambulatory Care in Safety-Net Clinics. Safety-net health-care clinics serve as important sources of ambulatory care for the uninsured and other population groups that lack access to office-based and hospital-based providers due to financial, geographic, or other barriers to care. These clinics rely on support from a variety of sources, including governmental funding, private charitable contributions, volunteer labor, and sliding-scale patient fees to deliver care to these population groups. Some of these clinics receive support through the federal Community Health Center program, which provides grants to more than 1200 health centers and 3000 individual clinic sites to deliver comprehensive primary care services to populations residing in medically underserved areas of the United States and its territories. Other clinics receive special support through other federal programs such as those targeting rural health centers, school-based health centers, and clinics that serve the residents of public housing facilities. A number of state and local governments also maintain programs that provide financial support to safety-net clinics. Many communities are also served by “free clinics” that rely primarily on voluntary clinical labor and on donations collected by community-based and faith-based organizations. In some communities, local public health agencies provide some preventive and primary care services such as immunizations, chronic disease screenings, and prenatal and well-child care. In some cases, universities sponsor safety-net health

1226

Health-Care Planning, Organization, and Evaluation

clinics that offer free ambulatory care as well as training opportunities for medical, nursing, dental, and other health professions students. Similarly, some community hospitals sponsor free primary care clinics as a strategy to reduce overcrowding in their emergency departments.

Long-Term Care Providers Long-term care providers represent one of the largest components of the U.S. health-care system after hospital-based and physician-based care are considered, with nursing home care alone accounting for 7% of the nation’s total health-care expenditures.6 Long-term care encompasses a broad spectrum of services delivered in both institutional and ambulatory care settings and designed to assist patients with health-related impairments in their ability to perform routine activities of daily living. Institutional settings for long-term care include nursing homes, assisted living centers, and board and care facilities. Ambulatory providers of long-term care include home care providers, visiting nurses associations, adult day care centers, and respite care programs. Many patients also receive long-term care services from informal caregivers including spouses, parents, and children, but the economic value of these services is typically not included in estimates of national long-term care spending. Coordinating these different types of long-term care and ensuring that patients receive the most appropriate types and levels of care are

continuing challenges for the nation’s health-care system. Financing these different components of long-term care remains problematic as well, particularly in view of the aging American population and the growing numbers of people who require this care. The nursing home is the most costly and visible component of the long-term care continuum. Nearly 1.5 million residents receive care in the nation’s 16,000 nursing homes, most of whom are over 75 years of age, female, suffer from multiple chronic conditions, and have severe limitations in activity (Table 74-4).3 Although many nursing homes are small, there is a growing trend toward larger homes and toward ownership by multihome not-for-profit and for-profit entities. Most long-term care services are not covered by Medicare, the federal health program that provides health-care coverage for elderly and permanently disabled populations in the United States. Medicare provides only short-term coverage for services provided by rehabilitation units, skilled nursing facilities, and home health agencies. For longer-duration care in nursing homes and other care settings, patients must rely on their own financial assets or on private longterm care insurance until those resources are depleted and patients become eligible for Medicaid, the program for low-income populations that is jointly administered by the federal and state governments. Financial support for nursing home care is limited under Medicaid

TABLE 74-4. U.S. NURSING HOME RESIDENTS 65 YEARS AND OLDER, 1973–99 Residents Resident Characteristics

1973–74

1985

1995

Residents per 1,000 population 1997

1999

1973–74 1985

1995

1997

1999

Age 65 years and over, age adjusted 65 years and over, crude

— 961,500

— 1,318,300

— 1,422,600

— 1,465,000

— 1,469,500

58.5 44.7

54.0 46.2

45.9 42.4

45.3 43.4

43.3 42.9

65–74 years 75–84 years 85 years and over

163,100 384,900 413,600

212,100 509,000 597,300

190,200 511,900 720,400

198,400 528,300 738,300

194,800 517,600 757,100

12.3 57.7 257.3

12.5 57.7 220.3

10.1 45.9 198.6

10.8 45.5 192.0

10.8 43.0 182.5

65 years and over, age adjusted 65 years and over, crude

— 265,700

— 334,400

— 356,800

— 372,100

— 377,800

42.5 30.0

38.8 29.0

32.8 26.1

32.0 26.7

30.6 26.5

65–74 years 75–84 years 85 years and over

65,100 102,300 98,300

80,600 141,300 112,600

79,300 144,300 133,100

80,800 159,300 132,000

84,100 149,500 144,200

11.3 39.9 182.7

10.8 43.0 145.7

9.5 33.3 130.8

9.8 34.6 119.0

10.3 30.8 116.5

65 years and over, age adjusted 65 years and over, crude

— 695,800

— 983,900

— 1,065,800

— 1,092,900

— 1,091,700

67.5 54.9

61.5 57.9

52.3 53.7

51.9 55.1

49.8 54.6

65–74 years 75–84 years 85 years and over

98,000 282,600 315,300

131,500 367,700 484,700

110,900 367,600 587,300

117,700 368,900 606,300

110,700 368,100 612,900

13.1 68.9 294.9

13.8 66.4 250.1

10.6 53.9 224.9

11.6 52.7 221.6

11.2 51.2 210.5

65 years and over, age adjusted 65 years and over, crude

— 920,600

— 1,227,400

— 1,271,200

— 1,294,900

— 1,279,600

61.2 46.9

55.5 47.7

45.4 42.3

44.5 43.0

41.9 42.1

65–74 years 75–84 years 85 years and over

150,100 369,700 400,800

187,800 473,600 566,000

154,400 453,800 663,000

160,800 464,400 669,700

157,200 440,600 681,700

12.5 60.3 270.8

12.3 59.1 228.7

9.3 44.9 200.7

10.0 44.2 192.4

10.0 40.5 181.8

65 years and over, age adjusted 65 years and over, crude

— 37,700

— 82,000

— 122,900

— 137,400

— 145,900

28.2 22.0

41.5 35.0

50.4 45.2

54.4 49.4

55.6 51.1

65–74 years 75–84 years 85 years and over

12,200 13,400 12,100

22,500 30,600 29,000

29,700 47,300 45,800

31,400 51,900 54,100

30,300 58,700 56,900

11.1 26.7 105.7

15.4 45.3 141.5

18.4 57.2 167.1

19.2 60.6 186.0

18.2 66.5 183.1

Male

Female

White

Black or African American

Notes: Excludes residents in personal care or domiciliary care homes. Sources: Hing E, Sekscenski E, Strahan G. The National Nursing Home Survey: 1985 summary for the United States National Center for Health Statistics. Vital Health Stat. 1989;13(97) and Centers for Disease Control and Prevention, National Center for Health Statistics, National Nursing Home Survey for other data years. Health, United States, 2004.

74 and is widely viewed as inadequate to support the staffing levels, physical environments, and range of services and activities that would be necessary to ensure high-quality care. Many state Medicaid programs are now experimenting with various forms of home-based and community-based alternatives to nursing home care with the goal of reducing the costs of care and improving quality of care and patient satisfaction. Some of these experiments are now including consumerdirected care models that offer expanded opportunities for patients to decide how best to use their long-term care benefits, including using funds to reimburse family members and other lay-persons as caregivers. Improvements in other aspects of the long-term care continuum are also moving forward. Hospice providers deliver services to terminally ill patients in caring and medically supportive environments using a multispecialty approach in both institutional and home settings. Home health providers and assisted living facilities have expanded rapidly in recent years, and several state Medicaid programs are now testing ways of positioning these services as cost-effective alternatives to nursing homes. The federal government continues to experiment with all-inclusive care programs that coordinate a comprehensive array of services for long-term care patients who are eligible for both Medicare and Medicaid. Additionally, various types of continuing care facilities have emerged in recent years, although most of these are designed to serve higher-income private-pay patients rather than lower-income Medicaid recipients. Despite some progress, serious challenges remain concerning how to finance longterm care services for the aging baby boom population and how to coordinate the various components of this care to achieve desired health and economic outcomes.

Mental Health and Substance Abuse Service Providers Mental health and substance abuse care providers represent another major component of the U.S. health-care system, accounting for nearly $33 billion of the nation’s $1.5 trillion in health-care expenditures for 2002.6 Like long-term care, mental health care encompasses a broad spectrum of services delivered in both institutional and ambulatory care settings. Institutional care providers include specialized psychiatric hospitals, psychiatric units of general hospitals, nursing homes, board and care facilities, and residential substance abuse treatment centers. In the ambulatory care arena, primary care physicians play key roles in diagnosing mental health and substance abuse disorders and in managing routine mental health conditions, while more specialized office-based care is provided by psychiatrists, psychologists, social workers, family counselors, and other health professionals. Community mental health centers and outpatient substance abuse treatment centers are also important sources of ambulatory care for these populations. Mental health services are generally provided through parallel public and private subsystems, with only those individuals having private insurance or sufficient resources for self-pay receiving care through the private subsystem. These patients are more likely to receive care from private-practice psychiatrists and other professionals, private mental health hospitals, and private substance abuse treatment facilities. Employees in many large and mid-sized firms may also obtain access to private mental health and substance abuse providers through the employee assistance programs offered by these firms. By contrast, patients who are uninsured, covered by Medicaid, or who exhaust their private insurance benefits typically rely on a patchwork of government-owned mental health hospitals, community mental health centers, and a variety of community-based not-forprofit providers. Many of these providers rely heavily on financial support from federal programs such as the Community Mental Health Services Block Grant and the Substance Abuse Prevention and Treatment Block Grant. Hospital emergency departments also frequently serve as providers of last resort for patients with acute mental health and substance abuse problems who lack other sources of care. Unfortunately, correctional facilities have also become common sources of care for patients with severe and poorly managed mental health and substance abuse problems, where services are delivered through local jail health systems as well as state and federal prison health systems.

The American Health-Care System: Structure and Function

1227

Pharmacy Providers and Suppliers Pharmaceutical therapies continue to be one of the fastest growing components of modern medical practice, and therefore the organizations and professionals involved in prescribing, distributing, and dispensing drugs have become increasingly important components of the health- care system. Between 1995 and 2002, national expenditures for prescription drugs grew faster than expenditures for any other type of health care, and by 2002, drug expenditures accounted for 11% of the nation’s total health-care spending.6 A variety of factors are driving the increased utilization of prescription drugs, including the availability of new drugs to treat an expanding array of health conditions, increased marketing of new and existing drugs to physicians and consumers, and a growing body of evidence demonstrating the effectiveness of drug therapies in treating a variety of common conditions ranging from heart disease and hypertension to diabetes and asthma. The delivery system for prescription drugs includes the manufacturers that are responsible for producing and marketing these products, the physicians and advanced practice nurses who prescribe them for patients, and the pharmacists who are responsible for dispensing drugs as well as educating patients about drug therapy choices and proper drug usage. A variety of intermediaries are involved in drug purchasing and distribution as well, including pharmacy benefit managers (PBMs) who work on behalf of health insurers and employers to establish policies on which drugs should be covered and to negotiate pricing arrangements with manufacturers. Drug dispensing is carried out through an array of different organizations including local retail pharmacies, national chain pharmacies, mail order pharmacies, and pharmacies operated by individual health plans and hospitals. In recent years, specialty pharmacy organizations have emerged that manage the drug purchasing, dispensing, and administration processes for high-cost medications and those that are difficult to store or administer, such as biologicals and other products that require intravenous administration. The growing importance of prescription drugs in modern medical care has raised concerns about population groups that lack access to these products, including the uninsured as well as the elderly and disabled populations covered by Medicare. Most private health insurance plans include coverage for prescription drugs, as do state Medicaid programs, but the federal Medicare program historically has not included an outpatient prescription drug benefit. In response, many state governments have created pharmacy assistance programs (PAPs) that provide the uninsured and low-income Medicare beneficiaries with financial assistance in purchasing needed prescription drugs. Some states have gone farther in adopting policies that would allow states to negotiate discounts with drug manufacturers for drugs needed by their residents who lack drug coverage or who are covered by Medicaid. Still other states and some local governments are exploring options for allowing their residents to purchase drugs from Canada and other foreign countries where drug prices are lower, and then reimporting these drugs to the United States The federal government also maintains several targeted programs to assist disadvantaged populations in obtaining needed medications, including the AIDS Drug Assistance Program (ADAP) that assists HIV and AIDS patients and the 340B Drug Pricing Program that allows community health centers to purchase discounted medications for their uninsured patients. The U.S. Congress passed legislation in 2003 that created an outpatient prescription drug benefit for Medicare beneficiaries. This benefit, which went into effect in 2006, is administered by private health insurers and prescription drug plans. Beyond pharmacy, a variety of other health-care providers play important roles in delivering health services within the health-care system. These include providers of dental care, vision services, nutritional assessment and counseling, genetic counseling, and the rapidly growing field of complementary and alternative medical services. Other organizations specialize in providing support services that facilitate access to care, such as emergency and nonemergency medical transportation and language translation services. Finally, a wide array of organizations participate in the health-care system as suppliers of health-related products and equipment, including wheelchairs and

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other durable medical equipment; orthotics, prosthetics, and other assistive devices; implantable therapeutic devices such as pacemakers and defibrillators; clinical laboratory and imaging equipment; and health information technology such as electronic medical records and telemedicine applications. By continually bringing new and improved products to market, these suppliers of medical technologies, devices, and equipment are major forces of change in medical practice.

The Health-Care Workforce The health-care system is the single largest industry in the United States, providing a total of 12.9 million jobs nationwide. About 518,000 establishments make up the employer base for the health industry, three-fourths of which are the offices of physicians, dentists, and other health professionals. Hospitals constitute only 2% of all health services establishments, but they employ 41% of all workers in the industry (Table 74-5).10 The federal Bureau of Labor Statistics projects that about 16% of all new wage and salary jobs created between 2002 and 2012 will be in the health services industry, representing a total of 3.5 million jobs—more than any other industry. This projected job growth is attributed to continued growth in demand for health services as the American population becomes older and as improvements in health and medical care allow more Americans to live longer but with more health conditions and disabilities that require care. Professional occupations such as physicians, registered nurses, dentists, therapists, and social workers account for three-fourths of all the jobs in the health-care industry. The remaining one-quarter of jobs include clinical service occupations such as nursing aides and therapist assistants, administrative and clerical workers, and management occupations.

Physicians Over the past half-century, the American health-care system has oscillated between concerns about physician shortages and concerns about over-supply. In the early 1960s, the perception of physician shortages led to the growth of medical school classes and the building of new medical schools. Foreign medical school graduates were also viewed as additional sources of personnel for the United States. In 1963, the Health Professions Educational Assistance Act was passed to provide funds to medical schools based on enrollments and for grants and loans for the construction of new medical education facilities. This legislation marked the first instance of direct federal involvement in medical education financing. Previous attempts at federal intervention in medical education had been blocked by both organized medicine TABLE 74-5. PERCENT DISTRIBUTION OF WAGE AND SALARY EMPLOYMENT AND ESTABLISHMENTS IN HEALTH SERVICES, 2002 Establishment Type Health services, total Hospitals, public and private Nursing and residential care facilities Offices of physicians Offices of dentists Home health-care services Offices of other health practitioners Outpatient care centers Other ambulatory health-care services Medical and diagnostic laboratories

Establishments

Employment

100.0 1.9

100.0 40.9

11.7 37.3 21.6 2.8

22.1 15.5 5.9 5.5

18.2 3.1

3.9 3.3

1.5

1.5

1.9

1.4

Source: Bureau of Labor Statistics, U.S. Department of Labor. Career Guide to Industries, 2004–05 Edition Health Services, on the Internet at http://www.bls. gov/ oco/cg/cgs035.htm (visited August 29, 2005).

and medical schools themselves. The incentives contained in the 1963 legislation were effective in increasing the number of medical school graduates, with new graduates doubling between 1965 and 1980. But in the early 1980s, however, industry observers were raising concerns that the earlier policies on medical education overcorrected the nation’s physician supply. The American Medical Association and other industry groups had predicted an over-supply of physicians within the U.S. health-care system for the past quarter century, and had worked to limit the number of new physicians produced by U.S. medical schools. In 1980, the Graduate Medical Education National Advisory Committee projected that by 1990 a surplus of 70,000 physicians would exist.11 As a result, medical schools began reducing class sizes and immigration laws were revised to eliminate preferential treatment for foreign medical graduates. A later study published in 1995 predicted a surplus of 165,000 physicians by the year 2000, in part due to the growth of managed care and its emphasis on steering patients to primary care physicians and restricting unnecessary access to specialists.12 The physician surplus never materialized, however. The American population has continued to grow, as has utilization of physician services. Health insurers have scaled back the use of restrictive managed care techniques in response to consumer preferences for direct access to specialists. Moreover, continued innovations in medical technology and practice have kept the physician workforce busy with new services and procedures ranging from heart stents to bariatric surgery. In fact, several recent studies warn of a looming physician shortage. The nation now has more than 800,000 active physicians, up from 500,000 twenty years ago (Table 74-6).9 But this supply is projected to begin shrinking in about 10 years as doctors from the baby boom generation retire in large numbers—just as demand for physician services is likely to spike upward as large cohorts of Americans become eligible for Medicare. Moreover, pressures from rising practice expenses and the costs of medical malpractice insurance are leading physicians in some communities to retire early. In response, the Council on Graduate Medical Education recently produced a study for Congress that recommends training 3000 additional physicians per year in U.S. medical schools to address the looming shortage.13 Even the American Medical Association has abandoned its long-standing opposition to producing more physicians. There are also concerns about the distribution of physicians across specialties and across geographic areas. During the 1990s, primary care physicians appeared to be in short supply relative to specialists, especially in light of the movement toward managed care and its heightened roles for primary care physicians as gatekeepers and care managers. Efforts to correct this specialty imbalance included federal training grants for new residency training in primary care specialties. For the most part, however, the bias toward specialty practice has persisted due to the higher earnings potential in many specialty areas compared to primary care practice. Rising levels of medical student debt and increasing medical practice expenses and malpractice insurance costs have reinforced this bias. Even more difficult to address is the maldistribution of physicians in rural versus urban areas and in wealthy versus lower-income communities. Physicians tend to locate where they want to live and where their earning potential is greatest rather than where unmet needs exist. Rural and inner-city communities face persistent difficulties recruiting and retaining physicians due to their lower incomes, greater professional isolation, higher charity care burden, and perceived quality of life issues. Several federal and state programs exist to encourage physicians to practice in rural and urban underserved areas. Several states have loan repayment programs for medical students that agree to practice in these areas after graduation. The federal National Health Service Corps provides similar incentives. Other programs are designed to expose medical students to the professional rewards of practicing in underserved areas, or to recruit medical students from among the residents of these areas, with the expectation that participants would be more likely to return to practice in these areas after medical school. Unfortunately many of these programs have had only limited success.

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The American Health-Care System: Structure and Function

1229

TABLE 74-6. U.S. PHYSICIANS ACCORDING TO ACTIVITY AND PLACE OF EDUCATION, 1970–2002 Physician Characteristics

1970

1975

1980

1985

1990

1995

Doctors of medicine Doctors per 100,000 population

334,028 16.4

393,742 15.3

467,679 20.6

552,716 20.7

615,421 24.7

720,325 24.2

Professionally active

310,845

340,280

414,916

497,140

547,310

Place of medical education: U.S. medical graduates International medical graduates

256,427 54,418

— —

333,325 81,591

392,007 105,133

Activity: Nonfederal Patient care Office-based practice

281,344 255,027 188,924

312,089 287,837 213,334

397,129 361,915 271,268

General and family practice

50,816

46,347

Cardiovascular diseases Dermatology Gastroenterology Internal medicine Pediatrics Pulmonary diseases

3882 2932 1112 22,950 10,310 785

General surgery Obstetrics and gynecology Ophthalmology Orthopedic surgery Otolaryngology Plastic surgery Urological surgery Anesthesiology Diagnostic radiology Emergency medicine Neurology Pathology, anatomical/clinical Psychiatry Radiology Other specialty

2000

2001

2002

813,770 28.9

836,156 29.4

853,187 29.6

625,443

690,128

709,168

717,549

432,884 114,426

481,137 144,306

525,691 164,437

537,529 171,639

544,779 172,770

475,573 431,527 329,041

526,835 487,796 359,932

604,364 564,074 427,275

672,987 631,431 490,398

693,358 652,328 514,016

699,249 658,123 516,246

47,772

53,862

57,571

59,932

67,534

70,030

71,696

5046 3442 1696 28,188 12,687 1166

6725 4372 2735 40,514 17,436 2040

9054 5325 4135 52,712 22,392 3035

10,670 5996 5200 57,799 26,494 3659

13,739 6959 7300 72,612 33,890 4964

16,300 7969 8515 88,699 42,215 6095

16,991 8199 8905 94,674 44,824 6596

16,989 8282 9044 96,496 46,097 6672

18,068 13,847 7627 6533 3914 1166 4273

19,710 15,613 8795 8148 4297 1706 5025

22,409 19,503 10,598 10,719 5262 2437 6222

24,708 23,525 12,212 13,033 5751 3299 7081

24,498 25,475 13,055 14,187 6360 3835 7392

24,086 29,111 14,596 17,136 7139 4612 7991

24,475 31,726 15,598 17,367 7581 5308 8460

25,632 32,582 15,994 17,829 7866 5545 8636

24,902 32,738 16,052 18,118 8001 5593 8615

7369 896 — 1192 2993 10,078 5781 12,400

8970 1978 — 1862 4195 12,173 6970 15,320

11,336 4190 — 3245 5952 15,946 7791 24,064

15,285 7735 — 4691 6877 18,521 7355 28,453

17,789 9806 8402 5587 7269 20,048 6056 22,784

23,770 12,751 11,700 7623 9031 23,334 5994 29,005

27,624 14,622 14,541 8559 10,267 24,955 6674 35,314

28,868 15,596 15,823 9156 10,554 25,653 6830 37,233

28,661 15,896 16,907 9034 10,103 25,350 6916 34,084

Hospital-based practice Residents and interns Full-time hospital staff Other professional activity

66,103 45,840 20,263 26,317

74,503 53,527 20,976 24,252

90,647 59,615 31,032 35,214

102,486 72,159 30,327 44,046

127,864 89,913 37,951 39,039

136,799 93,650 43,149 40,290

141,033 95,125 45,908 41,556

138,312 92,935 45,377 41,118

141,877 96,547 45,330 41,126

Federal Patient care Office-based practice Hospital-based practice Residents and interns Full-time hospital staff Other professional activity

29,501 23,508 3515 19,993 5388 14,605 5993

28,191 24,100 2095 22,005 4275 17,730 4091

17,787 14,597 732 13,865 2427 11,438 3190

21,567 17,293 1156 16,137 3252 12,885 4274

20,475 15,632 1063 14,569 1725 12,844 4843

21,079 18,057 — 18,057 2702 15,355 3022

19,381 15,999 — 15,999 600 15,399 3382

20,017 16,611 — 16,611 739 15,872 3406

20,182 16,701 — 16,701 390 16,311 3481

19,621 358 3204

21,449 26,145 5868

25,744 20,629 6390

38,646 13,950 2980

52,653 12,678 2780

72,326 20,579 1977

75,168 45,136 1098

81,520 38,314 2947

84,166 49,067 523

Number of Doctors of Medicine

Inactive Not classified Unknown address

Sources: American Medical Association (AMA) Distribution of physicians in the United States, 1970; Physician distribution and medical licensure in the US, 1975; Physician characteristics and distribution in the US, 1981, 1986, 1989, 1990, 1992, 1993, 1994, 1995–96, 1996–97, 1997–98, 1999, 2000–2001, 2001–2002, 2002–2003, 2003–2004, 2004 editions, Department of Physician Practice and Communications Information, Division of Survey and Data Resources, AMA. (Copyrights. 1971, 1976, 1982, 1986, 1989, 1990, 1992, 1993, 1994, 1996, 1997, 1999, 2000, 2001, 2002, 2003, 2004: Used with the permission of the AMA) Health, United States, 2004.

Nursing Registered nurses constitute the largest health-care profession with 2.3 million members, and over the next 10 years more new jobs are expected to be created for nurses than for any other health profession.14 About half of registered nursing jobs are in hospitals, in both inpatient and outpatient departments (Table 74-7). Many other nurses work in offices of physicians, nursing care facilities, home

health-care services, outpatient care centers, and public health agencies. About one in five nurses works part-time. The three primary educational paths to registered nursing are a bachelor’s degree, an associate degree, and a diploma. The diploma historically has been offered in hospital-based training programs, whereas the other degrees have been offered in college and university-based programs. Since the 1980s, the nursing profession has

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Health-Care Planning, Organization, and Evaluation

TABLE 74-7. U.S. REGISTERED NURSES BY EMPLOYMENT SETTING 2002 Employment

Projected 2012 Employment

Change, 2002–2012

Percent Distribution

Number Distribution

Percent

Number

2,284,459 1,123,488 195,914 163,923 126,889 111,324 64,336 63,952

100.00 49.18 8.58 7.18 5.55 4.87 2.82 2.8

2,907,614 1,355,775 305,331 183,786 172,669 177,700 100,278 64,534

100.00 46.63 10.5 6.32 5.94 6.11 3.45 2.22

623,156 232,286 109,417 19,864 45,779 66,376 35,942 582

27.3 20.7 55.8 12.1 36.1 59.6 55.9 0.9

52,081 51,187

2.28 2.24

55,670 74,786

1.91 2.57

3589 23,599

6.9 46.1

50,238

2.2

54,205

1.86

3967

7.9

Industry

Number

Total employment, all workers Hospitals, private Offices of physicians Local government hospitals Nursing care facilities Home health-care services Employment services State government hospitals Local government, excluding education and hospitals Outpatient care centers Federal Government, excluding Postal Service

Percent

Source: U.S. Bureau of Labor Statistics. Nursing Occupation Report. Washington, DC: BLS; 2005.

promoted university-educated nurses over diploma nurses in state licensing and credentialing programs, leading the numbers of diploma graduates to decline. To assist registered nurses, an auxiliary profession exists in the form of the licensed practical nurse, which requires a year of training in a vocational program. Additionally, higher-level professional categories exist in the form of advancedpractice nursing, which requires significant postbaccalaureate training and may include a master’s or doctoral degree. Advanced-practice nurses such as nurse practitioners and clinical nurse specialists enjoy a greater degree of professional autonomy and assume higher overall levels of patient care responsibility than do registered nurses. The health-care industry has periodically confronted times of apparent shortage in the supply of nurses. Nursing shortages are attributable to a variety of factors. Many nurses leave the field of practice prematurely due to salary constraints, stressful work environments, and limited opportunities for professional advancement. Moreover, the downsizing that occurred in the U.S. hospital industry during the 1980s and 1990s has required nurses to care for larger numbers of more acutely ill patients during generally shorter lengths of stay. Moreover, the efforts of some hospitals to contain costs by replacing registered nurses with LPNs and nurses aides served to reduce morale and job satisfaction among many nurses. More recently, the upsurge in hospital utilization and the efforts of many hospitals to expand their facilities and clinical services have caused the demand for nurses to outstrip the existing supply in many communities, leading to heightened competition for nurses and rising nursing compensation. The growing body of evidence concerning the effects that nurse staffing levels have on quality of care and health outcomes in hospitals and other health-care settings has also stimulated additional demand for nurses within the health-care industry. In response, nursing schools across the country have taken steps to increase their enrollment, often with financial support from area hospitals or special governmental programs. However, the production of new nursing graduates remains constrained by the availability of graduate-degree nursing faculty to teach in these schools.

Other Clinical Personnel Nonphysician health professionals such as nurse practitioners and physician assistants have assumed expanding responsibilities within the health-care system in recent decades. Nurse practitioners are registered nurses who receive 1–2 years of additional clinical training and sometimes a master’s degree. Physician assistants typically receive training through a 2-year university-based program that may result in a bachelor’s or master’s degree. Both of these professionals

provide patient care relatively autonomously but generally under the general direction of a physician. Some practice settings such as medical groups, community health centers, and staff-model HMOs use these professionals as lower-cost “physician extenders” to perform routine clinical services that physicians would otherwise provide, thereby freeing up physician time to provide more complex care. In some cases these professionals have been used to staff clinics in underserved geographic areas where physicians were unavailable, thereby expanding access to care. The use of nurse practitioners and physician assistants has been limited by professional and political struggles over where and under what circumstances they can practice. State medical societies have aggressively sought to limit their scope of practice and their ability to practice independently of physicians. Public and private insurance programs have also been reluctant to allow these professionals to directly bill for their services, in part due to concerns that these professionals will generate new and duplicative health-care costs rather than substitute for more costly physician services. Nevertheless, a growing body of evidence suggests that in appropriate practice settings these professionals can provide high-quality care at lower cost than care delivered by physicians alone. Other professional components of the health-care workforce include dentists, dental hygienists, podiatrists, psychologists, social workers, pharmacists, therapists, nutritionists, audiologists, and optometrists. To support this professional workforce, an expanding array of technical workers practice within the health-care system, contributing specialized knowledge and skills in the application of medical technologies and equipment. These workers include medical and radiological technicians, nuclear medicine technicians, sonographers, laboratory technicians, surgical technicians, and cardiovascular technicians. A variety of clinical service support staff also assist the health professions workforce, including nursing assistants and aides, home health aides, physical and occupational therapy assistants and aides, and pharmacy assistants and aides.

Health-Care Purchasers Expenditures for health care in the United States totaled more than $1.5 trillion in 2002, more than any other industrialized country on a per capita basis or as a percentage of the gross domestic product (Table 74-8).15 Private health insurance remains the single largest source of these funds, accounting for about 36% of all personal health-care expenditures. The federal government pays for about 34% of these expenditures through the Medicare program, the federal

74

The American Health-Care System: Structure and Function

TABLE 74-8. HEALTH-CARE EXPENDITURES IN THE UNITED STATES AND SELECTED COUNTRIES, 1960–2001 Country

1960

1970

1980

1990

2000

2001

Health Expenditures as a Percent of Gross Domestic Product Australia Austria Belgium Canada Czech Republic Denmark Finland France Germany

4.1 4.3 — 5.4 — — 3.8 — —

— 5.3 4.0 7.0 — — 5.6 — 6.2

7.0 7.6 6.4 7.1 — 9.1 6.4 — 8.7

7.8 7.1 7.4 9.0 5.0 8.5 7.8 8.6 8.5

8.9 7.7 8.6 9.2 7.1 8.3 6.7 9.3 10.6

9.2 7.7 9.0 9.7 7.3 8.6 7.0 9.5 10.7

Greece Hungary Iceland Ireland Italy Japan Korea Luxembourg Mexico Netherlands

— — 3.0 3.7 — 3.0 — — — —

6.1 — 4.7 5.1 — 4.5 — 3.6 — —

6.6 — 6.2 8.4 — 6.4 — 5.9 — 7.5

7.4 — 8.0 6.1 8.0 5.9 4.8 6.1 4.8 8.0

9.4 6.7 9.3 6.4 8.2 7.7 5.9 5.6 5.6 8.6

9.4 6.8 9.2 6.5 8.4 8.0 — — 6.0 8.9

New Zealand Norway Poland Portugal Slovak Republic Spain Sweden Switzerland Turkey United Kingdom United States

— 2.9 — — — 1.5 — 4.9 — 3.9 5.1

5.1 4.4 — 2.6 — 3.6 6.7 5.6 2.4 4.5 7.0

5.9 6.9 — 5.6 — 5.4 8.8 7.6 3.3 5.6 8.8

6.9 7.7 5.3 6.2 — 6.7 8.2 8.5 3.6 6.0 12.0

8.0 7.6 6.0 9.0 5.7 7.5 8.4 10.7 — 7.3 13.3

8.1 8.0 6.3 9.2 5.7 7.5 8.7 11.1 — 7.6 14.1

Per Capita Health Expenditures Australia Austria Belgium Canada Czech Republic Denmark Finland France Germany

$87 64 — 107 — — 54 — —

— $159 130 255 — — 161 — 223

$658 662 576 709 — 819 509 — 824

$1300 1204 1245 1674 575 1453 1295 1509 1600

$2363 2170 2260 2580 987 2398 1699 2387 2780

$2513 2191 2490 2792 1106 2503 1841 2561 2808

Greece Hungary Iceland Ireland Italy Japan Korea Luxembourg Mexico Netherlands New Zealand Norway Poland Portugal Slovak Republic Spain Sweden Switzerland Turkey

— — 45 36 — 26 — — — — — 46 — — — 14 — 138 —

98 — 129 99 — 130 — 148 — — 177 132 — 46 — 83 270 292 23

348 — 576 452 — 523 — 606 — 668 458 632 — 265 — 328 850 891 75

695 — 1377 719 1321 1082 354 1501 276 1333 937 1363 259 611 — 813 1492 1836 171

1556 817 2605 1793 2060 2002 893 2719 492 2348 1611 2755 572 1519 641 1497 2195 3160 —

1511 911 2643 1935 2212 2131 — — 536 2626 1710 2920 629 1613 682 1600 2270 3322 —

(Continued)

1231

1232

Health-Care Planning, Organization, and Evaluation TABLE 74-8. HEALTH-CARE EXPENDITURES IN THE U.S. AND SELECTED COUNTRIES, 1960–2001 (Continued) Country

1960

1970

1980

1990

2000

2001

United Kingdom United States —Data not available

74 143

144 348

445 1067

977 2738

1813 4670

1992 5021

Sources: All countries except United States from the Organization for Economic Cooperation and Development Health Data File 2003, following the annual update, www.oecd.org/els/health; United States data from the Centers for Medicare & Medicaid Services, Office of the Actuary, National Health Statistics Group, National Health Expenditures, 2002. Internet address: cms.hhs.gov/ statistics/nhe. Health, United States, 2004.

share of the Medicaid and State Children’s Health Insurance (SCHIP) programs, and through health insurance programs for federal employees, the active-duty military, and veterans. Approximately 11% of the nation’s health-care expenditures are paid by state and local governments, mostly for Medicaid and SCHIP recipients but also for health insurance for government employees. Consumers pay the remaining 16% of the nation’s health-care expenditures through out-of-pocket costs, including the self-pay payments made by uninsured patients as well as the deductibles and copayments incurred by patients covered by private or public health insurance programs. National health spending increased at double-digit annual rates of growth for much of the period following the creation of the federal Medicare and Medicaid programs in 1965. However, spending slowed during the 1990s, a fact attributed at least in part to the emergence of managed care plans in the private health insurance industry and their use of cost containment techniques such as selective contracting with health-care providers, preauthorization requirements for high-cost services, and capitated payment methods for hospitals and physicians. These managed care techniques were also introduced into many state Medicaid programs and into the federal Medicare program on an optional basis. During the late 1990s, mounting public and professional dissatisfaction with managed care and its restrictions on health-care utilization led many private health insurers to scale back the use of these techniques. Since then, health-care spending has returned to double-digit annual rates of growth.

Private Health Insurance Most individuals have some type of health insurance, although the number of Americans without health insurance coverage has continued to grow over the past decade (Table 74-9). Most individuals obtain private health insurance through an employer, with the employer paying part of the premium and the employee also contributing toward the premium through a payroll deduction. Individuals without access to employer-provided health insurance may purchase an individual policy directly from a private health insurance carrier. Individual policies are generally more costly than group insurance policies obtained through an employer because of the increased administrative costs involved in marketing and processing individual policies and because of the increased financial risk entailed in individual policies. Private health insurers gradually became the predominant method for financing health care during the 1900s. Initially commercial insurance companies were reluctant to offer insurance for healthcare expenditures because of concerns that it would attract only the sick (termed adverse selection) and encourage subscribers to overconsume health services (termed moral hazard). In the absence of commercial insurance policies, the fore-runners to the Blue Cross and Blue Shield health insurance plans were created during the Great Depression to allow individuals with limited incomes to prepay for health care they may need in the future. Hospitals and later physicians in many communities supported the emergence of these not-for-profit plans because of their ability to improve financial access to healthcare services and reduce unpaid hospital bills. Employers began offering subsidized health insurance as a benefit to their employees

in large numbers during World War II, when federal wage and price controls prevented employers from using wages to compete for scarce labor. Federal tax policies strengthened interest in employer-provided health insurance by making health insurance contributions exempt from employers’ payroll tax obligations as well as employees’ income tax obligations. As demand for private health insurance grew, commercial insurers rapidly entered the market for selling group health insurance policies because of the diminished potential for adverse selection among relatively young and healthy workers and their families. By the early 1950s, more individuals received insurance coverage from commercial insurers than from Blue Cross and Blue Shield plans. The policies sold by both types of insurance carriers were indemnity policies that reimbursed subscribers for their health-care expenses based on an established percentage of the usual, customary, and reasonable (UCR) charge that prevailed in the local area. Any difference between the provider’s actual charge and the carrier’s UCR-based reimbursement was borne by the subscriber as an out-of-pocket cost. By the 1950s, many indemnity policies provided coverage for both hospital and physician services. Rapidly rising health-care costs during the 1970s led employers— who paid most of the health insurance premiums for their employees— to search for strategies to reign in these costs. HMOs began to receive increasing attention as a lower-cost alternative to traditional indemnity insurance policies. HMOs contained costs by covering only those services delivered by a relatively limited network of physicians and hospitals. Rather than reimbursing subscribers for each service they receive based on a percentage of the UCR charge, HMOs frequently used capitated payment methods wherein providers agree to provide or arrange for all of the services needed by a defined panel of subscribers in exchange for fixed monthly payment per subscriber from the HMO. These methods created financial incentives for providers to reduce unnecessary service utilization and coordinate health-care delivery in order to keep health-care costs below their capitated payment rate. As an additional cost-saving mechanism, many HMOs also required subscribers to obtain a referral from their designated primary care physician before accessing services from specialists, hospitals, or other specialty providers. Federal legislation enacted during the 1970s encouraged the development of HMOs but indemnity health insurance remained dominant through the 1980s in most communities. As health-care costs continued to grow during the 1980s, several variants on the HMO concept emerged that collectively became known as managed care plans. Most of these plans sought to contain costs by selectively contracting with a limited network of physicians and hospitals that agreed to accept discounted payment arrangements in exchange for the prospect of increased patient volume. The least restrictive of these plans, known as preferred provider organizations (PPOs), typically allowed subscribers to access specialists without a referral from their primary care physician and offered subscribers the option of seeking care from providers not included in the plan’s network in exchange for paying higher out-of-pocket fees. Other plans, known as HMO point-of-service (POS) plans, required referrals for most specialist visits similar to the HMO design but offered out-of-network benefits similar to the PPO design. Managed

74

The American Health-Care System: Structure and Function

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TABLE 74–9. LACK OF HEALTH INSURANCE AMONG U.S. RESIDENTS UNDER 65 YEARS, 1984–2002 Characteristic

1984

1989

1994

1999

Total

29.8

33.4

40.0

Total, age adjusted Total, crude Under 18 years Under 6 years 6–17 years 18–44 years 18–24 years 25–34 years 35–44 years 45–64 years 45–54 years 55–64 years

14.3 14.5 13.9 14.9 13.4 17.1 25.0 16.2 11.2 9.6 10.5 8.7

15.3 15.6 14.7 15.1 14.5 18.4 27.1 18.3 12.3 10.5 11.0 10.0

17.2 17.5 15.0 13.4 15.8 21.7 30.8 21.9 15.9 12.0 12.5 11.2

Male Female

15.0 13.6

16.4 14.3

18.5 16.1

17.2 15.0

White only Black or African American only American Indian and Alaska Native only Asian only Native Hawaiian and Other Pacific Islander only 2 or more races Hispanic or Latino Mexican Puerto Rican Cuban Other Hispanic or Latino Not Hispanic or Latino White only Black or African American only All ages: Below 100 percent 100—149 percent 150—199 percent 200 percent or more Under 18 years: Below 100 percent 100—149 percent 150—199 percent 200 percent or more Geographic region Northeast Midwest South West Urban residence Within MSA Outside MSA

13.4 20.0 # 18.0 —

14.2 21.4 # 18.5 —

16.6 19.7 # 20.1 —

— 29.1 33.2 18.1 21.6 27.5 13.0 11.8 19.7

— 32.4 38.8 23.3 20.9 25.2 13.5 11.9 21.3

34.7 27.0 17.4 5.8

2000

2001

2002

39.2

40.6

16.2 16.1 11.0 9.7 11.7 21.7 29.3 22.3 16.7 12.3 13.0 11.0

16.6 16.5 10.7 9.1 11.5 22.5 28.2 23.8 17.8 13.1 14.1 11.6

17.8 15.8

17.2 15.1

18.2 15.1

14.6 19.5 38.3 16.4 ∗

15.2 20.0 38.2 17.3 ∗

14.7 19.3 33.4 17.1 ∗

15.3 19.3 38.7 17.2 ∗

— 31.8 36.2 15.7 27.4 30.7 15.5 14.4 19.3

16.8 33.9 38.0 19.8 19.7 30.8 13.5 12.1 19.4

18.4 35.4 39.9 16.4 25.2 32.7 14.1 12.5 20.0

18.6 34.8 39.0 16.0 19.2 33.1 13.4 11.9 19.2

19.2 33.8 37.0 19.5 20.5 32.9 14.0 12.6 19.2

35.8 31.3 21.8 6.8

33.1 35.0 26.1 9.2

35.6 34.7 27.2 9.1

35.2 35.2 27.2 10.0

34.0 32.0 26.5 9.9

31.4 32.8 25.6 10.9

28.9 22.8 12.7 4.2

31.6 26.1 15.8 4.4

22.1 27.7 19.1 7.1

22.3 24.2 19.1 5.4

21.8 25.1 17.6 6.5

20.6 19.4 17.3 5.8

16.9 19.2 14.2 6.7

10.1 11.1 17.4 17.8

10.7 10.5 19.4 18.4

13.6 12.2 21.0 20.4

12.2 11.5 19.8 18.6

12.1 12.3 20.4 20.2

11.6 11.7 20.0 18.6

12.7 12.4 20.2 18.8

13.3 16.4

14.9 16.9

16.7 19.0

15.3 18.9

16.3 18.8

15.6 18.5

16.1 18.9

Numbers in Millions 38.5 40.5 Percent of Population 16.1 16.8 16.1 16.8 11.9 12.4 11.0 11.7 12.3 12.8 21.0 22.0 27.4 29.7 22.1 22.7 16.3 16.8 12.2 12.7 12.8 12.8 11.4 12.5

# Estimates are available from the source upon request. ∗ Estimates have a relative standard error >30% and are considered unreliable Sources: Centers for Disease Control and Prevention, National Center for Health Statistics National Health Interview Survey, Health Insurance Supplements (1984, 1989, 1994–1996). Starting in 1997 data are from the family core questionnaires. Health, United States, 2004.

care plans also used a variety of administrative controls designed to limit health-care utilization and expenditures, including requiring physicians and/or subscribers to obtain preauthorizations, or medical necessity determinations, from the health plan before seeking specified high-cost services and procedures from hospitals and specialists. Enrollment in managed care plans grew rapidly during the late 1980s and early 1990s because of the relatively low insurance

premiums these plans offered employers and the relatively low outof-pocket costs they offered consumers compared to traditional indemnity insurance. Correspondingly, annual rates of growth in private health insurance premiums fell significantly during the 1990s. By the latter part of this decade, however, both consumers and providers began voicing complaints about the restrictions that these plans imposed on health-care choices. Faced with increasingly competitive labor markets, employers were pressured to offer less

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Health-Care Planning, Organization, and Evaluation

restrictive health insurance designs to their employees that included access to larger networks of providers and placed fewer restrictions on health-care utilization.16 At the same time, hospitals and physicians began negotiating more aggressively with health insurers for more favorable payment rates—including an end to capitated payments in many cases—as well as for fewer administrative requirements regarding referrals, preauthorizations, and medical necessity determinations. Growing public dissatisfaction with managed care plans also led state and federal policy makers to adopt regulatory limits on the use of containment techniques, including mandatory minimum hospital stays for selected procedures, mandatory coverage requirements for selected services, and any-willing-provider laws that limit selective contracting. In response, many managed care plans have scaled back these cost containment tools and moved to broader and more inclusive provider networks and traditional fee-for-service payment methods in order to retain their membership. In the wake of the managed care backlash, HMO enrollment has slowed and even declined in many communities while enrollment in less restrictive PPO insurance products has increased substantially. Since 2000, private health insurance premiums have resumed doubledigit annual rates of growth, placing renewed pressure on employers and insurers to find new ways of containing costs.17 Many smaller employers, unable to absorb the increased costs, have shifted more of the costs to consumers through increased payroll deductions for employee premium contributions and larger out-of-pocket costs for deductibles and copayments. As a consequence, larger numbers of employees are now declining to accept the insurance coverage offered by their employers because of the added costs entailed. Some small employers have chosen to discontinue insurance coverage for their employees’ spouses and dependents, while others have discontinued offering health insurance benefits altogether because of the rising costs. These developments are contributing to the rising numbers of individuals that lack health insurance coverage, which reached 45 million Americans in 2003. Private insurers and employers are currently pursuing two primary strategies for limiting the future growth of health-care costs and private health insurance premiums. First, these purchasers are investing more heavily in disease management programs and related care management initiatives designed to improve the likelihood that patients with identified health conditions and risks receive evidencebased standards of care and adhere to recommended self-care guidelines. These programs use a combination of interventions that are often tailored to a patient’s disease stage and level of risk, including printed health education materials, telephone outreach and follow-up, and provider notification and profiling. The most widely used diseasespecific programs currently target the most prevalent and costly health conditions, including diabetes, asthma, congestive heart failure, coronary artery disease, and depression. Other programs target patients with a variety of complex health conditions that result in high-cost episodes of care or sentinel events such as long hospital stays or repeated emergency department visits. A large number of specialty disease management vendors have emerged within the health-care system over the past decade to assist insurers and employers in implementing these programs. As a second cost-control strategy, purchasers have begun to experiment with new “consumer-driven” health insurance designs that require consumers to assume more responsibility for balancing issues of cost, choice, and quality when selecting among health-care providers and treatment alternatives. The most common designs take the form of a PPO health plan with a relatively large deductible that consumers must meet before services are covered by the plan. These high-deductible health plans are coupled with a spending account that consumers can use to pay health-care expenses before the deductible is met. The spending account may be funded with money contributed by the employer, by the employee, or both. A new law passed by Congress in 2003 allows consumers covered by high-deductible health plans to contribute funds to designated Health Savings Accounts (HSAs) on a pretax basis and to accumulate unused funds in the account from year to year. Proponents of these designs anticipate that

they will encourage consumers to be more economical in their healthcare decision-making and to shop for the best value among alternative providers and treatment options. To this end, health insurers are developing a variety of decision support tools and information resources for consumers to use, including cost estimators and reports containing quality measures for specific hospitals and physicians. One of the biggest limitations of these new products is the lack of accurate provider-specific information on health-care costs and prices so that consumers can factor this information into their decisions. Other observers fear that these plans will encourage consumers— especially those with low incomes—to forego needed health care once their spending accounts have been depleted, thereby contributing to the growing problem of underinsurance. Still others fear that these new insurance designs will contribute to adverse selection by attracting primarily young and healthy employees, leaving older and sicker individuals in traditional health plans and making these plans increasingly unaffordable to employers and consumers. To date, enrollment in these new insurance designs has been modest, so it remains unclear what impact they may have on the health-care system of the future.

Governmental Health Insurance The advent of public insurance programs during the 1960s, especially Medicare and Medicaid, ushered in major improvements in financial access to care for some of the nation’s most vulnerable populations, including the elderly, disabled, and poor. Both programs have been revised many times in response to cost containment pressures, quality and utilization concerns, and various political developments. More recently, the SCHIP was added by Congress in 1997 to expand coverage for low-income children, another vulnerable population that was not fully reached by the existing Medicaid program. These public programs not only supplement the private health insurance market by targeting populations that lack access to private coverage, but these programs also interact with this market in complex and sometimes unexpected ways. For example, efforts to expand coverage for lowincome, working adults and their children through Medicaid and SCHIP may “crowd out” the demand for private health insurance coverage among these populations and ultimately shift costs from the private sector to the public sector. Conversely, efforts to constrain costs in public sector programs like Medicare and Medicaid by limiting payments to hospitals and physicians may lead providers to increase the prices they negotiate with private insurers, thereby shifting costs from the public to the private sector. Medicare. Medicare is a federal health insurance program that serves three basic categories of beneficiaries: individuals age 65 and older, individuals who are permanently and completely disabled, and individuals with end-stage renal disease. The program has evolved over its 40-year history and now includes four major components. Part A provides coverage for short-stay hospital inpatient services, skilled nursing facilities, home health services, and hospice care. Part A coverage is financed through the Medicare Trust Fund which is funded from employer and employee payroll taxes. Coverage under Part A is mandatory for all eligibility groups, and beneficiaries are responsible for paying an out-of-pocket deductible for hospital care. Historically, payments to providers under Medicare Part A were based on a cost-based reimbursement system, but over time Medicare has adopted prospective payment methods for most services that pay providers a fixed amount for an episode of care regardless of the actual cost of care delivered. The fixed payment methods are tailored to specific types of diagnoses, services, and acuity levels and are adjusted for outlier cases that require more intensive care than the average patient. These methods create financial incentives for providers to reduce unnecessary and inappropriate care and minimize patient lengths of stay and readmissions. Such a system was implemented for inpatient hospital care in 1986 and extended to skilled nursing and home health during the late 1990s. Medicare’s second major component, Part B, covers physician care and other outpatient services. Part B is an optional benefit and

74 beneficiaries are responsible for paying a monthly premium for this coverage that is set to cover approximately 25% of the Part B costs. Physicians are paid using a modified fee-for-service methodology that adjusts payments to account for the time and resources required to deliver each service. This methodology, known as the Resource Based Relative Value Scale, is designed to reward physicians for performing timeintensive cognitive services that are common in primary care as opposed to purely procedure-based services that are common in specialty care. Both Part A and Part B leave Medicare beneficiaries exposed to significant out-of-pocket costs, including deductibles, copayments, and costs for noncovered services. Beneficiaries therefore have the option of purchasing private, supplementary health insurance coverage. These Medicare supplemental policies offer coverage for Medicare Part A deductibles and Part B copayments, and some policies offer additional coverage for services not covered by Medicare, including vision, and dental care. These policies are offered by a variety of private health insurance carriers and are regulated by state insurance departments. A third component of the Medicare program, Part C, covers an array of managed care plans that beneficiaries may choose to enroll in as an alternative to the traditional Medicare program. The Medicare program began experimenting with managed care plans on a voluntaryenrollment basis from the program’s very inception in 1965, and these options have evolved considerably over time. Medicare launched a major effort to expand managed care enrollment in Medicare in 1997 with the Medicare+Choice program, which authorized the creation of new plan options including HMOs, provider-sponsored plans, PPOs, and private fee-for-service plans. Because enrollment is voluntary, plans must compete to attract membership by offering additional benefits not available in the traditional Medicare program such as coverage for outpatient prescription drugs and expanded preventive and wellness services, and by offering lower premiums and out-of-pocket costs than are found in the traditional program. Plans must balance these benefits with the capitated payments they receive from Medicare, which are based on the average adjusted per-capita cost of serving beneficiaries in the traditional Medicare program and which vary by county. Managed care offerings and enrollment initially expanded under Medicare+Choice, but congressionally imposed limits on health plan payment updates ultimately led plans to scale back their benefits and pull out from a growing number of unprofitable counties. Nationally, Medicare enrollment in managed care plans dropped from 17% in 1999 to 12% in 2002. Most recently, Congress has attempted to revive managed care options for Medicare beneficiaries through the Medicare Advantage program created under the Medicare Modernization Act of 2003, which increases payment levels for private managed care plans and creates additional options for participating in Medicare as a private plan. The new program has attracted a number of health plans back into the Medicare market, but the long-term success of this program remains to be seen. The fourth and newest component of the Medicare program is Part D, which for the first time offers Medicare beneficiaries coverage for outpatient prescription drugs. This component was enacted as part of the Medicare Modernization Act of 2003 and took effect during 2006. As a voluntary component of the program, Medicare beneficiaries have the option to enroll in one of several private plans that offer prescription drug coverage that is compliant with the formulary requirements developed by Medicare. Options include a freestanding prescription drug plan that can be combined with the traditional Medicare program, as well as a variety of Medicare Advantage managed care plans that offer drug coverage along with other benefits. The Part D program also offers financial incentives to employers that currently offer their retirees a Medicare supplemental plan with prescription drug coverage, in order to encourage these employers to continue offering this coverage. The new Part D benefits promise to fill a longstanding gap in the Medicare benefit package, but its ultimate impact on the health-care system remains to be seen. Medicaid. Medicaid is now the single largest health-care program in the country, paying for medical and long-term care for more than

The American Health-Care System: Structure and Function

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53 million poor, elderly, and disabled Americans. It finances more than one-third of all births in the United States and pays the costs of almost two-thirds of the people in nursing homes.18 Because Medicare does not cover long-term care services and few individuals purchase private long-term care insurance, Medicaid is the nation’s single largest purchaser of long-term care, accounting for 43% of all spending on these services. The Medicaid program is jointly financed and administered by the federal government and individual state governments. Individual states provide partial funding for the program and agree to provide coverage for a minimum set of services and serve a minimum set of eligible recipients in order to receive federal matching funds. The states can choose to provide coverage for additional, optional services and for additional eligibility categories. The minimum services covered include inpatient and outpatient medical care, physician services, laboratory and imaging services, family planning services, mental health services, early childhood diagnostic screening and treatment services, and selected long-term care services including nursing home care and home health care. Optional services include rehabilitation care, dental care, and home and community-based long-term care services. The federal government requires that these services be provided to certain groups of low-income people, including the elderly, people with disabilities, children, and pregnant women and parents of children. People within these categories who have incomes below the historical eligibility criteria for cash assistance programs are considered mandatory for Medicaid coverage. Examples of mandatory eligibility groups include children in families with incomes below 100% of the federal poverty level (FPL), pregnant women with incomes below 133% of the FPL, and individuals with disabilities that receive cash assistance through the federal Supplemental Security Income (SSI) program. Other low-income population groups are considered optional, such as the disabled and elderly not eligible for SSI but below 100% of FPL, and nursing home residents not eligible for SSI but below 300% of the SSI eligibility level. Low-income adults under age 65 who are not living with a disability and are not caring for children generally do not qualify for coverage except through optional state waivers. When states choose to cover an optional eligibility group, these groups are usually eligible for the same set of benefits offered to mandatory groups. An exception is individuals covered under optional state Medically Needy categories. Individuals qualifying through these categories may have incomes above the state’s standard eligibility thresholds but when their medical expenditures are taken into account they fall below these thresholds. Many individuals with chronic health conditions requiring high-cost treatments, such as cancer, HIV/AIDS, and nursing home patients, fall into these categories. Under federal guidelines, states may provide a reduced benefit package for Medically Needy individuals that is typically limited to those services needed to address the relevant chronic health condition. The federal government matches the funds that states spend on their Medicaid programs using a match rate that is based on each state’s per capita income. The average federal matching rate was 57% in 2003 and ranged from 50% to 77% across states. Despite this significant federal subsidy, Medicaid programs represent a substantial and growing proportion of many states’ budgets. Rising health-care costs and increasing numbers of individuals eligible for Medicaid have caused the Medicaid program to become one of the largest budget items for many states, often rivaling or exceeding state education expenditures. In an effort to contain costs, a number of states have secured waivers from federal Medicaid program requirements that allow the states to implement key changes in the delivery and financing of health services for their Medicaid recipients. Many states have used these waivers to implement managed care programs for selected categories of Medicaid recipients, including arrangements that allow private HMOs and other managed care plans to enroll and arrange care for these recipients. Although experiences with Medicaid managed care have varied considerably across states, several

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Health-Care Planning, Organization, and Evaluation

of these programs have achieved considerable cost-savings while maintaining levels of access, quality, and patient satisfaction that are comparable to traditional fee-for-service programs. Some states have used the savings generated from their managed care programs to expand eligibility to additional population groups and to increase provider participation in Medicaid by raising payment levels. Likewise, many states have used waivers to implement programs that provide home and community-based long-term care services as lower-cost alternatives to nursing home care. Most recently, a number of states have used a new category of waivers under the federal Health Insurance Flexibility and Accountability (HIFA) initiative to implement more aggressive cost sharing provisions and management controls within their Medicaid programs in an effort to utilize contain costs. SCHIP. The State Children’s Health Insurance Program (SCHIP) was created by Congress in 1997 to expand health insurance coverage for low-income children not eligible for the traditional Medicaid program. SCHIP is the single largest expansion of health insurance coverage for children since the initiation of Medicaid in the mid1960s. Like Medicaid, SCHIP is jointly financed and administered by the federal government and individual state governments, but states have even broader discretion in setting policy regarding eligibility and services covered. SCHIP is designed to provide coverage to uninsured children who reside in families with incomes below 200% of the FPL or whose family has an income 50% higher than the state’s Medicaid eligibility threshold. Some states have expanded SCHIP eligibility beyond the 200% FPL limit, and others are covering entire families and not just children. SCHIP offers states three options when designing a program. The state can either (a) use SCHIP funds to expand Medicaid eligibility to children who previously did not qualify for the program; (b) design a separate children’s health insurance program entirely separate from Medicaid; or (c) combine both the Medicaid and separate program options. As of 1999, each of the 50 states had approved SCHIP plans in place. In addition to expanding eligibility, many states have used their SCHIP funds to implement statewide and community-based outreach and enrollment assistance activities, targeting eligible children who were not enrolled. States also increased access to coverage by designing streamlined enrollment strategies, such as creating simplified mail-in applications, eliminating the face-to-face interview and asset test requirements, adopting presumptive eligibility and 12-month continuous eligibility, and accelerating enrollment of uninsured children already participating in other means-tested programs such as food stamps or school lunch. As a result of these efforts, participation in Medicaid and SCHIP has grown substantially, reducing the number of uninsured children. Between 1996 and 2002, the uninsured rate among low-income children nationally dropped from 23% to 19%, largely due to increases in Medicaid and SCHIP coverage. Over the past few years, the economic downturn and resulting state budgetary shortfalls have forced states to slow spending on Medicaid and SCHIP. While some states are continuing to broaden access to coverage, many states have moved to restrict Medicaid and SCHIP enrollment for eligible children and parents. During 2003 and 2004, 23 states adopted policies that made it harder for eligible children and families to secure and retain coverage, including freezing enrollment, increasing premiums, and reversing previously simplified enrollment procedures.19 Most of these changes have been made in SCHIP rather than Medicaid programs, until recently states have had less flexibility to implement cost-sharing premiums, and enrollment freezes under Medicaid. As a result of these changes, SCHIP enrollment fell for the first time in the program’s history during the second half of 2003. Governmental health insurance programs for the poor and elderly perpetually face difficulties in securing the funding necessary to serve the populations that need this coverage. Adequate funding is especially difficult during periods of economic decline when job losses reduce access to private health insurance and constrict governmental

revenue streams. More persistent challenges loom for these programs due to the aging of the American population, continued escalation in health-care costs, and reductions in employer provision of health insurance for active workers as well as retirees. In response, more profound changes to these programs are likely to be necessary in the future. THE FUTURE

Although the American health-care system is a constantly evolving enterprise, many of its most severe problems and limitations tend to persist over time. Large numbers of Americans remain without adequate health insurance coverage and face financial and other barriers to health care. Health-care costs continue to rise rapidly and raise questions about the economic sustainability of the current system. And the quality and safety of health-care received by Americans often leaves much to be desired, all too often failing to conform to the evidence-based standards of care that are known to produce desired health outcomes. There are many activities underway at various levels within the system that appear to hold promise for improving system performance. For example, both private and public purchasers are investing in disease management interventions and health promotion programs designed to improve health outcomes, and some are experimenting with pay-for-performance programs that reward providers for improving the quality and efficiency of their practices. In turn, providers are implementing an expansive array of quality improvement and error reduction programs designed to improve the processes and outcomes of their care. And many providers have begun to adopt information technologies that can assist the health workforce in achieving these improvements, such as electronic medical records, disease registries, clinical decision support systems, and telehealth interventions. For the most part, however, the key actors within the health-care system are continuing down a path of individual, incremental change and reform. There is relatively little coordination and collaboration among the major purchasers and providers in carrying out their quality improvement activities, payment reforms, and information technology initiatives. As a result, many observers fear that these individual and isolated initiatives may not be sufficient to achieve meaningful change within the complex, interrelated, and dynamic health system that exists in the United States. Because no single organization or actor within society has full control over the health problems and threats that face the health-care system, effective solutions are likely to require multiorganizational and multisectoral efforts. Stronger policy action may be required at local, state, and federal levels to mobilize the collective action needed to address persistent deficits in health system performance. REFERENCES

1. William SJ, Torrens P. Introduction to Health Services, 5th ed. Albany, NY: Delmar Publishers; 2002. 2. Von Bertalanffy L. General Systems Theory: Foundations, Development, and Theory, New York: George Braziller; 1976. 3. National Center for Health Statistics. Health, United States, 2004, Hyattsville, MD: U.S. Public Health Service; 2005. 4. National Academy of Sciences Institute of Medicine. Crossing the Quality Chasm: A New Health System for the 21st Century, Washington, DC: National Academy Press; 2001. 5. Agency for Healthcare Research and Quality. National Healthcare Disparities Report, Rockville, MD: U.S. Department of Health and Human Services; 2004. 6. Smith C, Cowan C, Sensenig A, et al. Health spending slows in 2003. Health Affairs Vol. 24, Issue 1, 185–94. 7. Brewster LR, Rudell L, Lesser CS, et al. Emergency Room Diversions: A Symptom of Hospitals Under Stress. Community Tracking Study Issue Brief No. 38. Washington, DC: Center for Studying Health System Change; 2001.

74 8. Casalino LP, Devers KJ, Brewster LR, et al. Focused Factories? Physician-Owned Specialty Facilities. Health Affairs. 2003;22(6):56-67. 9. American Medical Association. Physician Characteristics and Distribution in the U.S., 2004 Edition. Chicago: AMA; 2005. 10. Bureau of Labor Statistics, U.S. Department of Labor, Career Guide to Industries, 2004–05 Edition, Health Services, Available at http:// www.bls.gov/oco/cg/cgs035.htm (last accessed August 29, 2005). 11. Report of the Graduate Medical Education National Advisory Committee: Summary Report. Washington, DC: U.S. Department of Health and Human Services; 1981. 12. Council on Graduate Medical Education. Sixth Report. Managed Health Care: Implications for the Physician Workforce and Medical Education. Washington, DC: U.S. Department of Health and Human Services; 1995. 13. Council on Graduate Medical Education. Sixteenth Report. Physician Workforce Policy Guidelines for the United States, 2000–2020. Washington, DC: COGME; 2005.

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14. Bureau of Labor Statistics. Career Guide to Industries, 2004–05 Edition, Health Services. Washington, DC: U.S. Department of Labor; 2005. 15. Smith C, Cowan C, Senseng A, et al. Health spending growth slows in 2003. Health Affairs. 2005; 24(1):185–94. 16. Mays GP, Hurley RE, Grossman JM. An Empty Toolbox? Changes in Health Plans’ Approaches for Managing Costs and Care. Health Services Research. Vol. 38, No. 1; 2003:375–394. 17. Mays GP, Claxton G. Managed Care Rebound: Recent Changes in Health Plans’ Cost Containment Strategies. Health Affairs. Web Exclusive Vol. W4, 2004;427–436. 18. Sommers A, Ghosh A, Rosseau D. Medicaid Enrollment and Spending by Mandatory and Optional Eligibility and Benefit Categories. Washington, DC: Kaiser Commission on Medicaid and the Uninsured; 2005. 19. Kaiser Commission on Medicaid and the Uninsured. Enrolling Uninsured Low-Income Children in Medicaid and SCHIP. Washington, DC: Kaiser Commission; 2005.

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F. Douglas Scutchfield • C. William Keck

John Last defines public health in his dictionary of epidemiology as, “Efforts organized by society to protect, promote, and restore the people’s health. It is the combination of science, skills and beliefs that is directed to the maintenance and improvement of the health of all the people through collective or social actions.”1 These efforts organized by society are focused on “creating conditions in which people can be healthy”—the mission of public health as defined by the Institute of Medicine (IOM) in its 1988 Report on the Future of Public Health,2 and confirmed in the IOM’s 2003 report, The Future of the Public’s Health in the 21st Century.3 The value of public health is unquestionable. Its prevention efforts are responsible for 25 years of the nearly 30 year improvement in life expectancy at birth in the United States over the past century. This is based on evidence that only about 5 years of the 30 year improvement are the result of medical care.4 Public health approaches carry significant potential for future contributions as well, since almost half of deaths in the United States are premature and result from preventable causes.5 Public health is practiced in a variety of settings and agencies, and by a variety of professionals. The work of many communitybased organizations or major not-for-profit voluntary organizations can certainly be characterized as the practice of public health. Their programs fit Last’s definition and are consistent with the mission statement articulated by the IOM. However, when we think of public health activities, we most often envision the constellation of activities of governmental public health agencies at the federal, state, and particularly, local levels. This is especially true since it is only official public health agencies that have statutory responsibility for the health status of the populations they serve. Legal authority for this responsibility is based on a variety of federal, state, and local ordinances, including the granting of police powers. A PUBLIC HEALTH RENAISSANCE?

It can be argued that public health in the United States is in the midst of a “renaissance” in several ways. The last several decades have seen a great deal of effort focused on defining the role of public health within the context of the health problems and health services existing in this country. There have also been significant changes in the way public health services are practiced and evaluated in a number of settings. Improvements in financial support and organizational structure for public health services have been less evident.

A Philosophic Renaissance The pace of change in understanding the place and role of public health in the United States has accelerated dramatically in recent years. Stimulated by the disturbing findings in the 1988 IOM report (public health system in disarray, no coherent vision or mission, disconnection from its academic base, etc.), and by the effort of the Clinton Administration to refine the health-care delivery system in the United States, public health professionals began a systematic review of their discipline and its place in this society. Adding to the impetus were the terrorist attacks of September 11, 2001, the subsequent anthrax scare, as well as the ever-expanding role of public health. Old understandings of illness and health have been increasingly synthesized and recast in a manner that clarified the inter-relatedness of social factors, cultural factors, genetics, behavior, illness care, and prevention. Public health is recognized as the discipline that spans almost all health discipline boundaries, and it is increasingly looked to for understanding and solutions for difficult problems, such as emerging infections, violence, etc. Some of the more important elements of the “philosophic renaissance” that followed included:

Public Health’s Three Core Functions In addition to proposing a national vision and mission statement for public health, the 1988 IOM Study Committee identified and proposed three core functions for public health departments.2 Described below, these functions have largely been accepted by the public health community: Assessment. Every public health agency should regularly and systematically collect, assemble, analyze, and make available information on the health of the community, including statistics on health status, community health needs, and epidemiologic and other studies of health problems. Policy Development. Every public health agency should exercise its responsibility to serve the public interest in the development of comprehensive public health policies by promoting the use of the scientific knowledge base in decision-making about public health and by leading in developing public health policy. Assurance. Public health agencies should assure their constituents that services necessary to achieve agreed upon goals are provided, either by encouraging actions by other entities, by requiring such action 1239

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through regulation, or by providing services directly. They should also involve key policy makers and the general public in determining a set of high-priority personal and community-wide health services that governments will guarantee to every member of the community, including subsidization of direct provision of personal health care. The assurance function is the most difficult of the three for many local health departments to comply with. Advocacy for access to illness care services for all is one thing, but providing those services for approximately 16% of the population (over 45 million people) is something else again in most public health settings. The resources for individual illness care essentially don’t exist in the public sector, and too much attention paid to that issue in public health agencies would diminish resources available for population-based preventive and regulatory activities. The 2003 IOM report faces the issue more directly by calling for universal access to health insurance in the United States.3

The Ten Essential Services The three core functions listed above were easily understood and embraced by public health professionals, but they meant little to legislators and the public at large. Because of the concern that public health would be ignored in efforts to redesign the health system in the United States, the U.S. Department of Health and Human Services convened a work group to determine how public health activities could be more clearly described. The three core functions were expanded to a list of Ten Essential Community Health Services that would more clearly define the services communities need in order to achieve high levels of healthfulness.6 Those Ten Essential Services are: 1. Monitor health status to identify community health problems. 2. Diagnose and investigate health problems and health hazards in the community. 3. Inform, educate, and empower people about health issues. 4. Mobilize community partnerships to identify and solve health problems. 5. Develop policies and plans that support individual and community health efforts. 6. Enforce laws and regulations that protect health and ensure safety. 7. Link people to needed personal health services and ensure the provision of health care when otherwise unavailable. 8. Ensure a competent public health and personal health workforce. 9. Evaluate effectiveness, accessibility, and quality of personal and population-based health services. 10. Research for new insights and innovative solutions to health problems. These essential services have become the central focal point for many public health activities, including evaluating the capacity of communities to assess their capacity for healthfulness, defining a public health research agenda, and providing a framework for determining the workforce competencies required to deliver them well. The relationships of the essential services to the IOM’s three core functions are illustrated in Fig. 75-1.

Council on Linkages between Public Health Practice and Academia In response to the finding that public health practice is “de-coupled” from its academic base, The Faculty/Agency Forum was established to address the educational and academic dimensions of the findings of the IOM. The Forum’s major accomplishment in 1993 was the development and publication of a compendium of competencies required for public health practice.7 After this group produced its report and went out of existence, the Council on Linkages Between Public Health Practice and Academia (COL) was formed to facilitate additional activities that would enhance the practice/academic connection. The COL is comprised of representatives from the major

Decision support

Planning & Detection, reporting, forecasting Record keeping & communication & indexing Health status monitoring and surveillance

Diagnose and investigate health problems and health hazards

Assessment

Analysis Conduct scientific investigations and support demonstration Assure capacity projects and competency of workforce

Human resources

Develop policies and plans that support health Enforce efforts regulations and standards

Policy development

Assurance

Evaluate effectiveness, accessibility, and quality

Networking Mobilize partnerships to solve problems and respond to disasters

Educate public about health issues Link people to services

Media and internet

Information & referral

Performance measurement

Figure 75-1. The relationship of the essential services to the Institute of Medicine (IOM’s) three core functions. The words and phrases in bold in the diagram were added by the Ohio Department of Health to suggest areas of emphasis for local health departments.

national public health professional organizations and certain federal governmental agencies involved in public health. A number of products and initiatives have emerged from this group. They include: 1. Delineation of workforce competencies: The COL, drawing on the work of the Forum and many others in the field, developed an improved list of public health workforce competencies required to deliver each of the ten essential services. The competencies can be viewed at: http://www.trainingfinder.org/ competencies/index.htm. 2. Improving the science base for community activities through community service guidelines: The COL piloted an effort to determine if it might be possible to develop community preventive service guidelines in the same way that the Clinical Preventive Services Guidelines were developed. The COL’s pilot efforts proved successful, and the Centers for Disease Control and Prevention (CDC) has taken on the task of examining the science base for community services. The first report is now available in book form and can also be viewed at http://www.thecommunityguide.org. 3. Defining a public health research agenda: Most of the research money in the United States is focused on the diagnosis and treatment of disease rather than health promotion, disease prevention, and public health service delivery. In an effort to modify that reality, the COL has engaged many interested in public health research in the effort of developing a research agenda. One approach is to review what we need to know to deliver the ten essential community services effectively so research dollars could be targeted to gaps in our knowledge. Another approach will be to review the work of the Community Health Services Guidelines Task Force, targeting research support to review program effectiveness where evidence is lacking. 4. Establishing practice coordinators at every school of public health: Working through the Association of Schools of Public Health, a COL agency member, a practice coordinator has been identified at each school of public health charged with improving their institution’s linkages with practice settings. Important contributions of the group include their promotion of the importance of scholarship in the area of public health practice,8 and the value of practice-based teaching for public health.9

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Structure and Function of the Public Health System in the United States

National Performance Standards The ten essential services, initially intended to describe the work of local health departments, have subsequently been recognized as a compilation of services that need to be available in communities for populations to be as healthy as possible. They certainly include many activities engaged in by health departments, but they also include activities of many other individuals, groups, agencies, and institutions. They, therefore, are now considered to be services provided by the Local Public Health System (LPHS), a term intended to include all agencies, institutions, and individuals providing health-related services. This broadens the concept of public health to include everyone involved in efforts to improve health status. National performance measures have been developed at the CDC to allow communities to measure their capacity to deliver the essential services. These measures can be viewed at www.cdc.gov/od/ocphp/nphpsp.

The Medicine/Public Health Initiative Medicine and public health have evolved into two distinct cultures in this country. Too often, these cultures have been at war with each other. The differences between the two professions remain quite apparent, but it is also clear that the differences are narrowing. The American Medical Association (AMA) and the American Public Health Association (APHA) have developed a medicine/public health initiative intended to draw the two professions more closely together where their agendas overlap, and agree to disagree where dissonance remains. The Journal of the American Medical Association prints many articles of relevance to public health, the AMA has taken many positions supporting traditional public health issues (tobacco, violence, gun control, etc.), and the APHA has reached out to clinicians to help deal with access to care issues.

National Association of County and City Health Officials In 1994, the National Association of County Health Departments (the national association for directors of county health departments) and the United States Conference of Local Health Officers (the national professional association for directors of city health departments) merged to become the National Association of County and City Health Officials. This organization grew in strength during the ensuing decade and it has become an important contributor to the development of strategies and tools for public health practice and an important force in the development of national public health policy.

National Association of Local Boards of Health Most local health departments are governed by a board of health. The large majority of board of health members have little or no background in the health sciences, and have relied on the health department they represent (sometimes with assistance from the relevant state health department) to inform them about the discipline of public health and their responsibilities to it. Some local state board of health associations were formed in the 1980s in early efforts to bring some organization, standardization, and support to this important component of the public health infrastructure. In November 1992, representatives of states with these kinds of organizations (Georgia, Illinois, North Carolina, Ohio, and Washington) came together to form the National Association of Local Boards of Health (NALBOH). Since its founding, NALBOH has grown rapidly, and now, among other activities, is a participant in providing training for local board of health members, in developing and using national performance standards, in tobacco control, and in developing academic/practice linkages.

Public Health Leadership Institutes Leadership was identified by the 1988 IOM report as an important need in public health practice. In response, the National Public Health Leadership Institute was developed with federal funding in 1991 to focus on identifying and training current and future public health leaders. The national program has since been joined by many statesponsored and academic institution programs focused on the same issues. There is a current urgency to this effort stimulated by data that

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suggests state governments could lose close to 45% of their public health workforce.10

The Need for an Accompanying Financial and Organizational Renaissance The progress made in understanding the value of public health to communities and individuals, and in describing the past and potential impact of the discipline, has been heartening. On the other hand, the continuing inability of the country to act to strengthen the financial underpinning and organization of its public health system makes it impossible for the discipline to reach its full potential to protect the public from disease and injury. Additional federal funding for terrorism preparation has been made available for state and most local health departments, and preparedness capacity has been measurably strengthened, especially in the area of communicable disease surveillance and control. This increase has occurred in an environment of decreasing overall resources at the federal level and in most states, however, with a resultant loss in overall capacity in many, if not most, public health jurisdictions. Little has changed with respect to the organization and governance of local health departments. Problem areas identified by the 1988 IOM study committee remain. The 2003 IOM report noted that the public health system that was in disarray in 1988 remained, in some important ways, in disarray in 2003. They noted the absence of fundamental reform of the statutory framework for public health in most of the country, and insufficient support for public health infrastructure. They noted mixed progress in improving capacity to address environmental issues, in building linkages with mental health, and in meeting health-care needs of the medically indigent. In addition, significant gaps remain in workforce capacity and competency, information and data systems, and the organizational capacities of state and local health departments and laboratories.3 Many local health departments remain too small and resource poor to meet the basic public health needs of the populations they serve. THE FEDERAL PUBLIC HEALTH ROLE

The federal government’s role in promoting and protecting the health of the public has evolved significantly over time. The 2003 IOM report notes the federal government has a limited role in the direct delivery of essential public health services, but plays a crucial role by acting in six main areas of population health: policy making, financing, public health protection, collection and dissemination of information about U.S. health and health-care delivery systems, capacity building for population health, and direct management of services.3 Based on a number of constitutional powers, including the power to “regulate Commerce . . . among several states,” the federal government involves itself in environmental protection, occupational health and safety, and food and drug purity.11 By setting conditions on the expenditure of federal funds, adjusting taxes on products to promote healthy use or discourage unhealthy use, and regulating business and persons whose activities may affect interstate commerce, the federal government can affect population health. Decisions by the judicial branch can also impact federal policy in many ways that affect health, such as upholding governmental power to protect people’s health, setting conditions on the receipt of public funds, and upholding a woman’s right to reproductive privacy.3

Organization The federal government is divided into three branches: the legislative, judicial, and executive. The legislative and judicial branches do play substantial roles in public health, but it is usually the activities of the executive branch that come to mind when considering the federal government’s role in improving public health. Within the executive branch, it is the Department of Health and Human Services (DHHS) which is the primary site of public health activities. Many of those activities are centered in one of the DHHSs component parts, the U.S.

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Public Health Service (PHS). There are, nonetheless, significant activities related to public health that occur in other branches of the executive branch. Examples include the Women, Infants, and Children Program (WIC) run by the Department of Agriculture (the largest public health program in the country in terms of dollars spent), the many pollution and contamination control programs run by the Environmental Protection Agency (EPA), the workplace safety programs run by the Occupational Safety and Health Administration (OSHA) which is part of the Department of Labor, and the health-care and public health services provided to active-duty military personnel by the Department of Defense.

The Department of Health and Human Services Public health-related activities and responsibilities are scattered throughout the federal government, but the principle federal agency for healthrelated programs is the Department of Health and Human Services (DHHS). DHHS is involved in policy making, financing of public health activities, public health protection, collection and dissemination of information, capacity building, and direct management of services.3 Many of these activities are located in various branches of the PHS. The PHS had its origins in the Marine Hospital Service in the late 1700s, created to meet the health-care needs of Merchant Marine seamen. The Service continued relatively unchanged until the turn of the twentieth century when it was renamed the Public Health Service and took on new responsibilities, most notably providing states with expertise to deal with major infectious disease epidemics.12 The PHS eventually became an arm of the DHHS after that cabinet department was formed, originally as the Department of Health, Education, and Welfare. The PHS consists of a series of operating agencies that have remained relatively intact through many changes in the federal executive establishment. The current operational arms of the PHS include the National Institutes of Health (NIH), the Centers for Disease Control and Prevention (CDC), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the Food and Drug Administration (FDA), the Agency for Toxic Substances and Disease Registry (ATSDR) (administered by the CDC), and the Substance Abuse and Mental Health Administration (SAMHA). These major agencies are subdivided into centers, institutes, and branches staffed with both commissioned officers of the PHS and civilian employees of the federal government. THE STATE PUBLIC HEALTH ROLE

The role of the states and territories in public health, as with the role of the federal government, has evolved over time. The IOM has also defined these responsibilities well. AS DEFINED BY THE INSTITUTE OF MEDICINE

The IOM report describes the duties of the state health department as: • Assessment of the health needs in the state based on statewide data collection • Assurance of an adequate statutory base for health activities in the state • Establishment of statewide health objectives, delegating power to locals as appropriate and holding them accountable • Assurance of appropriate organized statewide effort to develop and maintain essential, personal, educational, and environmental health services; provision of access to necessary services; and solution of problems inimical to health • Guarantee of a minimum set of essential health services • Support of local service capacity, especially when disparities in local ability to raise revenue and/or administer programs require subsidies, technical assistance, or direct action by the state to achieve adequate service levels2

Organization In order to fulfill these functions, the 50 states and 5 trusts (Guam, District of Columbia, American Samoa, Puerto Rico, and the Virgin Islands) have developed agencies to address them. In many cases these are not departments, so the Association of State and Territorial Health Officers refers to them as state health agencies (SHAs). There is substantial variability in the organizational structures of these agencies. In some cases the SHA is a cabinet-level office reporting directly to the governor—an arrangement encouraged by the IOM. In other circumstances the SHA functions are subsumed as part of a larger administrative organization, which often includes social services functions as well as health. These “umbrella” or “superagencies” carry titles such as Cabinet for Human Resources or Department of Health and Human Services. They are frequently led by political appointees who often have no substantive health expertise. These individuals report to their governors and are cabinet-level officers. In 2000, 20 states had the SHA in a superagency. This number decreased from 22 states in 1980, reversing a 40-year trend toward the establishment of superagencies.13

State Health Agency Activities The activities of SHAs vary considerably. For example, the IOM report recommended that Medicaid, environmental programs, and mental health services should be a part of the SHA’s function.2 That, however, is not the norm. In only five states is the SHA responsible for mental health services, and in only five states and three territories is the SHA responsible for Medicaid.13 In most states Medicaid management is the responsibility of the welfare agency. A case can certainly be made that subsuming the large budgets of Medicaid under the aegis of the SHA would allow the SHA to more closely integrate its public health functions with that of payment for medical care services. In fact, the group receiving the largest amount of public health services is women and children. Women and children also receive the a substantial portion of Medicaid expenditures, thus providing opportunity for synergy between these two governmental functions. Environmental health was traditionally a part of the SHA’s responsibility until the 1960s. At that point growing concern about environmental degradation led special interest groups and policy makers to give special attention to many environmental issues. The federal government had made the decision to create the Environmental Protection Agency in response to those same concerns, and most states followed the federal lead by creating a state environmental protection agency separate from the SHA with responsibility for many environmental issues. All states were given the opportunity to designate a lead environmental health agency. While some initially designated the SHA as the lead agency, the number so designated fell from 19 in 1978 to only 8 in 2000.13 Even though most major environmental concerns are dealt with by state environmental protection agencies, most SHAs have retained responsibility for some environmental health issues, such as food service, recreation facility inspections, investigation of chronic disease clusters that might have an environmental etiology, etc.

State Boards of Health One of the strong recommendations of the IOM regarded state boards of health. They felt, “. . . each state should have a state health council that reports regularly on the health of the state’s residents, makes health policy recommendations to the governor and legislature, promulgates regulations, reviews the work of the state health department, and recommends candidates for director of the department.”2 In 2000, 21 states had boards of health which were responsible for making policy, while 14 had boards which were advisory.13 It is more likely that existing boards of health have a policy-making function in states with a free-standing SHA than in those with a superagency. Only four states had a board which appointed the director of the SHA in 1992.14 The growing centralization of policy making in the executive branch

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and the perception that special interest groups, especially physicians, have “captured” them, has led to a decline in the power and influence of state boards of health.

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In the earlier half of the century, the director of health was a physician, frequently trained in public health, who held the job for a protracted period of time. In fact, many states had statutes that required the director to be a physician. That has changed over the years to the point that in 2000 only 25 states had that requirement.13 In many cases there is no statutory blockage to the governor appointing his or her cardiologist or campaign manager to the post. The “politization” of the position in many places has led to substantial turnover and a diminished desire on the part of qualified individuals to take such a position.

Delaware, Rhode Island, and Vermont). In seven states control is shared between the county and the state. Sixteen states are totally decentralized with local government operating the LHD, and another 16 states have a mix, where large jurisdictions run their own LHD, but the state directly runs smaller, more rural, LHDs.15 The IOM recommended that a single jurisdiction in a community be given the responsibility for providing public health services to decrease duplication and/or prevent confusion about responsibilities. As a corollary, it also recommended that jurisdictions too small to support an effective LHD consider linking with other communities to create district health departments.2 The IOM also recommended that boards of health should exist at the local level with responsibilities comparable to those it recommended for state boards.2 In 1992–93 (the most recent data available), approximately 73% of LHDs had a board of health, a slight increase from 70% in 1989.15

THE LOCAL PUBLIC HEALTH ROLE

Funding

Public Health Directors

Local health departments are the governmental entities closest to the populations needing services. The IOM felt that, “...no citizen from any community, no matter how small or remote, should be without protection, which is possible only through a local component of the public health delivery system.”2 This is a more modern reaffirmation of the need for, “a governmental presence at the local level (AGPALL).”2

As Defined by the Institute of Medicine The IOM defined the functions of official local public health agencies as assessment, policy development, and assurance. By assessment, the IOM meant the responsibility to develop or collect data and information that allows for analysis and understanding of the health status of the communities for which the agencies are responsible. The policy development function requires that public health agencies take the lead in developing policies and making decisions based on the best available scientific knowledge. Finally, the official public health agency has the responsibility to ensure that services necessary to achieve agreedupon health goals are provided.2 This can be done by providing the required services directly, or by encouraging their delivery by other agencies, groups, or individuals in the community. Guidance in this matter is provided by the 10 essential services described previously, and the Local Public Health System National Performance Standards. Particular services delivered by each local health department will depend on the needs of each community and decisions made locally about where those services can best be located.

Size of Local Health Departments State health agencies vary considerably from state to state, but there is even more variability in the approximately 3000 local public health departments in the United States. A periodic survey conducted by the National Association of County and City Health Officials (NACCHO) allows us to characterize the structure and function of local health departments (LHDs). Generally, LHDs serve small populations. Over two-thirds (69%) of LHDs serve a jurisdiction containing fewer than 50,000 people. In fact, 50% of LHDs serve less than 25,000 people. According to the survey, 60% of LHDs are county, 8% are multicounty, 7% are city/county, 10% are city, and 15% are town/township jurisdictions. Not surprisingly, the smaller jurisdictions have the fewest employees. LHDs that serve a population of less than 50,000 employ an average of 13.9 and a median of 8.5 FTEs.15

Organization and Structure The organizational relationships between the SHA and the LHDs also vary considerably. In 11 states the SHA is the LHD, or directly operates the LHD. Of these 11, four are very small states (Hawaii,

There are four major sources of funding for LHDs: local taxes, state grants, federal grants, and fees for service. Through the 1990s and into the current decade, there have been significant shifts in the portion of support coming from each area. By 2000, local revenues accounted for 44% of total LHD funding, up from 34% in 1992. State revenues comprised 30% of the revenue stream, down from 40% in 1992. Federal funding shrank from 6% in 1992 to only 3% in 2000, and fees for service rose to 19% of LHD budgets in 2000 from 17% in 1992. These changes probably represent, to some degree, the flattening of federal categorical grant dollars during this period,15 as well as increasingly tight state and federal budget allocations for public health. Neither the recent influx of bioterrorism preparedness funding to SHDs and LHDs, nor the continued decline of state and federal dollars in other areas of public health, are taken into account in these figures. Most LHDs serve jurisdictions that have small populations. Sixty-nine percent of health departments serve fewer than 50,000 residents, and 50% serve fewer than 25,000 people. The median average expenditure per year of departments serving 25,000 or fewer in 2000 was only $214, 658 and the median number of staff was just 8.5 FTEs.15 These are remarkably small numbers given the range of responsibilities shouldered by these agencies.

Leadership Leadership at the local level is more stable than it is in SHAs. The most recent data available is from 1992. At that time over 50% of LHD leaders had been in office longer than 5 years. In general, the smaller jurisdictions have the longest tenure and the largest health departments experience turnover rates comparable to those in SHAs. Approximately 37% of LHD directors have doctoral degrees, and only have 17% have public health practice degrees (MPH or DrPH).15

Services Despite the recommendation that a group of essential public health services be evident in every LHD, the evidence shows that there is great disparity in services offered. Most LHDs report that they offer clinical preventive services, such as adult immunizations (91%), childhood immunizations (89%), tuberculosis testing (88%), and HIV testing and counseling (64%). Most assess the extent to which clinical preventive services are provided in their communities (80%), and provide programs to fill gaps in those services. Communicable disease control services are commonly present (94%).15 Almost all public health departments provide some personal health services. In many cases, the health department is the provider of last resort, filling gaps in the private medical care system. Reimbursement for Medicaid-eligible clients often provides the funding base required for the department to maintain its services to the uninsured population. The growing trend in states to mandatory, Medicaid managedcare arrangements, however, has moved paying clients out of health

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departments into the private sector without reducing the need for care for the growing numbers of uninsured. This threatens the viability of one of our society’s “last resort” systems for the medically disenfranchised, and challenges both the private and public sectors to develop collaborative arrangements to assure continued access to needed personal health services. In testimony to this issue, between 1992 and 2001, LHDs reported significant reductions in the proportion of departments that offer personal health services: primary care from 30% to 18%, dental care from 45% to 30%, prenatal care from 64% to 41%, family planning from 68% to 58%, WIC from 78% to 55%, and EPSDT from 79% to 58%.15 Environmental issues are more clearly identified at the local level as the responsibility of the health department, in general, than they are at the state level. Most LHDs enforce state environmental laws (restaurant inspections, trailer park inspections, etc.), regulate private water and sewage systems, and enforce other local environmental ordinances. Confusion does sometimes occur when LHDs receive environmental complaints about problems when jurisdiction for dealing with those problems lies with others. It is then the job of the LHD to coordinate the response, and assure that the state or federal agency with jurisdiction follows through on investigation and resolution of the problem. ASSESSMENT AND MANAGEMENT TOOLS

Public health has benefited from the movement of a number of management tools from the private to the public sector over the past two to three decades. It has increased its capacity in recent years to deal with public health issues by successfully marrying good management mechanisms with new tools to describe and develop solutions for community health problems.

Setting National Objectives for 1990 One of the most important steps taken was to apply management by objectives and total quality management to public health. The notion to use measurable objectives to enhance the productivity of public health efforts at the federal level dates to the publication in 1979 of Healthy People: The Surgeon General’s Report on Health Promotion and Disease Prevention. This document laid out a series of goals for mortality reductions to be achieved in the United States by 1990 for four age groups: 1. a 35% reduction in infant mortality 2. a 20% reduction in mortality for children ages 1–14 years 3. a 20% death rate reduction for those between 15 and 24 years of age 4. a 25% reduction in adult mortality for those aged 25–65 years For those above age 65 it called for a reduction in disability days.16 The Public Health Service began examining health status determinants and developed information on 15 disease prevention/health promotion areas. With the help of outside experts, in 1979 the first draft of specific objectives for these 15 priority areas was developed. After considerable outside review, Health Promotion/Disease Prevention: Objectives for the Nation was published in 1981. It contained 226 objectives with targets for achievement by 1990 that were linked to the 15 priority areas. The objectives were grouped as improvement in health status, reduction of risks to health, increased awareness, improved and expanded preventive health services, and improved surveillance.17 This effort was moderately successful. Three of the four mortalityrelated goals were met or exceeded. Specifically, the infant and adult mortality goals were met, and the childhood mortality target was significantly exceeded. The mortality goal for adolescents was not met. Failure to achieve the goal was directly due to high rates of both unintentional (motor vehicle accidents) and intentional (homicide) fatal injuries in this age group.18

Thirty-two percent of the 228 objectives set for 1990 were met. Progress was made toward an additional 30%, and ground was either lost or no progress made in another 15%. Insufficient data was available to determine the status of the remaining 23% of the objectives.18 In general, however, the success of this project was remarkable. It established an agenda which the public health community could rally around, and served to energize and empower those who were committed to improving community health status.

Healthy People 2000 Because this project was so well received, the PHS began work in the late 1980s toward the establishment of a new set of objectives for the year 2000. It sought input even more broadly than it had previously, and in September, 1990, distributed Healthy People 2000: The National Health Promotion and Disease Prevention Objectives. This document contains three overarching goals: • Increase the span of healthy life • Reduce health disparities among Americans • Achieve access to preventive services for all Americans18 The 332 objectives contained in Healthy People 2000 address Health Promotion, Health Protection, Preventive Services, and Surveillance and Data Systems. They are grouped into 22 priority areas (see Table 75-1). Surveillance and Data Systems was included in this new version of national objectives in order to provide the foundation for tracking all of the objectives in an effort to minimize the problem of not being able to determine progress made on some of them. A Healthy People 2000 final review of progress in tracking these objectives yielded the following information: 68 objectives (21%) met the targets, 129 (41%) showed movement toward the targets, 35 objectives (11%) showed missed results, and 7 (2%) showed

TABLE 75-1. HEALTHY PEOPLE 2000 PRIORITY AREAS

Health Promotion 1. 2. 3. 4. 5. 6. 7. 8.

Physical activity and fitness Nutrition Tobacco Alcohol and other drugs Family planning Mental health and mental disorders Violent and abusive behavior Educational and community-based programs

Health Protection 9. 10. 11. 12. 13.

Unintentional injuries Occupational safety and health Environmental health Food and drug safety Oral health

Preventive Services 14. Maternal and infant health 15. Heart disease and stroke 16. Cancer 17. Diabetes and chronic disabling conditions 18. HIV infection 19. Sexually transmitted diseases 20. Immunization and infectious diseases 21. Clinical preventive services Surveillance and Data Systems 22. Surveillance and data systems Source: Public Health Service: Healthy People 2000: National Health Promotion and Disease Prevention Objectives. Washington, DC: U.S. Department of Health and Human Services, 1990.

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no change from the baseline. Only 47 objectives (15%) showed movement away from the targets, and 32 objectives (10%) did not provide sufficient data to be assessed.19

Healthy People 2010 The continued success of Healthy People 2000 prompted the creation of a new set of objectives for the year 2010. As with previous documents, this required the participation and input of a variety of constituencies and viewpoints. This report and its development were guided by the Institute of Medicine. As with the earlier objectives, this one begins with overarching goals. The first goal is to increase the quality and years of healthy life. This goal focuses on increasing life expectancy to more nearly that of other developed nations. It also includes a concern with the quality of life. While it is difficult to define, the notion is to use tools to document the increase in the quality-related years of life. The second goal is eliminating health disparities. There are continuing and significant differences in both length and quality of life based on several characteristics of populations, sex, gender, ethnicity, socioeconomic status, and so on. Healthy People 2010 commits us to decreasing those differences, to quote, “Healthy People 2010 is firmly dedicated to the principle that—regardless of age, gender, race or ethnicity, income, education, geographic location, disability, and sexual orientation—every person in every community across the Nation deserves equal access to comprehensive, culturally competent, communitybased health-care systems that are committed to serving the needs of the individual and promoting community health.”20 The document has 28 separate focus areas and 467 objectives distributed among these focus areas. These areas include very specific interventions or health problems in individuals or communities, such as cancer or physical activity. Others are focused on much broader areas, such as access to care or improving public health infrastructure. The 28 focus areas are listed in Fig. 75-2.20 One of the criticisms leveled at previous objectives is that there were too many, they had no priority and were hard to deal with given their number and variety.21 Given that criticism, the framers of Healthy People 2010 identified 10 leading health indicators from the 28 focus areas, these 10 are listed in Fig. 75-3.20 The establishment of measurable national health objectives coupled with regular tracking of progress made toward their accomplishment has proven to be a very effective way to focus the nation’s attention on health status. The objectives have brought a variety of governmental agencies together to determine approaches to protecting and improving health. They have also provided an opportunity for contributions to the process by nonpublic health organizations and agencies resulting in a prevention agenda that has a wide range of national support.

Figure 75-2. The document has 28 separate focus areas and 467 objectives distributed among these focus areas. These areas include very specific interventions or health problems in individuals or communities, such as cancer or physical activity. Others are focused on much broader areas, such as access to care or improving public health infrastructure. (Source: Healthy People 2010: Understanding and Improving Health. 2nd ed. U.S. Department of Health and Human Services, Washington, DC: U.S. Government Printing Office, November 2000; pp 17, 24.)20

Setting Local Objectives Setting national objectives is a very important step in preparing for an ordered process of allocating resources where the impact is likely to be greatest. It is the translation of those national objectives into action at the local level that actually assures progress toward meeting them.

Mobilizing for Action through Planning and Partnership The most recent tool for community health assessment and planning is Mobilizing for Action through Planning and Partnership (MAPP). This tool was developed through a collaborative effort of NACCHO and the CDC. The process of using MAPP is shown in the two graphics, Fig. 75-422 and Fig. 75-5.22 During the first phase those responsible for implementing MAPP get themselves prepared for the process. Embarking on MAPP is not to be taken lightly, as it requires substantial commitment from those who lead it and those involved in its various phases. The second step is the visioning process, attempting to describe what the community health should look like in ten years.

Figure 75-3. Framers of Healthy People 2010 identified 10 leading health indicators from the 28 focus areas. (Source: Healthy People 2010: Understanding and Improving Health. 2nd ed. U.S. Department of Health and Human Services, Washington, DC: U.S. Government Printing Office, November 2000; pp 17, 24.)20

1246

Health-Care Planning, Organization, and Evaluation

MAPP-Your community roadmap to health!

A healthier community

Action cycle uate implement plan Eval Formulate goals and strategies

Identify strategic issues

C ommun

ts

i t y t h e m es &

Com stat munity us a h sse ealth ssm ent

h alt nt he e lic ssm ub se l p as ca m Lo ste sy

Organize for success/partnership development

s es

ss

a Forc P assee of ch AP ssm an M en ge 4 t

Our vision

en

m

s trengths assessment

Figure 75-4. The most recent tool for community health assessment and planning is Mobilizing for Action through Planning and Partnership (MAPP). This tool was developed through a collaborative effort of NACCHO and the CDC.

Community themes & strengths assessment Partnership development

Organize for success

Visioning Four MAPP assessments Forces of change assessment

Identify strategic issues

Local public health system assessment

Formulate goals and strategies Evaluate

Plan Action

Implement

Community health status assessment Figure 75-5. The most recent tool for community health assessment and planning is Mobilizing for Action through Planning and Partnership (MAPP). This tool was developed through a collaborative effort of NACCHO and the CDC.

The next step is to complete the four community assessments which will characterize the community, its health status, assets, and infrastructure issues for solving community health problems. The four assessments are (a) community themes and strengths assessment, (b) local public health system assessment, (c) community health status assessment, and (d) forces of change assessment. Following those assessments, the MAPP process requires the identiďŹ cation of strategic community heath issues, then a formulation for goals and strategies to deal with these issues, and ďŹ nally, the action cycle. During this phase, participants plan, implement, and evaluate. These activities build upon one another in a continuous and interactive manner and ensure continued success. The NACCHO website which describes the MAPP process has many helpful tools and suggestions for those who wish to embark on the MAPP process. It is clear that this process is much improved over previous community health processes, but is still open for criticism and further development.23

Assessment Protocol for Excellence in Public Health MAPP builds on the experience of the Assessment Protocol for Excellence in Public Health (APEX/PH), which was the first major tool developed by NACCHO to address issues dealing with local community needs assessment. In order to assist LHDs with that task, the National Association of County Health Officials spearheaded a collaborative process in league with the CDC, the United States Conference of Local Health Officers, the American Public Health Association, the Association of State and Territorial Health Officials, and the Association of Schools of Public Health to develop the APEX/PH.24

75

Structure and Function of the Public Health System in the United States

The APEX/PH program is designed to help LHDs involve their communities in a process to assess community health status, identify and prioritize public health problems, and create a community plan for action. It contains three phases. Phase I is an assessment of internal organizational capacity of the department intended to identify strengths and weaknesses, particularly as they pertain to a department’s capacity to take the lead in the broader community assessment effort. Phase II, intended to be initiated after the department addresses weaknesses or concerns identified in Phase I, is the actual community assessment portion. Phase III is the implementation of the community health plan under the leadership of the LHD. The health officer is expected to combine the results of Phase I and Phase II in a manner that enhances the capacity of the health department to lead the community in directing its resources to most appropriately address the problems identified.

Planned Approach to Community Health During the 1980s, the CDC, encouraged by the evidence that community-based prevention programs were effective in reducing coronary heart disease risk factors, developed a protocol that could be locally applied to develop community-based health promotion programs. The Planned Approach to Community Health (PATCH) was designed as a working partnership between the CDC, SHA’s and communities to focus resources and activities on health promotion. There are five phases to the PATCH process: 1. Mobilizing the community—establishing a strong core of representative local support and participation in the process 2. Collecting and organizing data—gathering and analyzing local community opinion and health data for the purpose of identifying health priorities 3. Choosing health priorities—setting objectives and standards to denote progress and success 4. Intervention—design and implementation of multiple intervention strategies to meet objectives 5. Evaluation—continued monitoring of problems and intervention strategies to evaluate progress and detect need for change25

health problems. In addition to the epidemiology, biostatistics, environmental health, health behavior, and health systems management, the IOM also suggests that there are several additional areas where knowledge can assist us in understanding and dealing with disease. These areas include genomics, informatics, communication, cultural competency, community-based participatory research, global health, policy and law, and public health ethics. With the advent of new directions in disease etiology and intervention, these new content areas assume increased relevance for the public health practitioner.28 They suggest that we use the socioecological model for considering public health problems. This model, shown in Fig. 75-6,28 indicates that health and disease are dependent on risk factors or specific microbiologic agents, but those other areas, such as the family, the community, the work site, or the context in which we function, are also powerful determinants of disease. The science of this area of public health is rapidly developing and provides an important new source of information to be brought to bear on public health problems. The notion of community and the socioecological nature of disease also suggest that new ways of community involvement are key in community ownership and communities beginning to deal with these determinants of health. The use of democratic principles, deliberation, public judgment, and public acting has an important role in the new public health.23

The Place of Public Health in an Evolving System The United States is currently enduring a restructuring of its illness care system. Change is evolving based on a series of governmental and private policy decisions aimed at controlling illness care costs by applying market strategies to health care and improving the quality of care patients receive. Little attention is being paid to the more than 45 million Americans without health-care insurance, or the public health infrastructure. If our concern was for the health status of our population, reform of our “system” would be based on what should be done to create the

PATCH training has been provided by the CDC to 39 states and territories, and there are at least 130 operational programs.

Innate individual traits: age, sex, race, and biological factors

Healthy Cities The idea of Healthy Cities also emerged in the 1980s as a demonstration project of the European office of the World Health Organization. The project creates public, private, and voluntary partnerships which focus collective energies into coordinated, broad-based approaches to the resolution of community health problems. Each project is expected to attain four major goals: assure organizational capacity, enhance information, establish initiatives, and create networks.26 THE FUTURE

The health status of citizens of the United States has improved dramatically over the past several centuries. The bulk of that improvement is due to public health policies and actions.27 The major causes of disease and death have changed during that period, however, from communicable disease agents to behavioral and environmental factors that cause chronic illnesses or injuries. Approximately 70% of the resultant premature mortality currently suffered by the population of the United States is amenable to control using population-based strategies. There are also other areas which can, and will, contribute to the range of public health tools that we can use in dealing with community

1247

Over the life span

Individual behavior

Social, family, and community networks

Living and working conditions may include: • Psychosocial factors • Employment status and occupational factors • Socioeconomic status (income, education, occupation) c • The natural and built environments • Public health services • Health care services

Living an working conditions

Broad social,a economic, cultural, health,and environmental conditionsb and policies at the global, national, state,and loca levels

Figure 75-6. The socioecological model for considering public health problems. This model indicates that health and disease are dependent on risk factors or specific microbiologic agents, but those other areas, such as the family, the community, the work site or the context in which we function are also powerful determinants of disease.

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Health-Care Planning, Organization, and Evaluation

healthiest population possible. Following that concern to its logical ends would lead to the realization that improved health status depends on both illness care reform and public health reform. It is the responsibility of public health practitioners to help society understand that both disciplines are important, and that they should be integrated to provide a seamless web of services from health promotion through disease prevention to illness diagnosis and treatment accessible to all Americans. No one should be denied access to illness care, but it is population-based services that have the greatest potential to improve health status.

pursued in a manner that the technical capacity of public health workers is improved, and the knowledge of community public health problems is advanced. Students and faculty from educational settings teaching public health-related disciplines should be welcomed into LHDs for pragmatic practice experiences, and for access to data and systems to carry out research. Likewise, educational institutions should seek out the participation of practitioners in their teaching and research activities. Local health departments should be supportive of their employees who wish to receive further training while employed.

Strengthening Public Health for the Future

CONCLUSION

Public health departments face an operational environment that is more fluid than it has perhaps ever been. Rapid advances in technology and understanding of risks to health challenge agencies with minimal funding, training, and technical capacity to incorporate new methods into time-honored, traditional modes of operation. Federal and state comparative inattention to public health needs, coupled with the shift of resources and some responsibilities to private contracting insurance companies in many, especially urban, localities, create crises of role definition and funding. As often occurs, however, this period of relatively rapid change presents opportunities. The description of the core functions of public health has made basic public health roles and functions more easily understood and appreciated. The ascendency of concerns for costs and quality of health care brings new players to the scene who should be philosophically in tune with population risk reduction. The growing technical capacity to store, transmit, and analyze large bits of information brings new opportunities for interaction among public health professionals, and between the public health profession and the community. If public health departments can be flexible and adjust their services and activities to match the needs and opportunities now apparent, they will be in good position to serve well the communities that fund them. Basic to the successful LHD of the future will be its position as the health intelligence center of its constituency. The LHD must be the source of epidemiologically based thinking and analysis of its community’s approach to health problem solving. It must be the facilitator of strong and meaningful community participation in the assessment and prioritization of community health problems and issues. It must be a major participant in public policy decision-making relative to health, and it must deliver, and broker the delivery of, services needed by its constituency to maintain or regain health. And, of course, it must focus on health outcomes as the measure of the impact of interventions. It will be the rare LHD that has the resources available to it that are needed to carry out its community’s full public health agenda. To be successful, LHDs will have to build strong collaborative and cooperative linkages with a variety of other community agencies and institutions. These linkages might take the form of joint programming efforts, service and referral arrangements, contracts for services, conduits for funding, information-sharing agreements, etc. By acting as a broker to bring needed services together to meet identified community needs, the LHD can complete its role in assuring the community will have access to the services it needs. The proliferation of private, organized health-care delivery systems puts health departments into the position of deciding whether or not to partner with emerging managed care companies and/or to monitor their activities to assure that personal health services are available to all who need them in the community. It is far from clear how, or even if, this dual role can be successfully carried out. Circumstances are quite different community by community, and the many ways these issues will be addressed should be followed closely and evaluated rigorously. At the very least, essential public health services should not be compromised in the meantime. Also important for success will be the development of stronger linkages between public health agencies and their academic bases, particularly schools and programs of public health. This should be

Significant change is occurring in both the illness care system and the public health system. No one is clearly in charge of either. Consequently, there are remarkable opportunities for entrepreneurial efforts to reshape each. Those efforts are clearly evident in the illness care system. They are also present in the public health system, although not as visibly. If the public health leadership of the United States can move the public health system out of old molds that no longer serve it well, there is every reason to believe that public health can provide a valuable set of services to communities, and be recognized as having done so. Steady, measurable gains in community health status will be the ultimate marker of success. REFERENCES

1. Last JM. A Dictionary of Epidemiology, 2nd ed. New York: Oxford University Press; 1988. 2. Institute of Medicine, Committee for the Study of the Future of Public Health. The Future of Public Health. Washington, DC: National Academy Press; 1988. 3. Institute of Medicine, Committee on Assuring the Health of the Public in the 21st Century. The Future of the Public’s Health in the 21st Century. Washington, DC: National Academy Press; 2003. 4. Bunker JP, Frazier HS, Mosteller F. Improving health: measuring effects of medical care. Milbank Q. 1994;72:225–58. 5. Mokdad AH, et al. Actual Causes of Death in the United States, 2000. JAMA. March 10, 2004;291:1238–45. 6. Scutchfield FD, Keck CW. Concepts of Public Health Practice. Principles of Public Health Practice 2nd ed. Albany, NY: Delmar Publishers Inc; 2003:6–7. 7. Sorensen AA, Bialek RG. The Public Health Faculty/Agency Forum: Linking Graduate Education and Practice. Gainesville, FL: University Press of Florida; 1991. 8. The Association of Schools of Public Health Practice Coordinators. Demonstrating Excellence in Academic Public Health Practice. Washington, DC: Association of Schools of Public Health; 1999. 9. The Association of Schools of Public Health Practice Coordinators. Demonstrating Excellence in Practice-Based Teaching for Public Health. Washington, DC: Association of Schools of Public Health; 2004. 10. Association of State and Territorial Health Officials. State Public Health Employee Worker Shortage Report: A Civil Service Recruitment and Retention Crisis. Vol. 4. Washington, DC. 2004. 11. Gostin LO. Public Health Law: Power, Duty, Restraint. Berkely, CA: University of California Press; 2000. 12. Fee E. History and development of public health. In: Scutchfield FD, Keck CW, eds. Principles of Public Health Practice. Albany, NY: Delmar Publishers Inc;2003:11–30. 13. Dandoy S, Melton RA. The state public health department. In: Scutchfield FD, Keck CW, eds. Principles of Public Health Practice. Albany, NY: Delmar Publishers Inc;2003:105–22. 14. Degnon GK, Morelli V. 1992 Salary Survey. Washington, DC: Association of State and Territorial Health Officials; 1992.

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15. Milne TL. The local health department. In: Scutchfield FD, Keck CW, eds. Principles of Public Health Practice. Albany, NY: Delmar Publishers Inc;2003:123–39. 16. U.S. Department of Health and Human Services. Healthy People: The Surgeon General's Report on Health Promotion and Disease Prevention. DHEW Publication No. 79-55071. Washington, DC. U.S. Public Health Service;1979. 17. U.S. Department of Health Human Services. Health Promotion/ Disease Prevention: Objectives for the Nation. Washington, DC. Information Resources Press;1991. 18. U.S. Department of Health and Human Services, Public Health Service. Healthy People 2000: National Health Promotion and Disease Prevention Objectives. Government Printing Office;1990. 19. National Center for Health Statistics. Healthy People 2000 Final Review. Hyattsville, MD: Public Health Service; 2001: 382. Library of Congress Catalog Card Number 76-641496. 20. U.S. Department of Health and Human Services. Healthy People 2010: Understanding and Improving Health, 2nd ed. Washington, DC: U.S. Government Printing office; November 2000: 17, 24. 21. Davis RM. Healthy People 2010: National Health Objectives for the United States. BMJ. 28 November, 1998:317.

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22. National Association of County and City Health Officials. Mobilizing for Action through Planning and Partnerships. Washington, DC;2000. 23. Scutchfield FD, Ireson C, Hall L. The voice of the public in public health policy and planning: the role of public judgment. J Public Health Policy. 2004;197–205; discussion 206–10. 24. APEX/PH Assessment Protocol for Excellence in Public Health. Washington DC: National Association of County Health Officials; 1991. 25. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion. Planned Approach to Community Health: Guide for the Local Coordinator. Atlanta, GA;1993. 26. World Health Organization/EURO. Promoting Health in the Urban Context, Five Year Planning Framework, A Guide to Assessing Health Cities. Copehagen, Denmark;1998. 27. McKeown T. Medicine in Modern Society—Medical Planning Based on Evaluation of Medical Achievement. London, England: Allen & Vawin; 1966. 28. Gebbie K, Rosenstock L, Hernandez LM, eds. Who Will Keep the Public Healthy? Educating Public Health Professionals for the 21st century. Institute of Medicine of the National Academies. Washington, DC: The National Acadamies Press;2003:6–7.

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International and Global Health

76

Franklin M.M. White • Debra J. Nanan

International Health is a well-established branch of public health, with origins in the health situation of developing nations and the efforts of industrialized countries to assist them. It has always considered issues transcending national jurisdiction, for example, quarantine regulations. However, the field has recently extended to Global Health, emphasizing global cooperation for solutions. While problems like unsafe drinking water affect mainly local communities within countries, others have worldwide impact, for example, air pollution, drug trafficking, and tobacco marketing. Although local and national actions are essential, these also require additional global action, for example, Framework Convention on Tobacco Control.1 Regardless of the levels of solutions (local, national, international, global), at the core of the world’s health problems lie enormous inequities in economic and social conditions, and the right to health remains unfulfilled for most of the world’s people. Coherent country-specific, regional, or global health initiatives depend on priority setting that considers the magnitude of problems, and the availability of effective, affordable, and acceptable solutions. The process requires reliable health information to inform decisionmakers and guide managers in implementing sustainable programs. Many industrialized countries do not perform this process well, despite their resources and availability of choices. In developing countries, making the best possible decisions with more limited resources is even more critical, and requires building a research capacity to produce such health information.2 The 1990 Commission on Health Research for Development argued that developing countries allocate 2% of their health budgets on Essential National Health Research.3 The Global Forum for Health Research in 1999 noted the “10/90 disequilibrium”: only 10% of research is devoted to the health problems of 90% of the world’s population.4 This disequilibrium mirrors inequities in health worldwide: in 2003, the under-five mortality rate was 123 deaths per 1000 live births for low-income countries (LICs), while in high-income countries (HICs), the rate was 7 (Table 76-1). For all countries experiencing violent conflicts, child mortality rates have worsened: preventable infectious diseases (IDs) and malnutrition, often in combination, are the predominant underlying causes. Women are over 100 times more likely to die of pregnancy-related causes in developing than in developed countries. Of people in developing countries, more than half lack access to sanitation, a quarter lack clean water, a fifth lack access to health care of any kind, and a fifth experience inadequate nutrition. Economic disparities within and between countries are growing.5 Over a billion people live in extreme poverty despite the global economy doubling over the past 25 years to more than $25 trillion. For some LICs, historical dynamics complicate the situation. For centuries, powerful nations explored, conquered, and exploited world regions already inhabited by indigenous peoples; most of these nations today are donor countries. While colonialism produced benefits, for example, trade routes, and information exchange, many developing

countries still cope with its harmful legacies. In some settings, disparities arise from the colonial fragmentation or coalescence of peoples, sometimes with conflict along religious or tribal lines, for example, Palestine, Kashmir, and Rwanda. In permanently colonized lands, the poor health status of aboriginal peoples and some other minorities, for example, blacks and hispanics in the United States, reflect similar dynamics. People in rich countries can become indifferent to the widespread poverty and disease of developing nations, and to similar problems in their own. Yet, because such adverse conditions also diminish human dignity and can give birth to civil and global unrest, rich nations increasingly view global health investments as an extension of their foreign policy and security interests. Other motives exist: the growing global dimensions of health issues; the scientific challenge of unsolved and emerging health problems; the threat of IDs exported internationally, for example, severe acute respiratory syndrome (SARS), avian influenza, and Marburg haemorrhagic fever; and (not least) humanitarianism. GLOBALIZATION

This term refers to the growing interconnectedness of countries, centered around trade and the flow of ideas facilitated by communications technologies, cultural convergence, and common concerns for environmental and health impacts.6 In promoting more open trade, the International Bank for Reconstruction and Development (World Bank) and the International Monetary Fund (IMF) urge deregulated markets, subject to rules laid down by the World Trade Organization (WTO) through multilateral trade agreements, for example, corporate taxation concessions and investment incentives allied for relaxation of wage controls and workplace standards, and contraction of public sector spending.6 Some developing nations, for example, China and India, can compete in this environment––size and resources matter. Otherwise, nations with fragile economies may struggle in dependency relationships, often accumulating debt that reduces their capacity to meet human needs. It is argued that only where regulatory institutions are strong, domestic markets competitive, and social safety nets in place, will health benefits derive from globalization.7 The potential risks to LICs from trade-oriented initiatives were demonstrated during the era of structural adjustment programs (SAP) two decades ago. The IMF then argued that economic development eventually results in poverty reduction and improved health status; IMF requirements called for reducing public expenditures on education and health as a condition for development loans. This process resulted in reversing the social and health gains of many countries.8 The World Bank (WB) consequently came to recognize that strong state support is essential to education and health.9 Income gains accounted for only a fifth of life expectancy (LE) gains between 1960 and 1990; generation and application of new knowledge and female 1251

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1252 TABLE 76-1. SELECTED HEALTH AND DEVELOPMENT INDICATORS BY INCOME LEVEL, AND BY REGION FOR LOW AND MIDDLE INCOME LEVELS

Income Level (No. of Countries) Population (millions) GNI per capita (US$) LE at birth, sexes combined (years) TFR (births per woman) IMR (per 1 000 live births) <5 years mortality (per 1,000 children) Literacy, % ≥15 years*: males females % population access to improved water source*: urban rural

Lower Middle Income (56)

972

333

2,655

2,311

1,855

472

≥9,386

3,036–9,385

766–3,035

≤765

1,988

78

74

69

58

1.6

2.3

2.1

5

18

7

High Income (54)

Low Income (61)

Low and Middle Income Countries by Region

Upper Middle Income (37)

E. Asia & Pacific (24)

Europe & Central Asia (27)

Latin America & Caribbean (32)

Middle East & N. Africa (15)

South Asia (8)

Sub-Saharan Africa (48)

533

312

1,425

705

1,217

1,747

744

733

351

70

68

71

69

63

46

3.7

2.1

1.6

2.4

3.1

3.2

5.2

31

80

36

25

43

58

67

110

22

38

123

41

36

33

53

92

171

— —

90 90

88 86

68 48

90 86

98 96

86 88

82 61

73 44

71 58

100 98

96 —

94 71

89 70

71 69

92 80

98 69

96 78

93 80

82 46

Source: Data from 2005 World Development Indicators database, World Bank. Based on data reported as 2002 (*) and 2003. NOTE: GNI = Gross National Income, Atlas method; LE = Life Expectancy; TFR = Total Fertility Rate; IMR = Infant Mortality Rate; — = data not given.

76 education were more critical.10 The world should have learned that, in liberalizing trade, measures to protect the autonomy of national social and health policies must be respected. If health is a priority, it can be delivered; for example, health status in Cuba, excluded from mainstream globalization, is comparable to that of the United States, with per capita income less than a fifth. Public policies affecting health determinants underlie this success.11 How globalization plays out depends on how the process is managed. Under the WTO’s Trade-Related Aspects of Intellectual Property (TRIPS) Agreement (1994), drug patent protection trumps public health. Although the WTO Doha Declaration (2001) reaffirmed that TRIPS should not prevent poor countries from making essential drugs available to their people, successful applications of this principle so far remain few.5 Ideally, trade and health-related laws should work in harmony, for example, Rotterdam Convention on the Prior Informed Consent Procedure for Certain Hazardous Chemicals and Pesticides in International Trade (1998). A high level of compliance with such multilateral agreements can be achieved, a motivating factor being how a nation’s reputation is affected.12 Globalization will be optimized only when health becomes a central objective.13 CLASSIFICATIONS OF NATIONS

All classifications have advantages and limitations. The term “third world” originated in French (tiers monde) following World War II when politicians aligned countries into the “free world,” the “communist block,” or nonaligned states (“third world”). This construct is now obsolete, communism being a spent force and new geopolitical alignments forming. In 1980, the Brandt Commission envisioned a world divided into “North,” the industrialized nations (mostly Northern Hemisphere), and “South,” comprising most of Africa, Latin America, and South, Southeast, and Southwest Asia, the underdeveloped regions.14 While several “south” countries have transcended this status, the terminology remains relevant with renewed interest in the Commission’s goals.15 The terms “developing versus developed,” or “less developed versus more developed,” refer mainly to economic development. However, income-based groupings may be preferable. The WB classifies nations into four groups based on gross national income (GNI) per capita, using U.S. dollar equivalents (Table 76-1). Other classifications are also used, depending on the purpose. To compare disease burdens and expenditures, the World Health Organization (WHO; see International Health Agencies) groups nations as established market economies; former socialist economies of Europe; China and India as distinct entities due to population size; and the rest of the world by geographic region.16 The WHO also groups neighboring countries into regions, for example, Africa, Latin America and the Caribbean, and Eastern Mediterranean, for policy and programming purposes. The United Nations Children’s Fund (UNICEF), given its distinct mission, groups nations by their infant and early child mortality rates. INEQUALITIES AND THE HEALTH OF NATIONS

Of 6.3 billion people in the world (Table 76-1), 2.3 billion live in the poorest countries (LICs), 2.6 billion live in lower-middle income countries (LMICs), and 333 million in upper-middle income countries (UMICs). About 972 million people live in HICs, rich in part because of their access to or ability to exploit resources, for example, oil, and food. Restated, over 80% of people live in nations with access to less than 20% of the world’s wealth and productive capacity. More striking is that 2.5 million of the world’s poor collectively have less wealth than the world’s richest 400 individuals. Such gross inequalities should challenge the world community. That LE varies by more than 48 years among countries (Japan 81.5; Zambia 32.7), and 20 years or more within countries, is not inevitable.17 Social factors influence the occurrence of most forms of disease and lie at the root of health inequalities. In response to this global challenge, WHO recently launched a Commission on Social

International and Global Health

1253

Determinants of Health (2005) to review evidence, raise societal debate, and recommend policies to improve the health of vulnerable people; the thrust is to transform public health knowledge into political action.18 The Human Development Index (HDI) is a composite index developed by the United Nations Development Programme (UNDP), combining income, life expectancy, adult literacy, and schooling. Although controversial, the HDI helps to compare countries regarding their health and welfare. In 2002, Norway had the highest HDI (0.956) and Sierra Leone the lowest (0.273; rank 177).17 Four decades ago, China ranked below Pakistan on education although equal on per capita income.19 Pakistan today (HDI 0.497; rank 142) remains an LIC with an unfavourable health status.20 China (HDI 0.745; rank 94) is now a LMIC showing impressive gains. This did not happen by chance. In its process of socialist modernization, casting off feudalism and colonialism, China emphasized prevention, focused on rural areas (using “barefoot doctors”), and implemented a “one-child policy.”21 Now contemplating democratic reforms, while challenged by noncommunicable disease (NCD) risk factors, HIV/AIDS, and most recently SARS, how China now manages its health situation is of global interest. Today, several Asian nations, for example, Japan, Singapore, and South Korea, are at par with western economies. While often attributed to investment policies, savings incentives, and land and tax reforms, more critical to health are their public investment in education and technology, and degree of gender equity. Notwithstanding significant gains in the Americas, for example, Chile, Brazil, and Mexico, the situation is dire for the countries of sub-Saharan Africa and western Asia whose economic viability is overwhelmed by population growth outstripping resources, environmental degradation, poor planning and mismanagement, corruption, military conflict, and widespread preventable diseases.

International Health Agencies Health services in developing countries mostly reflect their own widely varying capacities. The international system plays an ancillary role, comprising four types of agency: multilateral, bilateral, nongovernmental, and other.

Multilateral Agencies Funded primarily by member governments, the lead agency of this type is WHO, headquartered in Geneva. Launched in 1948, under the aegis of the newly formed United Nations (UN), WHO is governed by a World Health Assembly composed of representatives from almost 200 member states. Its main task is to review and approve policies, program initiatives, and biennial budgets. WHO is primarily a coordinating agency, promoting technical cooperation among countries while facilitating training and technical assistance. Health data from member countries are analyzed and the resulting information disseminated globally; collaborative programs with member countries are performed by a Secretariat, supported by six regional offices with representatives in most countries. The organization’s achievements are impressive. Most notably, it spearheaded the global eradication of smallpox, accomplished in 1979.22 Similar initiatives for other conditions are underway. Nonetheless, such selective programming by WHO attracts debate given its broader mandate. WHO also suffers from unreliable funding; for example, the United States owed $2 billion in the late 1990s. In recent years, extrabudgetary sources (grants, contracts, donations) have exceeded the regular budget. While this diversification protects WHO against unstable government funding, extrabudgetary support is mostly restricted to particular programs, which may influence or distort priorities. Other multilateral agencies with health-related roles are UNICEF, UNDP, WB, UNAIDS (a separate agency since 1993, formerly the WHO Global Program on acquired immunodeficiency syndrome), the Food and Agriculture Organization (FAO), the United Nations Fund for Population Activities (UNFPA), the Office of the UN High

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Commissioner for Refugees (UNHCR), and the UN Fund for Drug Abuse Control (UNFDAC).

Bilateral Agencies In addition to supporting multilateral agencies, most industrialized nations also provide aid on a “country-to-country” basis, attempting to match a recipient’s needs with the donor’s objectives and capacity to assist, usually subject to political considerations. Smaller donors are geographically selective; for example, Australia emphasizes its Western-Pacific neighbors. Others emphasize their expertise; for example, the Netherlands supports water technologies. Some follow historical links; for example, France emphasizes its former colonies. Some both receive and donate international aid, for example, Cuba, and China. The United States links aid to democratic reforms and human rights, although restricting support for reproductive rights since 2001.23 Illustrating the flexibility of the bilateral system, other donor nations, for example, United Kingdom and Canada, compensate through unrestricted support for these rights. In 2004, only five countries met the UN target of contributing at least 0.7% of gross national product in official development assistance (ODA): Norway, Denmark, the Netherlands, Luxembourg, and Sweden. In contrast, the United States provided only 0.16%, and the U.K. 0.36%. Spain, Germany, France, Finland, Belgium, and the U.K. have pledged to reach the target by 2015. Donor countries often rely on their own expertise through competitive bidding to design, implement, and monitor projects funded under bilateral agreements, sometimes requiring that the donor’s own products and services be used. Thus, a significant proportion of aid budgets may be recycled within a donor’s economy. As each donor has its own motivation, priorities, and management style, competition and conflict can arise in some settings, revealing a need to improve donor coordination. It is critical that ODA is increased, effectively placed, and fairly counted, so as to help to build sustainable capacities for all the people of the world.

Foundation, Robert Wood Johnson Foundation, David and Lucille Packard Foundation, and Aga Khan Development Network. HEALTH REFORM AND FINANCING

In many developing countries, health and social development suffer from distortions in priority setting, fiscal allocations, and management. Neocolonial patterns are reflected in debt servicing and arms purchases (large donor countries are major suppliers), vastly exceeding the value of ODA and depleting national budgets. Given the consequently reduced national investment in health, private providers dominate with minimal regulation. Such situations have often arisen in virtual policy vacuums, with no explicit social development or health objectives, let alone comprehensive health sector planning. The widespread need for reform was recognized by the WB in their concept of “investing in health.”24 However, this idea is not widely accepted by political leaders even in some industrialized countries; for example, millions of Americans lack health insurance. In virtually all countries, “reform” is driven more by fiscal than health priorities. Lack of investment in health by many developing countries contributes to a “brain drain” that further diminishes their capacities while subsidizing the health systems of developed nations, some of which actively recruit this talent, for example, nurses and doctors. While health may be improved indirectly by investing in other sectors, for example, education, optimal outcomes require direct investment in the health sector. Assistance with health systems reform and human resources for health is an important responsibility for bilateral and multilateral aid agencies. There is a direct relationship between such investment and health outcomes.25

Public-Private Partnerships

International nongovernmental organizations (NGOs) are increasingly active in development work as the inadequacies of bilateral and multilateral responses become more apparent. Sometimes known as “people to people” aid, their activities are mostly specific, for example, targeting trachoma, and cataract, while some are general, for example, aid for orphans. Supported mainly by voluntary subscriptions or donations, some NGOs also act under contract to governments or other agencies. The largest NGO is the International Red Cross and Red Crescent movement, which has national counterparts within most countries. It is mandated under the Geneva Conventions to assist prisoners and civilians in armed conflicts, including visiting detainees and enabling them to communicate with the outside world, setting up surgical hospitals and emergency teams, rehabilitation of war-disabled persons, and providing independent information on prisoners and war victims. Other well-known international NGOs are Oxford Famine Relief (OXFAM), CARE International, Save the Children International Alliance, and World Vision. Medecins Sans Frontieres (MSF, Doctors Without Borders) was recently awarded the Nobel Peace prize (1999). Founded in France in 1971, MSF provides health aid to war victims, and assists in other health disasters and development initiatives. Smaller international NGOs also make highly valuable contributions, many operating within a country. Many exercise key advocacy roles, for example, to prevent violent conflicts, promoting gender equity. Despite good intentions, given sometimes conflicting priorities and mandates, and competition for resources, better coordination would help them become more effective.

In 1998, the Director-General of WHO advocated greater collaboration with the private sector.26 Perhaps inevitable given the global trend towards privatization and declining public sector funding, with this endorsement, public–private partnerships (PPPs) were ushered in to address a broader range of health initiatives. Beyond philanthropy, the private sector now had to help shoulder responsibility for the public good, or otherwise demonstrate the failure of privatization as sound public policy. Likewise, many public health managers had little option other than to develop such arrangements, despite their untested strengths and limitations. As a company’s first responsibility is to its shareholders, the potential for conflicts of interest was recognized, as was the need for WHO to ensure safeguards to protect the public interest.27 Large corporations gained access to certain areas of decisionmaking arguably greater than that of many countries. Major pharmaceutical and equipment manufacturing firms joined private foundations to become major players in the global development scene. While the impact of PPPs requires ongoing evaluation, some genuinely good work has emerged: subsidized products, distribution assistance, educational initiatives, and disease control ventures, for example, Global Alliance for Vaccines and Immunization and Medicines for Malaria Venture. In some instances, health services are to be strengthened, for example, Gates Foundation/Merck Botswana Comprehensive HIV/AIDS Partnership.28 However, WHO-facilitated PPPs generally emphasize specific disease interventions, and other PPP models seem better at health systems development; for example, BRAC (formerly Bangladesh Rural Advancement Committee), a people-centered national NGO, has developed an integrated and multidimensional health program that links foundations, governments, and communities, with notable success within the country.29

Other Agencies

Strategic Options

Both developed and developing country institutions, universities, laboratories, and consulting groups are active in bilateral initiatives, and some also work with multilateral agencies, for example, as WHO collaborating centers. Several philanthropic bodies contribute substantially to international health, for example, the Bill and Melinda Gates

The Alma Ata Conference sponsored by WHO and UNICEF in 1978 ushered in a new philosophy on health service development. With 134 countries represented, primary health care (PHC) was unanimously accepted as the key to attaining “by all peoples of the world by the year 2000 a level of health that will permit them to lead a

International Nongovernmental Organizations

76 socially and economically productive life”.30 The PHC strategy emphasized community participation, and included adequate nutrition, safe water, sanitation, maternal and child health, immunization, medical care for common illnesses, access to essential drugs, control of locally prevalent diseases, and health education. Countries were motivated to formulate PHC approaches, setting objectives based on their health profile and resources. However, lack of leadership and management skills in developing countries hampered progress towards this goal, and rather than taking on the task of building local capacity, the global agenda abruptly changed in 1979. A powerful counter movement questioned the feasibility of PHC, advocating an alternative strategy deemed “Selective Primary Health Care.”31 Buoyed by successful smallpox eradication, its goal was to control other important IDs, selected from a global list of 23.32 The guiding principle was interrupting transmission channels, not developing PHC systems from the ground up. Endorsing “selective PHC,” WHO launched globally coordinated, nationally administered, vertically integrated, and externally financed programs against mostly single diseases, for example, tuberculosis, leprosy, and malaria. Progress towards eradication of poliomyelitis and dracunculiasis demonstrated again that selective approaches can work. Developing countries quickly learned that selective programs attract funding, with little incentive for integration within broader programming; yet selective programs against every disease are unfeasible. Moreover, conditions dominating childhood morbidity and mortality (diarrheal diseases, acute respiratory infections, and malnutrition) are not efficiently addressed by selective PHC, and receive less funding. Regarding the NCD pandemic now dominating all regions except sub-Saharan Africa, lack of a broadly integrated PHC model hampers efforts to respond. At the “People’s Health Assembly” in Dhaka in 2000, delegates from 113 nations expressed disappointment over the unrealized goal of Alma Ata, and encouraged policy reflections “by” instead of “on behalf of” people, emphasizing the social and economic roots of ill health and poverty.33 There is clearly a need to restore balance between these two strategic visions. Integrated approaches have been advocated in all developing regions, and some show promise, for example, vitamin A supplementation within the Expanded Program on Immunization.34 Integrated Management of Childhood Illnesses (IMCI) promotes case management for common IDs and malnutrition, with health systems improvements involving families and communities; but IMCI has not succeeded when scaled to a national level.35 Community-directed treatment for the control of onchocerciasis, schistosomiasis, and intestinal helminths were shown to be functional strategies in poor rural communities in Africa.36 While addressing onchocerciasis as a target for eradication, Carter Center researchers recently reported that health workers engaged in other health activities performed better in control efforts than those involved solely in its control.37 Probably the best examples of integrated approaches are those addressing sexual and reproductive health (see Gender, later in this chapter). Integrated models for NCD, well tested in the WHO European Region’s CINDI network,38 are also of interest: Mauritius achieved impact on NCD risk factors with a policy and lifestyles approach;39 the Pan American Health Organization (PAHO/WHO) initiated the CARMEN network of projects in 1995;40 and in 2004, Pakistan launched an NCD Action Plan utilizing a PPP model.41 Despite the potential of these and other integrated models, they generally enjoy less political and funding support when compared with selective control models. Responsibility for general inaction in implementing more broadly-based PHC is shared at all levels. District health systems in all countries have, in principle, the potential to integrate medical and public health approaches at community level, consistent with the Alma Ata vision. But district health officers in developing countries are often selected based on seniority without adequate training, while public health specialists may be assigned to inappropriate tasks, for example, emergency clinics. Perhaps it was unrealistic to entrust the implementation of PHC strategy to this poorly managed local health

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system.20 With this backdrop, the merits of selective disease control became easier for the multilateral system to advocate and finance, and stays well within their remit. Citing the “disease-to-poverty” pathway, in 2001 the WHO Commission on Macroeconomics and Health gave timely support to the UN which then launched the Global Fund to Fight AIDS, Tuberculosis, and Malaria in 93 countries, committing an initial U.S. $1.5 billion by 2004, augmented in subsequent years.42 These are devastating conditions; for example, over the past two decades, more than 60 million people have become HIV-infected, and over three million have died from AIDS; in many countries health gains of the previous 50 years have been eroded; for example, in Botswana, adult HIV prevalence is 39%, and LE at birth is now below 40 years. However, despite this clear justification for the Global Fund, whenever selective goals receive massive support, alternative choices inevitably drop in priority; especially so in an era of ODA falling far short of the 0.7% which rich countries pledged to work towards in Monterrey and Johannesburg.5 The “poverty-to-disease” pathway also must be addressed, as recognized in 2005 when WHO launched The Commission on Social Determinants of Health.18 Focusing more on poverty reduction, the eight Millenium Development Goals (MDGs) adopted by the UN in 2000 committed members to tackle ill-health, gender inequality, lack of education, poor access to clean water, and environmental degradation. Three MDGs are directly health-related: reduce child mortality; improve maternal health; and combat HIV/AIDS, malaria, and other diseases.5 Critical needs such as health systems development, sexual and reproductive health, and NCDs were omitted, although countries may add their own goals. HEALTH TRANSITIONS

Epidemiologic transition theory combines the demographic transitions attributable to declining mortality and fertility rates, with shifts in variables that produce disease patterns. The process was experienced slowly by western societies over three centuries, accompanying improved literacy, hygiene, nutrition, and sanitation; medical interventions played a late role. The “classical” model of western Europe and North America revealed declining infant mortality, increased LE, and aging populations, with a gradual shift in predominance from IDs to NCDs and injuries. Less developed countries are undergoing faster transitions, the timing and pace of fertility decline varying with socioeconomic, medical, technological, and political settings. Variants of the theory help to characterize observed changes.43 The “accelerated/semiwestern model” applies to eastern Europe, Russia, and Japan: the disease pattern changes are attributed mainly to synergy between sanitation and disease control, for example, antibiotics, immunization, insecticides, and organized health care. A “rapid transitional variant” fits scenarios seen in fast industrializing or socially developing countries that are often small, for example, Hong Kong, Singapore, and Caribbean nations, where mortality declines began only in the third or fourth decade of the twentieth century, but once fertility then began falling, it did so rapidly. A “slow transitional variant” characterizes LICs in Africa, Asia, and Latin America, with moderate mortality declines and still high fertility associated with short LEs and young age structure, and slow socioeconomic development; a large NCD burden is superimposed on persistent heavy burdens from IDs and malnutrition. An “intermediate transitional variant” includes countries with patterns falling between rapid and slow models, having well-organized family planning programs, but coping with a considerable “double burden” of disease. Epidemiological transition theory helps explain existing patterns and disparities in international health, and provides an approach to modeling projections. Stages may overlap between or within countries; underlying processes may stagnate or even reverse; war, unfair trade, microbial resistance, systems failure, resource depletion, and environmental damage may be incorporated. Scenarios for sustained health can also be projected: this model calls for improved global governance, investment in social programs, sound resource and

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Health-Care Planning, Organization, and Evaluation used. The distribution of DALYs in 2002 due to three groups of conditions, for selected world regions, are presented in Table 76-2: Group I (communicable diseases, maternal and perinatal conditions, and nutritional deficiencies) accounts for below 10% in each developed region, but for almost 75% of DALYs in Africa. However, in all other developing regions, Group II (noncommunicable conditions) equals or exceeds the burden due to Group I. Health policies in poor countries, and at a global level, given the current preoccupation on IDs, must be quick to adapt or lose the opportunity to prevent much of the now burgeoning pandemic of NCDs and injuries. Differences also exist for indigenous populations.50 Wherever measured, for example, Australia, Canada, New Zealand, and the United States, aboriginal people experience lower LEs, higher infant mortality, higher rates for IDs and NCDs, and much higher rates of drug use, injuries, and suicide than general populations. Such gaps signal an urgent need to take action on the social causes that result in these health inequities.

environmental management, health systems adjusted to aging populations, and strategies to reduce disparities between rich and poor.44 Denoting transition variables as either determinants or consequences, or interpreting their interactions, is problematic. Furthermore, globalization forces may further distort current and future scenarios: rural to urban population drift, changing nutrition, and other lifestyle variables are dramatically transforming health patterns. The increasing prevalence of overweight or obesity, due to a shift from traditional diets low in fat and high in grains, to diets high in fats, processed foods, and meats, along with more sedentary living, is driving increasing rates of cardiovascular and metabolic disorders, for example, diabetes, especially in lower socioeconomic groups.45 In addition, NCDs are more likely to occur in adults who once suffered intrauterine growth retardation due to maternal undernutrition.46 The poorest LICs, mostly in Africa, already face a triple burden of communicable disease, NCDs, and sociobehavioural disorders; by 2020, NCDs will account for 70% of deaths in developing regions, injuries will rival infectious diseases in priority, and tobacco is expected to kill more people than any single disease, even HIV/AIDS.47

FOOD AND NUTRITION SECURITY

Global and Regional Health Profiles Nutrition throughout life determines growth, development, and disease susceptibility. Although enough food is produced to feed everyone, inequitable distribution results in hunger and malnutrition, affecting over 350 million people worldwide. Most vulnerable are the poor, the marginalized, women, children, and persons exposed to natural or manmade disasters. Children are most vulnerable and suffer irreversible growth retardation by stunting and wasting, and impaired cognitive development that affects them through life; females are almost twice as likely as males to experience malnutrition. Food security would exist when all people, at all times, have physical and economic access to sufficient, safe, and nutritious food to meet their dietary needs and preferences. Food insecurity results from unavailability, unstable supplies, insufficient purchasing power, inappropriate distribution, or inadequate household utilization. FAO classifies most of the developing world as “low income, food deficit countries” (LIFDCs) not producing enough food to feed their people and unable to afford importing sufficient amounts to close the gap.51 FAO estimates that 852 million people worldwide were undernourished in 2000–2002: 815 million in developing countries, 28 million in transitional countries, and 9 million in industrialized countries. The World Food Summit (1996) called for improving food security in over 80 LIFDCs by rapidly increasing food productivity; reducing year-to-year variability in production; and improving food access. The goal is to halve the number of malnourished people globally by

During the twentieth century, death rates fell and LEs rose first in the more developed countries, and then throughout the less developed world. In 1900, LE at birth was 45–50 years in the United States, Europe, Japan, and Australia. Today, LE in the United States is 77 years, while in Japan and many European countries, LE is over 80 years. However, Russia, Central Asian, and Eastern European states experienced declining LEs during the 1980s and 1990s when economic conditions deteriorated. Between 1990 and 2000, Russian male LE fell from 64 to 59 years, and female LE dropped about 2 years to 72 years.48 In Africa, adult mortality, following steady declines until the mid-1990s, sharply reversed; in parts of sub-Saharan Africa, current adult mortality rates now exceed the levels of three decades earlier, producing a rapid drop in LE in the 38 most-affected African countries, where nearly 10 years of LE will have been lost by 2020–2025, falling to age 40 or less in at least eight countries. Without HIV/AIDS, LE at birth in the African Region would have been almost 6.1 years higher in 2002. Healthy LE (HALE) converts total LE into equivalent years of “full health” by taking into account years lived in less than full health as a result of diseases and injuries.49 Globally, HALE varies even more than total LE, ranging from 41 years for sub-Saharan Africa to 71.4 years for western Europe in 2002. As LE at birth is heavily weighted by death at younger ages, to account for survivorship at older ages in various states of health, Disability Adjusted Life Years (DALYs) is an alternative health measure

TABLE 76-2. BURDEN OF DISEASE IN DALYs FOR DEVELOPED AND DEVELOPING REGIONS, BY NUMBER AND PERCENT ( ) Developing Regions

Developed Regions

Who Region

Africa

Americas

SE Asia

E Med

W Pacific

Americas

W Pacific

Europe

Population Total DALYs I. Communicable diseases, maternal and perinatal conditions, and nutritional deficiencies II. Noncommunicable conditions III. Injuries

672,238 361,376 265,722 (73.5)

518,971 98,719 23,544 (23.8)

1,590,832 426,573 184,649 (43.3)

502,824 139,079 64,373 (46.3)

1,562,136 248,495 53,358 (21.5)

333,580 46,868 3,106 (6.6)

155,400 16,384 929 (5.7)

877,886 150,322 14,037 (9.3)

64,851 (17.9) 30,803 (8.5)

59,855 (60.6) 15,319 (15.5)

186,376 (43.3) 55,547 (13.0)

57,223 (41.1) 17,481 (12.6)

159,791 (64.3) 35,347 (14.2)

39,217 (83.7) 4,545 (9.7)

13,827 (84.4) 1,627 (9.9)

115,339 (76.7) 20,945 (14.4)

Source: Constructed from Statistical Annexes, WHO Health Report 2004. NOTE: “Developed” versus “developing” based on WHO region and mortality rates for children <5 and adult males 15–59 years. Region abbreviations: SE Asia = South East Asia; E Med = Eastern Mediterranean; W Pacific = Western Pacific; Americas developed = Canada, Cuba, United States of America; W Pacific developed = Australia, Brunei Darussalam, Japan, New Zealand, Singapore.

76 2015, the underlying assumption being that barriers to food security can be overcome by economically viable and environmentally sustainable means; however, trade practices and policies associated with deregulated markets impede progress toward this goal. Though food and nutrition insecurity is generally declining worldwide, albeit slowly in South Asia, the problem is worsening in Africa due to civil conflicts, droughts, floods, and economic downturns. Estimates of undernourished people in Africa rose from 111 million in 1969–1971 to 204 million in 1999–2001. Food shortages are now so severe in East and Central Africa that they require regular international interventions. Rich country agricultural subsidies total over $300 billion annually, nearly six times the value of ODA.5 Food and nutrition security remain global ethical imperatives. WATER AND SANITATION

Over a billion people in developing countries lack access to safe water, and 2.4 billion lack access to adequate sanitation.5 In rural areas without distribution technology, fetching and carrying water, often performed by women and children, reduces the time available for other subsistence activities. In urban slums from Lima to Karachi, the poor suffer from exploitation by tanker “mafias” delivering water at prices up to 20 times that paid by those who enjoy a municipal supply; poor households spend up to 40% of their income on water.52 Most vulnerable are children, who suffer over three million deaths annually from preventable diseases due to lack of water, dirty water, and inadequate sanitation. Oral rehydration for diarrhea reaches only about half of those in need; without water for washing, skin and eye infections, for example, trachoma, can lead to blindness. Provision of hygiene education, water, and sanitation can reduce water-borne diseases.53 There is gross mismanagement of water resources virtually everywhere, and the abuse of water security as an instrument of conflict has increased exponentially.54 Of 30 such events over the past 20 years, half were military actions targeting water supplies, resulting in widespread waterborne diseases, affecting mainly infants and children; this form of biological warfare is not recognized under the Biological Weapons Convention (1972). Projections for 2025, if left unchecked, reveal that 40% of the world’s population will face a crisis of drinking water availability; water security is a global health issue. GENDER

Gender refers to social differences between women and men within and across cultures and that change over time: roles and responsibilities, opportunities and constraints, and needs and perceptions. Both sex (biological differences) and gender are determinants of health. Many health inequities stem from gender differences: in men, higher risk-taking, smoking and alcohol abuse; in women, reduced healthseeking behavior if community norms prevent mobility without a male escort, and lack of autonomy over sexual and reproductive health. In many LICs, gender-related health risks are much greater for women than for men: less access to resources; economic dependency; and lower status despite their contributions to home and community. In some cultures, the simultaneous burden of less-valued productive and reproductive roles places women at special risk, with systematic loss of life at all stages, as in South Asia: prenatal sex selection, infanticide, differential malnutrition, dowry and honor killings, unsafe birthing practices, and less access to health care, all reflected in persistently high male-female sex ratios.20 As poignantly asked by Amartya Sen: “Where are the 100 million missing women?”55 Addressing gender-based health issues entails improving the status of women and girls. Strategies include increasing the following: enrollment of girls in schools; access and availability of contraception; women’s share of nonfarm workforce; involvement of women in decision-making; gender as an explicit component of health research, interventions, systems reform, education, policies, and programs. The International Conference on Population and Development

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held in Cairo (1994) was critical in resetting the agenda. Signed by 179 governments, the plan of action helped to evolve reproductive services to better meet the needs of both women and men, replacing traditional family planning programs with broader services addressing sexuality, gender-based power, STDs, domestic violence, maternal mortality, and abortion.56 Developments since Cairo reveal encouraging examples of integrated interventions, evoking the Alma Ata approach to PHC, for example, Pakistan’s National Programme for Family Planning & Primary Health Care, now enjoying renewed support, NGO partnerships, and substantial bilateral assistance.57 Conservative governments, and some religious and special interest groups, have tried to overturn or revise elements of the Cairo agenda. However, governments increasingly are taking heed that a country’s social and economic development is often reflected in the status of their women. The emergence of women as national leaders, seen exponentially over the past decade, may signal an important global shift in attitudes.58 THE WAY FORWARD

Health is embodied within the Universal Declaration of Human Rights (1948). The WHO constitution also states: “The enjoyment of the highest attainable standard of health is one of the fundamental rights of every human being without distinction of race, religion, political belief, economic or social condition”; and yet, inequities in health most visibly mark these distinctions, and the right to health remains unfulfilled for most of the world’s people. To achieve health for all people requires better priority setting and investment in health determinants. It demands principled leadership, responsible governance, innovative management, and participation by people in making decisions affecting their health. In seeking global prosperity, we must not reduce health simply to economic equations or strategic choices. Rather, the way forward calls for health as a core value, in balance with development principles that are just, sustainable, and ethically sound. REFERENCES

1. Shibuya K, Ciecierski C, Guindon E, et al. WHO Framework Convention on Tobacco Control: development of an evidence-based global public health treaty. BMJ. 2003;327:154–7. 2. White F. Capacity-building for health research in developing countries: a manager’s approach. Pan Am J Public Health. 2002;12: 165–72. 3. Commission on Health Research for Development. Health Research: Essential Link to Equity in Development. New York: Oxford University Press; 1990. 4. Global Forum on Health Research. The 10/90 Report on Health Research 1999. Geneva: Global Forum on Health Research; 1999. 5. United Nations Development Programme. Human Development Report 2003. Millennium Development Goals: A Compact among Nations to End Human Poverty. New York: Oxford University Press; 2003. 6. McMichael A, Beaglehole R. The global context for public health. In: Beaglehole R, ed. Global Public Health. New York: Oxford University Press; 2003. 7. Collins T. Globalization, global health, and access to health care. Int J Health Plann Manage. 2003;18:97–104. 8. Loewenson R. Structural adjustment and health policy in Africa. Int J Health Serv. 1993; 23:717–30. 9. The World Bank. World Development Report 1997: The State in a Changing World. New York: Oxford University Press; 1997. 10. World Health Organization. The World Health Report 1999— making a difference. Geneva: World Health Organization; 1999. 11. Spiegel JM, Yassi A. Lessons from the margins of globalization: appreciating the Cuban health paradox. J Public Health Policy. 2004;25:85–110.

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12. Von Schirnding Y, Onizivu W, Adele AO. International environmental law and global public health. Bull World Health Organ. 2002;80:970–4. 13. Woodward D, Drager N, Beaglehole R, et al. Globalization and health: a framework for analysis and action. Bull World Health Organ. 2001;79:875–81. 14. Independent Commission on International Development Issues. North-South, a Programme for Survival: A Report of the Independent Commission on International Development Issues. Cambridge, Mass: MIT Press; 1980. 15. The Brandt 21 Forum. The Brandt Equation. 21st Century Blueprint for the New Global Economy 2002. Available at: http://www. brandt21 forum.info/. Accessed May 8, 2005. 16. Murray CJL, Lopez AD. Global Comparative Assessments in the Health Sector: Disease Burden, Expenditures and Intervention Packages. Geneva: World Health Organization; 1994. 17. United Nations Development Program. Human Development Report 2002. Deepening Democracy in a Fragmented World. New York: Oxford University Press; 2002. 18. Marmot M. Social determinants of health inequalities. Lancet. 2005; 365:1099–104. 19. Bryant J. Health & the Developing World. Ithaca and London: Cornell University Press; 1969. 20. John TJ, White F. Public health in South Asia. In: Beaglehole R, ed. Global Public Health. New York: Oxford University Press; 2003. 21. Lee L, Lin V, Wang R, et al. Public health in China: history and contemporary challenges. In: Beaglehole R, ed. Global Public Health. New York: Oxford University Press; 2003. 22. Hopkins JW. The eradication of smallpox: organizational learning and innovation in international health administration. J Dev Areas. 1988;22:321–32. 23. Crane BB, Dusenberry J. Power and politics in international funding for reproductive health: the U.S. Global Gag Rule. Reprod Health Matters. 2004;12:128–37. 24. The World Bank. World Development Report 1993: Investing in Health. New York: Oxford University Press; 1993. 25. Joint Learning Initiative. Human Resources for Health: Overcoming the Crisis. Cambridge, MA: Harvard University Press; 2004. 26. Bruntland GH. Message from the director-general. In: The World Health Report 1999—Making a Difference. Geneva: World Health Organization; 1999. 27. Buse K, Waxman A. Public-private health partnerships: a strategy for WHO. Bull World Health Organ. 2001;79:748–54. 28. Widdus R. Public-private partnerships for health: their main targets, their diversity, and their future directions. Bull World Health Organ. 2001;79:713–20. 29. BRAC. About BRAC. At a Glance. As of June 2003. Available at http://www.brac.net/aboutb.htm. Accessed May 3, 2005. 30. World Health Organization and UNICEF. Report of the International Conference on Primary Health Care, Alma-Ata, USSR September 6-12. Geneva: World Health Organization; 1978. 31. Walsh JA, Warren KS. Selective primary health care: an interim strategy for disease control in developing countries. NEJM. 1979; 301:967–74. 32. Walsh JA, Warren KS, eds. Strategies for Primary Health Care. Technologies Appropriate for the Control of Disease in the Developing World. Chicago: University of Chicago Press; 1986. 33. People’s Health Movement. People’s Charter for Health. Available at http://www.phmovement.org. Accessed May 3, 2005. 34. Ramakrishnan U, Darnton-Hill I. Assessment and control of vitamin A deficiency disorders. J Nutr. 2002;132(9):2947S–2953S. 35. Huicho L, Davila M, Campos M, et al. Scaling up integrated management of childhood illness to the national level: achievements and challenges in Peru. Health Policy Plan. 2005;20:14–24. 36. Ndyomugyenyi R, Kabatereine N. Integrated community-directed treatment for the control of onchocerciasis, schistomiasis and intestinal

37.

38.

39.

40.

41.

42.

43. 44.

45.

46. 47.

48.

49. 50. 51.

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helminths infections in Uganda: advantages and disadvantages. Trop Med Int Health. 2003;8:997–1004. Katabarwa MN, Habomugisha P, Richards FO, et al. Communitydirected interventions strategy enhances efficient and effective integration of health care delivery and development activities in rural disadvantaged communities of Uganda. Trop Med Int Health. 2005;10: 312–21. The World Health Organization Regional Office for Europe. Countrywide Integrated Noncommunicable Disease Intervention (CINDI) programme. Available at http://www.euro.who.int/eprise/main/ WHO/Progs/CINDI/Home. Accessed May 4, 2005. Dowse GK, Gareeboo H, Alberti KG, et al. Changes in population cholesterol concentrations and other cardiovascular risk factor levels after five years of the non-communicable disease intervention programme in Mauritius. BMJ. 1995;311:1255–9. Pan American Health Organization. About the CARMEN Initiative. Available at http://www.paho.org/English/HCP/HCN/IPM/cmn-about. htm. Accessed May 4, 2005. Nishtar S. The National Action Plan for the Prevention and Control of Non-communicable Diseases and Health Promotion in Pakistan— prelude and finale. J Pak Med Assoc. 2004;54(12 Suppl 3):S1–8. World Health Organization. Report of the Commission on Macroeconomics and Health. Macroeconomics and Health: Investing in Health for Development. Geneva: World Health Organization; 2001. Omran AR. The Epidemiological Transition in the Americas. Pan American Health Organization and University of Maryland; 1996. Martens P, Huynen M. A future without health? Health dimensions in global scenario studies. Bull World Health Organ. 2003;81: 896–901. World Health Organization. Obesity: Preventing and Managing the Global Epidemic. Report of a WHO Consultation on Obesity. Geneva, 3–5 June 1997. Geneva: World Health Organization; 1998. Stein CE, Fall CHD, Kumaran K, et al. Fetal growth and coronary heart disease in south India. Lancet. 1996;348:1269–73. World Health Organization. Health Transition. Available at http://www.who.int/trade/glossary/story050/en/. Accessed May 4, 2005. Population Reference Bureau staff. Transitions in World Population. Population Bulletin 59, No.1. Washington, DC: Population Reference Bureau; 2004. The World Health Organization. World Health Report 2003—Shaping the Future. Geneva: World Health Organization; 2003. Ring IT, Firman D. Reducing indigenous mortality in Australia: lessons from other countries. Med J Aust. 1998;169:528–33. Food and Agricultural Organization. The State of Food Security in the World 2004. Rome: Food and Agricultural Organization of the United Nations; 2004. Department for International Development. Guidance Manual on Water Supply and Sanitation Programmes. Loughborough University, UK: Water, Engineering and Development Centre; 1998. Nanan D, White F, Azam I, et al. Evaluation of a water, sanitation and hygiene education intervention on diarrhoea in northern Pakistan. Bull World Health Organ. 2003;81:160–65. White F. Water: life force or instrument of war? Lancet. 2002;360 (Suppl):S29–S30. Sen A. Development as Freedom. New York: Anchor Books; 1999. Haberland N, Measham D, eds. Responding to Cairo: Case Studies of Changing Practice in Reproductive Health and Family Planning. New York: Population Council; 2002. Ministry of Health Government of Pakistan. Programme for Family Planning & Primary Health Care. Available at http://www.phc. gov.pk/. Accessed May 4, 2005. White F. Women, Literacy, and Leadership. Harvard International Review. 2000; XXII,2:5–7.

77

Public Health Law Edward P. Richards, III • Katharine C. Rathbun

INTRODUCTION

Core public health—food and water sanitation, sewage and refuse disposal, vermin control, and the management of zoonosis and communicable diseases—depends on law as much as on science. From the Roman sewers and public water systems, and the Venetian 40-day interregnum for ships entering port, to the recent eradication of smallpox, public health depends on the power of the state. Public health authorities must seize property, close businesses, destroy animals, or involuntarily treat, or even lock away, individuals. Without the coercive power of the state, public health and modern society would be impossible. With the exception of its higher rates of HIV infection, the United States is similar to other developed countries. For the past 30 years, communicable diseases have been relatively well controlled, shifting the public focus to the problems of chronic diseases. The September 11, 2001, terrorist attacks on the United States, which were followed by several deaths from anthrax spores carried through the mail, refocused public opinion on public health and its role in protecting the nation from bioterrorism. The specter of bioterrorism, especially an attack with smallpox, has forced a reappraisal of the balance between individual liberty and public health authority. This chapter focuses on public health law in the United States. It reviews the constitutional basis for public health law, the routine practice of public health law as administrative law, and concludes with a discussion of the future of public health law, which includes the role of public health law in national security law.

PUBLIC HEALTH AND PRIMARY CARE

Public health law, as discussed in this chapter, deals with the role of the health department as a regulatory agency. If a health department also delivers primary care, it is a dual role department. When a health department provides health care to individuals, whether it is prenatal care, well-child checkups, or general primary care, the health department employees or contractors providing medical care must follow the same laws on privacy and patient autonomy as other health-care providers. As one example, a prenatal care clinic must comply with the provisions of the Health Insurance Portability and Accountability Act of 1996 (HIPAA).1 HIPAA limits the transfer of personal medical information without the patient’s consent, and sets out standards for how the privacy of that information must be protected. HIPAA does not apply to public health reporting or the handling of information for public health regulatory purposes. Specialty public health treatment programs, such as tuberculosis control, mix the personal medical care and public health regulatory roles. The basic patient medical information that is not necessary for

disease control (personal health information other than the diagnosis of the communicable disease) is treated the same as medical information in other clinical settings. Given the complexity of health-care privacy laws, it is critical that the disease control function be clearly separated from the medical services. In effect, the health department’s clinical care programs should be treated the same as clinical care programs run by other health-care providers. THE CONSTITUTIONAL BASIS FOR PUBLIC HEALTH LAW

In all societies, public health authority is derived from the basic power of the state to preserve itself: the right of societal self-defense.2 The Constitution grants the government broad, almost unlimited, public health powers because, when the Constitution was drafted, epidemic disease threatened the social order, not just the lives of individuals. 3 Pestilence was part of everyday colonial life, a constant threat that contributed to a life expectancy of only 25 years.4 Soon after the Constitution was ratified, an epidemic of yellow fever raged in New York and Philadelphia. The prevalent attitude of that period toward disease was captured in an argument before the Supreme Court: For 10 years prior, the yellow fever had raged almost annually in the city, and annual laws were passed to resist it. The wit of man was exhausted, but in vain. Never did the pestilence rage more violently than in the summer of 1798. The State was in despair. The rising hopes of the metropolis began to fade. The opinion was gaining ground, that the cause of this annual disease was indigenous, and that all precautions against its importation were useless. But the leading spirits of that day were unwilling to give up the city without a final desperate effort. The havoc in the summer of 1798 is represented as terrific. The whole country was roused. A cordon sanitaire was thrown around the city. Governor Mifflin of Pennsylvania proclaimed a non-intercourse between New York and Philadelphia.5

The government took such extreme actions because it feared that social order would collapse. Bioterrorism presents the same threats to modern society, and the legal authority to deal with bioterrorism is rooted in the same constitutional provisions that allowed these actions in 1798. The Constitution divides the government powers between the state and federal government. The federal government was given the power over foreign affairs and trade, war and insurrections, and the commerce between the states. The federal public health powers derive from the power to regulate trade and to control military threats and insurrections. Most of the public health powers were given to the states: 1259

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Every state has acknowledged power to pass, and enforce quarantine, health, and inspection laws, to prevent the introduction of disease, pestilence, or unwholesome provisions; such laws interfere with no powers of Congress or treaty stipulations; they relate to internal police, and are subjects of domestic regulation within each state, over which no authority can be exercised by any power under the Constitution, save by requiring the consent of Congress to the imposition of duties on exports and imports, and their payment into the treasury of the United States.6

These powers are called the police powers. The term police does not refer to police departments, which did not exist in their present form until much later. It refers to the older meaning of the word “police”— to keep order. The state’s police powers deal with general issues of public health and safety, not the punishment of criminals. Until the late 1800s, the federal government did little more than maintain quarantine stations and public health service hospitals. Even today, most public health and public health law is carried out by the states. The Constitution gives the states all the powers not reserved for the federal government that are not otherwise limited by the Constitution. These reserved powers—interstate commerce, foreign affairs— and constitutionally protected areas—criminal prosecution, free speech, equal protection, property rights—are the main limits on the state police powers.

Criminal Prosecution The Constitution provides its greatest protections for individuals who are accused of crimes. Threat of criminal prosecution triggers the constitutional provisions preventing unreasonable searches, protection against self-incrimination, the right to appointed counsel, and the other rights that attach when an individual is arrested. Public health agencies do not have to provide these protections as long as their intent is to prevent harm to the community, rather than to punish an individual or act as agents of the criminal justice system. Even when public health agencies isolate or quarantine individuals, they do not have to provide criminal law protections because their intent is to prevent harm to the community, not to punish the individual.7 Legislatures are sometimes tempted to use public health laws in place of criminal laws to avoid the constitutional protections required for prosecution. For example, if the government wants to search property or perform a medical test to collect evidence for criminal prosecution, the government must get a warrant. The government must present evidence to a judge that there is probable cause to suspect the specific individual of a crime and what type of evidence is being sought with the warrant. These warrants are not necessary for public health (administrative) searches. The Court struck down a program using public health powers to collect information about drug use by pregnant women because it was being used for criminal prosecution as well as public health purposes.8 The Court ruled that the government must get a probable cause warrant to use the information for criminal prosecution, even if there was also a valid public health purpose for collecting it. Bioterrorism investigations pose even more difficult coordination problems between public health and law enforcement because public health professionals want to control the threat to the community as quickly as possible, while law enforcement needs to protect the crime scenes while it waits to get proper warrants to gather evidence for criminal prosecutions.9

Equal Protection The Constitution does not allow public health laws to be used as an excuse for otherwise prohibited discrimination. For example, the Court struck down special building regulations for Chinese laundries because there was no evidence that Chinese laundries were any greater threat to the community than laundries owned by non-Chinese.10 However, public health laws can be constitutional when they have a differential impact on otherwise protected groups if there is evidence

that a disease is more prevalent in that racial or ethnic group. This is commonly seen in screening programs for genetic diseases, which can affect blacks, Jews, Amish, and other genetically distinct groups at very different rates.

Property Rights The Constitution requires that the government pay fair compensation for private property that is taken for public use. Persons whose property is being taken have a right to a hearing before the property is taken. At the hearing they may contest the basis for the taking and the price that is being paid. When property is seized and destroyed because it is a threat to the public health, such as spoiled food,11 or houses that need to be razed to stop an advancing fire,12 there is no right to a hearing before the action. There is no right to compensation because the property had no value, in one case, because it was spoiled, and in the other, because it would have been destroyed by the fire. However, if the government takes private property to use it in a public health emergency, such as turning a hotel into a quarantine facility the property owner may not have a right to hearing before the taking, but will probably have a right to be compensated for the use of the property.

Interstate Commerce and Foreign Affairs State laws that use public health enforcement to discriminate against out-of-state businesses are unconstitutional. Courts have struck down laws that imposed more stringent sanitary restrictions on out-of-state milk processors. Even if the restrictions are the same for in- and out-of-state businesses, the courts will strike down a law if it has a disparate impact on out-of-state business. 13 For example, a requirement that milk must be processed and delivered within 24 hours might prevent out-of-state dairies from selling milk in the state. This law would violate the Commerce Clause of the Constitution unless there is evidence that the 24-hour rule is necessary to protect the public health. Conversely, a Texas law that banned the import of Louisiana cattle was constitutional because Texas could show a real risk of anthrax in the Louisiana cattle.14 States are likewise prohibited from having special regulations for foreign trade and foreign visitors.

Freedom of Speech The First Amendment of the Constitution protects freedom of speech. This prevents the government from regulating publications that contain inaccurate or even dangerous health information, as long as the publication is not an advertisement for a product. For example, the government cannot regulate WWW sites that publish dangerous diet information unless the information is an advertisement for a product. The Supreme Court has broadened the protections for advertisements over the past decade.15 Now, if the advertisement is accurate, it cannot be banned, even if it encourages dangerous behavior such as buying beer with the highest alcohol content.16 PUBLIC HEALTH LAW AS ADMINISTRATIVE LAW

Administrative law is the law that governs state and federal agencies. It deals with the relationship between individuals and government, outside of the criminal justice system and the military.17 Public health law and the predecessors to public health agencies can trace their heritage to the colonial governments. Public health law is one of the earliest examples of administrative law in the United States.

Separation of Powers Administrative law arises out of the separation of government powers into the legislature, the executive (the president or governor), and the courts. The legislature passes the laws that give agencies their

77 powers and their budgets. The agencies that enforce laws, including public health agencies, are part of the executive branch of the government, and are under the political control of the executive branch. In the federal government, this is the president. In state governments, this is usually the governor, but states have other elected officials, such as the attorney general, who run their own agencies outside of the control of the governor. The legislature can also create independent agencies by having the executive appoint members of a board or commission to run the agency, and making the terms of office of the members such that no single governor or president can appoint all the members. The federal Securities and Exchange Commission is an independent agency. Some state and local health departments are run by a board of health, which makes them better insulated from political interference, but even with a board of health, state and local agencies are much less independent than federal independent agencies. The role of the courts in administrative law is to assure that the laws empowering the agency are constitutional, and that the agency carries out the laws in a way that is consistent with the intent of the legislature. The courts recognize that the executive branch is charged with overseeing the agencies, and that it is the executive branch that the voters expect to make the policy decisions that the agency carries out. If the agency action is constitutional and is consistent with the legislation that authorizes it, then the courts should defer to the agency and leave it to the voters to seek change from the legislature or the executive branch. This is the basis for the judicial deference to agencies that is discussed later.

Statutes and Regulations While the president and most governors have some power directly from the federal or state constitution that creates their office, most of the powers of the executive branch come from laws passed by the legislature. The legislature also creates agencies and assigns their powers. If the legislature wants to control agency, it passes very specific and detailed laws giving the agency narrow powers and specifying how those powers will be used. This limits agency discretion. The Americans with Disabilities Act is an example of a detailed statute that limits agency discretion. The legislature may want the agency to have discretion, often because the legislature does not want to make a difficult political decision. An example is the Federal Energy Regulatory Commission, which Congress left to decide whether cheap electric power is more important than plenty of electric power. The legislature will also give an agency broad discretion if the legislation involves technical standards which are based on expert judgment. Traditionally public health agencies were given very broad powers to do what was necessary to protect the public health. This reflected both the strong public support for the agencies and the recognition that public health decisions should be made by public health experts. These broad powers are most important when there are unexpected threats to the public health or in emergencies where the agency may have to change strategies based on the changing nature of the threat. Ironically, some proposals for strengthening state emergency powers laws, like the Model State Emergency Health Powers Act,18 try to specify how the emergency will be handled by listing actions that the agency must take. Since it is impossible to predict the proper actions in an emergency, requiring such specific actions can cripple the agency when it needs the most flexibility. The problem with broad grants of power is that they do not give the public and the regulated parties notice of what constitutes proper conduct. Since the legislature has the power to make specific rules, the courts have allowed this power to be given to the agency. Regulations must be published for public comment before being adopted, and many states provide for public hearings to discuss new regulations. This allows the agency the discretion to make and change rules, while giving the public and regulated parties detailed information about the public health standards and input into the standards. For example, the legislature gives the health department the general power over food sanitation, but leaves the detailed sanitation regulations to be promulgated

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by the agency, based on national standards. Regulations are easier and quicker to change than legislation and can be modified on an emergency basis. This is important when the health agency is dealing with problems such as emerging infectious diseases or changing standards of practice based on new scientific discoveries.

Administrative Searches Public health officials routinely enter private property to inspect for compliance with health standards and to access potential health hazards. Historically, the U.S. Supreme Court did not require any kind of warrant for these inspections. The court reasoned that the Constitutional requirement of a probable cause warrant was limited to criminal investigations.19 In the 1960s, concerned about possible harassment by health inspectors, the Court required that the public health department show some evidence of a public health purpose for an inspection. This is called an administrative or area warrant and it does not require any specific information about the individual properties being inspected.20 Instead, it describes the general area to be inspected and the reason, such as all the houses in a given neighborhood are to be inspected for rat infestations. If the premises being searched operates under a license or permit, the conditions of receiving the license or permit usually include allowing searches without notice or a warrant during regular business hours. Administrative searches sometimes turn up evidence of criminal conduct: can the health inspector call the police, and can the police use the evidence in court? If the criminal conduct is related to the activity being regulated by the agency, the evidence can usually be used in court.21 For example, if a restaurant inspector found that the chef was using black market seafood, this evidence could be used for criminal prosecution. If a rat inspector found the homeowner’s marijuana stash, this would have nothing to do with the search and it is unlikely that the courts would accept it as evidence. More importantly, health departments resist turning evidence over to the police because if the community sees health inspectors as agents of the police, it will make their work much more difficult and dangerous. If the police ask the health inspector to look for something, then the courts will find that the health inspector is acting for the police and thus cannot enter without a probable cause warrant. JUDICIAL REVIEW OF PUBLIC HEALTH ACTIONS

When public health agencies are acting within constitutional limits, the courts give them great flexibility and broad powers. The primary limit on public health agency power is set by the state legislature or local government: agencies only have the power that the legislature gives them. Traditional public health laws gave general, unlimited grants of power: the public health agency may do what is necessary to protect the public. All courts accept these broad grants of power. Such grants give the agency the maximum flexibility and power allowed under the U.S. and the appropriate state constitution. If the legislature limits the agency’s power, the agency cannot act beyond these limits, even if the Constitution would allow it greater powers. Sometimes these limits are found in other laws, such as privacy laws, rather than in the public health laws themselves. The second limit on agency power is its reasonableness. The courts require that public health actions be rationally related to the problem they seek to control. This does not require that the agency use the best or least restrictive strategy, but allows the agency or legislature to balance other factors, such as the cost and manpower needed. As long as the agency does not act in an arbitrary or capricious manner, the court will uphold its actions. For example, when New York moved to close the gay bathhouses to control the spread of HIV, this was opposed by the bathhouse owners and some public health experts who believed that it was better to leave the bathhouses open and use them to educate the patrons about safe sex. The court rejected this challenge to the agency’s decision, ruling:

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It is not for the courts to determine which scientific view is correct in ruling upon whether the police power has been properly exercised. The judicial function is exhausted with the discovery that the relation between means and ends is not wholly vain and fanciful, an illusory pretense. . . .22

The court deferred to the agency’s decision for three reasons: First, judges and juries do not have the expertise to make technical decisions so the courts delegate these to an agency or individual with expertise. This is especially important in areas such as public health which involve difficult policy choices that can affect the health of the population. Second, courts defer to agencies because it is efficient. The U.S. Supreme Court, in a case involving whether government disability claimants were entitled to a hearing before their claim was denied, ruled that the cost and delay of due process requirements had to be balanced against the probability that they help the agency make better decisions. The court found that the hearing would not improve the accuracy of the decisions very much, and the extra costs and delays would reduce the benefits available to other claimants.23 In public health emergencies, time can be more important than money, so the courts would be very unlikely to interfere with agency actions as the emergency was unfolding. As in the disability case, it would be more efficient to have hearings after the action, since in many cases the person would not contest the agency decision. The third reason courts defer to agencies is because it respects the constitutional separation of powers. The legislature gives agencies their powers and their budgets. The courts recognize that as long as the agency is acting constitutionally and its actions are rationally related to its mission, the executive branch should be allowed to set policy. If the voters do not like what the agency is doing, the remedy is through the political process, not the courts. Thus the most important limits on agency action are political. For public health departments, the public must support their actions or the legislature will limit them by law or by cutting the agency budget.

to mitigate a threat to the public health. These can range from an order to clean up garbage in a vacant lot to an order to show up for tuberculosis treatment. There may be a fine for violating an administrative order, but most enforcement of administrative orders depends on the cooperation of the affected individuals or businesses. Administrative orders are most effective when the violator holds a permit that may be suspended for not complying with the order. In other cases, if the violator does not comply with the order, the agency must ask a court to enforce the order. Public health agencies can use administrative orders to empower private entities to act in situations where they would otherwise be legally unable to act. As an example, the federal regulations on managing tuberculosis in hospitals require that the hospital have a process for quickly identifying and isolating persons with active tuberculosis. Assume a coughing patient is admitted to the hospital with respiratory distress. The history and x-ray are consistent with active pulmonary tuberculosis. The patient is put into respiratory isolation, but refuses to stay in the isolation room, preferring to pass the time drinking coffee in the cafeteria.25 The hospital has no legal right to isolate the patient against the patient’s will. The health department can order that the patient be isolated and direct the hospital to carry out the agency’s orders, thus allowing the hospital to use its personnel to confine the patient.

Direct Abatement The public health department can act on its own, if it has been given the authority to do so, to abate a public health problem. This is very common in environmental health. Health departments routinely mow weeds, board up or tear down dangerous buildings, and enter property to treat standing water that can breed mosquitoes. Direct abatement is generally used when the property owner cannot be located or refuses to comply with administrative orders. The costs of direct abatement may be billed to the owner or charged as a lien against property, which will be collected when the property is sold.

Public Health Law Tools The most important tool of effective public health practice is education. Public health depends on the voluntary cooperation and support of the community. In addition, however, public health agencies must also use the law to assure that individuals and businesses comply with public health laws. Public health officials have five primary enforcement tools:24 (a) permits, licenses, and registrations; (b) administrative orders; (c) direct abatement; (d) civil penalties; and (e) injunctions.

Permits Permits, licenses, and registrations are used to regulate routine activities that may pose a threat if they are carried out improperly. Food establishment permits are the most common public health example. Permits pose the fewest legal issues because they are prospective— the establishment must show that it meets the requirements before the permit is issued. The standards for the permitted activity are established by the legislative body, which usually specifies that the regulations will follow an approved national code and that special situations will be handled by the public health officer. To qualify for a permit, the applicant must agree to be bound by the standards for maintaining the permit. The applicant must agree to allow entry by the health inspectors, without notice or a warrant, to assure compliance with the applicable standards. The health officer will determine if the applicant meets the standards for a permit, and whether a permit should be revoked or denied because the permittee has violated these standards.

Administrative Orders Administrative orders are orders issued by a public health agency directly to an individual or a business requiring that actions be taken

Fines and Other Punishments Persons who violate public health administrative orders or statutes can be fined or jailed, after appropriate legal process. In most public health cases the fines are too small to be a deterrent and the municipal court judges who hear these cases are usually unwilling to jail a person for a public health violation. (As health officers quickly learn, it is hard to get judges to take “dog law” cases seriously.) However, fines and imprisonment are important enforcement tools for state and federal environmental quality laws because the fines can run to millions of dollars and the federal judges have no hesitation in ordering jail sentences.

Injunctions When a violator ignores administrative orders, when the violator has been incarcerated but the hazard has not been abated, or when the public health agency wants to mitigate a hazard prospectively, the proper remedy is an injunction. Unlike other legal proceedings where the court can only order fines or imprisonment, an injunction allows the court to give specific orders on what must be done or what is prohibited. In addition, the agency can often select the judge who will rule on the injunction. Courts can and do use fines, imprisonment, and other coercive strategies to enforce their injunctions. Courts may grant an injunction to prevent irreparable harm: harm that cannot be remedied by awarding monetary damages. For example, if a logging company mistakenly enters your land and begins to cut the trees, the court could order them to stop rather than just assuring that you get the market value of the wood. When a public health agency seeks an injunction, the courts will usually defer to the agency’s determination that the condition threatens the public health and that the injunction will remove this threat.

77 If there is an immediate threat, the court can order a temporary injunction on the evidence presented by the agency without waiting to hear from the other party. These are called ex parte proceedings. The court will order a hearing as soon as possible to allow the enjoined party to contest the injunction. Such emergency actions are used for threats such as tainted food or water, or a hazard such as a fire-weakened structure that threatens to fall. If the threat does not require emergency action, the opposing party must be given notice and be allowed to be heard in a court hearing before an injunction is granted. After the opposing party has been heard, the court may either dissolve the temporary injunction or enter a permanent injunction. Permanent injunctions are very important in public health enforcement because they are often the only way to deal with recalcitrant violators. PRIVACY, AUTONOMY, AND THE PUBLIC HEALTH

Protecting the public health often affects individual and institutional rights. The cost of pollution control can reduce the profitability of businesses, food sanitation rules increase the cost of building a restaurant, and concerns for problems such as mad cow disease can injure the livelihood of everyone in an industry. Yet the most difficult public health law issues are those involving the privacy and autonomy of individuals. While these questions once arose only in communicable disease control programs, privacy and autonomy questions also arise as public health becomes more involved with the control of lifestyle diseases such as smoking and obesity. PUBLIC HEALTH SURVEILLANCE

All public health begins with the collection and analysis of data about individual illness. In some cases this analysis can be done on anonymous data, but in most cases identified data is necessary for accurate analysis. The court explained the legal rationale for surveillance and using personal medical information in a case involving a typhoid carrier: The Sanitary Code which has the force of law . . . requires local health officers to keep the State Department of Health informed of the names, ages, and addresses of known or suspected typhoid carriers, to furnish to the State Health Department necessary specimens for laboratory examination in such cases, to inform the carrier and members of his household of the situation and to exercise certain controls over the activities of the carriers, including a prohibition against any handling by the carrier of food which is to be consumed by persons other than members of his own household. . . . Why should the record of compliance by the County Health Officer with these salutary requirements be kept confidential? Hidden in the files of the health offices, it serves no public purpose except a bare statistical one. Made available to those with a legitimate ground for inquiry, it is effective to check the spread of the dread disease. It would be worse than useless to keep secret an order by a public officer that a certain typhoid carrier must not handle foods which are to be served to the public.26

Medical care providers are the most common source of information, but reporting requirements for child abuse also include teachers and many others who would be in a position to notice abuse. Privacy advocates argue that individually identified information should not be reported without the individual’s permission. Given the sensitive nature of public health data, requiring the patient’s permission to report would seriously compromise the quality of the information. It could even lead to injuries if the report concerned communicable diseases or child abuse. After the U.S. Supreme Court found a right of privacy implicit in the Constitution,27 the court also recognized that this right of privacy must give way when necessary to protect the public health:

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Unquestionably, some individuals’ concern for their own privacy may lead them to avoid or to postpone needed medical attention. Nevertheless, disclosures of private medical information to doctors, to hospital personnel, to insurance companies, and to public health agencies are often an essential part of modern medical practice even when the disclosure may reflect unfavorably on the character of the patient. Requiring such disclosures to representatives of the State having responsibility for the health of the community, does not automatically amount to an impermissible invasion of privacy.28

All state constitutions also allow public health reporting of identified information, although at least one state still limits the right to collect information about HIV. All states require the reporting of child abuse, and most states also require the reporting of elder and spousal abuse, as well as violent or suspicious injuries, including all gunshot wounds, knifings, poisonings, serious motor vehicle injuries, and any other questionable wounds. Health-care providers and others making these reports cannot be held liable by the patient for incorrect reports, as long as the report was made in good faith. Failing to make a report can result in liability in many states if the injured person can show that the report was required and that the injury was caused by the failure to make the report.29 Knowingly reporting false data, such as an incorrect name when the patient’s real name is known, does not satisfy the duty to report, and the reporter can be disciplined by the state. In addition to requiring third parties to report public health conditions, public health agencies can carry out their own investigations. Infected individuals can be interviewed to determine where they contracted the disease and who they have been in contact with.30 These contacts will then be interviewed, without divulging the source of the contact information, to determine the spread of the disease. While the law would allow the punishment of persons who lie to disease investigators, in practice, investigations have historically been treated as voluntary. Investigations of serious outbreaks, such as smallpox, have used very intrusive techniques, including paying informers.31 In a bioterrorism investigation, it is likely that the police will apply criminal law investigation standards, which do require cooperation, and which punish false information.

Testing and Treatment Testing and screening are key strategies in accessing populations at risk for communicable disease. Screening systems, such as tuberculosis skin testing, are necessary to learn the prevalence of a disease in the community, to investigate specific outbreaks, and to identify individuals for treatment or restrictions. In most cases, individuals cooperate because of the benefit to themselves and to the community. When an individual does not cooperate, the agency may order them to submit to the test. While there are strict limits on involuntary testing when the results are to be used for criminal prosecution, public health agencies have great latitude to order testing for disease control,32 including testing of persons with religious objections to medical treatment.33 Many states require screening of pregnant women for syphilis to prevent congenital syphilis,34 and one state requires testing to prevent congenital HIV infection. Most states require screening of newborns to detect congenital illness such as hypothyroidism and phenylketonuria. The courts will order the involuntary treatment of prisoners and persons who are committed to mental institutions, but involuntary treatment is almost never used in routine public health when the case is a competent adult. (Treatment orders are commonly used to require the treatment of children against their parents’ wishes.) Instead, public health agencies will usually isolate an infectious person until the disease is resolved or the patient accepts treatment. In almost all cases, the patient prefers treatment to isolation. In a bioterrorism event involving a treatable infectious agent, mandatory treatment might be necessary because of limited isolation facilities.

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Vaccinations Vaccinations are a critical part of public health practice. Vaccinations eradicated smallpox and have dramatically reduced the morbidity and mortality of diseases such as measles, mumps, diphtheria, tetanus, and many others. Despite their value to the individual and to the public, vaccinations have always been controversial. The U.S. Supreme Court ruled on the constitutionality of mandatory vaccinations in 1905, and their ruling remains relevant today: We are not prepared to hold that a minority, residing or remaining in any city or town where smallpox is prevalent, and enjoying the general protection afforded by an organized local government, may thus defy the will of its constituted authorities, acting in good faith for all, under the legislative sanction of the state. If such be the privilege of a minority, then a like privilege would belong to each individual of the community, and the spectacle would be presented of the welfare and safety of an entire population being subordinated to the notions of a single individual who chooses to remain a part of that population.35

In 1905, the smallpox vaccine was known to be dangerous and the court appreciated that mandatory vaccination would injure many people. Smallpox vaccine is safer than it was in 1905, and other vaccines are very safe, compared to the risks they prevent. The state has clear authority to require vaccinations of adults and children, and there is no constitutional requirement that the state recognize religious or philosophical objections to vaccination.36 Unfortunately, mandatory vaccination is losing political support. Many states no longer require children to be vaccinated before entering public schools, allowing parents to refuse vaccination if they do not want them for their children. Emerging diseases, such as new flu agents, or the use of smallpox as a bioterrorism agent, could require large-scale vaccination campaigns, with the option of mandatory vaccinations. Official federal policy is that vaccinations would not be used in the event of a bioterrorism outbreak. In contrast, most states are prepared to use mandatory vaccinations for agents such as smallpox and are considering such requirements for other outbreaks. While mandatory vaccinations are legally allowed, such programs will be ineffective if the public is not educated to understand why mandatory vaccination is necessary.

Quarantine and Isolation From Leviticus and the Koran, to quarantine in fourteenth century Venice, 37 to the contemporary federal regulations on tuberculosis control,38 public health practice depends on the authority to impose restrictions on individuals to prevent them from spreading disease in the community. The common law provided severe punishment, including death, for breaking quarantine. 39 The legal authority (if not the punishment) is part of the state’s police power. In contemporary public health practice, isolation means to restrict the contact between an infected person and others, and quarantine means to restrict the uninfected contacts of an infected person. Informal isolation is widely used: sick children are told to stay home from school, adults with the flu are sent home from workplaces where they might endanger others, and individuals who are ill restrict their own contacts with persons they might infect. Public health departments will order isolation for persons with infectious tuberculosis, measles, and certain other communicable diseases. If these orders are not obeyed, the health department can ask the court to order the sheriff to return the person to a closed isolation facility. Quarantine is much less frequently used. The last large-scale quarantines in the United States were for polio in the 1950s. When there was a polio outbreak, public facilities were closed and travel from communities with the disease was limited. Individual or family quarantine is sometimes used for diseases such as measles, but generally only the infected individual is isolated.

Two factors have renewed concerns about implementing largescale isolation and quarantine programs. The first was bioterrorism fears, particularly of smallpox, after September 11, 2001. The second was the severe adult respiratory syndrome (SARS) outbreak in Canada and Asia in 2003, which forced the widespread use of both isolation and quarantine. This has raised concerns about whether the states have adequate laws to order large-scale restrictions. Since all states used these powers extensively from their founding until the 1950s, they all have the necessary authority, unless their legislature has changed the law since then. There has also been concern about the appropriate due process for instituting restrictions. Under the U.S. Constitution, isolation and quarantine can be ordered by the health department, although a court order will be necessary for persons who refuse to comply. There is no requirement for a hearing before the action. This is also true of old state public health laws, but some states have added due process requirements, such as a hearing before a person can be restricted. Once a person has been isolated or quarantined, the Constitution guarantees due process though a habeas corpus proceeding. Habeas corpus is the “Great Writ” from the English common law and means “bring me the body.” Habeas corpus requires that persons detained by the state be given a chance to answer the charges against themselves at a hearing before a judge, and that the state be required to show cause why the person should not be released. There is no bail for isolation or quarantine orders: To grant release on bail to persons isolated and detained on a quarantine order because they have a contagious disease which makes them dangerous to others, or to the public in general, would render quarantine laws and regulations nugatory and of no avail.40

The state may provide other mechanisms for a hearing in place of a habeas corpus proceeding, but if the state has no specific review process for isolation and quarantine, habeas corpus is always available. If the state requires a hearing before the restriction order, it will be very costly and time consuming for the agency, greatly complicating enforcement. If a large number of people are to be isolated or quarantined, even habeas corpus hearings may be difficult or impossible to arrange in a timely manner. The state may require persons who want to file a habeas corpus petition to first use an administrative review conducted by the health department.41 This review could determine the basic facts of the confinement and the applicable law, correct mistakes such as the quarantine of a person who was not exposed to the infection, and then prepare a report for the court to use if the person still wanted judicial review. Most problems could be solved with the administrative review, and the record would allow the court to review the case quickly. As long as the state is not acting in an arbitrary or capricious manner, the court will uphold the isolation or quarantine order. Of all the police powers, large-scale isolation and quarantine most depends on public cooperation. While law enforcement has a role in handling a small number of noncompliant individuals, if a community does not want to comply with the orders, there is little that can be done short of military occupation. As the SARS epidemic demonstrated, an effective large-scale isolation and quarantine program requires the community to assure that everyone has access to food, medical care, and compensation for lost time from work. Meeting these needs and educating the community ahead of time are much more important than questions of legal authority.

THE FUTURE OF PUBLIC HEALTH LAW

There was a consensus on public health law from the colonial period through the 1960s. Every adult in the United States had grown up in a world where communicable diseases were a major threat. As late as the mid-1950s, communities were isolated during polio epidemics, and while smallpox had not been seen in the United States since 1947,

77 it still existed in other parts of the world. While public health agencies protected individual privacy as much as possible, there was a societal consensus that individual rights had to give way to the protection of the public health. By the 1960s, the demographics of illness in the United States had already shifted from communicable diseases to chronic diseases. Smallpox immunizations were discontinued in the early 1970s, there were no more polio epidemics, tuberculosis was largely under control and routine TB screening was discontinued, and there were few reports of once common diseases such as cholera and malaria. By the 1980s, the fear of communicable diseases had faded, generally undermining the support for public health. The adoption of strict liability theories in tort law made it easier to win vaccine injury litigation, without regard to whether the claimed injuries were due to the vaccine. This fueled a vaccine litigation industry that uses its public relations resources to drown out the public health messages that vaccines for childhood diseases are safe and necessary. AIDS was viewed as a lifestyle disease, rather than a public health threat, and it was more than 15 years before many states started collecting the same personally identified data for HIV as they do for all other serious infectious diseases. As support for traditional public health waned, public health agencies became more involved in chronic disease epidemiology and prevention. While chronic diseases are the most serious threat to individual health, they pose a difficult problem for public health and public health law: the legal and ethical justifications for taking actions to prevent a person from spreading a communicable disease are very different from those for persuading a person to take better care of his or her own health. Some traditional public health strategies such as environmental modification—assuring safe drinking water and fortifying foods with vitamins—are also applicable to chronic diseases—making it more difficult to smoke in public places and providing more healthy choices in school lunches. Some are not: screening and treatment for tuberculosis is justified by public necessity, but would this justify screening and mandatory treatment for obesity? Should public health officials join with the same tort lawyers who attack vaccinations and other public health programs, just because they are now suing tobacco and food processors? The terrorist attacks on September 11, 2001, combined with the anthrax letters sent to public officials and media figures over the following few weeks, suddenly reminded the public of their fundamental fears of epidemic disease, whether driven by nature or bioterrorism. The SARS epidemic in 2003 reminded the public and policy makers that natural epidemics posed the same risks as bioterrorism and raised questions about the ability of the public health system to deal with a major disease outbreak. In particular, questions were raised about the ability of modern state public health laws to deal with large-scale quarantine and mandatory vaccinations. The smallpox vaccine program for healthcare workers that was launched early in 2003 was a failure.42 Public health law faces two challenges. First, obesity is joining smoking as a major preventable disease threat. These behaviors are dramatically increasing the incidence of chronic diseases such as diabetes, cardiac disease, and cancer. As diseases that are driven by environmental and cultural factors, their management will require public health law strategies, yet strategies that are very different from communicable disease control. Second, fears of bioterrorism and epidemic diseases such as SARS are driving states to pass very intrusive public health laws. Police and the national security agencies want to make public health an extension of homeland security, and use powers traditionally reserved for public health as part of the criminal law system. These pressures threaten to destroy the relationship of trust between public health agencies and their client populations, making public health practice much more difficult. Public health professionals, their lawyers, and the legislatures must look to the history of public health law and to administrative law principles if they are to meet these challenges. The need to protect the public from plagues, whether man-made or natural, must be balanced with the pervasive, if lower key, threat posed by preventable diseases. While bioterrorism is a real threat, it cannot be allowed to compromise the relationship between public health professionals and the public.

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Public health ultimately depends on public trust, and without that trust, even Draconian laws will not protect the public. REFERENCES

1. Public Law,104-91 (1996). 2. Richards EP. The Jurisprudence of Prevention: Society’s Right of self-defense Against Dangerous Individuals, Hastings Const L Q. 16:329–92 (1989). Available at http://biotech.law.lsu.edu/cphl/articles/ hastings/hastings-Contents.htm. 3. McNeill WH. Plagues and Peoples. New York: Doubleday; 1976. 4. Shattuck L. Report of the Sanitary Commission of Massachusetts 1850. Cambridge: Harvard University Press; 1948. Facsimile edition. Available at http://biotech.law.lsu.edu/cphl/history/books/sr/index.htm. 5. Smith v Turner, 48 U.S. (7 How.) 283, 340–41 (1849). 6. Holmes v Jennison, 39 U.S. (14 Pet.) 540, 616 (1840). 7. Bell v Wolfish, 441 U.S. 520 (1979). 8. Ferguson v City of Charleston, 532 U.S. 67 (2001). 9. Richards EP. Collaboration between Public Health and Law Enforcement: The Constitutional Challenge. Emerg Infect Dis. October 2002; 8(10): 1157–59. 10. Yick Wo v Hopkins, 118 U.S. 356 (1886). 11. North American Cold Storage Co. v Chicago, 211 U.S. 306 (1908). 12. Surocco v Geary, 3 Cal 69 (1853). 13. Baldwin v G. A. F. Seelig, Inc., 294 U.S. 511 (1935). 14. Smith v St. Louis & S.W. Ry. Co., 181 U.S. 248 (1901). 15. Central Hudson Gas & Elec. Corp. v Public Service Comm’n, 447 U.S. 557 (1980); Bolger v Youngs Drug Prods. Corp., 463 U.S. 60 (1983); and Greater New Orleans Broadcasting Ass’n v United States, 119 S. Ct. 1923 (1999). 16. Rubin v Coors Brewing Co., 514 U.S. 476 (1995). 17. Strauss P. Administrative Justice in the United States. 2nd Rev ed. Carolina Academic Press; May, 2002 18. Richards EP, Rathbun KC. Legislative Alternatives to the Model State Emergency Health Powers Act (MSEHPA), LSU Program in Law, Science, and Public Health White Paper #2, April 21, 2003 (unpaginated), published at http://biotech.law.lsu.edu/blaw/bt/MSEHPA_review.htm. 19. Frank v Maryland, 359 U.S. 360 (1959). 20. Camara v Municipal Court City And County, 387 U.S. 523 (1967); and See v Seattle, 387 U.S. 541 (1967). 21. New York v Burger, 482 U.S. 691 (1987); and People v Scott, 79 N.Y.2d 474, 593 N.E.2d 1328, 583 N.Y.S.2d 920 (N.Y. 1992). 22. City of New York v New Saint Mark’s Baths, 497 N.Y.S.2d 979, 983 (1986). 23. Mathews v Eldridge, 424 U.S. 319 (1976). 24. Grad FP. The Public Health Law Manual. 2nd ed. American Public Health Association; 1990. 25. Dooley SW, Villarino ME, Lawrence M, et al. Nosocomial Transmission of Tuberculosis in a Hospital Unit for HIV-Infected Patients. JAMA. 1992;267:2632–5. 26. Thomas v Morris, 286 N.Y. 266, 269, 36 N.E.2d 141, 142 (1941). 27. Griswold v Connecticut, 381 U.S. 479 (1965). 28. Whalen v Roe, 429 U.S. 589, 602 (1977); and Rollins v Ulmer, 15 P.3d 749 (Alaska 2001). 29. Derrick v Ontario Community Hospital, 47 Cal.App.3d 145, 120 Cal.Rptr. 566 (1975); and Landeros v Flood, 17 Cal. 3d 399, 551 P.2d 389, 131 Cal. Rptr. 69 (Cal.1976). 30. Potterat JJ, Spencer NE, Woodhouse DE, et al. Partner notification in the control of human immunodeficiency virus infection. Am J Pub Health. 1989;79(7):874–6. 31. Carrell S, Zoler ML. Defiant diseases: hard-won gains erode. Med World News. 1990;31(12):20–6. 32. Ex parte Woodruff, 210 P.2d 191 (Okla.Crim.App., 1949); Ex parte Fowler, 184 P.2d 814 (Okla.Crim.App., 1947); Reynolds v McNichols, 488 F.2d 1378 (10th Cir.(Colo.), Dec 13, 1973).

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33. Washington v Armstrong, 39 Wash. 2d 860, 239 P.2d 545 (Wa. 1952). 34. Rathbun KC. Congenital Syphilis (Review), Sexually Transmitted Diseases; April-June 1983;10:93–99. 35. Jacobson v Massachusetts, 197 U.S. 11 (1905). 36. Cude v State, 237 Ark. 927, 377 S.W.2d 816 (Ark. 1964). 37. Bolduan C, Bolduan N. Public Health and Hygiene. Philadelphia: WB Saunders; 1941. 38. Guidelines for Preventing the Transmission of Mycobacterium Tuberculosis in Health-Care Facilities, 59 FR 54242 (1994).

39. Blackstone W. Commentaries on the Common Laws of England. Chicago: University of Chicago Press; 1765: vol 4, chap13, 161. 40. Varholy v Sweat, 153 Fla. 571, 575, 15 So. 2d 267, 270 (1943). 41. Richards EP, Rathbun KC. Making state public health laws work for SARS outbreaks. Emerg Infect Dis. February, 2004;vol 10, #2:356–7. 42. Richards EP, Rathbun KC, Gold J. The Smallpox Vaccination Campaign of 2003: Why did it fail and what are the lessons for bioterrorism preparedness? La L Rev. 2005;64:904–51.

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Planning for Health Improvement: Models for Communities and Institutions K. Michael Peddecord

PLANNING AS A TOOL FOR CHANGING ORGANIZATIONS AND IMPROVING COMMUNITY HEALTH

Planning is the future-oriented, systematic process of determining a direction, setting goals, and taking actions to reach those goals. Planning is all about making change and is a basic management function essential to the success of all levels of an organization. This chapter provides an overview of planning definitions, issues, and tools or techniques. Several examples of models or frameworks for community health assessment and improvement efforts are provided along with references. A second goal is that readers develop an appreciation for the ambiguous nature of the planning vocabulary and recognize the need for clarifying understandings before venturing forth into planning, particularly when this activity involves a diverse group of professionals or community laypersons. While planning can be described in the terms of techniques and tools, it is often a very complicated social process that must be mastered by the successful manager and thriving organizations and or communities. One of the most essential of planning tools in public health is the ability to work with professional and community groups.

Planning in Context—The Continuous Improvement Cycle of Planning, Implementation, and Evaluation Planning is a core activity of what public health professionals, managers, and executives do. A generic or generalized model includes the steps or stages of understanding and engagement (“planning to plan”), needs assessment, setting goals and objectives, developing and intervention, fielding the intervention, and evaluating the results. Without planning and the formulation of explicit goals and objectives, evaluation becomes difficult, especially in larger organizations and in the community.1 Rather than a linear process, planning is best considered as part of a continuous improvement process that involves the iterative gathering of data, translating it into useful information, and using that information to make decisions.2

Need for a Common Vision and Language When beginning or reinvigorating the planning process, particularly in a setting with a diverse staff, it is essential to establish a common understanding of and language for the activities ahead. Picking a

model, and its associated vocabulary, will help provide a common framework. Training using the selected model and vocabulary also helps improve communication. A large number of models and tools are available to provide a roadmap, a language and common understanding of how to proceed. Since there is no one best model, it is more important to pick a model and move forward than to labor over what is the “best” model. While picking a model is an essential first step, ultimately, the success of the planning and improvement process is dependent on multiple factors such as leadership, hard work, resources, and luck. Considerations for selecting a model are included later in this chapter. As the planning process is initiated, and periodically throughout its life, it is important to assess the important underpinnings and environmental considerations in which the planning and improvement process is taking place. In the next section, salient factors that need to be understood and dealt with are described. This understanding will aid in selecting the planning model, modifying the model, selecting analytic and management tools, and setting the course of action for planning. CONSIDERATIONS FOR CHOOSING A MODEL AND MANAGING THE PROCESS FOR HEALTH PLANNING AND IMPROVEMENT

Sponsorship A sponsor gives legitimacy to the process. Every planning activity has one. The sponsor(s) may be some organization, group, legislative edict, or individual. At the institutional level, this may be the board of trustees, the chief executive, the medical staff chair, a program coordinator, or a department supervisor. In the community, the sponsor may be a community-based organization such as the heart association, a civic club, a church group, or a vocal community activist. At a governmental agency it may be a law or regulation, a mayor, or a local health officer. A well-funded foundation or a poorly funded hospital may sponsor and or initiate a planning process. Sponsors may have abundant or scarce resources. While some have legal authority, others may have only moral authority being empowered only by their interest in improving their lives and the lives of their community. Other sponsors may be motivated to improve their profits or survive in a competitive challenge. All of these factors need to be understood by those leading and seriously engaged in the planning process. 1267

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Stakeholders and Politics Stakeholders are individuals and organizations that have or may have a future interest in what your planning initiative is about. Since planning is as much a social and political as it is a technical process, all important stakeholders must be identified and dealt with. The level of interest exhibited by stakeholders can range from casual interest, to serious concern, to intimate involvement in the process and outcome. In addition to motivation to improve the health status of the community, improving one’s economic and power position will often explain each stakeholder’s interest level. Within an organization, particularly a larger agency such as a public health department, entrenched staff may see any change-producing process such as planning as a threat to the status quo. While a detailed discussion of organizational behavior and the politics of planning are beyond the scope of this chapter, leaders understand that change means discomfort. In many situations, expect that the stakeholder(s) may want to delay, obstruct, or subvert the planning process until they understand and or accept the potential change from their own perspective. It is essential to recognize that all participatory planning takes place in the context of an organizational culture and a history of relationships between internal and external stakeholders.3,4 Complications and conflicts often arise over disagreements on the scope of planning, strategies, and specific actions necessary to achieve goals. Combine conflicting economic incentives and egos, and the politics of planning takes on a life all its own. In a few situations, expect a few stakeholders to use their power to stop the planning and change process.

The Scope and Limits of Planning Planning, direction, and control are the basic functions of managers. It is somewhat artificial to separate planning from the day-to-day operations of an organization or the implementation of programs. However, as organizations become larger and work needs to be differentiated, planning may become a specialized task. While every management and supervisory text has chapters devoted to planning, the primary focus of planning texts for health facilities is often on broader institutional or “strategic” functions.5 Planning is also an important topic in other specialized books that focus on marketing6 or quality improvement.7

Focusing on Community Change: Comprehensive versus Narrow Planning? Systems theory can provide useful guidance to think how parts of the whole (subsystems) are connected.2 The concept is that, at some level, everything is connected to everything else. Realistically, however, it is impossible to plan for the “system” as a whole. However, attempting to describe and understand the workings and interactions of the entire system is usually a useful investment of time. After planners have a sense of how things work and interact, the problem can then be broken down into smaller parts. The planning of “subsystems” or sub-tasks can then proceed. Understanding how the “parts” work together or interact may also provide clues as to how to extend the planning process or at least communicate to “other subsystems.” The problem with isolating a subsystem is that subsystem exists within a larger system and problems often occur between well-planned subsystems. The key for the planner is to know how the subsystems interact and the extent of planning needed in the adjoining subsystems. The bottom line is that even if the planning focuses on a specific problem or issue, the planning process must recognize that this problem or issue does not exist in isolation. Planning, no matter how focused must deal with its environment.

Planning Models and Why You Need Them Planning Models: What Are They? Models are, at their core, extensive lists that described a schematic approach to studying, interacting with, and changing a system or situation. Example of systems may be individual behavior, an organization,

or a community. Most models have been developed based on experiences of workers in a particular field, most relevant to this chapter, community health improvement. Models can serve as guidebooks constructed by those who have traveled a similar road before. A planning model is also a paradigm (a way of thinking) that serves as a template that includes a set of assumptions, concepts, values, and practices. This paradigm can help construct a way of viewing reality for the community or an organization. Since a planning activity often brings together individuals with diverse backgrounds, interests, and agendas, as stated before, agreeing on a model to follow during the planning and improvement process is one of the most important steps in the early stages of the endeavor. While a model may not provide a completely unified vocabulary, it can provide a common understanding of the stages in a planning and improvement process.

MODELS VERSUS TOOLS

All models employ a wide range of tools to help complete the tasks along the way. A useful definition of a tool in this context is something regarded as necessary to the carrying out of one’s occupation or profession. A tool is something used in the performance of an operation, such as an instrument. Common planning tools are surveys, calculating risk ratios, archival research, process mapping, group management tools, and so on. Literally hundreds of tools exist ranging from common-sense approaches useful in managing group work to highly complex computer software used for modeling and statistical process control. The technical side of planning emphasizes learning how to select and use the proper tool for the task at hand. Textbooks from many academic disciplines teach us to understand and use various tools. Several websites also include “tool boxes” of use to those planning to change organizations or communities.8 Texts cited below, as well as other chapters of this book, describe myriad tools.

Choosing a Model As suggested earlier, the most important activity in the early phase of a planning activity is the choice of a model to follow. There is no easy formula or decision tree that would lead to the “best choice” model for a particular situation. Perhaps the best time spent early on in the planning process is to learn more about models for planning that are available. If the scope of the activity is defined in terms of a specific health problem or issue, then starting with a textbook may be productive. Also, looking for journal publications via Medline or postings on the Internet may be fruitful. In some instances, governmental agencies provide technical assistance and have published planning manuals to aid local agencies that are doing planning. For example, consider bioterrorism or emergency response. A web search will reveal planning guidelines or manuals for just this purpose. Telephoning funding agencies or engaging consultants with a broad or well-focused range of experience may also help identify appropriate options. There is no “one-size-fits-all model,” nor is there an evidence base that would suggest that one model is better that another. One text1 provides a summary of many of the more common health improvement planning models. A side-by-side comparison of the phases or steps in these models reveals a spectrum of choices from simple to those that provide guidance for dealing with issues at the individual, organizational, and community levels. While it is by no means exhaustive, the remainder of this chapter categorizes and describes a variety of available and well-used planning models. Since no comprehensive review, meta-website, or meta analysis of planning models exists (to this reviewer’s knowledge), readers are referred to a recent planning and evaluation text which provides a description of several commonly used models as well as a side-by-side comparison table for 11 different models.1

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Comprehensive Health Improvement Models These models are robust and useful in multiple situations. Most have been developed based on the developers’ or users’ experiences in multiple settings. All must be adapted to specific situations. Some uses (and published reports) may have an emphasis on consumer or stakeholder input. Other models may be developed from the perspective of the “responsible” agency and have an emphasis on the professional role and leadership. Textbooks, websites, and journal case studies suggest tools and techniques that will be useful in accomplishing the tasks needed in each phase of the planning, improvement, and evaluation process. Some texts include a complete sets of tools, computer files on CD, and website support.9 All models are useful in establishing a vocabulary and road map for the change process, be it at the community or organizational level. Comprehensive models implicitly or explicitly assume that there is a powerful and well-funded sponsor, often located in an agency or organization. These models also assume that there is a knowledgeable planner who will manage the process. PRECEDE-PROCEED is perhaps the most widely recognized model. Developed and tested by Green and colleagues over a number of years,9 this model has been widely used and well recognized based on the authors many texts used in health education and public health courses. PRECEDE includes five phases: social, epidemiological, behavioral and environmental, educational and ecological, and administrative assessment. The PROCEED phases include implementation, followed by process, impact, and outcome evaluations. The Multilevel Approach to Community Health (MATCH) was developed by the CDC in the form of intervention handbooks. It includes five phases of health goal selection, intervention planning, development, implementation, and evaluation. Each phase is broken down into steps. One strength of this model is the explicit recognition of interventions that focus on the multiple levels of individuals, organizations, and governments/communities.10 Mobilizing for Action through Planning and Partnership (MAPP) has been developed by the National Association of County and City Health Officials (NACCHO)11 with CDC and Health Resources and Services Administration (HRSA) funding. The MAPP model emphasizes the role of public health agencies in building community participation to planning and implementing effective, sustainable solutions to complex problems. Nine MAPP steps include: organizing for action, developing objectives and establishing accountability, developing action plans, reviewing action plans for opportunities for coordination, implementing and monitoring action plans, preparing for evaluation activities, focusing the evaluation, gathering credible evidence and justifying conclusions, and lastly, sharing lessons learned, and celebrating successes. This model builds on the Assessment Protocol for Excellence in Public Health (APEX-PH) that was introduced by NACCHO in 1991. The original APEX model was especially useful for building the planning capacity of a local health department as it prepares to work with the local hospitals and community-based organizations. Additional APEX steps include community engagement and completing the cycle of implementation and evaluation. Many of the methods and lessons from APEX have been subsumed by the MAPP model. The Protocol for Assessing Community Excellence in Environmental Health (PACE EH) is a model which focuses on environmental health planning and was also developed by NACCHO.12 The Community Tool Box is an expansive website developed by the Work Group on Health Promotion and Community Development at the University of Kansas.8 Developed as a resource for Health Communities projects, the Tool Box has been online since 1995. It includes a model for community health planning and development that is similar to MATCH and PRECEDE-PROCEED, but with an emphasis on organizational and leadership competencies needed to progress through the community health improvement cycle. Resources are arranged to provide guidance for tasks necessary to promote community health and development. Essentially an online textbook, sections include leadership, strategic planning, community

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assessment, grant writing, and evaluation. A framework for community health planning and improvement similar to other comprehensive models described above is provided on this website. Tools include step-by-step guidelines, case examples, checklists of points, and training materials. Also of use is a section on “best practices” with links to other knowledge bases that have collected information on best practices and evidence-based practices for general community health and focused areas such as HIV, chronic diseases, and substance abuse. OTHER PLANNING APPROACHES, MODELS, AND TOOLS

Social Marketing A number of health improvement planning and action models have roots in the communication and social marketing disciplines.6 Social marketing approaches follow the same generic steps as do the comprehensive health improvement models. However, marketing models emphasize the understanding of the audience and importance of crafting specific messages to various market segments within the community. These may be considered more programmatic models in that these models emphasize activities after the problem or need for a program has been determined. These models provide tools for developing, delivering, and evaluating interventions designed to change something at the individual, organizational, or community level. A comprehensive health communication model popularized by the CDC 13 is known as CDCynergy or Cynergy. Available on CD-ROM, its emphasis is on understanding communication audiences, segmentation techniques, and targeted communication strategies. Similar to comprehensive planning models described, it includes six phases, each with detailed steps. The CD-ROM includes extensive examples and supporting material to assist in developing targeted health communication campaigns. CDCynergy is by no means the only comprehensive communications model. For a number of years, the National Cancer Institute has promoted a model entitled Making Health Communications Work.14 Another example is the Social Marketing Assessment and Response Tool (SMART) model.15 These and other models have been developed based on experiences in multiple settings. NACCHO has also created a Public Health Communications toolkit to help local public health agencies develop messages. The website also includes links to promotional materials that have been developed by other public health departments.16

Strategic Planning Strategic planning implies that the planning process is significance. In concept, it is usually done by higher-level decisionmakers within the organization. The adjective “strategic” is often coupled with “long term or long range” to convey a since of importance. The result of this planning will be setting the organization’s overall directions and prioritizing major initiatives. In concept, strategic planning is a periodic, information driven, proactive, and systematic process that sets the overall business strategy of the organization for the years ahead.5 In reality, an organization’s strategic decisions are often made by distant legislators or regulators in far-off bureaucracies. Often, organizational leaders can only plan their reaction to these decisions. During the process, planners usually undertake what is commonly termed strengths, weaknesses, opportunities, and threats (SWOT) analysis, the assessment of strengths and weaknesses of the organization as well as the threats and opportunities presented in the operating environment or market. Most texts are based on a competitive model and devote considerable effort to the assessment of the competitors and what initiatives are likely to advance the planning organization’s position at the expense of competing organizations. Strategic planning models include provisions for developing action plans, performance information, accountability, and periodic evaluation.4

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Program Planning: Action Planning and Problem Solving Program and project planning are essential planning types which deal with policy and program implementation. Projects can be as massive as a new hospital or a nationwide immunization campaign or as limited as implementing a reengineered care process or new computer software system. Numerous management tools and techniques, such as decision support and project planning software, exist to aid in monitoring progress and optimizing project implementation. For many projects, there is no reason to reinvent the wheel. For planners, particularly those that are new to an organization, managers should learn from others. Abundant case studies have been published in practitioner-oriented journals.17 Some websites (including those cited in this chapter) now post volumes of content-specific information on topics ranging from planning for response to bioterrorism to pandemic influenza planning.18 Much of this information is in the form of how-to guides and checklists that can greatly accelerate the learning of managers and staff who are taking on the new project. In today’s connected, electronic, informationdriven world, it is sheer folly if any manager fails to learn from the experiences of others before embarking on implementing new projects and programs. Examples of resources useful in planning checklists, narrative insights, computer software, and other aids can be found on public health organization websites. While a complete review is beyond our scope, recent concern over emergency preparedness has lead to the provision of many planning resources. Some sites may have support and training services and websites with supporting resources.19 Planning guides for bioterrorism preparedness, such as NACCHO’s Preparing Your Local Public Health Agency for an Emergency Event,20 have been developed with CDC funding and tested in local health departments. An example of more specific resources would include the FluAid and FluSurge software programs to assist local planners in estimating the impact of a pandemic influenza strain. These are available for download.21

Information as a Basis for Better Community Health Gathering and transforming data into information that is useful in making decisions is at the core of any systematic planning process. Information may come from formal and informal sources or systems. For example, a formal system includes vital statistic systems and disease surveillance information systems.22 Much of the information from programs comes from management information systems. Such systems, automatic or manual, are seldom adequate to meet all of an organization’s needs for planning information. Planning always proceeds with less that perfect information. Filling serious deficiencies in information will occupy considerable planning resources. Recent initiatives in many states and local health departments have centered on making information available to health agencies and the public. The CDC’s Community Health Assessment Initiative supports development, implementation, and evaluation of tools, strategies, and approaches to improve the capacity of local public health agencies and communities to conduct effective community health assessments, and demonstrate how the resulting data have been used to affect public health programs and policies. Since 1992 the Initiative has supported the enhancement of electronic data systems that allow dissemination of health data using user-friendly, Internetbased, data query systems.23 Several exemplary systems include Utah’s Indicator-Based Information System for Public Health (IBISPH).24 Florida’s Community Health Assessment Resource Tool Set (CHARTS) is an interactive system that provides support for local health improvement initiatives using the Mobilizing for Action Through

Planning and Partnership model (MAPP).25 Information on other initiatives is linked from the CDC Assessment Initiative website.23 Unfortunately, not all states have information that is readily available to local planning efforts, thus many planning initiatives struggle to fill in their information gaps.

What Models Work Best? While it is necessary for every leader and manager to embrace the need to plan, there are few prescriptions for effective planning. The effectiveness of planning models is difficult to establish since the planning process does not lend itself to testing in the conventional, scientific, comparative approach that is used to establish an “evidence base” for the effectiveness of various interventions and technologies. Some models have been used extensively, and case studies of their use, almost always successful, have been published in professional journals. A critical element of comprehensive planning and improvement models is the engagement of the community. It is cliché but true to say that there is no one way to effectively do this “community thing.” What are the best practices? Several reviews have been devoted to the topic of community engagement and coalition building in public health settings26 and in more broadly defined communities.27,28 The consensus on what works offers no surprises. Leadership, undertaking action and achieving results, adequate technical assistance, feedback on progress, sustainable financial support are achieving outcomes that are associated with success. The unique situational factors, sometimes known as good or bad luck, as well as larger social and economic, factors, are also recognized as determinates of success or failure. The Community Tool Box includes a section on its website devoted to this question. The Turning Point Project, as part of its mission to transform and strengthen the public health system, gathered information on how to make governmental public health agencies more community based and collaborative.29 The Project’s approaches to engaging and sustaining community ownership and involvement in health improvement processes are detailed in an online report.30

Improving Planning: Both Leadership and Technical Skills are Needed for the Future Organizations that plan well at both the strategic and programmatic levels are likely to be the most successful. Some have suggested that governmental public health departments must be more concerned with steering rather than rowing,31 and will be primarily responsible for providing leadership to improve community health rather than providing direct services in the future.32 In this leadership role, the ability to engage other organizations and individuals in the community and to plan effectively becomes even more essential. At the local level there will be more effort needed on community-based rather than institutional and program planning. Without political and interpersonal skills, in addition to technical planning skills, it will be difficult to establish the credibility of the health department as a leader in community health improvement. This chapter has presented an overview of health planning models and current planning resources that may be useful at the community level. Other chapters in this text cover evaluation, policy development, and quality improvement, which provide additional tools and frameworks for planning. This text includes many epidemiological techniques which are essential tools for planning sound programs that are designed to improve community health. Effective planning is essential to improving the health of our communities and the effective operation of programs and organizations small and large. Devoting the necessary time and resources for planning is a challenge that leaders must meet if they are to improve the quality of our services and the health status of our communities.

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Public Health Leadership Development Kate Wright • Cynthia D. Lamberth

Changes and advancements in the science and practice of preventive medicine and public health increasingly require a systems approach to provide and ensure community health. This includes organizational changes in the delivery of preventive and curative services and interventions, an emerging priority for populationbased systems, partnerships among private and public health organizations and agencies, health information systems related to objectives and measurement of community health status1, and a focus on integrated emergency preparedness. Leaders in all sectors associated with ensuring the health of the public must improve the ability to develop complex integrated systems to address changing demands for critical services, including anticipating, preventing, responding to, and recovering from crisis events. Improved capacity requires leaders to ensure agency and workplace performance standards. Performance standards typically measure professional, disciplinary, technical, and management capacity to provide essential public health services. Ensuring these standards requires improving leadership competence and performance. This chapter discusses development and ongoing work of a national network of public health leadership institutes to ensure public health practitioners access to an integrated competency-based education system for public health leadership development. Recent reports and studies on the status of health personnel in the United States report important trends, including increasing demands for a competent public health workforce and for appropriately educated leadership.2 The identified shortage in public health workers includes calls for enhancing leadership capacity.3 The Institute of Medicine reports on the future of public health called for workforce capacity development to accommodate demands of emerging public health problems in an evolving public health system.4,5 The reports argued that public health will serve society effectively only if a more efficient, scientifically sound system of practitioner and leadership development is established. Demands on health leadership from all sectors require competence in systems thinking, design, and change dynamics. Often, however, public health leaders do not have access to or receive formal education in core public health practice or leadership skills. The Institute of Medicine report Who Will Keep the Public Healthy recommends that schools of public health increase the number of graduates who can assume system-level leadership positions, and recruit senior-level practitioners and mid-career professionals prepared for leadership positions. 6 Calls and support for improving workforce education and training have escalated during the last two decades, and more dramatically recently due to demands for crisis and emergency preparedness. As complexity of challenges increases, more resources to improve workforce and leadership capacity are required. The Health Resources Services Administration continues to support a national system of Public Health Education and Training Centers that provide competency-based core public health education.7 The Centers for Disease Control and Prevention (CDC) is expanding support for a national network of Centers for Public Health Preparedness that provides competency-based programs for improving capacity to anticipate, prevent, respond to, mitigate, and recover from bioterrorism and emergency events. The CDC also helps to foster a national agenda for public health leadership development, including providing support for public health leadership institutes and the National Public Health Leadership Development Network (NLN). In 2005, this expanding consortium consisted of 36 states, regional, national, and international institutes that collectively provided an integrated system for leadership development.8

THE NATIONAL PUBLIC HEALTH LEADERSHIP DEVELOPMENT NETWORK In 1991, the CDC began to support development of a national system of state, regional, and national public health leadership institutes. These 1- to 2-year programs provide practitioners with access to a unique professional development opportunity to enhance public health leadership competence. In 1994, the CDC sponsored a cooperative agreement with the Association of Schools of Public Health and Saint Louis University to establish the National Public Health Leadership Development Network (NLN). The purpose of the NLN is to improve capacity of and access to leadership development programs through expanding collaboration among academic and practice institute directors, alumni, and representatives of federal, professional, and private organizations.9 The Network, through sustained partnerships among schools of public health and state public health departments, is composed of 18 states, 9 regional (multistate), 4 national, and 3 international institutes. The national-level institutes include, in order of their establishment, The National Public Health Leadership Institute (PHLI), the CDC Leadership Institute, the National Health Education Leadership Institute, and the National Environmental Public Health Leadership Institute. Annual NLN conferences and meetings are held to accomplish strategic objectives. Recent accomplishments include: • Development of a Conceptual Model for Leadership Development10 • Development of the Public Health Leadership Competency Framework.11 • Development of an Evaluation Logic Model • Assessment of alumni network and development needs • Dissemination of best practices, methods, and instruments • Provision of technical assistance for development of new institutes • Advocacy for strategic workforce development • Advocacy for support and resource development • Formal linkages with national organizations to accomplish objectives Creation of the Conceptual Model, the Competency Framework, and models for program evaluation are fundamental to forming an integrated approach to leadership development.12

DEVELOPMENT OF THE LEADERSHIP COMPETENCY FRAMEWORK Continuing professional education has traditionally focused on the practice needs of individuals: their specialized practice area or technical expertise. This form of education has generally led to professional credentials or certification in the field of practice.13 Concern for the preparation and certification of leadership competence has led to increased demands for education and practice standards for leadership development.14 Identification of competence requirements is of particular concern because practitioners within public health are prepared in a wide array of professional programs or disciplines. In 1995, NLN academic and practice members, representing all leadership institutes, identified the lack of and need of a competency framework specific to professional preparation of public health leaders and for those who aspire to or hold public health leadership positions. The objective was to develop a competency framework for use by NLN institutes as a basis for design of core curriculum modules based

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on expected performance levels.15,16 Several existing competency frameworks were identified as a means to begin the process and confirm the need to develop a specific framework for public health leadership.17 The framework consists of 79 competencies and is reviewed and updated every 3–4 years. The 79 recommended competencies are divided into the following four competency areas: • Core Transformational Leadership Competencies: Personal mastery, including systems thinking, analytical and critical thinking processes, visioning of potential futures, strategic and tactical assessment, emotional intelligence, communication and change dynamics, and ethical decision-making and decisive action. • Legal and Political Competencies: Competence to facilitate, negotiate, and collaborate in an increasingly competitive and contentious political environment with complex multilevel crises and emergency events. • Trans-Organizational Competencies: The complexity of major public health problems and crisis or emergency events extend beyond the scope of any single stakeholder group, community sector, profession or discipline, organization, or government unit, thus leaders must have the ability and skills to be effective beyond organizational or system boundaries. • Team Leadership and Dynamics: Facilitation of learning teams or coalitions/networks to develop capacity and capability to develop integrated systems to accomplish mutual objectives. The Network serves as an efficient and effective means for producing core competencies and curriculum content from this common framework, determining levels of professional development and prerequisite criteria, and developing measurement and evaluation protocols. Measuring the effectiveness of leadership programs is accomplished through process, impact, and outcome evaluation.

Competencies are used to design standards to operationalize teaching objectives and create impact and outcome evaluation models, methods, and instruments. The NLN and several regional and state institutes have conducted various levels of evaluation.18,19 In 2005, the NLN created an evaluation logic model for use in design of leadership programs.20,21 Ultimately, the objective is to measure program impact and outcome to ensure competence and performance improvement measured by organizational performance standards.22 The possibility of certification or credentialing for different levels of the public health workforce is being discussed by various public health organizations, including the CDC, the National Association of County and City Health Officials, the Association of Schools of Public Health, and the American Public Health Association. Although there are no conclusions, there is general agreement that any system designed to accomplish this should be based on fundamental core and universal competency frameworks.23 There is also agreement that these competencies should include a set of leadership competencies required as core skills for the public health workforce. In addition, if various levels of public health workforce credentials are created, then there should be a distinct category for a high-level leadership credential. Interest in accreditation of local and state health departments has resulted in development of several voluntary and nonvoluntary models for local public health agencies.24,25 These models include an emphasis on performance standards and required education and training for specific levels of agency practitioners. Some of these models include a recommended education and training level for public health leadership. Although sometimes controversial, certification of local and state administrators is also germane to the need to formalize performance criteria for public health leaders in relation to accreditation of public health agencies. An established network of public health leadership development institutes is available to serve as an integrated national education and training infrastructure that provides required competency-based curriculum for voluntary or formal certification.

Policy Development Helen H. Schauffler

There are many different avenues for influencing policy development for public health and preventive medicine. In addition to policy decisions made by the U.S. Congress (the legislative branch of the federal government), public policy decisions affecting preventive medicine and public health are also made at the federal level in the executive branch (the Department of Health and Human Services, the Centers for Disease Control and Prevention, the Surgeon General’s Office, the Food and Drug Administration, etc.), at the state level in both the executive (governor’s office and state health department) and legislative branches, at the city and local levels of governments, and in the private sector in private associations, representing health-care organizations and professionals, and among health plans and employers.

AGENDA SETTING The process of agenda setting is key to initiating the policy development process.1,2 The formal policy agenda is defined as those issues to which policy makers will pay attention and take action. Thus, the first step in any policy development process is to get an issue on the formal policy agenda. Two of the most commonly used strategies for getting an issue on the policy agenda include (a) gaining inside access to decision-makers in the policy arena, and (b) organizing an outside initiative through grass-roots mobilization or coalition

building to call the issue to the attention of policy makers.1 These agenda-setting strategies can be used alone or in combination. Recently, both have been used successfully to influence the policy agenda for public health and preventive medicine.

Using Inside Access Strategies to Influence Policy Making During the 103rd Congress, effective inside access was achieved by state and local public health officials who met individually with their elected representatives in Congress to discuss the importance of securing stable and adequate funding for the core functions of public health under a reformed health-care system. Public health officials, both as constituents and leaders in their state and communities, bring credibility and lend importance to an issue and can facilitate translation of public health issues in terms that make them locally relevant to individual elected representatives.3

Using Outside Initiative Strategies to Influence Policy Making In 1994, the National Breast Cancer Coalition and other women’s groups organized a massive and effective postcard-writing campaign from women at the grassroots level all over the country

78 regarding the importance of covering mammography screening as a health insurance benefit under health-care reform in the 103rd Congress. U.S. senators and representatives reported receiving hundreds of postcards from their constituents calling their attention to this issue. Legislators care most about how an issue affects their constituents and will pay more attention to an issue if it comes from the grassroots. The state of Washington provides a model for how states may proceed, in the absence of reforms at the federal level, to put together a coalition of all of the key stakeholders in public health and engage in a productive planning process that produces tangible results. Washington state developed its own Public Health Improvement Plan in 1994, which was submitted to the state legislature and enacted into law in 1995.4 The plan was developed by the Washington state Department of Health and a Public Health Improvement Plan Steering Committee, representative of a broad coalition of public health and health-care organizations in the state. The coalition included representatives of the Department of Health, the state medical association, the association of community clinics, consumers, public health nursing directors, state legislators, schools of public health, labor unions, the state nurses’ association, local public health officials, the hospital association, the health-care purchasers’ association, and the Indian Health Service. The purpose of the plan was to help achieve three goals—stabilization of health-care costs, assurance of universal access to health care, and improvement of population health. The plan includes comprehensive recommendations for public health capacity, finance and governance of the public health system, and standards and strategies for addressing key public health problems. It served as the blueprint for state legislation enacted to reform Washington state’s public health system.

DIFFICULTIES IN GETTING PUBLIC HEALTH AND PREVENTIVE MEDICINE ON THE POLICY AGENDA For the last 10 years, public health and preventive medicine have had increased success in increasing awareness of the value and benefits of increasing access to preventive care, relying on a growing scientific evidence base that demonstrates the effectiveness and relative costeffectiveness of many preventive services. However, the relative importance of public health and preventive medicine in health policy development over the last decade is illustrated by estimates that less than 1% of total health expenditures in the United States is spent on population-based public health and prevention programs.5 There are many reasons for this neglect, including the bias toward the medical model in health policy development. One example that illustrates this struggle was the experience in trying to add preventive care as a benefit to the Medicare program.

Incremental Policy Development: Adding Prevention Benefits to the Medicare Program Perhaps the best example of how policy development for preventive medicine proceeds incrementally are the efforts over the last 30 years to add preventive services benefits to the Medicare program. The amendments to the Social Security Act, which authorized the Medicare program in 1965, include a provision (Section 1862) that prohibits reimbursement for any preventive care. The original Medicare program was based on the Blue Cross and Blue Shield programs operating at that time, where preventive care was not considered medically necessary. Preventive care is also neither unpredictable nor high cost, thus it was not considered to be appropriate for insurance coverage. Between 1965 and 1980, over 350 bills were introduced into the U.S. Congress proposing to add preventive care benefits under Medicare before one bill finally passed adding the pneumococcal vaccine as a covered benefit.5 Only incrementally and within the context of huge budget reconciliation bills were additional screening and immunization benefits added to the Medicare program between 1980 and 1992. And the only benefits that were added were those for which research had demonstrated not only their effectiveness, but their relative

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cost-effectiveness. The pneumococcal vaccine was shown to be costsaving to the Medicare program, while mammography and Pap smears were added later only when studies from the Office of Technology Assessment showed that they were relatively cost-effective.6 However, in the past decade huge gains have been realized in increasing access to preventive care under the Medicare program (Table 78-1). Since 1992 coverage has been added for (a) a “welcome physical”; (b) cardiovascular screening for cholesterol, HDL, and triglycerides; (c) pelvic exam; (d) colon cancer screening including fecal occult blood, flexible sigmoidoscopy, colonoscopy, and barium enema; (e) prostate cancer screening including a digital rectum exam and PSA test; (f) Hepatitis B vaccine; (g) bone mass measurement; (h) diabetes screening and management including fasting plasma glucose test, diabetes glucose monitors, test strips and lancets, and self-management training; (i) glaucoma screening tests; and (j) smoking cessation treatments including counseling for smoking and tobacco use and coverage of tobacco treatment medications under the new Part D prescription drug benefit. Table 78-1 describes what is covered, for whom, at what costs, and with what restrictions.

Key Factors Influencing Health Insurance Coverage of Preventive Care The key factors associated with successful policy development for adding prevention benefits in the Medicare program include an incremental approach of adding only a few benefits at a time, documented and scientific evidence of the effectiveness and cost-effectiveness of the preventive service, and sponsorship and leadership of key policy makers. Factors associated with failure include lack of active support from beneficiaries and health professionals, projected increases in costs to the medical care system associated with adding the benefit, and competing priorities on the policy agenda.

PREDICTING THE OUTCOMES AND DESIGNING SUCCESSFUL STRATEGIES FOR PREVENTION POLICY One of the most useful models for predicting the likely success or failure of proposed policies, and one that is also useful for designing more effective strategies for influencing the policy-making process, is James Q. Wilson’s model of concentrated and diffuse cost and benefits (Table 78-2).7 To apply Wilson’s model to a particular policy, one must identify the intended effects of the policy—who will benefit from the policy and who will bear the costs. In each case, one must also assess if the benefits and costs are concentrated or diffuse. Concentrated costs are those that are imposed on a well-organized, relatively small number of individuals or groups where the cost will be strongly felt. An example of a concentrated cost would be a tax policy requiring hospitals to contribute to a pool to support local public health activities. A diffuse cost, in contrast, is one where the cost burden is widely distributed among a large group of relatively unorganized individuals or groups, where the impact of the cost is relatively small. An example of a diffuse cost would be a small increase in the income tax or in insurance premiums to pay to support public health activities. Policies that rely on concentrated costs are always more difficult to adopt, as the group targeted to bear the cost is likely to organize strong opposition to the policy and will, more often than not, be successful in defeating it. The only case where this is not true is when the benefits are also concentrated and the group who will benefit is equally well organized and prepared to support the policy proposal. In this case, the victories are likely to be alternating. Policies that have concentrated benefits and diffuse costs are almost always winners, as the proponents are well organized, while those bearing the cost are not. Policies that have both diffuse benefits and costs proceed incrementally without strong or well-organized support or opposition. To be successful in developing policy for public health and preventive medicine, it is best to frame the policy and its impacts as having diffuse costs and concentrated benefits. Conversely, in trying to

TABLE 78-1. PREVENTIVE SERVICES COVERED UNDER THE MEDICARE PROGRAM, MARCH 2006 Preventive Service Welcome to Medicare Physical

Cardiovascular Screening Breast Cancer Screening

Services Covered Preventive physical exam, medical history, blood pressure, weight, height, vision test, electrocardiogram, immunizations, review of health, education, and counseling needs Screening for cholesterol level, HDL, and triglycerides after 12-hour fasting Screening mammograms

Cervical and Vaginal Cancer Screening

Pap test; pelvic exam

Colon Cancer Screening

Fecal occult blood test

Flexible sigmoidoscopy

Screening colonoscopy

Prostate Cancer Screening

Bone Mass Screening

Once in a lifetime

None

Every 5 years

20% of Medicare-approved amount with no Plan B deductible

Every 12 months for women age 40 and older, with one baseline mammogram for women ages 35–39 Every 24 months

None for the Pap lab test; 20% of the Medicare-approved amount with no Part B deductible for Pap test collection and pelvic exam None

20% of Medicare-approved amount after the yearly Part B deductible; 25% if done in a hospital 20% of Medicare-approved amount after the yearly Part B deductible; 25% if done in a hospital 20% of Medicare-approved amount after the yearly Part B deductible

Digital rectal exam

20% of Medicare-approved amount after the yearly Part B deductible None

Influenza Pneumococcal Hepatitis B Bone mass measurement test

Restrictions

Must first meet $124 Plan B deductible; 20% of the Medicare-approved amount above the deductible

Barium enema

Prostate Specific Antigen (PSA) test Vaccines

Cost-Sharing Required

None None 20% of the Medicare-approved amount after the yearly Part B deductible 20% of Medicare-approved amount after the yearly Part B deductible

Every 12 months for people age 50 and older

Definition of High Risk

Had colon cancer before; close relative with colorectal polyps or colorectal cancer; history of polyps; inflammatory bowel disease

Every 24 months

Every 24 months if high risk; once every 10 years if low risk, but not within 48 months of screening sigmoidoscopy May be used instead of sigmoidoscopy or colonoscopy. Every 24 months if high risk; every 48 months if low risk Every 12 months for men 50 and older Every 12 months for men 50 and older Once per year in fall or winter Once in a lifetime Persons at high risk for Hepatitis B Every 24 months

Persons with Hemophilia, ESRD, immunosuppression

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Diabetes Screening

Fasting plasma glucose test

None

Diabetes glucose monitors, test strips and lancets Self-management training

20% of Medicare-approved amount after the yearly Part B deductible 20% of Medicare-approved amount after the yearly Part B deductible 20% of Medicare-approved amount after the yearly Part B deductible

Glaucoma Test

Glaucoma eye exam

Smoking and Tobacco Use Cessation

Four counseling cessations per quit attempt. DeďŹ ned as face-to-face patient contact of either intermediate (greater than 3 minutes to 10 minutes) or intensive (greater than 10 minutes)

20% of Medicare-approved amount after the yearly Part B deductible

Tobacco cessation medications prescribed by a physician (e.g., nicotine replacement therapy, Zyban)

Part of Medicare Part D drug beneďŹ t; cost-sharing varies by plan

Up to two screenings per year for individuals at high risk; requires physician referral

Persons with high blood pressure, dyslipidemia, obesity, or history of high blood sugar

Every 12 months for persons at high risk

Persons with diabetes, a family history of diabetes, African American and over 50 years Persons who use tobacco and have a tobacco related disease or take therapeutic agents affected by tobacco use

Two attempts per year for highrisk persons or eight counseling sessions per year. May receive another eight sessions during a second or subsequent year after 11 months

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Health-Care Planning, Organization, and Evaluation TABLE 78-2. JAMES Q. WILSON MODEL OF CONCENTRATED AND DIFFUSE COST AND BENEFITS Concentrated Benefits Concentrated costs

Diffuse costs

Diffuse Benefits

(±) Alternating victories. Equally matched opponents. Battles between organized interest groups. (+) A winning policy. Organized support with little organized opposition.

(–) A losing policy. Organized opposition with little organized support. Need to reframe policy effects to get out of this box. (±) Incremental policy development, without strong, organized support or opposition.

Source: Data from Wilson JQ. The Politics of Regulation. New York: Basic Books, 1980:357–394.

defeat a proposed policy, it is best to frame the policy’s effects as having concentrated costs. The central challenge for public health is rooted in the fact that most public health programs, by definition, have diffuse benefits, making it very difficult to successfully organize political support for them.

IMPORTANCE OF PROBLEM DEFINITION IN POLICY DEVELOPMENT Also key to influencing the policy agenda is how a problem is defined.8 In times of budget constraint, programs that are seen as inexpensive or cost-saving are particularly popular among policymakers.2 If reforming and/or increased investment in public health and preventive medicine are portrayed as contributing toward lowering health-care costs, advocates may be more successful in capturing the attention of policy makers.9 In contrast, if public health is viewed as contributing toward increasing government expenditures and enlarging the role of government, it will be difficult to get the attention of policy makers in a political environment that seeks to reduce the role and size of government.

THE ROLE OF EVIDENCE-BASED GUIDELINES FOR PREVENTIVE MEDICINE POLICY: THE U.S. PREVENTIVE SERVICES TASK FORCE REPORT One of the greatest influences on health insurance policy for preventive medicine was the 1989 release of the U.S. Preventive Services Task Force Report, which established national guidelines for clinical preventive services.11 The report was prepared for the Department of Health and Human Services, and the Task Force recommendations were based on a rigorous review of the scientific evidence on the efficacy and effectiveness of 169 clinical preventive services. The reasons this report has been so influential are (a) the recommendations are grounded in health services research demonstrating the effects of preventive medicine, and (b) the report was developed by an independent task force, not associated with any one special interest or professional group. Clinical trials demonstrating the effectiveness and cost-effectiveness of specific preventive care measures are one of the most powerful tools for influencing purchaser and health plan decision makers to pay for and cover preventive medicine. The Task Force was updated in 1996 and updates on the evidence on specific services are continually published in the peer review literature. The Task Force Report has also had an influence in the development of quality measures to assess the performance of health plans. The National Committee for Quality Assurance (NCQA) defined seven of its nine quality measures in its Health Plan Employer Data and Information Set (HEDIS) 2.0, based on the recommendations for specific screening and immunization services in the U.S. Preventive Services Task Force Report.12 Employers, as purchasers of health care, have also relied on the U.S. Preventive Services Task Force Report to define standard benefits packages to be offered by health plans and to define performance standards for assessing the performance of health plans and the quality of care delivered to their employees.8

THE IMPORTANCE OF POPULATION-BASED DATA AND GOALS FOR PUBLIC HEALTH POLICY: HEALTHY PEOPLE 2000 Also important to furthering the development of public health policy in the last 10 years has been the development and release of the Healthy People 2000 goals and objectives for the nation.10 It not only documents the current health status of the U.S. population, but it establishes population-based goals to improving population health. Healthy People 2000 has provided the basis for establishing data systems at the national, state, and local levels for collecting and reporting on population data and has served as the benchmark against which to measure the influence of public health programs and health-care policies. The goals and objectives were developed between 1987 and 1990 using an extensive consultative and hearings process by the U.S. Public Health Service in partnership with the National Academy of Science and the Institute of Medicine.13 The impact of the goals and objectives has been far reaching. Congress has enacted three laws that incorporate the objectives, and 40 states have issued their own Healthy People 2000 plans, which have been used to build coalitions to improve public health and to improve data systems to monitor the health status of the population.10 The goals have also been widely adopted at the local level and by private and voluntary agencies. Even the quality measures for health plans developed by the National Committee for Quality Assurance were based in part on the Healthy People 2000 objectives to reward health plans for keeping populations healthy.14

NEW OPPORTUNITIES FOR POLICY DEVELOPMENT IN AN ERA OF ACCOUNTABILITY Perhaps the greatest opportunity for policy development that promotes public health and preventive medicine is the recent shift toward defining the problems in the health-care systems as ones of quality and accountability. As quality and “value” in the health-care system are increasingly defined as maintaining and improving the health of the population, monitoring changes in the health status of the population is necessary to ensure quality and accountability, and public health and preventive medicine become important players in the solution. Public health and preventive medicine offer expertise and experience in community-based prevention programs and population-based data collection and can take a leadership role in policy development in these areas. The clearest example of this shift toward increased accountability is the development of HEDIS measures by NCQA. The majority of the quality measures in HEDIS 2.0, 2.5, and 3.0 address provision of clinical preventive services in accordance with the U.S. Preventive Services Task Force recommendations. Health maintenance organizations (HMOs) all over the country are being evaluated against these measures, and their performance is being published in report cards made available to employers and the general public. In some instances, employers are requiring that HMOs guarantee their performance in meeting quality standards by placing a percentage of their premium at risk.9 Building requirements for collecting data, meeting performance standards, and adding economic incentives for performance guarantees into the contracts between HMOs and purchasers, including private employers, state Medicaid agencies, and federal Medicare contracts,

78 may be the most effective policy tools currently available for increasing appropriate provision of preventive care to the insured population.

ADDITIONAL PUBLIC POLICY TOOLS FOR PROMOTING PREVENTION AND PUBLIC HEALTH There are many additional policy tools that are effective in promoting population health.15 Taxation of unhealthy products (e.g., cigarettes and alcohol), regulation of individual and industry behaviors

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that will promote health and prevent disease (e.g., regulating helmet use and industrial environmental pollution), and public health education (e.g., media campaigns promoting good nutrition and physical activity) are all important tools that can contribute toward a more effective health-care system that promotes and maintains health.16 It is essential that policy for prevention and public health be developed at the national, state, local, and institutional levels and that it is developed based on a comprehensive model with policies that seek to influence the medical care system, communities, and governmental policies to promote population health and prevent disease.16

Quality Assurance and Quality Improvement Richard S. Kurz

Two recent IOM reports present a very mixed picture of quality in American health-care institutions.1,2 The second of these reports states that as many as 100,000 Americans may die from medical errors each year and that many of these circumstances are correctable. What needs to be changed to improve quality and how can we make these changes? In this section, two approaches to quality assessment will be discussed: quality assurance and quality improvement. Though similar regarding their emphasis on the process of providing health services, each approach differs in terms of its purpose and procedures. Quality assurance refers to “the formal and systematic exercise of identifying problems in medical care delivery, designing activities to overcome these problems, and carrying out follow-up steps to ensure that no new problems have been introduced and that corrective actions have been effective.”3 Quality improvement is “a management philosophy to improve the level of performance of key processes in the organization.”4 Using an approach adapted from Berwick,5 a context for and an analysis of each concept is presented. This approach is consistent with Donabedian’s categorization of the measurement of quality that is comprised of structure (personnel characteristics and institutional features), process (activities in providing care), and outcome (results of care) indicators.6

Knowing the Resources for What Works Operational and financial resources have been identified as essential for quality care in health services organizations. These are often viewed as structural concerns that are preconditions to the delivery of any services. Operational structures consist of physical facilities and personnel needed to accomplish the level of services that are desired. The earliest quality assessment procedures employed professional or organizational measures in developing licensure, certification, and accreditation for individuals, health-care institutions, and educational programs. The evidence is now clear that these aspects of providing care are necessary but not sufficient to assure high quality. For example, the major accreditation agencies for health-related organizations, the Joint Commission for the Accreditation of Healthcare Organizations (JCAHO) and the National Committee for Quality Assurance (NCQA), emphasize process and outcome rather than structural measures.

Knowing What Works Knowing what works requires information on the efficacy of specific technologies, pharmaceuticals, and clinical interventions under controlled conditions and on the effectiveness of medical and surgical treatments as well as diagnostic, preventive, and rehabilitative care in the course of practice.7 These approaches provide assessments of the

technical results of interventions or services as perceived by the developers or providers of the activity. The primary methodologies in the assessment of efficacy are clinical trials and sophisticated technology assessment techniques.8 The benefits of control in these approaches are balanced with the lack of generalizability resulting from restricted study groups of patients, the restrictions on delivery protocols used, and the limited outcomes addressed. Investigations of effectiveness of practitioners and organizations are referred to generically as “outcome research.” These studies consider the long- and short-term and broad and narrow results of care practices and interventions provided by specific practitioners or by specific types of organizations. Early outcome studies by Wennberg and others demonstrated that common procedures such as hysterectomy and hernia repair occurred much more frequently in some areas that others, even when these areas were not at great geographic distance from one another.9 The measures of these outcomes include mortality, morbidity, patient health status, and health-related quality of life indicators. For instance, the SF-36 Health Survey provides a multi-item scale which measures eight health concepts from the patient’s perspective (physical functioning, physical limitations, social functioning, bodily pain, mental health, emotional limitations, vitality, and general health perceptions).10 Substantial attention has been given to the measurement of outcomes, but equal or greater focus needs to be placed on extending this work to new clinical areas and translating existing findings into actions and disseminating them widely to the practice community.11 Knowing what works can also be assessed in terms of consumers’ perceptions of the services that they receive. This assessment may be of the technical care provided or of interpersonal relationships or amenities experienced.12 As health services organizations have experienced increased pressure to respond to consumer expectations, the distribution of patient or consumer satisfaction questionnaires has become routine and their methodologies increasingly diverse and sophisticated.13–15 At the community level, evaluation of services is conducted through report cards that are “standardized, publicly released reports on the quality of care.”16 Report cards have been developed for specific areas of care and types of health-care organizations.17 A widely cited example of these instruments is the Health Plan Employer Data and Information Set (HEDIS) which was developed to assess managed care plans and is employed by the NCQA.18

Using What Works Using what works or quality assurance implies a consideration of the process by which services are provided. The fundamental issue is the appropriateness of the care provided: (a) over use of services when

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other or no intervention would have been beneficial, (b) under use of the services that would benefit the patient, and (c) improper or incorrect use of beneficial care or prevention. Consideration of appropriateness leads directly to related questions of who determines what is appropriate care and who makes the judgment as to appropriateness in specific instances. Appropriateness is the aspect of quality assessment with which health-care professionals, especially physicians, are most comfortable if they maintain control of the process. Physicians are trained to determine what actions should be taken in specific situations and to take responsibility for their actions in each instance. Concurrent and post hoc assessments by committees in hospitals or other health services organizations are the routine means through which physicians and other professionals perform peer evaluation and discipline. State boards and hospital-utilization review programs have also attempted to maintain appropriate care. Quality assurance also includes malpractice litigation, insurer audits, and governmental investigations. All of these approaches employ retrospective review and assume that problems occur because of careless or incompetent care. In other words, these approaches attempt to identify “bad apples” and “improve quality by cutting off one tail of the bell-shaped curve of human performance.”19 The desire to improve quality assurance has led the Centers for Medicare and Medicaid Services (CMS) to develop quality initiatives for hospitals, nursing homes, and home health agencies. An initial strategy for hospitals was to develop Quality Improvement Organizations (QIOs) throughout the United States to replace the former professional review organizations, professional standards review organizations, and the experimental medical care review organizations. As no standard set of quality measures existed for hospitals, the CMS developed a consensus set of 10 clinical measures in conjunction with JCAHO and the QIOs. These measures are voluntarily reported by over 4000 hospitals as part of the Hospital Quality Alliance, a collaborative linking CMS and the national hospital and medical school associations. Ongoing research is assessing the effectiveness of these efforts.20 Although there are many approaches to assessing the appropriateness of care, perhaps the most extensively examined recently is the use of standards of care or practice guidelines. Standards of care are “statements describing specific diagnostic or therapeutic maneuvers that should or should not be performed in certain clinical circumstances.”21 Standards can be applied to a population of individuals in the community or to individual patients. The key question is do standards of care influence physician behavior and thus improve quality? There is limited evidence to date that this is the case.22 Chassin argues, however, that standards can be effective in changing physician behavior if guidelines regarding their construction and use are followed. These include (a) consensus and credibility concerning clinical content, (b) presentation in the context of a physician’s performance, (c) the legitimacy and focus of the presentation, for example, physician opinion leaders, and (d) reinforcement of the initial education, for example, academic detailing.21 How, then, should standards be developed and who should use them for what purposes? The dilemma in answering the first question is that efficacy research exists for a very limited number of clinical procedures, especially research applying the treatment in a clinical setting or linking it to specific effectiveness outcomes. Hence, although the best attempts to develop standards begin with a careful evaluation of the existing empirical literature, other consensus methods must be used to establish a standard of care. The Delphi methods used by the RAND Corporation produce appropriateness ratings similar to those based on research studies; however, the use of such reliable and valid consensus techniques is not always present in the development of standards of care.23 Although methods for assessing appropriateness based on judgments can be developed and used in clinical and research settings, for example, the Appropriateness Evaluation Protocol,24 substantial methodological study remains to be done. Despite the lack of agreement on how to establish standards, there is increasing demand for them. Insurers, private and governmental, seek standards as a basis for determining what care they will pay for, which health-care organizations they will use, and which treatments

they will cover in their policies. In addition, they provide a basis for external regulation of physician and hospital practice and internal assessment of the clinical care provided by physicians and other practitioners. The concern expressed by physicians regarding these multiple uses of standards of care is that treatment and prevention are constantly evolving processes based on research evidence and practice experience. The standard of care established today may not be appropriate to the care given tomorrow. It is this concern that has lead scholars, especially in the past 15 years, to study the question of how medicine can continually improve what it does.

Doing Well What Works Doing well what works results from a process of continuous quality improvement (CQI) or total quality management (TQM). The concepts and principles of CQI or TQM are based largely on the works of three scholars in the United States (W Edwards Deming,25 Joseph Juran,26 and Philip Crosby27) and two others from Japan (Genichi Taguchi and Kaoru Ishikawa).28 Donald Berwick and others have adapted these concepts for health services and public health organizations.29,30 As a management philosophy, the aspects of CQI require a significant shift in management behavior. In Table 78-3, these changes in management approach are summarized in seven principles adapted from Berwick and his associates’ work on a national demonstration project.29 In this approach, organizations emphasize the management of processes as system failures rather than the management of people. The vast majority of problems are said to result from failures in a process or the suppliers or inputs to it, while only a small minority occur from idiosyncratic events, including the behavior of individuals. Problems occur most frequently across functions as work moves from one area to another or as materials or products enter or leave the organization. Because of this fact, customers and suppliers should not be viewed as problems but as partners in the process of service delivery. The implementation of CQI in a health services organization results in a transformation that impacts all aspects of the organization. Deming described this change process as the integration of “profound knowledge” into management structures, policies, and procedures.31 As depicted in Fig. 78-1, traditional improvement is a function of professional knowledge comprised of information on discipline, subject matter, and values. In health care, quality assurance is a form of traditional improvement in which an individual’s failure to perform appropriately is viewed as correctable through greater professional training or better judgment based on professional standards or values. Quality improvement requires both professional knowledge and improvement knowledge. The first aspect of improvement knowledge, an appreciation for the system, implies the ability to answer three questions: why do we make what we make, how do we make what we make, and how do

TABLE 78-3. THE PRINCIPLES OF CONTINUOUS QUALITY IMPROVEMENT 1. Productive work is accomplished through processes. 2. Sound customer-supplier relationships are absolutely necessary for sound quality management. 3. The main source of quality defects is problems in the process. 4. Poor quality is costly. 5. Understanding the variability of processes is key to improving quality. 6. The modern approach to quality is thoroughly grounded in scientific and statistical thinking. 7. Total employee involvement is critical. 8. New organizational structures can help achieve quality improvement. Source: Adapted from Berwick DM, Godfrey AB, Roessner J. Curing Health Care: New Strategies for Quality Improvement. Chap. 3. San Francisco, CA: Jossey-Bass Publishers; 1991.

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Professional knowledge

Improvement knowledge

Discipline

System

Subject

Variation

Values

Psychology

Theory of knowledge

Traditional improvement

Continuous improvement

Figure 78-1. The aspects of Deming’s “profound knowledge.” (Source: Adapted from Batalden PB, Nolan TW. Knowledge for the leadership of continual improvement in healthcare. In: Taylor J, ed. AUPHA Manual. Gaithersburg, MD: Aspen; 1993.)

we improve what we make? An answer to the first of these questions requires knowledge of customer preferences and community needs; the second, knowledge of processes, their inputs and suppliers, the services provided, and their customers; and the third, knowledge of organizational vision, a plan for improvement, and an approach for design or redesign of key processes. Knowledge of variation requires an understanding of two types of causes for variation in processes. The first are special causes that are identifiable as resulting from specific and idiosyncratic problems of individuals, machines, or events. These causes if found should be removed immediately without the need for greater knowledge of the process. Common causes produce variation that is inherent to the elements of the process. In other words, to remove common causes of variation, the process must be studied thoroughly and the structure of the process, its inputs, and/or its suppliers must be changed. As outlined in Table 78-4, eight statistical procedures can be used to assist in the identification and resolution of process variation and, hence, to produce process improvement.32 The psychology of improvement is based on the power of intrinsic motivation. Goals may be achieved through competition and extrinsic reward, but also by working independently and in cooperation with others. The success and survival of an organization is more likely to be based on the work of cross-functional teams who understand how system processes work and are committed to a vision for the organization that advances it beyond its current reality. The final aspect of Deming’s profound knowledge is the use of a theory of knowledge. Improvement comes through the use of knowledge that allows us to predict the impact of changes. The theory of knowledge advocated for quality improvement is fundamentally the scientific method. Based on planning and study of the process, hunches or hypotheses are developed as to the causes of process

TABLE 78-4. SEVEN BASIC TOOLS FOR DATA ANALYSIS IN PROCESS IMPROVEMENT 1. Flow charts 2. Cause and effect (Fishbone or Ishikawa) diagrams 3. Pareto charts 4. Frequency distributions (histograms) 5. Scatter diagrams or regression analyses 6. Run charts 7. Control charts

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failures. These hunches are tested through small experiments based on existing or newly collected data. If a cause is identified, other experiments are attempted to continue the iterative process of improvement and knowledge gained is distributed to everyone in the organization. This approach to quality improvement has been called the Shewhart or the Plan, Do, Study, Act (PDSA) cycle. Many health services organizations have developed unique approaches for the implementation of CQI. One of the most widely recognized is the FOCUS-PDSA procedure developed and used by the former Hospital Corporation of America. The steps in this process can be illustrated with an example of process improvement completed by the Springfield/Greene County Department of Health (DOH) in Missouri. First, the DOH identified a process needing improvement (FIND). In the county, political concern had been expressed regarding the length of time needed to abate environmental hazards. Although many approaches had been used in the past to achieve the outcome of reduced abatement time, none had worked. A CQI approach was suggested and a team was organized, the members of which understood the process of hazard abatement from their participation in or supervision of it (ORGANIZE). To clarify their current knowledge of the process (CLARIFY), the team flow charted its steps and discovered the number of days that each step in the process required. Having described the process, the team undertook further investigation to discover what the causes of the delay were and which causes were the most important for reducing abatement time (UNDERSTAND). The team used Pareto charts and cause and effect diagrams to assist with this part of their work. Using this approach, the team discovered that the preparation of formal abatement requests through a typing pool and the search of courthouse records for property ownership were the most significant causes of abatement delay. Focusing on the second issue, the team attempted a modem connection to the records of the county utility company rather than the search of courthouse records to establish property ownership (SELECT). Having selected a potential solution, appropriate contacts were made with the utility company and a clerk was trained to make the modem connections and search the database (PLAN). Data was collected by the clerk on the length of time for discovery of ownership and presented in a simple bar graph comparing the length of time for utility company versus courthouse searches (DO). The analysis in this instance was simple and obvious. The average time for courthouse searches was three to five days and for utility database searches, 15 minutes (STUDY). Hence, approximately 4 days, on average, could be removed from each search. The DOH acted to train all clerks to do searches and expanded the investigation time of sanitarians that was formerly wasted in courthouse searches (ACT). Although this presentation of the abatement case is oversimplified, continuous quality improvement provided a systematic approach to process improvement, based on team knowledge rather than administrative authority. How effective has continuous improvement been in improving quality and controlling costs? Many scholars have described CQI implementation or presented normative explanations for its use; however, research regarding the impact of CQI on quality and costs is just beginning in the health services literature.33–35 Despite the fact that systematic study is advancing slowly in health care, the application of CQI in health-care organizations is occurring. To motivate change, the Baldrige Award provides national recognition to health-care (and industrial) organizations that achieve excellence on a set of established and validated criteria. To date, three healthcare organizations (the SSM Health System, the Baptist Hospital, Inc., and the Robert Wood Johnson University Hospital Hamilton) have won the award.36

Knowing the Purpose for Doing it Those involved in quality assurance and quality improvement must ultimately consider the purpose for quality assessment and the values underlying decisions. Unfortunately, this area has received little systematic attention in the literature. Berwick suggests that the issue can be addressed from an economic perspective. That is, to what extent is health care a social good, a product whose acquisition does not reduce one’s wealth? The answer to this question, Berwick believes,

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is intertwined with the distribution of insurance in our society. Brodeur provides a second approach for considering the purposes of quality assurance or improvement, ethical analysis.37 He believes that each management perspective has associated with it a set of more or less well-articulated values that provide the basis for an ethical analysis of how each approach views the nature of work. From this view, work as a group activity must not subjugate the value of the persons performing the work to organizational concerns for efficiency and productivity. CONCLUSION

In this section, the conceptualization, implementation, and significance of quality assurance and quality improvement are discussed

in the context of the range of approaches to quality assessment discussed in the literature. There is some evidence that quality assurance has not met expectations regarding its ability to change practitioner behavior although the concept has been implemented in several different ways and this variation is related to the inconsistency of results. Alternatively, although its detractors abound, research on quality improvement is beginning to demonstrate the potential of this approach for linking process and outcome of health services. Complete assessments of quality, however, require several approaches of efficacy, effectiveness, appropriateness, and efficiency studies. In addition, these investigations must identify how the structural, process, and outcome components of quality are related in the delivery of preventive and treatment services.

Public Health Management Tools Evaluation Thomas G. Rundall

Evaluation of health programs and policies is a fundamental competency for public health professionals.1–3 Building and maintaining an effective health-care system requires programs and policies that promote health and prevent disease in an effective and efficient manner. Evaluation is a process designed to collect and analyze information to determine program performance and improve it. This process involves a variety of concepts, methods, and analytic schemes to determine whether a given program is needed and likely to be used, whether it is appropriately designed to meet the targeted need, whether the program is implemented as planned, and whether the program actually does help people in need at a reasonable cost without undesirable side effects. Hence, evaluation is used to assist in health program planning, program quality assurance and improvement, and policy development. In planning an evaluation, the evaluator collaborates with other stakeholders to decide (a) what is the purpose of the evaluation, (b) what will be the focus of the evaluation, and (c) what specific evaluation model will guide the data collection and analysis.

PURPOSE OF THE EVALUATION Evaluations can be conducted for formative or summative purposes.4,5 Formative evaluation is done primarily for the purpose of providing program staff with information for making midstream alterations in the program to increase the likelihood of achieving desired outcomes. The primary purpose of summative evaluation is to provide information for decision makers with respect to whether the program in its final form, refined through the use of formative evaluation, is sufficiently superior to existing alternatives to justify the allocation of resources to its continuation and/or its adoption in other settings. Formative evaluation is most useful during the early implementation of a new program or as a means of reexamining an older program that stakeholders agree needs modification. Formative evaluations usually have three major components: (a) assessment of participant and staff satisfaction with features of the program, such as relevance and clarity of information presented, structure of the program, qualifications and skill of staff, and interpersonal dynamics among participants and staff; (b) assessment of the short-term cognitive (knowledge and awareness), affective (attitudes, motivation, and beliefs), or behavioral effects of the program; and (c) assessment of the sustainability of the program, including an appraisal of the current and future levels of participation in the program and an analysis of resource requirements.

Summative evaluation provides information about a health program’s effectiveness over a defined period of time, with a defined population, in one or more settings. Decision makers then use this information to help them decide whether to terminate a program, continue it, or expand it to new settings. Such evaluations should be conducted only when program managers are satisfied that the program is functioning as intended and that it is being properly delivered to participants.

Evaluation Focus Evaluations may focus on assessing program process, outcome, or impact.6,7 While the usage of these terms varies somewhat in the field, the following provides generally accepted descriptions of each type of evaluation. Process evaluation documents what is going on in the program and examines strengths and weaknesses of program components and activities. A process evaluation may include descriptions of the characteristics of those who use the program, patterns of use or attendance, characteristics of the program setting, satisfaction of participants and staff with the program, and the extent to which program components and activities are implemented as planned. Process is most useful as part of a formative evaluation. However, process evaluations are also useful in summative evaluations by helping the evaluator understand why certain effects were or were not observed. Outcome evaluations assess the effectiveness of a program in producing favorable cognitive, affective, and behavioral changes in the target population. While most commonly conducted as part of a summative evaluation, short-term assessments of outcomes are also used in formative evaluations. Impact evaluation assesses the effect of the program on more distal goals such as changes in health status and perceived quality of life. Because changes in these types of outcomes typically take a long time to achieve and to measure, the use of impact evaluation is normally restricted to summative evaluations. Although clarifying whether the evaluation is for formative or summative purposes and whether it will focus on program processes, outcomes, or impacts are important steps in planning an evaluation, there is still one other fundamental decision to be made: which model of evaluation practice is most appropriate for the program being evaluated?

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Models of Evaluation The modern era of program evaluation in the United States began in the early 1960s, when policymakers sought data on the effects of the huge federal investments that were made in health education, and social programs. Since that time, numerous approaches to evaluation have been developed. Four prominent models of evaluation are described below. Each of these models emphasizes a valuable aspect of evaluation. The specific questions being addressed by the evaluation and the opportunities and constraints present in the program setting will determine which model, or combination of models, is appropriate.8

Social Science Research Model In an attempt to develop a rigorous evaluation methodology, early evaluators borrowed heavily from the designs and methods used by social scientists to establish the causal effect of an independent variable on a dependent variable. Program evaluation was viewed as a specialized form of social science research. From this perspective, the success of a program is determined by forming two randomized groups, providing the service (treatment) to one group and using the second group to control for possible threats to internal and external validity.9–11 After implementation of the program, data on the appropriate dependent variables are collected from the members of each group. Statistical tests developed for basic research are applied to these data. If the difference between treatment and control group mean scores on a selected outcome measure is in the predicted direction and statistically significant, the program is considered a success. If the difference between the means is not statistically significant, the program is considered a failure. While the strength of this approach for the purposes of making causal interpretations is widely accepted, over time many stakeholders criticized this approach on a variety of grounds. For example, the social science approach was: often judged to be so time consuming that deadlines for making budgetary decisions about a program being evaluated could not be met, impractical to implement because randomization was not possible in many nonclinical settings, too focused on a small number of quantifiable outcomes, too reliant on statistical tests to determine program effectiveness, subject to incorrect interpretation, unable to provide information useful to managers for quality improvement purposes, and too costly.12

Goal-Based Evaluation In an effort to make evaluations more sensitive to the full range of expected program outcomes, evaluators often work with program staff to clearly state the goals and objectives for the program and then measure the extent to which these have been achieved. This approach provides program planners, with the opportunity to establish the criteria and standards to be used to determine program success. Further, qualitative goals and objectives can be stated, explicitly incorporating qualitative methods in evaluation research. This approach also has its drawbacks. It focuses so much attention on the stated program objectives that evaluators sometimes fail to come to understand why programs may or may not have achieved those objectives. Further, goal-based evaluations often fail to consider unanticipated beneficial or harmful effects of program activities.

Goal-Free Evaluation To avoid the pitfalls of goal-based evaluation, an evaluator might not build an evaluation’s design and measurement strategies around the stated goals of the program. A goal-free evaluation studies the program activities, staff, clients, program settings, and records to determine all the positive and negative effects of the program, without regard to the program’s stated objectives. This information is then communicated to program staff, clients, funding agencies, and other stakeholders, who decide whether the findings are compatible with the goals of the program and determine what adjustments should be made to improve the program.13

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Empowerment Evaluation New approaches to evaluation have emerged over the past decade explicitly incorporating a participatory and collaborative relationship between the evaluator and program stakeholders. When doing empowerment evaluation (also referred to as participatory action research, or community-based participatory research), the evaluator’s role includes consultation and facilitation directed toward developing the capabilities of the participating stakeholders to conduct evaluations on their own, to use the results effectively for advocacy and change, and to gain greater control over a program that affects their lives. The evaluation process, therefore, is directed not only at producing informative findings, but also at enhancing the self-development and political influence of the participants. As these themes imply, empowerment evaluation often involves those stakeholders who otherwise have little power in the program, usually the program recipients or intended beneficiaries.14 There is no one right way to do an evaluation. Successful evaluators tailor each evaluation to the questions that are important to program stakeholders and the opportunities and constraints present in the program setting. The specification of the evaluation’s purpose, focus, and data collection and analysis model must evolve from an evaluation planning process that will provide the evaluator with information essential to the design of the evaluation. There are six general steps in this process: (a) identification of stakeholders; (b) determination of the most important concerns of each stakeholder group; (c) assessment of the evaluability of the program (Is there sufficient agreement among stakeholders on the rationale for the program, the key evaluation questions, and the potential to make changes in the program to improve it, that justifies doing the evaluation?); (d) examination of the literature; (e) determination of the methodology to be used, including the research design, sampling, selection of criteria, data collection, and type of statistical analysis; and (f) preparation of a written proposal.15

The Special Case of Evaluations of Complex, Communitywide Interventions Communitywide health promotion and disease prevention programs are at the core of public health. These types of programs are aimed at modifying health risk behaviors and the conditions that produce and reinforce them. These activities often include communitywide health education programs and activities designed to change laws or regulatory policy in areas that affect health. Communitywide interventions are complex, because it is often difficult to define exactly what are the “active ingredients” of the intervention and how they relate to each other. Communitywide interventions often use multiple theories of change and channels of communication (including media advocacy), and often target healthy individuals as well as those in need. The distinguishing characteristic of communitywide interventions is that they attempt to improve health-related characteristics of the entire community. These interventions are typically implemented over several years, making it likely that non–program-related factors such as historical events and migration in and out of a community will affect program outcomes. These aspects of communitywide interventions make them difficult too evaluate. In recent years special research approaches have been developed to evaluate communitywide interventions, including random assignment of multiple communities to treatment and control conditions, combining cross-sectional and cohort research designs within communities, extensive monitoring of intervention processes, measurement of environmental variables, utilization of multiple data collection methodologies, and the use of randomized trial strategies that allow components of the intervention to take on different forms depending on local context.16–23 Evaluation is more than just research. It is fundamental to good management, and it is an essential part of the process of developing effective public policy. It is a complex enterprise, requiring researchers to balance the rigor of their research strategies with the relevance of their work for managers and policy makers. There are

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useful web-based “toolboxes” available to provide guidance and resources for public health practitioners interested in further developing their program and policy evaluation competencies (http:// www.cdc.gov/eval/framework.htm; http://www.eval.org/). These tools and the other resources identified in this chapter will help evaluation researchers to understand the opportunities and constraints associated with a given program and to use the concepts and methods introduced above to tailor an evaluation in such a way that a defensible assessment of program performance is produced. REFERENCES

Planning for Health Improvement: Models for Communities and Institutions 1. McKenzie JF, Neiger BL, Smeltzer JL, et al. Planning, Implementing and Evaluating Health Promotion Programs; A Primer, 4th ed. San Francisco: Pearson Benjamin Cummings; 2005. 2. Reeves PN, Cole R. Introduction to Health Planning, 4th ed. Arlington, VA: Information Resources Press; 1989. 3. Blum H L. Planning for Health: Generics for the Eighties, 2nd ed. New York: Human Sciences Press; 1981. 4. Pegels CC, Rogers KA. Strategic Management of Hospitals and Health Care Facilities. Rockville, MD: Aspen Publishers; 1988. 5. Bryson J. Strategic Planning for Public and Nonprofit Organizations. San Francisco: Jossey-Bass; 1988. 6. Kotler P, Roberto EL. Social Marketing: Strategies for Changing Public Behavior. New York: Collier Macmillan; 1989. 7. Juran JM. A History of Managing for Quality: The Evolution, Trends, and Future Directions of Managing for Quality. Milwaukee, WI: Am. Society for Quality Press; 1995. 8. University of Kansas, Lawrence; 2004. Work Group on Health Promotion and Community Development at the (U.S.A). Community Tool Box (CTB). Available at http://ctb.ku.edu/. Accessed May 14, 2007. 9. Green LW, Kreuter MW. Health promotion planning: an educational and ecological approach, 3rd ed. Mountain View, CA: Mayfield Pub. Co.; 1999. 10. Simons-Morton BB, Greene WH, Gottlieb NH. Introduction to health education and promotion, 2nd ed. Prospect Heights, IL: Waveland Press; 1995. 11. National Association of County and City Health Officials (NACCHO); 2004. Mobilizing for Action Through Planning and Partnership model (MAPP). Available at http://mapp.naccho.org/MAPP_ Home.asp. Accessed May 14, 2007. 12. National Association of County and City Health Officials (NACCHO); 2004. Community-based Environmental Health Assessment (CEHA) Program. PACE EH Resource Tool Kit. Available at http://www. naccho.org/topics/environmental/CEHA/documents/Part1.pdf. Accessed May 14, 2007. 13. Centers for Disease Control and Prevention; 2004. CDCynergy, a multimedia CD-ROM used for planning, managing, and evaluating public health communication programs. Available at http://www.cdc.gov/ healthmarketing/cdcynergy/index.htm. Accessed May 14, 2007. 14. National Cancer Institute (NCI). Making Health Communications Work (NIH Publication No. 02-5145). Washington, DC: U.S. Department of Health and Human Services; 2002. 15. Walsh DC, Rudd RE, Moeykens BA, et al. Social marketing for public health. Health Affairs. 1993;12:104–19. 16. National Association of County and City Health Officials (NACCHO); 2004. NACCHO Public Health Communications Toolkit. Available at http://www.naccho.org/advocacy/MarketingPublicHealth_toolkit_ overview.cfm. Accessed May 14, 2007. 17. Journal of Public Health Management and Practice. A turning Point for public health. (Editorial). J Public Health Manag Pract.2002;8:4–6. 18. Association of State Health Officers (ASTHO); 2004. Influenza pandemic planning for state health officials. Available at http://www. astho.org/pubs/PandemicInfluenza.pdf. Accessed May 14, 2007.

19. National Association of County and City Health Officials (NACCHO); 2004. Bioterrorism and Emergency Response Plan Clearinghouse. Bioterrorism Training Resources Library. Available at http://bt. naccho.org/. Accessed May 14, 2007. 20. National Association of County and City Health Officials (NACCHO); 2004. Preparing Your Local Public Health Agency for an Emergency Event. Available at http://bt.naccho.org/APC_Brochure.pdf. Accessed May 14, 2007. 21. Centers for Disease Control and Prevention; 2004. FluAid and FluSurge software programs. Available at http://www.cdc.gov/flu/ tools/fluaid/. Accessed May 14, 2007. 22. Teutsch S M, Elliot CR. Principles and Practice of Public Health Surveillance, 2nd ed. New York: Oxford University Press; 2000. 23. Centers for Disease Control and Prevention 2000. CDC Assessment Initiative, Accessing, interpreting, and communicating information to guide public health decision making. Available at http:// www.cdc.gov/ epo/dphsi/AI/ai-bg_new.htm. Accessed May 14, 2007. 24. Utah Department of Health and Environmental Services; 2004. Indicator-Based Information System for Public Health (IBIS-PH). Available at http://ibis.health.utah.gov/home/welcome.html. Accessed May 14, 2007. 25. Florida Department of Health Services; 2004. Florida’s Community Health Assessment Resource Tool Set (CHARTS) is an interactive system.Available at http://www.floridacharts.com/charts/chart.aspx. Accessed May 14, 2007. 26. Roussos ST, Faucett S. A review of collaborative partnerships a strategy for improving community health. Annual Review of Pubic Health. 2000;21:369–402. 27. Wolff T. Community coalition building—contemporary practice and research: Introduction. Am J Community Psychol. 2001;29:165–72. 28. Berkowitz B. Studying the outcomes of community-based coalitions. Am J Community Psychol. 2001;29:213–27. 29. Turning Point; 2004. The Turning Point Project. Available at http:// www.turningpointprogram.org. Accessed May 14, 2007. 30. National Association of County and City Health Officials (NACCHO); 2004. Turning Point’s approaches to engaging and sustain community ownership and involvement in health improvement, online report. Available at http://www.naccho.org/topics/infrastructure/ turningpoint/background.cfm. Accessed May 14, 2007. 31. Osborne DE, Gaebler T. Reinventing Government: How the Entrepreneurial Spirit is Transforming the Public Sector. Reading, MA: Addison-Wesley Pub. Co.; 1992. 32. Institute of Medicine, Committee for the Study of the Future of Public Health. The Future of the Public’s Health in the 21st Century. Washington, DC: National Academy Press; 2002.

Public Health Leadership Development 1. Wallace R. Public health and preventive medicine: trends and guideposts, In: Maxcy, Rosenau, Last. Public Health & Preventive Medicine. Stamford, CT: Appleton & Lange; 1998. 2. Public Health Workforce Study. Washington, DC: Bureau of Health Professions, Health Resources and Services Administration; Jan 2005. 3. Trends Alert: Public Health Worker Shortages. Lexington, KY: Council of State Governments; 2004. 4. Institute of Medicine. Committee for the study of the future of public health. The Future of Public Health. Washington, DC: The National Academies Press; 1988. 5. Institute of Medicine, Committee on assuring the health of the public in the 21st Century. The Future of the Public’s Health in the 21st Century. Washington, DC: The National Academies Press; 2003. 6. Institute of Medicine. Who Will Keep the Public Healthy? Educating Public Health Professionals for the 21st Century. Washington, DC: The National Academies Press; 2003. 7. U.S. Department of Health and Human Services. Available at http://bhpr.hrsa.gov/publichealth/phtc.htm. Accessed June 1, 2005.

78 8. National Public Health Leadership Development Network. Available at http://www.slu.edu/organizations/nln/. Accessed May 7, 2005. 9. National Public Health Leadership Development Network. Available at http://www.slu.edu/organizations/nln/. Accessed May 15, 2005. 10. Wright K, Rowitz L, Merkle. A conceptual model for public health leadership development. J Public Health Manag Pract. 2001;7(4):60–6. 11. Wright K, Rowitz L, Merkle A, et al. Competency development in public health leadership. Am J Public Health. 2000;90(8):1202–7. 12. National Public Health Leadership Development Network. Available at http://www.slu.edu/organizations/nln/. Accessed May 15, 2005. 13. Hunt ES. Higher Education and Employment: The Changing Relationship. Recent Developments in Continuing Professional Education. Country Study: United States. Paris, France: Organization for Economic Cooperation and Development; 1992. Report no. (OCDE/GD)(92) 21. 14. Senge PM. The leaders New Work: building learning organizations. Sloan Manage Rev. 1990;7–23. 15. Lovelace BE. A Model for Evaluating Competency-Based Instruction. Houston, TX: The Texas Higher Education Coordinating Board; 1993. 16. Klemp GO. Identifying, measuring and integrating competence. In: Pottinger M, Goldsmith E. Defining and Measuring Competence. San Francisco, CA: Jossey-Bass; 1979. 17. Public Health Faculty/Agency Forum, Public Health Competencies, School of Public Health, University of North Carolina, Doctorate in Public Health Leadership Competencies, Johns Hopkins University School of Hygiene and Public Health, Community Based Public Health Competencies, Association of Schools of Public Health Maternal and Child Health Council, Maternal and Child Health Competencies, and, Public Health Core Functions and Essential Services. 18. Umble KU, Steffen D, Porter J, et al. The National Public Health Leadership Institute: Evaluation of a Team-Based Approach to Developing Collaborative Public Health Leaders. Am J Public Health. 2005;(4):641–44. 19. Saleh SS, Williams D, Balougan M. Evaluating the effectiveness of public health leadership training: The NEPHLI Experience. Am J Public Health. 2004;94(7):1245–9. 20. Mains DA, Williams D. An Evaluation Framework to Assess the Impact of Public Health Leadership Training. Working Paper; August, 2004. 21. National Public Health Leadership Development Network. Available at http://www.slu.edu/organizations/nln/. Accessed May 15, 2005. 22. Strebler MT, Bevan S. Competence-Based Management Training. Parkstone, England: BEBC Distribution; 1996. Report no. 302. 23. Turnock BJ, Handler A. Is public health ready for reform? The case for accrediting local health departments. Public Health Manage Pract. 1996;2(3):41–5. 24. North Carolina Local Public Health Accreditation Program. Available at http://www.sph.unc.edu/nciph/consult/accred. Accessed May 7, 2005. 25. Michigan Local Public Health Accreditation. Available at http:// www.accreditation.localhealth.net. Accessed May 7, 2005.

Policy Development 1. Cobb R, Ross J, Ross MH. Agenda building as a comparative political process. Am Polit Sci Rev. 1976;70:126–38. 2. Kingdon JW. Agendas, Alternatives, and Public Policies. New York: Harper Collins;1984. 3. Scutchfield FD, Keck, ed. The Principles of Public Health Practice. Albany, NY: Delmar; 1997. 4. Washington State Department of Health. Public Health Improvement Plan. Olympia, WA: Washington Department of Health; November 29, 1994. 5. U.S. Department of Health and Human Services. For a Healthy Nation: Returns on Investment in Public Health. Washington, DC: Public Health Service; 1994. 6. Schauffler HH. Disease prevention policy under Medicare: an historical and political analysis. Am J Prev Med. 1993;9(2):71–7. 7. Wilson JQ. The Politics of Regulation. New York: Basic Books; 1980:357–94.

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8. Schauffler HH, Rodriguez T. Exercising purchasing power for preventive care. Health Affairs. 1996;15:74–85. 9. Omen GS. Prevention: Benefits, Costs and Savings. Washington, DC: Partnership for Prevention; 1994. 10. U.S. Public Health Service. Healthy People 2000: National Health Promotion and Disease Prevention Objectives. Washington, DC: U.S. Department of Health and Human Services; 1990. 11. U.S. Preventive Services Task Force. Guide to Clinical Preventive Services: An Assessment of the Effectiveness of 169 Interventions. Baltimore: Williams & Wilkins;1989. 12. National Committee on Quality Assurance. Health Plan Employer Data and Information Set (HEDIS), Version 2.0. Washington, DC: National Committee on Quality Assurance; 1993. 13. McGinnis J, Lee PR. Healthy People 2000 at Mid Decade. JAMA. 1995;273:1123–9. 14. Stone DA. Policy Paradox and Political Reason. Glenview, IL: Scott, Forseman; 1984 15. World Health Organization. Ottawa Charter for Health Promotion. An International Conference on Health Promotion. Ottawa, Ontario, Canada; November 17–21, 1986. 16. Schauffler HH, Faer M, Faulkner L, et al. Health promotion and disease prevention in health care reform. Am J Prev Med. 1994;10(Suppl): 1–35.

Quality Assurance and Quality Improvement 1. Committee on Quality of Health Care in America, Institute of Medicine. Crossing the Quality Chasm: A new Health System for the 21st Century. Washington, DC: National Academy Press; 2001. 2. Kohn LT, Corrigan JM, Donaldson MS, eds. To Err is Human: Building a Safer Health System. Washington, DC: National Academy Press; 2001. 3. Brook RH, Lohr KN. Efficacy, effectiveness, variations and quality: Boundary-crossing research. Med Care. 1985;23:710–22. 4. Flood AB, Shortell SM, Scott WR. Organizational performance: Managing for efficiency and effectiveness. In: Shortell S, Kaluzny A, eds. Health Care Management: Organizational Design and Behavior. Albany, NY: Delmar Publishers; 1994. 5. Berwick DM. Health services research and quality of care: Assignments for the 1990s. Med Care. 1989;27:763–71. 6. Donabedian A. Evaluating the quality of medical care. Milbank Memorial Fund Quarterly. 1966;44:166–206. 7. Guadagnoli E, McNeil BJ. Outcomes research: Hope for the future or latest rage? Inquiry. 1994;31:14–24. 8. Fineberg HV. Technology assessment: motivation, capability, and future direction. Med Care. 1985;23:663–71. 9. McPherson K, Wennberg JE, Hovind OB, et al. Small-area variations in the use of common surgical procedures: an international comparison of New England, England, and Norway. N Engl J Med. 1982;307:1310–4. 10. Ware J, Sherbourne C. The MOS 36-item short form health survey (SF-36): I. Conceptual framework and item selection. Med Care. 1992;30:473–83. 11. The Outcome of Outcomes Research at AHCPR: Final Report. Summary. Agency for Health Care Policy and Research, Rockville, MD. http://www.ahrq.gov/clinic/outcosum.htm 12. Wyszewianski L. Quality of care: Past achievements and future challenges. Inquiry. 1988;25:13–22. 13. Ross CK, Steward CA, Sinacore JM. A comparative study of seven measures of patient satisfaction. Med Care. 1995;33:392–406. 14. Babakus E, Mangold WG. Adapting the SERVQual scale to hospital services: An empirical investigation. Health Services Research. 1992;26:767–86. 15. Otani K, Kurz RS. The impact of nursing care and other healthcare attributes on hospitalized patient satisfaction and behavioral intentions. Journal of Healthcare Management. 2004;49: 181–96.

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16. Epstein A. Performance reports on quality — Prototypes, problems, and prospects. N Engl J Med. 1995;333:59–61. 17. Green J, Wintfeld N. Report cards on cardiac surgeons. N Engl J Med. 1995;332:1229–32. 18. Health Plan Employer Data and Information Set, National Committee for Quality Assurance, Washington, DC. http://www.ncqa.org/ Programs/HEDIS 19. Hsia D. Medicare quality improvement: Bad apples or bad systems. JAMA. 2003;289:354–6. 20. Hospital Quality Initiative Overview. Centers for Medicare and Medicaid Services, Washington, DC. http://www.cms.hhs.gov/quality/ hospital/PremierFactSheet.pdf 21. Chassin MR. Standards of care in medicine. Inquiry. 1988;25: 437–53. 22. Weingarten S. Assessing and improving quality of care. In: Williams SJ,Torrens PR. Introduction to Health Services. 6th ed. Albany, NY: Delmar; 2002, pp. 380–383. 23. Fink A. Consensus methods: Characteristics and guidelines for use. Am J Public Health. 1984;74:979–83. 24. Gertman PM, Restuccia JD. The appropriateness evaluation protocol: A technique for assessing unnecessary days of hospital care. Med Care. 1981;19:855–71. 25. Deming WE. Out of the Crisis. Cambridge, MA: M.I.T. Center for Advanced Engineering Study; 1986. 26. Juran JM. Juran on Planning for Quality. New York: The Free Press; 1988. 27. Crosby PB. Quality is Free: The Art of Making Quality Certain. New York: Mentor; 1979. 28. Jaeger BJ, Kaluzny AD, McLaughlin CP. TQM/CQI: From industry to health care. In: Continuous Quality Improvement in Health Care: Theory, Implementations, and Applications. CP McLaughlin and AD Kaluzny, eds. Gaithersburg, MD: Aspen; 1994. 29. Berwick DM, Godfrey AB, Roessner J. Curing Health Care: New Strategies for Quality Improvement. San Francisco, CA: Jossey-Bass Publishers; 1991. 30. Kaluzny A, McLaughlin CP, Simpson K. Applying total quality management concepts to public health organizations. Public Health Reports. 1992;107:257–64. 31. Batalden PB, Nolan TW. Knowledge for the leadership of continual improvement in healthcare. In: J Taylor, ed. Manual of Health Services Management. Gaithersburg, MD: Aspen; 1993. 32. Plsek PE. Techniques for managing quality. Hospital & Health Services Administration. 1995;40:50–79. 33. Shortell SM, O’Brien JL, Carman JM, et al. Assessing the impact of continuous quality improvement/total quality management: concepts versus implementation. Health Services Research. 1995;30: 377–401. 34. Olsson J, Eng L, Elg M, et al. Reflections on transnational transferability of improvement technologies: A comparison of factors for successful change in the United States and northern Europe. Qual Manag Health Care. 2003;12:259–69. 35. Shortell SM, Jones RH, Rademaker AW, et al. Assessing the impact of total quality management and organizational culture on multiple outcomes of care for coronary artery bypass graph surgery patients. Med Care. 2002;38:207–17. 36. Baldrige National Quality Program, National Institute of Standards and Technology, Gaithersburg, MD. http://www.quality.nist.gov 37. Brodeur D. Work ethics and CQI. Hospital & Health Services Administration. 1995;40:111–23.

Public Health Management Tools Evaluation 1. Institute of Medicine. Committee for the Study of the Future of Public Health. The Future of Public Health. Washington, DC: National Academy Press; 1988. 2. American Public Health Association: APHA’s vision: public health a reformed health care system. The Nation’s Health. 1993;23(6): 9–11. 3. Gebbie K, Rosenstock L, Hernandez LM. Who Will Keep the Public Healthy? Educating Public Health Professionals for the 21st Century. Washington, DC: National Academies Press; 2003. 4. Scriven M. The Logic of Evaluation. Inverness. CA: Edgepress; 1980. 5. Rossi PH, Lipsey MW, Freeman HE. Evaluation: A Systematic Approach, 5th ed. Newbury Park, CA: Sage Publications; 2004, pp. 34–7. 6. Rossi PH, Lipsey MW, Freeman HE. Evaluation: A Systematic Approach, 5th ed. Newbury Park, CA: Sage Publications; 2004, pp. 52–62. 7. Posavac EJ, Carey RG. Program Evaluation. 6th ed. Englewood Cliffs, NJ: Prentice Hall; 2003, pp 7–9. 8. Shadish WR, Cook TD, Leviton LC. Foundations of Program Evaluation. Newbury Park, CA: Sage Publications; 1991. 9. Campbell DT, Stanley JC. Experimental and Quasi-experimental Designs for Research. Chicago: Rand-McNally; 1963. 10. Cook TD, Campbell DT. Quasi-experimentation. Chicago: Rand-McNally; 1979. 11. Shadish WR, Cook TD, Campbell DT. Experimental and QuasiExperimental Designs for Generalized Causal Inference. Boston: Houghton-Mifflin; 2002. 12. Posavac EJ, Carey RG. Program Evaluation. 6th ed. Englewood Cliffs, NJ: Prentice Hall; 2003, p 25. 13. Scriven M. Evaluation Thesaurus, 4th ed. Newbury Park, CA: Sage Publications; 1991. 14. Fetterman DM, Kaftarian SJ, Wandersman A. Empowerment Evaluation: Knowledge and tools for Self-Assessment and Accountability. Thousand Oaks, CA: Sage Publications; 1996. 15. Posavac EJ, Carey RG. Program Evaluation, 6th ed. Englewood Cliffs, NJ: Prentice Hall; 2003, p 28–36. 16. Jackson C, Altman DG, Howard-Pitney B, et al. Evaluating community-level health promotion and disease prevention interventions. New Directions for Program Evaluation. 1989;43:19–33. 17. Mattson MA, Cummings KM, Lynn WR, et al. Evaluation plan for the Community Intervention Trial for Smoking Cessation (COMMIT). Int Q Community Health Educ. 1990–1991;11(3):271–90. 18. Wickizer TM, Von Korff M, Cheadle A, et al. Activating communities for health promotion: a process evaluation method. Am J Public Health. 1993;83(4):561–7. 19. The COMMIT Research Group: Community Intervention Trial for Smoking Cessation (COMMIT): I. Cohort results from a four-year community intervention. Am J Public Health. 1995;85(2):183–92. 20. The COMMIT Research Group: Community Intervention Trial for Smoking Cessation (COMMIT): II.Changes in adult cigarette smoking prevalence. Am J Public Health. 1995;85(2):193–200,183–92. 21. Hawe P, Shiell, Riley T. Complex interventions: How “Out of Control” can a Randomized Controlled Trial Be? BMJ. 2004;328:1561–3. 22. Glasgow RE, Vogt TM, Boles SM. Evaluating the public health impact of health promotion interventions: the RE-AIM Framework. Am J Public Health. 1999;89(9):1322–7. 23. Stead M, Hastings G, Eadie D. The challenge of evaluating complex interventions: a framework for evaluating media advocacy. Health Ed Res. 17(3):351–64.

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Disaster Preparedness and Response Theodore J. Cieslak • Scott R. Lillibridge • Trueman W. Sharp • George W. Christopher • Edward M. Eitzen

INTRODUCTION

The recent massive disaster brought about by the December 26, 2004, tsunami in the Indian Ocean was one of the most lethal, costly, and destructive in modern history. Some experts predict, however, that an ever-increasing global population, with its attendant strains on natural, technological, and human resources, portend even greater and more frequent disasters to come.1 These realizations, coupled with technological innovations, microbial engineering, increasingly sophisticated terrorist capabilities, and the ever-present danger of war and sectarian strife, call to mind the myriad problems associated with effective disaster planning and disaster response. Although disasters defy ready definition, and at least 35 different professions are involved in disaster assessment, study, and mitigation,2 a disaster might nonetheless be defined as a destructive event that results in the need for a wide range of emergency resources to assist and ensure the health and survival of the stricken population.3 Disasters can be natural or man-made, abrupt or insidious. Furthermore, disasters caused by man can include warfare and terrorism, as well as “technological” disasters (Table 79-1). “Natural” disasters, such as earthquakes, volcanic eruptions, hurricanes, floods, and the like, have been with us throughout history. The same can be said for warfare, and its accompanying destruction, disease outbreaks, and famine. Technological disasters have likewise been with us since the Industrial Revolution.4 Such disasters may involve explosions, fires, crashes, and chemical or radiological releases into the environment.5 More recently, the specter of man-made disasters related to terrorism and the deployment of weapons of mass destruction (WMDs) has focused considerable attention on public health and disaster preparedness. Disasters encompass a wide variety of events with multiple causes and consequences. Natural disasters are precipitated by the forces of nature and weather.6–8 Such disasters may be ongoing and insidious, as in the case of the famine of 1977 in Ethiopia, which followed successive years of drought.6 Most natural disasters occur suddenly, however, and often with little or no warning. The earthquake in Kobe, Japan, in 1995, which caused 5000 immediate deaths and created the need for an urgent and massive relief effort, is but one example among many.7 As technology rapidly evolves, so too does the inevitability of technology-related crises. Adverse health effects from technological disasters include those acute effects such as trauma, burns, and smoke inhalation injury, as well as those indirect effects related to environmental exposures to potentially contaminated soil, water, and food.8,9

An example is the 1986 radionuclide release from disabled reactor number 4 at Chernobyl in the former USSR. This disaster resulted in acute injuries, but more importantly it exposed more than 2 million people to radiation.10,11 Radiation exposures from this incident continue to result in a variety of adverse health effects, such as increased rates of thyroid cancer.12 Complex emergencies are the result of interrelated social, economic, and political problems and almost always involve armed confrontation.13 Warfare (and armed conflict) brings with it a unique set of disaster response challenges. In these increasingly common and often prolonged disasters, there is typically extensive destruction of social and public health infrastructure, large-scale population displacement, epidemic disease, and food shortages.17–19 Recent examples of complex emergencies include the humanitarian crises in Bosnia-Herzegovina, Rwanda, Somalia, Liberia, Cote d’Ivoire, Afghanistan, and East Timor, among many others. Terrorism is regarded by many as an escalating and evolving threat, and terrorists of today have unparalleled access to highly destructive technologies.14 Long a problem in some areas of the world, large-scale terrorism became a very real concern for Americans following the first attack on the World Trade Center in 1993. On March 20, 1995, an attack on the Tokyo subway system, perpetrated by the Japanese doomsday cult, Aum Shirykyo, demonstrated a willingness and capability on the part of terrorists to employ WMDs, in this case, a chemical weapon, the nerve agent, sarin.15 The following month, on April 19, 1995, large-scale terrorism came to the American heartland with the Oklahoma City bombings, significant also in that the perpetrators were Americans. Finally, the attacks on the World Trade Center and the Pentagon on September 11, 2001, and the release, the following month, of anthrax-contaminated mail, underscore the variety and adaptability of terrorist methodology. Moreover, they call to mind unique disaster response issues. Such issues include, in addition to conventional disaster response considerations, the need for rapid characterization of the offending agent, mass decontamination, ready access to antidotes and medications, specialized medical training, and proper protective equipment for emergency responders.

UNDERSTANDING DISASTERS

Natural Disasters. Over the past 20 years, natural disasters have affected at least 800 million people and caused well over 3 million deaths.16 Each week there is at least one natural disaster of sufficient magnitude to require external assistance from the international community. The incidence of natural disasters appears to be increasing,

1285 Copyright © 2008 by The McGraw-Hill Companies, Inc. Click here for terms of use.

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TABLE 79-1. DISASTERS Type of Disaster

Examples

Deaths

Comments

Natural Disasters Climatological Hurricanes, typhoons Tornadoes Floods Drought Blizzards Geological Earthquakes Tsunamis Volcanic eruptions

Mitch, Honduras, 1998 13 States in U.S., 4/3/1974 Monsoon, Bangladesh, 8/9/1988 Somalia, 1991–1993 Midwestern United States, 1930–1941 Eastern U.S., 3/12-14/1993

>11,000 330 >1300 ~400,000

Bam, Iran, 12/26/2003 Yerevan, Armenia, 12/7/1988 Indian Ocean, 12/26/2004 Mt Pinatubo, Philippines, 7/15/1991

>30,000 ~25,000 150–300,000 >800

Paraguay Supermarket, 8/1/2004 Lagos, Nigeria, 1/27/2002 Neishabour, Iran, 2/18/2004

>400 >1000 320

Bhopal, 12/3/1984 Chernobyl, 4/26/1986

>2000 31 claimed

Explosion triggered stampede, killing 1000 Runaway railcars loaded with fertilizer & petrol explode, destroy 5 villages ~150,000 injured >2 million exposed to radiation

Second World War

>40,000,000

30–50 wars ongoing at any given time

Aum Shinrykyo, Tokyo Anthrax Attacks, US, 10/2001

12 5

>5000 worried well WHO estimates 95,000 deaths possible under certain conditions 4 died from pilfered Cesium source at Goiania, Brazil, 1987

270

2–3 million homeless; damages >$5 billion 148 separate tornados; 5484 injured 30,000,000 left homeless Ongoing drought complicated by warfare Dustbowl destroyed 50 million acres $3–$6 billion in damages 30,000 injured; 75,000 homeless 400,000 homeless

Technological Disasters Fires Explosives Crashes Chemical exposures & spills Radiation exposures

Warfare Terrorism (CBRNE) Chemical Biological Radiological

No significant attacks thus far

Nuclear Explosive

None thus far Twin Towers, Pentagon, 9/11/2001

and the number of highly vulnerable persons in disaster-prone areas, particularly in the developing world, is at least 70 million people and growing.17,18 The devastating 2004 tsunami in the Indian Ocean, in which well over 150,000 persons were killed, illustrates the potential impact of a natural disaster on a population residing in a hazardous coastal region. Similarly, the earthquake in Bam, Iran, exactly 1 year earlier (on December 26, 2003), killed 30,000, injured another 30,000, and left 75,000 homeless, illustrating the perils of life in a highly earthquake-prone zone. Natural disasters may be associated with a wide variety of acute and long-term health effects. For example, volcanic eruptions may result in injury or death due to explosive blast effects, lava flow, falling debris, asphyxiating gases, or mudflows.19,20 For many months following an eruption, ash and other particulate matter vented from an active volcano may exacerbate respiratory illness in persons residing down-wind.21 Volcanic ash may contaminate soil and water, resulting in long-term toxic exposures to the population. One of the most unusual gas releases associated with volcanic activity occurred in 1986 in Cameroon.22 In this incident, carbon dioxide was release from an active volcano underneath Lake Nyos. The gas enveloped nearby villages and caused approximately 1700 deaths by asphyxiation. Volcanic ash in the atmosphere has also been known to cause engine shutdowns in commercial aircraft, leading to in-flight emergencies—a unique combination of natural and technological events interacting to produce the potential for catastrophe. Public health issues associated with floods extend beyond concerns for mortality due to drowning. In Bangladesh, the flooding which followed a 1991 tropical cyclone reduced the potability of water from wells and caused widespread outbreaks of diarrheal disease.23 Flooding may also result in increased numbers of breeding sites for mosquitoes and consequently, an increased risk of exposure to their associated diseases, such as malaria or dengue. Immediate public health actions required following a flood usually include vector control, the

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provision of potable water and food, and the restitution of vital environmental health services.24,25 Overall, however, early warning systems, improved evacuation plans, and the discouragement of settlement in flood-prone areas may have much greater potential to save lives than activities associated with external emergency response to flood disasters. The recent Indian Ocean tsunami illustrated the limitations of response activities in curtailing mortality during rapid flooding; most victims in this disaster were carried out to sea and drowned. Earthquakes typically cause traumatic injuries and deaths, as well as destroying buildings and infrastructure.26 The 1976 Tangshan Earthquake, for example, caused more than 200,000 sudden traumarelated deaths.27 Similarly, the relatively moderate (Richter Scale 6.6) earthquake in Bam in 2003 resulted in at least 30,000 deaths, largely due to trauma sustained when earth and mud buildings collapsed on inhabitants. In contrast to most floods (the recent Indian Ocean tsunami excepted), the morbidity and mortality of earthquakes is much more immediate. Deaths are primarily due to crush injuries and other trauma resulting from unstable, collapsing, or crumbling buildings. Earthquakes are not usually followed by longterm public health problems such as famine or epidemic diseases, although following the Northridge earthquake of 1994, a wide range of external primary care services were required by the population for up to 4 weeks. Other public health issues associated with earthquakes include concerns for the health of persons in shelters, occupational health protection for rescue workers, and the provision of mental services for survivors.28 Technological Disasters. Public health problems resulting from technological accidents, or from the unregulated and unsafe use of industrial technologies, are increasingly recognized as an important and increasingly common type of disaster.7,10 The nuclear reactor accident at Chernobyl, the toxic gas leak at Bhopal, India, the extensive chronic environmental pollution in several former Soviet block

79 nations, and the acute environmental catastrophe associated with the Exxon Valdez oil spill are but a few examples of the disastrous consequences that can ensue from technological disasters. The potential for harm from improper management of industrial technologies is a major concern in developed nations where at any given moment there are myriad complex industries in operation and tons of hazardous materials in transit through populated areas. Moreover, these hazardous materials can make attractive “weapons of opportunity” to would-be terrorists, who may be able to accomplish their objectives simply by opening the valve on a railroad tank car. In developing countries, these problems are exacerbated when rapid industrialization exceeds the development of counterbalancing safety controls. Technological disasters are usually the result of poor engineering, improper safety practices, or simple human error. However, natural disasters can be an important factor in precipitating a follow-up technological disaster. For example, gasoline fires that killed over 500 persons in Durunka, Egypt, in 1994 were the result of flash flooding that ruptured a fuel storage tank and carried burning petroleum into the nearby town.29 Such synergistic disasters have been termed NA-TECHs (Natural-Technological).30 In many locales, chemical plants, nuclear reactors, or other potentially dangerous industries are seated in geological regions that are highly vulnerable to natural disasters. Dealing with the consequences of a technological disaster or a NA-TECH presents many challenges. Recognizing the nature of the hazardous material involved, evacuating citizens after an accident, providing appropriate medical care for victims, and protecting emergency responders against hazardous exposures are but a few of the many challenges that emergency responders potentially face.31 In addition, because industrial disasters may leave toxic residues in the environment that pose ongoing threats to the health of populations, the initiation of chemical exposure and disease registries (in order to track adverse health effects of disaster victims over time) may be a fundamental component of emergency response. Clinical investigations following technical disasters may require assistance from laboratory scientists, toxicologists, and environmental epidemiologists. Public health prevention efforts include sound plant design and operation, safe disposal of waste products, thorough safety occupational programs, linkage to local emergency management operations, and proper site selection for industrial facilities. Warfare and Conflict-Related (Complex) Emergencies. Conflictrelated disasters are a growing phenomenon in the post-Cold War world. In the late 1970s there were approximately five conflict-related disasters per year, but by the early 2000s there were 15–20 per year. In 2003, the Office of Foreign Disaster Assistance of the U.S. Agency for International Development responded to at least 16 complex emergencies. The increase in conflict-related disasters closely relates to the number of armed conflicts in the world, which have likewise increased dramatically during the past two decades. Since 1980, there have been a couple of hundred major armed conflicts, and in 2003, there were 36 ongoing wars in 28 different nations.32 War has always been destructive, but in recent years the nature of armed conflict has become increasingly more devastating.39–42 In many conflicts today, there are eight to nine civilian deaths for every combatant death.33 Toole and Waldman have described the insidious cycle of armed confrontation, famine, and population displacement.34 In 1980 there were approximately 5 million refugees worldwide, but largely as a consequence of this cycle, there were approximately 17 million global refugees as of January 1, 2004, according to the United Nations High Commissioner for Refugees.35 In addition, there are tens of millions of internally displaced persons. The public health problems of refugees and displaced persons are often overwhelming. Crude mortality rates among refugees and displaced populations frequently rise dramatically above baseline levels, principally due to nutritional shortages, environmental problems, and preventable infectious diseases. Conflict-related disasters have similar effects on those who do not flee when infrastructure is destroyed or severely damaged, thereby limiting their access to food, potable water, refuse disposal, and basic medical services.

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During many conflicts today, international humanitarian law is unknown or disregarded, and human rights abuses are common. As a result, in some disasters, violence may be a direct and primary cause of morbidity and mortality.36,37 For example, while morbidity and mortality due to infectious diseases increased to some extent, deaths due to “ethnic cleansing” operations were by far the principal cause of death during the Bosnia and Kosovo conflicts.36,37 Similarly, the provision of emergency relief during conflict-related disasters can, in itself, be very dangerous.38 Many relief workers have been killed in recent years; their protection is often a major challenge of disaster relief operations. Relief organizations that wish to remain neutral and impartial can have tremendous difficulty operating in settings of armed confrontation. Unfortunately, the provision of humanitarian relief can easily be perceived as a partisan act, or can be manipulated for the benefit of different warring factions.39 In situations of conflict, traditional medical and public health interventions may not be effective in preventing injury and death. Indeed, some have argued that in certain situations emergency relief has served to exacerbate and prolong the conflict. Development initiatives, weapons control, conflict resolution, and other such measures may be more effective ways of preventing mortality in these situations. The role of relief organizations in preventing human rights abuses, including torture and genocide, is complex and uncertain. Nonetheless, international disaster operations today often require that nongovernmental relief organizations (NGOs) frequently work alongside military relief personnel and operations of wealthier nations. Often the militaries of these nations have robust capabilities which can be invaluable in disaster relief, such as food, transportation, medical care, and logistics; civilian NGOs are often unable to provide comparable levels of such relief. While those in the assisting military forces may see such roles as a natural extension of their capabilities, their activities have been known to foster jealousies and resentment among NGOs, which often view uniformed military responders as at least figuratively contributing to many of the types of disasters to which they respond (rightly or wrongly). Sensitivity to such dynamics among military disaster responders can go a long way toward heading off such tensions—abandonment of the “we’re in charge” mentality, the wearing of civilian clothes, a willingness to work cooperatively with civilian relief organizations, and a lack of arms, where possible, may further acceptance among both NGOs and the local population. One of the most extensive public health catastrophes today concerns the worldwide dissemination of land mines. It is estimated that 65–110 million land mines are scattered throughout more than 60 countries.40 These landmines can often persist and remain “armed” for decades. They impede the resettlement of displaced populations and serve to remove land from cultivation. Globally, landmines are responsible for more than 15,000 fatalities each year.40 With that said, many landmines are designed to maim; survivors typically require emergency surgical services and prolonged rehabilitation largely related to lower limb amputation. This has had devastating impact on the individuals, the economies, and the health-care systems of many developing nations. Countries affected by severe landmine problems in the wake of endemic warfare include Afghanistan, Mozambique, Angola, Rwanda, and nations of the former Yugoslavia. Terrorism. Terrorist attacks have recently captured the attention of the world’s citizenry and its media. Foremost among these attacks in recent memory, the assaults on the Pentagon and World Trade Center on September 11, 2001, resulted in 2992 deaths. While the numbers of casualties arising from most individual terrorist attacks, however, is still dwarfed by those due to natural disasters such as earthquakes, tsunamis, and floods, an increasing sophistication of terrorist methods and an increasing destructive capacity of terrorist weapons has caused terrorism, in the minds of many, to become the scourge of the twentyfirst century. Moreover, the cumulative toll of terrorism has been immense. From 1984–2000, an estimated 30,000–35,000 persons were killed by terrorists in Turkey alone.41 While small-scale terrorist endeavors, such as kidnappings and assassinations, have been with us for centuries, a recent emphasis on the possible employment of WMDs and the production of large numbers of casualties in a single

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event has caused terrorism to be considered a potential cause of largescale disasters; under ideal conditions (for the perpetrators), for example, the World Health Organization estimates that an anthrax attack on a large city in the developed world could produce as many as 95,000–100,000 deaths.42 The formerly held view that terrorists, motivated largely by political aims, avoided large numbers of casualties (as they would turn away potential supporters), has recently been supplanted, in many cases, by the religious or ideologically motivated views of groups such as al-Qaeda. These groups, in some cases, seem to have no hesitation about the production of massive numbers of casualties. While large numbers of casualties are possible, terrorism, by its very definition, is primarily designed to produce fear and panic in a population. The employment, or threat of employment, of unconventional and unfamiliar WMDs will only serve to heighten this fear. Many disaster planners employ the acronym CBRNE (chemical, biological, radiological, nuclear, explosive) to encompass these potential terrorist weapons. While each of these weapons brings with it unique, and often profound, disaster response considerations, it is the psychological and psychosocial impact that is likely to define a disaster associated with terrorism. DISASTER PLANNING

By their very definition, disasters have profound public health implications. Critical public health challenges following a disaster include the provision of basic life-sustaining commodities such as food, water, and shelter, and the establishment of essential curative and preventive medical services.43 In the past, public health and safety professionals and organizations concentrated their efforts primarily on emergency disaster relief. More recently, however, disaster preparedness, prevention, and mitigation have become increasingly important public health activities. Public health priorities for dealing with disasters should be determined by the predominant causes of morbidity and mortality for a particular type of disaster, and the best methods of prevention for the particular population involved.30 Effectively coping with disasters involves much more than the timely delivery of external emergency resources. Local vulnerabilities within a community, such as poverty, population density, type of construction, and a relative lack of disaster planning, may enhance the risk to a population to disasters. For example, the 1988 earthquake in Armenia resulted in more than 30,000 deaths while an earthquake of similar force, the 1989 Loma Prieta earthquake in California, resulted in less than 500 deaths.44,45 The low mortality associated with the Loma Prieta earthquake was thought to be due to enforcement of local building codes, better local emergency medical services (EMS), superior local disaster management services, and other communitybased prevention and mitigation activities.30,46

Although planning, preparation, and engineering controls can mitigate against a portion of the morbidity and mortality associated with disasters, human factors also play an aggravating role in almost all disasters, even natural ones. What is identified as the “disaster” is often better understood as a trigger event that exposes and exacerbates underlying societal problems and weaknesses. For example, in virtually every famine of the last 20 years, drought has been an important contributing factor, but food shortages have been primarily the result of armed conflict, inadequate economic and social systems, failed governments, and other man-made factors.47 The famine in Somalia48 from 1991 to 1993 and the ongoing famine and crisis in Darfur both highlight the dramatic amplification of drought by internecine clan warfare. Understanding the consequences of disasters, and effectively coping with them, requires looking well beyond the event itself. Coping with complex emergencies, as well as other disasters, is one of the great public health challenges of our time. There are a multitude of technical and logistical issues involved in providing lifesustaining services to large populations.49,50 Events during and after a disaster may not progress in a clear linear fashion; public health needs often evolve substantially.37 For example, priorities for refugees who have just arrived in a location (usually shelter, food, water, and basic medical care) are different from the needs of the same population a few months after a refugee camp has been established (family planning, medical care for more chronic problems, and rehabilitation). As with natural disasters, attention is increasingly being devoted toward prevention, early warning, and preparation activities. Because complex emergencies are usually the result of many years of deeply rooted social problems, effectively dealing with them requires that relief efforts be closely integrated with political, social, economic, military, cultural, and other activities. MEDICAL AND PUBLIC HEALTH ASPECTS OF DISASTER RESPONSE

The medical and public health response to a disaster can be envisioned as occurring on multiple levels. We find it useful to consider response needs on both a “micro” level (the level of the individual medical practitioner, where most needs involve traditional medical practices such as the provision of patient care) and a “macro” level (the level of public and governmental entities such as local, state, and federal public health authorities). Traditional medical response and the management of individual patients has been extensively reviewed elsewhere and is beyond the scope of this chapter.51,52 Here, we concentrate instead on the “macro” response of the Public Health Community at large and the many governmental and nongovernmental institutions that might be called upon to respond to, and mitigate the effects of, a natural or man-made disaster. In the United States, an evolving body of legislation (summarized in Table 79-2), culminating

TABLE 79-2. KEY DISASTER RESPONSE DOCTRINE, GUIDANCE, AND LEGISLATION Public Law 93–288 (PL 93–288) Robert T. Stafford Disaster Relief and Emergency Assistance Act (the Stafford Act; PL 100–707) The Federal Response Plan (FRP) Presidential Decision Directive 39 (PDD-39) PDD-62

PDD-63

The Nunn-Lugar-Domenici Act (an amendment to the Defense Authorization Act for FY97) The National Response Plan (NRP)

Provides legislative authority for Federal Government response to disasters Amends PL 93–288

Implements the Stafford Act Adds a Terrorism Annex to the FRP and divides response into phases of Crisis Management and Consequence Management Applies the Stafford Act to Unconventional and Terror Threats, Codifies the role of various Government Agencies in Terrorism Response Provides for the Protection of Critical National Infrastructure from Terror Threats, and specifically mentions Weapons of Mass Destruction (including Biological Weapons) Provided for training of First Responders in dealing with Weapons of Mass Destruction Supersedes the FRP and provides Federal Disaster Response efforts with a standardized National Incident Management Template

79 in the recent promulgation of a National Response Plan (NRP), now provides a framework for such disaster response. This framework forms the basis for a somewhat idealized planning and response effort, achievable, perhaps, in the United States and other developed nations. Efforts at disaster planning and response during complex emergencies and in developing nations obviously must be tempered with the realities of warfare, inadequate infrastructure, severe resource constraints, and all of the other myriad problems inherent in such settings. The institutional response to any disaster, natural or manmade, begins at the local level, and it is here that preparation efforts are perhaps most critical.53 It is also here that public health interventions will be implemented and the results of these implementations directly felt. Authorities at the California Emergency Medical Services Authority have recently identified 18 medical and public health functions, as well as 3 closely related response functions which should be considered in disaster planning and response at the local level (Table 79-3).54 1. Medical Needs Assessment. Prior to mobilizing an emergency response on behalf of a disaster-stricken population, information should be obtained regarding the extent of their immediate needs and the status of their supporting public health infrastructure. This task is accomplished through an organized needs assessment.55,56 The purpose of this initial assessment is to rapidly obtain objective, reliable, population-based information that describes a population’s specific need for various emergency relief services. Such an assessment should identify the extent of the needed response and the technical areas where specialized assistance is needed, and should suggest other areas where more focused health surveys or surveillance should be conducted (e.g., the nutritional status of the population and the status of water and sanitation). It is often impractical to evaluate the needs of all affected persons at a disaster site due to the size of the population and resource limitations. Relief personnel should instead sample representative cross sections from the affected population through a statistically valid sampling process using standardized assessment protocols.55–57 Such an activity requires knowledge

TABLE 79-3. LOCAL DISASTER MEDICAL AND PUBLIC HEALTH FUNCTIONS

Medical & Public Health Functions 1. Assessment of immediate health needs 2. Health surveillance & epidemiology 3. Identification of medical & health resources 4. Medical transportation 5. Patient distribution & evacuation 6. Pre-hospital emergency services 7. Hospital emergency services 8. In-hospital care 9. Out-of-hospital care 10. Temporary field treatment 11. Food safety 12. Management of hazardous agent exposure 13. Mental health 14. Medical & public health information 15. Vector control 16. Potable water 17. Waste management 18. Communicable disease control

Related Response Functions 29. Animal control 20. Coroner & mortuary services 21. Care and shelter Source: Adapted from information provided by the California Emergency Medical Services Authority.

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of the geographic distribution and size of the population, which may be obtained through census information, aerial photos, rapid surveys, and other sources. During sudden-impact disasters such as hurricanes, the initial assessment of the affected population should be completed as soon as possible, ideally within 24–48 hours.55,57 Slowly developing disasters such as endemic warfare and famines may require repeated emergency health assessments.56 2. Health Surveillance and Epidemiology. Public health surveillance is the logical continuation of the initial epidemiologic task of emergency health assessment. Surveillance systems should be established in sentinel sites (such as clinics) after disasters in order to monitor the health of the population and gauge the effectiveness of ongoing relief programs. This would be particularly important during the implementation of emergency programs that are likely to continue beyond the immediate aftermath of the disaster.58 Newer technologies such as e-mail, computers, and epidemiologic software permitted the rapid implementation of a statewide surveillance system in Iowa following the Great Flood of 1993.59 Among refugees in developing countries, critical public health surveillance targets include deaths, the appearance of malnourished children, and the occurrence of vaccine-preventable infectious diseases.56 Following a disaster, it is likely to be more effective to reestablish a preexisting surveillance system than to build a new system with external resources.60,61 Targeted investigations and surveys complement initial assessments and surveillance. For example, in some situations, the rapid assessment of the nutritional status of a population is a critical aspect of the development of appropriate relief programs.62 Investigation of outbreaks, surveys of vaccine coverage, and surveys for the prevalence of certain diseases are other common targets of more focused investigation. As public health information is collected through assessment and surveillance, relief interventions should be modified accordingly. In the absence of current data with which to evaluate the health of the target population, relief priorities and resources may easily become skewed.63,64 3. Identification of Medical and Health Resources. Medical and other health resources in a given locale should ideally be identified during the disaster planning process long before they might become needed in responding to an actual disaster. Personnel, equipment, and supplies available locally should be inventoried, and a realistic assessment made regarding ancillary resources which might readily be made available from state, regional, and federal sources. Memoranda of understanding (MOUs) and/or contracts should be proactively worked out between response agencies and local private sector institutions. A common problem concerning the preidentification of disaster response personnel surrounds the issue of “dual-hatting.” Recent disaster exercises have demonstrated that multiple agencies often rely on the same personnel to respond to a disaster.65 For example, a nurse in a local hospital may also serve as a military reservist and may also be a volunteer on a Disaster Medical Assistance Team (DMAT). When all three organizations rely on the presence of such a person, problems are sure to arise; such problems should be identified and resolved before a disaster occurs. On the other hand, in several response efforts, problems have arisen because of the presence of excessive numbers of well-intentioned but unneeded or poorly prepared volunteers and would-be providers. These “disaster tourists” sometimes consume more resources than they can provide.66 Thorough disaster planning includes plans for dealing with such problems. 4. Medical Transportation. Medical transportation assets should also ideally be identified during the disaster planning process before they are ever needed. Basic life support (BLS) and advanced life support (ALS) ground ambulances, as well as air ambulance resources should be catalogued and MOUs put in place during this planning process. Alternative sources of

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5.

6.

7.

8.

patient transport, such as bus companies, might also be examined. In developing nations and in resource-poor environments, primary reliance on such alternative methods of transport is often a necessity. Conversely, during many disasters, patients will arrive at treatment facilities by any means available. Following the sarin nerve agent attacks on the Tokyo subway system in 1995, over 4000 contaminated patients and “worried well” arrived at hospitals in private vehicles, despite the presence of a well-developed and available ambulance system.67 In contrast, only 452 victims arrived via ambulance. Similarly, the majority of victims of the 1995 Oklahoma City bombing arrived at hospitals in private vehicles.68 In a given disaster, the “worried well” may outnumber the actual sick and injured by a ratio of 10:1 or even 100:1, depending on the type of disaster. Larger numbers of “worried well” would be expected in the setting of a potential terrorist attack, where chemical, biological, or radiological contamination was a possibility. Disaster planners should be prepared for such eventualities. Patient Distribution and Evacuation. Regional disaster response plans will optimally plan for the rapid establishment of casualty collection and triage points, and project the number of casualties to be sent to each of the participating hospitals. These plans will ideally incorporate the emergency community, including ambulance assets for patient transportation. However, a major catastrophe may result in the destruction of hospitals, roads, bridges, and communications infrastructure. During the South Asia tsunami response of 2004–2005, portable military field hospitals were successfully deployed to bring medical assets to afflicted populations.69 This strategy moves medical assets into close proximity to those in need, and obviates a requirement to transport patients over long distances. Pre-Hospital Emergency Services. Sudden onset natural disasters have been the traditional model for understanding and organizing emergency relief services for disaster affected populations in the United States. For example, external medical services and rescue capabilities may be urgently needed after earthquakes to treat injured persons and to extract survivors trapped in collapsed buildings.44 This led to the development of specialized emergency services in many countries such as Urban Search and Rescue teams, which are designed to extract and treat entombed victims.26,70 Hospital Emergency Services. In a developed nation with established hospital facilities, the emergency department plays an important potential triage and treatment role in disaster response, especially the response to acute disasters such as earthquakes, fires, explosions, tornados, hurricanes, and the like. In such situations, however, emergency facilities can rapidly become overrun and resources exhausted. Moreover, in the event of a chemical attack or toxic exposure, emergency facilities can quickly become contaminated. During the 1995 sarin attack in Tokyo, staff exposure to sarin was a problem, as were the privacy issues raised by the requirement for large numbers of patients to undergo decontaminating showers.71 Prior planning can alleviate some of these problems. In the developing world and in chronic ongoing disasters such as famine and war, emergency facilities are likely to be unavailable or to play a lesser role. Proactive disaster response planning, nonetheless, must incorporate local emergency facilities into the planning process. In-Hospital Care. All hospitals should have plans in place in the event of a disaster. In fact, in the United States, the Joint Commission on the Accreditation of Healthcare Organizations (JCAHO) directs hospitals and other health-care institutions to conduct a hazard vulnerability analysis, develop an emergency management plan, and evaluate this plan annually.72 Such a plan could be implemented in the event of a disaster and must include an all-hazards command structure.

Many hospitals are now utilizing the “Hospital Emergency Incident Command System” (HEICS), which is designed to link with local governmental incident command systems.73 Another area of current concern relates to the need for planners to develop reasonable estimates and standards for bed requirements (by number and type) for various disasters, along with estimates (by number and specialty) of the supporting health-care providers necessary to staff those beds. 9. Out-of-Hospital Care. As is the case with hospitals, other medical and domiciliary facilities such as nursing homes, home health-care facilities, and community and public health clinics should also be prepared to respond in the event of a disaster. While such facilities may represent an important asset in times of crisis, they also pose unique problems. Whereas all hospitals have backup power generation capability, many outof-hospital care facilities do not. A large surge in emergency response calls and hospital activity during the August 2003 blackout on the U.S. eastern seaboard was attributed to the failure of respiratory devices and other medical equipment.74 Proactive community planning may help alleviate such problems and insure that out-of-hospital facilities remain an asset, rather than a burden, during a disaster. 10. Temporary Field Treatment. In certain disasters, medical treatment facilities may be rapidly overwhelmed or, worse yet, destroyed.75 Following the Gujarat earthquake of 2001, victims had to travel over 200 kilometers to reach unaffected hospitals in the “buffer zone.”66 Even in cases where treatment facilities are intact, prompt and proper treatment in the field may be necessary to save lives.76 In the United States, “strike teams” associated with the Metropolitan Medical Response System (see below) may provide such field treatment. In any case, local disaster plans must address the provision of temporary field treatment. 11. Food Safety. In the aftermath of mass casualty disasters, food processing and distribution may be seriously disrupted. Consequently, food distribution plans need to be incorporated into disaster response plans of governmental and non-governmental organizations. Lessons learned from the 2004 tsunami include the need to target food relief as a specific response, and the need to identify the most vulnerable populations (e.g., lactating women and those at the extremes of age). Challenges include the effective delivery of adequate quantities of food containing essential nutrients. Following the tsunami, multinational military services were instrumental in delivering food staples to afflicted populations. However, these consisted primarily of rice and noodles; there was concern regarding the delivery of protein, essential lipids, and vitamins.77 The use of prepackaged field rations may be a short-term solution. Another challenge is posed by the disruption of refrigeration and cooking in the wake of the disaster. An essential strategy involves educating the population at risk with a simple, straightforward message regarding the basics of food hygiene. Educational messages may be prepared well in advance, ready for distribution during crisis management. A fact sheet on food safety is available from the Centers for Disease Control and Prevention.78 Finally, the deliberate contamination of food has been used as a means of biological terrorism. Successful past attacks have utilized foods that are not cooked before consumption.79,80 These deliberate epidemics were not recognized until patients presented with illness, and future attacks of a similar nature are likely to be difficult to differentiate from sporadic point-source endemic food-poisoning events. Fortunately, the numbers of patients in previous intentional attacks have been relatively small; it is generally thought that this means of biological terrorism would be less effective than a well-executed aerosol attack. An effective response to a foodborne biological attack would utilize the same important steps used to counter naturally occurring foodborne epidemics:

79 recognition of the epidemic, identification of the etiologic agent, limitation of ongoing exposure, treatment of casualties, and prevention of future outbreaks.81 12. Management of Hazardous Agent Exposure. Hazardous materials may be released into the environment during natural disasters. Earthquakes, hurricanes, tornados, and floods may rupture petroleum and chemical storage tanks and overturn railroad stock; flooding may wash agricultural chemicals and fertilizers into drinking water supplies; infectious agents may even be released into the environment if hospital or scientific laboratories are damaged by earthquakes. Conversely, terrorist attacks may result in the intentional release of chemical, biological, or radiological agents into the environment. An important disaster response function involves the containment of such contamination. Since time is often critical in limiting the effects of such contamination, this function becomes, of necessity, a local responsibility. Local responders and governmental functionaries must have a basic understanding of hazardous agent management and response. 13. Mental Health. In addition to traditional public health concerns, disasters may present medical responders with patients who are suffering from complaints that are predominantly psychological in nature. In fact, mental health concerns may outweigh other medical concerns during the acute phase of disaster response.82 Such concerns may include the need for specialized psychological triage and treatment programs for victims. Emergency response personnel are also subject to short- and long-term effects as a result of stress imposed by the disaster and its response needs, particularly among persons required to be involved in postdisaster management of decedents.83 The psychological impact of disasters on children has only just begun to be documented but is clearly profound. Such impacts are likely to be even more significant if the disaster is produced by terrorism.84 Similarly, the appalling use of children as soldiers in many countries of the world will likely have long-term mental health consequences of unprecedented proportions.85 14. Medical and Public Health Information. One of the most important means of limiting the psychological trauma associated with a disaster is to provide timely, accurate, and relatively consistent information and risk communication. A disaster can provoke fear, uncertainty, and anxiety in the population, resulting in overwhelming numbers of patients seeking medical evaluation for unexplained symptoms, and demanding antidotes for feared exposure. Such a scenario could also follow a covert release when the resulting epidemic is characterized as the consequence of a bioterror attack. Symptoms due to anxiety and autonomic arousal, and side effects of postexposure antibiotic prophylaxis, may suggest prodromal disease due to biological agent exposure, and pose challenges in differential diagnosis. This “behavioral contagion” is best prevented by risk communication from health and government authorities which includes a realistic assessment of the risk (or lack thereof) of exposure, information about the resulting disease, and what to do and whom to contact for suspected exposure. Risk communication must be timely, accurate, consistent, and well coordinated, and the development of risk communication strategies, mechanisms, and messages prior to an event is strongly encouraged. As the epidemic subsides and public knowledge increases, public anxiety will decrease to realistic levels. This cycle of uncertainty, panic, response, and resolution occurred during the October 2001 anthrax bioterror attacks.86 The Centers for Disease Control and Prevention (CDC) has taken a proactive approach, featuring the development of Internet-accessible, agent-specific information packages for local public health authorities and the general public.87 Effective risk communication is predicated upon the preexistence of well-conceived risk communication plans and

15.

16.

17.

18.

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tactics. Similarly, plans must be made to rapidly deploy local centers for the initial evaluation and administration of postexposure prophylaxis (ideally decentralized to residential areas). Finally, plans must be made to proactively develop patient and contact tracing and vaccine screening tools, to access and rapidly distribute stockpiled vaccines and medications, and to identify and prepare local facilities and health-care teams for the care of mass casualties. The CDC smallpox response plan provides a template for such a coordinated, multifaceted approach. The benefits of farsighted planning and coordination were demonstrated by the efficient mass prophylaxis of over 10,000 individuals in New York City during the anthrax events of 2001.88 Vector Control. Certain disasters have been associated with a dramatic increase in the incidence of vector-borne disease. For example, following Hurricane Flora in 1963, a malaria epidemic occurred among the Haitian population.89 A similar increase in the incidence of malaria has been associated with the slowly developing El Nino “disaster.”90 The control of mosquitoes and other insect vectors is thus an important component of disease prevention following such disasters.91 Potable Water. Potable water is often the most important immediate relief commodity necessary for ensuring the survival of disaster-affected populations. Some water is necessary for drinking and cooking, but decreased water supplies also lead to inadequate personal hygiene. As a baseline, persons should have access to at least 15–20 liters of potable water per day.92,93 Heat stress and physical activity can substantially increase the human daily requirements for potable water to levels that are many times normal. Health authorities at disaster sites must plan for additional allotments of water to support clinical facilities and feeding centers and other public health activities. Waste Management. The proper management of human waste is also an important environmental health priority, particularly during disaster conditions. Earthquakes and floods frequently cause damage to sewage treatment facilities and cross-contamination of normally potable water sources. Consequently, the principal public health thrust of sanitation measures in emergency conditions is to reduce fecal contamination of food and water supplies. Communicable diseases that can be transmitted through contact with human feces include typhoid fever, cholera, bacillary and amoebic dysentery, hepatitis, polio, schistosomiasis, various helminth infestations, and viral gastroenteritis. Temporary latrines can be established in a disaster site in a variety of ways, including pits, trenches, and other chemical toilet methodologies.94 Communicable Disease Control. When infectious diseases occur after a disaster, they were almost invariably endemic before the disaster occurred. However, disaster conditions often serve to facilitate disease transmission and increase individual susceptibility to infection. Infectious diseases sometimes occur in a population that moves to a new location where an unfamiliar disease is endemic. For example, devastating malaria epidemics have occurred in nonimmune populations who were displaced to a malaria endemic area.95,96 The principal infectious disease problems in conflictrelated disasters have been measles, diarrheal diseases, acute respiratory infection, and malaria. During the Somali Famine (1991–1993), measles and diarrheal diseases accounted for the vast majority of the deaths among persons in temporary camps.48 Disease outbreaks during complex emergencies are usually the result of many factors, including a breakdown in environmental safeguards, crowding of persons in camps, lack of appropriate immunization programs, malnutrition, inadequate case finding, and limited availability of appropriate curative medical services. Despite the more limited potential for disease outbreaks following natural disasters, notable exceptions have occurred.

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During the Northridge Earthquake of 1995, the emergence of coccidiomycosis infections among emergency responders as a result of environmental contamination was a public health concern.97 Due to such threats and the propensity for epidemics to occur when the normal public health infrastructure has been damaged, it may be necessary to expand surveillance for certain diseases and rapidly institute appropriate disease control efforts following a disaster. Coping with infectious diseases following disasters involves a number of fundamental public health strategies applied to disaster settings. For example, in some settings, emergency measles vaccination programs, along with the administration of vitamin A, are critical and highly effective measures to prevent cases of measles and to reduce morbidity and mortality caused by this infection.98 With regard to diarrheal diseases, for which there are not effective immunizations, a combination of basic environmental measures to provide clean water and sanitation, plus rapid case finding and aggressive treatment (rehydration and, in some cases, appropriate antibiotics) can substantially reduce the consequences of diarrhea outbreaks. 19. Animal Control. Animal control issues frequently arise in the wake of a disaster. Carcasses can foul water supplies and spread disease. Surviving unsecured animals can serve as reservoirs for zoonotic disease outbreaks and contaminate water sources with urine and fecal matter.99,100 Animal deaths can result in ecological consequences and can represent the loss of a critical food source for a stricken population. Moreover, significant losses in the livestock industry can represent a major economic blow to the economies of many nations.101 Involving veterinary and animal husbandry personnel in disaster planning efforts at the local level can aid in ameliorating such consequences. 20. Coroner and Mortuary Services. Following a disaster, concerns often arise regarding the potential for disease transmission from decaying corpses. In reality, however, there is little evidence to suggest that serious epidemics arise from unburied corpses, and disease transmission following disasters is far more likely to be associated with survivors.102 Nonetheless, public concerns over dead and decaying bodies may present medical, psychological, and public relations problems. Local authorities must be prepared to address such concerns. Proactive planning in this regard (by designating temporary and makeshift morgues in advance, for example) may prevent the hasty and ill-conceived burial or cremation of remains before proper victim identification has been made. 21. Care and Shelter. Apart from access to water and food, shelter is often the most immediate need of disaster-stricken populations, particularly in cold weather. High mortality rates, particularly among the young and elderly, can occur when displaced populations are suddenly subjected to severe cold stress. Disaster planning efforts should include provisions for mass care and shelter, including shelter for the medically infirm. Typically, such provisions are made by nongovernmental agencies such as the Red Cross or Red Crescent. Medical planners should be prepared to support shelters with physician, nursing, and ancillary health support. Following some disasters, particularly conflict-related disasters, there may be substantially decreased availability of food, which can result in specific nutrient deficiencies, malnutrition, or outright starvation.50,103,104 Poor nutritional status increases susceptibility to communicable diseases such as measles and diarrhea. Indeed, the immediate cause of death in most malnourished persons is not usually starvation per se but, rather, infectious diseases.105 Emergency nutritional rehabilitation efforts for a starving population may involve a number of different types of programs to distribute food. During a food crisis, decisions must be made regarding whether emergency feeding programs should focus on widespread distribution of general

food rations, targeting specific food supplements to select highrisk groups (such as pregnant or lactating women), or on preparing food for consumption on-site in feeding centers. The type of food distributed is an important concern as well. Food must be culturally acceptable and must be nutritionally balanced. Donor-provided food has resulted in iatrogenic micronutrient deficiencies in some long-term relief operations.104 Sound program decisions should be based on information from rapid nutritional surveys as well as analyses of economic indicators that provide more detail on the nutritional status of the population and the context of the specific food shortage. During emergency famine relief, it is not the mere delivery of food to the disaster site that saves lives. The most rapid reduction in morbidity and mortality will occur when improvements in environmental health and communicable disease control accompany the restoration of proper nutritional resources.50,92,103 Because the lack of sufficient food in disasters is usually the result of many factors such as economic collapse, disruption of production, inadequate distribution, and other socioeconomic conditions, rather than a true lack of food, the long-term solution is in restoring an indigenous food economy, not in maintaining emergency feeding programs. STATE AND FEDERAL DISASTER RESPONSE (THE U.S. MODEL)

Prompt and competent disaster response at the local level has always been critical to preserving life, providing for public safety, and safeguarding public health. The response capabilities and organizational differences among the many thousands of local jurisdictions, however, have made standardization of disaster response plans, as well as communication among the various jurisdictions and response elements, quite problematic. Recently, the National Incident Management System and its component Incident Command System (ICS) has gained widespread acceptance as a standard model for response organization at local jurisdictions throughout the United States.106 Under the ICS, control of local response efforts rests with a designated local incident commander, typically the fire chief or chief of police. This incident commander can often summon groups of volunteer first responder and medical personnel, drawn from the Metropolitan Medical Response System (MMRS) under the auspices of the Department of Homeland Security’s (DHS) Office of Domestic Preparedness. As part of the MMRS, 122 local jurisdictions (as of this writing) have established emergency medical response capabilities. Under contract with local mayors, the MMRS elements can provide assistance with medical control, the extraction of victims, decontamination, triage, and medical treatment. While MMRS elements are able to respond to a range of disaster scenarios, the impetus for their formation has been recent awareness of the terrorist (particularly the WMD) threat, and the realization that response to a chemical, biological, or radiological event brings with it unique problems and requirements. The scene of a terrorist attack is, in addition to a disaster site, a crime scene. Handling of specimens originating from a potential terrorist event must, then, take into account proper evidence-handling procedures. Sampling should be coordinated with the local incident commander. The Association of Public Health Laboratories and the Centers for Disease Control and Prevention have developed a network of public and private laboratories, known as the “Laboratory Response Network,” prepared to respond to potential bioterrorist attacks in particular.107 Under this system, local hospital “Sentinel” (level A) laboratories would be capable of ruling out the presence of certain biological threat agents in clinical specimens. “Reference” (level B) laboratories in certain municipalities and regions would be capable of ruling in potential threat agents and performing susceptibility testing. More than 100 of these high-capability facilities now exist within established local public health, military, veterinary, agricultural, food, and water-testing laboratories throughout the United States. Similar facilities in Canada, Australia, and the United Kingdom serve an analogous purpose.

79 When response requirements exceed local capabilities, the local incident commander may request assistance from the state through the State Coordinating Officer (SCO). This SCO can then advise the governor to make available various state-level assets. These assets might include the law enforcement capabilities of the State Police and National Guard. Many state guards now include military “Weapons of Mass Destruction-Civil Support” (WMD-CS) teams, which can offer expert advice and provide liaison to more robust military assets at the federal level. These WMD-CS teams can also be prepositioned at “National Security Special Events,” such as political conventions, inaugurations, and other mass gatherings which might provide attractive targets to terrorists. Recently, such an employment was undertaken at the Super Bowl.108 In addition to WMD-CS teams, most state guards can provide public works assistance and mobile field hospitalization capability. Forensics laboratories are typically available through the state police or other state-level agencies. “Regional” (level C) laboratories, capable of providing sophisticated confirmatory diagnosis and typing of biological agents, are, in many cases, available through the State (and large city) Health Departments. When response requirements exceed the capabilities available at the state level, the state coordinating officer may contact the Federal Coordinating Officer (FCO). The FCO may activate a federal response under the auspices of the NRP.109 Under the NRP, federal consequence management is organized into 15 emergency support functions (ESFs), with each ESF being the responsibility of a specific federal agency. In addition, dozens of additional federal agencies can be tasked to provide assistance to these lead agencies. Federal disaster medical and public health support is provided for under ESF 8, and is primarily the responsibility of the Department of Health and Human Services. Among the 15 additional entities which support ESF 8 is the Department of Homeland Security, which oversees the Federal Emergency Management Agency (FEMA) and its National Disaster Medical System (NDMS).110 The NDMS includes numerous DMAT, consisting of trained medical volunteers that can arrive at a disaster site within 8–16 hours. The NDMS also includes a number of specialized teams, including Disaster Mortuary Operational Response Teams (DMORT), Veterinary Medical Assistance Teams (VMAT), National Pharmacy Response Teams (NPRT), and National Nurse Response Teams (NNRT). Finally, the NDMS is also capable of providing hospital bed capacity at numerous Department of Veterans Affairs, military, and civilian hospitals throughout the nation. Closely allied to the issue of medical and public health support are those of mass care, feeding, housing, and human services. These services, provided for under ESF 6 in the NRP, would be the primary responsibility of FEMA and the American Red Cross. Additionally, myriad other federal agencies would potentially contribute to disaster response. In the case of a potential bioterrorist attack, for example, the CDC, the United States Army Medical Research Institute of Infectious Diseases (USAMRIID), and the Department of Homeland Security’s National Biodefense Analysis and Countermeasures Center (NBACC) provide state-of-the-art “National Research” (level D) laboratories capable of sophisticated biological threat agent analysis. The Canadian Science Center for Human and Animal Health in Winnipeg provides a similar level of expertise. These labs, capable of banking strains, probing for genetic manipulations, and operating at Biosafety Level 4, would provide backup to regional laboratories at the state and large local health departments.121–123 Expert epidemiological consultation is also available from the CDC, and its Epidemic Intelligence Service (EIS), as are critical drugs and vaccines necessary to respond to a large-scale disaster. These pharmaceuticals are stockpiled at several locations throughout the country, available via the CDC’s Strategic National (Pharmaceutical) Stockpile (SNS) program for rapid deployment to an affected area.111 Release of stockpile components is currently controlled by the Department of Health and Human Services. An analogous asset, the National Emergency Services Stockpile System provides Canada with similar capabilities.

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TABLE 79-4. POINTS OF CONTACT AND TRAINING RESOURCES Local Law Enforcement Authorities∗ Local or County Health Department∗ State Health Department∗ Federal Emergency Management Agency: CDC Emergency Response Hotline: CDC Bioterrorism Preparedness & Response Program: CDC Emergency Preparedness Resources: Strategic National Stockpile: FBI (general point of contact): FBI (suspicious package info): Health Canada (suspicious package info): USAMRIID General Information: USAMRICD General Information: Armed Forces Radiobiology Research Institute: U.S. Army Medical NBC Defense Information:

http://www.fema.gov 770-488-7100 404-639-0385 http://www.bt.cdc.gov Access through State Health Dept 202-324-3000 http://www.fbi.gov/pressrel/ pressrel01/mail3.pdf http://www.hc-sc.gc.ca/english/ epr/packages.html http://www.usamriid.army.mil http://ccc.apgea.army.mil http://www.afrri.usuhs.mil http://www.nbc-med.org

∗

Clinicians and Response Planners are encouraged to post this list in an accessible location. Specific local and state points of contact should be included.

In the event of a disaster, and especially in the event of a terrorist attack employing WMDs, the military could provide several unique forms of assistance. In addition to laboratory support, biological threat evaluation and medical consultation are available through USA MRIID. Analogous chemical response capabilities are available through the U.S. Army Medical Research Institute for Chemical Defense (USAMRICD), and radiological capabilities are available through the Armed Forces Radiobiology Research Institute (AFRRI). Moreover, the military can provide advice and support to civilian authorities through the Chemical/Biological Rapid Response Team (CBRRT) and the Chemical/Biological Incident Response Force (CBIRF), a Marine Corps unit capable of reconnaissance, decontamination, and field treatment. Both the CBRRT and the CBIRF can be en route to a disaster site within a few hours of notification. Military support, when requested, would be subordinate to civilian authorities and would be tailored by the Joint Task Force for Civil Support, the component of the military’s Northern Command (NORTHCOM) designated to provide command and control for all military assets involved in disaster response missions and contingencies within the United States. Response to a disaster would likely constitute a complex undertaking requiring extensive cooperation among medical practitioners, civilian authorities, and officials at various levels of government. Health-care providers will require a thorough understanding of the principles of disaster medicine, basic trauma management, humanitarian relief operations, infection control procedures, and principles of personal protection. Moreover, they will also need a working knowledge of the components of our local, state, and federal response systems in order to function optimally in the event of an attack in their local area. Each practitioner and public health official should have a point of contact with such agencies and should be familiar with mechanisms for contacting them before a crisis arises. A list of useful points of contact is provided in Table 79-4. CONCLUSION

Many problems still remain in the effective implementation of emergency relief programs. In the Kurdish refugee crisis, despite a massive

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international relief effort, many deaths occurred due to preventable diarrheal disease.62 This mortality was in large part due to a failure to implement basic environmental health interventions and diarrhea control programs early enough in this particular crisis. During the 1994 Goma, Zaire, refugee emergency, as many as 50,000 persons died from cholera within the temporary camp system in only a matter of weeks,112 pointing out an urgent need for more intensive and focused training of relief workers to develop relevant expertise in the prevention and management of diarrheal diseases, as well as other essential elements of relief programs, such as measles immunization, public health surveillance, community outreach, and nutritional rehabilitation. A review of public health assessments and surveys conducted in Somalia demonstrated a lack of consistency in methodology, which led to difficulties in interpreting and acting upon critical public health data.113 Few training programs in Schools of Public Health have curricula that adequately cover the broad range of knowledge needed to cope with the public health issues associated with disaster-affected populations. Disasters do not affect all persons evenly. Thus, identifying and focusing on populations with special needs after disasters is a critical issue. For example, the unique concerns of women in disasters have become a greater focus in disaster relief in the last few years.114,115 Recent data suggests that in some disasters women have less access to medical care and other relief services.112 Additionally, while data is limited, pregnancy, sexually transmitted diseases, sexual abuse, and HIV infection are likely to be common issues among women,

especially refugees, in some disaster-affected populations. Few relief programs have sufficiently addressed these issues. The special problems of children in disasters are increasingly recognized.85,116 Children are much more vulnerable to many of the adverse health effects of disasters, such as malnutrition and infectious diseases. Additionally, the plight of unaccompanied children in Rwanda, and after the recent Indian Ocean tsunami, illustrated a problem common to many complex emergencies today.85 In disaster situations there are many other potentially vulnerable groups, such as members of a particular ethnic group, the elderly, and immigrants. The public health consequences of disasters are complex, multifactorial, wide ranging, and often long-lasting. Knowledge and experience from many health disciplines is needed for effective emergency response. Much needed health-care-related skills involve the disciplines of epidemiology, community health and primary care, environmental science, communicable disease control, and international health. Research is needed to develop standardized and valid assessment tools, reliable surveillance programs, low-technology environmental health interventions, and more effective intervention strategies. Unfortunately, the reality today is that many relief workers in the health sector, though well intentioned, are often recruited and deployed on short notice with little public health preparation or training. Schools of Public Health must continue to expand their training in the emergency skills that practitioners will need to deal with the public health needs of disaster-affected populations if the international community is to meet this challenge.

Maternal and Child Health Lewis H. Margolis • Alan W. Cross

INTRODUCTION

Maternal and Child Health (MCH) is the professional and academic field that focuses on the determinants, mechanisms, and systems that promote and maintain the health, safety, well-being, and appropriate development of children and their families in communities and societies, in order to enhance the future health and welfare of society and subsequent generations.1 This chapter provides an overview of MCH, highlighting the interactions among economic, social, cultural, educational, and health services factors that influence the population of children and families. In striving to assure the conditions for healthy mothers, women, and children, the field of maternal and child health focuses on four main strategies: (a) developing the public health infrastructure relevant to mothers and children; (b) providing population-based services; (c) offering enabling services; and (d) providing clinical services where gaps in availability are present.2 While maternal and child health issues are becoming increasingly globalized, the focus of this chapter is MCH in the United States. Most of the details of specific aspects of maternal and child health are covered in other chapters. HISTORY OF GOVERNMENT MCH SERVICES IN THE UNITED STATES

The health of women and children began to receive separate attention early in the twentieth century, in recognition of their greater vulnerability, particularly to socioeconomic and environmental forces, and the interdependence of the child’s health and that of the mother.3 In 1909 the first White House Conference on Child Health recommended the

formation of the Children’s Bureau, which, when established in 1912, proceeded to investigate the causes of maternal mortality (over 600 per 100,000 live births) and infant mortality (more than 100 per 1000 live births), as well as numerous other issues in social/economic welfare, education, and especially working conditions for children. The first federal support of maternal and child health services came with the Sheppard-Towner Act of 1921. By promoting birth registration and the establishment of maternal and child health divisions in many state and local health departments, this landmark legislation provides examples of both infrastructure building and population-based services. Title V of both Social Security Act of 1935 built upon the accomplishments of Sheppard-Towner, but also extended enabling and gapfilling services, especially to crippled children. Title V firmly established the principle of public responsibility for the health of mothers and children through a federal-state partnership. In the 1960s and early 1970s a host of additional programs were initiated by Congress, some through the mechanism of Title V and others through independent legislation. For example, Maternity and Infant Care Projects and Child and Youth Projects established relationships between Title V and individual communities, in contrast to states. Title XIX of the Social Security Act (Medicaid) and its childfocused Early and Periodic Screening, Diagnosis, and Treatment (EPSDT) vastly increased access to medical care for low-income children. Community Health Centers were developed to provide healthcare services, as well as enabling services for selected neighborhoods or catchment areas. Title X of the Public Health Services Act recognized a federal responsibility for providing family planning services, beginning in 1972. In the area of education, this period also witnessed the implementation of Head Start, which provided not only educational enrichment for low-income preschoolers, but also access to

79 health care. Similarly, the Education for All Handicapped Children Act (PL 94-142) (later renamed Individuals with Disabilities Education Act) created a right to a free education for children with disabilities. In the area of nutrition, programs such as the Women. Infants, and Children (WIC’s) Supplemental Food Program and enhanced school feeding programs sought to assure adequate nutrition, a cornerstone of health for children and mothers. Under President Reagan in the 1980s, what had become increasingly categorical maternal and child health services were reorganized into a Maternal and Child Health Services Block Grant. In return for more state autonomy and flexibility, states received less federal financial support for Title V services, and Title V funding has not kept pace either with inflation or a growing population with increasingly complicated needs and demands. The 1980s also witnessed increasing state autonomy and flexibility in other federal programs such as Medicaid. While improving access to care motivated many strategies during the 1960s and 1970s, efforts to control the rising costs of health services emerged in the 1980s and 1990s. Various models of managed care, for example, have been implemented in every state to attempt to control the escalating costs of Medicaid. Medicaid recipients have been shifted into managed care plans that for the most part restrict access to care through primary care providers. In many cases, health departments have assumed an oversight or accountability role to assure that managed care plans provide the agreed upon services for these high-risk populations. An example of cost control especially relevant to MCH was the limitation of postpartum hospital stays, even when providers and other caretakers counseled otherwise. Congress intervened with the passage of Newborns’ and Mothers’ Health Protection Act of 1996 (Public Law 104-204) which required a minimum stay of 48 hours. While MCH programs continue to provide gap-filling services and enabling services, much recent attention has focused on monitoring and evaluation through the development of national and state performance measures. Under the guidance of the Maternal and Child Health Bureau, state Title V programs have taken a leadership role in articulating needs, identifying strategies, and assessing the impact both of Title V and non-Title V programs on the well-being of mothers and children. It is important to underscore that Title V programs often identify needs and define a framework for action within a state, even though Medicaid and private insurance provide vastly more funding for actual clinical services. HEALTH INDICATORS

The development and continuous monitoring of health status indicators reflects one of the key infrastructure services at the core of maternal and child health. Many indicators are now routinely collected by a variety of health, economic, and social services agencies, but are routinely made available by the Maternal and Child Health Bureau, through the Title V Information System (https://perfdata.hrsa.gov/ mchb/mchreports/Search/search.asp). Although maternal mortality rates have reached a very low level (recently, about 11.8 deaths per 100,000 live births), this indicator can still serve as an important sentinel of failures in the health system. More generally, maternal health is better reflected in the population rates for a range of reproductive health outcomes: fertility (intended and otherwise), therapeutic abortion, birth, miscarriage, stillbirth, and especially low birth weight. Similarly, many process measures reflect the quality of maternity care: timing and quantity of prenatal care, place of delivery, attendant at delivery, vaginal or caesarian delivery, and complications (including those from nontherapeutic abortions). The infant mortality rate remains an important outcome measure for MCH. Linking infant birth and death records has added to the ability to assess factors associated with pregnancy outcome.4 The birth certificate form that was adopted in 1989 includes a wider array of information on both the mother and the child, offering opportunities

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for exploration of the relationships between sociodemographic factors, health and social services factors, and various pregnancy outcomes. Childhood morbidity is less routinely measured. Birth defect registries, neonatal intensive care use, discharge diagnoses, and national health surveys provide some estimates of morbidity. Immunization rates, school-based health data, and the data from such programs as EPSDT and Children With Special Health Care Needs (prior to the mid-1980s referred to as Crippled Children’s Programs) are also helpful indicators of child health, although they are not collected at either the state or national level as systematically as are infant birth data. Larger social and demographic changes are also important indicators of the status of mothers and children. Over the last 20 years there has been a dramatic increase in the percentage of mothers in the work force, creating challenges for families and service providers as the interests of mothers working outside the home have gained more prominence. The number of children in single parent families, either through divorce or the absence of marriage to begin with, continues to rise as do the numbers of homeless mothers and children. These social problems contribute directly or indirectly to most of the health problems of women and children. PRINCIPLES OF SERVICE DELIVERY

Several principles of service delivery stem from the unique focus of MCH on children and their families. Family-Centered Care. In a recently issued statement by the Maternal and Child Health Bureau, “Family-Centered Care assures the health and well-being of children and their families through a respectful family-professional partnership. It honors the strengths, cultures, traditions and expertise that everyone brings to this relationship. Family-Centered Care is the standard of practice which results in high quality services.”5 The child is not merely the passive recipient of the influences of the family, but, rather, plays an increasingly interactive role in the family, shaping in part the environment in which he or she lives. Similarly, the family works in partnership with the professionals providing services to children, especially where chronic diseases or disabling conditions are present. Developmental Perspective. The fetus and child are being continuously shaped by the normal developmental processes that result in a reasonably predictable series of changes from conception through adolescence. Progress over this course is a sensitive measure both of health and disease. Singular events or continuous disruption of normal development can have progressively magnifying adverse effects on the fetus or child. Because of the importance of development, prompt identification of problems and early and continuous intervention hold the greatest promise for achieving the best outcome. Health Promotion and Disease Prevention. Childhood is both a means to adulthood and an end in itself. There is great potential, therefore, for health promotion and disease prevention to benefit both the current child and the future adult. However, careful attention must be paid to the immediate implications of interventions that are aimed at preventing problems in the distant future, making sure that the desired long-term benefits are not counterbalanced by short-term hazards. CURRENT PRIORITIES

Preconceptional Health Promotion. Many of the critical phases of fetal development have already occurred before a woman is even aware that she is pregnant. Optimum fetal health, therefore, requires attention to maternal health and health-related behaviors even before conception. Efforts to counsel women before conception to avoid alcohol, drugs, tobacco, and other fetal hazards are currently being

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tested to determine the impact on pregnancy outcome.6 The demonstrated efficacy of periconceptional dietary folic acid in the prevention of neural tube defects has resulted not only in extensive health education campaigns about the importance of supplementation for women in their child-bearing years, but also mandated fortification of bread. Family Planning and Abortion. Optimum health for both mother and child has long been known to be related to maternal age, spacing of children, and the balance between family resources and family size. The ready availability of birth control and the option for abortion have provided means of achieving family planning, although financial, administrative, and clinical barriers continue to limit access.7 For example, despite the recommendations of the scientific advisory panel to the Food and Drug Administration that Plan B, a hormonal contraceptive that is effective in preventing pregnancy for up to 72 hours after sexual intercourse, be made available without prescription, political considerations have delayed implementation.8 Prenatal Care. Improving access to and quality of prenatal services continues to be a challenge with no obvious solution. Expansion of Medicaid to include women up to 185% (and beyond at state option) of the federal poverty level in comprehensive services has made prenatal care more accessible. Some states have developed innovative programs to improve quality and access for the poor, and many local community-based projects have also been created with these goals in mind. Perinatal health. The U.S. infant mortality rate has slowly declined, reaching a low of 6.8 per 1000 live births in 2001, and rising slightly to 7.0 per 1000 live births in 2002. The ranking of the United States continues to fall, however, compared to other nations, currently twenty-eighth in the world. Disparities among racial/ethnic groups in perinatal indicators is a major focus of research, both on epidemiological determinants of low birth weight and prematurity and interventions to continue and enhance the downward trends in these indicators. The United States lags behind all other developed countries in the provision of most services to mothers and children. Immunization. The past 10 years have witnessed critical new developments in this fundamental component of MCH. An acellular pertussis vaccine has greatly reduced the complications of the historical whole-cell vaccine.9 The use of conjugated vaccine against Hemophilus influenzae in infants as young as 2 months of age has significantly reduced the incidence of meningitis in infants. The hepatitis B vaccine is now widely used in the prevention both of hepatitis and the consequent hepatic cancer—both major problems, particularly in developing countries. The eradication of polio from the United States has led to a switch from oral polio vaccine to inactivated vaccines to reduce the incidence of paralytic reactions to the oral vaccine. Oral polio vaccine is still the vaccine of choice for global eradication.9 Children’s Injuries. Injuries are the leading cause of death from the age of 1 year throughout childhood, adolescence, and beyond. While the resources devoted to this major public health problem are not proportionate to the need, much progress has been made in reducing children’s injuries. For example, many states have implemented graduated driver license programs to introduce new young drivers to increasing risks gradually, resulting in dramatic reductions of 20–30% in teen crashes. Childcare. With the large proportion of families where both parents work outside the home or a single parent works outside the home, childcare remains central to the field of maternal and child

health. Oversight of health, safety, and educational performance necessitates collaboration among many professional and lay groups with interests in children, a convening role that is consistent with the definition of MCH. Child Abuse and Neglect. Abuse, including sexual abuse, continues as an important risk factor to the well-being of children, not only during childhood, but into their adult years. Reports of abuse and neglect persist at over 1%, but the incidence of these threats to children is likely much higher than the official reporting statistics would indicate. Children with Special Health Care Needs. Title V programs, as well as educators, health-care providers, and advocates, have devoted increasing attention to children who “have or are at increased risk for a chronic physical, developmental, behavioral, or emotional condition and who also require health and related services of a type or amount beyond that required by children generally.”10 With upward of 18% of U.S. children potentially with special needs, the infrastructure, population-based, enabling, and gap-filling approach of MCH is especially effective for these children and their families. In addition, Title V programs have taken a leadership role in defining and addressing the challenges associated with the transition from childhood to adulthood for individuals with special needs. Community-Based Social Support. Pregnant women and young children thrive best when they are surrounded by friends and relatives who provide companionship and assistance. As unwed motherhood becomes more common and the extended family further disintegrates, more young families face isolation and inadequate social supports. To remedy this, several programs have utilized home visitors to befriend and work closely with pregnant women and young families, offering the assistance and social support that are so often inadequate. Some of these programs have been able to demonstrate benefits in health and well-being associated with participation in the program.11,12

FUTURE DIRECTIONS

At the beginning of the twenty-first century, the field of MCH has perhaps devoted greater attention to developing the core functions of public health than any other field. The focus on community assessment, policy development, and assurance guides resource allocation decisions at the federal and state levels. Attention to the core functions, however, faces the challenges that come from the historical and ongoing tension in the United States between individual/private responsibility on the one hand and/or public responsibility for the well-being of mothers and children on the other. This stands in marked contrast to the approach taken toward the population of seniors. Whereas programs for children and families tend to fall within the purview of state governments and depend on discretionary funding, programs for seniors have become a federal responsibility through programs such as Old Age and Survivors Benefits, Medicare, and in the case of long-term care, Medicaid. In carrying out the core functions of public health, the field of MCH often makes contributions that are not readily visible to policy makers and taxpayers. As the demands for resources increase in a world defined by an aging population, external threats such as bioterrorism or pandemic infections diseases, federal priorities run the risk of being skewed toward those more apparent challenges. The role of the field of MCH is to build on its rich history by continuing to articulate the needs of the population of children and mothers with a commitment to the goal that any strong nation must appropriately invest in its future.

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Preventive Medicine Support of Military Operations Robert L. Mott

A corps of medical officers was not established solely for the purpose of attending the wounded and sick; the proper treatment of these sufferers is certainly a matter of a very great importance, and is an imperative duty, but the labors of Medical Officers cover a more extended field. The leading idea, which should be constantly kept in view, is to strengthen the hands of the Commanding General by keeping his army in the most vigorous health, thus rendering it, in the highest degree, efficient for enduring fatigue and privation and for fighting. ——Dr. Jonathan Letterman, Surgeon, Army of the Potomac, 1862 to 18641

By congressional statute, military commanders are responsible for the health of their commands. The command “surgeon” serves as the commander’s principal medical staff advisor, and in this role, he or she participates in the development of command plans and policies. The command surgeon, usually with the assistance of a staff preventive medicine officer, advises the commander on the health status of the command, threats to the health, and policies and practices to protect the health of military personnel and others associated with the operation. Preventive medicine programs for military units and personnel are designed to preserve and promote health and to prevent physical and mental diseases and disabilities. Knowledge of the environment in which the programs are to be effected is essential to assess the physical, chemical, and biologic hazards to which military personnel may be exposed. During military operations, besides the risk of injury from the weapons of war, principal hazards include accidents with machines, especially motor vehicles, explosives, and fire; exposures to noise, smoke, and toxic fumes; extremes of altitude, heat, and cold; and a host of infectious diseases, many with the capacity to produce catastrophic morbidity in deployed forces (e.g., malaria, dengue fever, and sand fly fever). The dissolution of the Soviet Union substantially altered the nature of the threat to global and U.S. national security, and along with it, the U.S. national military strategic response. U.S. military forces were formerly preoccupied with the potential for large-scale, highintensity armed conflicts, especially in the defense of Europe. The primary strategic concern has now shifted to the containment of regional ethnic and religious conflicts and to the prevention of terrorist attacks against U.S. interests, both at home and abroad. The use of commercial aircraft as terrorist weapons on September 11, 2001, followed closely by anthrax attacks in the eastern United States, dramatically elevated concerns about the use of weapons of mass destruction to include CBRNE. In addition, the nearly unprecedented destruction from hurricane Katrina in 2005 demonstrated the ongoing need for military support during domestic emergencies. The effect of these trends has been to increase the mission diversity of the U.S. Armed Forces to include not only fighting war, but also antiterrorism, peacekeeping, humanitarian assistance, domestic and international disaster relief, and support to civil authorities. This, in turn, requires the medical and preventive medicine capacity to provide highly flexible and mobile support over long distances and in widely diverse environments. FIELD PREVENTIVE MEDICINE ORGANIZATION

In “Joint” operations, such as Operation Iraqi Freedom, the deployed force will usually include combat elements from the Army, Marine

Corps, Air Force, and Navy. The Joint Task Force (JTF) will be tailored, or “task organized” with respect to the kinds of units and their size so as to be able to accomplish the mission articulated for it by the Joint Chiefs of Staff. Each combat unit (Army and Marine divisions; Air Force tactical fighter wings, etc.) has its own “organic” support elements (meaning support units that belong to the combat unit), including medical and preventive medicine units and personnel. At the combat unit level, preventive medicine capabilities include water testing for chlorine residuals and bacterial coliforms and limited vector control. Backing up the organic medical support units are additional medical units under the command and control of the JTF commander, and under the technical supervision of the JTF surgeon. These assets may include epidemiology, entomology, environmental sanitation, and environmental engineering capabilities. The Army also has established deployable laboratories which perform the functions of public health laboratories in the Theater of Operations. In addition, the Air Force maintains an aerial spray squadron, with aircraft configured to spray insecticide over large areas, should it become necessary to control widespread vector-borne disease outbreaks in the deployed force. DISEASE AND INJURY PREVENTION IN OPERATING FORCES

There are five key elements of the strategy for disease and injury prevention among forces deployed in field and combat operations: 1. Before force deployment, perform a medical threat assessment to determine the nature and magnitude of the disease and injury threats in the planned area of operations. 2. Identify the principal countermeasures that must be emphasized to reduce the threats to an acceptable level. 3. Promulgate countermeasures among the operating forces and train individuals and leaders in their use. 4. Enforce the countermeasures in the operational area. 5. Conduct medical surveillance to monitor the health of the deployed force and to identify events that require preventive medicine interventions.

Medical Threat Assessments The threats to health from disease and nonbattle injury (DNBI) in a deployed military force depend principally on the mission and composition of the force, the geographical area of operations, including the diseases that are endemic in the area, the time of year, and the intensity of the conflict. DNBI rates in past conflicts have invariably exceeded battle injury rates and have resulted from naturally occurring infectious diseases (e.g., malaria, dengue fever, and sand fly fever); environmental extremes of heat, cold, and altitude; motor vehicle accidents; athletic injuries; and psychological stresses. In operations in Bosnia and Iraq, industrial chemicals and radioactive waste were considered to be potential threat agents. During operations Desert Shield and Desert Storm, rates of hospitalization due to DNBI were extremely low in comparison with previous conflicts because of a unique set of favorable circumstances: (a) good medical intelligence about the area before the deployment; (b) sound preventive medicine policies that, for the most part, were rigorously subscribed to and enforced by unit commanders; (c) the religious proscriptions of the host nation; (d) a measured and unimpeded buildup phase; and (e) a relatively brief ground combat phase

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TABLE 79-5. U.S. ARMY DNBI RATES ∗ IN OPERATIONS FROM WWII THROUGH DESERT STORM Combat Troops World War II Korean War Vietnam Desert Shield Desert Storm

1.98 1.67 0.89 0.34 0.41

Support Troops 1.60 2.14 0.92 — —

∗

Per 1000 per day.

(Table 79-5).2 Decreasing DNBI rates continued in Operations Iraqi Freedom and Enduring Freedom (Afghanistan) even though there were multiple cases of cutaneous leishmaniasis3, diarrheal disease,4 eosinophilic pneumonia,5 and malaria.6 As a general rule, naturally occurring infectious diseases are likely to remain the most important causes of preventable medical noneffectiveness in most future overseas deployments. In past wars involving U.S. forces, infectious diseases have produced higher morbidity rates than battle injuries, and until World War II, higher mortality rates as well.7–9 The infectious diseases causing high morbidity among U.S. forces in past wars, arranged more or less in the relative order of their importance, are shown in Table 79-6.10 Because deployed troops usually must live and work under relatively primitive conditions, they are also at risk for “emerging” infectious diseases. As one example, hemorrhagic fever with renal syndrome due to Hantaan virus was first reported in Japanese and Soviet troops in Manchuria just before World War II, affected UN troops during the Korean War, and continues to be reported among Korean and U.S. soldiers in association with field operations along the demilitarized zone (DMZ) in South Korea.11 As a second example, cutaneous leishmaniasis due to Leishmania tropica was known to be endemic in the Persian Gulf region before the deployment of U.S. troops on Operations Desert Shield and Desert Storm. However, the capacity of the parasite to “visceralize” (i.e., to invade liver, spleen, and bone marrow) was not well documented before its appearance in returning U.S. troops.10 Cutaneous leishmaniasis was a significant cause of morbidity in Operation Iraqi Freedom, and its treatment often required medical evacuation to the United States.3 Wound infections with Acinetobacter baumannii in service members returning from the Middle East were also a challenge for clinicians, infection control, and preventive medicine personnel.12

TABLE 79-6. INFECTIOUS DISEASES CAUSING HIGH MORBIDITY IN U.S. FORCES IN PAST CONFLICTS: WORLD WAR II, KOREA, VIETNAM, OPERATION DESERT STORM, OPERATION IRAQI FREEDOM Acute respiratory disease and influenza Acute diarrheal disease Malaria Hepatitis Sexually transmitted diseases Arthropod borne diseases∗ Rickettsial diseases† Leptospirosis Leishmaniasis Schistosomiasis

All All WWII, Korea, Vietnam WWII, Korea, Vietnam WWII, Korea, Vietnam WWII, Vietnam WWII, Vietnam WWII, Vietnam WWII, Desert Storm, Iraqi Freedom WWII‡

Abbreviation: WWII, World War II. ∗ Especially dengue fever, sand fly fever, hemorrhagic fevers, encephalitides. † Principally scrub typhus, whose distribution is limited to parts of Asia and northern Australia. ‡ Principally in engineer bridge-building units in Luzon, Philippines. Source: Legters LJ, Department of Preventive Medicine and Biometrics, Uniformed Services University, Bethesda, MD, 1992.

The purpose of medical threat assessments is to help decide on the specific disease and injury countermeasures that must be planned for use by the force. The information needed to develop such assessments for a particular country or region is available from a variety of sources, including statistical reports of national and international health agencies, publications in general medical literature, medical historical data from previous operations in the area, and the unpublished observations of health-care personnel and epidemiologists working or visiting in the geographical areas of interest. In addition, in a number of widely dispersed geographical areas, the U.S. Army and Navy maintain medical research laboratories dedicated to the study of the epidemiology and prevention of regional medical problems of potential military importance. The U.S. Navy also maintains a number of Navy Environmental Preventive Medicine Units (NEPMUs) with regional responsibility for updated assessments of current health risks in areas of possible deployment of Navy and Marine forces. The collection and evaluation of medical information from these various sources and the preparation of a variety of medical information products for particular countries and regions are accomplished by the Armed Forces Medical Intelligence Center, the Defense Pest Management Information and Analysis Center of the Armed Forces Pest Management Board, and servicespecific preventive medicine organizations. The Army and Navy overseas laboratories and the NEPMUs are excellent sources of current information because they have personnel working “on the ground” in regions of interest, constantly updating the medical threat assessments. During the devastating tsunami in 2005, teams from overseas laboratories in Thailand and Indonesia conducted rapid public health assessments in support of the humanitarian response.13 The laboratories are also well placed to assist with surveillance for diseases, like avian influenza, which have outbreak and pandemic potential.

Identifying the Countermeasures and Promulgating the Force Preventive Medicine Program In military operations there are two general kinds of disease and injury countermeasures: those taken by or applied to individual soldiers and those taken by the unit and applied to the environment in which the unit is operating. Individual countermeasures are those that alter the individual in some way to increase refractoriness to the various risks, including immunizations, prophylactic drugs, insect repellents, protective clothing, and safety equipment. Environmental countermeasures are those directed at removal or attenuation of environmental risk factors, including measures directed at the provision of potable unit water supplies and sanitary food supplies, the sanitary disposal of wastes, and the control of disease vectors and animal reservoirs of disease. In addition, in the development and testing of major items of equipment (armored vehicles, artillery pieces, etc.), attention is paid to the design of the equipment so as to minimize the risk of injury from its use. For example, the ventilation system in the Bradley fighting vehicle (and other armored vehicles) is designed to rapidly remove from the troop compartment the smoke and gases generated by the combustion of ammunition propellants during weapons firing. In the highly mobile tactical operations characteristic of modern warfare, it is frequently necessary to place nearly total reliance for disease and injury prevention on individual countermeasures applied under the direction of the lieutenants and sergeants at the platoon and squad level. In more stable tactical situations and in rear areas, it is possible to place heavier reliance on environmental controls applied by the units themselves or by combat service support units (engineer, quartermaster, and medical) on an area basis. Besides the function of disease vector control, which is accomplished by specialized medical units, most environmental controls are the responsibility of nonmedical personnel and units. For example, in the Army, quartermaster units are responsible for food and water procurement and distribution. Medical personnel and units, to include Army veterinarians, retain responsibility for technical inspections to ensure compliance with prescribed sanitary standards. Malaria is perhaps the best example of a highly significant military disease problem that would receive the careful attention of preventive medicine planners during preparations for deployment to known

79 malaria-endemic areas. Decisions about the countermeasures to be employed by the force would be written into the medical annexes of the operations orders; these have the authority of command directives. These decisions would also represent the basis for procurement of medical supply items for use in the prevention and control of malaria, such as drugs for chemoprophylaxis and treatment, bed nets, and insecticides and insecticide dispersal equipment for mosquito control. A primary consideration would be the malaria chemoprophylactic regimen to be used by the force. Factors that would be taken into consideration in determining the malaria chemoprophylactic regimen include the malaria prevalence in the region, the predominant infecting species, and the prevalence of drug-resistant Plasmodium falciparum and Plasmodium vivax. Besides the chemoprophylactic regimen, other individual countermeasures against malaria that would be addressed include use of the standard-issue insect repellent (diethyltoluamide [DEET]), which would be used on exposed skin surfaces in conjunction with the permethrin-impregnated battle dress uniform (BDU), the proper wearing of the uniform (“shirts on, collars buttoned, sleeves rolled down, from dusk to dawn”), and the use of permethrin-treated bed nets in secure areas. Area malaria control programs in the operational area, including insecticide dispersal methods, would be devised based upon on-site professional entomological surveys conducted to determine the principal malaria vector species, their breeding sites, and adult mosquito biting and resting habits. Additional environmental controls that might be addressed include policies regarding campsite selection in relation to native villages, whose inhabitants might represent a reservoir of malaria infection, the use of indigenes in labor forces, and medical civic action programs directed at reduction of the size of the malaria reservoir though the identification and treatment of infected individuals.

Training Personnel to Use Countermeasures As noted, it is frequently necessary to rely almost entirely on individual countermeasures for disease and injury prevention in the early stages of deployments and during other kinds of offensive operations. During these periods, the combat service support units responsible for the implementation of area environmental controls ordinarily will be given a lower priority for transport than the combat elements. The medical personnel present in the forward areas will be those who are assigned to the combat units, and they will be more preoccupied with the care of combat casualties at the time than with the institution of environmental countermeasures. Moreover, it is during this period, in the disorganization of battle and before the construction of any permanent facilities, such as barracks, latrines, and mess halls, that troops are most vulnerable to vector-borne disease transmission, including diseases with the demonstrated capacity to produce catastrophic morbidity in fighting forces. The individual countermeasures determined to be necessary for use by the force must be integrated into predeployment training programs (see Table 79-7).14 Through repetition and constant

TABLE 79-7. INDIVIDUAL PREVENTIVE MEDICINE COUNTERMEASURES TO BE EMPHASIZED IN TROOP TRAINING EXERCISES Safety first: Use common sense during occupational and recreational activities Do not consume unapproved food, water, or ice Drink water frequently during the day Wash hands after using the latrine and before meals Take your malaria prevention pills when instructed to do so Wear permethrin-treated uniforms with trousers bloused and sleeves down Keep DEET insect repellent on exposed skin Sleep under a permethrin treated bed net Follow work-rest cycles to prevent heat injuries Avoid contact with all animals Defecate only in constructed latrines or designated areas Wear hearing protection during military operations

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reinforcement by the lieutenants and sergeants at platoon and squad level, it is to be expected that the application of individual countermeasures will become second nature among the troops. The principal prerequisite for ensuring that the desired health behaviors are incorporated into each individual soldier’s repertoire is to convince the lieutenant and sergeant leaders of small tactical units that the countermeasures are important to the success of their unit’s mission.

Rigorous Command Enforcement of Countermeasures Enforcement of the use of countermeasures is a command function. The appearance in a unit of cases of a specific disease that should have been prevented by the application of the command-directed countermeasures (e.g., cases of malaria that should have been prevented with the prescribed chemoprophylaxis) should bring about an epidemiological investigation to determine if the outbreak was due to unexpected failure of the prescribed countermeasures to prevent the cases (e.g., the malaria parasites are resistant to the prescribed chemoprophylaxis) or the result of command failure to enforce the countermeasures (e.g., soldiers are not taking the prescribed chemoprophylaxis). If the investigation shows that the cases are the result of failure of the prescribed countermeasures, then better methods must be decided upon and put in place quickly. If due to the latter, commanddirected disciplinary action may be warranted. In this connection, Field Marshall Sir William Slim, commander of the British Army in Burma in World War II, in his personal history of the period, stated: Good doctors are no use without discipline. More than half the battle against disease is fought, not by doctors, but by the regimental officers. . . . When mepacrine was first introduced . . . often the little tablet was not swallowed. An individual medical test in almost all cases will show whether it has been taken or not. . . . I, therefore, had surprise checks of whole units, every man being examined. If the overall result was less than ninety-five per cent positive I sacked the commanding officer. I only had to sack three; by then the rest got my meaning.15

Conducting Medical Surveillance Medical surveillance of the deployed force is necessary to continuously monitor the health status of the force, ensure that preventive medicine countermeasures are working, rapidly identify disease and injury threats that have the potential to compromise the combat effectiveness of the units, and if necessary, develop and recommend preventive medicine interventions to the appropriate unit commanders. As noted above, it is the commander who is ultimately responsible for the health of the command and the implementation of disease and injury countermeasures. Before Operations Desert Shield and Desert Storm, disease and injury surveillance programs during military operations were, for the most part, decentralized to brigade, regiment, and division level; were dependent upon the ad hoc, usually less than systematic observations of unit surgeons; and were frequently subject to reporting delays to higher headquarters, which prevented timely interventions from that level. During Operations Desert Shield and Desert Storm, U.S. Navy and Marine Corps medical personnel systematically recorded outpatient disease and injury data by category of illness or injury (heat and cold injury, diarrhea and gastrointestinal infections, dermatologic conditions, respiratory conditions, injury or orthopedic conditions, unexplained fever, sexually transmitted diseases, ophthalmologic conditions, psychiatric conditions, and other acute conditions) and reported these data weekly using a standard format. Unit strength figures were included in reports to permit the calculation of rates by unit, location, and in the aggregate. The system is credited with the identification of a force-wide diarrheal disease outbreak early in the operation related to the serving of fresh lettuce in U.S. Marine Corps field messing facilities; the lettuce was being provided along with other fresh foods by indigenous contractors outside the network of

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sources approved by the U.S. military. Rates had increased simultaneously throughout the force, exceeding 8% per week in some locations. A command decision was made to ban the use of lettuce in Marine Corps field messing facilities, which was followed by a precipitous decline in rates of diarrheal disease in the force to around 1% per week.16 Newer DNBI surveillance efforts rely on electronic medical records which allow the documentation, reporting, and analysis of specific diagnoses. This promising new program should improve the specificity and timeliness of disease reporting thereby facilitating outbreak response efforts. However, this system will also have limitations because case (numerator) data must still be combined with sometimes difficult to obtain population (denominator) data to permit the calculation of rates, and the electronic records may not be available at far forward levels of care and will be likely be impractical during intense combat operations.

OTHER MILITARY PREVENTIVE

MEDICINE MISSIONS The field missions described above are clearly important to military operations but they do not fully reflect the wide variety of activities that define military preventive medicine. Military preventive medicine professionals are also involved in policy and doctrine development at multiple levels within the Department of Defense; basic and applied research on infectious diseases, injuries, and environmental threats; managing the equivalent of county and state health departments; developing national- and international-level programs; teaching at the masters and doctorate levels; assisting with humanitarian assistance and disaster relief operations; and serving as medical executives in one of the largest health-care organizations in the world.

Public Health Workforce Kristine M. Gebbie

INTRODUCTION

The wide range of activities subsumed under the rubric of public health practice is provided by a workforce no less diverse. In the most recent effort to enumerate public health workers in the United States,1 448,254 were identified in federal, state, and local public health agencies; schools of public health; and in voluntary organizations actively collaborating in meeting public health needs, such as the American Red Cross and the March of Dimes (see Table 79-8). Compared to some sectors of the economy, the public health workforce is overwhelmingly professional (at least 40% can be identified as members of a professional category), enriched by a wide range of technicians (in laboratory, environment, and informatics, to name a few areas) and critical support staff in administrative, data entry, transportation, and other tasks. The discussion is complicated by the fact that in the enumeration process, over 24,000 professional staff (those with baccalaureate or higher education) could not be specifically identified, and nearly 98,000 workers could not be assigned even to a general category such as professional or technical. Whatever the detail, the actual workforce is larger than reported, as public health activities are spread across multiple agencies at all levels of government, only a few states have made efforts to identify all parts of the public health enterprise within the jurisdiction, data from local agencies are limited, and there is no agreed-upon definition of the full range of nongovernmental participants to include.

The Disciplines of Public Health The two largest groups of professionals identified in public health practice are public health nurses (50,000) and environmental health professionals (15,000). In addition to these, physicians, health educators, laboratory scientists, and epidemiologists are most likely to be mentioned as important contributors to public health. In the early history of public health, it was those with an environmental focus, including engineers, who made some of the most striking contributions, assuring that drinking water was safe, sewage systems installed, and waste products appropriately handled. As the specific causes of diseases became known in the first half of the twentieth century, physicians with public health training became more prominent, and measures of disease prevention such as isolation of infected persons, tracing of individual contacts, and vaccination became important tools. The complete list of professions associated with public health

practice includes all of those associated with medical care (dentist, pharmacist, physical and occupational therapist, psychologist), others less frequently seen in patient care settings (occupational health and industrial hygiene, law, veterinary medicine), and many with important analytic and data skills (biostatistics, economics, informatics). The professions in public health are supported by an impressive array of technicians and paraprofessionals as well. Laboratory technicians, dental technicians, computer technicians, community outreach workers, and environmental technicians are all represented. In addition, because much of public health depends on documentation and communication, there is a rich array of administrative and data management support staff. One of the complications in both describing and studying the public health workforce is that any one individual can often be described by several labels: the discipline in which he or she has formal training, the job title assigned by the employing agency, the functional activity in which the majority of time is spent, and the program in which this takes place. For example, an MD might be hired as a public health program specialist and spend the majority of time planning and conducting outbreak investigations in the sexually transmitted disease control program. Or a laboratory technician may be hired as an investigator and spend the majority of time visiting community-based laboratories to support a quality assurance program in lead testing. What unites all of these groups is the common attention to the health of populations, rather than individuals. The specific functions any one worker may be asked to fulfill are often not specific to the discipline in which he or she was trained, but rather a service to the community to which the world-view of that discipline can contribute. For example, in developing a community-wide health education program on reduction of tobacco use, physicians, health educators, environmental health specialists, nurses, and media specialists might all be employed under the programmatic title, “A Clean Indoor Air Team,” and would pool their various perspectives into a single programmatic effort that might eventually be carried out in a community through the media, volunteers, hospital staff, and public health nurses. Nurses provide one example of the diversity of public health work and workers. For over a hundred years public health nurses have been “promoting and protecting the health of populations using knowledge from nursing, social and public health sciences.”2 This effort has taken many forms, and led practitioners from crowded urban tenements to isolated farms to suburban workplaces, from healthy children to tubercular workers to the elderly seeking to maintain their

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TABLE 79-8. ESTIMATED NATIONAL PUBLIC HEALTH WORKFORCE BY LEVEL AND LOCATION OF EMPLOYMENT

Category

Federal Agencies

Officials and Administrators Professionals Technicians Protective Service Paraprofessionals Administrative Support Skilled Craft Service/Maintenance Category Unreported Volunteers

1152 58,897 11,695 429 1236 11,841 17 44 443 —

Total w/Volunteers Total w/o Volunteers

Voluntary Agencies — 8012 — — —

State and Territorial Agencies

Total

— — 7373 2,864,825

14,768 133,116 29,815 841 18,342 40,071 1166 4676 104,320 5

15,920 200,025 41,510 1270 19,578 51,912 1183 4720 112,136 2,864,830

85,754

2,880,210

347,120

3,313,084

85,754

15,385

347,115

448,254

Source: Health Resources and Services Administration. Enumeration 2000. New York: Columbia University School of Nursing; 2000.

independence. While it is difficult to say that there is a “typical” public health nurse, there are commonalities across many agencies of different sizes, serving diverse communities. Public health nurses are usually employed to work in those public health programs that require some contact with individuals, especially if that contact involves some aspects of “hands-on” clinical practice. This includes the staffing of immunization clinics, sexually transmitted disease and tuberculosis control programs, child and maternal health services, senior health promotion programs, and workplace health clinics. Nurses are also found in epidemiology programs, and working to assure the quality of day care centers, hospitals, and long-term care facilities through licensing and certification. In large health departments, a nurse might work exclusively in one or two program areas, and even in a limited part of the jurisdiction served. In many middlesized and most small departments, the nurse must be a generalist, moving day to day and hour by hour from program to program. Much of the apparent specialization and narrow targeting of work efforts is driven by the current approach to funding of public health, in which dollars are tied to very defined activities and population groups, rather than being available for more broad-based efforts to work with a population group or community to improve health overall. While complex models to explain the experience of health in populations (such as the Evans and Stoddard Field Model3) have only been in widespread use in recent years, public health professionals have understood that protecting the public health requires attention to individual and family circumstances, social and economic factors, and the full experience of the local community. The individual experiencing illness and seeking care may be the most visible evidence of the need for public health in a community, though individual medical care in response to symptoms is not central to public health practice. However, where there are large numbers of individuals uninsured or lacking primary care, public health departments have hired large numbers of physicians, physician assistants, nurse practitioners, and public health nurses to provide personal care services. There is no indication that this care has automatically been given in ways that differ in content or focus from that provided in any other ambulatory care practice. Having said that, it is also important to say that many health department-based primary care programs are different in their attention to prevention, to the special community needs of the populations seeking care, and to the potential for building new, better systems of care and prevention. As health departments have been a major source of primary care and prevention for the uninsured or other vulnerable populations, they have often supported the services by quietly riding on the economic coattails of Medicaid or other special funding sources. A maternalchild health-focused public health nurse or child health physician generating up to two-third or three-fourth of salary costs through billable services may well be supported to invest the remaining one-third to

one-fourth of time in improved community health systems. Absent the Medicaid resource, the health department may be unable to find the resource to continue these professionals even half time. Making the case for a community funding base for this shift is an important challenge to public health nurses across the country. The challenge is to ask the correct question, which is “how will I assure that care is available to those who lack it?”, not “how can I be sure that I am still here to give the care?” In the rush to downsize government and control spending for health and illness services, many fear that policy makers will inadvertently eliminate important community-based programs, such as health promotion to increase activity and reduce obesity.

Where is Public Health Practiced? The field of public health can be distinguished from other areas of health-related practice by the combined impact of three foci: prevention, community, and systems. While none of these is unique to public health, the combination is a particularly powerful one. Prevention is, of course, the historic defining feature of public health. As causal links and antecedents of disease have been understood, public health practitioners have taken steps to reshape exposure patterns, or strengthen resistance or eliminate causes of diseases. The earliest efforts were directed at infectious conditions, both before and after the introduction of protective immunizations and effective antibiotic treatment. More recently, prevention has extended to noninfectious diseases such as cancer and heart disease, and to injury, both unintentional and intentional. The expanding science base for prevention practice has supported provision of services in a variety of settings (home, school, workplace, health clinic) using multiple media (brochures, audio and video tapes, games, drama) and multiple reinforcers (public policy on tobacco control being a prime example). Emerging approaches such as harm reduction (seeking to achieve at least some movement toward more healthful choices even if full prevention of risk is not feasible) also play a part. Some prevention activities are directly provided to specific individuals, such as immunizations or prenatal care. Many others are provided to people at the population group or community level. In either case, public health is differentiated from the vast majority of health and illness care practice by the use of settings other than hospitals and doctors’ offices as the site of intervention. Schools and work sites, store-front clinics, homes, and shopping malls have also been used to assure that services and messages are available to people at the times and places where they will have the greatest impact in promoting health. The term community may well be overused; the fact that a health-related service is outside the four walls of a hospital does not make it a community service. Changes in medical and nursing practice have meant that many procedures previously requiring a hospital operating room or nursing care unit are performed in clinics or homes.

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For the public health worker, all activities are done in the context of community. Community means more than place, and may not occur in a single place. It also means relationship, whether one is considering an official geopolitical community, a neighborhood, or a community of affinity such as an advocacy or professional group. One widely used statement about public health in America4 captures the importance of relationships in the vision of “healthy people in healthy communities.” Related to the concept of community is that of systems, the notion that any one component of the community is tied in some way to all others, so that changes in any one component will lead sooner or later to some changes elsewhere. A focus on both prevention and community from a systems perspective pushes the practitioner to consider how the system relationships may be developed or strengthened, or how illness-fostering, noncommunity system elements may be reduced. Working with this perspective means that any work with an individual can be the source of data regarding the functioning of systems within the community, and lead to intervention at additional levels to promote healthy change. No one person can simultaneously work at all levels (individual, family, neighborhood, community-wide system), so the system of workers collaborating to assure that needed information flows among those performing different functions is an additional important part of the systems view. Given all of the above, it is impossible to define the public health workforce by the name on the employing agency door, though the largest concentration is reemployed by official public health agencies (local, regional, state, or federal).* Some community programs such as the not-for-profit community health centers and migrant health centers work with the community to improve health in ways that are clearly public health practice. The total number of public health workers reported is also deceptive in that the workers are not spread evenly in relation to the population. While the reported national ratio is 158 public health workers for each 100,000 in the population, in 2000 the range was from 37/100,000 (Pennsylvania) to 566/100,000 (South Carolina).5 While this does represent enormous variation in the assurance to the citizens that their health is being protected, caution should be exercised, as these variations are caused in part by state and local decisions to locate public health activities outside of identifiable public health agencies, by varying degrees of reliance on public health for clinical services, and on the lack of a standardized system for routine reporting on the public health workforce.

Degrees and Credentials Because of the myriad skills needed, entry routes to public health practice often do not include formal training in public health. For example, many experts in social dynamics of the populations most vulnerable to HIV infection (gay men, sex workers, injecting drug users) entered public health practice during the early years of the AIDS epidemic. As programs matured and workers considered promotions and career development, many of these have added public health training (formal or informal) and can now be found working in a wide range of programs. For the largest professional group, nurses, the picture can be most confusing. Nurses with the same legal credential to practice may have widely differing educations. Neither the associate degree nor diploma education includes public health as a required curriculum component. Basic education about public health nursing practice is included in the baccalaureate curriculum, and some public health systems have attempted to reserve the job title “public health nurse” for baccalaureate graduates only. Whatever their entry education, nurses employed to work in public health agencies or other entities with a focus on public health and the community *Because of the lack of clear definitions of public health positions, and the minimal attention to public health within the overall health system, there is no good, recent enumeration of the public health workforce. Efforts now underway within the Bureau of Health Professions, Health Resources and Services Administration, U.S. Department of Health and Human Services, should provide this needed data.

must master at least some content about population perspectives on health, epidemiology, health behavior and environmental influences on health.6,5 Advanced education for practice in communities is at least as confusing as entry-level education. Some public health nurses have studied in schools of public health, others in schools of nursing; some have degrees in both fields. Some physicians in public health practice are board certified in preventive medicine, but many others are pediatricians, obstetricians, or infectious disease specialists. As with entry-level education, the degrees and job titles alone do not identify whether the physician or nurse is practicing public health nursing or not. The answer to that question must be sought in questions of focus and goal. The Institute of Medicine considered the confusing picture of education for public health practice in the report Who Will Keep the Public Healthy?6 and provided some guidance for the field of public health education. The report acknowledges that the limited number of schools of public health, and the range of public health practice, mean that schools of public health should concentrate their efforts on those headed toward leadership positions, while expanding continuing education for the workforce generally, and working collaboratively with other schools (e.g., medicine, nursing, law) to improve the public health content included in their regular curricula. The report further suggested that the content of public health education at the graduate level be grounded in an ecological view of health (such as the determinants of the health model discussed above), emphasize practice, and work toward competency not only in the five classic areas of public health education (biostatistics, epidemiology, environmental health, social and behavioral science, and management) but in eight areas that have emerged as critical in the twenty-first century: cultural competency, communication, community-based participatory research, ethics, genomics, global health, informatics, and policy and law. Many public health workers are credentialed by an association or entity representing a single profession, such as public health nursing, preventive medicine, health education, or environmental health. Many others bring skills for which there is no specific national credential, such as epidemiology, public health law, or public health leadership. National public health associations have engaged in extensive dialogue over the last decade about the possibility of developing a single basic public health certification that could be used by any public health professional as an assurance of competency in the field. The American Public Health Association, the Association of State and Territorial Health Officials, the National Association of County and City Health Officials, the National Association of Local Boards of Health, and the U.S. Department of Health and Human Services (namely, the Centers for Disease Control and Prevention and the Health Resources and Services Administration) have all been actively involved, but resolution seems elusive. Questions include those about duplicate credentials for public health workers from existing specialties, the impact of a new credential on civil service employment systems, and the cost of a program of testing and issuing credentials. Further confusing the debate is an overlapping consideration of the accreditation of public health agencies. It is unlikely that this will be fully settled within another decade.

Current Challenges? The two most prominent practice challenges to the public health workforce today are those associated with continued efforts to reduce the size of government and those that result from overwhelming attention to specific issues without concern for fundamental infrastructure. A continuing feature of public life in the United States is concern that government has gotten “too big,” and that a goal for all elected officials is to substantially reduce the presence of government. This is easily translated into a reduction in the size of governmental agencies, the major expense of which is usually the workforce. Public health programs and activities have never been designed as entitlements, that is, services to which people are assured access by virtue of some identifying feature (e.g., Medicare for those over 65, Medicaid for those on

79 Aid to Families with Dependent Children, Social Security to workers over 65). Each public health program is reauthorized and refunded year to year, or at best, in a 5-year cycle. Few public health managers at any level of government have succeeded in presenting their programs as being exempt from cuts during recessions, or from across-the-board reductions. Further, public health practitioners have often failed to identify the conceptual basis of public health as being substantially different from the other “human service” programs with which they are often grouped organizationally. Because some public health activities are similar to individualized health services, there has also been pressure to either move them to the private sector or to make them financially self-supporting through fees. Public health professionals are only partially articulate in describing the population focus of public health, and in making certain that their efforts are truly driven by epidemiology and an interest in community systems toward actions that will raise the level of health in the whole community. The nationwide attention to emergency preparedness and the threats of deliberately caused disease outbreaks such as the anthrax events of late 2001 have been helpful in raising

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the profile of public health as a part of the community safety net, needing general revenue support to be ready to respond if needed. Unfortunately, the appropriations process at national and state levels has not made this new revenue additive. In many cases, agencies are the same size as before, with the same workforce being asked to assume more active roles in emergency preparedness and community response, while continuing the long-standing array of other public health services. Public health is by its nature the most interdisciplinary of practices. On a day-to-day or hour-to-hour basis, the activities of physicians, nurses, social workers, and sanitarians may appear identical. Yet each of these brings perspectives unique to a discipline, and each is important to the wide-ranging functions of public health. The challenges and opportunities of today are such that almost any profession may develop the needed public health understanding of the health of individuals, families, and communities essential to the accurate assessment of health concerns, the development of sound policy, and thus the assurance of continuing movement toward healthy people in healthy communities.

Family Planning Herbert B. Peterson • Andreea Creanga • Amy O. Tsui

“The Millennium Development Goals, particularly the eradication of extreme poverty and hunger, cannot be achieved if questions of population and reproductive health are not squarely addressed. And that means stronger efforts to promote women’s rights, and greater investment in education and health, including reproductive health and family planning.” United Nations Secretary-General Kofi A. Annan

Message to the Fifth Asian and Pacific Population Conference, December 2002

The CDC has declared family planning to be one of the key achievements in public health for the twentieth century.1 Milestones for this achievement include the arrest of Margaret Sanger for distributing information about birth control in 1914, the creation of the first state public health program to include contraception in 1936, the approval of oral contraceptives by the FDA in 1960, and the Supreme Court decision to declare unconstitutional state laws prohibiting contraceptive use by married couples in 1965 (Table 79-9). Family size declined in the United States from 3.5 children in 1900 to approximately 2 children at the end of the twentieth century. The success of family planning in achieving desired birth spacing and family size in the United States contributed to large decreases in both child mortality and maternal mortality in the twentieth century. In this chapter we provide the global context for family planning followed by an overview of family planning in the United States. We then discuss the safety, effectiveness, and use of contraceptive methods, with a focus on widely used methods and methods that are newly available in the United States. THE GLOBAL CONTEXT FOR FAMILY PLANNING

Of the estimated 6.2 billion people living on the planet, approximately one billion are women aged 15–49 who are married or in union. Data regarding contraceptive use are more available for these

women than for single women or for men. More than three-fifths (61% or about 635 million) of women who are married or in union are using contraception.2 The percent distribution of women using contraceptive methods varies by region, with a higher percentage (69%) of women using them in developed than in less-developed regions (59%). Further, the percentages of women using contraceptives are as high as 71% in Latin America and the Caribbean and as low as 27% in Africa. The great majority (approximately 90%) of women using contraception are relying on modern methods, with the most widely used method being female sterilization (21%), followed by IUDs (14%) and oral contraceptives (7%). While oral contraceptives and condoms are the most widely used methods in developed countries, by contrast, female sterilization and IUDs are the most widely used methods in developing countries. Contraceptive prevalence has been continually high in developed countries since the 1970s and has been increasing substantially over time in developing countries. The percentage of women who are married or in union and using contraception has increased by at least one percentage point per year since 1990 in over half (56%) of developing countries. However, despite the widespread availability and use of modern contraceptives, substantial unmet need remains. Of the estimated 705 million women aged 15–49 in developing countries, nearly 20% (137 million) who are at risk of unintended pregnancy and are not using any contraceptive methods; and a total of 201 million women in developing countries are estimated to have an unmet need for effective contraceptives.3 Unmet need remains particularly high in sub-Saharan Africa and South Asia. Meeting the global unmet need for contraceptive services would result in preventing an estimated 52 million unintended pregnancies annually, which would, in turn, prevent 23 million unplanned births, 22 million induced abortions, 7 million spontaneous abortions, 1.4 million infant deaths, and 142,000 pregnancy-related maternal deaths—53,000 from unsafe abortions and 89,000 from other causes. Provision of the additional contraceptive services necessary to meet this need, at a cost of approximately $3.9 billion per year, would prevent the loss of an estimated 27 million disability-adjusted life years.3 Worldwide, as many as 50% of all pregnancies are unplanned and 25% are unwanted.4 An estimated 50 million abortions are performed

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Health-Care Planning, Organization, and Evaluation TABLE 79-9. THE FIRST CENTURY OF FAMILY PLANNING IN THE UNITED STATES Year 1912 1916 1925 1928 1920–1930 1937 1942 1955 1960 1962 1965 1970 1972 1973 1976 1977 1990 1992 1992 1993 1997 2000 2001 2002 2003 2006

Event Margaret Sanger starts the birth-control movement in modern era The first family planning clinic opens in Brooklyn, New York First diaphragm is manufactured in the United States Ovulation timing is medically established Margaret Sanger continues to open more clinics and to promote contraception; physicians gain the right to prescribe contraceptive methods; public hospitals begin to provide family planning services Family planning is supported by the American Medical Association Planned Parenthood Federation of America is established The first National Fertility Survey is conducted The FDA approves the first birth control pill (Enovid) The Population Council organizes the first international conference on IUDs The law prohibiting contraceptive use for married people is declared unconstitutional Title X of the Public Health Service Act, the nation’s family planning program, is legislated Medicaid is authorized to fund family planning services Abortion is legalized by the Supreme Court (Roe vs. Wade) The FDA approves the first progesterone-releasing IUD (Progestasert) The Supreme Court rules that minors have a constitutional right to access contraception The FDA approves the first implantable contraceptive device (Norplant) The FDA approves Depo-Provera (progestin-only injectable contraceptive) The Supreme Court weakens abortion rights by allowing states to pass certain restrictions The FDA approves the female condom (Reality) The FDA approves the use of emergency contraception pills The FDA approves Lunelle (combined estrogen/progestin injectable contraceptive) and Mirena (levonorgestrel-releasing IUD) The FDA approves NuvaRing (combined estrogen/progestin contraceptive vaginal ring) The FDA approves Ortho-Evra (transdermal combined estrogen/progestin contraceptive patch) and removes Norplant from the market The FDA approves Seasonale (combined estrogen/progestin oral contraceptive for extended use) The FDA approves Implanon (etonogestrel releasing single implant system)

FDA—The Food and Drug Administration. Source: Adapted from CDC. Achievements in Public Health, 1900–1999. Family Planning. MMWR. 1999;48(47):1073–80.

each year with approximately 19 million considered by the World Health Organization (WHO) to be unsafe. Approximately 55,000 unsafe abortions occur each day, resulting in the deaths of at least 200 women. These deaths, over 95% of which occur in developing countries, account for approximately 13% of all maternal deaths.5 The International Conference on Population and Development, held in Cairo in 1994, has been considered a watershed event with respect to the role of family planning. Whereas previous similar efforts and viewpoints had largely focused on the population problem and demographic targets, the Cairo conference highlighted the important role that family planning plays in the context of social and economic development and created a series of goals regarding sexual and reproductive health and rights, including family planning—with a focus on empowering women.6 In 2005, United Nations Population Fund (UNFPA) affirmed that reproductive health, which includes family planning, “is not solely a health issue, but a matter of economic development, social justice, gender equality, and human rights.”7 FAMILY PLANNING IN THE UNITED STATES

Of the approximately 62 million women in the United States who are in their childbearing years, 43 million are sexually active and do not wish to become pregnant. Most women in the United States desire to have two or fewer children, and, to achieve this goal, most will require contraceptive protection for approximately three decades of their lifetimes. Among fertile, sexually active women who do not wish to become pregnant, 89% are estimated to be using a method of contraception.8 In 2002, among 38 million women using contraceptive methods in the United States, most were using oral contraceptives (30.6%), tubal sterilization (27.0%), male condoms (18.0%), or their partner’s vasectomy (9.2%). Less frequently used methods included depot medroxyprogesterone acetate injections (5.3%), withdrawal

(4.0%), IUDs (2.0%), periodic abstinence (1.6%), and progestin implants (1.2%). The choice of contraceptive method varied by age, with women under age 30 most likely to be using oral contraceptives, and women over age 35 most likely to be using sterilization. The choice of methods also varied by race, with oral contraceptives being the most popular method among white women and sterilization being the most popular method among black and Hispanic women.9 Although highly effective contraceptive methods are widely available in the United States, and overall contraceptive prevalence is high, a large number of unintended pregnancies occur each year. In 1998, 48% of the pregnancies in the United States were estimated to be unintended.10 In 2000, an estimated 6.4 million pregnancies resulted in 4.1 million live births, 1.3 million induced abortions, and one million spontaneous abortions. The overall pregnancy rate in 2000 (104 pregnancies per 1000 women aged 15–44 years) was 10% lower than that in 1990, while the teenage pregnancy rate (84.5 pregnancies per 1000 women aged 15–19 years) was 27% lower.11 Over half of the unintended pregnancies occur among women who do not use any method of contraception; the percentage of such women increased from 5.4% in 1995 to 7.4% in 2002.9 Contraceptive services in the United States are provided through both the public and private sectors. Public funding from the federal and state governments is primarily provided through Medicaid and the State Children’s Health Insurance Program (SCHIP), which, together, covered services for 6.5 million women in 2002.12 Medicaid, which provided 61% of public funding for family planning services in 2001,13 has been required to cover family planning services since 1972. While gaps in funding for family planning services remain for women without sufficient resources to pay for them, an increasing number of states have expanded Medicaid coverage through special initiatives that provide family planning services for women who would otherwise be ineligible for the broader Medicaid program.14 More than 7000 publicly funded clinics provide family planning services, and the

79 largest federal source of grants for such clinics is the Title X program, which was signed into law in 1970 and currently provides funds to over 4500 clinics. In 2003, among 61.7 million women of reproductive age, only 65% had private insurance.14 Although contraceptive coverage has improved recently in such plans, important gaps in coverage remain. Only 21 states have laws requiring insurers to provide comprehensive coverage for contraceptives if they otherwise cover prescription drugs and devices. The Equity in Prescription Insurance and Contraceptive Coverage Act, which was proposed to Congress in 1997 but has not been enacted, would require such coverage nationally for FDA-approved contraceptives. Insurance for federal employees covers all prescription contraceptives, and most employer-based insurance plans (90%) cover prescription contraceptives.8 Currently, insurers are less likely to cover newer approved methods such as the combined hormonal patch and vaginal ring than they are to cover oral contraceptives.15 Overall, where do women obtain family planning services? The answer depends heavily on income. In 1995, 70% of women with family incomes that are one and one-half times or more than the established level of poverty who make a family planning visit see a private provider compared with 42% of lower income women. Teenagers are less likely to visit a private provider (42%) for family planning. By contrast, family planning clients of public and other nonprivate providers are largely poor; 63% have incomes below the established level of poverty.16 CONTRACEPTIVE EFFECTIVENESS AND COST EFFECTIVENESS

In the United States, about half of all unintended pregnancies occur due to contraceptive failure.10 The effectiveness of contraceptives is assessed by measuring the number of unplanned pregnancies that occur during a specified period of exposure and use of a contraceptive method. Most methods have a low risk of failure if used perfectly, and this is why the most effective method for a woman is usually the method she or her partner can use correctly and consistently. There are two methods commonly used for measuring contraceptive effectiveness: the Pearl Index and life-table analysis. The Pearl Index is defined as the number of failures per 100 woman-years of exposure. The denominator represents the number of months or cycles of exposure from the onset of a method until an unintended pregnancy, discontinuation of the method, or completion of the study. The quotient is multiplied by 1200 if the denominator consists of months or by 1300 if cycles. However, the Pearl Index does not allow accurate comparisons at different durations of exposure, as it is usually calculated for a 1-year period. Life-table (or survival) analysis, on the other hand, calculates the failure rate for each month of use. A cumulative failure rate at various durations of exposure, such as 12, 18, 24, or 36 months, can then be calculated to compare across methods. Varying terms are used today to differentiate between contraceptive effectiveness with correct and incorrect use of the method. The best performance, based on correct and consistent use, is represented by the lowest expected failure rate, as compared to the usual experience, which includes both perfect and imperfect use, or a typical failure rate. Both the lowest expected and typical failure rates are determined in clinical trials, the former often measured among highly motivated subjects. Contraceptive failure occurs for a number of reasons, such as imperfect method use, frequency of intercourse, and fecundity patterns and is conditioned by such user characteristics as age, parity, marital status, and education. For most contraceptive methods, failure rates decline with duration of use, primarily because the users who are relatively more fecund, have higher intercourse frequency, or are less compliant with method use protocols will fail earlier. Data from the 1995 National Survey of Family Growth were used to estimate the number of contraceptive failures that a typical woman would experience in her life-time if she continuously used contraception from age 15 to 45 (except for the time of pregnancy after a contraceptive failure). If a typical woman continuously used reversible contraceptive methods

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over her reproductive lifetime, from ages 15 to 45, she would experience 1.8 contraceptive failures, whereas if she continuously used reversible methods and then sterilization, she would experience only 1.3 contraceptive failures.17 Contraceptive methods vary in effectiveness and in the determinants of effective use. While the effectiveness of some methods is highly dependent on proper use, the effectiveness of others is largely independent of the contraceptive user. Oral contraceptives, for example, are highly effective when used consistently and correctly, but substantially less effective when used typically. Other methods, such as intrauterine devices and progestin-only implants, are highly effective once they have been inserted properly. Trussell has estimated the effectiveness of contraceptive methods with perfect use and with typical use (which includes the experience of some who use the method consistently and correctly and others who do not).17 A 2004 cost-utility analysis found that all contraceptive methods resulted in cost savings and health gains (as measure by quality-adjusted life years) compared with nonuse of contraceptives.18 MEDICAL GUIDELINES FOR CONTRACEPTIVE USE

WHO has published two sets of guidelines that address safe and effective contraceptive use. The Medical Eligibility Criteria for Contraceptive Use, first published in 1996, provides recommendations regarding the medical appropriateness of contraceptive method use for women with medical problems or other selected characteristics. The third edition, published in 2004 (http://www.who.int/reproductive-health/publications/mec/index.htm) provides over 1700 recommendations with each contraceptive method/condition combination classified as either category 1, 2, 3, or 4 (Table 79-10). The Selected Practice Recommendations for Contraceptive Use provides guidance on how to use contraceptive methods once they have been deemed to be medically appropriate. The second edition of these guidelines, published in 2005 (http://www.who.int/reproductive-health/publications/spr/index.htm), provides guidance on clinical management issues that frequently arise in the provision of contraceptive services.

Combined Oral Contraceptives Oral contraceptives containing estrogens and progestins were first approved for use in the United States in 1960. The amount of estrogen and progestin used in combined oral contraceptives (COCs) has decreased substantially since that time, and the great majority of COCs that are prescribed currently contain 35 µg or less of ethinyl estradiol in combination with a progestin. COCs are either monophasic or multiphasic preparations with the former providing the same dose of hormones throughout the cycle and the latter providing varying doses. COCs are highly effective when taken properly, but 29% of COC users reported in the 1995 National Survey of Family Growth that they missed at least one pill in the prior 3 months of use. Health Benefits. The short- and long-term effects of COCs have been studied more thoroughly than those of any other drugs currently prescribed. On balance, most studies show that they are safe for the great majority of users. In fact, studies attempting to identify potentially harmful effects of oral contraceptives have documented important noncontraceptive health benefits. COCs have been found to reduce menstrual blood flow and dysmenorrhea and to lower the prevalence of iron deficiency anemia. Oral contraceptive users have a reduced risk of endometrial and ovarian cancers (Table 79-11). This protection is conferred after a minimum of 12 months of use and persists for long after discontinuation of use.19–21 Women with acne, hirsuitism, and endometriosis may experience improvements. Monophasic COC users also have a reduced risk of functional ovarian cysts but this benefit does not appear to pertain to low-dose multiphasic preparations. Several studies have suggested that COCs may protect women against colorectal cancer; but this potential benefit requires further study. In a meta-analysis of published data, the pooled relative risk of colorectal cancer for COC ever-use was 0.82

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TABLE 79-10. WHO MEDICAL ELIGIBILITY CRITERIA FOR CONTRACEPTIVE USE

WHO Category

Interpretation When Clinical Judgment is Available

Category 1 There is no restriction for the use of the contraceptive method.

Use the method in any circumstance

Category 2 The advantages of using the method generally outweigh the theoretical or proven risks. Category 3 The theoretical or proven risks usually outweigh the advantages of using the method. Category 4 The condition represents an unacceptable health risk if the contraceptive method is used.

Interpretation When Clinical Judgment is Limited

Example (Women with Headaches Who Want to Initiate Use of COC) Nonmigrainous headaches

Generally use the method

YES (Use the method)

Use of the method not usually recommended unless other more appropriate methods are not available or acceptable

Migraine headaches without aura Age < 35

NO (Do not use the method)

Migraine headaches without aura Age ≥ 35

Method should not be used

Migraine headaches with aura Any age

Source: WHO. Medical Eligibility Criteria for Contraceptive Use. 3rd ed. Geneva; 2004

(95% confidence interval (CI) = 0.74, 0.92). The protection was stronger for those who had used COCs within the previous 10 years.22 Health Risks. Despite its protective effects, use of the pill is not without risk. Oral Contraceptives and Venous Thromboembolism. Low-dose COCs are associated with an increased risk of venous thromboembolism (VTE).23 Most studies report that past users have no increased risk and the increased risk appears attributable to current oral contraceptive use. The use of COCs with second-generation progestins (levonorgestrel or norethisterone) is associated with a three to four-fold higher risk for VTE compared with nonusers, which is, nevertheless, substantially lower than the risk of VTE during pregnancy. When COCs with third-generation progestins (desogestrel or gestodene) are used, the risk of VTE appears to be about 1.5–1.8 times greater than that for users of formulations containing levonorgestrel,24 although the extent to which this is the case remains controversial. The presence of V Leiden factor mutations or protein S or C abnormalities significantly increases the risk of VTE in COC users— from 6 to 40 times higher than in nonusers without thrombophelia.24 Routine screening for thrombogenic mutations in all COC users, however, is not considered necessary because of the rarity of these conditions. Oral Contraceptives and Myocardial Infarction. Although studies of older, higher dose COCs found an increased risk of myocardial infarction and ischemic stroke, more recent studies of currently available low-dose COCs have been inconsistent, with some reporting no increase and others reporting up to a two- to fivefold increase TABLE 79-11. REDUCED INCIDENCE OF ENDOMETRIAL AND OVARIAN CANCER AFTER ORAL CONTRACEPTIVE USE Reduced Incidence after COCs Use For Cancer Type

4 years

8 years

12 years

p-value

Endometrial cancer Ovarian cancer

56% 41%

67% 54%

72% 61%

p<0.0001 p<0.0001

Source: The Practice Committee of the American Society for Reproductive Medicine, Hormonal Contraception. Recent Advances and Controversies. Fertil Steril. 2004;82(1):26–32.

in risk.24 A higher prevalence of women with risk factors for cardiovascular disease in the latter studies may explain the discrepancy.24 Women who smoke and use COCs have an increased risk of death from cardiovascular disease.25 For women under 35 years of age, the attributable risk of myocardial infarction for smokers who use COCs (35 per million woman-years) is tenfold greater than that for nonsmokers who use them (3 per million woman-years). For women over 35 years of age, the comparable attributable risks of myocardial infarction for women who smoke and who do not smoke are 396 per million woman-years and 31 per million woman-years, respectively (as seen in Table 79-12).21 The use of low-dose COCs by healthy women does not appear to increase the risk of hemorrhagic stroke.24 Oral Contraceptives and Liver Cancer. There is controversy regarding the relationship between COC use and development of liver cancer (hepatocellular carcinoma).26,27 The large Multicentre International Liver Tumor Study (MILTS) found no overall increase in risk or effect of duration of use; the only increase seen was in a small subgroup of women with negative serology for hepatitis B or C viruses and no history of cirrhosis. Any increase in the risk of COC use among this group of women at inherently very low risk of liver cancer would TABLE 79-12. ESTIMATED MYOCARDIAL INFARCTION INCIDENCE RATES AND ATTRIBUTABLE RISKS PER 106 WOMAN-YEARS ASSOCIATED WITH CURRENT COMBINED ORAL CONTRACEPTIVE USE BY AGE AND SMOKING STATUS AMONG EUROPEAN WOMEN. Incidence per 106 Woman-Years Age (Years) Women < 35 years Nonsmokers Smokers Women > 35 years Nonsmokers Smokers

Nonusers of COCs

Users of COCs

0.83 7.78

3.56 42.7

2.73 34.9

9.45 88.4

40.4 484.6

31.0 396.2

Attributable Risk

Source: WHO Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception Acute Myocardial Infarction and Combined Oral Contraceptives. Results of an International Multicentre Case-Control Study. Lancet. 1997;349(9060):1202–9.

79 result in a very small absolute increase in risk (an estimated one extra case per 1.5 million women-years of use in Germany).28 Oral Contraception and Breast Cancer. Despite more than 60 studies on the subject, the relationship between use of oral contraceptives and the risk of breast cancer remains controversial. A 1996 pooled analysis29 of 54 studies conducted in 25 countries that included 53,297 women with breast cancer and 100,239 women without breast cancer had four main findings. First, current or recent (within 10 years of stopping use) pill users had a small increase in risk of having breast cancer diagnosed (for current versus nonusers, RR was 1.24; 95% CI = 1.15–1.33). The increase for current users was seen for women with little pill use (less than 1 year) and did not increase with increasing durations of use.30 Second, past users (10 or more years after stopping use) had no increased risk. Third, the additional cancers identified were less advanced clinically than those in never users. Fourth, no subgroups of women were at increased risk for pill use. In particular, women with a family history of breast cancer were not at additional risk from pill use relative to women without such a history. These four findings suggest that either oral contraceptive users are more likely than nonusers to have existing breast cancers detected; that existing tumors are identified at an earlier stage in pill users; or that pill use accelerates tumor growth. By contrast, a 2002 U.S. study, which involved 4575 women with breast cancer and 4682 controls, concluded that among women 35–64 years of age, current and previous COC use was not associated with significantly increased risk of breast cancer; the relative risk did not increase consistently over longer periods of use or with higher doses of estrogen.31 Other recent studies have shown that the presence of inherited susceptibility to breast cancer or women who are carriers of BRCA1 or BRCA2 gene mutations have an increased risk of developing breast cancer during their life span.32 Moreover, women who are BRCA1 gene mutation carriers and users of high-dose COCs for more than 5 years before age 30 years are at high risk of being diagnosed with breast cancer before turning age 40.33 The influence of progestogen-only pills on a woman’s risk of breast cancer has been less well studied, but the limited available evidence suggests a similar effect to that for COCs. A national population-based case-control study in New Zealand found the relative risk of breast cancer in women who had used progestogen-only pills to be 1.1 (CI 95% = 0.73, 1.5), with recent users (within 10 years) having a higher risk and past users having no increase in risk.34 Oral Contraceptives and Cervical Cancer. The relationship between pill use and cervical cancer continues to be controversial. Observational studies of this relationship are difficult to interpret because of biases related to sexual behavior and the failure to control for the presence of the human papilloma virus (HPV) in most studies. Recently, a study carried out by the WHO’s International Agency for Research on Cancer (IARC) found that prolonged use of COCs increased the risk of cervical cancer up to three times in women with HPV infection who had taken oral contraceptives for 5–9 years and up to 4 times in women with HPV infection who had taken oral contraceptives for more than 10 years.35 WHO Recommendations. The WHO has recommended that women with the following conditions not use COCs: (a) breastfeeding in the first 6 weeks postpartum; (b) smoking more than 15 cigarettes per day and being age 35 or over; (c) multiple risk factors for arterial cardiovascular disease; (d) hypertension—more than 160/100 mmHg; (e) vascular disease; (f) a history or current deep venous thrombosis or pulmonary embolism; (g) following major surgery with prolonged immobilization; (h) known thrombogenic mutations (factor V Leiden, prothrombin mutation, protein C and S, and antithrombin deficiencies); (i) stroke; (j) complicated valvular heart disease; (k) migraine-headaches with aura at any age or without aura in women over age 35; (l) current or personal history of breast cancer; (m) diabetes with severe vascular complications of more than 20 years duration; (n) active viral hepatitis; (o) decompensated cirrhosis; or (p) benign or malignant liver tumors.36

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In 2003, the Food and Drug Administration approved Seasonale, a combined estrogen/progestin oral contraceptive for extended use. It involves a 91-day treatment cycle resulting in four menstrual periods per year if taken continuously. Menstruation occurs when the seven inert pills are taken within each cycle. Increased bleeding or spotting between periods may be expected, as compared to the standard 21- or 28-day birth control pill cycle, but tends to decrease with prolonged use.

Combined Injectable Contraceptives Injectable contraceptives containing both an estrogen and progestin provide an alternative for women who are candidates for combined oral contraception but do not want to take a pill daily. None are currently marketed in the United States. The method is highly effective (Fig. 79-1), but the user must return for injection every 30 days. The advantages of the monthly injection over the three-month, progestin-only formulation are a more rapid return to fertility upon discontinuation and more acceptable bleeding patterns while using the method.37 Health Effects. The method often causes changes in menstrual bleeding patterns during the initial three cycles of use, but after 6 months of use, most women report regular, acceptable bleeding patterns.38 Only 1% of users in the U.S. trial reported amenorrhea after the first month and 4% at 60 weeks of continuous use, results that are in contrast with the high frequency of amenorrhea associated with the use of depot medroxyprogesterone acetate (DMPA) (50% after 1 year of use).39,40 Weight gain is the leading cause of method discontinuation in U.S. trials. Long-term health effects have not been studied but are assumed to be similar to those of COCs.

Transdermal Patch A combined hormonal transdermal patch was approved by the FDA in 2002. It is a 20-cm2 system that releases 150 µg of norelgestromin and 20 µg of ethinyl estradiol daily. It is worn for 7 days, replaced with another patch for each of two consecutive additional 7-day periods, and then followed by a fourth patch-free week, during which time the woman has withdrawal menstrual bleeding. Data suggest that the use of this preparation may improve compliance relative to the daily pill taking required for proper use of COCs.41 Clinical trials suggest that women who weigh more than 90 kg may have a higher likelihood of contraceptive failure than women weighing 90 kg or less.42 Health Effects. The side-effect profile is similar to that for COCs; although nausea and mild breast discomfort were found to be more likely to occur in women using the patch than among those using the

Implants Vasectomy Tubal occlusion IUD (Cu releasing) POPs (breastfeeding) LAM Lunelle Depo-provera COCs Male condoms Diaphragms Female condoms Calendar Withdrawal Spermicides 0

5

10

15

20

25

30

35

Pregnancies per 100 women Typical use

Perfect use

Figure 79-1. Unintended pregnancy rate during the first year of use by contraceptive method used: United States. Rate is pregnancies per 100 women. (Source: Adapted from Trussell J. Contraceptive failure in the United States. Contraception. 2004;70:89–96.)

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pill; a statistically significant difference was shown only in cycles 1 and 2.43 Most skin reactions after patch application are mild. In early clinical trials reported to the FDA, about 2% of women withdrew from the trials because of patch irritation and about 5% had at least one patch that did not stay attached. Long-term health effects have not been assessed and are presumed to be similar to those for COCs; recent reports have raised questions regarding whether the patch carries a greater risk of VTE than COCs, but this aspect is unresolved.

Vaginal Ring A combined hormonal vaginal ring was approved by the FDA in 2001. It is a light-weight, 2-inch diameter, flexible ring made of ethylene vinyl acetate copolymer. The ring releases 120 µg of etonogestrel and 15 µg of ethinyl estradiol daily and is worn for 21 days, followed by 7 ring-free days during which menstruation occurs. A new ring is inserted at the end of each 28-day cycle. The method is highly effective17 (Figure 79-1). In a one-year multicenter study of over 2000 ring users, more than 90% indicated that the device was easy to insert and to remove.44 Health Effects. Problems such as vaginal discomfort, vaginal discharge, or vaginitis have been reported in 2–5% of European women using the vaginal ring.45 The expulsion rate is about 2%.46 In a oneyear, randomized trial that compared approximately 500 ring users to approximately 500 COC users, 71% in each group completed the trial. The groups had similar rates of reported side effects but the ring group reported more cases of vaginitis and leukorrhea. A total of 5% of ring users reported ring-related problems, including expulsion and interference with intercourse.47 Long-term health effects have not been assessed and are presumed to be similar to those for COCs.

Progestin-Only Contraceptives Progestin-only pills (POPs) are less popular than COCs, but they are suited for women who have contraindications for COCs (e.g., history of thrombosis, hypertension, or migraine headaches). They may be used by breastfeeding women who want an oral contraceptive, and their action is rapidly reversed soon after discontinuation. Ovulation is less reliably prevented with POPs as compared with COCs, and these so-called “mini-pills” may be less effective than COCs, particularly if pills are missed. Health Effects. The mini-pills have no estrogen-related risks, and overall, fewer and less serious complications when compared to COCs. The most common side-effects are changes in menstrual bleeding, especially irregular bleeding, intermenstrual bleeding and spotting, and amenorrhea. As for all progestin-only contraceptives, menstrual abnormalities are a major reason for discontinuation of use. The noncontraceptive benefits of POPs have not been as well studied as those for COCs, and the extent to which the benefits documented for COC use pertain is unclear.

Implantable Contraception The FDA has approved two levonorgestrel implants; one, a set of six silicone elastomer capsules, was approved in 1990 and marketed for approximately 10 years in the United States as Norplant. The other implant, approved in 1996, is a set of two silicone elastomer rods (Jadelle). Neither implant is currently available in the United States. Both implants are highly effective. The former implant (Norplant), although approved for 5 years of use, may be effective for up to 7 years of use. The effectiveness of this implant after 5 years is dependent on body weight; women weighing 70 kg or more at insertion or followup should be counseled regarding decreased effectiveness after 5 years (women weighing 80 kg or more should seriously consider having the implants removed after 4 years of use). The latter implant (Jadelle) is approved for only 5 years of use and is effective for a maximum of 5 completed years depending on body weight; women weighing 80 kg or more should also consider having the implants removed after 4

completed years of use.48 A single implant system (Implanon) has been developed that consists of a nonbiodegradable rod that releases the progestin, etonogestrel. It has been approved for 3 years of use in the European Union and was approved for 3 years of use by the FDA in 2006. At insertion, the implant releases approximately 60–70 µg of etonogestrel daily, with approximately 25–30 µg per day being released by the end of the third year. This implant is highly effective in suppressing ovulation. Health Effects. The main side effect of all available progestin-only implants is menstrual abnormalities. The great majority of women using a levonorgestrel implant will experience prolonged menstrual bleeding and intermenstrual spotting initially; by 5 years, most have regular bleeding, but a substantial minority will continue having irregular bleeding. By contrast, in the first 3 months of use of the etonogestrel implant, about 30% will have prolonged bleeding and 30–40% will become amenorrheic.49 The rate of prolonged bleeding decreases thereafter, but the rate of amenorrhea persists. A review of 55 observational studies50 provides evidence for the safety of these implants. While data regarding cardiovascular disease and cancer risks are limited, the available data find that, overall, implant users have no higher rates of major adverse outcomes than nonusers.50

Injectable Contraception In 1992, the FDA approved the use of injectable DMPA, marketed in the United States as Depo-Provera. When injected every 3 months, 150 mg of DMPA provides a high degree of protection from pregnancy— similar to that of the progestin-only implants and tubal sterilization. Health Effects. The main side effects of DMPA use are menstrual abnormalities, with most users becoming amenorrheic over time (55% of women by the end of the first year of use).51,52 In contrast to progestin-only implants, there is a delayed return to fertility with discontinuation of DMPA use, estimated at about 4 months longer than for women using combined oral contraceptives. Delays in return to fertility of up to 18 months have been reported.51 Another progestin-only injectable contraceptive that is not currently available in the United States contains norethisterone enantate (NET-EN) and is administered every 2 months. Findings among beagle dogs led to initial concerns regarding the possibility that use of DMPA may increase breast cancer risk. However, findings from a pooled analysis of data from the WHO and from New Zealand53 are reassuring. Overall, women who ever used DMPA had similar breast cancer risks as women who never used DMPA. However, the pattern of use made a difference; recent users of DMPA (use within 5 years) had an increased risk of breast cancer diagnosis, while past users (use more than 5 years previously) had no increased use. DMPA use creates a hypo-estrogenic state that results in a decrease in bone mineral density in some women. This effect appears at least largely reversible, as bone mineral density increases again when DMPA is discontinued. The effect on fracture risk for most women is expected to be small. However, it remains unclear whether use of DMPA among adolescents prevents potential attainment of peak bone mass and whether older women who reach menopause while using DMPA experience a recovery in bone mineral density before the marked bone loss associated with menopause occurs. Other contraceptive options should be considered for women at risk for osteoporosis.54

Intrauterine Devices Intrauterine devices (IUDs) are used by nearly 160 million women worldwide—making them the most popular nonpermanent method of contraception. In China, Egypt, and Uzbekistan, the IUD is the most popular form of contraception, accounting for upwards of two-fifths of all use.2 By contrast, only 2% of women using contraception in the United States were using IUDs in 2002.55

79 IUDs declined markedly in popularity during the 1980s in the United States after reports of pelvic infections associated with the Dalkon Shield—a device marketed in the 1970s which was later withdrawn from the market. Subsequently, studies in the late 1980s and 1990s showed that women at low risk of sexually transmitted diseases were at low risk for pelvic infections with use of IUDs. By that time, however, manufacturers had voluntarily stopped selling most types of IUDs in the United States, largely because of low profits and high costs of litigation. In 1989, a new copper IUD, the Copper T380A (ParaGard), was introduced to U.S. markets, and in 2000, the levonorgestrelreleasing intrauterine system (Mirena), which releases approximately 20 µg of levonorgestrel per day, was approved by the FDA. Both intrauterine contraceptives available in the United States are highly effective (Fig. 79-1). The copper IUD is approved for 10 years of use, but data suggest that the device remains effective for at least 12 years—with a cumulative 10-year failure rate of 2.1–2.8%.54 The levonorgestrel-releasing intrauterine system is approved for 5 years and has a cumulative 5-year failure rate of 0.7%.56 Health Effects. Although pregnancy rates are very low for IUD users, women who do become pregnant have a greater risk of ectopic pregnancy (5–8% of failures with the copper IUD are ectopic pregnancies), preterm labor, or spontaneous, septic abortion of an intrauterine pregnancy.46,57 The absolute risk of ectopic pregnancy is very low, however, approximately 1 per 1000 woman-years. The previous use of an IUD does not increase the risk of an ectopic pregnancy, and one WHO multicenter study has shown that women using IUDs are 50% less likely to have an ectopic pregnancy when compared to women using no contraception.51 The main side effects of both types of IUDs are menstrual abnormalities. The copper IUD is more likely to cause heavy and prolonged bleeding as well as intermenstrual spotting and dysmenorrhea, while the levonorgestrel intrauterine system is more likely to result in a reduction in menstrual blood loss over time. By 12 months of use, 20–60% of women using the levonorgestrel-releasing intrauterine system will become amenorrheic.51 Modern IUDs carry low risks of PID and infertility among women at low risk of sexually transmitted infections (STIs). WHO has summarized data from 12 randomized studies and one nonrandomized study and concluded that IUD users selected for low risk of STIs have little, if any, excess risk of PID. The overall rate of PID following 22,309 IUD insertions was 1.6 cases per 1000 woman-years of use. The risk of PID was highest (by greater than sixfold) during the first 20 days after insertion; after that time, the risk of PID was consistently low for up to 8 years of use.58 The use of prophylactic antibiotics prior to IUD insertion appears not to reduce this low insertion-associated risk among women at low risk for STIs.51 At least three observational studies have found no association between copper IUDs and the risk of infertility among nulligravid women at low risk for STIs.59–61 Although uterine perforation can occur with IUD insertion, this risk is low when proper techniques are used—at rates of approximately 1–2 perforations per 1000 insertions.56 WHO Recommendations. The WHO has recommended that women with the following conditions not have IUDs inserted: pregnant women, those developing postpartum or postabortum sepsis, those with an active pelvic infection, including purulent cervicitis, those with known or suspected gonorrheal or chlamydial infection, and those with uterine or cervical malignancy.36

Mechanical Barrier Methods and Spermicides The male latex condom is proven to be highly effective for preventing both unintended pregnancy (Fig. 79-1) and HIV infection when it is used consistently and correctly;62 inconsistent use, by contrast, is not a reliable prevention strategy for either purpose. Breakage rates of male latex condoms in the United States are low (about 2 condoms per 100 used).17 Studies of the polyurethane female condom (approved by the FDA in 1993) and polyurethane male condom are

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less complete, but they are expected to provide substantial protection against both pregnancy and HIV infection as well, when used consistently and correctly. Vaginal diaphragms—cervical caps—and spermicidal creams, foams, gels, films, and suppositories are also available as barrier contraceptive methods. All barrier contraceptives require substantial user motivation, and success in their use will be determined not only by motivation but also by user experience and skill. For example, perfect use of male condoms is associated with a pregnancy rate of about 2% in the first 12 months of use, which is lower than that for typical use of oral contraceptives (8%)—but typical condom use has a substantially higher failure rate (15%) than typical oral contraceptive use. Spermicides, when used alone, are the least effective barrier method and have a relatively high failure rate (15% in the first 12 months of use), even with perfect use.17 Health Effects. The risks associated with the use of barrier methods of contraception include primarily the risk of unintended pregnancy and minor side effects associated with the method. These complaints include vaginal or penile irritation by spermicides and discomfort from a diaphragm that is too large. True, allergic reactions to latex male condoms or cervical caps are uncommon, but they can occur.46 Diaphragm and spermicide users have an increased risk of urinary tract infections compared with women who do not use contraceptives, and diaphragm and cervical cap users have a relative increased risk of toxic shock syndrome,63 which can be reduced by leaving a diaphragm in for no longer than 24 hours and a cap in for no longer than 48 hours. The absolute risk of toxic shock syndrome associated with use of the cervical cap or diaphragm is small. While it was once hoped that use of spermicidal preparations containing nonoxynol 9 would reduce the risk of HIV infection, it is now clear that no such protection is offered. In fact, studies suggest that frequent use of spermicides may enhance the risk of acquiring HIV infection. Although one report raised concerns about a possible link between spermicide use and the risk of congenital defects, several larger and better designed studies demonstrated no association.23

Fertility Awareness-Based Methods The risk of an unintended pregnancy per each coital act is 17–30% in midcycle and less than 1% during menses.51 Natural family planning methods, known as fertility- awareness-based methods, are based on the observation of signs and symptoms of the woman during her fertile phase. These methods include both calendar-based method and symptoms-based methods. The calendar-based methods include the Calendar Rhythm Method and the Standard Days Method; the symptoms-based methods include the Cervical Mucus Method, the Symptothermal Method, and the Two Days Method. These methods use information to estimate the period of fertility (the fertile window) during which time intercourse should be avoided. Clearly, the effectiveness of fertility awareness-based methods depends heavily on the willingness and ability of couples to use the methods consistently and correctly. Even with perfect use, these methods are complicated by difficulty in reliably estimating the fertile window.

Lactational Amenorrhea Method On a worldwide scale, more births are prevented by breastfeeding than by any other method of contraception. Further, breastfeeding has important health benefits for the infant and the mother. The lactational amenorrhea method (LAM) is highly effective for women who are (a) amenorrheic; (b) fully or nearly fully breastfeeding; or (c) less than 6 months postpartum. While there is no known negative impact on a woman’s health to using LAM, certain conditions may impact the appropriateness of using this method, including maternal HIV infection, medications used during breastfeeding, and certain conditions affecting the newborn.36 Breastfeeding is not recommended for women using certain drugs that may harm infant health, and some infants may have disorders that make breastfeeding difficult

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or inappropriate.36 For most women and most infants, however, LAM is safe for both mother and infant, and highly effective.

Emergency Contraception

Female Sterilization

Emergency contraception involves the use of POPs, combined estrogen and progestin pills, or copper IUDs to prevent pregnancy shortly after unprotected intercourse. The most common POP regimen is the use of 1.5 mg of levonorgestrel, which is administered as a single dose or as two 0.75 mg pills given separately—one taken as soon as possible after unprotected intercourse and the other taken 12 hours after the first pill. The most common combined estrogen-progestin regimen is the use of two doses of pills, taken 12 hours apart, with each dose consisting of 100 µg of ethinyl estradiol and 0.5 mg of levonorgestrel. The combined regimen is highly effective, reducing the risk of pregnancy by at least 74%.64 The levonorgestrel-only regimen appears to be even more effective and results in fewer side effects.65 Use of emergency contraceptive pills will not disrupt a pregnancy after implantation has occurred. The effectiveness of emergency contraceptive pills decreases substantially over time after unprotected intercourse. Thus, when used, they should be taken as soon as possible after unprotected intercourse, ideally within 72 hours. The regimen appears to continue to provide at least some benefit when the first dose is taken up to 120 hours after intercourse. For women who are otherwise appropriate candidates for IUD use, and particularly for those desiring ongoing use of an IUD, the copper IUD is highly effective in reducing the risk of pregnancy when inserted within 5 days of unprotected intercourse. If an IUD is inserted more than 5 days after ovulation, it may disrupt an established pregnancy. Approved regimens for emergency use of oral contraceptives are listed in Table 79-13. Health Effects. The most common side effects of emergency contraceptive pills include nausea and vomiting and irregular vaginal bleeding. Nausea and vomiting occur less frequently with the levonorgestrel-only regimen than with the combined regimen. Less frequent side effects include breast tenderness, headache, and abdominal pain.

Sterilization Surgical sterilization is estimated to be the most prevalent form of contraception in the world. Globally, approximately 180 million women and 43 million men have undergone tubal sterilization and TABLE 79-13. APPROVED REGIMENS FOR ORAL CONTRACEPTIVE USE AS EMERGENCY CONTRACEPTION

Trade Name Plan—B Ovrette∗ Preven† Ovral∗,Ogestrel* Alesse, Levlite, Aviane, Lessina Nordette, Levlen, Levora Portia, Seasonale, Lo/Ovral∗ Low-Ogestrel∗, Cryselle∗ Triphasil, Tri-Levlen Trivora, Enpresse

Formulation per Dose

vasectomy, respectively. In 2002, 27% of U.S. women aged 15–44 reported having had a tubal sterilization, while 9% of them reported that they relied on their partner’s vasectomy for contraception.53

Pills per Dose

0.75 mg of levonorgestrel 0.75 mg of levonorgestrel 100 µg of ethinyl estradiol 0.50 mg of levonorgestrel 100 µg of ethinyl estradiol 0.50 mg of levonorgestrel 120 µg of ethinyl estradiol 0.60 mg of levonorgestrel

1 20 2

120 µg of ethinyl estradiol 0.50 mg of levonorgestrel

4

5 4

∗The progestin is norgestrel, which contains two isomers, only one of which is bioactive (levonorgestrel); the amount of norgestrel in each tablet is twice the amount of levonorgestrel. †Since 2004, Preven is no longer manufactured. Source: Adapted from Trussell J, Ellertson C, Stewart F, et al. The role of emergency contraception. Am J Obstet Gynecol. 2004;190:S30–8.

Approximately half of tubal sterilizations in the United States are performed in the immediate postpartum period by partial salpingectomy66 with most of the remainder being performed at a time unrelated to pregnancy via laparoscopy by application of coagulating current or mechanical clips or bands. Although most laparoscopic sterilizations in the United States are performed using general anesthesia, local anesthesia can also be used and carries lower anesthetic risks. A new tubal occlusion device that is placed hysteroscopically was approved by the FDA in 2002. Findings from the U.S. Collaborative Review of Sterilization—a large U.S. multicenter cohort study confirm that tubal sterilization is highly effective. Nevertheless, pregnancies occur more often than previously thought and can occur many years after the procedure.67 The 10-year cumulative probability of pregnancy was highest among women having sterilization by spring clip application (36.5 per 1000 procedures). Women sterilized at a young age (age 18–27) were 2.7 times as likely to become pregnant as women sterilized at older ages (age 34–44). This may be due to younger women being more fecund and remaining fecund for a longer period than older women. Among women sterilized at a young age, the 10-year cumulative probability of pregnancy was nearly 5.0% with two methods (54.3 per 1000 for bipolar coagulation and 52.1 per 1000 for spring clip application). In the unlikely event of pregnancy after tubal sterilization, there is a substantial increased risk of ectopic gestation. In the U.S. Collaborative Review of Sterilization, the proportion of pregnancies that were ectopic ranged from 65% (bipolar coagulation) to 15% (clip application), with the overall proportion increasing with time since sterilization (61% in years 4–10 after sterilization compared with 20% in years 1–3). The absolute risk of ectopic pregnancy after sterilization was low (7.3 per 1000 procedures), however, with a range from 1.5 to 17.1 per 1000 procedures, depending on the method of occlusion.68 Since ectopic pregnancies occurred in the study as late as the tenth year after sterilization, women of childbearing age who have signs or symptoms of ectopic pregnancy should be evaluated even if they had a tubal sterilization in the distant past. Health Effects. The risk of dying from tubal sterilization in the United States is estimated to be one to two deaths per 100,000 procedures.51,69 Complications from general anesthesia are the leading cause of death. Major complications from tubal sterilization are uncommon but may occur in as many as 1–2% of procedures. In the U.S. Collaborative Review of Sterilization, unintended major surgery after laparoscopic sterilization occurred in 0.9% of procedures and rehospitalization occurred in 0.6%. Risk factors for these complications included diabetes, general anesthesia, previous abdominal or pelvic surgery, and obesity.70 While the existence of a so-called post-tubal syndrome of menstrual abnormalities has been debated since the early 1950s, most recent findings argue strongly against any such syndrome.71 In the U.S. Collaborative Review of Sterilization, women at 5 years after sterilization were no more likely to have a syndrome of menstrual abnormalities than women whose husbands underwent vasectomy.72 Sterilization is intended to be permanent, and most women remain satisfied with their decision to have the procedure. However, regret at having undergone tubal sterilization is not rare, with women sterilized at a young age more likely to express later regret, regardless of the number of children they had at the time of sterilization.73 In the U.S. Collaborative Review of Sterilization, the 14-year cumulative probability of requesting information about reversal was 40% among women aged 18–24 at sterilization.74

Male Sterilization Most vasectomies are performed with either the no-scalpel technique (a small puncture) or through an incision under local anesthesia, using any of a series of available vas occlusion techniques. Most studies of

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the effectiveness of vasectomy are case series done by individual physicians or institutions; they do not allow for a comparison of the methods of vas occlusion. Such studies report failure rates of approximately 0.15% (Fig. 79-1),17 but the long-term effectiveness of vasectomy is less well studied than that for tubal sterilization. The risk of vasectomy failure is likely to vary by vasectomy technique. The risk of pregnancy after vasectomy can be reduced by avoiding unprotected intercourse until semen analysis, performed at 3 months or more after the procedure, has demonstrated vasectomy effectiveness.

infants of birth order five and greater.80 Birth spacing influences survival during the neonatal and postneonatal periods and throughout the years before the fifth birthday. In sum, family planning has a major impact on the health of individuals, families, and society. Major progress has been made over the last several decades in helping individuals to achieve their reproductive intentions, but there is substantial room for improvement. Continued progress will benefit both individual and public health.

Health Effects. The risk of death attributable to vasectomy is extremely low and clearly lower than that for tubal sterilization. Major morbidity is also uncommon. Although as many as 50% of men may experience minor complications, such as swelling of the scrotal tissue, bruising, and pain, these generally subside without treatment within 1–2 weeks after vasectomy.75 Hematoma formation and infection occur much less frequently (each in less than 5% of procedures) and generally are not serious. The long-term health effects of vasectomy are now well characterized. After studies in monkeys suggested a possible increase in risk of cardiovascular disease, numerous epidemiological investigations in men found that vasectomy does not increase the risk of atherosclerosis, myocardial infarction, coronary heart disease, or all-cause mortality.51,76 Although several studies in the early 1990s found an association between vasectomy and risk of prostate cancer, more recent studies provide strong evidence against any causal association.77,78 Questions remain regarding a possible post-vasectomy pain syndrome. Small surveys with low response rates and no comparison groups have reported rates of chronic epididymal, scrotal, or testicular pain in 2–15% of men after vasectomy.49 By contrast, The Health Status of American Men Study found a very low rate of epididymitis-orchitis at 12 months after vasectomy (24.7 per 10,000 person-years), which was approximately twice that for men who did not have a vasectomy (13.6 per 10,000 person-years).79

REFERENCES

CONCLUDING COMMENTS

If the prediction that there will be no fundamentally new approaches to family planning in the foreseeable future materializes, then individuals will be making choices about family planning from among existing options for some time. The health effects of contraceptive use have been studied far more extensively than most medical interventions, and the bottom line is clear—for most healthy women, the use of any method of contraception will be safer than the use of no contraceptive method. While some contraceptive methods require more effort to use properly than others, it is evident that consistent and correct use of contraceptives will maximize effectiveness and minimize side effects. It is also clear that the better informed people are about how best to achieve their reproductive intentions, the more likely they are to be able to do so. Helping individuals achieve their reproductive intentions will have profound effects on fertility, health, and society. Family planning can influence health by (a) permitting a woman to bear children at an age when the risk of health problems to her and her offspring is lowest; (b) permitting a couple to choose the number of children they wish to have; (c) permitting a couple to decide the spacing of their children; and (d) providing safe and effective measures of family planning that are part of a service program that includes information, education, and comprehensive preventive health services. The risk of health problems during pregnancy increases with age and with the number of pregnancies. The use of family planning enhances both maternal health and infant health by permitting women to delay the birth of their first child and to avoid childbearing in their later reproductive years, if so desired. Linked birth and infant death records in the United States show higher infant mortality rates for young mothers (ages 10–14) and for women in their later reproductive years (ages 35 and older). In addition, the risk of infant death is lowest for infants of second and third birth order, and highest for

Disaster Preparedness and Response 1. Kizer KW. Lessons learned in public health emergency management: personal reflections. Prehospital Disaster Med. 2000;15:209–14. 2. Alexander D. Terrorism, disasters, and security. Prehospital Disaster Med. 2003;28:165–9. 3. Lillibridge SR, Burkle FM, Noji EK. Disaster mitigation and humanitarian assistance training for uniformed service medical personnel. Mil Med. 1994;159:397–403. 4. Sanderson LM. Toxicologic disasters: natural and technologic. In: Sullivan JB, Krieger GR, eds. Hazardous Materials Toxicology, Clinical Principles of Environmental Health. Baltimore, MD: Williams & Wilkins; 1992:326–31. 5. Noji EK. Public health challenges in technological disaster situations. Arch Public Health. 1992;50:99–104. 6. Office of Foreign Disaster Assistance. Significant Disasters from 1990 to 1995—World Disaster Report. Washington, DC: Office of Foreign Disaster Assistance; 1996:84. 7. Logue JN. Disasters, the environment, and public health: improving our response. Am J Public Health. 1996;86:1207–10. 8. Baxter PJ. Review of major chemical incidents and their medical management. In: Murray V, ed. Major Chemical Disasters—Medical Aspects of Management. London: Royal Society of Medicine Services Limited; 1990:7–20. 9. Binder S. Deaths, injuries, and evacuations from acute hazardous materials releases. Am J Public Health. 1989;79:1042–4. 10. Fong F, Scrader DC. Radiation disasters and emergency department preparedness. Emerg Med Clin North Am. 1996;14:349–70. 11. Anspaugh LR, Catlin RJ, Goldman M. The global impact of the Chernobyl reactor accident. Science. 1988;242:1513–9. 12. Mahoney MC, Lawvere S, Falkner KL, et al. Thyroid cancer incidence trends in Belarus: examining the impact of Chernobyl. Int J Epidemiol. 2004;33:1025–33. 13. Burkle FM. Complex, humanitarian emergencies: I. Concepts and participants. Prehospital Disaster Med. 1995;10:36–42. 14. Laquer W. Postmodern terrorism. Foreign Aff. 1996;75:24–36. 15. Okumura T, Takasu N, Ishimatsu S, et al. Report on 640 victims of the Tokyo subway sarin attack. Ann Emerg Med. 1996;28:129–35. 16. Wasley A. Epidemiology in the disaster setting. Curr Issues Public Health. 1995;1:131–5. 17. United States Mission to the United Nations. Global Humanitarian Emergencies, 1996. New York: ESCSOC Section of the United States Mission to the United Nations 1996. 18. International Federation of Red Cross and Red Crescent Societies. World Disasters Report 1996. New York: Oxford University Press; 1996. 19. Baxter PJ, Ing RT, Falk H, et al. Medical aspects of volcanic disasters: an outline of the hazards and emergency response measures. Disasters. 1982;6:268–76. 20. Baxter PJ, Ing RT, Falk H, et al. Mount St Helens eruptions: the acute respiratory effect of volcanic ash in a North American community. Arch Environ Health. 1983;38:38–43. 21. Centers for Disease Control and Prevention. Surveillance for respiratory disease following eruptions of Mt St Helens. MMWR. 1980; 29:252.

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Health-Care Planning, Organization, and Evaluation

22. Baxter PJ, Kapila M, Mfonfu D. Lake Nyos disaster, Cameroon, 1986: the medical effects of large scale emission of carbon dioxide. BMJ. 1989;298:1437–41. 23. Bilqis AH, Hoque R, Bradley S, et al. Environmental health and the 1991 Bangladesh cyclone. Disasters. 1993;17:143–52. 24. Sommer AS, Mosley WH. East Bengal cyclone of November 1970. Lancet. 1972;1:1029–36. 25. Lillibridge SR. Managing the Environmental Health Aspects of Disasters: Water, Human Excreta, and Shelter. In: Noji EK, ed. Public Health Consequences of Disasters. New York: Oxford University Press; 1997:65–78. 26. Noji EK. The medical consequences of earthquakes: coordinating the medical and rescue response. Disaster Manag. 1991;4:32–40. 27. Office of Foreign Disaster Assistance. World Wide Disasters from 1900 to 1996. Washington, DC: Office of Foreign Disaster Assistance;1996. 28. Teeter DS. Illnesses and injuries reported at disaster application centers following the 1994 Northridge earthquake. Mil Med. 1996;161: 526–30. 29. Office of Foreign Disaster Assistance. Report of the Durunka oil fires. Washington, DC: Office of Foreign Disaster Assistance; 1994. 30. Noji EK. Disaster epidemiology. Emerg Med Clin North Am. 1996;14:289–300. 31. Lillibridge SR. Industrial disasters. In: Noji EK, ed. Public Health Consequences of Disasters. New York: Oxford University Press; 1997:354–72. 32. Project Ploughshares. Armed conflicts report 2004. Available at http://www.ploughshares.ca/content/ACR/ACR00/ACR04-Introduction.html. Accessed 14 April, 2005. 33. Sivard RL. World Military and Social Expenditures 1996. Washington, DC: World Priorities; 1996. 34. Toole MJ. The public health consequences of inaction: lessons learned responding to sudden population displacement. In: Cahill KM, ed. The Framework for Survival: Health, Human Rights, and Humanitarian Assistance in Conflicts and Disasters. New York: Basic Books; 1993:144–58. 35. United Nations High Commissioner for Refugees. Available at http://www.unhcr.ch/cgi-bin/texis/vtx/basics. Accessed 14 April, 2005. 36. Toole MJ, Galson S, Brady W. Are war and public health compatible? Lancet. 1993;341:1193–6. 37. Burkholder BT, Toole MJ. Evolution of complex disasters. Lancet. 1995;346:1012–5. 38. Sharp TW, DeFraites RF, Thornton SA, et al. Illness in journalists and relief workers during international relief efforts in Somalia, 1992–93. J Travel Med. 1995;2:70–6. 39. Cobey JC, Flanigan A, Foege WH. Effective humanitarian aid: our only hope for intervention in a civil war. JAMA. 1993;270:632–4. 40. Strada G. The horror of land mines. Sci Am. 1996;274:40–5. 41. Rodoplu U, Arnold J, Ersoy G. Terrorism in Turkey. Prehosp Disast Med. 2003;18:152–60. 42. World Health Organization. Health Aspects of Chemical and Biological Weapons. Geneva, Switzerland: World Health Organization; 1970:98–99. 43. SAEM Disaster Medicine White Paper Subcommittee. Disaster medicine: current assessment and blueprint for the future. Acad Emerg Med. 1995;12:1068–76. 44. Noji EK, Armenian HK, Oganessian A. Issues of rescue and medical care following the 1988 Armenian earthquake. Int J Epidemiol. 1993;22:1070–6. 45. Thiel CC, Schneider JE, Hiatt D, et al. 9-1-1 EMS process in the Loma Prieta earthquake. Prehospital Disaster Med. 1992; 348–58. 46. Schultz CH, Koenig KL, Noji EK. A medical disaster response to reduce immediate mortality after an earthquake. N Engl J Med. 1996;334:438–44. 47. Macrai J, Zwi AB. Food as an instrument of war in contemporary African famines: a review of the evidence. Disasters. 1992;16: 299–321.

48. Moore PS, Marfin AA, Quenemoen LE, et al. Mortality rates in displaced and resident populations of central Somalia during 1992 famine. Lancet. 1993;341:935–8. 49. Toole MJ, Waldman RJ. Refugees, displaced persons and relief today. Public Health Rev. 1996; :35–45. 50. Perrin P. War and Public Health. Geneva, Switzerland: International Committee of the Red Cross; 1996. 51. Cieslak TJ, Christopher GW, Eitzen EM. Bioterrorism alert for health care workers. In: Fong IW Alibek K, eds. Bioterrorism and Infectious Agents. New York: Springer Science & Business Media Inc; 2005:215–34. 52. Johannigman JA. Disaster preparedness: it’s all about me. Crit Care Med. 2005;33(suppl):S22–8. 53. Garrett LC, Magruder C, Molgard CA. Taking the terror out of bioterrorism: planning for a bioterrorist event from a local perspective. J Public Health Manag Pract. 2000;6:1–7. 54. Abbott D. Disaster public health considerations. Prehospital Disaster Med. 2000;15:158–66. 55. Lillibridge SR, Noji EK, Burkle FM. Disaster assessment: the emergency health evaluation of a population affected by a disaster. Ann Emerg Med. 1993;22:1715–20. 56. Toole MJ. The rapid assessment of health problems in refuge and displaced populations. Medi Glob Surviv. 1994;1:200–7. 57. Hlady WG, Quenemoen LE, Amenia-Cope RR, et al. Rapid needs assessment after Hurricane Andrew in South Florida using a modified cluster sample method. Ann Emerg Med. 1994;23:719–25. 58. Marfin AA, Moore J, Collins C, et al. Infectious disease surveillance during emergency relief to Bhutanese refugees in Nepal. JAMA. 1994;272:377–81. 59. O’Carroll PW, Friede A, Noji EK, et al. The rapid implementation of a statewide emergency health information system during the 1993 Iowa flood. Am J Public Health. 1995;85:564–7. 60. Armenian HK. Perceptions from epidemiologic research in an endemic war. Soc Sci Med. 1989;28:643–7. 61. Weinberg J, Simmonds S. Public health, epidemiology, and war. Soc Sci Med. 1995;40:1663–9. 62. Yip R, Sharp TW. Acute malnutrition and high childhood mortality related to diarrhea. JAMA. 1993;270:587–90. 63. Seaman J. Disaster epidemiology: or why most disaster relief is ineffective. Injury. 1990;21:5–8. 64. Hakewill PA, Moren A. Monitoring and evaluation of relief programmes. Trop Doct. 1991;21:24–8. 65. Lord EJ, Cieslak TJ. Joint regional exercise (“JREX”) 2000. Disaster Manag Response. 2004;2:24–7. 66. Roy N, Shah H, Patel V, et al. The Gujarat earthquake (2001) experience in a seismically unprepared area: community hospital medical response. Prehospital Disaster Med. 2002;17:186–95. 67. Okumura T, Suzuki K, Fukuda A, et al. The Tokyo subway sarin attack: disaster management, part 1: community emergency response. Acad Emerg Med. 1998;5:613–7. 68. Teague DC. Mass casualties in the Oklahoma City bombing. Clin Orthop Relat Res. 2004;422:77–81. 69. World Health Organization. South Asia earthquake and tsunamis. Inter-agency rapid health assessment-final report. Available at http://www.who.int/hac/crises/international/asia_tsunami/final_rep ort/en/index.html. Accessed 12 March, 2005. 70. Barbera JA, Lozano M. Urban search and rescue medical teams: FEMA task force system. Prehospital Disaster Med. 1993;8:88–92. 71. Okumura T, Takasu N, Ishimatsu S, et al. Report on 640 victims of the Tokyo subway sarin attack. Ann Emerg Med. 1996;28: 129–35. 72. Joint Commission on Accreditation of Healthcare Organizations. 2003 Hospital Accreditation Standards. Oakbrook Terrace, IL: JCAHO; 2003:221–4. 73. Zane RD, Prestipino AL. Implementing the hospital emergency incident command system: an integrated delivery system’s experience. Prehospital Disaster Med. 2004;19:311–7.

79 74. Prezant DJ, Clair J, Belyaev S, et al. Effects of the August 2003 blackout on the New York City healthcare delivery system: a lesson for disaster preparedness. Crit Care Med. 2005;33(suppl):S96–101. 75. Wolf Y, Bar-Dayan Y, Mankuta D, et al. An earthquake disaster in Turkey: assessment of the need for plastic surgery services in a crisis intervention field hospital. Plast Reconstr Surg. 2001;107:163–8. 76. Brugger H, Durrer B, Adler-Kastner L, et al. Field management of avalanche victims. Resuscitation. 2001;51:7–15. 77. World Health Organization. South Asia earthquake and tsunamis. Inter-agency rapid health assessment-final report. Food and Nutrition. Available at http://www.who.int/hac/crises/international/ asia_tsunami/final_report/en/index.html. Accessed 12 March, 2005. 78. Centers for Disease Control and Prevention. Fact Sheet. Food safety after a tsunami. Available at http://www.bt.cdc.gov/disasters/ tsunamis/foodsafety.asp. Accessed 12 March, 2005. 79. Török TJ, Tauxe RV, Wise RP, et al. A large community outbreak of salmonellosis caused by intentional contamination of restaurant salad bars. JAMA. 1997;278:389–95. 80. Kloavic SA, Kimura A, Simons SL, et al. An outbreak of Shigella dysenteriae Type 2 among laboratory workers due to intentional food contamination. JAMA. 1997;278:396–8. 81. Majkowski J. Strategies for rapid response to emerging foodborne microbial hazards. Emerg Infect Dis. 1997;3:551–4. 82. Burkle FM. Acute-phase mental health consequences of disasters: implications for triage and emergency medical services. Ann Emerg Med. 1996;28:119–28. 83. Ursano RJ, McCarroll JE. The nature of a traumatic stressor: handling dead bodies. J Nerv Ment Dis. 1990;178:396–8. 84. Schonfeld DJ. Supporting children after terrorist events: potential roles for pediatricians. Pediatr Ann. 2003;32:182–7. 85. UNICEF. The State of the World’s Children. New York: Oxford University Press; 1996. 86. Rundell JR, Christopher GW. Individual and group responses to bioterrorism agent exposure: differentiating manifestations of infection from psychiatric disorder and fears of having been exposed. In: Ursano RJ, Fullerton AE, Norwood CS, eds. Planning for the Psychological Effects of Bioterrorism: Individuals, Communities and the Public Health. Cambridge,MA University Press; 2003. 87. Centers for Disease Control and Prevention. Public health emergency preparedness and response. Available at http://www.bt.cdc.gov/. Accessed 31 August, 2003. 88. Blank S, Moskin LC, Zucker JR. An ounce of prevention is a ton of work: mass antibiotic prophylaxis for anthrax, New York City, 2001. Emerg Infect Dis. 2003;9:615–22. 89. Mason J, Cavalie P. Malaria epidemic in Haiti following a hurricane. Am J Trop Med Hyg. 1965;14:533–9. 90. Anonymous. El Nino and associated outbreaks of severe malaria in highland populations in Irian Jaya, Indonesia: a review and epidemiological perspective. Southeast Asian J Trop Med Public Health. 1999;30:608–19. 91. Centers for Disease Control and Prevention. Emergency mosquito control associated with Hurricane Andrew—Florida and Louisiana, 1992. MMWR. 1993;42:240–2. 92. UNICEF. Assisting in Emergencies: A Resource Handbook for UNICEF Field Staff. New York: UNICEF; 1992:34–365. 93. United Nations High Commissioner for Refugees. Water Manual for Refugee Situations. Geneva, Switzerland: United Nations High Commissioner for Refugees; 1992. 94. California Association of Environmental Health Administartors. Disaster Field Manual for Environmental Health Specialists, 1998. 95. Howard MJ, Brillman JC, Burkle FM. Infectious disease emergencies in disasters. Emerg Med Clin North Am. 1996;14:413–28. 96. Aghababian RV, Teuscher J. Infectious diseases following major disasters. Ann Emerg Med. 1992;21:362–7. 97. Centers for Disease Control and Prevention. Coccidioidomycosis following the Northridge earthquake. MMWR 1994;43:194–5.

Categorical Public Health Sciences

1313

98. Toole MJ, Steketee RW, Waldman RJ, et al. Measles prevention and control in emergency settings. Bull World Health Organ. 1989;67: 381–8. 99. Nagels JW, Davies-Colley RJ, Donnison AM, Muirhead RW. Faecal contamination over flood events in a pastoral agricultural stream in New Zealand. Water Sci Technol. 2002;45:45–52. 100. Sehgal SC, Sugunan AP, Vijayachari P. Outbraek of leptospirosis after the cyclone in Orissa. Natl Med J India. 2002;15:22–3. 101. Heath SE, Kenyon SJ, Zepeda-Sein CA. Emergency management of disasters involving livestock in developing countries. Rev Sci Tech. 1999;18:256–71. 102. Noji EK. Public health issues in disasters. Crit Care Med. 2005;33(suppl):S29–33. 103. Shears P. Epidemiology and infection in famine and disasters. Epidemiol Infect. 1991;107:241–51. 104. Toole MJ. Micronutrient deficiencies in refugees. Lancet. 1992;339: 1214–5. 105. Hansch S. How Many People Die of Starvation in Humanitarian Emergencies? Washington DC: Refugee Policy Group, 1995. 106. Emergency Management Institute. Incident Command System Independent Study Guide (IS-195). Washington DC: Federal Emergency Management Agency; January, 1998. 107. Gilchrist MJR. A national laboratory network for bioterrorism: evolution of a prototype network of laboratories for performing routine surveillance. Mil Med. 2000;165(suppl 2):28–31. 108. Kerry ME. 62nd civil support team supports the secret service in a national security special event. Army Chem Rev. 2002;PB 3-02-2: 13–16. 109. Department of Homeland Security. National Response Plan. November, 2004. 110. Moritsugu KP, Reutershan TP. The national disaster medical system: a concept in large-scale emergency medical care. Ann Emerg Med. 1986;15:1496–8. 111. Esbitt D. The strategic national stockpile: roles and responsibilities of health care professionals for receiving the stockpile assets. Disaster Manag Response. 2003;1:68–70. 112. Goma Epidemiology Group. Public health impact of the Rwandan refugee crisis: what happened in Goma, Zaire, in July, 1994? Lancet. 1995;345:339–45. 113. Boss LP, Toole MJ, Yip R. Assessments of mortality, morbidity, and nutritional status in Somalia during the 1991–1992 famine: recommendations for standardization of methods. JAMA. 1994;272:371–6. 114. Swiss S, Giller JE. Rape as a crime of war—a medical perspective. JAMA 1993;270:612–5. 115. Heise LL, Raikes A, Watts CH, et al. Violence against women: a neglected public health issue in less developed countries. Soc Sci Med. 1994;39:1165–79. 116. Cieslak TJ, Henretig FM. Ring-a-ring-a-roses: bioterrorism and its peculiar relevance to pediatrics. Curr Opin Pediatr. 2003;15:107–11.

Maternal and Child Health 1. Alexander GR. Maternal and child health (MCH). Encyclopedia of Health Care Management. Thousand Oaks, CA: Sage Publications; 2004. 2. Maternal and Child Health Bureau. Title V: A snapshot of Maternal and Child Health 2000. Rockville, MD: Health Resources and Services Administration; 2000. 3. Margolis LH, Cole G, Kotch J. Historical foundations of maternal and child health. In: Kotch J, ed. Maternal and Child Health Programs, Policies and Problems. Gaithersburg, MD: Aspen Publishers Inc.; 1997 (2nd ed, 2005). 4. Dollfus C, Patetta M, Siegel E, et al. Infant mortality: a practical approach to the analysis of the leading causes of death and risk factors. Pediatrics. 1990;86:176–83. 5. National Center for Family-Centered Care. Family-Centered Care for Children with Special Health Care Needs. Bethesda, MD: Association for the Care of Children’s Health; 1989.

1314

Health-Care Planning, Organization, and Evaluation

6. Centers for Disease Control and Prevention. Recommendations to improve preconception health and health care—United States: a report of the CDC/ATDSR Preconception Care Work Group and the Select Panel on Preconception Care. MMWR. 2006;55(No. RR-6). 7. Dailard C. Challenges Facing Family Planning Clinics and Title X. The Guttmacher Report on Public Policy; April 2001:8–11. 8. GAO. Food and Drug Administration Decision Process to Deny Initial Application for Over-the-Counter Marketing of the Emergency Contraceptive Drug Plan B Was Unusual. GAO-06-109, November 2005. 9. Pickering L, ed. Red Book: 2003 Report of the Committee on Infectious Diseases, 26th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2003. 10. McPherson M, Arango P, Fox H, et al. A new definition of children with special health care needs. Pediatrics. 1998;102:137–9. 11. Chapman J, Siegel E, Cross A: Home visitors and child health: analysis of selected programs. Pediatrics. 1990;85:1059–68. 12. Olds DL, Kitzman H: Can home visitation improve the health of women and children at environmental risk? Pediatrics. 1990;86: 108–16.

Preventive Medicine Support of Military Operations 1. Letterman J: Medical Recollections of the Army of the Potomac. New York: D. Appleton and Co.; 1866. 2. Withers BG, Erickson RL, Petruccelli BP, et al. Preventing disease and non-battle injuries in deployed units. Mil Med. 1994;159:39–43. 3. Weina PJ, Neafie RC, Wortmann G, et al. Old world leishmaniasis: an emerging infection among deployed U.S. military and civilian workers. CID. 2004;39:1674–80. 4. Sanders JW, Putnam SD, Frankart C, et al. Impact of illness and noncombat injury during operations Iraqi freedom and enduring freedom (Afghanistan). Am J Trop Med Hyg. 2005;73(4):713–9. 5. Shorr AF, Scoville SL, Cersovsky SB, et al. Acute eosinophilic pneumonia among U.S. military personnel deployed in or near Iraq. JAMA. 2004;292:2997–3005. 6. Kotwal RS, Wenzel RB, Sterling AS, et al. An outbreak of malaria in U.S. army rangers returning from Afghanistan. JAMA. 2005;293: 212–6. 7. Coates JB, Jr, Hoff EC, Hoff PM, eds. Preventive Medicine in World War II. Volume IV. Communicable Diseases Transmitted Chiefly through Respiratory and Alimentary Tracts. Washington, DC: Medical Department, United States Army, 1958. 8. Reister FA. Battle Casualties and Medical Statistics. U.S. Army Experiences in the Korean War. Washington, DC: The Surgeon General, Department of the Army; (Undated). 9. Washington Headquarters Services Directorate for Information, Operations and Reports, Department of Defense. U.S. Casualties in Southeast Asia. Statistics as of April 30, 1985. Washington, DC: Government Printing Office; 1985. 10. Lederberg J, Shope RE, Oaks SC, Jr (eds): Emerging Infections. Microbial Threats to Health in the United States. Committee on Emerging Microbial Threats to Health, Division of Health Sciences Policy, Division of International Health, Institute of Medicine, Washington, DC: National Academy Press, 1992. 11. Heymann DL, ed. Control of Communicable Diseases Manual. Washington, DC: American Public Health Association; 2004. 12. Acinetobacter baumannii infections among patients at military medical facilities treating U.S. service members, 2002–2004. MMWR. 2004;53(45):1063–6. 13. Rapid health response, assessment, and surveillance after a tsunami—Thailand, 2004–2005. MMWR. 2005;54(3):61–4. 14. U.S. Army Center for Health Promotion and Preventive Medicine. A Soldier’s Guide to Staying Healthy in Afghanistan and Pakistan. SHG 001-0302. 15. Slim W. Defeat into Victory. London: Cassell and Company; 1956. 16. Hanson K. Surveillance in action, U.S. Marine Corps Forces in the Persian Gulf War. In: Kelly PW, ed. Military Preventive Medicine:

Mobilization and Deployment. Washington, DC: Walter Reed Army Institute of Research; 2005.

Public Health Workforce 1. Health Resources and Services Administration. Enumeration 2000. New York: Columbia University School of Nursing; 2000. 2. American Public Health Association. The Definition and Role of Public Health Nursing: a Statement of APHA Public Health Nursing Section. Washington, DC: American Public Health Association; 1996. 3. Evans, RG, ML Barer, TR Marmor. Why Are Some People Healthy and Others Not? The Determinants of Health of Populations. New York: Aldine De Gruyter; 1994. 4. Public Health Functions Steering Committee. Public Health in America Statement, Fall, 1994. (Current members of this group include the American Public Health Association, the Association of Schools of Public Health, Association of State and Territorial Health Officers, National Association of County and City Health Officials, Environmental Council of the States, National Association of State Alcohol and Drug Abuse Directors, National Association of State Mental Health Program Directors, Partnership for Prevention and the Public Health Foundation.) 6. Pope AM, Snyder MA, Mood LH, eds. Nursing Health and Environment. Washington, DC: National Academy Press; 1995. 7. McNeil C Public Health Nursing within Core Public Health Functions Olympia, WA: Washington State Department of Health: July, 1993. 8. Gebbie K, Rosenstock L, Hernandez LM, eds. Who Will Keep the Public Healthy? Educating Public Health Professionals for the 21st Century. Washington, DC: National Academies Press; 2003.

Family Planning 1. Centers for Disease Control and Prevention. Achievements in public health, 1900–1999: family planning. Morb Mortal Wkly Rep. 1999; 48(47):1073–80. 2. World Contraceptive Use 2003. Available at http://www.un.org/esa/ population/publications/contraceptive2003/WallChart_CP2003_ pressrelease.htm. Accessed July 11, 2005. 3. Singh S, Darroch JE, Vlassoff M, et al. Adding It Up: The Benefits of Investing in Sexual and Reproductive Health Care. Washington, DC, and New York: The Alan Guttmacher Institute and UNFPA; 2004. 4. United Nations Population Fund. Available at http://www.unfpa.org/ mothers/contraceptive.htm. Accessed May 18, 2007. 5. World Health Organization. Abortion: A Tabulation of Available Data on the Frequency and Mortality of Unsafe Abortion. 3rd ed. Geneva, Switzerland: World Health Organization; 1997. 6. Rosenfield A, Schwartz K. Population and development—shifting paradigms, setting goals. N Engl J Med. 2005;352:647–9. 7. United Nations Population Fund. Reducing Poverty and Achieving the Millennium Development Goals: Arguments for Investing in Reproductive Health & Rights. New York: United Nations Population Fund; 2005. 8. Alan Guttmacher Institute. Facts in Brief: Contraceptive Use. New York: The Alan Guttmacher Institute. Available at http://www. agi-usa.org/pubs/fb_contr_use.html. Accessed July 16, 2005. 9. National Survey Family Growth, 2002. Available at http://www.cdc.gov/ nchs/about/major/nsfg/nsfgcycle6.htm. Accessed July 16, 2005. 10. Henshaw SK, Unintended pregnancy in the United States. Fam Plann Perspect. 1998;30:24–46. 11. Ventura SJ, Abma JC, Mosher WD, et al. Estimated Pregnancy Rates for the United States, 1990–2000: An Update. National vital statistics reports; vol 52 no 23. Hyattsville, MD: National Center for Health Statistics; 2004. 12. Alan Guttmacher Institute. Preventing unintended pregnancy in the U.S. 2004 Series, No.3. Available at http://www.agi-usa.org/pubs/ ib2004no3.pdf. Accessed July 16, 2005.

79 13. Sonfield A, Gold RB. Public Funding for Contraceptive, Sterilization, and Abortion Services, FY 1980-2001. New York: The Alan Guttmacher Institute; 2005. 14. Alan Guttmacher Institute. Medicaid: A Critical Source of Support for Family Planning in the United States. New York: The Alan Guttmacher Institute; 2005. 15. Kaunitz AM, Shields WC. Contraceptive equity and access in the United States: a 2005 update. Contraception. 2005;71:317–8. 16. Frost JJ. Public or private providers? U.S. women’s use of reproductive health services. Fam Plann Perspec. January/February 2001;33(1):4–12. 17. Trussell J. Contraceptive failure in the United States. Contraception. 2004;70:89–96. 18. Sonnenberg FA, Burkman RT, Hagerty CG, et al. Costs and net health effects of contraceptive methods. Contraception. 2004;69: 447–59. 19. Lee NC, et al. The reduction in risk of ovarian cancer associated with oral contraceptive use. N Engl J Med. 1987;316:650–5. 20. Kendrick JS, Lee NC, Wingo PA, et al. Oral contraceptive use and the risk of endometrial cancer. JAMA. 1987;257:796–800. 21. The Practice Committee of the American Society for Reproductive Medicine. Hormonal contraception: recent advances and controversies. Fertil Steril. 2004;82(1):26–32. 22. La Vecchia C, Altieri A, Franceschi S, et al. Oral contraceptives and cancer: an update, Drug Saf. 2001;24(10):741–54. 23. Farley TM, Meirik O, Chang CL, et al. Combined oral contraceptives, smoking, and cardiovascular risk. J Epidemiol Community Health. 1998;52(12):775–85. 24. Petitti DB. Clinical practice. Combination estrogen-progestin oral contraceptives. N Engl J Med. 2003;349(15):1443–50. 25. Schwingl PJ, Ory HW, Visness CM. Estimates of the risk of cardiovascular death attributable to low-dose oral contraceptives in the United States. Am J Obstet Gynecol. 1999;180:241–9. 26. Neuberger J, Forman D, Doll R, et al. Oral contraceptives and hepatocellular carcinoma. Br Med J. 1986;292:1355–7. 27. World Health Organization. Collaborative study of neoplasia and steroid contraceptives: combined oral contraceptives and liver cancer. Int J Cancer. 1989;43:254–9. 28. The Collaborative MILTS Project Team. Oral contraceptives and liver cancer: results of the multicentre international liver tumor study (MILTS). Contraception. 1997;56:275–84. 29. Collaborative Group on Hormonal factors in Breast Cancer: Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data in 53,297 women with breast cancer and 100,239 women without breast cancer from 54 epidemiological studies. Lancet. 1996;347:1713–27. 30. Collaborative Group on Hormonal factors in Breast Cancer: Breast cancer and hormonal contraceptives: further results. Contraception. 1996;54:1S–196S. 31. Marchbanks P, McDonald J, Wilson H, et al. Oral contraceptives and the risk of breast cancer. N Engl J Med. 2002;346:2025–32. 32. Grabrick DM, Hartmann LC, Cerhan JR, et al. Risk of breast cancer with oral contraceptive use in women with a family history of breast cancer. JAMA. 2000;284(14):1791–8. 33. Narod SA, Dube MP, Klijn J, et al. Oral contraceptives and the risk of breast cancer in BRCA1 and BRCA2 mutation carriers. J Natl Cancer Inst. 2002;94(23):1773–9. 34. Skegg DC, Paul C, Spears GF, et al. Progestogen-only oral contraceptives and risk of breast cancer in New Zealand. Cancer Causes Control. 1996;7(5):513–9. 35. Moreno V, Bosch FX, Muñoz N, et al. International Agency for Research on Cancer (IARC) Multicentre Cervical Cancer Study Group. Effect on oral contraceptives in women with human papilloma virus. Lancet. 2002;359:1085–92. 36. World Health Organization. Medical Eligibility Criteria for Contraceptive Use, 3rd ed, Geneva, Switzerland: World Health Organization; 2004. Available at http://www.who.int/reproductive-health/ publications/mec/mec.pdf.

Categorical Public Health Sciences

1315

37. Lunelle [package insert]. Peapack, NJ: Pharmacia Corp; 1999. 38. World Health Organization. Task force on research, on introduction, and transfer of technologies for fertility regulation, special programme of research, development, and research training in human reproduction, a multi-centered phase III comparative study of two hormonal contraceptive preparations given once-a-month by intramuscular injection, I: contraceptive efficacy and side effects. Contraception. 1988;37:1–20. 39. Kaunitz AM. Injectable contraception. In: Sciarra JJ, ed. Gynecology and Obstetrics. New York: Lippincott Williams & Wilkins; 1999:1–10. 40. Garceau RJ, Wajszczuk CJ, Kaunitz AM, et al. Bleeding patterns of women using Lunelle monthly contraceptive injections (medroxyprogesterone acetate and estradiol cypionate injectable suspension) compared with those of women using Ortho-Novum 7/7/7 (norethindrone/ethinyl estradiol triphasic) or other oral contraceptives. Contraception. 2000;62:289–95. 41. Jewelewicz R. New developments in topical estrogen therapy. Fertil Steril. 1997;67:1–12. 42. Zieman M, Guillebaud J, Weisberg E, et al. Contraceptive efficacy and cycle control with the Ortho Evra/Evra transdermal system: the analysis of pooled data. Fertil Steril. 2002;77(2 Suppl 2):S13–18. 43. Audet MC, Moreau M, Koltun WD, et al. ORTHO EVRA/EVRA 004 Study Group. Evaluation of contraceptive efficacy and cycle control of a transdermal contraceptive patch vs. an oral contraceptive: a randomized controlled trial. JAMA. 2001;285(18):2347–54. 44. Dieben TO, Roumen FJME, Apter D. Efficacy, cycle control, and user acceptability of a novel combined contraceptive vaginal ring. Obstet Gynecol. 2002;100:585–93. 45. Roumen FJ, Apter D, Mulders TM, et al. Efficacy, tolerability and acceptability of a novel contraceptive vaginal ring releasing etonogestrel and ethinyl oestradiol. Hum Reprod. 2001;16(3):469–75. 46. Hatcher RA, Nelson AL, Zieman M, et al. A Pocket Guide to Managing Contraception, 2002-2003. Tiger, GA: The Bridging the Gap Foundation; 2002. 47. Oddsson K, Leifels-Fischer B, de Melo NR, et al. Efficacy and safety of a contraceptive vaginal ring (NuvaRing) compared with a combined oral contraceptive: a 1-year randomized trial. Contraception. 2005;71(3):176–82. 48. World Health Organization. Selected Practice Recommendations for Contraceptive Use. Geneva, Switzerland: World Health Organization; 2004. Available at http://www.who.int/reproductive-health/ publications/ spr/index.htm. 49. Peterson HB, Curtis KM. Long-acting methods of contraception. N Engl J Med. 2005;353:2169–75. 50. Curtis KM. Safety of implantable contraceptives for women: data from observational studies. Contraception. 2002;65:85–96. 51. Speroff L, Darney PD. A clinical Guide for Contraception, 3rd ed. Baltimore: Williams &Wilkins; 2001. 52. The Essentials of Contraceptive Technology. A handbook for clinical staff. Center for Communication Programs. Johns Hopkins Population Information Program; 2003. 53. Skegg DLG, Noonan EA, Paul C, et al. Depot medroxyprogesterone acetate and breast cancer: a pooled analysis of World Health Organization and New Zealand studies. JAMA. 1995;273:799–804. 54. Food and Drug Administration. Black Box Warning Added Concerning Long-Term Use of Depo-Provera Contraceptive Injection. Available at http://www.fda.gov/bbs/topics/ANSWERS/2004/ ANS01325.html. Accessed November 17, 2004. 55. Mosher WD, Martinez GM, Chandra A, et al. Use of Contraception and Use of Family Planning Services in the United States: 1982–2002, Centers for Disease Control and Prevention, Advance Data From Vital and Health Statistics, Number 350, December 10, 2004. 56. Hatcher RA, Trussell J, Stewart F, et al, eds. Contraceptive technology, 17th ed. New York: Ardent Media, Inc; 1998. 57. Ory HW. The women’s health study: ectopic pregnancy and intrauterine contraceptive devices: new perspectives. Obstet Gyecol. 1981;57: 137–41.

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58. Farley TMM, Rowe PJ, Rosenberg MJ, et al. Intrauterine devices and pelvic inflammatory disease: an international perspective. Lancet. 1992;339:785–8. 59. Hubacher D, Lara-Ricalde R, Taylor DJ, et al. Use of copper intrauterine devices and the risk of tubal infertility among nulligravid women. N Engl J Med. 2001;345(8):561–7. 60. Cramer DW, Schiff I, Schoenbaum SC, et al. Tubal infertility and the intrauterine device. N Engl J Med. 1985;312(15):941–7. 61. Daling JR, Weiss NS, Metch BJ, et al. Primary tubal infertility in relation to the use of an intrauterine device. N Engl J Med.1985;312 (15):937–41. 62. Centers for Disease Control and Prevention. Available at http:// www.cdc.gov/nchstp/od/latex.htm. Accessed September 6, 2005. 63. Schwartz B, Gaventa S, Broome CV, et al. Nonmenstrual toxic shock syndrome associated with barrier contraceptives: report of a casecontrol study. Rev Infect Dis. 1989;(Suppl 1): S43–S49. 64. Trussell J, Vaughan B. Contraceptive failure, method-related discontinuation and resumption of use: results from the 1995 National Survey of Family Growth. Fam Plann Perspect. 1999;31:64–72, 93. 65. Trussell J, Ellertson C, Stewart F, et al. The role of emergency contraception, Am J Obstet Gynecol. 2004;190:S30–8. 66. Peterson HB. A 40–year-old woman considering contraception. JAMA. 1998;279:1651–8. 67. Peterson HB, Xia Z, Hughes JM, et al. The U.S. Collaborative Review of Sterilization Working Group. The risk of pregnancy after tubal sterilization: findings from the U.S. Collaborative Review of Sterilization. Am J Obstet Gynecol. 1996;174:1161–70. 68. Peterson HB, Xia Z, Hughes JM, et al. The U.S. Collaborative Review of Sterilization Working Group. The risk of pregnancy after tubal sterilization. N Engl J Med. 1997;336:762–7. 69. Escobedo LG, Peterson HB, Grubb GS, et al. Case-fatality rates for tubal sterilization in U.S. hospitals, 1979 to 1980. Am J Obstet Gynecol. 1989;160:147–50.

70. Jamieson DJ, Hillis SD, Duerr A, et al. Complications of interval laparoscopic tubal sterilization: findings from the United States collaborative review of sterilization. Obstet Gynecol. 2000;96(6): 997–1002. 71. Gentile GP, Kaufman SC, Helbig DW. Is there any evidence for a post-tubal sterilization syndrome? Fertil Steril. 1998;69:179–86. 72. Peterson HB, Jeng G, Folger SG, et al. The U.S. Collaborative Review of Sterilization Working Group. The risk of menstrual abnormalities after tubal sterilization. U.S. Collaborative Review of Sterilization Working Group. N Engl J Med. 2000; 343(23):1681–7. 73. Hillis SD, Marchbanks PA, Tylor LR, et al. The U.S. Collaborative Review of Sterilization Working Group. Poststerilization regret: findings from the United States Collaborative Review of Sterilization. Obstet Gynecol. 1999;93:889–95. 74. Schmidt JE, Hillis SD, Marchbanks PA, et al. The U.S. Collaborative Review of Sterilization Working Group. Requesting information about and obtaining reversal after tubal sterilization: findings from the U.S. Collaborative Review of Sterilization. Fertil Steril. 2000;74: 892–8. 75. Liskin L, Pile JM, Quillin WF. Vasectomy—safe and simple. Popul Rep D. 1983;4:61–100. 76. Peterson HB, Huber DH, Belker AM. Vasectomy: an appraisal for the obstetrician-gynecologist. Obstet Gynecol. 1990;76:568–72. 77. Cox B, Sneyd MJ, Paul C, et al. Vasectomy and risk of prostate cancer. JAMA. 2002;287:3110–5. 78. Bernal-Delgado E, Latour-Pérez J, Pradas-Arnal F, et al. The association between vasectomy and prostate cancer: a systematic review of the literature. Fertil Steril. 1998;70:191–200. 79. Massey FJ, Jr, Bernstein GS, O’Fallon WM, et al. Vasectomy and health—results from a large cohort study. JAMA. 1984;252: 1023–9. 80. Centers for Disease Control and Prevention. National infant mortality weekly report. MMWR. CDC Surveill Summ.1989; 38(3).

VII Injury and Violence

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Injury Control: The Public Health Approach

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Corinne Peek-Asa • Erin O. Heiden

INTRODUCTION

Injuries are a focus of public health practice because they pose a serious health threat, occur frequently, and are in most situations preventable.1 Preventing traumatic injuries and controlling their severity offer a cost-effective approach to improve the health status of populations. Injuries are a very broad group of afflictions, arising from many different activities and risk factors, and can affect all organ systems of the body. Since injuries are so diverse in mechanisms of occurrence, formulating an organized and structured approach to studying their incidence and prevention is helpful. Injuries affect people of all ages and range from minor cuts and bruises to major catastrophes that take thousands of lives. Some injuries may result in prolonged pain or lifelong disabilities that restrict an individual from performing personal, recreational, or work-related activities. Serious injuries affect more than the individual: they can destroy families and devastate communities as seen in recent earthquakes, hurricanes, and tsunamis. These events can leave individuals and societies with enormous medical costs, extensive rehabilitation needs, major lifestyle adjustments, and depression— losses that cannot easily, if ever, be recouped. However, the majority of injuries do not occur as a result of a catastrophic disaster; they are usually related to the activities of everyday life. For example, the annual number of deaths from motor vehicle crashes in the United States far exceeds that from airline crashes and natural disasters combined. Injuries disproportionately affect the young, the frail, and underserved populations. Because injuries disproportionately affect children and adolescents, they account for a high proportion of premature productive life lost and a large proportion of the number of school and workdays missed, and have become a large component of the medical care dollar expenditure per capita. The public is largely unaware of the preventable nature of many injuries. The most common reference to injurious events, “accidents,” evokes a feeling of chance, misfortune, and helplessness. Hence, the word “accident” should be avoided in discussing injury control, and instead, the focus should be on exposures to hazards and resulting injuries, as well as their preventability. In recent years, great strides have been made in injury prevention. In the last 75 years, the motor vehicle fatality rate per mile driven has decreased 90%, and this has occurred as the number of miles of driving has risen by more than 100%. Despite this decrease, motor vehicles remain the most common cause of injury death. Causes for the decreases seen include modifications in roadway environments and vehicle design, changes of hazardous behaviors, such as drunk driving, and policies that have regulated driving conditions. Preventive measures have been successful in reducing the incidence of drowning, poisoning, falls, and fires.

Despite successes in many areas of injury prevention, the potential of preventing traumatic injuries has not been realized. There remains much to be done. This chapter presents a short public health history of injuries, examines the magnitude and distribution of injuries in the United States, and outlines approaches to injury prevention and control. PUBLIC HEALTH HISTORY OF INJURIES

Injury prevention measures, such as the use of protective clothing in warfare, existed long before injuries were systematically studied. In the early 1940s, Cairnes and colleagues conducted one of the first epidemiologic studies to recognize the importance of using defined populations with comparison groups to compare head injury incidence between helmeted and unhelmeted motorcycle riders in the military.2,3 These studies demonstrated a decrease in head injuries among those riders wearing helmets. In 1949, John Gordon noted that injuries were patterned by age, gender, and other demographic factors, as well as by time and place.4 He recognized that “accidents” could be studied utilizing epidemiologic methods similar to those used in infectious or chronic disease prevention. In 1961, James Gibson defined the agent of injury as energy in its many forms.5 William Haddon Jr. placed this theory into a framework, which identified vehicles and vectors of injury occurrence, analogous to the models used for the study of infectious diseases.6–8 He recognized that injuries occur when energy delivered to a living host from a vehicle or vector exceeds human tolerance. He further categorized the energy-host interaction into (a) the energy delivered in excess of human tolerance, such as mechanical energy in motor vehicle crashes or in falls and (b) interference with energy use in normal metabolic functions, such as occurs in drowning or poisoning. Using these basic ideas as a framework, Haddon created a comprehensive matrix of host-energy interactions that is discussed later in this chapter.9 After surviving a crash in his trainer aircraft, Hugh DeHaven found a connection between his abdominal injuries and the shape and riveting location of his safety belt. DeHaven then studied ways in which engineering could reduce the severity of injuries during small aircraft and motor vehicle crashes.10 His work bred new studies on human tolerance to energy forces during many types of impacts. His approach using biomechanical principles coupled with epidemiologic evaluation is now prominent in motor vehicle crash research. Since these initial studies, the field of injury prevention has become more organized while maintaining an interdisciplinary focus. In 1985, the National Research Council released the landmark report 1319

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Injury in America, which identified priority areas for injury control activities and found that funding levels were not commensurate with the burden of the injury problem.11 Since that report, several other national efforts to prioritize injury-control activities have been conducted. The Institute of Medicine has released several important reports addressing injuries and trauma care, including the 1999 report Reducing the Burden of Injury.12 This report identified national priorities for surveillance, training and research, firearm prevention, trauma care systems, state infrastructure, and federal response. Recommendations from this report include expanding emergency department surveillance, the establishment of a national fatal intentional injury surveillance system, expansion of training activities for both research and practice, and increased coordination and support for agencies leading the field of injury control. Most recently, the Centers for Disease Control and Prevention supported research for the book Incidence and Economic Burden of Injuries in the United States, which identifies the financial burden of injuries in the United States.13 These landmark reports have helped bring attention to the injury problem and have been critical to the ongoing improvement and implementation of injury prevention and control programs. They have also argued strongly that a systematic approach to injury prevention, such as that defined by the public health model, provides a sustainable framework in which to address the problem. INJURY CONTROL AND THE PUBLIC HEALTH MODEL

Injuries and the Public Health Approach Injury prevention is well suited to the public health model, which advocates a cycle of surveillance, risk factor identification, and intervention implementation and evaluation. Injury surveillance provides an understanding of the incidence, trends, and magnitude of injuries. Surveillance also identifies specific populations that have a higher incidence of injuries. When developing an injury intervention strategy, surveillance can help identify injuries on which to focus prevention efforts. Priority can be given to the most prevalent injury causes, those that show an increasing incidence, or those that affect a population of special interest, such as children. It is important to examine surveillance data from the specific population that will be the focus of the intervention. However, local data, especially on nonfatal injuries, is often difficult to obtain. Thus, injury prevention programs are often prioritized on national data. The process of risk factor assessment helps identify individual or community factors that increase the risk for injury. Risk factors can be intrinsic, such as age or gender; behavioral, such as drinking and driving; or environmental, such as a poorly maintained roadway. Injury events are usually influenced by many risk factors, and these can be classified according to the causal model of injuries described later. Ideally, an intervention strategy is defined following careful surveillance and risk factor assessment. However, many interventions are implemented in the absence of such information, often because the information is not available or feasible to collect. Thus, many intervention programs are based on national trends. Intervention programs may focus on one population and risk factor, such as an educational campaign to increase the number of children adequately restrained in car seats. They might also target a broad population, such as environmental changes to the roadway. While broad programs might be more effective, they are also usually more expensive. An evaluation of the intervention strategy should accompany its implementation. A comprehensive evaluation should identify whether the program was implemented completely (process evaluation), determine if the intervention led to the desired change (impact evaluation), and finally, determine if the injury outcome of interest was achieved (outcome evaluation). Although evaluation is a crucial component of the public health approach, most intervention programs are not fully evaluated. Lack of funding, time, or expertise are some of the reasons that evaluations are not conducted.

Evaluation findings are important to understand the consequences of an intervention, and sometimes there are unintended detrimental consequences. The air bag is one example. The airbag is effective in reducing injuries among adults, especially in head-on collisions.14 However, surveillance of crash data indicated an increasing number of airbag-related injuries to children.15 Evaluation research indicated that children under 10 years of age who were riding in the right-front passenger seat have a 21% increased risk of fatality when an airbag was present.16 Since then, national campaigns to promote the placement of children in the back seat and efforts to design an air bag that is safe for children have helped reduce these events.17,18

A Causal Model for Injuries There are two main categories for injuries: unintentional and intentional. Unintentional injuries have no intentional motivation behind them and include the majority of injuries from traffic-related events, falls, fires, and drowning. Intentional injuries, on the other hand, have discernable human motivation and may be self-directed, such as suicide, or outwardly directed, such as homicide and assault. Although the number of intentional injuries is increasing more rapidly than unintentional injuries, unintentional injuries, currently and historically, have comprised a greater share of deaths and nonfatal injuries. Although there are many differences in the most effective approaches for the prevention and intervention of unintentional and intentional injuries, they share a common causal pathway. Traumatic injuries result from the transfer of energy to a human host. The traditional epidemiologic causal model for infectious diseases is easily adopted for traumatic injuries. In the traditional epidemiologic model for infectious diseases, microbes are the “agent” of infection and disease. In the epidemiologic model for traumatic injury, the “agent” of the injury is energy (Fig. 80-1). Energy can take many forms including mechanical, electrical, chemical, and thermal. An example of an agent-host interaction in the injury model is a motor vehicle crash, in which the energy exerted on the individual is mechanical. The environment refers to places where energy can be transmitted to a host. The potential for energy transfer exists everywhere, but its ability to cause injury is limited. For instance, the potential energy in a bullet causes injury only when the bullet is in motion and hits a human. The transfer of energy to a host is the necessary and sufficient cause of injury, but this transfer is affected by many other factors. Energy can be transferred to a host through vehicles or vectors. Vehicles are inanimate objects, such as a motor vehicle. Vectors are animate, such as another human being or an animal. For many injury causes, both vehicles and vectors are involved in energy transfer. For example, when an automobile crash occurs, the vehicles are the automobiles and the vectors are the drivers. The causal model is important because it depicts the many potential avenues for intervention. The environment is influenced by many physical, social, economic, demographic, and cultural factors. Modifying the environment can reduce the potential for energy transfer. Characteristics of vehicles and vectors can be modified to reduce the likelihood of causing an injury or to reduce the amount of energy transmitted. Even the host is an important focus for intervention. Only energy transmitted beyond the host’s tolerance causes an injury, and, therefore, not all

Environment

Reservoir

No injury

Vehicle

Agent

Agent, host, and environmental factors

Host

Injury

Vector Figure 80-1. Causal model for traumatic injuries.

80 exposures to energy result in noticeable injury. Humans have natural resistance to energy transfer, but the level of resilience varies over the population and depends on many factors. Intrinsic factors such as age and preexisting medical conditions can reduce resilience to energy transfer, as can extrinsic factors such as fatigue and alcohol use. Resilience can be increased through the use of protective devices or education to avoid potential injury-causing situations. SOURCES FOR INJURY DATA

Injury data is an important component in the cycle of surveillance, risk factor assessment, prevention, and evaluation. Data sources describing injuries are available on many levels, from broad national surveillance systems to local data. In general, the detail of information provided in a database decreases with the size of the surveillance system. A review by the Institute of Medicine12,19 identified 31 federally funded surveillance systems which address the incidence of injuries. The emergence of the Internet and improved computing power has made these databases easier to use and more accessible. Some specific data sources are described below.

Mortality Incidence data of fatal injuries in the United States are available from 1900 through the present in the Vital Statistics Records collected by the National Center for Health Statistics (NCHS). These data are collected from death certificates, and injuries are classified by the External Cause of Injury codes found in the International Classification of Diseases versions 9 and 10. The U.S. Vital Statistics Records are a good source for counts of fatal injuries by broadly defined causes as well as by age, race, and gender, but detailed information about the event and the types of injuries sustained is not available. Injury mortality rates from 1981 through 2003 can be obtained through WISQARS (Web-based Injury Statistics Query and Reporting System), maintained by the National Center for Injury Prevention and Control of the CDC (http://www.cdc.gov/ncipc/wisqars). In addition to overall injury mortality, several databases addressing specific causes of injury are maintained. The Fatal Accident Reporting System (FARS), developed in 1975 by the National Highway Traffic Safety Administration of the U.S. Department of Transportation, provides information on all motor vehicle crash-related fatalities in the United States. These standardized data on fatalities are collected from state and local police agency crash reports. Beginning in 1988, the National Automotive Sampling System (NASS) was designed to provide additional information on nonfatal crashes. The NASS includes two databases. The General Estimates System (GES) uses a nationally representative probability sample of approximately 55,000 police-reported crashes to estimate annual nonfatal crash injuries in the United States. The Crashworthiness Data System (CDS) provides detailed crash reconstruction data from a sample of approximately 5000 crashes. Since 1992, the Bureau of Labor Statistics has maintained the Census of Fatal Occupational Injuries (CFOI). The CFOI collects information from each state on work-related fatal injuries, comprised from death certificates, autopsy reports, media reports, and other sources. The National Safety Council also collects information on work-related fatalities. National estimates of homicide deaths in the United States beginning in 1976 are maintained by the Federal Bureau of Investigations Supplemental Homicide File. Information on the victim, incident, and offender involved in the homicide are included. Data through 1996 are available to download from the Bureau of Justice Statistics’ web page (http://www.ojp.usdoj.gov/bjs). Queries of databases describing perpetrators of crime are available on the same website through the Federal Justice Statistics Resource Center. The National Violent Death Reporting System (NVDRS) is a new initiative of the Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, to provide more detailed information about intentional traumatic injury deaths. After

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pilot testing in a few states, the system was established in 13 states20 and then expanded to 17 states. Each state links information from death certificates, medical examiner files, law enforcement records, and crime laboratories. Deaths occurring in the same incident are linked so event-level information is available.

Morbidity Information on hospital discharges, required for all accredited hospitals, is a source of national and community estimates of injury incidence. The National Hospital Discharge Survey conducted by the NCHS collects discharge data from each state to estimate national counts of injuries which require hospital admission. Discharge data is also usually available at the state and community levels. These data represent only the most severe injuries. National estimates of emergency department visits and physician’s office visits for injuries are available through surveys conducted by the NCHS, but there is no comprehensive national reporting system for these injuries. Queries of injury hospitalizations and emergency department visits are available from 2000 through 2004 on the WISQARS website (http://www.cdc.gov/ncipc/wisqars). The nonfatal injury data is a probability sample from approximately 60 U.S. emergency departments. National estimates of injury morbidity, as well as information about risk-taking behaviors and injury events, are available through national surveys. Two examples are the National Health Interview Survey, which measures many aspects of health status including a few variables addressing injuries, and the Behavioral Risk Factor Surveillance System (BRFSS), which collects information about risk-taking behaviors that are related to health outcomes. The BRFSS collects information on seat belt use, helmet use, drinking and driving, and other injury-related risk behaviors. These surveys are conducted at the state level using national probability sampling, so that pooled data has national representation. The National Crime Victimization Survey is conducted annually to determine incidence and outcomes from crime victimization. The National Nursing Home Survey provides information about injuries sustained by older persons residing in nursing homes. Many surveillance systems provide detailed information about specific types of injuries, exposures, and outcomes. The National Electronic Injury Surveillance System (NEISS) conducted by the U.S. Consumer Product Safety Commission gathers information about product-related injuries requiring hospital admission or emergency department treatment from a national sample of hospitals. Although the NEISS collects information only on product-related injuries, a subset of approximately 60 NEISS hospitals report on all traumatic injuries. This sample of hospitals is used to estimate overall nonfatal injury rates for the United States. Although the quality of injury data and access to it has improved dramatically over the last 20 years, there remain important gaps in injury surveillance. For example, few states have statewide databases for nonfatal occupational injuries or for Emergency Medical Services responses. Many types of injuries, such as those from natural disasters, and information about intentional injuries or occupational injuries, are difficult to identify in current national databases in which injuries can be identified. With an increasing focus on injury prevention within public health and preventive medicine, data is likely to improve in quality with easier access. INJURY INCIDENCE AND TRENDS

Mortality In 2003, unintentional injuries were the fifth leading cause of death in the United States. Unintentional injuries, however, were the leading cause of death for all those aged 1–44, and the third leading cause among those aged 45 through 54. Homicide is one of 10 leading causes of death for those aged 1 through 44, and the second leading cause of death for those aged 15 through 24. Suicide is one of the 10 leading causes of death for ages 10 through 64, and the second leading cause for those aged 25 through 34.

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50 40 30 20 10

19

81 19 82 19 83 19 84 19 85 19 86 19 87 19 88 19 89 19 90 19 91 19 92 19 93 19 94 19 95 19 96 19 97 19 98 19 99 20 00 20 01 20 02 20 03

0

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Figure 80-2. Age-adjusted mortality rates by year, United States, 1981–2003. (Source: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-Based Injury Statistics Query and Reporting System (WISQARS) [online]; 2005. Available at www.cdc.gov/ncipc/wisqars. Accessed 2006, April 27; from 1981 to 1998, ICD – 9CM coding was used; from 1999 to 2003 ICD–10CM coding was used.)

Overall, the injury mortality rate has decreased since the 1980s. Figure 80-2 shows the trends in injury mortality rates by intent from 1981 to 2003. Caution should be used in comparing rates from 1998 and prior with rates from 1999 to 2003 because beginning in 1999, mortality data used the International Classification of Disease—10th Revision (ICD-10) while mortality data from 1998 and prior used ICD-9. For all years, unintentional injuries make up the majority of injury deaths. From 1981 through 2003, the largest decreases in injury rates were for unintentional injuries, followed by homicide, while suicide rates remained largely unchanged. Injury mortality rates show characteristic patterns by age and gender (Fig. 80-3). For all age groups, the rate of injury mortality is higher for males than for females. Increased injury death rates in males have been attributed to increased risk-taking behavior, exposure to motor

vehicles, more hazardous occupations, and substance use. From age 15–64, the injury mortality rate for females is about one-third the injury mortality rate of males; after age 65, the injury mortality for females is approximately half the rate of males. The death rate from unintentional injuries among White males is almost twice that of White females, and the rate for Black males is almost three times that of Black females. The injury mortality rate is lower for those aged 5–14 years compared with the ages 1–4, and then increases sharply for both males and females to a rate of 93.5 and 27.4 per 100,000, respectively, from ages 15–24 (Fig. 80-3). The overall injury mortality rate for both sexes is 61.4 per 100,000 from ages 15–24 (not shown). Most of the increase during early adolescence can be attributed to motor vehicle crash-related injuries. Unintentional injuries account for the largest proportion of injuries across all years representing almost two-thirds of all injuries. The

450 Males

400

Females

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350

Figure 80-3. Injury mortality rates by age and gender, United States, 2003. (Source: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-Based Injury Statistics Query and Reporting System (WISQARS) [online]; 2005. Available at www.cdc.gov/ncipc/wisqars. Accessed 2006, April 27.)

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Mechanism of injury Figure 80-4. Age-adjusted injury mortality rates by mechanism and intent, United States, 2003. (Source: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-Based Injury Statistics Query and Reporting System (WISQARS) [online]; 2005. Available at www.cdc.gov/ncipc/wisqars. Accessed 2006, April 27.)

unintentional injury mortality rate remains between 50 and 65 deaths per 100,000 population until the increase at about age 65. Because injuries disproportionately affect the young, mortality rates, which are not age-adjusted, may not accurately reflect the role of injuries in killing the young. The leading causes of unintentional injury death from birth through age 5 are poisoning and drowning; the leading cause in the elderly is falls. Motor vehicle-related death rates are the highest of all injuries between the ages of 5 and 34, and peak between the ages of 15–24, the age group when young drivers are first licensed. Alcohol use is an important risk factor in motor vehicle crashes during these ages. Injury deaths from motor vehicles account for 28% of all injury deaths, followed by deaths due to firearms, poisonings, falls, and suffocation (Fig. 80-4). While over 90% of deaths due to motor vehicles and falls are unintentional, over 50% of deaths from firearms are due to suicide, and 40% are due to homicide (the intent of homicide includes a small proportion of deaths from legal intervention).

Approximately 50% of deaths from suffocation are suicides. Mortality rates due to falls are higher in the 65-plus age groups. The rate of firearm death is highest in the 15 through 34 age groups.

Hospital Admissions Injury mortality represents only a small proportion of total injury incidence. The relationship of injury deaths to nonfatal injuries of different severity levels is referred to as the “injury pyramid.” In 2003, there were 164,000 injury deaths, and over 1.9 million injury hospitalizations for a ratio of 1 death for every 12 hospitalizations. Nearly 27 million people were treated and released from emergency departments (EDs) during 2003, for a ratio of one death for every 152 ED visits that were treated and released. Hospitalization rates include injured persons who were admitted to a hospital for their injuries. In 2004, less than 10% of ED visits resulted in hospital admissions for age groups up to 65 (Fig. 80-5).

4500 Male

4000

Female

Figure 80-5. Injury hospitalizations by age and gender, United States, 2004. (Source: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. WebBased Injury Statistics Query and Reporting System (WISQARS) [online]; 2005. Available at www.cdc.gov/ ncipc/wisqars. Accessed 2006, April 27.)

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Figure 80-6. Injury hospitalizations by mechanism and intent, United States, 2004. (Source: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-Based Injury Statistics Query and Reporting System (WISQARS) [online]; 2005. Available at www.cdc.gov/ncipc/ wisqars. Accessed 2006, April 27.)

After 65, the rate of hospital admissions following ED visits for injury increased from 11% between ages 65 and 74 to almost 30% for age 85 and above. Among hospitalization rates for injuries in 2004, males had higher hospitalized injury rates up to age 65. Falls accounted for the largest proportion of hospitalizations with almost 40% attributed to falls (Fig. 80-6). Transportation and poisonings represented the next highest proportion of hospitalized injuries at 19% and 16%, respectively. As with injury mortality, unintentional injuries account for the largest proportion of hospitalized injuries overall and across most causes. Nearly all of the falls and the

transportation injuries are unintentional. However, nearly 50% of hospitalized poisonings are due to self-harm, and 43% of injuries characterized as struck by/against are intentional assaults.

Emergency Department Visits ED visits for injuries show less variation by age than mortality (Fig. 80-7). The high mortality rates among the elderly are more likely due to decreased injury resilience than increased injury rates, while younger people are more likely to sustain a nonfatal injury.

18,000 Male 16,000

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15–24

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Figure 80-7. Emergency department visits by age and gender, United States, 2004. (Source: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-Based Injury Statistics Query and Reporting System (WISQARS) [online]; 2005. Available at www.cdc.gov/ncipc/wisqars. Accessed 2006, April 27.)

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Overexertion

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Mechanism of injury Figure 80-8. Emergency department visits by mechanism and intent, United States, 2004. (Source: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-Based Injury Statistics Query and Reporting System (WISQARS) [online]; 2005. Available at www.cdc.gov/ncipc/wisqars. Accessed 2006, April 27.)

Among ED visits for injuries in 2004, males had higher injury rates up to age 65. The greatest disparity between males and females was among those 15–24, in which 16.8 of every 100 males and 11.8 of every 100 females had an injury-related ED visit. This age group had the highest rates for both males and females. The lowest rates for both males and females were for children less than 1 year and adults between ages 45–74. In 2004, unintentional injuries accounted for 67% of all injuryrelated deaths and 93% of classifiable injury-related ED visits in the United States (Fig. 80-8). Motor vehicle crashes accounted for 28% of injury fatalities but only 15% of ED visits. Falls represented 11% of fatal injuries and 27% of ED visits. The number of falls leading to fatality among the elderly, however, may be underestimated because deaths may be attributed to comorbid conditions.

Costs of Injuries The high costs associated with injuries have been recognized for many years. The economic costs of injuries can be measured in direct costs, such as those resulting from medical care expenditure, and indirect costs, such as those resulting from years of life lost, lost productivity, or property damage. In 1985, 57 million injuries resulted in an estimated total cost of $157.6 billion: $44.8 billion in direct costs, $64.9 billion in lost productivity, and $47.9 billion due to premature death.21 The Centers for Disease Control and Prevention estimates that the 50 million incident injuries that occurred in 2000 resulted in an estimated total cost of $406 billion: $80.2 billion in direct costs and $326 billion in productivity losses.12 Increased estimates from 1985 are due in part to better estimates of lost work time and societal costs for injuries. The costs for injuries, despite the fact that injury incidence has decreased, are growing, and this should provide a strong incentive for prevention. Injuries disproportionately occur among younger people, and the costs are also concentrated among the young. In 2000, individuals between 25 and 44 years of age represented 30% of the U.S. population, but 40% of the total lifetime costs for injuries.12 The cost of medical care increases with increasing injury severity. For motor vehicle-related injuries in 1990, the cost of medical care

averaged $18,585 for a moderate injury, $57,030 for a serious injury, and $249,753 for a critical injury.22 Indirect costs also increase with injury severity because extended treatment needs are greater, there is more loss of productivity, and disabilities are more common. Although fatalities often do not result in high medical costs, indirect costs due to premature loss of life can be extensive. For example, deaths due to drowning and poisoning have high societal costs because of the large number of affected children. THEORETICAL APPROACHES TO INJURY CONTROL

The main objectives of injury research are to prevent the occurrence of injuries and to reduce their level of severity. Limiting injury prevention strategies to any single aspect of the many causes of injuries is an ineffective and narrow approach; successful strategies will incorporate many countermeasures and involve many different professionals.23,24 Rather than “accident prevention,” the goal of injury prevention is better conceptualized by focusing on a general downshifting of severity over the entire spectrum of injuries. The phrase adapted by injury professionals to describe the desired effects of injury research is “injury control,” which embodies the goal of decreasing injuries through increased knowledge about risk factors, predicting injury occurrence, and active control of these factors. Unlike many chronic diseases, the agent of injury is usually known, and the mechanism of energy transfer from reservoir to host can be described with great detail. With the exception of some poisonings and burns, injuries usually occur immediately after exposure and have very short “latent” periods. This is different than infectious diseases and chronic conditions, in which symptoms may begin years after exposure. Within the framework of the public health model (Fig. 80-1), the primary focus of injury control is to identify sources of energy forces which cause injury, to define mechanisms of human exposure, and to identify precisely where interventions (countermeasures) may be introduced in the “natural history” of injury.

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Public health has defined three levels of prevention. Primary prevention aims to prevent the event which causes injury by eliminating the mechanisms of energy transfer or exposure. Traffic safety laws which prevent automobile crashes, fences around swimming pools which prevent submersion and drowning, locking devices on guns, and safety caps on poisonous substances are all examples of primary prevention which reduce or eliminate the chance of exposure. The goal of secondary prevention is to eliminate injuries or reduce injury severity once a potential injury-producing exposure has occurred. Motorcycle and bicycle helmets, seat belts, life vests, and bulletproof vests are examples of secondary prevention.25,26 It is important to note that some of the most effective secondary prevention strategies do not eliminate all injuries. For example, the motorcycle helmet is very effective in reducing head trauma in motorcycle crashes, but is not effective in preventing trauma to other body regions.27 Seat belts do not prevent all injuries in vehicle crashes; cuts, contusions, and extremity fractures are common among belted vehicle occupants because belts do not restrain the limbs.28,29 The crucial role of seat belts is to reduce severe injury to critical anatomic regions such as the head or chest, and for this purpose they are enormously effective. Tertiary prevention acknowledges that an injury has occurred, and aims to reduce the consequences of the injury. These efforts can include emergency response, trauma care, social work, and physical, occupational, and speech therapy. Some of the most important advances in injury prevention have occurred with the development of organized trauma care systems in the last decades.30 However, less attention has been focused on the emotional and psychological consequences, and subsequent recovery, from a severe injury. Specific injury prevention strategies can be divided into two very broad groups based on need for host actions. Passive intervention requires no input or action by the host and is usually accomplished by modifying the agent, vehicle, vector, or environment. Modifications in car design to improve brakes or increase energy absorption by the vehicle frame are two examples. Active intervention requires that the host take some type of action for the intervention to work. Seat belts and helmets are examples of active intervention. Just as effective injury control strategies must address multiple facets of injury occurrence, they should also incorporate active and passive intervention strategies to be fully effective. Passive intervention strategies are usually considered more effective, especially when compared to active interventions which require frequent or time-consuming action.31 Air bags, which require no driver action, will work in frontal crashes, whereas a seat belt can only be effective if the rider remembers to fasten it. The most effective prevention, however, is the combination of both approaches. The circumstances of specific types of injury must be considered when identifying injury control approaches. One framework for conceptualizing the many approaches to injury prevention is termed the “4 Es,” which consist of education, environmental modification, enforcement, and engineering. Education refers to efforts using educational messages to increase safe behavior among the intended audience. Of the four approaches, education is perhaps the most difficult to implement. Successful educational messages must be clear, appropriate for the audience, and must be periodically repeated to maintain behavior change. One important component of a successful educational campaign involves identifying the audience. For example, educating legislators regarding effective safety legislation may be more beneficial than broad communitybased education. One example was the implementation of the Poison Prevention Packaging Act, which also established state Poison Control Hotlines. These legislative approaches were only possible due to the availability of data to educate legislators about the risks for childhood poisonings, which were dramatically decreased following the legislation.32 Some community-based efforts, however, have shown success, such as programs that focus on decreasing childhood injuries.33,34 Many types of educational materials have been introduced, but most are not scientifically evaluated. One recent approach has been the broadcasting of Public Service Announcements stressing

safe behavior. The success of these programs is largely unknown, however, because few scientific evaluations have been undertaken. The effectiveness of environmental modification has been demonstrated through reduction in motor vehicle crashes following changes in the driving environment. Examples include skid-free road surfaces, cross slopes on curved roadways in areas with heavy rainfall, and separation barriers on freeways and two-way roads. Environmental modifications as simple as removing trees and adding guardrails can reduce traffic crashes in some areas by as much as 75%.35 Another example of successful environmental modification includes the introduction of pool-fencing barriers. Enforcement refers to legislative regulations and the enforcement of these activities. While legislatively mandated prevention activities have been highly successful, they can be controversial. The introduction of a mandatory helmet use law in California in 1992 led to a decrease in motorcycle fatalities of over 35% and a decrease in severe head injuries among injured motorcycle riders of over 50%.27 Efforts to repeal this law based on freedom of choice have continued since its inception. Another example of successful legislation has been the implementation of blood alcohol limits for drivers. The success of much legislation may be due in part to public recognition of the laws, and it is often this public recognition that leads to the legislation. Engineering advancements have been highly successful in reducing injuries. The most notable examples are the seat belt and airbag, which have been attributed with decreasing injuries in frontal collisions by over 50%.36 Many effective prevention measures have been introduced to motor vehicles without the consumer’s knowledge, including improvements in brakes, collapsible steering columns, and stronger head rests. As consumers of automobiles have started to demand safety in vehicle design, these improvements will likely continue. Although engineering measures tend to be very effective, they must be followed to determine if the engineering strategy introduces new injury risks. An example of this phenomenon involves the airbag, which has caused several fatalities among infants in car seats placed in the front passenger seat. One of the most successful theoretical approaches to injury prevention is the Haddon Matrix, developed by Dr William Haddon in the 1970s. The Haddon Matrix identifies three phases in an injury event and links approaches to prevent or reduce injury in each phase. This matrix was developed for application to countermeasures for highway safety but continues to be a useful theoretical framework for many types of injuries.8,9 The Haddon Matrix divides the timing of the injury event into three phases: preinjury, injury, and postinjury (Table 80-1). In the preinjury phase, the goal is primary prevention to eliminate any energy transfer to the host. Additional examples include fences around swimming pools which prevent submersion, trigger locks on guns, and safety caps on poisonous substances. These are all examples of countermeasures that reduce the chance of exposure to energy. In the injury phase, which represents secondary prevention, the goal is to eliminate or reduce the amount of energy absorbed by the host once an energy transfer has occurred. Postinjury interventions, also called tertiary prevention, reduce the consequences of the injury once an injuryproducing energy transfer has occurred. The Haddon Matrix categorizes interventions in each injury phase into those that affect the host, the vehicles or vectors in the causal pathway, and the environment. The environment is often separated into physical and socioeconomic components. While the Haddon Matrix is an important tool to recognize the many opportunities for prevention, it is not a useful tool in deciding which intervention approach to implement. In 1998, Dr Carol Runyan introduced a third dimension to the Haddon Matrix to assist in decision-making.37 The third dimension introduces value criteria to consider when choosing an intervention strategy, and includes such elements as anticipated effectiveness, cost, freedom, equity, stigmatization, preferences, and feasibility. These value criteria can be applied to interventions in each cell of the original Haddon Matrix to determine which approach is best suited for the specific problem.

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TABLE 80-1. THE HADDON MATRIX WITH ILLUSTRATIONS Factors Environment Phases

Human

Vector (Vehicle)

Physical

Socioeconomic

Preinjury

Alcohol intoxication

Injury

Low resistance to energy Conditions which affect energy tolerance

Instability in utility vehicles Sharp or pointed edges and surfaces Rapidity of energy reduction

Poor visibility of road hazards Flammable building materials Emergency medical response

Lack of knowledge regarding injury risks Lack of enforcement of safety belt legislation Lack of funding for emergency medical services and rehabilitation services

Postinjury

SOURCES TO IDENTIFY SUCCESSFUL

INJURY PREVENTION PROGRAMS The growth of the field has led to an increasing evidence base that identifies effective, replicable, and sustainable injury prevention and intervention measures. Increasing availability of peer-reviewed evaluations, systematic reviews, and best-practices guidelines help identify effective approaches to prevention.38,39 The Guide to Community Preventive Services: Systematic Reviews and Evidence– Based Recommendations (the Guide), developed by the Task Force on Community Preventive Services, includes some systematic reviews that address injury prevention topics.40 The Guide’s recommendations are primarily based on evidence of effectiveness, including the suitability of the study design, but they also assess the applicability of the intervention to other populations or settings, the economic impact, barriers observed in implementing the interventions, and whether the intervention had other beneficial or harmful effects.41 The Guide then provides a recommendation as to whether the approach is “strongly recommended,” “recommended,” has “insufficient evidence,” or is “discouraged.” The Guide has evaluated the use of child safety seats and safety belts, reducing alcohol-impaired driving, therapeutic foster care for the prevention of violence, early childhood home visitation programs, and firearm laws; these recommendations can be found at http://www.thecommunityguide.org/ default.htm. The Cochrane Collaboration provides scientific evidence-based reviews of health care interventions through the Cochrane Library.42,43 The Cochrane Injuries Group has published 57 reviews on the prevention, treatment, and rehabilitation of traumatic injuries. There are 13 reviews of general injury prevention interventions including fall-related injuries to older persons, pool fencing to prevent drowning in children, and interventions for promoting smoke alarm ownership and function. There are 16 reviews of prevention strategies to reduce traffic injuries, including graduated driver’s licensing, increasing pedestrian and bicyclist’s visibility to prevent crashes, and safety education of pedestrians. A list of reviews conducted by the Cochrane Injuries Group can be found at http://www.cochrane-injuries. lshtm.ac.uk. CONCLUSION

Injuries, which are frequent events with potentially devastating physical and emotional consequences, represent an underrecognized public health burden. Injury prevention measures represent an effective strategy to improve public health because, with the extremely short latency period between exposure and injury, the effects of intervention can be realized very quickly. This does not mean, however, that injury prevention strategies are simple. Most successes in reducing injury incidence have required multifaceted, interdisciplinary efforts. For example, the successful modifications of the roadway and vehicle environments that have led to reductions in motor vehicle crash-related

injuries and deaths required collaboration of legislators, urban planners, city councils, law enforcement, automobile manufacturers, engineers, and health professionals, among others. Prevention efforts focusing on the seat belt required engineering, education, legislative, and enforcement approaches.44 It was not until long after engineers designed seat belts that they were widely integrated into cars. Legislation was required first to get seat belts installed into cars, and then to get drivers and passengers to wear them. This required education of legislators to understand the scope of crash injuries, the promise of reducing them, as well as education of the public to understand the benefits of wearing seat belts and consequences for not wearing them, both legal and personal.45 Continued success in reducing injuries will require similar collaborative efforts, and preventive medicine specialists have a key role in this process as advocates for safety and injury prevention.

REFERENCES

1. Baker SP, O’Neill B, Ginsburg MJ, Guohua L. The Injury Fact Book. 2nd ed. New York: Oxford University Press; 1992. 2. Cairns H. Head injuries in motor-cyclists: the importance of the crash helmet. Br Med J. 1941;2:465–71. 3. Cairns H, Holbourn H. Head injuries in motor-cyclists: with special reference to crash helmets. Br Med J. 1943;1:591–8. 4. Gordon J. The epidemiology of accidents. Am J Public Health. 1949;39:504–15. 5. Gibson J. The contribution of experimental psychology to the formulation of the problem of safety: a brief for basic science. In: Behavioral Approaches to Accident Research. New York: Association for the Aid of Crippled Children; 1961. 6. Haddon W, Jr. A note concerning accident theory and research with special reference to motor-vehicle accidents. Ann N Y Acad Sc. 1963;107:635–46. 7. Haddon W Jr, Schuman E, Klein D. Accident Research: Methods and Approaches. New York: Harper & Row; 1964. 8. Haddon W, Jr. On the escape of tigers: an ecologic note. Am J Public Health. 1970;60:2229–34. 9. Haddon W, Jr. A logical framework for categorizing highway safety phenomena and activity. J Trauma. 1972;12:193–207. 10. DeHaven H. Beginnings of crash injury research. In: Brinkhaus K, ed. Accident Pathology. Washington, DC: U.S. Department of Transportation; 1968:FH 11–6595. 11. Committee on Trauma Research, Commission on Life Sciences, National Research Council and Institute of Medicine. Injury in America: A Continuing Public Health Problem. Washington, DC: National Academy Press, 1985. 12. Bonnie RJ, Fulco CE, Liverman CT, eds. Reducing the Burden of Injury: Advancing Prevention and Treatment. Washington, DC: National Academy Press, 1999.

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13. Finkelstein EA, Corso PS, Miller TR. Incidence and Economic Burden of Injuries in the United States. New York: Oxford University Press; 2006. 14. Zador PL, Ciccone MA. Automobile driver fatalities in frontal impacts: air bags compared with manual belts. Am J Pub Health. 1993;83:661–6. 15. Centers for Disease Control and Prevention. Warnings on interaction between air bags and rear-facing child restraints. Morb Mortal Wkly Rep. 1993;42:280–2. 16. Braver ER, Ferguson SA, Greene MA, et al. Reductions in deaths in frontal crashes among right front passengers in vehicles equipped with passenger airbags. JAMA. 1997;278(17):1437–9. 17. National Transportation Safety Board. Safety Recommendation, H-95-17. Washington, DC: 1995. 18. Martinez R. Improving air bags. Ann Emerg Med. 1996;28(6):709–10. 19. Annest JL, Conn JM, James SP. Inventory of Federal Data Systems in the United States for Injury Surveillance, Research, and Prevention Activities. Atlanta: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 1996. 20. Paulozzi LJ, Mercy J, Frazier L Jr, Annest JL. Centers for Disease Control and Prevention. CDC’s National Violent Death Reporting

System: background and methodology. Inj Prev. 2004;10:1;47–52. 21. Rice D, MacKenzie E. Cost of injury in the United States. A report to Congress, Institute for Health and Aging, University of California, and Injury Prevention Center. San Francisco, CA: The Johns Hopkins University; 1989. 22. Blincoe LJ, Faigin BM. The Economic Cost of Motor Vehicle Crashes, 1990. Washington, DC: U.S. Department of Transportation, National Highway Traffic Safety Administration, HS-807–876;1992. 23. National Committee for Injury Prevention and Control. Injury prevention: meeting the challenge. Am J Prev Med. 1989;5:3. 24. National Center for Injury Control. Injury Control in the 1990’s: A National Plan for Action. A Report to the Second World Conference on Injury Control. Maryland: Centers for Disease Control and Prevention, National Center for Injury Control; 1993. 25. U.S. General Accounting Office. Motorcycle Helmet Laws Save Lives and Reduce Costs to Society. Washington, D.C.: U.S. General Accounting Office, GAO/RCED-91-170; 1991. 26. Thomas S, Acton C, Nixon J, et al. Effectiveness of bicycle helmets in preventing head injury in children: case-control study. Brh Med J. 1994;308:173–7. 27. Kraus JF, Peek C, McArthur D, Williams A. The effects of the 1992 California Mandatory Motorcycle Helmet Use law on motorcycle crash fatalities and injuries. JAMA. 1994;272:1506–11. 28. Evans L. The Effectiveness of Safety Belts in Preventing Fatalities. Warren, MI: General Motors Research Publication, GMR-5088; 1985. 29. Evans L. Restraint effectiveness, occupant ejection from cars, and fatality reductions. Accid Anal Prev. 1990;22:167–75.

30. Pollock DA, McClain PW. Trauma registries: current status and future prospects. JAMA.1989;262:2280–3. 31. Waller JA. Injury Control: A Guide to the Causes and Prevention of Trauma. Lexington, MA: DC Health; 1985. 32. Chafee-Bahamon C, Lovejoy FH. Effectiveness of a regional poison center in reducing excess emergency room visits for children’s poisonings. Pediatrics. 1983;72:164–9. 33. Blomberg RD, Pruesser DF, Hale A, Leaf WA. Experimental Field Test of Proposed Pedestrian Safety Messages (vol 2). Child messages. Washington, DC: U.S. Department of Transportation; 1983. 34. DiGuiseppi CG, Rivara FP, Koepsell TD, Polissar L. Bicycle helmet use by children: evaluation of a community-wide campaign. JAMA. 1989;262;2256–61. 35. McFarland WF, Griffin LI, Rollins JB, et al. Assessment of Techniques for Cost-effectiveness of Highway Accident Countermeasures. Washington, DC: Federal Highway Administration; 1979. 36. National Highway Traffic Safety Administration. Final regulatory impact analysis: amendment to FMVSS 208 passenger car front seat occupant protection. Washington, DC: National Highway Traffic Safety Administration, U.S. Department of Transportation, HS-806572; 1984. 37. Runyan CW. Using the Haddon matrix: introducing the third dimension. Injury Prevention. 1998;4:302–07. 38. Cook DJ, Sackett DL, Spitzer WO. Methodological guidelines for systematic reviews of randomized control trials in health care for the Potsdam Consultation on Meta-Analysis. J Clin Epidemiol. 1995;48: 167–71. 39. Cooper H, Hedges LV, eds. The Handbook of Research Synthesis. New York: Russell Sage Foundation; 1994. 40. Poppaioanou M, Evans C, Jr. Development of the Guide to Community Preventive Services: a U.S. public health service initiative. J Public Health Manag Pract. 1998;4(S2):48–54. 41. Briss PA, Zaza S, Pappaioanou M, et al. Developing an evidencebased Guide to Community Preventive Services-Methods. Am J Prev Med. 2000;19(1S):35–43. 42. Bero L, Rennie D. The Cochrane Collaboration. Preparing, maintaining, and disseminating systematic reviews of the effects of health care. J Am Med Assoc, 1995;274:1935–8. 43. Cochrane Reviewers’ Handbook. 4.2.2. Available at http://www. cochrane.org/resources/handbook/hbook.htm. Accessed Apr 28, 2006. 44. Graham JD. Injuries from traffic crashes: meeting the challenge. Annu Rev Public Health. 1993;14:515–43. 45. Partyka SC, Womble KB. Projected Lives Saved from Greater Belt Use. National Center for Statistics & Analysis Research Notes. Washington, DC: National Highway Traffic Safety Administration; 1989.

Violence in the Family as a Public Health Concern

81

Irene Hanson Frieze • Jeremiah A. Schumm • Stacey L. Williams

Although the family can and often is a source of strength and support for many people, it can also be a source of victimization. Violence in family settings in the United States is believed to affect a large proportion of the population, although not all of this is severe violence. The Centers for Disease Control and Prevention (CDC) estimates that about 1.5 million women and more than 800,000 men are raped or physically assaulted by an intimate partner each year (http://www.cdc.gov/ncipc/factsheets/ipvfacts.htm).1 Such violence can be fatal. More than 10% of homicide victims are killed by an intimate partner.2 Other CDC data3 indicate that nearly 1 million children were confirmed by child protective agencies as victims of child abuse in 2002. This included neglect, physical abuse, sexual abuse, and emotional and psychological abuse. In this article, several different types of family violence are discussed, including couple violence, child abuse, sibling violence, and elder abuse. As will be seen, the more extreme forms of these forms of family violence are often found together in the same family. In the following sections, we first present data on what is known about family violence and then discuss strategies for how we might intervene or prevent forms of abuse. COUPLE VIOLENCE

Violence in couples is called intimate partner violence (IPV) by researchers today. Such violence can exist at various levels from extreme violence with serious injury, to relatively low-level forms of violence. In accord with the CDC definition, IPV can entail physical violence, sexual violence, threats of physical/sexual violence, and psychological or emotional abuse.4 The major public health concern is the most extreme and serious form of couple violence, now labeled as “intimate terrorism” by researchers.5,6 This is the type of situation that most people would associate with the battered woman. In the most typical pattern of such violence, a husband or male partner has become extremely violent toward his wife or female partner, using physical violence as well as psychological abuse or belittling of his partner.7 Such violence has become routine, and the woman lives in constant fear that something she might do will initiate another round of such violence. The female victim develops low self-esteem, after hearing so often that she deserves the violence she receives. She may fight back, but typically her resistance is ineffective in stopping the violence, and she often receives a more severe beating when she does try to respond with her own violence. She may seek help from the police or escape from a particularly violent incident and go to a shelter for battered women, but this typically does not stop the violence.

Such violence and the high levels of stress generated in the battered woman result in a weakened immune system for her. Her injuries mean that she has a heightened risk of hospital visits because of injury or illness.8 She likely experiences acute and chronic mental and physical health problems.7,9,10 She may also abuse alcohol or drugs. Attempted suicide may occur. The CDC estimates that physical assaults associated with IPV cost U.S. society over $6 billion in 2003 in direct costs associated with medical and mental health care, as well as additional indirect costs of lost productivity for the female victim of couple violence (http://www.cdc.gov/ncipc/factsheets/ipvfacts.htm). Along with problems for the battered woman, there are often other health concerns within this type of violent family. Often, the batterer is violent to the children as well, meaning that physical child abuse is also present. It is not unusual for the batterer to abuse alcohol or drugs. This creates an additional public health concern, addressed elsewhere in this book. Battered women remain in these abusive relationships for a variety of reasons.7 They may love their abuser, in spite of his violence. She may feel that he needs her and that she needs to remain with him because of this need. Another set of reasons involves feeling unable to live on her own (feelings that grow out of low self-esteem caused by psychological abuse), lack of financial resources to leave and live on her own or as a single parent (batterers typically control money within the couple and give her little access to funds), or lack of any social support network that might assist her in leaving. The lack of social support is again typical because batterers so often systematically cut off outside social contact for the battered women, and monitor their behavior to make sure she does not have outside friends or close family relationships. If the battered woman does actually try to break up the relationship, it is not uncommon for the batterer to try to find where she has gone and to threaten her if she is not willing to come back. Many women in this situation file for legal protection, but this is not always effective. Relationship violence tends to become even more severe during this breakup time, which also may be a risk factor for other forms of violence such as stalking.11 In some cases, the battered woman is able to successfully leave the relationship and develop a new life, but it is difficult. These women may feel that they are now stronger people because of being able to do this, which helps build their self-esteem. For those who don’t leave, there are a number of programs that have been developed to try to encourage the batterer to stop using violence. For example, Stosny12 developed a treatment program aimed at ending abusive behavior by enhancing the batterer’s compassion toward self and loved ones. Another approach seeks to eliminate abusive behaviors by increasing motivation toward nonviolence and 1329

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improving anger management and communication skills.13 Although these programs are shown to have some success in reducing violence,14 they have been criticized by those who view these types of programs as generally ineffective.15 CHILD ABUSE

Child abuse can take several forms.7 It can consist of high levels of physical violence, or of a caretaker failing to provide basic care of a child. The latter is known as neglect. Sexual abuse of a child is another form of child abuse. Sometimes, emotional abuse, such as belittling of a child, or lack of positive expressions of love or warmth is also defined as a form of child abuse. In this section we focus on physical violence and sexual abuse. Like wife battering, all forms of child abuse are often hidden, and we have no true estimates of any of the forms of child abuse identified above. All we can reliably know are the counts of cases that have been reported to authorities, and judged by social agencies to meet the standard of abuse or neglect. It is likely that this would be more likely to occur for poorer families who are already using other social services. Sexual and physical abuse prevalence is difficult to estimate because these forms of abuse often occur beyond public view. Perpetrators of sexual or physical abuse often isolate their victims and coerce them into silence. Therefore, estimations of sexual and physical abuse based on incidents reported to social agencies are likely to underestimate the true prevalence rates of these forms of abuse.16,17 The United States Department of Health and Human Services estimates that over 900,000 children a year are judged to be maltreated.3 The most common form of maltreatment was neglect (61%). Other forms of abuse identified included physical abuse (19%), sexual abuse (10%), and emotional abuse (5%). In addition, the CDC suggests that shaken-baby syndrome (SBS), affecting up to 1600 children a year, should be considered a form of child abuse.18,19 This involves violent shaking of an infant or small child and can result in serious injury or even death.

Physical Child Abuse Physical abuse of children is associated with injuries to children that require medical attention or that result in death.20 This type of definition excludes most types of spanking or other forms of mild physical violence that do not involve serious injury. Many people in the United States feel that it is perfectly acceptable, if not beneficial, to spank or use other physical punishment on children who disobey their parents.21 This means that one has to set a certain level of violence as meeting the criteria for child abuse. People may disagree on what an appropriate level might be. Similar difficulties exist with defining neglect. There are wide differences of opinion about how much supervision or help children of different ages need. What one person might label as neglect, another person might see as teaching a child to be independent. Parents who physically abuse their children are most likely to do this when under stress.7 Such stress can come from situations in the life of the parent, or from having a child with special needs who is difficult to care for. Other risk factors for physical child abuse include parental stress and lack of social support for the parents. Mothers who are depressed or anxious are more likely to be abusive. Parents with substance abuse problems are also more likely to physically abuse their children as well. Abuse is also associated with poor parenting skills.22 The physical child abuser often feels that his or her behavior is in response to a difficult child whose behavior cannot be controlled in any way except through parental violence. Programs that train parents to better understand their (false) assumptions about their children appear to have promise in helping these parents be less aggressive toward their children.23Abusive parents may have learned that such violence is appropriate parental behavior.7 Mothers or fathers who have grown up in families where they were abused may learn this pattern of interaction

between parents and children and use these same behaviors toward their own children when they become parents themselves. As mentioned earlier, battering men may be physically violent to children as well as to their partner. Battered women may also take out their own stress on their children through the use of physical violence. These women are often experiencing high levels of stress in their lives as they monitor their behavior to minimize being beaten by their partner. The evidence of both abusive men and their battered partners both being at high risk for child abuse means that severe couple violence is often associated with physical abuse of the children in the home, by the father or stepfather and/or the battered mother, or by both parents.24 Growing up in a violent household leads to a continuation of violent interactions in the home. The abused child learns that violence is a way of solving problems and interacting with loved ones. Abusive parental behavior is seen as the model for parent-child interaction, and physical violence in adults is seen as normal. Children growing up in violent homes are more likely to engage in partner violence themselves as adults.25 This intergenerational transmission of violence might be the outcome of children learning to engage in violence from observing this behavior in their parents.26 Being the recipient of physical abuse, especially from someone as important as a parent, is traumatic for the child.27 Abused children may not have their basic physical and emotional needs met, and they may come to fear or distrust others. They are at high risk for display of aggression toward other children and for other conduct disorders, anxiety, depression, and suicide.28 There can also be long-term health consequences. Many studies include any child identified as being maltreated, which would include those experiencing physical abuse as well as neglect or sexual abuse. Such children have been found to experience a range of health consequences and to engage in unhealthy behaviors as adults.18,29 This includes eating disorders, smoking, alcoholism and drug abuse, depression, and suicide.

Incest and Sexual Abuse of Children The general category of child sex abuse is quite broad and includes many different types of behavior. Technically, incest refers to sexual contact between biologically related family members such as parents and children or even siblings, but stepparents are often included as well in this category. In this section, we focus on incest and sexual abuse within the family. We further limit the discussion to examples of forced sexual contact, typically between a parent or much older sibling and a daughter or sister. The most common example of this situation is associated with the violent relationships mentioned earlier.7 The man who is highly physically abusive toward his wife or female partner is the most typical type of incest perpetrator. Growing up in this type of family, the child may not feel loved or close to either parent. As the daughter reaches puberty and her body develops, her father may find her very attractive. She reminds him of his wife when she was younger and more attractive. The father, feeling that his wife is not fulfilling him sexually, turns to his now adolescent daughter, and begins to be very loving toward her, essentially courting her. The daughter responds to this attention, feeling loved for the first time. Over time, he becomes more and more aggressive in his sexual requests, eventually seeking sexual intercourse with her. If the wife finds out, she may feel powerless to do anything, because of fears for her own safety. The daughter may not seek help, enjoying the attention and thinking her mother is just being jealous. Over time, as this situation evolves, the father begins to treat the daughter as a second wife. He becomes very jealous of her and may begin to be violent towards her. She may realize that this situation is not “normal” and may feel guilty for her loving feelings toward her father. As she tries to date boys her own age, she begins to fear her father’s anger. She may become pregnant or acquire a sexually transmitted disease. Finally, the situation becomes too difficult for her to cope with. She may run away from home, perhaps marrying a boy she has been

81 seeing secretly. Or, she may turn to prostitution to support herself on the street. Another possibility is disassociation or even the development of a split personality. None of these alternatives are good ones for her. She may seek outside help, but generally only if she fears her father will begin to sexually assault a younger sister.7 When the child is forced to participate in unwanted sexual activity, there can be long-term emotional and health consequences. Child sexual abuse is associated with adulthood depression and anxiety, substance abuse, suicidality, and interpersonal problems.30 Sexually abused individuals are also more likely to report physical health complaints as adults than those who were not abused.31 They are also more likely to engage in risky sexual behaviors as adults and to become infected with sexually transmitted diseases.32 These negative consequences are further compounded by sexual revictimization, which can reignite the negative sequelae associated with sexual abuse.33

Prevention of Child Abuse Primary and secondary prevention programs appear to have some promise for preventing various types of child abuse. Early support programs that target parents experiencing psychological distress and who have little or no social support have been shown to decrease rates of child abuse and neglect by these targeted parents.34 These programs typically include efforts to help improve parenting skills, increase social support, and decrease parents’ psychological distress. In addition, there is evidence that school-based prevention programs increase children’s knowledge and skills related to preventing sexual abuse, by being more aware of the fact that certain behaviors by adults may not be appropriate. A meta-analysis by Davis and Gidycz35 found school-based programs that afforded children the opportunity for physical involvement (e.g., role play) and that were targeted to preschool or early elementary students were most effective. Taken together, these findings suggest that abuse prevention efforts aimed at younger children or families are especially promising.

ELDER ABUSE AND SIBLING VIOLENCE

Like other forms of family violence, abuse of the elderly in the family is often hidden from others and is rarely reported to authorities. The National Center on Elder Abuse36 has been collecting data since 1986, based on surveys of adult protective service agencies, and reports an increasing number of reported cases, with nearly 300,000 reported cases in 1996, the last year in which data were available. The most common form of reported abuse was neglect, or inadequate physical care. Less than 20% of the cases involve physical violence. Taking money from the elderly is another form of abuse. The typical abuser is a family member who has the responsibility to care for the elder who is unable to care for herself or himself. This may be a spouse or a child, or another family member. Since this is so rarely reported, there is little formal data available, but there is belief that such abuse may be more likely in violent or abusive families.21 In one project administered in New York City by the Police Department and Victim Services, educational programs and home visits to teach people about the problem of elder abuse resulted in more reports of this problem, but had no clear effects of reducing the problem.37 Physical aggression among brothers and sisters is quite common. This can range from simple shoving or slapping to extreme violence using weapons.38 Like other forms of family violence, this behavior can result in extreme injuries, but the large majority of this does not have serious health consequences. Sibling aggression is considered abusive when there are large age or size differences between the siblings involved, with the older and bigger child being the aggressor, when the physical aggression is frequent and occurs over long periods of time, when the behavior is hidden from others, and when the victim is fearful or has other evidence of emotional or physical reactions to the aggression.21

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OTHER TYPES OF VIOLENCE IN THE FAMILY

This discussion has focused on extremely violent family interactions. There is a good deal of evidence that family members also engage in low-level, mild violence with each other. Researchers have begun to examine these less extreme forms of physical aggression recently in married couples and same-sex and heterosexual couples living together.39 A meta-analysis published by Archer40 of marital and dating violence studies found that women actually engage in more acts of physical aggression than men. Such data was difficult to relate to the work on battered women. But, further examination of these studies indicated that much of the “violence” consists of hitting, slapping, shoving, or other relatively minor acts of physical aggression. As Archer noted, the majority of those who do suffer injury from violent behavior of a romantic partner are women. But, at the same time, it is clear that there are some women who can and do engage in highly violent acts toward their partners. As researchers begin to reexamine the findings on couple violence, one of the questions being raised is whether low-level violence has health consequences. In one study attempting to answer this question, Williams and Frieze41 used data from the National Comorbidity Survey to look at the psychological consequences of mild and severe violence. It was found that even mild violence had some association with psychological distress and marital dissatisfaction, although women reacted more than men. At the same time, there was a small subsample that did not appear to have adverse reactions to couple violence. Further research is needed to better understand different types or patterns of couple violence. Furgusson and colleagues42 suggest that some important dimensions of violence are the level of overall violence, the frequency of the violence, and the level of injury. More nuanced analysis will also need to be applied to other forms of violence in the family. Finally, research that incorporates the full scope of couple violence is needed. Perhaps because physical violence is the most visible and the most obviously physically harmful, a large focus of assessment and research is physical violence. Yet, other forms of violence or abuse exist and can manifest as health symptoms as well. Studies find that emotional and sexual abuse can be just as deleterious as physical.43,44 Emotional abuse, coercive control, stalking, and sexual violence are understudied, particularly by public health researchers. Future nationally representative studies must assess these multiple dimensions of violence and the specific contexts in which they occur. Because population-based studies are better suited to answer questions about correlates of violence than are other types of study designs,45 more thorough assessment of violence will result in the most accurate information on prevalence and burden of disease linked to couple violence. Such studies also can contribute to efforts of ongoing surveillance.46

RISK FACTORS FOR FAMILY VIOLENCE

Risk factors are similar for all types of family violence. In terms of severe violence, males are more often perpetrators.5,6 Those of lower socioeconomic status (SES) tend to experience more frequent and severe violence than their higher SES counterparts.47–50 Further different health consequences of violence may exist for those of differing levels of SES due to variations in psychosocial resources, such as social support,51 which tend to be socially distributed. History of violence in families appears to be a risk factor for future violence. Exposure to violence as a child (whether personally or vicariously) is related to being in an abusive adult relationship.52 Studies are also increasingly showing that substance abuse is a strong risk factor for family violence occurrence.53 It is less clear what risk factors are for elder abuse; future research is needed. Moreover, although research finds risk factors for some aspects of family violence, causal factors still remain heavily debated, thus making intervention and prevention

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efforts difficult.54 Research must continue to uncover risk factors. White and Kowalski55 developed a useful framework for identifying potential factors that may increase risk for victimization. By identifying factors at sociocultural, social network, dyadic, situational, and interpersonal levels, we may be in a better position to address violence intervention and prevention. RESPONDING TO VIOLENCE IN FAMILIES

No epidemic has ever been successfully eliminated or controlled by treating those already infected or affected.56 Thus, primary prevention is crucial to address family violence. In traditional public health terms, primary prevention entails reducing the number of new cases by changing behavior or environmental factors. Although treatment for victims of violence is important, public health aims to prevent people from becoming injured in the first place and to prevent the perpetrators from ever resorting to violence. For example, it is important to have an adequate number of shelters for battered women, but if battering could be prevented in the first place, these shelters would not be needed. This focus on prevention does not in any way diminish the importance of providing care for victims or the importance of arresting and prosecuting perpetrators. Rather the approach complements the contributions of other fields such as criminal justice and medical care. Such prevention is more cost-effective than other types of interventions because the individual never develops the problem and therefore high cost of medical care is avoided.57 Prevention of violence follows the same public health approach that guides efforts to prevent infectious diseases, chronic diseases, and environmental and occupational health problems. Therefore, it is not difficult for public health workers to understand and work on violence prevention. In fact, public health practitioners can play an effective role in coordinating prevention programs. The prevention focus has several implications: 1. Interventions should be developed earlier on the pathway toward violence. In the area of couple violence, for example, interventions could target women who are in relationships with a high risk for physical violence, but in which physical violence has not yet occurred. This could involve intervening with couples who are newly married, engaged but not yet married, or with young men and women just beginning to date. Or it could mean pushing the intervention even further back in time to school-age children and starting to educate them about the risks of violence and how to avoid it. 2. Children should be involved in preventive programs. Young children and youth may be more receptive to preventive interventions, and behaviors learned early tend to endure. 3. New methods of delivering programs need to be developed. Traditionally, the criminal justice and police sectors have conceptualized violent situations as having a perpetrator and a victim. They often targeted some programs at perpetrators and others at victims. That approach makes sense after a violent incident has occurred. However, this way of identifying victims and perpetrators is not useful in the context of prevention programs designed to intervene before violence occurs. 4. Programs need to target increasingly broader and larger groups at multiple levels. After specific acts of violence have occurred, individual perpetrators and victims can be identified. If we wish to intervene preventively, then we can say that a certain group is at risk for violence, and we need to focus our interventions at members of this high-risk group, some of whom might otherwise become perpetrators or victims, but many of whom would not. Other interventions might be even more broadly targeted to a general population in an effort to achieve universal coverage. A large focus should be on expanding public awareness of couple violence, child abuse, and elder abuse, and emphasize the potential for violence in all of us, rather than attributing the problem to deviant and minority individuals.

5. Parents should get involved in prevention programs. Programs can provide parents with access to information about child development and about nonviolent methods of socializing their children. 6. Elder abuse should be an increasing focus given the changing demographics of the population. Given the lack of firm research findings in many areas, it is perhaps more appropriate to make proposals for future research than for practice and policy. The most critical need is information about the causes of elder abuse and effective methods of intervention. Suggestions for research include examining the content of abusive acts, the circumstances in which abuse occurs, and the patterns that might predict abusive acts against the elderly. Research on this form of family violence seems particularly salient due to the changing demographic and the increased number of elderly in the coming years. 7. Prevention efforts should consider that different forms of family violence co-occur within the same families. Strategies developed to intervene in and prevent family violence should not treat child abuse as separate from couple violence as separate from elder abuse. Those attending to the needs of a couple, for instance, might be wise to assess for child or elder abuse. Education and awareness campaigns should make clear the relationship between different forms of violence. Finally, future research should seek to uncover dynamics of violent families, not merely individuals. FINAL THOUGHTS

More than other branches of medicine, public health has a long tradition of working closely with community-based groups in prevention efforts. Such alliances are needed to develop successful action and creative programming to prevent violence. Systematic evaluation of programs that emphasize a partnership between researchers and practitioners using sophisticated techniques will be needed to determine the impact of the programs. Only through these efforts will we liberate citizens from coercion and control, a vital part of the public health mission. REFERENCES

1. Tjaden P, Thoennes N. Extent, Nature, and Consequences of Intimate Partner Violence: Findings from the National Violence against Women Survey. Washington, DC: Department of Justice; 2000. 2. Fox JA, Zawitz MW. Homicide Trends in the United States. Washington, DC: Department of Justice; 2004. 3. Department of Health and Human Services (DHHS). Child Maltreatment 2003. Washington, DC: Government Printing Office; 2005. Available at http://www.acf.hhs.gov/programs/cb/pubs/cm03/

index.htm. 4. Saltzman LE, Green YT, Marks JS, et al. Violence against women as a public health issue: comments from the CDC. Am J Prev Med. 2000;19:325–9. 5. Johnson MP. Patriarchal terrorism and common couple violence: two forms of violence against women. J Marriage Fam. 1995;75:283–94. 6. Johnson MP. Conflict and control: symmetry and asymmetry in domestic violence. In: Booth A, Crouter AC, et al., eds. Couples in Conflict. Mahwah, NJ: Lawrence Erlbaum Associates; 2001: 95–104. 7. Frieze IH. Hurting the One You Love: Violence in Relationships. Belmont, CA: Thompson/Wadsworth; 2005. 8. Coker AL, Smith PH, Bethea L, et al. Physical health consequences of physical and psychological intimate partner violence. Arch Fam Med. 2000;9:451–7. 9. Golding JM. Intimate partner violence as a risk factor for mental disorders: a meta-analysis. J Fam Violence. 1999;14:99–132. 10. Plichta SB. Intimate partner violence and physical health conse-

quences: policy and practice implications. J Interpersonal Viol. 2004;19:1296–323.

81 11. Williams SL, Frieze IH, Sinclair HC. Intimate stalking and partner violence. In: Hamel J, Nicholls T, eds. Family Therapy for Domestic Violence: A Practitioner’s Guide to Gender-Inclusive Research and Treatment, New York: Springer; 2007;109–23. 12. Stosny S. Treating Attachment Abuse: A Comparison Approach. New York: Springer; 1995. 13. Murphy CM, Scott E. Cognitive Behavior Therapy for Domestically Assaultive Individuals. Baltimore County: University of Maryland; 1996. Unpublished treatment manual. 14. Murphy CM, Stosny S, Morrel TM. Changes in self-esteem and physical aggression during treatment for partner violent men. J Fam Violence. 2005;20:201–10. 15. Jackson S. Analyzing the Studies. NIJ Special Report. Washington, DC: National Institute of Justice; 2003. 16. Widom CS, Shepard RL. Accuracy of adult recollections of child victimization: Part 1. Childhood physical abuse. Psychol Assess. 1996a;8:412–21. 17. Widom CS, Shepard RL. Accuracy of adult recollections of child victimization: Part 2. Childhood sexual abuse. Psychol Assess. 1996b;9: 34–46. 18. CDC. National center for injury prevention and control; 2006. Available at http://www.cdc.gov/ncipc/factsheets/cmfacts.htm. 19. National Center for Shaken Baby Syndrome website; 2005. Available at http://www.dontshake.com. 20. Straus MA, Gelles RJ, Steinmetz SK. Behind Closed Doors: Violence in the American Family. Garden City, NY: Doubleday; 1980. 21. Hines DA, Malley-Morrison K. Family Violence in the United States: Defining, Understanding and Combating Abuse. Thousand Oaks, CA: Sage; 2005. 22. Emery RE. Family violence. Am Psychol. 1989;44:321–8. 23. Bugental DB, Ellerson RC, Lin EK, et al. A cognitive approach to child abuse prevention. JFP. 2002;16:243–58. 24. Appel AE, Holden GW. The co-occurrence of spouse and physical abuse: a review and appraisal. JFP. 1998;12:578–99. 25. Stith SM, Rosen KH, Middleton KA, et al. Intergenerational transmission of spouse abuse: a meta-analysis. J Marriage Fam. 2000;62: 640–54. 26. Kwong MJ, Bartholomew K, Henderson AJZ, et al. The intergenerational transmission of relationship violence. JFP. 2003;17:288–301. 27. Duncan RD, Saunders BE, Kilpatrick DG, et al. Physical assault in childhood as a risk factor for post-traumatic stress disorder, major depressive episodes, and substance abuse: a national survey. Am J Orthopsych. 1996;160:1453–60. 28. Repetti RL, Taylor SE, Seeman TE. Risky families: family social environments and the mental and physical health of offspring. Psychol Bull. 2002;128:330–66. 29. Felitti V, Anda R, Nordenberg D, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. Am J Prev Med. 1998;14:245–58. 30. Beitchman JH, Zucker KJ, Hood JE, et al. A review of the long-term effects of childhood sexual abuse. Child Abuse Negl. 1992;16: 101–18. 31. McCauley J, Kern DE, Kolodner K, et al. Clinical characteristics of women with a history of childhood abuse. JAMA. 1997;277:1362–8. 32. Greenberg JB. Childhood sexual abuse and sexually transmitted diseases in adults: a review and implications for STD/HIV programmes. Int J STD AIDS. 2001;12:777–83. 33. Wyatt GE, Guthrie D, Notgrass CM. Differential effects of women’s child abuse and subsequent sexual revictimization. J Consult Clin Psychol. 1992;60:167–73. 34. Geeraert L, Van den Noorgate W, Grietens H, et al. The effects of early programs for families with young children at risk for physical child abuse and neglect: a meta-analysis. Child Maltreat. 2004;9:277–91.

Violence in the Family as a Public Health Concern

1333

35. Davis MK, Gidycz CA. Child sexual abuse prevention programs: a meta-analysis. J Clini Child Psychol. 2000;29:257–64. 36. National Center on Elder Abuse. Trends in elder abuse in domestic settings; 2006. Available at http://www.elderabusecenter.org/basic/ fact2.pdf. 37. Davis RC, Medina-Ariza J. Results from an Elder Abuse Prevention Experiment in New York City. Washington, DC: U.S. Department of Justice; 2001. 38. Straus MA, Gelles RJ. How violent are American families? Estimates from the national family violence resurvey and other studies. In: Hotaling GT, Finkelhor D, Kirkpatrick JT, Straus MA, eds. Family Abuse and Its Consequences: New Directions in Research. Beverly Hills, CA: Sage; 1990:14–36. 39. Frieze IH. Violence in close relationships—development of a research area: comment on archer (2000). Psychol Bull. 2000;126:681–4. 40. Archer J. Sex differences in aggression between heterosexual partners: a meta-analytic review. Psychol Bull. 2000;126;651–80. 41. Williams SL, Frieze IH. Patterns of violent relationships, psychological distress, and marital satisfaction in a national sample of men and women. Sex Roles. 2005;52:771–84. 42. Furgusson DM, Horwood LJ, Ridder EM. Partner violence and mental health outcomes in a New Zealand birth cohort. J Marriage Fam. 2005;67:1103–19. 43. Arias I, Pape KT. Psychological abuse: implications for adjustment and commitment to leave violent partners. Violence Vict. 1999;14:55–67. 44. Dutton MA, Goodman LA, Bennett L. Court-involved battered women’s responses to violence: the role of psychological, physical, and sexual abuse. Violence Vict. 1999;14:89–104. 45. Verhoek-Oftedahl W, Pearlman DN, Babcock JC. Improving surveillance of intimate partner violence by use of multiple data sources. Am J Prev Med. 2000;19:308–15. 46. Saltzman LE, Fanslow JL, McMahon PM, et al. Intimate Partner Violence Surveillance: Uniform Definitions and Recommended Data Elements, Version 1.0. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 1999. 47. Ceballo R, Ramirez C, Castillo M, et al. Domestic violence and women’s mental health in Chile. Psychol Women Q. 2004; 28:298–308. 48. Hotaling GT, Sugarman DB. A risk marker analysis of assaulted wives. J Fam Violence. 1990;5:1–13. 49. Kurz D. Old problems and new directions in the study of violence against women. In: Bergen RK, ed. Issues in Intimate Violence. Thousand Oaks, CA: Sage:1998:197–207. 50. Tolman RM, Rosen D. Domestic violence in the lives of women receiving welfare. Violence Against Women. 2001;7:141–58. 51. Williams SL, Mickelson KD. A psychosocial resource impairment model explaining partner violence and distress: moderating role of income. Am J Community Psychol. In press. 52. Aldarondo E, Sugarman DB. Risk marker analysis of the cessation and persistence of wife assault. J Consult Clini Psychol.1996;64:1010–19. 53. Murphy CM, Winters J, O’Farrell TJ, et al. Alcohol consumption and intimate partner violence by alcoholic men: comparing violent and non-violent conflicts. Psychol Addict Behav. 2005;19:35–42. 54. Wolfe DA, Jaffe PG. Emerging strategies in the prevention of domestic violence. Future Child. 1999;9:133–44. 55. White J, Kowalski RM. Male violence against women: an integrated perspective. In: Geen RG, Donnerstein E, eds. Human Aggression: Theories, Research, and Implications for Social Policy. San Diego, CA: Academic Press:1998:203–28. 56. Albee GW. Preventing psychopathology and promoting human potential. Am Psychol. 1982;37:1043–50. 57. Mercy JA, Krug EG, Dahlberg LL, et al. Violence and health: the United States in a global perspective. Am J Public Health. 2003; 93:256–61.

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Index

Page numbers followed by f or t indicate figures or tables, respectively.

A Abortion as determinant of fertility, 43 frequency, 1303–1304 spontaneous, pesticide exposure and, 719 Absorbed dose, 736t Absorption, of toxic substances, 510 Abstinence-only education, 162 Abuse alcohol. See Alcohol abuse and dependence child. See Child abuse domestic. See Violence, in the family elder, 1331 substance. See Substance abuse Acanthamoeba, 316–317 Acceleration, 910–911 Acceptable daily intake (ADI), 551 Acetaminophen, 1129 Acetic acid, 860 Acetylene, 622 Acquired immunodeficiency syndrome (AIDS). See Human immunodeficiency virus (HIV) infection Acrolein, 646–647 Acrylamide, 644–645, 870t Activation, 506 Activities of Daily Living (ADL) scale, 795 Acute airway reactivity. See Asthma/acute airway reactivity Acute myeloid leukemia, 959t, 960t, 961. See also Leukemia Acute poststreptococcal glomerulonephritis. See Glomerulonephritis, poststreptococcal Acute radiation syndrome, 738, 738t Acute renal failure, 1093. See also Renal disease Acute respiratory distress syndrome (ARDS), 1118–1119 Acute rheumatic fever, 242–244 clinical characteristics, 242, 243 diagnosis, 243 epidemiology, 242–243 incidence, 242, 1082 pathogenesis, 243 secondary prophylaxis after, 244 treatment, 243–244

Acute tubular necrosis, 1094 Acyclovir, 132, 236 ADA (Americans with Disabilities Act), 790, 798 Adducts, 520 Adequate intake (AI), 1195, 1196t ADI (acceptable daily intake), 551 ADL (Activities of Daily Living) scale, 795 Adolescents nonfatal occupational exposure, 835–836 nonfatal occupational injuries, 835, 835t occupational fatalities from injuries and exposures, 834–835 pregnancy in, 39, 46 sexually transmitted infections, 163 smoking in health effects, 963 prevalence and trends, 969, 969f suicide, 1166, 1168 Adverse events, medication-related case studies rotavirus vaccines and intussusception, 1208–1209 thiazolidinediones and hepatic failure, 1210–1211, 1211f, 1212f definition, 1206f incidence, 1208t, 1209f MedWatch, 1206, 1207f postmarketing surveillance program, 1205–1206, 1206f sources, 1208f types, 1208 Advertising of food, 1199 of tobacco products, 976, 979–980 Aedes aegypti, 81 Aerosols, 782 Aerospace medicine, 909–916 airline passengers jet lag, 915 patients as, 915 safety, 914–915, 914t airline personnel aging, 914 alcohol and tobacco use, 913 illness and disease, 913 medical services for, 913, 913t medication use, 913 work-rest cycles, 913–914 community and international health concerns

airliner environment, 916 disease transmission, 915 vector control, 915–916 definition, 909 environmental considerations “greenhouse effect,” 916 noise, 916 ozone depletion, 916 flight environment biodynamics, 910–911 biosphere, 910 oxygen systems, 910 space, 911 spatial disorientation, 911 future, 916 history of speciality, 909 operational characteristics civil aviation, 911–912 military aviation, 912 space operations, 912 training and education, 909 Affluence, 925 African tick bite fever, 363t, 364–365 Age as confounder of behavioral performance, 532 emergency department visits for injury and, 1324–1325, 1324f hospital admissions for injury and, 1323–1324, 1323f injury mortality and, 1322–1323, 1323f as mortality determinant, 44 psychiatric disorder incidence and, 1163 Age-related macular degeneration, 1155–1156 Age-specific death rate (ASDR), 41, 42t Age-specific fertility rate (ASFR), 41, 42t Agent Orange, 520, 521t, 680 Aging, 39, 46–47. See also Elderly persons Agriculture characteristics in U.S., 819–820 pesticide use in, 707–708 workers. See Farmworkers AHF (Argentine hemorrhagic fever), 353t, 354, 354f AI (adequate intake), 1195, 1196t AIDS. See Human immunodeficiency virus (HIV) infection Air pollution environmental, 700–701 effects, 701

1335 Copyright © 2008 by The McGraw-Hill Companies, Inc. Click here for terms of use.

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Index

Air pollution (Cont.): global patterns, 929 history, 700 modifiers, 700 ozone, 508 regulated pollutants, 700 sources, 700 indoor, 508–509, 701–703 chemicals, 701–702, 920, 921t dust, 920 effects, 702 exposure limits, 702 living agents, 701, 921 nitrogen dioxide, 508–509 prevention and control, 703 radon, 508, 920, 921t “sick building” syndrome and, 508–509 occupational, 691–699, 696–698t acute alveolar reactions and, 691–693, 692t asthma/acute airway reactivity and, 693–694, 696–698t chronic alveolar disease and, 693–694 chronic bronchitis and, 695, 698–699 lung cancer and, 699 Air travel. See also Aerospace medicine jet lag and, 915 for patients, 915 safety, 914–915, 914t tuberculosis transmission during, 257 Airborne contaminants, 782 Airborne precautions, 203t, 209 Alachlor, 870t Alanine aminotransferase (ALT), 1007 Albendazole for ascariasis, 478 for capillariasis, 479 for filariasis, 400 for hookworm disease, 476 for hydatid disease, 450 for pinworm, 479 for strongyloidiasis, 478 Alcohol abuse and dependence, 1001–1008 definitions, 1001–1002 economic impact, 1000, 1004, 1004t epidemiology, 1000–1001 mechanisms of dysfunction and damage, 1001, 1001f, 1002t morbidity and mortality, 1002–1003, 1002t prevalence, 1000, 1163t prevention strategies indicated interventions, 1007 legal accessibility, 1006 models, 1004, 1005t physical availability, 1006 price control, 1005–1006 selective efforts, 1006–1007 universal efforts, 1005 public health impact, 1003–1004, 1003t screening laboratory tools, 1007–1008 in primary care settings, 1007 questionnaires, 1007 treatment interventions, 1008 Alcohol consumption by airline personnel, 913 blood alcohol concentration, 1007 cancer risk and, 1053

cardiomyopathy and, 1083 categories hazardous, 999. See also Alcohol abuse and dependence safe, 999 coronary heart disease and, 1075–1076 as hypothermia risk factor, 731 in men, 1002–1003, 1002t in pregnancy, 1179 prevalence, 1000 smoking and, 959–960, 1053 in women, 1003 Alcohol Use Disorders Identification Test (AUDIT), 1007 Alcoholics Anonymous, 1008 Alcohols, 640–641 Aldehydes acrolein, 646–647 characteristics, 645 formaldehyde, 645–646 Alicyclic hydrocarbons, 622 Aliphatic amines, 653 Aliphatic hydrocarbons characteristics, 620 sources and uses, 620 toxic effects, 620–622 Alkanes, 619 Alkhurma virus, 353t, 358 Alkynes, 622 All Kids Count, 51, 52 Alleles, 64 Allergic pneumonitis, 694 Allyl alcohol, 641 Alpha error, 22 Alpha particles, 872t Alpha radiation, 736t. See also Ionizing radiation ALT (alanine aminotransferase), 1007 Aluminum exposure effects, 604–605 maximum contaminant levels in drinking water, 874t measurement, 604, 605 prevention, 605 sources, 604 Alzheimer’s disease aluminum accumulation in, 605 incidence, 1148 protective factors, 1148 risk factors, 1148 Amantadine, 124 Amblyopia, 1158 Ambulatory care services, 1223–1228 freestanding centers, 1225–1228 hospital-based, 1225 long-term care, 1226–1227, 1226t mental health and substance abuse services, 1227 office-based, 1223–1225 patient characteristics, 1224–1225t pharmacy providers and suppliers, 1227–1228 safety-net clinics, 1225–1226 types, 1223 AME (aviation medical examiner), 909. See also Aerospace medicine Amebiasis, 265t, 313–316 clinical characteristics, 265t, 315, 315t diagnosis, 265t, 315–316 epidemiology, 268t, 313–314, 314t immunology, 314

life cycle, 313 pathogenesis, 314–315 prevalence, 314 prevention, 316 treatment, 316, 316t Amebic meningoencephalitis, 316–317 clinical characteristics, 317 diagnosis, 317 epidemiology, 317 etiology, 316–317 life cycle, 317 pathogenesis, 317 prevention, 317 treatment, 317 American Medical Association (AMA), Guides to the Evaluation of Permanent Impairment, 800 American Public Health Association (APHA), ethics guidelines, 32 American Stop Smoking Intervention Study for Cancer Prevention (ASSIST), 974 American trypanosomiasis. See Chagas’ disease Americans with Disabilities Act (ADA), 790, 798 Amodiaquine, 378 Amosite, 568. See also Asbestos Amphetamines, 1014. See also Substance abuse Amyotrophic lateral sclerosis pesticide exposure and, 718–719 toxic exposures and, 1144 Anabolic steroids, 1014. See also Substance abuse Anal cancer, 160 Analgesic nephropathy, 1092–1093 Analytical study, 17 Anaplasmosis, human granulocytic, 367 Ancylostoma duodenale, 474. See also Hookworm disease Ancylostomiasis. See Hookworm disease Andrural typhus, 366–367 Anemia aplastic, benzene exposure and, 624 in hookworm disease, 475 Anesthetics, as drugs of abuse, 1014. See also Substance abuse Animal control, in disasters, 1292 Animal welfare/rights, 521–522 Anopheles mosquitos, 91 Anthophyllite, 569. See also Asbestos Anthrax, 427–430 clinical characteristics animal, 429 cutaneous, 428 gastrointestinal, 428–429 hematogenous, 429 inhalational, 428 diagnosis, 430 etiologic agent, 428 history, 427 immunization, 431 occurrence, 429–430 postexposure prophylaxis, 430 prevention and control, 430–431 transmission, 429 treatment, 430 Anthropometry, 763–764, 764f, 765f, 765t Antifol antimalarial drugs, 378 Antifungal drugs for aspergillosis, 465

Index for candidiasis, 462 for cryptococcosis, 463 for dermatophytoses, 471–473 for zygomycosis, 466 Antigenic drift, 121 Antigenic shift, 121 Antimicrobial drugs for acute rheumatic fever, 244 for amebiasis, 316, 316t for anthrax, 430 for brucellosis, 432 for diphtheria prophylaxis, 119 for endocarditis prophylaxis, 244 for GABHS prophylaxis, 242, 242t for H. influenzae infections, 125 for leprosy, 261–262 for leptospirosis, 435–436 for meningococcal disease prophylaxis, 247 for otitis media, 125, 205 for pertussis, 114 for plague, 372 for Q fever, 369 resistance, 84–85 for salmonellosis, 437 for sexually transmitted infection prophylaxis, 164 for shigellosis, 303–304 for streptococcal pharyngitis, 240 for traveler’s diarrhea, 92, 309 for tularemia, 427 for typhoid fever, 302 Antimony, 605, 869t Antimony compounds, 396–397 Antitoxin, diphtheria, 119 Antituberculosis drugs, 251–252 Antiviral drugs for cytomegalovirus infection, 236 for herpes simplex infections, 234 for herpes zoster, 132, 133 for HIV/AIDS, 193–195 for influenza, 124, 209 for severe acute respiratory syndrome, 207 for varicella, 132 Anxiety disorders, 1163t. See also Psychiatric disorders Aplastic anemia, benzene exposure and, 624 Apoptosis, 515 Apparent temperature, 726, 726f Arboviral diseases, 341–352, 343–346t diagnosis, 348, 349t by disease pattern. See also specific diseases arthritis, 346t, 351–352 central nervous system infections, 343–345t, 349–350 febrile illness, 346t, 351 epidemiology, 341–342 hosts, 347 prevention and control, 348 surveillance, 347–348 vector-host transmission cycles, 342 vectors, 342 viral recrudescence and survival strategies, 347 Arboviruses, 341, 342t ARDS (acute respiratory distress syndrome), 1118–1119 Arenaviruses, 342t, 352–355, 353t, 354t Argentine hemorrhagic fever, 353t, 354, 354f Bolivian hemorrhagic fever, 353–354, 353t

Lassa fever, 352–354, 353t lymphocytic choriomeningitis virus, 353t, 355 Sabia virus, 353t, 355 Venezuelan hemorrhagic fever, 353t, 355 Argentine hemorrhagic fever (AHF), 353t, 354, 354f Aristotle, 28 Aromatic hydrocarbons exposure, 623–628 benzene, 623–626 styrene, 628–629 toluene, 626–628 xylene, 628 Aromatic nitro- and amino-compound exposure, 650–653 4,4–diaminodiphenylmethane, 652 dinitrobenzene, 651 dinitrochlorobenzenes, 652 dinitrotoluene, 651 4,4’-methylene-bis-ortho-chloroaniline, 652–653 nitrobenzene, 651 nitrotoluene, 651 para-aminophenol, 652 paraphenylenediamine, 652 prevention and control, 653 tetranitromethylaniline, 653 toluylenediamine, 652 toxic effects, 650–651 trinitrotoluene, 651–652 xylidine, 652 Arsenic, 525, 525t, 605–606 exposure environmental contamination, 904 prevention, 606 sources, 605–606 maximum contaminant levels in drinking water, 869t toxic effects, 525, 525t, 606, 869t, 904 Artemisinin compounds, 380, 482 Arthritis. See also Osteoarthritis arboviruses causing, 351–352 rheumatoid, 1130 Arthropod vector-borne diseases, 341–401 arboviral diseases. See Arboviral diseases leishmaniasis, 394–397, 395t Lyme disease. See Lyme disease lymphatic filariasis. See Lymphatic filariasis malaria. See Malaria plague. See Plague Q fever, 368–369 rickettsial infections. See Rickettsial infections trypanosomiasis, 392–394 viral hemorrhagic fevers, 352–362 Asbestos, 567–577 asbestos minerals, 568–569 fibers and fibrils, 568 patterns of use, 569 removal, 569 sources, 568–569 uses, 569 biological effects, 569–570 cellular, 569 immune responses, 570 molecular, 569 target organ, 569–570, 570f transport of fibrils, 570 diseases associated with asbestosis, 571–575 cigarette smoking and, 569t, 574 clinical characteristics, 567, 573

1337

diagnosis, 571, 572f, 573f pathogenesis, 571, 574f physiological impairment, 573–574, 574f pleural effusions in, 574–575, 575f clinical recognition, 567 history, 567 lung cancer, 567–568, 576, 699 mesothelioma, 568, 575–576, 575f non-lung neoplasms, 568, 568t, 569t, 576 societal impact, 576–577 human exposure, 570–571 family members, 570 in schools and other buildings, 570–571, 701 workers, 570, 571f litigation regarding, 569, 577 maximum contaminant levels in drinking water, 869t regulations on workplace exposure, 577 smoking and, 569t, 574, 576 Ascariasis, 478 clinical presentation, 478 diagnosis, 478 epidemiology, 478 etiologic agent, 478 prevention and control, 478 treatment, 478 Ascaris lumbricoides, 478, 697t ASDR (age-specific death rate), 41, 42t Aseptic meningitis, 228–229 clinical illness, 228 diagnosis, 229 epidemiology, 228 etiologic agents, 229 prevention, 229 treatment, 229 ASFR (age-specific fertility rate), 41, 42t Asian flu pandemic, 121 Aspartate aminotransferase (AST), 1007 Aspergillosis, 464–465 clinical characteristics, 464 diagnosis, 464–465 epidemiology, 464 microbiology, 464 treatment, 465 Aspergillus, 464 Asphyxiant gases, 691, 692t Aspirin, Reye’s syndrome and, 122 Assessment Protocol for Excellence in Public Health (APEX/PH), 1246 ASSIST (American Stop Smoking Intervention Study for Cancer Prevention), 974 Asthma/acute airway reactivity in children genetic factors, 1116 incidence and prevalence, 1115, 1116f mortality rates, 1117 natural history, 1117 prevention, 1117 risk factors, 1115–1116, 1116t definition, 694 economic impact, 1117 incidence, 694, 1117 mortality, 1117 occupation-related diagnosis, 695 epidemiology, 694–695 etiologic agents, 695, 696–698t mechanisms, 695

1338

Index

Asthma/acute airway reactivity (Cont.): pesticide exposure, 713–714 prevention and control, 696 pesticide exposure and, 715–716 prevention, 1117 risk factors, 1117 smoking and, 962 swimming pool use and, 716 Atherosclerosis. See also Coronary heart disease diabetes and, 1107–1108 smoking and, 956–957 Atovaquone/proguanil for malaria prophylaxis, 91, 385t for malaria treatment, 378 Atrazine, 870t Atrial fibrillation, stroke risk and, 1145 Attack rate, 19 Attention, testing, 530 Attributable risk, 20 Attributable risk percent, 21 AUDIT (Alcohol Use Disorders Identification Test), 1007 Australian bat lyssaviruses, 420t Autoimmune disorders, silica exposure and, 597 Autonomy, 28 Autosomal chromosome disorders, 66 Autosomal dominant disorders, 67 Autosomal dominant polycystic kidney disease, 1092 Autosomal recessive disorders, 67 Avian influenza A epidemiology, 124 H5N1 clinical characteristics, 124 emergence, 81, 208–209 risk factors for infection, 124 Aviation. See Aerospace medicine; Air travel Aviation medical examiner (AME), 909. See also Aerospace medicine Azithromycin, for GABHS prophylaxis, 242t B BAC (blood alcohol concentration), 1007 Bacillary dysentery, 303. See also Shigellosis Bacillus anthracis, 428. See also Anthrax Bacillus Calmette-Guérin (BCG) vaccine in leprosy prevention, 263 tuberculin skin test interpretation and, 251 in tuberculosis prevention, 252 Bacillus cereus, 265t, 266t, 474, 848t, 849t Bacillus subtilis, 265t, 266t Bacteriocins, 860 Barbiturates, abuse, 1013–1014. See also Substance abuse Barium, 869t Basic needs theory, 943t Battered child. See Child abuse Battered women, 1329–1330 Bedrest, complications, 1187, 1188t Beef tapeworm, 447–448 Behavioral change, 941–948 interventional planning and evaluation design, 947 information sources, 947–948, 948t interventional strategies built environment, 947 classes and curricula, 945–946 mass media, 946–947

motivational interviewing, 945 policy, 947 print communications, 946 targeted electronic media, 946 theories Health Belief Model, 941–942 rationales for use, 941 self determination theory, 942–943, 942f, 943f social cognitive theory, 942 theory of reasoned action and planned behavior, 944–945, 945f transtheoretical model, 943–944, 943f, 944f Behavioral Risk Factor Surveillance System (BRFSS), 12, 40, 1321 Behavioral theory, 1016 Benchmark dose, 550–551 Beneficence, 28 Benign prostatic hyperplasia, 1096 Benzene, 623–626 exposure prevention and control, 626 sources, 623–624 maximum contaminant levels in drinking water, 870t toxic effects, 624–626, 870t Benzodiazepines, abuse, 1014. See also Substance abuse Bereavement, 1191 Beryllium maximum contaminant levels in drinking water, 869t sources, 606, 697t toxic effects, 606, 694, 869t Beta particles, 872t Beta-propiolactone, 643 Beta radiation, 736t. See also Ionizing radiation Bias, 21–22 Bidi smoking, 972 Biliary cancer, pesticide exposure and, 716, 717 Bioaccumulation, 866 Bioavailability definition, 506 environmental contaminant, 903 significance, 510 Biological agent risk assessment, 551 Biomarkers applications, 520 characteristics, 519–520 of effect, 564, 903 examples, 519t of exposure, 563–564, 564f, 903 for lead, 520. See also Lead for mercury, 520. See also Mercury of susceptibility, 564, 903 Biomass fuel combustion, 920, 921t Biomechanics, 763 Bioterrorism threats Bacillus anthracis, 427. See also Anthrax Coxiella burnetii, 369 infectious agents, 85 Biotransformation, 506 Birth defects, pesticide exposure and, 719–720 Bismuth subsalicylate, 92, 309 Bisphosphonates, 1127 Black lung disease. See Coal workers’ pneumoconiosis Bladder cancer

pesticide exposure and, 717 smoking and, 959–960, 959t, 960t Blindness. See also Visual disorders causes, 1153, 1154f definition, 1155 demographic factors, 1153, 1155f diabetes and, 1106 Blood alcohol concentration (BAC), 1007 Blood-borne diseases cytomegalovirus. See Cytomegalovirus (CMV) infection hepatitis B. See Hepatitis B hepatitis C. See Hepatitis C HIV. See Human immunodeficiency virus (HIV) infection malaria. See Malaria Blood flukes. See Schistosomiasis Blood pressure. See Hypertension Bloodstream infections, health care-associated, 334 Bolivian hemorrhagic fever, 353t, 354–355 Bone cancer, pesticide exposure and, 716 fractures in children, 1132–1133 in older adults, 1128, 1189, 1189f osteoporosis. See Osteoporosis Bordetella pertussis, 111, 206. See also Pertussis Borg perceived exertion scale, 766f Borrelia burgdorferi, 386–387, 387f. See also Lyme disease Botulism food-borne, 849t, 852–853 infant, 853 Bovine spongiform encephalopathy, 83, 1142 Brain cancer, pesticide exposure and, 716, 717 infection. See Encephalitis toxicant effects on. See Neurobehavioral toxicity Branch retinal vein occlusion, 1156 Brazilian hemorrhagic fever, 353t BRCA1/2 mutations, 1060–1061 Break-bone fever. See Dengue fever Breast cancer genetic factors, 1060–1061 oral contraceptives and, 1307 pesticide exposure and, 717 radiation exposure and, 739, 1054 reproductive factors, 1057 screening programs, 1064 sex steroid hormones and, 1055–1056 Breast-feeding benefits, 272 as determinant of fertility, 43 BRFSS (Behavioral Risk Factor Surveillance System), 12, 40, 1321 Bricklaying, silica exposure in, 592 Brill-Zinsser disease, 366 Bromate, 869t Brominated flame retardants environmental prevalence, 685 health effects, 685–686 human exposure, 686 production and use, 685 regulations, 686 Bronchiolitis, 205–206 Bronchitis, chronic, 695, 698–699 definition, 695

Index epidemiology, 699 natural history, 699 occupational exposures and, 695, 698–699 prevention and control, 699 smoking and, 695 surveillance, 699 Brucella, 431–432, 848t, 849t Brucellosis, 431–433 clinical characteristics, 432 etiologic agent, 431–432 history, 431 occurrence, 433, 848t, 849t prevention, 433 transmission, 432–433 Brugia spp., 398–399. See also Lymphatic filariasis Bubonic plague. See Plague Bunyaviruses, 342t, 353t, 358–362, 361t Crimean-Congo hemorrhagic fever, 359–360 hantavirus pulmonary syndrome, 360–362, 361t hemorrhagic fever with renal syndrome, 360 Rift Valley fever, 359 Burkitt’s lymphoma, 1058 1,3–Butadiene, 622 Byssinosis, 695 C Cadmium, 607 exposure prevention, 607 sources, 607 maximum contaminant levels in drinking water, 870t toxic effects, 607, 870t CAGE questionnaire, 1007 Calcitonin, 1127 Caliciviridae. See Noroviruses California encephalitis, 344t, 349 Campylobacter clinical characteristics, 265t, 851 epidemiological features, 266t, 848t, 851 fluoroquinolone-resistant, 85 prevention, 851 Canada, vital record linkage system in, 12 Cancer, 1047–1065. See also Carcinogens; specific cancers epidemiology age, 1048, 1049t classification, 1047 geography, 1049 magnitude of the problem, 1047 mortality and incidence in children, 1049t sources of data, 1047 specific neoplasms, 1047–1048, 1048t time trends, 1049–1052, 1050f, 1051f race, 1049, 1050t sex, 1049 etiology and primary prevention alcohol use, 1002t, 1053 criteria for causality, 1052 environmental pollution, 1053–1054 general considerations, 1052, 1061, 1061t genetic factors, 1060–1061, 1060t infectious agents, 160, 1057–1059 ionizing radiation exposure, 738–740, 739f, 740t, 1054–1055 nonionizing radiation exposure

electromagnetic fields, 747–748, 1055 radiofrequency/microwave radiation, 749 ultraviolet radiation, 744, 929, 1055 nutritional factors, 1059–1060 obesity, 1059–1060 occupational exposure industrial, 1053, 1054t in U.S.-hired farmworkers, 823 in women workers, 830 pesticide exposure, 716–717 physical activity, 1059–1060 reproductive factors, 1057 secondhand smoke, 964–966, 1053 sex hormones/oral contraceptives, 1055–1057, 1306–1307 tobacco use, 957–961, 957f, 959t, 960t, 1052–1053, 1053t protective factors, 1060 secondary prevention breast cancer, 1064 comprehensive programs, 1061–1062 evaluation of methods, 1063–1064 goals, 1062 overview of known causes, 1061, 1061t screening programs, 1062–1063 strategies, 1062 survivors, 1065 Candida, 462 Candidiasis, 461–462 clinical characteristics, 461–462 diagnosis, 462 epidemiology, 461 microbiology, 462 risk factors, 461–462 treatment, 462 Cannabinoids, 1013 Capillaria philippinensis, 479 Capillariasis, 479 clinical characteristics, 479 diagnosis, 479 epidemiology, 479 etiologic agent, 479 prevention and control, 479 treatment, 479 Caplan’s syndrome in coal workers’ pneumoconiosis, 585–586 in silicosis, 597 Carbofuran, 870 Carbohydrate-deficient transferrin (CDT), 1007 Carbohydrate intake, coronary heart disease and, 1075 Carbon dioxide, 691, 692t Carbon disulfide exposure, 649–650 effects, 524–525, 525t, 649–650 prevention, 650 sources, 649, 692t Carbon monoxide, 691, 692t Carbon tetrachloride, 631–632 exposure, 631–632 maximum contaminant levels in drinking water, 870t toxic effects, 631 Carcinogenesis, 518 Carcinogens. See also Cancer, etiology classification, 549, 550t in food, 1059 risk assessment dose-response assessment, 548 exposure assessment, 548–549

1339

hazard identification, 548 interpreting the model, 550 interspecies extrapolations, 549–550 landmarks, 549t risk characterization, 549 substances asbestos, 567–568, 568t, 576 benzene, 624–625 1.3–butadiene, 622 carbon tetrachloride, 630–631 chloroprene, 638–639 N, N-dimethylformamide, 643 ethylene dibromide, 637 ethylene oxide, 657–658 formaldehyde, 646 nitrosamines, 655–656 organic nitroso-compounds, 654 perchloroethylene, 634 silica, 597–598 styrene, 629 trichloroethylene, 633 vinyl chloride, 631 Cardiomyopathies, 1083–1084, 1083t Cardiovascular disease cardiomyopathies, 1083–1084, 1083t congenital heart disease, 1082–1083, 1083t coronary heart disease. See Coronary heart disease prevention, 1071, 1084 rheumatic heart disease, 1082 syphilitic heart disease, 1084 Carotid endarterectomy, 1147 Carrier, 274 Carson, Rachel, 506, 707 Case-control study, 17, 18t, 21t Case-fatality rate, 19 Cataract, 1153–1154 Causal association, 20, 21t Causality orientations theory, 943t CBPR. See Community-based participatory research CBR (crude birth rate), 40, 41, 42t CCHF (Crimean-Congo hemorrhagic fever), 353t, 359–360 CDCynergy, 1269 CDR (crude death rate), 40, 42t CDT (carbohydrate-deficient transferrin), 1007 Cellular phones, 749–750 Census, 39 Census of Fatal Occupational Injuries, 1321 Centers for Disease Control and Prevention (CDC), health care-associated infection prevention guidelines, 337 Central nervous system infections. See Encephalitis; Meningitis neurotoxicant effects on. See Neurobehavioral toxicity Cephalexin, for GABHS prophylaxis, 242t Ceramic fiber insulation, silica exposure from, 592 CERCLA (Comprehensive Emergency Response, and Compensation and Liability Act), 902 Cerebral palsy, 1140–1141 Cerebrovascular disease prevalence, 1139, 1141t, 1142t smoking and, 956 stroke, 1145–1147

1340

Index

Cervical cancer human papillomavirus infection and, 160 incidence, 160 oral contraceptives and, 1307 screening programs, 1064 sex steroid hormones and, 1057 smoking and, 959t, 960–961, 960t Cestode infections, 447–451 cysticercosis, 447–448 food-borne, 852 hydatid disease, 449–451 taeniasis, 447–448 Chagas’ disease, 392–393 biology and transmission, 392 clinical characteristics, 392 control, 393 diagnosis, 393 epidemiology, 392–393 treatment, 393 Chairs, ergonomics, 775–776 Chancroid, 168–169 Change processes of, 944t stages of, 944t transtheoretical model, 943–944 Change in rate, natural increase (CRNI), 41 Chemical exposures, 619–658. See also Carcinogens; Multiple chemical sensitivities brominated flame retardants, 685–686 environmental air, 508–509. See also Air pollution food, 509, 848t, 853. See also Food safety soil, 509. See also Soil water, 509. See also Water, contamination/pollution occupational, 697–698t organic compounds acids, anhydrides, lactones, and amides, 642–645 alcohols and glycols, 640–642 aldehydes, 645–647 alicyclic hydrocarbons, 622 aliphatic amines, 653 aliphatic hydrocarbons, 620–622 aromatic hydrocarbons, 628–629 aromatic nitro- and amino-compounds, 650–653 epoxy compounds, 656–658 esters, 647 ethers, 648–650 halogenated hydrocarbons, 629–638 ketones, 621, 647–648 organic nitroso-compounds, 653–656 organic solvents, 619–620 petroleum solvents, 622–623 pathophysiology cytochrome P450, 511–512 excretion route, 512–513 flavin-containing monooxygenases, 512 metabolic activation vs. detoxification, 511 phase II reactions, 512 toxicokinetics, 511 polychlorinated biphenyls, 525, 525t, 531–532, 675–677 polychlorinated dibenzofurans, 679–683 polychlorinated dioxins, 520, 521t, 679–680 CHEMTREC, 783 Chernobyl nuclear accident, 736

Chickenpox. See Varicella Chikungunya fever, 346t, 351–352 Chilblains, 730 Child abuse physical, 1330 prevention, 1331 as priority in maternal and child health, 1296 sexual, 1330–1331 Child labor, 832–836 artisanal miners in Nambija, Ecuador, 810–811 in U.S. current statistics, 833 definition, 832 historical perspective, 832–833 illegal, 834 injury prevention, 836 laws, 833–834 nonfatal occupational exposure, 835–836 nonfatal occupational injuries, 835, 835t occupational fatalities from injuries and exposures, 834–835 Children cancer epidemiology, 1048 incidence, 1049t pesticide exposure and, 716 cognitive disability. See Mental retardation employment. See Child labor heat-related illness, 727f, 728 hypothermia, 731–732, 731f musculoskeletal disorders developmental dysplasia/dislocation of the hip, 1133 fractures, 1132–1133 scoliosis, 1131–1132 slipped capital femoral epiphysis, 1132, 1132f respiratory diseases asthma, 1115–1117, 1116f, 1116t cystic fibrosis, 1114–1115 respiratory distress syndrome, 1113–1114 respiratory tract infections, 1115 secondhand smoke and, 964 with special health care needs, 1296 Chitin inhibitors, 713t Chlamydia infection epidemiology, 167 incidence, 156t in pregnancy, 161 prevalence, 167, 168t vaccine, 165 Chlamydia psittaci, 423–424 Chlamydia trachomatis, 1157 Chlordane, 871t Chlorinated hydrocarbon pesticides, 711, 713 Chlorine dioxide, 869t Chlorite, 869t Chlorobenzene, 871 Chloroform, 632 Chloroprene, 638–639 Chloroquine for malaria prophylaxis, 91, 385t for malaria treatment, 378 Chlorpyrifos, 711 Cholera, 304–307 clinical characteristics, 265t, 306, 850 diagnosis, 265t ecologic factors, 305–306

epidemiological features, 267t etiology, 304–305, 850 history, 305 immunization, 88–89, 274, 307 pathogenesis, 304–305 prevention and control, 307 susceptibility, 306 transmission, 267t, 306 treatment, 306–307 Cholesterol, coronary heart disease and, 1076 Chromium exposure prevention, 608 sources, 607–608, 697t maximum contaminant levels in drinking water, 870t toxic effects, 608, 870t Chromosomes anomalies in mental retardation, 1174–1177 ionizing radiation and, 736–737, 737f, 737t Chronic bronchitis. See Bronchitis, chronic Chronic disease. See also Disability cancer, 1047–1065 diabetes, 1101–1108 dietary factors, 1197 heart disease, 1071–1084 mental retardation, 1173–1180 musculoskeletal disorders, 1125–1134 neurological disorders, 1139–1148 psychiatric disorders, 1161–1168 renal and urinary tract disease, 1089–1098 respiratory diseases, 1113–1120 Chronic obstructive pulmonary disease (COPD), 1117–1118 definition, 1117 diagnosis, 1118 disability and, 1191 epidemiology, 1118 incidence, 961 mortality, 961, 1118, 1191 natural history, 1118, 1118f pathophysiology, 1117 risk factors, 1117 smoking and, 961–962, 1118 Chronic pelvic pain, 159–160 Chrysotile, 568. See also Asbestos Cidofovir, for cytomegalovirus, 236 Cigar smoking. See also Tobacco use cancer and, 958–959, 972, 1053 cardiovascular disease and, 955 chronic obstructive pulmonary disease and, 962 periodontal disease and, 962 trends, 971–972 Cigarette smoking. See Tobacco use Ciguatoxin, 848t, 853 Cinnabar. See Mercury Cities, world’s largest, 920t Civil aviation, 911–912. See also Aerospace medicine; Air travel Clarithromycin, 262 Clindamycin, 242t, 380 Clofazimine, 261, 261t Clonorchiasis, 445–447 clinical characteristics, 446 community patterns of infection and disease, 446 diagnosis, 446 etiologic agent, 445–446

Index geographic distribution, 446 prevention and control, 447 treatment, 446–447 Clostridium botulinum, 848t, 852–853 Clostridium difficile, 265t, 266t, 271t Clostridium perfringens, 265t, 266t, 848t, 851 Clostridium tetani, 115. See also Tetanus Clove cigarettes, 972 CMV. See Cytomegalovirus (CMV) infection Coal workers lung disease in, 583. See also Coal workers’ pneumoconiosis occupational safety and health legislation, 583–584, 584t Coal workers’ pneumoconiosis, 583–588 clinical characteristics, 586 definition, 584 environmental exposure and, 584, 585f epidemiology, 586–587, 587f history, 583 pathogenesis, 584–586, 585f prevention, 587–588, 588f Cobalt toxicity, 608–609, 694 Cocaine, 1014. See also Substance abuse Cognitive disability. See Dementia; Mental retardation Cognitive ergonomics, 763 Cognitive evaluation theory, 943t Cohort rate, 41 Cohort study, 17, 18t Cold-related illnesses, 729–732 cold stress indices, 729 epidemiology, 731–732, 731f frostbite, 730 hypothermia, 730 nonfreezing local tissue injury, 730 prevention, 732 seasonal trends, 728–729, 729f Collective effective dose, 736t Colorado tick fever, 343t, 351 Colorectal cancer genetic factors, 1061 pesticide exposure and, 716 screening programs, 1064 Committed effective dose, 736t Common cold, 203–204 Communicable diseases bioterrorism threats, 85 cancer and, 1057–1059 control in disease, 1291–1292 ethical issues, 28–29 methods, 77, 78t public health role, 78–79 public health systems for, 79 emerging threats antimicrobial drug resistance, 84–85 factors contributing to, 80t food-borne, 82–83 human immunodeficiency virus. See Human immunodeficiency virus overview, 79–80, 80t, 931 strategies for addressing, 85–87 tuberculosis. See Tuberculosis vector-borne, 81–82, 82f water-borne, 83 zoonotic, 80–81 food-borne. See Food-borne diseases

health care-associated. See Health careassociated infections international travel considerations. See Travel, international major problems, 77–78, 78t spread by close personal contact, 201–274 aseptic meningitis, 228–229 cytomegalovirus, 235–236 gastrointestinal infections. See Gastrointestinal infections herpes simplex virus infections. See Herpes simplex virus (HSV) infections infectious mononucleosis. See Infectious mononucleosis leprosy. See Leprosy meningococcal disease. See Meningococcal disease respiratory infections. See Respiratory infections tuberculosis. See Tuberculosis viral hepatitis hepatitis A. See Hepatitis A hepatitis B. See Hepatitis B hepatitis C. See Hepatitis C hepatitis delta. See Hepatitis delta hepatitis E. See Hepatitis E history, 211–212 non-A to E hepatitis, 228 vector-borne. See Arthropod vector-borne diseases water-borne. See Water-borne diseases zoonotic. See Zoonoses Community-based participatory research (CBPR) conceptualization, 59 definition, 59 empowerment and, 59–60 initiatives, 60–61 Community diagnosis, 14 Community empowerment, 60 Community health promotion. See Public health, holistic community approach Community Tool Box, 1269 Comprehensive Emergency Response, and Compensation and Liability Act (CERCLA), 902 Concentration, testing, 530 Condoms as contraceptive, 1309 for sexually transmitted infection prevention effectiveness, 164–165 use determinants, 164 use trends, 164 Conflict-related disasters, 1287. See also Disasters Confounding, 21 Congeners, 508 Congenital heart disease, 1082–1083, 1083t Congenital rubella syndrome, 108, 109t, 1179–1180 Congenital varicella syndrome, 130 Conservation medicine diclofenac and vulture decline, 555 organochlorines and avian reproduction, 555 West Nile virus, 555 Contact precautions, 203t, 209 Continuous quality improvement (CQI), 1278–1279, 1278t Contraception. See also Family planning

1341

cost-effectiveness, 1305 as determinant of fertility, 43 effectiveness, 1305, 1307t global context, 1303–1304 medical guidelines combined injectable contraceptives, 1307 combined oral contraceptives. See Oral contraceptives emergency contraception, 1308t, 1310 fertility awareness-based methods, 1309–1310 implantable contraception, 1308 injectable contraception, 1308–1309 intrauterine devices, 1309 lactational amenorrhea method, 1310 mechanical barriers and spermicides, 1309 progestin-only contraceptives, 1308 sterilization female, 1310 male, 1310–1311 transdermal patch, 1307–1308 vaginal ring, 1308 in U.S., 1304–1305 WHO guidelines, 1305, 1306t COPD. See Chronic obstructive pulmonary disease Copper maximum contaminant levels in drinking water, 870t, 871t toxic effects, 609, 870t Cor pulmonale, 595, 596–597 Coronary heart disease blood lipoproteins and, 1076 combined risk factors, 1081–1082 diabetes and, 1079, 1107–1108 dietary factors alcohol, 1075–1076 carbohydrates, 1075 dietary fats, 1073–1075, 1074t proteins, 1075 salt, 1076 epidemiology, 1071–1073, 1072t, 1073t genetic factors, 1081 hemostatic factors, 1080 hypertension and, 1079 mortality rates, 1072t, 1073t obesity/overweight and, 1077–1078 physical environment and, 1080 physical inactivity and, 1078 secondhand smoke and, 966–967 sex differential, 1080–1081 social support and, 1080 tobacco use and, 954–955, 1079–1080 Coronavirus. See Severe acute respiratory syndrome Correctional institutions, tuberculosis in, 256–257 Corynebacterium diphtheriae, 117, 206–207. See also Diphtheria Council on Linkages between Public Health Practice and Academia (COL), 1240 Coxiella burnetii, 368–369 Crashworthiness Data System (CDS), 1321 C-reactive protein, 1146 Cresolic pesticides, 714 Creutzfeldt-Jakob disease, 83, 852, 1142–1143 Crimean-Congo hemorrhagic fever (CCHF), 353t, 359–360 Cristobalite, 591, 599

1342

Index

CRNI (change in rate, natural increase), 41 CRNI (crude rate of natural increase), 40 Crocidolite, 568. See also Asbestos Cross-sectional study, 16–17 Crude birth rate (CBR), 40, 41, 42t Crude death rate (CDR), 40, 42t Crude rate of natural increase (CRNI), 40 Cruise ships’ diarrhea, 271–272 Cryptococcosis, 462–463 clinical characteristics, 462–463 diagnosis, 463 epidemiology, 462 microbiology, 463 treatment, 463 Cryptococcus neoformans, 463 Cryptosporidium, 322–323 clinical characteristics, 265t, 322 epidemiological features, 266t, 322 maximum contaminant levels in drinking water, 869t occurrence, 849t transmission, 322 treatment, 322–323 Cumulative incidence, 19, 20, 20t Current Population Survey, 40 Cutaneous anthrax, 428. See also Anthrax Cutaneous larva migrans, 474 Cyanide, 870t Cyclopropane, 622 Cyclospora, 323 clinical characteristics, 265t, 323 epidemiological features, 268t, 323, 849t transmission, 323 Cystic fibrosis, 1114–1115 Cysticercosis, 447–448 clinical characteristics, 447 diagnosis, 448 distribution, 447 etiologic agent, 447 prevention and control, 448 treatment, 448 Cytochrome P450 system, 511–512, 805 Cytomegalovirus (CMV) infection, 235–236 clinical characteristics, 235 diagnosis, 235 prevention, 235–236 in retinitis in HIV infection, 1157 transmission, 235 treatment, 236 D DALYS (disability adjusted life years), 796 Dapsone, 261, 261t Data collection in public health investigation, 17–18 in public health surveillance, 13 Data interchange technologies, 50–51 Data mining, 1209–1210, 1210t Data quality, 13 Data reporting, 13–14 DEET, 91, 714 Delta hepatitis. See Hepatitis delta Dementia diagnosis, 1147–1148 epidemiology, 1148 in HIV infection, 1141 incidence and prevalence, 1148, 1190, 1190f management, 1190

pesticide exposure and, 718 risk factors, 1148 Demographic equation, 41 Demographic transition theory, population growth, 45 Dengue fever, 346t, 351 clinical characteristics, 346t, 351 emergence, 81–82 epidemiology, 351, 353t precautions for travelers, 92–93 Dengue hemorrhagic fever, 353t, 356–357 Depo-medroxyprogesterone acetate (DMPA), 1305–1309 Depressants, 1013–1014 Depression. See also Psychiatric disorders in the elderly, 1189 historic trends, 1166 Dermatophytoses, 469–473 classification, 469, 470t definition, 469 expected trends, 473 incidence, 469 tinea capitis, 469–470 tinea corporis, 470–471 tinea cruris, 471–472, 471f tinea pedis, 472, 472f tinea unguium/onychomycosis, 472–473, 472f DES (diethylstilbestrol), 1056, 1057 Descriptive study, 16 Desertification, 930 Determinants, 6 Detoxification, 506 Developmental dysplasia/dislocation of the hip, 1133 Dextromethorphan, 1015 Diabetes, 1101–1108 classification, 1101, 1102f, 1103t complications atherosclerosis, 1107–1108 coronary heart disease, 1079, 1107 macrovascular disease, 1107–1108 neuropathy, 1107 renal disease, 1089–1090, 1106–1107 retinopathy, 1106, 1156 stroke, 1145 diagnosis, 1101–1102, 1103t future developments, 1108 heterogeneity in, 1102 mortality, 1106 screening, 1105–1106 type 1 clinical stages, 1102f epidemiology, 1102 genetic factors, 1102–1104, 1104t incidence, 1102, 1103f risk factors, 1104 treatment, 1104 type 2 clinical stages, 1102f epidemiology, 1105 genetic factors, 1105 metabolic syndrome and, 1101, 1102f prevention, 1105 risk factors, 1105 Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) alcohol abuse or dependence definition, 1000 approach, 1161

Dialysis aluminum toxicity in, 604–605 costs, 1097 technical developments, 1097 Dialysis centers, infections in, 335 4,4–Diaminodiphenylmethane, 652 Diarrhea. See also Food-borne diseases; Gastrointestinal infections in cholera. See Cholera in coccidial infections, 322–323 common causative agents, 265t E. coli. See Escherichia coli major clinical syndromes, 264 traveler’s. See Traveler’s diarrhea Diatomaceous earth, silica exposure from, 592 Diclofenac, vulture decline and, 555 Diet. See Food; Nutrition Dietary Reference Intakes, 1195–1196, 1196t Diethylcarbamazine, 400 Diethylene dioxide, 648–649 Diethylene glycol, 642 Diethylstilbestrol (DES), 1056, 1057 Diffuse parenchymal lung diseases, 1119–1120, 1119t Dilution ventilation, 786 N, N′–Dimethylacetamide, 644 Dimethylbenzene. See Xylene N, N-Dimethylformamide, 643 Dimethylsulfate, 647 Dinitrobenzene, 651 Dinitrochlorobenzenes, 652 Dinitrotoluene, 651 Dioxane. See Diethylene dioxide Dioxins. See Polychlorinated dioxins Diphtheria, 117–120 clinical characteristics, 118, 207 complications, 118, 207 diagnosis, 118 etiology, 117–118 immunization, 119–120, 210–211, 210t management of patient contacts, 119 occurrence, 118–119 pathogenesis, 117–118 transmission, 118, 206 treatment, 119, 207 Disability. See also Chronic disease in the aging population conditions causing arthritis, 1191. See also Osteoarthritis back pain, 1191. See also Low back pain chronic obstructive pulmonary disease, 1190–1191. See also Chronic obstructive pulmonary disease dementia, 1190, 1190f. See also Dementia depression, 1189 falls, 1188–1189 fractures, 1128, 1189 hearing impairment, 1189 heart failure, 1190 incontinence, 1189 Parkinson’s disease, 1190. See also Parkinson’s disease stroke, 1190. See also Stroke transitions, 1191 visual impairment, 1189 contributing factors disuse/deconditioning, 1187–1188, 1188t impairments and losses, 1187

Index demographic factors, 1185–1186, 1186f, 1186t early interventions and rehabilitation, 1188 prevention fall prevention strategies, 1128, 1128t physical activity, 1188 secular trends, 1186–1187, 1188f definition, 795, 1185 health care spending and, 1187t housing needs and, 922 measures Activities of Daily Living scale, 795, 1185 disability adjusted life years, 796 functional limitation model, 795 Instrumental Activities of Daily Living scale, 795, 1185 International Classification of Functioning, Disability, and Health, 795–796, 796f model, 1185, 1186f work and, 796. See also Workers, with disabilities Disability adjusted life years (DALYS), 796 Disasters, 1285–1294 characteristics, 1285, 1286t natural disasters, 927, 927t, 1285–1286 technological disasters, 1286–1287 terrorism, 1287–1288 warfare and conflict-related, 1287 definition, 1285, 1286t public health challenges local response, 1288–1292, 1289t animal control, 1291 care and shelter, 1291 communicable disease control, 1290–1291 coroner and mortuary services, 1291 food safety, 1290 hazardous agent exposure management, 1290 health surveillance and epidemiology, 1289 hospital emergency services, 1290 identification of medical and health resources, 1289 in-hospital care, 1290 medical and public health information, 1290 medical needs assessment, 1289 medical transportation, 1289–1290 mental health, 1290 out-of-hospital care, 1290 patient distribution and evacuation, 1290 pre-hospital emergency services, 1290 temporary field treatment, 1290 vector control, 1290 waste management, 1290 water quality management, 1290 planning, 1288 state and federal response, 1293–1294, 1293t Disease registries, 12 Dissociative anesthetics, 1014 Distribution, 6 Disuse/deconditioning, 1187–1188, 1188t Dix, Dorothea Lynde, 1167 DMPA (depo-medroxyprogesterone acetate), 1305–1309 DNA adducts, 563 DNA sequencing, 68

Doctors Without Borders, 1254 Domestic violence. See Violence, in the family Dose-response curve, 513, 513f Down syndrome, 66, 1174–1175 Doxycycline for leptospirosis, 436 for lymphatic filariasis, 400 for malaria prophylaxis, 91, 385t Dracunculiasis, 320–322 clinical characteristics, 320 diagnosis, 320 epidemiology, 320 eradication campaign, 321–322, 321f etiology, 320 prevention, 320–321 treatment, 320 Dracunculus medinensis, 320 Droplet precautions, 203t, 209 Drug abuse. See Substance abuse Drugs adverse events. See Adverse events, medication-related delivery systems, 1227 DT vaccine, 119–120, 210t DTaP vaccine, 119–120, 210t DTP vaccine, 119–120, 210t Dual energy x-ray absorptiometry, 1127–1128 Dust, occupational exposure, 696–697t Duvenhage virus, 420t E EAR (estimated average requirement), 1195, 1196t Earth Charter, 933t Earthquakes, 1286. See also Disasters Eastern equine encephalitis (EEE), 345t, 349 Ebola virus, 353t, 356 Echinococcus, 448–449. See also Hydatid disease Ecological study, 16 Economy class syndrome, 914–915 Ecosystems, 926t Ectopic pregnancy, 159 Ecuadorian Indians, 811–812 Effect biomarkers, 564 modification, 22, 22t Effective dose, 736t Effective temperature index, 725 Ehrlichiosis, human monocytic, 367 Elderly persons abuse, 1331 age-related macular degeneration, 1155–1156 cataracts, 1153–1154 disability in conditions causing arthritis, 1191. See also Osteoarthritis back pain, 1191. See also Low back pain chronic obstructive pulmonary disease, 1190–1191. See also Chronic obstructive pulmonary disease dementia, 1190, 1190f. See also Dementia depression, 1189 falls, 1188–1189 fractures, 1128, 1189 hearing impairment, 1189 heart failure, 1190 incontinence, 1189

1343

Parkinson’s disease, 1190. See also Parkinson’s disease stroke, 1190. See also Stroke transitions, 1191 visual impairment, 1189 contributing factors disuse/deconditioning, 1187–1188, 1188t impairments and losses, 1187 demographic factors, 1185–1186, 1186f, 1186t early interventions and rehabilitation, 1188 prevention fall prevention strategies, 1128, 1128t physical activity, 1188 secular trends, 1186–1187, 1188f foot disorders, 1130–1131 health care delivery comprehensive services, 1192–1193, 1193f geriatric medicine movement, 1191, 1192t geriatric strategies, 1191–1192, 1192f heat-related illness, 727–728 housing needs, 922 hypothermia, 731, 731f tuberculosis, 245 Electronic medical records, 52 Elephantiasis, 399 Emergency contraception, 1296, 1308t, 1310 Emerging Infections Program (EIP), 85–86, 86f Emphysema in COPD, 1117 silicosis and, 596 Empirical Bayesian Geometric Mean (EBGM), 1209–1210, 1210t Empowerment, 59–60 Enamel, silica exposure from, 592 Encephalitis California, 344t, 349 Eastern equine, 345t, 349 granulomatous amebic, 316–317 herpes simplex, 234 Japanese, 88–89, 344t, 349 measles, 101–102 Powassan, 344t, 349–350 St. Louis, 344t, 350 tick-borne, 93, 343t, 350 toxoplasmic, 442 Venezuelan equine, 345t, 350 West Nile. See West Nile virus Western equine, 343t, 350–351 Encephalopathy influenza-related, 122 in lead poisoning, 610 End-stage renal disease, 1096–1097, 1096f Endometrial cancer oral contraceptive use and, 1305, 1306t sex steroid hormones and, 1056 smoking and, 959t, 960t, 961 Endothall, 871t Endrin, 871t Energy shortages, 929 Entamoeba histolytica, 265t, 268t, 313–314. See also Amebiasis Enterobius vermicularis, 479 Enteroviruses, nonpolio in aseptic meningitis, 228–229 characteristics, 229 clinical illnesses, 230 diagnosis, 230 epidemiology, 230

1344

Index

Enteroviruses, nonpolio (Cont.): immunity, 229 prevention, 230 treatment, 230 types, 229 Environmental and occupational health air pollution. See Air pollution chemicals in food, 509 chemicals in soil, 509 in children. See Child labor current status, 503 in developing nations, 803–812 case studies children artisanal miners, Nambija, Ecuador, 810–811 San Quintín farmworkers, Mexico, 809–810 Texaco and the Ecuadorian Indians, 811–812 women maquiladora workers, Mexico, 811 Yakima Valley farmworkers, Washington State, 810 global context free trade agreements, 805–806 free trade zones, 806 hazard export, 806–807 maquiladoras, 806 multinational companies, 805 global disparities exposures, 804 public health policy implementation, 805 susceptibility, 804–805 technical resources, 805 global solutions policy initiatives, 807–808 public health initiatives, 808 U.S. solutions, 808–809 ethical issues, 29–30, 34 in farmworkers. See Farmworkers industrial hygiene. See Industrial hygiene occupational safety and health standards characteristics, 842–843 compliance, 843–844 consensus, 841–842 global, 844 hazardous waste and emergency response, 843 medical removal protection, 843 permanent, 842 permissible exposure limits, 843 temporary emergency, 842 threshold limit values, 843 risk assessment. See Risk assessment surveillance data analysis, 791–792 definition, 789 hazard, 789 health, 789 water pollution. See Water; Water quality management in women. See Women workers workplace health examinations biological monitoring, 790 ethical issues, 790–791, 791t general health appraisal, 790 legally mandated examinations, 790, 790t medical screening, 790 pre-placement, 789–790

program components, 791, 791t susceptibility screening, 790 Environmental justice, 803. See also Environmental and occupational health, in developing nations Environmental Protection Agency (EPA) carcinogen classifications, 550t drinking water regulations, 867, 868, 868t functions, 902 toxic exposure regulation, 522 Environmental tobacco smoke. See Secondhand smoke Epichlorohydrin, 656–657, 871t Epidemic polyarthritis, 346t, 352 Epidemic typhus, 365–366 Epidemiologic transition theory, 45, 1255–1256 Epidemiological analysis bias chance, 22 confounding, 21 effect modification, 22, 22t information bias, 21 selection bias, 21 comparison, 19–21, 20t definition, 19 description, 19 interpretation, 22–23 judgment in, 23 overview, 9 Epidemiological evaluation, 9, 23–24 Epidemiological investigation definition, 14–15 design analytical study, 17 case-control study, 17, 18t cohort study, 17, 18t cross-sectional study, 16–17 data gathering, 17–18, 18t descriptive study, 16 ecological study, 16 judgment in field investigations, 18–19 observational study, 17 overview, 8–9 preparation, 15 steps, 15–16, 15t Epidemiological method, 7–8 Epidemiology characteristics and practice foundations analysis. See Epidemiological analysis communication, 9 evaluation, 9, 23–24 information systems. See Public health informatics investigation. See Epidemiological investigation management and teamwork, 9 method, 7–8 presentation, 9 sequence, 8 surveillance. See Surveillance definition, 5, 6, 1239 ethical obligations, 32–34 history, 5–6 impartiality and advocacy, 33 public health applications epidemic control, 24 policy development, 24 program practices and operations, 24 relationship to other health professions

health policy, 9 health service and program management, 9 laboratory science, 9 statistics, 9 uses, 6t community assessment, 6–7 completion of clinical picture, 7 historical study, 6 individual chance assessment, 7 search for causes, 7 syndrome identification, 7 working of health services, 7 Epidermophyton, 469, 470t. See also Dermatophytoses Epilepsy, 1143 Epoxy compound exposure, 656–658 epichlorohydrin, 656–657 ethylene oxide, 657–658 glycidyl ethers, 658 Epstein-Barr virus, 230–231, 1057–1058 Equivalent dose, 735, 736t Ergonomics, 763–776 anthropometry, 763–764, 764f, 765f, 765t definition, 763, 764f fatigue and, 764–766, 766f specialty areas, 763 work-related musculoskeletal disorders and, 766–776. See also Musculoskeletal disorders, work-related Erysipelas, 241 Erythema marginatum, 243 Erythromycin, for GABHS prophylaxis, 242t Escherichia coli, 308–309 diffusely adherent, 309 enteroaggregative, 309 enterohemorrhagic, 265t, 266t, 308–309, 850–851 enteroinvasive, 309, 850 enteropathogenic, 308, 850 enterotoxigenic, 265t, 266t, 308 in food-borne disease, 850–851 incidence, 848t, 849t O157:H7, 82–83, 308, 850, 1094 in traveler’s diarrhea, 309 Esophageal cancer, smoking and, 958–960, 959t, 960t Esters, 647 Estimated average requirement (EAR), 1195, 1196t Estrogens. See also Oral contraceptives cancer risk and, 1055–1057 coronary heart disease and, 1079–1080 stroke risk and, 1146 Ethambutol, 361 Ethers, 648–650 carbon disulfide, 649–650 diethylene dioxide, 648–649 Ethics biomedical, 28 definition, 27 in public health. See Public health, ethical issues in research. See Research theories, 28 Ethnicity. See Race/ethnicity Ethylbenzene, 871t Ethylene chlorhydrin, 641 Ethylene dibromide, 637–638, 871t Ethylene dichloride, 636–637

Index Ethylene glycol, 641 Ethylene glycol ethers, 642 Ethylene oxide, 657–658 European bat lyssaviruses, 420t European Union, 805–806 Eutrophication, 866 Evaluation of complex, communitywide interventions, 1281–1282 focus, 1280 models empowerment, 1280 goal-based, 1280 goal-free, 1280 social science research, 1280 purpose, 1280 Evidence-based public health, 1024–1026, 1025t Excreter, 274 Exercise. See Physical activity Exposure biomarkers, 563–564 conceptual model, 563, 564f control, 785–787 measurements, 783–784 mixed, 784 by multiple routes, 785 variability, 784–785 Extremely low frequency electromagnetic fields biophysical effects, 748, 1055 epidemiological studies, 747–748 exposure limits, 750–751 sources and exposure, 747, 920 Eye disorders, pesticide exposure and, 719 F FAA (Federal Aviation Administration), 909, 912 Fair Labor Standards Act (FLSA), 833 Falls emergency department visits for, 1324–1325, 1325f hospitalizations for, 1324, 1324f incidence, 1188–1189 prevention, 1128, 1128t secondary consequences, 1189 Familial adenomatous polyposis, 1060t, 1061 Family planning. See also Contraception global context, 1303–1304 programs ethical issues, 34–35 sexually transmitted infections services, 158 in U.S., 1304–1305, 1304t Family violence child abuse. See Child abuse elder abuse, 1331 interventions, 1332 intimate partner, 1329–1330 low-level, 1331 risk factors, 1331–1332 Farmers, pesticide exposure in, 716–717 Farmworkers pesticide exposure in, 717, 823 in San Quintín, Mexico, 809–810 U.S.-hired, 820–824 acculturation, 823 characteristics, 820–821, 820t ethnicity, 821 health care access, 824

health status adverse reproductive outcomes, 823 cancer, 823 infectious diseases, 822 injuries and musculoskeletal disorders, 822–823 morbidity, 821–822, 822f mortality, 821 pesticide toxicity, 823 respiratory disease, 822 housing conditions, 824 organizations, 821 risk behaviors, 823, 824t utilization, 819–820, 820t Farr, William, 5 Fatal Accident Reporting System (FARS), 1321 Fatigue, work performance and, 764–766, 766f FCA (Functional Capacity Assessment), 800 FCE (Functional Capacity Evaluation), 800 FDA. See Food and Drug Administration Fear, biology of, 1030 Federal Aviation Administration (FAA), 909, 912 Federal Coal Mine Health and Safety Act, 583 Female condom, 1309 Fermentation, 860 Fertility, 41–43 behavioral determinants, 44t breast-feeding, 43 contraception, 43 frequency of intercourse, 43 induced abortion, 43 marriage or sexual union, 43 voluntary sterilization, 43 biologic determinants, 44t age within reproductive span, 43 involuntary infertility, 43 menarche and menopause, 43 ovulation, 43 spontaneous intrauterine mortality, 43 definition, 42–43 demographic measures, 41, 42t measurement, 41 pesticide exposure and, 720 smoking and, 963 teenage, public health issues, 39, 46 Fetal alcohol syndrome, 1179 Fetal tobacco syndrome, 963 Fever acute rheumatic. See Acute rheumatic fever African tick bite, 363t, 364–365 Chikungunya, 346t, 351–352 Colorado tick, 343t, 351 dengue. See Dengue fever hemorrhagic. See Hemorrhagic fever(s), viral Pontiac, 311, 312 Q. See Q fever Rift Valley, 81, 353t, 359 Rocky Mountain spotted, 363t, 364 sand fly, 346t, 351 scarlet, 240 typhoid. See Typhoid fever yellow. See Yellow fever Fiberglass, 578, 578f Fibers asbestos. See Asbestos human-made, 577–578 natural nonasbestos, 577 nonrespirable, 578 public health considerations

1345

control measures, 579 research, 579 respirable, 578–579 Fibrosis, chronic interstitial, 694 Fick’s law, 511 Field investigations, 18–19 Fillers, silica exposure from, 592 Filoviruses, 342t, 353t, 355–356 Ebola virus, 353t, 356 Marburg virus, 353t, 356 Fish consumption, benefits and risks, 547 shortages, 929 Fixed interval schedule-controlled paradigm (FISC), 527 Flame retardants, brominated. See Brominated flame retardants Flavin-containing monooxygenases, 512 Flaviviruses, 342t, 353t, 356–358 dengue hemorrhagic fever, 353t, 356–357 Kyasanur forest disease, 353t, 358 Omsk hemorrhagic fever, 353t, 358 yellow fever, 88, 353t, 357–358 Floods, 1286. See also Disasters FLSA (Fair Labor Standards Act), 833 Fluoridation, ethical issues, 30 Fluoride maximum contaminant levels in drinking water, 870t toxic effects, 870t Fluorocarbons, 639–640 Flying squirrel-associated typhus, 366 Focal segmental glomerulosclerosis, 1093 Folate deficiency, neural tube defects and, 1178 Food. See also Nutrition biologic amplification of toxins in the food chain, 509 carcinogens in, 1059 chemicals in, 509, 853 marketing in U.S., 1199 production in U.S., 1198 protective constituents, 1060 Food and Drug Administration (FDA) food safety regulations, 854 postmarketing safety surveillance program. See Postmarketing safety surveillance toxic exposure regulation, 522 Food-borne diseases. See also Gastrointestinal infections; Water-borne diseases common hazards bacteria, 848–851, 848t, 849t chemical intoxications, 848t, 853 microbial intoxications, 852–853 parasites, 848t, 849t, 852 physical hazards, 853 prions, 852 viruses, 848t, 849t, 851 contributing factors, 850t definition, 274 due to specific agents amebiasis. See Amebiasis Bacillus cereus, 265t, 266t, 474, 848t, 849t botulism, 849t, 852–853 Campylobacter. See Campylobacter cholera. See Cholera ciguatoxin, 848t, 853 clonorchiasis. See Clonorchiasis Clostridium botulinum, 848t, 852–853 Clostridium perfringens, 265t, 266t, 851

1346

Index

Food-borne diseases (Cont.): coccidial infections, 322–323 Cryptosporidium. See Cryptosporidium Cyclospora. See Cyclospora cysticercosis, 447–448 E. coli. See Escherichia coli giardiasis. See Giardiasis hepatitis A. See Hepatitis A Isospora, 323 listeriosis, 848t, 849t, 851 mushrooms, 848t noroviruses. See Noroviruses opisthorchiasis. See Opisthorchiasis prion, 83, 852 rotavirus. See Rotavirus Salmonella, nontyphoid. See Salmonellosis, nontyphoidal Salmonella typhi. See Typhoid fever shellfish toxin, 853 shigellosis, 850 Staphylococcus aureus, 848t, 852 taeniasis, 447–448 trichinellosis. See Trichinellosis typhoid fever. See Typhoid fever vibriosis, 850 yersiniosis, 310, 851 emerging, 82–83 incidence, 848, 848t, 849t location of outbreaks, 850t precautions for travelers, 92, 309 prevention and control, 86. See also Food safety Food insecurity, 1197, 1256–1257 Food safety, 847–89 consumer expectations, 847 in disasters, 1290 food plant sanitation equipment design, 855 facility design, 855 procedures, 855–856 food preservation asepsis/removal, 858 drying, 859 fermentation, 860 high temperature, 858–859, 858t irradiation, 860 low temperature, 859 modified atmosphere conditions, 858 preservatives, 859–860 principles, 857–858, 858t hazard analysis critical control point system, 856–857, 856t objectives, 847 regulation Food and Drug Administration, 854 good manufacturing practices, 854 international, 854 milk sanitation, 854 pest control, 854–855 prerequisite programs, 854 training and personal hygiene, 854 U.S. Department of Agriculture, 853–854 Foot disorders, in older adults, 1130–1131 Formaldehyde absorption, 646 carcinogenicity, 646 characteristics, 645 federal standard, 646 in indoor air pollution, 701, 702t, 920, 921t sources, 645–646

Foscarnet, 236 Founder effect, 65 Foundry work, silica exposure in, 591–592 Fractures in children, 1132–1133 in older adults, 1128, 1189, 1189f Fragile X syndrome, 1175–1177 Frailty, 1185. See also Disability, in the aging population Framework Convention for Tobacco Control (FCTC), 983 Francisella tularensis, 424–425. See also Tularemia Frank, Johann Peter, 5 Free radicals, 517 Free trade agreements, 805–806 Free trade zones, 806 Freon, 701–702 Frostbite, 730, 732 Fumigants, 713t, 714 Functional Capacity Assessment (FCA), 800 Functional Capacity Evaluation (FCE), 800 Fungi endemic infections, 461 occupational exposure, 696t opportunistic infections, 461–466 aspergillosis. See Aspergillosis candidiasis. See Candidiasis cryptococcosis. See Cryptococcosis zygomycosis. See Zygomycosis superficial infections. See Dermatophytoses Fungicides, 713t, 714 G Gamma glutamyltransferase (GGT), 1007 Gamma radiation, 736t. See also Ionizing radiation Ganciclovir, 236 Gases asphyxiant, 691, 692t definition, 782 irritant, 692t, 693 oxidant, 691–693, 692t Gastric cancer. See Stomach cancer Gastroesophageal reflux disease, smoking and, 962 Gastrointestinal anthrax, 428–429. See also Anthrax Gastrointestinal infections. See also Food-borne diseases; Water-borne diseases common causative agents, 265t. See also specific agents contagion risk, 264, 264t, 269, 269t epidemiologic approach by causative agent, 266–268t in the community, 270, 271t general considerations, 269–270 in health care settings, 271t, 272 information gathering, 270t notifiable diseases, 270t on passenger ships, 271–272 traveler’s diarrhea. See Traveler’s diarrhea major clinical syndromes, 264 occurrence and scope, 263–264 prevention enteric precautions, 273 specific interventions contact evaluation, 273 vaccines, 273–274

universal measures domestic and personal hygiene promotion, 273 measles immunization, 273 promotion of exclusive breast-feeding, 272 rotavirus immunization, 272–273 strategies, 272, 272t water and sanitation facilities improvement, 273 terminology, 274 Gender. See also Sex; Women workers as confounder of behavioral performance, 532 General Estimates System (GES), 1321 General fertility rate (GFR), 41, 42t Genes, ionizing radiation and, 736–737, 737f, 737t Genetic drift, 65 Genetics, 64–71. See also specific disorders disorders categories autosomal chromosomal disorders, 66 autosomal dominant disorders, 67 autosomal recessive disorders, 67 mitochondrial disorders, 68 multifactorial disorders, 68 sex chromosomal disorders, 66–67 X-linked dominant disorders, 68 X-linked recessive disorders, 67 incidence and prevalence, 63, 65–66 racial/ethnic disparities, 804–805 radiation exposure and, 736–737, 737t screening programs newborn, 70 prenatal, 70–71 social and ethical implications, 71–72 DNA tests for risk identification insurance industry and, 72 paternity, 72 social and ethical implications, 71–72 in the workplace, 72 familial clustering of disease associations between genotype and susceptibility, 69 characteristics, 68 common environmental exposure and, 69 heritability studies, 69 methods for determining mode of inheritance linkage analysis, 69 maternal effects analysis, 69 multifactorial model analysis, 69 segregation analysis, 69 sibling pair methods, 69–70 twin studies, 68–69 human gene map, 68 in populations inheritance and distribution, 64–65 mutation rate measurement, 64 sequencing, 68 services, 71 Genotoxicity, 516–517 Geriatric medicine, 1191–1193, 1192f, 1192t, 1193f. See also Elderly German measles. See Rubella GGT (gamma glutamyltransferase), 1007 Giardia duodenalis, 265t Giardia lamblia. See also Giardiasis characteristics, 317

Index incidence and frequency of food-borne disease from, 848t, 849t life cycle, 318 maximum contaminant levels in drinking water, 869t Giardiasis, 318–320 clinical characteristics, 265t, 318 control measures, 320 diagnosis, 318–319 epidemiology, 268t, 319 occurrence, 848t, 849t outbreaks, 319 pathogenesis, 318 treatment, 319 zoonosis, 319 Glass industry, silica exposure in, 592 Glaucoma, 1154–1155 Global change, 925–934 definition, 925 demographics, 930–931 desertification, 930 Earth Charter, 933t economic, social, and political, 931 emerging and remerging infections, 931. See also Communicable diseases, emerging threats environmental ethics, 932–933 environmental pollution, 930 global warming, 926–927, 927t, 928t grounds for optimism, 932 millennium development goals, 932t mitigation options, 934 ozone depletion, 916, 927–929 phenomena, 925–926 Precautionary Principle, 932–933 public health responses, 931–932, 931t resource depletion, 929 species extinction, 929–930 Global health, 1251. See also International health Global Outbreak Alert and Response Network (GOARN), 85 Global warming, 926–927, 927t, 928t Globalization, 1251–1253 Glomerulonephritis chronic idiopathic, 1091 IgA nephropathy, 1091 poststreptococcal, 244–245, 1091–1092 Glucuronidation, 512 Glutathione conjugation, 512 Glycidyl ethers, 658 Glycols diethylene glycol, 642 ethylene chlorhydrin, 641 ethylene glycol, 641 ethylene glycol ethers and derivatives, 642 Glyphosate, 871t Gonorrhea, 167–168 antimicrobial resistance, 168 epidemiology, 167–168 incidence, 156t in pregnancy, 161 prevalence, 168, 168t vaccine, 165 Good manufacturing practices, 854 Granulomatous amebic encephalitis (GAE), 316–317 Graunt, John, 5 Greenhouse effect, 916, 926, 928t

Grinding, silica exposure in, 592 Group A β-hemolytic Streptococcus (GABHS), 237–244 carriers, 238 disease reporting, 245 diseases caused by erysipelas, 241 necrotizing fasciitis, 241 pharyngitis, 239–240 clinical characteristics, 239 diagnosis, 204, 239–240 etiologic agents, 239 transmission, 239 treatment, 204, 239–240 pyoderma, 240–241 scarlet fever, 240 toxic shock syndrome, 241 history, 237 nonsuppurative sequelae acute poststreptococcal glomerulonephritis, 244–245, 1091–1092 acute rheumatic fever, 242–244, 1082 prevention in household contacts, 242, 242t typing genotypic methods, 238 phenotypic methods, 238 vaccine development, 245 virulence factors, 237–238 Guillain-Barré syndrome, 851 Guinea worm disease. See Dracunculiasis H HACCP (hazard analysis critical control point system), 856–857, 856t Haddon Matrix, 1326, 1327t Haemophilus influenzae, 125–127 antimicrobial resistance, 125 bacteriology, 125 immunity, 125–126 immunization, 126, 127, 210, 210t infections caused by clinical characteristics, 125 occurrence, 126–127, 126f pathogenesis, 125, 206 transmission, 126 treatment, 125 HAI. See Health care-associated infections Hallucinogens, 1014 Haloacetic acids, 869t Halofantrine, 380 Halogenated hydrocarbons, 629–640 carbon tetrachloride, 631–632 chloroform, 632 chloroprene, 638–639 effects, 630–631 ethylene dibromide, 637–638 ethylene dichloride, 636–637 fluorocarbons, 639–640 methyl bromide, 638 methyl chloride, 638 methyl chloroform, 634 perchloroethylene, 633–634 sources, 631 tetrachloroethane, 634 trichloroethylene, 632–633 vinyl chloride, 634–636, 636f vinyl trichloride, 634 vinylidene chloride, 636 Handicap, 1185

1347

Hands, work-related disorders. See Musculoskeletal disorders, work-related Hansen’s disease. See Leprosy Hantavirus pulmonary syndrome, 360, 362 Hantaviruses, 80, 361t Hardy-Weinberg equilibrium, 64 HAV. See Hepatitis A Hazard analysis critical control point system (HACCP), 856–857, 856t Hazardous waste, 901–908 agent-specific problems arsenic, 904 dioxin, 904–905 lead, 904 mercury, 905 mixtures, 905–906 organic chemicals, 904t polychlorinated biphenyls, 905 volatile organic compounds, 905 amount generated, 902 assessment of health hazard bioavailability, 903 biomarkers, 903 sediment, 903 characteristics, 901 definition, 901 OSHA standards, 843 radioactive, 907 regulation, 902 remediation, 906 research needs, 906–907 risk assessment, 906 transportation, 902 HBV. See Hepatitis B HCV. See Hepatitis C HDV. See Hepatitis delta Headaches, 1143–1144 Health behavior, 941–948 interventional planning and evaluation design, 947 information sources, 947–948, 948t interventional strategies built environment, 947 classes and curricula, 945–946 mass media, 946–947 motivational interviewing, 945 policy, 947 print communications, 946 targeted electronic media, 946 models Health Belief Model, 941–942 rationales for use, 941 self determination theory, 942–943, 942f, 943f social cognitive theory, 942 theory of reasoned action and planned behavior, 944–945, 945f transtheoretical model, 943–944, 943f, 944f Health Belief Model, 941–942 Health care-associated infections (HAI), 333–337 antimicrobial resistance, 335 by body site bloodstream, 334 pneumonia, 334–335 surgical site, 334 urinary tract, 334 definition, 333

1348

Index

Health care-associated infections (Cont.): emerging, 335 epidemiology, 333–334 gastrointestinal, 271t, 272 by health-care setting home care and outpatient, 335 long-term care facilities, 335 outpatient dialysis centers, 335 incidence, 333 infection control programs, 335–336 investigation, 336 prevention and control, 336 resources, 337 surveillance, 336 Health-care system, U.S., 1217–1236 complexity, 1217–1218 components ambulatory care providers freestanding centers, 1225 hospital-based, 1225 long-term care, 1226–1227, 1226t mental health and substance abuse services, 1227 office-based, 1223–1225 patient characteristics, 1224–1225t pharmacy providers and suppliers, 1227–1228 safety-net clinics, 1225–1226 types, 1223 hospitals admissions, length of stay, and outpatient visits, 1222t challenges, 1221–1222 history, 1218–1219 occupancy, 1220t structure, 1221 types, 1219–1221, 1220t, 1222t spending by types of care, 1218f future developments, 1236 health-care expenditures governmental health insurance Medicaid, 1235–1236 Medicare, 1234–1235 State Children’s Health Insurance Program, 1236 vs. other countries, 1231–1232t private health insurance, 1232–1234, 1233t statistics, 1230–1232 health-care workforce employment statistics, 1228, 1228t nurses, 1229–1230, 1230t other clinical personnel, 1230 physicians, 1228, 1229t performance and outcomes, 1218 quality assurance and improvement doing well what works, 1278–1279, 1278f, 1279t knowing resources for what works, 1277 knowing the purpose for doing it, 1279–1280 knowing what works, 1277 using what works, 1277–1278 Health Cities movement, 922 Health disparities, 55–59 barriers to reducing or eliminating, 59 conceptualization, 55–56, 56f determinants, 58–59 international context, 56. See also International health

inverse care law and, 56 measurement absolute vs. relative disparity, 57 adverse vs. favorable events, 58 choice points, 57, 58t guidelines, 57, 58t reference point, 57 weighing groups by size, 58 overview, 55 U.S. context, 56–57 Health education/health promotion. See Health behavior; Health literacy Health information, privacy issues, 30–31, 1259 Health insurance coverage among U.S. residents, 1233t governmental Medicaid, 1235–1236 Medicare, 1234–1235 State Children’s Health Insurance Program, 1236 private, 1232–1234 Health Insurance Portability and Accountability Act (HIPAA) confidentiality requirements, 31, 790 epidemiological research and, 31 public health reporting and, 1259 Health literacy definition, 1035 health activities and, 1036, 1037t health demands and, 1035–1036 implications for practitioners, 1038 for research, 1038 overview, 1035 skills, 1036, 1037t Health reports, 12 Health statistics, privacy issues, 30–31 Health surveys, 12, 40 Healthy Cities, 1247 Healthy People 2000, 1244–1245, 1244t, 1276 Healthy People 2010 focus areas, 1245f goals, 1245 health disparities goals, 55, 57, 1245 leading health indicators, 941, 1245f sexually transmitted infections objectives, 171t Hearing conservation programs, 760 neurotoxicant effect on, 528 testing, 528 Hearing loss in the elderly, 1189 noise-induced acceptable levels, 758–759 age-related hearing loss and, 759, 759t measurement, 756–757, 757f models, 759 pathogenesis, 755–756, 756f prevention, 759–760 susceptibility to, 757 Heart disease cardiomyopathies, 1083–1084, 1083t congenital, 1082–1083, 1083t coronary heart disease. See Coronary heart disease prevention, 1084 rheumatic, 1082 secondhand smoke and, 966–967

smoking and, 954–955 syphilitic, 1084 Heart failure, 1190 Heat index, 725–726 Heat-related illness, 725–728 epidemiology heat waves, 727 impact on elderly, 727–728, 727f risk factors, 728 heat cramps, 726 heat exhaustion, 726 heat stress, 725–726, 726f heat syncope, 726 heatstroke, 726 prevention, 728 reproductive effects, 727 Helicobacter pylori, cancer risk and, 1059 Helminth infections. See Nematode infections Helsinki Declaration, 32 Hemolytic uremic syndrome, 851–852, 1094 Hemorrhagic fever(s), viral, 352–362 arenaviruses, 352–355, 353t, 354f Argentine hemorrhagic fever, 353t, 354, 354f Bolivian hemorrhagic fever, 353–354, 353t Lassa fever, 352–354, 353t lymphocytic choriomeningitis virus, 353t, 355 Sabia virus, 353t, 355 Venezuelan hemorrhagic fever, 353t, 355 bunyaviruses, 342t, 353t, 358–362, 361t Crimean-Congo hemorrhagic fever, 359–360 hantavirus pulmonary syndrome, 360–362, 361t hemorrhagic fever with renal syndrome, 360 Rift Valley fever, 359 filoviruses, 342t, 353t, 355–356 Ebola virus, 353t, 356 Marburg virus, 353t, 356 flaviviruses, 342t, 353t, 356–358 dengue hemorrhagic fever, 353t, 356–357 Kyasanur forest disease, 353t, 358 Omsk hemorrhagic fever, 353t, 358 yellow fever, 88, 353t, 357–358 hantaviruses, 80, 360, 361t, 362 hosts, 353t transmission, 352 Hemorrhagic fever with renal syndrome, 360 Hepatitis, viral, 211–228 cancer and, 1058 diagnosis, 212 history, 211–212 morbidity and mortality, 212t non-A to E, 228 Hepatitis A (HAV), 212–216 clinical illness, 212, 851 diagnosis, 213 epidemiology transmission routes, 213 U.S., 213–215 worldwide, 213, 214f etiologic agent, 212 immunology, 213 incidence and prevalence, 171, 212t, 848t, 849t pathogenesis, 212–213, 851

Index prevention and control environmental measures, 215–216, 851 immunization, 88–89, 166, 215 postexposure prophylaxis, 215 Hepatitis B (HBV), 216–219 cancer risk and, 1058 clinical illness, 216 diagnosis, 217, 217t epidemiology transmission routes, 218 U.S., 219 worldwide, 218–219, 219f etiologic agent, 216 immunology, 216–217, 216f, 217f incidence and prevalence, 156t, 171, 212t liver cancer and, 160 pathogenesis, 216 prevention and control immune globulin, 220 immunization, 88–89, 166, 220 treatment, 220 Hepatitis C (HCV), 221–226 cancer risk and, 1058 clinical illness, 221 diagnosis, 221–224, 222f, 223f, 223t, 224f epidemiology transmission routes, 224 U.S., 225 worldwide, 224 etiologic agent, 221 immunology, 221 incidence and prevalence, 212t pathogenesis, 221 prevention and control, 225–226 treatment, 225–226 Hepatitis delta (HDV), 226–227 clinical illness, 226 diagnosis, 226 epidemiology, 226–227 etiologic agent, 226 immunology, 226 pathogenesis, 226 prevention and control, 227 Hepatitis E (HEV), 227–228 clinical illness, 227 diagnosis, 227 epidemiology, 227–228 etiologic agent, 227 pathogenesis, 227 prevention and control, 228 Hepatocellular carcinoma. See Liver cancer Heptachlor, 871t Heptachlor epoxide, 871t Herbicides, 713t, 714 Hereditary nonpolyposis colorectal cancer, 1060t, 1061 Heritability studies, 69 Herpes simplex virus (HSV) infections clinical manifestations, 233 diagnosis, 234 encephalitis, 234 epidemiology, 233 genital, 169–170, 233 clinical characteristics, 233 epidemiology, 169–170 incidence, 156t in pregnancy, 161 prevalence, 169–170 gingivostomatitis, 233

herpetic keratitis, 233 in immunocompromised host, 234 neonatal, 161, 233–234 pathogenesis, 233 prevention and control, 234 treatment, 234 types, 232–233 vaccine, 165–166, 234 Herpes zoster, 132–133 clinical characteristics, 132 epidemiology, 133 immunization, 133 treatment, 132, 133 Heterotrophic plate count, 869t HEV. See Hepatitis E Hexachlorobenzene, 713, 871t n-Hexane, 620–621 HHV-8 (human herpesviridae), 1058 Highly active antiretroviral therapy (HAART), 193 Hip developmental dysplasia/dislocation, 1133 fractures, in older adults, 1128, 1189, 1189f osteoarthritis, 1129 HIPAA. See Health Insurance Portability and Accountability Act Hippocrates, 5 Hispanic epidemiologic paradox, 823 HIV infection. See Human immunodeficiency virus (HIV) infection Hodgkin disease, 716, 717, 1058 Home care, infections in, 335 Homelessness psychiatric disorders and, 1166 in U.S., 919 worldwide, 919 Hookworm disease, 473–476 clinical presentation, 474–475 distribution, 473 epidemiology, 475 etiologic agents, 473–474 pathogenesis, 474 prevention and control, 475–476 Hormone replacement therapy, 1057–1058 Hospital-associated infections. See Health care-associated infections Hospitals admissions, length of stay, and outpatient visits, 1222t challenges, 1221–1222 in disaster response, 1290 history, 1218–1219 occupancy, 1220t records, 12 structure, 1221 types, 1219–1221, 1220t, 1222t Housing conditions mental health and, 921–922 statistical indicators, 922 worldwide, 919 Healthy Cities movement, 922 indoor environment biologic hazards, 921 physical hazards. See Air pollution, indoor socioeconomic factors, 921 special needs, 922 standards, 922 HPV. See Human papillomavirus

1349

HSV. See Herpes simplex virus (HSV) infections HTLV-1, 1059 Human Development Index (HDI), 1253 Human Genome Project, 68 Human granulocytic anaplasmosis, 363t, 367 Human herpesviridae (HHV-8), 1058 Human immunodeficiency virus (HIV) infection, 189–196 cancer risk and, 1058–1059 distribution of infection, 190 emergence, 83 ethical issues, 29 etiology, 189–190 history, 14, 189 incidence, 191–193, 191f, 192t, 194t leprosy and, 260–261 natural history, 190 neurological complications, 1141–1142 ophthalmic complications, 1157 opportunistic infections, 1141–1142 prevention and control, 194–195, 194t renal disease and, 1094 research issues, 195–196 sexually transmitted infections and, 161 surveillance, 190–193 toxoplasmosis and, 442 transmission, 190 treatment, 193–195 tuberculosis and, 249, 253–254 Human leukocyte antigen (HLA) genes, 1102–1103, 1104t Human monocytic ehrlichiosis, 363t, 367 Human papillomavirus (HPV) cancer and, 160, 1058 condom for reducing transmission, 165 epidemiology, 170 immunization, 166 incidence, 156t in pregnancy, 161 prevalence, 170 Hydatid disease, 449–451 clinical characteristics alveolar disease, 449–450 cystic disease, 449 polycystic disease, 450 diagnosis, 450 distribution, 449 etiologic agents, 448–449 prevention and control, 451 transmission, 449 treatment, 450–451 Hydrocarbons alicyclic, 622 aliphatic, 620–622 aromatic. See Aromatic hydrocarbons commercial mixtures of petroleum solvents, 622–623 halogenated. See Halogenated hydrocarbons organic solvents, 619–620 Hydrogen sulfide, 691, 692t Hypertension coronary heart disease and, 1079 in diabetes, 1090 renal disease and, 1090–1091 stroke risk and, 1145 Hypertrophic cardiomyopathy, 1083–1084 Hypothermia in the elderly, 731, 731f in infants and children, 731–732

1350

Index

Hypothermia (Cont.): pathogenesis, 730 risk factors, 731–732 treatment, 730 Hypoxia, in aviation, 910 I IADL (Instrumental Activities of Daily Living) scale, 795 ICF (International Classification of Functioning, Disability, and Health), 795–796, 796f IgA nephropathy, 1091 Illumination lighting recommendations, 746–747, 746t principles, 745–746 Immigration Reform and Control Act of 1986, 820 Immunization. See also Vaccine(s) legal issues, 1264 population-based registry, 51, 51t risks and benefits, 30 Immunotoxins, 516 Impairment, 1185 Imprinting, 67, 526 IMR (infant mortality rate), 41 Incest, 1330–1331 Incidence density, 19 Incontinence, in the elderly, 1189 Independent Medical Examination (IME), 800 Index case, 274 Industrial hygiene, 781–787. See also Environmental and occupational health definition, 781 hazard control education and training, 786–787 isolation, 785–786 material substitution, 785 personal protective equipment, 786, 844 principles and limitations, 785 process modification, 785, 843–844 ventilation, 786 hazard evaluation biological media measurements, 784 dermal and surface contamination, 784 environmental contaminant measurements, 783–784 exposure by multiple routes, 785 exposure history, 503, 504t exposure variability, 784–785 interpretation of exposure measurements, 784 mixed exposures, 784 principles, 783 unusual working conditions, 785 hazard recognition airborne concentration measures, 782 airborne contaminants, 782 classification, 782 information sources, 782–783 principles, 781–782 principles, 781 Infant(s) developmental dysplasia/dislocation of the hip, 1133 heat-related illness, 728 hypothermia, 731–732, 731f respiratory distress syndrome, 1113–1114 retinopathy of prematurity, 1157–1158 Infant botulism, 853

Infant mortality rate (IMR), 41 Infantile paralysis. See Poliomyelitis Infection(s), health care-associated. See Health care-associated infections Infection control programs components, 335–336 for tuberculosis, 256 Infectious diseases. See Communicable diseases Infectious mononucleosis, 230–232 clinical features, 231–232 complications, 232 diagnosis, 232 epidemiology, 231 etiologic agent, 230–231 pathogenesis, 231 prevention, 232 treatment, 232 Infertility as determinant of fertility, 43 pelvic inflammatory disease and, 159 pesticide exposure and, 720 Influenza, 120–123 antigenic drift, 121, 208f antigenic shift, 121, 208, 208f avian. See Avian influenza A clinical characteristics, 122 complications, 122 diagnosis, 122, 209 epidemiology, 120–121 etiologic agents, 121, 208 history, 120 H5N1. See Avian influenza A, H5N1 immunization adverse effects, 123 efficacy and effectiveness, 123 for international travel, 88–89 recommendations, 123, 123t, 209, 210t, 211 vaccine characteristics, 122–123, 209, 211 vaccine supply, 123–124 vaccine types, 209, 210t immunology, 122 pandemics, 121 surveillance, 121–122 treatment, 124, 209 Information bias, 21 Information Network for Public Health Officials (INPHO), 13 Information systems. See Public health informatics Informed consent ethical issues, 31 process and procedures, 31, 33t Infrared radiation, 747, 747t Infrasound, 760 Inhalational anthrax, 428. See also Anthrax Injuries. See also Violence in child workers, 834–836 data sources morbidity, 1321 mortality, 1321 incidence and trends by age and gender, 1322–1323, 1322f, 1323f, 1324f costs, 1325 emergency department visits, 1324–1325, 1324f, 1325f hospital admissions, 1323–1324, 1323f, 1324f by mechanism and intent, 1322–1323, 1323f, 1324f, 1325f

mortality rates, 1321–1323, 1322f, 1323f prevention and control effectiveness evaluation, 1326 Haddon Matrix, 1326, 1327t theoretical approaches, 1326–1327 public health history, 1319–1320 public health model, 1320–1321, 1320f in U.S.-hired farmworkers, 822–823 Insect repellents, 714 Institute of Medicine (IOM) duties of local health agencies, 1243 duties of state health departments, 1242 on health disparities, 55 mission of public health, 1239 public health leadership recommendations, 1271 public health recommendations, 1023 Instrumental Activities of Daily Living (IADL) scale, 795 International Agency for Research in Cancer (IARC), 549, 550t International Classification of Functioning, Disability, and Health (ICF), 795–796, 796f International health agencies bilateral, 1254 international nongovernmental organizations, 1254 multilateral, 1253 classification of nations, 1253 epidemiologic transition theory, 1255–1256 food and nutrition security, 1256–1257 future development, 1257 gender-based issues, 1257 global and regional health profiles, 1256, 1256t globalization and, 1251–1253 health and development indicators by income level, 1251 health reform and financing public-private partnerships, 1254 strategic options, 1254–1255 inequalities, 1252t, 1253 water and sanitation issues, 1257 International issues environmental justice in developing nations, 803–812 case studies children artisanal miners, Nambija, Ecuador, 810–811 San Quintín farmworkers, Mexico, 809–810 Texaco and the Ecuadorian Indians, 811–812 women maquiladora workers, Mexico, 811 Yakima Valley farmworkers, Washington State, 810 global context free trade agreements, 805–806 free trade zones, 806 hazard export, 806–807 maquiladoras, 806 multinational companies, 805 global disparities exposures, 804 public health policy implementation, 805 susceptibility, 804–805 technical resources, 805

Index global solutions policy initiatives, 807–808 public health initiatives, 808 U.S. solutions, 808–809 family planning, 1303–1304 tobacco use and production, 981–984, 982f, 984t travel-related. See Travel, international International Red Cross, 1254 International Space Station, 912 Interstitial lung diseases, 1119–1120, 1119t Intimate partner violence, 1329 Intrauterine devices, 1309 Intravenous drug abusers. See also Substance abuse hepatitis B transmission in, 218 hepatitis C transmission in, 224 renal disease in, 1093 tuberculosis in, 257 Inverse care law, 56 Iodine deficiency, 1178 Iodochlorhydroxyquin, 309 IOM. See Institute of Medicine Ionizing radiation, 735–741 adaptive responses, 740 effects acute radiation syndrome, 738, 738t carcinogenic, 738–739, 739f, 740t, 1054–1055 cytotoxic, 737–738 on genes and chromosomes, 736–737 of low-level exposure, 739–740 of prenatal exposure, 740 types, 736 environmental sources and levels, 735–736, 736t for food preservation, 860 physical properties, 735 protection from, 740 public health, 736f recommended exposure limits, 741t risk assessment, 551 visible light biologic effects, 745 units of measurement, 745 Iron deficiency, 609 fume, exposure limits, 609 toxicity, 609 Irradiation, food, 860 Irritant gases, 692t, 693 Isolation precautions, 203t Isolation programs, 1264 Isomers, 508 Isoniazid (INH) resistance, 248–249 for tuberculosis, 251 Isoprene, 622 Isopropyl alcohol, 641 Isospora, 323 Ivermectin, 400 for strongyloidiasis, 477 for trichuriasis, 477–478 J Japanese encephalitis, 88–89, 344t, 349 Japanese-river fever, 366–367 Jeryl Lynn vaccine, 106 Jet lag, 915

Job Site Evaluation (JSE), 800 Joint Commission on Accreditation of Healthcare Organizations (JCAHO), infection control guidelines, 337 Jones criteria, rheumatic fever, 243 Justice, 28 K Kant, Immanuel, 28 Kaposi’s sarcoma, 1058 Katayama fever, 480 Kepone, 713 Keratitis herpetic, 233 in leprosy, 258 Ketamine, 1014 Ketones, 621, 647–648 Kidney cancer smoking and, 959t, 960, 960t Kidney cancer, pesticide exposure and, 716 Kidney disease. See Renal disease Kidney stones, 1095 Klinefelter’s syndrome, 66 Knee, osteoarthritis, 1128–1129, 1129t Kwashiorkor, 1197 Kyasanur forest disease, 353t, 358 L Laboratory Response Network (LRN), 86 Lagos bat virus, 420t Land mines, 1287 Laryngitis, 204 Lasers, 745 Lassa fever, 352–354, 353t Lead exposure child development and, 531, 610, 1165–1166, 1179 environmental contamination, 904 limits, 610–611 pathophysiology, 610 prevention, 610–611 sources, 609–610 maximum contaminant levels in drinking water, 870t toxic effects, 610, 870t, 904 biomarkers, 520 neurobehavioral, 523, 525, 525t, 1165, 1179 Lead time bias, 1043 Legal issues. See also Public health law alcohol accessibility, 1006 child labor in U.S., 834 in workplace health examinations, 790, 790t Legionella, 311, 869t Legionellosis, 311–313 clinical characteristics, 311 diagnosis, 311, 312t microbiology, 311 prevention and control, 312–313 surveillance, 312 transmission, 312 treatment, 311–312 Leishmaniasis, 394–397, 395t clinical syndromes, 395t cutaneous, 395 mucosal, 395 visceral, 395–396 diagnosis, 396

1351

epidemiology, 394 genetic factors, 394 prevention and control, 398 transmission, 397–398 treatment, 396–397 Length bias, 1043 Leprosy, 258–262 clinical manifestations, 258 complications, 262–263 diagnosis, 258–259 epidemics, 259 epidemiology reservoir, 260 transmission, 259–260 etiologic agent, 258 geographic distribution, 259 history, 259 HIV and, 260–261 prevalence and incidence, 260 prevention and control, 263 treatment antileprosy drugs, 261–262, 261t reactions, 262 regimens, 261t, 262, 262t Leptospirosis, 434–437 clinical characteristics, 435 diagnosis, 435 etiologic agent, 434–435, 435f occurrence, 436 prevention and control, 436–437 transmission, 436 treatment, 435–436 Leukemia benzene exposure and, 624 extremely low frequency electromagnetic field exposure and, 747–748 pesticide exposure and, 716, 717 radiation exposure and, 738–739 smoking and, 959t, 960t, 961 Levonorgestrel implants, 1308 Li-Fraumeni syndrome, 1060, 1060t Lifting, 772–775, 772f, 773f, 773t, 774t, 775t Lindane, 713, 871t Linkage analysis, 69 Lipid peroxidation, 518 Lipoproteinosis, 694 Lipoproteins, coronary heart disease and, 1076 Listeria monocytogenes, 848t, 849t, 851 Listeriosis, 848t, 849t, 851 Liver failure, thiazolidinediones and, 1210–1211, 1211f, 1212f toxins and, 508 Liver cancer hepatitis and, 160, 1058 incidence, 160 oral contraceptive use and, 1306–1307 pesticide exposure and, 716, 717 screening programs, 1064–1065 Local health departments funding, 1243 Institute of Medicine definition of role, 1243 leadership, 1243 organization, 1243 services, 1243–1244 size, 1243

1352

Index

Long-term care facilities characteristics, 1226–1227 infections in, 335 resident demographics, 1226t Low back pain definition, 771 disability from, 771–772, 1191 incidence, 1125 management, 1125–1126, 1126t, 1191 prevention, 1125 risk factors, 1127 work-related lifting and, 772–775, 772f, 773f, 773t, 774t, 775t, 1125 posture and, 775 risk factors, 772 seated work and, 775–776 Low birth weight maternal smoking and, 959t, 963 mental retardation and, 1178 retinopathy of prematurity and, 1157–1158 Low-tar cigarettes, 969–970. See also Tobacco use Lowest observed adverse effect level (LOAEL), 551 LSD, 1014 Lung functional zones, 691, 692f response to gases and particles, 691, 693f. See also Air pollution Lung cancer asbestos exposure and, 567–568, 576 occupational exposures and, 699 pesticide exposure and, 716, 717 radiation exposure and, 1054 secondhand smoke and, 964–966 silicosis and, 598 smoking and, 957–958, 957f, 959t, 960t Lyme disease, 387–392 clinical characteristics, 388 diagnosis, 389, 389f ecology arthropod vectors, 387 environmental factors, 387 life cycle, 388, 388f vertebrate hosts, 387–388 epidemiology areas with unconfirmed endemicity, 391 emergence, 390–391 global distribution, 389 incidence in U.S., 390, 390f risk factors for infection, 391 transmission to humans, 389 etiology, 386–387, 387f prevention clinical interventions, 391 community interventions, 392 environmental modifications, 391–392 personal measures, 391 treatment, 389 Lymphatic filariasis biology and life cycles, 398–399, 398–401 clinical characteristics, 399 diagnosis, 399–400 distribution, 399 immunology, 399 prevention and control, 400–401 treatment, 400 Lymphocytic choriomeningitis, 353t, 355 Lymphogranuloma venereum, 169

Lymphoma Burkitt’s, 1058 non-Hodgkin, 716, 717 Lynch syndrome, 1061 Lyssavirus, 419, 420t M Macular degeneration, 1155–1156 “Mad as a hatter,” 1167 Malaria, 373–386 clinical characteristics, 376 complications, 376, 377 diagnosis antigen detection tests, 377–378 clinical, 377 microscopic, 377 molecular, 378 serologic, 378 drug-resistant, 85, 381 emergence, 84 etiology agent characteristics, 374t life cycle, 375–376, 375f routes of transmission, 374–375 vectors, 382t global distribution, 374, 374f, 381 pathogenesis, 376–377 prevalence, 373–374, 374f prevention and control case management, 384 chemoprophylaxis, 91–92, 384–385, 385t historical perspective, 383–384 personal protection measures, 91, 385 preventive treatment, 384–385 for travelers, 90–92 vaccine development and testing, 386 vector control, 385–386, 708–709 transmission endemicity levels, 381–382, 382t host factors, 382 nutrition and, 382–383 social and behavioral factors, 383 vector characteristics and, 381, 382t treatment amodiaquine, 378 antifol antimalarial drugs, 378 artemisinin compounds, 380 atovaquone, 378 chloroquine, 378 clindamycin, 380 halofantrine, 380 mefloquine, 380 piperaquine, 380 primaquine, 379–380 pyronaridine, 380 quinine, 378 strategy, 379t, 380–381 tetracyclines, 378–379 Maleic anhydride, 643 Malignant melanoma, 716, 717 Malnutrition, 1197. See also Nutrition Malta fever. See Brucellosis Managed care, 1233–1234 Manganese, 611 Mann, Horace, 1167 Mantoux test, 250–251 MAPP (Mobilizing for Action through Planning and Partnership), 1245–1246, 1246f, 1247f, 1269

Maquiladoras, 806, 811 Marasmus, 1197 Marburg virus, 353t, 356 Marijuana, 1013 Mass medication, ethical issues, 30 MAST (Michigan Alcoholism Screening Test), 1007 MATCH (Multilevel Approach to Community Health), 1269 Maternal and child health, 1294–1295. See also Pregnancy future directions, 1296 government services in U.S., 1294–1295 health indicators, 1295 principles of service delivery developmental perspective, 1295 family-centered care, 1295 health promotion and disease prevention, 1295 priorities child abuse and neglect, 1296 child care, 1296 children with special health care needs, 1296 children’s injuries, 1296 community-based social support, 1296 family planning and abortion, 1296 immunization, 1296 perinatal health, 1296 preconceptional health promotion, 1295–1296 prenatal care, 1296 Maternal mortality rate (MMR), 41, 42t Maximal medical improvement (MMI), 800 Maximum contaminant level (MCL) drinking water, 869–873t, 874t establishment, 875–876 Maximum contaminant level goal (MCLG), 875 MCS. See Multiple chemical sensitivities Measles, 101–105 clinical characteristics, 101 complications, 101–102 control and elimination in U.S., 104 worldwide, 105 diagnosis, 102 etiologic agent, 102 immunization active immunity, 103 contraindications, 103–104 disease incidence and, 104, 104f indications, 103 for international travel, 88 passive immunity, 102 risks and benefits, 30, 273 immunology, 102 Mebendazole for ascariasis, 478 for hookworm disease, 476 for pinworm, 479 for trichuriasis, 478–479 Medecins Sans Frontieres, 1254 Medicaid, 1235–1236 Medical removal protection, 843 Medicare history of program, 1234–1235 preventive benefits coverage, 1273, 1274–1275t structure, 1235

Index Medications adverse events. See Adverse events, medication-related delivery systems, 1227 Mediterranean spotted fever, 363t, 364 MedWatch, 1206, 1207f Mefloquine for malaria prophylaxis, 91, 385t for malaria treatment, 380 MEK (methyl-ethyl ketone), 621 Memory/learning, testing, 530 Men who have sex with men (MSM) HIV prevention and control, 194 sexually transmitted infections prevention, 163–164 Menarche, 43 Meningitis aseptic, 228–229 H. influenzae, 125, 127 meningococcal, 246 Meningococcal disease, 246–248 carriers, 246 clinical characteristics, 246 immunity, 246 immunization, 88, 89, 247–248 occurrence, 247 prevention, 247–248 transmission, 246–247 Meningoencephalitis, amebic. See Amebic meningoencephalitis Menopause, 43 Menstruation, 487–489, 488t Mental health. See Psychiatric disorders Mental retardation, 1173–1180 classification, 1173, 1174t community services, 1180 definition, 1173 epidemiology, 1174, 1175t etiology chromosomal anomalies Down syndrome, 66, 1174–1175 fragile X syndrome, 1175–1177 environmental toxins lead, 1179 maternal alcohol use, 1179 infections, 1178–1179 nutritional folate deficiency, 1178 iodine deficiency, 1178 phenylketonuria, 1177 premature birth, 1178 trauma, 1179 incidence and prevalence, 1173–1174, 1176t prevention, 1179–1180 Mercury, 525, 531, 611–612 exposure environmental contamination, 905 measurement, 611–612 occupational limits, 612 prevention, 612 sources, 611–612 teratology, 531 maximum contaminant levels in drinking water, 870t toxic effects, 612, 870t in children, 612 neurobehavioral, 525, 525t, 612 teratogenic, 531 Mesothelioma, 575–576

asbestos exposure and, 568 incidence, 576 pathogenesis, 575–576, 575f treatment, 576 Meta-analysis, 23–24 Metabolic syndrome, 1101 Metal exposure, 603–616 aluminum, 604–605 antimony, 605 arsenic, 525, 525t, 605–606 beryllium, 606 cadmium, 607 chromium, 607–608 cobalt, 608–609 definition, 603 diagnosis, 604 in food, 848 iron, 609 lead. See Lead manganese, 611 mercury. See Mercury molybdenum, 613 nickel, 613–614 osmium, 614 platinum, 614 prevention, 603–604 selenium, 614–615 silver, 615 sources, 603, 604t thallium, 615 tin, 615 toxic effects, 525, 603–604 uranium, 615–616 vanadium, 616 zinc, 616 Methane, 691, 692t Methemoglobin, 650–651 Methicillin-resistant S. aureus (MRSA), 84, 335 Methoxychlor, 871t Methyl alcohol, 640 Methyl bromide, 638, 714 N-Methyl-carbamates, 711, 713t Methyl chloride, 638 Methyl chloroform, 634 Methyl-ethyl ketone (MEK), 621 Methyl-heptyl ketone, 621 Methyl isobutyl ketone, 647 Methyl-n-butyl ketone (MnBK), 648 Methylbenzene. See Toluene N-Methyl-D-aspartate (NMDA) receptors, 523 4,4’-Methylene-bis-ortho-chloroaniline (MOCA), 652–653 Methylmercury. See also Mercury in fish, 547, 612 metabolism, 612 neurobehavioral toxicity, 525, 531, 612 teratogenic effects, 531 Methylphenidate, 1014 1–Methyl-phenyl-1,2,3,6–tetrahydropyridine (MPTP), 525 Metronidazole, 316, 319 Michigan Alcoholism Screening Test (MAST), 1007 Microsporum, 469, 470t. See also Dermatophytoses Microwave radiation epidemiologic studies, 749 exposure limits, 750–751

1353

for food preservation, 860 sources and exposures, 748–749 Migraine, 1143–1144 Migrant workers. See Farmworkers Migration definition, 45 global patterns, 930–931 measurement, 41, 44–45 public health and, 39, 45, 46 Military operations aviation, 912. See also Aerospace medicine disease and injury prevention measures command enforcement of countermeasures, 1299 countermeasure identification, 1298–1299, 1299t medical surveillance, 1299–1300 medical threat assessments, 1297–1298, 1298t training personnel on countermeasures, 1299, 1299t field preventive medicine organization, 1297 risk assessment applications, 546 Milk sanitation, 854 Mill, John Stuart, 28 Millennium Development Goals, 932, 932t Miners’ black lung. See Coal workers’ pneumoconiosis Mines coal. See Coal workers dust exposure in, 591 Minocycline, 261–262 Mite-born typhus, 366–367 Mitochondrial disorders, 68 Mitsuda skin test, 259 MMI (maximal medical improvement), 800 MMR (maternal mortality rate), 41, 42t MMR vaccine, 103–104, 106, 109 MMWR (Morbidity and Mortality Weekly Report), 14 MnBK (methyl-n-butyl ketone), 648 Mobilizing for Action through Planning and Partnership (MAPP), 1245–1246, 1246f, 1247f, 1269 MOCA (4,4’-Methylene-bis-orthochloroaniline), 652–653 Mokola virus, 420t Mold disease, 694 Molecular cloning, 68 Molybdenum toxicity, 613 Monitoring the Future (MTF), 1015, 1016f Monkeypox, 80 Monod’s sign, 464 Monosodium glutamate, 848t Mood disorders, 1163t. See also Psychiatric disorders Morality, 27 Morbidity and Mortality Weekly Report (MMWR), 14 Mortality determinants age, 41 cause of death, 41 public health, 41 race/ethnicity, 41 region/area, 41 sex, 41 social and economic conditions, 41 measurement, 41 seasonal trends, 728–729, 729f

1354

Index

Mosquitos as arbovirus vector, 342 natural habitats, 342 personal protection measures, 91 Motivational interviewing, 945 Motor function neurotoxicant effect on, 528–529 testing, 528–529 MPTP (1–methyl-pheny-1,2,3,6– tetrahydropyridine), 525 MRSA (methicillin-resistant S. aureus), 84, 335 MSM. See Men who have sex with men MTF (Monitoring the Future), 1015, 1016f Multifactorial genetic disorders, 68 Multifactorial model analysis, 69 Multilevel Approach to Community Health (MATCH), 1269 Multinational companies, 805 Multiple chemical sensitivities (MCS), 687–690 definition, 687 diagnosis, 687–688 epidemiology, 688–689 natural history, 689 pathogenesis, 688 prevention, 690 treatment, 689 Multiple endocrine neoplasia, 1060t, 1061 Multiple myeloma, 716, 717 Multiple sclerosis, 1144–1145 Mumps, 105–107 clinical characteristics, 105–106 complications, 106 diagnosis, 105 etiologic agent, 105 immunization, 106 occurrence, 106–107, 107f Murine typhus, 366 Musculoskeletal disorders, 766–776, 1125–1133 in children developmental dysplasia/dislocation of the hip, 1133 fractures, 1132–1133 scoliosis, 1131–1132 slipped capital femoral epiphysis, 1132, 1132f foot disorders in older adults, 1130–1131 incidence, 1125, 1126f, 1126t low back pain, 1125–1126, 1126t neck pain, 1126–1127 osteoarthritis, 1128–1129 osteoporosis, 1127–1128 paraplegia and quadriplegia, 1131 rheumatoid arthritis, 1130 work-related, 766–776 characteristics, 766 in farmworkers, 822–823 low back pain, 771–776 management issues, 776 neck pain, 1127 upper extremity, 766–771 exposure limits, 770–771, 771f, 771t intervention and evaluation of control methods, 771 job analysis, 767 morbidity, 766–767 risk factors, 767 surveillance, 767 work factor analysis, 767–770, 768f, 768t, 769f

worker input, 770, 770f in women, 829 Mushroom toxicity, 848t Mutagenesis, 516 Mutation, gene. See also Genetics definition, 64 rate in humans, 64–65 spectrum, 516 Mycobacterium bovis, 257 Mycobacterium leprae, 258. See also Leprosy Mycobacterium tuberculosis, 248–249. See also Tuberculosis Mycoses. See Fungi Mycotoxin, 694 N Naegleria fowleri, 316–317 Nambija, Ecuador, 810–811 Nasopharyngeal cancer Epstein-Barr virus and, 1058 pesticide exposure and, 717 National Agricultural Workers Survey (NAWS), 820–821, 820t National Ambulatory Medical Care Survey (NAMCS), 12 National Association of County and City Health Officials, 1241 National Association of Local Boards of Health, 1241 National Automotive Sampling System (NASS), 1321 National Center for Health Statistics (NCHS), 12 National Death Index (NDI), 12 National Drinking Water Contaminant Candidate List, 874, 875t National Electronic Disease Surveillance System (NEDSS), 52 National Electronic Injury Surveillance System (NEISS), 1321 National Electronic Surveillance System (NETSS), 13 National Health and Nutrition Examination Survey (NHANES), 40 National Health-care Safety Network (NHSN), 336 National Health Information Infrastructure (NHII), 52–53 National Health Interview Survey (NHIS), 40 National Hospital Discharge Survey (NHDS), 12 National Institute for Occupational Safety and Health (NIOSH), 782–783 National Nosocomial Infections Surveillance System (NNIS), 334, 336 National Notifiable Disease Surveillance System (NNDSS), 157 National Nursing Home Survey, 12 National Pesticides Telecommunications Network Hotline, 783 National Primary Drinking Water Regulations, 868, 869–873t National Public Health Leadership Development Network, 1271 National Public Health Leadership Institute, 1241 National Secondary Drinking Water Regulations, 868, 874t National Survey of Family Growth (NSFG), 12, 40 National Survey on Drug Use and Health (NSDUH), 1015, 1016f

National Toxicology Program (NTP), 521 National Violent Death Reporting System, 1321 Natural disasters, 927, 927t, 1285–1286, 1286t. See also Disasters Natural resources damage assessment, 555 depletion, 929, 929t ecosystems, 926t Necator americanus, 474. See also Hookworm disease Necatoriasis. See Hookworm disease Neck pain, 1126–1127 Necrotizing fasciitis, 241 Negative predictive value, 1044 Neisseria meningitidis, 245–246. See also Meningococcal disease Nematode infections, 473–479 ascariasis, 478 capillariasis, 479 food-borne, 852 hookworm disease. See Hookworm disease pinworm infection, 479 strongyloidiasis, 476–478 trichinellosis. See Trichinellosis trichuriasis, 478–479 Neonatal herpes, 161 Neonatal varicella, 129 Neoplasms, 1047. See also Cancer Nephropathy. See Renal disease Nerve growth factors, 526 Neural cell adhesion molecules, 531 Neural tube defects, 1178 Neurobehavioral toxicity, 523–533 animal models, 526–527 conditioning studies, 526–527 discrimination conditions, 527 fixed interval schedule-controlled paradigm, 527 imprinting, 526 intracerebral injection, 527 learning and memory tasks, 526 naturalistic studies, 527 open field exploratory behavior, 527 parental recognition, 526 biochemical mechanisms, 525–526 nerve growth factors, 526 neuropeptides, 526 neurotransmitters, 525–526 receptor biology, 526 thyrotropin-releasing hormone, 526 cognitive evaluation, 529–532 attention/concentration, 530 confounders of performance age and gender, 532 language and culture, 532 learning and experience, 532 physical condition, 532 interview, 529 memory and learning, 530 neurobehavioral testing, 529 overall intellectual ability, 525t, 530 personality, mood, and affect, 529 psychometric tests, 529–530 psychomotor functions, 525t, 530 temporal properties of performance, 530 test batteries, 530–531 future research directions, 532–533 overview, 523 psychiatric disorders and, 1165

Index sensory system evaluation, 527–529 basal ganglia, 529 cerebellar function, 529 hearing, 528 motor function, 528–529 olfaction, 528 position sense and vestibular function, 528 taste, 528 temperature, 528 touch and vibratory sensation, 528 vision, 527–528 stress and, 532 target nervous system components autonomic nervous system, 524 basal ganglia, 524 central nervous system, 524 hypothalamic-pituitary-adrenal axis, 524 peripheral nervous system, 524 teratology lead and child development, 531 methylmercury, 531 neural cell adhesion molecules, 531 polychlorinated biphenyls, 531–532 toxins, 525t carbon disulfide, 524–525 chemicals, 1144 metals, 525, 1144 pesticides, 525 solvents, 524 Neuroblastoma, pesticide exposure and, 716 Neurological disorders, 1139–1148 Alzheimer’s disease, 605, 1147–1148 cerebral palsy, 1140–1141 Creutzfeldt-Jakob disease, 83, 852, 1142–1143 dementia, 718, 1141, 1147–1148 diabetic neuropathy, 1107 headaches, 1143–1144 HIV infection and, 1141–1142 incidence, 1139 mortality, 1139, 1140t multiple sclerosis, 1144–1145 neurotoxic. See Neurobehavioral toxicity Parkinson’s disease, 718, 1147 prevalence, 1139, 1141t, 1142t seizure disorders, 1143 stroke, 956, 1145–1147 West Nile virus. See West Nile virus Neuropathy diabetic, 1107 in HIV infection, 1141 pesticide exposure and, 719 Neuropeptides, 526 Neurotransmitters, 525–526 Newborn screening programs benefits, 70 disadvantages, 70 expansion, 70 NGOs (nongovernmental organizations), 1254 Nickel exposure allergy, 613 effects, 613 measurement, 613 occupational limits, 612 prevention, 614 sources, 613 Nicotine. See Tobacco use Night soil, collection and disposal, 890. See also Water quality management

Nipah virus, 80 Nitrates maximum contaminant levels in drinking water, 870t as preservatives, 860 toxic effects, 870t Nitric oxide, 518, 526 Nitrites maximum contaminant levels in drinking water, 870t as preservatives, 860 toxic effects, 870t Nitrobenzene, 651 Nitrosamines, 653–655 chemical structure, 653 effects, 654–655 environmental, 655–656 history, 653 Nitrotoluene, 651 NMDA (N-methyl-D-aspartate) receptors, 523 No observable effect level (NOEL), 551 No observed adverse effect level (NOAEL), 551 Noise, 755–760 from aircraft, 916 effects on hearing, 755–756, 756f individual variations in susceptibility, 757 on other bodily functions, 760 permanent threshold shift, 755–756, 756f temporary threshold shift, 755, 756f hearing loss induced by acceptable levels, 758–759 age-related hearing loss and, 759, 759t measurement, 756–757, 757f models, 759 pathogenesis, 755–756, 756f prevention, 759–760 susceptibility to, 757 measurement, 758 standards, 757–758 Non-A to E hepatitis, 228 Non-Hodgkin lymphoma, 716, 717 Non-maleficence, 28 Nongovernmental organizations (NGOs), 1254 Nongranulomatous alveolitis, 694 Nonionizing radiation, 743–751 exposure limits, 750–751 extremely low frequency electromagnetic fields biophysical effects, 748, 1055 epidemiological studies, 747–748 exposure limits, 750–751 for food preservation, 860 forms, 743, 744t future research, 751 infrared radiation, 747, 747t microwave radiation, 748–749 mobile phones and towers, 749–750 radiofrequency radiation, 748–749 sources and exposure, 747 ultraviolet radiation biological effects, 743–744, 929, 1055 protection from, 744–745, 744t, 745t sources and exposures, 743, 744t visible light illumination principles, 745–746 lighting recommendations, 746–747, 746t Nonoxynol-9, 164, 1309 Nonsteroidal anti-inflammatory drugs (NSAIDs)

1355

nephrotoxicity, 1092–1093 for osteoarthritis, 1129 Noroviruses clinical characteristics, 265t, 851 emergence, 83 epidemiological features, 266t, 848t, 849t, 851 North American Free Trade Agreement (NAFTA), 806 North Asian tick typhus, 365 North Queensland tick typhus, 365 Norwalk-like viruses. See Noroviruses Nosocomial infections. See Health care-associated infections Nuclear Regulatory Commission (NRC), 907 Nurse practitioners, 1230 Nurses educational paths, 1229–1230 by employment setting, 1229, 1230t public health, 1300–1301 shortages of, 1230 Nursing homes funding, 1226–1227 resident characteristics, 1226t Nutrition assessment of status community, 1200, 1200t individuals and populations, 1199–1200, 1199t national monitoring, 1200 cancer risk and, 1059–1060 chronic disease and, 1197 coronary heart disease and, 1073–1076 deficiencies, 1196–1197 diabetes risk and, 1104, 1105 dietary recommendations barriers to implementation demand for convenience and low cost, 1199 environment of food choice, 1199 food marketing, 1199 food production, 1198 current consensus, 1198, 1198f goals and guidelines, 1197–1198 dietary requirements and allowances, 1195–1196, 1196t policy recommendations, 1200–1201, 1201t O Obesity cancer risk and, 1059–1060 coronary heart disease risk and, 1077–1078 diabetes risk and, 1105 prevalence, 1077, 1077t, 1105 Observational study, 17 Obstructive sleep apnea. See Sleep apnea syndrome Occupational health. See Environmental and occupational health Occupational hygiene. See Industrial hygiene Occupational low back pain. See Low back pain Occupational Safety and Health Act, 841–842 Occupational Safety and Health Administration (OSHA) consensus standards, 841–842 hazard identification standards, 782 hazardous waste and emergency response standards, 843 mandated medical examinations, 790, 790t toxic exposure regulation, 522

1356

Index

Odds ratio, 20 Office of the National Coordinator for Health Information Technology (ONCHIT), 53 Ofloxacin, 261, 261t Olefins, 622 Olfactory sense neurotoxicant effect on, 528 testing, 528 Omsk hemorrhagic fever, 353t, 358 Onchocerciasis, 1157 Onychomycosis, 472–473 clinical presentation and diagnosis, 472–473, 472f, 473f epidemiology, 472 prevention and control, 473 Open field exploratory behavior, 527 Opioid abuse, 1014. See also Substance abuse Opisthorchiasis, 445–447 clinical characteristics, 446 community patterns of infection and disease, 446 diagnosis, 446 etiologic agent, 445–446 geographic distribution, 446 prevention and control, 447 treatment, 446–447 Oral cancer, 958–960, 959t, 960t Oral contraceptives cancer risk and, 1055–1057, 1306–1307, 1306t characteristics, 1305 coronary heart disease and, 1081 health benefits, 1305–1306, 1306t myocardial infarction and, 1306, 1306t stroke risk and, 1146 venous thromboembolism and, 1306t WHO recommendations, 1307 Oral rehydration solution, 306–307 Organic nitroso-compounds chemical structure, 653 environmental, 655–656 history, 653 toxic effects, 654–655 Organic solvents, 619–620, 905. Organismic integration theory, 943t Organizational empowerment, 60 Organochlorines, 555 Organophosphates, 710–711, 713t Oropouche fever, 346t, 351 Orthomyxoviridae, 121 Oseltamivir, 124, 209 OSHA. See Occupational Safety and Health Administration Osmium, 614 Osteoarthritis, 1128–1129 disability from, 1128, 1191 etiology, 1128 incidence, 1128 prevalence, 1129 risk factors, 1128–1129 screening, 1129 treatment, 1129, 1129t Osteoporosis fracture incidence and, 1189, 1189f pathogenesis, 1127 prevention, 1127–1128 Otitis media, 204–205 diagnosis, 204–205

etiologic agents, 204 H. influenzae, 125 S. pneumoniae, 137, 206 incidence, 204 pathogenesis, 204 treatment, 125, 205 Outcome research, 1277 Outpatient settings, infections in, 335 Ovarian cancer oral contraceptive use and, 1305, 1306t reproductive factors, 1057 sex steroid hormones and, 1056 Ovulation, 43 Oxamyl, 871t Oxidant gases, 691–693, 692t Oxidative stress, 517 Ozone depletion, 916, 927–929 environmental, 508 indoor, 702t P p53 gene, 516–517 Pancreatic cancer pesticide exposure and, 716, 717 smoking and, 959t, 960, 960t Pandemics cholera, 305 influenza, 121 plague, 370 Pap smear, 1064 Para-aminophenol, 652 Paraffins, 620 Paramyxovirus in measles, 102 in mumps, 105 Paraphenylenediamine, 652 Paraplegia, 1131 Paraquat, 714 Parasitic disease amebiasis. See Amebiasis amebic meningoencephalitis, 316–317 Parkinson’s disease etiology, 1147 incidence, 1147, 1190 pesticide exposure and, 718 symptoms, 1147 treatment, 1190 Passenger ships’ diarrhea, 271–272 Passive smoke. See Secondhand smoke PCBs. See Polychlorinated biphenyls PCP (phencyclidine), 1014 Pearl Index, 1305 Pelvic inflammatory disease incidence, 159 sexually transmitted infections and, 159 Penicillin, 242t Pentachlorophenol, 872t Peptic ulcer disease, smoking and, 962 Pepto Bismol. See Bismuth subsalicylate Perchloroethylene, 633–634 Period rate, 41 Periodontal disease, smoking and, 962 Peripheral vascular disease diabetes and, 1107 smoking and, 955–956 Permethrin, 91 Permissible exposure limits, 843 Perniosis, 730

Personal Information Protection and Electronic Documents Act (PIPEDA), 31 Personal protective equipment, 786, 844 Pertussis, 111–114 antimicrobial resistance, 114 chemoprophylaxis, 114 clinical characteristics, 111 complications, 111, 206 diagnosis, 112, 206 etiology, 111 future perspectives, 114 immunization, 113–114, 210–211, 210t immunology, 112 occurrence, 112f, 113, 113f pathogenesis, 111–112 transmission, 113 treatment, 114, 206 Pest control, in food processing, 854–855 Pesticides, 707–722 agricultural use, 707–708 biomonitoring, 710 chlorinated hydrocarbon, 711, 713 contaminants, 709–710 in developing countries, 715 drift episodes, 715 exposure to, 710 in farmworkers, 823 formulations, 709 fumigants, 714 fungicides, 714 health effects, 715–721 asthma, 715–716 breast cancer, 717 cancer in adults, 716–717 cancer in children, 716 chronic, 716 data sources, 716 delayed neuropathy, 719 endocrine, 720–721 long-term sequelae of acute poisoning, 718 neurological, 717, 718–719 Parkinson’s disease, 718 reproductive, 719–720 herbicides, 714 history, 707 ingredients, 709, 709t insect repellents, 714 intermediates, 710 N-methyl-carbamates, 711, 713t nonagricultural use, 708–709 organophosphates, 710–711, 713t paraquat, 714 phenolic and cresolic, 714 production, 707 pyrethrums/pyrethrins/synthetic pyrethroid, 713–714, 713t reentry poisoning, 715 regulation and controls bans and restrictions, 711, 712t, 721 federal and state administration and enforcement, 721 legislation, 721 worker protection standards, 721 residues in blood and urine, U.S. adults, 709t surveillance data, 714–715 toxicity categories, 710, 710t, 711t Petroleum solvents, 622–623 Pharmacy providers, 1227–1228

Index Pharyngeal cancer, smoking and, 958–960, 959t, 960t Pharyngitis, 204, 239–240 Phase II reactions, 512 Phencyclidine (PCP), 1014 Phenolic pesticides, 714 Phenylketonuria, 1177 Phthalic anhydride, 642–643 Physical activity cancer risk and, 1060 coronary heart disease and, 1078 diabetes risk and, 1105 in the elderly, 1188 stroke risk and, 1146 Physician assistants, 1230 Physicians, 1228, 1229t Physiologically based pharmacokinetic model (PBPK), 551 Picloram, 872t Pilots. See also Aerospace medicine aging, 914 alcohol and tobacco use, 913 illness and disease, 913 medical services for, 913, 913t medication use, 913 work-rest cycles, 913–914 Pinworm infection, 479 clinical characteristics, 479 diagnosis, 479 epidemiology, 479 etiologic agent, 479 prevention and control, 479 treatment, 479 Pipe smoking. See also Tobacco use cancer and, 958, 959, 972, 1053 cardiovascular disease and, 955 chronic obstructive pulmonary disease and, 962 periodontal disease and, 962 trends, 972 Piperaquine, 380 Piperazine, 478 Plague, 370–373 bubonic, 372 care of contacts, 373 clinical characteristics, 372 diagnosis, 372 etiology, 370 global distribution, 371, 371f history, 370 hospital procedures, 372–373 hosts, 370–371 in nature, 370 pneumonic, 372 prevention and control, 373 surveillance, 371–372 treatment, 372 vectors, 370 Planet Health, 946 Planned Approach to Community Health (PATCH), 1246–1247 Plasmodium infection. See Malaria Platinum, 614 Pneumococcal infections, 137–139 antimicrobial resistance, 139 bacteriemia, 206 immunoprophylaxis, 139, 209–210 occurrence, 137 pathogenesis, 138

risk factors for invasive disease, 138–139 serotypes causing, 137–138 Pneumoconiosis, coal workers’. See Coal workers’ pneumoconiosis Pneumoconiosis Field Research, 586, 587f Pneumonia diagnosis, 205 etiologic agents, 205 C. psittaci, 424 F. tularensis, 426 H. influenzae, 125 S. pneumoniae, 205 varicella, 129 incidence, 567 risk categories, 205 treatment, 205 ventilator-associated, 334–335 Pneumonic plague. See Plague Pneumonitis, allergic, 694 Poisons. See also Toxicology cellular, 515 metabolic, 515 Poliomyelitis, 133–137 epidemiology, 134 etiology, 134 history, 133–134 pathogenesis, 134 prevention and control consequences of oral vaccine use, 135 current U.S. vaccination policy, 135 global eradication initiative, 135–136, 136f immunization for international travel, 88 oral vaccine cessation planning, 136–137 vaccine development and use, 134–135 Poliovirus. See also Poliomyelitis characteristics, 134 vaccine-derived, 136–137, 137t Polychlorinated biphenyls (PCBs), 531–532, 675–676 chemical properties, 675 environmental contamination, 905 exposure limits, 675, 871t in fish, 547 global contamination, 675–676 history, 675 neurobehavioral toxicity, 525, 525t, 531–532 production ban, 675 toxicity human health effects, 676 mechanism, 676 public health impact, 676 Polychlorinated dibenzofurans, 679–683 chemical structure, 679 environmental levels, 683 exposure, 679–680 toxic effects, 679 Yusho incident, 680–682, 681f, 681t, 682f Polychlorinated dioxins, 679–680 Agent Orange, 520, 521t, 680 chemical structure, 679, 680t environmental contamination, 904–905 exposure, 679–680 toxic effects, 679–680 Pontiac fever, 311, 312. See also Legionellosis Population, 39–41 data sources census, 39 immigration reports, 40

1357

population-based surveys, 39 vital registries, 40 definition, 3 demographic measures composition, 41–42, 42f crude rates, 40 fertility, 41. See also Fertility growth. See Population growth migration, 41, 930. See also Migration mortality, 41. See also Mortality period and cohort rates, 41 standardized rates, 40–41 urban, 919, 920t Population attributable risk, 21 Population attributable risk percent, 21 Population growth, 45–47, 925, 930–931 consequences economic change, 45–46 environment, resources, and food, 46 determinants demographic transition, 45 epidemiologic transition, 45 measurements, 41 projecting change, 45 public health issues aging, 46–47 need for improved population health measures, 47 refugees and other migrants, 46 teenage fertility, 46 urbanization, 46 Population screening, 33–34 Pork tapeworm, 447–448 Position sense neurotoxicant effect on, 528 testing, 528 Positive predictive value, 1044 Post-herpetic neuralgia, 132 Post-kala-azar dermal leishmaniasis, 395–396 Post-polio syndrome, 133, 134 Postmarketing safety surveillance adverse events incidence, 1208–1209, 1208t, 1209f case studies rotavirus vaccines and intussusception, 1208–1209 thiazolidinediones and hepatic failure, 1210–1211, 1211f, 1212f data mining for, 1209–1210, 1210t MedWatch, 1206, 1207f process, 1205–1206 withdrawals from market, 2000–2005, 1208, 1209t Poststreptococcal glomerulonephritis, 1091–1092 Pottery industry, silica exposure in, 592, 598 Powassan encephalitis, 344t, 349–350 Power lines. See Extremely low frequency electromagnetic fields Praziquantel for hookworm disease, 476 for hydatid disease, 450 resistance, 482 for schistosomiasis, 481 Precautionary Principle, 932–933 PRECEDE-PROCEED model, 1025–1026, 1269 Pregnancy. See also Maternal and child health in adolescents, 39, 46 alcohol use in, 1179

1358

Index

Pregnancy (Cont.): cytomegalovirus infection in, 235 ectopic, 159 hepatitis B screening in, 220 measles in, 102 rubella in, 108, 109t sexually transmitted infections in, 160–161 smoking during, 963 toluene abuse in, 627 toxoplasmosis in, 441 varicella in, 129–130 working conditions during, 830 Prenatal screening indications family history, 71 increased maternal age, 71 neural tube defects, 71 public health-based, 71 Preservatives, food, 859–860 Preterm delivery, maternal smoking and, 963 Preterm infants mental retardation in, 1178 retinopathy of prematurity, 1157–1158 Prevention. See specific disorders Preventive health. See Behavioral change; Health behavior Primaquine for malaria prophylaxis, 91–92 for malaria treatment, 379–380 Primary amebic meningoencephalitis (PAM). See Amebic meningoencephalitis Prions, 83, 852 Privacy, of health records, 30–31 Probability, 22 Progestin-only contraceptives, 1308 Propionate salts, 860 Propionic acid, 860 Prostate cancer, 1095–1096 diagnosis, 1096 incidence, 1095 pesticide exposure and, 717 risk factors, 1095–1096 screening programs, 1064 sex steroid hormones and, 1057 symptoms, 1096 treatment, 1096 Prostate-specific antigen (PSA), 1096 Prostatic hyperplasia, 1096 Protective association, 20, 21t Protein-energy malnutrition, 1197. See also Nutrition Protozoan infections food-borne, 852 giardiasis. See Giardiasis toxoplasmosis. See Toxoplasmosis Psittacosis, 423–424 bacteriology, 423–424 clinical characteristics, 424 diagnosis, 424 prevention and control, 424 public health significance, 424 transmission, 424 treatment, 424 Psychiatric disorders, 1161–1168 clinical characteristics, 1166 epidemiology comparative studies, 1162–1163 patient characteristics, 1161–1162

prevalence and incidence, 1162, 1162t, 1163t tools, 1161 etiology physical environment homelessness, 1166 lead exposure in children, 1165–1166 occupational exposures, 1165 social environment community-wide trauma, 1165 personal adversities and strain, 1165 health-care service providers, 1227 historical trends depression, 1166 psychosis, 1166 suicide, 1166 identification of new syndromes, 1166–1167 preventive interventions, 1168 risk factors age, 1163 familial aggregation, 1164 marital status, 1164 physical health status, 1164 race/ethnicity, 1164 season of birth, 1164 sex, 1163 social class, 1163–1164 treatment, 1167–1168 Psycho-organic syndrome, 620 Psychological empowerment, 60 Pteropus fruit bats, 80 Public health assessment and management tools evaluation of complex, communitywide interventions, 1280–1281 focus, 1280 models, 1280 purpose, 1280 Healthy People 2000, 1244–1245, 1244t, 1276 Healthy People 2010. See Healthy People 2010 local objectives Assessment Protocol for Excellence in Public Health, 1246 Healthy Cities, 1247 Mobilizing for Action through Planning and Partnership, 1245–1246, 1246f, 1247f Planned Approach to Community Health, 1246–1247 national objectives for 1990, 1244 quality assurance and improvement doing well what works, 1278–1279, 1278f, 1279t knowing resources for what works, 1277 knowing the purpose for doing it, 1279–1280 knowing what works, 1277 using what works, 1277–1278 definition, 3 epidemiology applications in epidemic control, 24 policy development, 24 program practices and operations, 24 ethical issues communicable disease control, 28–29 educating and socializing students, 37

environmental health, 29–30 in health education/health promotion, 34 informed consent, 31, 33t in international health, 35 methods, 36 in occupation health, 34 in population policies and family planning programs, 34–35 principles, 27–28 in research conflicts of interest, 33 ethics review, 32–33, 33t impartiality and advocacy, 33 policy statements, guidelines and codes of conduct, 32 population screening, 33–34 in resource allocation, 35 risks and benefits, 30–31 future developments public health’s role, 1247–1248 socioecological model, 1247, 1247f strengthening role of public health, 1248 holistic community approach core functions and essential services, 1024t evidence-based decision making, 1024–1026, 1025t infrastructure, 1024 socioecological model, 1023–1024 Steps to a Healthier US, 1024 information systems. See Public health informatics Institute of Medicine statements, 1023, 1024t law. See Public health law leadership development competency framework, 1271–1272 National Public Health Leadership Development Network, 1271 need for, 1271 mission, 1239 as mortality determinant, 44 paternalism and, 35–36 philosophical basis, 36–37 planning. See Public health planning policy development agenda setting, 1272–1273 getting issues on agenda, 1273 new opportunities, 1276–1277 outcome prediction, 1273, 1276t preventive benefits added to Medicare, 1273 problem definition, 1276 role of evidence-based guidelines, 1276 tools for promoting prevention, 1277 responses to global change, 931–932, 931t structure and function core functions, 1239–1240 Council on Linkages between Public Health Practice and Academia, 1240 essential services, 1240, 1240f federal public health role, 1241–1242 financial issues, 1241 local public health role funding, 1243 Institute of Medicine definition, 1243 leadership, 1243 organization, 1243 services, 1243–1244 size of local health departments, 1243 medicine/public health initiative, 1241

Index National Association of County and City Health Officials, 1241 National Association of Local Boards of Health, 1241 national performance standards, 1241 public health leadership institutes, 1241 state public health role Institute of Medicine definition, 1242 organization, 1242 public health directors, 1243 state boards of health, 1242–1243 state health agency activities, 1242 trends, 3–4 workforce current challenge, 1302–1303 degrees and credentials, 1302 disciplines, 1300–1301, 1301t practice locations, 1301–1302, 1301t Public health informatics challenges for future, 53–54 data interchange technologies, 50–51 enterprise architecture, 50 historical context, 49–50 lessons learned, 53 medical care information system needs, 52 national health information system needs, 52–53 public health information system needs, 51–52, 51t public health system needs, 50 public health worker needs, 51, 51t Public Health Information Network (PHIN), 52 Public health law as administrative law administrative searchers, 1261 separation of powers, 1260–1261 statutes and regulations, 1261 constitutional basis criminal prosecution, 1260 equal protection, 1260 foreign affairs, 1260 freedom of speech, 1260 history, 1259–1260 interstate commerce, 1260 property rights, 1260 future developments, 1264–1265 judicial review of public health actions, 1261–1262 primary care and, 1259 privacy and autonomy issues, 1263 public health surveillance and quarantine and isolation, 1264 requirements for health-care providers, 1263 testing and treatment, 1263 vaccinations, 1264 tools administrative orders, 1262 direct abatement, 1262 fines and other punishments, 1262 injunctions, 1262–1263 permits, 1262 Public health planning approaches information as basis for better community health, 1270 program planning, 1270 social marketing, 1269 strategic planning, 1269

leadership and technical skills for, 1270 models comprehensive health improvement, 1269 Community Tool Box, 1269 Mobilizing for Action through Planning and Partnership (MAPP), 1245–1246, 1246f, 1247f, 1269 Multilevel Approach to Community Health (MATCH), 1269 PRECEDE-PROCEED, 1025–1026, 1269 need for, 1268 selection, 1268, 1270 vs. tools, 1268 process management scope and limits, 1268 sponsorship, 1267 stakeholders and politics, 1268 as tool for changing organizations, 1267 Pulmonary thromboembolism, 1119, 1119t Pyoderma, streptococcal, 240–241 Pyrantel pamoate, 476 for ascariasis, 478 for pinworm, 479 Pyrethrins, 713–714, 713t Pyrethroids, 713–714 Pyrethrums, 713, 713t Pyronaridine, 380 Q Q fever, 368–369 bioterrorism/biowarfare use, 369 clinical characteristics, 368–369 diagnosis, 369 epidemiology, 368 history, 368 immunization, 369 treatment, 369 Quadriplegia, 1131 Quality assurance and improvement doing well what works, 1278–1279, 1278f, 1279t knowing resources for what works, 1277 knowing the purpose for doing it, 1279–1280 knowing what works, 1277 using what works, 1277–1278 Quality-of-life (QOL) measures, 3 Quarantine, 1264 Quarries, silica exposure in, 591, 597–598 Quartz, 591 Quinine, 378 Quinolone antibiotics for traveler’s diarrhea, 92 for typhoid fever, 302 R Rabies, 419–423 clinical disease in animals, 421 in humans, 421 control, 423 diagnosis, 421 distribution, 419, 420t epidemiology, 419–420, 420t immunization postexposure, 422, 422t preexposure, 422–423 rabies immune globulin, 422 for travel, 88–89 veterinary, 423

1359

prevention, 421–423 transmission, 420–421 Race/ethnicity cancer incidence and, 1049, 1050t definition, 58 diabetes and, 1105 as health disparity determinant, 58–59, 804. See also Workers, in developing nations as mortality determinant, 44 psychiatric disorder incidence and, 1164 Radiation. See Ionizing radiation; Nonionizing radiation Radioactive wastes, 907 Radioactivity, 736t Radiofrequency radiation epidemiological studies, 749 exposure limits, 750–751 sources and exposures, 748–749 Radionuclides maximum contaminant levels in drinking water, 872t toxic effects, 872t Radium, 872t Radon, 508, 702, 702t Raloxifene, 1127 Ras oncogenes, 556 Receiver operating characteristic (ROC), 1044 Recommended Dietary Allowance (RDA), 1195, 1196t Record linkage, 11–12 Reduced penetrance, 67 Reference dose (RfD), 551 Refractive error, 1158 Refugees, 39, 46. See also Migration Rehydration therapy, 306–307 Reiter’s syndrome, 851 Relocation, 1191 Renal disease, 1089–1094 acute renal failure, 1093 analgesic nephropathy, 1092–1093 autosomal dominant polycystic kidney disease, 1092 in diabetes, 1089–1090, 1106–1107 end-stage, 1096–1097, 1096f future developments, 1097–1098 glomerulonephritis chronic idiopathic, 1091 IgA nephropathy, 1091 poststreptococcal, 1091–1092 hemolytic uremic syndrome, 851–852, 1094 HIV infection and, 1094 hypertensive, 1090–1091 overview, 1089 substance abuse and, 1093–1094 Reoviridae, 342t Research conflicts of interest, 33 ethics review, 32–33, 33t impartiality and advocacy, 33 policy statements, guidelines and codes of conduct, 32 population screening, 33–34 Resource, Conservation, and Recovery Act (RCRA), 902 Respiratory diseases, 1113–1120 acute respiratory distress syndrome, 1118–1119

1360

Index

Respiratory diseases (Cont.): asthma. See Asthma/acute airway reactivity in children asthma, 1115–1117, 1116f, 1116t cystic fibrosis, 1114–1115 respiratory distress syndrome, 1113–1114 respiratory tract infections, 1115 chronic obstructive pulmonary disease. See Chronic obstructive pulmonary disease diffuse parenchymal lung diseases, 1119–1120, 1119t infections. See Respiratory infections mortality, 1113, 1114t pathogenesis, 1114t pulmonary thromboembolism, 1119, 1119t secondhand smoke and, 964–966 sleep apnea syndrome, 1120 tobacco use and. See Tobacco use worldwide incidence, 1113, 1114t Respiratory distress syndrome, 959t, 1113–1114 Respiratory infections, 201–211 in children, 1115 emergent influenza. See Influenza SARS coronavirus. See Severe acute respiratory syndrome incidence, 201 major syndromes bronchiolitis, 205–206 common cold, 203–204 diphtheria. See Diphtheria otitis media. See Otitis media pertussis. See Pertussis pneumonia. See Pneumonia sore throat, 204 pathogenesis, 202–203 pathogens, 204f prevention and control diphtheria, tetanus, pertussis vaccine, 119–120, 210–211, 210t H. influenzae vaccine, 126, 127, 206, 210, 210t influenza vaccine. See Influenza, immunization isolation precautions, 203t, 209 pneumococcal vaccine, 139, 209–210, 210t significant pathogens B. pertussis, 111, 206 C. diphtheriae, 117, 206–207 H. influenzae. See Haemophilus influenzae S. pneumoniae. See Streptococcus pneumoniae transmission, 203, 203t Respiratory protective devices, 786 Respiratory tract anatomy, 202 mechanisms of defense, 202 normal flora, 202 Retinal vein occlusion, 1156 Retinitis, cytomegalovirus, 1157 Retinopathy diabetic, 1106, 1156 of prematurity, 1157–1158 from retinal vein occlusion, 1156 Retirement, 1191 Retroviruses human immunodeficiency virus. See Human immunodeficiency virus (HIV) infection

Reye’s syndrome case definition, 492 etiology, 492 influenza and, 122 Rhabdoviridae, 342t Rheumatic fever. See Acute rheumatic fever Rheumatic heart disease, 1082 Rheumatoid arthritis, 1130 Rickettsial infections, 362–368 anaplasmosis, 367–368 diagnosis, 362 ehrlichioses, 367 natural history, 362 Orientia group, 366–367 pathogens, 362, 363t prevention and control, 363–364 spotted fever group, 363t, 364–365 treatment, 362–363 typhus group, 365–366 Rickettsialpox, 363t, 365 Rifampin for H. influenzae prophylaxis, 127 for leprosy, 261, 261t resistance, 248–249 for tuberculosis, 251 Rift Valley fever clinical characteristics, 359 emergence, 81 epidemiology, 353t, 359 Rimantadine, 124 Risk assessment applications energy and transportation, 547 future use of contaminated sites, 546–547 military, 546 terrorism and preparedness, 546 veterinary, 546 balancing risks and costs, 547 biological agent, 551 for carcinogens classification, 549, 550t dose-response assessment, 548 exposure assessment, 548–549 hazard identification, 548 interpreting the model, 550 interspecies extrapolations, 549–550 landmarks, 549t risk characterization, 549 conservation medicine, 555 definition, 545 ecological, 554–555 epidemiologic and experimental information for dose-duration, 552 extreme value theorem, 552 maximally tolerated dose, 552 susceptibility, 552 uncertainty, 552 framework, 545, 546f future priorities, 556 harmonization of methods, 555–556 identification of acceptable risks, 547–548, 548t individual vs. collective, 552 junk science and, 555 limitations, 552 natural resource damage assessment, 555 for noncancer endpoints calculations, 551

modeling, 550 physiologically based, pharmacokinetic models, 551 receptor kinetics and gene expression, 551 terminology benchmark dose, 550–551 conservative, 551 LOEAL, 551 NOEL and NOAEL, 551 reference dose, 551 safety factor, 551 purposes, 545 radiation, 551 research venues, 555 value, 545 Risk communication biology of fear, 1030 challenges, 553 definition, 1029–1030 evolution, 1029–1030 media coverage of risk, 554 models, 553–554 recommendations, 1032–1034 risk comparisons, 554 risk perception and, 552–553, 553t characteristics catastrophic vs. chronic, 1032 control benefit, 1031 dread, 1032 fairness/equity, 1032 familiar vs. new, 1032 future generations, 1032 imposed vs. voluntary, 1031 natural vs. human-made, 1031–1032 personal risk, 1032 personification, 1032 risk vs. benefit, 1031 trust, 1031 uncertainty, 1032 general heuristics anchoring and adjustment, 1031 availability, 1031 framing, 1031 optimism, 1030 representativeness, 1031 stakeholders and citizens’ advisory boards, 554 temporal characterization of risk, 554 Risk difference, 20 Risk perception, 552–553, 553t. See also Risk assessment; Risk communication River blindness, 1157 ROC (receiver operating characteristic), 1044 Rocky Mountain spotted fever, 363t, 364 Rodenticides, 713 Ross River virus infection, 346t, 352 Rotavirus characteristics, 265t epidemiological features, 266t, 849t immunization, 272–273 vaccine, withdrawal from market, 1208–1209 Rubella, 108–110 clinical characteristics postnatal infection, 108 prenatal infection, 108, 109t complications, 108 diagnosis, 108 etiologic agent, 108 immunization, 109–110

Index immunology, 108 occurrence, 108–109, 109f S Sabia virus, 353t, 355 Sabin vaccine, 134 Safe Water Drinking Act, 868, 868t Safety factor (SF), 551 Salk vaccine, 134 Salmonella, nontyphoid, 265t, 437, 439t, 848t, 849t. See also Salmonellosis, nontyphoidal Salmonella typhi, 265t, 301. See also Typhoid fever Salmonellosis, nontyphoidal, 437–439 clinical characteristics, 265t, 437, 850 diagnosis, 437 etiologic agents, 437 institutional, 438 occurrence, 438–439, 438f, 439f, 439t, 848t, 849t prevention, 439–440, 850 transmission, 266t, 437–438, 850 treatment, 437 Salt intake, coronary heart disease and, 1076 San Quintín, Baja California Norte, 809–810 Sand fly fever, 346t, 351 Sanger, Margaret, 1303 Sanitation, in food processing equipment design, 855 facility design, 855 procedures, 855–856 SARS. See Severe acute respiratory syndrome Scarlet fever, 240 Schistosoma, 480, 1059 Schistosomiasis, 480–482 cancer risk and, 1059 clinical characteristics, 480–481 diagnosis, 481 distribution, 480 etiologic agent, 480 pathogenesis, 480 prevention and control chemotherapy, 482 considerations for travelers, 93 education, 482 sanitation and water supply, 482–483 snail control, 482 vaccine development, 483 treatment, 481–482 Schools, asbestos exposure in, 570–571 Scoliosis, 1131–1132 Screening assessment of tests, 1043–1044 for cancer secondary prevention breast cancer, 1064 cervical cancer, 1064 colorectal cancer, 1064 evaluation of programs, 1063–1064 gastric cancer, 1064 liver cancer, 1064–1065 planning programs, 1062–1063 prostate cancer, 1064 definition, 1043 for diabetes, 1105–1106 Scrombotoxin, 848t, 853 Scrub typhus, 366–367 Seafood toxins, 848t, 853 Seated work, back pain and, 775–776

Secondhand smoke constituents, 964, 965t eliminating exposure, 975, 977–978 health effects in adults, 964, 966 cardiovascular disease, 966–967 in children, 964 lung cancer, 964–966, 1053 respiratory disease, 964–966 sinus cancer, 966 sudden infant death syndrome, 964 Sediment contamination, 903 Segregation analysis, 69 Seizure disorders, 1143 Selection bias, 21 Selenium, 614–615, 870t Self determination theory, 942–943, 942f, 943f Sensitivity, 1043 Sensory system testing, 527–529 basal ganglia, 529 cerebellar function, 529 hearing, 528 motor function, 528–529 olfaction, 528 position sense and vestibular function, 528 taste, 528 temperature, 528 touch and vibratory sensation, 528 vision, 527–528 Serostatus Approach to Fighting the Epidemic (SAFE), 195 Serotonin, 526 Severe acute respiratory syndrome (SARS), 207–208 clinical characteristics, 207 emergence, 81, 207 etiologic agent, 207 incidence, 207 transmission, 207 treatment, 207–208 Sex. See also Women workers anthropometric differences, 765t, 828 cancer incidence/mortality and, 1048t, 1049, 1050t, 1051t coronary heart disease and, 1080–1081 emergency department visits for injury and, 1324f, 1325 health inequities and, 1257 hospital admissions for injury and, 1323f injury mortality and, 1322–1323, 1322f as mortality determinant, 44 occupational disease susceptibility and, 828 psychiatric disorder incidence and, 1163 Sex chromosomal disorders, 66–67 Sex chromosome disorders, 66–67 Sex steroid hormones, cancer risk and, 1055–1057 Sexual abuse, of children, 1330–1331 Sexually transmitted infections (STIs), 155–171. See also specific infections consequences adverse perinatal outcomes, 160–161 female reproductive morbidity, 159–160 neoplasia, 160 synergy with HIV, 161 economic burden, 155 epidemiology chancroid, 168–169 chlamydia, 167

1361

gonorrhea, 167–168 herpes simplex, 169–170 lymphogranuloma venereum, 169 syphilis, 168 trichomoniasis, 169, 170t viral hepatitis, 171 Healthy People 2010 objectives, 171t incidence, 155, 156t international travel and, 93 prevention and control measures abstinence, 162 antimicrobial prophylaxis, 164 behavioral interventions adolescents, 163 heterosexual adults, 163 men who have sex with men, 163–164 risk reduction counseling, 163 condoms, 164–165 partner notification/contact tracing, 166–167 topical microbicides, 164 vaccines FDA-approved, 166 investigational, 165–166 public health programs clinical services community-based clinics, 158 private sector settings, 158–159 public clinics, 158 disease intervention services, 157 federal, 155–156 funding, 156–157 information and data systems, 157–158 infrastructure, 156, 156t state and local, 156 workforce, 157 transmission dynamics, 162 SF (safety factor), 551 Shellfish toxin, 853 Shigella, 303, 848t, 849t Shigellosis, 303–304 bacteriology, 303 clinical characteristics, 265t, 303 diagnosis, 265t, 303 epidemiological features, 267t occurrence, 304, 848t, 849t prevention and control, 304 transmission, 304 treatment, 303–304 Shingles. See Herpes zoster Sibling pair studies, 69–70 “Sick building” syndrome, 508–509 SIDS (sudden infant death syndrome), 959t, 963, 964 Significance testing, 22 Silent Spring, 506, 707 Silica. See also Silicosis cancer and exposure to, 597–598 characteristics, 591 occupational standards for exposure, 599 Silicolipoproteinosis, 593, 594 Silicosis, 591–599 clinical features, 594–595 complications, 596–597 diagnosis computed tomography, 598 differential, 598 history, 598 radiographic findings, 595–596, 595f, 596f, 597f, 598

1362

Index

Silicosis (Cont.): experimental studies, 593–594 history, 591 incidence and prevalence, 592–593 lung cancer and, 598 pathogenesis, 593–594 pathology, 594 prevention and control, 599 prognosis, 599 pulmonary function in, 596 treatment, 599 work exposure and, 591–592, 597–598 Silver, 615 Simazine, 872t Sindbis virus, 346t, 352 Sinus cancer, 966 Skin cancer, 744 Sleep apnea syndrome alcohol use and, 1001 characteristics, 1120 incidence, 1120 Sleeping sickness, 394 Slipped capital femoral epiphysis, 1132, 1132f Slums, 919 Smallpox, 30 Smokeless tobacco. See also Tobacco use cancer and, 958, 972 cardiovascular disease and, 955 periodontal disease and, 962, 972 trends in use, 972 Smoking. See Tobacco use Snow, John, 5, 49 Social cognitive theory, 942, 1017 Social learning theory, 1016–1017 Social Security Disability Insurance, 798–799 Socioeconomic status as health disparity determinant, 59 psychiatric disorder incidence and, 1163 Soft tissue sarcoma, 716, 717 Soil chemicals in, 509 diseases borne by, 93 Solvents abuse, 1014 neurobehavioral toxicity, 524, 525t Sore throat, 204 Space. See also Aerospace medicine environmental characteristics, 911 operations, 912 Spanish flu pandemic, 120 Species extinction, 929–930 Specificity, 1044 Spina bifida, 1178 Spinal cord injuries, 1131 SSPE (subacute sclerosing panencephalitis), 102 St. Louis encephalitis, 344t, 350 Stages of change, 943–944, 943f Standards, for occupational safety and health characteristics, 842–843 compliance, 843–844 consensus, 841–842 global, 844 hazardous waste and emergency response, 843 medical removal protection, 843 permanent, 842 permissible exposure limits, 843 temporary emergency, 842 threshold limit values, 843

Staphylococcus aureus in food-borne disease, 848t, 852 methicillin-resistant. See Methicillin-resistant S. aureus in toxic shock syndrome, 484. See also Toxic shock syndrome, staphylococcal vancomycin-intermediate, 84, 335 vancomycin-resistant, 84 State Children’s Health Insurance Program, 1236 State health agencies activities, 1242 Institute of Medicine definition of role, 1242 organization, 1242 public health directors, 1243 state boards of health, 1242–1243 Statins, in stroke prevention, 1146 Statistical power, 22 Sterilization as determinant of fertility, 43 female, 1310 male, 1310–1311 Stillbirth, pesticide exposure and, 719 Stimulant abuse, 1014. See also Substance abuse STIs. See Sexually transmitted infections Stomach cancer H. pylori infection and, 1059 pesticide exposure and, 717 screening programs, 1064 smoking and, 959t, 960–961, 960t Streptococcus classification, 237, 238t in food-borne disease, 848t, 849t group A β-hemolytic (GABHS). See Group A β-hemolytic Streptococcus history, 237 Streptococcus pneumoniae. See also Pneumococcal infections antimicrobial resistance, 85, 205, 206 diseases caused by, 206 immunization, 139, 209–210, 210t pathophysiology, 206 serotypes, 137–138 Streptococcus pyogenes. See Group A β-hemolytic Streptococcus Stress health effects in women, 829–830 psychiatric disorder incidence and, 1165 Stressors, 506 Stroke, 1145–1147 classification, 1145 disability following, 1190 economic costs, 1145 incidence and prevalence, 1145 mortality, 1145 prevention, 1146–1147 protective factors, 1146 risk factors, 1145–1146 tobacco use and, 956, 1145 Strongyloides stercoralis, 476, 477f Strongyloidiasis, 476–478 clinical presentation, 477 diagnosis, 477 epidemiology, 476 etiologic agent, 476, 477f prevention and control, 478 treatment, 477–478 Study on Efficacy of Nosocomial Infection Control (SENIC), 333 Styrene, 628–629, 872t

Subacute sclerosing panencephalitis (SSPE), 102 Substance abuse. See also Intravenous drug abusers alcohol. See Alcohol abuse and dependence drugs of abuse anabolic steroids, 1014–1015 cannabinoids, 1013 depressants, 1013–1014 dissociative anesthetics, 1014 hallucinogens, 1014 inhalants, 626–627, 1014 opioids and morphine derivatives, 1014 over-the-counter drugs, 1015 pharmacology, 1013–1015 stimulants, 1014 epidemiology, 1015, 1016f etiology behavioral theory, 1016 developmental perspective, 1015–1016, 1017f social cognitive theory, 1017 social learning theory, 1016–1017 health-care service providers, 1227 interventions community-based, 1020 family-based, 1019–1020 ineffective, 1020–1021 program delivery, 1021 school-based, 1020 prevalence, 1163t renal disease and, 1093 risk and protective factors, 1017–1019, 1018f, 1019f Sudden infant death syndrome (SIDS), 959t, 963, 964 Suicide, 1166, 1168 Sulfite esters, 713t Superfund, 902 Supplemental Security Income Program (SSI), 799 Surgical site infections, 334 Surveillance, 9–14 case studies AIDS epidemic, 14 community diagnosis, 14 cycle, 10, 10t definition, 8, 9–10 legal issues, 1263–1264 in occupational health, 789 purposes, 10 system characteristics, 10–11 data collection, 13 data quality, 13 data reporting, 13–14 data sources disease registries, 12 health reports, 12 health surveys, 12, 40 hospital records, 12 vital statistics, 11–12, 40 dissemination, 14 Surveys, population-based Current Population Survey, 40 health surveys, 40 Susceptibility biomarkers, 564 definition, 506 Swimming pools, asthma and, 716

Index Sydenham’s chorea, 243 Syphilis, 160, 168 cardiovascular complications, 1084 congenital, 160 epidemiology, 168 incidence, 156t prevalence, 168 Systematic reviews, 23–24 T Taenia saginata, 447–448 Taenia solium, 447–448 Taeniasis, 447–448 clinical characteristics, 447 diagnosis, 448 distribution, 447 etiologic agent, 447 prevention and control, 448 treatment, 448 Talc, 577 Tampons, 491 Taste neurotoxicant effect on, 528 testing, 528 TB. See Tuberculosis Technological disasters, 1286–1287, 1286t. See also Disasters Tenofovir, 195 Teratogenesis, 517 Teriparatide, 1127 Terrorism. See also Disasters casualties from, 1287–1288 risk assessment and preparedness, 546 types, 1286t Testicular cancer pesticide exposure and, 717 sex steroid hormones and, 1057 Tetanus, 115–117 clinical characteristics, 115 diagnosis, 115 etiology, 115 immunization boosters, 116 complications, 116 for international travel, 88 preexposure, 116, 210t in wound management, 116, 117t neonatal prevention, 117 occurrence, 115–116 pathogenesis, 115 treatment, 117 Tetrachloroethane, 634 Tetrachloroethylene, 872t Tetracyclines, 378–379 Tetranitromethylaniline, 653 Texaco, in Ecuador, 811–812 TFR (total fertility rate), 41 TGF-α (transforming growth factor-alpha), 594 Thallium, 615, 870t Theory of reasoned action and planned behavior, 944–945, 945f Thermal stratification, 866 Thermoregulation, 725 Thiabendazole, 478 Thiazolidinediones, hepatic failure and, 1210–1211, 1211f, 1212f Thimerosal, 122 Threshold, 506 Threshold limit values, 843

Thrombotic thrombocytopenic purpura, 851 Thyroid cancer, radiation exposure and, 739, 1055 Thyrotropin-releasing hormone, 526 Tick-borne encephalitis, 343t, 350 Ticks. See also Arthropod vector-borne diseases characteristics, 342 as Lyme disease vector, 387, 387f, 388, 388f as tularemia vector, 426 Tin, 615 Tinea capitis, 469–470 clinical presentation and diagnosis, 469–470, 470f epidemiology, 469 prevention and control, 470 Tinea corporis, 470–471 clinical presentation and diagnosis, 470–471, 471f epidemiology, 470 prevention and control, 471 Tinea cruris, 471 clinical presentation and diagnosis, 471, 471f epidemiology, 471 prevention and control, 471–472 Tinea pedis, 472 clinical presentation and diagnosis, 472, 472f epidemiology, 472 prevention and control, 472 Tinea unguium, 472–473 clinical presentation and diagnosis, 472–473, 472f, 473f epidemiology, 472 prevention and control, 473 Tobacco use asbestos exposure and, 568, 569t, 574, 576 cessation interventions advertising bans, 976 challenges, 984–985, 985t clinical treatment, 972–973 community-based, 974 countermarketing, 976 current status comprehensive programs, 978–979 insurance coverage for treatment, 978 quitlines, 978 performance measures, 973–974 price increases, 975 quitlines, 976 treatment cost reductions, 976 warning labels, 980 chemical constituents of smoke, 965t economic costs, 954 economic factors, 980–981 health effects cancer acute leukemia, 961 bladder and renal, 959–960 cervical, 961 endometrial, 961 lung, 957–958, 957f mortality, 959t, 960t, 1052–1053, 1053t oral, laryngeal, and esophageal, 958–960 pancreatic, 961 cardiovascular disease cerebrovascular disease, 956, 1145 coronary heart disease, 954–955, 1079–1080 pathophysiology related to smoking, 956–957

1363

peripheral vascular disease, 955–956 chronic bronchitis, 695 chronic obstructive pulmonary disease, 961–962 fetal, of maternal smoking, 963 gastrointestinal disease, 962 mortality, 953–954, 954f oral disease, 962 of secondhand smoke. See Secondhand smoke in young people, 963 industry lawsuits, 980 international perspective, 981–984, 982f, 984t in pregnancy, 963 prevention strategies challenges, 984–985, 985t countermarketing campaigns, 974–975 current status advertising restrictions, 977 comprehensive programs, 978–979 minors’ access restriction, 978 smoke-free indoor air policies, 977–978 tobacco excise taxes, 977 effectiveness, 976–977 minors’ access restrictions, 975 price increases, 974 school-based programs, 975 smoke-free policies in school, 975 protobacco influences advertising and promotion, 979–980 smoking in movies, 979–980 trade policies and, 981 trends cigarette characteristics, 969–970 potential reduced exposure products, 971 prevalence in adolescents and children, 969, 969f prevalence in adults, 967–969, 967f, 968f workplace issues, 981 Togaviridae, 108, 342t Tolerable upper intake level (UL), 1195, 1196t Toluene, 626–628 abuse, 626–627 characteristics, 626 exposure monitoring, 628 prevention and control, 627–628 sources, 626–627, 628 maximum contaminant levels in drinking water, 872t toxic effects, 626–627, 872t Toluylenediamine, 652 Total fertility rate (TFR), 41 Total quality management (TQM), 1278–1279, 1279f Touch neurotoxicant effect on, 528 testing, 528 Toxaphene, 872t Toxic shock syndrome staphylococcal, 484–491 clinical features, 490 definition, 484t diagnosis, 484, 490–491, 491t epidemic behavior, 485 etiologic agent, 484–485 geographic distribution, 485 history, 483 incidence and prevalence, 485, 485f

1364

Index

Toxic shock syndrome (Cont.): menstrual, 487–489, 488t, 491 nonmenstrual, 489 pathogenesis, 489–490 postoperative, 489 postpartum, 489 prevention and control, 491 risk factors age, 487 race, 487 sex, 487 surveillance, 483–484 temporal distribution, 485–487, 486f transmission, 489 streptococcal, 241 Toxicity, 515–521 biomarkers, 519–520, 519t clinical evaluation, 519 definition, 506 factors modifying, 508 mechanisms, 505, 506f, 515–518 apoptosis vs. necrosis, 515 cellular poisons, 515 endocrine disruptors, 517 enzyme induction, 515–516 genotoxins, 516–517 immunotoxins, 516 lipid peroxidation, 518 macromolecular binding, 515 metabolic poisons, 515 nitric oxide, 518 oxidative stress and free radicals, 517 receptors and ligands, 516 reproductive effects, 517 sensitizers, 516 teratogenesis, 517 metal exposure. See Metal exposure neurobehavioral. See Neurobehavioral toxicity testing bioassays, 521 human exposure studies, 521 transgenic and knockout mice, 521 Toxicokinetics, 511 Toxicology, 505–533 animal welfare/rights issues, 521–522 biomarkers, 519–520, 519t branches, 505–506 carcinogenesis, 518 causality, 520 chemical principles, 508 chemicals in the environment air, 508–509 food, 509 soil, 509 water, 509 clinical evaluation, 519 definition, 505 evolutionary basis, 506 exposure to toxic substances absorption, 510 acute vs. chronic, 510, 510t assessment, 509–510, 510t bioavailability, 510 defenses, 513 susceptibility, 515 time-dose interactions, 511 in utero exposure, 510 future directions imaging, 522

nanotechnology, 523 toxic environments, 523 toxicogenomics, 522–523 history, 505 interactions and mixtures, 518–519 mechanisms of toxicity. See Toxicity, mechanisms neurobehavioral toxicity. See Neurobehavioral toxicity pathophysiology cytochrome P450, 511–512 excretion route, 512–513 flavin-containing monooxygenases, 512 metabolic activation vs. detoxification, 511 phase II reactions, 512 toxicokinetics, 511 pharmacodynamics composite curves, 514, 514f dose-response curve, 513, 513f endpoints, 513 hormesis, 514 latency, 514–515 reversibility, 515 susceptibility, 515 thresholds, 514, 514f precautionary approach, 522 product substitution, 522 regulation of toxic exposure, 522 stressors, 506 terminology, 506 toxic agent classification, 507–508 toxicity testing. See Toxicity, testing Toxins, classification, 506–508 Toxoplasma gondii, 440, 441f, 849t Toxoplasmosis, 440–443 clinical characteristics, 440–442 congenital, 441 diagnosis, 442 epidemiology, 442 etiologic agent, 440, 441f prevention, 443 treatment, 442–443 TQM (total quality management), 1278–1279, 1279f Trachoma, 1157 Transforming growth factor-alpha (TGF-α), 594 Transtheoretical model, 943–944, 943f, 944f Travel, international, 88–93 environmental adaptations for, 88–93, 93 illness after return, 93 immunizations for recommended, 88–90 required, 88 routine, 87–88 timing of vaccine administration, 90 malaria protection, 90–92 sexually transmitted disease precautions, 93 soil- and water-borne disease, 93 traveler’s diarrhea. See Traveler’s diarrhea vector-borne diseases, 92–93 Traveler’s diarrhea definition, 270 etiology, 92, 270, 309 incidence, 92 prevention chemoprophylaxis, 92, 309 food and water precautions, 92, 309 regional differences, 270 treatment, 92, 309

Trench foot, 730 Trichinella, 443, 444t, 848t, 849t Trichinellosis, 443–445 clinical characteristics, 443–444 diagnosis, 444–445 epidemiology, 443 etiologic agent, 443, 444t occurrence, 848t, 849t prevention and control, 445 treatment, 445 Trichloroethylene characteristics, 632 exposure, 632, 633 maximum contaminant levels in drinking water, 872t metabolism, 632 toxic effects, 632–633, 872t Trichomoniasis epidemiology, 169 incidence, 156t prevalence, 169, 170t Trichophyton, 469, 470t. See also Dermatophytoses Trichuriasis, 478–479 clinical characteristics, 478 diagnosis, 478 epidemiology, 478 etiologic agent, 478 prevention and control, 479 treatment, 478–479 Trichuris trichiura, 478–479 Tridymite, 591, 599 Trimellitic anhydride, 643 Trinitrotoluene, 651–652 Trisomy 13, 66 Trisomy 18, 66 Trisomy 21. See Down syndrome Tropical pulmonary eosinophilia, 399 Tropical typhus, 366–367 Trypanosoma cruzi, 392 Trypanosomiasis African, 394 American. See Chagas’ disease Tsutsugamushi disease, 366–367 Tuberculin skin test (TST), 249, 250–251 Tuberculosis (TB), 248–257 bovine, 257 clinical characteristics, 250 diagnosis blood analysis, 251 chest radiograph, 250 cultures, 250 genotyping, 251 sputum examination, 250 tuberculin skin test, 250–251 drug-resistant, 85, 248–249, 254 emergence, 84 epidemiology in correctional institutions, 256–257 in the elderly, 245 in foreign-born immigrants to the U.S., 255 in health care workers, 256 history, 253 in IV drug abusers, 245 nosocomial transmission, 255–256 transmission during airline flights, 245 U.S. trends, 253 worldwide, 254–255 HIV and, 249, 253–254

Index immunization, 88–89, 252 incidence, 84, 84f microbiology, 248 pathogenesis, 249 reporting verified cases, 251 risk factors for active infection, 249, 249t silicosis and, 596 transmission, 249–250 treatment active disease, 251–252 adherence issues, 252 latent disease, 252 Tularemia, 425–427 clinical manifestations, 426 diagnosis, 426–427 epidemiology geographic distribution, 425, 425f populations affected, 425 sources of infection, 425–426 etiologic agent, 424–425 prevention and control, 427 treatment, 427 Tumor(s), 1047. See also Cancer Tumor suppressor genes, 516–517 Tungsten exposure, 694 Turbidity, drinking water, 869t Turner’s syndrome, 66 Twin studies, 68–69 Type I error, 22 Typhoid fever, 301–303 bacteriology, 301 carriers, 302 clinical characteristics, 265t, 301 diagnosis, 301–302 immunization, 73–74, 88–89, 302–303, 302t occurrence, 302, 438f transmission, 266t, 302 treatment, 302 Typhus, 365–367 epidemic, 365–366 flying squirrel-associated, 366 immunization, 88–89 murine, 366 scrub, 366–367 U UL (tolerable upper intake level), 1195, 1196t Ultrasound, 760 Ultraviolet radiation (UVR), 743–745 biological effects, 743–744, 929, 1055 for food preservation, 860 protection from, 744–745, 744t, 745t sources and exposures, 743, 744t Uncertainty factor (UF), 551 United Farmworkers Union, 821 United Nations Draft Principles on Human Rights and the Environment, 803 Framework Convention on Tobacco Control, 27 Upper extremity, work-related disorders. See Musculoskeletal disorders, work-related Uranium, 615–616, 699, 872t Urbanization public health issues, 39, 46 worldwide, 919, 920t Urinary incontinence, 1189 Urinary tract disease

benign prostatic hyperplasia, 1096 future developments, 1097–1098 infections. See Urinary tract infections prostate cancer. See Prostate cancer urinary stones, 1095 Urinary tract infections diagnosis, 1095 health care-associated, 334, 1095 incidence, 1094 pathogenesis, 1094–1095 treatment, 1095 U.S. Department of Agriculture, 853–854 U.S. Department of Health and Human Services, 1242 U.S. Department of Transportation, toxic exposure regulation, 522 U.S. Preventive Services Task Force, 194t V Vaccine(s). See also Immunization anthrax, 431 cholera, 88–89, 307 diphtheria, 119–120, 210–211, 210t H. influenzae, 126, 127, 210, 210t hepatitis A, 88–89, 166, 215 hepatitis B, 88–89, 166, 210 herpes simplex, 165–166, 234 HIV, 195 human papillomavirus, 166 influenza. See Influenza, immunization for international travel recommended, 88–90 required, 88 routine, 87–88 timing of vaccine administration, 90 Japanese encephalitis, 88–89 malaria, 386 measles. See Measles, immunization meningococcal disease, 88, 247–248 mumps, 106 pertussis, 113–114, 210–211, 210t pneumococcal, 139, 209–210, 210t poliomyelitis. See Poliomyelitis, prevention and control Q fever, 369 rabies, 88–89 rotavirus, 273 rubella, 109–110 for sexually transmitted infections, 165–166 smallpox, 30 tetanus. See Tetanus, immunization tuberculosis, 88–89, 251, 252 typhoid fever, 88–89, 302–303, 302t typhus, 88–89 varicella. See Varicella, immunization yellow fever, 88, 357–358 Vaccine-derived poliovirus, 136–137, 137t Vanadium, 616 Vancomycin-intermediate S. aureus (VISA), 84, 335 Vancomycin-resistant S. aureus (VRSA), 84 Vapors, 782 Varicella, 128–132 clinical characteristics, 129 complications, 129 congenital, 130 epidemiology, 130 etiology, 128 future public health needs, 133

1365

immune response, 128 immunization active, 130 contraindications, 132 efficacy and effectiveness, 131 passive, 132 persistence of vaccine-induced immunity, 130–131 postexposure, 132 recommendations, 128, 130 safety, 131–132 isolation guidelines, 132 laboratory tests, 128–129 neonatal, 129–130 public health significance, 127–128 treatment, 132 Varicella zoster virus, 128. See also Herpes zoster; Varicella Vasectomy, 1310–1311 Vector-borne diseases. See Arthropod vectorborne diseases Venezuelan equine encephalitis, 345t, 350 Venezuelan hemorrhagic fever, 353t, 354–355 Venous thromboembolism, 1119, 1119t, 1306 Ventilation, for workplace hazard control, 786 Ventilator-associated pneumonia, 334–335 Vermiculite, 577 Vertical equity, 56 Vestibular function neurotoxicant effect on, 528 testing, 528 Veterinary medicine, risk assessment applications, 546 Vibrio cholerae. See also Cholera classification, 304–305 O139, 83, 305 occurrence, 848t, 849t Vibrio spp., 265t, 266t, 848t, 849t, 850 Vinyl benzene. See Styrene Vinyl bromide, 636 Vinyl chloride exposure, 636 maximum contaminant levels in drinking water, 872t metabolism, 635 toxic effects, 634–635, 872t Vinyl trichloride, 634 Vinylidene chloride, 636 Violence. See also Injuries emergency department visits by mechanism, 1325, 1325f in the family, 1329–1332 child abuse. See Child abuse elder abuse, 1331 interventions, 1332 intimate partner, 1329–1330 low-level, 1331 risk factors, 1331–1332 hospital admission rates by mechanism, 1324, 1324f mortality rates by mechanism, 1322–1323, 1323f Virginity pledges, 162 VISA (vancomycin-intermediate S. aureus), 84, 335 Visible light biologic effects, 745 illumination principles, 745–747 units of measurement, 745

1366

Index

Vision neurotoxicant effect on, 527–528 testing, 527–528 Visual disorders, 1153–1158. See also Blindness amblyopia, 1158 cataract, 1153–1154 in diabetes, 1106, 1156 in the elderly, 1189 in HIV infection, 1157 incidence, 1153, 1154t macular degeneration, 1155–1156 onchocerciasis, 1157 refractive error, 1158 retinal disease, 1106, 1156–1157 retinopathy of prematurity, 1157–1158 trachoma, 1157 xerophthalmia, 1157 Vital record linkage, 11–12 Vital statistics as population data source, 40 in surveillance system, 11–12 Vital Statistics Report, 14 Vitamins. See also Nutrition as cancer protective factor, 1060 as stroke protective factor, 1146 Volatile organic compounds (VOCs), 619–620, 905 Von Hippel-Lindau syndrome, 1060t, 1061 VRSA (vancomycin-resistant S. aureus), 84 W Wakana disease, 474 Warfare, 1287. See also Disasters; Military operations Waste classification and properties, 901 liquid. See Water quality management Water conservation practices, 865t consumption in U.S., 863, 864t, 865t contamination/pollution chemical, 869–872t, 877–878 critical areas, 876–877 groundwater, 509 maximum contaminant levels, 869–872t microbial, 869t, 877, 877t radiologic, 872t, 878 surface water, 509 wastewater disposal and, 509, 891 functions, 863 international issues, 1257 properties, 864 shortages, 929, 929t sources groundwater, 866 ocean and brackish waters, 866 protection, 867–868 rainwater, 864 selection, 867 surface water, 864–866 water cycle, 865f water reclamation and reuse, 867 systems, 863–864 Water-borne diseases. See also Gastrointestinal infections definition, 274 due to specific agents amebiasis, 314–316 cholera. See Cholera

coccidial infections, 321–322 Cryptosporidium. See Cryptosporidium dracunculiasis, 320–321 E. coli. See Escherichia coli giardiasis. See Giardiasis Legionnaire’s disease, 311–313 shigellosis. See Shigellosis typhoid fever. See Typhoid fever emerging, 83 precautions for travelers, 93, 309 surveillance, 878–879 susceptible populations, 884–885, 884f trends drinking water-associated, 879–882, 879f, 880f, 881f recreational water-associated, 882–884, 882f, 883f Water pollution. See Water, contamination/ pollution Water quality management in disasters, 1291 engineered water purification adsorption, 889–890 chlorine, 889 coagulation, 886 corrosion inhibition, 889 disinfection, 888 distribution systems, 890 filtration, 887–888 oxidizing chemicals, 888 ozone, 888 sedimentation, 886–887 sludge management, 887 structural profile, 886f international issues, 1257 public health issues, 898 regulations determination of new standards, 874–876, 875t development, 874 Environmental Protection Agency, 868, 868t National Drinking Water Contaminant Candidate List, 874, 875t National Primary Drinking Water Regulations, 868t, 869–873t National Secondary Drinking Water Regulations, 868, 874t Safe Drinking Water Act, 868 wastewater collection and disposal drainage of buildings, 891, 892f drainage of towns, 891–892 industrial wastewaters, 893 night soil collection and disposal, 890 quantity and composition, 892–893 water pollution and, 891 wastewater treatment processes biological treatment, 893–894, 895f chemical coagulation and flocculation, 893 disinfection, 896 preliminary treatment, 893 sedimentation, 893 sludge digestion, 896–897 sludge disposal, 897 sludge drying, 897 sludge management, 896 sludge treatment, 896, 896f stabilization ponds, 894 tertiary treatment, 894–896

wastewater disposal, 897–898 wastewater reclamation, 898 water and wastewater treatment adsorption, 885 coagulation, 885 disinfection, 885 distillation, 885 filtration, 885 flocculation, 885 gas exchange, 885 ion exchange, 885 sedimentation, 885 Weil’s disease. See Leptospirosis West Nile virus characteristics, 343t differential diagnosis, 343t emergence, 81, 82f, 1143 prevention and control, 1143 risk assessment, 555 symptoms, 350, 1143 transmission, 350 Western equine encephalitis, 343t, 350–351 Wet-bulb globe temperature, 725–726 Whitehead, Margaret, 56 WHO. See World Health Organization Whooping cough. See Pertussis Wilms’ tumor genetic factors, 1061 pesticide exposure and, 716 Wind chill, 729, 730f Women workers biological factors, 828 job characteristics, 827–828, 828t in maquiladoras in Mexico, 811 occupational health problems cancer, 830 musculoskeletal disorders, 829 reproductive problems, 830 stress-related, 829–830 violence, 830 research methods, 829 social roles and employment patterns, 828 Woolsorter’s disease, 427. See also Anthrax Work disability, 796. See also Workers, with disabilities Work physiology, 763 Work-rest cycles, for aviators, 914–915 Workers coal. See Coal workers in developing nations, 803–812 case studies children artisanal miners, Nambija, Ecuador, 810–811 San Quintín farmworkers, Mexico, 809–810 Texaco and the Ecuadorian Indians, 811–812 women maquiladora workers, Mexico, 811 Yakima Valley farmworkers, Washington State, 810 environmental and occupational health issues U.S. solutions, 808–809 global context free trade agreements, 805–806 free trade zones, 806 hazard export, 806–807

Index maquiladoras, 806 multinational companies, 805 global disparities exposures, 804 public health policy implementation, 805 susceptibility, 804–805 technical resources, 805 global solutions policy initiatives, 807–808 public health initiatives, 808 with disabilities, 795–801. See also Disability accommodations to enable work, 800 assessment of ability to work, 800 causes, 797t clinicians’ roles, 799 definitions, 796 demographics, 796–797, 797t employment among, 797–798 medical care, 799 policies income support, 798–799 nondiscrimination, 798 rehabilitation and training, 798 prevention and wellness, 801 psychological care, 800 rehabilitation, 799–800 on farms. See Farmworkers smoking effects, 978 women. See Women workers Worker’s Compensation, 799 Workforce Investment Act, 798 Workplace. See also Environmental and occupational health health examinations in biological monitoring, 790 ethical issues, 790–791, 791t general health appraisal, 790 legally mandated examinations, 790, 790t medical screening, 790 preplacement, 789–790 program components, 791, 791t susceptibility screening, 790 smoking policies, 977–978

World Bank classification of nations, 1252t, 1253 tobacco policy, 983 World Health Organization (WHO) classification of nations, 1253 contraceptive use guidelines, 1305, 1306t, 1307 health disparities definition, 56 required immunizations by country, 88 structure and function, 1253 World Trade Organization (WTO), 805 Wounds surgical, infections, 334 tetanus prophylaxis, 116, 117t Wucheria bancrofti, 398–399. See also Lymphatic filariasis X X-linked dominant disorders, 68 X-linked mental retardation, 1175–1177 X-linked recessive disorders, 67 Xenobiotics definition, 506 sequestration, 512 Xerophthalmia, 1157 Xylene, 628, 872t Xylidine, 652 XYY syndrome, 66 Y Yakima Valley, Washington, 810 Yellow fever, 357–358 clinical characteristics, 357 immunization, 88, 357–358 transmission, 353t, 357 treatment, 357 Yersinia enterocolitica, 310, 848t, 849t, 851 Yersinia pestis, 370. See also Plague Yersinia pseudotuberculosis, 310 Yersiniosis, 310, 851 bacteriology, 310 clinical characteristics, 310, 851 epidemiology, 310 prevention, 310, 851

1367

Youth Risk Behavior Surveillance System (YRBSS), 40 Yusho incident, 680–682, 681f, 681t, 682f Z Zanamivir, 124 Zeolites, 577 Zidovudine, 191 Zinc, 616 Zoonoses, 419–451 bacterial anthrax. See Anthrax brucellosis. See Brucellosis leptospirosis. See Leptospirosis nontyphoidal salmonellosis. See Salmonellosis, nontyphoidal psittacosis, 423–424 tularemia. See Tularemia cestode cysticercosis, 447–448 hydatid disease. See Hydatid disease taeniasis, 447–448 definition, 80 emerging, 80–81 nematodes. See Nematode infections protozoan toxoplasmosis. See Toxoplasmosis trematode clonorchiasis, 445–447 opisthorchiasis, 445–447 viral avian influenza A. See Avian influenza A hantavirus, 80, 361t monkeypox, 80 Nipah virus, 80 rabies. See Rabies severe acute respiratory syndrome. See Severe acute respiratory syndrome Zygomycosis, 465–466 clinical characteristics, 465 diagnosis, 465–466 epidemiology, 465 microbiology, 465 treatment, 466