PAN UK - Pesticide News - Issue 91

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The journal of Pesticide Action Network UK An international perspective on the health and environmental effects of pesticides Quarterly

March 2011

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Pesticides News No 91 Editorial 2 Bees

Erratum

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17 PN89 Factsheet – Which Pesticides are

Honey bees – an indicator species in decline

10 Bee-toxic pesticides are causing a buzz 11 The London Mayor’s new campaign for a bee-friendly capital

Integrated pest management 6

Promoting IPM in Illinois childcare centres

banned in Europe?

European regulation 18 Still no EU agreement to reduce dependency on biocides

Factsheet 20 Imidacloprid

Biocontrol

News

12 Could knotweed’s reign of terror be

10 UN says bee decline is global trend 19 Beekeepers expose weaknesses in EU

over?

Latin America 14 Continued poisoning and protest force change in Latin America

Climate change 16 Pesticide use and climate change – are they decoupled?

pesticide assessments

19 Ecological agriculture can double food production says UN

Book reviews 23 ENDURE network for diversifying crop protection

23 Systemic pesticides: a disaster in the making

Pesticide Action Network UK Development House 56-64 Leonard Street London EC2A 4LT, UK Tel +44 (0)20 7065 0905 Fax +44 (0)20 7065 0907 Email admin@pan-uk.org

www.pan-uk.org www.pan-international.org links to all PAN Regional Centres

Over the past four years US beekeepers have seen unprecedented annual overwintering losses of between 29% and 36% Photo: PANNA

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Editorial

Pesticides News 91

Populations of bees and other pollinators are in rapid decline all over the world. While the causes of this are many and complex, there is little doubt that the growing use of systemic neonicotinoid insecticides is contributing.

This issue of Pesticides News includes a number of articles exploring the relationship between pesticides and pollinators.

On page 3, Heather Pilatic of PAN North America provides an update on the situation in the US where beekeepers have witnessed overwintering losses of 29%-36% each year for the last four years. She highlights concerns over the ‘fast tracking’ of problem pesticides by the US EPA which released two neonicotinoids – imidacloprid and clothianidin – onto the US market in recent years with ‘conditional registrations’.

The EU process for assessing the impact of pesticides on bees has also come in for criticism from beekeepers and the NGO Corporate Europe Observatory who have joined together to complain about pesticide industry involvement in the assessment process (page 19).

But politicians are waking up to the problem. Some 70 UK MPs have signed up to a motion to restrict neonicotinoids in the UK (page 10), and London Mayor Boris Johnson has launched an initiative to promote community beekeeping and make London a ‘bee-friendly’ city (page 11).

We also include a factsheet on imidacloprid (page 20). This neonicotinoid is on the world’s pesticide ‘bestseller’ list with sales of around US$1 billion in 2009. Howver, it has been implicated in declines in bees and its use has been restricted in some European countries including France and Germany.

Many commentators have predicted that the temperature rises and changes to weather patterns predicted in the coming decades will result in increased pesticide use. However Lars Neuminster, believes this does not have to be the case. He points out that socio-economic and regulatory factors have a greater impact on pesticide use than climate. He proposes that effective government policies to reduce pesticide use could more than offset increased pressure from climate change (page 16).

Integrated pest management (IPM) is mostly associated with agricultural systems, but on page 6 we report on the adoption of IPM in childcare centres in Illinois.Young children are particularly susceptible to damage from pesticides, so it is refreshing to read of a successful programme to reduce their exposure.

Online subscription Subscribers can now benefit from an online searchable version of Pesticides News (September 1993 to the current issue) with the following username and password (changed twice a year): Username: subscriber Password: carbaryl

Meanwhile pesticide poisonings continue to cause problems in Latin America. On page 14 we report on the outcry from citizens and NGOs that has led governments to take steps to ban some of the most harmful substances.

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ASIA/PACIFIC PAN Asia and the Pacific PO Box 1170 10850 Penang, Malaysia Tel: (60-4) 657 0271 Fax: (60-4) 658 3960 panap@panap.net www.panap.net

EUROPE PAN Europe is facilitated

by PAN UK and PAN Germany www.pan-europe.info elliott@pan-europe.info PAN Germany Nernstweg 32 22765 Hamburg, Germany Tel: (49-40) 399 191022 Fax: (49-40) 390 7520 info@pan-germany.org www.pan-germany.org www.pan-international.org links to all PAN Regional Centres

Who’s who at Pesticide Action Network UK Dr Keith Tyrell Director Nick Mole Policy Officer Dr Roslyn McKendry Editor, Pesticides News Phil Monday Project Officer (Africa Liaison) Dr Stephanie Williamson International Project Officer (Food and Farming) Ruth Beckmann Project Information Officer Liz Kabiro Finance and Admin Manager Geremew Tereda Accounts Articles published in Pesticides News promote health, safety, environmental commitment and alternatives to pesticides as well as debate. The authors’ views are not necessarily those of the Pesticide Action Network UK. Initials at the end of articles refer to staff contributions to Pesticides News.

Abbreviations and acronyms used ACP Advisory Committee on Pesticides CRA Comparative Risk Assessment EA Environment Agency (UK) EC European Commission EPA Environmental Protection Agency (US) EU European Union FAO Food and Agriculture Organisation of the United Nations FFS Farmer Field School FSA Food Standards Agency HSE Health and Safety Executive ILO International Labour Organisation IPM Integrated pest management LD50 lethal dose for 50% of population µg/kg parts per billion MRLs Maximum Residue Limits mg/l parts per million NGO Non government organisation OECD Organisation of Economic Cooperation and Development OP Organophosphate (pesticide) PAN Pesticide Action Network PIC Prior Informed Consent PN Pesticides News UNEP United Nations Environment Programme

© Pesticide Action Network UK

Pesticide Action Network – Regional Centres AFRICA PAN Africa BP 15938, Dakar-FANN Senegal Tel: (221) 33 825 4914 Fax: (221) 33 825 1443 panafrica@pan-afrique.org www.pan-afrique.org

March 2011

LATIN AMERICA RAPAL (PAN Latin America) Coordinadora Regional Av. Providencia No365, depto. No41 Providencia, Santiago de Chile Tel/Fax: (56-2) 341 6742 rapal@rapal.cl www.rap-al.org NORTH AMERICA PAN North America 49 Powell St., 5th Floor San Francisco, CA 94102, US Tel: (1-415) 981 1771 Fax: (1-415) 981 1991 panna@panna.org www.panna.org

Please credit Pesticide Action Network UK when quoting articles ISSN 0967-6597 Printed on recycled paper

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Bees

Pesticides News 91

March 2011

Honey bees – an indicator species in decline The role of neonicotinoid insecticides in the global demise of bee populations remains controversial. Heather Pilatic of PAN North America summarises and tracks the emergence of neonicotinoids in the United States where weakened regulations have fast-tracked them into the marketplace.

Of the 100 species providing 90% of the world’s food, over 70 are bee pollinated, making managed bees the most economically valuable pollinator worldwide1. In the United States alone, honey bee pollination services are estimated at $15-$20 billion per year, and the crop acreage requiring these services stands at an all-time high – even as bee populations are dramatically declining2. While US honey bee populations have been decreasing at a rate of about 1% per year since the 1950s, over the last five years the bee keeping industry has seen unprecedented annual losses each winter. Overwintering losses of 32%, 36%, 29% and 34% for 2006-20073, 2007-20084, 2008-20095, and 2009-20106, respectively, have been reported. These figures are over double the 15% that is considered an acceptable annual loss7.

While previous US bee population declines have been largely attributed to the decreasing popularity of bee keeping, variations in data collection, fluctuations in the price of ‘renting’ pollinators, and changes in import and export regulations, losses since 2006 cannot be attributed to any of these causes8. In fact, US bee keeping is increasing in popularity, and the 2007 US Agricultural Census, reported a dramatic increase in the number of honey producing colonies being managed. It is likely that beekeepers, fearing heavy losses, have begun overwintering more colonies to ensure that they have enough bees to meet the spring pollination demands9.

Annual hive losses of 29-36% cannot be sustained, and many US beekeepers contend that even these figures significantly underestimate the losses they have been taking since 200610. US commercial beekeepers report that their industry is on the verge of collapse, and since wild pollinators are also dying off, farmers who rely on pollination services are increasingly concerned. Although pollination biologists doubt that this will directly result in a food security crisis, it is likely that crop yields will decline, and so, more acres of land – along with increasingly scarce fresh water resources – will need to be put into agricultural production in order to meet demand for food and fibre11.

Equally concerning from a biodiversity and conservation biology point of view is the

fact that honey bees are understood to be a keystone, indicator species. Their decline points to, and will likely precipitate, larger ecosystemic degradation. Scientists from around the world have accordingly been mobilized to investigate the recent drop-off in honey bee populations. In the wake of intensive research and public attention, a global controversy has emerged over the role of pesticides. On one side are the pesticide industry and the scientists funded by them, and on the other are the beekeepers, environmentalists and independent scientists.

Colony collapse disorder Colony Collapse Disorder, or CCD, is the name given to this recent, mysterious decline in honey bee populations. While pollinators have long faced a number of threats, CCD is defined by a sudden and perplexing combination of symptoms: colonies found empty; no sign of the dead bees; evidence that the loss of adult bees from colonies was rapid; and a lack of kleptoparasitism in dead hives despite the presence of surplus honey and pollen stores12.

An individual beekeeper may lose upwards of 90% of their colonies after having been hit with CCD. The prevailing consensus is that CCD is a result of several factors, and that the combined and synergistic effects of co-factors, acting together, is pushing bee colonies over their health threshold, causing sudden collapse. Controversy hinges largely on the relative importance of each co-factor. Key suspects include habitat loss, pathogens (mites, parasites and fungi) and pesticides. In addition, centuries of breeding large numbers of domesticated bees from relatively few queens (in the US, it is estimated that most commercial hives come from as few as 500 breeder queens) has led to diminished genetic variability and with that greater susceptibility to being overcome with disease.

While each of these co-factors has been present for some time, beekeepers point to the relatively recent introduction of systemic neonicotinoid insecticides as a critical, potentiating co-factor. Systemic pesticides are applied at the root (often as seed coating or a soil soak), taken up through the plant’s vascular system and are subsequently found in

The decline of the honey bee may be a sign of wider ecological degradation Photo: Yvan Leduc

pollen, nectar and guttation droplets13.

Neonicotinoid insecticides also accumulate in the environment because they persist in the soil, often for many years. This persistence, coupled with neonicotinoids’ systemic mode of action mean that translocation from treated to untreated plants is an additional concern.

Bees and other pollinators thus face chronic, sub-lethal exposures and many independent scientists posit that this is undermining honey bee health by disrupting their immune system, reproductive system and/or neurobehavioural systems. Science has shown that micro-doses of imidacloprid disrupt bee mobility, orientation, foraging and learning14. Developing science further shows that doses so small as to be virtually undetectable compromise honey bee immunity, allowing various infectious pathogens to invade15. Immunosuppressive effects of these and other pesticides are significant because part of the difficulty in defining the etiology of CCD has consisted in the disorder’s inconsistency: no one infectious pathogen is associated with CCD, nor is the presence of any single pesticide. But higher overall levels of pathogens are linked with the disorder, leading many to suspect that immune system disruption lies at its root.

Neonicotinoids Since their introduction in the 1990s, the use of neonicotinoids has grown dramatically. As insects developed resistance to older classes of pesticides like organophosphates, pyrethroids and carbamates, and regulatory pressures discouraged their use, the neonicotinoids rapidly became the most important new class of synthetic insecticides of the last three decades. In 2008, they accounted for nearly 17% of the global pesticide market16.

Imidacloprid and clothianidin are two of the most common and are known to be highly acutely toxic to bees. Over 120 countries use imidacloprid alone under the Bayer label on more than 140 crop varieties, as well as on termites, flea collars and home garden landscaping. In the US, imidacloprid and clothianidin are used as seed treatments on most conventional corn. Covering over 88 million acres of countryside, corn is by far the most widely planted crop in the US. Because corn is wind pollinated it must produce pollen in

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Bees

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Number of colonies (in millions)

Figure 1. Numbers of managed honey bee colonies in the US, 1940-2009*

Year * Bee population data for this figure were taken from revised USDA NASS archived documents.

NASS surveys were not collected from 1983-1986, so population figures from 1982-1985 are unknown.

National Agricultural Statistics Service (2010) Honey. http://usda.mannlib.cornell.edu/MannUsda/viewDocumentInfo.do?documentID=1191

abundance and bees exploit this rich protein source, bringing in more than their daily need and storing a large surplus for later use. Many commercial honey bees also feed on corn syrup over the winter.

Neonicotinoids are nicotine-like, neurotoxic insecticides that bind to niconitic acetylcholine receptors in insects’ brains. Bees have a particular genetic vulnerability to these and other pesticides: compared to other insects, they have more nicotinic acetylcholine receptors; fewer genes for, and therefore lower capacity for detoxification; and since bees have more learning and memory genes than other insects, they are more vulnerable to disruption of these sophisticated capacities17.

Symptoms of neonicotinoid pesticide poisoning are heavily dependent on the dosage and consistency of that dosage. For example, if a bee comes into direct contact with the pesticide, or a guttation droplet from a plant treated with a pesticide, death can occur within minutes18. If a bee experiences sub-chronic or acute exposure through pesticide-laden pollen or brood-comb, several effects are still seen: impaired communication and hindered navigation ability make it difficult for forager bees to locate nectar sources; decreased longevity and a disruption in the brood cycle forces nurse bees to become field bees before they are fully mature; and micro-doses can result in impaired immune system function.

Effects of other pesticides

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Commercial honey bees face an array of other non-neonicotinoid pesticides19. Beekeepers treat their hive with miticides to fight off pathogens. Acute bee-kills are still reported as growers apply highly bee-toxic pyrethroids and other pesticides on or near bloom as bees are foraging. And bee researchers are increas-

ingly concerned about fungicide exposures, particularly in combination with the rest of the pesticide load carried by bees.

Independent research from both the US and abroad demonstrates that the abundance of pesticides in hives is having a negative impact on colony health. For instance, fungicides were not previously thought to be toxic to bees, but they can interfere with the microbes that break down pollen in the insect’s guts, compromising nutrient absorption and longterm health. One study shows that a common fungicide in combination with imidacloprid multiplies the effect of the latter 1,000-fold20.

The spread of crops genetically engineered (GE) to be herbicide resistant also has potential impacts. These crops have increased the use of broad-spectrum herbicides eliminating many blooming plants from field borders, irrigation ditches, and from crop fields themselves. The reduction in plant diversity and abundance due to the increased use of RoundUp (active ingredient: glyphosate) on GE crops is difficult to quantify. However, reduced food availability may damage honey bee health.

The French example French beekeepers were the first to experience widespread hive collapses in July 1994, days after sunflower crops came into bloom.

These sunflowers had been treated with a new insecticide, Gaucho (active ingredient: imidacloprid). By 1997, half of France’s sunflower seeds were being treated with this product.

Between 1996 and 1999, France’s honey production dropped by more than half, from 110,000 tons to 50,000 tons. The National Union of French Beekeepers (UNAF) reported having lost one-third of their hives when they lobbied the French agriculture ministry

March 2011

in 1997. The following year French researchers conducted a number of studies into imidacloprid’s effects on honey bees. The results of this research, carried out at Boulogne University and the Institut National Recherche Agricole contradicted the safety claims made by imidacloprid’s manufacturer, Bayer Crop Science. The French researchers looked at the effects of low doses of imidacloprid and found that as little as 6 ppb (parts per billion) could impair the foraging behaviour of the bees. Bayer had claimed that 50 100 ppb imidacloprid was safe for bees.

French regulatory authorities opted to continue trials without suspending imidacloprid. The beekeepers (UNAF) and allied organisations protested on the streets in Paris in December 1998. They appealed to the Minister of Agriculture, who could overrule the regulatory authorities. On 22 January 1999 the Minister suspended imidacloprid use on sunflowers until research proved it safe (this suspension was upheld in 2000). This marked the first time the principle of precaution had been used in France in a decision to remove a pesticide from the market. (The precautionary principle states that if there are reasonable scientific grounds for believing that a new product may not be safe, it should not be used until there is convincing evidence that the risks are outweighed by the benefits.)

Imidacloprid has been banned as a sunflower seed dressing in France since 1999 and in 2003 was also banned on sweet corn and canola (oilseed rape). Bayer's application for approval of clothianidin was rejected by French authorities. This ban is still in place and appears to be working: by 2006/07 bee deaths had fallen to less than 10%21.

Clothianidin and other neonicotinoids are banned for use on corn seed in Italy as well.

Bayer’s annual sales of these blockbuster products nevertheless remain brisk. In 2010, global sales of imidacloprid earned Bayer Cropscience $830 million, and clothianidin, $267 million. Imidacloprid is the company’s best-selling product and among the most widely used insecticides in the US.

US emergence While CCD was named and diagnosed in the US in 2006, retrospective investigations showed that symptoms began emerging around 2004. During this window, a number of shifts in US pesticide regulatory policy and application practice were put in place. Under the Bush administration, tolerances (lower limits) for bee-toxic pesticides were arbitrarily increased and the increased use of ‘emergency exemptions’ and ‘conditional registrations’ fast-tracked approval of suspect neonicotinoids like imidacloprid and clothianidin, bringing both to market before safety testing had been completed. The head of the US Environmental Protection Agency (US EPA) under Bush’s presidency, Stephen Johnson, made a concerted and successful effort to speed up the ‘emergency exemption’ approval process beginning around 2002. And ‘conditional registrations’ have long been over-used by the agency.

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Bees The US EPA is supposed to license (‘register’) pesticides only if they meet standards for protection of environment and human health. However, this is frequently breached.

For example, the EPA relies on industry-funded science that is often shielded from peer review and public scrutiny by claims of ‘confidential business information.’ Pesticide law further allows the EPA to effectively waive the scientific review process and grant a ‘conditional’ registration when health and safety data are lacking in the case of a new pesticide, allowing companies to sell a pesticide before the EPA gets safety data. The company is supposed to submit the data by the end of the conditional registration period, but often they do not. Conditional registrations account for 2/3 of current pesticide product registrations.

It is a common practice for the EPA’s Office of Pesticide Programs, to afford rapid market access for products that remain in use for many years before they are tested. Of the 16,000 current product registrations: 11,000 (68%) have been conditionally registered; almost 8,200 products have been conditionally registered (‘CR status’) since 2005; approximately 5,400 products have had CR status since 2000; and over 2,100 products have had CR status since 199022. Imidacloprid and clothianidin both entered the US market as conditional registrations.

Since 2000, virtually all conventional corn seed has been treated with one or more insecticide seed treatments, and from about the mid-2000s, often one to three fungicides.

From about 2004, and roughly coinciding with the emergence of CCD, corn seed companies in the US began marketing seeds treated with a 5-X rate of neonicotinoids (1.25 mg/seed, compared to the traditional 0.25 mg/seed). For example, 80% of the corn seed sold in 2007 by corn seed market-leader Pioneer Hi-Bred was treated with clothianidin plus two fungicides (the systemic azoxystrobin, and fludioxonil). Pioneer first sold seeds treated with the 5-X rate of clothianidin in 200423. Further, beekeepers and scientists reporting their experiences in the field say that spray tank mixes of other pesticides were increasingly combined with fungicides in a deliberate attempt to increase the toxicity of those applications beginning in the early- to mid-2000s. As a matter of practice and policy, the pesticide load faced by US honey bees increased dramatically just as the first symptoms of CCD were setting in.

The clothianidin controversy In December 2010, Pesticide Action Network North America (PANNA) joined US beekeepers and the non-governmental organisation Beyond Pesticides in publicising a leaked EPA memo which revealed that the field study on the basis of which clothianidin was granted conditional registration had been found by the Agency to be scientifically unsound for purposes of registration24. Although the agency originally accepted the field study (conducted by Bayer Crop Science, the registrant) in 2007, subsequent review in the context of registering the pesticide for expanded

Pesticides News 91

uses led the Agency to quietly downgrade the study in a 2 November 2010 memo, which was then passed to beekeeper Tom Theobald by a source within EPA. The Bayer field study is deeply flawed on a number of counts, according to practicing beekeepers: it tests the wrong crop, for an insufficient time period under conditions that allow for no control colonies. (Both control and test colonies had access to treated and untreated crops.) The study’s authors nevertheless concluded that ‘Exposure to clothianidin seed-treated canola has no long-term impact on honey bees.’25 One leading bee scientist said that the Bayer field study was so obviously flawed that he ‘immediately thought it invalid.’ The Canadian regulatory agency with whom US EPA was jointly assessing clothianidin rejected the study upon first review. EPA granted clothianidin full registration in April 2010, and has, in the wake of this controversy, refused to revisit that decision despite the fact that hundreds of thousands of concerned citizens have rallied around US beekeepers in asking EPA to take decisive action.

The ripple effects have gone international.

In January of 2011, the UK House of Commons held a hearing on the contributions of neonicotinoids to pollinator decline, citing the clothianidin controversy in the US as a precipitating occasion. International partners have gathered over a million signatures asking EPA to ban neonicotinoids in order to protect US honey bee populations. PANNA has continued in the intervening months to work with beekeepers and partner organizations in pressing for immediate remedy.

References 1. Kluser S et al., Global Honey Bee Colony Disorder and Other Threats to Insect Pollinators, UNEP Emerging Issues, 2010.

2. Status of Pollinators in North America: A report commissioned by the National Research Council, National Academies Press, 2007.

3. vanEngelsdorp D, Underwood R, Caron D and Hayes Jr J, An estimate of managed colony losses in the winter of 2006-2007: A report commissioned by the Apiary Inspectors of America, American Bee Journal (147) 599-603, 2007 4. vanEngelsdorp D, Hayes Jr J, Underwood R, Caron D and Pettis J, A survey of honey bee colony losses in the US, Fall 2007 to Spring 2008, PLoS ONE 3: e4071, 2008.

Accessible at doi:10.1371/ journal.pone.0004071 5. vanEngelsdorp D, Evans JD, Saegerman C, Mullin C, Haubruge E, Nguyen BK, Frazier M, Frazier J, Cox-Foster D, Chen Y, Underwood R, Tarpy DR, Pettis JS, Colony Collapse Disorder: A descriptive study, PloS ONE 4(8): e6481, 2009.

Accessible at doi:10.1371/journal.pone.0006481 6. vanEngelsdorp D, Hayes Jr J, Underwood RM, Pettis JS, A survey of honey bee colony losses in the United States, Fall 2008 to Spring 2009, Journal of Apicultural Research 49 (1) 7-14, 2010.

Accessible at doi:10.3896/IBRA.1.49.1.03 7.vanEngelsdorp D, Hayes Jr J, Underwood RM, Dewey C, Pettis JS, A survey of honey bee colony losses in the USA, Fall 2009 to Winter 2010, Journal of Apicultural Research 50 (1) 1-10, 2011.

Accessible at doi: 10.3896/IBRA.1.50.1.01 8. vanEngelsdorp D, Hayes Jr J, Underwood RM, Dewey C, Pettis JS, A survey of honey bee colony losses in the USA, Fall 2009 to Winter 2010, Journal of Apicultural Research 50 (1) 1-10, 2011.

Accessible at doi: 10.3896/IBRA.1.50.1.01

March 2011

9. vanEnglesdorp D, Meixner MD, A historical review of managed honey bee populations in Europe and the United States and the factors that may affect them, Journal of Invertebrate Pathology (103) s80-s95, 2010.

10. Kremen C, Honey Bee Pollination Crisis, Commonwealth Club, 13 January, 2009.

Accessible at http://fora.tv/2009/01/13/Claire_Kremen_Honey_Be e_Pollination_Crisis 11. Spivak M, Mader E, Vaughan M, et al., The plight of the bees, Environmental Science and Technology (45) 34-38, 2011.

12. Vanengelsdorp D, Evans JD, Saegerman C, Mullin C, Haubruge E, et al. (2009) Colony Collapse Disorder: A Descriptive Study. PLoS ONE 4(8): e6481. doi:10.1371/journal.pone.0006481 13. Girolami V, Mazzon L, Squartini A, et al., Translocation of neonicotinoid insecticides from coated seeds to seedling guttation drops: a novel way of intoxication for bees, Journal of Economic Entomology 102 (5) 1808-1815, 2009.

14. Kindemba V (2009) The impact of neonicotinoid insecticides on bumblebees, Honey bees and other nontarget invertebrates report, http://www.buglife.org.uk/ Resources/Buglife/Neonicotinoid%20insecticides% 20report.pdf 15. Alaux C, et al., Interactions between Nosema microspores and a neonicotinoid weaken honeybees (Apis mellifera), Environmental Microbiology, 12 (3) 774-782, 2010.

16. Jeshcke P, Nauen R. Neonicotinoids – from zero to hero in insecticide history. Pest Management Science. 68 (11): 1084 - 98, 2008.

17. Jones AK, Raymond-Delpech V, Thany SH, Gauthier M and Sattelle DB. The nicotinic acetylcholine receptor gene family of the honey bee, Apis mellifera. Genome Research 2006, 16(11), 1422-30.

18. Op cit 13 19. Mullin CA, Frazier M, Frazier JL, et al., High levels of Miticides and Agrochemicals in North American Apiaries: Implications for Honey Bee Health, PLoS ONE 5(3) e9754, 2010.

Accessible at doi:10.1371/journal.pone.0009754 20. Iwasa T, Motoyama N, Ambrose JT, Roe RM. (2003) Mechanism for the differential toxicity of neonicotinoid insecticides in the honey bee, Apis mellifera, Crop Prot. 23, 371–378.

21. Soil Association, Bee briefing: The evidence that neonicotinoids are implicated in colony collapse disorder in honey bees, and should be banned in the UK, 2009. Accessible at http://www.soilassociation.org/LinkClick.aspx?fileti cket=RXLEm9WXrHk%3d&tabid=439 22. http://switchboard.nrdc.org/blogs/mwu/NRDC nanosilver CR Docket ID EPA-HQ-OPP-20091012.pdf 23. Benbrook C (2008) Prevention, not profit, should drive pest management, Pesticide News 82.

24. See www.panna.org for supporting documentation and more background.

25. Cutler GC, Scott-Dupree CD. (2007) Exposure to clothianidin seed-treated canola has no long-term impact on honey bees, Journal of Economic Entomology, 100, 765–772.

Heather Pilatic, PhD, Co-Director, Pesticide Action Network North America (PANNA); heather@panna.org This article was written with research assistance from Neva Jacobs, a Sustainable Food Systems programme intern at PANNA

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Integrated pest management

Promoting IPM in Illinois childcare centres Increasingly government and NGO recommendations and legislation are promoting adoption of IPM in schools and childcare facilities to prevent children's exposure to pesticides. However childcare providers often lack the information and confidence needed to implement these changes, despite the fact that young children are at their most vulnerable. A study was carried out to evaluate a successful IPM training programme in the Illinois childcare sector in the United States. Debby Mir, Yoram Finkelstein and Gayle Tulipano report on its successes.

Toxic chemicals are insidious in our modern world and few have been fully evaluated for their ecological or reproductive impacts1. Pesticides and their degradation products are ubiquitous in homes, schools and the environment. Even banned pesticides remain an integral part of our body burden.

In the past ten years there has been increasing attention to pesticide use and children's exposure in schools, but childcare centres are less aware of potential impacts despite the greater vulnerability of younger children. Younger children engage in more hand-to-mouth behaviour making oral contact more likely, they also have high metabolic and respiratory rates, and their immature organs are especially vulnerable. Paradoxically, pesticides including disinfectants are heavily used and even mandated in homes and childcare settings in order to provide a safe and sanitary environment. There is sufficient evidence that pesticide exposure causes illnesses and can irreversibly affect neurological development, yet parents, childcare workers and management are generally poorly informed and untrained in safe pesticide practices.

Federal government legislation, oversight and support for reducing exposure to pesticides are fragmented, precarious and often unfunded. However, many US states have enacted laws promoting safe pest control in and around schools and childcare facilities. Non-governmental organizations (NGOs) and academic institutions have also taken up the challenge, partnering with government agencies to promote integrated pest management (IPM), an approach which focuses on eliminating pests by minimizing their access to food, water, and hiding places.

Pesticide regulation In the US the number of registered pesti-

6 cide active ingredients increased from 875

in 1997 to 1,360 in 2009. Some have been banned or their use restricted when research revealed potential risks to health or the environment2,3,4. However, illegal use of pesticides remains widespread in and around schools5,6.

The EU is taking an aggressive approach towards regulating pesticides based on the Precautionary Principal that requires reproductive and developmental neurotoxicity (DNT) testing to protect children. In contrast, the US EPA Office of Pesticide Programs (OPP) depends primarily on data provided by industry petitioners, mostly carried out on adult animals and often from a single species. This means that, in the US, children are being exposed to toxic pesticides pending proof of health impacts. US manufacturers are not required to conduct pre-market toxicity testing, DNT testing or low level exposure studies in the absence of positive findings in initial tests. Thus manufacturers can avoid even basic testing on immature animals7,8.

Lack of data on children Researchers have an incomplete understanding of the impact of pesticides on children. For ethical and practical reasons most human studies have evaluated farmers, pesticide applicators and other groups occupationally exposed to higher concentrations than the normal population.

Epidemiology studies are often marred by incomplete or inaccurate information on the cause of death and do not distinguish between the effects of active and ‘inert’ ingredients present in a commercial product. Case studies are subject to low participation rates, poor recall bias, and problems of follow-up. In addition, due to the pervasive low level exposure an unexposed control population does not exist9. The relevance of these studies to children is questionable. A common maxim in pedi-

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March 2011

atrics is that children are not small adults.

They may be impacted by pesticide residues from different sources, exposure pathways and concentrations than adults in the same scenario10,11,12.

The extent and severity of acute pesticide poisonings is underestimated. Many poisoning victims never receive medical attention and many illnesses related to pesticide exposure go unreported as such. The World Health Organization estimate one million serious unintentional poisonings annually (hospital data), while the number of less severe or chronic poisonings is much higher13. One US study showed that most pesticide poisoning incidents involve children with a mean age of five and a median age of three years (Minnesota). In an Italian study 48% of those affected were under five years old (Milan)14,15. An additional study noted a significant increase in pesticide-related illnesses in pre-school and school-aged children during 1998200216. No information was found for childcare facilities.

Infants and children are particularly vulnerable to pesticide impacts because of their physiology, metabolism and behaviour. Children are more likely to absorb pesticide residues while playing in- and out-of-doors because of their proportionately larger exposed skin surface and handto-mouth behaviours. Children are closer to the ground, have faster heart and respiration rates, their livers excrete less efficiently and their skin is more permeable than that of adults. They ingest more pesticides residues in food and drink because of their higher caloric intake per kilogramme of body weight, and they consume less varied and more processed foods. Critical neurodevelopmental processes in the human nervous system are especially at risk from toxins during the first three years of life and impaired processes can later lead to diseases with a long latency period17,18,19,20,21.

A comprehensive review of pesticide research presented a range of illnesses and symptoms in children associated with pesticide exposure, and points to links between genetic and environmental factors.

Pesticide exposure contributed to kidney, brain and haematologic tumours, leukaemia, soft tissue sarcoma, as well as developmental and neuropsychological deficits such as developmental delays, learning disabilities, attention deficit hyperactivity disorder (ADHD), autism and behavioural disorders22.

Exposure in childcare centres Multiple risk factors and synergism between them determine the impact of pesticides. Exposure is often underestimated as pesticides which degrade in sunlight may persist indoors and adhere to dust and surfaces23,24,25. One study found associations between early onset asthma and exposure to cockroaches, herbicides and insecticides during the first year of life; and attendance at childcare within the first four months of

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Integrated pest management life26. This highlights the challenges in maintaining a pest-free, safe and sanitary childcare environment.

Approximately seven million US children (35%) under the age of five regularly spend up to ten hours a day in non-relative care27,28. Licensed childcare providers generally meet minimum mandated educational and training requirements, which focus on early childhood development, legal issues and general health, safety and nutrition29,30. A national survey found 63% of childcare centres reported using pesticides while at least one type of pesticide was detected in over 89% of centres tested31.

IPM implementation The US EPA has encouraged but not legislated school IPM since the early 1990's.

Growing public concern over pesticide exposure and recognition that the government is failing to protect children resulted in an uneven state response and increasing pressure for a federal law mandating IPM in all schools by 2015. In the interim, 35 states have implemented programmes for safe pesticide use in and around schools and childcare centres, partnering with government health and education institutions and NGOs focusing on IPM. States vary considerably in their interpretation and implementation of IPM with regard to key components: IPM policy statement, prior and post notification of pesticide use, and pesticide restrictions. Approximately 400 school districts contract out to pest management companies that rely on biological controls32,33.

Unlike state-operated public schools, childcare centres are not centrally regulated and are harder to influence34. A review of 17,000 school districts found that state laws recommending but not mandating IPM were ineffective, with the exception of a pilot project in Indiana34. Surveys assessing the efficacy of mandated IPM in California and Massachusetts (Boston city) childcare centres found widespread violations and lack of supervision or enforcement mechanisms36,37.

Fournier and Johnson worked with government and academic institutes to implement IPM in three Indiana pilot school corporations and four childcare facilities38.

The intensive project included over 300 staff trainings, site inspections, and ongoing communications with directors/principals and service staff. Results indicated that staff reduced clutter, replaced paper containers with plastic, pest-proofed facilities and installed pest sighting logs and monitoring devices.

However, schools had difficulty maintaining staff cooperation especially with reporting requirements. Childcare centres were even more challenged due to high management and staff turnover and a hectic work environment with young children.

Poorly stored arts and crafts materials provided good pest habitats. A common problem was poor coordination with outside

cleaning and pest management contractors unfamiliar with IPM who preferred familiar chemicals and misplaced traps. Without extensive oversight, childcare centres had difficulties maintaining standard operating procedures.

Introducing IPM in Illinois childcare centres The Safer Pest Control Project (SPCP) is an NGO spearheading the drive for safe pesticide legislation for schools and childcare centres to protect the approximately 285,000 children in 12,000 licensed childcare centres in Illinois. Amendments to the Child Care Act of 1969 to address safe pesticide applications were unanimously passed in 2004, but no funding was provided initially for implementing these programmes. In response, SPCP created the Partnership for Childcare IPM and raised private funds to provide the needed outreach and training to move childcare centres from a pesticide to an IPM-based pest management system. Partners in the environmental, health and education fields included the Department of Children and Family Services (DCFS), Department of Public Health (DHS), and the Illinois Network of Child Care Resource and Referral Agencies (R&R) network (Figure 1).

The SPCP Partnership model was based on systemic solutions with goals and actions designed to integrate IPM into the existing structure for childcare centres. The strategy was to provide IPM training to the supervisory bodies (partners) as well as to childcare management and staff in order to provide a legal incentive (licensing) and ongoing monitoring without encurring additional costs39,40. Those trained included

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March 2011

providers of continuing education (R&R), licensing inspectors (DCFS), and health professionals (DPH) in close contact with childcare centres. SPCP created materials which outlined the IPM programme and its training components, and IPM questions were included on licensing forms for childcare centres41. Essentially, SPCP developed a training paradigm for sustainable IPM adoption. In 2004, the US EPA Partnerships to Reduce Pesticide Risk Programs funded the initiative.

The training programme was based on SPCP's experience in promoting IPM in schools and public housing projects. The single session training was advertised on the SPCP website (www.spcp.org) and promoted by the Partners with an emphasis on reaching underserved communities most vulnerable to the health effects of pesticides. No childcare centre was refused training for lack of funds. Partners often provided the venues and training consisted of a PowerPoint presentation addressing pest and pesticide health risks, the new IPM law requirements, and IPM solutions and was followed by a question and answer session. Trainees received an IPM binder and were encouraged to complete a background survey in return for an IPM toolkit with samples and training material.

Evaluating SPCP training In 2007, a pre-tested survey was mailed out to all 3,364 licensed Illinois childcare centres to evaluate pest problems and IPM perceptions and knowledge, with an additional section for SPCP-trained childcare centres to assess the efficacy of the training. Follow-up phone calls were made to all SPCP-trained childcare centres and one in ten of the remaining childcare centres.

Figure 1. SPCP and partners promote IPM in childcare facilities

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Integrated pest management Data was verified by cross-checking with related questions, comments and early training records and data. The response rate was 9.4% (316 childcare centres), including 69 SPCP-trained centres. The data was analyzed for three groups (SPCP trained, aware of IPM from other sources, unaware of IPM), and between pre- and post-training for the SPCP-trained groups.

The survey had 24 questions with sections for additional comments. The questions were designed to characterise the childcare centres, staff knowledge and confidence in IPM, source of knowledge, extent of pest problems, pest control practices, knowledge and confidence in complying with the IPM law, and interest in web-based training. A separate set of questions for SPCP-trained providers assessed IPM action uptake post-training, use of SPCP materials, whom they discussed IPM with (dissemination), and use of IPM at home. As an incentive, participants were entered into a prize draw.

Census data indicated that the trained childcare centres are mostly located in significantly poorer, less educated neighborhoods with a higher percentage of minorities and families living with young children (less than five years old) under the poverty line. While SPCP offered IPM training to all childcare centres, the free training enabled childcare providers in underprivileged neighbourhoods to meet their licensing training requirements; childcare providers in higher socio-economic localities could alternatively hire pest control contractors already meeting the new IPM law requirements. Partners might also have selectively recruited these childcare centres that otherwise would be unlikely to receive IPM training.

Trained childcare centres were significantly more confident in their understanding of IPM and IPM law and appreciated its benefits while 17% of childcare centres had no knowledge of IPM. Most trained childcare centres (70%) agreed on the ease of implementing IPM, approximately half agreed IPM takes little time and one-third that IPM controlled pests or saved money.

Importantly, trained childcare workers were significantly less likely to use pesticide sprays, a cornerstone of IPM training

Pesticides News 91

because of the potential harm to children (Table 1). Furthermore, for trained childcare workers there was a positive relationship between no pesticides spraying and using rodent monitoring traps.

The remaining analysis focused on pest frequency and IPM practices in trained childcare centres pre- and post-training.

Post-training, more childcare workers reported significantly fewer pests, were more confident about understanding IPM law requirements, used IPM at home, and were almost twice as likely to select recommended IPM actions. Some of the recommended new practices were specific to IPM such as ‘assign an IPM coordinator’, and others depended on the severity of existing problems ‘patch holes around pipes’. Over half of trained childcare workers adopted preventative measures to prevent pest entry such as patching holes around pipes, cleaning behind appliances and controlling clutter, while only one-third adopted new management or pesticide control practices (Table 2). Childcare workers interpreted ‘notify parents before spraying’ differently, indicating this was unnecessary as spraying was conducted on weekends or vacations when no children were present.

The questionnaire also looked at items used from SPCP training and with whom trained providers discussed IPM. Trained providers were more likely to use the sticky traps (50%) than IPM notification guidelines (34%), checklist (29%) or pest sighting log (24%) while only six percent used the PowerPoint presentation for internal training. Providers were most likely to discuss IPM with staff (79%), and less with parents (32%), pest management contractors (29%), DCSF (22%) or other providers (21%). Almost all childcare workers were interested in online continued IPM training.

Lessons learned The study confirmed the need for IPM training given the low interest and understanding of the benefits of IPM even in childcare centres claiming IPM knowledge from other sources. Trained providers reported fewer pests compared to childcare centres with no training. The highest participation in SPCP training was from child-

March 2011

care centres in socio-economically disadvantaged neighbourhoods with perhaps more compromised buildings, where IPM can provide more dramatic results in safe pest control. Almost all childcare workers, trained and untrained, expressed high interest and indicated they had the capacity for continued computer-based IPM training.

Training increased providers' confidence and proficiency in implementing IPM and oversight of pest control contractors, though not all practices taught or tools provided were used. In particular, one-third of childcare workers discussed IPM with persons other than staff, changed their pest control measures or used monitoring and reporting documents. The low rate of monitoring agrees with the intensively supported Indiana childcare study suggesting that in the absence of legal oversight, most providers are unlikely to use monitoring data to guide their pest control actions.

However, training was associated with a decrease in pesticide spraying intensity and an increase in the alternative use of baits (safer).

The most common IPM practices adopted were preventive and sanitary, blocking pest entry (patching holes) and removing access to food and shelter (controlling clutter, cleaning hard-to-reach areas). Blocking pest entry was a one-time effort bringing quick results. More stringent cleaning could easily be incorporated into daily routines, either by staff or a cleaning crew, and with supervision was sustainable. Most important was the high motivation, expressed through unsolicited telephone and written comments, to adopt IPM, as a means for providers to protect the health and safety of the children under their care. While this study makes a strong argument for continued IPM training we have to remember why this is important: the 316 childcare centres that responded to the survey are in charge of the care, health and well-being of approximately 27,424 children, in only 2.5% of Illinois childcare centres42.

In 2008, SPCP won an US EPA Environmental Justice Achievement Award for its work to reduce children's exposure to pesticides in childcare centres.

Table 1. IPM perception, knowledge and actions relative to information source Source IPM information IPM perception/actions Confidence - know IPM well Confidence - know IPM law IPM is easy to use IPM controls pests IPM saves money IPM takes little time High use pesticide sprays Use insect/rodent monitoring traps

8

SPCP trained

Number

%

87 88 90 90 90 90 67 90

91 92 71 32 32 47 14 48

IPM information from elsewhere Agree with statement Number % 167 165 170 170 170 170 119 170

49 65 28 14 14 20 47 82

Spearman's rho (1-tailed) * significant at the 0.01 level ** significant at the 0.05 level

No IPM information Number

%

52 53 55 55 55 55 42 55

2 30 0 0 0 2 25 18

Significance

** ** ** ** ** ** ** *

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Table 2. New action taken at childcare centres following IPM training Preventative measures

Pesticide control practices

Programme management

Item

Item

Item

% Uptake

% Uptake

% Uptake

Assigned an IPM coordinator

32

Stopped spraying

27

Patch holes around pipes

60

Use pest sighting logs

32

Use baits instead of sprays

41

Install door sweeps for gaps

30

Use monitor traps

29

Notify parents before spraying

31

Control clutter

60

Create notification procedures

28

Clean behind appliances

56

No change

19

No change

14

Bibliography 1. Doyle J (2004) Trespass Against Us: Dow Chemical and the Toxic Century. Monroe, ME: Common Courage Press/Environmental Health Fund 2. Colborn T and Short P (1999) Pesticide use in the US and policy implications: A focus on herbicides, Toxicology and Industrial Health, 15: 241-276.

3. Pesticide Action Network North America (PANNA) (2009) Pesticide Registration Information for United States, http://www.pesticideinfo.org/Detail_Country.jsp?Co untry=United States [accessed 25 Jan 2011] 4. Weschler CJ (2008) Changes in indoor pollutants since the 1950s, Atmospheric Environment 43: 153–169.

5. Health Hazard Evaluation (HHE) of Andrew Jackson Junior High School (1991) NIOSH, HETA 89-183-2101, http://www.cdc.gov/niosh/hhe/reports/pdfs/19890183-2101.pdf; The Chlordane Pest Problem (n.d.)

Chem-Tox.Com Researching Effects of Chemicals and Pesticides upon Health, http://www.chemtox.com/chlordane/ 6. Green TA and Gouge DH (2009) School IPM 2015: A Strategic Plan for Integrated Pest Management in Schools in the United States, http://www.ipmcenters.org/pmsp/pdf/ USschools PMSP.pdf [accessed 14.04.2010] 7. Gilbert SG. (2005) Ethical, Legal, and Social Issues: Our Children’s Future, NeuroToxicology 26 (2005) 521–530.

8. Lanphear BP, Vorhees CV and Bellinger DC (2005) Protecting Children from Environmental Toxins. PLoS Medicine, http://www.plosmedicine.org/article/info:doi/10.137 1/ journal.pmed.0020061 2(3):203–4 [accessed 14.04.2010].

9. Sanborn M, Cole D, Kerr K, Vakil C, Sanin LH, Bassil K (2004) Pesticides Literature Review, The Ontario College of Family Physicians, http://www.cfpc.ca/local/files/Communications/Curr ent%20Issues/Pesticides/Final%20Paper%2023APR 2004.pdf; 186 p. [accessed 14.04.2010].

10. Op cit 8 11. Op cit 9 12. Garry VF (2004) Pesticides and Children, Toxicology and Applied Pharmacology 198: 152– 163.

13. Jeyaratnam J (1990) Acute pesticide poisoning: a major global health problem. World Health Statistics Quarterly, 43(3):139-44.

14. Olson DK, Sax L, Gunderson P, Sioris L (1991) Pesticide Poisoning Surveillance through Regional Poison Control Centers, Am J Public Health.

81(6):750-3.

15. Davanzo F, Travaglia A, Chiericozzi M, Dimasi V, Sesana F, Faraoni L, et al. (2001) Pesticide

No change

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poisoning referred to the poison center of Milan in 1995–1997. Ann 1st Super Santa: 37:127–31.

16. Alarcon WA, Calvert GM, Blondell JM, Mehler LN, Sievert J, Propeck M, et al. (2005) Acute illnesses associated with pesticide exposure at schools. J Am Med Assoc (JAMA): 294(4):455–65.

17. Chaisson Christine and Gina Solomon (2001) Children's Exposure to Toxic Chemicals – Modeling their World to Quantify the Risks: Session V Summary and Research Needs, Neurotoxicology 22:563-565.

18. Committee on Pesticides in the Diets of Infants and Children (1993) Pesticides in the Diets of Infants and Children. National Research Council, www.nap.edu/catalog.php?record_ id=2126#toc; 1993 [accessed 14.04.2010].

19. Op cit 8 20. Landrigan PJ, Claudio L, Markowitz SB, Berkowitz GS, Brenner BL, Romero H, Wetmur JG, et al. (1999) Pesticides and inner-city children: exposures, risks, and prevention. Environmental Health Perspectives, http://www.ncbi.nlm.nih.gov/ pmc/articles/ PMC1566233/: 107(suppl. 3):431–7 [accessed 14.04.2010].

21. Op cit 12 22. Op cit 9 23. Cohen-Hubal EA, Egeghy PP, Leovic KW, Akland GG. (2006) Measuring potential dermal transfer of a pesticide to children in a childcare center. Environ Health Perspect:114(2):264–9.

24. Fenske RA, Chensheng L, Simcox NJ, Loewenherz C, Touchstone J, Moate TF, et al.

(2000) Strategies for assessing children’s organophosphorus pesticide exposures in agricultural communities. J Expo Anal Environ Epidemiol: 10:662–71.

25. Goldman L, Eskenazi B, Bradman A, Jewell NP. (2004) Risk behaviors for pesticide exposure among pregnant women living in farmworker households in Salinas, California. Am J Ind Med: 45(6):491–9.

26. Salam MT, Li Y, Langholz B, Gilli FD. (2004) Early-life environmental risk factors for asthma: findings from the Children’s Health Study. Environ Health Perspect: 112(6): 760–5.

27. Tulve N, Jones P, Nishioka M, Fortmann R, Croghan C, Zhou JY, et al. (2006) Pesticide measurements from the first national environmental health survey of child care centers using a multiresidue GC/MS analysis method. Environ Sci Technol, 2006; 40:6269–74.

28. Lauglin L (2010) Who's Minding the Kids?

Child Care Arrangements: Spring 2005/Summer 2006, Household Economic Studies, Current Population Reports, U.S. Department of Commerce, Economics and Statistics Administration, U.S. Census Bureau: 70-121, http://www.census.gov/prod/2010pubs/p70-121.pdf 29. USEPA (last updated 4 Dec 2010), Healthy

School Environments, http://www.epa.gov/schools/ [accessed 25 January 2011] 30. Op cit 27 31. Op cit 27 32. Piper C, Owens K. Are schools making the grade? School districts nationwide adopt safer pest management policies. Pesticides and You – Beyond Pesticides/National Coalition Against the Misuse of Pesticides 2002;22(3):11–20.

33. Owens, Kagen (2010) The Schooling of State Pesticide Laws - 2010 Update, Pesticides and You, 29(3): 9-20, http://www.beyondpesticides.org/ schools/publications/Schooling2010.pdf 34. Rosenberg R (2008) Reducing Pesticide Exposure in Illinois Childcare Center, Safer Pest Control Project (internal memo) 35. Op cit 34 36. Bradman A, Dobson CM, Leonard V (2010) Pest Management and Pesticide Use in California Child Care Centers, UC Berkeley School of Public Health, http://apps.cdpr.ca.gov/schoolipm/childcare/pest_m gt_childcare.pdf, [accessed 25 January 2011] 37. Testa, Karen (2004) Audit finds schools ignoring pesticide protection law, Herald-Tribune Southwest Florida, http://www.ipminstitute.org/ Articles/schools_ignore_pesticide_law_article.htm [accessed 25 January 2011] 38. Fournier A, Johnson T. (2003) Implementation of Pilot Integrated Pest Management Programs in Indiana Schools and Child Care Facilities, Executive Summary. IPM School Technical Resource Center, http://extension.entm.purdue.edu/schoolipm/ Update%20May%202003/IDEM%20Pilot%20repor t%20fin.htm [accessed 19.04.2010].

39. US EPA, 2009 40. Mir DF, Finkelstein Y, Tulipano GD. Impact of integrated pest management (IPM) training on reducing pesticide exposure in Illinois childcare centers (2010) Neurotoxicology (5):621-6.

41. Op cit 35 42. Op cit 41

Professor Yoram Finkelstein, MD, PhD, Head, Unit and Service of Neurology and Toxicology, Shaare Zedek Med. Ctr., yoramf@ekmd.huji.ac.il Debby Mir, PhD, Department of Environmental Sciences and Environment and Society Group, Tel Hai Academic College, Upper Galilee 12210, Israel, debbymir@gmail.com Gayle Tulipano, BA, Northeastern Illinois University, Chicago, gayo63@yahoo.com

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Bees

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Bee-toxic pesticides are causing a buzz A group of controversial pesticides are causing a buzz in the UK. In the last month they have made front page news and have been debated by MPs in the Houses of Parliament. They are the neonicotinoids, a group of chemicals that have become controversial due to the increasing evidence demonstrating their impacts on bees.

Vicky Kindemba of Buglife reports.

Neonicotinoids are synthetic chemicals related to nicotine that are highly toxic to insects. Their most common use in the UK is as a coating for agricultural seeds and to treat potting compost. They are also present in a range of products commonly found on supermarket and garden centre shelves.

They spread through the plant and eventually contaminate the nectar and pollen of the flowers. As pollen and nectar provide a food source for bees, this means their food becomes contaminated with neonicotinoids.

A regulatory approvals process assesses the risks of pesticides to non-target insects including honey-bees. In 2009, the nongovernmental organisation Buglife wrote a report on neonicotinoids, The impact of neonicotinoid insecticides on bumblebees, Honey bees and other non-target invertebrates, reviewing the tests carried out on the impacts of imidacloprid (the most commonly used neonicotinoid) on honey bees and on the process required to gain regulatory approval. The report concluded that the methods used to test the effects of imidacloprid on honey bees were inadequate, failing to properly test all parts of the honey bees’ life cycle and also overwintering bees, the

impacts of sub-lethal effects and potential poisoning routes.

While neonicotinoids are unlikely to be the complete explanation for Colony Collapse Disorder in the honey bee, they could be a key contributory factor and may well be part of the reason for widespread declines in wild pollinator populations.

These ongoing declines in the numbers of pollinators are disastrous and could potentially cause crops to fail in the future.

However this issue is not just about honey bees. The majority of our commercial crops are pollinated by wild insects such as bumblebees and hoverflies. Many of these species have suffered massive declines in recent years and may also be at risk from neonicotinoids.

In 2009 Buglife submitted their report to the UK government (Defra) along with four key asks: ● to review the inclusion of imidacloprid, other neonicotinoids and another insecticide fipronil on the positive list of authorised substances in Annex I of Directive 91/414 ● to review existing neonicotinoid and fipronil products authorised for outdoor use in the UK

UN says bee decline is global trend

10

Bee populations are in decline across the globe and without urgent action this trend will continue with devastating consequences for food security according to a new report from the United Nations Environment programme (UNEP)1.

The report identifies a dozen factors ranging from habitat loss to fungal infection that lie behind the crash, but also highlights agricultural intensification and the growing use of systemic insecticides – including the neonicotinoids imidacloprid, clothianidin, and thiamethoxam – as key problems.

It says that more care needs to be taken in the choice, timing and application of insecticides and other chemicals.

While the study focuses on the impacts on bees, UNEP thinks that wild pollinator species are also at risk and are likely to be experiencing similar declines. It points out that while managed hives can be moved out of harm's way, ‘wild populations [of pollinators] are completely vulnerable’. It says

that Bees should be considered an indicator of environmental health and provide an early warning of wider impacts on animal and plant life. It says that measures to boost pollinators should not only improve food security but also help other economically and environmentally-important plants and animals.

Dr Peter Neumann of the Swiss Bee Research Centre, one of the report’s authors said: The transformation of the countryside and rural areas in the past half century or so has triggered a decline in wild-living bees and other pollinators. Society is increasingly investing in 'industrial-scale' hives and managed colonies to make up the shortfall and going so far as to truck bees around to farms and fields in order to maintain our food supplies.

1. Global honey bee colony disorders and other threats to insect pollinators http://www.unep.org/ dewa/Portals/67/pdf/Global_Bee_Colony_Disorder_ and_Threats_insect_pollinators.pdf

Photo: Ben Hamers

until the reviews are completed a precautionary suspension of all existing approvals for products containing neonicotinoids and fipronil where these products have been authorised for outdoor use in the UK ● the development of international methodologies for assessing the effects of systemic pesticides and sub-lethal impacts on invertebrates A year and four months later Buglife has only received a letter outlining a few of the government’s conclusions from their partial assessment in July last year. However, Buglife still has not received a complete response to their report. While the UK government stalls, new evidence of the negative impacts of neonicotinoids continues to mount, for example evidence of their toxicity even at very low levels, evidence that concentrations in Dutch rivers are impacting invertebrates, and evidence that honey bees resistance to disease is weakening. Recent research demonstrated an interaction between honey bee pathogen Nosema and a neonicotinoid chemical1. With the growing scientific evidence so the media interest increases and the concern of the general public becomes stronger. The opposing arguments gradually weaken.

A group of environmental NGOs including Buglife, PAN UK and the Bumblebee Conservation Trust are continuing to put pressure on the government regarding this issue and have initiated a letter-writing campaign to MPs on the Buglife website www.buglife.org.uk under conservation and campaigns. One MP, due to his concern instigated an Early Day Motion regarding neonicotinoids and as result 64 MPs have signed the EDM so far – this is 10% of all MPs. However, more MPs need to show their support to put pressure on the government to ensure that this problem is not forgotten about. Buglife would like everyone to help by getting involved in a letter-writing campaign and to make their local MP aware of neonicotinoids and their impacts on bees. ●

1. Alaux et al. (2010) Interactions between Nosema microspores and a neonicotinoid weaken honeybees (Apis mellifera). Environmental Microbiology. 12 (3). 774-782.

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Bees

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March 2011

The London Mayor’s new campaign for a bee-friendly capital The Mayor of London, Boris Johnson, has turned his attention to protecting the beleaguered honey bee. His new Capital Bee campaign seeks to promote community-run beekeeping and to make London a ‘bee-friendly’ city. Pamela Brunton reports.

In December a group of luminaries gathered on London’s Southbank to shine a light on the darker issues facing bees and other pollinators in these environmentally troubled times. For the first time, academics, scientists, politicians and community groups came together to debate the role of London’s urban beekeepers in securing a brighter future for the capital’s bees.

The London Bee Summit 2010 launched the Capital Bee campaign at the Royal Festival Hall in the week before Christmas. This is a new initiative managed

by Sustain, the alliance for better food and farming. It is part of the existing Capital Growth scheme, which aims to help create 2,012 new community food growing spaces by the end of 2012. Capital Growth is a partnership initiative between London Food Link, the Mayor of London, Boris Johnson and the Big Lottery’s Local Food Fund.

Capital Bee promotes community-run beekeeping in London and campaigns for a bee-friendly city. The project is running a competition to give community groups the hives, special suits and bees, training and support they need to start beekeeping. The project also encourages residents to make London a city in which bees and other pollinators can thrive: it asks people to grow more of their own vegetables, use less pesticide in their gardens, buy organic food,

Tasting London honey at the London Bee Summit

look out for local honey and look after their local parks by signing up to PAN UK’s new London Parks Campaign, to ask councils to reduce the use of pesticides in our shared green spaces.

Cities can be particularly good for bees.

London bees have a wide range of forage, as the gardens and green spaces contain a rich variety of trees and flowers. This, and the slightly milder weather, means that the foraging season is longer and usually more productive than in rural areas. The use of pesticides tends to be more tightly controlled in urban areas which also makes city gardens and green spaces more bee-friendly. But it is not a wholly rosy picture. Wild bees need places to nest and to spend the winter safely. When their natural habitats are lost, for instance if lawns or tarmac replace wild spaces full of plants and shrubs, wild bee populations also decline.

Capital Growth is setting up more food growing spaces, which will provide food for the bees too; meanwhile, the Mayor’s Urban Greening team is creating new habitats across the city to help bees and other pollinators and provide Londoners with healthy parks and green spaces It is testimony to how important beekeeping has become to London residents that the London Bee Summit was heavily over-subscribed with standing room only

Photo: Pamela Brunton

Nick Mole of PAN UK speaks at the London Bee Summit 2010 Photo: Pamela Brunton

on the day, and plenty of people to fill it. It is also telling that the loudest cheers were reserved for two people: PAN UK’s Nick Mole, who gave a rousing speech on the role of pesticides in bee decline, challenging the government’s weak strategy (which had been released the day before the Summit); and Heidi Hermann from the Natural Beekeeping Trust, who suggested that bee decline indicated problems with the way we currently manage both honey bees and their environment.

Meanwhile, environment minister Lord Henley had opened the Summit by excusing himself from the honey tasting, but he got a taste of the public’s frustration as audience members asked why neonicotinoid pesticides have been banned in Germany but not in the UK and why, despite warnings from the British Medical Council, the public will not have to be notified when pesticides are sprayed.

Responsibility was the message of the day. All the speakers were clear; from the British Beekeepers’ Associations Tim Lovett and the London Beekeepers’ Associations vice-chair Karin Courtman, to Dr Outhwaite at Greenwich University and head master Tim Baker at Charlton Manor Primary: we have a shared responsibility to make sure that the city – and the country – is a healthy place for bees. This may mean making sure that beekeeping practice is fit for purpose in the face of contemporary challenges like disease, environmental pollution or insufficient food supply (forage); or ensuring that we grow more bee-friendly plants with less chemicals; or putting aside differences to make sure that support networks for new beekeepers, like the allimportant local associations, can respond to the resurgence of interest in urban beekeeping. Whoever you are, it seems, there is something you can do to help the bees today.

More information about Capital Bee can be found at: www.capitalbee.org The notes and presentations from the London Bee Summit 2010 are available at: www.capitalgrowth.org/summit/

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Biocontrol

Pesticides News 91

Could knotweed’s reign of terror be over?

Introduced into Europe almost 200 years ago, Japanese knotweed has been naturalised since the 1880s. It is highly invasive and difficult to eradicate and is dreaded by horticulturalists and homeowners alike.

Djami Djeddour and Richard Shaw of CABI now report a promising new biocontrol agent. Could this spell the end for Japanese knotweed?

The scourge of Britain’s gardeners, land managers and developers alike, Japanese knotweed (Fallopia japonica), famously dubbed by the press as the ‘concrete-cracking superweed’, has very few admirers.

Native to Eastern Asia, this hardy, herbaceous perennial is thought to have been introduced to the United Kingdom from Japan, by Phillip Von Siebold, in the early nineteenth century and it soon became a highly sought after, fashionable ornamental.

In the UK, its history and fall from grace has been well documented1; By the late 1880’s it had naturalised in the wild and subsequently its expansion has been rapid and widespread and it is now present in most regions of the country2. Japanese knotweed’s invasive success can be attributed in part to its opportunistic nature and physical adaptability; in Japan it is equally at home on lowland riverine gravel, roadside ditches and rich pastureland as on high altitude, inhospitable volcanic lava fields where it is often the primary coloniser. This innate tolerance is exaggerated further in its new environment because the natural predators, competitors, and pathogens which keep it in check in its native range are absent in the area of introduction, affording it a superior competitive advantage over our native species.

Its spread in the UK is all the more impressive when one considers that it has

been achieved by vegetative reproduction; University of Leicester biologists established that the Japanese knotweed introduced to Europe was one of the biggest females in the world – a male-sterile clone which has spread solely through rhizome and stem fragments, usually as a consequence of disturbances like flood events as well as human activity and movement of contaminated soil.

Japanese knotweed is ‘illegal to cause to grow in the wild’ under the 1981 UK Wildlife and Countryside Act, and its disposal is subject to legislation. An official Environment Agency knotweed management best practice guide has been issued in the UK3,4 to help deal with the challenging minefield of available control options. So dreaded is knotweed that some bank policies preclude money lending to house buyers if it has been detected on the land or even within a set distance5,6.

A recent economic review7 of the cost of invasive non native species to the British economy estimated the total annual cost of Japanese knotweed as £179 million whilst the cost of national control, were it to be attempted, is estimated to exceed £1.5 billion8. Its invasiveness also poses significant problems to the rest of Europe and to the United States. Knotweed's impacts are as diverse as the habitats it invades – not only does it pose structural and aesthetic problems

March 2011

in the built environment and affect floral and faunal biodiversity and ecosystem functions by forming dominant monocultures, it can also exacerbate flood risk and undermine riverbank protection in riparian systems. The European Union Water Framework Directive demands that member nations’ waterways achieve ‘good ecological status’ by 2015.

Whilst there will always be some debate over what ‘good’ means and whether invasive non-native species should be included in assessments there is no getting away from the fact that a canal with a 30cm, bank-tobank mat of a floating weed stretching for kilometres cannot attain this benchmark. The arsenal of available chemicals for use near water is limited and the numbers of countries permitting any chemical use near water even smaller. Furthermore, chemical treatments often prove to be ineffective unless treatment is judiciously and laboriously repeated for several years. With conventional methods of control proving costly and largely ineffective and a sway of opinion calling for reduced use of pesticides in the environment, a project to investigate the potential for biological control was initiated in 2003 with funding from a consortium of sponsors.

Predators versus aliens Classical biological control of weeds, or ‘classical biocontrol,’ is a management approach that involves the introduction of specialist plant-feeding insects or fungal pathogens to temper the growth or spread of an invasive plant. It is based on the principle that specialized, co-evolved natural enemies keep a plant species in check in the native range and can be deliberately released in the invasive range, to help restore the balance and reduce the abundance of a weed below an ecological or economic threshold.

Although a relatively new weed management approach for Europe it is one which has been successfully implemented for over a century in over 70 countries, on more than 1,300 occasions, against more than 130 weed targets and has proved a highly efficient and cost-effective approach. For example, an economic review of Australian classical weed biocontrol programmes9 highlights an outstanding benefit/cost ratio of 23:1.

Despite these successes and the absence of any non target effects that had not been predicted by the science, there is an unfortunate but natural tendency for the disastrous and unregulated introductions of the past to be confused with contemporary biocontrol efforts. Today’s programmes are based on extensive and rigorous scientific studies which are vetted by regulatory peer reviews and subject to stringent international protocols and risk assessments before any releases can be authorised.

History of the project

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The insect psyllid, Aphalara itadori, was released into the wild at specific sites.

Photo: CABI

From 2000 to 2007, repeated survey missions to Japan were carried out, concentrating on the Island of Kyushu from 2003 onwards, after it was confirmed by Leicester University that Nagasaki Prefecture was the

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Biocontrol likely origin of the clonal biotype introduced into the UK and Europe. Working in collaboration with Kyushu University, these expeditions, coupled with thorough literature reviews, revealed that over 186 species of phytophagous insects and more than 40 species of fungi were recorded from knotweed in its native range. For an organism even to be considered a potential biocontrol, it must first be proven to be highly hostspecific, but before this laborious process can begin, a test plant list must be drawn up based primarily on the phylogeny of the target plant, representing all native related species, and historically including species which have economic or commercial importance and may be more distantly related. This internationally recognized process for prioritizing test plants, the ‘Centrifugal Phylogenetic System’ of Wapshere10, resulted in the selection of 89 plant species. Those natural enemies which showed the most promise in the field were then subjected to host range testing in a Defra-licensed quarantine facility in the UK11. These studies establish the agent's suitability by demonstrating that it is effective against the target invasive and poses no threat to other non target plants.

After years of testing, during which time many species failed the rigorous testing, two potential agents, one fungus and one insect, were found to be consistently specific to knotweed. With the fungus proving a challenging organism to work with, faster progress was made with the research on the insect psyllid (Aphala itadori) such that in 2009, an application was made to release it into the wild in Great Britain under the Wildlife and Countryside Act 1981, as well as under the Plant Health Regulations through a Pest Risk Analysis. In March 2010, in a huge milestone for biocontrol of weeds in Europe, and following public and scientific consultation periods as well as peer review, approval was granted by the UK governement’s Department for Food, Agricuture and Rural Affairs (Defra) for the psyllid to be released at specially chosen sites. Up until then, no official releases of biocontrol agents against weeds had been made in the EU and as such, the regulatory framework in the UK was far from straightforward and, at times, less than appropriate.

What can we expect?

The psyllid is a sap–sucking insect and it is the nymph stages which cause the most damage to knotweed plants. Impact studies in the laboratory have shown that even in relatively low numbers they are able to stunt growth and reduce photosynthetic ability.

Knotweed’s strength lies in its powerhouse of reserves below ground which it accumulates throughout the season and stores in its extensive rhizome system; by interfering with its nutrient assimilation and storage system, the psyllids should cause the plants to grow less vigorously, lose their competitive edge and be much more susceptible to management.

Pesticides News 91

Following their release in April, a spell of unseasonably cold weather meant that knotweed plants in the release sites were compromised and the release had to be repeated later in the year. Monitoring at the sites indicated that the number of psyllids was low however and consequently additional field-caged studies were carried out to record non-target impact, if any, under conditions with higher psyllid density than was established in the field. Results continued to confirm the insect’s host specificity and the absence of non-target impact, particularly on the native red data book species, Fallopia dumetorum.

The psyllid's progress will continue to be monitored, but as with all biocontrol programmes it will take time before we know if it has established successfully, and the overall effect on the wider knotweed problem could take up to ten years to be become evident. In effect the same rules apply to the psyllid as to all non-native species following introduction into a new area; their establishment and spread will be subject to a number of limiting abiotic and biotic factors or ‘barriers’12. Indeed, many new arrivals fail to establish and it reportedly took eight attempts for the grey squirrel to be established in the UK and we all know how successful and widespread it subsequently became.

A weakness with classical biological control of weeds lies in its unpredictability, not in safety but in efficacy. Biocontrol history is strewn with both promising agents which failed to live up to their potential as well as candidates which exceeded all expectations turning out to be ‘silver bullets’. In the case of the knotweed psyllid the scientific evidence suggests that it will be a safe and effective agent but the proof of the pudding will be in the eating. If the psyllid reduces the impact of knotweed on the UK economy by 1% it will have paid for the research in one year. It is hoped that it will in fact have a much bigger impact and that traditional management techniques will be made more effective against a weaker foe. In the built environment however, where developers need rapid results and eradication is the stated aim rather than the control the psyllid would deliver, it is anticipated that additional control measures will still be needed.

Further releases are planned for 2011 (subject to approval) on a wider scale, so there is a good chance that Japanese knotweed in Britain will eventually lose the upper hand after almost 200 years of dominance13.

Other targets for biocontrol There are plenty of other good targets for classical biocontrol in Europe14 and work is focusing on aquatic and riparian weeds driven by the demands of the EU’s Water Framework Directive and strengthened by the restriction on chemical use on or near water. Targets in the sights of European biocontrollers include the following (their potential biocontrol agents in brackets): Himalayan balsam (rust fungus), Floating

March 2011

pennywort (weevil, fly, rust), Australian swamp stonecrop (weevil), Curly water weed (fly), Floating fairy fern (ordinarily resident weevil) and giant hogweed (different strains of a leafspot fungus).

Using nature to control nature can seem both illogical and frightening to people but the use of natural enemies to control weeds around the world has been shown to be a worthwhile and safe endeavour. This technique provides an alternative and sustainable tool to limit our reliance on chemical and physical control of large scale invasions of environmental weeds and challenges the temptation to just give up in the face of unfavourable odds and limitless expenditure.

References 1. Bailey JP, Conolly AP 2000. Prize-winners to pariahs—a history of Japanese knotweed s.l.

(Polygonaceae) in the British Isles. Watsonia 23, 93–110.

2. Preston CD, Pearman DA, Dines TD, 2002. New Atlas of the British and Irish Flora. Oxford University Press, Oxford.

3. Environment Agency, 2007. Managing Japanese knotweed on development sites, 2007. Available from: http://www.environmentagency.gov.uk/static/documents/Leisure/japnkot_1_ a_1463028.pdf (accessed 12 February, 2011).

4. Welsh Development Agency, 1998. The Eradication of Japanese Knotweed: Model Tender Document. Welsh Development Agency, Cardiff.

5. Daily Telegraph, 13 March, 2010 http://www.telegraph.co.uk/property/propertynews/7 436431/Mortgages-refused-over-invasive-weed.html 6. The Metro, 26 May 2010 http://www.metro.co.uk/news/828020-bank-refusesmortgage-to-landowner-because-of-weeds 7. Williams F, Eschen R, Harris A, Djeddour D, Pratt C, Shaw R, Varia S, Lamontagne-Godwin J, Thomas SE, Murphy ST 2010. The economic cost of invasive non-native species to Great Britain.

CABI report, 198pp.

8. Defra, 2003. Review of non-native species policy—report of the working group.PB8072.

9. Palmer WA, Heard TA, Sheppard AW 2010. A review of Australian classical biological control of weeds programs and research activities over the past 12 years. Biological Control 52, Issue 3, Pages 271287.

10. Wapshere A, 1974. A strategy for evaluating the safety of organisms for biological weed control.

Annals of Applied Biology 77, 201–211.

11. Shaw RH, Bryner S, Tanner R 2009. The life history and host range of the Japanese knotweed psyllid, Aphalara itadori Shinji: Potentially the first classical biological weed control agent for the European Union. Biological Control 49: 105-113.

12. Richardson DM, Pysek P, Rejmánek M, Barbour MG, Panetta FD and West CJ 2000. Naturalization and invasion of alien plants: concepts and definitions. Diversity and Distributions 6, 93-107.

13. The Daily Telegraph, 1 February 2011 http://www.telegraph.co.uk/gardening/8293993/Japa nese-knotweed-might-just-have-met-its-match.html 14. Sheppard AW, Shaw RH and Sforza, R (2006).

Top 20 environmental weeds for classical biological control in Europe: A review of opportunities, regulations and other barriers to adoption. Weed Research 46 (1), 1-25.

Djami Djeddour and Richard Shaw are both Principal Investigators at CABI and have 30 years combined weed biocontrol experience; d.djeddour@cabi.org; r.shaw@cabi.org

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Latin America

Pesticides News 91

Continued poisonings and protest force change in Latin America Over recent months, PAN Latin America Regional Centre has collated reports of numerous poisoning incidents in South America, Central America and the Caribbean. Increasing protests by citizens’ groups, along with concerns from health and environmental officials, is finally leading to changes in government attitudes, with a series of harmful active ingredients to be banned. Stephanie Williamson reports.

Through its active network of member NGOs, community groups and academics in 17 countries, PAN Latin America (RAPAL) performs an invaluable task of disseminating information on pesticide poisoning incidents reported in national media and on research on impacts on health and environment in the region.

Since January 2010, nine mass poisoning cases involving dozens of people and three cases of individual or family fatal poisonings have been reported from ten countries, as summarised in Table 11. The cir-

cumstances of these incidents demonstrate clearly that despite relatively sophisticated legislation on pesticide controls in these countries, their enforcement is woefully neglected. Indirect exposure of workers and residents to pesticide application operations on large farms is a common scenario, often linked to non-compliance with safety rules.

Another common cause is the use of active ingredients known to be harmful, particularly organophosphate and carbamate insecticides. In two major incidents, negligence at pesticide formulation plants

March 2011

led to release of toxic material, affecting the health of local residents. A further two cases involved acute and fatal poisoning of family members who ate contaminated food. Although the main stories to hit the headlines are of mass intoxications, there are likely to be thousands of less visible incidents affecting individuals and communities, on a daily basis across the continent.

In December 2010, the United Nations Food and Agriculture Organisation called on countries in Latin America and the Caribbean to take action to improve controls on pesticides and better protect consumer and farm family health, given the increase in pesticide use in the region.

According to World Health Organisation data, almost three million poisoning cases occur each year in Latin America, especially of women and children in rural areas. In El Salvador, poisoning statistics just published for 2009 indicate an average of four to five people are poisoned each day, with a national total of 1,639 cases and 22 fatalities. Officials described an upward trend in incidence, with most fatalities linked to pesticide application without adequate protection. Chile’s 2009 data show an excess of 700 cases, including three major poisonings of workers. RAPAL Chile estimates an annual figure of 3,000 cases is nearer the truth, as for each reported case, four remain unreported in official figures.

Increasing reliance on pesticides, by farms large and small, is also related to chronic health problems and environmental

Table 1. Serious poisoning incidents reported by RAPAL since January 2010

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Country/Region Date

Incident

Chile, Valparaiso

17 Jan 2011

Residents of Hijuelas suffered poisoning symptoms several hours after pesticides sprayed by helicopter in Chuico Blanco avocado farm. Adults and children affected by eye and throat irritation, vomiting, headache and respiratory difficulties. Local fire service identified methoxyfenozide as one of the compounds applied, although this is not irritant. Authorities withdrew emergency services but others suspect more harmful pesticides were also in the spray mix.

Paraguay, Curuguaty

13 Jan 2011

Ten people, including children, from Yeruti neighbourhood presented symptoms of pesticide inhalation, with abnormal blood tests, and five hospitalised for further examination. Three days earlier a young man was brought dead to hospital, after suffering high fever, stomach pain and vomiting. Affected families blame regular spraying in nearby soya fields. Authorities are investi gating further people affected.

Chile, Linares

7 Jan 2011

Seven women workers suffered nausea, dizziness, vomiting and skin itching while picking cranberries on Alto Los Lomas farm. Health services confirm pesticide intoxication, probably due to spraying of organophosphate insecticide phosmet in a neighbouring field.

Ecuador, Guayas

30 Nov 2010

At least 66 people suffered acute poisoning symptoms after dimethoate insecticide applied in rice in La Victoria parish. Health authorities confirmed 36 people required hospitalisation due to fainting and convulsions and 30 were treated for milder symptoms. Affected witnesses said farm operators ignored their pleas to stop spraying.

Costa Rica, Guanacaste

13 Oct 2010

Over 65 workers from a company growing GM cotton suffered poisoning symptoms the day following spraying on Las Loras farm, Puntarenas. Most presented serious respiratory problems and allergic reactions, high blood pressure, skin rashes and dizziness and were taken to local clinics, with two people needing intensive care. Witnesses described a strong wind blowing dust from the sprayed cotton fields shortly before workers fell ill. Organophosphates were suspected as responsible.

Dominican Republic

Oct 6, Sep 2010 13 year old boy died in hospital due to organophosphate poisoning, after eating possibly contaminated rice pudding. The case is under police investigation. One month earlier, three children died from methomyl poisoning, confirmed by postmortem tests. Police investigating whether food poisoning was accidental or deliberate. Authorities concerned about lack of awareness of pesticide hazards in farming communities.

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Latin America

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March 2011

Colombia, Boyacá

Aug 12 2010

At least 42 children suffered acute inhalation symptoms (nausea, headache, eye irritation and stomach cramps) in Tutazá municipality after a potato field sprayed next to their school.

Health authorities then checked all the pupils and two were hospitalised. Epidemiological investigation confirmed the incident was due to poor spraying practice.

El Salvador

Jul 9 2010

Two children died and five other family members hospitalised after eating maize tortillas made from treated seed destined for planting. Maize seed treated with carbamate insecticide is distributed by government for peasant farmers but not intended for human consumption. Doctors confirmed that this was not the first such case. Relatives recounted how the father told his wife to cook the treated maize seed, as they had nothing else to eat.

Venezuela, Aragua

Jun 14 2010

Mass poisoning incident in Villa Cura causes diarrhoea, vomiting, fainting, allergic swelling in lips and throat and migraine in hundreds of local residents as toxic gas escapes from seed company SEFLOARCA premises. Over 400 are hospitalised in one night and further affected people treated over next few days. Emergency services find methamidophos insecticide was being used by a pesticide formulation unit on the premises, despite registration for this pesticide being withdrawn some months earlier.

Costa Rica, Guanacaste

Jun 10 2010

28 women suffered poisoning on cotton plantation Caballo Blanco shortly after starting work. All were given emergency medical attention for respiratory problems, headache, fainting, and eight were hospitalised. Unofficial sources said malathion and acephate insecticides sprayed on cotton the day before were likely causes.

Argentina, Santa Fe

Apr 30 2010

Truckdriver working for Bunge commodities multinational died after fumigating his truckload of soya before entering port area. Colleagues reported he was ordered to have his cargo treated with gas fumigant aluminium phosphide while he was in the front cab. Minutes later he collapsed with convulsions, dying before the ambulance arrived. Days later another Bunge truck driver was hospitalised with acute poisoning, and drivers complain that they are expected to eat and sleep in their trucks after fumigation.

Mexico, Puebla

Mar 24 2010

Explosion in pesticide factory owned by Dragón Group in Izúcar de Matamoros released 300kg dimethoate insecticide, poisoning 750 inhabitants. Local authorities closed factory but company transported over 3,500 tons of material to its other production sites in Mexico. In 1991 a similar explosion took place in another pesticide factory belonging to the same company, releasing 30,000 litres of toxic material. Dragón Group had previously been accused of violating environmental protection laws by Federal Environment Procurator in 2009.

Chile, O'Higgins

Jan 22 2010

40 seasonal workers tending grapevines in Santa Rosa export estate were poisoned by drift from spray plane. Women workers suffered dizziness, fainting and vomiting and health services confirm they were affected by a fungicide application two hours earlier, although law sets a minimum of four hours re-entry period in treated fields. A second application took place while they were working just 5m away, covering them in a cloud of drift. Chilean Insurance Association claims the women suffered a 'collective attack of anxiety'.

contamination, particularly in large expanses of soya cropping in Paraguay, Argentina and Uruguay [PN81 pp12-15; PN82 pp911; PN85 p5]. A new Brazilian study from Mato Grosso Federal University analysed data from state clinics and found that peo-

ple living close to large acreages growing soya, maize and cotton are three times more likely to suffer pesticide-related ill health, including diarrhoea, fainting, cardiac and respiratory problems, than less-exposed people. The authors warn of a timebomb of

Table 2. Regulatory changes in Latin America Country

Change in pesticide regulation

Brazil

Cancels approval for methamidophos, all uses to be prohibited by Jun 2012. Endosulfan withdrawal announced, with all uses to be phased out

by Jul 2013.

Paraguay

Government regulator announces prohibition decision on endosulfan at RAPAL seminar. Use in horticulture prohibited from Nov 2010 and on arable crops within 2 years.

Ecuador

Prohibits all WHO Class Ia and Ib pesticides from Oct 2010.

Chile

New controls on aerial spraying from May 2011, including 200m mini mum buffer zone and all operations to be notified to authorities in advance.

Argentina

Government decrees in Sep 2010 all printed and audiovisual pesticide advertisements must carry message on danger posed to health and environment. National Ombudsman recommends reclassification of pesticides to include chronic health hazards.

Panama

Prohibits all use and import of carbofuran products from end 2010.

chronic health problems for farm workers, their families and rural residents who take their drinking water from wells and streams contaminated with pesticide residues.

Pesticide use in Brazil has almost doubled in ten years and in 2009 the country became the world’s largest consumer of pesticides, selling over one million tons and ‘beating’ the US annual consumption rate for the first time. Applications in 2009-10 averaged 22.3kg per hectare, with more than half the total volume applied on soya, giving the lie to the pesticide reduction claims of GM soya2.

However, a growing movement in rural communities and supported by activists, academics and some public sector professionals is challenging government complacency, pushing for far stricter controls on pesticide use and policy changes. A National Network of Agrotoxics Victims exists in Paraguay, demanding penalties for farmers that violate pesticide application laws. In Mexico, a Citizens Council was set up in the wake of the explosion at the Matamoros factory and has organised protest marches, while a Committee for the SEFLOARCA Victims in Villa de Cura, Venezuela, took to the streets to demand the government sue the company responsible

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Climate change

Pesticides News 91

Pesticide use and climate change – are they decoupled?

Many commentators speculate that the increasing temperatures and rising CO2 levels associated with climate change will increase pest and disease pressures on crops forcing farmers to use more pesticides.

Lars Neumeister questions this assumption pointing out that there are many factors influencing pesticide use. Drawing on data from Scandinavia he suggests that regulation and policy instruments can have a greater influence on pesticide use than climate change.

Conventional farmers usually apply pesticides against weeds, diseases and pests.

However, the quantities of pesticides used are influenced by many factors: financial resources, expected yields and commodity prices, agrochemical industry marketing, availability, education levels, crop management and, last but not least, the presence of weeds, diseases, pests and their natural enemies. Since the latter are all influenced by weather and by changes in climate1,2, many commentators have speculated on the potential impact of climate change on pesticide use.

A number of authors have constructed models to predict the impact of various factors on pesticide use. For example, Tilman and colleagues foresee a 2.4 to 2.7-fold increase in global pesticide use by 2050 mainly due to population growth and the conversion of natural ecosystems to agriculture3. However, these authors do not consider the effects of climate change.

Chen and McCarl investigated the relationship of temperature, precipitation and pesticide costs for several crops in the United States and concluded that increases in rainfall lead to increases in average pesticide costs for corn, cotton, potatoes, soybeans, and wheat, while hotter weather increases pesticide costs for corn, cotton, potatoes, and soybeans but decreases the cost for wheat. A simulation by the same authors applying a different climate change scenario showed uniform increases in average

pesticide costs for corn, soybeans, cotton, and potatoes and mixed results for wheat4.

However, climate change is only one of many variables affecting pesticide use.

Koleva and Schneider (2009)5 and Koleva and colleagues (2010)6 have constructed a number of models of US agriculture under climatic change. In one of their models both the direct and indirect costs of increased pesticide use driven by climate change were fully internalized via economic instruments such as pesticide taxes. Under this scenario they predicted that pesticide application rates would actually decline despite climate change7.

Figure 1 shows the variation in insecticide sales in Norway during the period from 1991 to 2008. It compares this with the deviation in temperature away from the average annual temperature (calculated by averaging annual temperatures in the years 1961-1990)8,9. The data show that while the temperature in the years from 2000 to 2008 were always higher than in previous decades, insecticide sales dropped sharply.

When calculating the correlation coefficient (r), it turns out that temperature is – against any logic – negatively correlated with insecticides sales (r = -0.49; p<0.05), which implies that increasing temperature reduced insecticide sales. A similar trend can be observed in Denmark10. What happened?

In 1991, Norway introduced a pesticide tax of 2% of the product’s retail price as part of a pesticide reduction programme. In

continued from p15

16

for the methamidophos gas leak. In Uruguay, El Salvador and Argentina NGOs collaborate with local researchers and regional public agencies to collect data on pesticide environmental exposure and damage. Table 2 summarises recent regulatory changes achieved thanks to mounting public pressure in the continent, combined with evidence-based research and advocacy. The RAPAL network continues to lobby for elimination of WHO Class Ia and Ib compounds, endosulfan and paraquat, as

regional priorities, along with a ban on aerial spraying and tougher sanctions on noncompliance with national laws.

References 1. All information compiled from individual news items on PAN Latin America website news section (in Spanish) http://www.rapal.org/index.php?seccion=8&f=news_list.php&offse t=5 2. Brasil, mayor consumidor mundial de agrotoxicos (2011). RAPAL ENLACE magazine, 91 p27

March 2011

1999, the tax model was changed to a riskbased tax such that more toxic pesticides were subject to higher taxes11,12 and pesticide sales dropped considerably. Pesticide sales data may not be the best indicator of pesticide use, but better Norwegian data, such as the treatment frequency are not available13. It is very likely that the large reduction in sales after 2000 translated into a use reduction. Considering that the Norwegian tax rate is bound to the toxicity, a replacement of high dosage-low toxicity insecticides with low dosage-high toxicity insecticide is not a possible explanation for the reduction.

The data from Norway (and Denmark) support the idea that taxes, which can be used as instruments to internalize external costs, override the potential impacts of climate change.

A literature review looking at the ecological effects of climate change on pests, weeds and diseases and natural enemies was inconclusive14. While elevated CO2 enhances the growth of most crops (C3 plants), the protein concentration decreases.

This could mean that herbivores simply consume more plant material to receive the same amount of protein (compensatory feeding). This is frequently observed for some insect species, but not for others. The low quality food (lower protein content) seems to have adverse effects on the fecundity of later generations for some species.

Increased temperature might outweigh some effects of elevated CO2, but experiments combining both parameters have been rare. In addition, natural enemy populations would hypothetically adjust to potentially higher pest populations, but this has not been investigated. Little ecological research has been conducted on weed populations and plant diseases under climate change. There is no evidence that elevated CO2 and elevated (mean) temperature as projected by the Intergovernmental Panel on Climate Change (IPCC) for the next 50 years will cause tremendous new pest problems, especially if farmers respect basic crop management measures.

By contrast the data from Scandinavia suggest that pesticide use is largely decoupled from climate and even from biotic factors. Certainly, there are weeds, pests and diseases, but the rate of pesticide use is more a function of social and economic factors than environmental factors. Otherwise farming without the use of pesticides, as in the past, or on organic farms, would not be possible. Education, agronomy, economy and policy are the main drivers of pesticide use.

Education has been shown to influence pesticide use15. The researchers investigated 61 Integrated Pest Management (IPM) projects in 21 developing countries. In five projects, pesticide use was cut by 93.3% (±6,7%), but yields declined only by 4.2% (±5%). In 47 projects pesticide use declined by 70.8% (±3.9) and yields increased by 41.6% (±10.5). In 10 projects, mainly zerotillage and conservation agriculture pro-

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Climate change

Pesticides News 91

Temperature deviation* (oC)

Sales of insecticide (tonnes)

Figure 1: Insecticide sales and deviation from average temperature of previous 30 years, Norway 1991-2008

*these figures represent the deviation in temperature from the average annual temperature over the previous 30 year period (1961-1990)

jects, pesticide use, as well as yields increased. In those IPM projects, where pesticide use was considerably reduced, pests, weeds and diseases did not simply disappear, but the crops were managed differently making many pesticide applications redundant. It has been shown on a large scale in China that simple agronomic measures such as mixing varieties reduced rice blast severity by 94% and increased yield by 89%16.

Conversion to cost-cutting zero-tillage, which is very popular in the United States, Europe and South America often leads to increasing pesticide use, especially when crop rotation is limited. Weeds in such systems are usually controlled with herbicides, since tillage as a weed control tool is reduced or abandoned. In addition, pressure from certain fungi, such as Fusarium can increase significantly17,18,19. A new type of decoupling of production and nature emerged through the introduction of genetically engineered crops. In particular, growing herbicide-resistant crops such as corn, cotton, soybeans and rape seed has increased the usage and intensity of specific herbicides and led to the development of resistant ‘superweeds’, which are controlled with additional herbicides20,21,22.

Climate change may pose new challenges to agriculture, but will not automatically lead to higher pesticide use. Quite the opposite, the potential to reduce pesticide use has not been fully explored.

References 1. Goudriaan J and Zadoks JC (1995): Global Climate Change: Modelling the potential Responses of Agroecosystems with special reference to Crop Protection.

Environmental Pollution 87: 215-224.

2. Patterson DT, Westbrook JK, Joyce RJV and

Rogasik J (1999): Weeds, Insects, and Diseases.

Climatic Change 43: 711-727.

3. Tilman D, Fargione J, Wolff B, D’Antonio C, Dobson A, Howarth R, Schindler D, Schlesinger WH, Simberloff D and Swackhamer D (2001): Forecasting Agriculturally Driven Global Environmental Change.

Science 292:281–284.

4. Chen CC and McCarl BA (2001): An Investigation of the Relationship between Pesticide Usage and Climate Change. Climatic Change 50:475–48.

5. Koleva NG, Schneider UA (2009): The impact of climate change on the external cost of pesticide applications in US agriculture: International Journal of Agricultural Sustainability7 (3): 203-216.

6. Koleva NG, Schneider UA and Tol RSJ (2010): The impact of weather variability and climate change on pesticides application in the US - An empirical investigation.International Journal of Ecological Economics and Statistics (18): S10.

7. Koleva NG, Schneider UA & McCarl BA (2009): Pesticide externalities from the US agricultural sector – The impact of internalization, reduced pesticide application rates, and climate change. Working Paper FNU177 Research unit Sustainability and Global Change, Hamburg University and Centre for Marine and Atmospheric Science. Hamburg.

8. State of the Environment Norway (2010): Excel table ‘Middeltemperatur_N_og _globalt_2009.xls’ received per e-mail from Gro.Haram@klif.no February 2nd 2010.

9. Mattilsynet (2009): Omsetningsstatistikk for plantevernmidler. Plantevernmiddel-statistikk several files for 1991-2008 at: http://www.mattilsynet.no/planter/ plantevernm idler/st atistikk/ omsetningsstatis tikk_for_plantevernmidler_61713.

10. Annex II in Neumeister L (2010): Climate Change and Crop Protection - Anything can happen. Pesticide Action Network Asia and the Pacific, Penang and Cancun.

11. Sæthre MG, Ørpen HM and Hofsvang T (1999): Action programmes for pesticide risk reduction and pesticide use in different crops in Norway.

CropProtection 18:207-215.

March 2011

12. NFSA (2005): Guidelines for a Banded Pesticide Tax Scheme, Differentiated According to Human Health and Environmental Risks. Norwegian Food Safety Authority (NFSA).

13. NFSA, personal communication 14. Neumeister L (2010): Climate Change and Crop Protection - Anything can happen. Pesticide Action Network Asia and the Pacific, Penang and Cancun.

15. Pretty JN, Noble AD, Bossio D, Dixon J, Hine RH, Penning de Vries FWT, Morison JIKL (2006): Resource-conserving agriculture increases yields in developing countries. Environmental Science and Technology 40 (4):1114-1119.

16. Zhu Y, Chen H, Fan J, Wang Y, Li Y, Chen J, Fan J, Yang S, Hu L, Leungk H, Mewk TW, Tengk PS, Wang Z and Mundt CC (2000): Genetic diversity and disease control in rice. Nature 406:718-722.

17. Johal GS and Huber DM (2009): Glyphosate effects on diseases of plants. European Journal of Agronomy 31:144–152.

18. Fernandez MR, Zentner RP, Basnyat P, Gehl D, Selles F and Huber D (2009): Glyphosate associations with cereal diseases caused by Fusarium spp. in the Canadian Prairies. European Journal of Agronomy 31:133–143.

19. Dill-Macky R and Jones RK (2000): The Effect of Previous Crop Residues and Tillage on Fusarium Head Blight of Wheat. Plant Disease 84 (1):71-76.

20. Johnson WG, Davis VM, Kruger GR and Weller SC (2009): Influence of glyphosate-resistant cropping systems on weed species shifts and glyphosate-resistant weed populations. European Journal of Agronomy 31:162–172.

21. Benbrook C (2009): Impacts of Genetically Engineered Crops on Pesticide Use in the United States: The First Thirteen Years. The Organic Center. http://www.organic-center.org/reportfiles/ 13Years20091126_FullReport.pdf.

22. Op cit 17

Lars Neumeister (MSc. Global Change Management) is an independent pesticide expert; lars.neumeister@pestizidexperte.de

PN89 Factsheet – Which Pesticides are banned in Europe?

CORRECTION. In this factsheet, PAN UK gave the impression that all uses of maleic hydrazide have been banned. In fact, choline, potassium and sodium salts of maleic hydrazide (containing no more than 1 mg/kg of free hydrazine expressed on the basis of the acid equivalent) have been granted EU approval for agricultural use since 2004. We apologise for any confusion caused and have corrected the factsheet accordingly. We have also deleted entries for haloxyfop-P, malathion and methomyl which have regained EU agricultural approval under Directive 91/414 over the last 18 months, although still featuring as banned pesticides on the EU EDEXIM database on which our factsheet is based. The corrected version of the factsheet, with a more detailed explanatory note, is available online to subscribers at http://www.pan-uk.org/pnarchive/pn89september-2010

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Biocides

Pesticides News 91

Still no EU agreement to reduce dependency on biocides EU biocide legislation is currently being revised. However, a coalition of environmental and health NGOs coordinated by PAN Germany have branded the proposed revisions as ‘weak and inadequate to protect people or the environment from potentially toxic biocides’.

They are calling on the European Parliament and the Council of Ministers to introduce requirements to promote non-chemical alternatives to biocides and to substitute toxic biocides with non- or less toxic products. Christian Schweer reports.

Biocides are mainly used for hygiene, disinfection, preservation, urban pest control and antifouling. They are subject to different regulation from the pesticides used to protect crops but often contain the same active substances. Many biocides pose risks to human health and the environment because they are carcinogenic, disrupt hormones, or are toxic to aquatic life or reproduction.

New biocide legislation needed

18

In 1998 the European Union (EU) initiated a process of harmonising biocide regulations across Member States by establishing provisions for an EU-wide authorisation system for biocidal products marketed within Europe (Directive 98/8/EC).

However, the process has several shortcomings. For example, imported biocidal-treated articles are not regulated. In addition, implementation of the regulations has been seriously delayed such that the majority of biocidal products currently on sale still have not been officially reviewed or authorised.

In 2009 the European Commission (EC) proposed a draft review of the Directive to address some of its shortcomings. The European Parliament (EP) added a number of revisions and amendments to the EC’s proposal and passed it to the EU Council of Ministers (Ministerial representatives of all EU Member States) who agreed to it on 20 December 2010.

However, in their current state the proposals focus on simplifying the authorisation system at the cost of protecting human health and the environment. There will be a second reading of the proposal by all three elements of the EU (Parliament, Commission and Council) who will likely reach agreement on it later this year.

In its current format the Environment Ministers have suggested a range of amendments to the current proposals for approval, product authorisation, sale and use.

Approvals The Council reaffirms the current principle that active substances intended for use in biocidal products need to be approved and included in a ‘positive list’ established at EU level. However, the Environment Ministers have put forward several problematic amendments.

Hazardous biocides are not effectively restricted the criteria for approval are not binding: there are provisions for circumstances under which certain criteria can be bypassed ● before the procedure for approval is complete an active substance can be included in the ‘positive list’ if it is expected to meet the conditions for inclusion ● highly hazardous substances such as carcinogenic, endocrine disruptive or persistent, bio-accumulative and toxic (PBT) substances are not explicitly excluded (cut-off) from approval even if sound alternatives are available ● the Environment Ministers reject the EP's and Commission's proposal to replace developmental, immuno-toxic and neurotoxic biocides linked to serious threats for vulnerable groups like children. If the risk of human exposure is deemed neglible such substances may receive approval ● the Council will not ensure that biocides in nano-form will be adequately assessed.

Although the Ministers want to introduce provisions for a separate assessment of such substances they do not specify the methods, timeline or work programme for phasing in these provisions. ●

Product authorisations Under current regulations active ingredients are approved at EU level and individual products subsequently authorised at national level.

The Commission proposes that this remains unchanged. But at the same time Council are

March 2011

proposing several additional options.

EU-wide authorisations that manufacturers should be able to choose between national-level, or EU-level product authorisation ● that there should be mutual (parallel) recognition of authorisation. Under the current system a particular product formulation approved in one country will not necessarily receive approval in a second. Under the new proposals national-level authorisation granted by any Member State would allow the product to be marketed throughout the EU provided the formulation was deemed to be the same.

These proposed modifications would limit the ability of national authorities to prevent certain products from being used in their country and challenge the enforcement of more strict protection standards in their territory. Problematic antibacterial cleaners associated with antimicrobial resistance, or insecticides containing highly hazardous, neurotoxic substances will be able to get an EU-wide authorisation once authorisation in a single Member State has been obtained. Such a permit would be valid for the UK and Germany (and all other Member States) and the relevant national authorities would not be able to refuse or adapt an authorisation, even if the product might pose a serious risk for the citizens and ecosystems of their countries.

Only the EU can decide about restrictions, such as on marketing and areas of application. ●

Derogations The planned criteria for the authorisation system are ambiguous. On the one hand it is encouraging that the Council supports considering non-chemical alternatives, the risks of mixture effects of biocides and risks to vulnerable groups. However, these provisions are weakened or challenged by other amendments. The Council introduces a derogation clause such that there are circumstances under which a product will not have to fulfil all criteria. Hence, a product might be placed on the market even if it poses a risk to drinking water or to vulnerable groups. The quality standards of the Water Framework Directive do not have to be considered for all relevant areas (such as, water bodies which are not used for drinking water extraction) and there is no specific risk assessment for products with nanomaterials. Furthermore, there is no mechanism to promote the development of a pool of non-chemical options in order to reduce dependency on hazardous substances. Such a mechanism is necessary if substitution is to work.

Sale No real transparency for consumers Currently, a warning label is not mandated

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Biocides on all biocidal products. The Council suggests additional label requirements which may include a warning phrase to protect vulnerable groups from adverse effects of hazardous products. The Ministers are also in favour of labelling all biocidal-treated articles to indicate that the relevant article is treated with a biocide and including a web address where further information can be obtained. In addition, articles should only include active substances which are approved for the EU market, another new and essential requirement. On the other hand the proposals do not ensure that the label has to be provided on the package and there is no requirement to indicate if nanomaterials are used in the product.

Use Effective preventive measures will be not ensured The proposals pay very little attention to the use phase which is the time when the public are most likely to come into contact with biocides. PAN would like to see the development of legislation tackling the use phase and providing guidance and regulation on, for example, training requirements for people using professional biocides, information for the public when biocides are being used, information for the public on alternatives to biocides at the point of sale.

PAN calls for alternatives The second reading of the EU biocide regulation will probably start later this year. It is essential that the Council improves its proposal. The European Parliament has submitted several promising amendments to be considered. In particular, the following amendments should be supported: ● human health and the environment shall be protected from the adverse effects of biocides. This shall be the main purpose of the regulation. ● highly hazardous biocides shall be banned and exemptions shall be applied only in exceptional cases (only in the absence of alternatives, cases of real emergency and in the area affected). It is necessary to stipulate substitution plans when granting such cases. ● EU-wide mandatory measures shall be established in order to promote non-chemical preventive measures and alternatives to biocides. It is essential to embed such provisions in the Directive for the sustainable use of pesticides by 2013 at the latest. ● national authorities shall have the competence to refuse any product if it poses a risk for human health and the environment on the member state’s territory.

For more information: www.pan-germany.org/gbr/project_work/ biocide_policy_europe.html christian.schweer@pan-germany.org

Pesticides News 91

March 2011

Beekeepers expose weaknesses in EU pesticide assessments The European Commission relies too heavily on advice from pesticide firms when deciding on how to measure the impacts of pesticides on bees according to a new report1.

Written by the campaigning NGO Corporate Europe Observatory (CEO) and the European Beekeeping Coordination (EBC) – a collection of professional beekeeping organisations – the study complains that pesticide firms are too heavily represented in the advisory bodies that the European Commission relies on to guide its evaluation of pesticides.

The European Commission relies heavily on outside experts when developing new legislation and when deciding how pesticides should be evaluated. In the case of bees, it has turned to the International Commission on Plant Bee Relationships (ICPBR) to help develop guidance on assessing pesticide impacts. This body was set up in the 1950s to share research and information on bees and plants. It is made up of scientists, government officials and increasingly, says CEO, representatives of the pesticide industry. The report points out that pesticide company employees make up six of the 17 members of the three working groups charged with examining the impacts of pesticides on bees, and what is more, that some of these individuals sit on more than one working group. ‘[Pesticide companies] have been invited to shape the guidelines that will be used to assess their own products’, says the report. ‘This is a typical case of the fox guarding the henhouse.’

The beekeepers, for their part, complain that the criteria that the ICPBR have come

up with to evaluate pesticides simply does not stack up. For example, the ICPBR has proposed that a 30% loss of bee brood is ‘normal’, but the beekeepers point out that this scale of loss from a single factor (pesticide use) is not normal. This level of damage, on top of all other factors that cause brood loss, would make beekeeping unsustainable.

The report also highlights that the ICPBR ignores chronic impacts of pesticide exposure. This is a major failing given that much of the concern around the impact of systemic neocotinoid insecticides has focused on the cumulative impacts of repeated small doses. Neither are the beekeepers happy at the way the ICPBR appears to focus on the impact on individual bees rather than bee colonies. They point out that even if the pesticides do not kill the bees, they can interfere with their communication and behaviour and disrupt the colonies making them unviable.

CEO and ECB want to see these shortcomings addressed and going forward want greater involvement by independent experts and stakeholders from outside the pesticide industry in the evaluation of pesticide impacts on bees.

‘Allowing the industry to self-regulate carries a clear risk of profit coming before precaution,’ says the report. ‘It should not be possible for companies to develop the rules made to regulate their own harmful products.’

1. Is the future of bees in the hands of the pesticides lobby? By Corporate Europe Observatory and European Beekeeper Coordination http://www.corporateeurope.org/system/files/files/ar ticle/The+Future+of+Bees+-+ENG.pdf

Ecological agriculture can double food production says UN Small scale farmers can double food production within five to ten years by adopting agroecological methods according to a new report by the UN. The study1, based on a review of scientific literature concludes that agroecology outperforms conventional farming in regions where the poorest people live and where there is greatest stress on food production.

‘Today’s scientific evidence demonstrates that agroecological methods outperform the use of chemical fertilizers in boosting food production where the hungry live – especially in unfavorable environments,’ said Olivier De Schutter, UN Special Rapporteur on the right to food and author of the report. ‘Conventional farming relies on expensive inputs, fuels climate change and is not resilient to climatic shocks. It simply is not the best choice anymore.’

He pointed to studies that have shown that agroecological projects spread over 57 developing countries have delivered an average yield increase of 80%. In Africa, the performance is even more impressive with average yield increases of 117%.

As well as increased yields, agroecology leads to less pesticide use, saving farmers money and offering significant health benefits. The report points to a 92% reduction in insecticide use in rice farming in projects in Indonesia, Vietnam and Bangladesh.

The UN is calling for more support for small farmers’ organisations and greater emphasis on policies to support agricultural research and extension services.

1. Agroecology and the right to food http://www.srfood.org/images/stories/pdf/officialrep orts/20110308_a-hrc-16-49_agroecology_en.pdf

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Factsheet

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Imidacloprid

March 2011

Figure 1. Comparison between imidacloprid and nicotine

Imidacloprid is a systemic insecticide of the neonicotinoid family. It is widely used across the world and has a relatively low human toxicity. However, there is increasing concern over evidence suggesting impacts on bee populations and target pest resistance.

A relatively new insecticide, imidacloprid has been registered for use in the UK since 19931 and in the US since 19942. Launched in 1991, imidacloprid is currently manufactured by Aimco, Bayer CropScience, Hesenta, Jiangsu Yangnong, Sharda and Tide3, but is principally a product of Bayer CropScience who have registered products in over 100 countries (including; Brazil, Canada, Europe, India, Japan, Korea, Mexico and USA)4. Reported as the ‘best selling product’ in Bayer’s 2010 annual press release5, imidacloprid’s immediate future looks bright.

Products In the UK there are currently 35 imidacloprid-containing products registered for either amateur or professional use6. Product names include Admire, Amuse, Baytan, Secure, Bug Free Extra, Chinook, Gaucho, Imidachem, Imidasect, Jive, Merit Turf, Mido, Neptune, Nuprid, Picus, Provado, Raxil secur, Tripod Plus and Valiant7. Outside the UK imidacloprid may be sold under alternative product names: Aeris, CropStar, Imprimo, Monceren G, Montur, Prestige8.

In these products imidacloprid may be mixed in varying concentrations with a range of other active ingredients including thiodicarb (carbamate), tefluthrin (pyrethroid), pencycuron (urea), beta-cyfluthrin (pyrethroid), cyfluthrin (pyrethroid)9. Each will impart its own unique toxicology over and above that of imidacloprid.

Imidacloprid is available in a range of formulations which may contain different ‘inert’ ingredients and suit different application methods10,11. The following ‘inerts’ have been identified from Bayer material safety reports12,13: ● crystalline quartz silica: classed as a known carcinogen to humans by the International Agency for Research on Cancer, causing lung cancer and emphysema (obstructive airway disease) and has caused genetic damage to laboratory test mammals and exposed people ● naphthalene: listed by the National Toxicology Program as having clear evidence of carcinogenic activity (via inhalation)

Application Imidacloprid has become one of the most widely used insecticides14, used for variety of applications to protect crops against biting insects (such as water weevil, termites and Colorado beetle15) and sucking insects (such as hoppers, aphids, thrips and whitefly).

Imidacloprid has three mechanisms of application, which are as a seed coating, a foliar treatment and a soil treatment16. These treatments are extensively used in agriculture, protecting different crops including; citrus, coffee, cotton, fruits, grapes, potatoes, rice, soybeans, sugarcane, tobacco and vegetables17. Products licensed in the UK primarily treat; hops, barley, oats, wheat, oilseed rape and sugar beet18. Imidacloprid

Table 1. Summary of imidacloprid status (2010)26,27

20

Regulation

Rating

PAN Dirty Dozen

None

PAN Bad actor

None

PAN Groundwater Contaminant

Potential*

Prior Informed Consent (PIC)

None

Persistent Organic Pollutants (POP)

None

Long Range Transboundary Air Pollution (LRTAP)

None

World Health Organisation (WHO) (acute toxicity)

II – Moderately hazardous

Carcinogenicity

US EPA Class E (no carcino genicity to humans)24

Endocrine disrupter

None

Toxicity to Bees

Listed by US EPA, UK PSD

Dietary reference dose (RfD)

0.057mg/kg/day25

*listed as potential groundwater contaminant by PAN http://www.pesticideinfo.org/Docs/ ref_regulatoryCA.html#PANGWrating

products are also used domestically as lawn and turf products and ornamental plant treatments.

Mode of action Imidacloprid is an insecticide of the chemical class neonicotinoid, with similarities to and originating from the natural chemical nicotine (Figure 1). Imidacloprid is a synthetic derivative of nicotine, an alkaloid obtained from plants in the Solanaceae family, which mimic acetylcholine binding with its receptor in the post-synaptic membrane at the neuromuscular junction. It is a systemic insecticide that translocates rapidly through plant tissues following application19. Effective from both contact and ingestion, its action both agonises and antagonises nerve impulses causing convulsions then death.

Shown to exhibit selective toxicity, imidacloprid has a greater effect on insects than mammals, which is attributed to differences in the binding affinity or potency at the postsynaptic membrane20.

Regulatory status Imidacloprid is in the EU list of approved pesticide active ingredients, under annex 1 of EU directive 91/41421,22. Imidacloprid containing products are registered for use in the UK23. It is also registered for use in Australia, Cambodia, Cameroon, Canada, Cyprus, Denmark, Finland, Germany, Greece, Hungary, India, Madagascar, Netherlands, New Zealand, Philippines, Portugal, South Africa, Tanzania, United States and Viet Nam.

France In 1999 a temporary suspension was placed on some imidacloprid-containing products in France after strong lobbying action in Paris by the beekeeping trade union (UNAF)28. The suspension (upheld in 2000) specifically stopped the use of ‘Gaucho’ and ‘Regent’ as sunflower seed dressings following a crash in the bee population in 1994, the year that imidacloprid was introduced as an active ingredient in seed dressing29. France’s council of state judged (most recently in 2006) that con-

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Factsheet

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March 2011

Table 2. Precautionary labelling according to the global harmonized system High Toxicity

Moderate toxicity

Acute Oral LD50 Inhalation LC50

Low Toxicity

Very Low toxicity

380-650 mg/kg *

41

69 g/m3 (aerosol)

> 2.0 mg/l (>2.0 mg/l) (dust)

Dermal LD50

> 5323 mg/kg

Primary Eye Irritation

Minimal effects clearing in less than 24 hours

Primary Skin Irritation

effects at >5000 mg/kg, some mild, slight irritation at 72 hours

Precautionary labelling according to the Globally Harmonised System (GHS)42. Data are from INCHEM’s toxicology research on lethal dose 50% (LD50), lethal concentration 50% and external testing on rats43. It is adapted from the National Poison Information Center44 and the US EPA45.

ditions for authorisation had not been fulfilled, compelling suspension until the completion of an EU review30. In 2006 European beekeepers association demanded an EU wide withdrawal of bee toxic pesticides; this request has been ignored.

Germany In May 2008, Germany also temporarily suspended eight seed treatments containing neonicotinoids alongside other seed treatment pesticides after reported colony loss31, only to withdraw the ban on four pesticides in July fearing crop pest infestation32.

European Union In Europe imidacloprid’s application guidelines were amended in 2008 following growing fears of adverse effects on bee populations. In 2010 the European Parliament’s Agricultural Committee adopted a resolution on bee protection, amending the use of four insecticides including imidacloprid. The commission emphasised the prevention of accidental release via ‘dust drift in seed treatments’33.

UK In the UK, imidacloprid is one of the 40 chemicals identified by the Chemicals Regulation Directorate (previously the Pesticides Safety Directorate) as toxic to bees34. The British Crop Production Council suggests restricted use on flowering crops or weeds to prevent contact with foraging bees.

The British Beekeepers Association have indicated that imidacloprid may be a cause of colony collapse, although describe the evidence as ‘anecdotal’35. The Cooperative, as part of its ‘Plan-Bee’ campaign (initiated in 2009), restricted the use of some neonicotinoids on some crops and are investing in honeybee decline research36.

Acute toxicity in mammals Imidacloprid has a lower acute toxicity to mammals than insects (see mode of action), but acute symptoms are still perceptible from tests. In Table 2 the precautionary labelling is shown and annotated with the derived lethal doses from experiments on rats as given by the INCHEM report to World Health Organisation (WHO)37. The key points from

the table show that when imidacloprid is orally ingested it is likely to be harmful to health (WHO rating moderate38). Testing on rats found alterations in behaviour and mobility with trembling and spasms39.

Inhalation of contaminated dust is considered slightly toxic but in aerosol form is reported as highly toxic40.

Other veterinary reports have found hypersensitivity of the skin following dermal application to treat dogs with very high oral exposures often leading to lethargy, vomiting and diarrhoea46.

Acute human poisonings have been reported ● after accidental inhalation to 17.8% imidacloprid a farm worker was described as disorientated, agitated, incoherent, sweating and breathless47 ● after oral ingestion of 9.6% imidacloprid in N-methyl pyrrolide solution a 69 year old woman suffered severe cardiac toxicity and death 12 hours after exposure48

Chronic toxicity in mammals Chronic oral feeding experiments in preliminary testing by Bayer found that feeding rats for three months with imidacloprid would reduce body weight, damage the liver and reduce blood clotting at doses of 61mg/kg/day for males and 420 mg/kg/day for females. These effects are noted as reversible with the exception of minor blood abnormalities. The experiment concluded that the NOAEL (No Observable Adverse Effect Level) was 14 mg/kg/day49. In other experiments chronic feeding of rats caused thyroid abnormalities50. Chronic dermal exposure of rabbits using an imidacloprid paste over 15 days had no effect51. There are no publically available chronic studies of commercial imidacloprid products52.

Reproductive and teratogenic effects In a series of product tests submitted to WHO

by Bayer, imidacloprid was found to effect female rats and embryo development minimally. High doses caused maternal toxicity with reduced embryo development leading to some abnormal bone growth53. Testing on rabbits gave similar results54.

Cancer The International Agency for Research on Cancer (IARC) has not evaluated imidacloprid. The United States Environmental Protection Agency (US EPA) rates it in group E, ‘no evidence of carcinogenicity’ based on studies using rats55.

Ecotoxicology Birds Acute oral toxicity was found to vary between bird species with an LD50 (lethal dose 50%) of 31 mg/kg in Japanese quail and 152 mg/kg in bobwhite quail56. The EPA has noted ‘levels of concern’ being exceeded for songbirds57.

Fish Imidacloprid is acutely toxic to fish at high concentrations. LC50 values for 96 hour exposure for golden orfe (Leucisus idus) is reported as 237mg/l, and for rainbow trout (Oncorhyncus mykiss) as 211 mg/l58.

Aquatic invertebrates have shown signs of risk in a couple of studies59.

Bees Imidacloprid is highly toxic to bees60. Oral LD50 values for bees range from 3.7 to 40.9 ng per bee, and contact toxicity values range form 59.7 to 242.6 ng per bee61. Bees may be exposed to imidacloprid in a number of ways but primarily through consumption of plant products. Imidacloprid is applied to soil or is used to coat seeds. It is taken up by the roots of plants and translocated around the plant’s ending up in the pollen and nectar62. Bees will consequently be exposed when they consume pollen and nectar. They may also be exposed to sprays contaminating the surface of flowers where they are foraging. Separate studies found that imidacloprid, even at very low doses, impairs the bee’s neural capacity, and reduces the bee’s ability to navigate back to the hive63. Small doses may also be able to compromise the honey bee immune system making them more vulnerable to pathogens64.

Honey bee populations are in global decline with colonies crashing at unprecedented rates. It has been hard for researchers to pinpoint the cause of this global phenomenon but exposure to imidacloprid and other neonicotinoids may be one of several contributing factors.

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Factsheet Pesticide resistance Resistance to an active ingredient is of serious concern. Recently, studies of brown plant hoppers, commonly treated on rice crops with imidacloprid, have shown them to develop resistance65. A similar UK experiment found whitefly to have resistance at slightly lower than recommended application concentrations66. Both studies agree on the need for ‘better pesticide management’ to ensure effective use. The University of Missisouri has also demonstrated cross-resistance, where organophosphate-resistant thrips displayed stronger resistance to imidacloprid67.

Environmental fate Environmental fate studies have been carried out by Bayer68. In soil imidacloprid is degraded by bacteria through aerobic metabolites and photo-degradation at the surface with an average first order half-life of between 7-146 days (dependent on organic content). This metabolises imidacloprid to carbon dioxide and non-extractable particles, with all metabolites having a lower toxicity then the Imidacloprid is parent chemical69. hydrophilic and in water is non-persistent, readily degrading by photolysis.

Imidacloprid has ‘very low’ relative vapour pressure, restricting movement and volatilisation. Imidacloprid shows no tendency for bioaccumulation and has a low ‘octanolwater’ coefficient.

22

References 1. Agrow, No.188, July 23 1993, p18.

2. US EPA, pesticides registration review, Imidacloprid summary document, December 2008, http://www.epa.gov/oppsrrd1/registration_review/i midacloprid/index.htm [Accessed 9/01/2011] 3. Tomlin CDS. The Pesticide Manual, A World Compendium, 14th ed.; British Crop Protection Council: Surrey, England, 2006; pp 598-599.

4. Bayer CropScience (2010), Crop protection, insecticides, Imidacloprid, www.bayercropscience. com/bcsweb/cropprotection.nsf/id/imidacloprid.htm ?open&l=EN&ccm=200020010 [Accessed 04/01/2011] 5. Bayer CropScience Key Facts & Figures (2010), p17, www.bayercropscience.com/bcsweb/ cropprotection.nsf/id/EN_Key_Facts_Figures_2010/ $file/BCS_Facts-and-Figures_2009-2010.pdf [Accessed 18/12/2010] 6. Chemicals Regulation Directorate (CRD) (2011), Directorate of the Health and Safety Executive (HSE), www.pesticides.gov.uk/databases.asp [Accessed 05/01/2011] 7. CRD, Op cit 6 8. Bayer, Op cit 5 9. Bayer, Op cit 4 10. EPA, Op cit 2 11. Bayer, Op cit 4 12. Caroline Cox (2001) Imidacloprid, Journal of Pesticide Reform, National Coalition for Alternatives to Pesticides, www.pesticide.org/getthe-facts/pesticide-factsheets [Accessed 04/01/2011] 13. Cox, Op Cit 12 14. Tomlin, Op cit 3 15. Tomlin, Op cit 3 16. Bayer, Op cit 4 17. Bayer, Op cit 4 18. CRD, Op cit 6 19. Lainsbury MA (2010) The UK Pesticide Guide 2010, Britist Crop Protection Council: Surrey,

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England, pp387 - 388 20. Chao SL and Casida JE (1997) Interaction of imidacloprid metabolites and analogs with the nicotinic acetylcholine receptor of mouse brain in relation to toxicity. Pest. Biochem. Physiol., 58, 77–88.

21. Tomlin, Op Cit 3 22. European Commission (2008) Final, Review report for the active substance Imidacloprid 26/09/08, Directorate E.3 Chemical, Contaminants, Pesticides SANCO/108/08 – rev1 http://ec.europa.eu/food/plant/protection/evaluation/ existactive/list-imidacloprid_en.pdf [accessed 05/02/10] 23. CRD, Op cit 6 24. EPA, Op cit 2 25. Imidacloprid (2005) pesticide tolerances for Emergency Exemptions. Fed. Regist. Oct 12, 2005, 70 9195), 59268-59276 26. PAN UK, List of Lists – 3rd edition 2009, PAN UK briefing paper 27. PAN North America, pesticide database: Imidacloprid (2010) www.pesticideinfo.org/Detail_Chemical.jsp?Rec_Id =PC35730#ChemID [Accessed 14/01/2011] 28. PAN UK, June 2007, Pesticide News 76, Elliot Cannell, ‘France withdraws gaucho’, pp4-5 29. White G (2011) Concern over Imidacloprid Systemic Insecticide used on Oilseed Rape in UK, British Beekeepers Association reviewed 2011http://www.britishbee.org.uk/articles/imidaclop rid.php [Accessed 05/02/2011] 30. PAN UK, Op cit 28 31. PAN UK, June 2008, Pesticide News 80, Germany bans bee-killing pesticides, p11 32. Agrow (2008) Germany lifts suspension of four STs for use on oilseed rape, Agrow world protection news No 547, 11/07/2008, p13 33. Jackie Bird (2010) EU amends insecticide use to protect bees, Agrow world crop protection news No 588, 26/03/2010, p12 34. UK PSD (2008) Assessment of the impact of crop protection in the UK of the ‘cut off’ criteria and substitution in the proposed Regulation of the European Parliament and the Council concerning the placement of plant protection products on the market, the UK Pesticides Saftey Directorate (PSD), http://www.pesticides.gov.uk/ uploadedfiles/Web_Assets/PSD/Imapct_report_(Ma y_2008).pdf [Accessed 05/02/2011] 35. Bird, Op cit 33 36. Agrow (2009) BCPC criticises Co-op block on neonicotinoids, Agrow world crop protection news, No 561, 13/02/2009, p10 37. Reported in Gervais JA, Luukinen B, Buhl K, Stone D. (2010) Imidacloprid Technical Fact Sheet; National pesticide Information Centre, Oregon State University Extension services. http://npic.orst.edu/factsheets/imidacloprid.pdf [Accessed 20/01/2011] 38. PAN UK, Op cit 26 39. JMPR (2001) Pesticides and Biocides Division, Federal Institute for Health Protection of Consumers and Veterinary Medicine, Berlin, Germany, INCHEM,www.inchem.org/ documents/jmpr/jmpmono/2001pr07.htm#2.2.1 [Accessed 20/01/2011] 40. Label Review Manual (2007) U.S. Environmental protection Agency, Office of prevention, Pesticides and Toxic Substances, Office of Pesticide programs. www.epa.gov/oppfead1/ labeling/lrm/chap-07.pdf [Accessed 20/01/2011] 41. Tomlin, Op cit 3 42. Globally Harmonized System (GHS) for Classification and Labeling of Chemicals (2010), US Environmental protection agency, pesticide: international activities www.epa.gov/oppfead1/ international/globalharmon.htm [Accessed 20/01/2011] 43. JMPR, Op cit 39 44. Gervais et al, Op cit 37

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45. LRM, Op cit 40 46. Wismer T (2004) Novel Insecticides, Clinical Veterinary Toxicology; Plumlee, K. H, Ed; Mosby: St. Louis, MO pp 184-185 47. Agarwai R (2008) Severe neuropsychiatric manifestations and Rhabdomyolysisin patient with imidacloprid poisoning. Am. J. Emerg. Med. 25, 844-856 48. Huang N, Lin S, Chou C, Hung Y, Chung H and Huang S (2006) Fatal ventricular fibrillation in a patient with Imidacloprid poisoning. Am. J. Emerg. Med. 24, 844-856 49. Gervais, Op cit 37 50. Cox, Op cit 12 51. Bayer, Op cit 3 52. Cox, Op cit 12 53. Becker H, Vogel W and Terrier C (1988) Embryotoxicology study (including teratogenicity) with NTN 33893 technical in rats. Unpublished Report no. R4582, submitted to WHO by Bayer AG, Mannheim, Germany. INCHEM Toxicological Evaluations: Imidacloprid; International Programme on Chemical Safety, World Health Organisation: Geneva, Switzerland 54. Op cit 53 55. EPA, Op cit 2 56. Tomlin, Op cit 3 57. US EPA (1993) Ecological effects preliminary review. NTN No. 420553-09. Washington, D.C. Mar 27 58. Tomlin, Op cit 3 59. Cox, Op cit 12 60. US EPA Op cit 2 61. Schmuck R, Schoning R, Stork A and Schramel O. Risk posed to honeybees (Apis mellifera L, Hymenoptera) by an imidacloprid seed dressing of sunflowers. Pest Management Science (2001) 57, 225-238.

62. Tomlin, Op cit 3 63. Kindemba V (2009) The impact of neonicotinoid insecticides on bumblebees, Honey bees and other nontarget invertebrates report, http://www.buglife.org.uk/ Resources/Buglife/Neonicotinoid%20insecticides% 20report.pdf 64. Alaux C, et al., Interactions between Nosema microspores and a neonicotinoid weaken honeybees (Apis mellifera), Environmental Microbiology, 12 (3) 774-782, 2010.

65. Wang Y, Chen J, Zhu YC, Ma C, Huang Y and Shen J (2008) Susceptibility to neonicotinoids and risk of resistance development in the brown planthopper, Nilaparvatalugens(Homoptera: Delphacidae) Pest Management Science 64:1278–1284 (2008) 66. Gorman K, Devine G, Bennison J, Coussons P, Punchard N and Denholm I (2007) Report of resistance to the neonicotinoidinsecticide imidacloprid in Trialeurodesvaporariorum (Hemiptera: Aleyrodidae) 67. Zhao GY, Liu W, Brown JM and Knowles CO (1995) Insecticide Resistance in Field and Laboratory Strains of Western Flower Thrips (Thysanoptera: Thripidae) Journal of Economic Entomology, Volume 88, Number 5, October 1995 , pp1164-1170(7) 68. Bayer CropScience (2002) Pflanzenschutz,(environmental fate) special edition vol. 55 www.bayercropscience.com/bcsweb/ cropprotection.nsf/id/1stArticle2002_EN?open&l=E N&ccm=300030020 [Accessed 19/01/2011] 69. Liu W, Zheng W, Ma Y and Liu KK. (2006) Sorption and degredation of Imidacloprid in soil and water. Journal of Environmental Science and Health, Part B, 41(5) pp623-634.

This factsheet was prepared by Alastair Relf, an intern at PAN UK

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Resources ENDURE network for diversifying crop protection This European research programme has compiled a wealth of information on pest management methods, IPM and methods for reducing pesticide use. Drawing on expertise from 17 research institutes in northern, central and eastern and Mediterranean Europe, ENDURE produced a series of case studies on IPM methods available or under field testing. It also provided estimates of current adoption and identified factors driving or hindering their wider use. The grapevine case study, for example, covers: reducing herbicide use with cover cropping and tillage; Decision Support Systems; mating disruption for control of grape berry moths; use of microbial biocontrol agents; and new resistant grape varieties. Other studies look at: potato diseases; Integrated Weed Management; maize-based rotations; tomato (whitefly); wheat diseases; winter-based arable rotations; and bananas (Canaries and Caribbean). Broader studies describe IPM training and the role of consumer demands and supermarkets in stimulating IPM. These studies can be downloaded from http://www.endure-network.eu/endure_ publications/endure_publications2 The ENDURE Information Centre is a central point of reference for extending expert knowledge, recommendations and advice, based on several hundred research and advisory publications on all aspects of IPM use across Europe. You can search via a crop/pest or disease/country/control method combination to find validated IPM measures including prevention, chemical pest and disease control as well as non-chemical alternatives. The practicability of each method is classed as Experimental or Ready to Use. The database contains 322 records on nonchemical alternatives, for example, biofumigation for controlling root diseases on carrot.

English summaries are provided with links to the original source document at http://www. endureinformationcentre.eu/ The ENDURE Network of Advisers (ENA) is a forum for sharing knowledge across Europe. It is free of charge and open to any farm advisers, state or private, working with farmers on a daily basis and membership provides the opportunity to share IPM experiences and help more growers in Europe to practically implement IPM-related recommendations. ENA members will also be able to test new recommendations under ‘real life’ conditions. http://www.endure-network.eu/

Systemic pesticides: a disaster in the making Many possible causes of the global decline in bee populations have been posited, among them pesticides, and the systemic neonicotinoid pesticides in particular. Henk Tennekes' book brings together in a new

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way several strands of evidence about the potential harms of these insecticides, and joins the voices of campaigning organisations in calling for a ban. He also makes a compelling case for urgent action to halt declines in insect and bird populations.

However, overall the book lacks coherence, and, with a disappointingly brief discussion, it is not clear how Tennekes arrives at his exclusive focus on neonicotinoids as the cause of these declines. With its curious juxtaposition of scientific report and vivid landscape paintings, the question also arises of who the book is for.

The book is essentially in two parts. The first sets out the case against imidacloprid and other neonicotinoid pesticides. A toxicologist, Tennekes argues that chronic, low level exposure to imidacloprid is more significant than previously thought. He proposes that imidacloprid obeys ‘Haber's rule’, that is, the product of concentration and exposure time produces a constant toxic effect. This kind of relationship is seen in some carcinogens, which bind irreversibly to a cell receptor, so that the effects are cumulative. Tennekes states that the mode of action of imidacloprid involves ‘virtually irreversible’ binding to receptors in the nervous system of insects, and therefore toxicity is cumulative in the same way.

Tennekes’ lengthy exposition of Haber's rule is fairly impenetrable to the average lay reader, and (to this non-chemist, non-mathematician reviewer) seems not to be essential to the take-home message, which is that where a chemical shows this kind of doseresponse relationship, given a long enough time period, even tiny doses may ultimately be harmful (Tennekes says that there may be no safe dose). ‘Thus, low environmental concentrations of these insecticides (that may not be acutely toxic) could be detrimental to many aquatic and terrestrial invertebrate species in the long term, in particular because [neonicotinoids] are persistent in soil and stable to breakdown by water and their toxicity to invertebrates may be reinforced by exposure time.’

The question is whether this rule applies to imidacloprid. There is some evidence that it does: the author cites one study showing such a relationship for imidacloprid toxicity to midges, and another, looking at aquatic invertebrates, yielding very similar, though not identical, relationships.

Tennekes also compiles several other strands of evidence on imidacloprid. It is widely used and persistent in soil and water, with high leaching potential. He provides data showing that imidacloprid contamination of surface waters in Holland in some areas exceeds acceptable limits to a staggering degree, in the worst case by a factor of several thousand. It would be interesting to know more about what is going on here: there is clearly a serious environmental problem which needs addressing urgently.

There is also evidence that low concentrations of imidacloprid may have harmful sub-lethal effects, affecting bees’ foraging and learning behaviour. Taken altogether,

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these points build a case that imidacloprid is at the very least a serious cause for concern; at worst, it could indeed be a ‘disaster in the making’. Some of Tennekes’ points have been disputed elsewhere; he makes no mention of these controversies here1.

The second, longer part of the book surveys changes in insect-eating bird populations in different habitats in Holland, and also (in less detail) in Britain, France, Germany and Switzerland. There is an impressive array of data, though it is not made clear how the data has been selected.

Some of the detail on bird feeding and reproductive habits brings to life what is generally a very dense read; some photos of the species mentioned would have been a nice addition. With a few exceptions this part of the book makes gloomy reading. It is clear that insect and bird populations are dwindling rapidly, though this is hardly news.

Tennekes concludes: ‘Ground and surface water contamination with persistent insecticides that cause irreversible and cumulative damage to…insects must lead to an environmental catastrophe. The data presented here show that it is actually taking place before our eyes, and that it must be stopped.’

Tennekes raises valid concerns, adding to the debate on neonicotinoids. In particular the data on contamination in Dutch surface water is very concerning and raises questions over why this is happening and how widespread a problem it is. However, Tennekes does not sufficiently make the connection between the first and second parts of the book. The data are baldly presented with very little discussion. In a few instances there is circumstantial evidence of an association with neonicotinoid use, but multiple factors could be involved in the declines (and in a few cases, increases) in bird populations. Some are given a brief mention: habitat loss in urban areas; changes in agricultural practices, including more intensive use of herbicides as well as insecticides; industrial pollutants. In many cases the declines predate the introduction of neonicotinoids in 1991. Whilst this does not, of course, preclude a role for neonicotinoids, it is clear that other factors are at work.

Indeed, in the current focus on neonicotinoids amongst campaigning organisations, it is important not to lose sight of other issues.

The data he presents from France and Germany, both of which have restricted the use of imidacloprid, does not suggest that wildlife populations have begun to recover.

Tennekes' failure to engage with these wider issues is curious, and weakens his case, as it could be argued that neonicotinoid pesticides play only a minor role.

1. Maus C, Nauen R. Response to the publication: Tennekes HA (2010): The significance of the Druckrey-Küpfmüller equation for risk assessment – The toxicity of neonicotinoid insecticides to arthropods is reinforced by exposure time.

Toxicology (2010), doi:10.1016/j.tox.2010.11.014 Henk Tennekes, The systemic insecticides: a disaster in the making, (2010) 72pp, ebook 9.95 euros; hardcover 29.95 euros http://www.disasterinthemaking.com/

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Pesticide Action Network UK PAN UK – Making a difference Pesticide Action Network UK works to eliminate the dangers of toxic pesticides, our exposure to them, and their presence in the environment where we live and work. Nationally and globally we promote safer alternatives, the production of healthy food and sustainable farming.

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