The Effects of Air Pollution on Cardiovascular Health

Alex Behram

Abstract: Research indicates that that air pollution can have adverse effects on cardiovascular health. This paper evaluates the different types of air pollutants: gaseous pollutants, particulate matter, and metals, their sources, and the potential health hazards they pose to our cardiovascular health.

Introduction: Air pollution comes from a variety of different sources, including a mix of natural and human-generated emissions. Most of the air pollution we face comes from either vehicular sources, such as cars, planes, and trains, or stationary sources, such as power plants and other industrial facilities. Other sources of pollution, such as those created by agricultural work or those created by natural events like wildfires, are much less significant and do not create ongoing air pollution problems.1 Air Pollution is made up of various primary pollutants, such as nitrogen oxides (NOx), sulfur dioxide (SO2), and carbon monoxide (CO), as well as secondary pollutants such as ozone (O3). Air pollution also contains volatile and semivolatile organic aerosol compounds such as benzene, toluene, xylene, 1,3-butadiene, and polycyclic aromatic hydrocarbons.iii Particulate matter (PM) in the air is categorized into 3 categories: coarse particles (aerodynamic-mass median diameter, <10 μm [PM10]), fine particles (<2.5 μm [PM2.5]), and ultrafine particles (<0.1 μm [PM0.1]). iii Additionally, toxic metals such as lead, mercury, arsenic, and cadmium are also emitted into the air in industrial settings.iii CVD is the leading cause of death globally, accounting for upwards of 30% of all global deaths each year.2 Recent studies have suggested that gaseous pollutants, PM, and metals are all dangerous parts of air pollution which can have detrimental health risks, most notably an increased risk for Cardiovascular Disease (CVD).3 A study done by the Global Burden of Disease found that pollution was responsible for 9 million deaths in 2019, with 61.9% of those deaths caused by CVD. The two primary types of CVD associated with pollution are ischemic heart disease, which contributed to 31.7% of the CVD deaths related to pollution in 2019, and stroke, which contributed to 27.7% of the deaths related to pollution in 2019.iii Although studies have verified the effects of these compounds on increasing the risk of CVD, more research must be done to understand the mechanisms by which these compounds cause an increased risk of CVD.

Gaseous Pollutants: Gaseous pollutants commonly come from mobile and industrial sources. Primary gaseous pollutants, such as NOx, SO2, and CO are toxic on their own; however, they are also used in the formation of O3. The primary gaseous pollutants undergo a photochemical reaction with sunlight, volatile organic compounds, and other gaseous precursors to form ozone (See Figure 1).4

Figure 1: This graphic depicts the photochemical reaction in the atmosphere with primary gaseous pollutants and volatile organic compounds to form ozone.5

These primary gaseous pollutants, as well as ozone, have been linked to cardiovascular toxicity.vi Analyses have found a strong relationship between short-term exposure to ozone and acute myocardial infarction (MI, known colloquially as a heart attack). vi Individual gaseous pollutants affect cardiovascular tissues differently. Exposure to ozone impairs pulmonary gas exchange and leads to increasing myocardial (heart) work, which leads to an increased risk of MI. Conversely, SO2 exposure reduces cardiac vagal control, which increases susceptibility to ventricular arrhythmias.vi Although studies have established the effects of exposure to these gaseous pollutants, it remains unclear what mechanisms cause the exposure to these pollutants to be so detrimental to cardiovascular health.6

Particulate Matter: PM varies in its chemical composition depending on its source and location. PM is most concerning in urban and industrial area. The main source of PM in these places is combustion, whether it be from mobile vehicles or industrial facilities. Combustion-derived PM contains elemental and organic carbon, as well as mineral dusts, sea salt, ammonium, nitrates, and sulfates. Moreover, much of the PM formed in these industrial and urban areas come from vehicular exhaust, and much of the PM from these sources, especially those from diesel vehicles, are PM0.1, the smallest form thereof. These particles’ chemical composition, high surface area to mass ratio, and ability to penetrate deeply into the body suggest that these particles gave greater toxicity when compared to other sizes and sources of PM.7 A study done by Peters et al in the greater Boston area found a positive correlation between an exposure to an elevated concentration of PM2.5 and acute MI onset, highlighting its toxic effect to cardiovascular health. They discovered that an hourly change of 25 μg/m3 in PM2.5 concentration led to an increase in the odds ratio of MI just hours after exposure to it (See Figure 2).8

Figure 2: This graph shows the change in odds of experiencing acute MI over the course of hours after exposure to an elevated concentration of PM2.5. It depicts a positive association between exposure to an increased concentration of PM2.5 and MI risk. vii

Although a positive correlation between increased PM exposure and CVD risk has been proven, it remains unclear what mechanism causes PM exposure to lead to CVD risk. A study done by O’Toole et al found that exposure to elevated levels of PM2.5 depletes circulating endothelial progenitor cells (EPCs) while increasing the platelet activation and plasma levels of highdensity lipoproteins.ix These changes in the circulatory system are linked to an increased risk of CVD, specifically risks to vascular dysfunction and endothelial injury, which are strongly linked to an effect of elevated PM exposure. However, they discovered that the decrease in EPC levels can be reversed, with the associated vascular injuries thus also reversible. Despite this, they concluded that the depletion of EPCs is likely correlated with other changes in lipids and protein levels in the cardiovascular system, which leads to vascular injury induced by PM. More research must be done to understand the mechanisms behind elevated PM exposure and an increase in CVD risk.9

Metals: Heavy metals such as cadmium, lead, and mercury are air pollutants commonly emitted as a result of industrial activity. They eventually make their way into soil and bodies of water, where they accumulate and make their way into the food-chain.10 Exposure to these metals, either in the air or through the food chain (as a result of air pollution), can cause severe risk of CVD. Cadmium is typically found in contaminated soils and tobacco smoke. Experimental evidence has liked cadmium exposure to increased risk of artery disease, peripheral arterial disease, stroke, and other CVDs, even at very low exposures.iii Lead air pollution primarily comes from industrial sources such as smelters and waste incinerators, as well as the combustion of leaded gasoline and aviation fuel.11 Exposure to lead has been widely known to have adverse health effects. It leads to an increased risk of hypertension, and studies on animals have shown that lead exposure leads to increased blood pressure, thus increasing risk of CVD.iii Mercury is another toxic metal air pollutant, which is vaporized into the air

1 Where Does Air Pollution Come From? (n.d.). Retrieved from https://www.nps.gov/subjects/air/sources.htm 2 Cardiovascular diseases (CVDs). (n.d.). Retrieved from https://www.who.int/news-room/factsheets/detail/cardiovascular-diseases-(cvds) 3 Rajagopalan, Sanjay, and Philip J. Landrigan. “Pollution and the Heart.” New England Journal of Medicine, edited by Dan L. Longo , vol. 385, no. 20, Massachusetts Medical Society, 11 Nov. 2021, pp. 1881–1892. Crossref, doi:10.1056/nejmra2030281. 4 Bourdrel, T., Bind, M.-A., Béjot, Y., Morel, O., & Argacha, J.-F. (2017). Cardiovascular effects of air pollution. In Archives of Cardiovascular Diseases (Vol. 110, Issue 11, pp. 634–642). Elsevier BV. https://doi.org/10.1016/j.acvd.2017.05.003 5 Amann, Markus & Derwent, Dick & Forsberg, Bertil & Hänninen, Otto & Hurley, Fintan & Krzyzanowski, Michal & de Leeuw, Frank & Liu, Sally & Mandin, Corinne & Schneider, Jürgen & Schwarze, Per & Simpson, David. (2008). Health risks of ozone from long-range transboundary air pollution. 6 Bhatnagar, A. (2006). Environmental Cardiology. In Circulation Research (Vol. 99, Issue 7, pp. 692–705). Ovid Technologies (Wolters Kluwer Health). https://doi.org/10.1161/01.res.0000243586.99701.cf during processes such as the combustion of coal. It eventually precipitates into aqueous bodies, where it is converted into the highly toxic methylmercury. This methylmercury makes its way through the food chain, and humans eventually consume it. Recent data suggests that exposure increases the risks of death from CVD and MI. However, CVD is not the only effect of exposure to these toxic metals, as exposure can also cause cancer, neurobehavioral disorders, and renal disease.iii

Conclusion: Exposure to different types of air pollution, whether it be primary or secondary gaseous pollutants, PM, or heavy metals, can be particularly harmful to cardiovascular health and can increase the risk of getting a heart attack, stroke, or other CVD. Further research still needs to be done in order to understand the mechanisms behind what makes exposure to these different types of air pollution lead to an increased risk of CVD; however, current evidence clearly demonstrates that in order to reduce CVD, we must reduce air pollution.

7 Miller, M. R., & Newby, D. E. (2019). Air pollution and cardiovascular disease: car sick. In Cardiovascular Research. Oxford University Press (OUP). https://doi.org/10.1093/cvr/cvz228 8 Peters, A., Dockery, D. W., Muller, J. E., & Mittleman, M. A. (2001). Increased Particulate Air Pollution and the Triggering of Myocardial Infarction. In Circulation (Vol. 103, Issue 23, pp. 2810–2815). Ovid Technologies (Wolters Kluwer Health). https://doi.org/10.1161/01.cir.103.23.2810 9 O’Toole, T. E., Hellmann, J., Wheat, L., Haberzettl, P., Lee, J., Conklin, D. J., Bhatnagar, A., & Pope, C. A., III. (2010). Episodic Exposure to Fine Particulate Air Pollution Decreases Circulating Levels of Endothelial Progenitor Cells. In Circulation Research (Vol. 107, Issue 2, pp. 200–203). Ovid Technologies (Wolters Kluwer Health). https://doi.org/10.1161/circresaha.110.222679 10 Health risks of heavy metals from long-range transboundary air pollution (2007). (2017, March 18). Retrieved from https://www.euro.who.int/en/healthtopics/environment-and-health/airquality/publications/pre2009/health-risks-of-heavy-metalsfrom-long-range-transboundary-air-pollution-2007 11 Department of Health. (n.d.). Retrieved from https://www.health.ny.gov/environmental/lead/sources.h tm#air