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Is There A Link Between Air Pollution And Heart Disease Air pollution can pose serious danger to the environment, and it can also be a major risk factor for diseases including respiratory infections, lung cancer and even heart disease. World Health Organization (WHO) estimates that indoor air pollution cause approximately 2 million deaths mostly in developing countries, and urban outdoor air pollution cause about 1.3 million deaths worldwide each year. In 2012, researchers from Tel Aviv University found that air pollution not only impacts cardiac events like heart attack and stroke, but also causes recurrences over the long term. The paper was presented at the San Diego Epidemiological Meeting of the American Heart Association in March and the Annual Meeting of the Israeli Heart Society in April. Their findings indicated that patients, who had heart attack before and lived in the most polluted areas, were 43 percent more likely to have a second heart attack or suffer congestive heart failure, and 46 percent more likely to suffer a stroke when compared to patients living in the lowest polluted areas. The study also found that patients exposed to air pollution were 35 percent more likely to die in the almost 20 year period following their first heart attack than those who were exposed to lower levels of pollution.
On April 23, 2013, a paper published in ‘PLOS Medicine’ by researchers from University of Michigan School of Public Health reported that long-term exposure to air pollution might be linked to heart attacks and strokes by speeding up atherosclerosis (hardening of the arteries). The study showed that higher concentrations of fine particulate air pollution (PM2.5) were associated with a faster thickening of the inner 2 layers of the common carotid artery (an important blood vessel that provides blood to the head, neck and brain). On the other hand, the researchers also found reduction of the fine particulate air pollution over time was linked to slower progression of blood vessel thickness. Fine particulate matter (PM2.5) are particles with a diameter of less than 2.5 micrometers or 1/30th the width of a human hair. It is mainly produced by motor vehicles, power plants, and other combustion sources. It has long been thought that there is a link between exposure to these particles and cardiovascular disease, but results from previous studies were inconclusive. 5,362 people, ages between 45 and 84 from 6 United States metropolitan areas as part of the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), were followed. At the beginning of the study, all the participants had no signs of cardiovascular disease. The air pollution levels estimated at each person’s house were associated with 2 ultrasound measurements of the blood vessels, separated by about 3 years. Analysis showed that, on average, the thickness of the carotid vessel increased by 14 micrometers each year, after adjusting for other factors like smoking. The blood vessels thickened faster for those people exposed to higher levels of residential fine particulate air pollution than others living in the same metropolitan area. By linking these findings with other results from the same population, the researchers also found that persons living in a more polluted part of town might have a 2 percent higher risk of stroke as compared to people in a less polluted part of the same metropolitan area. Undoubtedly, the new findings help understand how exposures to air pollution may cause the increases in heart attacks and strokes observed by other studies, and they provided further evidence of the health impacts of poor air quality. However, the association between particulates and carotid artery thickness could not prove that PM2.5 is the contributing factor. While PM2.5 might well be an indicator of other components of pollution such as nitrogen oxides, carbon monoxide or ozone, it might also be a surrogate for ultra-fine particulates. Hence, future studies of concurrent pollution factors are necessary to resolve the likely mechanistic rationale for these effects.
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