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Cardiovascular Disease as a Risk Factor for Enhanced Susceptibility to Air Pollutants
Citation:
DEVLIN, R. B. Cardiovascular Disease as a Risk Factor for Enhanced Susceptibility to Air Pollutants. Presented at American Association of Aerosol Research, San Diego, CA, March 22 - 26, 2010.
Impact/Purpose:
This presentation will focus on better understanding why people with pre-existing cardiovascular disease (CV) are a susceptible population, as well as whether exposure to air pollutants can cause progression of cardiovascular disease.
Description:
Adverse health effects caused by airborne particular matter (PM) are restricted primarily to susceptible populations. The actual risk of anyone individual is quite small, but because of the large number of exposed people, the overall population risk is significant. Ferreting out which individuals are at greatest risk is one of the challenges of PM research. Individuals may be at risk for a variety of reasons, including pre-existing disease (cardiovascular, pulmonary), genetics, age, lifestyle factors, geographical location that may lead to increased exposure, etc. Most PM susceptibility research has focused on studies of people with pre-existing disease. This presentation will focus on better understanding why people with pre-existing cardiovascular disease (CV) are a susceptible population, as well as whether exposure to air pollutants can cause progression of cardiovascular disease. It is complementary to another presentation focusing on enhanced responsiveness of people with asthma and diabetes to air pollution. The original epidemiology studies linked day-to-day variations in PM with increases in mortality and morbidity in older individuals with CV. More recent epidemiological studies have better characterized subgroups of people with CV disease that may be targeted by PM, as well as demonstrating increased risk of cardiac arrhythmias in people with CV disease. Panel studies have extended the epidemiological findings by pointing to biological mechanisms that may be associated with the response of people with CV to air pollutants such as systemic inflammation, changes in autonomic nervous system control of heart rate, increase in prothombogenic potential of the blood, and vascular enodothelial cell dysfunction. These findings in humans are supported by recent findings in animal models which demonstrate an augmentation of PM effects in ischemic animals, vascular disease progression in atherosclerotic mice, exacerbated pathophysiology in hyper-lipidemic rabbits, greater pulmonary edema and injury in stroke-prone rats, and autonomic dysregulation and increased cardiac arrhythmias in hypertensive rats. Although most research has focused on PM as a causative agent, recent studies have suggested that other air pollutants such as ozone may also cause mortality in some people with CV disease. Additionally both human and animal studies suggest that chronic exposure to air pollutants can cause the progression of CV disease. According to the American Heart Association, 35 % of all deaths in 2005 were due to CV disease in the U.S. and greater than 36 % of all adults (80 million people) suffered from CV disease in 2006. The pronounced adverse effects of air pollutants in individuals with CV disease are thus a major public health problem. An increased understanding of how pollutants target those individuals with CV disease will potentially lead to improvements in public health by decreasing morbidity and mortality associated with exposure to air pollutants. This abstract of a proposed presentation does not necessarily reflect EPA policy