Air pollution is responsible worldwide for 9-12 million deaths annually. The major contributor to air pollution is particulate matter ≤2.5 µg per cubic meter of air (PM2.5) from vehicles, industrial emissions, and wildfire smoke. United States ambient air standards recommend annual average PM2.5 concentrations of ≤12 μg/m³ while European standards allow an average annual PM2.5 concentration of ≤20 μg/m3. However, significant PM2.5 cardiovascular and pulmonary health risks exist below these concentrations. Chronic PM2.5 exposure significantly increases major cardiovascular and pulmonary event risks in Americans by 8 to more than 20% for each 10-μg/m3 increase in PM2.5. PM2.5-induced increases in lipid peroxidation, induction of vascular inflammation and endothelial cell injury initiate and propagate respiratory diseases, coronary and carotid atherosclerosis. PM2.5 can cause atherosclerotic vascular plaque rupture and myocardial infarction and stroke by activating metalloproteinases. This article discusses PM2.5 effects on the cardiovascular and pulmonary systems, specific PM2.5 pathophysiologic mechanisms contributing to cardiopulmonary disease, and preventive measures to limit the cardiovascular and pulmonary effects of PM2.5.
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