Particulate air pollution and coronary heart disease

Abstract

Air pollution poses a significant health risk. The article focuses on the adverse effects of air pollution on the cardiovascular system. Short-term and long-term studies clearly indicate that relatively modest exposures to particulate matter in the ambient air are associated with increased morbidity and mortality due to coronary heart disease. In humans, inhalational exposure to particulate air pollutants decreases heart rate variability, causes ST-segment depression and endothelial dysfunction, increases blood pressure and blood coagulability, and accelerates the progression of atherosclerosis. Mechanisms of air pollution-induced cardiotoxicity include increased generation of reactive oxygen species followed by activation of proinflammatory and prothrombotic pathways. In experimental settings, ultrafine air pollutants instilled directly into the cardiac vasculature depress cardiac contractility and decrease coronary flow. Both effects are attenuated by the use of a free radical scavenger. Reactive oxygen species-related mechanisms of air pollution cardiotoxicity might become a valid target in developing new pharmacological strategies aimed at decreasing adverse effects of air pollution during extreme episodes (fires, earthquakes, industrial accidents, acts of terrorism). Educating patients and the general population on the negative cardiovascular effects of air pollution might be helpful in decreasing the risk of developing air pollution-related coronary heart disease.