Air pollution exposure is associated with an increased risk of acute and chronic cardiovascular mortality. Recent observations have implicated fine particulate matter (PM(2.5)) as one of the most important pollutants. Inhalation of PM(2.5) causes acute pulmonary inflammation and oxidative stress. The subsequent generation of a systemic inflammatory response could link air pollution exposure with the development of cardiovascular disease. Human experiments have demonstrated pro-arrhythmic alterations in cardiac autonomic tone, increased blood pressure, higher serum C-reactive protein levels, and alterations in blood rheology favoring coagulation following controlled pollution exposures or in relation to elevated ambient PM(2.5) levels. Recent studies have also uncovered several harmful impacts on the systemic vasculature, including the triggering of acute vasoconstriction and the enhanced development of atherosclerosis. Many questions, however, remain unanswered and future studies will be required to clarify the relevant biologic mechanisms and to identify the specific constituents responsible for mediating the adverse health impacts.
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