Acute and chronic exposure to elevated levels of fine airborneparticulate matter (PM) is associated with an increase in theincidence of adverse cardiovascular events,1,2 atherogenesis, cardiovasculardisease (CVD) risk, and cardiovascular mortality. In urbanenvironments, fine PM (PM with aerodynamic diameter of2.5 m [PM2.5]) is generated mostly by fossil fuel combustion inautomobiles or by industrial processes. Although several mechanismshave been proposed to account for the link between PMexposure and CVD risk, endothelial dysfunction has emerged as akey feature of PM toxicity. Inhalation of concentrated PM2.5induces acute conduit artery vasoconstriction in humans and chronicdeficits in endothelium-mediated vasodilation in mice.1,2The adult endothelium is a differentiated cell layer thatprovides a nonthrombotic interface between parenchymal cellsand peripheral blood. Defects in its function arise because of theupregulated expression of proinflammatory and prothrombotic moleculesor from defective, endogenous repair capacity. Evidencefrom multiple studies suggests that the endothelium is continuall ……
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