Document Type



Cardiology; Office of the Provost


Air pollution, especially exposure to particulate matter 2.5 (PM2.5), has been associated with an increase in morbidity and mortality around the world. Specifically, it seems that PM2.5 promotes the development of cardiovascular risk factors such as hypertension and atherosclerosis, while being associated with an increased risk of cardiovascular diseases, including myocardial infarction (MI), stroke, heart failure, and arrhythmias. In this review, we seek to elucidate the pathophysiological mechanisms by which exposure to PM2.5 can result in adverse cardiovascular outcomes, in addition to understanding the link between exposure to PM2.5 and cardiovascular events. It is hypothesized that PM2.5 functions via 3 mechanisms: increased oxidative stress, activation of the inflammatory pathway of the immune system, and stimulation of the autonomic nervous system which ultimately promote endothelial dysfunction, atherosclerosis, and systemic inflammation that can thus lead to cardiovascular events. It is important to note that the various cardiovascular associations of PM2.5 differ regarding the duration of exposure (short vs long) to PM2.5, the source of PM2.5, and regulations regarding air pollution in the area where PM2.5 is prominent. Current strategies to reduce PM2.5 exposure include personal strategies such as avoiding high PM2.5 areas such as highways or wearing masks outdoors, to governmental policies restricting the amount of PM2.5 produced by organizations. This review, by highlighting the significant impact between PM2.5 exposure and cardiovascular health will hopefully bring awareness and produce significant change regarding dealing with PM2.5 levels worldwide.


Issue and pagination are not provided by the author/publisher.

Publication (Name of Journal)

International Journal of Cardiology Cardiovascular Risk and Prevention