PM(2.5) and cardiovascular diseases: State-of-the-Art review

Air pollution, especially exposure to particulate matter 2.5 (PM(2.5)), has been associated with an increase in morbidity and mortality around the world. Specifically, it seems that PM(2.5) 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 PM(2.5) can result in adverse cardiovascular outcomes, in addition to understanding the link between exposure to PM(2.5) and cardiovascular events. It is hypothesized that PM(2.5) 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 PM(2.5) differ regarding the duration of exposure (short vs long) to PM(2.5), the source of PM(2.5), and regulations regarding air pollution in the area where PM(2.5) is prominent. Current strategies to reduce PM(2.5) exposure include personal strategies such as avoiding high PM(2.5) areas such as highways or wearing masks outdoors, to governmental policies restricting the amount of PM(2.5) produced by organizations. This review, by highlighting the significant impact between PM(2.5) exposure and cardiovascular health will hopefully bring awareness and produce significant change regarding dealing with PM(2.5) levels worldwide.