Anthropogenic ambient fine particulate matter less than 2.5 µm (PM2.5) air pollution from fossil fuel combustion (eg, coal-fired power plants and traffic) ranks among the leading causes of worldwide morbidity and mortality.1 In agreement with figures from the World Health Organization (http://www.who.int/topics/global_burden_of_disease/en/), estimations indicate that approximately 3.15 million deaths per year are attributable to PM2.5. This alarming figure exceeds that of many more widely recognized risk factors (eg, hypercholesterolemia) and unfortunately is estimated to double by 2050.1 However, perhaps underappreciated by health care professionals and the general populace alike is that the largest portion of ambient PM2.5–induced health effects are owing to cardiovascular events. Short-term elevations in PM2.5 increase the risk for myocardial infarctions, strokes, heart failure, arrhythmias, and cardiac death.2,3 Longer-term exposures synergistically increase this acute risk and can even potentiate the development of chronic cardiometabolic conditions including diabetes and hypertension. As such, both the American Heart Association and European Society of Cardiology have formally recognized ambient PM2.5 as a major cardiovascular risk factor.2,3