Inhalation of ultrafine and fine particulate matter disrupts systemic vascular function

This study investigated the effects of particulate matter (PM) with aerodynamic diameter 0.02-1 mu m (noted as PM1) inhalation during exercise on conduit artery and microvascular function. Inhalation of internal combustion-derived PM is associated with cardiovascular mortality and morbidity. Direct action of PM on the vascular endothelium is likely, as a substantial fraction of ultrafine PM translocates from the alveoli to the circulatory system. Sixteen intercollegiate athletes performed 30 min of exercise while inhaling low or high PM1. Flow-mediated brachial artery dilation (FMD) using high-resolution ultrasonography with simultaneous measurements of forearm oxygen kinetics using near infrared spectrophotometry (NIRS) was done before and after exercise. Basal brachial artery vasoconstriction was found after high PM1 exercise (4.0%, 4.66 +/- 0.609 to 4.47 +/- 0.625 mm diameter; p = .0002), but not after low PM1 exercise (-0.3%, 4.66 +/- 0.626 to 4.68 +/- 0.613 mm diameter). FMD was impaired after high PM1 exercise (6.8 +/- 3.58% for preexercise FMD and 0.30 +/- 2.74% for postexercise FMD, p = .0001), but not after low PM1 exercise (6.6 +/- 4.04% for preexercise FMD and 4.89 +/- 4.42% for postexercise FMD). Reduction in forearm muscle reperfusion estimated by reoxygenation slope-to-baseline after 4 min cuff ischemia was observed for high PM1 exercise (55% vs. 3%, p =. 0006); no difference was noted for low PM1 exercise. Brachial artery FMD was significantly correlated to muscle reoxygenation slope-to-baseline (r = .50, p = .005). Acute inhalation of high [PM1] typical of urban environments impairs both systemic conduit artery function and microcirculation. The observed decrease reoxygenation slope-to-baseline after cuff release is consistent with reduced blood flow in the muscle microvasculature.