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 μm (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 PM ₁ 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.