Inhalation of Ultrafine and Fine Particulate Matter Disrupts Systemic Vascular Function

Abstract

This study investigated the effects of particulate matter (PM) with aerodynamic diameter 0.02-1 μm (noted as PM 1 ) 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 PM 1 . 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 PM 1 exercise (4.0%, 4.66 ± 0.609 to 4.47 ± 0.625 mm diameter; p = .0002), but not after low PM 1 exercise (−0.3%, 4.66 ± 0.626 to 4.68 ± 0.613 mm diameter). FMD was impaired after high PM 1 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 PM 1 exercise (55% vs. 3%, p = .0006); no difference was noted for low PM 1 exercise. Brachial artery FMD was significantly correlated to muscle reoxygenation slope-to-baseline (r = .50, p = .005). Acute inhalation of high [PM 1 ] 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.

Ultrafine and Fine Particulate Matter Inhalation Decreases Exercise Performance in Healthy Subjects

“…The near abolishment of FMD was accompanied by a 55% decrease in muscle reoxygenation slope-to-baseline measured by near-infrared spectroscopy (NIRS) after release of artery occlusion and is consistent with compromised reperfusion. This study (19) supported a constrictive response from PM 1 inhalation in the microvasculature that was independent of the observed brachial artery vasoconstriction. Calculation of the return slope of reoxygenation (mMÁs 21 ) to baseline after cuff ischemia (19) provided a rate of decreased reperfusion of the muscle tissue (after 30 minute exercise breathing high PM 1 ) that should be proportional to blood flow.…”

“…Instead, these results support a response initiated from the first high (PM 1 ) exposure trial that affected muscle perfusion in the second high (PM 1 ) trial 3 days later. We previously reported diminished flow-mediated vasodilation (FMD) after 30 min of running while breathing high (PM 1 ), suggesting a PM 1 -induced disruption of normal endothelial-mediated vasodilation (19). The near abolishment of FMD was accompanied by a 55% decrease in muscle reoxygenation slope-to-baseline measured by near-infrared spectroscopy (NIRS) after release of artery occlusion and is consistent with compromised reperfusion.…”

Indoor and outdoor sources of size-resolved mass concentration of particulate matter in a school gym—implications for exposure of exercising children

“…Research into fine and/or ultrafine particulate pollution and exercise has shown both increased genotoxic (Vaclavik-Bräuner et al 2007) and cardiovascular (Rundell et al 2007;Mittleman 2007) risk with increasing aerosol concentrations. During aerobic exercise, inhaled air is taken in predominantly through the mouth, and there is a major increase in minute ventilation and diffusion capacity.…”

Environmental determinants of blood pressure, arterial stiffness, and central hemodynamics

“…Regarding the mechanism involved, particulate matter inhalation has been associated with important alterations of the vascular tone [20,21], the endothelial function [22], the autonomic-nervous system [23], the endogenous fibrinolysis [19] and the systemic inflammation [24], factors that may potentially interact with the arterial wave reflection mechanisms. It could be hypothesized that the effect of PM 10 concentration on the magnitude of the reflection wave could be attributed to a heightened adrenergic-mediated vasoconstriction of the microvascular tree, or to an impaired endothelium-dependent microvascular vaosoconstriction.…”