Diesel exhaust inhalation elicits acute vasoconstriction in vivo

Traffic-related air pollution is consistently associated with cardiovascular morbidity and mortality. Recent human and animal studies suggest that exposure to air pollutants affects vascular function. Diesel exhaust (DE) is a major source of traffic-related air pollution.

Our goal was to study the effects of short-term exposure to DE on vascular reactivity and on mediators of vascular tone.

In a double-blind, crossover, controlled exposure study, 27 adult volunteers (10 healthy and 17 with metabolic syndrome) were exposed in randomized order to filtered air (FA) and each of two levels of diluted DE (100 or 200 microg/m(3) of fine particulate matter) in 2-hr sessions. Before and after each exposure, we assessed the brachial artery diameter (BAd) by B-mode ultrasound and collected blood samples for endothelin-1 (ET-1) and catecholamines. Postexposure we also assessed endothelium-dependent flow-mediated dilation (FMD).

Compared with FA, DE at 200 microg/m(3) elicited a decrease in BAd (0.11 mm; 95% confidence interval, 0.02-0.18), and the effect appeared linearly dose related with a smaller effect at 100 microg/m(3). Plasma levels of ET-1 increased after 200 microg/m(3) DE but not after FA (p = 0.01). There was no consistent impact of DE on plasma catecholamines or FMD.

These results demonstrate that short-term exposure to DE is associated with acute endothelial response and vasoconstriction of a conductance artery. Elucidation of the signaling pathways controlling vascular tone that underlie this observation requires further study.