|dc.description.abstract||BACKGROUND: 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.
OBJECTIVES: Our goal was to study the effects of short-term exposure to DE on vascular reactivity
and on mediators of vascular tone.
METHODS: 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 μg/m3 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).
RESULTS: Compared with FA, DE at 200 μg/m3 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
μg/m3. Plasma levels of ET-1 increased after 200 μg/m3 DE but not after FA (p = 0.01). There was
no consistent impact of DE on plasma catecholamines or FMD.
CONCLUSIONS: 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.||en_US