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Alon Peretz,¹ Jeffrey H. Sullivan,¹ Daniel F. Leotta,² Carol A. Trenga,¹ Fiona N. Sands,¹ Jason Allen,¹ Chris Carlsten,^1,3 Charles W. Wilkinson,⁴ Edward A. Gill,³ and Joel D. Kaufman^1,3

¹Occupational and Environmental Medicine Program, Department of Environmental and Occupational Health Sciences, ²Department of Surgery (Vascular Surgery), ³Department of Medicine, and ⁴Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington, USA

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.

Key words: air pollution, brachial artery, catecholamines, endothelin-1, vasoconstriction. Environ Health Perspect 116:937–942 (2008) . doi:10.1289/ehp.11027 available via http://dx.doi.org/ [Online 18 March 2008]

Address correspondence to J.D. Kaufman, University of Washington Occupational and Environmental Medicine Program, Department of Environmental and Occupational Health Sciences, Box 35469, 4225 Roosevelt Way NE, Suite 100, Seattle, WA 98105 USA. Telephone: (206) 616-3501. Fax: (206) 897-1991. E-mail: joelk@u.washington.edu

We thank J. Stewart for conducting and controlling the exposures to diesel exhaust, M. Paun for ultrasound imaging of the brachial artery, M. Aulet and S. Jarvis for coordinating and conducting recruitments and exposure sessions, J. Wilkerson for processing of blood samples, C. Sikkema for catecholamine and neuropeptide measurements, and all the study participants who contributed their time to the study.

This study was supported by grants R830954 and R827355 from the U.S. Environmental Protection Agency and grants K24ES013195, K23ES011139, P30ES07033, and M01RR-00037 from the National Institutes of Health and the National Institute of Environmental Health Sciences. Catecholamine and neuropeptide assays were performed at the Geriatric Research, Education and Clinical Center at the VA Puget Sound Health Care System, and that work was supported in part by the U.S. Department of Veterans Affairs.

The authors declare they have no competing financial interests.

Received 29 October 2007 ; accepted 18 March 2008.