Published ahead of print on April 19, 2007, doi:10.1164/rccm.200606-872OC Am. J. Respir. Crit. Care Med., Volume 176, Number 4, August 2007, 395-400 A more recent version of this article appeared on August 15, 2007
Submitted on June 29, 2006 Persistent Endothelial Dysfunction Following Diesel Exhaust Inhalation in ManHakan Tornqvist1,1 Department of Respiratory Medicine and Allergy, Umea University, Umea, Sweden, 2 Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom, 3 Department of Medicine, Umea University, Umea, Sweden, 4 Free Radical Research Facility, UHI Millennium Institute, Inverness, United Kingdom, 5 ELEGI Colt Laboratory, Centre for Inflammation Research, University of Edinburgh, Edinburgh, United Kingdom * To whom correspondence should be addressed. E-mail: anders.blomberg{at}lung.umu.se.
Rationale
Exposure to combustion-derived air pollution is associated with an early (1-2 hours) and sustained (24 hour) rise in cardiovascular morbidity and mortality. We have previously demonstrated that inhalation of diesel exhaust causes an immediate (within 2 hours) impairment of vascular and endothelial function in man.
Objective
To investigate the vascular and systemic effects of diesel exhaust 24 hours following inhalation in man.
Methods
Fifteen healthy men were exposed to diesel exhaust (particulate concentration, 300 µg/m3) or filtered air for one hour in a double-blind randomised crossover study. Twenty-four hours following exposure, bilateral forearm blood flow, and inflammatory and fibrinolytic markers were measured before and during unilateral intra-brachial bradykinin (100-1000 pmol/min), acetylcholine (5-20 µg/min), sodium nitroprusside (2-8 µg/min) and verapamil (10-100 µg/min) infusions.
Measurements and Main Results
Resting forearm blood flow, blood pressure and basal fibrinolytic markers were similar 24 hours following either exposure. Diesel exhaust increased plasma cytokine concentrations (tumor necrosis factor- Key words: air pollution; endothelium; blood flow; inflammation; diesel exhaust
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and interleukin-6; P<0.05 for both) but appeared to reduce acetylcholine (P=0.01) and bradykinin (P=0.08) induced forearm vasodilatation. In contrast, there were no differences in either endothelium-independent (sodium nitroprusside and verapamil) vasodilatation or bradykinin-induced acute plasma tissue plasminogen activator (t-PA) release.
Conclusions
Twenty-four hours after diesel exposure, there is a selective and persistent impairment of endothelium-dependent vasodilatation that occurs in the presence of mild systemic inflammation. These findings suggest that combustion-derived air pollution may have important systemic and adverse vascular effects for at least 24 hours following exposure.
