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Persistent Endothelial Dysfunction in Humans after Diesel Exhaust Inhalation

¹ Department of Respiratory Medicine and Allergy, Umeå University, Umeå, Sweden; ² Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom; ³ Department of Medicine, Umeå University, Umeå, Sweden; ⁴ Free Radical Research Facility, UHI Millennium Institute, Inverness, United Kingdom; and ⁵ ELEGI Colt Laboratory, Centre for Inflammation Research, University of Edinburgh, Edinburgh, United Kingdom

Correspondence and requests for reprints should be addressed to Anders Blomberg, M.D., Ph.D., Department of Respiratory Medicine and Allergy, Umeå University Hospital, SE-901 85 Umeå, Sweden. E-mail: anders.blomberg{at}lung.umu.se

Rationale: Exposure to combustion-derived air pollution is associated with an early (1–2 h) and sustained (24 h) rise in cardiovascular morbidity and mortality. We have previously demonstrated that inhalation of diesel exhaust causes an immediate (within 2 h) impairment of vascular and endothelial function in humans.

Objectives: To investigate the vascular and systemic effects of diesel exhaust in humans 24 hours after inhalation.

Methods: Fifteen healthy men were exposed to diesel exhaust (particulate concentration, 300 µg/m³) or filtered air for 1 hour in a double-blind, randomized, crossover study. Twenty-four hours after exposure, bilateral forearm blood flow, and inflammatory and fibrinolytic markers were measured before and during unilateral intrabrachial bradykinin (100–1,000 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 after either exposure. Diesel exhaust increased plasma cytokine concentrations (tumor necrosis factor- 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 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 after exposure.

Key Words: air pollution • endothelium • blood flow • inflammation • diesel exhaust

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject The link between ambient particulate matter air pollution and cardiorespiratory mortality and morbidity is well established. However, the biological mechanisms underlying the cardiovascular effects of particulate matter air pollution are largely unknown. What This Study Adds to the Field Exposure to diesel exhaust causes a selective impairment of vascular endothelial function, which persists up to 24 hours after exposure. Adverse cardiovascular effects of combustion-derived pollution may be mediated through prolonged detrimental vascular effects.

 

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