Diesel Exhaust Inhalation Causes Vascular Dysfunction and Impaired Endogenous Fibrinolysis

N. L. Mills
2005 Circulation  
Background-Although the mechanisms are unknown, it has been suggested that transient exposure to traffic-derived air pollution may be a trigger for acute myocardial infarction. The study aim was to investigate the effects of diesel exhaust inhalation on vascular and endothelial function in humans. Methods and Results-In a double-blind, randomized, cross-over study, 30 healthy men were exposed to diluted diesel exhaust (300 g/m 3 particulate concentration) or air for 1 hour during intermittent
more » ... ercise. Bilateral forearm blood flow and inflammatory factors were measured before and during unilateral intrabrachial bradykinin (100 to 1000 pmol/min), acetylcholine (5 to 20 g/min), sodium nitroprusside (2 to 8 g/min), and verapamil (10 to 100 g/min) infusions 2 and 6 hours after exposure. There were no differences in resting forearm blood flow or inflammatory markers after exposure to diesel exhaust or air. Although there was a dose-dependent increase in blood flow with each vasodilator (PϽ0.0001 for all), this response was attenuated with bradykinin (PϽ0.05), acetylcholine (PϽ0.05), and sodium nitroprusside (PϽ0.001) infusions 2 hours after exposure to diesel exhaust, which persisted at 6 hours. Bradykinin caused a dose-dependent increase in plasma tissue plasminogen activator (PϽ0.0001) that was suppressed 6 hours after exposure to diesel (PϽ0.001; area under the curve decreased by 34%). Conclusions-At levels encountered in an urban environment, inhalation of dilute diesel exhaust impairs 2 important and complementary aspects of vascular function in humans: the regulation of vascular tone and endogenous fibrinolysis. These important findings provide a potential mechanism that links air pollution to the pathogenesis of atherothrombosis and acute myocardial infarction. (Circulation. 2005;112:3930-3936.) Key Words: air pollution Ⅲ endothelium Ⅲ blood flow Ⅲ fibrinolysis A ir pollution is a major cause of cardiovascular morbidity
doi:10.1161/circulationaha.105.588962 pmid:16365212 fatcat:7gisgfstnfguvgjbmlrj2nkfqm