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Citation
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HERO ID
95757
Reference Type
Journal Article
Title
Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis
Author(s)
Mills, NL; Tornqvist, H; Robinson, SD; Gonzalez, M; Darnley, K; Macnee, W; Boon, NA; Donaldson, K; Blomberg, A; Sandstrom, T; Newby, DE
Year
2005
Is Peer Reviewed?
Yes
Journal
Circulation
ISSN:
0009-7322
EISSN:
1524-4539
Volume
112
Issue
25
Page Numbers
3930-3936
Language
English
PMID
16365212
DOI
10.1161/CIRCULATIONAHA.105.588962
Web of Science Id
WOS:000234058200016
URL
http://www.ncbi.nlm.nih.gov/pubmed/16365212
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Abstract
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 microg/m3 particulate concentration) or air for 1 hour during intermittent exercise. Bilateral forearm blood flow and inflammatory factors were measured before and during unilateral intrabrachial bradykinin (100 to 1000 pmol/min), acetylcholine (5 to 20 microg/min), sodium nitroprusside (2 to 8 microg/min), and verapamil (10 to 100 microg/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 (P<0.0001 for all), this response was attenuated with bradykinin (P<0.05), acetylcholine (P<0.05), and sodium nitroprusside (P<0.001) infusions 2 hours after exposure to diesel exhaust, which persisted at 6 hours. Bradykinin caused a dose-dependent increase in plasma tissue plasminogen activator (P<0.0001) that was suppressed 6 hours after exposure to diesel (P<0.001; 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.
Keywords
air pollution; endothelium; blood flow; fibrinolysis
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