Document Detail


Exposure to nitrogen dioxide is not associated with vascular dysfunction in man.
MedLine Citation:
PMID:  20047363     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Exposure to air pollution is associated with increased cardiorespiratory morbidity and mortality. It is unclear whether these effects are mediated through combustion-derived particulate matter or gaseous components, such as nitrogen dioxide. OBJECTIVES: To investigate the effect of nitrogen dioxide exposure on vascular vasomotor and six fibrinolytic functions. METHODS: Ten healthy male volunteers were exposed to nitrogen dioxide at 4 ppm or filtered air for 1 h during intermittent exercise in a randomized double-blind crossover study. Bilateral forearm blood flow and fibrinolytic markers were measured before and during unilateral intrabrachial infusion of bradykinin (100-1000 pmol/min), acetylcholine (5-20 microg/min), sodium nitroprusside (2-8 microg/min), and verapamil (10-100 microg/min) 4 h after the exposure. Lung function was determined before and after the exposure, and exhaled nitric oxide at baseline and 1 and 4 h after the exposure. RESULTS: There were no differences in resting forearm blood flow after either exposure. There was a dose-dependent increase in forearm blood flow with all vasodilators but this was similar after either exposure for all vasodilators (p > .05 for all). Bradykinin caused a dose-dependent increase in plasma tissue-plasminogen activator, but again there was no difference between the exposures. There were no changes in lung function or exhaled nitric oxide following either exposure. CONCLUSION: Inhalation of nitrogen dioxide does not impair vascular vasomotor or fibrinolytic function. Nitrogen dioxide does not appear to be a major arbiter of the adverse cardiovascular effects of air pollution.
Authors:
Jeremy P Langrish; Magnus Lundb?ck; Stefan Barath; Stefan S?derberg; Nicholas L Mills; David E Newby; Thomas Sandstr?m; Anders Blomberg
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Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Inhalation toxicology     Volume:  22     ISSN:  1091-7691     ISO Abbreviation:  Inhal Toxicol     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-18     Completed Date:  2010-04-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8910739     Medline TA:  Inhal Toxicol     Country:  England    
Other Details:
Languages:  eng     Pagination:  192-8     Citation Subset:  IM    
Affiliation:
Centre for Cardiovascular Sciences, University of Edinburgh, United Kingdom.
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MeSH Terms
Descriptor/Qualifier:
Adult
Air Pollutants, Occupational / metabolism,  toxicity*
Blood Cell Count
Cross-Over Studies
Double-Blind Method
Endothelium, Vascular / drug effects,  pathology
Exercise / physiology
Fibrinolysis / drug effects
Hemodynamics / drug effects
Humans
Inhalation Exposure
Lung / drug effects
Male
Nitrogen Dioxide / metabolism,  toxicity*
Oxidants, Photochemical / metabolism,  toxicity*
Plasminogen Activators / metabolism
Respiratory Function Tests
Spirometry
Thrombosis / blood
Vascular Diseases / chemically induced*,  epidemiology,  pathology
Young Adult
Grant Support
ID/Acronym/Agency:
FS/07/048//British Heart Foundation
Chemical
Reg. No./Substance:
0/Air Pollutants, Occupational; 0/Oxidants, Photochemical; 10102-44-0/Nitrogen Dioxide; EC 3.4.21.-/Plasminogen Activators

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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