Document Detail


Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation.
MedLine Citation:
PMID:  21753226     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIM: Exposure to road traffic and air pollution may be a trigger of acute myocardial infarction, but the individual pollutants responsible for this effect have not been established. We assess the role of combustion-derived-nanoparticles in mediating the adverse cardiovascular effects of air pollution.
METHODS AND RESULTS: To determine the in vivo effects of inhalation of diesel exhaust components, 16 healthy volunteers were exposed to (i) dilute diesel exhaust, (ii) pure carbon nanoparticulate, (iii) filtered diesel exhaust, or (iv) filtered air, in a randomized double blind cross-over study. Following each exposure, forearm blood flow was measured during intra-brachial bradykinin, acetylcholine, sodium nitroprusside, and verapamil infusions. Compared with filtered air, inhalation of diesel exhaust increased systolic blood pressure (145 ± 4 vs. 133 ± 3 mmHg, P< 0.05) and attenuated vasodilatation to bradykinin (P= 0.005), acetylcholine (P= 0.008), and sodium nitroprusside (P< 0.001). Exposure to pure carbon nanoparticulate or filtered exhaust had no effect on endothelium-dependent or -independent vasodilatation. To determine the direct vascular effects of nanoparticulate, isolated rat aortic rings (n= 6-9 per group) were assessed in vitro by wire myography and exposed to diesel exhaust particulate, pure carbon nanoparticulate and vehicle. Compared with vehicle, diesel exhaust particulate (but not pure carbon nanoparticulate) attenuated both acetylcholine (P< 0.001) and sodium-nitroprusside (P= 0.019)-induced vasorelaxation. These effects were partially attributable to both soluble and insoluble components of the particulate.
CONCLUSION: Combustion-derived nanoparticulate appears to predominately mediate the adverse vascular effects of diesel exhaust inhalation. This provides a rationale for testing environmental health interventions targeted at reducing traffic-derived particulate emissions.
Authors:
Nicholas L Mills; Mark R Miller; Andrew J Lucking; Jon Beveridge; Laura Flint; A John F Boere; Paul H Fokkens; Nicholas A Boon; Thomas Sandstrom; Anders Blomberg; Rodger Duffin; Ken Donaldson; Patrick W F Hadoke; Flemming R Cassee; David E Newby
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Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't     Date:  2011-07-13
Journal Detail:
Title:  European heart journal     Volume:  32     ISSN:  1522-9645     ISO Abbreviation:  Eur. Heart J.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-02     Completed Date:  2012-01-31     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  8006263     Medline TA:  Eur Heart J     Country:  England    
Other Details:
Languages:  eng     Pagination:  2660-71     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Air Pollutants / toxicity
Animals
Aorta / drug effects
Blood Pressure / drug effects*
Carbon / toxicity*
Cross-Over Studies
Double-Blind Method
Forearm / blood supply
Humans
Inhalation Exposure / adverse effects*
Male
Muscle Contraction / drug effects
Muscle, Smooth, Vascular / drug effects
Nanoparticles / toxicity*
Rats
Vasoconstrictor Agents / pharmacology
Vasodilation / drug effects*
Vasodilator Agents / pharmacology
Vehicle Emissions / toxicity*
Young Adult
Grant Support
ID/Acronym/Agency:
FS/10/024/28266//British Heart Foundation; PG/10/42/28388//British Heart Foundation; RG/10/9/28286//British Heart Foundation; //British Heart Foundation; //Chief Scientist Office
Chemical
Reg. No./Substance:
0/Air Pollutants; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 0/Vehicle Emissions; 7440-44-0/Carbon
Comments/Corrections
Comment In:
Eur Heart J. 2011 Nov;32(21):2613-5   [PMID:  21753227 ]

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


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