期刊
EUROPEAN HEART JOURNAL
卷 32, 期 21, 页码 2660-2671出版社
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehr195
关键词
Air pollution; Diesel exhaust; Nanoparticles; Endothelium; Blood flow
资金
- British Heart Foundation Centre of Research Excellence
- UK National Health Service (NHS) Research Scotland (NRS), through NHS Lothian
- Chief Scientist Office
- British Heart Foundation [PG/10/009, FS/10/024, PG/05/003]
- UK. Dutch Ministry of Housing, Spatial Planning and Environment (VROM), the Netherlands
- British Heart Foundation [FS/10/024/28266, RG/10/9/28286, PG/10/42/28388] Funding Source: researchfish
- Medical Research Council [G9900991B] Funding Source: researchfish
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.
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