Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation

The BHF/University Centre for Cardiovascular Science, Edinburgh University, The Queens Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.
European Heart Journal (Impact Factor: 15.2). 07/2011; 32(21):2660-71. DOI: 10.1093/eurheartj/ehr195
Source: PubMed


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.
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.
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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    • "For example, constriction of systemic or intrapulmonary arteries (IPA), rise in blood viscosity and alteration in heart rate variability in response to UPM exposure have been reported (Brook et al., 2002; Huang et al., 2002; Peters et al., 1997; Pope et al., 2004b). Vasoconstriction may result from alteration of the endothelium-derived nitric oxide (NO)-cGMP-dependent relaxant pathway (Miller et al., 2009; Mills et al., 2011; Nurkiewicz et al., 2004). Ex vivo, acetylcholine is usually used to trigger the release of NO by endothelial cells, and therefore to study the NO-cGMP relaxation pathway. "
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