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

Abstract

AimExposure 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 resultsTo 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.ConclusionCombustion-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.

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

“…Observations in healthy young volunteers exposed to pure elemental carbon particles implied that heart function was not affected by these controlled exposures. This was confirmed by a very similar exposure in a study (Mills et al, 2011) that looked at measurements of arterial stiffness and blood clothing in healthy subjects. The presence of a susceptible population has not been shown, and no studies could be identified that have applied exposure periods longer than 2 hours.…”

“…The effects of ultrafine carbon particles were observed in both heart rate variability and cardiac repolarization, but there were no changes in soluble markers of either systemic inflammation or coagulation. In a more recent study, no vascular impairment or effect on blood clotting were observed in volunteers exposed for 2 hours to 70 µg/m 3 of ultrafine carbon particles (Mills et al, 2011). In this same study, and in Lucking et al (2011), it was shown that removing the particles from diluted diesel engine exhaust also prevented adverse effects on the cardiovascular system.…”

“…A few recently published clinical studies support pre-2005 studies that suggested increasing evidence for ultrafine particles in eliciting health effects during and after 2-hour exposure periods Langrish et al, 2009;Mills et al, 2011). However, most studies were performed with a mixture of particles and gases, which do not allow statements to be made about the contributions of ultrafine particles.…”

“…Also, volatile organic compounds are able to form PM (Robinson et al, 2007;Jimenez et al, 2009) In addition, studies of human beings and diesel engine exhaust and clean carbon particles (Mills et al, 2011) strongly suggest that organic chemical compounds on the surface of the carbon particles are responsible for immediate cardiovascular responses. Interestingly, reducing the amount of soot can lead to an increase in NO 2 , but the net effect is still reduced adverse effects on health (Lucking et al, 2011).…”

Human inhalation exposure to iron oxide particles

“…The authors are not aware of any published human inhalation studies using iron oxide nanoparticles. However, several controlled human inhalation studies have exposed volunteers to other ultrafine particles [57][58][59][60][61][62][63][64][65][66]. In addition, many human inhalation studies have been conducted using Technegas or 99m Tc labeled ultrafine carbon particles; however, this literature is beyond the scope of this review.…”