Particle Traps Prevent Adverse Vascular and Prothrombotic Effects of Diesel Engine Exhaust Inhalation in Men

Abstract

Background-In controlled human exposure studies, diesel engine exhaust inhalation impairs vascular function and enhances thrombus formation. The aim of the present study was to establish whether an exhaust particle trap could prevent these adverse cardiovascular effects in men. Methods and Results-Nineteen healthy volunteers (mean age, 25Ϯ3 years) were exposed to filtered air and diesel exhaust in the presence or absence of a particle trap for 1 hour in a randomized, double-blind, 3-way crossover trial. Bilateral forearm blood flow and plasma fibrinolytic factors were assessed with venous occlusion plethysmography and blood sampling during intra-arterial infusion of acetylcholine, bradykinin, sodium nitroprusside, and verapamil. Ex vivo thrombus formation was determined with the use of the Badimon chamber. Compared with filtered air, diesel exhaust inhalation was associated with reduced vasodilatation and increased ex vivo thrombus formation under both low-and high-shear conditions. The particle trap markedly reduced diesel exhaust particulate number (from 150 000 to 300 000/cm 3 to 30 to 300/cm 3 ; PϽ0.001) and mass (320Ϯ10 to 7.2Ϯ2.0 g/m 3 ; PϽ0.001), and was associated with increased vasodilatation, reduced thrombus formation, and an increase in tissue-type plasminogen activator release. Conclusions-Exhaust particle traps are a highly efficient method of reducing particle emissions from diesel engines. With a range of surrogate measures, the use of a particle trap prevents several adverse cardiovascular effects of exhaust inhalation in men. Given these beneficial effects on biomarkers of cardiovascular health, the widespread use of particle traps on diesel-powered vehicles may have substantial public health benefits and reduce the burden of cardiovascular disease. Clinical Trial Registration-http://www.clinicaltrials.gov. Unique identifier: NCT00745446. (Circulation. 2011;123:1721-1728.) Key Words: air pollution Ⅲ endothelium Ⅲ thrombosis T here is a robust and consistent association between air pollution and cardiorespiratory morbidity and mortality. [1][2][3][4] These harmful effects are most strongly associated with exposure to traffic-derived fine particles (particulate matter [PM] with a mean diameter Ͻ2.5 m [PM 2.5 ]) that originate predominantly from diesel engine exhaust emissions. 5 Diesel engines are popular because of their reliability, efficiency, and relatively low running costs. However, they generate up to 100 times more fine particles than petroleum engines of a similar size and contribute substantially to the global burden of PM air pollution. Editorial see p 1705 Clinical Perspective on p 1728According to the World Health Organization, air pollution is responsible for at least 800 000 premature deaths worldwide each year, with an average loss of life of 1 year. 6 The long-term risk of cardiovascular death rises by 76% for each 10-g/m 3 increase in PM 2.5 . 7,8 Short-term exposure has been linked to the triggering of acute myocardial infarction, 9 with patients 3 times more likely to be expo...

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

“…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. The difference is explained by the differences in composition, with black carbon particles (soot) being rich in (semi)volatile organic particles and metals.…”

“…This is an important paper, as this result contrasts markedly with the group's previous findings using diesel exhaust containing high concentrations of NO 2 . A subsequent paper, examining the vascular and prothrombic effects of diesel exhaust (300 µg/m 3 for 1 hour), with and without inclusion of a particle trap, demonstrated that a reduction of particle number and mass concentration, in the absence of changes in nitrogen oxides, was associated with reduced adverse cardiovascular outcomes (Lucking et al, 2011). This was interpreted as strongly supporting the view that fine particles, and not NO 2 , were driving the previously reported cardiovascular effects, especially as NO 2 concentrations increased almost five-fold with the particle trap.…”

“…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).…”

Endothelial Function

“…[61][62][63] Several studies have linked air pollution to endothelial dysfunction. 64,65 In a mouse model, air pollution induced insulin resistance and endothelial dysfunction. 66 This effect was attributable to increased adipose tissue inflammation, which has been linked to the pathogenesis of diabetes mellitus.…”

European Perspectives

“…This research demonstrates how interventions can make a real difference to cardiovascular health." 5 Professor Newby was also involved in another intervention study in 2008 examining the impact of the smoking ban in Scotland that also generated positive results. 6 The Study of Public Place Intervention on Tobacco Exposure (STOPIT), led by Professor Jill Pell, MD, FFPHM (see http://circ.ahajournals.org/content/120/6/f31), at the University of Glasgow, Glasgow, Scotland, found a 17% reduction in cases of myocardial infarction presenting to hospital after the smoking ban in public places came into force compared to before the ban.…”