Inhalation of diesel exhaust increases ex vivo thrombus formation and causes in vivo platelet activation in man. These findings provide a potential mechanism linking exposure to combustion-derived air pollution with the triggering of acute MI.

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...