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July 13th, 2011:

PM2.5 Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation

Air pollution is increasingly recognized as an important and modifiable risk factor for cardiovascular disease.1 Acute exposure has

been linked to a range of adverse cardiovascular events, including hospital admissions with angina,2myocardial infarction,3 and

heart failure,4 and long-term exposure increases the lifetime risk of death from coronary heart disease.5 Long-term residential

exposure to air pollution is also associated with the extent of atherosclerosis in the carotid and coronary blood vessels.6 – 12

These associations are strongest for fine particulate matter (PM2.5) air pollution that arises from a variety of sources, including

the combustion of diesel fuel by automobiles. This important source of PM2.5 is thought to explain the association between transient

exposure to road traffic and the triggering of acute myocardial infarction.13


Inhalation of dilute diesel exhaust (but not the associated gaseous pollutants or carbon nanoparticles alone) impairs vascular function

in man. These findings suggest that the adverse vascular effects of diesel exhaust are predominately mediated by combustion-derived

particles and provide a rationale for testing environmental health interventions to reduce particulate emissions to establish

whether they can reduce the incidence of cardiovascular events.

Download PDF : eurheartj.ehr195.full