Key result
Particulate-induced oxidative stress emerges as a key driver of air pollution's cardiovascular toxicity.
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Air pollution has been estimated to be responsible for several millions of deaths worldwide per year, the majority of which have been attributed to cardiovascular causes. The particulate matter in air pollution has been shown impair vascular function, increase blood pressure, promote thrombosis and impair fibrinolysis, accelerate the development of atherosclerosis, increase the extent of myocardial ischaemia, and increase susceptibility to myocardial infarction. The pathways underlying these effects are complex and poorly understood; however, particulate-induced oxidative stress repeatedly emerges as a potential mechanism in all of these detrimental cardiovascular actions. The present mini-review will use diesel exhaust as an example of a pollutant rich in combustion-derived nanoparticles, to describe the potential by which oxidative stress could drive the cardiovascular effects of air pollution.
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Mark R. Miller (2014) conducted a review in Cardiovascular disease associated with particulate air pollution. Particulate air pollution (e.g., diesel exhaust nanoparticles) was evaluated. Particulate-induced oxidative stress is a potential primary mechanism driving the detrimental cardiovascular actions of air pollution, such as those from diesel exhaust nanoparticles.
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