Air pollution and cardiovascular disease

Air pollution is associated with increased cardiovascular morbidity and mortality. Recent experimental and epidemiologic studies show that particulate matter (PM) air pollution with PM10 or inhalable (thoracic) particles (mean aerodynamic diameter < 10 microm) is most consistently linked with acute and chronic cardiovascular effects. Fine (PM2.5) and ultrafine (PM0.1) particles (aerodynamic diameter < 2.5 and < 0.1 microm) are able to reach the small airways and terminal alveoli, and PM0.1 can also be translocated directly into the systemic circulation. PM2.5 and PM0.1 are mainly formed by fossil fuel combustion and are the main components of exhaust emissions from motor vehicles. A variety of biological mechanisms responsible for adverse cardiovascular outcomes associated with PM have been described, including the release of pro-oxidative and pro-inflammatory mediators from the lungs into the circulation, autonomic nervous system imbalance, and the direct actions on the heart and vasculature of ultrafine particles translocated into the systemic circulation. The induction of oxidative stress by these particles may be central to all of these putative pathways that trigger coagulation and thrombosis, increased heart rate and reduced heart rate variability, endothelial dysfunction, arterial vasoconstriction, apoptosis, and hypertension. In chronic exposures these alterations favor the development and progression of atherosclerosis and possibly of hypertension in the long term, and in the short term acute exposures contribute to plaque instability, affect various traditional risk factors and trigger acute cardiovascular events (myocardial ischemia and infarction, stroke, heart failure, arrhythmias, and sudden death), particularly in high-risk subjects. There are currently also significant concerns with the risks of engineered nanoparticles.