Cardiovascular effects of ambient particulate air pollution exposure.

Abstract

An association between high levels of air pollutants and human disease has been known for more than half a century. Air pollution is composed of a heterogeneous mixture of compounds including ozone (O3), carbon monoxide (CO), sulfur dioxide (SO2), nitrogen oxides (NOx), liquids, and particulate matter (PM). Substantial epidemiological evidence implicates air pollution, particularly PM, as a major risk factor with serious consequences on human health.1–3 Of particular interest in PM are the particles that are ≤10 μm in diameter (PM10) because they are the PM that ultimately enters the lungs.4 PM is further divided into coarse (10 to 2.5 μm; PM10–2.5), fine (<2.5 μm; PM2.5), and ultrafine (<0.1 μm; PM0.1) particles.1 These particles are composed of solid and liquid components that originate from vehicle exhaust, road dust, smokestacks, forest fires, windblown soil, volcanic emissions, and sea spray. Particle size, surface area, and chemical composition determine the health risk posed by PM. Particulate and gaseous pollutants coexist in the air and may induce adverse health effects, whereas compelling data implicate PM as a major perpetrator of various types of human disease. PM rarely exists by itself within the ambient environment because gaseous and semivolatile/volatile compounds (ie, aldehydes and polycyclic aromatic hydrocarbons) are constantly changing and interacting. Many of these vapor-phase compounds attach to the surface of PM and/or by themselves form secondary aerosol particles. Because of their small size, PM2.5 and PM0.1 are inhaled deeply into the lungs, with a portion depositing in the alveoli and entering the pulmonary circulation and presumably the systemic circulation. The adverse effects of PM on the cardiovascular system have been established in a series of major epidemiological and observational studies.5–9 Although life expectancy has been improved significantly since air pollution levels …