Air Pollution and Cardiovascular Disease

Abstract

Numerous epidemiological studies report consistent associations between exposure to urban air pollution and cardio-respiratory morbidity and mortality. One of the important discoveries of these epidemiological studies during the last decade was that the increased mortality associated with enhanced air pollution exposure was not due only to pulmonary diseases, but mainly to cardiovascular diseases. (Zanobetti et al. 2003, Samet et al. 2000, Dockery et al. 1993, Jerrett et al. 2005, Pope et al. 2004a, Pope et al. 2002, Simkhovich, Kleinman and Kloner 2008, Nawrot, Nemmar and Nemery 2006, Hoek et al. 2002, Katsouyanni et al. 2001, Dominici et al. 2003). The focus in the initial epidemiological research was directed towards the association between both short-term and long-term exposure to air pollution and arterial cardiovascular effects, such as myocardial infarction. These landmark studies, in the beginning of the 90's, were quickly followed by experimental studies in humans and in rodents, to unravel the underlying pathophysiological mechanisms. The number of publications in this field increased exponentially, so that by the beginning of 2011, a search through PubMed using the MeSH terms 'air pollution' and 'cardiovascular disease' retrieved almost 1300 hits. Ambient environmental air pollutants include gaseous (carbon monoxide, nitrogen oxides, sulfur dioxide, ozone) and particulate components. The particulate component, particulate matter (PM), is subdivided based on size ranges into 'thoracic particles' (PM10, with a mean aerodynamic diameter 2.5 μm and <10 μm), 'fine particles' (PM2.5, <2.5 μm), and ultra-fine particles (UFP, <0.1 μm). Although exposure to some gaseous components has been linked to cardiovascular events, the larger body of evidence points towards the deleterious effects of the particulates in air pollution. Therefore, this chapter will focus mainly on the cardiovascular morbidity induced by PM exposure. Active cigarette smoking has been established as a major independent cause of cardiovascular disease (HHS 2004). The inhaled dose of fine particles from ambient air pollution, as from secondhand cigarette smoke, is extremely small compared with that from active cigarette smoking. Accordingly, the estimated relative risks from active smoking, even at relatively light smoking levels, are substantially larger than the risks from ambient air pollution or secondhand smoke. However, the risks induced by these latter 2 types of exposure are higher than would be expected from a simple linear extrapolation based on the amount of inhaled PM from active smoking (Pope et al. 2009), and have important public health implications (Nawrot et al. 2011).