Particulate air pollution, systemic oxidative stress, inflammation, and atherosclerosis

Abstract

Air pollution has been associated with significant adverse health effects leading to increased overall morbidity and mortality of worldwide significance. Epidemiological studies have shown that the largest portion of air pollution-related mortality is due to cardiovascular diseases, predominantly those of ischemic nature. Human studies suggest an association with atherosclerosis and increasing experimental animal data support that this association is likely to be causal. While both gasses and particles have been linked to detrimental health effects, more evidence implicates the particulate matter (PM) components as major responsible for a large portion of the proatherogenic effects. Multiple experimental approaches have revealed the ability of PM components to trigger and/or enhance free radical reactions in cells and tissues, both ex vivo as well as in vivo. It appears that exposure to PM leads to the development of systemic prooxidant and proinflammatory effects that may be of great importance in the development of atherosclerotic lesions. This article reviews the epidemiological studies, experimental animal, and cellular data that support the association of air pollutants, especially the particulate components, with systemic oxidative stress, inflammation, and atherosclerosis. It also reviews the use of transcriptomic studies to elucidate molecular pathways of importance in those systemic effects.

Fig. 1

Potential mechanisms how exposure to PM leads to CV disease. Three main pathways could mediate PM-related cardiovascular effects: (1) induction of autonomic nervous system imbalance, (2) development of pulmonary oxidative stress and inflammation with systemic “spill-over” of inflammatory mediators (e.g., cytokines, activated cells), (3) translocation of particles and/or chemical constituents to the systemic circulation. CHF congestive heart failure, CV cardiovascular, CVA cerebrovascular accident, EC endothelial cells, IHD ischemic heart disease, PVD peripheral vascular disease. Pulmonary inflammation may range from activation of inflammatory molecular pathways without histological evidence of it to overt infiltration by inflammatory cells. Taken from Araujo and Book (2011)