Center for Molecular Medicine & Genetics, Department of Immunology and Microbiology, The Wayne State University School of Medicine, Detroit, MI 48201, USA; Division of Cardiovascular Medicine, Davis Heart & Lung Research Institute, College of Medicine, Division of Environmental Health Sciences, College of Public Health, The Ohio State University, Columbus, OH 43210, USA
Received February 21, 2010, accepted March 5, 2010, available online March 15, 2010
Abstract: Epidemiological studies have shown strong link between air pollution and the increase of cardio-pulmonary mortality and morbidity. In particular, inhaled airborne particulate matter (PM) exposure is closely associated with the pathogenesis of air pollution- induced systemic diseases. In this study, we exposed C57BL/6 mice to environmentally relevant PM in fine and ultra fine ranges (diameter < 2.5 µm, PM2.5) using a "real-world" airborne PM exposure system. We investigated the pathophysiologic impact of PM2.5 exposure in the animal model and in cultured primary pulmonary macrophages. We demonstrated that PM2.5 exposure increased the production of reactive oxygen species (ROS) in blood vessels in vivo. Furthermore, in vitro PM2.5 exposure experiment suggested that PM2.5 could trigger oxidative stress response, reflected by increased expression of the anti-oxidative stress enzymes superoxide dismutase-1 (SOD-1) and heme oxygenase-1(HO-1), in mouse primary macrophages. Together, the results obtained through our “real- world” PM exposure approach demonstrated the pathophysiologic effect of ambient PM2.5 exposure on triggering oxidative stress in the specialized organ and cell type of an animal model. Our results and approach will be informative for the research in air pollution- associated physiology and pathology. (IJPPP1002002).
Key words: Air pollution; airborne particulate matter; oxidative stress; reactive oxygen species; animal model