Real-world exposure of airborne particulate matter triggers oxidative stress in an animal model.

Epidemiological studies have shown a 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 C57BIV6 mice to environmentally relevant PM in fine and ultra fine ranges (diameter < 2.5 μm, PM(2.5)) using a "real-world" airborne PM exposure system. We investigated the pathophysiologic impact of PM(2.5) exposure in the animal model and in cultured primary pulmonary macrophages. We demonstrated that PM(2.5) exposure increased the production of reactive oxygen species (ROS) in blood vessels in vivo. Furthermore, in vitro PM(2.5) exposure experiment suggested that PM(2.5) could trigger oxidative stress response, reflected by an 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 PM(2.5) 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.