10th International Aerosol Conference September 2 - September 7, 2018 America's Center Convention Complex St. Louis, Missouri, USA
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Seasonal Variations in Fine Particle Composition from Beijing Prompt Oxidative Stress Response In Vivo and In Vitro
MICHAL PARDO, Fanfan Xu, Xinghua Qiu, Tong Zhu, Yinon Rudich, Weizmann institute of science, Israel
Abstract Number: 271 Working Group: Aerosol Toxicology
Abstract Exposure to air pollution can induce oxidative stress, inflammation and adverse health effects. To understand how seasonal and chemical variations drive health impacts, we investigated indications for oxidative stress and inflammation in mice and cell culture exposed to water and organic extracts from urban fine particles/PM2.5 (particles with aerodynamic diameter ≤ 2.5 μm) collected in Beijing, China. The heating season (HS, winter and part of spring) PM2.5 samples contained more pollutants than the non-heating season (NHS, summer and part of spring and autumn) PM2.5. The HS samples had high content of dissolved metals in the water extracts and polycyclic aromatic hydrocarbons (PAHs) in the organic extracts compared to the non-heating samples. An increased inflammatory response was detected in the lung and liver following exposure to the organic extracts compared to the water extracts, mostly in the HS PM2.5. While suppressed antioxidant response was observed in the lung, it was activated in the liver, again, more in the HS extracts. Nrf2 transcription factor, a master regulator of stress response that controls the basal oxidative capacity and induces the expression of antioxidant response, and its related genes were also induced. In the liver, elevated levels of lipid peroxidation adducts were measured, which correlated well with histologic analysis that revealed morphologic features of cell damage and proliferation, indicating oxidative and toxic damage. In addition, expression of genes related to detoxification of PAHs was observed. Lung alveolar cells silenced for nrf2 (siNrf2) demonstrated increased susceptibility to PM-induced cell death and a higher capacity to generate reactive oxygen species. Seahorse XFe96 Analyzer of siNrf2 cells showed involvement of the mitochondria, and a higher lipid peroxidation levels than their controls which were even more salient after exposure to PM. Altogether, the study suggests that the acute effects of PM2.5 can vary seasonally with stronger health effects in the HS than in the NHS in Beijing. These changes are attributed to the high content of PAH due to coal and biomass burning for residential heating. The signaling mechanisms of air pollution involves Nrf2 and the mitochondria.