Abstract

Overproduction of reactive oxygen species (ROS) induced by atmospheric particles and subsequent inflammatory responses are considered as one of the most important pathological mechanisms with regard to the adverse effects of air pollution exposure. In this study, fine particulate matter (PM 2.5 ) samples were collected at a rural site in Guanzhong Basin, Northwest China, in both summer (August 3–23, 2016) and winter (January 5–February 1, 2017). Then, human bronchial epithelial BEAS-2B cells were exposed to the PM 2.5 , cultured for 24 h, and then assayed for particle-induced ROS and three inflammatory factors (tumor necrosis-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ)) in vitro . The oxidative potential (OP) induced by winter PM 2.5 samples was higher than that induced by summertime samples, whereas inflammatory values showed contrasting seasonal variations. Both OP and inflammatory factors were significantly correlated with most chemical compounds in winter, but not in summer, which was thought to be related mainly to the higher contribution from secondary aerosols formed during the warm season. Source apportionment results showed secondary aerosols formation have significant contribution to OP of PM 2.5 in both seasons, but the dominant oxidation processes is different. Secondary nitrates-related process was the major contributors regulating the OP in winter; however, secondary sulfates formation were mainly responsible for the ROS responses in summer. For primary emission, biomass burning, rather than coal emission or vehicle exhaust, was the significant source for OP of PM 2.5 in winter. In most cases, the source contribution of each inflammatory factor was similar to that of the ROS. Our results highlighted the significant health risk of atmospheric aerosols from biomass burning in the rural regions of Guanzhong Basin, Northwest China.