FANGXIA SHEN, Fobang Liu, Xiangyu Zhang, Jing Li, Kira Ziegler, Ting Zhang, Tianle Zhu, Manabu Shiraiwa, Haijie Tong, Maosheng Yao, Ulrich Pöschl, Kurt Lucas, Beihang University
Abstract Number: 678 Working Group: Health Related Aerosols
Abstract China has experienced frequently serious haze weather in recent years. Strong association between haze events and respiratory as well as cardiovascular disease was reported. Although fine particulate matter (PM2.5) was shown to play a crucial role in the higher incidence and exacerbation of respiratory diseases, the key underlying mechanisms are still not well understood. In our study, PM2.5 samples were collected during a haze period in winter 2016 of Beijing, China. Characterization of the PM2.5 samples were performed, including ions, metals, redox activity and particle-bound LPS. We measured inflammatory cytokine releases from human macrophages that were exposed to the water elution of PM2.5 from distinct days. Additionally we mixed (spiked) these PM2.5 extracts with lipopolysaccharide (LPS), to mimic the inflammatory conditions in sick individual's respiratory tract with a high bacterial load. Differential cellular inflammatory signals, i.e., interleukin 8 (IL-8), IL-1Β and tumor necrosis factor (TNF), were observed upon exposure to the PM2.5 from same volume of air but from distinct days at sub-toxic levels. Compared to the macrophages treated with PM2.5 alone, up to 13-folds more IL-8 were released from macrophages treated with PM2.5 spiked with LPS (100 pg/mL). Moreover, changes in the expression of oxidative stress-related genes were observed to depend on PM2.5 mass levels. When spiked with LPS at 100 pg/mL, 2.5-folds higher up-regulation of the gene superoxide dismutase 2 (SOD2) was observed for the sample collected from polluted day compared to that from clean day. Our results suggest that particle-bound LPS as well as lung-resident LPS along with other constitutes mediates the PM2.5-related inflammatory effects, thereby contributing to the deterioration of existing chronic respiratory disease, like COPD. This work highlights the need to consider the biological fraction of PM2.5 such as LPS when assessing its health effects.