AAAR 37th Annual Conference October 14 - October 18, 2019 Oregon Convention Center Portland, Oregon, USA
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Organic Extracts of PM2.5 in Seoul Mediates Neutrophilic Inflammation and Aging in Lung Epithelial Cells
JIEUN PARK, Kyoung-Hee Lee, Jongbae Heo, Chang-Hoon Lee, Seung-Muk Yi, Chul-Gyu Yoo, Seoul National University, Seoul, Korea
Abstract Number: 834 Working Group: Aerosol Exposure
Abstract Ambient fine particulate matter with an aerodynamic diameter of 2.5 µm or less (PM2.5) is well known to be associated with adverse health effects. Several studies have been providing evidence that PM2.5 leads to inflammatory response by provoking oxidative stress. Airway epithelial cells are the first line of defense against the inhaled PM2.5 and key effector cells in the pathogenesis of several lung diseases. The objective of this study was to assess the effect of non-polar organic compounds of PM2.5 (high concentration events in Seoul) in lung epithelial cells.
PM2.5 samples were collected for 24-hr in Seoul, South Korea. Selected twelve samples for the PM2.5 events included four seasons and punched filters (4cm x 4cm) were extracted to be used for non-polar organic compound analysis and in vitro experiments. Organic compounds were analyzed using a GC-MS.
The organic extracts of PM2.5 samples were exposed to BEAS-2B. The results showed that the extracts specifically induced IL-8 production, but not IL-1β, IL-6, TNF-α, and IL-17. The PM2.5 samples activated extracellular signal-regulated kinase (ERK) and pretreatment of ERK inhibitor (U0126) completely suppressed PM2.5-induced release of IL-8, which suggest that PM2.5-induced IL-8 production is dependent on ERK activation. Aging in lung epithelial cells impairs lung function. We found that PM2.5 significantly increased the expression of aging markers such as p21 and p27. ERK activation, IL-8 production, and up-regulation of aging markers were also observed in primary human airway epithelial cells. These results positively correlated with the level of PAHs and n-Alkanes in PM2.5.
Our findings suggest that non-polar organic compounds of PM2.5 mediate neutrophilic inflammation and aging and chemical composition of organic compounds might be important to determine the toxicity of PM2.5 in respiratory system.