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Inflammation Response of Water-Soluble Fractions in Atmospheric Fine Particulates: A Seasonal Observation in 10 Large Chinese Cities

Author:
Ma, Huimin, Li, Jun, Wan, Cong, Liang, Yaohui, Zhang, Xiangyun, Dong, Guanghui, Hu, Liwen, Yang, Boyi, Zeng, Xiaowen, Su, Tao, Lu, Shaoyou, Chen, Shejun, Khorram, Mahdi Safaei, Sheng, Guoying, Wang, Xinming, Mai, Bixian, Yu, Zhiqiang, Zhang, Gan
Source:
Environmental science & technology 2019 v.53 no.7 pp. 3782-3790
ISSN:
1520-5851
Subject:
DNA methylation, aerosols, biomass burning, carbohydrate structure, cities, coal, combustion, endotoxins, gene expression, genes, human health, inflammation, interleukin-6, interleukin-8, ions, lead, metalloids, nuclear magnetic resonance spectroscopy, organic carbon, particulates, risk, seasonal variation, secretion, toxicity, water solubility
Abstract:
Spatiotemporal trends in pro-inflammatory (interleukin (IL)-6 and IL-8) release after exposure to the water-soluble fractions of PM₂.₅ sampled in 10 large Chinese cities over 1 year were investigated. Chemical components (water-soluble ions, metal(loid) elements, water-soluble organic carbon (WSOC), humic-like substances (HULIS), and endotoxins) in PM₂.₅ samples were measured, and the molecular structure of WSOC was also analyzed by nuclear magnetic resonance. Changes in DNA methylation and gene expression of candidate genes were also evaluated to explore the potential mechanisms. PM₂.₅ from southern cities induced lower pro-inflammatory responses compared to those from northern cities. Seasonal differences in toxicity were noted among the cities. IL-6 was significantly correlated with HULIS (as the main fraction of WSOC with oxygenated carbohydrate structures characteristic), Pb, and endotoxin. Furthermore, DNA methylation and gene expression changes in RASSF2 and CYP1B1 were related to pro-inflammatory secretion. Certain components of PM₂.₅, rather than PM₂.₅ mass itself, determine the pro-inflammatory release. In particular, HULIS, which originated from primary biomass burning and residual coal combustion, and secondary organic aerosols, appear to be the key component in PM₂.₅ to induce human health risk.
Agid:
6355783