The acute effects of fine particulate matter constituents on circulating inflammatory biomarkers in healthy adults

• Published in: The Science of the total environment 2020-03, Vol.707, p.135989, Article 135989
• Main Authors: Zhang, Qingli, Niu, Yue, Xia, Yongjie, Lei, Xiaoning, Wang, Weidong, Huo, Juntao, Zhao, Qianbiao, Zhang, Yihua, Duan, Yusen, Cai, Jing, Ying, Zhekang, Li, Shanqun, Chen, Renjie, Fu, Qingyan, Kan, Haidong
• Format: Article
• Language: English
• Subjects: Adult; Air Pollutants; Air Pollution; Biomarkers; Chemical constituents; China; Environmental Exposure; Fine particulate matter; Humans; Panel study; Particulate Matter - analysis; Systemic inflammation
• ISSN: 0048-9697; 1879-1026
• DOI: 10.1016/j.scitotenv.2019.135989

Systemic inflammation is considered one of the key mechanisms in the development of cardiovascular diseases induced by fine particulate matter (PM2.5) air pollution. However, evidence concerning the effects of various PM2.5 constituents on circulating inflammatory biomarkers were limited and inconsistent. To evaluate the associations of short-term exposure to a variety of PM2.5 constituents with circulating inflammatory biomarkers. We conducted a panel study from May to October 2016 among 40 healthy adults in Shanghai, China. We monitored the concentrations of 27 constituents of PM2.5. We applied linear mixed-effect models to analyze the associations of PM2.5 and its constituents with 7 inflammatory biomarkers, and further assessed the robustness of the associations by fitting models adjusting for PM2.5 mass and/or their collinearity. Benjamini-Hochberg false discovery rate was used to correct for multiple comparisons. The associations of PM2.5 were strongest at lag 0 d with tumor necrosis factor-α (TNF-α), at lag 1 d with interleukin-6, interleukin-8, and interleukin-17A, at lag 02 d with monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1). After correcting for multiple comparisons in all models, Cl−, K+, Si, K, As, and Pb were significantly associated with interleukin-8; SO42− and Se were marginally significantly associated with interleukin-8; SO42−, As, and Se were marginally significantly associated with TNF-α; and Si, K, Zn, As, Se, and Pb were marginally significantly associated with MCP-1. Our results suggested that some constituents (SO42−, Cl−, K+, and some elements) might be mainly responsible for systemic inflammation triggered by short-term PM2.5 exposure. [Display omitted] •It remains unclear how PM2.5 constituents affect systemic inflammation differently.•27 constituents and 7 inflammatory biomarkers were evaluated in Shanghai, China.•SO42−, Cl−, K+ and some elements may be responsible for inflammation.