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

Background 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. Objectives To evaluate the associations of short-term exposure to a variety of PM2.5 constituents with circulating inflammatory biomarkers. Methods 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. Results 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. Conclusions 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.