Atmospheric fine particulate matter (PM2.5) is a serious threat to human health. As a toxicant constituent, metal leads to significant health risks in a population, but exposure to PM2.5-bound metals and their biological impacts are not fully understood. In this study, we determined the metal contents of PM2.5 samples collected from a typical coal-burning city and then investigated the metabolic distributions of six metals (Zn, Pb, Mn, As, Cu, and Cd) following PM2.5 inhalation in mice in different developmental windows. The results indicate that fine particles were mainly deposited in the lung, but PM2.5-bound metals could reach and gather in secondary off-target tissues (the lung, liver, heart and brain) with a developmental window-dependent property. Furthermore, elevations in triglycerides and cholesterol levels in sensitive developmental windows (the young and elderly stages) occurred, and significant associations between metals (Pb, Mn, As and Cd) and cholesterol in the heart, brain, liver and lung were observed. These findings suggest that PM2.5 inhalation caused selective metal metabolic distribution in tissues with a developmental window-dependent property and that the effects were associated with lipid alterations. This provides a foundation for the underlying systemic toxicity following PM2.5 exposure based on metal components.
Keywords: Atmospheric fine particulate matter (PM(2.5)) exposure; Different developmental windows; PM(2.5)-bound metal metabolic distribution; Triglycerides and cholesterol alteration.
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