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Heavy metals bound to fine particulate matter from northern China induce season-dependent health risks: A study based on myocardial toxicity

Zhang, Yingying, Ji, Xiaotong, Ku, Tingting, Li, Guangke, Sang, Nan
Environmental pollution 2016 v.216 pp. 380-390
anthropogenic activities, apoptosis, burning, cadmium, cardiovascular diseases, children, chromium, coal, cobalt, copper, droplets, heavy metals, in vitro studies, inflammation, lead, manganese, mortality, nickel, particulates, rats, reactive oxygen species, risk, risk assessment, spring, toxic substances, toxicity, winter, zinc, China
Substantial epidemiological evidence has consistently reported that fine particulate matter (PM2.5) is associated with an increased risk of cardiovascular outcomes. PM2.5 is a complex mixture of extremely small particles and liquid droplets composed of multiple components, and there has been high interest in identifying the specific health-relevant physical and/or chemical toxic constituents of PM2.5. In the present study, we analyzed 8 heavy metals (Cr, Ni, Cu, Cd, Pb, Zn, Mn and Co) in the PM2.5 collected during four different seasons in Taiyuan, a typical coal-burning city in northern China. Our results indicated that total concentrations of the 8 heavy metals differed among the seasons. Zn and Pb, which are primarily derived from the anthropogenic source, coal burning, were the dominant elements, and high concentrations of these two elements were observed during the spring and winter. To clarify whether these heavy metals in the locally collected PM2.5 were associated with health effects, we conducted health risk assessments using validated methods. Interestingly, Pb was responsible for greater potential health risks to children. Because cardiovascular disease (CVD) is a main contributor to the mortality associated with PM2.5 exposure, we performed experimental assays to evaluate the myocardial toxicity. Our in vitro experiments showed that the heavy metal-containing PM2.5 induced season-dependent apoptosis in rat H9C2 cells through a reactive oxygen species (ROS)-mediated inflammatory response. Our findings suggested that heavy metals bound to PM2.5 produced by coal burning play an important role in myocardial toxicity and contribute to season-dependent health risks.