Few studies have focused on the impact of particulate matter (PM) exposure with respect to the relationship between PM-induced inflammation and the levels of trace metals in tissues and organs. In this study, C57BL/6 male mice were exposed to ambient air alongside control mice breathing air filtered through a high-efficiency particulate air (HEPA) filter. In both groups, mRNA levels of pro- and anti-inflammatory cytokines were measured after 4, 8 and 12 weeks together with the trace metal contents of the lungs, heart, liver, hippocampus and blood. PM exposure resulted in a general upward trend in the levels of pro-inflammatory cytokines in lung, heart, liver and hippocampus. By contrast, IL-10 mRNA expression varied depending on the organ, with a continuous upward trend in heart and liver and an up-regulation at 8 weeks followed by a down-regulation at 12 weeks in lung and hippocampus. The disturbed homeostasis of inflammatory cytokines was accompanied by changes in trace metal levels in the mice. These alterations may have constituted a compensatory effect conferring protection from inflammatory damage. However, prolonged PM exposure finally resulted in the deficiency of several essential trace metals in the lungs and hippocampus, which may have contributed to the observed histological changes typical of an inflammatory response.
Keywords: Homeostasis; Inflammatory cytokine; Particulate matter; Trace metal.
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