Copper in airborne fine particulate matter (PM2.5) from urban sites causes the upregulation of pro-inflammatory cytokine IL-8 in human lung epithelial A549 cells.

Abstract

Fine atmospheric particles, such as PM2.5, are strongly related to the onset and exacerbation of inflammatory responses leading to the development of respiratory and cardiovascular diseases. PM2.5 is a complex mixture of tiny particles with different properties (i.e., size, morphology, and chemical components). Moreover, the mechanism by which PM2.5 induces inflammatory responses has not been fully elucidated. Therefore, it is necessary to determine the composition of PM2.5 to identify the main factors causing PM2.5-associated inflammation and diseases. In the present study, we investigated PM2.5 from two sites (Fukue, a remote monitoring site, and Kawasaki, an urban monitoring site) with greatly different environments and PM2.5 compositions. The results of ICP-MS and EDX-SEM indicated that PM2.5 from Kawasaki contained more metals and significantly induced the expression of the pro-inflammatory cytokine gene IL-8 compared to the PM2.5 from Fukue. We also verified the increased secretion of IL-8 protein from exposure to PM2.5 from Kawasaki. We further investigated their effects on inflammatory response and cytotoxicity using metal nanoparticles (Cu, Zn, and Ni) and ions and found that the Cu nanoparticles caused a dose-dependent increase in IL-8 expression together with significant cell death. We also found that Cu nanoparticles enhanced the secretion of IL-8 protein. These results suggest that Cu in PM2.5 is involved in lung inflammation.