Oxidative stress indices induced by industrial and urban PM2.5-bound metals in A549 cells

The detrimental effects of atmospheric fine particulate matter (PM2.5) on human health are of major global concern. PM2.5-bound metals are toxic compounds that contribute to cellular damage. To investigate the toxic effects of water-soluble metals on human lung epithelial cells and their bioaccessibility to lung fluid, PM2.5 samples were collected from both urban and industrial areas in the metropolitan city of Tabriz, Iran. Oxidative stress indices, including proline content, total antioxidant capacity (TAC), cytotoxicity, and DNA damage levels of water-soluble components of PM2.5, were evaluated. Furthermore, an in vitro test was conducted to assess the bioaccessibility of various PM2.5-bound metals to the respiratory system using simulated lung fluid. PM2.5 average concentrations in urban and industrial areas were 83.11 and 97.71 μg/m3, respectively. The cytotoxicity effects of PM2.5 water-soluble constituents from urban areas were significantly higher than in industrial areas and the IC50 was found to be 96.76 ± 3.34 and 201.31 ± 5.96 μg/mL for urban and industrial PM2.5 samples, respectively. In addition, higher PM2.5 concentrations increased the proline content in a concentration-dependent manner in A549 cells, which plays a protective role against oxidative stress and prevents PM2.5-induced DNA damage. Also, the partial least squares regression revealed that Be, Cd, Co, Ni, and Cr, were significantly correlated with DNA damage and proline accumulation, which caused cell damage through oxidative stress. The results of this study showed that PM2.5-bound metals in highly polluted metropolitan city caused substantial changes in the cellular proline content, DNA damage levels and cytotoxicity in human lung A549 cells.