Abstract：To investigate the effects and mechanisms of PM2.5 and its typical components on cellular senescence in lung tissue, human fetal lung fibroblast cells (MRC-5) were exposed to SRM1649a as PM2.5 standard, carbon black FW200 as the core particle, and benzo[a]pyrene (B[a]P) as the main organic component, respectively. The experiments were conducted to assess the cellular senescence of MRC-5 cells by measuring SA-β-Gal activity and clarify the mechanism of cellular senescence induced by intracellular reactive oxygen levels, DNA damage and mitochondrial membrane potential. It was showed that the treatment of SRM1649a and B[a]P significantly increased the proportion of cellular senescence in MRC-5 cells with no obvious effect on cellular viability, whereas cellular senescence was not remarkably changed in the FW200-exposed group. Mechanism studies indicated that FW200 treatment caused only DNA damage rather than cellular senescence, while exposure to B[a]P induced cellular senescence by triggering changes in ROS levels. Furthermore, the mixture SRM1649a could lead to DNA double-strand breaks and decrease the mitochondrial membrane potential, which induced cellular senescence in terms of DNA damage and mitochondrial dysfunction. These results suggested that the toxic effects induced by the main components of PM2.5 were different, and synergistic promoting effects are manifested in PM2.5 as the mixture.
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