Exposure to polycyclic aromatic hydrocarbons derived from vehicle exhaust gas induces premature senescence in mouse lung fibroblast cells.

Long-term exposure to vehicle exhaust gas may lead to various age-associated disorders, including cardiovascular disease and cancer. Polycyclic aromatic hydrocarbons (PAHs) belong to an important class of carcinogens, which are released into the environment by vehicles and are detectable at high levels in Chinese urban areas. However, whether vehicle exhaust gas (EG), and in particular the PAHs derived from EG, are able to induce cell senescence remains unclear. In the present study, vehicle EG and pure PAHs were used as pollution sources to investigate the effects of long-term exposure to PAH on the cellular processes occurring in mouse lung fibroblast cells (mLFCs). Using cell proliferation and apoptosis assays, it was demonstrated that benzopyrene (BaP) suppressed the proliferation of mLFCs, and benzanthracene (BaA) and BaP induced cell apoptosis. Molecular analysis suggested that long-term exposure to BaA and BaP was able to increase the protein expression levels of p53, p21 and the apoptotic factors involved in the caspase cascade, including caspase-3 and -9. Notably, the present study suggested that PAH exposure was able to promote cell senescence in mLFCs by activating the ATM serine/threonine kinase/H2A histone family member X pathway. The present study may provide novel insights into the underlying mechanism of vehicle EG and PAHs in promoting the development of age-associated diseases.