Epidemiological　studies　have　corroborated　that　respiratory　diseases,　including　lung　cancer,　are　related　to　fine　particulate　matter　(＜2.5　mu　m)　(PM2.5)　exposure.　The　toxic　responses　of　PM(2.5)are　greatly　influenced　by　the　source　of　PM2.5.　However,　the　effects　of　PM(2.5)from　Beijing　on　bronchial　genotoxicity　are　scarce.　In　the　present　study,　PM(2.5)from　Beijing　was　sampled　and　applied　in　vitro　to　investigate　its　genotoxicity　and　the　mechanisms　behind　it.　Human　bronchial　epithelial　cells　16HBE　were　used　as　a　model　for　exposure.　Low　(67.5　mu　g/mL),　medium　(116.9　mu　g/mL),　and　high　(202.5　mu　g/mL)　doses　of　PM(2.5)were　used　for　cell　exposure.　After　PM(2.5)exposure,　cell　viability,　oxidative　stress　markers,　DNA　(deoxyribonucleic　acid)　strand　breaks,　8-OH-dG　levels,　micronuclei　formation,　and　DNA　repair　gene　expression　were　measured.　The　results　showed　that　PM(2.5)significantly　induced　cytotoxicity　in　16HBE.　Moreover,　the　levels　of　reactive　oxygen　species　(ROS),　malondialdehyde　(MDA),　and　cellular　heme　oxygenase　(HO-1)　were　increased,　and　the　level　of　glutathione　(GSH)　was　decreased,　which　represented　the　occurrence　of　severe　oxidative　stress　in　16HBE.　The　micronucleus　rate　was　elevated,　and　DNA　damage　occurred　as　indicators　of　the　comet　assay,　gamma-H2AX　and　8-OH-dG,　were　markedly　enhanced　by　PM2.5,　accompanied　by　the　influence　of　8-oxoguanine　DNA　glycosylase　(OGG1),　X-ray　repair　cross-complementing　gene　1　(XRCC1),　and　poly　(ADP-ribose)　polymerase-1　(PARP1)　expression.　These　results　support　the　significant　role　of　PM(2.5)genotoxicity　in　16HBE　cells,　which　may　occur　through　the　combined　effect　on　oxidative　stress　and　the　influence　of　DNA　repair　genes.