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Although the strongly causal associations were between fine particulate matter (PM_2.5) and cardiovascular disease, the toxic effect and potential mechanism of PM_2.5 on heart was poorly understood. Thus, the aim of this study was to evaluate the cardiac toxicity of PM_2.5 exposure on human cardiomyocytes (AC16). The cell viability was decreased while the LDH release was increased in a dose-dependent way after AC16 exposed to PM_2.5. The reactive oxygen species (ROS) generation and production of malondialdehyde (MDA) were increased followed by the decreasing in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). The damage of mitochondria was observed by ultra-structural analysis and MMP measurement. The apoptotic rate of AC16 were markedly elevated which was triggered by PM_2.5. In addition, the proteins involved in mitochondria- mediated apoptosis pathway were …