In this study, the authors investigated the role of reactive oxygen species (ROS) in inducing A549 apoptosis by activated mitochondria apoptosis pathway in chrysotile asbestos. Human lung epithelial cell (A549) cells were exposed to different concentrations of chrysotile asbestos dust and, on such a basis, the authors conducted detection of cell viability by MTT assay and detection of cell apoptosis rate, intracellular ROS level and mitochondrial membrane potential by flow cytometry before and after pretreatment of N-acetyl-l-cysteine (NAC) of ROS inhibitor, and then performed determination of caspase-3 and p53 protein expression level by Western blot. The experimental results show that chrysotile asbestos dust can reduce the survival rate of A549 cells and present the effectiveness relationship between the time and the dose. NAC could significantly reduce intracellular ROS level, prevent mitochondrial membrane potential declining, lower the expression level of caspase-3, p53 protein, and inhibit the occurrence of some cell apoptosis. The results indicate that ROS could activate mitochondrial apoptotic pathway by raising p53 protein expression and thus induce apoptosis of A549 cells.