In this study, A549 cells were exposed to PM_2.5 dust-fall of different concentrations. MTT assay was used to evaluate cell viability. Cell morphology was observed through Scanning Electron Microscopy (SEM). Flow cytometry was used to detect the cell cycle induced by PM_2.5. Then the expression levels of p53, p21, CDK1, c-myc and lncRNA H19 were detected by RT-PCR, and cyclin B1 was measured by Western-blot. In addition, the expression of p53, c-myc and CDK1 in A549 cell was detected after transferring H19 siRNA, with the purpose of investigating the mechanism of A549 cell cycle arrest induced by PM_2.5. The results showed that, compared with the control group, A549 cell viability was declined in a dose-dependent manner and time-dependent effect. It was observed that cell morphology was changed and the cell membrane surface adsorbed a large amount of dust particles. The proliferation of A549 cells was inhibited in G2/M phase after being treated by PM_2.5 for 24 h, and the expression of CDK1 and cyclin B1 was decreased by increasing the expression of p53, p21 and H19. In addition, the expression of H19 was successfully inhibited by transferring H19 siRNA, and then the expression of CDK1 was further decreased. It is inferred that exposure to PM_2.5 could inhibit the expression of CDK1 and cyclin B1 by activating p53 and p21 activity, induce G2/M phase arrest, and finally inhibit A549 cell proliferation. In addition, after being exposed to PM_2.5, lncRNA H19 may play a specific oncogenes role in treated cells in that it participated in the cell cycle progression by binding to p53 and c-myc, and hence low expression of H19 caused G2/M phase arrest more obviously.