Chrysotile asbestos from four major mining areas in China was selected to prepare inhalable dust with particle size less than 10 μm. Male Wistar rats were exposed by non-exposure tracheal instillation and weighed and sacrificed at the time in 1, 3 and 6 months. The lung tissues were quickly separated, the lung morphology was observed and weighed, and the lung organ coefficient was calculated. The pathological changes of lung tissue were observed by light microscopy with HE staining, and the expression of p53 and p16 genes were determined by RT-PCR to investigate the biosafety of chrysotile fiber in China. The results show that the size of chrysotile fiber in the main mining areas was less than 10 μm, which could meet the standards of inhalable dust. The structure and active groups of the dust before and after grinding were not damaged. The body weight of the Wistar rats was significantly reduced, the lung weight was significantly increased, and the lung organ coefficient was increased. The lung tissues of Wistar rats in the exposed group showed severe pathological changes, and there were different degrees of congestion, edema, inflammatory cell infiltration and fibrosis. The expression of p53 and p16 genes in the lungs of Wistar rats exposed to 1~6 months was significantly decreased. Based on the above results, it was found that the inhalable fiber dust of chrysotile asbestos in four major mining areas in China damaged the lung tissue of Wistar rats in different degrees and ways. With the prolonged exposure time, the expression of p53 and p16 in the lung of Wistar rats was significantly decreased. It is inferred that the inhalable fiber dust of chrysotile asbestos in four major mining areas in China has the risk of lung cancer.