Objective To study the effects of chronic PM2. 5 exposure on lung inflammation and NLRP3inflammasome activation in mice, and to provide a new target for prevention and treatment of lung injury caused by PM2. 5.Methods Male C57BL/6J mice were exposed to two doses of PM2. 5 by tracheal instillation [2, 10 mg/ (kg.bw)], andthe control mice were instilled with normal saline. After mice had been instilled for 20 times (1 time every 3 days), bloodand lung tissues were collected. Blood cells were counted, and lung tissue macrophage levels were measured usingimmunofluorescence staining. Interleukin (IL)-1β and IL-18 levels and caspase-1 activity in lung tissues were determinedusing ELISA and caspase-1 activity measurement kits. The expression levels of NLRP3 inflammasome-associated mRNA inlung tissue were detected using real-time PCR. Results The two doses of PM2. 5 significantly reduced the percentage ofmonocytes ( P < 0. 01) and induced lung inflammation. The PM2. 5-treated mice had a higher percentage of neutrophils ( P < 0. 01), a higher in caspase-1 activity ( P < 0. 01), and a higher in mRNA expression of NLRP3 and ASC ( P < 0. 01) inlung tissues compared with the control mice. IL-1β and IL-18 levels in the lung tissues of the two PM2. 5-exposed groupswere significantly higher than those seen in the control group (both P < 0. 01). Conclusion Chronic PM2. 5 exposure may induce lung inflammation by activating the NLRP3 inflammasome in the lung tissue.