To study the effects of PM2.5 (particulate matter ＜2.5μm) on apoptosis and inflammatory response of RAW264.7 macrophages and the roles of inflammasome and ROS (reactive oxygen species). Methods RAW264.7 cells were divided into control group, PM2.5 group, PM2.5+TAK242 group, PM2.5+ROS(-) and PM2.5+ROS(+) groups. Cell activity was detected by CCK8, and intracellular ROS level was determined by ROS detection kit. Cell apoptosis was detected by flow cytometry, TLR4, NLRP1, NLRP3, NLRC4, AIM2 and Caspase-1 were detected by Western Blot, and IL-1β, IL-18 and IL-10 were detected by ELISA. Results PM2.5 can inhibit RAW264.7 activity in a concentration and time dependent manner, and promote macrophage apoptosis. Western Blot results showed that PM2.5 stimulated the expression of NLRP1, NLRP3, NLRC4 and AIM2 (P＜0.05), and TLR4 was also highly expressed(P＜0.05. ELISA showed that PM2.5 also promoted the secretion of pro-inflammatory cytokines IL-1β and IL-18 (P＜0.05), and inhibited the secretion of anti-inflammatory cytokines IL-10 (P＜0.05). After TAK242, TLR4 inhibitor,compared with PM2.5 group, the apoptosis rate was decreased(P＜0.05), and the polyinflammasomes and pro-inflammatory cytokines were also decreased (P＜0.05). PM2.5 increases the ROS level, and the apoptosis rate decreases after ROS inhibitors (P＜0.05). TLR4, polyinflammasomes and pro-inflammatory cytokines all decrease (P＜0.05), while ROS agonists show the opposite results. Conclusion PM2.5 promotes polyinflammasomes generation and induces RAW264.7 macrophages apoptosis and inflammatory response through TLR4/ROS pathway.