Objective To investigate the effect and mechanisms of PM2. 5 on atherosclerotic plaques in ApoE- knockout mice. Methods Thirty-two 8-week-old male ApoE^{- / -} mice were divided into two groups, both fed with a high-fat diet: a control group that was treated with normal saline by intratracheal instillation, and an experimental group that was exposed to PM2. 5 (30 mg / kg body weight) saline suspension by intratracheal instillation. We measured PM2. 5 in whole blood using inductively coupled plasma mass spectrometry (ICP-MS), and measured lipids and inflammatory factors using standard method . Echocardiography was used to evaluate cardiac function. The whole descending arteries were stained with Oil Red O, aortic roots were stained with Movat, and descending arteries were investigated using quantitative PCR. Results In the PM2. 5 group,We observed elevated heavy metal components (P < 0.05),but there was no significant change in heart function(P > 0.05),blood glucose and lipid levels(P > 0.05).We also observed elevated serum inflammatory factor levels (P < 0.05). In addition, the PM2. 5 group had larger atherosclerotic plaques (P < 0. 05), elevated levels of the inflammatory factors IL-6, TNF-α, and Lp-PLA2, and elevated levels of the NADPH oxidase subunits p22phox and p47phox (P < 0. 05). Conclusions In ApoE^{- / -} mice, PM2. 5 exposure is associated with increased inflammatory factors and oxidative stress, thus contributing to the progression of atherosclerosis.