Objective This study was designed to evaluate the effect of short-term exposure to the particulate matter with diameters that are generally 2. 5 μm and smaller (PM_{2. 5} ) on the rat uterine injury, and to determine its mechanism. Methods Thirty Sprague-Dawley rats were randomly divided into: a control group, a 1. 5 mg/ kg body-weight (bw) low-dose PM_{2. 5} exposure group and a 6 mg/ (kg·bw) high-dose PM_{2. 5} exposure group, all of which were followed for 30 days. The pathological uterine changes were observed with hematoxylin-eosin staining (HE staining). Uterine apoptosis was evaluated with the TUNEL method, and the expression levels of cleaved caspase-3 were measured. In addition, the mRNA expression levels of glucose-regulated protein 78 (GRP78), PER-like ER kinase (PERK), eukaryotic initiation factor 2α (eIF2α) and C/ EBP homologous protein (CHOP) were measured with quantitative real-time PCR, and the protein levels involved in the PERK-eIF2α-CHOP signal pathway were tested using western blot assay. Results After short-term exposure, PM_{2. 5} resulted in atrophy and vacuolization of endometrial epithelial cells and glands. The apoptosis rates were (9. 93±1. 66)%, (29. 40±6. 96)% and (43. 58±8. 23)% in the uteruses in the control, low-dose exposure and high-dose exposure groups, respectively. Furthermore, the apoptosis rate was significantly higher ( P <0. 05) in the two exposure groups than in the control group. At the same time, the cleaved caspase-3 protein expression levels in the two exposure groups were significantly increased ( P <0. 05). The results of qPCR and western blot showed that the mRNA and protein levels of GRP78, PERK, eIF2α and CHOP in the two exposure groups were significantly higher than those in the control group ( P <0. 05). Conclusions After short-term exposure to PM_{2. 5}, the uterine structure of the rats is damaged, possibly as a consequence of PM_{2. 5} inducing uterine cell apoptosis via ERs, mediated by the PERK- eIF2α-CHOP pathway.