Objective To investigate the toxic effects of acrylamide (ACR) on the lung tissue of mice and its possible mechanism of action. Methods 4-week-old SPF male mice were randomly divided into a control and two ACR groups (10 mg/ (kg·d)group and 20 mg/ (kg·d)group), with eight mice in each group. The control group was given conventional drinking water. In the ACR groups, the exposure concentration of ACR was prepared according to 5 mL of drinking water per day which was changed every 3 days for 4 weeks. At the end of the experiment, lung tissue was sectioned for histopathological analysis. Related indexes of oxidative damage were detected. Immunofluorescence and Western Blot were used to detect the expression of Nrf2-ARE-pathway-related proteins. Results Compared with the control group, the body weight of mice decreased gradually with an increase in ACR concentration (P< 0. 01). Histopathological analysis showed that bronchiolar epithelial hypertrophy, alveolar epithelial hyperplasia, and the alveolar cavity area were significantly reduced in the ACR group, and the pathological changes were more obvious in the 20 mg/ (kg·d) group. Compared with the control group, the activity of GSH-Px (P< 0. 05), SOD (P< 0. 05), and CAT (P< 0. 01) in lung tissue decreased with an increase in ACR concentration, while the content of MDA increased significantly (P< 0. 01). Immunofluorescence result showed that, compared with the control group, the ACR group’s expression of Nrf2 protein in the lung tissue was significantly increased, and the highest expression was found in the 10 mg/ (kg·d)group (P< 0. 001). The nuclear translocation phenomenon occurred, and expression of the chaperone protein Keap1 was significantly decreased, with the lowest expression found in the 10 mg/ (kg·d)group (P< 0. 001). Western Blot result showed that, compared with the normal control group, expression of the Nrf2 gene and its downstream antioxidant protein HO-1 was increased in the lung tissue of the ACR group, and the highest level was found in the 10 mg/ (kg·d) (P< 0. 01). Expression of the chaperone protein Keap1 was significantly decreased, and the lowest expression was found in 10 mg/ (kg·d)group (P< 0. 01), but the expression of NQO-1 gradually increased with increased ACR intake concentration (P< 0. 01). Conclusions Exposure of adolescent mice to ACR can lead to lung tissue injury, which may be related to a redoxic imbalance of the lung tissue.