Objective To establish and evaluate a mouse model of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS). Methods Forty BALB/ c mice were divided randomly into a control group and a CS group. Mice in the CS group were subjected to passive smoking for 20 weeks and a COPD model was established. Morphological changes in the organs and lung, heart, liver, and kidney fibrosis were observed by hematoxylin-eosin ( HE) and Masson staining. Lung, cardiac, and brain cognitive function were evaluated by pulmonary function testing, small-animal ultrasound, and Morris water maze trials. Tumor necrosis factor-α ( TNF-α), interleukin (IL)-6 and IL-1β levels in lung and brain tissues were detected by ELISA. Liver and renal functions were measured by biochemical method. Results The alveolar septum was narrowed or broken in mice in the CS group, and the adjacent alveolar cavity was enlarged and fused, consistent with the pathological changes of COPD. Neuronal degeneration and necrosis were observed in the hippocampus, but there were no significant morphological changes in other organs. Masson staining showed no obvious fibrosis in the lung, heart, liver, or kidney in CS-group mice. The result of pulmonary function tests showed that the forced expiratory volume in 0. 1 second / forced vital capacity(FEV 0. 1 / FVC) and dynamic compliance were significantly decreased in the CS group compared with the control group, while airway resistance was obviously increased. Cognitive impairment in mice in the CS group was confirmed in the Morris water maze trial. TNF-α, IL-6, and IL-1β levels in lung and brain tissues were higher in the CS group compared with the control group. There were no significant differences in cardiac, liver, and renal functions between the groups. Conclusions A mouse model of COPD can be established by CS exposure for 20 weeks. Lung histomorphology, lung function, brain cognitive function, and levels of inflammatory factors can be used as indicators to evaluate the success of the model.