The aim of this study is to investigate the protective effect and the underlying mechanism of bilirubin on lung tissue damage  via macrophage efferocytosis in smoking-exposed rats. Six-week-old healthy male Wistar rats were randomly divided into six groups of ten. The rat smoking model was established by twelve weeks＇ smoking. A smoking withdrawal model was established by twelve weeks of smoking followed by four weeks of withdrawal. Exogenous bilirubin was given in treatment groups before daily smoking exposure. Specimens were retained for pulmonary histology and histopathological analysis. ELISA was used for the detection of cytokine levels in bronchoalveolar lavage fluid (BALF) and FACS for the percentage of macrophages with efferocytosis. The results showed that after twelve weeks of smoking exposure, the emphysema model was successfully established, and the cigarette smoke exposure significantly increased the infiltration of inflammatory cells, the levels of inflammatory cytokines, and lung tissue damage (all P＜0.05). In addition, smoking also affected macrophage polarization towards the M1 type. Smoking also affected macrophage efferocytosis  (all P＜0.05). The inflammatory response and damage of lung tissue after four weeks of smoking withdrawal were moderately alleviated (all P＜0.05), but still existed. Exogenous bilirubin intervention reduced the infiltration of inflammatory cells, the secretions of partial inflammatory cytokines, and relieved lung tissue damage (all P＜0.05), which might correlate to its regulation on the macrophage polarization state and efferocytosis (all P＜0.05). In conclusion, bilirubin may alleviate lung tissue damage caused by cigarette smoke exposure via multiple mechanisms such as anti-inflammatory, antioxidant, and immunomodulatory. The discovery of the effect of bilirubin on the polarization state and efferocytosis of macrophages is complementary to the known functions of bilirubin and provides the theoretical basis and new ideas for the application of bilirubin to treat cigarette smoke-related inflammatory diseases.