Objective To develop a rat model of battleship fire?related smoke inhalation?induced acute lung injury using combustion of composite materials with a controllable temperature. Methods We designed a smoke?generating chamber and a test chamber. Sober rats were restricted to cages located inside the chamber during the experiments. In aim one, we investigated the survival rates at different inhalation times (15, 30, and 50 min). In aim two, we evaluated blood gas values, lung pathological scores, pro?inflammatory molecules, and protein concentrations in the bronchoalveolar lavage fluid, circulating white cells, and liver and renal functions at 1 h, 6 h, and 24 h after 30 min smoke inhalation. Results The survival rates at the different inhalation periods were 84. 21% (15 min), 25% (30 min), and 0% (50 min). There was a significant increase in carboxyhaemoglobin (COHB), lactate, and partial pressure of carbon dioxide (PCO2 ) at 1 h post injury ( P < 0. 05), which then gradually returned to normal. In the bronchoalveolar lavage fluid (BALF), the protein concentration and lung injury were score increased immediately after smoke inhalation, and persisted until 24 h. In the BALF, the total number of leukocytes cells significantly increased after smoke inhalation, while the proportion of macrophages significantly decreased at 6 h, then slightly recovered at 24 h; neutrophils showed the opposite trend. By western blot, there was a significant increase in signal pathway factors and inflammatory factors at 6 h recovery. There were no changes in the liver or renal functions after smoke inhalation. Conclusions This stable and reliable rat smoke inhalation injury model induced using our novel smoke generators is characterized by activation of inflammatory signaling pathways, inflammatory cell changes, and lung injury. This model may be useful for studies examining acute and chronic lung injury.