We have examined the effects of chlorine gas inhalation (110 and 140 ppm) on cardiovascular and pulmonary function in nine anaesthetised and mechanically ventilated pigs. Four additional pigs, which were similarly treated but not exposed to gas, served as controls. Severe pulmonary dysfunction developed when the animals were exposed to 100 l of 140 ppm chlorine gas for 10 min. Five of six animals died within 6 h of exposure. This dose induced a rapid drop in arterial oxygen tension (P < 0.001 compared with controls, ANOVA), a biphasic decline in lung compliance (P < 0.001) and a gradual increase in pulmonary vascular resistance (P < 0.001) that eventually caused a significant reduction in cardiac output (P < 0.05). Microscopic examination showed sloughing of the bronchial epithelium and early infiltration with leukocytes, but largely intact alveoli. The sequence of events and the microscopic appearance suggested that the initial stage of pulmonary dysfunction (the first 1 or 2 h) was the result of mismatching of ventilation and perfusion. This was followed at a later stage by interstitial oedema and migration of immunocompetent cells into the tissue. We conclude that exposure to 100 l of 140 ppm chlorine gas induces a severe stereotypic lung injury with high mortality within 6 h in this anaesthetised animal model.