This study was designed to investigate the pathogenesis of chlorine gas (Cl 2 ) induced acute lung injury and oedema.Isolated blood-perfused rabbit lungs were ventilated either with air (n=7) or air plus 500 parts per million (ppm) of Cl 2 (n=7) for 10 min.Capillary pressure, measured by analysing the pressure/time transients of pulmonary arterial, venous and double (both arterial and venous) occlusions, was unchanged in both groups. In Cl 2 -exposed lungs, the fluid filtration rate increased from -0.228±0.25 to 1.823±1.23 mL·min -1 ·100 g -1 (p<0.001) and the filtration coefficient increased from 0.091±0.01 to 0.259±0.07 mL·min -1 ·cmH 2 O -1 ·100 g -1 (p<0.001). No changes were observed in the control lungs. The extravascular lung water/blood-free dry weight ratio was 8.6±1.6 in the Cl 2 group and 4.0±0.5 in the control group (p<0.001), confirming that the increase in lung weight was related to accumulation of extravascular fluid.Although the alveolar flooding by oedema is explained, in part, by the Cl 2 -induced epithelial injury, our results suggest that Cl 2 exposure induces acute lung injury and oedema due to an increased microvascular permeability.