The role of free radicals in the precipitation of lung damage after hydrogen sulfide inhalation was investigated in rats, which were killed right after and in the 1st, 6th,12th, 24th, and 72nd hour after exposure to 100 and 220 ppm of hydrogen sulfide (H2S) for 3 hours respectively. Malondialdehyde(MDA) level in lung homogenate and in bronchoalveolar lavage fluid (BALF), protein content and the number of leucocytes and pulmonary alveolar macrophages (PAM) in BALF, superoxide dismutase(SOD),glutathione(GSH),and vitamin E(VE)level in lung tissue and blood were determined. It was found that H2S inhalation resulted in an increase of MDA level which occurred much earlier after exposure to 220 ppm than after exposure to 100 ppm. Protein content was increased in the 1st, 6th, and 12th hour after inhalation. The number of leucocytes and PAM were increased, which implies the existence of inflammatory response in the respiratory tract. SOD activity decreased in the early period after inhalation but significantly increased later. Both GSH and VE levels decreasedThese findings suggest that H2S inhalation induces an inflammatory response in the respiratory tract and an increase of free radical formation which in turn brings about exessive lipid peroxidation. It is concluded that free radical formation is a contributing factor of lung damages after H2S inhalation.