Selected cardiopulmonary variables were measured in anesthetized, male, White Leghorn type chickens before, during, and after 60 min exposure to various inhaled SO2 concentrations ranging from 0 to 5000 ppm. In one series of experiments, birds breathed through their nostrils and mouth; in a second series they breathed through a tracheal cannula. Exposure to 5000 ppm SO2 rapidly caused death in all birds with cannulated tracheae and in 4 of 5 birds with an intact respiratory system; one bird in each series of experiments died when exposed to 1000 ppm. Inhaling 100 ppm SO2 did not alter heart rate, blood pressure, tidal volume, respiratory frequency, or arterial blood gases and pH. Airway resistance was decreased by inhaling 500 ppm SO2 and was initially decreased but later greatly increased by inhaling 1000 ppm. Respiratory frequency and minute volume were decreased and PaCO2 was increased by inhaling 1000 ppm. The cardiopulmonary responses to inhaling 5000 ppm were generally augmentations of those responses which occurred when 1000 ppm was inhaled. The SO2 could not be detected in caudal thoracic or abdominal air sac gas at any concentration inhaled but vascular congestion and areas of brown discoloration appeared in the lungs of all birds that inhaled 5000 ppm and some that inhaled 1000 ppm. Mucous secretion in the trachea increased in some birds that inhaled 500 ppm SO2 and in most that inhaled higher concentrations. Chickens appear to have more tolerance for inhaled SO2 than most mammals but the pollutant gas at high concentrations detrimetally affects the cardiopulmonary system.