As part of a study of human organ O₂ tolerance, lung flow-volume and spirometric measurements were performed repeatedly before, during, and after continuous O₂ exposures at 1.5, 2.0, and 2.5 ATA for average durations of 17.7, 9.0, and 5.7 h, respectively (effects of O₂ breathing at 3.0 ATA for 3.5 h were reported previously; J. M. Clark, R. M. Jackson, C. J. Lambertsen, R. Gelfand, W. D. B. Hiller, and M. Unger. J. Appl. Physiol. 71: 878-885, 1991). Additional measurements of pulmonary mechanical function, gas exchange, and alveolar inflammatory cells were obtained before and after O₂ exposure. Rates of pulmonary symptom development and lung volume reduction increased progressively with elevation of O₂ pressure. Average rates of vital capacity reduction over a useful range of O₂ pressures provided a valuable general description of pulmonary O₂ tolerance in humans. However, the existence of multiple pulmonary effects of O₂ toxicity and the complexity of their interactions require awareness that deviations from the average relationships may occur in different individuals or under varying conditions of O₂ exposure and subsequent recovery. The associated pulmonary function deficits may represent responses to a composite of direct and indirect effects of O₂ poisoning, along with related consequences and subsequent reactions to those effects.