The effects of short‐term exposure to ozone on control and elastase‐induced emphysematous rats were examined to investigate whether emphysema would change the pulmonary susceptibility to oxidant air pollution. Emphysema was induced in rats after a single intratracheal instillation of 0.2 IU elastase/g body weight. Histologically, panacinar emphysema was apparent at 2, 4, 8, and 76 wk, that is, the total duration of the experiment. The diagnosis was confirmed by morphometry: the mean linear intercepts (MLI) of elastase‐treated rats were significantly increased at all observation times, whereas the internal surface areas (ISA) of the elastase‐treated rats were significantly decreased. In addition, pulmonary function tests provided supportive evidence for the diagnosis of emphysema. Respiratory system compliance and functional residual capacity showed a significant increase in elastase‐treated rats. No differences in inspiratory capacity or in forced vital capacity between control rats and elastase‐treated rats were observed. The above data are indicative for a rat model for elastase‐induced emphysema. Short‐term exposure to ozone of elastase‐treated rats revealed panacinar emphysema, including an inflammatory response in the centroacinar region. No differences in MLI as well as in ISA between ozone‐exposed rats (with or without emphysema) and their respective controls were observed. Short‐term exposure to ozone induced an identical, significant increase in protein content, lactate dehydrogenase, glucose‐6‐phosphate dehydrogenase, and glutathione peroxidase activities in lungs of normal and emphysematous rats. Moreover, these results strongly suggest that emphysematous rats are not more susceptible to ozone than nonemphysematous rats.