Nasal, tracheal and bronchoalveolar injuries resulting from acute ozone exposure of rats were investigated by permeability changes.99mTc‐labeled diethylenetriaminepen‐taacetate (DPTA) and125l‐labeled bovine serum albumin (BSA) were selectively instilled into localized airway regions of anesthetized rats exposed to 0.8 ppm O3or clean air for 2 h. Transmucosal transfer of the radiolabeled tracers was detected by counting the radioactivity in blood samples collected at short postinstillation time intervals. Permeability measurements were made on d 0, 1, and 2 after O3exposure to analyze the extent and persistence of tissue injury in the nasal, tracheal, and bronchoalveolar regions. Normal mucosal permeability was low in nose, intermediate in bronchoalveolar zone, and high in trachea. The O3‐related injury, reflected by elevated permeability, was substantial in the trachea and bronchoalveolar zone but was minimal in the nose immediately after the exposure. Abnormal permeability persisted for less than 24 h in the trachea but for more than 24 h in the bronchoalveolar zone. The results are consistent with the properties of O3of causing greater injury in the smaller airways and the alveolar zone than in the trachea.