Effects of Acute Exposure to O3On Rats: Sequence of Epithelial and Inflammatory Changes in the Distal Airways

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Abstract
This study involves the analysis of the sequence of changes in lung epithelial permeability, free cells in the airways, prostaglandin E2 (PGE2) levels, polymorphonuclear leukocyte (PMN) flux, and alveolar lesions in rats exposed to 0.8 ppm ozone (O3) for 3 h and then studied at 4-h intervals up to 24 h postexposure. Protein content of the bronchoalveolar lavage (BAL) increased immediately after O3 exposure and returned to control levels by 16 h postexposure. Albumin concentration in the BAL also increased with time after O3 exposure, but the increase was more gradual than the protein increase. The lower albumin concentrations at 20 and 24 h postexposure were still higher than the control levels. While the total protein in the BAL could be attributed to tissue injury and increased transmucosal transport, the albumin primarily reflected elevated transport from the serum. Total cells in the BAL decreased immediately after the O3 exposure, but returned to near normal levels by 4 h. PGE, levels did not change significantly after O3 exposure. PMNs in the lung sections increased in number with time, peaked at 8 h, and returned to normal levels by 76 h following O3 exposure. The data suggest that the permeability changes may be produced by the direct toxic effects of O3 on the airway epithelia, but the PMNs contribute to the injury process, especially at the later stages. Lung lesions, represented by the thickening of the alveolar septae and increased cellularity, were present at 72 h postexposure and increased with time, thus coinciding with declining permeability at the later stages. The morphological changes lag behind the functional perturbations and appear to represent a phase of functional recovery.