Pulmonary epithelial permeability in rats exposed to O3

Abstract

Measurements of pulmonary epithelial permeability were made in rats exposed for 2 h to either purified air or ozone (O ₃ ) at concentrations of 0.8 or 2 ppm. [ ^99m Tc]Dieth‐ylenetriaminepentaacetate ([ ^99m Tc]DTPA) (492 daltons) and ¹²⁵ l‐labeled bovine serum albumin (T ¹²⁵ /]BSA) (69,000 daltons) were injected intravenously, and the lungs were lavaged 6 min later. In rats exposed to air, transfer of the larger tracer molecule (BSA) from blood to the lavage fluid was less than that of the smaller molecule (DTPA) when the amount of tracer in the lavage fluid was calculated as percent of the counts in femoral artery blood 5 min after injection, i.e., 1 min prior to lavage. In rats exposed to O ₃ , alveolar permeability increased in a dose‐related fashion, the increase under all exposure conditions was greater for the smaller molecule than for the larger one, and the permeability was reversible with time. The increase in permeability from blood to air was comparable to the increase from air to blood reported earlier (Bhalla et al., 1986). The increased permeability provided an early and reliable indicator of short‐term O ₃ exposure effect in rats. Autoradiography by electron microscopy identified multiple pathways for BSA transfer from blood to the alveolar space. Crains produced by [ ¹²⁵ /]BSA were localized over endothelial and epithelial cell surfaces, were associated with cytoplasmic vesicles, were over cell surface invaginations, and were found in the cytoplasm of apparently degenerating cells. Although defects in tight junctions of alveolar type I cells were observed in lungs of rats exposed to O ₃ , auto‐radiographic grains also appeared in intercellular spaces, with the intercellular junctions remaining intact.