Transport of macromolecules and particles at target sites for deposition of air pollutants.

This study analyzed rats' nasal, tracheal and bronchoalveolar epithelial permeability to macromolecules after they were exposed, in 2- or 4-hour periods of rest or exercise, to ozone (O3) (0.6, 0.8 or 2 ppm), nitrogen dioxide (NO2) (2.5, 6 or 12 ppm) or formaldehyde (10 ppm). Exercise was performed on a treadmill operated at a speed that led to a 2-fold increase in oxygen consumption. Histopathologic and electron microscopic cytochemical and autoradiographic studies were performed to identify the structural aspects of mucosal response. In rats not exposed to pollutants, the quantity of macromolecular tracers (99mTc-DTPA, 125I-BSA) in blood sampled 6, 7, 8, 9 and 10 minutes after a slow 5-minute instillation of comparable quantities of tracer molecules in the lumen of each zone, was lowest in nasal, highest in tracheal, and intermediate in the bronchoalveolar region. Exposure of resting rats to O3 did not affect nasal permeability, but tracheal and bronchoalveolar permeabilities increased by 2-fold 1 hour after the exposure. In rats exposed at rest to O3, tracheal permeability was no longer elevated 24 hours after exposure, but bronchoalveolar permeability remained elevated at 24 hours after exposure and was normal at 48 hours. Exposure during exercise increased the effect of O3 in the trachea and in the bronchoalveolar zone. However, exercise also prolonged the duration of the O3 effect on the tracheal zone from 1 hour to 24 hours and, in the bronchoalveolar zone, from 24 hours to 48 hours. Histologically, focal inflammatory lesions in the alveolar zone were maximal at 48 hours after a 4-hour resting exposure to O3. After exposure during exercise, the area of lung involved by lesions increased 4- to 7-fold above the lesion-bearing area in rats exposed while resting. By electron microscopy, horseradish peroxidase (HRP) was localized in epithelial intercellular spaces, but not in the apical tight junctions, of tracheal epithelial cells from O3-exposed rats; no HRP was found in intercellular spaces in controls. The number of HRP-containing endocytic vesicles in tracheal epithelial cells was 2-fold greater in rats exposed to O3 than in control rats. This 2-fold increase in vesicles presumed to be transporting HRP matches the 2-fold increase in transfer of DTPA from the tracheal lumen to the blood. Electron microscopic autoradiography revealed 125I-BSA accumulation in subepithelial connective tissue, and electron microscopic cytochemistry identified accumulation of HRP not only between cells but also at the basal lamina.(ABSTRACT TRUNCATED AT 400 WORDS)