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

Abstract

This study involves the analysis of the sequence of changes in lung epithelial permeability, free cells in the airways, prostaglandin E2 (PC€;J levels, polymorphonuclear leukocyte (PMN) flux, and alveolar lesions in rats exposed to 0.8 ppm ozone (03 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 0, 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 0, exposure, but returned to near normal levels by 4 h. PGE, levels did not change significantly after 0, exposure. PMNs in the lung sections increased in number with time, peaked at 8 h, and returned to normal levels by 76 h following 0, exposure. The data suggest that the permeability changes may be produced by the direct toxic effects of 0, 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

Permeability, inflammation and oxidant status in airspace epithelium exposed to ozone

“…Ã Po0:05 and ÃÃ Po0:01 compared with breathing air for 1 h. to 0.8 ppm ozone, permeability to 99m Tc-DTPA and BAL, it was suggested that the neutrophil influx occurred as a consequence of the increased permeability, rather than causing the increased permeability. 23 Ozone-induced permeability in rats, exposed to 0.8 ppm for 2 h, was inhibited by pretreatment with cyclophosphamide, FPL 55712 (a leukotriene D 4 antagonist) and indomethacin. 5 Neutrophils from ozone exposed rats have been shown to alter epithelial resistance in vitro, but only when stimulated with PMA or FMLP.…”

Particulate Matter in Polluted Air May Increase Biomarkers of Inflammation in Mouse Brain

“…Samples were collected during mouse exposures, and the impactor stages were extracted in distilled water. Ovalbumin extracted from the impactor stages was analyzed using a bicinchonicinic acid procedure (Bhalla and Young, 1992) with absorbance measured at 562 nm. Animals were sacrificed 1 day after the second antigen challenge.…”

Respiratory Tract Responses to Repeated Inhalation of an Oxidant and Acid Gas-Particle Air Pollutant Mixture

“…Epithelial permeability. Permeability of the nasal epithelium was measured at 1 h following the last exposure (Bhalla et al, 1986, Bhalla andYoung, 1992). Animals were anesthetized with 73 mg/kg sodium pentobarbital, polyethylene tubing (PE-90) was placed in the trachea, and a polyethylene catheter (P-10) was placed in the femoral artery.…”

“…Lactate dehydrogenase was analyzed spectrophotometrically by enzymatic conversion of pyruvate to lactate in the presence of NADH (Sigma Chemical, St. Louis, MO). Albumin concentration was evaluated with an enzyme-linked immunosorbent assay (ELISA) as described by Bhalla and Young (1992).…”