Journal of Applied Physiology, Vol 81, Issue 3 1143-1149, Copyright © 1996 by American Physiological Society

ARTICLES

Regional clearance of solute from the respiratory epithelia: 18-20 h postexposure to ozone

W. M. Foster and P. T. Stetkiewicz
Department of Environmental Health Sciences, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland 21205, USA. mfoster@welchlink.welch.jhu.edu

Exposure of humans to ambient levels of ozone causes inflammatory changes within lung tissues. These changes have been reported for the "initial" (1- to 3-h) and "late" (18- to 20-h) postexposure periods. We hypothesized that at the late period when protein and cellular markers of inflammation in bronchoalveolar lavage remain abnormal, permeability of respiratory epithelia would be altered. To test this, we measured by gamma-camera imagery the clearance kinetics in healthy subjects (n = 9) of 99mTc-labeled solute [diethylenetriaminepentaacetic acid (DTPA)] that was deposited by aerosol onto epithelial surfaces 19 +/- 1 h after a single exposure to ozone (O3; 130 min at ambient levels between 150 and 350 parts per billion and alternate periods of rest and moderate exercise) or filtered air. At the late period, the lung clearance of 99mTc-DTPA over a 120-min period was significantly increased, i.e., 0.732%/min for O3 exposures compared with 0.661%/min for filtered-air exposures (P < 0.05). Regional analysis demonstrated that 99mTc-DTPA clearance from the periphery (excluding the lung hilum) and lung apexes were significantly increased by O3 but changes in clearance for the base of the lung were not significant. The forced expiratory volume in 1 s at the late time after O3 was slightly but significantly reduced (-2.1%) from preexposure levels. There was no relationship between the functional changes observed acutely after exposure to O3 and subsequent changes in 99mTc-DTPA clearance or forced expiratory volume in 1 s observed at the late period. These results suggest that epithelial permeability of the lung is altered 18-20 h post-O3; this injury is regional, and the lung base appears to have a different time course of response or is in an adapted state with respect to O3 exposure.

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