Regional clearance of solute from the respiratory epithelia: 18-20
hours post-exposure to ozone.
W., Michael Foster, Pamela T. Stetkiewicz.
DEPARTMENT OF ENVIRONMENTAL HEALTH SCIENCES, SCHOOL OF HYGIENE AND
PUBLIC HEALTH, THE JOHNS HOPKINS UNIVERSITY, BALTIMORE, MD 21205
APStracts 3:0156A, 1996.
Exposure of humans to ambient levels of ozone causes inflammatory
changes within lung tissues. These changes have been reported for the
`initial'(1-3 hr), and `late' (18-20 hr) postexposure periods. We
hypothesized that at the late period when protein and cellular
markers of inflammation in broncho-alveolar lavage remain abnormal,
permeability of respiratory epithelia would be altered. To test this,
we measured by [delta]-camera imagery the clearance kinetics in
healthy subjects (n=9) of 99mTc-labeled solute (diethylenetriamine
pentaacetate, DTPA) that was deposited by aerosol onto epithelial
surfaces 19+/-1 hr after a single exposure to O3 (130 min at ambient
levels between 150-350 ppb 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 increased, i.e., 0.732 % x min-1
for ozone exposures as compared to 0.661 % x min-1 for filtered air
exposures (significant, p<0.05). Regional analysis demonstrated
that 99mTc-DTPA clearance from the periphery (excludes the lung
hilum) and lung apices were significantly increased by ozone; but
changes in clearance for the base of the lung were not significant.
The forced expiratory volume in 1 sec (FEV1) at the late time after
O3 was slightly, but significantly reduced (-2.1%) from pre-exposure
levels. There was no relationship between the functional changes
observed acutely after exposure to O3, and subsequent changes in
99mTc-DTPA clearance or FEV1 observed at the late period. These
results suggest that epithelial permeability of the lung is altered
18-20 hr 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.
Received 6 September 1995; accepted in final form 27 February
1996.
APS Manuscript Number A979-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96