||Chronic exposure to ozone causes restrictive lung disease /
Grose, E. C. ;
Costa, D. L. ;
Hatch, G. E. ;
Miller, F. J. ;
Graham, J. A.
||Health Effects Research Lab., Research Triangle Park, NC. Environmental Toxicology Div. ;Duke Univ., Durham, NC. Dept. of Medicine. ;Northrop Services, Inc., Research Triangle Park, NC.
|| U.S. Environmental Protection Agency, Office of Research and Development, Health Effects Research Laboratory, Environmental Toxicology Division,
Lung diseases ;
Pulmonary fibrosis ;
Air pollution effects(Humans)
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
||11 pages ; 28 cm
A chronic study to determine the progression and/or reversibility of ozone-induced lung disease was conducted. Male rats were exposed to a diurnal pattern of ozone (O3) for 1 week, 3 weeks, 3 months, 12 months, or 18 months. The occurrence of chronic lung disease was determined by structural and functional endpoints. Structural, a biphasic response was observed with an initial acute inflammatory response after 1 week of exposure, a reduced acute response after 3 weeks of exposure, and an epithelial and interstitial response observed after 3 months which persisted or increased in intensity up to 18 months of exposure. Functional studies showed a persistence of decreased total lung capacity and residual volumes at 3, 12, and 18 months of exposure, a response indicative of restrictive lung disease. Biochemical changes in antioxidant metabolism were also observed after 12 and 18 months of exposure. Most significant changes were resolved after the clean air recovery period. The study has shown that chronic exposure to O3 causes restrictive lung disease as characterized by the development of focal interstitial fibrosis.