Record Display for the EPA National Library Catalog


OLS Field Name OLS Field Data
Main Title Does chronic ozone exposure lead to lung disease. {microfiche}
Author Costa, D.L. ; Hatch, G. E. ; Crapo., J. D.
CORP Author Duke Univ. Medical Center, Durham, NC. Center for Extrapolation Modelling.;Health Effects Research Lab., Research Triangle Park, NC. Environmental Toxicology Div.
Publisher . Duke University Medical Center
Year Published 1991
Report Number EPA-R-813113; EPA/600/D-90/168
Stock Number PB91-132993
Additional Subjects Ozone ; Respiratory diseases ; Rats ; Biochemistry ; Blood proteins ; Exposure ; Air pollution effects(Humans) ; Respiratory function tests ; Health hazards ; Basement membrane ; Bronchoalveolar lavage fluid ; Fibrosis
Library Call Number Additional Info Location Last
NTIS  PB91-132993 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 01/01/1988
Collation 11 p.; 28 cm.
The potential role of ozone (O3) in the induction of chronic lung diseases remains unclear. Using an ambient profile adopted from aerometric data from the Southwest Air Basin, rats were exposed to O3 for up to 18 months before assessments of pulmonary structure, function and biochemistry. Small, but significant alterations in lung function were observed at 52 and 78 weeks of exposure which were consistent with an overall 'restrictive' functional lesion; these effects subsided during the post-exposure in clean air. Evidence of augmented lung permeability to plasma proteins and shifts in the antioxidant balance of lung tissues, free cells and lavage fluids were consistent with chronic oxidant stress. EM-morphometry revealed alterations in proximal bronchoalveolar epithelia and interalveolar interstitium which largely resolved during clean air post-exposure. However, fibrotic activity within the epithelial basement membrane and interstitium persisted. These collective data suggest that chronic exposure to O3 in an ambient exposure pattern induces alterations of lung infrastructure at presumptive O3 deposition sites resulting in functional and biochemical consequences.