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RECORD NUMBER: 24 OF 35

OLS Field Name OLS Field Data
Main Title Morphological Effects of Prolonged Exposure to Ozone and Sulfuric Acid Aerosol on the Rat Lung.
Author Moore, P. F. ; Schwartz, L. W. ;
CORP Author California Univ., Davis.;Health Effects Research Lab., Research Triangle Park, NC.
Year Published 1981
Report Number EPA-68-02-2496; EPA-600/J-81-519;
Stock Number PB82-154857
Additional Subjects Toxicology ; Respiratory system ; Ozone ; Sulfuric acid ; Lung ; Rats ; Laboratory animals ; Exposure ; Aerosols ; Morphology ; Pathology ; Reprints ; Acids ; Toxic substances ; Synergism
Holdings
Library Call Number Additional Info Location Last
Modified
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Status
NTIS  PB82-154857 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 06/23/1988
Collation 18p
Abstract
The purpose of this study was to determine the pulmonary effects of a combination of ozone (0.5 ppm) and sulfuric acid aerosol (1 mg/cu. m.) and to assess the possibility of interactive effects. Groups of Sprague-Dawley rats were continously exposed to the pollutants, either individually or combined, for 3, 50, 9O, or 180 days. After 180 days of exposure, additional groups breathed clean air for a further 62 days. Morphological evaluation included light microscopy, autoradiography, scanning electron microscopy (SEM), and transmission electron microscopy. Quantification of pulmonary centriacinar inflammatory cell response was performed by SEM. The results clearly demonstrated that exposure to 0.5 ppm ozone for 180 days resulted in a persistent inflammatory response in the pulmonary centriacinar region together with a structural modification of the terminal bronchiole - proximal alveolar duct junction. Sulfuric acid aerosol did not induce pulmonary morphological changes, nor did it potentiate lesions produced by simultaneous ozone exposure. After termination of the 62-day postexposure period, ozone and ozone plus sulfuric acid postexposure rats demonstrated a marked diminution in the intensity of the pulmonary centriacinar inflammatory response and a partial restoration of normal centriacinar structure.