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RECORD NUMBER: 10 OF 37

OLS Field Name OLS Field Data
Main Title Effects of Inhalation of Ethylene Dichloride on Pulmonary Defenses of Mice and Rats.
Author Sherwood, R. L. ; O'Shea, W. ; Aranyi, C. ; Graham, J. A. ;
CORP Author IIT Research Inst., Chicago, IL.;Health Effects Research Lab., Research Triangle Park, NC.
Year Published 1987
Report Number EPA/600/J-87/321;
Stock Number PB88-196035
Additional Subjects Ethylene ; Chlorohydrocarbons ; Respiratory diseases ; Streptococcal infections ; Respiratory infections ; Rats ; Mice ; Ethane ; Respiration ; Toxicity ; Lymphocytes ; Reprints ; Ethylene dichlorides ; Hydrocarbons(Chlorinated) ; Lung diseases ; Pulmonary alveoli
Holdings
Library Call Number Additional Info Location Last
Modified
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Status
NTIS  PB88-196035 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 09/04/1988
Collation 8p
Abstract
The effects of single or multiple 3-hr inhalation exposures to ethylene dichloride (dichloroethane or DCE) on macrophage functions and pulmonary defense were evaluated. Single exposures to the TLV level of DCE (10 ppm) resulted in decreased pulmonary bactericidal activity and increased susceptibility to mortality from Streptococcus 2 zooepidemicus respiratory infection. Streptococcal-induced mortality was also increased after a single exposure to 5 ppm DCE. No increase in mortality was observed following single or 5 consecutive daily exposures to 2.5 ppm DCE. Single exposures to 10 ppm DCE significantly decreased the number of cells recovered by pulmonary lavage but did not affect alveolar macrophage inhibition of the proliferation of a tumor target cell in vitro, or the in vitro phagocytosis of (51)Cr-chicken red blood cells. The activity of the ectoenzyme leucine aminopeptidase was increased in alveolar macrophages of DCE-exposed mice. It is hypothesized that exposure of mice to DCE for 3-hr results in increased susceptibility to pulmonary bacterial infection by altering the functioning of the resident alveolar macrophage population. (Copyright (c) 1987 by Academic Press, Inc.)