Record Display for the EPA National Library Catalog


OLS Field Name OLS Field Data
Main Title Comparative Immunosuppression of Various Glycol Ethers Orally Administered to Fisher 344 Rats.
Author Smialowicz, R. J. ; Williams, W. C. ; Riddle, M. M. ; Andrews, D. L. ; Luebke, R. W. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. ;ManTech Environmental Technology, Inc., Research Triangle Park, NC.
Publisher c1992
Year Published 1992
Report Number EPA/600/J-92/230;
Stock Number PB92-195833
Additional Subjects Toxicology ; Immunosuppression ; Antibody formation ; Lipopolysaccharides ; Rats ; Alcohol dehydrogenase ; Enzyme inhibitors ; Ethylene glycol ; Reprints ; Glycol ethers ; 4-methylpyrazole
Library Call Number Additional Info Location Last
NTIS  PB92-195833 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 08/22/1992
Collation 9p
Oral dosing of adult male F344 rats with the glycol ether 2-methoxyethanol (ME) or its principal metabolite 2-methoxyacetic acid (MAA) results in the suppression of the primary plaque-forming cell (PFC) response to trinitrophenyl-lipopolysaccharide (TNP-LPS). In the present study, the PFC response to TNP-LPS was used to evaluate the immunotoxic potential of ethylene glycol (EG) as well as the glycol ethers 2-methoxyethyl acetate (MEA), 2-(2-methoxyethoxy) ethanol, bis(2-methoxyethyl) ether, 2-ethoxyethanol and its principal metabolite 2-ethoxyacetic acid, 2-ethoxyethyl acetate, and 2-butoxyethanol relative to ME and MAA. Rats were immunized with TNP-LPS and then exposed 4 and 28 hr later to 50, 100, 200, or 400 mg/kg of glycol ether or EG. Three days following immunization, the PFC response to TNP-LPS was determined. In addition to ME and MAA, only MEA, which was as effective as ME, suppressed the PFC response to TNP-LPS. Concomitant administration of the alcohol dehydrogenase inhibitor 4-methylpyrazole with ME or MEA prevented suppression of the PFC response by these glycol ethers. (Copyright (c) 1992 by the Society of Toxicology.)