Record Display for the EPA National Library Catalog

RECORD NUMBER: 5 OF 15

OLS Field Name OLS Field Data
Main Title Genotoxicity of Acrylic Acid, Methyl Acrylate, Ethyl Acrylate, Methyl Methacrylate, and Ethyl Methacrylate in L5178Y Mouse Lymphoma Cells (Journal Version).
Author Moore, M. M. ; Amtower, A. ; Doerr, C. L. ; Brock, K. H. ; Dearfield, K. L. ;
CORP Author Environmental Health Research and Testing, Inc., Research Triangle Park, NC.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1988
Year Published 1988
Report Number EPA-68-02-4031; EPA/600/J-88/063;
Stock Number PB89-110357
Additional Subjects Toxicity ; Acrylates ; Methacrylates ; Mutagens ; Cytogenetics ; Acrylic acids ; Carboxylic acids ; Carboxylic acid esters ; Lymphomas ; Cells(Biology) ; Chromosome abnormalities ; Reprints ; Methyl acrylate ; Ethyl acrylate ; Methyl methacrylate ; Ethyl methacrylate ; CAS 79-10-7 ; CAS 96-33-3 ; CAS 140-88-5 ; CAS 80-62-6 ; CAS 97-63-2 ; Propenoic acid ; Propenoic acid/(methylester) ; Propenoic acid/(ethylester) ; Propenoic acid/methyl-(methylester) ; Propenoic acid/methyl-(ethylester)
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NTIS  PB89-110357 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 03/14/1989
Collation 17p
Abstract
A series of monomeric acrylate/methacrylate esters (methyl acrylate, ethyl acrylate, methyl methacrylate, and ethyl methacrylate) as well as acrylic acid were examined for genotoxic activity in L5178Y mouse lymphoma cells without exogenous activation. All five compounds induced concentration dependent increases in mutant frequency. Small-colony, TFT-resistant mutants were primarily induced which suggest that these compounds may act via a clastogenic mechanism. The prediction was confirmed by the finding that all five compounds produced gross aberrations in mouse lymphoma cells. The two acrylates were much more potent in their response than acrylic acid. The two methacrylates required larger quantities of compound to induce a positive response. The evidence suggests that the genotoxicity of these compounds is most likely due to a clastogenic mechanism.