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Tumorigenesis and Genotoxicity of Ethyl Carbamate and Vinyl Carbamate in Rodent Cells¹

Health Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711 and Cincinnati, Ohio 45268 [J. W. A., M. A. P., L. C. B., A. G. S., S. N.]; Department of Pathology, Medical College of Ohio at Toledo, Toledo, Ohio 43699 [G. D. S.]; Northrop Environmental Sciences, Research Triangle Park, North Carolina 27709 [G. G. H.]; Environmental Health Research and Testing, Inc., Research Triangle Park, North Carolina 27709 [Y. S., J. A. C]

Vinyl carbamate (VC) is a suspect metabolic intermediate in ethyl carbamate (EC) carcinogenesis. In the present studies, EC and VC were evaluated for their relative abilities to induce adenomas and sister chromatid exchanges (SCEs) in lung cells of A/J, C3HeB/FeJ, and C57BL/6J strain mice. For both end points, animals were administered a single i.p. injection of the test chemical. Percentage of mice with adenomas and number of adenomas per mouse were compared among the three strains 24 weeks following exposure to EC or VC. Although the relative order of strain sensitivity was the same for both chemicals: A/J > C57BL/6J > C3HeB/FeJ, VC was much more potent than EC. For SCE analysis of primary lung cells cultured from treated animals, EC and VC showed potency differences similar to those observed for tumorigenesis. All three mouse strains revealed significant dose-dependent increases in SCE frequency. However, there was no strain specificity for this effect. SCE persistence over time was also compared in treated A/J and C57BL/6J mice. Although EC- and VC-induced SCE frequencies declined over a 2-week observation period, again, there was no strain specificity for this effect. VC was also tested for enhancement of SA7 virus transformation of Syrian hamster embryo cells. Significant concentration-dependent increases in cell transformation frequency were observed.

¹ The research described in this article has been reviewed by the Health Effects Research Laboratory, U.S. Environmental Protection Agency and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.

² To whom requests for reprints should be addressed, at Mutagenesis and Cellular Toxicology Branch (MD-68), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711.

³ Parts of this work conducted at the Medical College of Ohio were supported by U.S. Environmental Protection Agency Cooperative Agreement No. CR-807671.

⁴ L. C. B. is supported by a National Academy of Sciences National Research Council Fellowship.

Received 4/10/86. Accepted 6/19/86.

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