Vinyl chloride induces hepatic angiosarcomas, which are otherwise rare malignancies. The biochemical basis involves the formation of the epoxide, which reacts with DNA to give approximately 98% of the 7-(2-oxoethyl) adduct (4) of dGuo plus small amounts of the etheno derivatives of dGuo, dCyd, and dAdo. The carcinogenicity is generally ascribed to the etheno adducts, not 4, because 4 has been shown to disappear from cells rapidly and to have negligible mutagenicity, which argues against its biological importance, whereas etheno adducts are both persistent and mutagenic. It has also been shown that apurinic sites derived from 4 are unlikely to be crucial lesions. A confounding factor with regard to the etheno hypothesis is that etheno adducts arise in unexposed cells by reactions of various lipid peroxidation products. The present study explores the possibility that a major contributor to the carcinogenicity of vinyl chloride may be formamidopyrimidine (FAPy) 12, N-[2-amino-6-[(2-deoxy-beta-D-erythro-pentofuranosyl)amino]-3,4-dihydro-4-oxo-5-pyrimidinyl]-N-(2-oxoethyl)-formamide, which can arise by ring opening of 4, although its formation has not been observed until the present study. N7 adduct 4 undergoes deglycosylation to give 7-(2-oxoethyl)-Gua (13) in acid and imidazolium ring-opening to 12 in base. At pH 7.4, both processes occur with the formation of 12 representing approximately 10% of the product mixture. FAPy 12 spontaneously cyclizes to 22, which upon mild acid treatment yields the deglycosylation product 2-amino-3,4,7,8-tetrahydro-7-hydroxy-4-oxopteridine-5(6H)-carbaldehyde (14). The structure of 14 has been established by NMR and mass spectroscopy and by independent synthesis. Reaction of the epoxide of crotonaldehyde with dGuo failed to give either 13 or 14, indicating that both compounds are unique products of the reactions of dGuo with the epoxides of vinyl monomers. Although FAPy 12 was found to be unstable, carbinolamine 22 arising from cyclization of 12 may be an important contributor to the carcinogenicity of vinyl chloride.