For definition of Groups, see Preamble Evaluation.
VOL.: 63 (1995) (p. 443)
Chem. Abstr. Name: Acetic acid, ethenyl ester
5.1 Exposure data
Vinyl acetate is used in the production of a wide range of polymers, including polyvinyl acetate, polyvinyl alcohol, polyvinyl acetals, ethylene-vinyl acetate copolymers and polyvinyl chloride-vinyl acetate copolymers, which are widely used in the production of adhesives, paints and food packaging.
Human exposure to vinyl acetate occurs mainly by inhalation or dermal contact during production of the monomer or during production of polymers and water-based paints.
5.2 Human carcinogenicity data
The available data were too limited to form the basis for an evaluation of the carcinogenicity of vinyl acetate to humans.
5.3 Animal carcinogenicity data
Vinyl acetate was tested in one experiment in mice and in one experiment in rats by inhalation. No treatment-related increase in tumour incidence was observed in mice; in rats, an increased incidence of nasal cavity tumours was found in animals of each sex. No increase in tumour incidence was found in rats administered vinyl acetate in the drinking-water in utero and then for life.
5.4 Other relevant data
Vinyl acetate is rapidly metabolized by esterases in human blood and animal tissues to acetaldehyde and acetic acid.
Vinyl acetate irritates the eye and respiratory system. Respiratory distress is seen after subchronic exposure by inhalation. Other effects included nasal irritation, nasal mucosal metaplasia, tracheal metaplasia and bronchitis or bronchiolitis. After chronic exposure by inhalation, changes were observed in the lung. Non-neoplastic effects, atrophic and regenerative changes, were seen in the nasal cavity. After chronic exposure via the drinking-water, the only effects observed were decrements in body weight at high doses.
There are no data on the effects of vinyl acetate on human reproduction. A two-generation study in rats showed evidence of parental toxicity and decreased fertility at the highest dose tested. Oral administration of vinyl acetate to rats during pregnancy did not result in maternal or developmental toxicity, whereas exposure by inhalation induced maternal toxicity, retarded embryonic growth and minor skeletal alterations at the highest dose tested.
Vinyl acetate induced sperm abnormalities and sister chromatid exchange in rodents exposed in vivo; micronuclei were induced in bone marrow but not in meiotic cells. No DNA binding was seen in rat hepatocytes. In human lymphocytes in vitro, vinyl acetate produced chromosomal aberrations, micronuclei, sister chromatid exchange and DNA cross-links. It enhanced viral transformation and sister chromatid exchange in mammalian cells in vitro, and it induced DNA-protein cross-links in rat nasal epithelial cells in vitro. Vinyl acetate did not induce mutation in bacteria but induced DNA-protein cross-links in plasmid DNA. The primary metabolite of vinyl acetate, acetaldehyde, is genotoxic in a wide range of assays.
There is inadequate evidence in humans for the carcinogenicity of vinyl acetate.
There is limited evidence in experimental animals for the carcinogenicity of vinyl acetate.
Vinyl acetate is possibly carcinogenic to humans (Group 2B).
In making the overall evaluation, the Working Group took into account the following evidence:
(i) Vinyl acetate is rapidly transformed into acetaldehyde in human blood and animal tissues.
(ii) There is sufficient evidence in experimental animals for the carcinogenicity of acetaldehyde (IARC, 1987). Both vinyl acetate and acetaldehyde induce nasal cancer in rats after administration by inhalation.
(iii) Vinyl acetate and acetaldehyde are genotoxic in human cells in vitro and in animals in vivo.
For definition of the italicized terms, see Preamble Evaluation.
Previous evaluation: Suppl. 7 (1987) (p. 73)
See Also: Toxicological Abbreviations