Abstract
Acrylic acid (AA), ethyl acrylate (EA) and n-butyl acrylate (BA) are widely used in the production of plastics, coatings and acrylic fibres. Occupational exposure occurs primarily via inhalation and/or skin contact.
In chronic inhalation experiments EA and BA did not induce neoplastic changes in rats and mice (Klimisch and Reininghaus 1984; Miller et al. 1985). Additional investigations showed that AA and BA were not carcinogenic in mice after chronic dermal application (De Pass et al. 1984). However, recently other authors reported a weak carcinogenic potential of AA and BA after chronic dermal administration to mice (Cote et al. 1986). The conditions of the latter study lead to the suggestion that the observed tumours had developed secondarily due to the local irritating and corrosive properties of AA and BA.
This view is supported by the negative results of AA, EA and BA in the conventional Ames test (Waegemaekers and Bensink 1984). Mutagenicity data in mammalian cell systems of EA were equivocal (Henschler 1986) and were lacking for AA and BA. For this reason the mutagenic potential of AA and BA was investigated in Syrian hamster embryo fibroblasts (SHE cells). DNA repair (UDS assay), chromosomal changes (micronucleus assay) and morphological transformation were chosen as biological endpoints.
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Wiegand, H.J., Schiffmann, D. & Henschler, D. Non-genotoxicity of acrylic acid and n-butyl acrylate in a mammalian cell system (SHE cells). Arch Toxicol 63, 250–251 (1989). https://doi.org/10.1007/BF00316378
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DOI: https://doi.org/10.1007/BF00316378