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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Williams, Gary M. Iatropoulos, Michael J. |
| Description | Country affiliation: United States Author Affiliation: Williams GM ( New York Medical College, Department of Pathology, Chemical Safety Laboratory, Valhalla, NY 10595, USA. gary_williams@nymc.edu) |
| Abstract | Ethyl acrylate (EA) is an acrylic monomer used in the manufacture of a variety of polymers and copolymers as components of many commercially important products. Human exposure to EA occurs primarily in the workplace via inhalation or dermal contact. In F344 rat and B6C3F(1) mouse studies of EA carcinogenicity conducted by the National Toxicology Program [National Toxicology Program, NTP, 1986. Carcinogenesis Studies of Ethyl Acrylate (CAS No. 140-88-5) in F344/N Rats and B6C3F(1) Mice (Gavage Studies) (Tech. Rep. Ser. No. 259; NIH Publication No. 87-2515), Research Triangle Park, NC, USA], the only increased tumor incidences was in squamous cell papillomas and carcinomas of the forestomach, when EA was administered by gavage in corn oil at 100 or 200mg/kg/day (high dose; HD). The neoplasms were preceded by forestomach irritation, inflammation, hyperkeratosis and hyperplasia of the forestomach mucosa. In studies in which rats and mice were exposed at comparable doses to EA in drinking water, by inhalation, or by dermal application, no neoplasms in the forestomach or in any other tissue were reported. EA exhibited clastogenicity and related mutagenicity in vitro, but was non-genotoxic in vivo, including in the forestomach of treated rats. The in vitro clastogenicity response correlates well with cellular toxicity, mediated by non-protein sulfhydryl depletion and mitochondrial impairment. Thus, the carcinogenicity in the forestomach can be ascribed to a non-genotoxic mode of action (MOA). The forestomach mucosal hyperplastic and even dysplastic changes, observed chronically, were reversible, provided the HD exposure was not longer than 6months. This again supports a non-genotoxic MOA. In addition, the route and rate of EA exposure in rodents for forestomach neoplasia are irrelevant to potential human exposure, since humans do not have forestomach and are not exposed to EA by oral bolus. Thus, the weight of evidence indicates that the tumors produced in the rodent carcinogenicity studies arise from conditions that are irrelevant for human risk assessment. |
| File Format | HTM / HTML |
| ISSN | 02732300 |
| Issue Number | 1 |
| Volume Number | 53 |
| e-ISSN | 10960295 |
| Journal | Regulatory Toxicology and Pharmacology |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2009-02-01 |
| Publisher Place | Netherlands |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Pharmacology Acrylates Toxicity Carcinogens Mutagens Administration & Dosage Animals Carcinoma, Squamous Cell Chemically Induced Female Humans Male Mice Mice, Inbred Icr Occupational Exposure Adverse Effects Papilloma Rats Rats, Inbred F344 Rats, Sprague-dawley Risk Assessment Species Specificity Stomach Neoplasms Journal Article Research Support, Non-u.s. Gov't Review |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine Toxicology |
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