Abstract
Ethylene oxide (ETO) is considered by the International Agency for Research on Cancer (IARC) to be a known genotoxic human carcinogen (IARC, 1994). However, ETO is introduced into the food supply in trace quantities through fumigation in some countries to sterilize commodities that may have pathogenic bacterial contaminants. ETO is also formed from degradation of polymers, polysorbates and emulsifiers, as well as by endogenous gut microflora reactions involving ethylene. Due to its intrinsic cancer hazard, it is appropriate that attention be paid to minimizing consumer exposure to unnecessary ETO residues.The status of ETO was upgraded by the IARC from Group 2A to Group 1 (carcinogenic in humans) in 1994 due to increasing epidemiological and occupational evidence of carcinogenicity and laboratory genetic toxicity studies showing that ETO was a genotoxic carcinogen capable of causing tumors in both animals and humans. The evidence of carcinogenicity in laboratory animals comes largely from inhalation studies (NTP, 1985a; Snellings et al., 1984), but the designation by IARC is not qualified by the route of exposure. Furthermore, oral exposure data in laboratory animals have yielded stomach and systemic tumors (Dunkelberg, 1982). It has been assumed, for the purposes of some risk assessments, that ETO is a human carcinogen by ingestion (Fowles et al., 2001). Structurally similar chemicals such as formaldehyde and propylene oxide are also probable human carcinogens. When comparing the potency of ETO in laboratory animals and human epidemiological studies, agencies have concluded that the potency of ETO was comparable in animals and humans (California Air Resources Board (CARB), 1987). The USEPA and the State of California have designated ETO a carcinogen and ETO air emissions by facilities are subject to tight regulatory controls.
Published Version
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