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Only blood GSH levels remained depressed in mice 48 hours after exposure to ethylene oxide. The results indicate a marked species difference between rats and mice regarding the effects of ethylene oxide exposure on blood GSH levels. 1 Inhalation Exposure No studies were located regarding excretion of ethylene oxide in humans after inhalation exposure. 5%), and expired ethylene oxide (1%). Cumming et al. (1981) reported that ethylene oxide was rapidly eliminated by mice that had been exposed to radio-labeled ethylene oxide.

Hepatic total microsomal protein, cytochrome b5, NADPH-cytochrome c reductase and NADHferricyanide reductase were not affected. The activity of hepatic heme oxygenase showed a two-fold increase. These results suggest that the heme moiety of hepatic cytochrome P-450 was primarily affected by exposure of ethylene oxide and the cellular heme balance in liver was altered. Nakashima et al. (1987) found that in rats exposed to ethylene oxide for 12 weeks, the concentration of the reduced form of glutathione (GSH) in the liver was not significantly different from that of controls.

1977; Woodard and Woodard 1971). 4 years) who were challenged with a single dermal application of 1% ethylene oxide. Dermal application studies using human volunteers by Sexton and Henson (1950) and Shupack et al. (1981) however, have provided some evidence that ethylene oxide is a skin sensitizer. A case study of a hospital patient diagnosed with allergic contact dermatitis in response to ethylene oxide also suggests skin sensitization (Alomar et al. 1981). However, ethylene chlorhydrin may also have contacted the patient's skin.

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Toxicological profiles - Ethylene oxide

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