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Description of key information

Short description of key information on bioaccumulation potential result: 
A reliable with restrictions study (Nomeir et al, 1995) has been provided for the determination of the basic toxicokinetics of 2,3-epoxypropanol. This study was undertaken to compare the disposition characteristics of glycidol in Fischer 344 rats following oral (where glycidol is exposed to stomach HCI) or intravenous (i.v.) (bypass stomach HCI) administration. The rats were subjected to a single exposure either orally or intravenously. This study demonstrates that the disposition characteristics of glycidol were similar following oral and i.v. administration. Also, the conversion of glycidol to a-chlorohydrin by HCI in the stomach was quantitatively insignificant.
Two additional supporting investigations are presented to indicate the degree of metabolism and to identify possible metabolites.

Key value for chemical safety assessment

Bioaccumulation potential:
low bioaccumulation potential

Additional information

The study by Nomeir et al. was carried out to determine the comparitive disposition of 2,3-epoxy-1-propanol (glycidol) in rats following oral and intravenous administrations. This study demonstrates that the disposition characteristics of glycidol were similar following oral and i.v. administration. Also, the conversion of glycidol to a-chlorohydrin by HCI in the stomach was quantitatively insignificant.There is low bioaccumulation potential based on the study results.

The study by Jones and O'Brian was provided to help determine the basic toxicokinetics of 2,3 -epoxypropanol. The excretion of beta-chloropropionic acid in urine from rats treated with 36Cl-chloride and glycidol was studied. Male Wistar rats (250 - 280 g b.w.), pretreated with 4 doses i.p. of each 10 uCurie 36Cl-chloride, received 3 doses of 100 mg/kg b.w. glycidol each.

Glycidol administered i.p. to male rats is converted to epichlorohydrine which is oxidised to chloropropionic acid.

The study by Patel et al was provided to help determine the basic toxicokinetics of 2,3 -epoxypropanol.

Allyl alcohol was oxidised to acrolein in the presence of NAD in 9000 g supernatants or cytosol from liver, but not lung. However, in liver and lung microsomes incubated with allyl alcohol and NADP, glycidol was detected as intermediary product. After an initial formation, its concentration steadily decreased with further incubation time. Glycerol was rapidly formed from glycidol when this was added to lung or liver microsomes, probably by enzymatic hydrolysis by microsomal epoxide hydrase. Glycidol and its oxidation product, glycidaldehyde, were both also found to be substrates of lung and liver cytosolic GSH-S-epoxidetransferases, the activity in liver preparations being much higher.

Glycidol is an alkylating agent which reacts readily with glutathione. It causes a decrease in glutathione content in rat liver, probably reflecting its binding to glutathione. In rats, it is metabolized to oxidative and glutathione-derived products. No toxicokinetic data on humans were available.