Registration Dossier
Registration Dossier
Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.
The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.
Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 203-459-7 | CAS number: 107-07-3
Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
Additional information
In NTP TR 275 a summary is given of avaialable literature on toxicokinetics (page 20 -21):
"No reports were found on the kinetics of the dermal absorption of 2-chloroethanol or on the tissue distribution of 2-chloroethanol following dermal absorption. After a single oral dose of an aqueous solution of [1,2 -14C-2 -chloroethanol (5 or 50 mg/kg) was administered to adult male Wistar rats, 77%-80% of the administered radioactivity was recovered in the urine within 24 hours (Grunow and Altmann, 1982). In the same time period, another 3%-5% was recovered in the feces and expired air. No unchanged 2 -chloroethanol was recovered in either feces or urine; expired 14C was all in the form of 14CO2. Peak levels of radioactivity were found in blood 1 hour after administration; these levels were reduced by 50% after approximately 4 hours. About 90% of the radioactivity in the urine was in the form of thiodiacetic acid and thiodiacetic acid, the latter probably formed by the oxidation of the former metabolite.
Johnson (1965) suggested that the toxicity of 2 -chloroethanol was due to the formation of chloroacetaldehyde by the test animal in amounts greater than could be detoxified by glutathione (GSH). 2-Chloroethanol is known to be a substrate for the purified cytoplasmic alcohol dehydrogenase of human liver (Blair and Vallee, 1966), rat liver, or yeast (Johnson, 1967). Johnson (1967) demonstrated the in vivo and in
vitro formation of S-carboxymethyl-GSH in livers of rats dosed with 2-chloroethanol. S-Carboxymethyl-GSH is presumably formed from GSH and chloroacetaldehyde, the dehydrogenation product of 2-chloroethanol; S-formylmethyl-GSH is the presumed intermediate. Grunow and Altmann (1982) reported finding thiodiacetic acid and thionyldiacetic acid in the urine of rats given an oral dose of 2 -chloroethanol; both and are derivable
from S-carboxymethylcysteine, the hydrolysis and deamination product of S-carboxymethyl-GSH. Thiodiacetic acid has been shown to be a metabolite of compounds that have the general property of being converted to chloroacetaldehyde; these compounds include vinyl chloride (Green and Hathway, 1975, 1977; Watanabe et al., 1976), 1,2-dichloroethanol (Yllner, 1971), and vinylidene chloride (Jones and Hathway, 1978).
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
