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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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.

Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

Key value for chemical safety assessment

Additional information

No metabolism data is available for this substance. The main metabolic pathway for metabolism of ethylene glycol monoalkyl ethers is oxidation via alcohol and aldehyde dehydrogenases (ALD/ADH) that leads to the formation of an alkoxy acid. Alkoxy acids are the only toxicologically significant metabolites of glycol ethers that have been detected in vivo. Methoxy acetic acid, a metabolite of ethylene glycol methyl ether, is a known testicular toxicant in rats, and butoxyacetic acid, a metabolite of ethylene glycol butyl ether, causes hemolysis of rodent red blood cells. The principal metabolite of 2-(2-(2 -methoxyethoxy)ethoxy)ethanol is believed to be 2-[2-(2- methoxyethoxy)ethoxy] acetic acid. Although ethylene glycol, a known kidney toxicant, has been identified as an impurity or a minor metabolite of glycol ethers in animal studies, it does not appear to contribute to the toxicity of glycol ethers. Some glycol ethers have been shown to undergo conjugation with sulfate and glucuronic acid, and the alkoxyacetic acid metabolites may conjugate with glycine (rodents) or glutamine (humans). Conjugation is regarded as a pathway of detoxification.

An in vitro study determined that the permeability of 2-(2-(2 -methoxyethoxy)ethoxy)ethanol, the lowest molecular weight component of this substance, to human skin is quite low. The permeability co-efficient was determined to be 34 +/-7.7ug/cm2/hr, which is around 1.5% of the skin penetration rate of the shorter chain glycol ether ethylene glycol methyl ether. Exposure to the substance caused slight deterioration of skin barrier properties as quantified by the damage ration (rate of permeation of tritiated water through the skin before and after exposure.). Larger molecules in this homologous series will have even slower diffusion rates.

Discussion on bioaccumulation potential result:

No metabolism or toxicokinetic data is available for this substance. The main metabolic pathway for metabolism of ethylene glycol monoalkyl ethers is oxidation via alcohol and aldehyde dehydrogenases (ALD/ADH) that leads to the formation of an alkoxy acid. Alkoxy acids are the only toxicologically significant metabolites of glycol ethers that have been detected in vivo. Methoxy acetic acid, a metabolite of ethylene glycol methyl ether, is a known testicular toxicant in rats, and butoxyacetic acid, a metabolite of ethylene glycol butyl ether, causes hemolysis of rodent red blood cells. The principal metabolite of 2-(2-(2 -methoxyethoxy)ethoxy)ethanol is believed to be 2-[2-(2- methoxyethoxy)ethoxy] acetic acid. Although ethylene glycol, a known kidney toxicant, has been identified as an impurity or a minor metabolite of glycol ethers in animal studies, it does not appear to contribute to the toxicity of glycol ethers. Some glycol ethers have been shown to undergo conjugation with sulfate and glucuronic acid, and the alkoxyacetic acid metabolites may conjugate with glycine (rodents) or glutamine (humans). Conjugation is regarded as a pathway of detoxification.