Registration Dossier

Administrative data

Link to relevant study record(s)

Description of key information

Glycol ether acetates are rapidly hydrolyzed to their corresponding glycol ethers by carboxylesterases. This occurs in a variety of tissues, including blood and of factory mucosa and as a result, both the toxicity as well as patterns of metabolic elimination are nearly identical for glycol ethers and their acetates. 

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

The parent glycol ethers are substrates for alcohol dehydrogenase (ADH) which catalyzes the conversion of their terminal alcohols to aldehydes. Further conversion by aldehyde dehydrogenase produces alkoxyacetic acids. The conversion by ADH and the resulting toxicity of the glycol ether can be blocked by pyrazole and other ADH inhibitors. Alcohol also inhibits this conversion. The higher molecular weight glycol ethers, (di- and triethylene glycol ethers), are believed to be poor substrates for ADH and are partially cleaved by the action of P-450 isozymes.Alkoxyacetic acids are significant if not major urinary metabolites of glycol ethers in both animals and humans and are the only toxicologically significant metabolites that have been detectedin vivo. Although indirect evidence suggests that the aldehydes form underin vivoconditions, these have not yet been detected in whole animal studies.In animal studies, ethylene glycol has been identified as a minor metabolite of glycol ethers. Sulfate and glucuronide conjugation of the parent glycol ethers has been reported as have the glycine (rodents) and glutamine (humans) conjugates of the alkoxyacetic acid metabolites.The formation of ethylene glycol under normal conditions of exposure is unlikely to contribute to the toxicity of glycol ethers. None of the other conjugates that have been identified has been associated with a toxicological response, and the formation of these is presumed to represent detoxification