Monoalkyl ethers are metabolised via alcohol dehydrogenase to their respective alkoxyacetic acids, e.g., methoxyacetic acid (MAA) from EGME, ethoxyacetic acid (EAA) from EGEE and butoxyacetic acid (BAA) from EGBE. Glycol ether acetates are believed to be metabolised by the same mechanisms as the glycol ethers after hydrolysis of the ester moiety (Groeseneken et al., 1987). Treatment with alcohol dehydrogenase inhibitors, such as pyrazole, blocks conversion of the glycol ether to the alkoxyacetic acid metabolite (Moss et al., 1985; Ghanayem et al., 1987).

Although the majority of the work on urinary metabolites has been carried out in exposed workers, the same compounds (i.e., the alkoxyacetic acids) have also been found in the urine (Rambourg-Schepens et al., 1988; Gijsenbergh et al., 1989) and blood (Gualtieri et al., 1995) of individuals who have ingested large quantities of glycol ether-containing products.

There may be a minor metabolic pathway (Laitinen et al., 1996) through ethylene glycol, glycoaldehyde, glycolic acid and glyoxylic acid to oxalic acid, although this has been disputed (Browning and Curry, 1994). Oxalate crystals have been found in the urine in some cases of acute glycol ether ingestion (Nitter-Hauge, 1970; Rambourg-Schepens et al., 1988) and in the kidneys at biopsy (Nisse et al., 1998). However, oxalate has not been detected in most cases of glycol ether poisoning (Nitter-Hauge, 1970; Gijsenbergh et al., 1989; McKinney et al., 2000), nor has it been demonstrated in animal studies (Truhaut et al., 1979). Methanol is another possible product of metabolism if there is cleavage of the ether linkage (Browning and Curry, 1994). Ethylene glycol and methanol are not usually detected after ingestion of glycol ether (Young and Woolner, 1946; Nitter-Hauge, 1970; Gualtieri et al., 1995; Wermuth and Furbee, 1997; McKinney et al., 2000). However, there are a small number of cases where ethylene glycol has been detected following ingestion of a large quantity of a glycol ether. The ethylene glycol concentrations reported were 1.1 g/l (Litowitz et al., 1991) and 0.31 g/l (Nisse et al., 1998). Serious toxicity may occur with ethylene glycol concentrations above 200 mg/l. The primary metabolic pathway (to alkoxyacetic acids) may become saturated following ingestion of a large quantity of glycol ether (Rambourg-Schepens et al., 1988) and this may account for the presence of ethylene glycol and oxalate in some cases.

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