Ethylene glycol is the primary ingredient (up to 95%) in antifreeze. It sometimes is consumed intentionally as an alcohol substitute by alcoholics and is tempting to children and pets because of its sweet taste. Intoxication by ethylene glycol itself causes inebriation and mild gastritis; more importantly, its metabolic products cause metabolic acidosis, renal failure, and death. Other glycols may also produce toxicity (Table II–24).
Table II-24 Other Glycols |Favorite Table|Download (.pdf)
Table II-24 Other Glycols
Toxicity and Comments
Diethylene glycol (DEG)
Highly nephrotoxic. Renal failure, coma, metabolic acidosis, and death have been reported after ingestion as well as repeated dermal application in patients with extensive burn injuries. Most reported incidents were from adulteration of consumer products or medications. Gastritis, hepatitis, pancreatitis, and delayed neurologic sequelae also reported after ingestion. Metabolic acidosis may be delayed longer than 12 hours after ingestion. Estimated human lethal dose is 0.05–2.0 g/kg. Calcium oxalate crystal formation documented in animals but not humans after fatal exposure. The metabolism of DEG is unclear; however, a case report documents a good outcome with fomepizole. Molecular weight is 106.
Ethanol and fomepizole may be effective. Hemodialysis indicated for patients with anuric renal failure or severe metabolic acidosis nonresponsive to medical treatments.
Dioxane (dimer of ethylene glycol)
May cause coma, liver and kidney damage. The vapor (>300 ppm) may cause mucous membrane irritation. Dermal exposure to the liquid may have a defatting action. Metabolites unknown. Molecular weight is 88.
Role of ethanol and fomepizole is unknown, but they may be effective.
Relatively low toxicity. Central nervous system depression, hepatic injury, and renal damage have occurred in animal studies after massive exposures. There is a human report of acute renal failure, polyneuropathy, and myopathy after an ingestion of dipropylene glycol fog solution but no reports of acidosis or lactate elevation. Molecular weight is 134.
Supportive care. There is no role for ethanol therapy.
Ethylene glycol monobutyl ether (EGBE, 2-butoxyethanol, butyl cellosolve)
Clinical toxic effects include lethargy, coma, anion gap metabolic acidosis, hyperchloremia, hypotension, respiratory depression, hemolysis, renal and hepatic dysfunction; rare disseminated intravascular coagulation (DIC), noncardiogenic pulmonary edema, and acute respiratory distress syndrome (ARDS). Oxalate crystal formation and osmolar gap elevation have been reported, but not in all cases. Serum levels in poisoning cases have ranged from 0.005 to 432 mg/L. Butoxyethanol is metabolized by alcohol dehydrogenase to butoxyaldehyde and butoxyacetic acid (BAA); however, the affinity of alcohol dehydrogenase for butoxyethanol is unknown. Molecular weight is 118.
Ethanol, fomepizole, and hemodialysis may be effective.
Ethylene glycol monoethyl ether (EGEE, 2-ethoxyethanol, ethyl cellosolve)
Calcium oxalate crystals have been reported in animals. Animal studies indicate that EGEE is metabolized in part to ethylene glycol; however, the affinity of alcohol dehydrogenase is higher for EGEE than for ethanol. One patient developed vertigo, unconsciousness, metabolic acidosis, renal insufficiency, hepatic damage, and neurasthesia after ingesting 40 mL. Teratogenic effect has been reported in humans and animals. ...