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Diethylene glycol is a common industrial solvent with physical and chemical properties similar to propylene glycol. (Chap. 55) Substitution of diethylene glycol for propylene glycol in oral elixirs has repeatedly caused epidemics of mass poisoning (Chap. 2). Patients develop neurologic symptoms and acute renal injury that often progresses to renal failure.

Diethylene glycol (DEG) is produced by the condensation of two ethylene glycol molecules with an ether bond,1 yielding a molecular weight of 106 Da. It was first isolated in 1869 and has been used in industry and manufacturing since 1928.1 Since then it has found use as an antifreeze, as a finishing agent for wool, cotton, silk and other fabrics, and in dye manufacturing. DEG is chemically inert, does not ignite at normal temperatures, and has a higher boiling point than ethylene glycol (EG).17,43 Its other physical properties are quite similar to EG, including a sweet taste.17,43 It is often used as an intermediate in the production of polymers, higher glycols, morpholine, and dioxane.26 Its physical properties enable it to serve as an excellent solvent for water-insoluble substances including drugs. This unfortunate use has accounted for the overwhelming majority of reported cases of illness.4,6,7,9,11,12,14,15,21,23,29–33,36,38,43 In these recurring events, DEG was substituted for a safe and appropriate diluent such as glycerin or propylene glycol. Other causes of DEG-associated illness have resulted from the intentional addition of DEG to wine as a sweetening agent40,41 and ingestion of radiator fluid or antifreeze,27 brake fluid,5 Sterno,34 a "fog solution,"16 cleaning solutions,1 wallpaper stripper,25 and as a substitute for ethanol.44


Diethylene glycol is rapidly absorbed after ingestion and distributed primarily based on blood flow, with the kidneys receiving the most DEG, followed by the brain, the spleen, liver, and muscles.17 The degree of protein binding and the volume of distribution (Vd) in humans is unknown but the Vd in the rat is approximately 1 L/kg.17 Maximal DEG concentrations likely occur within 1 to 2 hours postingestion.17,43 In both rats and dogs, as much as 30% of a given dose is converted to 2-(hydroxy) ethoxyacetic acid (HEAA).10,26 In rats, there does not appear to be other metabolites although it is unclear if humans metabolize DEG by similar mechanisms.17 Several early rat studies reported that oxaluria or calcium oxalate crystal formation occurred in renal tubules.18,24,28 This limited evidence suggested that perhaps the ether bond joining the 2 ethylene glycol molecules was cleaved. This could then result in ethylene glycol-associated glycolate, glyoxylate and oxalate formation and the subsequent adverse health effects associated with ethylene glycol toxicity. (Chap. 107). Although this hypothesis for the pathophysiology of DEG induced renal toxicity remained popular for many ...

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