the world, the information available regarding human toxicity is limited. Some authors suggest the minimum toxic dose is estimated at 0.14 mg/kg of body weight and the lethal dose is between 1.0 and 1.63 g/kg of body weight, while some suggest the LD50 in adults is of ~1 mL/kg, and others suggest this is the LD30. Because of its adverse effects on humans, diethylene glycol is not allowed for use in food and drugs (in many countries). The U.S. Code of Federal Regulations allows no more than 0.2% of diethylene glycol in polyethylene glycol when the latter is used as a food additive. The Government of Australia does not allow DEG as a food additive due to its toxicity; it is only allowed at less than 0.25% w/w of DEG as an impurity of polyethylene glycol (PEG) even in toothpaste. Diethylene glycol has "moderate to low" acute toxicity in animal experiments. The LD50 for small mammals has been tested at between 2 and 25 g/kg, less toxic than its relative ethylene glycol, but still capable of causing toxicity in humans (in high concentration only). It appears diethylene glycol may be more hazardous to humans than implied by oral toxicity data in laboratory animals. Toxicokinetics Although there is limited information about toxicokinetics in humans, observations in mass poisonings and experimental studies suggest the following information: Absorption and distribution The principal method of absorption is through oral ingestion. Dermal absorption is very low, unless it is administered on broken or damaged skin. After ingestion, DEG is absorbed through the gastrointestinal tract and distributed by the bloodstream throughout the body, reaching peak blood concentrations within 30 to 120 minutes. Once DEG reaches the liver, it is metabolized by enzymes. Metabolism and elimination At first, scientists thought that DEG metabolized into ethylene glycol, which is poisonous due to the metabolic production of glycolic acid, glyoxylic acid, and ultimately oxalic acid. The major cause of ethylene glycol toxicity is the accumulation of glycolic acid in the body, but the accumulation of calcium oxalate crystals in the kidneys can also lead to acute kidney failure. In the case of DEG, observations demonstrated there were no calcium oxalate crystal deposits in the kidneys, implying ethylene glycol is not on the DEG metabolic pathway. Rat models suggest DEG is metabolized in the liver by enzyme NAD-dependent alcohol dehydrogenase (ADH) into a hydrogen ion, NADH and 2-hydroxyethoxyacetaldehyde (C4H8O3). Shortly