Re: Case closed!!

If it is glycolic acid then why doesn't the ingredient list say that. Okay, lets say it is glycolic acid then. I will say that you and Dupont (the world's largest manufacturer of glycolic acid) think that it is a relatively non toxic chemical. Personally I don't trust Dupont. See next post for one of many reasons why. Also, many toxicologists and certainly detox specialists along with environmental medicine Docters would disagree with Dupont's status of non toxicity.

Here is an exerpt of data from a medical poisoning center on Ethylene Glycol. Pay particular attention to metabolites formed as the liver attempts to break it down.

Synonyms, Key Words, and Related Terms: EG, radiator fluid, antifreeze, glycolic acid, GA

Background: Several toxic alcohols are of medical importance. Principal ones include ethanol, ethylene glycol (EG), methanol, and isopropanol. This article discusses EG, the common component of radiator fluid.
EG is the major ingredient of almost all radiator fluid products in the US. It is used to increase the boiling point and decrease the freezing point of radiator fluid, which circulates through the automotive radiator. These changes to the boiling and freezing points result from the colligative properties of the solute (ie, they are dependent on the number of particles in solution). Hence, ethylene glycol is added to prevent the radiator from overheating or freezing, depending on the season. Fluorescein dye also is added to radiator fluid to help identify the source of a leak. The fluorescein in the fluid fluoresces when viewed under ultraviolet light.

Ethylene glycol is sweet tasting, which accounts for the attraction that some animals have toward it. Most veterinarians are very familiar with ethylene glycol toxicity, particularly when dogs are exposed to radiator fluid.

Ethylene glycol is not an uncommon cause of overdose in American EDs (553 cases were reported to the American Association of Poison Control Centers in 1994), and rapid intervention often makes an important difference in the outcome of EG toxicity.


Pathophysiology: Each of the toxic alcohols mentioned above (parent compounds) exert most of their toxicity by conversion to metabolites. While the parent compound, EG, may cause some alteration of mental status, it is a relatively nontoxic compound unmetabolized. The metabolites cause the distinctive toxicity associated with this compound.

Knowing the pathway of ethanol metabolism is necessary to properly understand EG toxicity. Ethanol is metabolized by the enzyme alcohol dehydrogenase (ADH) pathway, which is located in the liver and gastric mucosa, and the cytochrome P-450 mixed function oxidase (MFO) system in the liver. The MFO component is subject to greater inducibility than ADH.

As with ethyl alcohol and methanol, EG is metabolized via ADH to form glycoaldehyde. Through interaction with aldehyde dehydrogenase, EG is then metabolized to glycolic acid (GA). A profound acidosis often ensues and is attributable to the GA in circulation. The patient may develop hyperventilation resulting from acidemia. The glycolate is transformed into glyoxylic acid. At this point, the molecule may be transformed into to the highly toxic oxalate or into the safer glutamate or alpha-ketoadipic acid metabolites. Formation of these safer metabolites may be promoted by the administration of particular vitamins. With the formation of oxalate crystals in the urine, calcium oxalate crystals form and accumulate in blood and other tissues. Precipitation of calcium oxalate in the renal cortex results in decreased glomerular filtration and renal insufficiency. Calcium is consumed in circulation, and hypocalcemia may occur.

The rate-dependent step for EG metabolism is the ADH-catalyzed step. Ethyl alcohol binds much more easily to ADH than ethylene glycol or methanol do. Because ethanol is the preferential substrate for ADH, metabolism of EG may be essentially blocked by the presence of ethanol. This is the basis of one therapy used in the US (see Emergency Department Care).