What is the pathophysiology of methanol alcohol toxicity?

Updated: Jan 05, 2021
  • Author: Michael D Levine, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
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Methyl alcohol (methanol; CH3 OH) is widely used as an industrial and marine solvent and paint remover. It is also used in photocopying fluid, shellacs, and windshield-washing fluids. Although toxicity primarily occurs from ingestion, it can also occur from prolonged inhalation or skin absorption. [6, 7, 8, 9]  

Methanol is rapidly absorbed from the gastric mucosa, and achieves a maximal concentration 30-90 minutes after ingestion. [10]  Methanol is primarily metabolized in the liver via alcohol dehydrogenase into formaldehyde. Formaldehyde is subsequently metabolized via aldehyde dehydrogenase into formic acid, which ultimately is metabolized to folic acid, folinic acid, carbon dioxide, and water. A small portion is excreted unchanged by the lungs.

Formic acid is responsible for the majority of the toxicity associated with methanol. Without competition for alcohol dehydrogenase, methanol undergoes zero-order metabolism, and is thus is excreted at a rate of 8.5 mg/dL/h to 20 mg/dL/h. Once methanol experiences competitive inhibition, from either ethanol or fomepizole, the metabolism changes to first order. In this later scenario, the excretion half-life ranges from 22-87 hours.

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