EC Pharmacology and Toxicology

Background: Methanol and ethylene glycol are highly toxic alcohols that undergo biotransformation to metabolites more hazardous than the parent compounds, resulting in severe clinical outcomes including high mortality and disability.

Objective: To analyze scientific literature on the epidemiology and the pathogenetic mechanisms underlying the toxicity of acute methanol and ethylene glycol intoxication.

Materials and Methods: A systematic review of literature from PubMed, Scopus, and RSCI bibliographic databases was conducted. A systematic search was used.

Results: Evidence demonstrates that methanol and ethylene glycol remain significant causes of mass poisoning with severe sequelae in the twenty-first century. Methanol-related mass poisonings are documented in various countries worldwide on an almost annual basis and are typically characterized by high mortality rates. Ethylene glycol, employed by unscrupulous manufacturers in certain pharmaceutical formulations, has precipitated several mass poisonings among pediatric populations. This review presents legislative and regulatory frameworks from multiple countries that restrict the use of methanol and ethylene glycol in industrial and commercial product manufacturing. Toxicological profiles of methanol and ethylene glycol are provided, encompassing their toxicity, toxicokinetics, and biotransformation within the organism. The toxic mechanism of methanol is primarily attributed to its toxic metabolites-formaldehyde and formic acid. Similarly, the toxic effects of ethylene glycol are mediated by its metabolic products, including glycolaldehyde, glyoxal, glycolic acid, and glyoxylic acid. Metabolites of both methanol and ethylene glycol are capable of inducing cellular damage through mitochondrial dysfunction, activation of lipid peroxidation pathways, and depletion of the glutathione antioxidant system, culminating in dysregulation of multiple biochemical systems.

Conclusion: Methanol and ethylene glycol poisoning constitute a substantial proportion of substance-abuse-related and accidental exposures, particularly in countries with limited medical awareness. These poisonings cause significant morbidity and mortality, especially when antidote therapy is unavailable. Toxicity results from metabolite formation-formaldehyde and formic acid (methanol) and oxalates (ethylene glycol)-which precipitate metabolic acidosis and damage the optic nerves and kidneys. Prompt ethanol antidote therapy substantially reduces mortality.

Limitations: Incomplete data from certain regions, underreporting of cases, and lack of recent literature on the September 2025 Leningrad Region incident.

Keywords: Methanol; Ethylene Glycol; Toxic Alcohols; Acute Poisoning; Alcohol Poisonings Epidemiology; Toxic Metabolites; Mechanisms of Toxic Action; Review

Abbreviations: ADH: Alcohol Dehydrogenase; ALDH: Aldehyde Dehydrogenase; ATP: Adenosine Triphosphate; BAS: Biologically Active Substances; CNS: Central Nervous System; DNA: Deoxyribonucleic Acid; NAD: Nicotinamide Adenine Dinucleotide; RSCI: Russian Science Citation Index

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