Ethanol

CAS RN: 64-17-5

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: Found primarily in alcoholic beverages. Also found in a variety of over-the-counter products, including some cough/cold medicines, perfumes, colognes, mouthwashes, food flavorings (eg, vanilla extract), and hand sanitizers. Also used clinically as a treatment of ethylene glycol or methanol poisonings.
    • B) PHARMACOLOGY: When used therapeutically, ethanol's high affinity for alcohol dehydrogenase inhibits the metabolism of methanol and ethylene glycol.
    • C) TOXICOLOGY: Ethanol enhances the inhibitory effects of GABA at the GABA-A receptor. It also competitively inhibits the binding of glycine at the NMDA receptor, disrupting excitatory glutaminergic neurotransmission. The net result is CNS depression. Chronic ethanol use causes desensitization and down-regulation of GABA-A receptors and NMDA up-regulation. Abrupt cessation of ethanol use then causes a hyperexcitable state, producing ethanol withdrawal syndrome. Please refer to the ALCOHOL WITHDRAWAL SYNDROMES management for further information.
    • D) EPIDEMIOLOGY: Extremely common exposure that rarely results in morbidity or death. However, ethanol frequently precipitates traumatic injury.
    • E) WITH POISONING/EXPOSURE
      • 1) MILD TO MODERATE TOXICITY: Intoxication, euphoria, ataxia, nystagmus, disinhibition, aggressive behavior, nausea, vomiting, flushing, and supraventricular tachyarrhythmias (primarily atrial fibrillation) can develop.
      • 2) SEVERE TOXICITY: Coma, respiratory depression, pulmonary aspiration, hypoglycemia, and hypothermia can occur. Abrupt cessation of chronic ethanol use causes withdrawal, manifested by hypertension, tachycardia, tremors, seizures, and in severe cases, delirium.
0.2.3 VITAL SIGNS
  • 0.2.3.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Hypothermia is common. Hypotension and tachycardia may be present. Bradypnea may occur early, and tachypnea may develop in cases of metabolic acidosis. Elevated body temperature and labored breathing (possibly from aspiration) have been reported in infants.
0.2.20 REPRODUCTIVE HAZARDS
  • A) Women who consume ethanol during pregnancy may give birth to a child with Fetal Alcohol Syndrome. No safe consumption level is known.
0.2.21 CARCINOGENICITY
  • 0.2.21.1 IARC CATEGORY
    • A) IARC Carcinogenicity Ratings for CAS64-17-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) Not Listed
  • 0.2.21.2 HUMAN OVERVIEW
    • A) Alcohol consumption has been associated with various cancers, including liver, esophageal, breast, prostate, and colorectal cancer.
0.2.22 GENOTOXICITY
  • A) Ethanol caused DNA damage in a rat model and Saccharomyces cerevisiae, DNA repair in Escherichia coli, and DNA inhibition in human lymphocytes. It caused mutations in E coli, Salmonella typhimurium, Aspergillus nidulans, and S cerevisiae. Ethanol has been positive on cytogenetic analysis in human fibroblasts, leukocytes, and lymphocytes; in rats and mice; and in hamster embryo and ovary cells.
  • B) A positive micronucleus test was observed in mice and in dog lymphocytes. The dominant lethal test was positive in mice; sperm morphology was observed in mice, and ethanol was positive for gene conversion/mitotic recombination in A nidulans.
  • C) Ethanol has caused sister chromatid exchange in human lymphocytes, in hamster ovary cells, and in mice. It also caused sex chromosome loss/nondisjunction in A nidulans, in Drosophila melanogaster, and in mice.
Find more information on this substance at: PubChem, PubMed