Ethanol

CAS RN: 64-17-5

Toxicity Summary

IDENTIFICATION AND USE: Ethanol is a clear, colorless, very mobile liquid. It is used in alcoholic beverages in suitable dilutions, and as a reagent in synthetic organic chemistry and chromatography, as well as industrial and laboratory organic solvent. Other uses are in manufacture of denatured alcohol, pharmaceuticals (rubbing compounds, lotions, tonics, colognes), in perfumery. Octane booster in gasoline. Pharmaceutic aid (solvent). HUMAN STUDIES: Ethanol is a central nervous system (CNS) depressant. It enhances the inhibitory effects of gamma-aminobutyric acid (GABA) at the GABA-A receptor and competitively inhibits the binding of glycine at the N-methyl-d-aspartate receptor (it disrupts excitatory glutaminergic neurotransmission). Ethanol also stimulates release of other inhibitory neurotransmitters, such as dopamine and serotonin. The most common clinical signs of ethanol toxicosis are ataxia, lethargy, vomiting, and recumbency. In more severe cases, hypothermia, disorientation, vocalization, hypotension, tremors, tachycardia, acidosis, diarrhea, respiratory depression, coma, seizures, and death may occur. Alcohol is directly irritating to the stomach and causes vomiting. High ethanol blood levels also stimulate emesis. The concern with vomiting during intoxication is that at high blood ethanol concentrations, the muscles that control the epiglottis become slow to react or even paralyzed. This increases the risk for aspiration. Ethanol intoxication reduces peripheral oxygen delivery and metabolism and causes mitochondrial oxidative dysfunction, potentially resulting in shock or hypoxia in an acutely intoxicated patient. Hypothermia may result from multiple mechanisms. Peripheral vasodilation, CNS depression, ethanol interference with the thermoregulator mechanism, and/or impaired behavioral responses to a cold environment all lead to a lowered body temperature. Moderate ethanol intake appears to reduce the risk of myocardial infarction and other heart diseases. However, high spirits consumption was associated with increased risk of cancer mortality in women. Consumption of alcoholic beverages (beer, in particular) is associated with an increased risk for rectal but not colon cancer. Beer is a commonly consumed alcoholic beverage among reproductive-age adults. Beer drinking males have an increased risk of contributing to pregnancy waste. Women consume beer before and after pregnancy recognition. Binge drinking appears to be a common drinking behavior, and those who binge drink have an increased risk of impaired fetal growth and offspring behavior. Beer consumption by lactating women might temporarily impair motor function of nursing infants. The rate of ethanol metabolism varies among individuals. Studies of twins indicate that interindividual variability in the rate of ethanol metabolism may be genetically controlled. The main pathway for ethanol oxidation in humans is to acetaldehyde via alcohol dehydrogenase pathway. Acetaldehyde is oxidized further to acetic acid by aldehyde dehydrogenase. Asians are known to be sensitive to the health effects of ethanol; the sensitivity has been attributed to different forms of the enzyme acetaldehyde dehydrogenase. Alcohol ingestion by Asians resulted in marked elevations of blood acetaldehyde levels ranging from 0.4 to 3 mg/L, and individuals developed facial flushing and tachycardia as a direct consequence of elevated blood acetaldehyde levels. ANIMAL STUDIES: A drop full-strength ethanol on rabbit eyes causes reversible injury graded only 3 on a scale of 10 after 24 hr. Application of 70% alcohol to rabbit corneas injures and temporarily loosens the corneal epithelium, but the recovery is complete. When rats were dosed with ethanol by oral gavage with 8 to 15 g/kg/day over 4 months and fed a diet containing 25% of total calories as fat, focal necrosis, inflammation, and fibrosis were observed in the liver. Nine baboons fed ethanol at 50% of total calories developed fatty liver, and four animals developed hepatitis within 9 to 12 months. Rabbits exposed to saturated vapors of ethanol for periods ranging from 25 to 365 days developed cirrhosis of the liver. Rats were given a single intraperitoneal dose of diethylnitrosamine followed by treatment with ethanol in drinking water for 12 to 18 months. Ethanol was an effective promoter of liver tumors. Cynomolgus monkeys administered up to 5 g/kg bw ethanol daily on gestation days 20-150 revealed an increase in pregnancy wastage (abortions and still births) but no structural malformation or facial change. Ethanol, and not acetaldehyde, has been implicated as the causative agent of the teratogenic effects in laboratory animals. Oral coadministration of 100 mg/kg of 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, with 6 g/kg of ethanol intraperitoneally on gestation day 10 dramatically increased the embryotoxicity of ethanol in mice. Ethanol is not mutagenic in Salmonella typhimurium strains TA 97, TA 98, TA 100, TA 1535, TA 1537, or TA 1538 in the presence or absence of metabolic activation. In the presence of a metabolic activation system, ethanol is slightly mutagenic to Salmonella strain TA 102, a strain considered to respond to the presence of oxygen radicals. Ethanol did not induce mutations in mouse lymphoma L5178Y TK+/- cells and did not induce micronuclei in Chinese hamster V79 cells in the absence of metabolic activation. No chromosomal aberrations or sister chromatid exchanges were observed in Chinese hamster ovary cells treated with ethanol. ECOTOXICITY STUDIES: The zebrafish were exposed to different concentrations (control, 0.01, 0.1, and 1%) of ethanol from blastula stage to 144 hour-post-fertilization (hpf). No effect on survival was observed except the 1% ethanol group suffered 89% mortality during 108-120 hpf. No developmental defects were observed at the 0.01 and 0.1% concentrations, but significantly higher deformity rates occurred with 1% ethanol. Hyperactivity and less tortuous swimming paths were observed in all ethanol concentrations.
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