| GHS 分類 | DangerH225: Highly Flammable liquid and vapor [Danger Flammable liquids]P210, P233, P240, P241, P242, P243, P280, P303+P361+P353, P370+P378, P403+P235, and P501 (click each P-code to see the statement)This chemical does not meet GHS hazard criteria for < 0.1% (5 of 13886) of reports.H225 (> 99.9%): Highly Flammable liquid and vapor [Danger Flammable liquids] |
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| 規制情報 | Chemical: EthanolRegulation (EC) No 1831/2003 (amended)Ethanol is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Ethanol are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)Status: No longer Valid Update: 11-01-2016 https://echa.europa.eu/registration-dossier/-/registered-dossier/6310Ethanol: HSNO Approval: HSR001144 Approved with controlsThe New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.) |
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| その他の安全情報 | IMAP assessments - Ethanol: Human health tier II assessment |
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| 輸送ラベル（DOT） | Flammable Liquid |
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| 火災危険 | Excerpt from ERG Guide 127 [Flammable Liquids (Water-Miscible)]:FLAMMABLE. Flashback along vapor trail may occur. Vapor may explode if ignited in an enclosed area. (USCG, 1999)· HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames.Highly flammable. Vapour/air mixtures are explosive. Risk of fire and explosion on contact with incompatible substances. See Chemical Dangers. |
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| 火災の可能性 | Flammable liquid when exposed to heat or flame ... . |
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| 健康有害性 | Excerpt from ERG Guide 127 [Flammable Liquids (Water-Miscible)]:VAPOR: Irritating to eyes, nose and throat. LIQUID: Not harmful. (USCG, 1999)· Inhalation or contact with material may irritate or burn skin and eyes. |
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| 有害性の概要 | Drinking alcoholic beverages is a known human carcinogen listed by the International Agency for Research in Cancer (IARC) and the National Toxicology Program (NTP). Alcohol consumption causes cancers of the oral cavity, pharynx, larynx, oesophagus, colorectum, liver (hepatocellular carcinoma) and female breast. [Reference #2] That ethyl alcohol is unlikely to be an occupational carcinogen is reflected by its classification as 5 by MAC. MAC defines 5 as, Substances with carcinogenic and genotoxic effects, the potency of which is considered to be so low that, provided the MAK and BAT values are observed, no significant contribution to human cancer risk is to be expected. Drinking alcoholic beverages is also a reproductive hazard, causing fetal alcohol syndrome. Low level occupational exposures are not likely to harm the fetus. [Frazier, p. 175-7] Inhalation of high concentrations can cause CNS depressionAn eye and respiratory tract irritant[ICSC] Suspected germ cell mutagen (3B)[MAK] Causes non-immunological contact urticaria[Kanerva, p. 219] |
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| 輸送番号・ガイド（DOT） | 1170 1271987 127 |
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| FDA 要件 | Substance added directly to human food affirmed as generally recognized as safe (GRAS).Ethanol is an indirect food additive for use only as a component of adhesives. |
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| 反応性グループ | Alcohols and Polyols |
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| UN 分類 | UN Hazard Class: 3UN Pack Group: II |
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| Special Reports | Kuhn C et alBuzzed. The Straight Facts About The Most Used and Abused Drugs From Alcohol to Ecstasy 4th ed (2014)Handbook features the most recent discoveries about drugs, including new information about biological and behavioral changes in addiction, the prescription-drug abuse epidemic, distinctive drug effects on the adolescent brain, and a perspective on legal trends.Sato C et alAlcohol Relat Dis Gastroenterol: p.172-84 (1985). A review with many references on the interactions of ethanol with drugs and xenobiotics. The effects of ethanol on absorption, plasma protein binding, hepatic blood flow, distribution, hepatic uptake, and phase I & II hepatic metabolism are briefly summarized and the clinical relevance of the observed changes is discussed.Lieber CS, Leo MAFalk Symp 39 Hepatology: 15-36 (1985). A review with 60 references on the direct effects of ethanol on vitamin A metabolism and resulting alterations of hepatic vitamin A levels even at early stages of alcohol liver injury. Implication with regard to vitamin A therapy in alcoholics and possible vitamin A toxicity were also discussed.USEPA/Office of Pesticide ProgramsReregistration Eligibility Decision Document - Aliphaatic Alcohols, EPA 738-R-95-013 (April 1995). The RED summarizes the risk assessment conclusions and outlines any risk reduction measures necessary for the pesticide to continue to be registered in the USA.[Available from, as of October 11, 2017: http://www.epa.gov/pesticides/reregistration/status.htm] |
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| 消火 | Excerpt from ERG Guide 127 [Flammable Liquids (Water-Miscible)]:Use water spray, powder, alcohol-resistant foam, carbon dioxide. In case of fire: keep drums, etc., cool by spraying with water. |
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| 応急処置措置 | Fresh air, rest.Remove contaminated clothes. Rinse skin with plenty of water or shower.First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.Rinse mouth. Give one or two glasses of water to drink. Refer immediately for medical attention. |
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| 漏出応急措置 | · CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. |
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| 応急処置 | Excerpt from ERG Guide 127 [Flammable Liquids (Water-Miscible)]:EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.General First Aid:(General first aid procedures) |
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| 安全保管 | Fireproof. Separated from : see Chemical Dangers. |
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| 暴露管理・個人防護 | · Wear positive pressure self-contained breathing apparatus (SCBA).27314.0 [ppm]200.0 [ppm] |
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| 消火手順 | Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Solid streams of water may be ineffective. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Use "alcohol" foam, dry chemical or carbon dioxide. |
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| 保管条件 | Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage. Hygroscopic. Storage class (TRGS 510): Flammable liquidsKeep tightly closed, cool and away from flame.Storage temp: ambient. Venting: open (flame arrester) or pressure vacuum.Protect containers against physical damage. Underground storage tanks outside the building is preferred for use of large quantities. Small amt may be stored outside the building in the original shipping containers. ... Should not be stored with perchlorates, peroxides, chromic acid and nitric acid. |
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| 清掃方法 | ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Remove all sources of ignition. Evacuate personnel to safe areas. Beware of vapors accumulating to form explosive concentrations. Vapors can accumulate in low areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Contain spillage, and then collect with an electrically protected vacuum cleaner or by wet-brushing and place in container for disposal according to local regulations.Land spill: Apply appropriate foam to diminish vapor and fire hazard.Water spill: Use natural barriers or oil spill control booms to limit spill travel. Allow to aerate.Air spill: Apply water spray or mist to knock down vapors. |
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| 非火災時の漏出対応 | Excerpt from ERG Guide 127 [Flammable Liquids (Water-Miscible)]: |
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| 処分方法 | SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air qualitypotential migration in air, soil or watereffects on animal, aquatic and plant lifeand conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.Product: Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Contaminated packaging: Dispose of as unused product.SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.The following wastewater treatment technologies have been investigated for ethanol: Biological Treatment. |
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| 漏出処分 | Remove all ignition sources. Ventilation. Do NOT wash away into sewer. Collect leaking and spilled liquid in covered containers as far as possible. Absorb remaining liquid in inert absorbent. Wash away remainder with plenty of water. Store and dispose of according to local regulations. |
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| 体内負荷 | Ethanol was detected at levels of 13-1000 ppb in the exhaled breath of 64 human subjects(1). |
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| Treatment | If you suspect someone has alcohol poisoning, call for an ambulance to take them to a hospital. While you're waiting: try to keep them sitting up and awake, give them water if they can drink it. If they've passed out, lie them on their side in the recovery position and check they're breathing properly, keep them warm and stay with them and monitor their symptoms. Acute alcohol poisoning is a medical emergency due to the risk of death from respiratory depression and/or inhalation of vomit if emesis occurs while the patient is unconscious and unresponsive. Emergency treatment for acute alcohol poisoning strives to stabilize the patient and maintain a patent airway and respiration, while waiting for the alcohol to metabolize. Emergency treatment in a hospital can involve: 1) treating hypoglycaemia (low blood sugar) with 50 ml of 50% dextrose solution and saline flush, as ethanol induced hypoglycaemia is unresponsive to glucagon2) Administration of the vitamin thiamine to prevent Wernicke-Korsakoff syndrome, which can cause a seizure3) application of haemodialysis if the blood concentration is dangerously high (>400 mg%), and especially if there is metabolic acidosis and 4) Providing oxygen therapy as needed via nasal cannula or non-rebreather mask. |
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| 相互作用 | Mass methanol poisonings present a serious problem for health systems worldwide, with poor outcome associated with delayed treatment. Positive pre-hospital serum ethanol concentration may have predictive value as the prognostic factor of the treatment outcome. We studied the effect of positive serum ethanol level on admission to hospital on survival in patients treated during the Czech methanol outbreak during 2012-2014. Cross-sectional cohort study was performed in 100 hospitalized patients with confirmed methanol poisoning. Pre-hospital ethanol was administered in 42 patients (by paramedic/medical staff to 30 patients and self-administered by 12 patients before admission)58 patients did not receive pre-hospital ethanol. Forty-two patients had detectable serum ethanol concentration on admission to hospital [median 18.3 (IQR 6.6-32.2) mmol/cu dm]. Pre-hospital ethanol administration by paramedic/medical staff had a significant effect on survival without visual and CNS sequelae when adjusted for arterial blood pH on admission (OR 8.7395 % CI 3.57-21.34p < 0.001). No patients receiving pre-hospital ethanol died compared with 21 not receiving (p < 0.001). Positive serum ethanol concentration on admission to hospital was a predictor for survival without health sequelae when adjusted for arterial blood pH (OR 8.1095 % CI 2.85-23.02p < 0.001). The probability of visual and CNS sequelae in survivors reduced with increasing serum ethanol concentration on admission.Most cocaine abusers also abuse alcohol, but little is known about interactions that promote co-abuse. These experiments in rhesus monkeys determined the effects of >8 weeks of ethanol(EtOH) consumption on cocaine self-administration (n=6), effects of dopamine (DA) receptor antagonists on cocaine reinforcement (n=3-4 per drug) and the ability of the D2-like DA receptor agonist quinpirole to elicit yawning (n=3). Monkeys self-administered cocaine (0.0-1.0mg/kg/injection, i.v.) under a 300-s fixed-interval schedule and the above-listed variables were measured before EtOH exposure. Next, monkeys consumed a sweetened, 4% EtOH solution in the home cage under binge-like conditions: 1 hr, 5 days/week with daily intake equaling 2.0 g/kg EtOH. After approximately 8 weeks, measures were re-determined, then EtOH drinking was discontinued. Finally, acute effects of EtOH on cocaine self-administration were determined by infusing EtOH (0.0-1.0g/kg. i.v.) prior to cocaine self-administration sessions (n=4). In five of six monkeys, EtOH drinking increased self-administration of low cocaine doses but did not alter reinforcing effects of higher doses. Self-administration returned to baseline after EtOH access was terminated (n=3). Effects of DA receptor antagonists on cocaine self-administration were not consistently altered after EtOH consumption, but the ability of quinpirole to induce yawning was enhanced in two of three monkeys. Acute EtOH infusions only decreased self-administration of lower cocaine doses. Taken together, the data suggest that long-term EtOH exposure can increase sensitivity to cocaine, possibly by increasing D3 receptor sensitivity. Data do not support a role for acute pharmacological interactions in promoting cocaine/EtOH co-abuse.Binge drinking is a common pattern of ethanol consumption among young people. Binge drinkers are especially susceptible to brain damage when other substances are co-administered, in particular 3,4 methylendioxymethamphetamine (MDMA). The aim of the present work was to study the mechanisms implicated in the adaptive changes observed after administration of these drugs of abuse. So, we have evaluated the cardiac sympathetic activity and the expression and activation of heat shock protein 27 (HSP27), after voluntary binge ethanol consumption, alone and in combination with MDMA. Both parameters are markers of stressful situations and they could be modified inducing several alterations in different systems. Adolescent mice received MDMA, ethanol or both (ethanol plus MDMA). Drinking in the dark (DID) procedure was used as a model of binge. Noradrenaline (NA) turnover, tyrosine hydroxylase (TH), TH phosphorylated at serine 31 and HSP27 expression and its phosphorylation at serine 82 were evaluated in adolescent mice 48 hr, 72 hr, and 7 days after treatments in the left ventricle. NA and normetanephrine (NMN) were determined by high-performance liquid chromatography (HPLC)TH and HSP27 expression and phosphorylation were measured by quantitative blot immunollabeling using specific antibodies. Ethanol and MDMA co-administration increased NA turnover and TH expression and phosphorylation versus the consumption of each one of these drugs. In parallel with the described modifications in the cardiac sympathetic activity, our results showed that binge ethanol+MDMA exposure is associated with an increase in HSP27 expression and phosphorylation in the left ventricle, supporting the idea that the combination of both drugs exacerbates the cellular stress induced by ethanol or MDMA alone.Factors affecting vitamin D metabolism may preclude anti-carcinogenic effects of its active metabolite calcitriol. Chronic ethanol consumption is an etiological factor for breast cancer that affects vitamin D metabolismhowever, the mechanisms underlying this causal association have not been fully clarified. Using a murine model, we examined the effects of chronic moderate ethanol intake on tumoral and renal CYP27B1 and CYP24A1 gene expression, the enzymes involved in calcitriol synthesis and inactivation, respectively. Ethanol (5% w/v) was administered to 25-hydroxyvitamin D3-treated or control mice during one month. Afterwards, human breast cancer cells were xenografted and treatments continued another month. Ethanol intake decreased renal Cyp27b1 while increased tumoral CYP24A1 gene expression. Treatment with 25-hydroxyvitamin D3 significantly stimulated CYP27B1 in tumors of non-alcohol-drinking mice, while increased both renal and tumoral CYP24A1. Coadministration of ethanol and 25-hydroxyvitamin D3 reduced in 60% renal 25-hydroxyvitamin D3-dependent Cyp24a1 upregulation (P<0.05). We found 5 folds higher basal Cyp27b1 than Cyp24a1 gene expression in kidneys, whereas this relation was inverted in tumors, showing 5 folds more CYP24A1 than CYP27B1. Tumor expression of the calcitriol target cathelicidin increased only in 25-hydroxyvitamin D3-treated non-ethanol drinking animals (P<0.05). Mean final body weight was higher in 25-hydroxyvitamin D3 treated groups (P<0.001). Overall, these results suggest that moderate ethanol intake decreases renal and tumoral 25-hydroxyvitamin D3 bioconversion into calcitriol, while favors degradation of both vitamin D metabolites in breast cancer cells. The latter may partially explain why alcohol consumption is associated with vitamin D deficiency and increased breast cancer risk and progression.For more Interactions (Complete) data for Ethanol (137 total), please visit the HSDB record page. |
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| 標的器官 | Eyes, skin, respiratory system, central nervous system, liver, blood, reproductive system |
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| 健康影響 | Acute: At 0.1% blood alcohol levels individuals experience CNS depression, nausea, possible vomiting, impaired cognition and impaired motor and sensory function. Accidents or injury can also occur due to the side effects of loss of coordination, slowed reaction time, sleepiness and impaired judgment. At >0.14% blood alcohol levels there is decreased blood flow to the brain. At greater than 0.3% blood alcohol there is a marked degree of stupefaction and possible unconsciousness. At levels greater than 0.4% there is a risk of death. Acute consumption leading to blood alcohol levels greater than 0.5% is almost universally fatal.
Chronic: high levels of alcohol consumption are associated with an increased risk of alcoholism, malnutrition, chronic pancreatitis, alcoholic (fatty) liver disease, and cancer. Frequent drinking of alcoholic beverages has been shown to be a major contributing factor in cases of elevated blood levels of triglycerides. In addition, damage to the central nervous system and peripheral nervous system can occur from chronic alcohol abuse. The long-term use of alcohol is capable of damaging nearly every organ and system in the body. The developing adolescent brain is particularly vulnerable to the toxic effects of alcohol. In addition, the developing fetal brain is also vulnerable, and fetal alcohol syndrome (FAS) may result if pregnant mothers consume alcohol. The net effect of alcohol consumption on global human health is quite detrimental, with an estimated 3.8% of all global deaths and 4.6% of global disability-adjusted life-years attributable to alcohol. Ethanol is considered a teratogen (causing fetal alcohol syndrome) and a Group 1 carcinogen because of the carcinogenicity of acetaldehyde (a major metabolite of alcohol). |
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| 生態毒性値 | Toxicity Threshold (Cell Multiplication Inhibition Test) Scenedesmus quadricauda (green algae) 5000 mg/LToxicity Threshold (Cell Multiplication Inhibition Test) Microcystis aeruginosa (algae) 1450 mg/LToxicity Threshold (Cell Multiplication Inhibition Test): Uronema parduczi Chatton-Lwoff (protozoa) 6120 mg/LToxicity Threshold (Cell Multiplication Inhibition Test) Entosiphon sulcatum (protozoa) 65 mg/LFor more Ecotoxicity Values (Complete) data for Ethanol (53 total), please visit the HSDB record page. |
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| 環境中動態 | TERRESTRIAL FATE: Based on a classification scheme(1), a log Koc value of 0.20(2), indicates that ethanol is expected to have very high mobility in soil. Volatilization of ethanol from moist soil surfaces is expected(SRC) given a Henry's Law constant of 5.0X10-6 atm-cu m/mole(3). Ethanol is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 59.3 mm Hg at 25 °C(4). Ethanol, present at 100 mg/L, reached 89% of its Theoretical BOD in 2 weeks using an activated sludge inoculum at 30 mg/L in the Japanese MITI test(5). Ethanol, present at 100 mg/L, was completely degraded in 5-8 days in an aerobic sandy soil/groundwater microcosm(6).AQUATIC FATE: Based on a classification scheme(1), a log Koc value of 0.20(2), indicates that ethanol is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon a Henry's Law constant of 5.0X10-6 atm-cu m/mole(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 5 and 39 days, respectively(SRC). Ethanol is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). According to a classification scheme(5), an estimated BCF of 3(SRC), from its log Kow of -0.31(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low. Biodegradation of ethanol in water is expected based on degradation half-lives on the order of a few days in aquatic studies conducted using microcosms constructed with a low organic sandy soil and groundwater(8).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), ethanol, which has a vapor pressure of 59.3 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase ethanol is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC)the half-life for this reaction in air is estimated to be 5 days(SRC), calculated from its rate constant of 3.27X10-12 cu cm/molecule-sec at 25 °C(3). Ethanol does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC). |
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| 食品調査値 | Ethanol was identified, not quantified, as a volatile plant isolate in soy beans(1). Ethanol was detected at levels of 250-980 ppb (common beans), 4900 ppb (split peas) and 2900 ppb (lentils)(2). Ethanol was identified, not quantified, as a volatile flavor component in fried bacon(3) and mountain Beaufort cheese (French Alps, summer and winter)(4). Ethanol was detected at levels of 140 to 890 mg/kg in fermented soybean curds(5). Ethanol was identified, not quantified, as a volatile component of pine sprout tea and pine needle tea(6). Ethanol is produced in the manufacture of alcohol, whiskey and gin(7). A standard drink in the US is equal to 14.0 grams (0.6 ounces) of pure alcohol as typically found in 12-ounces of beer (5% alcohol)8-ounces of malt liquor (7% alcohol)5-ounces wine (12% alcohol)1.5-ounces or a "shot" of 80-proof distilled spirits or liquor (e.g. , gin, rum, vodka, or whiskey)(8). In 14 honey spirit samples collected from market or artisan Portuguese producers, the alcohol concentration was 28.0-53.0%, most of this alcohol is reported as ethanol(9).Ethanol concentration was measured using two different methods in nine different wine styles with the following results(1):[Table#230]Ethanol is ... present to extent of 3-6% by vol in naturally fermented beers and ales, 10-12% in wines and 20-60% in distilled beverages. |
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| 有害作用 | Neurotoxin - Acute solvent syndromeDuring the liver's conversion of ethanol to acetaldehyde, the electron carrier NAD+ donates 2 electrons to this reaction. In the process, NAD+ is reduced to NADH, increasing the NADH/NAD+ ratio in the hepatocytes. |
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| 暴露経路 | The substance can be absorbed into the body by inhalation of its vapour and by ingestion.inhalation, ingestion, skin and/or eye contactOral, rapidly absorbed. Blood alcohol level and the time necessary to achieve it are controlled largely by the rapidity and extent of ethanol consumption. (T10) |
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| 毒性の概要 | The CIR Expert Panel concluded that Alcohol Denat.... denatured with t-Butyl Alcohol, Denatonium Benzoate, Diethyl Phthalate, or Methyl Alcohol are safe in the practices of use and concentration as described in this safety assessment, and, that Denatonium Benzoate is safe as a denaturant. The CIR Expert Panel concluded that the available data are insufficient to support the safety of Alcohol Denat.... denatured with Quassin, Brucine, and Brucine Sulfate in cosmetic products, and that the available data are insufficient to support the safety of Quassin, Brucine, and Brucine Sulfate as denaturants.Ingredients for which the data are insufficient and their use in cosmetics is not supportedIDENTIFICATION 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 ethanolthe 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.Alcohol intoxication causes CNS depression by enhancing the inhibitory effect of GABA on its receptors. Alcohol also inhibits the effects of glutamate on NMDA receptors, resulting in disinhibition and a blunted mental state. Ethanol intoxication manifests as slurred speech, stupor, and gait abnormalities. Severe intoxication may even result in a coma.Alcohol binds to the GABA(A) receptors (delta subunit), NMDA receptors, Glycine receptors, Serotonin receptors, Acetylcholine receptors, L-channel calcium channels and GIRK channels. Ethanol acts in the central nervous system primarily by binding to the GABAA receptor, increasing the effects of the inhibitory neurotransmitter GABA. Ethanol within the human body is converted into acetaldehyde by alcohol dehydrogenase. Acetaldehyde is linked to most of the clinical effects of alcohol. It has been shown to increase the risk of developing cirrhosis of the liver and multiple forms of cancer. During the metabolism of alcohol via the respective dehydrogenases, NAD (Nicotinamide adenine dinucleotide) is converted into reduced NAD. Normally, NAD is used to metabolise fats in the liver, and as such alcohol competes with these fats for the use of NAD. Prolonged exposure to alcohol means that fats accumulate in the liver, leading to the term 'fatty liver'. Continued consumption (such as in alcoholism) then leads to cell death in the hepatocytes as the fat stores reduce the function of the cell to the point of death. These cells are then replaced with scar tissue, leading to the condition called cirrhosis. |
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| 生態毒性抜粋 | /AQUATIC SPECIES/ Ethanol and dimethylsulfoxide (DMSO) are commonly used as carrier solvents for lipophilic chemicals in aquatic toxicity bioassays. However, very little information has been reported on the behavioral effects of these solvents. In this study, /the authors/ examined the effects of ethanol and DMSO on development and locomotor activity by a zebrafish embryo-larval bioassay. The zebrafish were exposed to different concentrations (control, 0.01, 0.1, and 1%) of ethanol or DMSO from blastula stage to 144 hour-post-fertilization (hpf). Hatchability, survival, and abnormalities were monitored every 12 hr, and locomotor activity of the larvae was analyzed at 144 hpf. Hatchability was not affected by the ethanol or DMSO treatments. No effect on survival was observed except the 1% ethanol group suffered 89% mortality during 108-120 hpf. No developmental defects were observed in any of the solvents at the 0.01 and 0.1% concentrations, but significantly higher deformity rates occurred with 1% ethanol and DMSO groups. Hyperactivity and less tortuous swimming paths were observed in all ethanol and DMSO concentrations. .../AQUATIC SPECIES/ 24-hr LC50 value for rainbow trout in flow-through bioassay system at 10 °C was 11200 mg/L. Ethanol at about 0.26 of the fingerling LC50, affected cardiovascular and respiratory system in adults. Slight ventilation rate and buccal pressure amplitude depression occurred in initial stages of 24 hr exposure. Q-T interval decreased. |
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| FIFRA 要件 | Residues of ethyl alcohol are exempted from the requirement of a tolerance when used in accordance with good agricultural practice as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops or to raw agricultural commodities after harvest. Use: solvent, cosolvent. Limit: None.Residues of ethyl alcohol are exempted from the requirement of a tolerance when used in accordance with good agricultural practice as inert (or occasionally active) ingredients in pesticide formulations applied to animals. Use: Solvent, cosolvent. Limit: None.Residues of the following chemical substances are exempted from the requirement of a tolerance when used in accordance with good manufacturing practice as ingredients in an antimicrobial pesticide formulation, provided that the substance is applied on a semi-permanent or permanent food-contact surface (other than being applied on food packaging) with adequate draining before contact with food. (a) The following chemical substances when used as ingredients in an antimicrobial pesticide formulation may be applied to: Food-contact surfaces in public eating places, dairy-processing equipment, and food-processing equipment and utensils. Ethanol is included on this list. Limits: None.Residues of the following chemical substances are exempted from the requirement of a tolerance when used in accordance with good manufacturing practice as ingredients in an antimicrobial pesticide formulation, provided that the substance is applied on a semi-permanent or permanent food-contact surface (other than being applied on food packaging) with adequate draining before contact with food. ... (c) The following chemical substances when used as ingredients in an antimicrobial pesticide formulation may be applied to: Food-processing equipment and utensils. Ethanol is included on this list. Limits: None.For more FIFRA Requirements (Complete) data for Ethanol (6 total), please visit the HSDB record page. |
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| 大気基準 | This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Ethanol is produced, as an intermediate or a final product, by process units covered under this subpart. |
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