The following information has been extracted from our CHEMINFO database, which also contains hazard control and regulatory information. [More about...] [Sample Record]

Access the complete CHEMINFO database by contacting CCOHS Client Services.


CHEMINFO Record Number: 423
CCOHS Chemical Name: Ethanol

Absolute alcohol
Anhydrous ethanol
Ethanol denatured
Ethyl alcohol
Ethyl hydrate
Ethyl hydroxide
Fermentation alcohol
Grain alcohol
Methyl carbinol

Chemical Name French: Alcool éthylique
Chemical Name Spanish: Alcohol etílico
CAS Registry Number: 64-17-5
UN/NA Number(s): 1170
RTECS Number(s): KQ6300000
EU EINECS/ELINCS Number: 200-578-6
Chemical Family: Saturated primary aliphatic alcohol / primary alkanol / primary alkyl alcohol / ethanol / ethyl alcohol
Molecular Formula: C2-H6-O
Structural Formula: CH3-CH2-OH


Appearance and Odour:
Colourless, clear, volatile liquid with a sweet, ethereal odour like wine or whiskey (62-64). Denatured ethanol may have an unpleasant odour. Hygroscopic (absorbs moisture from the air) (65,66)

Odour Threshold:
Reported values vary widely; 49-716 ppm (geometric mean: 180 ppm) (detection); 100 ppm (recognition) (63)

Warning Properties:
GOOD - TLV is 5 to 10 times the odour threshold.

Ethanol is available commercially in the anhydrous form (absolute alcohol or 100% ethanol) and as various proofs or percentages of ethanol-water, the most common being 190 proof or 95%. If ethanol is used for purposes other than as a beverage, it is denatured by addition of substances, such as methanol, 2- propanol, ethyl acetate, methyl isobutyl ketone, heptane or kerosene, to make the product undesirable for human consumption. See reference 65 for a more complete list of denaturants. Completely denatured alcohol (CDA) and specially denatured alcohols (SDA) are available.(62,67) The physical properties given in this CHEMINFO record are for the pure, anhydrous alcohol and/or 95% alcohol. Physical properties can vary depending on whether ethanol is anhydrous, mixed with water, the percentage composition, and whether it is denatured and the type of denaturant used.

Uses and Occurrences:
Ethanol is a component of alcoholic beverages, such as beer, wine and spirits. It is used as a solvent, mainly in the manufacture of toiletries and cosmetics, surface coatings, inks, detergents and household cleaners, external pharmaceuticals, insecticides and disinfectants, and in food and drug processing; as a raw material to produce various chemical, such as acetic acid, ethyl acetate, ethyl acrylate, and other ethyl esters, ethylamine, glycol ethers, ethylene and butadiene; in the manufacture of drugs and medicinal chemicals, plastics, lacquers, dyes, polishes, plasticizers, perfumes, cosmetics and explosives; and as a motor fuel.(62,64,67) Can also be used as an antiseptic.(65)


Colourless, clear, volatile liquid with a sweet, ethereal odour like wine or whiskey. Hygroscopic. FLAMMABLE LIQUID AND VAPOUR. Vapour is slightly heavier than air and may spread long distances. Distant ignition and flashback are possible. Mild central nervous system depressant following ingestion or very high vapour concentrations. May cause headache, nausea, dizziness, drowsiness, incoordination and confusion. Causes eye irritation. SUSPECT MUTAGEN - May cause inheritable genetic damage, based on animal data. Aspiration hazard. Swallowing or vomiting of the liquid may result in aspiration into the lungs.


Effects of Short-Term (Acute) Exposure

Ethanol readily forms high vapour concentrations. However, harmful effects are unlikely to occur since it provides good warning of exposure. Aerosols and vapours are irritating to the nose and throat well above the odour threshold (approximately 100-180 ppm) and well below exposures expected to cause the effects typically associated with alcohol ingestion.
A 30-minute exposure to 1800 to 2000 ppm ethanol aerosol caused coughing, dry throat and temporary bronchial constriction.(58) In other studies, brief exposure to very high levels (5300-10600 ppm (cited as 10-20 mg/L)) produced temporary irritation of the nose and coughing. At 16000 ppm (cited as 30 mg/L), continuous irritation of nose, with coughing was observed and 21300 ppm (cited as 40 mg/L) was considered to be intolerable for even a short period of time.(16)
Symptoms of alcohol intoxication which develop following the ingestion of alcoholic beverages containing ethanol have been well described in the literature (see "Ingestion" below). Similar effects are not expected to occur following inhalation of ethanol, unless the victim is knocked down or unable to remove themselves from exposure to high concentrations. Individuals with repeated exposure to ethanol can develop tolerance to its effects. In this case, higher exposure may be required to produce effects which were previously observed at lower exposures.
One historical study has described symptoms such as headaches and slight numbness (approximately 1380 ppm for 30 minutes); sensations of warmth/cold (from 3340 ppm for 100 minutes); difficulty breathing, drowsiness and fatigue (from 8840 ppm for 60 minutes) in volunteers.(2,3) The validity of this study has been questioned, since subsequent studies have shown that it is unlikely that these effects would have been observed at the low concentrations cited.(3,16)

Skin Contact:
Ethanol is either not irritating or only mildly irritating to the skin, based on human and animal information. No irritation was produced in 16 volunteers following application of 0.5 mL of 95% ethanol, using a modified Draize test.(42) Mild irritation has been observed in animal tests.
Absorption of ethanol through the skin is minimal.(3) Harmful effects would not be expected by this route of exposure.

Eye Contact:
Depending upon concentration, direct contact with the liquid is expected to produce moderate to severe irritation, based on animal information. Exposure to high vapour concentrations can produce mild irritation. High vapour concentrations (7000-10000 ppm) have caused stinging and watering of the eyes which increased in intensity with passing time and persisted throughout the exposure. There was no subsequent eye damage noted. Exposure to 2500 ppm had no effect on the eyes.(5,16)

Due to the relatively low oral toxicity of ethanol, it is unlikely that toxic effects would result from accidental occupational ingestion. Evidence from animal studies and human consumption of alcoholic beverages demonstrates that ingestion of large amounts causes depression of the central nervous system (CNS) with symptoms such as lack of coordination, impaired vision, reduced reaction time, slurred speech, impaired judgement, nausea/vomiting and unconsciousness progressing to death from respiratory or circulatory failure.(2,49) For an average adult, the fatal ingested dose is approximately 1 L (approximately 2 pints) of 40-55% ethanol (the percentage found in whiskey, gin, rum, vodka, or brandy) consumed within a few minutes.(49)
Based on animal evidence and its physical properties, ethanol can be aspirated into the lungs during ingestion or vomiting. Aspiration can cause potentially fatal injury to the lungs.

Effects of Long-Term (Chronic) Exposure

Occupational exposures which principally occur by inhalation and skin contact do not result in as high absorption of ethanol as that which occurs from drinking alcoholic beverages.(2,3) Ethanol vapours and mists produce irritation, thus limiting long-term inhalation exposure. Ethanol is not readily absorbed through the skin.

SKIN IRRITATION: Long-term or repeated contact may result in dermatitis (dry, red, cracked skin). Repeated application of 10% ethanol, under cover, to 8 volunteers for 21 days produced redness and hardening of the skin during the final 7 days of exposure.(42)

SKIN SENSITIZATION: Ethanol is not a clear occupational skin sensitizer. Approximately 20 cases of ethanol allergic skin reactions confirmed by positive patch tests have been identified. In most cases, exposure to ethanol was not occupational.(9,10,12,13,51-54,59,60) In some cases, a previous history of allergies was also identified.(53,54,59) One limited study suggests that contact sensitivity to ethanol may be related to an ethnic sensitivity, similar to the Oriental ethnic sensitivity to skin flushing following ingestion of alcoholic beverages.(55) Another report suggests that some of the cases may actually be a non-allergic wheal reaction (non-allergic contact urticaria).(12)
In the three occupational exposure cases located, patch testing with ethanol proved positive. Prior history of allergies was not discussed for any of the cases.(9,10,61) Therefore, no firm conclusions can be drawn from these reports.
In one sensitization study, 6/93 volunteers developed delayed allergic skin reactions.(11) In another study, sensitization was not produced in any of 94 subjects tested.(8) These results indicate that ethanol may be a weak skin sensitizer.

HUMAN POPULATION STUDIES: No conclusions about the potential long-term health effects of ethanol can be drawn from a mortality study of ethanol production workers. Workers were exposed to strong sulfuric acid at the same time and it appears that this chemical is more likely to have caused the health effects observed.(15)

LONG-TERM INGESTION: Long-term ingestion of alcoholic beverages containing ethanol has been clearly associated with significant health problems, including cirrhosis of the liver and diseases of the gastrointestinal, cardiovascular, respiratory, and nervous systems. Mental problems include a wide range of neurological changes, depression and other mental disorders.(17,48,49) There are no cases or studies reported of similar long-term health effects resulting from occupational exposure to ethanol.


Occupational exposure to ethanol has not been associated with carcinogenicity. The International Agency for Research on Cancer (IARC) has has classified alcoholic beverages as carcinogenic to humans (Group 1), based on tumours of the oral cavity, pharynx, larynx, esophagus, liver, colorectum, and female breast. Because the positive associations were generally noted with different types of alcoholic beverages and in view of the carcinogenicity of ethanol in animals, IARC has also classified ethanol in alcoholic beverages as carcinogenic to humans (Group 1).(96) Oral exposure to alcoholic beverages containing ethanol is not relevant to occupational exposures.

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

IARC has classified ethanol in alcoholic beverages as Group 1 (carcinogenic to humans).

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as not classifiable as a human carcinogen (A4).

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

NTP has listed consumption of alcoholic beverages as a known human carcinogen.

Teratogenicity and Embryotoxicity:
There are no reports of adverse effects on pregnancy following occupational exposures. It is well documented that exposure to ethanol through the ingestion of alcoholic beverages during pregnancy can cause significant harmful effects in unborn children. Certain physical malformations, stillbirths, low birth weight, and neurological, behavioural and intelligence deficits have been observed in the children of mothers who have consumed alcohol during pregnancy. The most severe group of effects is commonly referred to as Fetal Alcohol Syndrome (FAS). The lower limit of alcohol ingestion necessary to cause FAS has not been determined, but is associated with the consumption of large amounts of alcohol or chronic alcoholism in the mother. Reduced birth weight is a less severe effect and the lower limit of alcohol ingestion associated with this effect appears to be approximately two drinks per day on average.(46) Effects have not generally been seen with alcoholic beverage intake of about one drink per day.(17)
Animal evidence also clearly demonstrates that ingestion of ethanol can cause embryotoxicity, teratogenicity and fetotoxicity in the presence of maternal toxicity. No effects were observed in one study with very high inhalation exposures, despite the observation of significant harmful effects in the mothers.

Reproductive Toxicity:
There are no reports of adverse effects on pregnancy following occupational exposures. Reproductive effects have been observed in people who have consumed large amounts of alcoholic beverages which contain ethanol. Human population studies have shown testicular atrophy and sperm effects in alcoholic men, but these effects are generally accompanied by the cirrhosis of the liver. Some studies have shown early menopause in alcoholic women.(45) It is not possible to draw firm conclusions about the potential reproductive toxicity of ethanol from these studies because of design limitations. For example, often only a very small number of people were studied and alcoholics are commonly exposed to other harmful chemicals (for example, through smoking or second-hand smoking). Furthermore, these effects cannot be related to people who are occupationally exposed to ethanol because the nature and degree of exposure is significantly different.
Effects on reproductive organs, including decreased testicular weight, decreased numbers of motile sperm, decreased ovarian function and irregular fertility cycles, have been observed in animals given very large oral doses of ethanol. However, no confirmed effects on fertility or reproductive capability have been observed.

Ethanol is considered a very toxic mutagen, because it has caused mutations in both the germ cells and somatic cells of live animals. These effects were observed following exposure of the animals to very high, oral doses of ethanol. There are no reports of mutagenic effects in people with occupational exposures. Mutagenic effects, such as increased frequencies of chromosomal aberrations, sister chromatid exchanges and aneuploidies have been observed in the white blood cells of alcoholics. However, it is not possible to conclusively relate these effects directly to ethanol exposure, because of other potential causes, such as smoking and exposure to other potentially harmful chemicals at the same time.

Toxicologically Synergistic Materials:
Most information about the interactions of ethanol with other chemicals results from studies involving alcohol consumption and exposure to chemicals. Occupational exposure to ethanol would be much lower and any interactive effects would be substantially reduced or absent. Ethanol increases liver metabolism and thus increases the metabolism of some organic compounds. It may also compete for metabolic sites thus interfering with the metabolism of other compounds.(2,7)
Ethanol has been associated with an increase in the toxicity of many chemicals including other alcohols, ketones (e.g. acetone and methyl ethyl ketone), benzene, toluene, halogenated hydrocarbons (e.g. carbon tetrachloride, trichloroethylene, chloroform, and methylene chloride), aromatic amines and nitrosamines.(2,4,7,14) In particular, it enhances the activity of many chemicals which are harmful to the liver (hepatotoxic agents).(2) There is also a synergistic effect between ethanol and certain metals (e.g. cobalt, manganese and mercury) or compounds containing these metals.(7)
Some chemicals (e.g. thiuram disulfides or "antabuse" , dimethylformamide and cyanamide) can decrease or slow the metabolism of ethanol thereby increasing the toxic effects of ethanol.(7)

Potential for Accumulation:
Ethanol does not accumulate. It is readily absorbed by the oral or inhalation routes of exposure, but skin uptake is low. Human absorption of vapours has been reported to be 33-62%, and independent of air concentration and ventilation rate. Most ethanol is metabolized before it is eliminated. It is metabolized primarily by the liver to acetaldehyde, which in turn is converted to acetic acid or acetate, which is oxidized to carbon dioxide, which is exhaled. Only small amounts are eliminated unchanged in exhaled air, urine or perspiration. The rate of metabolism varies between individuals and, in the case of animals, between species.(2,3,17)


This material is flammable. Take proper precautions to ensure your own safety before attempting rescue (e.g. remove any souces of ignition). If symptoms develop, remove source of contamination or have victim move to fresh air. If symptoms persist, obtain medical advice.

Skin Contact:
No health effects expected. If contact occurs, flush with lukewarm, gently flowing water for 5 minutes or until the chemical is removed.

Eye Contact:
Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 20 minutes, or until the chemical is removed, while holding the eyelid(s) open. Take care not to rinse contaminated water into the unaffected eye or onto the face. Obtain medical attention immediately.

NEVER give anything by mouth if the victim is rapidly losing consciousness, is unconscious or is convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. Have victim drink 240 to 300 mL (8 to 10 oz.) of water to dilute material in the stomach. If vomiting occurs naturally, have victim lean forward to reduce risk of aspiration. Obtain medical attention immediately.

First Aid Comments:
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.
NOTE: Denatured alcohol often contains other potentially toxic ingredients. The first aid procedures recommended should be appropriate for the product as a whole, not just the ethanol component.


Flash Point:
13 deg C (55.4 deg F) (closed cup) (100%) (67)

Lower Flammable (Explosive) Limit (LFL/LEL):
3.3% (62); 4.3% (62) (100%)

Upper Flammable (Explosive) Limit (UFL/UEL):
19% (62) (100%)

Autoignition (Ignition) Temperature:
363 deg C (685 deg F) (100%) (68); 423-425 deg C (793.4-797 deg F) (100%) (62,67)

Sensitivity to Mechanical Impact:
Not sensitive. Stable material.

Sensitivity to Static Charge:
Will not accumulate static charge. The electrical conductivity of ethanol (1.345 pS/m X 10(5) at 25 deg C) is high.(69,70) Mixtures of ethanol vapour and air at concentrations in the flammable range may be ignited by a static charge of sufficient energy.

Combustion and Thermal Decomposition Products:
Toxic, irritating chemicals.(66)

Fire Hazard Summary:
Flammable liquid. Can release vapours that form explosive mixtures with air at, or above, 13 deg C. Vapour is slightly heavier than air and can travel a considerable distance to a source of ignition and flash back to a leak or open container. Can accumulate in confined spaces, resulting in a toxicity and flammability hazard. Closed containers may rupture violently when exposed to fire or excessive heat for a sufficient period of time.

Extinguishing Media:
Carbon dioxide, dry chemical powder, alcohol foam or polymer foam. Water may be ineffective because it will not cool ethanol below its flash point. Fire fighting foams are the extinguishing agent of choice for most flammable liquid fires. However, alcohols are water-soluble and will break down the common foams.(66)

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or protected location. Approach fire from upwind to avoid toxic decomposition products.
Stop leak before attempting to stop the fire. If the leak cannot be stopped, and if there is no risk to the surrounding area, let the fire burn itself out. If the flames are extinguished without stopping the leak, vapours could form explosive mixtures with air and reignite. Water can extinguish the fire if used under favourable conditions and when hose streams are applied by experienced firefighters trained in fighting all types of flammable liquid fires. If possible, isolate materials not yet involved in the fire, and move containers from fire area if this can be done without risk, and protect personnel. Otherwise, fire-exposed containers or tanks should be cooled by application of hose streams and this should begin as soon as possible and should concentrate on any unwetted portions of the container. If this is not possible, use unmanned monitor nozzles and immediately evacuate the area. If a leak or spill has not ignited, use water spray in large quantities to disperse the vapours and toprotect personnel attempting to stop a leak. Water spray can be used to dilute spills to nonflammable mixtures and flush spills away from ignition sources. Solid streams of water may be ineffective and spread material. For a massive fire in a large area, use unmanned hose holder or monitor nozzles; if this is not possible withdraw from fire area and allow fire to burn. Stay away from ends of tanks, but be aware that flying material from ruptured tanks may travel in any direction. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank due to fire.
As in any fire, firefighters may enter the area if positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) and full Bunker Gear is worn.


NFPA - Health: 2 - Intense or continued (but not chronic) exposure could cause temporary incapacitation or possible residual injury.
NFPA - Flammability: 3 - Liquids and solids that can be ignited under almost all ambient temperature conditions.
NFPA - Instability: 0 - Normally stable, even under fire conditions, and not reactive with water.


Molecular Weight: 46.07

Conversion Factor:
1 ppm = 1.88 mg/m3; 1 mg/m3 = 0.532 ppm at 25 deg C (calculated)

Physical State: Liquid
Melting Point: -114 to -114.5 deg C (-173.2 to - 174 deg F) (Freezing point) (62,67,70)
Boiling Point: 78.3 deg C (173 deg F) (100%) (62,69,70); 78.15 deg C (172.7 deg F) (95%) (67)
Relative Density (Specific Gravity): 0.789 at 20 deg C (water = 1) (100%) (62,69,70); 0.816 at 15.6 deg C (water = 1) (95%) (62)
Solubility in Water: Soluble in all proportions at 20 deg C (62)
Solubility in Other Liquids: Soluble in all proportions with ethers, ketones, hydrocarbons, acids, esters, glycols, other alcohols and many other organic solvents (69)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = -0.32 (measured) (71)
pH Value: Not available. Ethanol is a very weak acid.(72,73)
Vapour Density: 1.59 (air = 1) (66,69)
Vapour Pressure: 5.9 kPa (44.3 mm Hg) at 20 deg C (69)
Saturation Vapour Concentration: 58300 ppm (5.8%) at 20 deg C (calculated)
Evaporation Rate: 2.4 (n-butyl acetate = 1); 8.3 (diethyl ether = 1) (69)
Critical Temperature: 243.1 deg C (469.6 deg F) (62)

Other Physical Properties:
ACIDITY: Very weak acid and very weak base; pKa = 16 (72,73)
VISCOSITY-DYNAMIC: 1.17-1.21 mPa.s (1.17-1.21 centipoises) at 20 deg C (62,69,70)
VISCOSITY-KINEMATIC: 1.48-1.53 mm2/s (1.48-1.53 centistokes) at 20 deg C (calculated)
SAYBOLT UNIVERSAL VISCOSITY: Approximately 30.9 Saybolt seconds at 37.8 deg C (100 deg F) (calculated)
SURFACE TENSION: 22.4 mN/m (22.4 dynes/cm) at 20 deg C (70,74)
CRITICAL PRESSURE: 6384 kPa (63 atm.) (62,70)


Normally stable

Hazardous Polymerization:
Does not occur

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.

STRONG OXIDIZING AGENTS (e.g. chromium trioxide, chlorine oxides, nitrosyl perchlorate, nitric acid and permanganates) - may react violently or explosively. Increased risk of fire and explosion.(64,66,75)
HYDROGEN PEROXIDE - mixtures of concentrated peroxide and ethanol can be detonated by shock or heat.(75)
PERCHLORIC ACID, METAL PERCHLORATES (e.g. silver perchlorate), MERCURIC NITRATE, SILVER NITRATE, SILVER and NITRIC ACID, or SILVER OXIDE and AQUEOUS AMMONIA - may form shock-sensitive or explosive compounds.(68,75)
ALKALI METALS (e.g. sodium or potassium) - reaction may be explosive due to the formation of hydrogen-air mixtures, unless air is excluded.(66)
BROMINE PENTAFLUORIDE, DISULFURYL DIFLUORIDE or BROMIDES - reaction may be vigorous or violent with risk of fire and explosion.(66,68,75)
PHOSPHORUS (III) OXIDE - ignites readily at normal temperatures.(75)
POTASSIUM TERT-BUTOXIDE - contact of solid butoxide with ethanol vapour caused ignition.(75)
ACIDS, ACID ANHYDRIDES, or ACID CHLORIDES - reaction may be vigorous or violent, with the evolution of heat.(66,75)

Hazardous Decomposition Products:
None reported

Conditions to Avoid:
Sparks, open flames, heat and other ignition sources

Corrosivity to Metals:
Not corrosive to cast iron, steel stainless steel, copper and its alloys, nickel and its alloys and aluminum.(76) May react with hot aluminum.(64)


LC50 (mouse): Approximately 21000 ppm (4-hour exposure); cited as 39 g/m3 (4-hour exposure) (1, unconfirmed)

LD50 (oral, rat): 7060 mg/kg (41); 10600 mg/kg (41); 13660 mg/kg (37)
LD50 (oral, mouse): 3450 mg/kg (1, unconfirmed)
LD50 (oral, guinea pig): 5560 mg/kg (37)

Eye Irritation:

Concentrated ethanol is a moderate to severe eye irritant.

Application of 0.1 mL of undiluted ethanol caused moderate injury in rabbits (scored up to 5 where 5 is severe injury; graded 3/10).(38) In other studies, application of 0.1 mL of 90% ethanol produced severe irritation in rabbits and 95% ethanol produced mild to moderate irritation in rabbits.(39,40) There have been extensive studies of the visual and ocular effects produced with short-term and long-term ethanol intoxication.(5) These effects are not reported here as they are not relevant to occupational exposure.

Skin Irritation:

Concentrated ethanol is a mild skin irritant.

In a modified Draize test, application of 95% ethanol produced no irritation to intact skin and only very mild irritation to abraded (damaged) skin of rabbits.(39) Application of 0.5 mL of 95% ethanol, under cover, produced mild irritation in rabbits.(42) In one unconfirmed study, application of 20 mg produced moderate irritation after 24 hours in rabbits in a standard Draize test.(1)

Effects of Short-Term (Acute) Exposure:

Short-term inhalation studies showed no effects in rats exposed to 3260 ppm for 6 hours or to 10750 ppm for 0.5 hours. At higher exposures or longer exposure times, increasing signs of depression of the central nervous system (CNS) were observed. Effects included drowsiness, muscle weakness, incoordination, unconsciousness and death. Similar results were observed in other species.(2) Exposure to 27300 ppm produced a reduced respiratory rate in 50% of the mice tested (RD50).(47) This study was designed to evaluate the relative degree of sensory irritation (irritation of the nose, throat and respiratory tract). These results indicate that ethanol is a relatively weak sensory irritant.

CNS effects have also been observed in animals given oral doses of ethanol in many studies. In one study, dogs orally dosed with ethanol (3000 mg/kg in single dose or repeated for 7 days) showed changes in kidney function.(56) In a study designed to test aspiration risk, aspiration of 0.2 mL of 100% ethanol produced death in 5/10 rats. Aspiration of 0.2 mL of 70% ethanol in water on produced death in 1/10 rats.(35)

Effects of Long-Term (Chronic) Exposure:

Major effects observed following long-term inhalation or ingestion are on the liver and pancreas, with only minor other changes reported.

No harmful effects were observed in rats, guinea pigs, rabbits, monkeys and dogs exposed continuously by inhalation for 90 days to 46 ppm ethanol.(36) Guinea pigs also showed no harmful effects following intermittent inhalation exposure to 3000 ppm of a product largely composed of ethanol for 10.5 weeks.(43) In other continuous exposure studies, where rats were exposed to high levels (8000-13300 ppm), liver changes were noted, as well as reduced numbers of cells in the spleen, thymus and bone marrow.(3) Exposure of rabbits to saturated vapours (approximately 58000 ppm) for 25-365 days caused liver damage (cirrhosis of the liver).(2)

Baboons fed high dietary levels (80 mL/kg/day (equivalent to 63000 mg/kg/day)) of ethanol developed fatty livers and, in some cases, hepatitis with 9-12 months exposure.(57) Long-term oral dosing studies using rats have shown consistent liver damage (fatty infiltration, focal necrosis, inflammation and/or fibrosis).(2) Oral exposure of rats to 1% or 3% ethanol in semisynthetic liquid diets for two years produced damage to the nerves of the extremities (peripheral nerve degeneration) in both sexes. Liver injury, bile duct injury, inflammation of the pancreas and/or increased cell growth (hyperplasia) was observed in males. Increased cell growth in the adrenal and thyroid glands and inflammation of the clitoral gland was noted in females.(22) Reports of effects on the immune system are inconclusive. Immune system effects were observed in one strain of rats exposed to high dietary levels (35%) of ethanol for 6 weeks, while another strain showed no significant effects. The authors conclude that susceptibility to the immune system effects may be genetically linked.(18)

Skin Sensitization:
Ethanol had no effect in the mouse ear sensitization assay (2,6) and failed to produce sensitization in five different tests using guinea pigs.(8)

The International Agency for Research on Cancer (IARC) has determined that there is sufficient evidence for the carcinogenicity of ethanol in experimental animals.(96)
The potential carcinogenicity of ethanol has been evaluated in numerous studies using mice, rats and hamsters. IARC reviewed the available studies and determined that, for the most part, conclusions could not be drawn due to deficiencies in study design.(17) However, since this IARC evaluation was made the evidence for the carcinogenicity of ethanol in experimental animals has become stronger. Administration of ethanol in drinking-water caused a dose-related increase in the incidence of hepatocellular adenomas and carcinomas in male mice, an increased incidence of head and neck carcinomas in male and female rats, an increased incidence of fore-stomach carcinomas, testicular interstitial-cell adenomas, and osteosarcomas of the head, neck, and other sites in male rats, and of mammary adenocarcinomas in female rats. In most of the studies in which it was co-administered with known carcinogens, ethanol enhanced the carcinogenic effect.(96)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
The harmful effects of ethanol administration to pregnant animals are well documented. Effects have included fetotoxicity (e.g. delayed growth), embryotoxicity (e.g. increased prenatal mortality), and teratogenicity (e.g. malformations of the central nervous system, facial structures, heart, limbs and urogenital system). The minimum dose required to produce these effects varies and determination of this dose is complicated by factors such as the duration and route of exposure and the stage of pregnancy during which the ethanol is administered. For example, long-term exposure during pregnancy produces effects at lower doses than short-term exposure. Most studies involving oral exposure to ethanol have involved very large doses which have also produced significant maternal toxicity.(17,27,28,34) The lowest reported dose which caused teratogenicity in rats is approximately 316 mg/kg (cited as 0.4 mL/kg).(44) No firm conclusions can be drawn from this study since the authors did not conduct a full evaluation of maternal toxicity. Inhalation exposure to levels as high as 20000 ppm has not produced any statistically significant teratogenic effects despite severe maternal toxicity (unconsciousness).(26) In a related study, male and female rats were exposed to 16000 or 10000 ppm for 6 weeks before mating with untreated rats. Pregnant rats were exposed throughout pregnancy. Despite the presence of measurable neurochemical effects, there were no behavioural effects observed in the offspring of exposed male or female rats.(24)

Reproductive Toxicity:
Effects on reproductive organs, including decreased testicular weight, decreased numbers of motile sperm, decreased ovarian function and irregular fertility cycles, have been observed in animals given large oral doses of ethanol. However, no confirmed effects on fertility or reproductive capability have been observed.(2,17) In a well-conducted continuous breeding study, mice were exposed to 5, 10 or 15% ethanol in water (approximately 8500, 16000 and 20000 mg/kg/day). No effects on fertility and only minor reproductive effects were observed (reduced sperm motility and increased time between litters).(23) Male and female rats with inhalation exposure to 10000 or 16000 ppm ethanol for 6 weeks prior to mating showed no effect on fertility.(24) In a poorly designed study, 10 male rats dosed with 20% ethanol in drinking water for 60 days showed statistically significant testicular effects and an increased rate of fetal death in all 3 post-exposure matings. Observations of reduced fertility were not statistically significant.(25) In another poorly designed study, 10 female rabbits administered 5 mL/100 g of 10% ethanol and then mated, were determined to be infertile.(50) No conclusions can be drawn from these studies due to the small number of animals used and the fact that only a single dosing group was used.

Ethanol is mutagenic, based on positive results (dominant lethality, aneuploidy, sister chromatid exchanges) obtained in the germ cells and somatic cells of tests using live animals. These effects have been observed at very high doses. The mutagenicity of ethanol has been extensively studied and reviewed.(17,30-33)
Statistically significant dominant lethal mutations were observed when male mice were orally exposed to 0.1 mL of 40 or 60% ethanol (reported doses of 1240 or 1860 mg/kg/day) for 3 days and then mated. The response was dose-related with the Dominant Lethal Mutation Index 30.6 and 46.3 for the 40% ethanol and 57.4 and 67.3 for the 60% ethanol.(81) Positive results were obtained for dominant lethal mutations in two other studies.(82,89) A dose-related, statistically significant increase in aneuploidy was observed in the germ cells of male mice following a single oral dose of 0.8 mL of 12.5% or 15% ethanol (approximately 4000 or 4800 mg/kg).(84) Positive results were also obtained for aneuploidy in the germ cells of mice and hamsters in two other studies.(83,86) Male rats were exposed to 12000-16000 mg/kg (cited as 12-16 g/kg) ethanol in their diets for 6 weeks. Significantly increased numbers of micronucleated bone marrow cells were observed in the ethanol fed rats.(85) Statistically significant sister chromatid exchanges were observed in the peripheral lymphocytes, but not the bone marrow, of rats exposed to 10 or 20% ethanol (approximately 10000 or 20000 mg/kg/day) as their only liquid supply for 3 or 6 weeks.(88) Statistically significant sister chromatid exchanges were observed in the bone marrow of male mice when 10 or 20% ethanol (approximately 20000 or 40000 mg/kg/day) was given as the only liquid supply for 3-16 weeks.(87)
Positive and negative results have been obtained in cultured mammalian cells and bacteria.(17,30-33)


Selected Bibliography:
(1) RTECS database record for ethyl alcohol. Last updated: 9704
(2) Lington, A.W., et al. Alcohols. In: Patty's industrial hygiene and toxicology. 4th ed. Edited by G.D. Clayton et al. Volume II. Toxicology. Part D. John Wiley and Sons, 1994. p. 2585-2622
(3) Criteria Group for Occupational Standards, National Institute of Occupational Health. Consensus report for ethanol vapors. In: Scientific basis for Swedish occupational standards XI. Edited by P. Lundberg. Arbete och Halsa. No. 8 (1991). p. 120-125
(4) Youssef, A., et al. Comparative lethality of methanol, ethanol and mixtures in female rats. Journal of Applied Toxicology. Vol. 12, no. 3 (June 1992). p. 193-197
(5) Grant, W.M., et al. Toxicology of the Eye. 4th ed. Charles C. Thomas, 1993. p. 71-81
(6) Descotes, J. Identification of contact allergens: the mouse ear sensitization assay. Journal of Toxicology - Cutaneous and Ocular Toxicology. Vol. 7, no. 4 (Dec. 1988). p. 263-272
(7) Hills, B.W., et al. The interaction of ethyl alcohol and industrial chemicals. American Journal of Industrial Medicine. Vol. 3 (1982). p. 321- 333
(8) Marzulli, F., et al. Validation of guinea pig tests for skin hypersensitivity. In: Dermatotoxicology. 2nd ed. Edited by F.N. Marzulli, et al. Hemisphere Publishing Corporation, 1983. p. 237-250
(9) Patruno, C., et al. Allergic contact dermatitis due to ethyl alcohol. Contact Dermatitis. Vol. 31, no. 2 (Aug. 1994). p. 124
(10) Fregert, S., et al. Alcohol dermatitis. Acta Dermato-Venereologica. Vol. 49, no. 5 (1969). p. 493-497
(11) Stotts, J., et al. Induction of human skin sensitization to ethanol. The Journal of Investigative Dermatology. Vol. 69, no. 2 (Aug. 1977). p. 219-222
(12) Ophaswongse, S., et al. Alcohol dermatitis: allergic contact dermatitis and contact urticaria syndrome: a review. Contact Dermatitis. Vol. 30, no. 1 (Jan. 1994). p. 1-6
(13) Fregert, S., et al. Dermatitis from alcohols. Journal of Allergy. Vol. 34, no. 5 (Sept.-Oct. 1963). p. 404-408
(14) Hartmann, R.J., et al. Effect of exposure to toluene and ethanol alone or in combination on a match-to-sample discrimination task in the juvenile baboon. Proceedings of the Western Pharmacology Society. Vol. 27 (Jan. 1984). p. 251-253
(15) Teta, M.J., et al. Mortality study of ethanol and isopropanol production workers at two facilities. Scandinavian Journal of Work, Environmental and Health. Vol. 18, no. 2 (Apr. 1992). p. 90-96
(16) Lester, D., et al. The inhalation of ethyl alcohol by man I. Industrial hygiene and medicolegal aspects. II. Individuals treated with tetraethylthiuram disulfide. Quarterly Journal of Studies on Alcohol. Vol. 12 (1951). p. 167-178
(17) International Agency for Research on Cancer. IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 44. Alcohol drinking. World Health Organization, 1988
(18) Razani-Boroujerdi, S., et al. Alcohol-induced changes in the immune response: immunological effects of chronic ethanol intake are genetically regulated. Toxicology and Applied Pharmacology. Vol. 127, no. 1 (July 1994). p. 37-43
(19) Anderson, L.M., et al. Characterization of ethanol's enhancement of tumorigenesis by N-nitrosodimethylamine in mice. Carcinogenesis. Vol. 13, no. 11 (Nov. 1992). p. 2107-2111
(20) Schwarz, M., et al. The mechanism of cocarcinogenic action of ethanol in rat liver. In: Models, mechanisms and etiology of tumour promotion. IARC Scientific Publication Number 56. International Agency for Research on Cancer, 1984. p. 83-90
(21) Radike, M.J., et al. Effect of ethanol on vinyl chloride carcinogenesis. Environmental Health Perspectives. Vol. 41 (Oct. 1981). p. 59-62
(22) Holmberg, B., et al. A two-year carcinogenicity study of peroral administration of ethyl alcohol in semisynthetic liquid diet to Sprague-Dawley rats. Arbete och Halsa. No. 7 (1994)
(23) Lamb IV, J. Ethanol. Environmental Health Perspectives. Vol. 105, suppl. 1 (Feb. 1997). p. 199-205, 309-310
(24) Nelson, B.K., et al. Neurochemical, but not behavioral, deviations in the offspring of rats following prenatal or paternal inhalation exposure to ethanol. Neurotoxicology and Teratology. Vol. 10, no. 1 (1988). p. 15-22
(25) Mankes, R.F., et al. Paternal effects of ethanol in the Long-Evans rat. Journal of Toxicology and Environmental Health. Vol. 10, no. 6 (Dec. 1982). p. 871-878
(26) Nelson, B.K., et al. Teratological assessment of methanol and ethanol at high inhalation levels in rats. Fundamental and Applied Toxicology. Vol. 5, no. 4 (Aug. 1985). p. 727-736
(27) Mankes, R.F., et al. Acute embryopathic effects of ethanol in the Long- Evans rat. Journal of Toxicology and Environmental Health. Vol. 11, no. 4 (Apr. 1983). p. 583-590
(28) Chernoff, G.F. The fetal alcohol syndrome in mice: an animal model. Teratology. Vol. 15, no. 3 (1977). p. 223-230
(29) Hood, R.D., et al. Lack of prenatal effects of maternal ethanol consumption in CD-1 mice. Toxicology Letters. Vol. 4 (1979). p. 79-82
(30) Waters, M.D., et al. The genetic toxicology of Gene-Tox non- carcinogens. Mutation Research. Vol. 205, nos. 1-4 (May 1988). p. 139-182
(31) Obe, G., et al. Genetic effects of alcohol. International Commission for Protection Against Environmental Mutagens and Carcinogens. ICPEMC Working Paper No. 15/1. Mutation Research. Vol. 186, no. 3 (1987). p. 177-200
(32) Anonymous. Conclusions on the genotoxicity of alcohol and recommendations for further work. International Commission for Protection Against Environmental Mutagens and Carcinogens (ICPEMC). Mutation Research. Vol. 186, no. 3 (1987). p. 175-176
(33) Halkka, O., et al. Alcohol as a mutagen in vivo and in vitro. In: Genetic damage in man caused by environmental agents. Edited by K. Berg. Academic Press Inc., 1979. p. 327-334
(34) Blakley, P.M. Experimental teratology of ethanol. Issues and Reviews in Teratology. Vol. 4 (1988). p. 237-282
(35) Gerarde, H.W., et al. The aspiration hazard and toxicity of a homologous series of alcohols. Archives of Environmental Health. Vol. 13 (Oct. 1966). p. 457-461
(36) Coon, R.A., et al. Animal inhalation studies on ammonia, ethylene glycol, formaldehyde, dimethylamine and ethanol. Toxicology and Applied Pharmacology. Vol. 16, no. 3 (May 1970). p. 646-655
(37) Smyth, Jr., H.F., et al. The single dose toxicity of some glycols and derivatives. Journal of Industrial Hygiene and Toxicology. Vol. 23, no. 6 (June 1941). p. 259-268
(38) Carpenter, C.P., et al. Chemical burns of the rabbit cornea. American Journal of Ophthalmology. Vol. 29 (1946). p. 1363-1372
(39) Guess, W.L. Tissue reactions to 2-chloroethanol in rabbits. Toxicology and Applied Pharmacology. Vol. 16, no. 2 (Mar. 1970). p. 382-390
(40) Guillot, J.P., et al. Evaluation of the ocular-irritation potential of 56 compounds. Food and Chemical Toxicology. Vol. 20, no. 5 (1982). p. 573- 582
(41) Wiberg, G.S., et al. Increased ethanol toxicity in old rats: changes in LD50, in vivo and in vitro metabolism, and liver alcohol dehydrogenase activity. Toxicology and Applied Pharmacology. Vol. 16, no. 3 (May 1970). p. 718-727
(42) Phillips, II, L., et al. A comparison of rabbit and human skin response to certain irritants. Toxicology and Applied Pharmacology. Vol. 21 (1972). p. 369-382
(43) Smyth, Jr., H.F., et al. Inhalation experiments with certain lacquer solvents. The Journal of Industrial Hygiene. Vol. 10, no. 8 (Oct. 1928). p. 261-271
(44) Mankes, R.F., et al. Teratogenic and reproductive effects of ethanol in Long-Evans rat. Journal of Toxicology and Environmental Health. Vol. 10, no. 2 (1982). p. 267-276
(45) Gavaler, J.S., et al. Reproductive consequences of alcohol abuse: males and females compared and contrasted. International Commission for Protection Against Environmental Mutagens and Carcinogens. ICPEMC Working Paper No. 15/7. Mutation Research. Vol. 186, no. 3 (1987). p. 269-277
(46) Streissguth, A.P., et al. Alcohol and pregnancy: an overview and an update. Substance and Alcohol Actions/Misuse. Vol. 4, nos. 2-3 (1983). p. 149-173
(47) Kane, L.E., et al. Evaluation of sensory irritation from some common industrial solvents. American Industrial Hygiene Association Journal. Vol. 41, no. 6 (June 1980). p. 451-454
(48) Ahmed, F.E. Toxicological effects of ethanol on human health. Critical Reviews in Toxicology. Vol. 25, issue 4 (July 1995). p. 347-367
(49) Ethyl alcohol. In: Clinical toxicology of commercial products. 5th ed. Edited by R.E. Gosselin, et al. Williams and Wilkins, 1984. p. III- 166 to III-171
(50) Chaudhury, R.R., et al. Effect of alcohol on the fertility of female rabbits. Journal of Endocrinology. Vol. 34 (1966). p. 275-276
(51) Van Ketel, W.G., et al. Contact dermatitis from ethanol. Contact Dermatitis. Vol. 1 (1975). p. 7-10
(52) Kanzaki, T., et al. Late phase allergic reaction of the skin to ethyl alcohol. Contact Dermatitis. Vol. 25, no. 4 (1991). p. 252-253
(53) Rilliet, A., et al. Alcohol contact urticaria syndrome (immediate-type hypersensitivity): case report. Dermatologica. Vol. 161 (1980). p. 361-364
(54) Melli, M.C., et al. Sensitization from contact with ethyl alcohol. Contact Dermatitis. Vol. 14, no. 5 (May 1986). p. 315
(55) Wilkin, J.K., et al. Ethnic contact urticaria to alcohol. Contact Dermatitis. Vol. 12, no. 2 (Feb. 1985). p. 118-120
(56) Sargeant, W.Q., et al. The effects of acute and chronic alcohol administration on renal hemodynamics and monovalent ion excretion. Journal of Pharmacology and Experimental Therapeutics. Vol. 188, no. 2 (1974). p. 461- 471
(57) Lieber, C.S., et al. Experimential production of fatty liver, hepatitis, and cirrhosis in sub-human primates fed ethanol with adequate diets. Proceedings of the National Academy of Science. USA. Vol. 72, no. 2 (Feb. 1975). p. 437-441
(58) Zuskin, E., et al. Lung function changes by ethanol intoxication. Clinical Allergy. Vol. 11, no. 3 (May 1981). p. 243-248
(59) Drevets, C.C., et al. Dermatitis from alcohol. The Journal of Allergy. Vol. 32, no. 4 (July-Aug. 1961). p. 277-282
(60) Martin-Scott, I. Contact dermatitis from alcohol. British Journal of Dermatology. Vol. 72 (1960). p. 372-373
(61) Haxthausen, H. Allergic eczema caused by ethyl alcohol: elicited both by epicutaneous and by internal application. Acta Dermato-Venereologica. Vol. 25 (1944). p. 527-528
(62) Logsdon, J.E. Ethanol. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 9. John Wiley and Sons, 1994. p. 812-860
(63) Odor thresholds for chemicals with established occupational health standards. American Industrial Hygiene Association, 1989. p. 18, 57-58
(64) Emergency action guide for ethyl alcohol. Association of American Railroads, Mar. 1995
(65) Budavari, S, ed. The Merck index: an encyclopedia of chemicals, drugs, and biologicals. 12th ed. Merck and Co., Inc., 1996. p. 641-642
(66) The Sigma-Aldrich library of chemical safety data. Ed. II. Vol. 1. Sigma- Aldrich, 1988. p. 1568A
(67) Kosaric, N, et al. Ethanol. In: Ullmann's encyclopedia of industrial chemistry. 5th revised ed. Vol. A 9. VCH Verlagsgesellschaft, 1987. p. 587-653
(68) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 325; NFPA 491
(69) Stoye, D, et al. Solvents. In: Ullmann's encyclopedia of industrial chemistry. 5th revised ed. Vol. A 24. VCH Verlagsgesellschaft, 1993. p. 448-453, 479, 483-486
(70) Dean, J.A. Lange's handbook of chemistry. 14th ed. McGraw-Hill, Inc., 1992. p. 1.200, 5.106, 6.139, 8.163
(71) Leo, A., et al. Partition coefficients and their uses. Chemical Reviews. Vol. 71, no. 6 (Dec. 1971). p. 558
(72) Morrison, R.T., et al. Organic chemistry. 4th ed. Allyn and Bacon, 1983. p. 201-202, 500-501
(73) Pine, S.H., et al. Organic chemistry. 4th ed. McGraw-Hill Book Company, 1980. p. 200
(74) Jasper, J.J. Surface tension of pure liquid compounds. In: Compilation of data of some 2200 pure liquid compounds. Journal of Physical and Chemical Reference Data. Vol. 1, no. 4 (1972). p. 852, 965
(75) Urben, P.G., ed. Bretherick's handbook of reactive chemical hazards. 5th ed. Vol. 1. Butterworth-Heinemann Ltd., 1995. p. 343-345
(76) Corrosion data survey: metals section. 6th ed. National Association of Corrosion Engineers, 1985. p. 54-3 to 55-3
(77) NIOSH pocket guide to chemical hazards. National Institute to Occupational Safety and Health, June 1994. p. 132-133
(78) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002
(79) European Economic Community. Commission Directive 93/72/EEC. Sept. 1, 1993
(80) Report on Carcinogens. 11th ed. US Department of Health and Human Services, Public Health Service, National Toxicology Program
(81) Badr, F.M., et al. Evaluation of the mutagenic effects of ethyl alcohol by different techniques. Adv. Exper. Med. Biol. Vol. 85A (1977). p. 25-26
(82) Washington, W.J., et al. Ethanol-induced late fetal death in mice exposed around the time of fertilization. Mutation Research. Vol. 147 (1985). p. 205-210
(83) Kaufman, M.H. Ethanol-induced chromosomal abnormalities at conception. Nature. Vol. 302. p. 258-260
(84) Hunt, P.A. Ethanol-induced aneuploidy in male germ cells of the mouse. Cytogenetics and cell genetics. Vol. 44 (1987). p. 7-10
(85) Baraona, E., et al. Cytogenetic damage of bone marrow cells produced by chronic alcohol consumption. Life Sciences. Vol. 19 (1981). p. 1797-1802
(86) Daniel, A. and Roane, D. Aneuploidy induced by ethanol during spermatogenesis in the Chinese hamster. [Abstract]. Mutation Research. Vol. 164 (1986). p. 193
(87) Obe, G., et al. Induction of chromosomal aberrations in peripheral lymphocytes of human blood in vitro, and of SCEs in bone-marrow cells of mice in vivo by ethanol and its metabolite acetaldehyde. Mutation Research. Vol. 68 (1979). p. 291-294
(88) Tates, A.D., et al. Cytogenetic effects in hepatocytes, bone-marrow cells and blood lymphocytes of rates exposed to ethanol in drinking water. Mutation Research. Vol. 29 (1980). p. 285-288
(89) James, D.A., et al. Analysis of results from a collaborative study of the dominant lethal assay. Mutation Research. Vol. 97 (1982). p. 303-314
(90) Occupational Safety and Health Administration (OSHA). Ethyl Alcohol. In: OSHA Analytical Methods Manual. Revision Date: Oct. 31, 2001. Available at: <>
(91) National Institute for Occupational Safety and Health (NIOSH). Alcohols I. In: NIOSH Manual of Analytical Methods (NMAM(R)). 4th ed. Edited by M.E. Cassinelli, et al. DHHS (NIOSH) Publication 94-113. Aug. 1994. Available at: <>
(92) National Institute for Occupational Safety and Health (NIOSH). Volatile Organic Compounds (Screening). In: NIOSH Manual of Analytical Methods (NMAM(R)). 4th ed. Edited by M.E. Cassinelli, et al. DHHS (NIOSH) Publication 94-113. Aug. 1994. Available at: <>
(93) Jacobs, G.A. OECD eye irritation tests on three alcohols: acute toxicity data. Journal of the American College of Toxicology. Part B. Vol. 1 (1990). p. 56-57
(94) Jacobs, G.A., et al. OECD skin irritation tests on three alcohols. Journal of the American College of Toxicology. Vol. 11 (1992). p. 733
(95) European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC). Eye irritation reference chemicals data bank. 2nd ed. Technical Report No. 48 (2). ECETOC, June 1998. p. 62
(96) International Agency for Research on Cancer (IARC). Alcoholic beverage consumption. IARC, Feb 6-13, 2007. Accessed: July 2007. Available at: <>

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.

Review/Preparation Date: 1997-12-02

Revision Indicators:
Acute exposure (inhalation) 2001-04-01
WHMIS (effects) 2001-04-01
WHMIS (proposed class) 2001-04-01
Emergency overview 2001-04-01
Handling 2001-05-01
TDG 2002-05-29
US transport 2002-12-10
NFPA (health) 2003-04-17
PEL transitional comments 2003-12-19
PEL-TWA final 2003-12-19
WHMIS classification comments 2003-12-22
Important New Information 2003-12-22
Resistance of materials for PPE 2004-04-06
Mutagenicity 2004-04-19
Passive Sampling Devices 2005-04-04
Sampling/analysis 2005-04-04
Bibliography 2007-07-17
Carcinogenicity 2007-07-17
WHMIS detailed classification 2007-07-17
Toxicological info 2007-07-17

©2007 Canadian  Centre  for  Occupational  Health  &  Safety  E-mail:  Fax: (905) 572-2206  Phone: (905) 572-2981  
Mail:  250  Main  Street  East,  Hamilton  Ontario  L8N  1H6