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| SECTION 1. CHEMICAL IDENTIFICATION |
| CHEMINFO Record Number: |
30 |
| CCOHS Chemical Name: |
Acetone |
- Synonyms:
-
Dimethyl formaldehyde
Dimethylketal
Dimethyl ketone
Ketone propane
beta-Ketopropane
Methyl ketone
2-Propanone
Pyroacetic acid
Pyroacetic ether
| Chemical Name French: |
Acétone |
| Chemical Name Spanish: |
Acetona |
| CAS Registry Number: |
67-64-1 |
| UN/NA Number(s): |
1090 |
| RTECS Number(s): |
AL3150000 |
| EU EINECS/ELINCS Number: |
200-662-2 |
| Chemical Family: |
Saturated aliphatic ketone / alkanone |
| Molecular Formula: |
C3-H6-O |
| Structural Formula: |
CH3-C(=O)-CH3 |
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- Appearance and Odour:
- Clear, colourless, volatile liquid with a mildly pungent, characteristic sweet, slight aromatic, fruity odour.(50-52)
- Odour Threshold:
- Reported values vary widely; 3.6-653 ppm (geometric mean: 62 ppm) (detection); 33-699 ppm (geometric mean: 130 ppm) (recognition) (52)
- Warning Properties:
- NOT RELIABLE - some reported odour threshold values are about the same magnitude as the TLV. Acetone has been reported to diminish the sense of smell and adaptation to smell and irritation has occurred.(7,53)
- Composition/Purity:
- Available commercially in grades of greater than 99% purity, with the remainder being mainly water (less than 0.5 wt%). Other impurities present depend on the method of manufacture and may include very small amounts of phenol and benzene.
- Uses and Occurrences:
- Used as a solvent in formulations for surface coatings and related washes and thinners, mainly for acrylic and nitrocellulose lacquers and paints; as a spinning solvent in the manufacture of cellulose acetate; as a solvent in the manufacture of pharmaceuticals and cosmetics; as a solvent for adhesives, contact cements, printing inks, gums, waxes, resins, fats, greases, oils and dyestuffs; for degreasing wool and degumming silk; in extraction processes; in the manufacture of smokeless powder; as a cleaning solvent in the electronics industry; and as a carrier for acetylene in cylinders. Used as a chemical intermediate for methyl methacrylate, methacrylic acid, methyl isobutyl ketone, bisphenol A, and aldol chemicals, such as diacetone alcohol and isophorone; also used to make functional compounds, such as antioxidants, herbicides, higher ketones, condensates with formaldehyde or diphenylamine, and vitamin intermediates.(50,51,54)
Acetone is a natural product of metabolism in the body and virtually every organ and tissue, and the blood contains some acetone. Other natural sources include forest fires, volcanoes and metabolism of vegetation, insects and higher animals.(6,50)
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| SECTION 3. HAZARDS IDENTIFICATION |
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- EMERGENCY OVERVIEW:
- Clear, colourless, volatile liquid with a mildly pungent, characteristic sweet, slight aromatic, fruity odour. EXTREMELY FLAMMABLE LIQUID AND VAPOUR. Vapour is heavier than air and may spread long distances. Distant ignition and flashback are possible. Mild central nervous system depressant. Very high concentrations may cause headache, nausea, dizziness, drowsiness, incoordination and confusion. Causes eye irritation. Aspiration hazard. Swallowing or vomiting of the liquid may result in aspiration into the lungs.
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Effects of Short-Term (Acute) Exposure
- Inhalation:
- In one study, volunteers exposed to concentrations up to 500 ppm reported no harmful effects.(1) In other studies, concentrations of approximately 300- 500 were reported to cause slight irritation of the nose and throat.(2,3,4) Exposure to 250 ppm for 4 hours has caused mild effects on performance in some behavioural tests (auditory tone discrimination and a mood test).(5) As concentrations approach 1000 ppm, noticeable irritation has occurred and some people have reported headaches, light-headedness and tiredness.(3,4,6) Inhalation of concentrations higher than 2000 ppm can cause dizziness, a feeling of drunkenness, drowsiness, nausea and vomiting. Unconsciousness may result if exposure is extremely high (greater than 10000 ppm). Intolerable nose and throat irritation would also occur at these concentrations.(6) Even higher concentrations can cause collapse, coma and death.
Tolerance to the effects of acetone can develop.(3,6,7) Tolerance means that, with repeated exposures, higher concentrations are required to produce symptoms which had previously been observed at lower concentrations.
One case report describes two men who were working in a confined space with extremely high acetone concentrations (measured at 12000 ppm, 3 hours after the accident). Low concentrations (up to 50 ppm) of trichloroethane were also detected. After working in the area 4 hours, the men noticed irritation of the throat, headache, weakness in the legs and a feeling of drunkenness. The men then left the area for 1 hour. Upon returning, one man collapsed and the other felt faint. Rescuers, who were exposed for 2 to 3 minutes, experienced symptoms similar to the workers. The man who lost consciousness regained consciousness a short time later but was confused, drowsy, unsteady on his feet, felt nauseated and was vomiting. The other man had, at this point, also lost consciousness and was vomiting. Both men fully recovered.(8)
A single case report suggests slight kidney and liver damage may have occurred following a severe exposure to acetone.(6 unconfirmed, 9) There are insufficient details available to draw conclusions from this report.
- Skin Contact:
- Acetone is either slightly irritating or not irritating, based on animal and limited human information. Application of 1 mL of acetone in a small glass tube to six male volunteers for 30 or 90 minutes resulted in only mild redness and swelling at 90 minutes.(10)
The risk of developing health effects following the absorption of acetone through unbroken skin is very slight. There are several reports of people, usually young children, becoming ill following skin exposure to acetone while lightweight casts were being put on broken limbs. The symptoms experienced were similar to those described following high inhalation exposures. In all cases, a large amount of acetone came into contact with the skin for several hours and inhalation exposure may also have occurred.(11) These reports are not considered relevant to people exposed to acetone at work.
- Eye Contact:
- Acetone vapour causes mild irritation at concentrations of around 500 ppm.(2,3) Irritation is very noticeable at 1000 ppm.(12) Liquid acetone is severely irritating, based on animal and limited human information. In 3 human cases, acetone caused corneal injury which completely healed within 48 hours.(13) In one unusual case, liquid acetone was held directly on the eye for a long time. In this particular case, there was permanent damage to the eye, with clouding of the cornea.(14)
- Ingestion:
- Ingestion is not a typical route of occupational exposure. Several studies report no effects or minor effects (slight drowsiness) in people who ingested up to 20 grams/day for several days.(6) Animal toxicity information also suggests that acetone is not very toxic following ingestion.
If acetone is aspirated (breathed into the lungs during ingestion or vomiting) it can cause severe, life-threatening lung injury. Animal information suggests that acetone would be difficult to aspirate because it evaporates so quickly. Based on its physical properties, acetone can be aspirated into the lungs during ingestion or vomiting.
One case report describes a man who intentionally drank 200 mL (about 7 ounces) of acetone. Within one hour, he had flushed cheeks and appeared drunk. His breathing was shallow and his throat red and swollen. He soon lapsed into coma and did not regain consciousness for 12 hours. Four weeks later, he developed symptoms similar to diabetes (increased urination, thirst and blood sugar levels). The patient fully recovered within 5 months after the incident.(15)
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Effects of Long-Term (Chronic) Exposure
- SKIN: Prolonged or repeated contact may cause defatting of the skin and produce dermatitis (dryness, irritation, redness and cracking).
INHALATION: Most human population studies indicate that acetone would not produced significant health effects following long-term exposure. In a series of studies, no statistically significant differences in causes of death or clinical laboratory results were observed in 948 employees exposed to up to 1070 ppm acetone over 23 years. Another study which reviewed 18 years of industrial experience with employees in a cellulose acetate production facility did not show an increased incidence of illness. One other study did not find significant changes in clinical chemistry tests conducted on 60 employees who had worked at least 5 years in the acetate fibre manufacturing industry (exposures of 550-1050 ppm).(6)
No conclusions can be drawn from other reports which have described effects following long-term acetone exposure. These reports are limited by factors such as the small number of workers studied, the fact that other exposures may have contributed to or caused the observed effects and/or possible self- reporting biases. In one study, 110 men were exposed to a mean concentration of 361 ppm acetone for an average of 14.9 years. These men reported more heavy headedness, nausea, faintness, weight loss, eye irritation than a comparison group with no acetone exposure. They also did not perform as well on some neurobehavioural tests (reaction time and digit span tests).(16) A few historical reports have also described long-term exposure effects such as irritation of the airways, throat, stomach and occasionally, dizziness, attacks of giddiness and a loss of strength.(17,18)
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- Carcinogenicity:
-
- There is no human information. Animal information suggests that acetone is not carcinogenic.
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- The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.
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- The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as not classifiable as a human carcinogen (A4).
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- The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.
- Teratogenicity and Embryotoxicity:
- No conclusions can be drawn based on the limited human information available. Animal information suggests that acetone would only cause developmental effects in the presence of maternal toxicity.
A study of 891 women who worked or were working in the semiconductor industry showed an increased risk of miscarriages among fabrication workers. Seven chemicals were strongly associated with the increased risk of miscarriage, one of which was acetone.(20) No conclusions can be drawn from this study because of factors such as the small number of workers studied and the concurrent exposure to other potentially harmful chemicals. There is insufficient information available to evaluate a Russian study that reports increased complications of pregnancy and reduced birth weight in children of mothers exposed to acetone.(21)
- Reproductive Toxicity:
- It is not possible to conclude that acetone is a reproductive toxin based on the information located.
A study of 25 men exposed to acetone and styrene during the manufacture of reinforced plastics showed an increased percentage of abnormal sperm head shape in exposed workers compared to controls.(19) No conclusions can be drawn from this study because of factors such as the small number of workers studied and the concurrent exposure to other potentially harmful chemicals. One animal study showed sperm effects, in the presence of kidney damage.
- Mutagenicity:
- There is no human information available. Negative results have been obtained in tests using cultured human cells.(6) Negative results have also been obtained in a study which used live animals, cultured mammalian cells and bacteria.
- Toxicologically Synergistic Materials:
- Acetone has increased the liver toxicity of chemicals, such as carbon tetrachloride, chloroform, trichloroethylene, bromodichloromethane, dibromochloromethane, N-nitrosodimethylamine and 1,1,2-trichloroethane, the lung toxicity of styrene and the toxicity of acetonitrile and 2,5-hexanedione in laboratory animals.(6,22-27) It appears to inhibit the metabolism and elimination of ethyl alcohol, thereby potentially increasing its toxicity.(23) Acetone can either increase or decrease the toxicity of 1,2-dichlorobenzene, depending on the concentration of acetone used.(6)
- Potential for Accumulation:
- Acetone is a normal by-product of mammalian metabolism and is found in virtually every organ and tissue, and in the blood. Acetone can enter the body by inhalation, ingestion or skin contact. Acetone is metabolized by a number of routes to compounds, which are used by the body to make glucose and other products of intermediary metabolism, with the generation of carbon dioxide. Acetone is excreted both unchanged, and following metabolism, mainly as carbon dioxide. The main route of excretion is in the expired air, with very little excreted in the urine. Respiratory excretion is complete within 20 hours after inhalation. The amount of unchanged acetone excreted in the urine increases with increasing exposure concentration and duration, and with exercise during exposure.(6,23,28)
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| SECTION 4. FIRST AID MEASURES |
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- Inhalation:
- If symptoms are experience, 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.
- Ingestion:
- 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.
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| SECTION 5. FIRE FIGHTING MEASURES |
- Flash Point:
- -18 deg C (0 deg F) (closed cup) (50,56,57)
- Lower Flammable (Explosive) Limit (LFL/LEL):
- 2.5% at 25 deg C (50,56)
- Upper Flammable (Explosive) Limit (UFL/UEL):
- 12.8% at 25 deg C (50,56)
- Autoignition (Ignition) Temperature:
- 465 deg C (869 deg F) (56); 538-540 deg C (1000.4-1004 deg F) (50,58)
- Sensitivity to Mechanical Impact:
- Not sensitive. Stable material.
- Sensitivity to Static Charge:
- Will not accumulate static charge. The electrical conductivity of acetone (5.5-6 X 10(6) pS/m at 25 deg C) is high.(50,51,57) Mixtures of acetone 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.(56,59)
- Fire Hazard Summary:
- Extremely flammable liquid. Material will readily ignite at room temperature. Vapour is 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. Even dilute solutions of acetone in water may be flammable.
- Extinguishing Media:
- Carbon dioxide, dry chemical powder, "alcohol" foam, polymer foam. Water may be ineffective because it will not cool acetone below its flash point. Fire fighting foams are the extinguishing agent of choice for most flammable liquid fires.(59)
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- 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.
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| NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION |
| NFPA - Health: |
1 - Exposure would cause significant irritation, but only minor 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. |
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| SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES |
- Conversion Factor:
- 1 ppm = 2.37 mg/m3; 1 mg/m3 = 0.422 ppm at 25 deg C (calculated)
| Physical State: |
Liquid |
| Melting Point: |
-94.6 deg C (-138.3 deg F) (freezing point) (50,56) |
| Boiling Point: |
56.2 deg C (133.2 deg F) at 760 mm Hg (51,56) |
| Relative Density (Specific Gravity): |
0.791 at 20 deg C (water = 1) (51,57) |
| Solubility in Water: |
Soluble in all proportions (50,51,56) |
| Solubility in Other Liquids: |
Soluble in all proportions in ethanol and other lower molecular weight alcohols, diethyl ether, other ethers, benzene, chloroform, carboxylic acids, dimethylformamide, other polar organic solvents, and most oils. It is miscible in limited proportions in nonpolar solvents, such as hydrocarbons.(51,54,56) |
| Coefficient of Oil/Water Distribution (Partition Coefficient): |
Log P(oct) = -0.24 (measured) (54,61) |
| pH Value: |
Not available. Acetone is a very weak acid.(60) |
| Vapour Density: |
2.0 (air = 1) (51) |
| Vapour Pressure: |
24 to 24.7 kPa (180 to 185.3 mm Hg at 20 deg C (50,51,56) |
| Saturation Vapour Concentration: |
Approximately 240000 ppm (24%) at 20 deg C (calculated) |
| Evaporation Rate: |
5.6 (n-butyl acetate = 1); 2.0 (diethyl ether = 1) (58) |
| Critical Temperature: |
235.1 deg C (455.2 deg F) (50,51,57) |
- Other Physical Properties:
- ACIDITY: Very weak acid; pKa = 20 (54,60)
VISCOSITY-DYNAMIC: 0.32 mPa.s (0.32 centipoise) at 20 deg C (50,51,57)
VISCOSITY-KINEMATIC: 0.40 mm2/m (0.40 centistokes) at 20 deg C (calculated)
SURFACE TENSION: 23.7 mN/m (23.7 dynes/cm) at 20 deg C (50,58)
CRITICAL PRESSURE: 4701 kPa (46.4 atm.) (50,57)
TRIPLE POINT: -94.7 deg C (-138.5 deg F) (50)
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| SECTION 10. STABILITY AND REACTIVITY |
- Stability:
- Normally stable. Prolonged exposure to direct sunlight may result in the formation of carbon monoxide.(51)
- 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. bromine, chromium trioxide, chromyl chloride, nitric acid, nitric acid-sulfuric acid mixture, nitrosyl perchlorate or permonosulfuric acid) - may react violently or explosively, with increased risk of fire .(55,56,62)
HYDROGEN PEROXIDE - readily form explosive cyclic peroxides.(62)
STRONG REDUCING AGENTS (e.g. phosphorus, tin (II) chloride, metal hydrides) - may react violently. Increased risk of fire.(59)
HEXACHLOROMELAMINE or TRICHLOROMELAMINE - violent reaction with ignition. May explode if amounts are large and confined.(55)
HALOGINATED SOLVENT/ALKALI MIXTURES (e.g. chloroform or bromoform and potassium hydroxide) - may react violently, with evolution of heat.(55,62)
POTASSIUM TERT-BUTOXIDE - contact of solid butoxide with acetone vapour caused ignition.(55,62)
BASES (including alkalis, such as sodium hydroxide) - violent reaction may occur, with heat and pressure.(59)
SULFUR DICHLORIDE - reaction may be vigorous.(62)
- Hazardous Decomposition Products:
- None reported
- Conditions to Avoid:
- Sparks, open flames, heat and other ignition sources; prolonged exposure to direct sunlight.
- Corrosivity to Metals:
- Not corrosive to carbon steel, stainless steel, cast iron, copper and its alloys, nickel and its alloys, and aluminum.(50,63)
- Stability and Reactivity Comments:
- Attacks many forms of plastics and rubber, including rayon.(56)
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| SECTION 11. TOXICOLOGICAL INFORMATION |
- LC50 (male rat): 30000 ppm (4-hour exposure); cited as 71000 mg/m3 (4-hour exposure) (29)
LC50 (male mouse): 18600 ppm (4-hour exposure); cited as 44000 mg/m3 (4-hour exposure) (29)
- LD50 (oral, female rat): 5800 mg/kg (24)
LD50 (oral, mature rat): 6700 mg/kg (cited as 8.5 mL/kg) (31)
LD50 (oral, newborn rat): 1750 mg/kg (cited as 2.2 mL/kg) (31)
LD50 (oral, mouse): 3000 mg/kg (32,unconfirmed)
- LD50 (dermal, rabbit): Greater than 16000 mg/kg (cited as 20 mL/kg) (30)
- Eye Irritation:
- Undiluted acetone is a severe eye irritant.
- Application of 0.005 mL of undiluted acetone produced severe irritation in rabbits (graded 5/10).(30) In a standard Draize test, application of 0.1 mL undiluted acetone resulted in severe irritation in rabbits, while 1-30% solutions resulted in minimal irritation.(33) In a modified Draize test, application of 0.1 mL undiluted acetone was reported to cause corrosive eye injury in rabbits.(34)
- Skin Irritation:
- Undiluted acetone is not irritating to the skin.
- Uncovered application of 0.01 mL undiluted acetone produced no irritation in rabbits (graded 1/10).(30) Acetone was also not irritating in guinea pigs.(35)
- Effects of Short-Term (Acute) Exposure:
-
- Inhalation:
- Numerous studies have evaluated the effects of acetone on the central nervous system (CNS). The concentration of acetone that causes unconsciousness depends on the both the amount of acetone and the length of exposure. In general, acetone concentrations in excess of 8000 ppm are required to produce symptoms, regardless of the exposure duration and species tested. Drowsiness, incoordination, loss of reflexes, unconsciousness, respiratory failure and death have been observed following acetone exposure.(6)
Several studies have evaluated behavioural responses in animals following acetone exposure (for example, avoidance/escape behaviours). The results of these studies have been variable and it is not possible to draw a clear description of the possible effects of acetone.(6) In one study, 10700 ppm was the acetone concentration required to reduce a behavioural response in mice by 50%. Acetone was the least potent of the chemicals tested in this study.(36)
The concentration of acetone which reduces the respiratory rate of mice by 50% (RD50) was reported to be 23480 ppm in one study (37) and 77516 ppm in another (38). The RD50 is a measure of sensory irritation (nose, throat and respiratory irritation). These results indicate that acetone is a weak sensory irritant.
- Skin Contact:
- Application of 0.5 mL to the skin over 3 to 8 weeks produced cataracts in the eyes of guinea pigs. In a later study, conducted similarly, acetone produced cataracts in guinea pigs, but not rabbits.(41) Statistical analysis of the data was not conducted. The development of cataracts may be an effect specific to guinea pigs.(6)
- Ingestion:
- Oral exposure to large doses of acetone in drinking water for 14 days has produced mild toxicity in rats and mice. Compared to controls, male rats receiving approximately 4300 or 7000 mg/kg/day and female rats given 8500 mg/kg/day had lower mean body weights. No significant changes in body weight were observed in mice. Kidney and liver weights were higher for exposed rats and mice. Slight liver injury was observed in female mice exposed to 5500 mg/kg/day and male mice exposed to 6300 mg/kg/day.(39)
In a study designed to evaluate the aspiration risk, acetone was found to evaporate too quickly to be aspirated. However, if ingested very quickly, acetone can be an aspiration hazard.(40)
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- Effects of Long-Term (Chronic) Exposure:
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- Long-term studies have not shown significant harmful effects following oral or inhalation exposures.
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- Inhalation:
- No significant harmful effects were observed in rats exposed by inhalation to 19000 ppm intermittently for 8 weeks.(42)
- Ingestion:
- Mild harmful effects were observed in rats and mice exposed to high oral doses for 13 weeks.(39) Rats were exposed to up to approximately 3400 mg/kg/day for 13 weeks. Rats receiving the high dose had decreased body weight and liver and kidney weights were increased in rats receiving 1600 mg/kg/day or greater. Changes consistent with macrocytic anemia were observed at 400 mg/kg/day (males) and 1600 mg/kg/day (males and females). Kidney damage was observed in males.(39) However, this kidney effect may be specific to male rats and not relevant to other species or sexes. Mice were similarly exposed. Liver weights were increased and spleen weights decreased in females given the high dose.(39)
No significant behavioural changes were observed in male rats administered 0.5% acetone in their drinking water for 6 weeks.(26) Neurotoxic effects (e.g. peripheral neuropathy) were not observed in rats exposed to 0.5-1% acetone in their drinking water for 12 weeks.(43)
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- Skin Sensitization:
- Negative results were obtained in the Mouse Ear Sensitization test.(44)
- Carcinogenicity:
- Acetone has been used as a vehicle in dermal studies using mice. Mice generally received one or two 0.2 mL applications/week for 6 months to 2 years without an increased incidence of tumours.(6,39)
- Teratogenicity, Embryotoxicity and/or Fetotoxicity:
- The available information suggests that inhalation of acetone can cause fetotoxicity in rats and mice and embryotoxicity in mice, but only in the presence of maternal toxicity.
- Rats were exposed by inhalation to 440, 2200 or 11000 ppm acetone on days 6-19 of pregnancy. Signs of toxicity (body weight effects) were observed in mothers exposed to the highest concentration. The only statistically significant effect observed in the offspring was fetotoxicity (reduced fetal weight) in the high exposure group.(45)
Mice were exposed by inhalation to 440, 2200 or 6600 ppm acetone on days 6-17 of pregnancy. The high exposure group animals were initially exposed to 11000 ppm for one day and then the concentration was decreased to 6600 ppm because the mice experienced severe narcosis. Minimal maternal toxicity (increased liver weight) was then observed at 6600 ppm. Fetotoxicity (reduced fetal weight) and slight, but statistically significant, embryotoxicity (fetal deaths) were observed in the high exposure group.(45)
In a preliminary screening test (the Chernoff/Kavlock test), acetone was administered orally at a dose of 3500 mg/kg/day to female mice on days 6-15 of pregnancy. In this study, the results indicated that acetone warranted high priority for additional developmental testing.(46) No other conclusions can be drawn from this study. No conclusions can be drawn from one other study because the animals were exposed to acetone and several other potentially harmful chemicals at the same time.(47)
- Reproductive Toxicity:
- Sperm effects have been observed in rats already experiencing kidney damage. No effects on fertility have been observed.
- Rats and mice were exposed to up to 50000 ppm acetone in drinking water for 13 weeks. Sperm motility was decreased and the percentage of abnormal sperm was increased in male rats, at the high dose (approximately 4300 mg/kg/day). These same male rats had experienced kidney damage. Similar effects were not observed in the mice.(39)
No effects on reproductive or testicular toxicity were observed in male rats exposed to 0.5% acetone in their drinking water for 6 weeks.(25)
- Mutagenicity:
- Negative results were obtained in the peripheral blood cells of mice that received 5000-20000 ppm acetone in drinking water for 13 weeks.(39)
- Negative results have been obtained in tests using cultured mammalian cells and bacteria.(6,32,39,48) Positive and negative results have been obtained in one studies using yeast.(6,49)
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| SECTION 16. OTHER INFORMATION |
- Selected Bibliography:
- (1) DiVincenzo, G.D., et al. Exposure of man and dog to low concentrations of acetone vapor. American Industrial Hygiene Association Journal. Vol. 34, no. 8 (August, 1973). p. 329-336
(2) Nelson, K.W., et al. Sensory response to certain industrial solvent vapors. Journal of Industrial Hygiene and Toxicology. Vol. 25, no. 7 (September, 1943). p. 282-285
(3) Matsushita, T., et al. Experimental studies for determining the MAC value of acetone: 2. Biological reactions in the "six-day exposure" to acetone. Japanese Journal of Industrial Hygiene (Sangyo Igaku). Vol. 11, no. 10 (October, 1969). p. 507-515
(4) Matsushita, T., et al. Experimental studies for determining the MAC value of acetone: 1. Biological reactions in the "one-day exposure" to acetone. Japanese Journal of Industrial Hygiene (Sangyo Igaku). Vol. 11, no. 9 (September, 1969). p. 477-485
(5) Dick, R.B., et al. Neurobehavioural effects of short duration exposures to acetone and methyl ethyl ketone. British Journal of Industrial Medicine. Vol. 46, no. 2 (February, 1989). p. 111-121
(6) Morgott, D.A. Acetone. In: Patty's industrial hygiene and toxicology. 4th edition. Edited by G.D. Clayton, et al. Volume II. Toxicology. Part A. John Wiley and Sons, Inc., 1993. p. 149-281
(7) Wysocki, C.J., et al. Acetone odor and irritation thresholds obtained from acetone-exposed factory workers and from control (occupationally unexposed) subjects. American Industrial Hygiene Association Journal. Vol. 58, no. 10 (October, 1997). p. 704-712
(8) Ross, D.S. Acute acetone intoxication involving eight male workers. Annals of Occupational Hygiene. Vol. 16, no. 1 (April, 1973). p. 73-75
(9) Henschler, D. Acetone (Aceton). In: Gesundheitsschaedliche Arbeitstoffe, 1979. Vol. 1, 7th issue, A. p. 1-4. Verlag Chimie GmbH, 1979. (HSE translation no. 10670, February, 1984)
(10) Lupulescu, A.P., et al. An electron microscopic study of human epidermis after acetone and kerosene administration. Journal of Investigative Dermatology. Vol. 60, no. 1 (1973). p. 33-45
(11) Harris, L.C., et al. Acute acetone poisoning caused by setting fluid for immobilizing casts. British Medical Journal. (November, 8, 1952). p. 1024-1026
(12) Raleigh, R.L., et al. Effects of short, high-concentration exposures to acetone as determined by observations in the work area. Journal of Occupational Medicine. Vol. 14, no. 8 (August, 1972). p. 607-610
(13) McLaughlin, R.S. Chemical burns of the human cornea. American Journal of Ophthalmology. Vol. 29, no. 11 (November, 1946). p. 1355-1362
(14) Grant, W.M., et al. Toxicology of the Eye. 4th edition. Charles C. Thomas, 1993. p. 55-56
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(16) Satoh, T., et al. Cross-sectional study of effects of acetone exposure on workers' health. Proceedings of the 9th International Symposium on Epidemiology in Occupational Health, September 23-25, 1992, Cincinnati, Ohio. p. 407-412. NIOSH Publication No. 94-112. International Commision on Occupational Health, National Institute for Occupational Safety and Health, 1994.
(17) Vigliana, E.C., et al. Experiences of the Clinics del Lavoro with some maximum concentrations of poisons of industry at the place of work (MAK). (English translation of: Erfahrungen der Clinica del Lavoro mit einigen maximalen Arbeitsplatzkonzentrationen (MAK) von Industriegiften. Archiv fur Gewerbepathologie und Gewerbehygiene. Vol. 13 (1955). p. 528-534)
(18) Parmeggiani, L., et al. Occupational poisoning with acetone: clinical disturbances, investigations in work rooms and physiopathological research. Medicina del Lavoro. Vol. 45, no. 8-9 (1954). p. 431-468 (English translation: NIOSHTIC Control Number: 00031405)
(19) Jelnes, J.E. Semen quality in workers producing reinforced plastic. Reproductive Toxicology. Vol. 2, nos. 3/4 (1988). p. 209-212
(20) Swan, S.H., et al. Historical cohort study of spontaneous abortion among fabrication workers in the semiconductor health study: agent-level analysis. American Journal of Industrial Medicine. Vol. 28, no. 6 (December, 1995). p. 751-769
(21) Nizaeva, I.V. On hygienic assessment of acetone. (English translation of: K gigienicheskoi otsenke atsetona. Gigiena Truda i Professional'nye Zabolevaniya (Labor Hygiene and Occupational Diseases). Vol. 26, no. 6 (1982). p. 24-28) (HSE translation no. 13720 A, February, 1990)
(22) Hewitt, W.R., et al. Nephrotoxic interactions between ketonic solvents and halogenated aliphatic chemicals. Fundamental and Applied Toxicology. Vol. 4, no. 6 (December, 1984). p. 902-908
(23) Anonymous. Acetone. Dangerous Properties of Industrial Materials Report. Vol. 4, no. 3 (May/June, 1984). p. 9-23
(24) Freeman, J.J., et al. Acetone potentiation of acute acetonitrile toxicity in rats. Journal of Toxicology and Environmental Health. Vol. 15, no. 5 (1985). p. 609-621
(25) Larsen, J.J., et al. Infertility in rats induced by 2,5-hexanedione in combination with acetone. Pharmacology and Toxicology. Vol. 69, no. 1 (July, 1991). p. 43-46
(26) Ladefoged, O., et al. Acetone potentiation and influence on the reversibility of 2,5-hexanedione-induced neurotoxicity studied with behavioural and morphometric methods in rats. Pharmacology and Toxicology. Vol. 74, no. 4-5 (April-May, 1994). p. 294-299
(27) Charbonneau, M., et al. Influence of acetone on the severity of the liver injury induced by haloalkane mixtures. Canadian Journal of Physiology and Pharmacology. Vol. 69, no. 12.(December, 1991). p. 1901-1907
(28) Agency for Toxic Substances and Disease Registry. Toxicological profile for acetone. TP-93/01. US Department of Health and Human Services, May, 1994.
(29) Safronov, N.S., et al. Comparative acute inhalation toxicity of aliphatic aldehydes and ketones according to exposure time. Current Toxicology. Vol. 1, no. 1 (1993). p. 47-51
(30) Smyth, Jr., H.F., et al. Range-finding toxicity data: list VI. American Journal of Industrial Hygiene. Vol. 23 (March-April, 1962). p. 95- 107
(31) Kimura, E.T., et al. Acute toxicity and limits of solvent residues for sixteen organic solvents. Toxicology and Applied Pharmacology. Vol. 19, no. 4 (August, 1971). p. 699-704
(32) RTECS database record for acetone. Last updated: 9704.
(33) Kennah II, H.E., et al. An objective procedure for quantitating eye irritation based upon changes of corneal thickness. Fundamental and Applied Toxicology. Vol. 12, no 2 (February, 1989). p. 258-268
(34) Morgan, R.L., et al. Prediction of ocular irritation by corneal pachymetry. Food and Chemical Toxicology. Vol. 25, no. 8 (August, 1987). p. 609-613
(35) Anderson, C., et al. Animal model for assessment of skin irritancy. Contact Dermatitis. Vol. 15, no. 3 (September, 1986). p. 143-151
(36) Glowa, J.R., et al. Behavioral toxicology of volatile organic solvents: IV. Comparisons of the rate-decreasing effects of acetone, ethyl acetate, methyl ethyl ketone, toluene, and carbon disulfide on schedule-controlled behavior of mice. Journal of the American College of Toxicology. Vol. 6, no. 4 (1987). p. 461-469
(37) De Ceaurriz, J.C., et al. Sensory irritation caused by various industrial airborne chemicals. Toxicology Letters. Vol. 9, no. 2 (1981). p. 137-143
(38) Kane, L.E., et al. Evaluation of sensory irritation from some common industrial chemicals. American Industrial Hygiene Association Journal. Vol. 41, no. 6 (June, 1980). p. 451-454
(39) Dietz, D. Toxicity studies of acetone (CAS no. 67-64-1) in F344/N rats and B6C3F1 mice (drinking water studies). NIH Publication No. 91-3122. National Toxicology Program, US Department of Health and Human Services, January 1991.
(40) Panson, R.D., et al. Aspiration toxicity of ketones. Clinical Toxicology. Vol. 17, no. 2 (1980). p. 271-317
(41) Rengstorff, R.H., et al. Cataracts induced in guinea pigs by acetone, cyclohexanone and dimethyl sulfoxide. Edgewood Arsenal technical report: EATR 4550. Edgewood Arsenal Research Laboratories, Department of the Army, August, 1971
(42) Bruckner, J.V., et al. Evaluation of toluene and acetone inhalant abuse: II. Model development and toxicology. Toxicology and Applied Pharmacology. Vol. 61, no. 3 (December, 1981). p. 302-312
(43) Spencer, P.S., et al. On the specific molecular configuration of neurotoxic aliphatic hexacarbon compounds caused central-peripheral distal axonopathy. Toxicology and Applied Pharmacology. Vol. 44, no. 1 (April, 1978). p. 17-28
(44) Descotes, J. Identification of contact allergens: the mouse ear sensitization assay. Journal of Toxicology - Cutaneous and Ocular Toxicology. Vol. 7, no. 4 (December, 1988). p. 263-272
(45) Mast, T.J., et al. Inhalation developmental toxicology studies: teratology study of acetone in mice and rats. Final report. No. NIH-Y01-ES-7- 153. Contract DE-AC06-76RLO 1830. National Toxicology Program, National Institute of Environmental Health Sciences, November, 1988
(46) Environmental Health Research and Testing, Inc. Screening of priority chemicals for reproductive hazards: benzethonium chloride (CAS No. 121-54-0), 3-ethoxy-1-propanol (CAS No. 111-35-3), acetone (CAS No. 67-64-1). Final report. Contract No.: 200-85-2735. EHRT Project No.: ETOX-85-1002. National Institute for Occupational Safety and Health, April 22, 1987
(47) Tachi, N., et al. Fetotoxic effects of exposure to the vapor of organic solvents from a synthetic adhesive in mice. Bulletin of Environmental Contamination and Toxicology. Vol. 53, no. 3 (September, 1994). p. 471-478
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(49) Zimmerman, F.K., et al. Acetone, methyl ethyl ketone, ethyl acetate, acetonitrile and other polar aprotic solvents are strong inducers of aneuploidy in Saccharomyces cerevisiae. Mutation Research. Vol. 149 (1985). p. 339-351
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(53) Amoore, J.E. Effects of chemical exposure on olfaction in humans. In: Toxicology of the nasal passages. Edited by C.S. Barrow. Hemisphere Publishing Corporation, 1984. P. 155-190
(54) HSDB record for acetone. Last revision date: 97/03/24
(55) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 325; NFPA 491
(56) Emergency action guide for acetone. Association of American Railroads, January, 1988
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(59) The Sigma-Aldrich library of chemical safety data. Edition II. Volume 1. Sigma- Aldrich, 1988. p. 20A
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(66) European Communities. Commission Directive 98/98/EC. December 15, 1998
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(69) 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. 157-158
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- 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: 1997-11-26 |
- Revision Indicators:
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| Respiratory guidelines |
1997-12-01 |
| Transport (US) |
1998-02-01 |
| TLV comments |
1998-08-01 |
| EU Class |
2000-04-01 |
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2000-04-01 |
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2000-04-01 |
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2000-04-01 |
| Resistance of materials for PPE |
2004-04-06 |
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2005-03-30 |
| Sampling/analysis |
2005-03-30 |
| Teratogenicity/embryotoxicity |
2005-10-07 |
| Reproductive toxicity |
2005-10-07 |
| Bibliography |
2006-03-30 |
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