Everything You Need to Know About Acetone

Acetone is a common Household Toxic Chemical The complete guide to acetone, 2-Propanone, Dimethyl keton structure with complete Acetone MSDS information

Acetone

Public Health Statement for Acetone

CONTENTS:

Summary

What is acetone?

What happens to acetone when it enters the environment?

How might I be exposed to acetone?

How can acetone affect my health?

How likely is acetone to cause cancer?

Is there a medical test to show whether I've been exposed to acetone?

Has the federal government made recommendations to protect human health?

Glossary

References

Contact Information

ACETONE MSDS Information

SUMMARY:

Exposure to acetone results mostly from breathing air, drinking water, or coming in contact with products or soil that contain acetone. Exposure to moderate-to-high amounts of acetone can irritate your eyes and respiratory system, and make you dizzy. Very high exposure may cause you to lose consciousness. This chemical has been found in at least 572 of 1,416 National Priorities List sites identified by the Environmental Protection Agency.

What is acetone?

Acetone is a manufactured chemical that is also found naturally in the environment. It is a colorless liquid with a distinct smell and taste. It evaporates easily, is flammable, and dissolves in water. It is also called 2-Propanone, Acetone, Dimethyl keton, 2-Propanone, AI3-01238, Aceton [German, Dutch, Polish] , Acetone , Acetone (natural), CCRIS 5953, Caswell No. 004, Chevron acetone, Dimethyl ketone, Dimethylformaldehyde, Dimethylketal, EINECS 200-662-2 , EPA Pesticide Chemical Code 004101, FEMA No. 3326, HSDB 41, Ketone propane, Ketone, dimethyl, Methyl ketone, NSC 135802, Propanone, Pyroacetic acid, Pyroacetic ether, RCRA waste number U002, beta-Ketopropane, 2-Propanone, Acetone, 2-Propanone, Acetone, Acetone [UN1090] [Flammable liquid], Methyl ketone, RCRA waste no. U002, UN1090

Acetone is used to make plastic, fibers, drugs, and other chemicals. It is also used to dissolve other substances.

It occurs naturally in plants, trees, volcanic gases, forest fires, and as a product of the breakdown of body fat. It is present in vehicle exhaust, tobacco smoke, and landfill sites. Industrial processes contribute more acetone to the environment than natural processes.

What happens to acetone when it enters the environment?

A large percentage (97%) of the acetone released during its manufacture or use goes into the air.
In air, about one-half of the total amount breaks down from sunlight or other chemicals every 22 days.
It moves from the atmosphere into the water and soil by rain and snow. It also moves quickly from soil and water back to air.
Acetone doesn't bind to soil or build up in animals.
It's broken down by microorganisms in soil and water.
It can move into groundwater from spills or landfills.
Acetone is broken down in water and soil, but the time required for this to happen varies.

How might I be exposed to acetone?

Breathing low background levels in the environment.
Breathing higher levels of contaminated air in the workplace or from using products that contain acetone (for example, household chemicals, nail polish, and paint).
Drinking water or eating food containing acetone.
Touching products containing acetone.
For children, eating soil at landfills or hazardous waste sites that contain acetone.
Smoking or breathing secondhand smoke.

How can acetone affect my health?

If you are exposed to acetone, it goes into your blood which then carries it to all the organs in your body. If it is a small amount, the liver breaks it down to chemicals that are not harmful and uses these chemicals to make energy for normal body functions. Breathing moderate- to-high levels of acetone for short periods of time, however, can cause nose, throat, lung, and eye irritation; headaches; light-headedness; confusion; increased pulse rate; effects on blood; nausea; vomiting; unconsciousness and possibly coma; and shortening of the menstrual cycle in women.

Swallowing very high levels of acetone can result in unconsciousness and damage to the skin in your mouth. Skin contact can result in irritation and damage to your skin.

The smell and respiratory irritation or burning eyes that occur from moderate levels are excellent warning signs that can help you avoid breathing damaging levels of acetone.

Health effects from long-term exposures are known mostly from animal studies. Kidney, liver, and nerve damage, increased birth defects, and lowered ability to reproduce (males only) occurred in animals exposed long-term. It is not known if people would have these same effects.

How likely is acetone to cause cancer?

The Department of Health and Human Services, the International Agency for Research on Cancer, and the Environmental Protection Agency (EPA) have not classified acetone for carcinogenicity.

Acetone does not cause skin cancer in animals when applied to the skin. We don't know if breathing or swallowing acetone for long periods will cause cancer. Studies of workers exposed to it found no significant risk of death from cancer.

Is there a medical test to show whether I've been exposed to acetone?

Methods are available to measure the amount of acetone in your breath, blood, and urine. The test can tell you how much acetone you were exposed to, although the amount that people have naturally in their bodies varies with each person. The tests can't tell you if you will experience any health effects from the exposure.

The test must be performed within 2-3 days after exposure because acetone leaves your body within a few days. These tests are not routinely performed at your doctor's office, but your doctor can take blood or urine samples and send them to a testing laboratory.

Has the federal government made recommendations to protect human health?

The EPA requires that spills of 5,000 pounds or more of acetone be reported.

The Occupational Safety and Health Administration (OSHA) has set a maximum concentration limit in workplace air of 1,000 parts of acetone per million parts of air (1,000 ppm) for an 8-hour workday over a 40-hour week to protect workers. The National Institute for Occupational Safety and Health (NIOSH) recommends an exposure limit of 250 ppm in workplace air for up to a 10-hour workday over a 40-hour workweek.

Glossary

< Carcinogenicity: Ability to cause cancer.

Evaporate: To change into a vapor or a gas.

Ingesting: Taking food or drink into your body.

Long-term: Lasting one year or longer.

References

Agency for Toxic Substances and Disease Registry (ATSDR). 1994. Toxicological Profile for acetone. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service.

Where can I get more information?

ATSDR can tell you where to find occupational and environmental health clinics. Their specialists can recognize, evaluate, and treat illnesses resulting from exposure to hazardous substances. You can also contact your community or state health or environmental quality department if you have any more questions or concerns.

For more information, contact:

Agency for Toxic Substances and Disease Registry
Division of Toxicology
1600 Clifton Road NE, Mailstop F-32
Atlanta, GA 30333
Phone: 1-888-42-ATSDR (1-888-422-8737)
FAX: ��(770)-488-4178
Email: ATSDRIC@cdc.gov

ACETONE MSDS Information

Contents:

Human Health Effects
Emergency Medical Treatment
Animal Toxicity Studies
Metabolism/Pharmacokinetics
Pharmacology
Environmental Fate & Exposure
Environmental Standards & Regulations
Chemical/Physical Properties
Chemical Safety & Handling
Occupational Exposure Standards
Manufacturing/Use Information
Laboratory Methods
Special References
Synonyms and Identifiers

Information Provided By:
U.S. National Library of Medicine,
8600 Rockville Pike, Bethesda, MD 20894,
National Institutes of Health,
Department of Health & Human Services

Toxicity Summary:

Exposure to acetone results from both natural and anthropogenic sources. Acetone also occurs as a metabolic component in blood, urine and human breath. ... Acetone is one of three ketone bodies that occur naturally throughout the body. It can be formed endogenously in the mammalian body from fatty acid oxidation. Fasting, diabetes mellitus and strenuous exercise increase endogenous generation of acetone. Under normal conditions, the production of ketone bodies occurs almost entirely within the liver and to a smaller extent in the lung and kidney. ... Products are excreted in the blood and transported to all tissues and organs of the body where they can be used as a source of energy. Two of these ketone bodies, acetoacetate and beta-hydroxybutyrate, are organic acids that can cause metabolic acidosis when produced in large amounts, as in diabetes mellitus. ... Endogenous acetone is eliminated from the body either by excretion in urine and exhaled air or by enzymatic metabolism. ... Acetone is rapidly absorbed via the respiratory and gastrointestinal tracts of human and laboratory animals, as indicated by the detection of acetone in blood within 30 min of inhalation exposure and 20 min of oral administration. ... The nasal cavities of human and laboratory animals appear to have a limited ability to absorb and excrete acetone vapor, compared with the remainder of the respiratory tract. Acetone is uniformly distributed among non-adipose tissues and does not accumulate in adipose tissue. ... Acetone is rapidly cleared from the body by metabolism and excretion. ... Exhalation is the major route of elimination for acetone and its terminal metabolite (carbon dioxide), and the fraction of administered acetone that is exhaled as unchanged acetone is dose-related. Urinary excretion of acetone and its metabolites occurs but this route of elimination is minor ... Exogenously supplied acetone enters into many metabolic reactions in tissues throughout the body, but the liver appears to be the site of most extensive metabolism. Carbon from orally administered acetone has been detected in cholesterol, amino acids, fatty acids and glycogen in rat tissues, urea in urine and unchanged acetone and CO2 in exhaled breath. Metabolically, acetone is degraded to acetate and formate ... Oral LD50 values in adult rats are in the range of 5800-7138 mg/kg. ... Experimental animal data characterizing the effects of long term oral or inhalation exposure to acetone are not available, due probably to its low toxicity and its endogenous characteristics. ... Pretreatment of rodents with acetone enhances the hepatotoxic effects of a number of compounds, notably halogenated alkanes. ... Acetone is not considered to be genotoxic or mutagenic. ... In a study of pregnant rats and mice exposed to acetone vapor during days 6-19 of gestation, slight developmental toxicity was observed ... Reports of other reproductive effects of acetone include observations of testicular effects and changes of sperm quality in rats ... Acetone has been used extensively as a solvent vehicle in skin carcinogenicity studies and is not considered carcinogenic when applied to the skin. Acetone is relatively less toxic than many other industrial solvents; however, at high concentrations, acetone vapor can cause CNS depression, cardiorespiratory failure and death. Acute exposures of humans to atmospheric concentrations ... have been reported to produce either no gross toxic effects or minor transient effects, such as eye irritation. More severe transient effects (including vomiting and fainting) were reported for workers exposed to acetone vapor concentrations ... for about 4 hr. Acute exposures to acetone have also been reported to alter performances in neurobehavioral tests in humans. ... Females ... were reported to suffer menstrual irregularities.
[Environmental Health Criteria 207: Acetone. pp. 1-7 (1998) by the International Programme on Chemical Safety (IPCS) under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation and the World Health Organization.]**QC REVIEWED**

Evidence for Carcinogenicity:

CLASSIFICATION: D; not classifiable as to human carcinogenicity. BASIS FOR CLASSIFICATION: Based on lack of data concerning carcinogenicity in humans or animals. HUMAN CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY DATA: None.
[U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Acetone (67-64-1) Available from: http://www.epa.gov/ngispgm3/iris" target=new on the Substance File List as of March 15, 2000]**PEER REVIEWED**

A4; Not classifiable as a human carcinogen.
[ American Conference of Governmental Industrial Hygienists TLVs and BEIs. Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinatti, OH, 2005, p. 10]**QC REVIEWED**

Human Toxicity Excerpts:

EFFECTS SIMILAR TO ETHYL ALCOHOL ... BUT ANESTHETIC POTENCY IS GREATER. 10-20 ML TAKEN BY MOUTH WITHOUT ILL EFFECT. IN ACUTE CASES A LATENT PERIOD MAY BE FOLLOWED BY RESTLESSNESS AND VOMITING LEADING TO HEMATEMESIS AND PROGRESSIVE COLLAPSE WITH STUPOR.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-168]**PEER REVIEWED**

WORKERS HAVING BEEN EXPOSED TO 1000 PPM, 3 HR/DAY FOR 7-15 YEARS, ALSO COMPLAINED OF CHRONIC INFLAMMATION OF AIRWAYS, STOMACH AND DUODENUM; SOME OF THEM COMPLAINED OF DIZZINESS & ASTHENIA. SIMILAR COMPLAINTS WERE REPORTED AFTER EXPOSURE ... TO 700 PPM.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 38]**PEER REVIEWED**

PROLONGED OR REPEATED SKIN CONTACT MAY DEFAT THE SKIN & PRODUCE DERMATITIS.
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4720]**PEER REVIEWED**

... Onset of hepatorenal lesions in two men & two women acutely exposed to acetone /is described/. One person had inhaled acetone vapors whereas the others had ingested acetone. Clinical manifestation of liver injury was observed in all four workers & renal lesions were detected in two.
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4725]**PEER REVIEWED**

Repeated exposure to 25-920 ppm: chronic conjunctivitis, pharyngitis, bronchitis, gastritis, and gastroduodenitis. /Route not specified/
[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983., p. 150]**PEER REVIEWED**

SYMPTOMATOLOGY (acute intoxication): 1. Early emotional lability: exhilariation, boastfulness, talkativeness, remorse, and belligerency. 2. Impaired motor coordination: slowed reaction time, slurred speech, ataxia. 3. Sensory disturbances: diplopia, vertigo. 4. Flushing of face, rapid pulse, sweating. 5. Nausea and vomiting. Eventual incontinence of urine and feces. 6. Drowsiness, stupor and finally coma, with impaired or absent tendon reflexes. Convulsive episodes may indicate hypoglycemia. /Ethyl alcohol/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-169]**PEER REVIEWED**

SYMPTOMATOLOGY (acute intoxication): 7. Pupils dilated or normal. 8. Peripheral vascular collapse (shock): hypotension, tachycardia, cold pale skin, hypothermia. 9. Slow stertorous respirations. 10. Death from respiratory or circulatory failure or from aspiration pneumonitis. 11. During convalescence: postalcoholic headache and gastritis; infections (for example, pneumonia, septicemia); alcoholic psychoses (for example, delirium tremens). /Ethyl alcohol/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-169]**PEER REVIEWED**

Acute acetone intoxication was reported in a 10-year old boy who wore a hip cast set with a mixture of 90% acetone, 9% pentane and 1% methyl salicylate. The following symptoms were described: restlessness, headache, vomiting (positive benzidine for blood), stupor, blood pressure 80/60, rapid and irregular respiration rate.
[American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 10]**PEER REVIEWED**

A total of 659 males occupationally exposed to acetone and other solvents were divided into nine unrelated groups working in plastic boat, chemical, plastic button, paint, and shoe factories. Urine samples were collected at the beginning of the workshift and at the end of the first half of the shift. A close relationship (correlation coefficient always above 0.85) between the average environmental solvent concentration (mg/cu m) measured in the breathing zone and the urinary concentration of unchanged solvent (ug/l) was observed. A Biological Equivalent Exposure Limit (56 mg/l) corresponding to the environmental Threshold Limit Value (58 mg/l) was recommended for acetone. The biological exposure data for urine collected over 4 hr during random sampling for at least 1 yr could be used to evaluate long-term exposure and probability of non-compliance for individual or groups of workers.
[Ghittori S et al; Am Ind Hyg Assoc J 48 (9): 786-90 (1987)]**PEER REVIEWED**

Direct contact of acetone with the eyes may produce irritation and corneal injury.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 1(78) 186]**PEER REVIEWED**

High vapor concentrations will produce anesthesia.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 1(78) 186]**PEER REVIEWED**

Acetone can be placed among solvents of comparatively low acute and chronic toxicities. Acetone does not have sufficient warning properties to prevent repeated exposures to vapors which may have adverse effects. There has been no reports that prolonged inhalation of low vapor concentrations result in any serious chronic effects in humans.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 1(78) 186]**PEER REVIEWED**

Severe toxic effects: 4,000 ppm= 9,650 mg/cu m, 60 minutes; symptoms of illness: 800 ppm= 1,930 mg/cu m, 60 minutes.
[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983., p. 150]**PEER REVIEWED**

Toxic concn in human blood: 200.0-300.0 ug/ml (20.0-30.0 mg %); lethal concn in human blood: 550.0 ug/ml (55.0 mg %)
[Winek, C.L. Drug and Chemical Blood-Level Data 1985. Pittsburgh, PA: Allied Fischer Scientific, 1985., p. 1]**PEER REVIEWED**

Symptoms following acute acetone ingestion include nausea, vomiting, gastric hemorrhage, sedation, respiratory depression, ataxia, and paresthesia. Depression resembles alcoholic stupor, but its onset is quicker than that with ethanol. Coughing and bronchial irritation may be the only clues to ingestion of quantities that are too small to produce sedation. Hyperglycemia and ketonemia with acidosis that resembles acute diabetic coma may be present.
[Gossel, T.A., J.D. Bricker. Principles of Clinical Toxicology. 3rd ed. New York, NY: Raven Press, Ltd., 1994., p. 89]**PEER REVIEWED**

EXPOSURE FOR 15 MINUTES TO 1660 PPM CAUSES IRRITATION OF EYES AND NOSE ...
[Thienes, C., and T.J. Haley. Clinical Toxicology. 5th ed. Philadelphia: Lea and Febiger, 1972., p. 137]**PEER REVIEWED**

Human Toxicity Values:

In children 2 to 3 ml/kg is considered to be toxic.
[Gossel, T.A., J.D. Bricker. Principles of Clinical Toxicology. 3rd ed. New York, NY: Raven Press, Ltd., 1994., p. 89]**PEER REVIEWED**

Skin, Eye and Respiratory Irritations:

EXPOSURE FOR 15 MINUTES TO 1660 PPM CAUSES IRRITATION OF EYES AND NOSE ...
[Thienes, C., and T.J. Haley. Clinical Toxicology. 5th ed. Philadelphia: Lea and Febiger, 1972., p. 137]**PEER REVIEWED**

Medical Surveillance:

Urinary glucaric acid and the ratio between 6-beta-OH-cortisol and 17-OH-corticosteroids were determined in chemical workers exposed to styrene greater than or equal to 164 mg/cu m, and acetone greater than or equal to 571 mg/cu m, and in a control group. Exposed workers had significantly higher excretion of glucaric acid and a higher ratio. ... Urinary mercapturic acids were also increased. Simultaneous styrene and acetone exposure induces mono-oxygenases in humans. ...
[Dolara P et al: Annals of Occupat Hyg 27 (2): 183-8 (1983)]**PEER REVIEWED**

Probable Routes of Human Exposure:

NIOSH (NOES Survey 1981-1983) has statistically estimated that 1,510,107 workers (466,677 of these are female) are potentially exposed to Acetone in the US(1). Occupational exposure may be through inhalation and dermal contact with this compound at workplaces where acetone is produced or used(SRC). The 8 hour TWA exposure to acetone was in the range of 0-70,000 umols/cu m in a survey of 659 occupationally exposed male subjects working in shoe, plastics and chemical plants in Italy (2). Workers in a Japanese acetate fiber producing plant had detectable levels of acetone in urine samples between 1 and 160 mg/l(3). The average TWA exposure to acetone in 7 spray painting and glue spraying plants was 0.9, 3.2, 2.3 0.9 and 5.6 ppm for higher-aromatic paint spraying, lower-aromatic paint spraying, glue spraying, solvent wiping, and paint mixing respectively(4).
[(1) NIOSH; National Occupational Exposure Survey (NOES) (1983) (2) Ghittori S et al; Am Ind Hyg Assoc J 48: 786 (1987) (3) Fujino A et al; Br J Ind Med 49: 654-57 (1992) (4) Whitehead LW et al; Am Ind Hyg Assoc J 45: 767-72 (1984)]**PEER REVIEWED**

The general population may be exposed to acetone through the use of commercially available products containing this compound such as paints, adhesives, cosmetics, and rubber cements(SRC). Exposure will also arise from inhalation of ambient air, ingestion of drinking water, and food that contains acetone(SRC). The average blood concn of acetone in 600 non-occupationally exposed persons in the US was 3,100 ppb(1).
[(1) Ashley DL et al; Clin Chem 40: 1401-04 (1994)]**PEER REVIEWED**

Body Burden:

Acetone was detected in the expired breath of 23 of 26 smokers and 42 of 43 nonsmokers in the US(1). Acetone was ubiquitous in the expired air from a carefully selected urban population of 54 normal healthy non-smoking people (387 samples) with a geometric mean concn of 101.3 ng/l(2). Acetone loss in the urine is generally 1 mg/24 hr for a normal adult but is about 50 mg in children(3,4). Acetone was detected in the expired breath of children in 2 classrooms in France at an average concn of 800 ng/l(5).
[(1) Gordon SM; J Chromatogr 511: 291-302 (1990) (2) Krotoszynski BK et al; J Anal Toxicol 3: 225-34 (1979) (3) Harper HA; Review of Physiological Chemistry 12th ed p. 303 (1969) (4) White WL et al; Chemistry for Medical Technologists 3rd ed Mosby Co St Louis, MO (1970) (5) Cailleux A et al; Chromatographia 37: 57-59 (1993)]**PEER REVIEWED**

Average Daily Intake:

AIR INTAKE (assume air concn of 0.05-20 ppb): 24-960 mg; WATER INTAKE - insufficient data; FOOD INTAKE - insufficient data. (SRC)
**PEER REVIEWED**

Emergency Medical Treatment:

Antidote and Emergency Treatment:

For immediate first aid: Ensure that adequate decontamination has been carried out. If victim is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep victim quiet and maintain normal body temperature. Obtain medical attention. /Ketones and related compounds/
[Bronstein, A.C., P.L. Currance; Emergency Care for Hazardous Materials Exposure. 2nd ed. St. Louis, MO. Mosby Lifeline. 1994., p. 237]**PEER REVIEWED**

For basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilation if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary. ... For contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport. ... Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Ketones and related compounds/
[Bronstein, A.C., P.L. Currance; Emergency Care for Hazardous Materials Exposure. 2nd ed. St. Louis, MO. Mosby Lifeline. 1994., p. 237]**PEER REVIEWED**

Animal Toxicity Studies:

Toxicity Summary:

Evidence for Carcinogenicity:

CLASSIFICATION: D; not classifiable as to human carcinogenicity. BASIS FOR CLASSIFICATION: Based on lack of data concerning carcinogenicity in humans or animals. HUMAN CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY DATA: None.
[U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Acetone (67-64-1) Available from: http://www.epa.gov/ngispgm3/iris on the Substance File List as of March 15, 2000]**PEER REVIEWED**

Non-Human Toxicity Excerpts:

SUMMARY OF RESULTS OF SINGLE EXPOSURES OF ANIMALS TO THE VAPORS: MICE 20,256 PPM, 1.5 HR: CNS DEPRESSION. MICE 46,000 PPM, 1 HR: FATAL. RATS 126,600 PPM, 1.75-2.25 HR: FATAL. RATS 42,200 PPM, 1.75-2.0 HR: LOSS OF CORNEAL REFLEX. GUINEA PIGS 20,000 PPM, 8-9 HR: LOSS OF REFLEXES.
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4721]**PEER REVIEWED**

/INVESTIGATORS/ ... STUDIED THE EFFECTS ON CATS OF REPEATED EXPOSURES TO ACETONE VAPORS. THEY USED DOSES OF 3 TO 5 MG/L (1265 TO 2110 PPM) AND OBSERVED NO ILL EFFECTS OTHER THAN SLIGHT IRRITATION OF THE EYES AND NOSE.
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4721]**PEER REVIEWED**

/Investigators/ ... reported that acetone produced moderate corneal injury to rabbit eyes. /Others/ ... reported mild ocular edema. Small multiple doses of acetone admin percutaneously (0.5 ml) or sc (0.05 ml) over a period of 3 to 8 wk produced cataracts in guinea pigs. ... No cataracts were seen in control animals. ... In a subsequent study conducted similarly, acetone produced cataracts in guinea pigs, but not in rabbits.
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4721]**PEER REVIEWED**

... GRANULAR DEGENERATION IN LESS SEVERE /INTOXICATIONS/, AND NECROSIS OF TUBULAR EPITHELIUM /IN MORE SEVERE INTOXICATIONS/ /OF KIDNEYS/ WERE /OBSERVED/ IN DOGS/. ... /OTHER WORK INDICATED/ LESIONS OF THE CONVOLUTED TUBULES, SOME FATTY INFILTRATION /OF THE KIDNEYS/ IN 1 CAT FOLLOWING INHALATION OF 75,900 PPM ... ALBUMINURIA /WAS SEEN/ IN SOME ... ANIMALS SUBJECTED TO INHALATION.
[Browning, E. Toxicity and Metabolism of Industrial Solvents. New York: American Elsevier, 1965., p. 418]**PEER REVIEWED**

WITH ACUTE INTOXICATION PRELIMINARY /SPECIES NOT SPECIFIED/ SYMPTOMS OF ... /CNS DEPRESSION/ ARE IRRITATIVE--SALIVATION, LACRIMATION, GIDDINESS, ATAXIA, TWITCHINGS & CONVULSIONS. ... AFTER IV & IM INJECTION FALL IN BLOOD PRESSURE ... /WAS/ REGARDED AS PRIMARILY DUE TO DECREASE IN CARDIAC OUTPUT.
[Browning, E. Toxicity and Metabolism of Industrial Solvents. New York: American Elsevier, 1965., p. 417]**PEER REVIEWED**

MALE MICE & RATS WERE EXPOSED FOR VARYING TIME PERIODS TO VAPOR LEVELS OF 12,600-50,600 PPM ACETONE. UNCONDITIONED PERFORMANCE & REFLEX TESTS WERE USED TO MEASURE CNS DEPRESSION. ANIMALS BREATHING ACETONE TOOK 9 HR TO RECOVER FROM 5 MIN EXPOSURE. BLOOD LEVELS WERE RELIABLE DEPRESSION INDEX.
[BRUCKNER JV, PETERSON RG; TOXICOL APPL PHARMACOL 61 (1): 27-37 (1981)]**PEER REVIEWED**

A SHORT INHALATION EXPT WAS PERFORMED ON MICE USING VARIOUS INDUSTRIAL AIRBORNE CHEMICALS, INCL ACETONE. FOR EACH CMPD SYSTEMATIC DETERMINATION OF CONCN ASSOC WITH A 50% DECR IN RESP RATE WAS USED FOR COMPARISONS. DATA MAY HELP ESTABLISH WORKPLACE TLV'S.
[DE CEAURRIZ JC ET AL; TOXICOL LETT 9 (2): 137-43 (1981)]**PEER REVIEWED**

Sensitivity of developing chicken embryos to various solvents was investigated. Acetone (0.10 ml/egg injected) significantly reduced the percentage hatchability & caused a high embryonic mortality during the first wk of incubation.
[Ameenuddin S, Sunde ML; Proc Soc Exp Biol Med 175 (2): 176-8 (1984)]**PEER REVIEWED**

10.5 day-old rat embryos were cultured for 2 days in whole rat serum containing 0.1, 0.5, & 2.5 vol% of acetone. No adverse effects occurred at 0.1% concn. The order of increasing embryotoxicity & dysmorphogenesis of the studied liquids was corn oil < acetone/corn oil < dimethyl sulfoxide < ethanol, acetone < Tween 80. Any of the water miscible solvents (at 0.1%) met the criteria of a nontoxic & nonteratogenic water insol cmpd delivery system for in vitro embryo culture.
[Kitchin KT, Ebron MT; Toxicology 30 (1): 45-57 (1984)]**PEER REVIEWED**

Hepatocytes from young male rats were incubated in acetone in closed vessels fitted with side arms for serial sampling for approx 5 hr at 37 deg C with gentle shaking under an oxygen:carbon dioxide atmosphere. Parameters evaluated were glutamate-oxaloacetate transaminase & lactate dehydrogenase release from cells, trypan blue exclusion, cell count, urea synthesis capability, & steady-state ATP levels. Acetone /10 mM/ was without effect /in LDH or GOT release/. Isolated hepatocyte suspensions are useful for identification of cytotoxins in general & hepatotoxins in particular, but their capability for yielding a quantitative index of cytotoxic potential for diverse chemical species remains to be demonstrated.
[Story DL et al; J Toxicol Environ Health 11 (4-6): 483-501 (1983)]**PEER REVIEWED**

Acetone (reagent grade) was evaluated by the standard plate incorporation method in the Ames Salmonella reverse mutation assay with strains TA98, TA100, TA1535, TA1537, & TA1538. Experiments were done in triplicate with & without metabolic activation (S9 fractions from Aroclor-treated Sprague-Dawley rats). Results were negative in these strains.
[De Flora S et al; Mutat Res 133 (3): 161-98 (1984)]**PEER REVIEWED**

At a concn of 8,100 mg/l of acetone, there was an approximate 50% inhibition of ammonia oxidation of Nitrosomonas.
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 114]**PEER REVIEWED**

Acetone was used as a solvent control in this experiment and 0.2 ml was applied to the shaved dorsa of 50 male and 50 female SHEL:CF1,SPF mice once per week from six weeks of age to two years. All dead and dying animals were autopsied as well as all animals still alive at 2 years. Local irritation was noted at the application site of a few animals. One subcutaneous fibrosarcoma observed in one male was considered ... to be incidental. There were 17/50 tumors in the males and 13/50 tumors in the females, considered to be a normal rate for this strain (primarily tumors of the lymphoreticular or hematopoietic system). A second study using 100 mice for each sex, and identical treatment and autopsy regimens resulted in negative results for the skin and similar background rates for tumors of the lymphoreticular or hematopoietic systems, ie: 30/100 for males and 29/100 for the females.
[Zakova N et al; Fd Chem Toxic 23: 1081-9 (1985)]**PEER REVIEWED**

The frequency of recessive chlorophyll and embryonic lethals included by N-methyl-N'-nitro-N-nitrosoguanidine in Arabidopsis thaliana was markedly increased when exposure of the seeds to N-methyl-N'-nitro-N-nitrosoguanidene (3 hr) was carried out in the presence of 4-12% acetone, 4-16% ethanol, or 8-32% dimethylformamide. The enhancement of N-methyl-N'-nitro-N-nitrosoguanidene mutagenicity was proportional to the concentrations of these organic solvents. In contrast, none of the solvents, when applied at the same conditions and doses, influenced the mutagenic activity of N-methyl-N-nitrosourea. The solvents without mutagens did not influence the spontaneous rate of mutations and revealed no or very weak toxic effect as measured by the seed germination.
[Gichener T et al; Mutat Res 192 (1): 31-5 (1987)]**PEER REVIEWED**

Female Sprague-Dawley-rats were given 0.5, 1, or 2.5 ml/kg of acetone once by gavage. Sodium phenobarbital (SPB), 100 mg/kg, was administered once a day for 3 days. The animals were killed 24 hours after the last dose. Livers were homogenized and microsomes were prepared by differential centrifugation. Microsomal lipids were extracted with a 2 to 1 chloroform methanol mixture. The extracted samples were assayed for total phosphate or resuspended in saline and assayed for cholesterol. Treatment with acetone did not cause alterations in the concentrations of total phospholipid (TPL) and total cholesterol (TC) in microsomal membranes. Acetone had no effect on microsomal N-demethylation of aminopyrine, however, at the high dose, it significantly increased the metabolism of acetonitrile to cyanide. Acetone did not significantly change the concentration of cytochrome p450.
[Hayes EP et al; Toxicol Lett 31: 139-45 (1986)]**PEER REVIEWED**

The purpose of this study was to determine if acetone could alter the acute nephrotoxicity produced by the experimental fungicide N-(3,5-dichlorophenyl)succinimide. Male Fischer 344 rats were administered acetone (1, 5 or 10 mmol/kg) or acetone vehicle (corn oil, 10 mg/kg) orally followed 16 hr later by a single intraperitoneal injection of N-(3,5-dichlorophenyl)succinimide (0.2 or 0.4 mmol/kg) or N-(3,5-dichlorophenyl)succinimide vehicle (sesame oil, 2.5 ml/kg) and renal function was monitored at 24 and 48 hr. Acetone (1 or 5 mmol/kg) did not alter N-(3,5,-dichlorophenyl)succinimide (0.2 mmol/kg) induced renal effects while acetone (10 mmol/kg) pretreatment attenuated N-(3,5-dichlorophenyl)succinimide (0.4 mmol/kg) induced increases in blood urea nitrogen (BUN) concentration and kidney weight but had no effect on N-(3,5,-dichlorophenyl)succinimide (0.4 mol/kg) induced changes in urine volume or content, organic ion accumulation by renal cortical slices or renal morphology.
[Lo HH et al; Toxicol Lett 38 (1-2): 161-8 (1987)]**PEER REVIEWED**

The effects of combinations of chemicals known to individually induce aneuploidy were tested on the diploid Saccharomyces-cerevisiae strain D61.M. Exponential phase cultures of the yeast were treated with nocodazole, ethyl acetate, acetone, and methyl ethyl ketone alone or in combination, incubated at 28 degrees C for 4 hours, held in an ice bath for 16 hours, incubated at 28 degrees C for an additional 4 hours, and then diluted and plated onto selective media. Treatment of yeast strain D61.M with mixtures containing nocodazole levels too low to induce aneuploidy and ineffective low levels of the solvents ethyl acetate, acetone, and methyl ethyl ketone was highly effective in inducing aneuploidy. The synergistic effect did not depend on the cold holding period during treatment.
[Mayer VW, Goin CJ; Mutat Res 187: 21-30 (1987)]**PEER REVIEWED**

In studies of acetone-potentiated liver injury induced by haloalkanes, acetone is usually given by gavage, whereas industrial exposure to acetone normally occurs by inhalation. It was of interest to verify if the route of administration influences the potentiation. Male Sprague-Dawley rats were exposed for 4 hr to acetone vapors or treated orally with acetone; the minimal effective dose levels for potentiating CCl4-induced liver injury were estimated to be 2500 ppm and 0.25 mg/kg, respectively. Groups were treated with acetone using 0.4, 1, 2, 4, or 6 times the minimal effective dose. Half of each group was killed at various time intervals after treatment for blood acetone measurements by gas chromatography; the other half was challenged with CCl4 (0.1 ,l/kg, ip) 18 hr after acetone, and killed 24 hr later. Plasma alanine aminotransferase (ALT) activity and bilirubin concentrations were measured. Inhalation and oral administration of acetone both potentiated CCl4 toxicity. Rats exposed repetitively to acetone vapors (10 daily exposures) and subsequently challenged with CCl4 exhibited liver toxicity that was not significantly different from that of rats subjected to a single exposure. Correlations between ALT activities and maximal bloodacetone concentrations were found to be linear (positive) and significant for both routes. For a given blood acetone concentration, however, toxicity was least severe following acetone exposure by inhalation.
[Charbonneau M et al; Toxicol Appl Pharmacol 84 (2): 286-94 (1986)]**PEER REVIEWED**

The susceptibility of New Zealand White rabbits and albino guinea pigs to the cataractogenic effects of dermal acetone treatments. Male and female rabbits treated with 1 ml of acetone 3 days/wk for 3 weeks showed no lens abnormalities during the 6 month observation period. Male and female guinea pigs were treated with 0.5 ml of acetone 5 days/wk for 6 weeks and examined with an ophthalmoscope and slip lamp at regular intervals for 1 yr post-treatment. By 3 months post-treatment, cataracts were observed in 30% of the test animals and none of the control animals. The ascorbate levels in aqueous humor specimens from the test throughout the 1 yr observed period. It was concluded that the development of cataracts in guinea pigs was species specific and related to ascorbate synthesis.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 239]**PEER REVIEWED**

The reproductive effects of acetone in male Wistar rats administered 0.5% acetone in their drinking water for 6 wk. On fifth week of treatment, the rats were allowed to mate with untreated females and the number of matings were recorded together with the number of pregnancies and the number of fetuses per pregnancy. The absolute weight of the testes was measured along with the diameter of the seminiferous tubules in the treated and control rats. Semiquantitative histopathological scoring was used to detect any effects on vacuole formation, chromatic margination, epithelial disruption, multinucleated giant-cell formation, intracellular debris, or atrophy of the testes. None of these measures of reproductive and testicular toxicity were affected by the acetone treatment relative to the control animals.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 242]**PEER REVIEWED**

The avoidance and escape behavior of female Carworth rats exposed to acetone vapors for 10 days at 4 hr/day (180). Groups of animals were trained to avoid (conditioned response) or escape (unconditioned response) a shock stimulus by climbing a pole situated in a test chamber with an electric grid on the floor. Each animal was evaluated before and after daily acetone exposures of 3000, 6000, 12,000, and 16,000 ppm. The 3000 ppm exposure were without effect on all exposure days, the 6000 ppm exposure inhibited the avoidance but not the escape response, and the two highest exposures inhibited both responses. Normal responses were obtained after three days of exposure to 6000 and 12,000 ppm, which indicated adaptation and tolerance developed on repeated exposure to acetone vapors.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 176]**PEER REVIEWED**

Groups of male Sprague-Dawley rats were exposed for 3 hr to acetone concentrations of 12,600, 19,000, 25,300, and 50,600 ppm. The degree of /CNS depression/ was measured at regular intervals during and after the exposure by performing five tests (wire maneuverability, visual pacing, grip strength, tail pinch, and righting reflex) that measured unconditioned performance and involuntary reflex. Each animal was scored between 0 and 8 on each of these tests, and the individual results were averaged to obtain a mean performance score. Performance scores showed a dose-related decline at all but the highest acetone exposure level. Animals exposed to 50,600 ppm of acetone died within 2 hr of initiating the exposure. The performance score for the group of rats exposed to 19,000 ppm of acetone returned to the preexposure level after 9 hr, whereas the group exposed to 25,300 ppm of acetone required 21 hr before its performance score returned to base-line levels.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 176]**PEER REVIEWED**

Single-dose oral lethality studies have been performed in mice, rats, and rabbits. A 14-day oral LD50 of 10.7 ml/kg (8.5 g/kg) and 95% confidence limits of 7.7 to 15.0 ml/kg (6.2 to 11.9 g/kg) for female Carworth-Wistar rats was reported. Using the same test conditions and test species, ... the LD50 value was found to be 12.6 ml/kg (9.8 g/kg) and the 95% confidence limits to be 10.6 to 14.9 ml/kg (8.5 to 11.9 g/kg). ... An oral LD50 value of 5.3 g/kg for an unstated sex and strain of rabbit and an LD50 value between 4 and 8 g/kg for an unstated sex and strain of mouse was reported. Using male ddY mice, ... the oral LD50, of acetone was found to be 90.39 mmol/kg (5.25 g/kg) with 95% confidence limits of 61.68 to 132.5 mmol/kg (3.58 to 7.70 g/kg).
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 180]**PEER REVIEWED**

A group of male baboons was exposed continuously (24 hr/day) to 500 ppm acetone for 7 days. The percentage of correct and incorrect responses was recorded along with the time necessary to respond precisely to a stimulus-induced discrimination task that resulted in a food reward when performed correctly. The acetone exposure caused no change in the number of correct responses, a highly variable change in the number of extra incorrect responses, and a consistent increase in the response time relative to control values. The authors did not measure blood or urine acetone levels; however, the uninterrupted exposure undoubtedly resulted in an extremely high acetone body burden. Acetone exposures were performed at 150 ppm for times ranging from 30 min to 4 hr.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 178]**PEER REVIEWED**

Male Swiss mice were placed in a container of water and the lag time between water contact and the initiation of swimming behavior was measured relative to a control group. A nominal concentration of 2000 ppm caused no change in swimming behavior, whereas concentrations ranging from about 2600 to 3000 ppm caused the swimming lag time to decrease up to 59%.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 178]**PEER REVIEWED**

National Toxicology Program Studies:

... The potential for acetone to cause developmental toxicity was assessed in Sprague-Dawley rats exposed to 0, 440, 2200, or 11000 ppm, and in Swiss (CD-1) mice exposed to 0, 440, 2200, and 6600 ppm acetone vapors, 6 hr/day, 7 days/week. Each of the four treatment groups consisted of 10 virgin females (for comparison), and approximately 32 positively mated rats or mice. Positively mated mice were exposed on days 6-17 of gestation (dg), and rats on 6-19 days of gestation. The day of plug or sperm detection was designated as 0 days of gestation. ... Pregnant rats did not exhibit overt symptoms of toxicity other than statistically significant reductions for the 11,000 ppm group in body weight. (14, 17, 20 days of gestation), cumulative weight gain from 14 days of gestation onward, uterine weight and in extragestational weight gain. (EGWG - maternal body weight (20 days of gestation) uterine weight - maternal body weight (0 days of gestation.) Mean body weights of treated virgin females were also reduced, but not significantly. There were no maternal deaths and the mean pregnancy rate was greater than or equal to 93% in all groups. No affect was observed in the mean liver or kidney weights of pregnant dams, the organ to body weight ratios, the number of implantations, the mean percent of live pups/litter, the mean percent of resorptions/litter, or the fetal sex ratio. However, fetal weights were significantly reduced for the 11,000 ppm exposure group relative to the 0 ppm group. The incidence of fetal malformations was not significantly increased by gestational exposure to acetone vapors, although the percent of litters with at least one pup exhibiting malformations was greater for the 11,000 ppm group than for the 0 ppm group, 11.5 and 3.8%, respectively. The diversity of malformations observed in the 11,000 ppm group was greater than that found in the lower dose groups or in the 0 ppm group. There was no increase in the incidence of fetal variations, reduced ossification sites, or in the mean incidence of fetal variations per litter. Analysis of rat plasma samples 30 min post-exposure showed an increase in plasma acetone levels which correlated with increasing exposure concentration. Acetone levels dropped to control levels by 17 hr post-exposure for all exposure groups except the 11,000 ppm group. Plasma acetone-levels for this group were still slightly elevated with respect to the controls at 17 hr post-exposure. The concentration of plasma acetone levels at either 30 min or 17 hr post exposure did not increase over gestation regardless of the exposure concentration. Neither exposure to acetone vapor, nor advancing gestation resulted in alterations of the plasma levels for the other two ketone bodies, acetoacetic acid and b-hydroxybutyric acid, with respect to control animals. Swiss (CD-1) mice exhibited severe ... /CNS depression/ at the 11,000 ppm acetone concentration; consequently, the high exposure concentration was reduced to 6600 ppm acetone after one day of exposure. No further overt signs of toxicity were observed and there were no maternal deaths. No treatment- related effects on maternal or virgin body weight, maternal uterine weight, or on extragestational weight gain were noted in mice. There was a treatment-correlated increase in liver to body weight ratios in pregnant dams which may have been indicative of an induction of the p450 monooxygenase enzyme system. The mean pregnancy rate for all mated mice was greater than or equal to 85% in all groups. There was no effect on the number of implantations per dam, on any other reproductive indices, or on the fetal sex ratio. Developmental toxicity was observed in mice in the 6,600 ppm exposure group as; 1) a statistically significant reduction in fetal weight, and 2) a slight, but statistically significant increase in the percent incidence of late resorptions. However, the increase in the incidence of late resorptions was not sufficient to cause a decrease in the mean number of live fetuses per litter. The incidence of fetal malformations or variations in mice was not altered by exposure to acetone vapors at any of the levels employed. It may be concluded from the results of this study that the 2,200 ppm acetone level was the no observable effect level (NOEL) in both the Sprague-Dawley (CD) rat and the Swiss (CD-1) mouse for developmental toxicity. Furthermore, since only minimal maternal toxicity was observed at 11,000 ppm acetone for rats and 6,600 ppm acetone for mice, it is possible that the actual maternal NOEL is somewhat greater than 2,200 ppm.
[Department of Health & Human Services/National Institute of Environmental Health Sciences, National Toxicology Program; Inhalation Developmental Toxicity Studies: Acetone (CAS # 67-64-1) in Mice and Rats, NTP Study No. TER87140 (Mice), TER87036 (Rats) (November, 1988) available at http://ntp.niehs.nih.gov as of August 14, 2002]**QC REVIEWED**

Non-Human Toxicity Values:

LD50 Rat oral 10.7 ml/kg
[Budavari, S. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 1996., p. 12]**PEER REVIEWED**

Ecotoxicity Values:

LC50 JAPANESE QUAIL ORAL GREATER THAN 40,000 PPM, IN DIET, AGE 14 DAYS, (NO MORTALITY TO 40,000 PPM)
[Hill, E.F. and Camardese, M.B. Lethal Dietary Toxicities of Environmental Contaminants and Pesticides to Coturnix. Fish and Wildlife Technical Report 2. Washington, DC: United States Department of Interior Fish and Wildlife Service, 1986., p. 22]**PEER REVIEWED**

LC50 RING-NECKED PHEASANT ORAL GREATER THAN 40,000 PPM, IN DIET, AGE 10 DAYS, (NO MORTALITY TO 40,000 PPM)
[U.S. Department of the Interior, Fish and Wildlife Service, Bureau of Sports Fisheries and Wildlife. Lethal Dietary Toxicities of Environmental Pollutants to Birds. Special Scientific Report - Wildlife No. 191. Washington, DC: U.S. Government Printing Office, 1975., p. 8]**PEER REVIEWED**

LC50 SALMO GAIRDNERI (RAINBOW TROUT) 5,540 MG/L/96 HR @ 12 DEG C (95% CONFIDENCE LIMIT 4,740-6,330 MG/L), WT 1.0 G /STATIC BIOASSAY/
[U.S. Department of Interior, Fish and Wildlife Service. Handbook of Acute Toxicity of Chemicals to Fish and Aquatic Invertebrates. Resource Publication No. 137. Washington, DC: U.S. Government Printing Office, 1980., p. 81]**PEER REVIEWED**

LD100 Asellus aquaticus 3 ml/l (within 3 days of exposure) /Conditions of bioassay not specified/
[Erben R, Beader B; Poljopr Sumar 29 (2): 105-14 (1983)]**PEER REVIEWED**

LD100 Gammarus fossarum 10 ml/l (within 48 hr) /Conditions of bioassay not specified/
[Erben R, Beader B; Poljopr Sumar 29 (2): 105-14 (1983)]**PEER REVIEWED**

LC50 Pimephales promelas 8,120 mg/l/96 hr /Conditions of bioassay not specified/
[Veith GD et al; Can J Fish Aquat Sci 40 (6): 743-8 (1983)]**PEER REVIEWED**

LC50 Daphnia magna 10 mg/L 24 to 48-Hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 116]**PEER REVIEWED**

LC50 Brine shrimp 2,100 mg/L 24 to 48-Hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 116]**PEER REVIEWED**

LC50 Mosquito fish 13,000 mg/L 24 to 96-Hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 116]**PEER REVIEWED**

LC50 Lepomis macrochirus (bluegill sunfish) 8,300 mg/L 96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 116]**PEER REVIEWED**

LD50 Goldfish 5,000 mg/L 24-hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 116]**PEER REVIEWED**

LC50 Poecilia reticulata (guppy) 7,032 mg/l 14 day /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 116]**PEER REVIEWED**

LC50 Mexican axolotl 20,000 mg/l (3-4 weeks after hatching) 48 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 116]**PEER REVIEWED**

LC50 Clawed toad 24,000 mg/l (3-4 weeks after hatching) 48-hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 116]**PEER REVIEWED**

LC50 fingerling trout 6,100 mg/l 24-hr /Flow-through bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 116]**PEER REVIEWED**

Metabolism/Pharmacokinetics:

Metabolism/Metabolites:

Two pathways for the conversion of acetone to glucose are proposed, the methylglyoxal & the propanediol pathways. The methylglyoxal pathway is responsible for the conversion to acetol, acetol to methylglyoxal, & subsequent conversion of methylglyoxal to glucose. The propanediol pathway involves the conversion of acetol to L-1,2-propanediol by an as yet unknown process. L-1,2-propanediol is converted to L-lactaldehyde by alcohol dehydrogenase, & L-lactaldehyde is converted to L-lactic acid by aldehyde dehydrogenase. Expression of these metabolic pathways in rat appears to be dependent on the induction of /acetone/ oxygenase & acetol monooxygenase by acetone.
[Casazza JP et al; J Biol Chem 259 (1): 231-6 (1984)]**PEER REVIEWED**

HEPATIC NAD-DEPENDENT ALCOHOL DEHYDROGENASE ... ENZYME IS CAPABLE OF CATALYZING REVERSE REACTION IN WHICH ... ACETONE ... /IS REDUCED TO ALCOHOL/.
[Testa, B. and P. Jenner. Drug Metabolism: Chemical & Biochemical Aspects. New York: Marcel Dekker, Inc., 1976., p. 310]**PEER REVIEWED**

Acetone may be converted to 1,2-propanediol which enters the glycolytic pathway & possibly the one carbon pool. Acetone has been shown to be converted to lactate in mice. The rate-limiting step appears to be the conversion of acetone to a hydroxylated intermediate. Rats & mice exposed to 30 mg/l of acetone, & rabbits & guinea pigs exposed to 72 mg/l for 2 hr, had increased levels of acetone, acetoacetic acid, & beta-hydroxybutyric acid in the blood & urine immediately after exposure & 24 hr later.
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4726]**PEER REVIEWED**

Acute admin of acetone to rats resulted in measureable levels of isopropanol in blood. Metabolism of acetone to isopropanol was different in normal & diabetic animals. Blood levels of isopropanol reached a max at 2 g/kg dose in normal rats, but there was a 2-phase response in diabetic rats. In a second series of experiments, acetone was admin on alternate days for a wk. In spite of this chronic admin, there was no enhancement of acetone metabolism to isopropanol.
[Lewis GD et al; J Forensic Sci 29 (2): 541-9 (1984)]**PEER REVIEWED**

The metabolic mechanism responsible for the incorporation of acetone into the glucose and amino acids of lactating cows. Normal and spontaneously ketotic cows (unspecified type) were given a single bolus iv dose of [2-14(C)] acetone. The casein and lactose isolated from milk specimens were digested to obtain their constituent amino acids and hexoses. The glucose and galactose from lactose were labeled to the same degree, indicating that the galactose was derived from labeled glucose. The labeling intensity in the amino acids from casein increased in the following order:glycine < serine < aspartic acid < glutamic and that 40 to 70% of the end genous acetone was metabolized in the citric acid cycle through a common precursor, oxaloacetate. It was concluded that the utilization of acetone for glucose synthesis was not enhanced in ketotic cows and that the glucose from acetone constituted a small and insignificant portion of the total production.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 210]**PEER REVIEWED**

Absorption, Distribution & Excretion:

ACETONE IS ONE OF THE LEAST HAZARDOUS INDUSTRIAL SOLVENTS, BUT IS HIGHLY VOLATILE AND MAY BE INHALED IN LARGE QUANTITIES. IT MAY BE ABSORBED INTO THE BLOOD THROUGH THE LUNGS AND DIFFUSED THROUGHOUT THE BODY. SMALL QUANTITIES MAY BE ABSORBED THROUGH THE SKIN.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 38]**PEER REVIEWED**

LARGE QUANTITIES OF ACETONE ARE RAPIDLY EXCRETED FOLLOWING EXPOSURE. ONLY A SMALL AMT IS REDUCED. EXCRETION MAINLY VIA LUNGS AND URINE ... ACETONE ABSORBED DURING 8 HOURS AT 200 PPM WILL BE COMPLETELY METABOLIZED OR EXCRETED WITHIN 16 HOURS ...
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 38]**PEER REVIEWED**

... THE AMT OF ACETONE ABSORBED WHEN FOOT OF ANIMAL WAS IMMERSED /WAS ESTIMATED/ BY MEASURING AMT EXHALED AND THAT PRESENT IN BLOOD.
[Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 1727]**PEER REVIEWED**

ACETONE, BECAUSE OF ITS SOLUBILITY IN WATER, IS READILY ABSORBED INTO BLOOD STREAM AND THUS IS TRANSPORTED RAPIDLY THROUGHOUT BODY. ... A MAN BREATHING AN ESTIMATED CONCN OF 22 MG/L (9300 PPM) FOR 5 MIN ABSORBED 71% OF INHALED ACETONE; 2 MEN BREATHING 11 MG/L ... FOR 15 MIN ABSORBED 76-77% ...
[Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 1729]**PEER REVIEWED**

... EXCRETION ... IN HUMANS IS RAPID FOR 8 HR AFTER A SINGLE ORAL DOSE BUT WAS NOT COMPLETE IN 24 HR. ... THE RATIO OF EXCRETION ... WAS APPROX 40-70% IN BREATH, 15-30% IN THE URINE, AND 10% OF TOTAL EXCRETED THROUGH SKIN.
[Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 1730]**PEER REVIEWED**

In order to verify the relationship between urinary acetone concentrations and corresponding mean environmental concentrations in the breathing zone, the urinary concentration of acetone was measured in subjects experimentally or occupationally exposed to acetone. Fifteen healthy volunteers were exposed to acetone vapor concentrations of 56 to 500 ppm/cu m in an exposure chamber for 2 hours at rest or during alternating rest and light physical exercise. The urinary elimination of acetone was also studied in 104 workers occupationally exposed to acetone. The ratio of alveolar concentration to environmental concentration averaged approximately 0.28, and the relative uptake averaged 53%. The urinary acetone concentration showed a linear relationship to the corresponding environmentally time weighted average concentration in both the experimentally exposed subjects and the occupationally exposed subjects. There was also a linear relationship between the amount of acetone absorbed and the urinary concentrations of acetone.
[Pezzagno G et al; Scand J Work Environ Health 12: 603-8 (1986)]**PEER REVIEWED**

The upper respiratory tract (URT) deposition of acetone was studied in vivo in male Syrian golden hamsters and in vitro using nasal tissue homogenates. A steady state for acetone deposition was obtained within 3 minutes in hamsters exposed to 1030 mg/cu m. Nasal perfusion of 0.046 ml/min (95% confidence limit, 0.035-0.58 ml/min) was calculated. The effect of flow rate on URT was described by a ventilation perfusion model. Acetone was not metabolized by in vitro homogenates.
[Morris JB, Cavanagh DG; Fundam Appl Toxicol 9 (1): 34-40 (1987)]**PEER REVIEWED**

Mechanism of Action:

Levels of endogenous acetone in fasted rats correlated with 3-4-fold increase in nitrosodimethylamine demethylase (NDMAd) activity. A dose-response experiment showed endogenous levels of acetone to be capable of causing at most 40% of the induction in fasted rats. This suggests that other ketone bodies or factors may have contributed to the induction.
[Miller KW, Yang CS; Arch Biochem Biophys 229 (2): 483-91 (1984)]**PEER REVIEWED**

... /IT WAS/ SUGGESTED THAT INJURIOUS EFFECT OF ACETONE ON EYE /OF RABBITS/ WAS CAUSED BY DEHYDRATION OF SCLERA WHICH RESULTED IN GELATINOUS FLOCCULATION AND OPACITY OF SCLERA.
[Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 1728]**PEER REVIEWED**

Interactions:

Pretreatment with acetone for 6 days (one-tenth the LD50) potentiated acute ethanol toxicity in rats. ... /Investigators/ ... demonstrated that acetone pretreatment potentiates chlorinated hydrocarbon toxicity. ... Acetone protected animals against electroshock or isonicotinic acid hydrazide-induced convulsions. Acetone ... enhanced the hepatotoxicity of 1,1-dichloroethylene (200 ppm) in rats.
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4727]**PEER REVIEWED**

PRETREATMENT OF MICE WITH ACETONE GREATLY REDUCED THE MINIMUM MUTAGENICALLY EFFECTIVE CONCN OF DIMETHYLNITROSAMINE (DMN) IN SALMONELLA TYPHIMURIUM TA92. THE RESULTS OF THE HOST-MEDIATED ASSAYS SUBSTANTIALLY DIFFERED FROM THOSE OF THE IN VITRO ACTIVATION ASSAYS (A) IN THE RELATIVELY LOW DOSE OF DMN REQUIRED FOR MUTAGENICITY TO OCCUR & (B) IN THE LACK OF POTENTIATION BY ACETONE PRETREATMENT. ACETONE EVEN LED TO A MARGINAL DECREASE IN MUTAGENICITY OF DIMETHYLNITROSAMINE.
[GLATT H ET AL; CARCINOGENESIS (LONDON) 2 (10): 1057-61 (1981)]**PEER REVIEWED**

Pretreatment of rats with acetone potentiated the hepatotoxicity of n-nitrosodimethylamine as indicated by plasma glutamic-pyruvatic transaminase levels & histological data. Pretreatment with acetone (2.5 ml/kg) & 2 days of fasting caused a 2-fold potentiation of n-nitrosodimethylamine-induced plasma glutamic-pyruvatic transaminase elevation. Centrilobular necrosis produced by n-nitrosodimethylamine was more severe after pretreatment with inducers. N-nitrosodimethylamine treatment also decreased hepatic microsomal demethylase activity. Thus, n-nitrosodimethylamine demethylase is responsible for the activation of n-nitrosodimethylamine in vivo to a toxic intermediate, & induction of this enzyme activity potentiates n-nitrosodimethylamine hepatotoxicity.
[Lorr NA et al; Toxicol Appl Pharmacol 73 (3): 423-31 (1984)]**PEER REVIEWED**

Treatment of rats with acetone (2.5-5 ml/kg, intragastric) caused a 3-4.5-fold enhancement in reduced nicotinamide adenine dinucleotide-dependent nitrosodimethylamine demethylase (NDMAd) activity. This was accompanied by only moderate incr in gross cytochrome p450 content & reduced nicotinamide adenine dinucleotide-cytochrome c reductase & 261% incr in ethoxycoumarin O-dealkylase activity. The treatment enhanced the metabolism of nitrosomethylethylamine, nitrosomethylbenzylamine, & nitrosomethylaniline, although to lesser extents than with nitrosodimethylamine. Observations suggest that the enhanced nitrosodimethylamine demethylase was due to induction of 1 or more specific p450 isozyme(s) by pretreatment with acetone or isopropanol. Treatment induced proteins with molecular weights of 50,000 & 52,000 which were in the range of known p450 isozymes. The induction of these proteins & nitrosodimethylamine demethylase activity was inhibited by cobaltous chloride & cycloheximide. The induced microsomes had a peak at 450.6 nm, different from 450.0 nm peak of control microsomes. When added to the incubation mixture, acetone & isopropanol inhibited nitrosodimethylamine demethylase activity. Isopropanol was more potent than acetone.
[Tu YY et al; Chem-Biol Interact 44 (3): 247-60 (1983)]**PEER REVIEWED**

... Pretreatment of rats with acetone (15 mmol/kg, po) markedly potentiated the hepatotoxic response to bromodichloromethane and dibromochloromethane ... /in male Sprague-Dawley rats/.
[Hewitt WR et al: Toxicol Lett 16 (3-4): 285-96 (1983)]**PEER REVIEWED**

Chloroform-induced hepato- and nephrotoxicity was evaluated in male, Fischer 344 rats pretreated with various dosages (1.0 to 15.0 mmol/kg, po) of acetone, 2-butanone, 2-pentanone, 2-hexanone, or 2-heptanone. Chloroform ... produced extensive tubular and centrilobular necrosis when administered to ketone-pretreated rats. The relationship between ketone dosage and the magnitude of the potentiated response was non-linear. Maximum potentiation of chloroform toxicity occurred in the dose range of 5.0-10.0 mmol ketone/kg. Ketone dosages > 10.0 mmol/kg were associated with a reduction in the degree of chloroform injury. At the lowest ketone dosage (1.0 mmol/kg), potentiating capacity appeared to be related to ketone C skeleton length. No differences were discernable between ketones at dosages of 5.0-10.0 mmol/kg. ...
[Brown EM, Hewitt WR; Toxicol Appl Pharm 76 (3): 437-53 (1984)]**PEER REVIEWED**

The influence of organo-antimony and organo-bismuth compounds was determined. Significant antagonistic and synergistic solvent-compound interactions occurred when the acetone concentrations exceeded 0.4% (vol/vol). At < 0.4%, only additive responses were observed. The fungitoxicity of the test compounds was determined by using acetone as the carrier solvent at a final concn of 0.1% (vol/vol). Trivalent organo-bismuth compounds were the most fungitoxic. ...
[Burrell RE et al; J Agric Food Chem 31 (1): 85-8 (1983)]**PEER REVIEWED**

The toxicity of 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, and aldrin to sugarcane leafhopper (Pyrilla perpusilla) depended on the solvent used; ie, the insecticides were more effective when dissolved in ethanol, than in methanol, followed by acetone.
[Gupta M, Ahmed I; Pesticides 18 (10): 50-1 (1984)]**PEER REVIEWED**

Acetone has the ability to induce the enzymatic activity of a specific constitutive cytochrome p450 isozyme that plays an important role in the metabolism of endogenous and exogenous substrates. A considerable amount of information is available on the physiological function and toxicologic consequence of p450 induction by acetone. Because acetone is metabolized by the same p450 isozyme that is induced following high-dose administration the auto-inductive increase in cytochrome p450 levels provides a mechanism for increasing the elimination of acetone when high body burdens develop. The pretreatment of laboratory animals with acetone can also potentiate or antagonize the acute effects of known systemic toxicants that are metabolized by the induced p450 isozyme. The potentiation observed following acetone administration has involved treatments with known nephrotoxins and hepatotoxins; the potentiating effects were generally quantitative in nature and involved an increase in the extent of damage without altering the types of tissues or organs affected. Minimally effective dose thresholds have been shown to exist for the induction of cytochrome p450 by acetone.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 187]**PEER REVIEWED**

Pharmacology:

Therapeutic Uses:

Anti-Infective Agents, Local; Pharmaceutic Aids; Solvents
[National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)]**QC REVIEWED**

PHARMACEUTICAL AID (SOLVENT)
[Budavari, S. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 1996., p. 12]**PEER REVIEWED**

Interactions:

Environmental Fate & Exposure:

Environmental Fate/Exposure Summary:

Acetone's production and use as a solvent for fats, oils, waxes, resins, rubbers, plastics, pharmaceuticals and rubber cements may result in its release to the environment through various waste streams. Its use as an extracting reagent and starting material or intermediate in the manufacture of chemical products will also lead to its release to the environment. Acetone occurs naturally as a metabolic byproduct of plants and animals and is released into the atmosphere by volcanoes and forest fires. Based on an experimental vapor pressure of 231 mm Hg at 25 deg C, acetone is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase acetone is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals with an estimated atmospheric half-life of 71 days. Acetone also undergoes photodecomposition by sunlight with an estimated half-life of about 80 days. Acetone is expected to have very high mobility in soils based upon an estimated Koc value of 1. Volatilization from dry soil surfaces is expected based upon the vapor pressure of this compound. Volatilization from moist soil surfaces is also expected based upon the measured Henry's Law constant of 1.87X10-5 atm-cu m/mol. This compound is expected to biodegrade under aerobic and anaerobic conditions. In water, acetone is not expected to adsorb to suspended solids or sediment based upon its estimated Koc value. Volatilization from water surfaces is expected to be an important environmental fate process given its estimated Henry's Law constant. Estimated half-lives for a model river and model lake are 38 and 333 hours, respectively. Experimentally determined volatilization half-lives in a shallow stream were measured in the range of 8-18 hours. Bioconcentration in aquatic organisms is considered low based upon an estimated BCF value of 1. Occupational exposure may be through inhalation and dermal contact with this compound at workplaces where acetone is produced or used. The general population may be exposed to acetone through the use of commercially available products containing this compound such as paints, adhesives, cosmetics, and rubber cements. Exposure will also arise from inhalation of ambient air, ingestion of drinking water, and food that contains acetone. (SRC)
**PEER REVIEWED**

Probable Routes of Human Exposure:

Body Burden:

Average Daily Intake:

AIR INTAKE (assume air concn of 0.05-20 ppb): 24-960 mg; WATER INTAKE - insufficient data; FOOD INTAKE - insufficient data. (SRC)
**PEER REVIEWED**

Natural Pollution Sources:

/Component/ of oxidation of humic substances.
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 112]**PEER REVIEWED**

Acetone has been produced by the fermentation of west coast kelp.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 15(81) 294]**PEER REVIEWED**

Acetone occurs naturally as a metabolic byproduct of plants and animals and is released into the atmosphere by volcanoes and forest fires(1).
[(1) Graedel TE et al; Atmospheric Chemical Compounds. NY,NY: Academic Press p. 263 (1986)]**PEER REVIEWED**

Artificial Pollution Sources:

Emissions from wood-burning fireplaces were measured. Acetone was one of the compounds identified.
[Lipari F et al; Environ Sci Technol 18 (5): 326-30 (1984)]**PEER REVIEWED**

Acetone's production and use as a solvent for fats, oils, waxes, resins, rubbers, plastics, pharmaceuticals and rubber cements(1,2) will result in its release to the environment through various waste streams(SRC). Its use as an extracting reagent and starting material or intermediate in the manufacture of chemical products(1) will also lead to its release to the environment(SRC).
[(1) Budvari S; Merck Index, 12th ed, Whitehouse Station,NJ: Merck & Co. p. 1773 (1996) (2) Stoye D; Ullmann's Encycl Indust Chem 5th ed Deerfield,FL: VCH Publ A24: 489 (1993)]**PEER REVIEWED**

Environmental Fate:

TERRESTRIAL FATE: Based on a recommended classification scheme(1), an estimated Koc value of 1(SRC), determined from an experimental log Kow of -0.24(2), and a recommended regression-derived equation(3), indicates that acetone is expected to have very high mobility in soil(SRC). Volatilization of acetone from moist soil surfaces(SRC) is expected given the measured Henry's Law constant of 1.87X10-5 atm-cu m/mole(4). Volatilization from dry soil surfaces is expected based upon the experimental vapor pressure of 232 mm Hg at 25 deg C(5,SRC). Acetone is expected to biodegrade under both aerobic and anaerobic conditions as indicated by numerous screening tests(6-9).
[(1) Swann RL et al; Res Rev 85: 23 (1983) (2) Hansch C et al; Exploring QSAR Hydrophobic, Electronic and Stearic Constants Washington,DC: Amer Chem Soc (1995) (3) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington,DC: Amer Chem Soc pp. 4-9 (1990) (4) Benkelberg HJ et al; J Atmos Chem 20: 17-34 (1995) (5) Alarie Y et al; Toxicol Appl Pharmacol 134: 92-99 (1995) (6) Suflita JM, Mormile MR; Environ Sci Technol 27: 976-78 (1993) (7) Waggy GT et al; Environ Toxicol Chem 13: 1277-80 (1994) (8) Schwartz LJ; Appl Biochem Biotechnol 28/29: 297-305 (1991)(9) Chou WL et al; Bioeng Symp 8: 391-414 (1979)]**PEER REVIEWED**

AQUATIC FATE: Based on a recommended classification scheme(1), an estimated Koc value of 1(SRC), determined from an experimental log Kow of -0.24(2), and a recommended regression-derived equation(3), indicates that acetone will not adsorb to suspended solids and sediment in water(SRC). Acetone is expected to volatilize from water surfaces(3,SRC) based on the measured Henry's Law constant of 1.87X10-5 atm-cu m/mole(4). Estimated half-lives for a model river and model lake are 38 and 333 hours, respectively(3,SRC). Experimentally determined volatilization half-lives in a shallow stream were measured in the range of 8-18 hours(5-7). Biodegradation of this compound is expected, but volatilization has been shown to be the primary removal process of acetone in water(5-7). According to a classification scheme(8), an estimated BCF value of 1(3,SRC), from an experimental log Kow(2,SRC), suggests that bioconcentration in aquatic organisms is low(SRC).
[(1) Swann RL et al; Res Rev 85: 23 (1983) (2)Hansch C et al; Exploring QSAR Hydrophobic, Electronic and Stearic Constants Washington,DC: Amer Chem Soc (1995) (3) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington,DC: Amer Chem Soc pp. 4-9 (1990) (4) Benkelbberg HJ et al; J Atmos Chem 20: 17-34 (1995) (5) Rathbun RE et al; J Hydrol 104: 181-209 (1988) (6) Rathbun RE et al; J Hydrol 123: 225-42 (1991) (7) Rathbun RE et al; Environ Pollut 79: 153-62 (1993) (8) Franke C et al; Chemosphere 29: 1501-14 (1994)]**PEER REVIEWED**

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), acetone, which has an experimental vapor pressure of 231 mm Hg at 25 deg C(2), will exist solely as a vapor in the ambient atmosphere. Vapor-phase acetone is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be about 71(3,SRC) days. The average rate constant for the photodissociation of acetone by natural sunlight in the lower troposphere was measured as 1X10-7 sec-1(4). This corresponds to a half-life of about 80 days(4).
[(1) Bidleman TF; Environ Sci Technol 22: 361-367 (1988) (2) Alarie Y et al; Toxicol Appl Pharmacol 134: 92-99 (1995) (3) Atkinson R; J Phys Chem Ref Data (1989) (4) Meyrahn H et al; J Atmos Chem 4: 227-91 (1986)]**PEER REVIEWED**

Environmental Biodegradation:

Biological oxygen demand: (Theoretical) 122%, 5 days
[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5., p. ]**PEER REVIEWED**

The percent theoretical BOD of acetone in water seeded with settled domestic sewage was 56%, 76%, 83% and 84%, over 5, 10, 15 and 20 day incubation periods(1). Percent theoretical BOD's of acetone in a raw sewage inocula were reported as 37% and 81% over 5 and 20 day incubation periods respectively(2), 54% over a 5 day incubation period(3), 71% over a 7 day incubation period(4), 55% and 72% over 5 day and 10 day incubation periods respectively(5) and 38% over a 5 day incubation period(6). Acetone was shown to be readily biodegradable under anaerobic conditions(7-9). The percent theoretical methane recovery of acetone in an anaerobic aquifer was 89% over a 3 week incubation period following a 25 day acclimation period(9).
[(1) Waggy GT et al; Environ Toxicol Chem 13: 1277-80 (1994) (2) Young RHF, et al; J Water Pollut Contr Fed 40: 354-68 (1968) (3) Bridie Al, et al; Water Res 13: 627-30 (1979) (4) Helfgott TB et al; An Index of Refactory Organics USEPA-600/2-77-174 (1977) (5) Lamb CB, Jenkins GF; Proc 8th Industrial Waste Conf, Purdue Univ p. 326-9 (1952) (6) Vaishnav DD et al; Chemosphere 16: 695-703 (1987) (7) Schwartz LJ; Appl Biochem Biotechnol 28/29: 297-305 (1991) (8) Chou WL et al; Bioeng Symp 8: 391-414 (1979) (9) Suflita JM, Mormile MR; Environ Sci Technol 27: 976-78 (1993)]**PEER REVIEWED**

Environmental Abiotic Degradation:

The rate constant for the vapor-phase reaction of acetone with photochemically-produced hydroxyl radicals has been measured as 2.26X10-13 cu cm/molecule-sec at 25 deg C(1). This corresponds to an atmospheric half-life of about 71 days at an atmospheric concn of 5.0X10+5 hydroxyl radicals per cu cm(1,SRC). The average rate constant for the photodissociation of acetone by natural sunlight in the lower troposphere was measured as 1X10-7 sec-1(2). This corresponds to a half-life of about 80 days(2). When water containing acetone is treated with chlorine for disinfection purposes, the acetone can react with the hypochlorite ion formed by the hydrolysis of chlorine leading to the production of trichloromethane(3). This reaction is strongly pH dependent and is expected to have a significant effect only at pH values of 6-7(3).
[(1) Atkinson R; J Phys Chem Ref Data (1989) (2) Meyrahn H et al; J Atmos Chem 4: 227-91 (1986) (3) Stevens AA et al; J Am Water Works Assoc 68: 615-20 (1976)]**PEER REVIEWED**

Environmental Bioconcentration:

An estimated BCF value of 1 was calculated for acetone(SRC), using an experimental log Kow of -0.24(1) and a recommended regression-derived equation(2). According to a classification scheme(3), this BCF value suggests that bioconcentration in aquatic organisms is low(SRC).
[(1) Hansch C et al; Exploring QSAR Hydrophobic, Electronic and Stearic Constants Washington,DC: Amer Chem Soc (1995)(2) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington,DC: Amer Chem Soc pp. 5-4, 5-10 (1990) (3) Franke C et al; Chemosphere 29: 1501-14 (1994)]**PEER REVIEWED**

Soil Adsorption/Mobility:

The Koc of acetone is estimated as approximately 1(SRC), using an experimental log Kow of -0.24(1) and a regression-derived equation(2,SRC). According to a recommended classification scheme(3), this estimated Koc value suggests that acetone is expected to have very high mobility in soil(SRC). Acetone showed no adsorption to montorillonite, kaolinite clay, or stream sediment(4,5).
[(1) Hansch C et al; Exploring QSAR Hydrophobic, Electronic and Stearic Constants Washington,DC: Amer Chem Soc (1995) (2) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington,DC: Amer Chem Soc pp. 4-9 (1990) (3) Swann RL et al; Res Rev 85: 23 (1983) (4) Rathbun RE et al; Chemosphere 11: 1097-114 (1982) (5) Wolfe TA et al; J Water Pollut Control Fed 58: 68-76 (1986)]**PEER REVIEWED**

Volatilization from Water/Soil:

The Henry's Law constant for acetone was measured as 1.87X10-5 atm-cu m/mole(SRC) at 25 deg C(1). This value indicates that acetone will volatilize from water surfaces(2,SRC). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec) is estimated as approximately 38 hours(2,SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec) is estimated as approximately 333 hours(2,SRC). Volatilization rate constants of a model stream (234 m long, water velocity 0.67 m/min) were measured in the range of 8.23X10-4 min-1 to 11.1X10-4 min-1(3). These rate constants correspond to volatilization half-lives of about 10-14 hours(3). Similar experiments in the same stream measured acetone volatilization rate constants in the range of 6.22X10-4 min-1 to 14.5X10-4 min-1(4,5). These rate constants correspond to volatilization half-lives of about 8-18 hours(4,5). Acetone is expected to volatilize from dry soil surfaces given its experimental vapor pressure(1,SRC).
[(1) Benkelbberg HJ et al; J Atmos Chem 20: 17-34 (1995) (2) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington,DC: Amer Chem Soc pp. 15-1 to 15-29 (1990) (3) Rathbun RE et al; J Hydrol 104: 181-209 (1988) (4) Rathbun RE et al; J Hydrol 123: 225-42 (1991) (5) Rathbun RE et al; Environ Pollut 79: 153-62 (1993)]**PEER REVIEWED**

Environmental Water Concentrations:

A concentration of 0.6 g/l of acetone was found in a sample of a one-year old leachate from a ... sanitary landfill.
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 114]**PEER REVIEWED**

DRINKING WATER: Acetone was identified, not quantified, in 10 out of 10 drinking water samples collected in the US(1). Acetone was identified, not quantified, in the drinking water of New Orleans, LA(2), Seattle, WA(3) and Tuscaloosa, AL(4). Acetone was detected in a drinking water well in New Jersey at a concn of 3,000 ppb(5). Six drinking water wells in the vicinity of a landfill contained 0.2 to 0.7 ppb of acetone(6). An unspecified concn of acetone leached from a section of high density polyethylene tubing supplying drinking water in Paris(7). Acetone was detected in the municipal wells in Waite Park, MN at concns between 74-3,300 ug/l(8).
[(1) Fielding M, Packman RF; J Inst Water Eng Sci 31: 353-75 (1977) (2) USEPA; New Orleans Area Water Supply Study. Draft Analytical Report by the Lower Mississippi River Facility, Slidell (1974) (3) Keith LH et al; Identification of Organic Pollut Water Ann Arbor, MI pp.329-73 (1976) (4) Bertsch W et al; J Chromatog 112: 701-18 (1975) (5) Rao PSC et al; Soil Crop Sci Soc Fl Proc 44: 1-8 (1985) (6) Dewalle FB, Chain ESK; J Am Water Works Assoc 73: 206-11 (1981) (7) Anselme C et al; Sci Total Environ 47: 371-84 (1985) (8) Minnesota Dept of Health; Health assessment for Waite Park ground water contamination site, Waite Park, Minnesota, Region 5. CERCLIS No MND981002249, PB90-107475 (1990)]**PEER REVIEWED**

GROUNDWATER: Acetone was detected in groundwater near a chemical manufacturing facility in Michigan at a maximum concn of 1,600 ug/l(1). Acetone was detected in groundwater in NJ at a concn of 3,000 ug/l(2). Acetone was detected at a concn of 620 ppb in the groundwater at the Lipari landfill, NJ(3). Acetone was detected at a concn of 11 ug/l in the on-site wells and 0.19 ug/l in the off-site groundwater near a manufacturing facility in MI(4). Acetone was identified, not quantified, in 12.4% of the groundwater samples at 1