Acetone Sources, Testing, Air Purification, and Health Information


Acetone is a common household toxic chemical that may reduce your indoor air quality after being released from such products as paint, nail polish, secondhand cigarette smoke, and many household chemical products.

This page will answer all your questions about Acetone, including what the common sources in your home are, the best way to test your air for Acetone, the best chemical air purifier to clean your air of most fumes, and health / exposure information.

The complete guide to acetone,  2-Propanone, Dimethyl keton structure with complete Acetone MSDS information







The Best Chemical Air Purifier for Acetone Removal, Odor Control, and Particle Filtration:
IQAir GC Multigas Air Purifier


The best air purifier for controlling Acetone fumes that may be continuously reintroduced into rooms from source materials such as nail polish and paint is one that has a high amount of special chemical gas filtering media such as Activated Carbon Potassium Permanganate filtration such as what is found in professional gas mask cartridges.


Since tiny gas molecules such as Acetone and Formaldehyde will pass right through HEPA filters, air cleaners for Acetone removal must contain advanced gas filters besides just efficient air purifier HEPA filters which catch the tiniest of particulates, but not gases.


With this in mind, the best of breed air purifier for Acetone removal from indoor air is IQAir GC Chemisorber Multigas or VOC. It is proven to be one of the most effective air cleaners on the market today and will likely clean your air of both solids and gases such as Acetone and Formaldehyde with the highest efficiency compared to other air purifiers.


IQ Air GC Chemisorber contains an impressive 12 pounds of the advanced Carbon-Potassium Permanganate filter media and has a very sophisticated gas filtration cartridge system plus highly efficient HEPA filtration for the removal of the tiniest of solid particulates as well.


IQAir GC Multigas Air Purifier: Powerfully Efficient Air Cleaning of Solids and Gases


  1. Chemical Vapors Such as from Acetone and Formaldehyde Are Destroyed Via Oxidation Inside Active Alumina Pellet Filter Media

  2. Micro-charged Filtration Technology With Charged Fiber Structure for Particle Elimination

  3. Ultra-small Nano-particle Filtration of Solid Indoor Air Pollutants Such as Viruses, Smoke, and Microorganisms

  4. Advanced Activated Carbon Cartridge Filtration for Adsorption of Odors and Volatile Organic Compounds

  5. Efficiently filters out mold spores, pet dander, wildfire / cooking / cigarette smoke, pollen, most odors, chemical molecules such as Benzene, and most general indoor air pollutants.

  6. The IQ Air GC MultiGas is a Top Rated Air Purifier for Multiple Chemical Sensitivity (MCS).











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


If you are concerned about Acetone odors or fumes, toxic black mold, toxins from cigarette smoke, or if you would like to know which of over 400 volatile organic compounds such as Acetone may be contaminating your indoor air, I recommend you easily and accurately test your indoor air using a high quality indoor air quality test kit


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.

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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.

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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.

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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.

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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.

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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.

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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.

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Glossary

Evaporate: To change into a vapor or a gas.

Ingesting: Taking food or drink into your body.

Long-term: Lasting one year or longer.

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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.

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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

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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:

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 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**

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:

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**

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:

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**

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 178 sites in the US(5) and in the groundwater of a waste disposal facility in SC(6). The average concn of acetone in groundwater sampled at 5 wood treatment facilities was 20 ug/l(7). Acetone was detected in the groundwater of a coal strip-mine in Ohio at concns of 1,300 mg/l and 2,700 ug/l(8).
[(1) USEPA; Superfund Record of Decision: Cordova Chemical Site, North Muskgon, MI. USEPA/ROD/RO5-89/111 (1989) (2) Jury WA et al; Ecosystem 99: 119-64 (1987) (3) USEPA; Superfund Record of Decision: Lipari Landfill Mantau Township, NJ. USEPA/ROD/RO2-88/074 (1988) (4) USEPA; Superfund Record of Decision: US Aviex, MI USEPA/ROD/RO5-88/073 (1988) (5) Plumb RHJR; Groundwater Monit Rev 7: 94-100 (1987) (6) ATSDR; Public health assessment for Carolawn, Fort Lawn, Chester County, South Carolina, Region 4, CERCLIS No. SCD980558316. Addendum. NTIS PB93-146249 (1993) (7) Rosenfeld JK, Plumb RHJR; Groundwater Monit Rev 11: 133-40 (1991) (8) USEPA; Superfund Record of Decision: Summit National Site, Deerfield OH. USEPA/ROD/R85-88/068 (1988)]**PEER REVIEWED**

SURFACE WATER: Five of nine sites in Lake Michigan contained 1-4 ppb acetone(1). In a survey of 14 heavily industrialized river basins in the USA (204 samples), 33 contained detectable amounts of acetone including 18 of 31 sites in the Chicago area and the Illinois River basin, 8 of 30 sites in the Delaware River basin, 1 of 45 sites in the Mississippi River basin, 3 of 27 sites in the Ohio River basin, and 3 of 15 west coast sites(2). Acetone was identified, not quantified, in the Black River in Tuscaloosa, AL(3), and the Cuyahoga River in the Lake Erie basin(4). Acetone was detected in the Potomac River at a concn of less than 40 ug/l(5).
[(1) Konasewich D et al; Great Lake Water Qual Board (1978) (2) Ewing BB et al; Monitoring to Detect Previously Unrecognized Pollutants in Surface Waters Appendix USEPA-560/6-77-015 (1977) (3) Berstch W et al; J Chromatog 112: 701-18 (1975) (4) Great Lakes Water Quality Board Ontario; An inventory of chemical subtances identified in the Great Lakes ecosystem volume 1 - Summary. Report to the Great Lakes Water Quality Board. Windsor Ontario, Canada p. 195 (1983) (5) Hall LWJR et al; Aquat Toxicol 10: 73-99 (1987)]**PEER REVIEWED**

SEAWATER: Samples of seawater and surface slicks taken from Biscayne Bay and the Florida Current contained 39.6 and 89.7 ppb of acetone, respectively(1). Grab samples of surface water from the Straits of Florida and the Eastern Mediterranean contained 20 and 28 ppb of acetone, respectively(2). Samples of ocean water taken at 1,200 m depths contained unspecified concns of acetone(2).
[(1) Seba DB, Corcoran EF; Pestic Monit J 3: 109-3 (1969) (2) Corwin JF; Bull Mar Sci 19: 504-9 (1969)]**PEER REVIEWED**

RAIN/SNOW: 50 ppb of acetone was detected in one of 6 samples tested at 5 cities in California(1). An unspecified concn of acetone was detected in rain in Japan(2). Acetone/acrolein was detected in rainfall in Los Angeles, CA at a concn of 0.05 ug/ml and in ice at Urban Fairbanks, AK at a concn of 0.21 umols/ml(3). Acetone was identified, not quantified, in rainfall in Germany(4). Acetone was detected in the clouds (460 ng/l) and rainfall (0.5 ng/l) at a state park in North Carolina(5).
[(1) Grosjean D, Wright B; Atmos Environ 17: 2093-6 (1983) (2) Kato T et al; Yokohama Kokuritsu Daigaku Kankyo Kagaku Kenkyu Senta Kiyo 6: 11-20 (1980) (3) Mazurek MA, Simoneit BRT; CRC Crit Rev Environ Control 16: 140 (1986) (4) Levson K et al; Chemosphere 21: 1037-61 (1990) (5) Aneja VP et al; J Air Waste Manag Assoc 43: 1239-44 (1993)]**PEER REVIEWED**

Effluent Concentrations:

Acetone was detected in the effluent of a chemical plant located in Sweden at a concn of 5.5 kg/cu m(1). Acetone was detected in the effluent of municipal landfill sites in North America at concns of 6,838 ppb and 32,500 ppb(2). Acetone was identified, not quantified in the emissions of new carpets(3), automobiles(4,5) and common household waste(6-9). Acetone was detected in the effluent from a solid waste composting plant at concns of 6,100 ug/cu m(tipping area), 7,800 ug/cu m(indoor air), 9,200 ug/cu m(fresh compost), 9,500 ug/cu m(middle age compost), 6,100 ug/cu m(old compost) and 2,300 ug/cu m(curing region)(10). Acetone was identified, not quantified, in the emissions of 314 out of 1,005 common household products(11). Acetone was detected in the effluent of a waste incinerator in Germany at a concn of 17.6 ug/cu m(12). Acetone was detected in the emissions of a photocopying machine at rates of less than 100 ug/hr to 2,200 ug/hr(13). Acetone was detected at a concn of 25 ug/cu m in the emissions of a composting facility in Virginia(14).
[(1) Brorson T et al; Environ Toxicol Chem 13: 543-52 (1994) (2) Brosseau, Heitz M; Atmos Environ 25A: 1473-77 (1994) (3) Hodgeson AT et al; J Air Waste Manage Assoc 43: 316-24 (1993) (4) Sawyer RF; Environ Health Perspect 101: 5-12 (1994) (5) Harley RA et al; Environ Sci Technol 26: 2395-2408 (1992) (6) Wilkins CK, Larsen K; J High Resol Chromatogr 18: 373-77 (1995) (7) Wilkins K, Larsen K; Chemosphere 31: 3225-36 (1995) (8) Wilkins K, Larsen K; Chemosphere 32: 2049-55 (1996) (9) Wilkins K; Chemosphere 29: 47-53 (1994) (10) Eitzer BD; Environ Sci Technol 29: 896-902 (1995) (11) Sack TM et al; Atmos Environ 26A: 1063-70 (1992) (12) Jay K, Stieglitz L; Chemosphere 30: 1249-60 (1995) (13) Leovic KW et al; J Air Waste Manage Assoc 46: 821-29 (1996) (14) Vandurme GP et al; Water Environ Res 64: 19-27 (1992)]**PEER REVIEWED**

Acetone was detected in the leachate of several municipal landfills at concns between 6-4,400 ug/l(1). Acetone was detected in the wastewater of a truck parts producing plant in Michigan at a concn of 44.5 ug/l(2). Acetone was detected in the effluent of an unauthorized hazardous waste disposal facility in New Jersey at a concn of 480 ug/l(3). Acetone was detected at a concn of 46.6 ppb in the leachate of a landfill in Delaware containing industrial and municipal waste(4). Acetone was detected at concns between 0.05-62 mg/l and 0.14-44 mg/l in the leachate of industrial landfills and municipal landfills in the US(5). Acetone was detected in the leachate of a landfill in Connecticut at a concn of 3,500 ug/l(6).
[(1) Christensen TH et al; Crit Rev Environ Sci Technol 24: 119-202 (1994) (2) USEPA; Superfund Record of Decision: Kysor Industrial, Cadillac, MI. USEPA/ROD/R05/-89/113 (1989) (3) USEPA; Superfund Record of Decision: Lang Property, Pemberton Township, NJ. USEPA/ROD/R05/-89/113 (1987) (4) Dewalle FB, Chian Esk; J Am Water Works Assoc 73: 206-11 (1981) (5) Brown KW, Donnelly KC; Haz Waste Haz Mater 5: 1-30 (1988) (6) Sawhney BL; pp 447-74 in Reactions and Movements of Organic Chemicals in Soils SSSA Special Pub No 22 (1989)]**PEER REVIEWED**

In gasoline exhaust: 2.3-14.0 ppm (partly propionaldehyde)
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 113]**PEER REVIEWED**

Sediment/Soil Concentrations:

Acetone was detected in the soil of a coal strip mine in Ohio at mean concns of 9,484 ug/kg (surface soil), 2,263 ug/kg (2-4 feet), 9644 ug/kg (4-6 feet), 5,272 ug/kg (6-8 feet)(1). Acetone was identified, not quantified, in the sediment and subsurface soil of a gravel mine in Tennessee(2). Acetone was detected at an average concn of 736 ug/kg in the soil of an unauthorized hazardous waste disposal facility in New Jersey(3).
[(1) USEPA; Superfund Record of Decision: Summit National Site, Deerfield OH. USEPA/ROD/R85-88/068 (1988) (2) USEPA; Superfund Record of Decision: Galloway Ponds Site, Galloway, TN. USEPA/ROD/R04-86/013 (1987) (3) USEPA; Superfund Record of Decision: Lang Property Pemberton Township, NJ USEPA/ROD/R02-86/031 (1987)]**PEER REVIEWED**

Atmospheric Concentrations:

SOURCE DOMINATED: Acetone was detected at 22 source dominated sites in the USA at a median concn of 0.350 ppb and a maximum concn of 53 ppb(1). Acetone was detected at concns between 2.3-3.3 ppb near the Texaco Refinery in Tulsa, OK(2).
[(1) Brodzinsky R, Singh HB; Volatile Organic Chemicals in the Atmos SRI International Contract 68-02-3452 (1982) (2) Arnts RR, Meeks SA; Atmos Environ 15: 1643-51 (1981)]**PEER REVIEWED**

URBAN/SUBURBAN: Acetone was detected at a concn of 1-8 ppb in Denver, CO(1). Acetone was detected at mean concns of 13.9 ppb in Boston, MA, 34.5 ppb(2) and 6.1 ppb(3) in Houston, TX and 12 ppb in Tucson, AZ(4). The average concn of acetone/formaldehyde at 4 southern California locations was 0.30 ppb(5). Acetone was detected at a concn of 2.07 ppb in Columbus, OH(6). The average concn of acetone at 5 sites in Stockholm was between 4.04-19.40 ppb(7).
[(1) Anderson LG et al; Isr J Chem 34: 341-53 (1994) (2) Kelly TJ et al; Environ Sci Technol 27: 1146-53 (1993) (3) Lagrone FS; Environ Sci Technol 25: 366-68 (1991) (4) Snider JR, Dawson GA; J Geophys Res, D: Atmos 90: 3797-805 (1985) (5) Grosjean E et al; Environ Sci Technol 30: 2687-2703 (1996) (6) Spicer CW et al; Atmos Environ 30: 3443-56 (1996) (7) Jonsson A et al; Environ Int 11: 383-92 (1985)]**PEER REVIEWED**

INDOOR AIR: Acetone was detected at an average concn of 39 ug/cu m at 14 homes and buildings in Italy(1). Acetone was detected in 2 buildings in Portland, OR at concns between 14.9-66.0 ug/cu m and 7.4-33.9 ug/cu m(2). Acetone was detected in a building in Switzerland at a concn of 7,763 ug/cu m(3). Acetone was detected at a concn of 10 and less than 1 ng/l in 2 elementary school classrooms in France(4).
[(1) Debortoli M et al; Environ Int 12: 343-50 (1986) (2) Hodgeson AT et al; J Air Waste Manage Assoc 41: 1461-68 (1991) (3) Rothweiler H et al; Atmos Environ 26A: 2219-25 (1992) (4) Cailleux A et al; Chromatographia 37: 57-59 (1993)]**PEER REVIEWED**

RURAL/REMOTE: Acetone was detected at an average concn of 14.72 ng/l in the air of a state park in North Carolina(1). Acetone was identified, not quantified, in the air of a German forest(2). Acetone was detected at concns between 0.39-3.26 ppb and 0.72-3.81 ppb in Egbert Ontario and Dorset Ontario respectively(3). Acetone was detected at a mean concn of 1,140 parts per trillion in Eastern Canada(4). Acetone was detected at a mean concn of 2.6 ppb at 2 rural sites in AZ(5) and 5.1 ppb in Rio Blanco county, CO(6). The acetone concn in air at Pt Barrow, AK (22 measurements) ranged from 0.3 to 2.9 ppb, with a mean concn of 1.21 ppb(7). Acetone was detected at a concn of 1.9 ppb in the Jones State Forest near Houston, TX(8).
[(1) Aneja VP et al; J Air Waste Manag Assoc 43: 1239-44 (1993) (2) Helmig D et al; Chemosphere 19: 1399-1412 (1989) (3) Shepson PB et al; Atmos Environ 25A: 2001-15 (1991) (4) Singh HB et al; J Geophys Res 99: 1805-19 (1994) (5) Snider JR, Dawson GA; J Geophys Res, D: Atmos 90: 3797-805 (1985) (6) Arnts RR, Meeks SA; Atmos Environ 15: 1643-51 (1981) (7) Cavanagh LA et al; Environ Sci Technol 3: 251-7 (1969) (8) Seila RL; Non-urban Hydrocarbon concns in Ambient Air North of Houston, TX USEPA USEPA-500/3-79-010 p.38 (1979)]**PEER REVIEWED**

Food Survey Values:

Acetone was identified, not quantified, in the volatiles of kiwi fruit(1,2), blue cheese(3), raw chicken(4), cured pork(5), chickpea seeds(6), nectarines(7), mutton, chicken and beef(8). Acetone has been identified, not quantified, as a volatile component of baked potatoes(9), roasted filberts(10), dried beans and legumes(11), and French cognac(12).
[(1) Bartley JP, Schwede AM; J Agric Food Chem 37: 1023-25 (1989) (2) Tatsuka K et al; J Food Sci 38: 2176-80 (1990) (3) Day EA, Anderson DF; J Agric Food Chem 13: 2-4 (1965) (4) Grey TC, Shrimpton DH; Brit Poultry Sci 8: 23-33 (1967) (5) Hinrichsen LL, Anderson HJ; J Agric Food Chem 42: 1537-42 (1994) (6) Rembold H et al; J Agric Food Chem 37: 659-62 (1989) (7) Takeoka GR et al; J Agric Food Chem 36: 553-60 (1988) (8) Shahidi F et al; CRC Crit Rev Food Sci Nature 24: 141-243 (1986) (9) Coleman EC et al; J Agric Food Chem 29: 42-8 (1981) (10) Kinlin TE et al; J Agric Food Chem 20: 1021 (1972) (11) Lovegren NV et al; J Agric Food Chem 27: 851-3 (1979) (12) TerHeide R et al; pp. 249-81 in Anal Foods Beverages, Chavalambous G, ed. NY,NY: Academic (1978)]**PEER REVIEWED**

Plant Concentrations:

Acetone is emitted from Bay Leaf Willows, European Firs and Evergreen Cyprus(1).
[(1) Singh HB, Zimmerman PB; Adv Environ Sci Technol 24: 177-235 (1992)]**PEER REVIEWED**

Milk Concentrations:

Acetone was identified, not quantified, in human milk from Bayonne, NJ, Jersey City, NJ, Pittsburgh, PA and Baton Rouge, LA(1). Acetone was identified, not quantified, in all 8 samples of mother's milk analyzed from 4 industrial urban areas in the USA(2). Acetone was identified, not quantified from milk samples in Australia(3).
[(1) Erickson MD et al; Acquisition and chemical analysis of mother's milk for selected toxic substances. USEPA-560/13-80-029. Washington DC: US EPA Off Pestic Toxic Subst (1980) (2) Pellizzari ED et al; Bull Environ Contam Toxicol 28: 322-8 (1982) (3) Urbach G; J Chromatogr 404: 163-74 (1987)]**PEER REVIEWED**

Other Environmental Concentrations:

Cigarette smoke - 1,100 ppm
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 113]**PEER REVIEWED**

Acetone was detected in cigarette smoke at a concn of 1,620 ug per cigarette(1).
[(1) Otson R, Fellin P; pp. 335-421 in Gas Pollut: Charact Cycl, Nriagu JO ed. NY,NY: John Wiley & Sons (1992)]**PEER REVIEWED**

Environmental Standards & Regulations:

CERCLA Reportable Quantities:

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 5000 lb or 2270 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).
[40 CFR 302.4 (7/1/96)]**PEER REVIEWED**

RCRA Requirements:

F003; When acetone is a spent solvent, it is classified as a hazardous waste from a nonspecific source (F003), as stated in 40 CFR 261.31, and must be managed according to State and/or Federal hazardous waste regulations.
[40 CFR 261.31 (7/1/96)]**PEER REVIEWED**

U002; As stipulated in 40 CFR 261.33, when acetone, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).
[40 CFR 261.33 (7/1/96)]**PEER REVIEWED**

Atmospheric Standards:

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). These standards implement Section 111 of the Clean Air Act and are based on the Administrator's determination that emissions from the SOCMI cause, or contribute significantly to, air pollution which may reasonably be anticipated to endanger public health or welfare. The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Acetone is produced, as an intermediate or final product, by process units covered under this subpart. These standards of performance become effective upon promulgation but apply to affected facilities for which construction or modification commenced after January 5, 1981.
[40 CFR 60.489 (7/1/86)]**PEER REVIEWED**

State Drinking Water Guidelines:

(FL) FLORIDA 700 ug/l
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**QC REVIEWED**

(MA) MASSACHUSETTS 3000 ug/l
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**QC REVIEWED**

(MN) MINNESOTA 700 ug/l
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**QC REVIEWED**

(NH) NEW HAMPSHIRE 700 ug/l
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**QC REVIEWED**

(WI) WISCONSIN 1000 ug/l
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**QC REVIEWED**

(ME) MAINE 700 ug/l
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines (11/93), p. ]**QC REVIEWED**

Allowable Tolerances:

Residues of acetone are exempted from the requirement of a tolerance when used as a solvent, cosolvent in accordance with good agricultural practices as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops or to raw agricultural commodities after harvest.
[40 CFR 180.1001(c) (7/1/96)]**PEER REVIEWED**

Chemical/Physical Properties:

Molecular Formula:

C3-H6-O
**PEER REVIEWED**

Molecular Weight:

58.08
[Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 76th ed. Boca Raton, FL: CRC Press Inc., 1995-1996., p. 3-284]**PEER REVIEWED**

Color/Form:

Colorless liquid
[Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993, p. 9]**PEER REVIEWED**

Odor:

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

Taste:

PUNGENT, SWEETISH
[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**

Boiling Point:

56.0 DEG C @ 760 MM HG
[Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 76th ed. Boca Raton, FL: CRC Press Inc., 1995-1996., p. 3-284]**PEER REVIEWED**

Melting Point:

-94.8 DEG C
[Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 76th ed. Boca Raton, FL: CRC Press Inc., 1995-1996., p. 3-284]**PEER REVIEWED**

Critical Temperature & Pressure:

Critical temperature: 455 deg F= 235 deg C= 508 deg K; critical pressure: 46.4 atm
[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**

Density/Specific Gravity:

0.7899 AT 20 DEG C/4 DEG C
[Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 76th ed. Boca Raton, FL: CRC Press Inc., 1995-1996., p. 3-284]**PEER REVIEWED**

Dissociation Constants:

pKa = 20
[Serjeant EP, Dempsey B; Ionisation constants of organic acids in aqueous solution. IUPAC Chem Data Ser No.23. NY,NY: Pergamon pp.989 (1979)]**PEER REVIEWED**

Heat of Combustion:

Liquid: -1787 kJ/mol (-427 kcal/mol)
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 178]**PEER REVIEWED**

Heat of Vaporization:

220 Btu/lb= 122 cal/g
[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**

Octanol/Water Partition Coefficient:

Log Kow= -0.24
[Hansch, C., Leo, A., D. Hoekman. Exploring QSAR - Hydrophobic, Electronic, and Steric Constants. Washington, DC: American Chemical Society., 1995., p. 6]**PEER REVIEWED**

Solubilities:

SOLUBLE IN BENZENE
[Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 76th ed. Boca Raton, FL: CRC Press Inc., 1995-1996., p. 3-284]**PEER REVIEWED**

MISCIBLE WITH WATER, ALCOHOL, DIMETHYLFORMAMIDE, ETHER
[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**

MISCIBLE WITH CHLOROFORM, MOST OILS
[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**

Spectral Properties:

INDEX OF REFRACTION: 1.3588 AT 20 DEG C/D
[Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 76th ed. Boca Raton, FL: CRC Press Inc., 1995-1996., p. 3-284]**PEER REVIEWED**

IR: 77 (Sadtler Research Laboratories IR Grating Collection)
[Weast, R.C. and M.J. Astle. CRC Handbook of Data on Organic Compounds. Volumes I and II. Boca Raton, FL: CRC Press Inc. 1985., p. V2 158]**PEER REVIEWED**

UV: 89 (Sadtler Research Laboratories Spectral Collection)
[Weast, R.C. and M.J. Astle. CRC Handbook of Data on Organic Compounds. Volumes I and II. Boca Raton, FL: CRC Press Inc. 1985., p. V2 158]**PEER REVIEWED**

NMR: 9288 (Sadtler Research Laboratories Spectral Collection)
[Weast, R.C. and M.J. Astle. CRC Handbook of Data on Organic Compounds. Volumes I and II. Boca Raton, FL: CRC Press Inc. 1985., p. V2 158]**PEER REVIEWED**

MASS: 30 (Atlas of Mass Spectral Data, John Wiley & Sons, New York)
[Weast, R.C. and M.J. Astle. CRC Handbook of Data on Organic Compounds. Volumes I and II. Boca Raton, FL: CRC Press Inc. 1985., p. V2 158]**PEER REVIEWED**

Intense mass spectral peaks: 43 m/z, 58 m/z
[Pfleger, K., H. Maurer and A. Weber. Mass Spectral and GC Data of Drugs, Poisons and their Metabolites. Parts I and II. Mass Spectra Indexes. Weinheim, Federal Republic of Germany. 1985., p. 19]**PEER REVIEWED**

Surface Tension:

0 deg C: 26.2 mN/m; 20 deg C: 23.7 mN/m; 40 deg C: 21.2 mN/m
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 177]**PEER REVIEWED**

Vapor Pressure:

231 mm Hg at 25 deg C
[Boublik T et al; The vapor pressures of pure substances: selected values of the temperature dependence of the vapour pressures of some pure substances in the normal and low pressure region. Vol. 17. Amsterdam, Netherlands: Elsevier Sci. Publ (1984)]**PEER REVIEWED**

Viscosity:

0.32 cP at 20 deg C
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 177]**PEER REVIEWED**

Other Chemical/Physical Properties:

Saturation concentration: 553 g/cu m
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 112]**PEER REVIEWED**

Specific heat of liquid: 2.6 J/g (0.62 cal/g) at 20 deg C; specific heat of vapor: 92.1 J/(mol x k) (22.0 cal/mol x k) at 102 deg C; electric conductivity: 5.5x10-8 sec/cm at 25 deg C; heat of formation at 25 deg C: gas -216.5 kJ/mol, liquid: -248 kJ/mol.
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 177-178]**PEER REVIEWED**

Heat of fusion: 23.42 cal/g
[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**

Partition coefficients at 37 deg C for acetone into blood = 245; into oil = 86.
[Sato A, Nakajima T; Scand J Work Environ Health 13: 81-93 (1987)]**PEER REVIEWED**

Henry's Law constant = 1.87X10-5 atm-cu m/mole at 25 deg C
[Benkelbberg HJ et al; J Atmos Chem 20: 17-34 (1995)]**PEER REVIEWED**

Chemical Safety & Handling:

DOT Emergency Guidelines:

Fire or explosion: HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion hazard indoors, outdoors or in sewers. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water.
[U.S. Department of Transportation. 2000 Emergency Response Guidebook. RSPA P 5800.8 Edition. Washington, D.C: U.S. Government Printing Office, 2000,p. G-127]**QC REVIEWED**

Health: Inhalation or contact with material may irritate or burn skin and eyes. Fire may produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control may cause pollution.
[U.S. Department of Transportation. 2000 Emergency Response Guidebook. RSPA P 5800.8 Edition. Washington, D.C: U.S. Government Printing Office, 2000,p. G-127]**QC REVIEWED**

Public safety: CALL Emergency Response Telephone Number. ... Isolate spill or leak area immediately for at least 25 to 50 meters (80 to 160 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering.
[U.S. Department of Transportation. 2000 Emergency Response Guidebook. RSPA P 5800.8 Edition. Washington, D.C: U.S. Government Printing Office, 2000,p. G-127]**QC REVIEWED**

Protective clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Structural firefighters' protective clothing will only provide limited protection.
[U.S. Department of Transportation. 2000 Emergency Response Guidebook. RSPA P 5800.8 Edition. Washington, D.C: U.S. Government Printing Office, 2000,p. G-127]**QC REVIEWED**

Evacuation: ... Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
[U.S. Department of Transportation. 2000 Emergency Response Guidebook. RSPA P 5800.8 Edition. Washington, D.C: U.S. Government Printing Office, 2000,p. G-127]**QC REVIEWED**

Fire: CAUTION: All these products have a very low flash point: Use of water spray when fighting fire may be inefficient. Small fires: Dry chemical, CO2, water spray or alcohol-resistant foam. Large fires: Water spray, fog or alcohol-resistant foam. Use water spray or fog; do not use straight streams. Move containers from fire area if you can do it without risk. Fire involving Tanks or Car/Trailer loads: Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
[U.S. Department of Transportation. 2000 Emergency Response Guidebook. RSPA P 5800.8 Edition. Washington, D.C: U.S. Government Printing Office, 2000,p. G-127]**QC REVIEWED**

Spill or leak: ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. A vapor suppressing foam may be used to reduce vapors. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. Use clean non-sparking tools to collect absorbed material. Large spills: Dike far ahead of liquid spill for later disposal. Water spray may reduce vapor; but may not prevent ignition in closed spaces.
[U.S. Department of Transportation. 2000 Emergency Response Guidebook. RSPA P 5800.8 Edition. Washington, D.C: U.S. Government Printing Office, 2000,p. G-127]**QC REVIEWED**

First aid: Move victim to fresh air. Call 911 or emergency medical service. Apply artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Wash skin with soap and water. Keep victim warm and quiet. Ensure that medical personnel are aware of the material(s) involved, and take precautions to protect themselves.
[U.S. Department of Transportation. 2000 Emergency Response Guidebook. RSPA P 5800.8 Edition. Washington, D.C: U.S. Government Printing Office, 2000,p. G-127]**QC REVIEWED**

Odor Threshold:

WATER: 20 MG/L (OR 20 PPM, W/V); AIR: 13 UL/L (OR 13 PPM, V/V).
[AMOORE JE, HAUTALA E; J APPL TOXICOL 3 (6): 272-90 (1983)]**PEER REVIEWED**

Odor low: 47.5 mg/cu m; Odor high: 1613.9 mg/cu m
[Ruth JH; Am Ind Hyg Assoc J 47: A-142-51 (1986)]**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**

Fire Potential:

Highly flammable liquid. Dangerous disaster hazard due to fire and explosion hazard ...
[Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 19]**PEER REVIEWED**

NFPA Hazard Classification:

Health: 1. 1= Materials that, on exposure, would cause irritation, but only minor residual injury, including those requiring the use of an approved air-purifying respirator. These materials are only slightly hazardous to health and only breathing protection is needed.
[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National Fire Protection Association, 1997., p. 325-10]**QC REVIEWED**

Flammability: 3. 3= This degree includes Class IB and IC flammable liquids and materials that can be easily ignited under almost all normal temperature conditions. Water may be ineffective in controlling or extinguishing fires in such materials.
[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National Fire Protection Association, 1997., p. 325-10]**QC REVIEWED**

Reactivity: 0. 0= This degree includes materials that are normally stable, even under fire exposure conditions, and that do not react with water. Normal fire fighting procedures may be used.
[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National Fire Protection Association, 1997., p. 325-10]**QC REVIEWED**

Flammable Limits:

LOWER LIMIT 2.15%; UPPER LIMIT 13.0%
[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. 4723]**PEER REVIEWED**

Flash Point:

-20 DEG C (-4 DEG F) (CLOSED CUP)
[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National Fire Protection Association, 1997., p. 325-10]**QC REVIEWED**

0 deg F (closed cup)
[Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 18]**PEER REVIEWED**

Autoignition Temperature:

869 DEG F
[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**

Fire Fighting Procedures:

Evacuation: If fire becomes uncontrollable or container is exposed to direct flame - consider evacuation of one-third mile radius.
[Association of American Railroads. Emergency Handling of Hazardous Materials in Surface Transportation. Washington, DC: Association of American Railroads, Bureau of Explosives, 1994., p. 4]**PEER REVIEWED**

If material is on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Solid streams of water may be ineffective. Cool all affected containers with flooding quantities of water and apply water from as far a distance as possible. Use alcohol foam, carbon dioxide, or dry chemical.
[Association of American Railroads. Emergency Handling of Hazardous Materials in Surface Transportation. Washington, DC: Association of American Railroads, Bureau of Explosives, 1994., p. 4]**PEER REVIEWED**

Flammable. Flashback along vapor trail may occur. Vapor may explode if ignited in an enclosed area. Extinguish with dry chemical, alcohol foam, or carbon dioxide. Water may be ineffective on fire. Cool exposed containers with water.
[Prager, J.C. Environmental Contaminant Reference Databook Volume 1. New York, NY: Van Nostrand Reinhold, 1995., p. 80]**PEER REVIEWED**

Firefighting Hazards:

FLASHBACK ALONG VAPOR TRAIL MAY OCCUR.
[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**

Explosive Limits & Potential:

Highly flammable liquid. Dangerous disaster hazard due to fire and explosion hazard ...
[Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 19]**PEER REVIEWED**

UPPER 12.8%, LOWER 2.6%.
[Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 18]**PEER REVIEWED**

VAPOR MAY EXPLODE IF IGNITED IN AN ENCLOSED AREA.
[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**

Hazardous Reactivities & Incompatibilities:

MIXTURE OF ACETONE & CHLOROFORM IN A RESIDUE BOTTLE EXPLODED. SINCE ADDITION OF CHLOROFORM TO ACETONE IN PRESENCE OF A BASE WILL RESULT IN A HIGHLY EXOTHERMIC REACTION, IT IS THOUGHT THAT A BASE MAY HAVE BEEN IN THE BOTTLE.
[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National Fire Protection Association, 1997., p. 491-8]**QC REVIEWED**

ACETONE MAY FORM EXPLOSIVE MIXTURES WITH CHROMIC ANHYDRIDE, CHROMYL CHLORIDE, HEXACHLOROMELAMINE, HYDROGEN PEROXIDE, NITRIC ACID, ACETIC ACID, NITRIC ACID & SULFURIC ACID, NITROSYL CHLORIDE, NITROSYL PERCHLORATE, NITRYL PERCHLORATE, PERMONOSULFURIC ACID, POTASSIUM TERT-BUTOXIDE, THIODIGLYCOL & HYDROGEN PEROXIDE.
[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National Fire Protection Association, 1997., p. 491-8]**QC REVIEWED**

AN EXPLOSION OCCURRED DURING AN ATTEMPT TO PREPARE BROMOFORM FROM ACETONE BY THE HALOFORM REACTION. ACETONE IGNITED WHEN IT WAS ACCIDENTALLY SPLASHED INTO A SULFURIC ACID-DICHROMATE SOLUTION.
[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National Fire Protection Association, 1997., p. 491-8]**QC REVIEWED**

Oxidizers, acids.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 2]**QC REVIEWED**

Potentially explosive reaction with nitric acid + sulfuric acid, bromine trifluoride, nitrosyl chloride + platinum, nitrosyl perchlorate, chromyl chloride, thiotrithiazyl perchlorate, and (2,4,6-trichloro-1,3,5-triazine + water). Reacts to form explosive peroxide products with 2-methyl-1,3-butadiene, hydrogen peroxide, and peroxomonosulfuric acid. Ignites on contact with activated carbon, chromium trioxide, dioxygen difluoride + carbon dioxide, and potassium-t-butoxide. Reacts violently with bromoform, chloroform + alkalies, bromine, and sulfur dichloride. Incompatible with CrO, (nitric + acetic acid), NOCl, nitryl perchlorate, permonosulfuric acid, NaOBr, (sulfuric acid + potassium dichromate), (thio-diglycol + hydrogen peroxide), trichloromelamine, air, HNO3, chloroform, and H2SO4.
[Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 19]**PEER REVIEWED**

Prior History of Accidents:

The wreck of the MV Ariadne, a Panamanian flag container ship, is examined as a case study of a hazardous substance emergency response in a third world country. /The ship/, carrying a cargo of heavy fuel oil, tetraethyl lead, xylene, toluene, methyl isobutyl ketone, butyl acetate, ethyl acetate, and acetone was grounded while departing the harbor of Mogadishu, Somalia. The Somalian government requested a team of technical advisors to help respond appropriately to the emergency. The major issues addressed by the advisory team were the need for additional salvage equipment and expertise, the danger of toxic fumes from the fire and explosions aboard the ship, the presence and possible release of tetraethyl lead, possible port blockage by the wreck, recovery of the chemical drums, and the extent of environmental damage caused by the release of oil, pesticides, and tetraethyl lead into the harbor. ...
[Heare SF et al; 1986 Hazard Matl Spill Conf p.12-18 (1986)]**PEER REVIEWED**

Immediately Dangerous to Life or Health:

2500 ppm (IDLH based on a 10% of the lower explosive limit for safety considerations even though the relevant toxicological data indicated that irreversible health effects or impairment of escape existed only at higher concentrations.)
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 2]**QC REVIEWED**

Protective Equipment & Clothing:

Protective equipment made from natural rubber, viton, neoprene, polyvinyl alcohol, neoprene/natural rubber, or nitrile have breakthrough times less (usually significantly less) than one hour reported by (normally) two or more testers.
[ACGIH; Guidelines Select of Chem Protect Clothing Volume #1 Field Guide p.68 (1983)]**PEER REVIEWED**

Protective clothing made from polyethylene or chlorinated polyethylene; the data suggests breakthrough times of approximately an hour or more.
[ACGIH; Guidelines Select of Chem Protect Clothing Volume #1 Field Guide p.68 (1983)]**PEER REVIEWED**

No data is available regarding break-through times for clothing made from styrene-butadiene rubber, nitrile/polyvinyl chloride, or polyurethane.
[ACGIH; Guidelines Select of Chem Protect Clothing Volume #1 Field Guide p.68 (1983)]**PEER REVIEWED**

Wear appropriate eye protection to prevent eye contact.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 3]**QC REVIEWED**

Wear appropriate personal protective clothing to prevent skin contact.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 3]**QC REVIEWED**

Recommendations for respirator selection. Max concn for use: 2500 ppm. Respirator Class(es): Any chemical cartridge respirator with organic vapor cartridge(s). May require eye protection. Any powered, air-purifying respirator with organic vapor cartridge(s). May require eye protection. Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted organic vapor canister. Any supplied-air respirator. May require eye protection. Any self-contained breathing apparatus with a full facepiece.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 3]**QC REVIEWED**

Recommendations for respirator selection. Condition: Emergency or planned entry into unknown concn or IDLH conditions: Respirator Class(es): Any self-contained breathing apparatus that has a full facepiece and is operated in a pressure-demand or other positive pressure mode. Any supplied-air respirator that has a full facepiece and is operated in pressure-demand or other positive pressure mode in combination with an auxiliary self-contained breathing apparatus operated in pressure-demand or other positive pressure mode.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 3]**QC REVIEWED**

Recommendations for respirator selection. Condition: Escape from suddenly occurring respiratory hazards: Respirator Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted organic vapor canister. Any appropriate escape-type, self-contained breathing apparatus.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 3]**QC REVIEWED**

Preventive Measures:

Personnel protection: Avoid breathing vapors. Keep upwind. Do not handle broken packages without protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water.
[Association of American Railroads. Emergency Handling of Hazardous Materials in Surface Transportation. Washington, DC: Association of American Railroads, Bureau of Explosives, 1994., p. 4]**PEER REVIEWED**

Direct contact with the skin should be avoided. Acetone should never be used as a cleaning agent for the skin.
[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**

A major concern in the painting studio is solvents, /including acetone/. ... Precautions include ... use of dilution and local exhaust ventilation, control of storage areas, disposal of solvent soaked rags in covered containers, minimizing skin exposure and the use of respirators and other personal protective equipment. The control of fire hazards is also important, since many of the solvents are highly flammable.
[Hart C; J Environ Health 49 (5): 282-86 (1987)]**PEER REVIEWED**

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants.
**PEER REVIEWED**

If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. Attempt to stop leak if without undue personnel hazard. Use water spray to disperse vapors and dilute standing pools of liquid.
[Association of American Railroads. Emergency Handling of Hazardous Materials in Surface Transportation. Washington, DC: Association of American Railroads, Bureau of Explosives, 1994., p. 4]**PEER REVIEWED**

Contact lenses should not be worn when working with this chemical.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 3]**QC REVIEWED**

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.
**PEER REVIEWED**

The worker should immediately wash the skin when it becomes contaminated.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 3]**QC REVIEWED**

Work clothing that becomes wet should be immediately removed due to its flammability hazard.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 3]**QC REVIEWED**

Keep away from plastic eyeglass frames, jewelry, pens and pencils, rayon stockings and other rayon garments.
[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**

Shipment Methods and Regulations:

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
[49 CFR 171.2 (7/1/96)]**PEER REVIEWED**

The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.
[IATA. Dangerous Goods Regulations. 38th ed. Montreal, Canada and Geneva, Switzerland: International Air Transport Association, Dangerous Goods Board, January, 1997., p. 89]**PEER REVIEWED**

The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.
[IMDG; International Maritime Dangerous Goods Code; International Maritime Organization p.3020 (1988)]**PEER REVIEWED**

Storage Conditions:

Store acetone in closed containers, and keep away from heat, sparks, and flames.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 1(78) 187]**PEER REVIEWED**

Acetone is stored in steel tanks
[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**

Disposal Methods:

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number F003, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.
[40 CFR 240-280, 300-306, 702-799 (7/1/96)]**PEER REVIEWED**

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U002, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.
[40 CFR 240-280, 300-306, 702-799 (7/1/96)]**PEER REVIEWED**

Incineration: Spray into a furnace. Incineration will become easier by mixing with a more flammable solvent.
[United Nations. Treatment and Disposal Methods for Waste Chemicals (IRPTC File). Data Profile Series No. 5. Geneva, Switzerland: United Nations Environmental Programme, Dec. 1985., p. 75]**PEER REVIEWED**

Acetone is a good candidate for fluidized bed incineration with a temperature of 450-980 deg C and with residence times for liquids and gases: seconds.
[USEPA; Engineering Handbook for Hazardous Waste Incineration p.3-10 (1981) EPA 68-03-3025]**PEER REVIEWED**

Acetone is a good candidate for rotary kiln incineration with a temperature of 820-1,600 deg C and with residence time for liquids and gases: seconds.
[USEPA; Engineering Handbook for Hazardous Waste Incineration p.3-10 (1981) EPA 68-03-3025]**PEER REVIEWED**

Acetone is a good candidate for liquid injection incineration with a temperature of 650-1,600 deg C with a residence time of 0.1-2 seconds.
[USEPA; Engineering Handbook for Hazardous Waste Incineration p.3-10 (1981) EPA 68-03-3025]**PEER REVIEWED**

This compound should be susceptible to removal from waste water by air stripping.
[USEPA/ORD; Innovative and Alternative Technology Assessment Manual pp.3-5, 3-11,12 (1980) EPA 430/9-78-009]**PEER REVIEWED**

Small amounts can be burned after pouring on dry sand. Larger quantities can be atomized into an approved type combustion chamber.
[Prager, J.C. Environmental Contaminant Reference Databook Volume 1. New York, NY: Van Nostrand Reinhold, 1995., p. 78]**PEER REVIEWED**

Occupational Exposure Standards:

OSHA Standards:

Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 1000 ppm (2400 mg/cu m).
[29 CFR 1910.1000 (7/1/98)]**QC REVIEWED**

Vacated 1989 OSHA PEL TWA 750 ppm (1800 mg/cu m); STEL 1000 ppm (2400 mg/cu m) is still enforced in some states.
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 359]**QC REVIEWED**

Threshold Limit Values:

8 hr Time Weighted Avg (TWA): 500 ppm; 15 min Short Term Exposure Limit (STEL): 750 ppm.
[ 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**

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**

Biological Exposure Index (BEI): Determinant: acetone in urine; Sampling Time: end of shift; BEI: 50 mg/l. The determinant is nonspecific, since it is also observed after exposure to other chemicals.
[ 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. 90]**QC REVIEWED**

NIOSH Recommendations:

Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 250 ppm (590 mg/cu m).
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 2]**QC REVIEWED**

Immediately Dangerous to Life or Health:

2500 ppm (IDLH based on a 10% of the lower explosive limit for safety considerations even though the relevant toxicological data indicated that irreversible health effects or impairment of escape existed only at higher concentrations.)
[NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997., p. 2]**QC REVIEWED**

Other Occupational Permissible Levels:

Exposure limits: France, TWA limits - 1,800 mg/cu m (1983).
[Institut National de Research et de S'ecruit'e; Acetone 1-4 (1987)]**PEER REVIEWED**

Manufacturing/Use Information:

Major Uses:

SOLVENT FOR FATS, OILS, WAXES, RESINS, RUBBER, PLASTICS, LACQUERS, VARNISHES, RUBBER CEMENTS
[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**

MFR MESITYL OXIDE, ACETIC ACID, DIACETONE ALCOHOL, CHLOROFORM, IODOFORM, BROMOFORM
[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**

MFR EXPLOSIVES, AIRPLANE DOPES, RAYON, ISOPRENE, PHOTOGRAPHIC FILMS, STORING ACETYLENE GAS
[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**

EXTRACTION OF VARIOUS PRINCIPLES FROM ANIMAL AND PLANT SUBSTANCES; IN PAINT & VARNISH REMOVERS; PURIFYING PARAFFIN
[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**

HARDENING AND DEHYDRATING TISSUES
[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**

NAIL POLISH REMOVER
[Haddad, L.M., Clinical Management of Poisoning and Drug Overdose. 2nd ed. Philadelphia, PA: W.B. Saunders Co., 1990., p. 701]**PEER REVIEWED**

CHEM INT FOR METHYL METHACRYLATE, METHACRYLIC ACID & HIGHER METHACRYLATES, METHYL ISOBUTYL KETONE, METHYL ISOBUTYL CARBINOL, BISPHENOL A, ISOPHORONE; SPINNING SOLVENT IN MFR OF CELLULOSE ACETATE; SOLVENT FOR ADHESIVES & PRINTING INKS, ACETYLENE
**PEER REVIEWED**

Manufacture of smokeless powder.
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 112]**PEER REVIEWED**

Acetone is used for the production of modacrylic fibers, for either wet spinning or dry spinning.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 1(78) 380]**PEER REVIEWED**

Acetone is used as a raw material in the manufacturing of acetic anhyride.
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 145]**PEER REVIEWED**

Preparation of vitamin intermediates.
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 192]**PEER REVIEWED**

Acetone is used as a brine for low temperature heat transfer in indirect refrigeration.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 20(82) 91]**PEER REVIEWED**

The evaporation rate of acetone makes it quite useful for cleaning and drying precision parts.
[American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 6]**PEER REVIEWED**

Manufacturers:

Allied-Signal, Inc, Hq, Columbia Road and Park Avenue, Morristown, NJ 07960, (201) 455-2000; Engineered Materials Sector; Production site: Philadelphia, PA 19137
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

Eastman Chemical Company, Hq, 343 State Street, Rochester, NY 14650, (716) 724-4000; Eastman Chemical Products, Inc; Tennessee Eastman Company; Production site: Kingsport, TN 37662
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

General Electric Company, Hq, 3135 Easton Turnpike, Fairfield, CT 06431, (203) 373-2211; GE Plastics, One Plastics Avenue, Pittsfield, MA 01201; Production site: Mount Vernon, IN 47620
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

Georgia Gulf Corporation, Hq, 400 Perimeter Center Terrace, Suite 595, Atlanta, GA 30348, (404) 395-4500; Production site: Bound Brook, NJ 08805
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

The Goodyear Tire & Rubber Company, Hq, 1144 East Market Street, Akron, OH 44316, (216) 796-2121; General Products Division; Production site: Bayport, TX 77058
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

JLM Chemicals Company, 3350 West 131st Street, P.O. Box 598, Blue Island, IL 60406. (708)388-9373
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

Shell Oil Company, Hq, One Shell Plaza, Houston, TX 77252-2463; Shell Chemical Company, division (address same as Hq); Production sites: Deer Park, TX 77536 (Houston Plant); Wood River, IL 62095
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

Texaco, Inc, Hq, 2000 Westchester Avenue, White Plains, NY 10650, (914) 253-4000; Subsidiary: Texaco Chemical Company, 4800 Fournace Place, Bellaire, TX 77401, (713) 666-8000; Production site: El Dorado, KS 67042
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

Union Carbide Corporation, Hq, Old Ridgebury Road, Danbury, CT 06817, (203) 794-2000; Chemicals and Plastics Business Group; Solvents and Coatings Materials Division; Production site: Institute, WV 25103
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

Aristech Chemical Corp, Hq, 600 Grant St, Pittsburgh, PA 15219, (412) 433-2747; Production site: Haverhill, OH 45638
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

Dow Chemical USA, Hq, 2020 Dow Center, Midland, MI 48674, (517) 636-1000; Production site: Oyster Creek, TX 77541
[SRI. 1996 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1996., p. 427]**PEER REVIEWED**

Methods of Manufacturing:

(1) BY DESTRUCTIVE DISTILLATION OF WOOD. (2) BY DISTILLATION OF CALCIUM ACETATE. (3) BY FERMENTATION OF CORN PRODUCTS BY SELECTED BACTERIA. (4) BY CATALYTIC OXIDATION OF ISOPROPYL ALCOHOL, CUMENE, OR NATURAL GAS.
[Browning, E. Toxicity and Metabolism of Industrial Solvents. New York: American Elsevier, 1965., p. 413]**PEER REVIEWED**

MOST USA/ACETONE/PRODUCTION BASED ON CUMENE PROCESS /IN WHICH/ BENZENE AND PROPYLENE ARE REACTED TO FORM CUMENE. CUMENE IS THEN OXIDIZED WITH AIR /TO PRODUCE/ CUMENE HYDROPEROXIDE /WHICH/ IS THEN DECOMPOSED OR CLEAVED WITH ACID TO YIELD PHENOL AND ACETONE.
[CHEMICAL PRODUCTS SYNOPSIS: ACETONE, 1984]**PEER REVIEWED**

General Manufacturing Information:

DISINFECTANT WHEN USED IN HIGH CONCENTRATIONS, BEING RAPIDLY BACTERICIDAL FOR MICROCOCCUS AUREUS, BUT NOT SPORICIDAL, THOUGH IT INDUCES DELAY IN THE GROWTH OF SPORES.
[Browning, E. Toxicity and Metabolism of Industrial Solvents. New York: American Elsevier, 1965., p. 413]**PEER REVIEWED**

EXXON AT BAYWAY, NJ AND UNION CARBIDE AT PENUELAS, PR ARE ON STANDBY. MONSANTO, CHEVRON, SHELL AND CYANAMID HAVE CLOSED APPROXIMATELY 445 MILLION LB OF ACETONE CAPACITY SINCE 1982
[CHEMICAL PROFILE: ACETONE, (1985)]**PEER REVIEWED**

DURING 1984, APPROXIMATELY 15% OF US ACETONE OUTPUT WAS DERIVED FROM ISOPROPANOL
[CHEMICAL PRODUCTS SYNOPSIS: ACETONE, 1984]**PEER REVIEWED**

0.40-0.45 kg of acetone per kg of cumene are produced as a coproduct with phenol via cumene peroxidation route. Stated in terms of phenol, one kg of phenol production will result in 0.6 kg of acetone.
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 181]**PEER REVIEWED**

Acetone is a co-product of liquid-phase-oxidation of butane. It may be produced from isobutane, an impurity present in all commercial butane.
[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 12(80) 842]**PEER REVIEWED**

Impurities:

PURITY: TECHNICAL AND REAGENT : 99.5% PLUS 0.5% WATER.
[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 chief impurity in acetone ... water. Acetone contains no oxidizable impurities, and the color of a few drops of permanganate is retained for several hours.
[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**

Consumption Patterns:

25% FOR METHYL METHACRYLATE; 14% FOR METHYL ISOBUTYL KETONE; 10% AS COATING SOLVENT; 10% FOR OTHER ORGANIC CHEMS; 6% IN PHARMACEUTICAL MANUFACTURE; 5% FOR METHACRYLIC ACID AND HIGHER METHACRYLATES; 5% FOR BISPHENOL-A; 4% FOR CELLULOSE ACETATE SPINNING; 21% FOR MISC (1973)
**PEER REVIEWED**

33% METHYL METHACRYLATE, METHACRYLIC ACID AND HIGHER METHACRYLATES; 17% SOLVENTS; 10% MIBK; 9% BISPHENOL-A; 7% ALDOL CHEMICAL; 6% PHARMACEUTICALS AND COSMETICS; 2% METHYL ISOBUTYL CARBENOL; 4.5% EXPORTS; 11.5% MISC (1985)
[CHEMICAL PROFILE: ACETONE, 1985]**PEER REVIEWED**

CHEMICAL PROFILE: Acetone. Methylmethacrylate, methacrylic acid and higher methacrylates, 34%; coatings solvent, 15%; bisphenol-A, 12%; MIBK (methyl isobutyl ketone), 10%; solvent for cellulose acetate, 5%; drug and pharmaceutical applications, 5%; miscellaneous chemical and solvent uses, 6%; exports, 5%.
[Kavaler AR; Chemical Marketing Reporter 232 (12): 70 (1987)]**PEER REVIEWED**

CHEMICAL PROFILE: Acetone. Demand: 1986: 1,936 million lb; 1987: 2,050 million lb; 1991 /projected/: 2,140 million lb.
[Kavaler AR; Chemical Marketing Reporter 232 (12): 70 (1987)]**PEER REVIEWED**

Demand 1995: 2.76 billion pounds; 1996: 2.72 billion pounds; 2000 (projected) 3.2 billion pounds.
[Kavaler AR; Chemical Marketing Reporter. Sept. 2, 1996]**PEER REVIEWED**

U. S. Production:

(1972) 7.74X10+11 G
**PEER REVIEWED**

(1975) 7.45X10+11 G
**PEER REVIEWED**

(1984) 7.90X10+11 g
[USITC, SYN ORG CHEM-US PROD/SALES 1984 p.256]**PEER REVIEWED**

(1984) 5.58X10+10 g
[USITC, SYN ORG CHEM-US PROD/SALES 1984 p.256]**PEER REVIEWED**

(1987) 9.5X10+5 tons
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 186]**PEER REVIEWED**

United States acetone production 1,102,426X10+3 kg
[United States International Trade Commission. Synthetic Organic Chemicals - United States Production and Sales, 1993. USITC Publication 2810, Nov. 1994. Washington, D.C., p. 3-61]**PEER REVIEWED**

(1990) 2.33 billion lb
[Chem & Engineering News 70 (15): 17 (4/13/92)]**PEER REVIEWED**

(1992) 2.43 billion lb
[Chem & Engineering News 72 (15): 13 (4/11/94)]**PEER REVIEWED**

(1991) 2.35 billion lb
[Chem & Engineering News 71 (15): 11 (4/12/93)]**PEER REVIEWED**

(1993) 2.46 billion lb
[Chem & Engineering News 72 (15): 13 (4/11/94)]**PEER REVIEWED**

U. S. Imports:

(1972) 1.18X10+10 G
**PEER REVIEWED**

(1975) 1.36X10+9 G
**PEER REVIEWED**

(1983) 2.48X10+6 g
[USITC. IMPORTS OF BENZENOID CHEMICALS AND PRODUCTS 1983 p.7]**PEER REVIEWED**

(1987) 7.5X10+4 tons
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 186]**PEER REVIEWED**

U. S. Exports:

(1972) 4.11X10+10 G
**PEER REVIEWED**

(1975) 2.93X10+10 G
**PEER REVIEWED**

(1984) 3.76X10+10 g
[BUREAU OF THE CENSUS: US EXPORTS 1984 p.2-77]**PEER REVIEWED**

(1987) 1.18X10+5 tons
[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New York, NY. John Wiley and Sons, 1991-Present., p. V1 186]**PEER REVIEWED**

Laboratory Methods:

Clinical Laboratory Methods:

A gas chromatographic method for determining acetone in biological tissues is described. Solvent was extracted with nitrogen gas from specimen & adsorbed on porous polymer (Porapak Q). Concentrations ranging between 17 nmol/g tissue in nonexposed animals & 1.8 mumol/g tissue in exposed mice were determined.
[Holm S, Lundgren E; Anal Biochem 136 (1): 157-60 (1984)]**PEER REVIEWED**

Analytic Laboratory Methods:

ANALYTE: ACETONE. MATRIX: AIR. PROCEDURE: ADSORPTION ON CHARCOAL, DESORPTION WITH CARBON DISULFIDE, GC. RANGE: 1200-4500 MG/CU M. SENSITIVITY: 0.082
[U.S. Department of Health and Human Services, Public Health Service. Centers for Disease Control, National Institute for Occupational Safety and Health. NIOSH Manual of Analytical Methods, 3rd ed. Volumes 1 and 2 with 1985 supplement, and revisions. Washington, DC: U.S. Government Printing Office, February 1984., p. 1300-1]**PEER REVIEWED**

A procedure for the determination of volatile compounds in fish tissue is described. Characterization is by gas chromatography/mass spectrometry using a fused-silica capillary column.
[Hiatt MH; Anal Chem 55 (3): 506-16 (1983)]**PEER REVIEWED**

Emissions of organic compounds from shale oil waste waters were investigated by using headspace & purge & trap sampling followed by analysis by gas chromatography with mass spectral & flame ionization. Acetone was identified.
[Hawthrone SB, Sievers RE; Environ Sci Technol 18 (6): 483-90 (1984)]**PEER REVIEWED**

EPA Method 1624 - Volatile Organic Compounds By GC/MS: Grab samples in municipal and industrial discharges are collected. If residual chlorine is present, add sodium thiosulfate. Extraction is performed by a purge and trap apparatus. An isotope dilution gas chromatography/ mass spectrometry method for the determination of volatile organic compounds in municipal and industrial discharges is described. Unlabeled acetone has a minimum level of 50 ug/l and a mean retention time of 565 sec.
[40 CFR 136 (7/1/86)]**PEER REVIEWED**

Method 8240A - Volatile Organics by gas chromatography/mass spectrometry (GC/MS). Packed column technique.
[USEPA/Office of Solid Waste (OSW); Test Methods for Evaluating Solid Waste, Physical/Chemical Methods SW846 Methods (1986)]**PEER REVIEWED**

Sampling Procedures:

Activated charcoal, Ambersorb XE-348, and Amberlites XAD-2, XAD-4, and XAD-7 were evaluated as solid adsorbents for work-room air sampling of acetone, methyl ethyl ketone, methyl isobutyl ketone, methyl n-butyl ketone, cyclohexanone and isophorone. Activated charcoal had good capacity for the compounds investigated, but most ketones decomposed on this adsorbent during storage. Ambersorb XE-348 also showed good capacity for most of the ketones and decomposition was insignficant.
[Levin JO, Carleborg L; Ann Occup Hyg 31 (1): 31-8 (1987)]**PEER REVIEWED**

Special References:

Special Reports:

DHHS/NTP; NTP Report on the Toxicity Studies of Acetone in F344/N Rats and B6C3F1 Mice (Drinking Water Studies) NTP TOX 3 NIH Pub No. 91-3122

DHHS/ATSDR; Toxicological Profile for Acetone (1994) ATSDR/TP-93/01

Synonyms and Identifiers:

Synonyms:

ACETON (GERMAN, DUTCH, POLISH)
**PEER REVIEWED**

AI3-01238
**PEER REVIEWED**

Caswell No. 004
**PEER REVIEWED**

DIMETHYL KETONE
**PEER REVIEWED**

EPA Pesticide Chemical Code 004101
**PEER REVIEWED**

KETONE, DIMETHYL
**PEER REVIEWED**

KETONE PROPANE
**PEER REVIEWED**

BETA-KETOPROPANE
**PEER REVIEWED**

METHYL KETONE
**PEER REVIEWED**

PROPANONE
**PEER REVIEWED**

2-propanone
**PEER REVIEWED**

Shipping Name/ Number DOT/UN/NA/IMO:

UN 1090; Acetone

IMO 3.1; Acetone

Standard Transportation Number:

49 081 05; Acetone

EPA Hazardous Waste Number:

U002; A toxic waste when a discarded commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate.

F003; A hazardous waste from nonspecific sources when a spent solvent.





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