ACETONE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
IDENTIFIERS
SYNONYM REFERENCE
- (Ashford, 1994; Bingham et al, 2001; RTECS , 2002)
USES/FORMS/SOURCES
Acetone, the simplest aliphatic ketone, is widely used as industrial solvent and chemical intermediate (Ashford, 1994; ATSDR, 1994; Budavari, 2000; Hathaway et al, 1996; HSDB, 2002; ILO, 1998; Verschueren, 2001): Acetone is used in the manufacture of diacetone alcohol; acetylene; acetic anhydride; methyl isobutyl alcohol; methyl isobutyl ketone; methyl isobutyl carbinol; methyl isobutyl ketone; methacrylic acid; methyl methacrylate; bisphenol-A; chloroform; iodoform; isophorone; isoprene; bromoform; smokeless powder; explosives; lubricating oils; paints; varnishes; lacquers; printing inks; sealants; adhesives; cellulose resins; cellulose acetate; nitrocellulose; modacrylic fibers; rayon; artificial silk; synthetic leather; polyurethane foam; photographic films. It is used also for purifying paraffin, and hardening and dehydrating tissues when preparing histological laboratory samples.
Acetone is useful in storing acetylene gas because it takes up approximately 24 times its volume of the gas. The gas is dissolved in acetone which is absorbed into porous cellular material, filling the interior of an acetylene cylinder. This storage method allows shipping of 250 psig (1724 kPa) at 70 degrees F (21.1 degrees C) (Budavari, 2000). Acetone is used in the production of drugs of abuse (Lewis, 2000a) and in the preparation of vitamin intermediates (e.g., vitamin C) (Bingham et al, 2001; HSDB, 2002). Acetone is used as a solvent for cements in the leather and rubber industries (ACGIH, 1991a). It is used for cleaning and drying parts of precision equipment (ATSDR, 1994; ACGIH, 1991a; Lewis, 1997). Acetone is the primary chemical in some fingernail polish removers, paint removers, and varnish removers (Hathaway et al, 1996). It can be used as a brine for low temperature heat transfer agent in indirect refrigeration (HSDB, 2002). OTHER: Acetone can accumulate in the blood of patients undergoing long term (10 hours) isoflurane anesthesia with a closed system (Straub & Hausdorfer, 1993). Patients with acetone concentrations of more than 10 mg/L prior to the onset of anesthesia had higher serum acetone concentrations at the end of 10 hours than did patients with serum acetone levels less than 10 mg/L at the onset of anesthesia.
There are multiple grades of acetone: technical, CP, NF, electronic, and spectrophotometric (Lewis, 1997).
Two main processes are used in large-scale commercial production. The first, and by far the most common, is cumene oxidation through the acid-catalyzed hydrolytic cleavage of cumene hydroperoxide. The second process involves the catalytic dehydrogenation or oxidation of isopropyl alcohol (Bingham et al, 2001). Vapor-phase oxidation of butane also produce acetone (Lewis, 1997). Methods (such as biofermentation, propylene oxidation, and diiospropylbenzene oxidation) are either experimental or account for a very small percentage of production worldwide (Bingham et al, 2001). Acetone is produced endogenously as a normal by-product of metabolism from the breakdown and utilization of stored fats and lipids. Pregnancy, postnatal growth, high fat consumption, dieting lactation, vigorous physical exercise, perinatal development, alcoholism, diabetes mellitus, hypoglycemia, prolonged vomiting, acute trauma, and inborn errors of metabolism can all affect the level of acetone production (Bingham et al, 2001; Baselt, 1997).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: In industry used as a solvent and chemical intermediate. Also used in some nail polish removers, and paint and varnish removers.
- TOXICOLOGY: Lipid soluble solvent, causes CNS effects similar to ethanol.
- EPIDEMIOLOGY: Common inadvertent exposure in the home, significant toxicity is rare. Deliberate inhalation abuse occurs but is not common. Systemic toxicity most commonly occurs after ingestion or prolonged or high concentration inhalation; rarely after extensive dermal exposure.
MILD TO MODERATE INTOXICATION: Mild CNS depression, mild metabolic acidosis, nausea, vomiting, hyperglycemia and ketosis (mimicking diabetic ketoacidosis) may be seen, most often after ingestions, but occasionally after inhalation or severe dermal exposure. SEVERE INTOXICATION: Severe CNS depression, coma, seizures, tachycardia, hypotension, gastrointestinal bleeding, and respiratory depression are rare effects seen with serious intoxication, most commonly after ingestion. INHALATION: Nausea, vomiting, headache, excitement, faintness, fatigue, and bronchial irritation may result from inhalation exposure. With high concentration exposures, systemic toxicity can occur similar to that seen with ingestion. DERMAL: Repeated dermal exposure to liquid acetone can cause defatting and drying of the skin, and brittle nails. Chemical burns may develop after prolonged exposure. Systemic toxicity after dermal exposure is rare, but may occur if large surface areas are exposed to high concentrations, primarily in young children due to larger surface area to volume and more rapid dermal penetration. OCULAR: Acetone and its vapors are mildly irritating to the eyes and mucous membranes. Corneal erosions are a rare effect after high concentration exposure.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
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.
ACUTE CLINICAL EFFECTS
TOXICOLOGY: Lipid soluble solvent, causes CNS effects similar to ethanol. EPIDEMIOLOGY: Common inadvertent exposure in the home, significant toxicity is rare. Deliberate inhalation abuse occurs but is not common. Systemic toxicity most commonly occurs after ingestion or prolonged or high concentration inhalation; rarely after extensive dermal exposure. MILD TO MODERATE INTOXICATION: Mild CNS depression, mild metabolic acidosis, nausea, vomiting, hyperglycemia and ketosis (mimicking diabetic ketoacidosis) may be seen, most often after ingestions, but occasionally after inhalation or severe dermal exposure. SEVERE INTOXICATION: Severe CNS depression, coma, seizures, tachycardia, hypotension, gastrointestinal bleeding, and respiratory depression are rare effects seen with serious intoxication, most commonly after ingestion. INHALATION: Nausea, vomiting, headache, excitement, faintness, fatigue, and bronchial irritation may result from inhalation exposure. With high concentration exposures, systemic toxicity can occur similar to that seen with ingestion. DERMAL: Repeated dermal exposure to liquid acetone can cause defatting and drying of the skin, and brittle nails. Chemical burns may develop after prolonged exposure. Systemic toxicity after dermal exposure is rare, but may occur if large surface areas are exposed to high concentrations, primarily in young children due to larger surface area to volume and more rapid dermal penetration. OCULAR: Acetone and its vapors are mildly irritating to the eyes and mucous membranes. Corneal erosions are a rare effect after high concentration exposure.
METABOLIC ACIDOSIS: Mild metabolic acidosis has been reported after significant oral, dermal and inhalation exposures (van Wijngaarden et al, 1995; Gitelson et al, 1966; Gamis & Wasserman, 1988).
Tachycardia and hypotension have been reported with severe intoxication (Harris & Jackson, 1952; Hift & Patel, 1961; Gamis & Wasserman, 1988).
DERMATITIS: It is a mild irritant and may cause erythema, drying, scaling, peeling and burning as well as nail brittleness and peeling after repeated application (Kechijian, 1991; van Wijngaarden et al, 1995). CHEMICAL BURNS: Superficial dermal burns have occurred following occupational exposure to acetone (Piatkowski et al, 2007).
NAUSEA AND VOMITING: Nausea, vomiting, and rarely hematemesis has developed after dermal and inhalational exposure to an acetone-containing liquid which was used to set orthopedic plaster casts (Hift & Patel, 1961; Harris & Jackson, 1952; Strong, 1944). Nausea and vomiting has occurred after exposure to acetone vapors in excess of 12,000 parts per million (ppm) (Ross, 1975).
CORNEAL IRRITATION: Prolonged eye contact with liquid acetone has resulted in permanent corneal opacity in one case and temporary corneal opacity in another case (Grant & Schuman, 1993). Eye injury is unlikely from vapor concentrations which are tolerable to humans (Grant & Schuman, 1993). IRRITATION: Splash contact with acetone causes immediate stinging, followed by mild epithelial injury which resolves in a day or two (Grant & Schuman, 1993). NOSE IRRITATION: Transient nasal irritation can occur with brief exposure to vapor concentrations of 500 parts per million (ppm) to greater than 1000 ppm (Nelson et al, 1943; Raleigh & McGee, 1972). THROAT IRRITATION: If ingested, erythema, irritation and erosions of the oral pharynx may be present (Gitelson et al, 1966). Vapors are mildly irritating, generally at concentrations of 500 parts per million or greater (DiVincenzo et al, 1973; Raleigh & McGee, 1972).
KETOSIS: Hyperglycemia and ketosis (acetone and acetoacetate) mimicking diabetic ketoacidosis have developed after ingestion of acetone (Gitelson et al, 1966; Gamis & Wasserman, 1988). Hyperglycemia, polyuria, and polydipsia persisted for several days following ingestion of sake (rice wine) and liquid cement which contained acetone, cyclohexanone and methyl ethyl ketone (Sakata et al, 1989), and after dermal and inhalational exposure to an acetone-based cast lacquer (Hift & Patel, 1961).
RHABDOMYOLYSIS: Following occupational inhalational and dermal exposure to acetone, a man developed rhabdomyolysis and acute renal failure. The rhabdomyolysis and renal failure resolved with normalization of laboratory parameters following supportive therapy, including continuous veno-venous hemofiltration (Piatkowski et al, 2007).
COMA: Depression of the central nervous system can occur. Sedation, ataxia, nystagmus, coma and other effects have been reported (Zettinig et al, 1997; Hathaway et al, 1996a; Lewis, 2000). SEIZURE: Repeated episodes of gagging, hypotonia, unresponsiveness, eye deviation, and focal tonic clonic activity were reported in a 17-month-old girl who was repeatedly poisoned with acetone by her mother (Knapp et al, 1997). In another case, a toddler developed tonic-clonic seizures after ingesting almost 6 ounces of a fingernail polish remover which contained 65% acetone and 10% isopropanol. Seizures may have occurred secondary to hypoxemia (Gamis & Wasserman, 1988). HYPERESTHESIA: After ingesting 200 mL of acetone, an adult developed hyperesthesia of the legs and an abnormal gait. Symptoms resolved 2 months later (Gitelson et al, 1966). NEUROBEHAVIORAL EFFECTS: Inhalation of small amounts of acetone may decrease auditory tone discrimination ability and may cause slight mood changes (Dick et al, 1988; Dick et al, 1989).
RESPIRATORY DEPRESSION: High vapor concentrations can produce CNS depression and unconsciousness. Exposure by any route which results in significant CNS depression may cause respiratory depression as a secondary effect (Hathaway et al, 1996a; Ross, 1975). KUSSMAUL'S RESPIRATION: Deep, irregular and rapid respirations may develop in patients with severe intoxication (Harris & Jackson, 1952; Hift & Patel, 1961). UPPER RESPIRATORY TRACT IRRITATION: Mucous membrane irritation may occur with exposure to vapor concentrations in excess of 1000 ppm (Raleigh & McGee, 1972).
CHRONIC CLINICAL EFFECTS
- There have been no reported permanent injuries from industrial use of acetone despite years of use (Lewis, 2000).
- Acetone is rapidly eliminated from the body, but slowly enough that it may accumulate over the work week and return to normal levels over the weekend (Clayton & Clayton, 1993). Studies of human volunteers have shown that acetone can accumulate in the body with repeated exposures to more than approximately 1200 parts per million (ppm) for an individual at rest and approximately 400 ppm for a person engaged in moderate exercise; blood acetone levels reached a plateau of approximately 180 mg/L after 2 days of exposure (Haggard et al, 1944). Urinary acetone levels did not return to baseline after a day's exposure when exposure exceeded 300 ppm, but peak levels on the second day were comparable to those on the first (Satoh et al, 1995). A theoretical multi-compartment model does not predict accumulation of acetone in the blood from one week to another at simulated occupational exposure to airborne concentrations as high as 2000 ppm, but there was accumulation during the work week at the highest exposure level (Kumagai & Matsunaga, 1995).
- Symptoms of chronic occupational exposure include loss of appetite, heartburn, eye irritation, bronchitis, and gastritis. In a controlled exposure to 500 parts per million (ppm) for 6 days, the subjects complained of irritation of the mucous membranes, heavy eyes, headache, and weakness, and there were changes in blood values (Parmeggiani & Sassi, 1954)
- Several occupational studies have shown that chronic exposure to acetone appears to cause no permanent adverse health effects. Studies of 948 workers exposed to acetone at levels up to 1070 parts per million (ppm) over a 23-year period found no differences in mortality rates from all deaths, heart disease, or cancer compared with the US population (Ott et al, 1983a, 1983b, 1983c).
- Workers have reported symptoms of eye and throat irritation, nausea, headache, weakness, drowsiness, dizziness, and vertigo when exposed to acetone at airborne concentrations in the range of 309 to 918 parts per million (ppm) for up to 3 hours over 7 to 15 years, and at a second site where levels ranged from 84 to 147 ppm (Parmeggiani & Sassi, 1954; Vigliani & Zurlo, 1955).
- Other workers exposed to higher levels had no adverse effects except for transient irritation at airborne concentrations greater than 2500 parts per million (ppm) (Oglesby et al, 1949). No differences in clinical laboratory and hematologic values were seen between two groups of workers exposed to "low" levels of acetone (range, 549 to 653 ppm) or "high" levels (range, 948 to 1048 ppm) and an unexposed control group (pp 137-141).
- In a cross-sectional study of 110 male workers exposed to acetone at airborne concentrations in the range of 19.6 to 1018 parts per million, dose-related effects related to the past 6 months' exposure include heavy or vague feeling in the head, faintness, nausea, weight loss, and slow healing of an external wound. Reaction times and digit span scores were lower in the exposed workers, but not in a clearly dose-related fashion (Satoh et al, 1996).
- There has been one case of cataracts attributed to occupational acetone exposure because of its similarity to cataracts in diabetics (Mayou, 1932). Studies of groups of persons occupationally exposed to acetone have not revealed cataracts, however.
- Repeated administration of acetone can induce a several-fold increase in activity of CYP2E1 in rat and rabbit liver, which is involved in acetone metabolism, as well as metabolism of other substances. The liver and kidney are the primary target organs for chronic exposure to acetone in experimental animals; generally, increased organ weight occurs, possibly as a consequence of induction of cytochrome P450 in the liver and acceleration of spontaneous kidney abnormalities (Morgott, 1993). Chronic exposure to acetone at a concentration of 1% in the drinking water was more effective than a single intragastric dose of 5 mL/kg in inducing cytochrome P450 CYP2E1 in mouse liver (Forkert et al, 1994).
- Repeated exposures even to relatively high doses of acetone have generally not produced permanent effects in experimental animals. Rats exposed to 19,000 parts per million of acetone by inhalation 5 days/week for 8 weeks had no signs of acute toxicity other than slightly less weight gain than controls (Bruckner & Peterson, 1981).
- Acetone did not induce central or peripheral nerve damage in rats exposed to 0.5% in the drinking water for 8 weeks, followed by 1% for 4 weeks (Spencer et al, 1978). Mice given 400 mg/kg/day of acetone subcutaneously showed normal neurologic functionality in movement and nerve conduction velocities (Misumi & Nagano, 1984).
- Cataracts developed in guinea pigs, but not in rabbits, several months after treatment with acetone (dermal and subcutaneous) for a minimum of 3 weeks; the induction of cataracts was ascribed to low levels of ascorbate induced by acetone (Rengstorff et al, 1972; Rengstorff & Khafagy, 1985). This work is considered controversial, however, and no cataracts were found in guinea pigs on low or high ascorbate diets given 0.5 mL acetone dermally 5 days/week for 6 months (Taylor et al, 1993). Cataracts have not been seen in cases of human acetone exposure (Grant & Schuman, 1993).
- Acetone caused damage to the liver, kidneys, pancreas, and adrenal cortex in dogs (Viale & Pende, 1948). When given to male rats in the drinking water at levels as high as 5000 parts per million for 13 weeks, acetone was associated with changes in the blood similar to those seen in megaloblastic anemia (Dietz et al, 1991).
- Dermal application of acetone inhibited B-cell immunity against sheep red blood cells, but not against TNP-LPS antigen, in SSIN mice. Development of T-cells was not affected (Singh et al, 1996).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give 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. In case of burns, immediately cool affected skin for as long as possible with cold water. Do not remove clothing if adhering to skin. Keep victim warm and quiet. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
FIRST AID INHALATION EXPOSURE INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm. If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
DERMAL EXPOSURE DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999). Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL EXPOSURE Because of the potential for CNS depression, DO NOT induce emesis. Activated charcoal is of limited utility in adsorbing acetone; routine administration is not recommended.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
The lowest reported lethal dose in humans (unreported route): 1159 mg/kg (RTECS , 2002). Lethal concentration in human blood: 550 mcg/mL (55 mg%) (HSDB , 2002).
MAXIMUM TOLERATED EXPOSURE
No toxic effects were reported in adults after oral administration of 40 to 80 mg/kg (Haggard et al, 1944). The ingestion of 200 mL produced coma, hyperglycemia, and acetonuria in an adult (Gitelson et al, 1966). This would approximate a dose of 2 to 3 mL/kg. No signs or symptoms of toxic effects occurred in subjects who were exposed to 100 parts per million (ppm) or 500 ppm of acetone for 2 to 4 hours (DiVincenzo et al, 1973). Several human studies have reported that up to 8 hours of exposure to acetone vapors of 1000 parts per million or less has produced only slight, transient irritation of the eyes, nose and throat (Krasavage et al, 1982). Concentration of acetone in expired air and blood correlated positively with the degree of exposure. Eye irritation may be expected at concentrations of 1000 to 6000 parts per million (ppm). CNS depression is likely to occur at concentrations in excess of 10,000 ppm (Baselt, 2000). Based on acute acetone intoxication cases, blood levels in excess of 1000 mg/L are necessary to cause unconsciousness in humans (Bingham et al, 2001). CASE REPORTS Exposure to greater than 12,000 parts per million (ppm) acetone and 50 ppm 1,1,1-trichloroethane resulted in transient throat and eye irritation, nausea, vomiting, confusion, drowsiness, unconsciousness (1 case), chest tightness, dizziness, inebriation, weakness, headache, dizziness, malaise and light-headedness among 8 workers. The duration of exposure ranged from a few minutes to several hours. The authors attributed the symptoms to acetone (Ross, 1975).
Suspected ingestion of almost 6 ounces (180 mL) of a fingernail polish remover (65% acetone, 10% isopropyl alcohol) resulted in severe toxicity (ie, seizures, CNS and respiratory depression, hypothermia, hyperglycemia, ketonemia, acidosis) in a 30-month-old child (Gamis & Wasserman, 1988). In children, ingestion of 2 to 3 mL/kg is considered toxic (HSDB , 2002).
- Carcinogenicity Ratings for CAS67-64-1 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Acetone ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Acetone EPA (U.S. Environmental Protection Agency, 2011): Not applicable. This substance was not assessed using the EPA's 1986 cancer guidelines. ; Listed as: Acetone IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Acetone MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS67-64-1 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 0.9 mg/kg-day
Inhalation: Drinking Water:
LC50- (INHALATION)MOUSE: 44 g/m(3) for 4H ((Bingham et al, 2001a); CHRIS, 2002; IPCS, 1998; OHM/TADS, 2002; RTECS, 2002)
LC50- (INHALATION)RAT: 50,100 mg/m(3) for 8H ((Bingham et al, 2001a); CHRIS, 2002; IPCS, 1998; OHM/TADS, 2002; RTECS, 2002) 76,000 mg/m(3) for 4H (IPCS, 1998) 16,000 mg/m(3) for 4H (OHM/TADS, 2002) 18,000,000 mg/m(3) (OHM/TADS, 2002) female: 21,150 ppm (Bingham et al, 2001a)
LD50- (ORAL)DOG: LD50- (SKIN)GUINEA_PIG: LD50- (INTRAPERITONEAL)MOUSE: LD50- (ORAL)MOUSE: 5800 mg/kg: behavioral changes 3 g/kg male, 5.2 g/kg (Bingham et al, 2001)
LD50- (ORAL)RABBIT: 5300 mg/kg (OHM/TADS, 2002) 9700 mg/kg (OHM/TADS, 2002) 5340 mg/kg 5.3 g/kg (Bingham et al, 2001a)
LD50- (SKIN)RABBIT: greater than 16,000 mg/kg for 14D (OHM/TADS, 2002) male: greater than 15.8 g/kg (Bingham et al, 2001a)(Bingham et al, 2001)
LD50- (INTRAPERITONEAL)RAT: 1.3 g/kg (Bingham et al, 2001a) 0.61 g/kg (Bingham et al, 2001a)
LD50- (INTRAVENOUS)RAT: LD50- (ORAL)RAT: newborn: 1726 mg/kg (IPCS, 1998) 14-day-old: 4393 mg/kg (IPCS, 1998) young adult: 7138 mg/kg (IPCS, 1998) older adult: 6667 mg/kg (IPCS, 1998) 5800 mg/kg: weight loss and prostration (IPCS, 1998) 9.8 g/kg (Bingham et al, 2001) 7.3 g/kg (Bingham et al, 2001) male: 9.75 g/kg (Bingham et al, 2001) female: 8.5 g/kg (Bingham et al, 2001) female, 10.0 g/kg (Bingham et al, 2001)
LDLo- (INTRAPERITONEAL)DOG: LDLo- (ORAL)DOG: LDLo- (SUBCUTANEOUS)DOG: LDLo- (SUBCUTANEOUS)GUINEA_PIG: LDLo- (INTRAVENOUS)MOUSE: LDLo- (INTRAVENOUS)RABBIT: LDLo- (SKIN)RABBIT: LDLo- (INTRAPERITONEAL)RAT: TCLo- (INHALATION)HUMAN: 500 ppm: sensory and respiratory systems changes male: 440 mcg/m(3) for 6M: CNS changes male: 10 mg/m(3) for 6H: biochemical changes male: 12,000 ppm for 4H: nausea and muscle weakness
TCLo- (INHALATION)RAT: 199 mg/m(3) for 8H/45D: intermittent: muscle contraction 19,000 ppm for 3H/8W: intermittent: changes in brain weight
TDLo- (ORAL)HUMAN: TDLo- (ORAL)MOUSE: TDLo- (ORAL)RAT: male: 273 g/kg at 13 W prior to mating: spermatogenesis 273 g/kg for 13W continuous: changes in liver and bladder weights, normocytic anemia
CALCULATIONS
1 part per million (ppm) = 2.411 mg/m(3) (Verschueren, 2001) 1 ppm = 2.38 mg/m(3) (at 68 degrees F and 760 mmHg)(NIOSH , 2002) 1 mg/m(3) = 0.421 ppm (at 25 degrees C) (IPCS, 1998) 1 mg/m(3) = 0.415 ppm (Verschueren, 2001)
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS67-64-1 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS67-64-1 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS67-64-1 (National Institute for Occupational Safety and Health, 2007):
Listed as: Acetone REL: TWA: 250 ppm (590 mg/m(3)) STEL: Ceiling: Carcinogen Listing: (Not Listed) Not Listed Skin Designation: Not Listed Note(s):
IDLH: IDLH: 2500 ppm Note(s): [10%LEL]
- OSHA PEL Values for CAS67-64-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
Listed as: Acetone Table Z-1 for Acetone: 8-hour TWA: ppm: 1000 mg/m3: 2400 Ceiling Value: Skin Designation: No Notation(s): Not Listed
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS67-64-1 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS67-64-1 (U.S. Environmental Protection Agency, 2010):
Listed as: 2-Propanone Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Acetone Final Reportable Quantity, in pounds (kilograms): Additional Information: The following spent non-halogenated solvents and the still bottoms from the recovery of these solvents. (F003) Listed as: Acetone Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS67-64-1 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS67-64-1 (U.S. Environmental Protection Agency, 2010b):
Listed as: Acetone P or U series number: U002 Footnote: Listed as: 2-Propanone P or U series number: U002 Footnote: Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.
- EPA SARA Title III, Extremely Hazardous Substance List for CAS67-64-1 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS67-64-1 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS67-64-1 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS67-64-1 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1090 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1090 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS67-64-1 (NFPA, 2002):
Listed as: Acetone Hazard Ratings: Health Rating (Blue): 1 Flammability Rating (Red): 3 (3) Flammable. Liquids and solids that can be ignited under almost all ambient temperature conditions. Including liquids with a flash point below 73 degrees F and a boiling point above 100 degrees F, solid materials which form coarse dusts that burn rapidly without becoming explosive, materials which burn rapidly by reason of self-contained oxygen (ie, organic peroxides), and materials which ignite spontaneously when exposed to air.
Instability Rating (Yellow): 0 Oxidizer/Water-Reactive Designation: Not Listed
-HANDLING AND STORAGE
HANDLING
- When handling acetone, workers should keep it away from plastic eyeglass frames, jewelry, pens, pencils, and clothing material made of rayon (HSDB , 2002).
STORAGE
Acetone is stored in steel containers (eg, tank cars, trucks, and returnable barrels/drums) or glass bottles (HSDB , 2002; OHM/TADS , 2002). Containers should also be equipped with open (flame arrester) or pressure-vacuum venting systems (CHRIS , 2002).
- ROOM/CABINET RECOMMENDATIONS
Atmospheres that contain acetone vapors are classified as Class 1 Group D. Explosive venting of storage areas and good ventilation are recommended (OHM/TADS , 2002). Underground storage is preferred (OHM/TADS , 2002).
Keep away from sparks, fire, and other ignition sources (AAR, 2002; (Budavari, 2000). Store away from acids or oxidizing materials (OHM/TADS , 2002). Acetone ignites on contact with (HSDB , 2002; ITI, 1995; NFPA, 2002a; Urben, 1999): Acetone reacts violently/explosively on contact with (HSDB , 2002; ITI, 1995; Lewis, 2000; NFPA, 2002a; Urben, 1999): acetic acid bromine bromine trifluoride bromoform bromoform + potassium hydroxide chloroform + alkalies chloroform + solid potassium hydroxide or calcium hydroxide chromic anhydride chromyl chloride hexachloromelamine hydrogen peroxide 2-methyl-1,3-butadiene nitric acid nitrosyl chloride nitrosyl perchlorate nitryl perchlorate peroxomonosulfuric acid platinum + nitrosyl chloride potassium tert-butoxide thiodiglycol + hydrogen peroxide thiotriazyl perchlorate thiotrithiazyl perchlorate trichloromelamine sodium hypobromite sodium hypoiodite sulfur dichloride sulfuric acid + nitric acid water + 2,4,6-trichloro-1,3,5-triazine
Acetone is incompatible with (HSDB , 2002; ILO , 1998; ITI, 1995; Lewis, 2000): chloroform chromium oxide chromyl anhydride chromyl chloride decaborane hexachloromelamine nitric acid nitric acid + acetic acid nitrosyl chloride nitryl perchlorate permonosulfuric acid sodium hypobromite sulfuric acid + potassium dichromate sulfuric acid thio-diglycol + hydrogen peroxide 1,1,1-trichloroethane trichloromelamine
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
- Wear appropriate chemical protective clothing and equipment, including respiratory protection, at all times when working with or near acetone (AAR, 2000).
- Acetone is reported as mildly irritating to the eyes: at 2000 to 3000 parts per million, it caused eye irritation that resolved after exposure ceased (IPCS, 1998).
- Acetone is absorbed through the skin (IPCS, 1998). Prolonged repeat exposure will cause defatting, drying, and cracking (CHRIS , 2002; IPCS, 1998). However, acetone is not a skin sensitizer (IPCS, 1998). Acetone is very volatile, and small amount of accidental contamination will evaporate quickly from the skin, and as such, does not pose a significant hazard (CHRIS , 2002).
Skin contact with acetone should be prevented. Do not handle broken, damaged, or leaking packages containing acetone unless wearing adequate chemical protective clothing (AAR, 2000; (NIOSH , 2002). Due to the acetone's flammability, work clothing that becomes wet with acetone should be removed and replaced immediately (HSDB , 2002; NIOSH , 2002). Skin that comes into contact with this chemical should be flushed with running water for at least 15 minutes (AAR, 2000).
- Acetone is readily absorbed from the lung (Bingham et al, 2001; HSDB , 2002). Inhalation of its vapors can cause headaches, excitement, and it can act as an anesthetic at very high concentrations (CHRIS , 2002; Lewis, 1998). It can irritate the nose, throat, trachea, and lungs: at 1660 parts per million, acetone caused nose irritation after 15 minutes (HSDB , 2002). However, the effect on respiratory system is temporary, and acetone is not a respiratory tract sensitizer (CHRIS , 2002; IPCS, 1998).
EYE/FACE PROTECTION
- Wear safety goggles, face splash shield, or other appropriate eye protection, to prevent eye contact with acetone (CHRIS , 2002; NIOSH , 2002).
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
- In order to assess the service life of a respirator cartridge, a theoretical model was applied to various acetone/styrene binary assault systems. The styrene concentration was varied between 228 to 1578 parts per million (ppm) and the range of acetone concentrations was 92 to 985 ppm. For the acetone/styrene system a displacement (from the carbon) of previously adsorbed acetone molecules by styrene molecules was observed. Acetone breakthrough was observed to occur first at all concentrations studied. The service life of respirator cartridges is significantly shortened by the displacement phenomenon (Yoon et al, 1992).
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 67-64-1.
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004) 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.
Acetone is a highly flammable liquid. Do not extinguish fire involving this compound unless flow can be stopped (AAR, 2000; Budavari, 2000). Water, applying from as far a distance as possible, can be used in flooding quantities as a fog and for cooling containers not yet on fire (AAR, 2000). Acetone ignites on contact with (HSDB, 2004; ITI, 1995; NFPA, 2002a; Urben, 1999): Acetone may accumulate static electrical charges, and thus cause ignition of its own vapors (Pohanish & Greene, 1997).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS67-64-1 (NFPA, 2002):
Listed as: Acetone Flammability Rating: 3 (3) Flammable. Liquids and solids that can be ignited under almost all ambient temperature conditions. Including liquids with a flash point below 73 degrees F and a boiling point above 100 degrees F, solid materials which form coarse dusts that burn rapidly without becoming explosive, materials which burn rapidly by reason of self-contained oxygen (ie, organic peroxides), and materials which ignite spontaneously when exposed to air.
- INITIATING OR CONTRIBUTING PROPERTIES
Acetone has a flashpoint ranging from -24 degrees C to -9.4 degrees C and poses a great combustion hazard (OHM/TADS , 2002; IPCS, 1998; ITI, 1995).
- FIRE CONTROL/EXTINGUISHING AGENTS
- FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
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.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
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.
- NFPA Extinguishing Methods for CAS67-64-1 (NFPA, 2002):
- Alcohol foam, dry chemical, or carbon dioxide may be used to fight fire involving acetone (AAR, 2000; OHM/TADS , 2002). Because acetone floats and mixes with water, straight hose streams of water may scatter and spread the fire and should not be used (CHRIS , 2002).
EXPLOSION HAZARD
- Explosion limits in air: 2.6 to 12.8 percent (Lewis, 2000).
- Acetone can react vigorously on contact with oxidizing materials, causing explosion danger (Lewis, 2000).
- Acetone reacts violently/explosively on contact with (HSDB, 2004; ITI, 1995; Lewis, 2000; NFPA, 2002a; Urben, 1999):
acetic acid bromine bromine trifluoride bromoform bromoform + potassium hydroxide chloroform + alkalies chloroform + solid potassium hydroxide or calcium hydroxide chromic anhydride chromyl chloride hexachloromelamine hydrogen peroxide 2-methyl-1,3-butadiene nitric acid nitrosyl chloride nitrosyl perchlorate nitryl perchlorate peroxomonosulfuric acid platinum + nitrosyl chloride potassium tert-butoxide thiodiglycol + hydrogen peroxide thiotriazyl perchlorate thiotrithiazyl perchlorate trichloromelamine sodium hypobromite sodium hypoiodite sulfur dichloride sulfuric acid + nitric acid water + 2,4,6-trichloro-1,3,5-triazine
- Due to its volatility, acetone may be dangerous if it is drawn into water intakes and it may explode if used in boiler water (CHRIS , 2002; OHM/TADS , 2002).
DUST/VAPOR HAZARD
- Acetone is readily absorbed from the lung (Bingham et al, 2001; HSDB, 2004). Inhalation of its vapors can cause headaches, excitement, and it can act as an anesthetic at very high concentrations (CHRIS , 2002; Lewis, 1998). It can irritate the nose, throat, trachea, and lungs: at 1660 ppm, acetone caused eye and nose irritation after 15 minutes (HSDB, 2004). However, the effect on the respiratory system is temporary, and acetone is not a respiratory tract sensitizer (CHRIS , 2002; IPCS, 1998).
- Acetone vapors are heavier than air and may travel to the source of ignition and flash back. Water spray may be used to disperse and knock down vapors (AAR, 2000).
- Acetone vapors are irritating and may explode if ignited in an enclosed area (CHRIS , 2002).
- Acetone may accumulate static electrical charges, and thus cause ignition of its own vapors (Pohanish & Greene, 1997).
REACTIVITY HAZARD
- Acetone ignites on contact with (HSDB, 2004; ITI, 1995; NFPA, 2002a; Urben, 1999):
- Acetone reacts violently/explosively on contact with (HSDB, 2004; ITI, 1995; Lewis, 2000; NFPA, 2002a; Urben, 1999):
acetic acid bromine bromine trifluoride bromoform bromoform + potassium hydroxide chloroform + alkalies chloroform + solid potassium hydroxide or calcium hydroxide chromic anhydride chromyl chloride hexachloromelamine hydrogen peroxide 2-methyl-1,3-butadiene nitric acid nitrosyl chloride nitrosyl perchlorate nitryl perchlorate peroxomonosulfuric acid platinum + nitrosyl chloride potassium tert-butoxide thiodiglycol + hydrogen peroxide thiotriazyl perchlorate thiotrithiazyl perchlorate trichloromelamine sodium hypobromite sodium hypoiodite sulfur dichloride sulfuric acid + nitric acid water + 2,4,6-trichloro-1,3,5-triazine
- Acetone is incompatible with (HSDB, 2004; ILO , 1998; ITI, 1995; Lewis, 2000):
chloroform chromium oxide chromyl anhydride chromyl chloride decaborane hexachloromelamine nitric acid nitric acid + acetic acid nitrosyl chloride nitryl perchlorate permonosulfuric acid sodium hypobromite (sulfuric acid + potassium dichromate) sulfuric acid thio-diglycol + hydrogen peroxide 1,1,1-trichloroethane trichloromelamine
- Acetone may accumulate static electrical charges, and thus cause ignition of its own vapors (Pohanish & Greene, 1997).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- LARGE SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
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.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering.
- "If fire becomes uncontrollable or container is exposed to direct flame, consider evacuation of one-third mile radius" (AAR, 1994).
- "If material is leaking (not on fire) consider evacuation from downwind area based on amount of material spilled, location and weather conditions" (AAR, 1994).
- AIHA ERPG Values for CAS67-64-1 (AIHA, 2006):
- DOE TEEL Values for CAS67-64-1 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Acetone TEEL-0 (units = ppm): 200 TEEL-1 (units = ppm): 200 TEEL-2 (units = ppm): 3200 TEEL-3 (units = ppm): 5700 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS67-64-1 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
Listed as: Acetone Proposed Value: AEGL-2 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-2 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape.
Listed as: Acetone Proposed Value: AEGL-3 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.
Listed as: Acetone Proposed Value: AEGL-1 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.
- NIOSH IDLH Values for CAS67-64-1 (National Institute for Occupational Safety and Health, 2007):
IDLH: 2500 ppm Note(s): [10%LEL]
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004) 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.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004)
Ventilate area of spill to disperse fumes (Sittig, 1991). Absorb acetone on paper, evaporate on a glass or iron dish in a hood, and then burn the paper (ITI, 1995)
LARGE SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 127 (ERG, 2004) Ventilate area of spill to disperse fumes (Sittig, 1991). Stop leak if it can be done so without personnel hazard; keep material out of water sources and sewers. Standing pools of liquid may be diluted with water spray. Dikes can be built to control flow. Water spray can be used to disperse and knock down vapors (AAR, 2000).
When water containing acetone is disinfected using chlorine, trichloromethane can be produced from the reaction of acetone with the hypochlorite ion formed by chlorine hydrolysis. This reaction is heavily dependent on pH and is expected to have an effect at pH 6 to 7 (Howard, 1990). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
Acetone is a good candidate for disposal through incineration; fluidized bed incineration, rotary kiln incineration, and liquid injection incineration are all viable methods (HSDB, 2004). (ITI, 1995). Acetone should be susceptible to removal from waste water using air stripping (HSDB, 2004).
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- The general public is exposed to atmospheric concentrations of acetone resulting from auto exhaust, solvent vapors, tobacco smoke, and fireplace emissions. Exposure through dermal contact from the use of consumer products, such as solvents, may also occur (Howard, 1990).
- AIR: Acetone is a common air contaminant. Acetone may be released into the environment as stack emissions and fugitive emissions (Howard, 1990; Lewis, 2000).
Acetone is a product of the photo-oxidation of some alkanes (such as propane) and alkenes found in urban air. It is also released from volcanoes and in forest fires. Exposure to acetone can occur from auto exhaust, tobacco smoke, and fireplaces. It is a metabolic product of plants and animals (including humans). It can also be found in microorganisms (ATSDR, 1994; Bingham et al, 2001; Howard, 1990). Tropospheric photooxidation of alkanes and alkenes accounts for 50% of the estimated annual emissions; whereas natural events accounts for 47% of the acetone emitted (Bingham et al, 2001). Several consumer products such as nail polish removers, carpet backing, paint removers, and liquid/paste waxes or polishes all contribute to atmospheric emissions of acetone (ATSDR, 1994). Acetone levels in indoor air are generally higher than those found outdoors (Bingham et al, 2001).
- WATER: Acetone may be released into the environment in wastewater during its production and use. Acetone may also leach into groundwater sources from municipal and industrial landfills (ATSDR, 1994; Howard, 1990). Drinking water may also contain acetone because of leaching from polyethylene distribution pipes (ATSDR, 1994).
- SOIL: Acetone readily leaches into soils from landfills. Other sources for acetone released to soil include disposal of agricultural and food wastes, animal waste, atmospheric wet deposition, and household septic tank effluents (IPCS, 1998).
- OTHER: Acetone has been detected in onions, apples, beans, peas, grapes, cauliflower, tomato, morning glory, and wild mustard (ATSDR, 1994; Howard, 1990).
ENVIRONMENTAL FATE AND KINETICS
In the air, acetone is lost by photolysis and reaction with photochemically-produced hydroxyl radicals. The estimated half-life from these combined processes is 22 days with shorter estimates in summer and longer in winter (Howard, 1990). This relatively long half-life allows acetone to be transported long distances from its emission source (ATSDR, 1994). The slow removal from the troposphere indicates that acetone is relatively un-reactive and a minor contributor to urban ozone and peroxylacyl nitrate concentrations (Bingham et al, 2001). Acetone is also expected to be removed through wet deposition (Howard, 1990). This compound has a UV absorption band at 270 nm that extends to approximately 330 nm, but ranks low in photochemical reactivity based on criteria such as ozone production (Howard, 1990). Hydroxyl Radical Reaction Half-life: 31 days (Bingham et al, 2001) Atmospheric Photolysis Half-life: 80 days (Bingham et al, 2001) The photooxidation half-life ranges from 279 hours (11.6 days) to 2790 hours (116 days) (Howard, 1991).
SURFACE WATER Acetone is removed from water predominately by biodegradation. Acetone does not adsorb significantly to sediment due to its high water solubility (ATSDR, 1994; Bingham et al, 2001; Howard, 1990). The surface water half-life ranges from a low of 24 hours (1 day) to a high of 168 hours (7 days)(Howard, 1991). Aqueous Photolysis Half-life: 40 days (Bingham et al, 2001) River Volatilization Half-life: 6 days (Bingham et al, 2001) Lake Volatilization Half-life: 100 days (Bingham et al, 2001) The photooxidation half-life ranges from a low of 9.92 x 10(4) hours (11.3 years) to a high of 3.97 x 10(6) hours (453 years) (Howard, 1991).
GROUND WATER
TERRESTRIAL Acetone will leach into the ground where it is expected to biodegrade rapidly. It is also expected to volatilize readily from soil surfaces due to its miscibility in water, low adsorption to soil, and high vapor pressure (Howard, 1990). The half-life in soil ranges from 24 hours (1 day) to 168 hours (7 days) (Howard, 1991).
ABIOTIC DEGRADATION
- Acetone rapidly biodegrades in soil and water. Biodegradation is expected to be the predominant removal mechanism in water. It does not adsorb to sediments due to it high water solubility. It has low adsorptive capability in soil and will volatilize from surface soil based on the high vapor pressure. In air, acetone can be removed by wet deposition, or it will undergo photodegradation by photolysis or reaction with photochemically-produced hydroxyl radicals. Acetone has a relatively long half-life of 22 days, allowing airborne transport away from the release point (Bingham et al, 2001; ATSDR, 1994; Howard, 1990).
BIODEGRADATION
- Although acetone readily biodegrades in both aerobic and anaerobic conditions, it is thought to be toxic to microorganisms at high concentrations (Howard, 1990).
- Aqueous Biodegradation Half-life: 0.6 days (Bingham et al, 2001)
- The aerobic half-life for aqueous biodegradation ranges from a low of 24 hours (1 day) to a high of 168 hours (14 days) (Howard, 1991).
- The anaerobic half-life for aqueous biodegradation ranges from a low of 96 hours (4 days) to a high of 672 hours (28 days) (Howard, 1991).
- Soil Biodegradation Half-life: 7 days (Bingham et al, 2001)
BIOACCUMULATION
ENVIRONMENTAL TOXICITY
- Acetone may be dangerous to aquatic life in very high concentrations (CHRIS , 2002).
LC50 - (ORAL) JAPANESE QUAIL, 14 days old: >40,000 ppm (HSDB, 2004) LC50 - (ORAL) RING-NECKED PHEASANT, 10 days old: >40,000 ppm (HSDB, 2004) LC50 - RAINBOW TROUT (Salmo gairdneri): 6100 mg/L for 24H -- in flow-through nominal condition at pH 8.0 and 10 degrees C with water hardness of 90 mg/L (IPCS, 1998) LC50 - RAINBOW TROUT (Salmo gairdneri), 1.0 gram in weight: 5540 mg/L for 96H -- in static condition at 12 degrees C (HSDB, 2004) LC50 - RAINBOW TROUT, fingerlings: 6486 ppm -- at 12 degrees C (OHM/TADS, 2002) LC50 - BLEAK (Alburnus alburnus): 11,000 mg/L for 96H -- in static nominal condition at pH 7.8 and 10 degrees C (IPCS, 1998) LC50 - MOSQUITO FISH (Gambusia affinis): 13,500 mg/L for 24H -- in static nominal condition at pH between 8.0 and 8.5 and temperature between 23 and 27 degrees C with water hardness less than 100 mg/L (IPCS, 1998) LC50 - MOSQUITO FISH (Gambusia affinis): 13,000 mg/L for 48H -- in static nominal condition at pH between 8.0 and 8.5 and temperature between 23 and 27 degrees C with water hardness less than 100 mg/L (IPCS, 1998) LC50 - MOSQUITO FISH (Gambusia affinis): 13,000 mg/L for 96H -- in static nominal condition at pH between 8.0 and 8.5 and temperature between 23 and 27 degrees C with water hardness less than 100 mg/L (IPCS, 1998) LC50 - FATHEAD MINNOW (Pimephales promelas): >100 mg/L for 96H -- in static nominal condition at pH between 6.5 and 8.5 (IPCS, 1998) LC50 - FATHEAD MINNOW (Pimephales promelas): 6290 mg/L for 96H -- at pH 7.62 and 24 degrees C with water hardness of 44.0 mg/L (IPCS, 1998) LC50 - FATHEAD MINNOW (Pimephales promelas): 6880 mg/L for 96H -- at pH 6.93 and 25 degrees C with water hardness of 53.5 mg/L (IPCS, 1998) LC50 - FATHEAD MINNOW (Pimephales promelas): 8120 mg/L for 96H -- at pH 7.58 and 25 degrees C with water hardness of 48.5 mg/L (IPCS, 1998) LC50 - BLUEGILL SUNFISH (Lepomis macrochirus): 8300 mg/L for 96H -- in static nominal condition at 18 degrees C with water hardness of 10 mg/L (IPCS, 1998) LC50 - GOLDFISH: 5000 mg/L for 24H (HSDB, 2004) LC50 - GUPPY (Poecilia reticulata): 7032 mg/L for 14D (HSDB, 2004) LC50 - FISH (Brachydanio rerio): 8100 mg/L for 96H (Verschueren, 2001) LC50 - MEXICAN AXOLOTL, 3 to 4 weeks after hatching: 20,000 mg/L for 48H (HSDB, 2004) LC50 - CLAWED TOAD, 3 to 4 weeks after hatching: 24,000 mg/L for 48H (HSDB, 2004) LC50 - FINGERLING TROUT: 6100 mg/L for 24H -- in flow-through condition (HSDB, 2004) LC50 - BRINE SHRIMP (Artemia salina): 2100 mg/L for 24H -- in static nominal condition (IPCS, 1998) LC50 - BRINE SHRIMP (Artemia salina): 6010 mg/L for 24H -- in static nominal condition at pH 7.4 and 12 degrees C with water hardness of 40 mg/L (IPCS, 1998) LC50 - BRINE SHRIMP (Artemia salina): 5540 mg/L for 96H -- in static nominal condition at pH 7.4 and 12 degrees C with water hardness of 40 mg/L (IPCS, 1998) LC50 - COPEPOD (Nitocra spinipes): 16,700 mg/L for 96H -- in static nominal condition at pH 7.8 and 10 degrees C (IPCS, 1998) LC50 - CRUSTACEAN (Streptocephalus rubricandatus): 64,300 mg/L for 24H -- in static nominal condition at pH 7.8 and 25 degrees C with water hardness of 250 mg/L (IPCS, 1998) LC50 - ASIATIC CLAM (Corbicula manilensis): >20,000 mg/L for 96H -- in static nominal condition at 16 degrees C with water hardness of 16 to 26 mg/L (IPCS, 1998) LC50 - CLAM, egg: >100 ppm for 48H (OHM/TADS, 2002) LC50 - CLAM, larva: >100 ppm for 288H (OHM/TADS, 2002) LC50 - OYSTER, egg: >100 ppm for 48H (OHM/TADS, 2002) LC50 - SNAIL (Helisoma trivolvis): >100 mg/L for 96H -- in static nominal condition at pH between 6.5 and 8.5 and 20 degrees C (IPCS, 1998) LC50 - SEGMENTED WORM (Lumbriculus variegatus): >100 mg/L for 96H -- in static nominal condition at pH between 6.5 and 8.5 and 20 degrees C (IPCS, 1998) LC50 - SIDE SWIMMER (Gammarus fasciatus): >100 mg/L for 96H -- in static nominal condition at pH between 6.5 and 8.5 and 20 degrees C (IPCS, 1998) LC50 - FLATWORM (Dugesia tigrina): >100 mg/L for 96H -- in static nominal condition at pH between 6.5 and 8.5 and 20 degrees C (IPCS, 1998) LC50 - PILLBUG (Asellus intermedius): >100 mg/L for 96H -- in static nominal condition at pH between 6.5 and 8.5 and 20 degrees C (IPCS, 1998) LC50 - WATER FLEA (Daphnia magna): 10 mg/L for 24H -- in nominal condition (IPCS, 1998) LC50 - WATER FLEA (Daphnia magna): 4068 mg/L for 24H -- in static nominal condition at pH 8.2 and 25 degrees C with water hardness of 90 to 110 mg/L (IPCS, 1998) LC50 - WATER FLEA (Daphnia magna): 10 mg/L for 24 to 48H (Verschueren, 2001) LC50 - WATER FLEA (Daphnia magna): 10 mg/L for 48H (IPCS, 1998) LC50 - WATER FLEA (Daphnia magna): 9218 mg/L for 48H -- in static nominal condition at pH 8.2 and 25 degrees C with water hardness of 90 to 110 mg/L (IPCS, 1998) LC50 - WATER FLEA (Daphnia magna): 12,100-13,300 mg/L for 48H -- in nominal condition (IPCS, 1998) LC50 - WATER FLEA (Daphnia magna): >100 mg/L for 96H -- in nominal condition at pH between 6.5 and 8.5 and 20 degrees C (IPCS, 1998) LC50 - WATER FLEA (Daphnia pulex): 8800 mg/L for 48H -- in nominal condition (IPCS, 1998) LC50 - WATER FLEA (Daphnia cuculata): 7460-7810 mg/L for 48H -- in nominal condition (IPCS, 1998) LC50 - WATER FLEA (Cesiodaphnia dubia): 8098 mg/L for 48H -- in nominal condition at pH 8.2 and 25 degrees C with water hardness of 90 to 110 mg/L (IPCS, 1998) LC50 - WATER FLEA (Cesiodaphnia dubia): 6693 mg/L for 240H -- in nominal condition at pH 8.2 and 25 degrees C with water hardness of 90 to 110 mg/L (IPCS, 1998) EC50 - WATER FLEA (Daphnia magna): >10,000 mg/L for 24H -- in immobilization condition (IPCS, 1998) EC50 - WATER FLEA (Daphnia magna): 13,500mg/L for 48H -- in nominal condition at pH 7.7 and 22 degrees C with water hardness of 154.5 mg/L (IPCS, 1998) EC50 - ALGA (Rhaphidocellis subcapitata): 7000 mg/L for 72H (Verschueren, 2001) EC50 - BACTERIUM (Vibrio fisheri): 85,000 mg/L for 15 minutes -- in Microtox test (Verschueren, 2001) EC50 - BACTERIUM (Photobacterium phosphoreum): 12,900 mg/L for 5 minutes -- in Microtox test (Verschueren, 2001) EC50 - BACTERIUM (Photobacterium phosphoreum): 8600 mg/L for 5 minutes -- in Microtox test (Verschueren, 2001) TLm - MOSQUITO FISH: 13,000 ppm for 48H -- in turbid water at 23-27 degrees C (CHRIS , 2002; OHM/TADS, 2002) TLm - HARLEQUIN FISH: 5700 ppm for 24H (OHM/TADS, 2002) TLm - BLUEGILL: 8300 ppm for 96H (OHM/TADS, 2002) TLm - DAPHNIA: 10 ppm for 48H (OHM/TADS, 2002) TLm - BRINE SHRIMP: 2100 ppm for 24H -- in static conditions (OHM/TADS, 2002) CV50 - RAINBOW TROUT (Salmo gairdneri): 36,500 mg/L for 24H -- at 18 degrees C (IPCS, 1998)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Acetone is a clear, colorless, volatile, and highly flammable liquid with a pungent and sweetish taste. It has an odor that has been described as fruity, characteristic ethereal, fragrant, and mint-like (Ashford, 1994; Budavari, 2000; HSDB , 2002; Lewis, 2000).
VAPOR PRESSURE
- 60 mmHg (at -2 degrees C) (OHM/TADS , 2002)
- 70 mmHg (at 0 degrees C) (Bingham et al, 2001)
- 89 mmHg (at 5 degrees C) (Verschueren, 2001)
- 180 mmHg (at 20 degrees C) (ACGIH, 1991; Harbison, 1998)
- 181.72 mgHg (at 20 degrees C) (IPCS, 1998)
- 182 mmHg (at 20 degrees C) (Clayton & Clayton, 1993)
- 185 mmHg (at 20 degrees C) (Bingham et al, 2001)
- 240 hPa (at 20 degrees C) (Lewis, 2000)
- 231 mmHg (at 25 degrees C) (HSDB , 2002)
- 270 mmHg (at 30 degrees C) (Verschueren, 2001)
- 184 mmHg (at 39.5 degrees C) (Sage, 1997)
- 400 mmHg (at 39.5 degrees C) (Lewis, 1996; OHM/TADS , 2002)
- 410 mmHg (at 40 degrees C) (Bingham et al, 2001)
SPECIFIC GRAVITY
- NORMAL TEMPERATURE AND PRESSURE
- OTHER TEMPERATURE AND/OR PRESSURE
0.7899 (at 20/4 degrees C) (HSDB , 2002) 0.791 (at 20/20 degrees C) (Clayton & Clayton, 1994) 0.792 (at 20/20 degress C) (ITI, 1995; Lewis, 1997)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
DENSITY
- NORMAL TEMPERATURE AND PRESSURE
(25 degrees C; 77 degrees F and 760 mmHg) 0.778 g/mL (ACGIH, 1991) 0.78440 g/mL (ATSDR, 1994; Clayton & Clayton, 1993; IPCS, 1998)
- OTHER TEMPERATURE AND/OR PRESSURE
0.780 g/cm(3) (at 30 degrees C) (Bingham et al, 2001) 0.784 g/cm(3) (at 25 degrees C) (Bingham et al, 2001) 0.78033 g/mL (at 30 degrees C) (ATSDR, 1994; IPCS, 1998) 0.78998 g/mL (at 20 degrees C) (ATSDR, 1994; IPCS, 1998) 0.7990 g/mL (at 20 degrees C) (Clayton & Clayton, 1993) 0.790 g/cm(3) (at 20 degrees C) (Bingham et al, 2001) 0.7972 g/mL (at 15 degrees C) (Lewis, 2000)
FREEZING/MELTING POINT
-94 degrees C (Budavari, 2000; ACGIH, 1991) -94.3 degrees C (Lewis, 1997; ITI, 1995) -94.6 degrees C (Lewis, 2000) -94.7 degrees C (at 760 mmHg) (Clayton & Clayton, 1993) -94.8 degrees C (HSDB , 2002) -95.35 degrees C (IPCS, 1998) -95.4 degrees C (Clayton & Clayton, 1994)
BOILING POINT
- 56.5 degrees C (ACGIH, 1991; Budavari, 2000)
- 56.2 degrees C (at 760 mmHg) (IPCS, 1998; ITI, 1995)
- 56.1 degrees C (OHM/TADS , 2002)
- 56 degrees C; 133 degrees F (at 760 mmHg) (HDSB, 2002; (NFPA, 2002a)
FLASH POINT
- -24 degrees C (OHM/TADS , 2002)
- -20 degrees C; -4 degrees F (closed cup) (ATSDR, 1994; ILO , 1998; ITI, 1995)
- -17 degress C (tag closed cup) (Bingham et al, 2001)
- -17.7 degrees C; 0 degrees F (closed cup) (Budavari, 2000; IPCS, 1998; Lewis, 2000)
- -17.2 degrees C; 1 degrees F (closed cup) (CHRIS, 20002)
- -9.4 degrees C; 15 degrees F (open cup) (IPCS, 1998; ITI, 1995)
- -9.0 degrees C (cleveland open cup) (Bingham et al, 2001)
AUTOIGNITION TEMPERATURE
- 465 degrees C; 869 degrees F (color) (ILO , 1998; Lewis, 2000; NFPA, 2002a)
- 537 degrees C; 1000 degrees F (Lewis, 1997)
- 537.8 degrees C (ITI, 1995)
- 603 degrees C (OHM/TADS , 2002)
EXPLOSIVE LIMITS
12.8% (IPCS, 1998; NFPA, 2002a) 13.0% (ATSDR, 1994; Bingham et al, 2001)
SOLUBILITY
infinitely soluble in water (Bingham et al, 2001; OHM/TADS , 2002) and lighter than water (AAR, 2000; (CHRIS , 2002)
Acetone is freely miscible with alcohol, dimethylformamide, chloroform, ether, and most oils and is soluble in benzene (Ashford, 1994; Budavari, 2000; Lewis, 1997).
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow = -0.24 (Bingham et al, 2001)
HENRY'S CONSTANT
- 6.8x10(-6) atm-m(3)/mol (Ehrenfeld et al, 1986)
- 1.87X10(-5) atm-m(3)/mole (measured) (at 25 degrees C) (HSDB , 2002)
- 3.67x10(-5) atm-m(3)/mol (Howard, 1990)
- 4.26x10(-5) atm-m(3)/mol (IPCS, 1998)
- 2.05 atm (Bingham et al, 2001)
SPECTRAL CONSTANTS
OTHER/PHYSICAL
0.2 to 1.5 ppm (Harbison, 1998) 4ppm; 9.5 mg/m(3) (detection) (IPCS, 1998) 13 ppm (volume by volume); 13 mcL/L (AQUIRE, 1997; (HSDB , 2002) 13 to 20 ppm; 30 to 48 mg/m(3) (absolute) (ATSDR, 1994; IPCS, 1998) 100 to 140 ppm; 237 to 332 mg/m(3) (100% odor recognition) (ATSDR, 1994; IPCS, 1998) 200 to 400 ppm (ACGIH, 1991) Editor's Note: Adaptation to the odor of acetone occurs quickly both during an exposure and between exposure sessions. In addition, differences in sensitivity can also be observed as a function of sex and age (Bingham et al, 2001). Water: 20 ppm (weight by volume); 20 mg/L (HSDB , 2002; IPCS, 1998)
553 g/m(3) (at 20 degrees C) (HSDB , 2002; Verschueren, 2001) 825 g/m(3) (at 30 degrees C) (Verschueren, 2001)
23.2 dyn/cm (at 20 degrees C) (Clayton & Clayton, 1993) 26.2 mN/m (at 0 degrees C) (HSDB , 2002) 23.7 mN/m (at 20 degrees C) (HSDB , 2002) 21.2 mN/m (at 40 degrees C) (HSDB , 2002)
1.3560 (Clayton & Clayton, 1993) 1.3591 (at 20 degrees C) (Budavari, 2000; Lewis, 1997; ITI, 1995) 1.3588 (at 20 degrees C/d) (HSDB , 2002) 0.3587 (at 20 degrees C) (Clayton & Clayton, 1993)
- NUCLEAR MAGNETIC RESONANCE
0.32 cP (at 20 degrees C) (HSDB , 2002) 0.303 cP (at 25 degrees C) (IPCS, 1998)
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