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ACETONE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Acetone is a solvent.

Specific Substances

    1) Acetone
    2) Dimethylformaldehyde
    3) Dimethyl ketal
    4) Dimethyl ketone
    5) Ketone propane
    6) Methyl ketone
    7) Propanone
    8) Pyroacetic acid
    9) Pyroacetic ether
    10) Beta ketopropane
    11) 2-propanone
    12) CAS 67-64-1
    13) ACETON
    1.2.1) MOLECULAR FORMULA
    1) C3H6O CH3COCH3

Available Forms Sources

    A) FORMS
    1) There are multiple grades of acetone: technical, CP, NF, electronic, and spectrophotometric (Lewis, 1997).
    a) The commercial grade of acetone is generally 99.5 percent pure and contains less than 0.4 percent water and 0.1 percent organic matter (Bingham et al, 2001).
    B) SOURCES
    1) 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).
    2) 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).
    3) 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).
    C) USES
    1) 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):
    a) 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.
    2) 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).
    3) 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).
    4) Acetone is used as a solvent for cements in the leather and rubber industries (ACGIH, 1991a).
    5) It is used for cleaning and drying parts of precision equipment (ATSDR, 1994; ACGIH, 1991a; Lewis, 1997).
    6) Acetone is the primary chemical in some fingernail polish removers, paint removers, and varnish removers (Hathaway et al, 1996).
    7) It can be used as a brine for low temperature heat transfer agent in indirect refrigeration (HSDB, 2002).
    8) 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.

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: In industry used as a solvent and chemical intermediate. Also used in some nail polish removers, and paint and varnish removers.
    B) TOXICOLOGY: Lipid soluble solvent, causes CNS effects similar to ethanol.
    C) 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.
    D) WITH POISONING/EXPOSURE
    1) 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.
    2) 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.
    3) 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.
    4) 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.
    5) OCULAR: Acetone and its vapors are mildly irritating to the eyes and mucous membranes. Corneal erosions are a rare effect after high concentration exposure.
    0.2.20) REPRODUCTIVE
    A) Acetone has not caused teratogenic effects in mice and rat studies. Spermatogenesis, including sperm morphology, motility, and count, has been observed in rats. Post-implantation mortality has been noted in mammals (species unspecified).

Laboratory Monitoring

    A) Monitor blood glucose, serum bicarbonate and acetone, and urine ketones in patients with moderate to severe symptoms.
    B) Monitor mental status and vital signs. Evaluate patients with significant CNS depression for respiratory depression and the ability to protect their airway.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE POISONING
    1) Generally requires no specific intervention. Administer intravenous fluids and antiemetics as necessary.
    B) MANAGEMENT OF SEVERE POISONING
    1) Administer intravenous 0.9% saline for hypotension or persistent tachycardia. Endotracheal intubation and mechanical ventilation may be required in patients with CNS or respiratory depression. Evaluate for gastrointestinal bleeding after large ingestion.
    C) DECONTAMINATION
    1) EMESIS: Emesis is not recommended because of the potential for CNS depression and subsequent aspiration.
    2) Activated charcoal is of limited utility; routine use is not recommended.
    3) Consider insertion of a nasogastric tube to aspirate stomach contents only after recent, large acetone ingestions.
    D) ENHANCED ELIMINATION
    1) Hemodialysis enhances clearance of acetone, but is almost never indicated. It may be considered in patients with hemodynamic instability or acidosis not responding to supportive care.
    E) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients with inadvertent exposures to small quantities of household products can be monitored at home.
    2) OBSERVATION CRITERIA: Symptomatic patients and those with deliberate or large exposures should be referred to a healthcare facility.
    3) ADMISSION CRITERIA: Admit patients with persistent CNS depression, hypotension, persistent tachycardia, or gastrointestinal bleeding to an intensive care setting.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for patients with severe manifestations such as coma, hypotension, or gastrointestinal bleeding.
    F) TOXICOKINETICS
    1) Well absorbed orally; dermal and inhalation absorption occur, but rarely cause systemic toxicity. Volume of distribution 0.8 L/kg. Mostly excreted unchanged, primarily by the lungs, to a lesser extent renally. Limited metabolism to acetate and formate. Half life is about 4 hours at low levels of exposure, increases to 19 to 31 hours after large exposures.
    G) DIFFERENTIAL DIAGNOSIS
    1) Diabetic ketoacidosis. Ethanol or isopropanol intoxication.
    0.4.3) INHALATION EXPOSURE
    A) Remove from exposure. Administer oxygen if respiratory distress develops. Treat wheezing or persistent coughing with inhaled beta agonists.
    0.4.4) EYE EXPOSURE
    A) Irrigate eyes with 0.9% saline after splash exposures. Perform a slit lamp exam in patients with persistent irritation. Refer to an ophthalmologist if corneal injury is present.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Remove contaminated clothing and wash exposed skin with soap and water. An emollient cream may provide symptomatic relief in patients with irritation or defatting dermatitis.

Range Of Toxicity

    A) Ingestion of 200 mL (2 to 3 mL/kg) produced coma, hyperglycemia, and acetonuria in an adult.
    B) In a 30-month-old child, approximately 180 mL of nail polish remover (65% acetone, 10% isopropyl alcohol) caused severe toxicity (ie, seizures, CNS and respiratory depression, hypothermia, hyperglycemia, ketonemia, acidosis).
    C) Ingestion of small amounts of acetone (volume and concentration) such as that found in fingernail preparations generally does not cause significant toxicity except in very young children.

Clinical Effects

Summary Of Exposure

    A) USES: In industry used as a solvent and chemical intermediate. Also used in some nail polish removers, and paint and varnish removers.
    B) TOXICOLOGY: Lipid soluble solvent, causes CNS effects similar to ethanol.
    C) 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.
    D) WITH POISONING/EXPOSURE
    1) 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.
    2) 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.
    3) 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.
    4) 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.
    5) OCULAR: Acetone and its vapors are mildly irritating to the eyes and mucous membranes. Corneal erosions are a rare effect after high concentration exposure.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CORNEAL IRRITATION
    a) LIQUID: Prolonged eye contact with liquid acetone has resulted in permanent corneal opacity in one case and temporary corneal opacity in another case. Cellulose acetate was present in the acetone solution and may have contributed to the ocular effects (Grant & Schuman, 1993).
    b) VAPORS: Eye injury is unlikely from vapor concentrations which are tolerable to humans . One case of injury to the corneal epithelium has been reported in a human who was exposed to acetone vapor and acetaldehyde. Acetaldehyde was considered the cause of the corneal damage (Grant & Schuman, 1993).
    c) CASE REPORT: Bilateral corneal erosion occurred in a 49-year-old man following occupational exposure to acetone (Piatkowski et al, 2007).
    d) ANIMALS (LIQUID): Temporary edema, corneal epithelium irregularity, and discoloration of the stroma occurred in rabbit eyes exposed to several drops of acetone (Grant & Schuman, 1993). Recovery occurred by 2 to 5 days. A severe reaction of the rabbit eye to undiluted acetone has also been reported (Carpenter & Smyth, 1946).
    e) ANIMALS (VAPORS): Injury to the corneal epithelium and conjunctiva has occurred in experimental animals exposed to uncomfortably high concentrations (Grant & Schuman, 1993).
    2) IRRITATION
    a) LIQUID: Splash contact with acetone causes immediate stinging, followed by mild epithelial injury which resolves in a day or two (Grant & Schuman, 1993).
    b) VAPORS: Acetone vapors are irritating to the eyes (Hathaway et al, 1996a). Brief exposure to vapor concentrations of 500 to greater than 1000 parts per million have caused subjective complaints of eye irritation (Nelson et al, 1943; Raleigh & McGee, 1972).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Brief exposure to vapor concentrations of 500 parts per million (ppm) to greater than 1000 ppm can cause transient nasal irritation (Nelson et al, 1943; Raleigh & McGee, 1972). No symptoms occurred at vapor concentrations of 100 ppm to 500 ppm (DiVincenzo et al, 1973).
    2) The acetone odor is detected at concentrations of 200 parts per million (ppm) to 500 ppm (DiVincenzo et al, 1973; Raleigh & McGee, 1972), but many individuals do not notice the odor until air concentrations reach or exceed 1000 ppm (Raleigh & McGee, 1972).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Mucus membrane irritation may occur with ingestion or vapor inhalation.
    2) ERYTHEMA: 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).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Tachycardia may develop with severe poisoning (Harris & Jackson, 1952; Hift & Patel, 1961; Gamis & Wasserman, 1988).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension has been reported with severe poisoning (Harris & Jackson, 1952; Gamis & Wasserman, 1988; Knapp et al, 1997).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) TACHYCARDIA
    a) ANIMAL STUDY: Acetone increased the atrial contraction rate and stimulated norepinephrine release in isolated rat hearts (Chentanez et al, 1987).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) INJURY OF UPPER RESPIRATORY TRACT
    1) WITH POISONING/EXPOSURE
    a) No adverse effects have been reported in 1 study involving exposure to vapor concentrations of 100 to 500 parts per million (ppm) (DiVincenzo et al, 1973). Mucous membrane irritation may occur with exposure to vapor concentrations in excess of 1000 ppm (Raleigh & McGee, 1972). A sensation of chest tightness was reported in a worker who was believed to have been exposed to acetone vapors in excess of 12,000 ppm during three 2-minute periods. The symptoms lasted 4 hrs (Ross, 1975).
    B) ACUTE RESPIRATORY INSUFFICIENCY
    1) WITH POISONING/EXPOSURE
    a) High vapor concentrations can produce CNS depression and unconsciousness (Hathaway et al, 1996a; Ross, 1975). Exposure by any route which results in significant CNS depression may cause respiratory depression as a secondary effect.
    b) CASE REPORT: Severe respiratory and central nervous system depression developed in a 30-month-old boy who had ingested an unknown quantity of an acetone-based (65% acetone and 10% isopropyl alcohol) fingernail polish remover. Intubation and mechanical ventilation were required (Gamis & Wasserman, 1988).
    c) CASE REPORT: Intubation and mechanical ventilation were required for 14 hours in a 42-year-old man who ingested approximately 800 mL of acetone (Zettinig et al, 1997).
    d) CASE REPORT: A 49-year-old man developed edema and reddish epithelium of the bronchial tree following inhalational exposure of acetone. Bronchoscopy confirmed the diagnosis of inhalation injury, and mechanical ventilation was required due to impaired oxygenation of the patient. The patient also developed rhabdomyolysis and acute renal failure, which resolved following supportive therapy, including continuous veno-venous hemofiltration (Piatkowski et al, 2007).
    C) HYPERVENTILATION
    1) WITH POISONING/EXPOSURE
    a) KUSSMAUL'S RESPIRATION: Deep, irregular and rapid respirations may develop in patients with severe intoxication (Harris & Jackson, 1952; Hift & Patel, 1961).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) Depression of the central nervous system can occur. Sedation, ataxia, nystagmus, coma and other effects have been reported (van Wijngaarden et al, 1995; Zettinig et al, 1997; Gitelson et al, 1966; Ross, 1975; Gamis & Wasserman, 1988; Hathaway et al, 1996a; Lewis, 2000).
    B) ABNORMAL BEHAVIOR
    1) WITH POISONING/EXPOSURE
    a) 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).
    b) CASE SERIES: One hundred thirty-seven human volunteers were tested for neurobehavioral performance changes and biochemical indicators during and after a short duration (4 hour) exposure to either acetone at 250 parts per million (ppm), methylethyl ketone (MEK) at 200 ppm, acetone at 125 ppm with MEK at 100 ppm, or a chemical placebo. Ethanol (95%, 0.84 mL/kg) was used as a positive control. Blood and breath concentrations during and after exposure did not demonstrate any interaction between the two solvents, nor were statistically significant sex differences during uptake or elimination. Only the 250 ppm acetone exposure produced small but statistically significant differences from controls in two measures of the auditory tone discrimination task, and on the anger-hostility scale (males only) of the psychological "Profile of Mood states (POMS) test". Ethanol at 0.07 to 0.08 percent blood concentration caused significant decrements on both the auditory tone and tracking tests in the dual task (Dick et al, 1988; Dick et al, 1989).
    C) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT (RARE): Tonic-clonic seizures developed in a 30-month-old child who may have ingested 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).
    b) CASE REPORT: 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).
    D) HYPERESTHESIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT (RARE): Hyperesthesia of the legs and an abnormal gait developed in a 42-year-old man after ingesting 200 mL of acetone. Symptoms had resolved 2 months later (Gitelson et al, 1966).
    E) CEREBRAL EDEMA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 31-year-old woman presented with lethargy and increased muscle tone in the upper extremities. Fluid-attenuated inversion recovery images (FLAIR) revealed bilateral hyperintensities of the putamina, globi pallidi, and thalami extending to the brain stem, and apparent diffusion coefficient (ADC) maps indicated the presence of vasogenic edema. Laboratory analysis revealed serum acetone and isopropanol levels of 836 mg/L (200-fold above normal) and 10 mg/L (5-fold above normal), respectively. With supportive care, the patient's serum acetone level decreased and her symptoms gradually resolved without neurologic sequelae (Kallenberg et al, 2008).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting have developed after dermal and inhalational exposure to an acetone-containing liquid which was used to set plaster casts (Strong, 1944; Harris & Jackson, 1952; Hift & Patel, 1961) and after exposure to acetone vapors in excess of 12,000 parts per million (ppm) (Ross, 1975). No nausea and vomiting was reported in individuals exposed to concentrations slightly greater than 1000 ppm (Raleigh & McGee, 1972).
    B) HEMATEMESIS
    1) WITH POISONING/EXPOSURE
    a) Hematemesis has been reported in two patients who developed persistent vomiting after significant dermal and inhalational exposure. The patients had been exposed to an acetone-containing fluid which was used to set their orthopedic casts (Strong, 1944; Harris & Jackson, 1952; Hift & Patel, 1961)
    b) CASE REPORT: Grossly bloody gastrostomy drainage and guaiac positive stools were reported in a 17-month-old girl who was repeatedly poisoned with acetone by her mother (Knapp et al, 1997).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) Kidney damage may occur (Lewis, 2000).
    B) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 49-year-old man developed mild rhabdomyolysis and acute renal failure following occupational inhalational and dermal exposure to acetone. Five days postexposure, laboratory data revealed elevated creatine kinase levels (1712 units/L) and mild myoglobinuria (220 mcg/L), as well as elevated creatinine and urea levels. The rhabdomyolysis and renal failure resolved with normalization of laboratory parameters following supportive therapy, including continuous veno-venous hemofiltration (Piatkowski et al, 2007).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) 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; Sakata et al, 1989).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Mild irritant effects in humans may include erythema, drying, scaling, peeling and burning (Kechijian, 1991; van Wijngaarden et al, 1995). Dermatitis and skin defatting may also occur (Harbison, 1998).
    B) NAIL FINDING
    1) WITH POISONING/EXPOSURE
    a) Nail brittleness and peeling can develop after repeated application (Kechijian, 1991).
    C) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Superficial dermal burns, involving the face, neck, and upper extremities, occurred in a 49-year-old man following occupational exposure to acetone. The burns covered 18% of his total body surface area (Piatkowski et al, 2007).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DERMATITIS
    a) RABBITS: Mild reactions have been reported in the standard draize test and in the open draize test in rabbits (RTECS , 1995).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 49-year-old man developed rhabdomyolysis and acute renal failure following occupational inhalational and dermal exposure to acetone. Five days postexposure, laboratory data revealed elevated creatine kinase levels (1712 units/L) and mild myoglobinuria (220 mcg/L), as well as elevated creatinine and urea levels. The rhabdomyolysis and renal failure resolved with normalization of laboratory parameters following supportive therapy, including continuous veno-venous hemofiltration (Piatkowski et al, 2007).

Reproductive

    3.20.1) SUMMARY
    A) Acetone has not caused teratogenic effects in mice and rat studies. Spermatogenesis, including sperm morphology, motility, and count, has been observed in rats. Post-implantation mortality has been noted in mammals (species unspecified).
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) There are suggestive reports of acetone being linked with complications of pregnancy and birth defects (Nizjaeva, 1982), interference with the menstrual cycle at 1000 parts per million (Anon, 1975), low hemoglobin levels and miscarriages (Malysheva, 1974), and CNS birth defects (Holmberg, 1977). These reports are either anecdotal or involve mixed exposures, such that a cause-and-effect relationship between human reproductive effects and exposure to acetone cannot be determined. In a more recent occupational study, risks of miscarriages and birth defects, verified by hospital records, were not increased by laboratory work with acetone during pregnancy (Axelsson et al, 1984). Details on exposures have generally been lacking in these studies.
    B) ANIMAL STUDIES
    1) Animal studies have been negative when chick eggs were injected prior to incubation or in vitro mutagenicity was studied (AMA, 1985). Teratogenicity studies in rats and mice have been negative (Schardein, 1993).
    2) Acetone itself was not teratogenic in mice and rats by inhalation at doses up to 6600 parts per million (ppm) and 11,000 ppm, respectively, although resorptions were increased in the highest dosage groups (Mast et al, 1988).
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) Acetone freely crosses the placenta in humans and has been found at higher levels in the fetus than in the mother (Dowty, 1976). Similar findings have been noted in experimental animals (Nizyaeva & Silanteva, 1984). Acetone in the maternal urine has correlated with higher perinatal mortality (Naeye, 1981); this may be related to complications from gestational diabetes.
    B) ANIMAL STUDIES
    1) Post-implantation mortality was noted in mammals (RTECS , 2002).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS67-64-1 (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):
    1) Not Listed
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) Acetone is not classifiable as to human carcinogenicity, based on a lack of data concerning carcinogenicity in humans or animals (IRIS , 1995). No listing for acetone has been found in summaries by the International Agency for Research on Cancer (IARC) and the National Toxicology Program (NTP) (IARC, 1987; US DHHS, 1994).
    2) Deaths from all types of cancer were lower than expected in a group of 948 workers exposed to acetone levels up to 1070 parts per million for periods up to 23 years, compared to the US population (Ott et al, 1983a, 1983b, 1983c).
    3) A retrospective study of cancer deaths in the rubber industry showed a relationship between exposure to acetone and lymphatic leukemia, but the exposures were mixed with other solvents (Wilcosky, 1984).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Acetone has been used as a solvent for test vehicles in lifetime rodent carcinogenicity studies; the incidence of tumors in acetone-treated animals has not differed from untreated controls (Van Duuren et al, 1978; Zakova et al, 1985; Ward et al, 1986; Peristianis et al, 1988). Acetone has not caused cancer in animals, either in the hamster cheek pouch assay (Odukoya & Shklar, 1984) or when painted on the skin of mice for 1 year (Depass, 1984).
    2) Acetone was inactive as a tumor promotor in mice when 0.1 mL was applied to the skin 3 times per week for 441 days; it may have actually suppressed development of tumors induced by 7,12-dimethylbenz(a)anthracene (DMBA) (Van Duuren et al, 1971). It also prevented development of tumors in mice if applied to the skin prior to DMBA (Weiss et al, 1988). However, it has accelerated the action of other carcinogens on the skin (Bradbury, 1941; Slaga & Fischer, 1983).

Genotoxicity

    A) Acetone caused sex chromosome loss/nondisjunction in S. cerevisiae and was positive on cytogenic analysis in hamster fibroblasts.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor blood glucose, serum bicarbonate and acetone, and urine ketones in patients with moderate to severe symptoms.
    B) Monitor mental status and vital signs. Evaluate patients with significant CNS depression for respiratory depression and the ability to protect their airway.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Measurement of serum/urine acetone and blood glucose, can be used to monitor the initial severity of ingestion or inhalation as well as subsequent improvement.
    B) LABORATORY INTERFERENCE
    1) Acetone will interfere with some laboratory tests: bromosulfophthalein, phenolsulfonphthalein, inositol, metformin, phenformin, and methionine give false positive values with acetone present.
    2) Acetone interferes with the colorimetric determination of serum creatinine (used in most Autoanalyzer(R) systems) resulting in falsely elevated values (Hawley & Falko, 1982). If the urinalysis and BUN are not consistent with acute renal failure, then acetone may be considered responsible for the elevated serum creatinine.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Urinary acetone can be used to monitor acetone concentrations.
    2) Urinary unaltered acetone concentration may be a good indicator of workplace exposure since it has a linear relationship to both amounts of acetone absorbed and average environmental concentration (Pezzagno et al, 1986; Fujino et al, 1992).

Methods

    A) OTHER
    1) Acetest(R) tablets may be useful to check the urine and/or serum.
    2) Since acetone is excreted by the lungs, the odor of acetone is usually found on the patient's breath.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Admit patients with persistent CNS depression, hypotension, persistent tachycardia, or gastrointestinal bleeding to an intensive care setting.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Ingestion of small amounts of acetone, such as that found in fingernail preparations, generally does not cause significant toxicity, except in very small children. These children may be watched at home.
    1) Warn parents to watch for lethargy, ataxia, and incoherent speech.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for patients with severe manifestations such as coma, hypotension, or gastrointestinal bleeding.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) The prolonged elimination half life of acetone may require medical supervision for up to 30 hours in symptomatic patients, especially children (Ellenhorn & Barceloux, 1988a).
    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) The prolonged elimination half life of acetone may require medical supervision (up to 30 hours) in symptomatic patients, especially children (Ellenhorn & Barceloux, 1988a).

Monitoring

    A) Monitor blood glucose, serum bicarbonate and acetone, and urine ketones in patients with moderate to severe symptoms.
    B) Monitor mental status and vital signs. Evaluate patients with significant CNS depression for respiratory depression and the ability to protect their airway.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
    B) ACTIVATED CHARCOAL
    1) Activated charcoal is of limited utility in the treatment of acetone ingestion. Routine pre-hospital administration of activated charcoal is not recommended.
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS
    1) Emesis is not recommended because of the potential for CNS depression and subsequent aspiration.
    B) ACTIVATED CHARCOAL
    1) Usual doses of activated charcoal are unlikely to adsorb a clinically important amount of acetone. Use of activated charcoal should only be considered in circumstances where the potential benefit outweighs the risk (primarily concern about toxic coingestants).
    2) IN VITRO STUDY: A 20:1 ratio (gram for gram) of activated charcoal to acetone bound 92% of acetone in water. A 10:1 ratio of activated charcoal to acetone bound 75% of the acetone, and ratios of 5:1 or less bound up to about 43% of acetone in water (Burkhart & Martinez, 1992). Thus, 80 g of activated charcoal would adsorb about 75% of the acetone in a 10-mL ingestion of 100% acetone (nail polish remover may contain 50% to 100% acetone).
    C) NASOGASTRIC ASPIRATION
    1) Consider insertion of a nasogastric tube to aspirate stomach contents in patients with large, recent ingestions. Evaluate the patient's ability to protect the airway and the need for endotracheal intubation first.
    6.5.3) TREATMENT
    A) SUPPORT
    1) In general, ingestion of small amounts of acetone (volume and concentration), such as that found in fingernail preparations, will not require treatment.
    2) Treat patients symptomatically.
    B) MONITORING OF PATIENT
    1) Monitor blood glucose, serum acetone, urine acetone, and arterial pH in symptomatic patients.
    2) Monitor urine output and fluid intake. Maintain adequate hydration with intravenous fluids, as necessary.
    C) DIETARY FINDING
    1) Adjust diet depending on degree of gastroesophageal irritation.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: 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, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) HEMOPERFUSION
    1) Hemoperfusion is NOT effective for acetone elimination. It failed to decrease acetone levels in one reported case (Sakata et al, 1989).
    B) HEMODIALYSIS
    1) Hemodialysis has been shown to enhance elimination of acetone in patients with isopropanol intoxication. In one report, the average dialysance of isopropyl alcohol and acetone were 137 and 165 mL/minute, respectively (Rosansky, 1982). It should generally only be considered in patients with hemodynamic compromise unresponsive to supportive care.
    C) HYPERVENTILATION
    1) Since acetone is eliminated unchanged in breath, careful hyperventilation may increase elimination in comatose intubated patients (Zettinig et al, 1997). Efficacy of this procedure has not been established.

Range Of Toxicity

Summary

    A) Ingestion of 200 mL (2 to 3 mL/kg) produced coma, hyperglycemia, and acetonuria in an adult.
    B) In a 30-month-old child, approximately 180 mL of nail polish remover (65% acetone, 10% isopropyl alcohol) caused severe toxicity (ie, seizures, CNS and respiratory depression, hypothermia, hyperglycemia, ketonemia, acidosis).
    C) Ingestion of small amounts of acetone (volume and concentration) such as that found in fingernail preparations generally does not cause significant toxicity except in very young children.

Minimum Lethal Exposure

    A) ADULT
    1) The lowest reported lethal dose in humans (unreported route): 1159 mg/kg (RTECS , 2002).
    2) Lethal concentration in human blood: 550 mcg/mL (55 mg%) (HSDB , 2002).

Maximum Tolerated Exposure

    A) ADULT
    1) No toxic effects were reported in adults after oral administration of 40 to 80 mg/kg (Haggard et al, 1944).
    2) 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.
    3) 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).
    4) 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.
    5) 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).
    6) 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).
    7) CASE REPORTS
    a) 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).
    B) PEDIATRIC
    1) 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).
    2) In children, ingestion of 2 to 3 mL/kg is considered toxic (HSDB , 2002).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) NORMAL LEVELS (NON-TOXIC): Acetone is produced endogenously and as a metabolite of isopropyl alcohol. Endogenous blood acetone levels can range up to 10 mg/L in healthy adults (Baselt, 2000).
    2) KETOACIDOSIS: Acetone levels during diabetic or fasting ketoacidosis can range from 100 to 700 mg/L (Ramu et al, 1978; Lewis, 1984).
    3) A blood level of 2500 mg/L was associated with lethargy and unsteadiness in a patient with suspected acetone ingestion. The patient had a history of chronic ethanol abuse (Ramu et al, 1978).
    4) Blood acetone levels of 330 mg/L did not result in intoxication in volunteers exposed to acetone by inhalation or ingestion (Haggard et al, 1944) .

Workplace Standards

    A) ACGIH TLV Values for CAS67-64-1 (American Conference of Governmental Industrial Hygienists, 2010):
    1) 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.
    a) Adopted Value
    1) Acetone
    a) TLV:
    1) TLV-TWA: 500 ppm
    2) TLV-STEL: 750 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: BEI
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.
    c) TLV Basis - Critical Effect(s): URT and eye irr; CNS impair; hematologic eff
    d) Molecular Weight: 58.05
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:
    b) Under Study
    1) Acetone
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s):
    d) Molecular Weight:
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS67-64-1 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Acetone
    2) REL:
    a) TWA: 250 ppm (590 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 2500 ppm
    b) Note(s): [10%LEL]
    1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

    C) Carcinogenicity Ratings for CAS67-64-1 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Acetone
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Acetone
    3) EPA (U.S. Environmental Protection Agency, 2011): Not applicable. This substance was not assessed using the EPA's 1986 cancer guidelines. ; Listed as: Acetone
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Acetone
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS67-64-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Acetone
    2) Table Z-1 for Acetone:
    a) 8-hour TWA:
    1) ppm: 1000
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 2400
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 1297 mg/kg
    2) male: 3.1 g/kg (Bingham et al, 2001a)
    B) LD50- (ORAL)MOUSE:
    1) 5800 mg/kg: behavioral changes
    2) 3 g/kg
    3) male, 5.2 g/kg (Bingham et al, 2001)
    C) LD50- (INTRAPERITONEAL)RAT:
    1) 1.3 g/kg (Bingham et al, 2001a)
    2) 0.61 g/kg (Bingham et al, 2001a)
    D) LD50- (ORAL)RAT:
    1) newborn: 1726 mg/kg (IPCS, 1998)
    2) 14-day-old: 4393 mg/kg (IPCS, 1998)
    3) young adult: 7138 mg/kg (IPCS, 1998)
    4) older adult: 6667 mg/kg (IPCS, 1998)
    5) 5800 mg/kg: weight loss and prostration (IPCS, 1998)
    6) 9.8 g/kg (Bingham et al, 2001)
    7) 7.3 g/kg (Bingham et al, 2001)
    8) male: 9.75 g/kg (Bingham et al, 2001)
    9) female: 8.5 g/kg (Bingham et al, 2001)
    10) female, 10.0 g/kg (Bingham et al, 2001)
    E) TCLo- (INHALATION)HUMAN:
    1) 500 ppm: sensory and respiratory systems changes
    2) male: 440 mcg/m(3) for 6M: CNS changes
    3) male: 10 mg/m(3) for 6H: biochemical changes
    4) male: 12,000 ppm for 4H: nausea and muscle weakness
    F) TCLo- (INHALATION)RAT:
    1) 199 mg/m(3) for 8H/45D: intermittent: muscle contraction
    2) 19,000 ppm for 3H/8W: intermittent: changes in brain weight

Pharmacology Toxicology

Toxicologic Mechanism

    A) CARDIAC EFFECTS: In rats, the increase in atrial contraction rate (ACR) caused by acetone in the range 10 to 210 nanometers may be partly due to an increase in norepinephrine release from the sympathetic nerve terminals in the atrium (Chentanez et al, 1987).
    B) HEPATOTOXIC POTENTIATION BY KETONES: In a rat model, acetone potentiates the hepatotoxicity of chloroform and carbon tetrachloride (Hewitt et al, 1986) 1987; (Charbonneau et al, 1986) 1988).
    C) Acetone induces changes in microsomal metabolism (Lieber et al, 1988; Puntarulo & Cederbaum, 1988) (Hankakoshi et al, 1988). It does not affect hepatic glutathione levels (Hewitt et al, 1987), nor does it decrease the oxidation capacity of hepatic enzymes (Kanofsky & Axelrod, 1986).

Physicochemical

Physical Characteristics

    A) 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).

Molecular Weight

    A) 58.08

Other

    A) ODOR THRESHOLD
    1) 0.2 to 1.5 ppm (Harbison, 1998)
    2) 4ppm; 9.5 mg/m(3) (detection) (IPCS, 1998)
    3) 13 ppm (volume by volume); 13 mcL/L (AQUIRE, 1997; (HSDB , 2002)
    4) 13 to 20 ppm; 30 to 48 mg/m(3) (absolute) (ATSDR, 1994; IPCS, 1998)
    5) 100 to 140 ppm; 237 to 332 mg/m(3) (100% odor recognition) (ATSDR, 1994; IPCS, 1998)
    6) 200 to 400 ppm (ACGIH, 1991)
    7) 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).
    8) Water: 20 ppm (weight by volume); 20 mg/L (HSDB , 2002; IPCS, 1998)

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