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Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
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ACETONE

BACKGROUND INFORMATION

PHYSICAL AND CHEMICAL PROPERTIES

Structural formula:

CH3COCH3

Molecular weight:

58.08

Chemical name:

2-Propanone

Synonyms:

Acetone; dimethyl ketone; dimethyl ketal; −ketopropane

CAS number:

67641

Melting point:

−95.35°C

Boiling point:

56.2°C

Density:

0.7899 (20°/4°)

Index of refraction:

1.3588 (20°/0°)

Vapor pressure:

226.3 mm Hg (25°C)

Flash point:

Tag closed cup; −4°F (−20°C); tag open cup, −2°F (−19°C)

Fire point:

−2°F (−19°C)

Flammable limits in air:

2.6–12.8% by volume; autoignition temperature, 1,000°F (538°C)

Solubility:

Miscible with water in all proportions; miscible with alcohol, dimethylformamide, chloroform, ether, and most oils

Stability:

Chemically stable liquid

General characteristics:

A colorless liquid with a pungent odor and taste; volatile and extremely flammable; forms explosive mixtures with air or oxygen.

Other chemical properties:

Forms crystalline compounds with alkali bisulfites; reducing agents convert it to isopropyl alcohol (Hays, 1958).

Conversion factors:

ppm=0.42 (mg/m3)

mg/m3=2.38 (ppm)

OCCURRENCE AND USE

Acetone occurs naturally, being found in plants and animals, such as fowl and fish (Walter et al., 1975). It is the only methyl ketone detected in animal tissues. In some pathologic conditions associated with excessive fat catabolism, mammals accumulate acetone; acetoacetate and ß-hydroxybutyrate are then found as “ketone bodies” or “acetone bodies” in the blood.

Acetone is used as a solvent for resins, lacquers, oils, fats, waxes, rubber cements, plastics, cotton, cellulose acetate, and acetylene. It is used in the production of ketene, acetic anhydride, methyl methacrylate, diacetone alcohol, methyl isobutyl ketone, isophorone, chloroform, iodoform, and vitamin C. It is used in the paint, lacquer, and varnish industry; in the rubber, plastics, dyeing,

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

celluloid, photographic, and explosives industries; and in the manufacture of artificial silk and leather.

Acetone may be found in such products as solvents, cooking fuels, corn remover, drawing inks, fuel-system deicer, glue, nail-polish remover, paint-brush cleaners, paint and varnish removers, and china, film, fishing-rod, metal, plastic, and shoe cements. U.S. production of acetone in 1973 was a billion pounds.

SUMMARY OF TOXICITY INFORMATION

EFFECTS ON HUMANS

Several pertinent examples of effects on humans of uncontrolled and controlled exposure to acetone are listed in Tables 2 and 3.

EFFECTS ON ANIMALS

Acute, Subchronic, and Chronic Exposure

Results of acute, subchronic, and chronic exposure of animals to acetone are summarized in Table 4. Excretion of this relatively nontoxic substance prevents its accumulation, unless doses are overwhelming. The rate of elimination is about 2.3%/h (Haggard et al., 1944).

Carcinogenicity, Mutagenicity, and Teratogenicity

McLaughlin et al. (1963) injected 0.05 ml of undiluted acetone into the yolk sac of fertile chick eggs before incubation. The hatch yield was 70%, with no evidence of teratogenicity. The same investigators (1964) similarly injected 39 and 78 mg of acetone into the yolk sac of fertile chick eggs before incubation. The hatch yields were 80% and 50%, respectively, again with no evidence of teratogenicity.

Caujolle et al. (1966) exposed 72- and 96-h-old chick embryos to various doses of acetone. The LD50 and ED50 values for malformations were 48.6 mg and 18.0 mg, respectively, for the 72-h-old embryos and 28.7 mg and 25.0 mg for the 96-h-old embryos.

Park and Koprowska (1968) painted the cervical tissue of virgin C3H/HcJ mice with acetone for up to 5 mo; no tumors resulted. A 1% solution of benzo[a]pyrene in acetone induced invasive carcinoma in all the test animals.

Mazzucco (1975) reported that acetone, often used as a vehicle for skin carcinogens, did not lower the skin collagen content of mice (unlike benzene and toluene). Stenback et al. (1977) reported that p-amino-o-nitrophenol, p-phenylenediamine, and sodium thioglycollate were nontoxic when applied to mouse and rabbit skin in acetone solution.

In a study of the carcinogenic potential of prostaglandins, control male albino Swiss mice treated topically with only acetone

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

exhibited no tumors, whereas experimental mice treated with combinations of 3-methylcholanthrene and prostaglandins in acetone solution developed tumors (Lupulescu, 1978).

McCann et al. (1975) tested acetone for mutagenicity in the Salmonella/microsome test and found it to be without effect.

PHARMACOKINETICS

Absorption and Distribution

An acetone inhalation study was performed in man (100–500 ppm) and beagles (100, 500, and 1,000 ppm) for 2–4 h (DiVincenzo et al., 1973). In both species, the acetone concentrations in the breath and blood were directly proportional to the magnitude of exposure, and the acetone half-life in blood (3 h) was the same for both man and dog. Exercise significantly increased the extent of acetone absorption in man. Blood acetone in man increased sharply during exposure and reached maximums in 2 h of 2 mg/L and 10 mg/L in subjects exposed at 100 and 500 ppm, respectively. The acetone excreted 24 h after exposure was only a fraction of the quantity absorbed. Results of routine biochemical tests were unaffected in the human subjects by any of the exposures used. The beagles absorbed approximately 5 times more acetone than man under comparable conditions (expressed as amount absorbed per kilogram of body weight).

Rats were given various doses of acetone intraperitoneally to determine tissue absorption and distribution patterns 1–2 h after treatment (Haggard et al., 1944). At 100 mg/kg, blood acetone was 113 mg/L, tissue acetone was 90 mg/kg, and acetone was metabolized and eliminated in urine and expired air at 10 mg/kg. At 500 mg/kg, the corresponding figures were 570 mg/L, 464 mg/kg, and 30 mg/kg; and at 1,000 mg/kg, they were 1,150 mg/L, 941 mg/kg, and 59 mg/kg. At 2,000 mg/kg, blood and tissue concentrations were almost double those at 1,000 mg/kg, but the amount eliminated was 4 times as large. Three rats at rest were given acetone orally at 40, 50, and 60 mg/kg. At the lowest dose, blood acetone reached 41 mg/L; tissue acetone, about 34 mg/kg; and acetone was metabolized or eliminated at about 3 mg/kg. At 60 mg/kg, the corresponding figures were 63 mg/L, 53 mg/kg, and 7 mg/kg. Acetone clearance from the blood of a 68-kg man given acetone orally at 80 mg/kg was determined from alveolar air concentrations and compared with the rat clearance rate. Blood acetone started at 72 mg/L, and disappeared in 27 h; in rats, disappearance took only 10.5 h.

Mongrel dogs exposed to acetone vapor at 140–310 ppm (0.36–0.80 μg/ml) retained 52% at respiratory rates of 5–18/min (Egle, 1973). Retention was lower (42%) in an animal whose respiratory rate was higher (21–40/min). Total retention of acetone at respiratory rates of 10–15/min increased significantly (p<0.01) from 52% at vapor concentrations of 180–280 ppm (0.46–0.72 mg/ml) to 59% at concentrations of 530–680 ppm (1.35–1.75 mg/ml).

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×
Metabolism and Excretion

Four rats were given acetone intraperitoneally at 3,000 mg/kg within a few minutes (Haggard et al., 1944). After a 4-h period for distribution of the acetone, blood was withdrawn successively from different rats at intervals of up to 47 h. In the first 15 h, acetone was lost at about 100 mg/L per liter of blood, with smaller and decreasing losses up to virtually complete disappearance by 47 h.

These same authors reported that in simulated industrial exposures at 5.35 mg/L (in air) for 8 h/d for 9 d, it was observed that acetone accumulated if the amount of acetone absorbed in the first 8 h exceeded the amount that could be eliminated during the following 16 h in ambient air. At the next 8-h challenge, blood acetone increased over that of the earlier exposure. In humans exposed to acetone at 1, 3, and 5 mg/L (420, 1,270, and 2,100 ppm) in ambient air, the relation of exposure to blood acetone after 8 h was as follows:

Exposure, ppm

Blood Acetone Concentration, mg/L

420

30

1,270

99

2,100

162

Blood acetone in the subject who had 162 mg/L 8 h after the first exposure decreased to 79 mg/L on 16-h recovery. After a second 8-h exposure, it increased to 180 mg/L and decreased to 89 mg/L on 16-h recovery. After a third 8-h exposure, blood acetone increased to 182 mg/L and decreased to 91 mg/L after 16 h.

INHALATION EXPOSURE LIMITS

Table 5 lists the recommended occupational exposure limits for acetone in various countries. The American Conference of Governmental Industrial Hygienists (1980) recommends a threshold limit value-time weighted average (TLV-TWA) concentration for acetone of 750 ppm on the basis of data suggesting that only mild irritation has been observed at exposures below 1,000 ppm.

On the basis of odor perception threshold, Tkach (1968) suggested that the minimal perceptible acetone concentration should be 1.096 mg/m3 for the most sensitive persons.

COMMITTEE RECOMMENDATIONS

EXPOSURE LIMITS

In 1958, the Committee recommended the following maximal concentrations of acetone for various durations of exposure (Hays, 1958):

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

Concentration, ppm

Duration of Exposure

15,000

1 h

10,000

4 h

5,000

8 h

300

1 wk

100

30 d

40

60 d

25

90 d

These concentrations were derived from the estimated maximal amount of acetone that could be absorbed during the exposure, assuming 100% absorption from the respiratory tract. These recommendations were applicable for single exposures during the stated duration of exposure.

In 1966, the Committee suggested the following EELs and CEL for acetone:

60-min EEL:

15,000 ppm

24-h EEL:

2,000 ppm

90-d CEL:

300 ppm

Nelson et al. (1943) concluded that 500 ppm was the highest tolerable concentration of acetone for an 8-h exposure, on the grounds that 500 ppm produced eye, nose, and throat irritation in experimental subjects. These sensory responses were unpleasant, but not necessarily “toxic.” The data suggested that a 90-d continuous exposure not exceed 200 ppm.

Haggard et al. (1944) reported no indications of toxicity in exposures of men to acetone at 2,100 ppm (5 mg/L) in air for 8 h/d. They considered this an upper limit of exposure. They also considered a blood content of 340 mg/L as an upper limit. These authors also reported that 1.0 mg/L in air resulted in 8 mg/L in blood when exposure was for 1 h and the subjects were at rest. If this relation is linear, 42 mg/L in air would result in 340 mg/L in blood; this concentration would equal 17,500 ppm for men at rest or 8,750 ppm for men at exercise.

Raleigh and McGee (1972) studied the effects of exposures of filter press operators to acetone. Their data supported a TLV of 1,000 ppm. Both subjective and objective test data were obtained. Vigliani and Zurlo (1955) reported that Italian workers exposed to 700–1,000 ppm for 3 h/d over 7–15 yr showed inflammation of the respiratory tract, stomach, and duodenum and occasional attacks of giddiness and asthenia. At 1,000 ppm, they excreted acetone at 160 mg/L in urine. By the morning after exposure, they excreted acetone at 10 mg/L. These investigators, reporting from the Workers Clinic in Milan, recommended 500 ppm as a maximal exposure concentration for workers (8 h/d). Under these circumstances, 1,000 ppm would be tenable as an EEL for 24 h.

If 1.34 mg/L in urine equals 1.00 mg/L in blood (from Haggard et al., 1944), then 160 mg/L in urine equals 119 mg/L in blood at 1,000 ppm in air (3-h exposure), and 2,807 ppm in air equals 334 mg/L in blood (upper limit of Haggard et al., 3 h.), and 8,421 ppm equals 334

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

mg/L in blood (1 h). Thus, the data of both Haggard et al. (1944) and Vigliani and Zurlo (1955) suggest a concentration of about 8,500 ppm as a 1-h EEL for moderately active men.

The data of Vigliani and Zurlo (1955) also support a figure of 200 ppm for a 90-d GEL as do those of Nelson et al. (1943). Additional support for this concentration is provided by the data of Raleigh and McGee (1972) on repeated exposures to acetone in the work place.

To summarize, the Committee currently recommends the following:

60-min EEL:

8,500 ppm

24-h EEL:

1,000 ppm

90-d GEL:

200 ppm

RESEARCH RECOMMENDATIONS

Because of the wide use of acetone (1.9 billion pounds in 1973), it is suggested that information on the following subjects be obtained:

Cataract formation: The marked ability of acetone to produce cataracts in the guinea pig suggests that chronically exposed workers be examined to determine whether man is similarly affected.

Chronic health effects in workers: Available data are insufficient for determining chronic health effects in workers.

Reproduction: Information on reproductive effects of acetone in animals and man is incomplete.

Skin effects: Acetone is a cutaneous irritant. Data are required to determine methods for avoiding exposures that lead to dermatitis.

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

TABLE 2

Effects on Humans of Uncontrolled Exposure to Acetone

No.a

Age, yra

Sexa

Agentsa

Concentrationa

Durationa

Clinical Effects

Pathologya

Ref.

1

12

ND

Damp acetone dressing

ND

ND

Death

ND

Cossmann (1903), as quoated by Lehmann and Flury (1943)

2

18, 19

F

Acetone vapor and MEKb vapor

330–500 ppm (acetone),

400–500 ppm (MEK)

1 d

Gastric distress and fainting in 1 worker, fainting and seizure in 1 worker

ND

Smith and Mayers (1944), as quoted by Walter et al. (1975)

ND

ND

ND

Acetonec

1,000 ppm

3 h/d for 7–15 yr

Chronic inflammation of respiratory tract, stomach, and duodenum; occasional attacks

At end of shift, acetone exhaled at 0.2 mg/L of air and present in urine at 160 mg/L; next morning, acetone exhaled at 0.3 ng/L and in urin at 10 mg/L.

Vigliani and Zurlo (1955)

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

No.a

Age, yra

Sexa

Agentsa

Concentrationa

Durationa

Clinical Effects

Pathologya

Ref.

4

30–57

M

Acetone vapor

12,000 ppm

4–5 h

Weakness of extremities, headache, eye irritation, light-headedness, feelings of drunkenness and vertigo

Acetone in 2 workers’ urine at 2.4 mg/100 ml 45 min after immobilization; in other 2 workers’ urine at 0.5–1.3 mg/100 ml up to 7 d after exposure

Ross (1973) as quoted by Walter et al. (1975)

1

48

M

Commercial organic solvent containing benzene, methanol, and acetone

ND

2.3 h

Death

Epiglottic hyperemia, abundant pulmonary edema, negative results in tissues analyzed for common toxicants

Winek et al. (1973)

9

4

ND

M

Acetone vapor exposure of filter press operators

1,006 ppm (average)

6 h/d for 2–3 yr

Slight eye, nose and throat irritation at 1.000–1,500 ppm

No remarkable findings

Raleigh and McGee (1972)

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

No.a

Age, yra

Sexa

Agentsa

Concentrationa

Durationa

Clinical Effects

Pathologya

Ref.

8

30–57

M

Acetone vapor

12,000 ppm (TLV, 1,000)

0.5 d

Irritation of mucous membranes of eyes, nose, and throat; nausea and vomiting

Acetone in urine at 4–7 mg/100 ml at initial consultation, at 0.39–1.29 mg/100 ml 7 d after exposure

Rosa (1975)

1

41

M

Acetone vapor

ND

3 mo; 40% of time was spent fitting polyvinyl chloride piping (cleaned with acetone and other solvents)

Hyposmia and parosmia associated with solvent exposure; otherwise, normal reaults of physical examination

Inability to identify standard solutions by smell; improved after exposure ended

Emmett (1976)

4

ND

F(2),

M(2)

Acetone vapor and liquid

ND

Acute

Death

Lesions of the parenchymal organs, e.g., liver and kidneys

Mirchev (1978)

aND=no data available.

bMEK=methyl ethyl ketone.

cMight not have been “pure” exposure.

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

TABLE 3

Effects on Humane of Controlled Exposure to Acetone

No.a

Age, yra

Sexa

Agents

Concentration

Duration

Clinical Effectsa

Pathology

Ref.

6

ND

M

Acetone

1 ml applied to the forearm surface

90 min

ND

Mild cutaneous edema and hyperemia with moderate layer disorganization; electron microscope showed disrupted desmosomes and keratin, vacuolization, and organelle changes; cell damage primarily in the stratum corneum and stratum spinosum

Lupulescu et al., 1973, as quoted by Walter et al. (1975)

24

18–28

M

Acetone gas

250–270 ppm, 500–750 ppm

6 h, with 1 h free from exposure after the first 3 h (2 d)b

Period of heartbeat in 500 ppm group shortened, that in control group (no exposure) lengthened

Galvanic skin reflex decreased in exposed groups; cerebral activities higher in exposed groups than control group

Suzuki (1973)

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

No.a

Age, yra

Sexa

Agents

Concentration

Duration

Clinical Effectsa

Pathology

Ref.

10

18–25

M, F

Acetone vapor

127–131 ppm

4 h

ND

Acetone concentration in expired air decreased slowly after cessation of exposure; much retained acetone eliminated through lungs as unchanged solvent; mean retention of acetone after 2-h exposure 17.6 ±5.1% in men, 11.3 ±5.4% in women; acetone uptake higher in men than in women; respiratory excretion, 16.3±2.8%

Nomiyama and Nomiyama (1974 a, b)

ND

ND

ND

Acetone (percutaneous absorption)

Topical application to 12.5 cm2 of skin

2 h/d for 4 consecutive days, 4 h/d for 4 consecutive days

Fairly rapid skin penetration of acetone; concentration of acetone in blood, alveolar air, and urine decreased rapidly to normal value by next morning

2 h/d: acetone in blood, alveolar air, and urine at 5–12 μg/ml, 5–12 ppm, and 8–14 μg/ml, respectively; 4 h/d: acetone in blood, alveolar air, and urine at 26–44 μg/ml, 25–34 ppm, and 29–41 μg/mlb

Fukabori et al. (1979)

aND=no data available.

b2-h application to 12.5 cm2 of skin corressponds to about 2-h exposure at 50–150 ppm in air.

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

TABLE 4

Effects on Animals of Exposure to Acetone

Compound Puritya

Species, Strain, Sex, Numbera

Route of Administration

Dosea

Durationa,b

Effects

Reference

“pure, undiluted”

Rat, rabbit, dog; ND ND; 35 rats, 14 rabbits, 8 dogs

Intravenous (also by stomach tube in rabbits)

Rats 4,000–8,700 mg/kg; rabbits 790–7900 mg/kg; dogs, ND

Effects usually noted immediately

Maximal tolerated dose for rats was 4,000 mg/kg; and minimal lethal dose, 5,000 mg/kg or more; 2 rabbits given 3,950 mg/kg intravenously died at end of 50–85 sec injection period; injection into anesthetized dogs decreased blood pressure

Walton et al., (1928) as quoted by Walter et al. (1975)

ND

Rabbit, ND, ND, ND

Inhalation

ND

ND

Loss in weight, in some cases to 1/3 original; symptoms of intoxication included irritation, CNS disturbances, decreases in RBC and Hb, and increases in urobilin

Bassi and Ghezzi (1936) as quoted in Chemical Abstracts (1937).

ND

Guinea pig, ND, F, 10

Inhalation

20,000 ppm

24.4 h

8 of 10 animals died during or soon after exposure ended; by 865 min after exposure, 10 animals were comatose; gradual but regular slowing in heart rate

Specht et al. (1939)

Specht et al. (1940) as quoted by Walter et al. (1975)

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

Compound Puritya

Species, Strain, Sex, Numbera

Route of Administration

Dosea

Durationa,b

Effects

Reference

ND

Rat, ND, ND, ND

Inhalation

2,110–126,000 ppm

ND

At 42,000 ppm, death in 4.5–5.5 h; at 84,000 ppm, in 2.5–3 h; at 126,000 ppm, in 1.75–2.25 h

Haggard et al. (1944) as quoted by Walter et al. (1975)

ND

Rabbit, albino, ND, ND

Topical application to eyes

0.005 ml

1 min

Corneal injury covering 3/4 of eye surface or more severe damage covering smaller area

Carpenter and Smyth (1946) as quoted by Walter et al. (1975)

ND

Rabbit, ND M+F, 4 each

Intracranial injection

700 mg/kg

4–6 times on alternate days

Convulsions followed each injection within 5–15 sec; examination of ether-extracted brains suggested that acetone directly or indirectly caused brain fat dissolution, leading to demyelination and other insulation defects

Anderson (1949) as quoted by Walter et al. (1975)

ND

Rat, ND, M+F, 10

Oral

490 mg/kg

ND

Isonicotinic acid hydrazide-induced convulsions and maximal electroshock seizures completely inhibited; against electroshock scizures, acetone ED50 was 220 mg/kg, TD50 was 2,450 mg/kg, and the LD50 was 3,460 mg/kg

Kohli et al. (1967) as quoted by Walter et al. (1975)

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

Compound Puritya

Species, Strain, Sex, Numbera

Route of Administration

Dosea

Durationa,b

Effects

Reference

ND

Rat, Sprague-Dawley, M, 6–12

Oral

ND

ND

Ataxia, dyspnea, and cyanosis at 3,950 mg/kg in young adults; maximal permissible limit for single oral exposure is approx. 4.0 mg/kg for rats

Kimura et al. (1971) as quoted by Walter et al. (1975)

ND

Guinea pig, random-bred, albino, M+F, 28

Topical application onto clipped skin of dorsal thorax or subcutaneously (0.05 ml 1:1 acetone/saline or 0.05 ml 5% acetone in saline)

1 ml

2 times/d

5 d/wk for 4 or 8 wk; controls received saline in an identical manner or nothing (exposure acute and subchronic)

Cataracts in 9 of 28 guinea pigs over a period of 3–8 wk; lens changes began as early as 8 wk and as late as 6 mo and consisted of subcapsular foci or extensive vacuolated areas extending from periphery toward lens center; histologic appearance of lenses similar to that of senile cataracts and some forms of diabetic cataracts

Rengstorff et al. (1971)

Acetone vapor, obtained by passing air through pure acetone at 0°C

Dog, mongrel M+F, ND, (12–26 kg)

Inhalation

0.36–0.80 μg/ml

ND (type of exposure unknown)

Uptake of acetone by total respiratory tract 65–70%

Egle (1973)

Acetone as 25% solution in water

Rat, Sprague-Dawley, M, ND, (180–235 g)

Oral

2.5 mg/kg

0–40 h elapsed between exposure and sacrifice (type of exposure unknown)

Pretreatment with acetone increased hepatic microsomal activity, as shown by increased capacity to bind 14CCl4 and l4CHCl3 covalently and to N-demethyllate DMN.

Sipes et al. (1973)

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

Compound Puritya

Species, Strain, Sex, Numbera

Route of Administration

Dosea

Durationa,b

Effects

Reference

ND

(probably absolute acetone)

Rabbit, New Zealand White, M 5 F, 20 (10 test, 10 control)

Application directly onto akin of dorsal thorax

1 ml

3 times/wk for 3 wk (controls received saline in an identical manner)

None developed lens abnormalities during 6 mo observation period

Rengstorff et al. (1974)

Insecticides in acetone solution

Mice, ND, F, ND

Dermal and oral

0.1 ml dermally in acetone at 1 mg/kg

Sacrificed 5, 15, 30, and 60 min; 8 and 48 h after application

Penetration of acetone twice as rapid through the GI tract as dermally

Ahdaya et al. (1978)

Diterpene esters in acetone solution

Mice, albino LACA, F, 6

Topical administration to inner surface of one ear (other ear used as control)

5 1 of various dilutions

Observation periods of 30 min-24 h

Persistent inflammatory changes

Evans and Schmidt (1979)

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

Compound Puritya

Species, Strain, Sex, Numbera

Route of Administration

Dosea

Durationa,b

Effects

Reference

ND

Rat, Sprague-Dawley, M, ND

Inhalation

12,600–50,600 ppm

3 h/d

5 d/wk for 8 wk (exposure subchronic)

No residual toxic effects, according to biochemical assays and histopathoiogic examination of of sacrified specimens

Bruckner and Peterson (1978)

ND

Rat, ND ND, ND

Inhalation

1.657 kg/m3

90 d (exposure chronic)

Disordered antagonist muscle activity and decreased serum cholinesterase activity and urinary coproporphyrin levels

Osintseva et al. (1967)

aND=no data available.

bType of exposure acute, unless otherwise noted.

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

TABLE 5

Occupational Exposure Limits for Acetone

Country

Concentration,a mg/m3

Year

Ref.

United States

2,400 (TWA)

1974

Winell, 1975

East Germany

2,400 (TWA)

1974

Winell, 1975

West Germany

1,000 (TWA)

1973

Winell, 1975

Sweden

1,200 (TWA)

1975

Winell, 1975

Czechoslovakia

800 (TWA)

1969

Winell, 1975

USSR

200 (C)

1972

Winell, 1975

Italy

1,000 (TWA)

1975

Soc. Ital. Di Med. Del Lav., 1975

Japan

1,200 mg/m3 (TWA)

1964

Japan Assoc. Ind. Hlth., 1971

aTWA=time-weighted average concentration; C=ceiling concentration.

Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

REFERENCES

American Conference of Governmental Industrial Hygientists. 1980. Documentation of the Threshold Limit Values. 4th ed. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists.

Anderson, C.L. 1949. Experimental production of convulsive seizures. J. Nerv. Ment. Dis. 109:210–219.

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Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
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Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

Nomiyama, K., and Nomiyama, H. 1974. Respiratory elimination of organic solvents in man. Benzene, toluene, n-hexane, trichloroethylene, acetone, ethyl acetate and ethyl alcohol. Int. Arch. Arbeitsmed. 32:85–91.


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Suggested Citation:"Acetone." National Research Council. 1984. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/689.
×

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