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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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,
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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).
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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):
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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)
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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)
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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)
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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)
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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)
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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)
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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)
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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. Ahdaya, S.M., Shah, P.V., and Guthrie, F.E. 1978. Comparative penetration (in vivo) of insecticides through the skin and gastrointestinal tract of mice. Toxicol. Appl. Pharmacol. 45:320, abstr. no. 235. Bassi, U., and Ghezzi, G. 1936. Experimental studies on intoxication with acetone. Med. Lav. 27:225–239. [Chem. Abs. 31:80269, 1937] Bruckner, J.V., and Peterson, R.G. 1978. Effect of repeated exposure of mice and rats to concentrated toluene and acetone vapors. Toxicol. Appl. Pharmacol. 45:359, abstr. no. 328. Carpenter, C.P., and Smyth, H.F., Jr. 1946. Chemical burns of the rabbit-cornea. Am. J. Ophthalmol. 29:1363–1372. Caujolle, F., Huron, R., Moulas, F. and Cros, S. 1966. Statistical comparison of the teratogenic actions of two products. Ann. Pharm. Franc. 24:23–28. [Chem. Abs. 65:4468g, 1966] Cossmann. 1903. Azetonvergiftung nach Anlegung eines Zelluloid-Mullverbandes. Munch. Med. Wochenschr. 50:1556–1557. DiVincenzo, G.D., Yanno, F.J., and Astill, B.D. 1973. Exposure of man and dog to low concentrations of acetone vapor. Am. Ind. Hyg. Assoc. J. 34:329–336. Egle, J.L., Jr. 1973. Retention of inhaled acetone and ammonia in the dog. Am. Ind. Hyg. Assoc. J. 34:533–539. Emmett, E.A. 1976. Parosmia and hyposmia induced by solvent exposure. Brit. J. Ind. Med. 33:196–198. Evans, F.J., and Schmidt, R.J. 1979. An assay procedure for the comparative irritancy testing of esters in the tigliane and daphnane series. Inflammation (N.Y.) 3:215–223. Fukabori, S., Nakaaki, K., and Tada, O. 1979. On the cutaneous absorption of acetone. Rodo Kagaku 55:525–32. [Chem. Abs. 92:70603x, 1980] Haggard, H.W., Greenberg, L.A., and Turner, J.McC. 1944. The physiological principles governing the action of acetone together with determination of toxicity. J. Ind. Hyg. Toxicol. 26:133–151.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Hays, H.W. 1958. Report on Acetone. Prepared by Toxicological Information Center. National Academy of Sciences, Washington, D.C. [9 p.] Japan Association of Industrial Health. 1971. Recommendations for permissible concentrations, etc. Jpn. J. Ind. Health 13:475–484. Kimura, E.T., Ebert, D.M., and Dodge, P.W. 1971. Acute toxicity and limits of solvent residue for sixteen organic solvents. Toxicol. Appl. Pharmacol. 19:699–704. Kohli, R.P., Kishor, K., Dua, P.R., and Saxena, R.C. 1967. Anticonvulsant activity of some carbonyl-containing compounds. Indian J. Med. Res. 55:1221–1225. Lehmann, K.B., and Flury, F., eds. 1943. Toxicology and Hygiene of Industrial Solvents. Baltimore: Williams and Wilkins. [378 p.] Lupulescu, A. 1978. Enhancement of carcinogenesis by prostaglandins. Nature 272:634–636. Lupulescu, A.P., Birmingham, D.J., and Pinkus, H. 1973. An electron microscopic study of human epidemis after acetone and kerosene administration. J. Invest. Dermatol. 60:33–45. Mazzucco, K. 1975. Effect of some solvents (benzene, toluene, acetone) used for carcinogens on the collagen content of mouse dosral skin. Oesterr. Z. Onkol. 2:49–51. [Chem. Abs. 85:187512p, 1976] McCann, J., Choi, E., Yamasaki, E., and Ames, B. 1975. Detection of carcinogens as mutagens in the Salmonella/microsome test: Assay of 300 chemicals. Proc. Natl. Acad. Sci. USA 72:5135–5139. McLaughlin, J., Jr., Marliac, J.-P., Verrett, M.J., Mutchler, M.K., and Fitzhugh, O.G. 1963. The injection of chemicals into the yolk sac of fertile eggs prior to incubation as a toxicity test. Toxicol. Appl. Pharmacol. 5:760–771. McLaughlin, J., Jr., Marliac, J.-P., Verrett, M.J., Mutchler, M.K., and Fitzhugh, O.G. 1964. Toxicity of fourteen volatile chemicals as measured by the chick embryo method. Am. Ind. Hyg. Assoc. J. 25:282–284. Mirchev, H. 1978. Hepatorenal lesions in acute acetone poisoning. Vutr. Boles. 17(2):89–92. Nelson, K.W., Ege, J.F., Jr., Ross, M., Woodman, L.E., and Silverman, L. 1943. Sensory response to certain industrial solvent vapors. J. Ind. Hyg. Toxicol. 25:282–285. Nomiyama, K., and Nomiyama, H. 1974. Respiratory retention, uptake, and excretion of organic solvents in man. Benzene, toluene, n-hexane, trichloroethylene, acetone, ethyl acetate and ethyl alcohol. Int. Arch. Arbeitsmed. 32:75–83.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 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. Osintseva, V.P., Pogosyan, U.G., and Kolbasova, O.D. 1967. Experimental resorptive effect of small concentrations of acetone and phenol on the organism. Sb. Tr. Inst. Epidemiol. Gig. Arm. SSR No. 5:358–362. [Chem. Abs. 71:104901b, 1969] Park, H.-Y., and Koprowska, I. 1968. A comparative in vitro and in vivo study of induced cervical lesions of mice. Cancer Res. 28:1478–1489. Raleigh, R.L., and McGee, W.A. 1972. Effects of short, high-concentration exposures to acetone as determined by observation in the work area. J. Occup. Med. 14:607–610. Rengstorff, R.H., Petrali, J.P., and Sim, V.M. 1971. Cataracts induced in guinea pigs by acetone, cyclohexanone, and dimethyl sulfoxide. Edgewood Arsenal Technical Report, Edgewood Arsenal, Maryland. Rengstorff, R.H., Petrali, J.P., and Sim, V.M. 1974. Attempt to induce cataracts in rabbits by cutaneous application of acetone. Edgewood Arsenal, Aberdeen Proving Ground, Maryland. Ross, D.S. 1975. Acute acetone intoxication: Case history. Occup. Health 27:120–124. Ross, D.S. 1973. Acute acetone intoxication involving eight male workers. Ann. Occup. Hyg. 16:73–75. Sipes, I.G., Stripp, B., Krishna, G., Maling, H.M., and Gillette, J.R. 1973. Enhanced hepatic microsomal activity by pretreatment of rats with acetone or isopropanol. Proc. Soc. Exp. Biol. Med. 142: 237–240. Smith A.R., and Mayers, M.R. 1944. Poisoning and fire hazards of butanone and acetone. Ind. Bull. (N.Y. State Dept. Labor) 23:173–176. Societa Italiana di Medicina del Lavoro. 1975. Associazione Italiana degli Igienisti Industriali. Valori Limite Ponderati degli Inquinanti Chimici e Particolati degli Amgienti di Lavoro Per Il. 1975. Med. Lav. 66:361–371. Specht, H., Miller, J.W., and Valaer, P.J. 1939. Acute response of guinea pigs to the inhalation of dimethyl ketone (acetone) vapors in air. U.S. Publ. Health Repts. 54:944–954. Specht, H., Miller, J.W., and Valaer, P.J. 1940. Acute response of guinea pigs to the inhalation of ketone vapors. Natl. Inst. Health Bull. No. 176. [66 p.]
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Stenback, F.G., Rowland, J.C., and Russell, L.A. 1977. Non-carcinogenicity of hair dyes: Lifetime percutaneous applications in mice and rabbits. Food. Cosmet. Toxicol. 15:601–606. Suzuki, H. 1973. An experimental study on physiological functions of the autonomic nervous system of man exposed to aceton[e] gas. Jpn. J. Ind. Health 15:147–164. [In Japanese with English summary] Tkach, N.Z. 1968. Combined effects of low acetone and acetophenone concentrations in the air of the living organism, in B.S.Levin, U.S.S.R. Literature on Air Pollution and Related Occupational Diseases—Volume 17: The Biological Effects and Hygienic Importance of Atmospheric Pollutants: Book 10. Washington, D.C. p. 108–117. Vigliani, E.C., and Zurlo, N. 1955. Experiences of the Clinica del Lavoro with some maximum concentrations of poisons of industry at the place of work. Transl. from: Arch. Gewerbepathol. Gewerbehyg. 13: 528–534. Walton, D.C., Kehr, E.F., and Loevanhart, A.S. 1928. A comparison of the pharmacological actions of diacetone alcohol and acetone. J. Pharmacol. Exp. Ther. 33:175–183. Walter, P., Craigmill, A., and Dukick, A. 1975. Methyl Ketone Toxicity. (Acetone, methyl ethyl ketone, diacetone alcohol, methyl isobutyl ketone and methyl n-butyl ketone). A Monograph prepared for the Consumer Product Safety Commission, Bureau of Biomedical Science, Bethesda, Maryland. [117 p.] Winek, C.L., Collom, W.D., and Davis, E.R. 1973. Accidental solvent fatality. Clin. Toxicol. 6:23–27. Winell, M. 1975. An international comparison of hygienic standards for chemicals in the work environment. AMBIO 4:34–36.
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Representative terms from entire chapter: