Acetone
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~RfPsoT:1
ACETONE
CASRN: 67-64-1
Human Health Effects:
Toxicity Summary:
Exposure to acetone
results from both natural and anthropogenic sources. Acetone
also occurs as a metabolic component in blood, urine and human breath. ... Acetone
is one of three ketone bodies that occur naturally throughout the body. It can
be formed endogenously in the mammalian body from fatty acid oxidation. Fasting,
diabetes mellitus and strenuous exercise increase endogenous generation of acetone.
Under normal conditions, the production of ketone bodies occurs almost entirely
within the liver and to a smaller extent in the lung and kidney. ... Products
are excreted in the blood and transported to all tissues and organs of the body
where they can be used as a source of energy. Two of these ketone bodies,
acetoacetate and beta-hydroxybutyrate, are organic acids that can cause
metabolic acidosis when produced in large amounts, as in diabetes mellitus. ...
Endogenous acetone is eliminated from
the body either by excretion in urine and exhaled air or by enzymatic
metabolism. ... Acetone is rapidly
absorbed via the respiratory and gastrointestinal tracts of human and laboratory
animals, as indicated by the detection of acetone
in blood within 30 min of inhalation exposure and 20 min of oral administration.
... The nasal cavities of human and laboratory animals appear to have a limited
ability to absorb and excrete acetone
vapor, compared with the remainder of the respiratory tract. Acetone
is uniformly distributed among non-adipose tissues and does not accumulate in
adipose tissue. ... Acetone is rapidly
cleared from the body by metabolism and excretion. ... Exhalation is the major
route of elimination for acetone and
its terminal metabolite (carbon dioxide), and the fraction of administered acetone
that is exhaled as unchanged acetone
is dose-related. Urinary excretion of acetone
and its metabolites occurs but this route of elimination is minor ...
Exogenously supplied acetone enters
into many metabolic reactions in tissues throughout the body, but the liver
appears to be the site of most extensive metabolism. Carbon from orally
administered acetone has been detected
in cholesterol, amino acids, fatty acids and glycogen in rat tissues, urea in
urine and unchanged acetone and CO2 in
exhaled breath. Metabolically, acetone
is degraded to acetate and formate ... Oral LD50 values in adult rats are in the
range of 5800-7138 mg/kg. ... Experimental animal data characterizing the
effects of long term oral or inhalation exposure to acetone
are not available, due probably to its low toxicity and its endogenous
characteristics. ... Pretreatment of rodents with acetone
enhances the hepatotoxic effects of a number of compounds, notably halogenated
alkanes. ... Acetone is not considered
to be genotoxic or mutagenic. ... In a study of pregnant rats and mice exposed
to acetone vapor during days 6-19 of
gestation, slight developmental toxicity was observed ... Reports of other
reproductive effects of acetone
include observations of testicular effects and changes of sperm quality in rats
... Acetone has been used extensively
as a solvent vehicle in skin carcinogenicity studies and is not considered
carcinogenic when applied to the skin. Acetone
is relatively less toxic than many other industrial solvents; however, at high
concentrations, acetone vapor can
cause CNS depression, cardiorespiratory failure and death. Acute exposures of
humans to atmospheric concentrations ... have been reported to produce either no
gross toxic effects or minor transient effects, such as eye irritation. More
severe transient effects (including vomiting and fainting) were reported for
workers exposed to acetone vapor
concentrations ... for about 4 hr. Acute exposures to acetone
have also been reported to alter performances in neurobehavioral tests in
humans. ... Females ... were reported to suffer menstrual irregularities.
Evidence for Carcinogenicity:
CLASSIFICATION: D; not classifiable as to
human carcinogenicity. BASIS FOR CLASSIFICATION: Based on lack of data
concerning carcinogenicity in humans or animals. HUMAN CARCINOGENICITY DATA:
None. ANIMAL CARCINOGENICITY DATA: None.
A4; Not classifiable as a human carcinogen.
Human Toxicity Excerpts:
EFFECTS SIMILAR TO ETHYL ALCOHOL ... BUT
ANESTHETIC POTENCY IS GREATER. 10-20 ML TAKEN BY MOUTH WITHOUT ILL EFFECT. IN
ACUTE CASES A LATENT PERIOD MAY BE FOLLOWED BY RESTLESSNESS AND VOMITING LEADING
TO HEMATEMESIS AND PROGRESSIVE COLLAPSE WITH STUPOR.
WORKERS HAVING BEEN EXPOSED TO 1000 PPM, 3
HR/DAY FOR 7-15 YEARS, ALSO COMPLAINED OF CHRONIC INFLAMMATION OF AIRWAYS,
STOMACH AND DUODENUM; SOME OF THEM COMPLAINED OF DIZZINESS & ASTHENIA.
SIMILAR COMPLAINTS WERE REPORTED AFTER EXPOSURE ... TO 700 PPM.
PROLONGED OR REPEATED SKIN CONTACT MAY DEFAT
THE SKIN & PRODUCE DERMATITIS.
... Onset of hepatorenal lesions in two men
& two women acutely exposed to acetone
/is described/. One person had inhaled acetone
vapors whereas the others had ingested acetone.
Clinical manifestation of liver injury was observed in all four workers &
renal lesions were detected in two.
Repeated exposure to 25-920 ppm: chronic
conjunctivitis, pharyngitis, bronchitis, gastritis, and gastroduodenitis. /Route
not specified/
SYMPTOMATOLOGY (acute intoxication): 1. Early
emotional lability: exhilariation, boastfulness, talkativeness, remorse, and
belligerency. 2. Impaired motor coordination: slowed reaction time, slurred
speech, ataxia. 3. Sensory disturbances: diplopia, vertigo. 4. Flushing of face,
rapid pulse, sweating. 5. Nausea and vomiting. Eventual incontinence of urine
and feces. 6. Drowsiness, stupor and finally coma, with impaired or absent
tendon reflexes. Convulsive episodes may indicate hypoglycemia. /Ethyl alcohol/
SYMPTOMATOLOGY (acute intoxication): 7. Pupils
dilated or normal. 8. Peripheral vascular collapse (shock): hypotension,
tachycardia, cold pale skin, hypothermia. 9. Slow stertorous respirations. 10.
Death from respiratory or circulatory failure or from aspiration pneumonitis.
11. During convalescence: postalcoholic headache and gastritis; infections (for
example, pneumonia, septicemia); alcoholic psychoses (for example, delirium
tremens). /Ethyl alcohol/
Acute acetone
intoxication was reported in a 10-year old boy who wore a hip cast set with a
mixture of 90% acetone, 9% pentane and
1% methyl salicylate. The following symptoms were described: restlessness,
headache, vomiting (positive benzidine for blood), stupor, blood pressure 80/60,
rapid and irregular respiration rate.
A total of 659 males occupationally exposed to
acetone and other solvents were
divided into nine unrelated groups working in plastic boat, chemical,
plastic button, paint, and shoe
factories. Urine samples were collected at the beginning of the workshift and at
the end of the first half of the shift. A close relationship (correlation
coefficient always above 0.85) between the average environmental solvent
concentration (mg/cu m) measured in the breathing zone and the urinary
concentration of unchanged solvent (ug/l) was observed. A Biological Equivalent
Exposure Limit (56 mg/l) corresponding to the environmental Threshold Limit
Value (58 mg/l) was recommended for acetone.
The biological exposure data for urine collected over 4 hr during random
sampling for at least 1 yr could be used to evaluate long-term exposure and
probability of non-compliance for individual or groups of workers.
Direct contact of acetone
with the eyes may produce irritation and corneal injury.
High vapor concentrations will produce
anesthesia.
Acetone
can be placed among solvents of comparatively low acute and chronic toxicities. Acetone
does not have sufficient warning properties to prevent repeated exposures to
vapors which may have adverse effects. There has been no reports that prolonged
inhalation of low vapor concentrations result in any serious chronic effects in
humans.
Severe toxic effects: 4,000 ppm= 9,650 mg/cu
m, 60 minutes; symptoms of illness: 800 ppm= 1,930 mg/cu m, 60 minutes.
Toxic concn in human blood: 200.0-300.0 ug/ml
(20.0-30.0 mg %); lethal concn in human blood: 550.0 ug/ml (55.0 mg %)
Symptoms following acute acetone
ingestion include nausea, vomiting, gastric hemorrhage, sedation, respiratory
depression, ataxia, and paresthesia. Depression resembles alcoholic stupor, but
its onset is quicker than that with ethanol. Coughing and bronchial irritation
may be the only clues to ingestion of quantities that are too small to produce
sedation. Hyperglycemia and ketonemia with acidosis that resembles acute
diabetic coma may be present.
EXPOSURE FOR 15 MINUTES TO 1660 PPM CAUSES
IRRITATION OF EYES AND NOSE ...
Human Toxicity Values:
In children 2 to 3 ml/kg is considered to be
toxic.
Skin, Eye and Respiratory Irritations:
EXPOSURE FOR 15 MINUTES TO 1660 PPM CAUSES
IRRITATION OF EYES AND NOSE ...
Medical Surveillance:
Urinary glucaric acid and the ratio between
6-beta-OH-cortisol and 17-OH-corticosteroids were determined in chemical
workers exposed to styrene greater than or equal to 164 mg/cu m, and acetone
greater than or equal to 571 mg/cu m, and in a control group. Exposed workers
had significantly higher excretion of glucaric acid and a higher ratio. ...
Urinary mercapturic acids were also increased. Simultaneous styrene and acetone
exposure induces mono-oxygenases in humans. ...
Probable Routes of Human Exposure:
NIOSH (NOES Survey 1981-1983) has
statistically estimated that 1,510,107 workers (466,677 of these are female) are
potentially exposed to Acetone in the
US(1). Occupational exposure may be through inhalation and dermal contact with
this compound at workplaces where acetone
is produced or used(SRC). The 8 hour TWA exposure to acetone
was in the range of 0-70,000 umols/cu m in a survey of 659 occupationally
exposed male subjects working in shoe, plastics and chemical
plants in Italy (2). Workers in a Japanese acetate fiber producing plant had
detectable levels of acetone in urine
samples between 1 and 160 mg/l(3). The average TWA exposure to acetone
in 7 spray painting and glue spraying plants was 0.9, 3.2, 2.3 0.9 and 5.6 ppm
for higher-aromatic paint spraying,
lower-aromatic paint spraying, glue
spraying, solvent wiping, and paint
mixing respectively(4).
The general population may be exposed to acetone
through the use of commercially available products containing this compound such
as paints, adhesives, cosmetics, and
rubber cements(SRC). Exposure will also arise from inhalation of ambient air,
ingestion of drinking water, and food that contains acetone(SRC).
The average blood concn of acetone in
600 non-occupationally exposed persons in the US was 3,100 ppb(1).
Body Burden:
Acetone
was detected in the expired breath of 23 of 26 smokers and 42 of 43 nonsmokers
in the US(1). Acetone was ubiquitous
in the expired air from a carefully selected urban population of 54 normal
healthy non-smoking people (387 samples) with a geometric mean concn of 101.3 ng/l(2).
Acetone loss in the urine is generally
1 mg/24 hr for a normal adult but is about 50 mg in children(3,4). Acetone
was detected in the expired breath of children in 2 classrooms in France at an
average concn of 800 ng/l(5).
Average Daily Intake:
AIR INTAKE (assume air concn of 0.05-20 ppb):
24-960 mg; WATER INTAKE - insufficient data; FOOD INTAKE - insufficient data. (SRC)
Animal Toxicity Studies:
Toxicity Summary:
Exposure to acetone
results from both natural and anthropogenic sources. Acetone
also occurs as a metabolic component in blood, urine and human breath. ... Acetone
is one of three ketone bodies that occur naturally throughout the body. It can
be formed endogenously in the mammalian body from fatty acid oxidation. Fasting,
diabetes mellitus and strenuous exercise increase endogenous generation of acetone.
Under normal conditions, the production of ketone bodies occurs almost entirely
within the liver and to a smaller extent in the lung and kidney. ... Products
are excreted in the blood and transported to all tissues and organs of the body
where they can be used as a source of energy. Two of these ketone bodies,
acetoacetate and beta-hydroxybutyrate, are organic acids that can cause
metabolic acidosis when produced in large amounts, as in diabetes mellitus. ...
Endogenous acetone is eliminated from
the body either by excretion in urine and exhaled air or by enzymatic
metabolism. ... Acetone is rapidly
absorbed via the respiratory and gastrointestinal tracts of human and laboratory
animals, as indicated by the detection of acetone
in blood within 30 min of inhalation exposure and 20 min of oral administration.
... The nasal cavities of human and laboratory animals appear to have a limited
ability to absorb and excrete acetone
vapor, compared with the remainder of the respiratory tract. Acetone
is uniformly distributed among non-adipose tissues and does not accumulate in
adipose tissue. ... Acetone is rapidly
cleared from the body by metabolism and excretion. ... Exhalation is the major
route of elimination for acetone and
its terminal metabolite (carbon dioxide), and the fraction of administered acetone
that is exhaled as unchanged acetone
is dose-related. Urinary excretion of acetone
and its metabolites occurs but this route of elimination is minor ...
Exogenously supplied acetone enters
into many metabolic reactions in tissues throughout the body, but the liver
appears to be the site of most extensive metabolism. Carbon from orally
administered acetone has been detected
in cholesterol, amino acids, fatty acids and glycogen in rat tissues, urea in
urine and unchanged acetone and CO2 in
exhaled breath. Metabolically, acetone
is degraded to acetate and formate ... Oral LD50 values in adult rats are in the
range of 5800-7138 mg/kg. ... Experimental animal data characterizing the
effects of long term oral or inhalation exposure to acetone
are not available, due probably to its low toxicity and its endogenous
characteristics. ... Pretreatment of rodents with acetone
enhances the hepatotoxic effects of a number of compounds, notably halogenated
alkanes. ... Acetone is not considered
to be genotoxic or mutagenic. ... In a study of pregnant rats and mice exposed
to acetone vapor during days 6-19 of
gestation, slight developmental toxicity was observed ... Reports of other
reproductive effects of acetone
include observations of testicular effects and changes of sperm quality in rats
... Acetone has been used extensively
as a solvent vehicle in skin carcinogenicity studies and is not considered
carcinogenic when applied to the skin. Acetone
is relatively less toxic than many other industrial solvents; however, at high
concentrations, acetone vapor can
cause CNS depression, cardiorespiratory failure and death. Acute exposures of
humans to atmospheric concentrations ... have been reported to produce either no
gross toxic effects or minor transient effects, such as eye irritation. More
severe transient effects (including vomiting and fainting) were reported for
workers exposed to acetone vapor
concentrations ... for about 4 hr. Acute exposures to acetone
have also been reported to alter performances in neurobehavioral tests in
humans. ... Females ... were reported to suffer menstrual irregularities.
Evidence for Carcinogenicity:
CLASSIFICATION: D; not classifiable as to
human carcinogenicity. BASIS FOR CLASSIFICATION: Based on lack of data
concerning carcinogenicity in humans or animals. HUMAN CARCINOGENICITY DATA:
None. ANIMAL CARCINOGENICITY DATA: None.
A4; Not classifiable as a human carcinogen.
Non-Human Toxicity Excerpts:
SUMMARY OF RESULTS OF SINGLE EXPOSURES OF
ANIMALS TO THE VAPORS: MICE 20,256 PPM, 1.5 HR: CNS DEPRESSION. MICE 46,000 PPM,
1 HR: FATAL. RATS 126,600 PPM, 1.75-2.25 HR: FATAL. RATS 42,200 PPM, 1.75-2.0
HR: LOSS OF CORNEAL REFLEX. GUINEA PIGS 20,000 PPM, 8-9 HR: LOSS OF REFLEXES.
/INVESTIGATORS/ ... STUDIED THE EFFECTS ON
CATS OF REPEATED EXPOSURES TO ACETONE
VAPORS. THEY USED DOSES OF 3 TO 5 MG/L (1265 TO 2110 PPM) AND OBSERVED NO ILL
EFFECTS OTHER THAN SLIGHT IRRITATION OF THE EYES AND NOSE.
/Investigators/ ... reported that acetone
produced moderate corneal injury to rabbit eyes. /Others/ ... reported mild
ocular edema. Small multiple doses of acetone
admin percutaneously (0.5 ml) or sc (0.05 ml) over a period of 3 to 8 wk
produced cataracts in guinea pigs. ... No cataracts were seen in control
animals. ... In a subsequent study conducted similarly, acetone
produced cataracts in guinea pigs, but not in rabbits.
... GRANULAR DEGENERATION IN LESS SEVERE
/INTOXICATIONS/, AND NECROSIS OF TUBULAR EPITHELIUM /IN MORE SEVERE
INTOXICATIONS/ /OF KIDNEYS/ WERE /OBSERVED/ IN DOGS/. ... /OTHER WORK INDICATED/
LESIONS OF THE CONVOLUTED TUBULES, SOME FATTY INFILTRATION /OF THE KIDNEYS/ IN 1
CAT FOLLOWING INHALATION OF 75,900 PPM ... ALBUMINURIA /WAS SEEN/ IN SOME ...
ANIMALS SUBJECTED TO INHALATION.
WITH ACUTE INTOXICATION PRELIMINARY /SPECIES
NOT SPECIFIED/ SYMPTOMS OF ... /CNS DEPRESSION/ ARE IRRITATIVE--SALIVATION,
LACRIMATION, GIDDINESS, ATAXIA, TWITCHINGS & CONVULSIONS. ... AFTER IV &
IM INJECTION FALL IN BLOOD PRESSURE ... /WAS/ REGARDED AS PRIMARILY DUE TO
DECREASE IN CARDIAC OUTPUT.
MALE MICE & RATS WERE EXPOSED FOR VARYING
TIME PERIODS TO VAPOR LEVELS OF 12,600-50,600 PPM ACETONE.
UNCONDITIONED PERFORMANCE & REFLEX TESTS WERE USED TO MEASURE CNS
DEPRESSION. ANIMALS BREATHING ACETONE
TOOK 9 HR TO RECOVER FROM 5 MIN EXPOSURE. BLOOD LEVELS WERE RELIABLE DEPRESSION
INDEX.
A SHORT INHALATION EXPT WAS PERFORMED ON MICE
USING VARIOUS INDUSTRIAL AIRBORNE CHEMICALS,
INCL ACETONE. FOR EACH CMPD SYSTEMATIC
DETERMINATION OF CONCN ASSOC WITH A 50% DECR IN RESP RATE WAS USED FOR
COMPARISONS. DATA MAY HELP ESTABLISH WORKPLACE TLV'S.
Sensitivity of developing chicken embryos to
various solvents was investigated. Acetone
(0.10 ml/egg injected) significantly reduced the percentage hatchability &
caused a high embryonic mortality during the first wk of incubation.
10.5 day-old rat embryos were cultured for 2
days in whole rat serum containing 0.1, 0.5, & 2.5 vol% of acetone.
No adverse effects occurred at 0.1% concn. The order of increasing
embryotoxicity & dysmorphogenesis of the studied liquids was corn oil < acetone/corn
oil < dimethyl sulfoxide < ethanol, acetone
< Tween 80. Any of the water miscible solvents (at 0.1%) met the criteria of
a nontoxic & nonteratogenic water insol cmpd delivery system for in vitro
embryo culture.
Hepatocytes from young male rats were
incubated in acetone in closed vessels
fitted with side arms for serial sampling for approx 5 hr at 37 deg C with
gentle shaking under an oxygen:carbon dioxide atmosphere. Parameters evaluated
were glutamate-oxaloacetate transaminase & lactate dehydrogenase release
from cells, trypan blue exclusion, cell count, urea synthesis capability, &
steady-state ATP levels. Acetone /10
mM/ was without effect /in LDH or GOT release/. Isolated hepatocyte suspensions
are useful for identification of cytotoxins in general & hepatotoxins in
particular, but their capability for yielding a quantitative index of cytotoxic
potential for diverse chemical species
remains to be demonstrated.
Acetone
(reagent grade) was evaluated by the standard plate incorporation method in the
Ames Salmonella reverse mutation assay with strains TA98, TA100, TA1535, TA1537,
& TA1538. Experiments were done in triplicate with & without metabolic
activation (S9 fractions from Aroclor-treated Sprague-Dawley rats). Results were
negative in these strains.
At a concn of 8,100 mg/l of acetone,
there was an approximate 50% inhibition of ammonia oxidation of Nitrosomonas.
Acetone
was used as a solvent control in this experiment and 0.2 ml was applied to the
shaved dorsa of 50 male and 50 female SHEL:CF1,SPF mice once per week from six
weeks of age to two years. All dead and dying animals were autopsied as well as
all animals still alive at 2 years. Local irritation was noted at the
application site of a few animals. One subcutaneous fibrosarcoma observed in one
male was considered ... to be incidental. There were 17/50 tumors in the males
and 13/50 tumors in the females, considered to be a normal rate for this strain
(primarily tumors of the lymphoreticular or hematopoietic system). A second
study using 100 mice for each sex, and identical treatment and autopsy regimens
resulted in negative results for the skin and similar background rates for
tumors of the lymphoreticular or hematopoietic systems, ie: 30/100 for males and
29/100 for the females.
The frequency of recessive chlorophyll and
embryonic lethals included by N-methyl-N'-nitro-N-nitrosoguanidine in
Arabidopsis thaliana was markedly increased when exposure of the seeds to
N-methyl-N'-nitro-N-nitrosoguanidene (3 hr) was carried out in the presence of
4-12% acetone, 4-16% ethanol, or 8-32%
dimethylformamide. The enhancement of N-methyl-N'-nitro-N-nitrosoguanidene
mutagenicity was proportional to the concentrations of these organic solvents.
In contrast, none of the solvents, when applied at the same conditions and
doses, influenced the mutagenic activity of N-methyl-N-nitrosourea. The solvents
without mutagens did not influence the spontaneous rate of mutations and
revealed no or very weak toxic effect as measured by the seed germination.
Female Sprague-Dawley-rats were given 0.5, 1,
or 2.5 ml/kg of acetone once by gavage.
Sodium phenobarbital (SPB), 100 mg/kg, was administered once a day for 3 days.
The animals were killed 24 hours after the last dose. Livers were homogenized
and microsomes were prepared by differential centrifugation. Microsomal lipids
were extracted with a 2 to 1 chloroform methanol mixture. The extracted samples
were assayed for total phosphate or resuspended in saline and assayed for
cholesterol. Treatment with acetone
did not cause alterations in the concentrations of total phospholipid (TPL) and
total cholesterol (TC) in microsomal membranes. Acetone
had no effect on microsomal N-demethylation of aminopyrine, however, at the high
dose, it significantly increased the metabolism of acetonitrile to cyanide. Acetone
did not significantly change the concentration of cytochrome p450.
The purpose of this study was to determine if acetone
could alter the acute nephrotoxicity produced by the experimental fungicide
N-(3,5-dichlorophenyl)succinimide. Male Fischer 344 rats were administered acetone
(1, 5 or 10 mmol/kg) or acetone
vehicle (corn oil, 10 mg/kg) orally followed 16 hr later by a single
intraperitoneal injection of N-(3,5-dichlorophenyl)succinimide (0.2 or 0.4 mmol/kg)
or N-(3,5-dichlorophenyl)succinimide vehicle (sesame oil, 2.5 ml/kg) and renal
function was monitored at 24 and 48 hr. Acetone
(1 or 5 mmol/kg) did not alter N-(3,5,-dichlorophenyl)succinimide (0.2 mmol/kg)
induced renal effects while acetone
(10 mmol/kg) pretreatment attenuated N-(3,5-dichlorophenyl)succinimide (0.4 mmol/kg)
induced increases in blood urea nitrogen (BUN) concentration and kidney weight
but had no effect on N-(3,5,-dichlorophenyl)succinimide (0.4 mol/kg) induced
changes in urine volume or content, organic ion accumulation by renal cortical
slices or renal morphology.
The effects of combinations of chemicals
known to individually induce aneuploidy were tested on the diploid
Saccharomyces-cerevisiae strain D61.M. Exponential phase cultures of the yeast
were treated with nocodazole, ethyl acetate, acetone,
and methyl ethyl ketone alone or in combination, incubated at 28 degrees C for 4
hours, held in an ice bath for 16 hours, incubated at 28 degrees C for an
additional 4 hours, and then diluted and plated onto selective media. Treatment
of yeast strain D61.M with mixtures containing nocodazole levels too low to
induce aneuploidy and ineffective low levels of the solvents ethyl acetate, acetone,
and methyl ethyl ketone was highly effective in inducing aneuploidy. The
synergistic effect did not depend on the cold holding period during treatment.
In studies of acetone-potentiated
liver injury induced by haloalkanes, acetone
is usually given by gavage, whereas industrial exposure to acetone
normally occurs by inhalation. It was of interest to verify if the route of
administration influences the potentiation. Male Sprague-Dawley rats were
exposed for 4 hr to acetone vapors or
treated orally with acetone; the
minimal effective dose levels for potentiating CCl4-induced liver injury were
estimated to be 2500 ppm and 0.25 mg/kg, respectively. Groups were treated with acetone
using 0.4, 1, 2, 4, or 6 times the minimal effective dose. Half of each group
was killed at various time intervals after treatment for blood acetone
measurements by gas chromatography; the other half was challenged with CCl4 (0.1
,l/kg, ip) 18 hr after acetone, and
killed 24 hr later. Plasma alanine aminotransferase (ALT) activity and bilirubin
concentrations were measured. Inhalation and oral administration of acetone
both potentiated CCl4 toxicity. Rats exposed repetitively to acetone
vapors (10 daily exposures) and subsequently challenged with CCl4 exhibited
liver toxicity that was not significantly different from that of rats subjected
to a single exposure. Correlations between ALT activities and maximal
bloodacetone concentrations were found to be linear (positive) and significant
for both routes. For a given blood acetone
concentration, however, toxicity was least severe following acetone
exposure by inhalation.
The susceptibility of New Zealand White
rabbits and albino guinea pigs to the cataractogenic effects of dermal acetone
treatments. Male and female rabbits treated with 1 ml of acetone
3 days/wk for 3 weeks showed no lens abnormalities during the 6 month
observation period. Male and female guinea pigs were treated with 0.5 ml of acetone
5 days/wk for 6 weeks and examined with an ophthalmoscope and slip lamp at
regular intervals for 1 yr post-treatment. By 3 months post-treatment, cataracts
were observed in 30% of the test animals and none of the control animals. The
ascorbate levels in aqueous humor specimens from the test throughout the 1 yr
observed period. It was concluded that the development of cataracts in guinea
pigs was species specific and related to ascorbate synthesis.
The reproductive effects of acetone
in male Wistar rats administered 0.5% acetone
in their drinking water for 6 wk. On fifth week of treatment, the rats were
allowed to mate with untreated females and the number of matings were recorded
together with the number of pregnancies and the number of fetuses per pregnancy.
The absolute weight of the testes was measured along with the diameter of the
seminiferous tubules in the treated and control rats. Semiquantitative
histopathological scoring was used to detect any effects on vacuole formation,
chromatic margination, epithelial disruption, multinucleated giant-cell
formation, intracellular debris, or atrophy of the testes. None of these
measures of reproductive and testicular toxicity were affected by the acetone
treatment relative to the control animals.
The avoidance and escape behavior of female
Carworth rats exposed to acetone
vapors for 10 days at 4 hr/day (180). Groups of animals were trained to avoid
(conditioned response) or escape (unconditioned response) a shock stimulus by
climbing a pole situated in a test chamber with an electric grid on the floor.
Each animal was evaluated before and after daily acetone
exposures of 3000, 6000, 12,000, and 16,000 ppm. The 3000 ppm exposure were
without effect on all exposure days, the 6000 ppm exposure inhibited the
avoidance but not the escape response, and the two highest exposures inhibited
both responses. Normal responses were obtained after three days of exposure to
6000 and 12,000 ppm, which indicated adaptation and tolerance developed on
repeated exposure to acetone vapors.
Groups of male Sprague-Dawley rats were
exposed for 3 hr to acetone
concentrations of 12,600, 19,000, 25,300, and 50,600 ppm. The degree of /CNS
depression/ was measured at regular intervals during and after the exposure by
performing five tests (wire maneuverability, visual pacing, grip strength, tail
pinch, and righting reflex) that measured unconditioned performance and
involuntary reflex. Each animal was scored between 0 and 8 on each of these
tests, and the individual results were averaged to obtain a mean performance
score. Performance scores showed a dose-related decline at all but the highest acetone
exposure level. Animals exposed to 50,600 ppm of acetone
died within 2 hr of initiating the exposure. The performance score for the group
of rats exposed to 19,000 ppm of acetone
returned to the preexposure level after 9 hr, whereas the group exposed to
25,300 ppm of acetone required 21 hr
before its performance score returned to base-line levels.
Single-dose oral lethality studies have been
performed in mice, rats, and rabbits. A 14-day oral LD50 of 10.7 ml/kg (8.5
g/kg) and 95% confidence limits of 7.7 to 15.0 ml/kg (6.2 to 11.9 g/kg) for
female Carworth-Wistar rats was reported. Using the same test conditions and
test species, ... the LD50 value was found to be 12.6 ml/kg (9.8 g/kg) and the
95% confidence limits to be 10.6 to 14.9 ml/kg (8.5 to 11.9 g/kg). ... An oral
LD50 value of 5.3 g/kg for an unstated sex and strain of rabbit and an LD50
value between 4 and 8 g/kg for an unstated sex and strain of mouse was reported.
Using male ddY mice, ... the oral LD50, of acetone
was found to be 90.39 mmol/kg (5.25 g/kg) with 95% confidence limits of 61.68 to
132.5 mmol/kg (3.58 to 7.70 g/kg).
A group of male baboons was exposed
continuously (24 hr/day) to 500 ppm acetone
for 7 days. The percentage of correct and incorrect responses was recorded along
with the time necessary to respond precisely to a stimulus-induced
discrimination task that resulted in a food reward when performed correctly. The
acetone exposure caused no change in
the number of correct responses, a highly variable change in the number of extra
incorrect responses, and a consistent increase in the response time relative to
control values. The authors did not measure blood or urine acetone
levels; however, the uninterrupted exposure undoubtedly resulted in an extremely
high acetone body burden. Acetone
exposures were performed at 150 ppm for times ranging from 30 min to 4 hr.
Male Swiss mice were placed in a container of
water and the lag time between water contact and the initiation of swimming
behavior was measured relative to a control group. A nominal concentration of
2000 ppm caused no change in swimming behavior, whereas concentrations ranging
from about 2600 to 3000 ppm caused the swimming lag time to decrease up to 59%.
National Toxicology Program Studies:
... The potential for acetone
to cause developmental toxicity was assessed in Sprague-Dawley rats exposed to
0, 440, 2200, or 11000 ppm, and in Swiss (CD-1) mice exposed to 0, 440, 2200,
and 6600 ppm acetone vapors, 6 hr/day,
7 days/week. Each of the four treatment groups consisted of 10 virgin females
(for comparison), and approximately 32 positively mated rats or mice. Positively
mated mice were exposed on days 6-17 of gestation (dg), and rats on 6-19 days of
gestation. The day of plug or sperm detection was designated as 0 days of
gestation. ... Pregnant rats did not exhibit overt symptoms of toxicity other
than statistically significant reductions for the 11,000 ppm group in body
weight. (14, 17, 20 days of gestation), cumulative weight gain from 14 days of
gestation onward, uterine weight and in extragestational weight gain. (EGWG -
maternal body weight (20 days of gestation) uterine weight - maternal body
weight (0 days of gestation.) Mean body weights of treated virgin females were
also reduced, but not significantly. There were no maternal deaths and the mean
pregnancy rate was greater than or equal to 93% in all groups. No affect was
observed in the mean liver or kidney weights of pregnant dams, the organ to body
weight ratios, the number of implantations, the mean percent of live
pups/litter, the mean percent of resorptions/litter, or the fetal sex ratio.
However, fetal weights were significantly reduced for the 11,000 ppm exposure
group relative to the 0 ppm group. The incidence of fetal malformations was not
significantly increased by gestational exposure to acetone
vapors, although the percent of litters with at least one pup exhibiting
malformations was greater for the 11,000 ppm group than for the 0 ppm group,
11.5 and 3.8%, respectively. The diversity of malformations observed in the
11,000 ppm group was greater than that found in the lower dose groups or in the
0 ppm group. There was no increase in the incidence of fetal variations, reduced
ossification sites, or in the mean incidence of fetal variations per litter.
Analysis of rat plasma samples 30 min post-exposure showed an increase in plasma
acetone levels which correlated with
increasing exposure concentration. Acetone
levels dropped to control levels by 17 hr post-exposure for all exposure groups
except the 11,000 ppm group. Plasma acetone-levels
for this group were still slightly elevated with respect to the controls at 17
hr post-exposure. The concentration of plasma acetone
levels at either 30 min or 17 hr post exposure did not increase over gestation
regardless of the exposure concentration. Neither exposure to acetone
vapor, nor advancing gestation resulted in alterations of the plasma levels for
the other two ketone bodies, acetoacetic acid and b-hydroxybutyric acid, with
respect to control animals. Swiss (CD-1) mice exhibited severe ... /CNS
depression/ at the 11,000 ppm acetone
concentration; consequently, the high exposure concentration was reduced to 6600
ppm acetone after one day of exposure.
No further overt signs of toxicity were observed and there were no maternal
deaths. No treatment- related effects on maternal or virgin body weight,
maternal uterine weight, or on extragestational weight gain were noted in mice.
There was a treatment-correlated increase in liver to body weight ratios in
pregnant dams which may have been indicative of an induction of the p450
monooxygenase enzyme system. The mean pregnancy rate for all mated mice was
greater than or equal to 85% in all groups. There was no effect on the number of
implantations per dam, on any other reproductive indices, or on the fetal sex
ratio. Developmental toxicity was observed in mice in the 6,600 ppm exposure
group as; 1) a statistically significant reduction in fetal weight, and 2) a
slight, but statistically significant increase in the percent incidence of late
resorptions. However, the increase in the incidence of late resorptions was not
sufficient to cause a decrease in the mean number of live fetuses per litter.
The incidence of fetal malformations or variations in mice was not altered by
exposure to acetone vapors at any of
the levels employed. It may be concluded from the results of this study that the
2,200 ppm acetone level was the no
observable effect level (NOEL) in both the Sprague-Dawley (CD) rat and the Swiss
(CD-1) mouse for developmental toxicity. Furthermore, since only minimal
maternal toxicity was observed at 11,000 ppm acetone
for rats and 6,600 ppm acetone for
mice, it is possible that the actual maternal NOEL is somewhat greater than
2,200 ppm.
Non-Human Toxicity Values:
LD50 Rat oral 10.7 ml/kg
Ecotoxicity Values:
LC50 JAPANESE QUAIL ORAL GREATER THAN 40,000
PPM, IN DIET, AGE 14 DAYS, (NO MORTALITY TO 40,000 PPM)
LC50 RING-NECKED PHEASANT ORAL GREATER THAN
40,000 PPM, IN DIET, AGE 10 DAYS, (NO MORTALITY TO 40,000 PPM)
LC50 SALMO GAIRDNERI (RAINBOW TROUT) 5,540
MG/L/96 HR @ 12 DEG C (95% CONFIDENCE LIMIT 4,740-6,330 MG/L), WT 1.0 G /STATIC
BIOASSAY/
LD100 Asellus aquaticus 3 ml/l (within 3 days
of exposure) /Conditions of bioassay not specified/
LD100 Gammarus fossarum 10 ml/l (within 48 hr)
/Conditions of bioassay not specified/
LC50 Pimephales promelas 8,120 mg/l/96 hr
/Conditions of bioassay not specified/
LC50 Daphnia magna 10 mg/L 24 to 48-Hr
/Conditions of bioassay not specified/
LC50 Brine shrimp 2,100 mg/L 24 to 48-Hr
/Conditions of bioassay not specified/
LC50 Mosquito fish 13,000 mg/L 24 to 96-Hr
/Conditions of bioassay not specified/
LC50 Lepomis macrochirus (bluegill sunfish)
8,300 mg/L 96 hr /Conditions of bioassay not specified/
LD50 Goldfish 5,000 mg/L 24-hr /Conditions of
bioassay not specified/
LC50 Poecilia reticulata (guppy) 7,032 mg/l 14
day /Conditions of bioassay not specified/
LC50 Mexican axolotl 20,000 mg/l (3-4 weeks
after hatching) 48 hr /Conditions of bioassay not specified/
LC50 Clawed toad 24,000 mg/l (3-4 weeks after
hatching) 48-hr /Conditions of bioassay not specified/
LC50 fingerling trout 6,100 mg/l 24-hr
/Flow-through bioassay/
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
Two pathways for the conversion of acetone
to glucose are proposed, the methylglyoxal & the propanediol pathways. The
methylglyoxal pathway is responsible for the conversion to acetol, acetol to
methylglyoxal, & subsequent conversion of methylglyoxal to glucose. The
propanediol pathway involves the conversion of acetol to L-1,2-propanediol by an
as yet unknown process. L-1,2-propanediol is converted to L-lactaldehyde by
alcohol dehydrogenase, & L-lactaldehyde is converted to L-lactic acid by
aldehyde dehydrogenase. Expression of these metabolic pathways in rat appears to
be dependent on the induction of /acetone/
oxygenase & acetol monooxygenase by acetone.
HEPATIC NAD-DEPENDENT ALCOHOL DEHYDROGENASE
... ENZYME IS CAPABLE OF CATALYZING REVERSE REACTION IN WHICH ... ACETONE
... /IS REDUCED TO ALCOHOL/.
Acetone
may be converted to 1,2-propanediol which enters the glycolytic pathway &
possibly the one carbon pool. Acetone
has been shown to be converted to lactate in mice. The rate-limiting step
appears to be the conversion of acetone
to a hydroxylated intermediate. Rats & mice exposed to 30 mg/l of acetone,
& rabbits & guinea pigs exposed to 72 mg/l for 2 hr, had increased
levels of acetone, acetoacetic acid,
& beta-hydroxybutyric acid in the blood & urine immediately after
exposure & 24 hr later.
Acute admin of acetone
to rats resulted in measureable levels of isopropanol in blood. Metabolism of acetone
to isopropanol was different in normal & diabetic animals. Blood levels of
isopropanol reached a max at 2 g/kg dose in normal rats, but there was a 2-phase
response in diabetic rats. In a second series of experiments, acetone
was admin on alternate days for a wk. In spite of this chronic admin, there was
no enhancement of acetone metabolism
to isopropanol.
The metabolic mechanism responsible for the
incorporation of acetone into the
glucose and amino acids of lactating cows. Normal and spontaneously ketotic cows
(unspecified type) were given a single bolus iv dose of [2-14(C)] acetone.
The casein and lactose isolated from milk specimens were digested to obtain
their constituent amino acids and hexoses. The glucose and galactose from
lactose were labeled to the same degree, indicating that the galactose was
derived from labeled glucose. The labeling intensity in the amino acids from
casein increased in the following order:glycine < serine < aspartic acid
< glutamic and that 40 to 70% of the end genous acetone
was metabolized in the citric acid cycle through a common precursor,
oxaloacetate. It was concluded that the utilization of acetone
for glucose synthesis was not enhanced in ketotic cows and that the glucose from
acetone constituted a small and
insignificant portion of the total production.
Absorption, Distribution & Excretion:
ACETONE
IS ONE OF THE LEAST HAZARDOUS INDUSTRIAL SOLVENTS, BUT IS HIGHLY VOLATILE AND
MAY BE INHALED IN LARGE QUANTITIES. IT MAY BE ABSORBED INTO THE BLOOD THROUGH
THE LUNGS AND DIFFUSED THROUGHOUT THE BODY. SMALL QUANTITIES MAY BE ABSORBED
THROUGH THE SKIN.
LARGE QUANTITIES OF ACETONE
ARE RAPIDLY EXCRETED FOLLOWING EXPOSURE. ONLY A SMALL AMT IS REDUCED. EXCRETION
MAINLY VIA LUNGS AND URINE ... ACETONE
ABSORBED DURING 8 HOURS AT 200 PPM WILL BE COMPLETELY METABOLIZED OR EXCRETED
WITHIN 16 HOURS ...
... THE AMT OF ACETONE
ABSORBED WHEN FOOT OF ANIMAL WAS IMMERSED /WAS ESTIMATED/ BY MEASURING AMT
EXHALED AND THAT PRESENT IN BLOOD.
ACETONE,
BECAUSE OF ITS SOLUBILITY IN WATER, IS READILY ABSORBED INTO BLOOD STREAM AND
THUS IS TRANSPORTED RAPIDLY THROUGHOUT BODY. ... A MAN BREATHING AN ESTIMATED
CONCN OF 22 MG/L (9300 PPM) FOR 5 MIN ABSORBED 71% OF INHALED ACETONE;
2 MEN BREATHING 11 MG/L ... FOR 15 MIN ABSORBED 76-77% ...
... EXCRETION ... IN HUMANS IS RAPID FOR 8 HR
AFTER A SINGLE ORAL DOSE BUT WAS NOT COMPLETE IN 24 HR. ... THE RATIO OF
EXCRETION ... WAS APPROX 40-70% IN BREATH, 15-30% IN THE URINE, AND 10% OF TOTAL
EXCRETED THROUGH SKIN.
In order to verify the relationship between
urinary acetone concentrations and
corresponding mean environmental concentrations in the breathing zone, the
urinary concentration of acetone was
measured in subjects experimentally or occupationally exposed to acetone.
Fifteen healthy volunteers were exposed to acetone
vapor concentrations of 56 to 500 ppm/cu m in an exposure chamber for 2 hours at
rest or during alternating rest and light physical exercise. The urinary
elimination of acetone was also
studied in 104 workers occupationally exposed to acetone.
The ratio of alveolar concentration to environmental concentration averaged
approximately 0.28, and the relative uptake averaged 53%. The urinary acetone
concentration showed a linear relationship to the corresponding environmentally
time weighted average concentration in both the experimentally exposed subjects
and the occupationally exposed subjects. There was also a linear relationship
between the amount of acetone absorbed
and the urinary concentrations of acetone.
The upper respiratory tract (URT) deposition
of acetone was studied in vivo in male
Syrian golden hamsters and in vitro using nasal tissue homogenates. A steady
state for acetone deposition was
obtained within 3 minutes in hamsters exposed to 1030 mg/cu m. Nasal perfusion
of 0.046 ml/min (95% confidence limit, 0.035-0.58 ml/min) was calculated. The
effect of flow rate on URT was described by a ventilation perfusion model. Acetone
was not metabolized by in vitro homogenates.
Mechanism of Action:
Levels of endogenous acetone
in fasted rats correlated with 3-4-fold increase in nitrosodimethylamine
demethylase (NDMAd) activity. A dose-response experiment showed endogenous
levels of acetone to be capable of
causing at most 40% of the induction in fasted rats. This suggests that other
ketone bodies or factors may have contributed to the induction.
... /IT WAS/ SUGGESTED THAT INJURIOUS EFFECT
OF ACETONE ON EYE /OF RABBITS/ WAS
CAUSED BY DEHYDRATION OF SCLERA WHICH RESULTED IN GELATINOUS FLOCCULATION AND
OPACITY OF SCLERA.
Interactions:
Pretreatment with acetone
for 6 days (one-tenth the LD50) potentiated acute ethanol toxicity in rats. ...
/Investigators/ ... demonstrated that acetone
pretreatment potentiates chlorinated hydrocarbon toxicity. ... Acetone
protected animals against electroshock or isonicotinic acid hydrazide-induced
convulsions. Acetone ... enhanced the
hepatotoxicity of 1,1-dichloroethylene (200 ppm) in rats.
PRETREATMENT OF MICE WITH ACETONE
GREATLY REDUCED THE MINIMUM MUTAGENICALLY EFFECTIVE CONCN OF DIMETHYLNITROSAMINE
(DMN) IN SALMONELLA TYPHIMURIUM TA92. THE RESULTS OF THE HOST-MEDIATED ASSAYS
SUBSTANTIALLY DIFFERED FROM THOSE OF THE IN VITRO ACTIVATION ASSAYS (A) IN THE
RELATIVELY LOW DOSE OF DMN REQUIRED FOR MUTAGENICITY TO OCCUR & (B) IN THE
LACK OF POTENTIATION BY ACETONE
PRETREATMENT. ACETONE EVEN LED TO A
MARGINAL DECREASE IN MUTAGENICITY OF DIMETHYLNITROSAMINE.
Pretreatment of rats with acetone
potentiated the hepatotoxicity of n-nitrosodimethylamine as indicated by plasma
glutamic-pyruvatic transaminase levels & histological data. Pretreatment
with acetone (2.5 ml/kg) & 2 days
of fasting caused a 2-fold potentiation of n-nitrosodimethylamine-induced plasma
glutamic-pyruvatic transaminase elevation. Centrilobular necrosis produced by n-nitrosodimethylamine
was more severe after pretreatment with inducers. N-nitrosodimethylamine
treatment also decreased hepatic microsomal demethylase activity. Thus, n-nitrosodimethylamine
demethylase is responsible for the activation of n-nitrosodimethylamine in vivo
to a toxic intermediate, & induction of this enzyme activity potentiates n-nitrosodimethylamine
hepatotoxicity.
Treatment of rats with acetone
(2.5-5 ml/kg, intragastric) caused a 3-4.5-fold enhancement in reduced
nicotinamide adenine dinucleotide-dependent nitrosodimethylamine demethylase (NDMAd)
activity. This was accompanied by only moderate incr in gross cytochrome p450
content & reduced nicotinamide adenine dinucleotide-cytochrome c reductase
& 261% incr in ethoxycoumarin O-dealkylase activity. The treatment enhanced
the metabolism of nitrosomethylethylamine, nitrosomethylbenzylamine, &
nitrosomethylaniline, although to lesser extents than with nitrosodimethylamine.
Observations suggest that the enhanced nitrosodimethylamine demethylase was due
to induction of 1 or more specific p450 isozyme(s) by pretreatment with acetone
or isopropanol. Treatment induced proteins with molecular weights of 50,000
& 52,000 which were in the range of known p450 isozymes. The induction of
these proteins & nitrosodimethylamine demethylase activity was inhibited by
cobaltous chloride & cycloheximide. The induced microsomes had a peak at
450.6 nm, different from 450.0 nm peak of control microsomes. When added to the
incubation mixture, acetone &
isopropanol inhibited nitrosodimethylamine demethylase activity. Isopropanol was
more potent than acetone.
... Pretreatment of rats with acetone
(15 mmol/kg, po) markedly potentiated the hepatotoxic response to
bromodichloromethane and dibromochloromethane ... /in male Sprague-Dawley rats/.
Chloroform-induced hepato- and nephrotoxicity
was evaluated in male, Fischer 344 rats pretreated with various dosages (1.0 to
15.0 mmol/kg, po) of acetone,
2-butanone, 2-pentanone, 2-hexanone, or 2-heptanone. Chloroform ... produced
extensive tubular and centrilobular necrosis when administered to ketone-pretreated
rats. The relationship between ketone dosage and the magnitude of the
potentiated response was non-linear. Maximum potentiation of chloroform toxicity
occurred in the dose range of 5.0-10.0 mmol ketone/kg. Ketone dosages > 10.0
mmol/kg were associated with a reduction in the degree of chloroform injury. At
the lowest ketone dosage (1.0 mmol/kg), potentiating capacity appeared to be
related to ketone C skeleton length. No differences were discernable between
ketones at dosages of 5.0-10.0 mmol/kg. ...
The influence of organo-antimony and organo-bismuth
compounds was determined. Significant antagonistic and synergistic
solvent-compound interactions occurred when the acetone
concentrations exceeded 0.4% (vol/vol). At < 0.4%, only additive responses
were observed. The fungitoxicity of the test compounds was determined by using acetone
as the carrier solvent at a final concn of 0.1% (vol/vol). Trivalent organo-bismuth
compounds were the most fungitoxic. ...
The toxicity of
1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, and aldrin to sugarcane
leafhopper (Pyrilla perpusilla) depended on the solvent used; ie, the
insecticides were more effective when dissolved in ethanol, than in methanol,
followed by acetone.
Acetone
has the ability to induce the enzymatic activity of a specific constitutive
cytochrome p450 isozyme that plays an important role in the metabolism of
endogenous and exogenous substrates. A considerable amount of information is
available on the physiological function and toxicologic consequence of p450
induction by acetone. Because acetone
is metabolized by the same p450 isozyme that is induced following high-dose
administration the auto-inductive increase in cytochrome p450 levels provides a
mechanism for increasing the elimination of acetone
when high body burdens develop. The pretreatment of laboratory animals with acetone
can also potentiate or antagonize the acute effects of known systemic toxicants
that are metabolized by the induced p450 isozyme. The potentiation observed
following acetone administration has
involved treatments with known nephrotoxins and hepatotoxins; the potentiating
effects were generally quantitative in nature and involved an increase in the
extent of damage without altering the types of tissues or organs affected.
Minimally effective dose thresholds have been shown to exist for the induction
of cytochrome p450 by acetone.
Pharmacology:
Therapeutic Uses:
Anti-Infective Agents, Local; Pharmaceutic
Aids; Solvents
PHARMACEUTICAL AID (SOLVENT)
Interactions:
Pretreatment with acetone
for 6 days (one-tenth the LD50) potentiated acute ethanol toxicity in rats. ...
/Investigators/ ... demonstrated that acetone
pretreatment potentiates chlorinated hydrocarbon toxicity. ... Acetone
protected animals against electroshock or isonicotinic acid hydrazide-induced
convulsions. Acetone ... enhanced the
hepatotoxicity of 1,1-dichloroethylene (200 ppm) in rats.
PRETREATMENT OF MICE WITH ACETONE
GREATLY REDUCED THE MINIMUM MUTAGENICALLY EFFECTIVE CONCN OF DIMETHYLNITROSAMINE
(DMN) IN SALMONELLA TYPHIMURIUM TA92. THE RESULTS OF THE HOST-MEDIATED ASSAYS
SUBSTANTIALLY DIFFERED FROM THOSE OF THE IN VITRO ACTIVATION ASSAYS (A) IN THE
RELATIVELY LOW DOSE OF DMN REQUIRED FOR MUTAGENICITY TO OCCUR & (B) IN THE
LACK OF POTENTIATION BY ACETONE
PRETREATMENT. ACETONE EVEN LED TO A
MARGINAL DECREASE IN MUTAGENICITY OF DIMETHYLNITROSAMINE.
Pretreatment of rats with acetone
potentiated the hepatotoxicity of n-nitrosodimethylamine as indicated by plasma
glutamic-pyruvatic transaminase levels & histological data. Pretreatment
with acetone (2.5 ml/kg) & 2 days
of fasting caused a 2-fold potentiation of n-nitrosodimethylamine-induced plasma
glutamic-pyruvatic transaminase elevation. Centrilobular necrosis produced by n-nitrosodimethylamine
was more severe after pretreatment with inducers. N-nitrosodimethylamine
treatment also decreased hepatic microsomal demethylase activity. Thus, n-nitrosodimethylamine
demethylase is responsible for the activation of n-nitrosodimethylamine in vivo
to a toxic intermediate, & induction of this enzyme activity potentiates n-nitrosodimethylamine
hepatotoxicity.
Treatment of rats with acetone
(2.5-5 ml/kg, intragastric) caused a 3-4.5-fold enhancement in reduced
nicotinamide adenine dinucleotide-dependent nitrosodimethylamine demethylase (NDMAd)
activity. This was accompanied by only moderate incr in gross cytochrome p450
content & reduced nicotinamide adenine dinucleotide-cytochrome c reductase
& 261% incr in ethoxycoumarin O-dealkylase activity. The treatment enhanced
the metabolism of nitrosomethylethylamine, nitrosomethylbenzylamine, &
nitrosomethylaniline, although to lesser extents than with nitrosodimethylamine.
Observations suggest that the enhanced nitrosodimethylamine demethylase was due
to induction of 1 or more specific p450 isozyme(s) by pretreatment with acetone
or isopropanol. Treatment induced proteins with molecular weights of 50,000
& 52,000 which were in the range of known p450 isozymes. The induction of
these proteins & nitrosodimethylamine demethylase activity was inhibited by
cobaltous chloride & cycloheximide. The induced microsomes had a peak at
450.6 nm, different from 450.0 nm peak of control microsomes. When added to the
incubation mixture, acetone &
isopropanol inhibited nitrosodimethylamine demethylase activity. Isopropanol was
more potent than acetone.
... Pretreatment of rats with acetone
(15 mmol/kg, po) markedly potentiated the hepatotoxic response to
bromodichloromethane and dibromochloromethane ... /in male Sprague-Dawley rats/.
Chloroform-induced hepato- and nephrotoxicity
was evaluated in male, Fischer 344 rats pretreated with various dosages (1.0 to
15.0 mmol/kg, po) of acetone,
2-butanone, 2-pentanone, 2-hexanone, or 2-heptanone. Chloroform ... produced
extensive tubular and centrilobular necrosis when administered to ketone-pretreated
rats. The relationship between ketone dosage and the magnitude of the
potentiated response was non-linear. Maximum potentiation of chloroform toxicity
occurred in the dose range of 5.0-10.0 mmol ketone/kg. Ketone dosages > 10.0
mmol/kg were associated with a reduction in the degree of chloroform injury. At
the lowest ketone dosage (1.0 mmol/kg), potentiating capacity appeared to be
related to ketone C skeleton length. No differences were discernable between
ketones at dosages of 5.0-10.0 mmol/kg. ...
The influence of organo-antimony and organo-bismuth
compounds was determined. Significant antagonistic and synergistic
solvent-compound interactions occurred when the acetone
concentrations exceeded 0.4% (vol/vol). At < 0.4%, only additive responses
were observed. The fungitoxicity of the test compounds was determined by using acetone
as the carrier solvent at a final concn of 0.1% (vol/vol). Trivalent organo-bismuth
compounds were the most fungitoxic. ...
The toxicity of
1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, and aldrin to sugarcane
leafhopper (Pyrilla perpusilla) depended on the solvent used; ie, the
insecticides were more effective when dissolved in ethanol, than in methanol,
followed by acetone.
Acetone
has the ability to induce the enzymatic activity of a specific constitutive
cytochrome p450 isozyme that plays an important role in the metabolism of
endogenous and exogenous substrates. A considerable amount of information is
available on the physiological function and toxicologic consequence of p450
induction by acetone. Because acetone
is metabolized by the same p450 isozyme that is induced following high-dose
administration the auto-inductive increase in cytochrome p450 levels provides a
mechanism for increasing the elimination of acetone
when high body burdens develop. The pretreatment of laboratory animals with acetone
can also potentiate or antagonize the acute effects of known systemic toxicants
that are metabolized by the induced p450 isozyme. The potentiation observed
following acetone administration has
involved treatments with known nephrotoxins and hepatotoxins; the potentiating
effects were generally quantitative in nature and involved an increase in the
extent of damage without altering the types of tissues or organs affected.
Minimally effective dose thresholds have been shown to exist for the induction
of cytochrome p450 by acetone.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Acetone's
production and use as a solvent for fats, oils, waxes, resins, rubbers,
plastics, pharmaceuticals and rubber cements may result in its release to the
environment through various waste streams. Its use as an extracting reagent and
starting material or intermediate in the manufacture of chemical
products will also lead to its release to the environment. Acetone
occurs naturally as a metabolic byproduct of plants and animals and is released
into the atmosphere by volcanoes and forest fires. Based on an experimental
vapor pressure of 231 mm Hg at 25 deg C, acetone
is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase acetone
is degraded in the atmosphere by reaction with photochemically-produced hydroxyl
radicals with an estimated atmospheric half-life of 71 days. Acetone
also undergoes photodecomposition by sunlight with an estimated half-life of
about 80 days. Acetone is expected to
have very high mobility in soils based upon an estimated Koc value of 1.
Volatilization from dry soil surfaces is expected based upon the vapor pressure
of this compound. Volatilization from moist soil surfaces is also expected based
upon the measured Henry's Law constant of 1.87X10-5 atm-cu m/mol. This compound
is expected to biodegrade under aerobic and anaerobic conditions. In water, acetone
is not expected to adsorb to suspended solids or sediment based upon its
estimated Koc value. Volatilization from water surfaces is expected to be an
important environmental fate process given its estimated Henry's Law constant.
Estimated half-lives for a model river and model lake are 38 and 333 hours,
respectively. Experimentally determined volatilization half-lives in a shallow
stream were measured in the range of 8-18 hours. Bioconcentration in aquatic
organisms is considered low based upon an estimated BCF value of 1. Occupational
exposure may be through inhalation and dermal contact with this compound at
workplaces where acetone is produced
or used. The general population may be exposed to acetone
through the use of commercially available products containing this compound such
as paints, adhesives, cosmetics, and
rubber cements. Exposure will also arise from inhalation of ambient air,
ingestion of drinking water, and food that contains acetone.
(SRC)
Probable Routes of Human Exposure:
NIOSH (NOES Survey 1981-1983) has
statistically estimated that 1,510,107 workers (466,677 of these are female) are
potentially exposed to Acetone in the
US(1). Occupational exposure may be through inhalation and dermal contact with
this compound at workplaces where acetone
is produced or used(SRC). The 8 hour TWA exposure to acetone
was in the range of 0-70,000 umols/cu m in a survey of 659 occupationally
exposed male subjects working in shoe, plastics and chemical
plants in Italy (2). Workers in a Japanese acetate fiber producing plant had
detectable levels of acetone in urine
samples between 1 and 160 mg/l(3). The average TWA exposure to acetone
in 7 spray painting and glue spraying plants was 0.9, 3.2, 2.3 0.9 and 5.6 ppm
for higher-aromatic paint spraying,
lower-aromatic paint spraying, glue
spraying, solvent wiping, and paint
mixing respectively(4).
The general population may be exposed to acetone
through the use of commercially available products containing this compound such
as paints, adhesives, cosmetics, and
rubber cements(SRC). Exposure will also arise from inhalation of ambient air,
ingestion of drinking water, and food that contains acetone(SRC).
The average blood concn of acetone in
600 non-occupationally exposed persons in the US was 3,100 ppb(1).
Body Burden:
Acetone
was detected in the expired breath of 23 of 26 smokers and 42 of 43 nonsmokers
in the US(1). Acetone was ubiquitous
in the expired air from a carefully selected urban population of 54 normal
healthy non-smoking people (387 samples) with a geometric mean concn of 101.3 ng/l(2).
Acetone loss in the urine is generally
1 mg/24 hr for a normal adult but is about 50 mg in children(3,4). Acetone
was detected in the expired breath of children in 2 classrooms in France at an
average concn of 800 ng/l(5).
Average Daily Intake:
AIR INTAKE (assume air concn of 0.05-20 ppb):
24-960 mg; WATER INTAKE - insufficient data; FOOD INTAKE - insufficient data. (SRC)
Natural Pollution Sources:
/Component/ of oxidation of humic substances.
Acetone
has been produced by the fermentation of west coast kelp.
Acetone
occurs naturally as a metabolic byproduct of plants and animals and is released
into the atmosphere by volcanoes and forest fires(1).
Artificial Pollution Sources:
Emissions from wood-burning fireplaces were
measured. Acetone was one of the
compounds identified.
Acetone's
production and use as a solvent for fats, oils, waxes, resins, rubbers,
plastics, pharmaceuticals and rubber cements(1,2) will result in its release to
the environment through various waste streams(SRC). Its use as an extracting
reagent and starting material or intermediate in the manufacture of chemical
products(1) will also lead to its release to the environment(SRC).
Environmental Fate:
TERRESTRIAL FATE: Based on a recommended
classification scheme(1), an estimated Koc value of 1(SRC), determined from an
experimental log Kow of -0.24(2), and a recommended regression-derived
equation(3), indicates that acetone is
expected to have very high mobility in soil(SRC). Volatilization of acetone
from moist soil surfaces(SRC) is expected given the measured Henry's Law
constant of 1.87X10-5 atm-cu m/mole(4). Volatilization from dry soil surfaces is
expected based upon the experimental vapor pressure of 232 mm Hg at 25 deg
C(5,SRC). Acetone is expected to
biodegrade under both aerobic and anaerobic conditions as indicated by numerous
screening tests(6-9).
AQUATIC FATE: Based on a recommended
classification scheme(1), an estimated Koc value of 1(SRC), determined from an
experimental log Kow of -0.24(2), and a recommended regression-derived
equation(3), indicates that acetone
will not adsorb to suspended solids and sediment in water(SRC). Acetone
is expected to volatilize from water surfaces(3,SRC) based on the measured
Henry's Law constant of 1.87X10-5 atm-cu m/mole(4). Estimated half-lives for a
model river and model lake are 38 and 333 hours, respectively(3,SRC).
Experimentally determined volatilization half-lives in a shallow stream were
measured in the range of 8-18 hours(5-7). Biodegradation of this compound is
expected, but volatilization has been shown to be the primary removal process of
acetone in water(5-7). According to a
classification scheme(8), an estimated BCF value of 1(3,SRC), from an
experimental log Kow(2,SRC), suggests that bioconcentration in aquatic organisms
is low(SRC).
ATMOSPHERIC FATE: According to a model of
gas/particle partitioning of semivolatile organic compounds in the
atmosphere(1), acetone, which has an
experimental vapor pressure of 231 mm Hg at 25 deg C(2), will exist solely as a
vapor in the ambient atmosphere. Vapor-phase acetone
is degraded in the atmosphere by reaction with photochemically-produced hydroxyl
radicals(SRC); the half-life for this reaction in air is estimated to be about
71(3,SRC) days. The average rate constant for the photodissociation of acetone
by natural sunlight in the lower troposphere was measured as 1X10-7 sec-1(4).
This corresponds to a half-life of about 80 days(4).
Environmental Biodegradation:
Biological oxygen demand: (Theoretical) 122%,
5 days
The percent theoretical BOD of acetone
in water seeded with settled domestic sewage was 56%, 76%, 83% and 84%, over 5,
10, 15 and 20 day incubation periods(1). Percent theoretical BOD's of acetone
in a raw sewage inocula were reported as 37% and 81% over 5 and 20 day
incubation periods respectively(2), 54% over a 5 day incubation period(3), 71%
over a 7 day incubation period(4), 55% and 72% over 5 day and 10 day incubation
periods respectively(5) and 38% over a 5 day incubation period(6). Acetone
was shown to be readily biodegradable under anaerobic conditions(7-9). The
percent theoretical methane recovery of acetone
in an anaerobic aquifer was 89% over a 3 week incubation period following a 25
day acclimation period(9).
Environmental Abiotic Degradation:
The rate constant for the vapor-phase reaction
of acetone with photochemically-produced
hydroxyl radicals has been measured as 2.26X10-13 cu cm/molecule-sec at 25 deg
C(1). This corresponds to an atmospheric half-life of about 71 days at an
atmospheric concn of 5.0X10+5 hydroxyl radicals per cu cm(1,SRC). The average
rate constant for the photodissociation of acetone
by natural sunlight in the lower troposphere was measured as 1X10-7 sec-1(2).
This corresponds to a half-life of about 80 days(2). When water containing acetone
is treated with chlorine for disinfection purposes, the acetone
can react with the hypochlorite ion formed by the hydrolysis of chlorine leading
to the production of trichloromethane(3). This reaction is strongly pH dependent
and is expected to have a significant effect only at pH values of 6-7(3).
Environmental Bioconcentration:
An estimated BCF value of 1 was calculated for
acetone(SRC), using an experimental
log Kow of -0.24(1) and a recommended regression-derived equation(2). According
to a classification scheme(3), this BCF value suggests that bioconcentration in
aquatic organisms is low(SRC).
Soil Adsorption/Mobility:
The Koc of acetone
is estimated as approximately 1(SRC), using an experimental log Kow of -0.24(1)
and a regression-derived equation(2,SRC). According to a recommended
classification scheme(3), this estimated Koc value suggests that acetone
is expected to have very high mobility in soil(SRC). Acetone
showed no adsorption to montorillonite, kaolinite clay, or stream sediment(4,5).
Volatilization from Water/Soil:
The Henry's Law constant for acetone
was measured as 1.87X10-5 atm-cu m/mole(SRC) at 25 deg C(1). This value
indicates that acetone will volatilize
from water surfaces(2,SRC). Based on this Henry's Law constant, the
volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind
velocity of 3 m/sec) is estimated as approximately 38 hours(2,SRC). The
volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind
velocity of 0.5 m/sec) is estimated as approximately 333 hours(2,SRC).
Volatilization rate constants of a model stream (234 m long, water velocity 0.67
m/min) were measured in the range of 8.23X10-4 min-1 to 11.1X10-4 min-1(3).
These rate constants correspond to volatilization half-lives of about 10-14
hours(3). Similar experiments in the same stream measured acetone
volatilization rate constants in the range of 6.22X10-4 min-1 to 14.5X10-4
min-1(4,5). These rate constants correspond to volatilization half-lives of
about 8-18 hours(4,5). Acetone is
expected to volatilize from dry soil surfaces given its experimental vapor
pressure(1,SRC).
Environmental Water Concentrations:
A concentration of 0.6 g/l of acetone
was found in a sample of a one-year old leachate from a ... sanitary landfill.
DRINKING WATER: Acetone
was identified, not quantified, in 10 out of 10 drinking water samples collected
in the US(1). Acetone was identified,
not quantified, in the drinking water of New Orleans, LA(2), Seattle, WA(3) and
Tuscaloosa, AL(4). Acetone was
detected in a drinking water well in New Jersey at a concn of 3,000 ppb(5). Six
drinking water wells in the vicinity of a landfill contained 0.2 to 0.7 ppb of acetone(6).
An unspecified concn of acetone
leached from a section of high density polyethylene tubing supplying drinking
water in Paris(7). Acetone was
detected in the municipal wells in Waite Park, MN at concns between 74-3,300 ug/l(8).
GROUNDWATER: Acetone
was detected in groundwater near a chemical
manufacturing facility in Michigan at a maximum concn of 1,600 ug/l(1). Acetone
was detected in groundwater in NJ at a concn of 3,000 ug/l(2). Acetone
was detected at a concn of 620 ppb in the groundwater at the Lipari landfill,
NJ(3). Acetone was detected at a concn
of 11 ug/l in the on-site wells and 0.19 ug/l in the off-site groundwater near a
manufacturing facility in MI(4). Acetone
was identified, not quantified, in 12.4% of the groundwater samples at 178 sites
in the US(5) and in the groundwater of a waste disposal facility in SC(6). The
average concn of acetone in
groundwater sampled at 5 wood treatment facilities was 20 ug/l(7). Acetone
was detected in the groundwater of a coal strip-mine in Ohio at concns of 1,300
mg/l and 2,700 ug/l(8).
SURFACE WATER: Five of nine sites in Lake
Michigan contained 1-4 ppb acetone(1).
In a survey of 14 heavily industrialized river basins in the USA (204 samples),
33 contained detectable amounts of acetone
including 18 of 31 sites in the Chicago area and the Illinois River basin, 8 of
30 sites in the Delaware River basin, 1 of 45 sites in the Mississippi River
basin, 3 of 27 sites in the Ohio River basin, and 3 of 15 west coast sites(2). Acetone
was identified, not quantified, in the Black River in Tuscaloosa, AL(3), and the
Cuyahoga River in the Lake Erie basin(4). Acetone
was detected in the Potomac River at a concn of less than 40 ug/l(5).
SEAWATER: Samples of seawater and surface
slicks taken from Biscayne Bay and the Florida Current contained 39.6 and 89.7
ppb of acetone, respectively(1). Grab
samples of surface water from the Straits of Florida and the Eastern
Mediterranean contained 20 and 28 ppb of acetone,
respectively(2). Samples of ocean water taken at 1,200 m depths contained
unspecified concns of acetone(2).
RAIN/SNOW: 50 ppb of acetone
was detected in one of 6 samples tested at 5 cities in California(1). An
unspecified concn of acetone was
detected in rain in Japan(2). Acetone/acrolein
was detected in rainfall in Los Angeles, CA at a concn of 0.05 ug/ml and in ice
at Urban Fairbanks, AK at a concn of 0.21 umols/ml(3). Acetone
was identified, not quantified, in rainfall in Germany(4). Acetone
was detected in the clouds (460 ng/l) and rainfall (0.5 ng/l) at a state park in
North Carolina(5).
Effluent Concentrations:
Acetone
was detected in the effluent of a chemical
plant located in Sweden at a concn of 5.5 kg/cu m(1). Acetone
was detected in the effluent of municipal landfill sites in North America at
concns of 6,838 ppb and 32,500 ppb(2). Acetone
was identified, not quantified in the emissions of new carpets(3),
automobiles(4,5) and common household waste(6-9). Acetone
was detected in the effluent from a solid waste composting plant at concns of
6,100 ug/cu m(tipping area), 7,800 ug/cu m(indoor air), 9,200 ug/cu m(fresh
compost), 9,500 ug/cu m(middle age compost), 6,100 ug/cu m(old compost) and
2,300 ug/cu m(curing region)(10). Acetone
was identified, not quantified, in the emissions of 314 out of 1,005 common
household products(11). Acetone was
detected in the effluent of a waste incinerator in Germany at a concn of 17.6 ug/cu
m(12). Acetone was detected in the
emissions of a photocopying machine at rates of less than 100 ug/hr to 2,200 ug/hr(13).
Acetone was detected at a concn of 25
ug/cu m in the emissions of a composting facility in Virginia(14).
Acetone
was detected in the leachate of several municipal landfills at concns between
6-4,400 ug/l(1). Acetone was detected
in the wastewater of a truck parts producing plant in Michigan at a concn of
44.5 ug/l(2). Acetone was detected in
the effluent of an unauthorized hazardous waste disposal facility in New Jersey
at a concn of 480 ug/l(3). Acetone was
detected at a concn of 46.6 ppb in the leachate of a landfill in Delaware
containing industrial and municipal waste(4). Acetone
was detected at concns between 0.05-62 mg/l and 0.14-44 mg/l in the leachate of
industrial landfills and municipal landfills in the US(5). Acetone
was detected in the leachate of a landfill in Connecticut at a concn of 3,500 ug/l(6).
In gasoline exhaust: 2.3-14.0 ppm (partly
propionaldehyde)
Sediment/Soil Concentrations:
Acetone
was detected in the soil of a coal strip mine in Ohio at mean concns of 9,484 ug/kg
(surface soil), 2,263 ug/kg (2-4 feet), 9644 ug/kg (4-6 feet), 5,272 ug/kg (6-8
feet)(1). Acetone was identified, not
quantified, in the sediment and subsurface soil of a gravel mine in
Tennessee(2). Acetone was detected at
an average concn of 736 ug/kg in the soil of an unauthorized hazardous waste
disposal facility in New Jersey(3).
Atmospheric Concentrations:
SOURCE DOMINATED: Acetone
was detected at 22 source dominated sites in the USA at a median concn of 0.350
ppb and a maximum concn of 53 ppb(1). Acetone
was detected at concns between 2.3-3.3 ppb near the Texaco Refinery in Tulsa,
OK(2).
URBAN/SUBURBAN: Acetone
was detected at a concn of 1-8 ppb in Denver, CO(1). Acetone
was detected at mean concns of 13.9 ppb in Boston, MA, 34.5 ppb(2) and 6.1
ppb(3) in Houston, TX and 12 ppb in Tucson, AZ(4). The average concn of acetone/formaldehyde
at 4 southern California locations was 0.30 ppb(5). Acetone
was detected at a concn of 2.07 ppb in Columbus, OH(6). The average concn of acetone
at 5 sites in Stockholm was between 4.04-19.40 ppb(7).
INDOOR AIR: Acetone
was detected at an average concn of 39 ug/cu m at 14 homes and buildings in
Italy(1). Acetone was detected in 2
buildings in Portland, OR at concns between 14.9-66.0 ug/cu m and 7.4-33.9 ug/cu
m(2). Acetone was detected in a
building in Switzerland at a concn of 7,763 ug/cu m(3). Acetone
was detected at a concn of 10 and less than 1 ng/l in 2 elementary school
classrooms in France(4).
RURAL/REMOTE: Acetone
was detected at an average concn of 14.72 ng/l in the air of a state park in
North Carolina(1). Acetone was
identified, not quantified, in the air of a German forest(2). Acetone
was detected at concns between 0.39-3.26 ppb and 0.72-3.81 ppb in Egbert Ontario
and Dorset Ontario respectively(3). Acetone
was detected at a mean concn of 1,140 parts per trillion in Eastern Canada(4). Acetone
was detected at a mean concn of 2.6 ppb at 2 rural sites in AZ(5) and 5.1 ppb in
Rio Blanco county, CO(6). The acetone
concn in air at Pt Barrow, AK (22 measurements) ranged from 0.3 to 2.9 ppb, with
a mean concn of 1.21 ppb(7). Acetone
was detected at a concn of 1.9 ppb in the Jones State Forest near Houston,
TX(8).
Food Survey Values:
Acetone
was identified, not quantified, in the volatiles of kiwi fruit(1,2), blue
cheese(3), raw chicken(4), cured pork(5), chickpea seeds(6), nectarines(7),
mutton, chicken and beef(8). Acetone
has been identified, not quantified, as a volatile component of baked
potatoes(9), roasted filberts(10), dried beans and legumes(11), and French
cognac(12).
Plant Concentrations:
Acetone
is emitted from Bay Leaf Willows, European Firs and Evergreen Cyprus(1).
Milk Concentrations:
Acetone
was identified, not quantified, in human milk from Bayonne, NJ, Jersey City, NJ,
Pittsburgh, PA and Baton Rouge, LA(1). Acetone
was identified, not quantified, in all 8 samples of mother's milk analyzed from
4 industrial urban areas in the USA(2). Acetone
was identified, not quantified from milk samples in Australia(3).
Other Environmental Concentrations:
Cigarette smoke - 1,100 ppm
Acetone was detected in cigarette smoke at a concn of 1,620 ug
per cigarette(1).
Environmental Standards & Regulations:
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are
required to notify the National Response Center (NRC) immediately, when there is
a release of this designated hazardous substance, in an amount equal to or
greater than its reportable quantity of 5000 lb or 2270 kg. The toll free number
of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202)
426-2675. The rule for determining when notification is required is stated in 40
CFR 302.4 (section IV. D.3.b).
RCRA Requirements:
F003; When acetone
is a spent solvent, it is classified as a hazardous waste from a nonspecific
source (F003), as stated in 40 CFR 261.31, and must be managed according to
State and/or Federal hazardous waste regulations.
U002; As stipulated in 40 CFR 261.33, when acetone,
as a commercial chemical product or
manufacturing chemical intermediate or
an off-specification commercial chemical
product or a manufacturing chemical
intermediate, becomes a waste, it must be managed according to Federal and/or
State hazardous waste regulations. Also defined as a hazardous waste is any
residue, contaminated soil, water, or other debris resulting from the cleanup of
a spill, into water or on dry land, of this waste. Generators of small
quantities of this waste may qualify for partial exclusion from hazardous waste
regulations (40 CFR 261.5).
Atmospheric Standards:
This action promulgates standards of
performance for equipment leaks of Volatile Organic Compounds (VOC) in the
Synthetic Organic Chemical
Manufacturing Industry (SOCMI). These standards implement Section 111 of the
Clean Air Act and are based on the Administrator's determination that emissions
from the SOCMI cause, or contribute significantly to, air pollution which may
reasonably be anticipated to endanger public health or welfare. The intended
effect of these standards is to require all newly constructed, modified, and
reconstructed SOCMI process units to use the best demonstrated system of
continuous emission reduction for equipment leaks of VOC, considering costs, non
air quality health and environmental impact and energy requirements. Acetone
is produced, as an intermediate or final product, by process units covered under
this subpart. These standards of performance become effective upon promulgation
but apply to affected facilities for which construction or modification
commenced after January 5, 1981.
State Drinking Water Guidelines:
(FL) FLORIDA 700 ug/l
(MA) MASSACHUSETTS 3000 ug/l
(MN) MINNESOTA 700 ug/l
(NH) NEW HAMPSHIRE 700 ug/l
(WI) WISCONSIN 1000 ug/l
Allowable Tolerances:
Residues of acetone
are exempted from the requirement of a tolerance when used as a solvent,
cosolvent in accordance with good agricultural practices as inert (or
occasionally active) ingredients in pesticide formulations applied to growing
crops or to raw agricultural commodities after harvest.
Chemical/Physical Properties:
Molecular Formula:
C3-H6-O
Molecular Weight:
58.08
Color/Form:
Colorless liquid
Odor:
Fruity odor
Taste:
PUNGENT, SWEETISH
Boiling Point:
56.0 DEG C @ 760 MM HG
Melting Point:
-94.8 DEG C
Critical Temperature & Pressure:
Critical temperature: 455 deg F= 235 deg C=
508 deg K; critical pressure: 46.4 atm
Density/Specific Gravity:
0.7899 AT 20 DEG C/4 DEG C
Dissociation Constants:
pKa = 20
Heat of Combustion:
Liquid: -1787 kJ/mol (-427 kcal/mol)
Heat of Vaporization:
220 Btu/lb= 122 cal/g
Octanol/Water Partition Coefficient:
Log Kow= -0.24
Solubilities:
SOLUBLE IN BENZENE
MISCIBLE WITH WATER, ALCOHOL,
DIMETHYLFORMAMIDE, ETHER
MISCIBLE WITH CHLOROFORM, MOST OILS
Spectral Properties:
INDEX OF REFRACTION: 1.3588 AT 20 DEG C/D
IR: 77 (Sadtler Research Laboratories IR
Grating Collection)
UV: 89 (Sadtler Research Laboratories Spectral
Collection)
NMR: 9288 (Sadtler Research Laboratories
Spectral Collection)
MASS: 30 (Atlas of Mass Spectral Data, John
Wiley & Sons, New York)
Intense mass spectral peaks: 43 m/z, 58 m/z
Surface Tension:
0 deg C: 26.2 mN/m; 20 deg C: 23.7 mN/m; 40
deg C: 21.2 mN/m
Vapor Pressure:
231 mm Hg at 25 deg C
Viscosity:
0.32 cP at 20 deg C
Other Chemical/Physical Properties:
Saturation concentration: 553 g/cu m
Specific heat of liquid: 2.6 J/g (0.62 cal/g)
at 20 deg C; specific heat of vapor: 92.1 J/(mol x k) (22.0 cal/mol x k) at 102
deg C; electric conductivity: 5.5x10-8 sec/cm at 25 deg C; heat of formation at
25 deg C: gas -216.5 kJ/mol, liquid: -248 kJ/mol.
Heat of fusion: 23.42 cal/g
Partition coefficients at 37 deg C for acetone
into blood = 245; into oil = 86.
Henry's Law constant = 1.87X10-5 atm-cu m/mole
at 25 deg C
Chemical Safety & Handling:
DOT Emergency Guidelines:
Fire or explosion: HIGHLY FLAMMABLE: Will be
easily ignited by heat, sparks or flames. Vapors may form explosive mixtures
with air. Vapors may travel to source of ignition and flash back. Most vapors
are heavier than air. They will spread along ground and collect in low or
confined areas (sewers, basements, tanks). Vapor explosion hazard indoors,
outdoors or in sewers. Those substances designated with a "P" may
polymerize explosively when heated or involved in a fire. Runoff to sewer may
create fire or explosion hazard. Containers may explode when heated. Many
liquids are lighter than water.
Health: Inhalation or contact with material
may irritate or burn skin and eyes. Fire may produce irritating, corrosive
and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire
control may cause pollution.
Public safety: CALL Emergency Response
Telephone Number. ... Isolate spill or leak area immediately for at least 25 to
50 meters (80 to 160 feet) in all directions. Keep unauthorized personnel away.
Stay upwind. Keep out of low areas. Ventilate closed spaces before entering.
Protective clothing: Wear positive pressure
self-contained breathing apparatus (SCBA). Structural firefighters' protective
clothing will only provide limited protection.
Evacuation: ... Fire: If tank, rail car or
tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all
directions; also, consider initial evacuation for 800 meters (1/2 mile) in all
directions.
Fire: CAUTION: All these products have a very
low flash point: Use of water spray when fighting fire may be inefficient. Small
fires: Dry chemical, CO2, water spray
or alcohol-resistant foam. Large fires: Water spray, fog or alcohol-resistant
foam. Use water spray or fog; do not use straight streams. Move containers from
fire area if you can do it without risk. Fire involving Tanks or Car/Trailer
loads: Fight fire from maximum distance or use unmanned hose holders or monitor
nozzles. Cool containers with flooding quantities of water until well after fire
is out. Withdraw immediately in case of rising sound from venting safety devices
or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For
massive fire, use unmanned hose holders or monitor nozzles; if this is
impossible, withdraw from area and let fire burn.
Spill or leak: ELIMINATE all ignition sources
(no smoking, flares, sparks or flames in immediate area). All equipment used
when handling the product must be grounded. Do not touch or walk through spilled
material. Stop leak if you can do it without risk. Prevent entry into waterways,
sewers, basements or confined areas. A vapor suppressing foam may be used to
reduce vapors. Absorb or cover with dry earth, sand or other non-combustible
material and transfer to containers. Use clean non-sparking tools to collect
absorbed material. Large spills: Dike far ahead of liquid spill for later
disposal. Water spray may reduce vapor; but may not prevent ignition in closed
spaces.
First aid: Move victim to fresh air. Call 911
or emergency medical service. Apply artificial respiration if victim is not
breathing. Administer oxygen if breathing is difficult. Remove and isolate
contaminated clothing and shoes. In case of contact with substance, immediately
flush skin or eyes with running water for at least 20 minutes. Wash skin with
soap and water. Keep victim warm and quiet. Ensure that medical personnel are
aware of the material(s) involved, and take precautions to protect themselves.
Odor Threshold:
WATER: 20 MG/L (OR 20 PPM, W/V); AIR: 13 UL/L
(OR 13 PPM, V/V).
Odor low: 47.5 mg/cu m; Odor high: 1613.9
mg/cu m
Skin, Eye and Respiratory Irritations:
EXPOSURE FOR 15 MINUTES TO 1660 PPM CAUSES
IRRITATION OF EYES AND NOSE ...
Fire Potential:
Highly flammable liquid. Dangerous disaster
hazard due to fire and explosion hazard ...
NFPA Hazard Classification:
Health: 1. 1= Materials that, on exposure,
would cause irritation, but only minor residual injury, including those
requiring the use of an approved air-purifying respirator. These materials are
only slightly hazardous to health and only breathing protection is needed.
Flammability: 3. 3= This degree includes Class
IB and IC flammable liquids and materials that can be easily ignited under
almost all normal temperature conditions. Water may be ineffective in
controlling or extinguishing fires in such materials.
Reactivity: 0. 0= This degree includes
materials that are normally stable, even under fire exposure conditions, and
that do not react with water. Normal fire fighting procedures may be used.
Flammable Limits:
LOWER LIMIT 2.15%; UPPER LIMIT 13.0%
Flash Point:
-20 DEG C (-4 DEG F) (CLOSED CUP)
0 deg F (closed cup)
Autoignition Temperature:
869 DEG F
Fire Fighting Procedures:
Evacuation: If fire becomes uncontrollable or
container is exposed to direct flame - consider evacuation of one-third mile
radius.
If material is on fire or involved in fire: Do
not extinguish fire unless flow can be stopped. Use water in flooding quantities
as fog. Solid streams of water may be ineffective. Cool all affected containers
with flooding quantities of water and apply water from as far a distance as
possible. Use alcohol foam, carbon dioxide, or dry chemical.
Flammable. Flashback along vapor trail may
occur. Vapor may explode if ignited in an enclosed area. Extinguish with dry chemical,
alcohol foam, or carbon dioxide. Water may be ineffective on fire. Cool exposed
containers with water.
Firefighting Hazards:
FLASHBACK ALONG VAPOR TRAIL MAY OCCUR.
Explosive Limits & Potential:
Highly flammable liquid. Dangerous disaster
hazard due to fire and explosion hazard ...
UPPER 12.8%, LOWER 2.6%.
VAPOR MAY EXPLODE IF IGNITED IN AN ENCLOSED
AREA.
Hazardous Reactivities & Incompatibilities:
MIXTURE OF ACETONE
& CHLOROFORM IN A RESIDUE BOTTLE EXPLODED. SINCE ADDITION OF CHLOROFORM TO ACETONE
IN PRESENCE OF A BASE WILL RESULT IN A HIGHLY EXOTHERMIC REACTION, IT IS THOUGHT
THAT A BASE MAY HAVE BEEN IN THE BOTTLE.
ACETONE
MAY FORM EXPLOSIVE MIXTURES WITH CHROMIC ANHYDRIDE, CHROMYL CHLORIDE,
HEXACHLOROMELAMINE, HYDROGEN PEROXIDE, NITRIC ACID, ACETIC ACID, NITRIC ACID
& SULFURIC ACID, NITROSYL CHLORIDE, NITROSYL PERCHLORATE, NITRYL PERCHLORATE,
PERMONOSULFURIC ACID, POTASSIUM TERT-BUTOXIDE, THIODIGLYCOL & HYDROGEN
PEROXIDE.
AN EXPLOSION OCCURRED DURING AN ATTEMPT TO
PREPARE BROMOFORM FROM ACETONE BY THE
HALOFORM REACTION. ACETONE IGNITED
WHEN IT WAS ACCIDENTALLY SPLASHED INTO A SULFURIC ACID-DICHROMATE SOLUTION.
Oxidizers, acids.
Potentially explosive reaction with nitric
acid + sulfuric acid, bromine trifluoride, nitrosyl chloride + platinum,
nitrosyl perchlorate, chromyl chloride, thiotrithiazyl perchlorate, and
(2,4,6-trichloro-1,3,5-triazine + water). Reacts to form explosive peroxide
products with 2-methyl-1,3-butadiene, hydrogen peroxide, and peroxomonosulfuric
acid. Ignites on contact with activated carbon, chromium trioxide, dioxygen
difluoride + carbon dioxide, and potassium-t-butoxide. Reacts violently with
bromoform, chloroform + alkalies, bromine, and sulfur dichloride. Incompatible
with CrO, (nitric + acetic acid), NOCl, nitryl perchlorate, permonosulfuric
acid, NaOBr, (sulfuric acid + potassium dichromate), (thio-diglycol + hydrogen
peroxide), trichloromelamine, air, HNO3, chloroform, and H2SO4.
Prior History of Accidents:
The wreck of the MV Ariadne, a Panamanian flag
container ship, is examined as a case study of a hazardous substance emergency
response in a third world country. /The ship/, carrying a cargo of heavy fuel
oil, tetraethyl lead, xylene, toluene, methyl isobutyl ketone, butyl acetate,
ethyl acetate, and acetone was
grounded while departing the harbor of Mogadishu, Somalia. The Somalian
government requested a team of technical advisors to help respond appropriately
to the emergency. The major issues addressed by the advisory team were the need
for additional salvage equipment and expertise, the danger of toxic fumes from
the fire and explosions aboard the ship, the presence and possible release of
tetraethyl lead, possible port blockage by the wreck, recovery of the chemical
drums, and the extent of environmental damage caused by the release of oil,
pesticides, and tetraethyl lead into the harbor. ...
Immediately Dangerous to Life or Health:
2500 ppm (IDLH based on a 10% of the lower
explosive limit for safety considerations even though the relevant toxicological
data indicated that irreversible health effects or impairment of escape existed
only at higher concentrations.)
Protective Equipment & Clothing:
Protective equipment made from natural rubber,
viton, neoprene, polyvinyl alcohol, neoprene/natural rubber, or nitrile have
breakthrough times less (usually significantly less) than one hour reported by
(normally) two or more testers.
Protective clothing made from polyethylene or
chlorinated polyethylene; the data suggests breakthrough times of approximately
an hour or more.
No data is available regarding break-through
times for clothing made from styrene-butadiene rubber, nitrile/polyvinyl
chloride, or polyurethane.
Wear appropriate eye protection to prevent eye
contact.
Wear appropriate personal protective clothing
to prevent skin contact.
Recommendations for respirator selection. Max
concn for use: 2500 ppm. Respirator Class(es): Any chemical
cartridge respirator with organic vapor cartridge(s). May require eye
protection. Any powered, air-purifying respirator with organic vapor cartridge(s).
May require eye protection. Any air-purifying, full-facepiece respirator (gas
mask) with a chin-style, front- or back-mounted organic vapor canister. Any
supplied-air respirator. May require eye protection. Any self-contained
breathing apparatus with a full facepiece.
Recommendations for respirator selection.
Condition: Emergency or planned entry into unknown concn or IDLH conditions:
Respirator Class(es): Any self-contained breathing apparatus that has a full
facepiece and is operated in a pressure-demand or other positive pressure mode.
Any supplied-air respirator that has a full facepiece and is operated in
pressure-demand or other positive pressure mode in combination with an auxiliary
self-contained breathing apparatus operated in pressure-demand or other positive
pressure mode.
Recommendations for respirator selection.
Condition: Escape from suddenly occurring respiratory hazards: Respirator
Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a
chin-style, front- or back-mounted organic vapor canister. Any appropriate
escape-type, self-contained breathing apparatus.
Preventive Measures:
Personnel protection: Avoid breathing vapors.
Keep upwind. Do not handle broken packages without protective equipment. Wash
away any material which may have contacted the body with copious amounts of
water or soap and water.
Direct contact with the skin should be
avoided. Acetone should never be used
as a cleaning agent for the skin.
A major concern in the painting studio is solvents, /including acetone/.
... Precautions include ... use of dilution and local exhaust ventilation,
control of storage areas, disposal of solvent soaked rags in covered containers,
minimizing skin exposure and the use of respirators and other personal
protective equipment. The control of fire hazards is also important, since many
of the solvents are highly flammable.
SRP: Local exhaust ventilation should be
applied wherever there is an incidence of point source emissions or dispersion
of regulated contaminants in the work area. Ventilation control of the
contaminant as close to its point of generation is both the most economical and
safest method to minimize personnel exposure to airborne contaminants.
If material not on fire and not involved in
fire: Keep sparks, flames, and other sources of ignition away. Keep material out
of water sources and sewers. Build dikes to contain flow as necessary. Attempt
to stop leak if without undue personnel hazard. Use water spray to disperse
vapors and dilute standing pools of liquid.
Contact lenses should not be worn when working
with this chemical.
SRP: The scientific literature for the use of
contact lenses in industry is conflicting. The benefit or detrimental effects of
wearing contact lenses depend not only upon the substance, but also on factors
including the form of the substance, characteristics and duration of the
exposure, the uses of other eye protection equipment, and the hygiene of the
lenses. However, there may be individual substances whose irritating or
corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn.
In any event, the usual eye protection equipment should be worn even when
contact lenses are in place.
The worker should immediately wash the skin
when it becomes contaminated.
Work clothing that becomes wet should be
immediately removed due to its flammability hazard.
Keep away from plastic eyeglass frames,
jewelry, pens and pencils, rayon stockings and other rayon garments.
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a
hazardous material for transportation in commerce unless that person is
registered in conformance ... and the hazardous material is properly classed,
described, packaged, marked, labeled, and in condition for shipment as required
or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA)
Dangerous Goods Regulations are published by the IATA Dangerous Goods Board
pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry
carrier regulations to be followed by all IATA Member airlines when transporting
hazardous materials.
The International Maritime Dangerous Goods
Code lays down basic principles for transporting hazardous chemicals.
Detailed recommendations for individual substances and a number of
recommendations for good practice are included in the classes dealing with such
substances. A general index of technical names has also been compiled. This
index should always be consulted when attempting to locate the appropriate
procedures to be used when shipping any substance or article.
Storage Conditions:
Store acetone
in closed containers, and keep away from heat, sparks, and flames.
Acetone
is stored in steel tanks
Disposal Methods:
Generators of waste (equal to or greater than
100 kg/mo) containing this contaminant, EPA hazardous waste number F003, must
conform with USEPA regulations in storage, transportation, treatment and
disposal of waste.
Generators of waste (equal to or greater than
100 kg/mo) containing this contaminant, EPA hazardous waste number U002, must
conform with USEPA regulations in storage, transportation, treatment and
disposal of waste.
Incineration: Spray into a furnace.
Incineration will become easier by mixing with a more flammable solvent.
Acetone
is a good candidate for fluidized bed incineration with a temperature of 450-980
deg C and with residence times for liquids and gases: seconds.
Acetone
is a good candidate for rotary kiln incineration with a temperature of 820-1,600
deg C and with residence time for liquids and gases: seconds.
Acetone
is a good candidate for liquid injection incineration with a temperature of
650-1,600 deg C with a residence time of 0.1-2 seconds.
This compound should be susceptible to removal
from waste water by air stripping.
Small amounts can be burned after pouring on
dry sand. Larger quantities can be atomized into an approved type combustion
chamber.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr
Time Weighted Avg: 1000 ppm (2400 mg/cu m).
Vacated 1989 OSHA PEL TWA 750 ppm (1800 mg/cu
m); STEL 1000 ppm (2400 mg/cu m) is still enforced in some states.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA): 500 ppm; 15 min
Short Term Exposure Limit (STEL): 750 ppm.
A4; Not classifiable as a human carcinogen.
Biological Exposure Index (BEI): Determinant: acetone
in urine; Sampling Time: end of shift; BEI: 50 mg/l. The determinant is
nonspecific, since it is also observed after exposure to other chemicals.
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr
Time-Weighted Avg: 250 ppm (590 mg/cu m).
Immediately Dangerous to Life or Health:
2500 ppm (IDLH based on a 10% of the lower
explosive limit for safety considerations even though the relevant toxicological
data indicated that irreversible health effects or impairment of escape existed
only at higher concentrations.)
Other Occupational Permissible Levels:
Exposure limits: France, TWA limits - 1,800
mg/cu m (1983).
Manufacturing/Use Information:
Major Uses:
SOLVENT FOR FATS, OILS, WAXES, RESINS, RUBBER,
PLASTICS, LACQUERS, VARNISHES, RUBBER CEMENTS
MFR MESITYL OXIDE, ACETIC ACID, DIACETONE
ALCOHOL, CHLOROFORM, IODOFORM, BROMOFORM
MFR EXPLOSIVES, AIRPLANE DOPES, RAYON,
ISOPRENE, PHOTOGRAPHIC FILMS, STORING ACETYLENE GAS
EXTRACTION OF VARIOUS PRINCIPLES FROM ANIMAL
AND PLANT SUBSTANCES; IN PAINT &
VARNISH REMOVERS; PURIFYING PARAFFIN
HARDENING AND DEHYDRATING TISSUES
NAIL POLISH REMOVER
CHEM INT FOR METHYL METHACRYLATE, METHACRYLIC
ACID & HIGHER METHACRYLATES, METHYL ISOBUTYL KETONE, METHYL ISOBUTYL
CARBINOL, BISPHENOL A, ISOPHORONE; SPINNING SOLVENT IN MFR OF CELLULOSE ACETATE;
SOLVENT FOR ADHESIVES & PRINTING INKS, ACETYLENE
Manufacture of smokeless powder.
Acetone
is used for the production of modacrylic fibers, for either wet spinning or dry
spinning.
Acetone
is used as a raw material in the manufacturing of acetic anhyride.
Preparation of vitamin intermediates.
Acetone
is used as a brine for low temperature heat transfer in indirect refrigeration.
The evaporation rate of acetone
makes it quite useful for cleaning and drying precision parts.
Manufacturers:
Allied-Signal, Inc, Hq, Columbia Road and Park
Avenue, Morristown, NJ 07960, (201) 455-2000; Engineered Materials Sector;
Production site: Philadelphia, PA 19137
Eastman Chemical
Company, Hq, 343 State Street, Rochester, NY 14650, (716) 724-4000; Eastman Chemical
Products, Inc; Tennessee Eastman Company; Production site: Kingsport, TN 37662
General Electric Company, Hq, 3135 Easton
Turnpike, Fairfield, CT 06431, (203) 373-2211; GE Plastics, One Plastics Avenue,
Pittsfield, MA 01201; Production site: Mount Vernon, IN 47620
Georgia Gulf Corporation, Hq, 400 Perimeter
Center Terrace, Suite 595, Atlanta, GA 30348, (404) 395-4500; Production site:
Bound Brook, NJ 08805
The Goodyear Tire & Rubber Company, Hq,
1144 East Market Street, Akron, OH 44316, (216) 796-2121; General Products
Division; Production site: Bayport, TX 77058
JLM Chemicals
Company, 3350 West 131st Street, P.O. Box 598, Blue Island, IL 60406.
(708)388-9373
Shell Oil Company, Hq, One Shell Plaza,
Houston, TX 77252-2463; Shell Chemical
Company, division (address same as Hq); Production sites: Deer Park, TX 77536
(Houston Plant); Wood River, IL 62095
Texaco, Inc, Hq, 2000 Westchester Avenue,
White Plains, NY 10650, (914) 253-4000; Subsidiary: Texaco Chemical
Company, 4800 Fournace Place, Bellaire, TX 77401, (713) 666-8000; Production
site: El Dorado, KS 67042
Union Carbide Corporation, Hq, Old Ridgebury
Road, Danbury, CT 06817, (203) 794-2000; Chemicals
and Plastics Business Group; Solvents and Coatings
Materials Division; Production site: Institute, WV 25103
Aristech Chemical
Corp, Hq, 600 Grant St, Pittsburgh, PA 15219, (412) 433-2747; Production site:
Haverhill, OH 45638
Dow Chemical
USA, Hq, 2020 Dow Center, Midland, MI 48674, (517) 636-1000; Production site:
Oyster Creek, TX 77541
Methods of Manufacturing:
(1) BY DESTRUCTIVE DISTILLATION OF WOOD. (2)
BY DISTILLATION OF CALCIUM ACETATE. (3) BY FERMENTATION OF CORN PRODUCTS BY
SELECTED BACTERIA. (4) BY CATALYTIC OXIDATION OF ISOPROPYL ALCOHOL, CUMENE, OR
NATURAL GAS.
MOST USA/ACETONE/PRODUCTION
BASED ON CUMENE PROCESS /IN WHICH/ BENZENE AND PROPYLENE ARE REACTED TO FORM
CUMENE. CUMENE IS THEN OXIDIZED WITH AIR /TO PRODUCE/ CUMENE HYDROPEROXIDE
/WHICH/ IS THEN DECOMPOSED OR CLEAVED WITH ACID TO YIELD PHENOL AND ACETONE.
General Manufacturing Information:
DISINFECTANT WHEN USED IN HIGH CONCENTRATIONS,
BEING RAPIDLY BACTERICIDAL FOR MICROCOCCUS AUREUS, BUT NOT SPORICIDAL, THOUGH IT
INDUCES DELAY IN THE GROWTH OF SPORES.
EXXON AT BAYWAY, NJ AND UNION CARBIDE AT
PENUELAS, PR ARE ON STANDBY. MONSANTO, CHEVRON, SHELL AND CYANAMID HAVE CLOSED
APPROXIMATELY 445 MILLION LB OF ACETONE
CAPACITY SINCE 1982
DURING 1984, APPROXIMATELY 15% OF US ACETONE
OUTPUT WAS DERIVED FROM ISOPROPANOL
0.40-0.45 kg of acetone
per kg of cumene are produced as a coproduct with phenol via cumene peroxidation
route. Stated in terms of phenol, one kg of phenol production will result in 0.6
kg of acetone.
Acetone
is a co-product of liquid-phase-oxidation of butane. It may be produced from
isobutane, an impurity present in all commercial butane.
Impurities:
PURITY: TECHNICAL AND REAGENT : 99.5% PLUS
0.5% WATER.
The chief impurity in acetone
... water. Acetone contains no
oxidizable impurities, and the color of a few drops of permanganate is retained
for several hours.
Consumption Patterns:
25% FOR METHYL METHACRYLATE; 14% FOR METHYL
ISOBUTYL KETONE; 10% AS COATING
SOLVENT; 10% FOR OTHER ORGANIC CHEMS; 6% IN PHARMACEUTICAL MANUFACTURE; 5% FOR
METHACRYLIC ACID AND HIGHER METHACRYLATES; 5% FOR BISPHENOL-A; 4% FOR CELLULOSE
ACETATE SPINNING; 21% FOR MISC (1973)
33% METHYL METHACRYLATE, METHACRYLIC ACID AND
HIGHER METHACRYLATES; 17% SOLVENTS; 10% MIBK; 9% BISPHENOL-A; 7% ALDOL CHEMICAL;
6% PHARMACEUTICALS AND COSMETICS; 2% METHYL ISOBUTYL CARBENOL; 4.5% EXPORTS;
11.5% MISC (1985)
CHEMICAL
PROFILE: Acetone. Methylmethacrylate,
methacrylic acid and higher methacrylates, 34%; coatings
solvent, 15%; bisphenol-A, 12%; MIBK (methyl isobutyl ketone), 10%; solvent for
cellulose acetate, 5%; drug and pharmaceutical applications, 5%; miscellaneous chemical
and solvent uses, 6%; exports, 5%.
CHEMICAL
PROFILE: Acetone. Demand: 1986: 1,936
million lb; 1987: 2,050 million lb; 1991 /projected/: 2,140 million lb.
Demand 1995: 2.76 billion pounds; 1996: 2.72
billion pounds; 2000 (projected) 3.2 billion pounds.
U. S. Production:
(1972) 7.74X10+11 G
(1975) 7.45X10+11 G
(1984) 7.90X10+11 g
(1984) 5.58X10+10 g
(1987) 9.5X10+5 tons
United States acetone
production 1,102,426X10+3 kg
(1990) 2.33 billion lb
(1992) 2.43 billion lb
(1991) 2.35 billion lb
(1993) 2.46 billion lb
U. S. Imports:
(1972) 1.18X10+10 G
(1975) 1.36X10+9 G
(1983) 2.48X10+6 g
(1987) 7.5X10+4 tons
U. S. Exports:
(1972) 4.11X10+10 G
(1975) 2.93X10+10 G
(1984) 3.76X10+10 g
(1987) 1.18X10+5 tons
Laboratory Methods:
Clinical Laboratory Methods:
A gas chromatographic method for determining acetone
in biological tissues is described. Solvent was extracted with nitrogen gas from
specimen & adsorbed on porous polymer (Porapak Q). Concentrations ranging
between 17 nmol/g tissue in nonexposed animals & 1.8 mumol/g tissue in
exposed mice were determined.
Analytic Laboratory Methods:
ANALYTE: ACETONE.
MATRIX: AIR. PROCEDURE: ADSORPTION ON CHARCOAL, DESORPTION WITH CARBON
DISULFIDE, GC. RANGE: 1200-4500 MG/CU M. SENSITIVITY: 0.082
A procedure for the determination of volatile
compounds in fish tissue is described. Characterization is by gas
chromatography/mass spectrometry using a fused-silica capillary column.
Emissions of organic compounds from shale oil
waste waters were investigated by using headspace & purge & trap
sampling followed by analysis by gas chromatography with mass spectral &
flame ionization. Acetone was
identified.
EPA Method 1624 - Volatile Organic Compounds
By GC/MS: Grab samples in municipal and industrial discharges are collected. If
residual chlorine is present, add sodium thiosulfate. Extraction is performed by
a purge and trap apparatus. An isotope dilution gas chromatography/ mass
spectrometry method for the determination of volatile organic compounds in
municipal and industrial discharges is described. Unlabeled acetone
has a minimum level of 50 ug/l and a mean retention time of 565 sec.
Method 8240A - Volatile Organics by gas
chromatography/mass spectrometry (GC/MS). Packed column technique.
Sampling Procedures:
Activated charcoal, Ambersorb XE-348, and
Amberlites XAD-2, XAD-4, and XAD-7 were evaluated as solid adsorbents for
work-room air sampling of acetone,
methyl ethyl ketone, methyl isobutyl ketone, methyl n-butyl ketone,
cyclohexanone and isophorone. Activated charcoal had good capacity for the
compounds investigated, but most ketones decomposed on this adsorbent during
storage. Ambersorb XE-348 also showed good capacity for most of the ketones and
decomposition was insignficant.
Special References:
Special Reports:
DHHS/NTP; NTP Report on the Toxicity Studies
of Acetone in F344/N Rats and B6C3F1
Mice (Drinking Water Studies) NTP TOX 3 NIH Pub No. 91-3122
DHHS/ATSDR; Toxicological Profile for Acetone
(1994) ATSDR/TP-93/01
Synonyms and Identifiers:
Synonyms:
ACETON (GERMAN, DUTCH, POLISH)
**PEER REVIEWED**
AI3-01238
**PEER REVIEWED**
Caswell No. 004
**PEER REVIEWED**
DIMETHYL KETONE
**PEER REVIEWED**
EPA Pesticide Chemical
Code 004101
**PEER REVIEWED**
KETONE, DIMETHYL
**PEER REVIEWED**
KETONE PROPANE
**PEER REVIEWED**
BETA-KETOPROPANE
**PEER REVIEWED**
METHYL KETONE
**PEER REVIEWED**
PROPANONE
**PEER REVIEWED**
2-propanone
**PEER REVIEWED**
Shipping Name/ Number DOT/UN/NA/IMO:
UN 1090; Acetone
IMO 3.1; Acetone
Standard Transportation Number:
49 081 05; Acetone
EPA Hazardous Waste Number:
U002; A toxic waste when a discarded
commercial chemical product or
manufacturing chemical intermediate or
an off-specification commercial chemical
product or a manufacturing chemical
intermediate.
F003; A hazardous waste from nonspecific sources when a spent solvent.
Administrative Information:
Hazardous Substances Databank Number:
41
Last Revision Date: 20030214
Last Review Date: Reviewed by SRP on 9/18/1997
Update History:
Complete Update on 02/14/2003, 1 field
added/edited/deleted.
Complete Update on 11/08/2002, 1 field added/edited/deleted.
Complete Update on 10/31/2002, 2 fields added/edited/deleted.
Complete Update on 08/06/2002, 1 field added/edited/deleted.
Complete Update on 07/22/2002, 2 fields added/edited/deleted.
Complete Update on 01/18/2002, 4 fields added/edited/deleted.
Field Update on 01/14/2002, 1 field added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 05/16/2001, 1 field added/edited/deleted.
Complete Update on 05/15/2001, 1 field added/edited/deleted.
Complete Update on 11/14/2000, 2 fields added/edited/deleted.
Complete Update on 03/24/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 01/11/2000, 7 fields added/edited/deleted.
Field Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 06/03/1999, 1 field added/edited/deleted.
Complete Update on 03/19/1999, 1 field added/edited/deleted.
Complete Update on 03/17/1999, 1 field added/edited/deleted.
Complete Update on 03/01/1999, 1 field added/edited/deleted.
Complete Update on 01/20/1999, 1 field added/edited/deleted.
Complete Update on 11/16/1998, 1 field added/edited/deleted.
Complete Update on 11/12/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 01/26/1998, 80 fields added/edited/deleted.
Field Update on 10/17/1997, 1 field added/edited/deleted.
Field Update on 09/17/1997, 1 field added/edited/deleted.
Complete Update on 03/27/1997, 2 fields added/edited/deleted.
Complete Update on 03/11/1997, 2 fields added/edited/deleted.
Complete Update on 02/24/1997, 1 field added/edited/deleted.
Complete Update on 07/22/1996, 5 fields added/edited/deleted.
Complete Update on 04/12/1996, 1 field added/edited/deleted.
Complete Update on 04/11/1996, 1 field added/edited/deleted.
Complete Update on 04/09/1996, 8 fields added/edited/deleted.
Field Update on 01/18/1996, 1 field added/edited/deleted.
Complete Update on 11/10/1995, 1 field added/edited/deleted.
Complete Update on 01/18/1995, 1 field added/edited/deleted.
Complete Update on 12/19/1994, 1 field added/edited/deleted.
Complete Update on 11/18/1994, 1 field added/edited/deleted.
Complete Update on 10/11/1994, 1 field added/edited/deleted.
Complete Update on 08/31/1994, 1 field added/edited/deleted.
Complete Update on 06/28/1994, 1 field added/edited/deleted.
Complete Update on 06/08/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 08/24/1993, 1 field added/edited/deleted.
Complete Update on 08/07/1993, 1 field added/edited/deleted.
Complete Update on 08/04/1993, 1 field added/edited/deleted.
Complete Update on 04/30/1993, 1 field added/edited/deleted.
Complete Update on 02/28/1993, 2 fields added/edited/deleted.
Field Update on 01/22/1993, 1 field added/edited/deleted.
Field update on 12/10/1992, 1 field added/edited/deleted.
Field Update on 09/03/1992, 1 field added/edited/deleted.
Complete Update on 08/17/1992, 3 fields added/edited/deleted.
Field Update on 05/29/1992, 1 field added/edited/deleted.
Field Update on 04/16/1992, 1 field added/edited/deleted.
Complete Update on 03/19/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 09/26/1991, 2 fields added/edited/deleted.
Complete Update on 05/31/1991, 1 field added/edited/deleted.
Complete Update on 10/10/1990, 2 fields added/edited/deleted.
Complete Update on 04/16/1990, 2 fields added/edited/deleted.
Complete Update on 01/11/1990, 2 fields added/edited/deleted.
Field update on 12/29/1989, 1 field added/edited/deleted.
Complete Update on 05/05/1989, 1 field added/edited/deleted.
Complete Update on 12/28/1988, 79 fields
GLCC
RELATED TOXIC SUBSTANCES FOUND IN THE CAMP POND AND CAMP WATER WELL 2003 AND
2004