Information Regarding Acetone and Paint (Industrial Coatings)
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~rqxBHy:1
ACETONE
CASRN: 67-64-1
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).
Manufacturers :
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
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)
Consumption Patterns :
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%.
Effluent Concentrations :
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).
Analytic Laboratory Methods :
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.
Major Uses :
EXTRACTION OF VARIOUS PRINCIPLES FROM ANIMAL
AND PLANT SUBSTANCES; IN PAINT &
VARNISH REMOVERS; PURIFYING PARAFFIN
Human Toxicity Excerpts :
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.
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 :
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).
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.
Non-Human Toxicity Excerpts :
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.
Non-Human Toxicity Excerpts :
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.
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.
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).
GLCC
RELATED TOXIC SUBSTANCES FOUND IN THE CAMP POND AND CAMP WATER WELL 2003 AND
2004