OECD SIDSACETONE

FOREWORDINTRODUCTIONACETONE
CAS N°: 67-64-1

UNEP PUBLICATIONSOECD SIDSACETONE

SIDS Initial Assessment Report(SIAR) for the
9th SIAM
Place: Paris, France
Date: June 29-30, 1999
July 1, 1999

Chemical Name:

Acetone

CAS No:67-64-1

Sponsor Country:

USA

National SIDS Contact Point in Sponsor Country:
Dr. Oscar Hernandez
Director, Risk Assessment Division
U.S. Environmental Protection Agency
Office of Pollution Prevention and Toxics (7403)
401 M Street, S.W.
Washington, DC 20460
Telephone:(202) 260-1835
Email: hernandez.oscar@epa.gov

HISTORY:
This high production volume (HPV) chemical was assigned to the USA in Phase 4 of theOECD HPV voluntary testing program. A SIDS Dossier was prepared by the Chemical
Manufacturer's Association and submitted to the National SIDS Contact Point (USA) on
March 14, 1997. The draft SIAR was reviewed on March 7, 1998 at SIAM 7 and theconclusions on the environment were accepted. Modifications to the health part were madein accordance with the comments received from the participants.

COMMENTS:
Deadline for Circulation:
Date of Circulation:

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OECD SIDSACETONE
SIDS INITIAL ASSESSMENT PROFILECAS No.

67-64-1

CHEMICAL NAME

Acetone

STRUCTURAL FORMULA

CH3-CO-CH3
RECOMMENDATIONS

The chemical is currently of low priority for further work

SHORT SUMMARY OF CONCLUSIONS OF INITIAL ASSESSMENT WHICH
SUPPORTS THE RECOMMENDATIONS
Summary of hazard assessment

The acute toxicity is low. Acetone is not a skin irritant or sensitiser but is a defatting agent to theskin. Acetone is an eye irritant. The subchronic toxicity of acetone has been examined in miceand rats that were administered acetone in the drinking water and again in rats treated by oral
gavage. Acetone-induced increases in relative kidney weight changes were observed in male andfemale rats used in the oral 13-week study. Acetone treatment caused increases in the relative
liver weight in male and female rats that were not associated with histopathologic effects and theeffects may have been associated with microsomal enzyme induction. Hematologic effects
consistent with macrocytic anemia were also noted in male rats along with hyperpigmentation in
the spleen. The most notable findings in the mice were increased liver and decreased spleen
weights. Overall, the no-observed-effect-levels in the drinking water study were 1% for male rats
(900 mg/kg/d) and male mice (2258 mg/kg/d), 2% for female mice (5945 mg/kg/d), and 5% forfemale rats (3100 mg/kg/d). For developmental effects, a statistically significant reduction in
foetal weight, and a slight, but statistically significant increase in the percent incidence of later
resorptions were seen in mice at 15,665 mg/m3 and in rats at 26,100 mg/m3. The no-observableeffect level for developmental toxicity was determined to be 5220 mg/m3 for both rats and mice.
Teratogenic effects were not observed in rats and mice tested at 26,110 and 15,665 mg/m3,
respectively. Lifetime dermal carcinogenicity studies in mice treated with up to 0.2 mL of acetone
did not reveal any increase in organ tumor incidence relative to untreated control animals.
The scientific literature contains eight different studies that have measured either the neurobehavioural performance or neurophysiological response of humans exposed to acetone. Effectlevels ranging from about 600 to greater than 2375 mg/m3 have been reported. Neurobehavioral
studies with acetone-exposed employees have recently shown that 8-hr exposures in excess of2375 mg/m3 were not associated with any dose-related changes in response time, vigilance, or
digit span scores. Clinical case studies, controlled human volunteer studies, animal research, andoccupational field evaluations all indicate that the NOAEL for this effect is 2375 mg/m3 orgreater.
Acetone has been tested in a wide variety of aquatic and terrestrial species. Acute toxicity to fish
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ranges from an LC50 of 6,070 mg/L for Brook trout to 15,000 mg/l for Fathead minnow. The
lowest LC50 for aquatic invertebrates is 2,100 mg/L, ranging to 16,700 mg/L. The NOEC’s for
toxicity to aquatic plants range from 5,400-7,500 mg/L. The chronic NOEC for Daphnia is 1,660
mg/L. Tests using Ring-neck pheasant and Japanese quail produced no adverse effects at 40,000
mg/kg. In summary, ecotoxicity testing shows that acetone exhibits a low order of toxicity.
An assessment factor of 100 was used to calculate a predicted no effect concentration (PNEC) for
acetone in an aqueous environment, because acute toxicity data were available for algae,
crustaceans, and fish. The lowest PNEC value for these species was calculated to be 21 mg/L
when using the LC50 value of 2100 mg/L for marine brine shrimp.
Summary of general exposure information

Worldwide production capacity of acetone was 3.8 million tonnes in 1995 with the actual volume
produced being somewhat less at 3.7 million tonnes. Production capacity in the United States
constituted about 33% (1.3 million tonnes) of the global capacity, while Western Europe and Asia
(including Japan) were about 31% (1.2 million tonnes) and 19% (0.7 million tonnes),
respectively. Major end uses of acetone can be divided into three separate categories as: i) a
chemical feedstock, ii) a formulating solvent for commercial products, and iii) an industrial
process solvent. Acetone can be found in wide variety of consumer and commercial products but
only a few are known to contain high concentrations. These include paints and paint-related
products, such as paint thinners, finger nail polish removers, automotive waxes and tar removers.
PECs have been derived based on the results from air and water monitoring data. The PEClocal(2500 µg/L [water], 10,000 µg/m3 [air]) and PECglobal (50 µg/L [water], 10 µg/m3 [air]) values areintended to represent plausible worst case environment concentrations on a global and regional
scale.
High concentrations of acetone can be detected in a variety of occupational environments (up to2876 mg/m3 at cellulose acetate factory). The predominant route of both occupational andconsumer exposure is through vapor inhalation. The estimated human exposure (EHE) value forworkplace employees is 1780 mg/m3. Using a USEPA modelling programme entitled SCIES(Screening Consumers Inhalation Exposure Software), a scenario intended to represent a likely
indoor consumer use of a product (45 min application of a spray contact adhesive that contained
21% acetone) predicted a short-term exposure (EHE) value of 900 mg/m3 for the consumer use of
the product.

IF FURTHER WORK IS RECOMMENDED – INDICATE ITS NATURE
None recommended

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OECD SIDSACETONE
FULL SIDS SUMMARYCAS NO: 67-64-1

SPECIESPROTOCOL

RESULTSPHYSICAL-CHEMICAL
2.1

Freezing. Point-94.6 °C

2.2

Boiling Point

56.1 °C at 760 mm Hg

2.3

Vapor Pressure

182 mm Hg at 20 °C
400 mm Hg at 39.5 °C

2.4Partition Coefficient-0.24 (Log Kow)

2.5

Water Solubility

100% at 20 °C

2.6

Flash Point

Cleveland open cup: -9 °C
Tag closed cup: -17 °C

2.7

Flammability

Lower limit : 2.2% (v/v) at 25 °C
Upper limit : 13.0% (v/v) at 25 °C

2.8

Autoignition Temperature

465 °C

2.9

Specific Gravity

0.791 at 20 °C

ENVIRONMENTAL
FATE/BIODEGRADATION
3.1.1

Calculated
Calculated

Undergoes slow photolysis
Water: T1/2 >43 hr
Air : T1/2 = 80 hr

Photodegradation

3.1.2

Stability in Water

SRC Program

Does not hydrolyze

3.1.3

Stability in Soil

SRC ProgramLog KOC = 0.30 (Calculated)

3.2

Monitoring Data

Water (µg/L):
residential well water : 2 - 7
sea water :5 - 53ground water :12 - 25
lake water:
1 - 50storm water runoff : 0 - 100
cloud water:
0 - 17,300
industrial wastewater : 138 - 37,709
landfill leachate: 50 - 62,000

Air (µg/m3):
inside office building : 7.1 - 28.5
inside home :9.5 - 81urban street :2.4 - 306
nonsmoking workplace : 4.7 - 415
inside aircraft cabin :7.1 - 560
human breath :230 - 11,285
smoking workplace :9.5 - 21,085

3.3

Transport/Distribution

Fugacity Level 1

Calculated
Measured

UNEP Publications

Distribution:
Air : 71.0%
Water : 28.6%
Soil : 0.0%
Partition Coefficients:
Octanol/Water : 0.58
Water/Air: 334

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OECD SIDSACETONEaerobic
anaerobic

3.4

Type of Biodegradation

3.5

Biodegradation

3.6

Oxygen Demand

Theoretical (ThOD): 2.20 g O2/g
Chemical (COD) : 2.00 g O2/g

3.7

Bioconcentration

Atlantic Cod BCF : 0.65

OECD 301D

Freshwater:
BOD5 : 14%
BOD15 : 74%
BOD28 : 74%
Seawater :BOD5 : 38%
BOD10 : 67%
BOD15 : 69%
BOD20 : 76%

ECOTOXICOLOGY
4.1

4.2

4.3

Acute/Prolonged Toxicity
to FishLC50 (mg/L) :Acute Toxicity to Aquatic
Invertebrates

LC50 (mg/L) :Toxicity to Aquatic Plants

NOEC (mg/L) :Fathead minnow : 15,000
Japanese medaka : 14,300
Mosquito fish
: 13,000
Goldfish: >5000
Golden orfe
: 9880Bluegill sunfish : 8300
Rainbow trout: 7400
Brook trout:
6070

Nitocra spinipes : 16,700
Daphnia magna : 15,800
Daphnia pulex :8800
Daphnia cucullata:
7635
Artemia salina :2100

Scenedesmus quadricauda :Selenastrum capricornutum :Chlorella pyrenoidosa:
Scenedesmus pannonicus:
Lemna gibba :5400
Lemna minor:
5400

4.4

4.5.2

4.6.1

4.6.2

6

Toxicity to Bacteria,
Diatoms, and Protozoa

NOEC (mg/L) :Chronic Toxicity to
Aquatic Invertebrates

NOEC (mg/L) :Toxicity to Soil Dwelling
Organisms

Escherichia coli :Nitzschia linearis :Skeletonema costatum
Chilomonas paramecium
Uronema parduczi
Pseudomonas putida
Microcystis aeruginosa
Entosiphon sulcatum

25,00011,610: 6000: 3520: 1710: 1700: 530: 28

Ceriodaphnia dubia : 1866
Daphnia magna : 1660

Predicted

NOEC (mg/L) :Lumbricus terrestris : >1000

NOEC (mg/L) :Toxicity to Terrestrial
PlantsRyegrass : >80
Radish : >80
Lettuce : >80
Corn : >80

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7500
7000
3400
4740

OECD SIDS
4.6.3

ACETONE

Toxicity to Other NonMammalian Terrestrial
Species

NOEC (mg/kg) :Japanese quail: >40,000
ring-neck pheasant : >40,000

TOXICOLOGY
5.1.1

Acute Oral Toxicity

rat
mouse
rabbit

LD50 : 8400 mg/kg
LD50 : 5250 mg/kg
LD50 : 5300 mg/kg

5.1.2

Acute Inhal. Toxicity

rat

LC50 : 50,000 mg/m3

5.1.3

Acute Dermal Toxicity

rabbit

LD50 : >15,700 mg/kg

5.2.1

Skin Irritation

rabbitnot irritating

5.2.2

Eye Irritation

rabbitDraizehighly irritating

5.2.3

Respiratory Irritation

mouse

RD50

weakly irritating

5.3

Sensitization

mouse

ear swelling

not sensitizing

5.4

Repeated Dose Toxicity

OECD 408

NOEL :
1% (2258 mg/kg/day)
2% (5945 mg/kg/day)NOEL :
1% (900 mg/kg/day)
5% (3100 mg/kg/day)mice : malemice : female

OECD 408
rat : male
rat : female

5.5

Genetic Toxicity In Vitro

OECD 471

bacterial test:
reverse mutation : neg. At 10 mg
yeast gene mutation : neg. at 5%
forward mutation : neg. At 500 mM
prophage induction : neg. at 10%

non-bacterial test :chromosomal aberration : neg. at 5 mg/mL
sister chromatid exchange : neg. at 5 mg/mL
cell transformation : neg. at 0.5%
alkaline elution : neg. at 1%
mouse lymphoma : neg. At 30 mg/mL
chromosomal malsegregation : pos. at 6.8%

5.6

Genetic Toxicity In Vivo
rat
mouse
hamster

OECD 474

embryo cell transformation assay :rat : negative at 0.1%
mouse : negative at 0.01%
micronucleus assay :negative at 865 mg/kg

5.7

Carcinogenicity

mouse

NOEL : 0.2 mL (dermal)

5.8

Toxicity to Reproduction

rat

NOEL : 0.5% (drinking water)

5.9

Developmental Toxicity/
Teratogenicity

rat
mouse

OECD 414

OECD 414

5.11

Experience with Human
Exposure

NOEL :
teratogenicity : >26,110 mg/m3
developmental : 5220 mg/m3
NOEL :
teratogenicity : >15,665 mg/m3
developmental : 5220 mg/m3
see SIAR text

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1.

ACETONE

IDENTITY

Acetone is a clear colorless liquid that is highly flammable and infinitely soluble with water.
Reagent grade acetone can contain up to 0.5% water as well as small amounts of other polar
solvents. Acetone vapors have a characteristic sweet and fruity odor at low concentrations. The
odor threshold for humans has been reported at values ranging from about 24 to 1615 mg/m3, with235 to 339 mg/m3 being the range of odor recognition thresholds for most people and 95 mg/m3
being the odor detection threshold for unadapted individuals (Devos et al., 1990; Leonardos et al.,1969).
Virtually every organ and tissue within the human body contains some acetone which is one ofthree biochemicals collectively referred to as ketone bodies. Acetone is produced within the bodyas a result of the breakdown and utilization of stored fats and lipids as a source of energy (Wieland,1968). Consequently, conditions such as strenuous physical exercise and prolonged dieting, whichlead to a break-down of fat within the body, may result in higher than average amounts of acetone
in the bloodstream (Williamson and Whitelaw, 1978). Measurable amounts of acetone arecontinuously being excreted in the breath and urine of humans as a result of its high volatility andsolubility in water (Wigaeus et al., 1981).

2.

GENERAL INFORMATION ON EXPOSURE

Worldwide production capacity of acetone was 3.8 million tonnes in 1995 with the actual volume
produced being somewhat less at 3.7 million tonnes (Bizzari, 1996). Production capacity in the
United States constituted about 33% (1.3 million tonnes) of the global capacity, while the capacity
in Western Europe and Asia (including Japan) was about 31% (1.2 million tonnes) and 19% (0.7
million tonnes), respectively. The average annual production of acetone is expected to rise at a
global rate of 3.3% until the year 2000.
Major end uses of acetone can be divided into three separate categories. These include use as: i) a
chemical feedstock, ii) a formulating solvent for commercial products, and iii) an industrial process
solvent. The majority of worldwide production is used as a feed-stock to prepare methyl
methacrylate/methacrylic acid and Bisphenol A (Bizzari, 1996). Several aldol chemicals, such as
methyl isobutyl ketone, methyl isobutyl carbinol, isophorone, and diacetone alcohol, are also
prepared directly from nascent acetone. Acetone has many favorable properties that make it usefulas a formulating solvent for a variety of paints, inks, resins, varnishes, lacquers, surface coatings,
paint removers, and automotive care products. As an industrial process solvent, acetone is used to
manufacture cellulose acetate yarn, polyurethane foam, vitamin C, and smokeless gun powder. At
least 75% of the acetone consumed in 1995 was used in captive processes for the preparation ofdownstream chemicals, while only about 12% was used as a formulating solvent for commercial
products.
Large-scale commercial production of acetone is generally accomplished by one of two processes.
The first, and by far the most common, is through the acid catalyzed hydro-lytic cleavage ofcumene hydroperoxide (Bizzari, 1996). Acetone and phenol are formed as co-products in thisreaction at a ratio of 0.61 to 1.00. The second process, catalytic dehydrogenation of isopropyl
alcohol, accounted for about 6% of the US production in 1995. Other methods, such as
biofermentation, propylene oxidation, and diisopropyl-benzene oxidation, are either experimental innature or account for a very small percentage of worldwide production.

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The release of acetone by chemical manufacturers’ and end users accounts for a very small
percentage (1%) of the estimated 40 million tonnes that are annually released to the environment(Table 1). Vegetative releases, forest fires, and other natural events account for nearly half (47%)
of the estimated annual emissions of acetone, with another 50% resulting from the troposphericphotooxidation of propane and other alkanes and alkenes (Singh et al., 1995). Since 1993, US
industries have not been required to report their TRI (Toxic Release Inventory) emissions ofacetone as required under SARA Title III, Section 313. In 1992, 2548 facilities reported a total
environmental release of 60,904 tonnes of acetone with 60,904 tonnes emitted to the air, 454 tonnes
to water, 254 tonnes to land, and 1446 tonnes injected underground (USEPA, 1994).
Table 1
Estimated average annual emissions of acetone from different sources
Global Annual Emissions (tonnes x 10-6)
Average
Range

AcetoneSourcePrimary Anthropogenic
stationary sources

0.5

0.4 - 0.7

mobile sources

0.3

0.2 - 0.3

Primary Biogenic
Vegetation

9

4 - 18

17
2
1
0.2
10
40

15 - 201-3
1-2
0.2 - 0.3
8 - 1230 - 46

Secondary Anthropogenic
propane oxidation
isobutane & isopropane oxidation
isobutene & isopropene oxidation
myrcene oxidation
Biomass Burning
Total

Acetone can be found as an ingredient in a variety of consumer products ranging from cosmetics toprocessed and unprocessed foods. Acetone has been rated as a GRAS (Generally Recognized asSafe) substance when present in beverages, baked goods, deserts, and preserves at concentrations
ranging from 5 to 8 mg/L (Oser and Ford, 1973). It can also be detected in measurable amounts inonions, grapes, cauliflower, tomatoes, milk, cheese, beans, peas, and other natural foods. Milk fromdairy cattle may contain very high levels of acetone, ranging as high as 225 mg/L for the milk fromhyperketo-nemic cows (Andersson and Lundström, 1984). Acetone has also been identified, but not
quantified, in air samples from numerous plants and microorganisms. In addition to its eliminationin the expired air of all mammals, acetone is excreted as a metabolic end-product by some bacteria(Clostridium butylicium), molds, fungi (Paecilaomyces variotii), and algae (Cryptomonas ovata
palustris) (George et al., 1983; Sunnesson et al., 1996; Collins and Kalnins, 1966).
Acetone is often detected as an end product of thermal combustion and biological decom-position.
Except for tree foliage, the release of acetone from living vegetation has been poorly quantified(Khalil and Rasmussen, 1992). Emissions from poultry manure (530 g/kg), backyard waste
incinerators (4.0 g/kg), pine wood combustion (2.8 g/kg), neoprene combustion (990 mg/kg), andwood burning stoves (145 mg/kg) have all been measured and reported (Smith et al., 1977; Yocum
et al., 1956; Hartstein and Forshey, 1974; Lipari et al., 1984).

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3.

ENVIRONMENT

3.1

Environmental Exposure
3.1.1

General Discussion

A level I fugacity analysis revealed that acetone preferentially locates in the air compart-ment whenreleased to the environment (Table 2). The fugacity analysis was based on the equilibrium
established after the release of 100 moles (5.8 kg) of acetone into the envi-ronment (Mackay andPaterson, 1981). A substantial amount of acetone can also be found in water, which is consistent
with the high water to air partition coefficient and its small, but detectable, presence in rain water,
sea water, and lake water samples. Very little acetone is expected to reside in soil, biota, or
suspended solids. This is entirely consistent with the physical and chemical properties of acetone
and with measurements showing a low propensity for soil absorption and a high preference formoving through the soil and into the ground water (Steinberg and Kreamer, 1993).
Table 2
State-state distribution of acetone in the environment
Environmental
Compartment

Mass
Distribution (%)

Air

71.00

Water

28.58

Sediment

0.01

Soil

0.00

Biota

0.00

suspended solids

0.00

Acetone meets the OECD definition of readily biodegradable which requires that the biologicaloxygen demand (BOD) is at least 70% of the theoretical oxygen demand (THOD) within the 28-day
test period (Table 3). Studies by the standard dilution method have shown greater than 75% of theacetone is biodegraded when using non-acclimated sewage seed from either a freshwater or a sea
water sanitary waste treatment plant. These results compare favorably with the values frombiodegradability tests performed according to OECD 301D guidelines. Using the OECD method,the BOD5, BOD15, and BOD28 for acetone were found to be 14%, 74%, and 74%, respectively(Waggy et al., 1994). The BOD5 of acetone has been measured by numerous investigators andproduced values ranging from about 23% to 83% depending on the test and the type of sewage seed.
The THOD of 2.20 g O2/g of acetone has been found to be only slightly greater than the measured
chemical oxygen demand (COD) value of 2.00 g O2/g of acetone (Price et al., 1974).
Studies with several different strains of anaerobic bacteria from municipal waste water treatment
plants have shown that acetone is completely degraded to CO2 following aceto-acetate formation
through an initial carboxylation reaction and incorporated into the carbon cycle (Platen and Schink,1989). Soil bacteria have also been shown to biode-grade acetone to CO2 (Taylor et al., 1980).

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Table 3The biological oxygen demand from acetone in water samples
SampleType

Biological Oxygen Demand (g )5 days 10 days 15 days 20 days

Author(s)(year)

freshwater

55

79

78

78

Lamb & Jenkins, 1952

freshwater

56

76

83

84

Price et al., 1974

saltwater

38

67

69

76

Price et al., 1974

Table 4Comparison of the environmental fate and removal processes for acetone
AcetoneRemoval Process

Approximate
Half-life (days)

Author(s)(year)

aqueous biodegradation
volatilization riversoil biodegradation
total tropospheric removalhydroxyl radical reaction
aqueous photolysis
atmospheric photolysis
volatilization lake

0.6
6
7
22
31
40
80
100

Rathbun et al., 1993
Howard et al., 1990
Sanders, 1995
Meyrahn et al., 1986
Meyrahn et al., 1986
Betterton, 1991
Meyrahn et al., 1986
Howard et al., 1990

Two processes govern the photochemical removal of acetone from the troposphere: reaction withhydroxyl radicals and photolysis. The two processes occur at about equal rates in clear unpolluted
skies yielding a total tropospheric lifetime of about 32 days (Meyrahn et al., 1986). The reaction
with hydroxyl radicals will predominate over photo-lysis in urban areas where hydroxyl radical
concentrations are greater, and during cloudy winter-time conditions where photodecomposition isminimal. Rain out and other forms of wet deposition are considered to be minor troposphericremoval processes (Chatfield et al., 1987). Calculated and measured rate constants have been used
to estimate the elimination half-life (t½= 0.693/kcalc) of acetone through various environmental
processes (Table 4). These data show that acetone is rapidly biodegraded in water and that this is
the dominant removal process in the environment. The slow removal of acetone from thetroposphere indicates that it is relatively non-reactive and a minor contributor to urban ozone andperoxyacyl nitrate (PAN) concentrations (Derwent et al., 1996).
3.1.2

Predicted Environmental Concentration

Measurable amounts of acetone can be found in both mobile and stationary emission sources(Table 5). The levels of acetone in the air from municipal landfills and cigarette smoke can be
relatively high, but they are minor contributors to the total global mass. The direct release ofacetone from vegetation is an important emission source that is often overlooked. In a qualitativeevaluation, acetone was found to be emitted from all 22 of the forest plant species examined(Isidorov et al., 1985).

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Background levels of acetone in the atmosphere have been assessed from both ground level andairborne monitoring stations located throughout the world. The average acetone concentrations atrural ground level sites are generally lower than the values reported for urban areas (Table 6). The
concentration of acetone in urban areas can show large unpre-dictable variations that are likely
related to the amount of vehicle traffic and to the emis-sion of precursor alkanes and alkenes(Zweidinger et al., 1988; Chatfield et al., 1987). Airborne measurements of acetone in the upper
troposphere and lower stratosphere reveal an average concentration of 190 to 285 ng/m3 in theseregions (Singh et al., 1995).
Table 5
Mobile and stationary emissions of acetone
Emission
SourceAirborne
Concentration (mg/m3)

Author(s)(year)

fuel or crude oil fire

0.02 - 0.16

Booher & Janke, 1997

automobile exhaust

0.09 - 4.50

Grimaldi et al., 1996

factory fence line

1.9 - 9.7

Hoshika et al., 1981

tree foliage

7.8 - 12.6

Khalil & Rasmussen, 1992

municipal landfill

15.7 - 77.1

Brosseau & Heitz, 1994

cigarette smoke

498 - 869

Euler et al., 1996

Acetone has routinely been detected in the expired air of humans and in the air samples from manydifferent occupied environments (Table 7). The levels in these samples can vary greatly, ranging
from a few µg/m3 to nearly 25 mg/m3. Cigarette smoking, emissions from furnishings andconstruction materials, and excretion by the lung are perhaps the greatest contributors to indoor
acetone levels. The acetone levels in indoor air are generally higher than those found outdoors(Jarke et al., 1981).
Table 6
Background levels of acetone in urban and rural air samples
Location

Background
Concentration (µµg/m3)

Range(µµg/m3)

Author(s)(year)

Smoky Mts, Tennessee
Copenhagen, Denmark
Point Barrow, Alaska
Waldhof, Germany
Central Ontario
Eastern Georgia
Los Angeles, California
Ispra, Italy
Donan, France
Athens, Greece
Columbus, Ohio----2.4
3.8
4.0
4.3
3.8
4.7
4.7
--5.0

1.7 - 9.5
0.5 - 5.2
0.7 - 6.9----0.0 - 15.9
0.2 - 15.2----1.7 - 18.3
0.0 - 21.8

Arnts & Meeks, 1981
Granby et al., 1997
Cavanagh et al., 1969
Solberg et al., 1996
Shepson et al., 1991
Lee et al., 1995
Grosjean et al., 1996
Solberg et al., 1996
Solberg et al., 1996
Kalabokas et al., 1997
Spicer et al., 1996

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Southern Germany
Western Colorado
Western Alabama
Sao Paulo, Brazil
Rome, Italy
Stockholm, Sweden
Vancouver, Canada
Boston, Massachusetts
Houston, Texas

6.2--10.0--16.1
9.5
19.2
32.0
81.9

0.5 - 11.4
2.4 - 8.3
0.7 - 5.2
0.5 - 7.4
10.0 - 21.8
1.7 - 24.2
8.3 - 30.9
9.7 - 64.0
29.4 - 223.1

Slemr et al., 1996
Goldan et al., 1995
Goldan et al., 1997
Grosjean et al., 1990
Possanzini et al., 1996
Jonsson et al., 1985
Li et al., 1997
Kelly et al., 1993
Kelly et al., 1993

Table 7
Acetone concentration range in various airborne samples
SampleType

Airborne
Concentration (µµg/m3)

Author(s)(year)

inside office building
inside home

7.1 - 28.5
9.5 - 81

Daisey et al., 1994
Lewis & Zweidinger, 1992

urban street

2.4 - 306

Jonsson et al., 1985

nonsmoking workplace

4.7 - 415

Heavner et al., 1996

inside aircraft cabin

7.1 - 560

Dechow et al., 1997

human breath

230 - 11,285

Crofford et al., 1977

smoking workplace

9.5 - 21,085

Heavner et al., 1996

Fugitive stack emissions have been used to estimate fence line concentrations of acetone at threeindustrial sites. Airborne emissions reported under USEPA SARA Title III section 313 for the year
1989 or 1990 were used in conjunction with the USEPAs ISCST (Industrial Source Complex ShortTerm) dispersion model to calculate the highest 24-hr concentration and the highest average annual
concentration of acetone at property sites beyond the fence line (Table 8). The highest averageannual concentration at the three industrial sites ranged from 4.3 to 9.3 mg/m3. Actual fence line
measurements of acetone at five locations outside of the Eastman Chemical Company site inKingsport, Tennessee showed that the average concentration ranged from 0.05 to 0.50 mg/m3 whichwere notably lower than the predicted 24-hr average.
Table 8
Fugitive emissions of acetone and the resulting maximum
predicted off-property concentrations
Company &Location
Eastman Chemical Co.
Kingsport, TN
Hoechst-Celanese Corp.
Narrows, WV
Hoechst-Celanese Corp.
Rock Hill, SC

Fence Line Concentration (mg/m3)
24-hr averageannual average

0.9

9.3

2.6

8.3

0.1

4.3

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OECD SIDSACETONE

Acetone has been found in surface and ground water samples at concentrations that were highly
dependent on the type of sample (Table 9). Ambient background levels of acetone are the result ofboth natural and commercial releases and are generally reflective of the physical processes affecting
absorption from the air, movement through soil, and micro-bial biodegradation. A search of theopen literature and the nearly 2000 entries in USEPAs STORET database revealed that acetone
levels in natural water and industrial monitoring wells rarely exceeded 1 mg/L.
A USEPA-sponsored survey has determined the acetone concentrations in the discharge from 4000
industrial and publicly owned wastewater treatment plants (Table 10). The highest recorded
individual concentration of 37.7 mg/L was found in the discharge from a paint and ink industry
facility; whereas, the highest median concentration of 2.5 mg/L was associated with printing andpublishing plants (Howard et al., 1990). The highest reported aqueous acetone concentration was
found in the wastewater from a specialty chemical manufacturing plant. Although wastewateracetone levels of about 200 mg/L were found in water samples from the primary influent at thewastewater treatment plant serving this manufacturing site, the levels in the receiving river waterand sediment beyond the treatment plant were below the analytical detection limit (Jungclaus et al.,1978). These results are in agreement with data showing that 94% of the acetone removed by apilot-scaled wastewater facility occurs during secondary treatment (Bhattacharya et al., 1996).
Table 9Acetone concentration range in different water samples
SampleType

AqueousConcentration (µµg/L)

Author(s)(year)

residential well water

2-7

Dewalle & Chain, 1981

sea water

5 - 53

Corwin, 1969

ground water

12 - 25

Sabel & Clark, 1984lake water

1 - 50Jungclaus et al., 1978

storm water runoff

0 - 100

Line et al., 1997

cloud water

0 - 17,300

Aneja, 1993

industrial wastewater

138 - 37,709

Howard et al., 1990

landfill leachate

50 - 62,000

Brown & Donnelly, 1988

Predicted environmental concentrations (PECs) of acetone have been derived from the air and water
monitoring data described above. The values listed in Table 11 have been taken from the publishedreport that best provide a plausible worst case environmental concentration on both a global andregional scale. The PEC(local) and PEC(global) air concen-trations of 10,000 and 10 µg/m3 were basedon factory fence line concentrations (Table 5; Hoshika et al., 1981) and ambient air concentrations
for a remote region in the western US (Table 6; Golden et al., 1995), respectively. The PEC(local)
and PEC(global) water con-centrations of 2500 and 50 µg/L represent the highest median acetone
concentration from an industrial wastewater treatment plant (Table 10; Howard et al., 1990) and thehighest reported natural water concentration of acetone from seawater (Table 9; Corwin, 1969).
3.2

Effects on the Environment
3.2.1

14

Aquatic Effects
UNEP Publications

OECD SIDSACETONEAs shown in Tables 12 and 13, acetone is minimally toxic to freshwater and marine or-ganisms
exposed for 1 to 10 days. Acute NOEC for vertebrate and invertebrate organ-isms were greaterthan 3500 mg/L and the LC50 values were generally greater than 10,000 mg/L. The marine brine
shrimp (Artemia salina) showed the greatest sensitivity to acetone with a 1-day LC50 value of 2100
mg/L.
When examined at a seawater concentration of 1.52%, acetone did not bioconcentrate in the tissues
or organs of the Atlantic cod (Gadus morhua) (Rustung et al., 1931). The 7-day EC50 values ofgreater than 10,000 mg/L and no observable effect levels of 5400 mg/L were similar for two speciesof aquatic duckweed, Lemna gibba and Lemna minor (Cowgill et al., 1991). The 10-day LC50
values for acetone in the 3-brood test with Daphnia magna and Ceriodaphnia dubia were 4068
mg/L and 6693 mg/L, respectively (Cowgill and Millazo, 1991). The maximum acceptableconcentration of acetone that did not affect the survival of Daphnia magna exposed for 28 days wasapproximately 2100 µL/L (1660 mg/L) (LeBlanc and Surprenant, 1983).
Table 10
Acetone concentrations in the discharge water from industrial
and public wastewater treatment plants
Industrial
Category

Number of Positive
Occurrences

Median Acetone
Concentration (µµg/L)

nonferrous metal
textile mills
inorganic chemicals
porcelain/enameling
pesticide manufacturing
oil and gas extraction
pulp and paper
leather tanning
pharmaceuticals
mechanical products
photographic industries
publicly owned treatment works
organic chemicals
plastics and synthetics
petroleum refining
organics and plastics
explosives
auto and other laundries
electronics
rubber processing
transportation equipment
paint and ink
coal mining
printing and publishing

2
4
8
4
7
5
6
4
6
6
1
40
1
10
14
24
23
2
12
1
6
22
1
7

6.6
11.0
13.8
14.7
52.7
59.2
59.8
74.7
75.4
84.4
94.9
96.8
113.9
164.1
166.9
374.4
388.0
437.5
441.2
604.4
616.7
894.9
2260.82501.2

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OECD SIDSACETONE
Table 11Predicted environmental acetone concentrations

3.2.2

Area

Concentration
Air (µµg/m3)

Concentration
Water (µµg/L)

PEC(local)

10,0002500

PEC(global)

10

50

Terrestrial Effects

The 5-day LC50 of acetone for Japanese quail (Coturnix coturnix japonica) and ring-neck pheasants(Phasianus colchicus) was greater than 40,000 mg/kg (Hill et al., 1975). The EPAs ECOSAR
program predicted a 14-day earthworm (Lumbricus terrestris) LC50 value of greater than 1000 mg/L
(Meylan and Howard, 1998). Acetone vapors were shown to be relatively toxic to two types insects
and their eggs. The time to 50% lethality (LT50) was found to be 51.2 hr and 67.9 hr when the flour
beetle (Tribolium confusum) and the flour moth (Ephestia kuehniella) were exposed to an airborne
acetone concentration of 61.5 mg/m3 (Tunç et al., 1997). The LT50 values for the eggs were30-50% lower than for the adult. The direct application of acetone liquid to the body of the insects
or surface of the eggs did not, however, cause any mortality.
The effects of acetone on the growth and germination of terrestrial plants and seeds has also been
examined (Gorsuch et al., 1990). A 168-hr exposure of ryegrass (Lolium perenne), radish(Raphanus sativus), and lettuce (Lactuca sativa) to acetone concen-trations as high as 80 mg/L did
not cause any effects. The IC50 value obtained when tobacco pollen (Nicotiana sylvestris) was
incubated with acetone for 18 hr was 20,500 mg/L (Kristen et al., 1994). This value, however,conflicts with the 2-hr NOEC of 12 mg/L for the germination of another tobacco plant species,
Nicotiana tabacum (Schubert et al., 1995).
Table 12
Acute and chronic toxicity of acetone to aquatic invertebrates
Species

Duration(hr)

NOEC(mg/L)

LC50(mg/L)

Author(s)(year)

240

---

4068

Cowgill & Milazzo,

240

1866

6693

Cowgill & Milazzo,

48

8500

15,800Sloof et al., 1983

48

5800

8800

Canton & Adema,

48

---

7635

Canton & Adema,

96

≥ 100

---

Ewell et al., 1986

96

≥ 100

---

Ewell et al., 1986

96

≥ 100

---

Ewell et al., 1986

Freshwater Organisms

Water flea
Daphnia magna
Water flea
Ceriodaphnia dubia
Water flea
Daphnia magna
Water flea
Daphnia pulex
Water flea
Daphnia cucullata
SnailPlanorbella trivolvis
Aquatic earthworm
Lumbriculus
Sideswimmer
Gammarus fasciatus
16

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OECD SIDSACETONE

Pillbug
Caecidotea
Flatworm
Dugesia

96

≥ 100

---

Ewell et al., 1986

96

≥ 100

---

Ewell et al., 1986

Harpacticoids
Nitocra spinipes
King crab
Lithodes antarcticus
Grass shrimp
Palaemonetes pugio
Brine shrimp
Artemia salina

96

---

16,700

Lindén et al., 1979

168

750

---

Lombardo et al., 1991

288

---

69,400Rayburn & Fisher,

24

---

2100

Price et al., 1974

Marine Organism

Table 13
Acute toxicity of acetone to aquatic vertebrates
Species

Duration(hr)

NOEC(mg/L)

LC50(mg/L)

Author(s)(year)

48

12,00015,000Sloof et al., 1983

96

---

9100

Cardwell et al., 1974

48

9500

14,300Sloof et al., 1983

96

10,00013,000

Wallen et al., 1957

24

5000

---

Bridié et al., 1979

96

---

6070

Cardwell et al., 1974

48

---

9880

Juhnke & Lüdemann,

96

3700

8300

Cairns & Scheier,

48

5700

7400

Sloof et al., 1983

96

---

11,000

Lindén et al., 1979

48

6700

9600

Sloof et al., 1983

48

11,50013,500Sloof et al., 1983

48

3500

7000

Sloof et al., 1983

48

12,00020,000Sloof & Baerselman,48

20,00024,000Sloof & Baerselman,

48

3500

15,000Sloof et al., 1983

48

8000

17,000Sloof et al., 1983

Freshwater Fish

Fathead minnow
Pimephales
Fathead minnow
Pimephales
Japanese medaka
Oryzias latipes
Mosquito fish
Gambusia affinis
Goldfish
Carassius auratus
Brook trout
Salvelinus fontinalis
Golden Orfe
Leuciscus idus
Bluegill sunfish
LepomisRainbow trout
Salmo gairdnerii
Bleak
Alburnus alburnus
Guppy
Poecilia reticulata
Hydra
Hydra oligactis
Pond snail
Lymnaea stagnalis

Freshwater Amphibians

Mexican axolotl
Ambystoma
African clawed toad
Xenopus leavis

Insects

Mosquito
Aedes aegypti
Mosquito
Culex pipens

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OECD SIDS
3.2.3

ACETONE
Other Effects

The ability of acetone to inhibit cell multiplication has been examined in a wide variety of
microorganisms (Table 14). The results have generally indicated mild to minimal toxicity with
NOECs greater than 1700 mg/L for exposures lasting from 6 hr to 4 days. Longer exposure periodsof 7 to 8 days with bacteria produced mixed results; but overall the data indicate a low degree of
toxicity for acetone. The only exception to these findings were the results obtained with theflagellated protozoa (Entosiphon sulcatum) which yielded a 3-day NOEC of 28 mg/L. This was
likely a spurious value, however, and the result could not be verified from the tests with otherspecies of protozoa.
The four species of green algae examined in the multiplication inhibition test were relatively
insensitive to the effects of acetone treatment. The lowest NOEC of 3400 mg/L was obtained
following the 48-hr treatment of Chlorella pyrenoidosa. The lowest NOEC for bacteria, in contrast,
was found to be 530 mg/L following the 192-hr treatment of Microcystis aeruginosa. The IC50
values for acetone have also been measured and compared using commercial and natural bacterial
test cultures. The IC50 value of 48,000 mg/L obtained using the Polytox™ test system was found tocompare favorably with the IC50 of 48,619 mg/L for an activated sludge test culture(Nirmalakhandan et al., 1994). The EC50 value for acetone in the Microtox™ test using the bacteria
Photobacterium phosphoreum was found to be about 14,000 mg/L (Chen and Que Hee, 1995).
Table 14
Acetone toxicity thresholds in the cell multiplication inhibition test
Species

Flagellated protozoa
Entosiphon sulcatum
Bacteria
Microcystis aeruginosa
Bacteria
Pseudomonas putida
Ciliated protozoa
Uronema parduczi
Green algae
Chlorella pyrenoidosa
Flagellated protozoa
Chilomonas
Green algae
Scenedesmus
Marine diatom
Skeletonema costatum
Green algae
Selenastrum
Green algae
Scenedesmus
dddiatomFreshwater
Nitzschia linearis
Bacteria
Escherichia coli

3.3
18

Duration(hr)

NOEC(mg/L)

Author(s)(year)

72

28

Bringmann & Kühn,

192

530

Bringmann & Kühn,

16

1700

Bringmann & Kühn,

20

1710

Bringmann & Kühn,

48

3400

Sloof et al., 1983

48

3520

Bringmann & Kühn,

48

4740

Sloof et al., 1983

120

6000

Cowgill et al., 1989

96

7000

Sloof et al., 1983

168

7500

Bringmann & Kühn,

120

11,610Patrick et al., 1968

1.5

25,000Reinhartz et al., 1987

Initial Assessment for the Environment
UNEP Publications

OECD SIDSACETONE

Considering the availability of acute data for algae, crustaceans, and fish an assessment factor of
100 was used to calculate a predicted no effect concentration (PNEC) for acetone in an aqueous
environment. Using the LC50 value of 2100 mg/L obtained with the marine brine shrimp (Artemia
salina), the lowest PNEC value for acetone was calculated to be 21 mg/L.
The lowest PNEC was compared to the PEC(local) and PEC(global) values for water (Table 11) to
calculate PEC/PNEC ratios. The PEC(global) of 50 µg/L produced a PEC/PNEC ratio of 0.002;
whereas, the PEC(local) value of 2500 µg/L yielded a ratio of 0.12. These margins of exposure areeach less than one; acetone was therefore judged to have low environmental risk potential.

4.

HUMAN HEALTH

4.1

Human Exposure

Virtually every organ and tissue within the human body contains some acetone, which is one ofthree biochemicals collectively referred to as ketone bodies. Measurable amounts of acetone arecontinuously being excreted in the breath and urine of humans as a result of its high volatility andsolubility in water (Brega et al., 1991). The acetone found in the body is produced in the liver
following the utilization of stored fats and lipids as a source of energy (Landau and Brunengraber,
1987). The ability of humans to naturally produce and dispose of acetone may to a large degree
explain its relatively low toxicity following external exposure to moderate amounts of the vapor or
liquid (Wigaeus et al., 1981; Haggard et al., 1944). The background levels of acetone in blood andurine can vary widely but tend to average 1 to 2 mg/L. The levels in expired alveolar air are,however, about 1000-fold lower at 1 µg/L (Morgott, 1993).
Exogenous exposures to acetone typically occur by the pulmonary route. The high blood- to-air
partition coefficient suggests that a large percentage of inhaled acetone will be absorbed into thebody; the occurrence, however, of a peculiar wash-in/wash-out effect effectively reduces the uptake
to about 50% (Johanson, 1991). The miscibility of acetone in the fluid layers lining the lungappears to be responsible for the wash-in/wash-out phenomenon. Under normal conditions acetone
is efficiently and effectively metabolized to a variety of products that are used as building blocks forthe synthesis of glucose, amino acids, and other more complex biochemicals (Argilés, 1986).
Sustained high blood levels of acetone can result in the induction of enzymes responsible for its
own metabolism and the metabolism of other chemicals (Koop and Casazza, 1985; Forkert et al.,1994). This compensatory response to high blood levels is responsible for the ability of acetone topotentiate the hepato- and nephrotoxicity of chemicals that undergo metabolic activation by
microsomal enzymes to form toxic metabolites.
4.1.1

Occupational Exposure

High airborne concentrations of acetone have been found in a variety of occupational environments(Table 15). These levels reflect the high volatility and low intrinsic toxicity which combine to
make acetone an attractive industrial process solvent. The predominant route of both occupationaland consumer exposure to acetone is through vapor inhalation. Oral and dermal uptake can occur,
but the body burden from these exposure routes is relatively small compared to respiratory
absorption. Impermeable gloves should be worn together with a supplied air respirator whenworking with liquid acetone or when the vapor concentration exceeds the occupational exposure
limit.

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OECD SIDSACETONE
Table 15
Exposure to acetone in various occupations
FactoryType

8-Hour TWA
Concentration (mg/m3)

Author(s)(year)

automotive repair shop

12 - 77

Winder & Turner, 1993

print shop

6 - 235

Nasterlack et al., 1994

electronics plant2 - 648

Hallock et al., 1993

fiberglass fabrication

40 - 1580

DeRosa et al., 1996

varnish production

5 - 1448

Franco et al., 1986

cellulose acetate factory

12 - 2876

Satoh et al., 1996

The estimated human exposure (EHE) value for workplace employees has been set at 1780 mg/m3
based on an examination of the data in Table 15. This exposure value for acetone also agrees wellwith the occupational exposure limits established in many countries and provides some assurance
that it represents a plausible worst case concentration.
4.1.2

Consumer Exposure

Acetone can be found in wide variety of consumer and commercial products but only a few are
known to contain high concentrations (Sack et al., 1992). These include paints and paint-related
products, such as paint thinners, finger nail polish removers, automotive waxes and tar removers(Table 16). Consumer exposures will most likely occur by the inhalation route and will be thegreatest for those using adhesives, automotive products, and paint-related products that contain ahigh percentage of acetone.
Table 16
Average acetone concentration in various consumer product categories
Product Categoryoils, greases & lubricantscleaners for electronic equipment
household cleaners & polishers
miscellaneous products
fabric & leather treatments
adhesive-related products
automotive products
paint-related products

NumberProduct
Average
Products Assayed Prevalence (%) Concentration (%)

71
111
463
76
91
69
111
167

5.3
16.1
10.8
17.2
14.6
24.3
22.7
51.5

0.2
0.3
0.3
7.4
12.9
18.8
28.1
29.3

Using a USEPA modelling program entitled SCIES (Screening Consumers Inhalation Exposure
Software), a 45-min exposure model was created for the application of a spray contact adhesive that
contained 21% acetone. This scenario was selected because it depicts a realistic short duration
exposure that involves the direct indoor air release of large amounts of acetone. Althoughconsumer products such as nail polish removers can contain 70 to 80% acetone, the resulting air
acetone concentrations are generally lower than those described in the following scenario because
20

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OECD SIDSACETONEof the small volumes of liquid typically applied. The spray contact adhesive scenario describes aplausible worst case consumer application where respirators may not be worn because of the shorttask duration and relatively low VOC content of the product.
SPRAY CONTACT ADHESIVE SCENARIO
Input Parameters
Use Rate
Mass of ProductDuration of Use
Zone 1 Volume
Whole House Volume
House Air Exchange Rate
User Inhalation Rate
User Inhalation Rate
Molecular Weight
Vapor Pressure
Weight Fraction
Starting Time

:
:
:
:
:
:
:
:
:
:
:
:

1 event/year
225.0 g0.66 hr40.0 m3
292.0 m3
0.20 room air exchanges/hr
1.20 m3/hr (during use)
1.10 m3/hr (after use)
58.08 g/mole
182 torr
0.210
9:00 AM

Output Summary
Evaporation Time
Release Time
Duration Following Use
Interval Between Uses

:
:
:
:

0.021 hr0.66 hr (duration of exposure)8759.34 hr
8760.00 hr

User Potential Dose Rate From Inhalation:
Non-User Potential Dose Rate From Inhalation :(mg/m3)
Concentration in Zone of Release :During period of use
During period after use
Concentration in Zone 2 :During period of use
During period after use

1264.3 mg/yr
561.6 mg/yr

Average(mg/m3)Peak

556.030.18

907.19847.86

10.90
0.07

27.75
82.90

The modelling results shown above indicate average and peak exposures to acetone of 556 and 907
mg/m3, respectively. The estimated short-term human exposure (EHE) value associated with theuse of consumer products was therefore set at the peak exposure concentration of 900 mg/m3 thatwas predicted in this scenario.
4.1.3

Indirect Exposure

Acetone levels in the body at any point in time are reflective of free fatty acid utilization andacetoacetate production by the liver. Consequently, many normal and abnormal physiological states
can appreciably increase the body burden of acetone through the process of ketogenesis. Children
and adolescents typically have higher acetone blood levels than adults due to their higher energy
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OECD SIDSACETONE

expenditure. In fact, 2 to 5 day old infants have been found to have acetone blood levels ranging as
high as 140 mg/L (Peden, 1964). Furthermore, vigorous exercise and the resulting utilization of
fatty acids as a fuel source can lead to a condition commonly called post-exercise ketosis that
results in a dramatic increase in blood ketone body concentrations. In addition to these normal
physiological conditions, there are a number of clinical states that can result in human ketosis. In
each of these conditions, the ketosis can be traced to the increased mobilization and utilization offree fatty acids by the liver. These conditions include pregnancy, fasting, prolonged vomiting, andalcoholism (Morgott, 1993).
Other clinical conditions, such as diabetic ketoacidosis and starvation, can lead to much larger
increases in blood acetone levels (Table 17). In each of these situations, the elevations in blood
acetone are typically accompanied by even larger increases in the remaining two ketone bodies,
acetoacetate and β-hydroxybutyrate (Sulway et al., 1971). Unlike acetone, however, these two
ketone bodies disrupt normal acid-base balance and cause many of the acute symptoms of diabetes
due to their ionization (Winek, 1976). Acetone, in contrast, is non-ionic and is produced together
with carbonic acid during the breakdown of acetoacetate (Koorevaar and Van Stekelenburg, 1976).
Because acetone has a normal physiological role in the body, the estimated short-term human
exposure (EHE) value for endogenous acetone was set at 10 mg/L, which represents the upper limit
for blood acetone in healthy individuals.
Table 17
Human plasma acetone concentrations expectedunder various exposure and health conditions
Physiological Stateor Condition

Plasma Concentration Range(mg/L)(mg %)(mM)

healthy

< 10

< 1.0

< 0.17

occupational exposure< 100< 10.0< 1.72diabetic ketoacidosis

100 - 700

10.0 - 70.0

1.72 - 12.04> 200> 20.0> 3.44

toxic exposure

4.2

Effects on Human Health

About twenty separate instances of human acetone poisoning have been reported in the medical
literature. Many of these case reports have involved patients seen in hospital emergency wards
following either accidental or intentional ingestion of acetone. The case reports provide a clear
picture of the signs, symptoms, and prognosis that accompany acute acetone intoxication. The mostnoticeable features of high exposures to acetone vapor are irritation to the eyes, nose, and throat. If
the exposure is extremely large, as in cases of accidental ingestion of liquid acetone, fatigue,
irritability, dizziness, and breathing irregularities may occur. When the poisoning is severe, these
symptoms may precede the development of gastrointestinal disturbances and a temporary loss of
consciousness. While many reports of severe acetone poisoning have been reported in theliterature, no deaths have ever been recorded.
The following three methods have been used to study the sensory irritation potential of acetone forthe eyes, nose, and throat: physiological techniques, psychophysical methods, and subjective ques22

UNEP Publications

OECD SIDSACETONEtionnaires. It is important to understand the differences between sensory irritation and bothsensitization and chemical irritation. Sensory irritation, known also as the "common chemical
sense" or chemesthesis, occurs when a vapor or gas interacts with trigeminal nerve receptors in theocular or nasal mucosa. Sensory irritation often occurs as a physical sensation that is describedusing a variety of terms including: pungency, piquancy, stinging, burning, and tickling.
Sensitization, in contrast, is an allergic reaction that is manifested through a either a cell-mediated(dermal sensitization) or a humoral response (pulmonary sensitization) by the immune system.
Chemical or primary irritation denotes an inflammatory reaction with localized redness andswelling. This type of irritation is found when a chemical solid or liquid makes direct contact withthe skin or eyes. Sensory irritation is a generally milder effect than either sensitization or chemical
irritation.
The studies listed in Table 18 were conducted both in the workplace using acetone-exposed
employees and in the laboratory using naive volunteers exposed to acetone in an inhalationchamber. The studies using objective physiological and psychophysical tech-niques showedacetone to be an extremely weak sensory irritant. Subjective symptom questionnaires, in contrast,
indicated that acetone was a sensory irritant at much lower vapor concentrations. Recent research
indicates that the irritancy responses observed using subjective symptom questionnaires are likely
caused by the odor of acetone (Dalton et al., 1997). Investigators have shown that both acetone andphenyl ethyl alcohol, a known non-irritant with a strong odor, produced subjective irritancy
responses in humans following a 20-min inhalation exposure at 1900 mg/m3. Objective
psychophysical methods, in contrast, showed little if any irritancy effect in humans exposed under
the same conditions.
The scientific literature contains eight different studies that have measured either theneurobehavioral performance or neurophysiological response of humans exposed to acetone. Manyof the early neurotoxicity studies with acetone were not amenable to reliable statistical analysis
because of the variability in the data and the inability to reproduce the results. A close inspection ofthese early investigations also reveals many problems with design, conduct, or interpretation thathinder their use.
Among more recent studies with acetone, NOAELs ranging from vapor concentrations of 600
mg/m3 to greater than 2375 mg/m3 have been reported. The wide range in effect levels are likely
due to statistical errors caused by large numbers of independent variables, analytical problems, andthe failure to use multiple concentrations to evaluate dose-response characteristics.
Neurobehavioral studies with acetone-exposed employees have recently shown that 8-hr exposures
up to 2375 mg/m3 were not associated with any dose-related changes in reaction time, vigilance, or
digit span scores (Satoh et al., 1996). When the test subjects were divided into three age groups, astatistically significant decrease in simple reaction time and digit span scores was observed in oneof the groups 30 to 44 years of age, but not in the older or younger age groups.
Table 18
Reported cases of human sensory irritation from acetone vapors
Test
MethodSubjective

Type of
Subjects

No Effect
Level (mg/m3)

Author(s)(year)

questionnairequestionnairequestionnaire

naive
workers
naive

475
< 595
595

Nelson et al., 1943
Satoh et al., 1996
Matsushita et al., 1969

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OECD SIDSACETONEquestionnairequestionnairequestionnairequestionnairequestionnaire

naive
workersboth
naive
workers

1185
1900
2375
2850
3560

DiVincenzo et al., 1973
Raleigh & McGee, 1972
Seeber et al., 1992
Stewart et al., 1975
Oglesby et al., 1949

naive
naive
naive
naive
workers
naive

7120
18,985> 23,730> 23,730> 35,600> 83,070

Roberts et al., 1996
Douglas, 1974)
Cometto-Muñiz et al.,Cometto-Muñiz et al.,
Wysocki et al., 1997
Wysocki et al., 1997

Objective

acoustic
spirometry
psychophysics
psychophysics
laterialization
laterialization
4.2.1

Acute Toxicity

The acute effects of a single exposure to acetone vapor have been examined in mice, rats, guinea
pigs, and cats. The adverse effects observed in laboratory animals are generally similar to the signsof central nervous system depression seen in cases of human intoxication. Vapor concentrations inexcess of 24,000 mg/m3 are generally required to elicit any sign of acute acetone intoxication inlaboratory animals. Animal studies have demonstrated that the acute narcotic effects of acetone arestrongly dependent upon both the length and magnitude of the exposure (Flury and Wirth, 1934;
Haggard et al., 1944; Kagen, 1924; Specht et al., 1939). Regardless of the species examined, thenarcotic effects of acetone tend to proceed through several distinct phases that can be described asfollows: drowsiness, lack of coordination, loss of autonomic reflexes, narcosis, respira-tory failure,and death.
The hallmark of animal studies with acetone is the extremely high vapor concentrations or longexposure duration needed to produce an adverse effect. An 8-hr inhalation LC50 value of 50,100
mg/m3 was reported for female rats (Pozzani et al., 1959). Single-dose oral lethality studies havealso been performed in rats, mice, and rabbits. The oral LD50 was found to be 10.7 mL/kg (8.5g/kg) in rats, 90.4 mmol/kg (5.25 g/kg) in mice, and greater than 5.3 g/kg in rabbits (Smyth et al.,
1962; Tanii et al., 1986; Krasavage et al., 1982). An examination of the oral LD50 values for maleand female rats from different age groups reveals that acetone is more acutely toxic for newborn
rats than for adults (Table 19). The LD50 values for rats aged 14 days and older were not, however,substantially different (Kimura et al., 1971).
Table 19
Acute lethality of acetone to Sprague-Dawley rats from different age groups

24

Age Group

WeightRange (g)LD50
(g/kg)

95% Confidence
Limits (g/kg)

newborn (24-48 hr)

5-8

2.8

2.1 - 4.8

immature (14 day)16 - 50

7.1

4.9 - 10.1

young adult80 - 160

11.5

8.6 - 15.3

old adult

300 - 470

10.7

9.8 - 11.8

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The ability of acetone to dehydrate and delipidate unprotected skin is well known from industrial
and laboratory experience. Laboratory animal studies have confirmed this ob-servation and also
shown a low potential for systemic toxicity following exposure by the dermal route. The 24-hr
dermal LD50 was found to be greater than 20 mL/kg (15.7 g/kg) in rabbits (Smyth et al., 1969).
4.2.2 Irritation/Sensitization
Acetone did not cause contact hypersensitization in the mouse ear swelling test or the guinea pig
maximization test (Descotes, 1988; Nakamura et al., 1994). The sensory irritation potential foracetone vapors was determined by measuring the concentration-related decline in the respiration
rate of mice. The RD50 values for acetone were found to be 183,970 mg/m3 and 55,725 mg/m3 in
two separate studies (Kane et al., 1980; De Ceaurriz et al., 1981).
Studies conducted in rabbits have generally shown that acetone can be a severe eye irritant whenapplied undiluted and left in contact with the cornea. Dilute aqueous solutions, however, areminimally irritating. Corneal thickness measurements three days after the treatment of rabbits with
0.1 mL of undiluted acetone produced severe eye irritation (Morgan et al., 1987). An acetone
concentration of 3.9 M (225 g/L) was found to cause a 50% increase in ocular edema after a 1-hr
exposure. Acetone treatment for up to several minutes was shown to destroy the corneal
epithelium, but not the corneal stroma. All injury to the corneal epithelium was reversible within 4
to 6 days. Acetone was not found to be a corrosive eye irritant (Märtins et al., 1992).
4.2.3 Repeated Dose Toxicity
The subchronic toxicity of acetone has been examined in rats following oral gavage and drinking
water consumption. In the gavage study, acetone was administered in water to male and female rats
for 90 consecutive days at dose levels of 100, 500, and 2500 mg/kg (Mayhew and Morrow, 1988).
The rats showed an increase in several hematological parameters and an increase in the serum
activity of three enzymes. Increases in the absolute liver and kidney weight were observed forfemale rats at the two highest dose levels. Increases in organ-to-body weight ratios were also
observed, but only at the highest dose level tested. Male rats administered 2500 mg/kg showed anincrease in organ-to-body weight ratios for the liver and kidney, but the absolute weights of theorgans were unaffected. No liver pathology was observed, however some histopatho-logicalabnormalities were observed in the renal tubular cells of male and female rats treated at the highdose.
In a more relevant study, acetone was administered in the drinking water of mice and rats for either
14 days or 13 weeks. The drinking water concentrations and calculated average daily doses ofacetone are presented in Table 20 (Dietz et al., 1991). No mouse or rat mortality was observed ineither the 14-day or the 13-week study. Overt clinical signs of toxicity were only observed in therats treated at the 10% level in the 14-day study. Acetone-induced increases in relative kidneyweight were observed in the male and female rats treated for 13 weeks. The kidney weight changes
were reportedly associated with a nephropathy that occurred spontaneously in untreated control rats.
The increases in the relative liver weight of male and female rats were not associated withhistopatho-logic changes and may have been caused by microsomal enzyme induction.
Hematologic effects consistent with macrocytic anemia were noted in male rats along withhyperpig-mentation in the spleen. The most notable findings in mice were increased liver anddecreased spleen weights, which were confined exclusively to female mice administered a 5%
concentration of acetone (Dietz, 1991). The authors concluded that the no-observed-effect-levelwas 1% for male rats and male mice, 2% for female mice, and 5% for female rats.
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Table 20
Time-weighted-average dose for male and female Fisher 344 rats andB6C3/F1 mice exposed to acetone in their drinking water

Water
14-Day Average Dose (mg/kg/day) 13-Week Average Dose (mg/kg/day)
Concentration
Rats
Rats
Mice
Mice
(%)
male female male
female male
female male
female

0.125
0.25
0.5
1.0
2.0
5.0
10.0

714
1616
2559
4312
6942

751
1485
2328
4350
8560

965
1569
1579
3023
3896
5481
6348
8804
10,314 12,725

200
400
900
1700
3400
-

200
600
1200
1600
3100
-

380
611
1353
2258
4858
-

892
2007
4156
5945
11,298-4.2.4 Reproduction/Devlopmental Toxicity
Acetone showed minimal reproductive and developmental effects in animals exposed either byinhalation or via drinking water.
No reproductive performance changes or testicular
histopathological effects were noted in male rats treated with 0.5% acetone in their drinking waterfor 6 weeks (Larsen et al., 1991). In another study, however, an acetone drinking water
concentration of 5% caused a mild decrease in testicular weight, a moderate increase in theincidence of abnormal sperm, and depressed sperm motility after 13 weeks of treatment (Dietz etal., 1991). These findings indicate that high concentrations of acetone can have a mild effect on rat
spermatogenesis.
The potential for acetone vapors to cause developmental effects was examined in virgin andpregnant rats and mice (Mast et al., 1988). Mated rats were exposed by inhalation to 1045, 5220, or
26110 mg/m3 of acetone on days 6 through 19 of gestation. Mice were ex-posed at concentrationsof 1045, 5220, or 15665 mg/m3 of acetone on days 6 through 17 of gestation. No effects were seenin the mean liver or kidney weights of pregnant dams, the organ-to-body weight ratios, the numberof implantations, the mean percentage of live pups per litter, the mean percentage of resorptions per
litter, or the fetal sex ratio. No treatment-related effects were seen in maternal or virgin bodyweight, or the maternal uterine weight of the treated mice. A treatment-related increase wasobserved in the liver-to-body weight ratios for pregnant dams. A statistically significant reduction
in fetal weight, and a slight, but statistically significant increase in the incidence of late resorptions
was also seen in mice exposed to 15,665 mg/m3 of acetone. The incidence of fetal malformations inmice was not altered by gestational exposure to acetone at any exposure concentration. The
no-observed-effect level for developmental toxicity was found to be 5220 mg/m3 for both rats andmice. Acetone did not produce any teratogenic effects at any of the exposure concentrations tested.
The no-observed-effect level for teratogenicity was, therefore, greater than or equal to15,665 mg/m3 for mice and 26,110 mg/m3 for rats.
4.2.5 Neurotoxicity
Mild neurobehavioral changes have been observed in rats repeatedly exposed to high vapor
concentrations of acetone. Female rats were exposed 4 hr/day for 2 weeks at acetone concentrationsof 7120, 14240, 28480, and 37975 mg/m3 were examined for their response to avoidance andescape stimuli before and after each exposure (Goldberg et al., 1964). Repeated daily exposures to
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14,240 mg/m3 of acetone produced an inhibition of avoidance behavior but did not produce any
signs of motor imbalance. Acetone concentrations of 28,480 and 37,975 mg/m3 produced ataxia inseveral animals after a single exposure, however, a rapid tolerance developed and ataxia was notseen on subsequent days. In a recent schedule controlled operant performance study, acetone did
not cause any permanent effects in rats exposed to the vapor for 13 weeks at 2375, 4750, and9495 mg/m3 (Christoph and Stadler, 1997).
4.2.6 Carcinogenicity
Information on the carcinogenicity of acetone is available from dermal studies performed in mice.
In each of these studies, acetone was used as the vehicle to evaluate the effects of a test chemical.
The test design therefore included untreated and vehicle-treated study groups. The carcinogenicityof acetone was evaluated in a group of 29 female ICR/Ha Swiss mice treated topically with 0.1 mLof acetone or 0.1 mL of an acetone-water mixture (9:1) three times per week for up to 424 days
(Van Duuren et al., 1978). Histopathological analysis of all major organs revealed a total of 14 lungtumors, one liver tumor, one forestomach tumor, and no skin tumors in the acetone andacetone/water treatment groups. Lung papillary tumors were seen in 37% of the untreated mice and
24% of the acetone or acetone-water treated mice. The incidence of forestomach tumors in acetone
or acetone-water treated mice was comparable to untreated mice. Except for one undifferentiatedmalignant liver tumor, which was not cited as a remarkable finding, the incidence of systemic
tumors in the acetone and acetone-water treated mice was not different from the backgroundincidence in untreated mice. In another study, the application of 0.2 mL of acetone to the shaved
dorsal skin of male and female CF1 mice once per week for two years had no effect on the survivalof the 300 animals tested (Zakova et al., 1985). Dermal inflammatory reactions (focal acanthosis,
dermal fibrosis) were seen in 6% of the animals and a fibrosarcoma was seen in one male mouse.
An historical analysis of the organ pathology observed in two previous dermal carcinogenicity
studies showed no evidence of a treatment-related increase in tumors or organ lesions from acetone(Ward et al., 1986). Sixty female SENCAR mice received 0.2 mL of acetone once or twice per
week for up to 92 weeks. The major organs and tissues from all of the animals were examined both
macroscopically and microscopically following necropsy. Fifty percent of the animals survived
past 96 weeks of age with 15 of the mice dying due to neoplastic lesions and 27 due tonon-neoplastic lesions.
4.2.7 Genotoxicity
Acetone has been repeatedly tested in a variety of prokaryotic and eukaryotic test systems withoutcausing genotoxic effects. Studies in the Salmonella assay have shown acetone to be nonmutagenic and to be an acceptable vehicle for dissolving and delivering water- insoluble chemicals
to the tester strains (Anderson and MacGregor, 1980). EPA-spon-sored studies have shown acetone
to be negative in Salmonella strains TA97, TA98, TA100, and TA1535 at levels up to 1 mg/plate(NTP, 1987). Subsequent studies then found that acetone was negative in strains TA92, TA94,
TA98, TA100, TA1535, and TA1537 at a concentration of 10 mg/plate (Ishidate et al., 1984).
Acetone was not geno-toxic to Schizosaccharomyces pombe either with or without metabolic
activation (Abbondandolo et al., 1980). Acetone induced aneuploidy, but not mitotic recombinationor point mutations, in Saccharomyces cerevisiae when tested at concentrations greater than 40
mg/mL using a cold-interruption procedure (Zimmermann et al., 1985). These effects were notobserved, however, when Saccharomyces cerevisiae was tested according to the standard overnightincubation procedure (Albertini, 1991).
Acetone did not produce genotoxic effects in an embryo cell transformation assay per-formed inrats and mice, and was also negative in a micronucleus assay using hamsters (Rhim et al., 1974;
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Basler, 1986). Acetone did not cause chromosomal aberrations or sister chromatid exchanges in
Chinese hamster ovary cells treated at concentrations up to 5 mg/mL (Loveday et al., 1990).
Acetone concentrations ranging from 10.5 to 20.9 mM (0.6 to 1.2 mg/mL) also did not cause
chromosomal aberrations or sister chromatid exchanges in cultured human lymphocytes (Norppa,
1981). Acetone did not cause point mutations at the thymidine kinase locus in L5178Y mouse
lymphoma cells treated at a level of 10 mg/mL (Amacher et al., 1980).
4.2.8 Epidemiology
An epidemiological evaluation of mortality and clinical laboratory data for 948 employees in a fiber
production plant exposed to 8-hr average acetone concentrations of 900, 1830, and 2540 mg/m3
over 23 years produced no unusual findings (Table 21). The liver enzymes, clinical chemistryvalues, and hematological parameters were all within normal range (Ott et al., 1983a,b,c). Standard
mortality ratios for death from all causes, cardio-vascular disease, and malignant neoplasms were
below expectations by 55%, 61%, and 43%, respectively.
Table 21Observed and expected mortality rates for men and women
occupationally exposed to acetone
Cause of
Death

Male Mortality Ratio
observed
expected

Female Mortality Ratio
observed
expected

all causes

24

53.8

3

6.7

malignant neoplasm

5

10.0

2

2.3

cardiovascular disease

15

40.4

2

2.8

Four health surveillance studies have been conducted on acetone-exposed employees from cellulose
acetate facilities located worldwide. The studies did not reveal any evidence of systemic toxicity or
dose-related adverse heath effects based on the results obtained from a wide variety of biochemicaland hematological tests (Table 22).
Table 22
Occupational health surveys with acetone exposed workers
Factory
Location

4.3
28

Number Employed Exposure
Examined (years)(mg/m3)

United800

UnitedStates
Italy

948

Japan

110

60

ClinicalMeasurements

Author(year)

hematology
Oglesby et al.,Unknown 1425 - 5100
& urinalysis
1949
Hematology, urinalysis,Ottetal., 1983< 23
900 - 2540
& mortality
Hematology, urinalysis,>51305 - 2490 & clinical chemistry Grampella et al.,1987
Hematology,
Satohet al., 1996
15
48 - 2415
immunology,& li i l h i

Initial Assessment for Human Health
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The inhalation EHE values for occupational and consumer groups have been set at 1780 and 900
mg/m3, respectively. The most critical effect of acetone inhalation for both industrial and consumer
contact is central nervous system depression. This endpoint was selected over the more commonly
reported sensory irritation effects based on the findings from a recently completed comprehensive
review of the odor and irritancy potential of acetone (Arts et al., 1998). The authors of this review
concluded that subjective reports of acetone’s irritancy were unreliable and likely related to its
distinctive odor. Furthermore, the authors determined that the true irritancy threshold for acetone
vapors was very high, ranging somewhere between 23,730 and 94,930 mg/m3. Clinical casestudies, controlled human volunteer studies, animal research, and occupational field evaluations all
indicate that the NOAEL for the CNS-related effects of acetone is about 2375 mg/m3. Acetone istherefore considered to have a low potential for neurological risk to humans.
In a subchronic drinking water study, renal toxicity and increased liver and decreased spleen
weights were observed. The reported NOAEL’s were 900mg/kg/d and 3,100 mg/kg/d for male andfemale rats, and 2,258 mg/kg/d and 5,945 mg/kg/d for male and female mice. Worst-case EHE’s ona body weight basis for occupational and consumer exposures are 254 mg/kg/d and 16 mg/kg/d,
respectively. Developmental toxicity and teratogenicity of acetone were measured in rats and mice.
For developmental endpoints the NOAEL in rats and mice is 5,220 mg/m3, while no teratogenic
effects were observed at the highest doses tested of 26,111 mg/ m3 in rats and 15,665 mg/m3 inmice. Acetone is therefore considered to have a low potential for renal damage and developmental
effects in humans.
The unconsciousness, respiratory distress, and vomiting associated with cases of accidental or
intentional exposure to acetone appear to occur when the blood levels are in excess of 1000 mg/L.
Likewise, the drowsiness observed in patients with uncontrolled diabetes mellitus has been
associated with acetone blood levels in excess of 150 mg/L. By com-parison, an 8-hr occupational
exposure to 1780 mg/m3 of acetone is expected to result in an acetone blood level of about 60 mg/L.
This shows that the blood levels associated with occupational exposures to acetone are below thosecausing central nervous system depression.

5.

CONCLUSIONS AND RECOMMENDATIONS

5.1

Conclusions

An examination of all available information on the biological activity of acetone indicates that thevapors are mildly toxic after both direct contact or systemic absorption. The primary effect of acutehigh-level exposure appears to be central nervous system depres-sion. Comparative studies withother solvents have shown that the irritative properties of acetone vapor are extremely mild and areoften confused with its odor. Although many cases of accidental or intentional human acetone
poisoning have occurred, no instances of death or permanent injury have been recorded.
Appreciable quantities of acetone are continually being produced and eliminated in the body as aresult of energy needs. Normal background levels in the blood can, therefore, dramaticallyfluctuate depending upon age, eating habits, and level of physical fitness.
The data indicate that acetone does not appear to pose a neurotoxic, carcinogenic, or reproductive
health hazard at the concentrations reported to be found in the environment. Information obtained
from occupationally exposed individuals, animal feeding studies, and in vitro screening assays
support this conclusion. The kidney appeared to be the most sensitive target tissue in the animalstudies. Acetone has also been tested in a wide variety of aquatic and terrestrial organisms and
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OECD SIDSACETONEproduced minimal to mild effects in every instance. The mild effects have allowed acetone to be
used as a carrier solvent for dissolving and testing less soluble chemicals. The preceding analysis
shows that acetone has a low potential for harming both human health and the environment.
5.2

Recommendations

Acetone has a low priority for further work. The health and environmental effects ofacetone have both been well studied.

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References
Abbondandolo, A., Bonatti, S., Corsi, C., Corti, G., Fiorio, R., Leporini, C., Mazzaccaro, A., Nieri,
R., Barale, R., and Loprieno, N. (1980). The use of organic solvents in mutagenicity testing. Mutat.
Res. 79,141-150.
Albertini, S. (1991). Reevaluation of the 9 compounds reported conclusive positive in yeast
Saccharomyces cerevisiae aneuploidy test systems by the Gene-Tox Program using strain D61.M ofSaccharomyces cerevisiae. Mutat. Res. 260,165-180.
Amacher, D.E., Pailler, S.C., Turner, G.N., Ray, V.A., and Salsburg, D.S. (1980). Point mutations
at the thymidine kinase locus in L5178Y mouse lymphoma cells. II. Test validation andinterpretation. Mutat. Res. 72,447-474.
Anderson, D. and MacGregor, D.B. (1980). The effect of solvents upon the yield of revertants in the
Salmonella/activation mutagenicity assay. Carcinogenesis 1,363-366.
Andersson, L. and Lundström, K. (1984). Milk and blood ketone bodies, blood isopropanol andplasma glucose in dairy cows; methodological studies and diurnal variations. Zentralbl. Vet. Med. A
31,340-349.
Aneja, V.P. (1993) Organic compounds in cloud water and their deposition at a remote continental
site. J. Air Waste Manage. Assoc. 43,1239-1244.
Argilés, J.M. (1986). Has acetone a role in the conversion of fat to carbohydrate in mammals?
Trends Biochem. Sci. 11,61-63.
Arnts, R.R. and Meeks, S.A. (1981). Biogenic hydrocarbon contribution to the ambient air ofselected areas. Atmos. Environ. 15,1643-1651.
Arts, J.H.E., Mojet, J., van Gemert, L.J., Emmen, H.H., Lammers, J.H.C.M., Marquart, J.,
Woutersen, R.A., and Feron, V.J. (1998). An analysis of human response to the irritancy of acetone
vapours. TNO Report V98.357. TNO Nutrition and Food Research Institute. Zeist, The
Netherlands.
Basler, A. (1986). Aneuploidy-inducing chemicals in yeast evaluated by the micronucleus test.
Mutat. Res. 174,11-13.
Betterton, E.A. (1991). The partitioning of ketones between the gas and aqueous phases. Atmos.
Environ. 25A,1473-1477.
Bhattacharya, S.K., Madura, R.L., Dobbs, R.A., Angara, R.V.R., and Tabak, H. (1996). Fate of
selected RCRA compounds in a pilot-scale activated sludge system. Water Environ. Res.
68,260-269.
Bizzari, S.N. (1996). CEH Marketing Research Report Acetone. Chemical Economics Handbook,
SRI International. Menlo Park, CA.
Booher, L.E. and Janke, B. (1997). Air emissions from petroleum hydrocarbon fires during controlled burning. Am. Ind. Hyg. Assoc. J. 58,359-365.
UNEP Publications

31

OECD SIDSACETONE

Brega, A., Villa, P., Quadrini, G., Quadri, A., and Lucarelli, C. (1991). High-performance liquid
chromatographic determination of acetone in blood and urine in the clinical diagnostic laboratory. J.
Chromatogr. 553,249-254.
Bridié, A.L., Wolff, C.J.M., and Winter, M. (1979). The acute toxicity of some petrochemicals togoldfish. Water Res. 13,623-626.
Bringmann, G. and Kühn, R. (1980). Comparison of the toxicity thresholds of water pollutants tobacteria, algae, and protozoa in the cell multiplication inhibition test. Water Res. 14,231-241.
Bringmann, G. and Kühn, R. (1978). Testing of substances for their toxicity threshold: Modelorganisms Microcystis (Diplocystis) aeruginosa and Secenedesmus quadricauda. Mitt. Int. Verein.
Limnol. 21,275-284.
Bringmann, G. and Kühn, R. (1977). Grenzwerte der Schadwirkung wassergefährdender Stoffe
gegen Bakterien (Pseudomonas putida) und Grünalgen (Scenedesmus quadricauda) im Zellvermehrungshemmtest. Z. Wasser Abwasser Forsch. 10,87-98 (German).
Brosseau, J. and Heitz, M. (1994). Trace gas compound emissions from municipal landfill sani-tarysites. Atmos. Environ. 28,285-293.
Brown, K.W. and Donnelly, K.C. (1988) An estimation of the risk associated with the organic
constituents of hazardous and municipal waste landfill leachates. Haz. Waste Haz. Mater. 5,1-30.
Cairns, J. and Scheier, A. (1968). A comparison of the toxicity of some common industrial waste
components tested individually and combined. Prog. Fish Culturist 30,3-8.
Canton, J.H. and Adema, D.M.M. (1978). Reproducibility of short-term and reproduction toxicity
experiments with Daphnia magna and comparison of the sensitivity of Daphnia magna with
Daphnia pulex and Daphnia cucullata in short-term experiments. Hydrobiologia 59,135-140.
Cardwell, R.D., Foreman, D.G., Payne, T.R., and Wilbur, D.J. (1974). Acute and chronic toxicity offour organic chemicals to fish. US Environmental Protection Agency, Envirogenics Contract 68-010711. Environmental Research Laboratory. Duluth, MN.
Cavanagh, L.A., Schadt, C.F., and Robinson, E. (1969). Atmospheric hydrocarbon and carbon
monoxide measurements at Point Barrow, Alaska. Environ. Sci. Technol. 3,251-257.
Chatfield, R.B., Gardner, E.P., and Calvert, J.G. (1987). Sources and sinks of acetone in the troposphere: Behavior of reactive hydrocarbons and a stable product. J. Geophys. Res. 92,4208-4216.
Chen, H.-F. and Que Hee, S.S. (1995). Ketone EC50 values in the Microtox test. Ecotoxicol.
Environ. Safety 30,120-123.
Christoph, G.R., Keller, D.A., and Stadler, J.C. (1997). Subchronic inhalation of acetone vapor:
Schedule-controlled operant behavior and time-course of blood acetone concentration in rats.
Toxicologist 17,63 (Abstract).
Collins, R.P. and Kalnins, K. (1966). Carbonyl compounds produced by Cryptomonas ovata var.
palustris. J. Protozool. 13,435-437.
32

UNEP Publications

OECD SIDSACETONE

Cometto-Muñiz, J.E. and Cain, W.S. (1993). Efficacy of volatile organic compounds in evoking
nasal pungency and odor. Arch. Environ. Health 48,309-314.
Cometto-Muñiz, J.E. and Cain, W.S. (1995). Relative sensitivity of the ocular trigeminal, nasal
trigeminal and olfactory systems to airborne chemicals. Chem. Senses 20,191-198.
Corwin, J.F. (1969). Volatile oxygen-containing organic compounds in sea water: Determination.
Bull. Marine Sci. 19,504-509.
Cowgill, U.M. and Milazzo, D.P. (1991). The sensitivity of Ceriodaphnia dubia and Daphnia
magna to seven chemicals utilizing the three-brood test. Arch. Environ. Contam. Toxicol.
20,211-217.
Cowgill, U.M., Milazzo, D.P., and Landenberger, B.D. (1991). The sensitivity of Lemna gibba G-3
and four clones of Lemna minor to eight common chemicals using a 7-day test. J. Water Pollut.
Control Fed. 63,991-998.
Crofford, O.B., Mallard, R.E., Winton, R.E., Rogers, N.L., Jackson, J.C., and Keller, U. (1977).
Acetone in breath and blood. Trans. Am. Clin. Climatol. Assoc. 88,128-139.
Daisey, J.M., Hodgson, A.T., Fisk, W.J., Mendell, M.J., and Ten Brinke, J. (1994). Volatile organic
compounds in twelve California office buildings: Classes, concentrations and sources. Atmos.
Environ. 28,3557-3562.
Dalton, P., Wysocki, C.J., Brody, M.J., and Lawley, H.J. (1997). Perceived odor, irritation andhealth symptoms following short-term exposure to acetone. Am. J. Ind. Med. 31,558-569.
De Ceaurriz, J.C., Micillino, J.C., Bonnet, P., and Guenier, J.P. (1981). Sensory irritation caused byvarious industrial airborne chemicals. Toxicol. Lett. 9,137-143.
Dechow, M., Sohn, H., and Steinhanses, J. (1997). Concentrations of selected contaminants in cabin
air of Airbus aircrafts. Chemosphere 35,21-31.
De Rosa, E., Cellini, M., Sessa, G., Scapellato, M.L., Marcuzzo, G., and Bartolucci, G.B. (1996).
The importance of sampling time and co-exposure to acetone in the biological monitoring ofstyrene-exposed workers. Appl. Occup. Environ. Hyg. 11,471-475.
Derwent, R.G., Jenkin, M.E., and Saunders, S.M. (1996). Photochemical ozone creation potentials
for a large number of reactive hydrocarbons under European conditions. Atmos. Environ.
30,181-199.
Descotes, J. (1988). Identification of contact allergens: The mouse ear sensitization assay. J.
Toxicol. Cut. Ocular Toxicol. 7,263-272.
Devos, M., Patte, F., Rouault, J., Laffort, P., and Van Gemert, L.J. (1990). In: Standardized Human
Olfactory Thresholds, p. 145. Oxford University Press. Oxford, United Kingdom.
Dewalle, F.B. and Chian, E.S.K. (1981). Detection of trace organic’s in well water near a solid
waste landfill. J. Am. Water Works Assoc. 73,206-211.

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33

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Dietz, D.D. (1991). Toxicity studies of acetone in F344/N rats and B6C3F1 mice (drinking waterstudies). US Dept. of Health Human Services Report, Report NIH 91-3122, pp. 1-38. National
Toxicology Program. Research Triangle Park, NC.
Dietz, D.D., Leininger, J.R., Rauckman, E.J., Thompson, M.B., Chapin, R.E., Morrissey, R.L., andLevine, B.S. (1991). Toxicity studies of acetone administered in the drinking water of rodents.
Fund. Appl. Toxicol. 17,347-360.
Di Vincenzo, G.D., Yanno, F.J., and Astill, B.D. (1973). Exposure of man and dog to low concentrations of acetone vapor. Am. Ind. Hyg. Assoc. J. 34,329-336.
Euler, D.E., Davé, S.J., and Guo, H. (1996). Effect of cigarette smoking on pentane excretion inalveolar breath. Clin. Chem. 42,303-308.
Ewell, W.S., Gorsuch, J.W., Kringle, R.O., Robillard, K.A., and Spiegel, R.C. (1986). Simultaneous
evaluation of the acute effects of chemicals on seven aquatic species. Environ. Toxicol. Chem.
5,831-840.
Flury, F. and Wirth, W. (1934). Zur Toxikologie der Lösungsmittel (Verschiedene Ester, Aceton,
Methylalkohol). Arch. Gewerbepath. Gewerhyg. 5,1 (German).
Forkert, P.G., Redza, Z.M., Mangos, S., Park, S.S., and Tam, S.-P. (1994). Induction and regulationof CYP2E1 in murine liver after acute and chronic acetone administration. Drug Metab. Dispos.
22,248-253.
Franco, G., Fonte, R., Tempini, G., and Candura, F. (1986). Serum bile acid concentrations as aliver function test in workers occupationally exposed to organic solvents. Int. Arch. Occup. Environ.
Health 58,157-164.
George, H.A., Johnson, J.L., Moore, W.E.C., Holdeman, L.V., and Chen, J.S. (1983). Acetone,
isopropanol, and butanol production by Clostridium beijerinckii (syn. Clostridium butylicium) and
Clostridium aurantibutyricum. Appl. Environ. Microbiol. 45,1160-1163.
Goldan, P.D., Kuster, W.C., and Fehsenfeld, F.C. (1997). Nonmethane hydrocarbon measure-ments
during the tropospheric OH photochemistry experiment. J. Geophys. Res. 102,6315-6324.
Goldan, P.D., Trainer, M., Kuster, W.C., Parrish, D.D., Carpenter, J., Roberts, J.M., Yee, J.E., andFehsenfeld, F.C. (1995). Measurements of hydrocarbons, oxygenated hydrocarbons carbon
monoxide, and nitrogen oxides in an urban basin in Colorado: Implications for emissions
inventories. J. Geophys. Res. 100,22771-22783.
Goldberg, M.E., Johnson, H.E., Pozzanni, U.C., and Smythe, H.F. (1964). Effect of repeatedinhalation of vapors of industrial solvents on animal behavior. I. Evaluation of nine solvent vapors
on pole-climb performance in rats. Am. Ind. Hyg. Assoc. J. 25,369-375.
Gorsuch, J.W., Kringle, R.O., and Robillard, K.A. (1990). Chemical effects on the germination andearly growth of terrestrial plants. In: Plants for Toxicity Assessment, W. Wang, J.W. Gorsuch, andW.R. Lower, eds., pp. 49-58, ASTM STP 1091. American Society of Testing Materials.
Philadelphia, PA.

34

UNEP Publications

OECD SIDSACETONE

Grampella, D., Catenacci, G., Garavaglia, L., and Tringali, S. (1987). Health surveillance inworkers exposed to acetone. In: Proceedings of the VII International Symposium on Occupational
Health in the Production of Artificial Organic Fibres. Wolfheze, Holland.
Granby, K., Christensen, C.S., and Lohse, C. (1997). Urban and semi-rural observations ofcarboxylic acids and carbonyls. Atmos. Environ. 31,1403-1415.
Grimaldi, F., Bacle, D., Bouthiba, M., Gouezo, F., Viala, A., Casabianca, S., Muls, E., Figos, J.,
Esberard, N., and Masquelez, N. (1996). Study of air pollution by carbonyl compounds in automobile exhaust. Pollut. Atmos. 149,68-76.
Grosjean, E., Grosjean, D., Fraser, M.P., and Cass, G.R. (1996). Air quality model evaluation datafor organics. 2. C1-C14 carbonyls in Los Angeles air. Environ. Sci. Technol. 30,2687-2703.
Grosjean, D., Miguel, A.H., and Tavares, T.M. (1990). Urban air pollution in Brazil: Acetaldehyde
and other carbonyls. Atmos. Environ. 24B,101-106.
Haggard, H.W., Greenberg, L.A., and Turner, J.M. (1944). The physiological principles governing
the action of acetone together with the determination of toxicity. J. Ind. Hyg. Toxicol. 26,133-151.
Hallock, M.F., Hammond, K., Kenyon, E., Smith, T., and Smith, E. (1993). Assessment of task andpeak exposures to solvents in the microelectronics fabrication industry. Appl. Occup. Environ. Hyg.
8,945-954.
Hartstein, A.M. and Forshey, D.R. (1974). Coal mine combustion products. Neoprenes, poly-vinyl
chloride compositions, urethane foam, and wood. US Department of the Interior, Report 7977.
Bureau of Mines. Pittsburgh, PA.
Heavner, D.L., Morgan, W.T., and Ogden, M.W. (1996). Determination of volatile organic
compounds and respirable suspended particulate matter in New Jersey and Pennsylvania homes andworkplaces. Environ. Int. 22,159-183.
Hill, E.F., Heath, R.G., Spann, J.W., and Williams, J.D. (1975). Lethal dietary toxicities ofenvironmental pollutants to birds. US Department of the Interior, Wildlife Report No. 191. Fish andWildlife Service. Washington, DC.
Hoshika, Y., Nihei, Y., and Muto, G. (1981). Pattern display for characterization of trace amountsof odorants discharged from nine odour sources. Analyst 106,1187-1202.
Howard, P.H., Sage, G.W., Jarvis, W.F., and Gray, D.A. (1990). Acetone. In: Handbook ofEnvironmental Fate and Exposure Data for Organic Chemicals, pp. 9-18. Lewis Publishers, Inc.
New York, NY.
Ishidate, M., Sofuni, T., Yoshikawa, K., Hayashi, M., Nohmi, T., Sawada, M., and Matsuoka, A.
(1984). Primary mutagenicity screening of food additives currently used in Japan. Food Chem.
Toxicol. 22,623-636.
Isidorov, V.A., Zenkevich, I.G., and Ioffe, B.V. (1985). Volatile organic compounds in theatmosphere of forests. Atmos. Environ. 19,1-8.
Jarke, F.H., Dravnieks, A., and Gordon, S.M. (1981). Organic contaminants in indoor air and theirrelation to outdoor contaminants. ASHRAE Trans. 87,153-166.
UNEP Publications

35

OECD SIDSACETONE

Johanson, G. (1991). Modelling of respiratory exchange of polar solvents. Ann. Occup. Hyg.
35,323-339.
Jonsson, A., Persson, K.A., and Grigoriadis, V. (1985). Measurements of some low molecularweight oxygenated, aromatic, and chlorinated hydrocarbons in ambient air and in vehicle emissions.
Environ. Int. 11,383-392.
Juhnke, I. and Luedemann, D. (1978). Ergebnisse der Untersuchung von 200 chemischen
Verbindungen auf akute Fishtoxizität mit dem Goldorftest. Z. Wasser Abwasser Forsch. 11,161-164(German).
Jungclaus, G.A., Lopez-Avila, V., and Hites, R.A. (1978). Organic compounds in an industrial
wastewater: A case study of their environmental impact. Environ. Sci. Technol. 12,88-96.
Kagan, E. (1924). Experimentelle Studien über den Einfluss technisch und hygienisch wichtiger
Gase und Dämfpe auf den Organismus. XXXVI. Aceton. Arch. Hyg. Berl. 94,41-53 (German).
Kalabokas, P., Hatzianestis, J., Bartzis, J., and Mimikos, N. (1997). Seasonal and diurnal variationof carbonyl compounds concentration levels in the atmosphere of the Athens basin. Fresenius
Environ. Bull. 6,172-177.
Kane, L.E., Dombroske, B.S., and Alarie, Y. (1980). Evaluation of sensory irritation from somecommon industrial solvents. Am. Ind. Hyg. Assoc. J. 41,451-455.
Kelly, T.J., Callahan, P.J., Piell, J., and Evans, G.F. (1993). Method development and field measurements for polar volatile organic compounds in ambient air. Environ. Sci. Technol. 27,1146-1153.
Khalil, M.A.K. and Rasmussen, R.A. (1992). Forest hydrocarbon emissions: Relationships between
fluxes and ambient concentrations. J. Air Waste Manage. Assoc. 42,810-813.
Kimura, E.T., Ebert, D.M., and Dodge, P.W. (1971). Acute toxicity and limits of solvent residue forsixteen organic solvents. Toxicol. Appl. Pharmacol. 19,699-704.
Koop, D.R. and Casazza, J.P. (1985). Identification of ethanol-inducible P-450 isozyme 3a as theacetone and acetol monooxygenase of rabbit microsomes. J. Biol. Chem. 260,13607-13612.
Koorevaar, G. and Van Stekelenburg, G.J. (1976). Mammalian acetoacetate decarboxylase activity.
Its distribution in subfractions of human albumin and occurrence in various tissues of the rat. Clin.
Chem. Acta 71,173-183.
Krasavage, W.J., O'Donoghue, J.L., and Di Vincenzo, G.D. (1982). Ketones. In: Patty's Industrial
Hygiene and Toxicology, G.D. Clayton and F.E. Clayton, eds., 3rd ed., Vol. IIC, pp. 4720-4727.
John Wiley & Sons, Inc. New York, NY.
Kristen, U., Kappler, R., and Van Aken, J.P. (1994). The pollen tube growth test (PTG-test).
Invittox Protocol 55,1-7.
Lamb, C.B. and Jenkins, G.F. (1952). BOD of synthetic organic chemicals. Proc. Ind. Waste Conf.
36,326-339.
36

UNEP Publications

OECD SIDSACETONE

Landau, B.R. and Brunengraber, H. (1987). The role of acetone in the conversion of fat tocarbohydrate. Trends Biochem. Sci. 12,113-114.
Larsen, J.J., Lykkegaard, M., and Ladefoged, O. (1991). Infertility in rats induced by 2,5-hexanedione in combination with acetone. Pharmacol. Toxicol. 69,43-46.
Le Blanc, G.A. and Surprenant, D.C. (1983). The acute and chronic toxicity of acetone, dimethylformamide, and triethylene glycol to Daphnia magna (Straus). Arch. Environ. Contam. Toxicol.
12,305-310.
Lee, Y.-N., Zhou, X., and Hallock, K. (1995). Atmospheric carbonyl compounds at a rural southeastern United States site. J. Geophys. Res. 100,25933-25944.
Leonardos, G., Kendall, D., and Barnard, N. (1969). Odor threshold determinations of 53 odorantchemicals. J. Air Poll. Control Assoc. 19,91-95.
Lewis, C.W. and Zweidinger, R.B. (1992). Apportionment of residential indoor aerosol VOC andaldehyde species to indoor and outdoor sources, and their source strengths. Atmos. Environ.
26A,2179-2184.
Li, S.-M., Anlauf, K.G., Wiebe, H.A., Bottenheim,, J.W., Shepson, P.B., and Biesenthal, T. (1997).
Emission rates and photochemical production efficiencies of nitrogen oxides, ketones, andaldehydes in the lower Fraser valley during the summer Pacific 1993 oxidant study. Atmos.
Environ. 31,2037-2048.
Lindén, E., Bengtsson, B.-E., Svanberg, O., and Sundström, G. (1979). The acute toxicity of 78
chemicals and pesticide formulations against two brackish water organisms, the bleak (Alburnus
alburnus) and the harpacticoid (Nitocra spinipes). Chemosphere 8,843-851.
Line, D.E., Wu, J., Arnold, J.A., Jennings, G.D., and Rubin, A.R. (1997). Water quality of firstflush runoff from 20 industrial sites. Water Environ. Res. 69,305-310.
Lipari, F., Dasch, J.M., and Scruggs, W.F. (1984). Aldehyde emissions from wood-burning fireplaces. Environ. Sci. Technol. 18,326-330.
Lombardo, R.J., Ferrari, L., and Vinuesa, J.H. (1991). Effects of lindane and acetone on thedevelopment of larvae of the southern king crab (Lithodes antarcticus Jaquinot). Bull. Environ.
Contam. Toxicol. 46,185-192.
Loveday, K.S., Anderson, B.E., Resnick, M.A., and Zeiger, E. (1990). Chromosome aberration andsister chromatid exchange tests in Chinese hamster ovary cells in vitro. V: Results with 46
chemicals. Environ. Mol. Mutagen. 16,272-303.
Mackay, D. and Paterson, S. (1981). Calculating fugacity. Environ. Sci. Technol. 15,1006-1014.
Märtins, T., Pauluhn, J., and Machemer, L. (1992). Analysis of alternate methods for determining
ocular irritation. Food Chem. Toxicol. 30,1061-1067.
Mast, T.J., Evanoff, J.J., Rommereim, R.L., Stoney, K.H., Weigel, R.J., and Westerberg, R.B.
(1988). Inhalation developmental toxicology studies: Teratology study of acetone in mice and rats.
UNEP Publications

37

OECD SIDSACETONE

National Institute of Environmental Health Sciences, National Toxicology Program, Contract DE
AC06-76RLO 1830. Pacific Northwest Laboratory, Battelle Memorial Institute. Richland, WA.
Matsushita, T., Yoshimune, A., Inoue, T., Yamada, S., and Suzuki, H. (1969). Experimental studies
for determining the MAC value of acetone. 1. Biologic reactions in the "one-day exposure" toacetone. Jpn. J. Ind. Health 11,477-485 (Japanese).
Mayhew, D.A. and Morrow, L.D. (1988). Ninety day gavage study in albino rats using acetone. US
Environmental Protection Agency, American Biogenics Corp., Contract No. 68-01-7075. Office ofSolid Waste. Washington, DC.
Meylan, W.M. and Howard, P.H. (1998). User’s guide for the ECOSAR class program. US
Environmental Protection Agency, Health and Environmental Review Division. Washington, DC.
Meyrahn, H., Pauly, J., Schneider, W., and Warneck, P. (1986). Quantum yields for the photodissociation of acetone in air and an estimate for the life time of acetone in the lower troposphere. J.
Atmos. Chem. 4,277-291.
Morgan, R.L., Sorenson, S.S., and Castles, T.R. (1987). Prediction of ocular irritation by corneal
pachymetry. Food Chem. Toxicol. 8,609-613.
Morgott, D.A. (1993). Acetone. In: Patty's Industrial Hygiene and Toxicology, G.D. Clayton and
F.E. Clayton, eds., 4th ed., Volume II, Part A, Chapter 5, pp. 149-281. John Wiley & Sons, Inc.
New York, NY.
NTP (1987). Cellular and genetic toxicology. In: National Toxicology Program Fiscal Year 1987
Annual Plan, pp. 43-96. US Department of Health and Human Services, National Toxicology
Program, Report No. NTP-87-001. National Institute of Environmental Health Sciences. Research
Triangle Park, NC.
Nakamura, A., Momma, J., Sekiguchi, H., Noda, T., Yamano, T., Kaniwa, M., Kojima, S., Tsuda,M., and Kurokawa, Y. (1994). A new protocol and criteria for quantitative determination ofsensitization potencies of chemicals by guinea pig maximization test. Contact Dermatitis 31,72-85.
Nasterlack, M., Triebig, G., and Stelzer, O. (1994). Hepatotoxic effects of solvent exposure aroundpermissible limits and alcohol consumption in printers over a 4-year period. Int. Arch. Occup.
Environ. Health 66,161-165.
Nelson, K.W., Ege, J.F., Ross, M., Woodman, L.E., and Silverman, L. (1943). Sensory response tocertain industrial solvent vapors. J. Ind. Hyg. Toxicol. 25,282-285.
Nirmalakhandan, N., Arulgnanendran, V., Mohsin, M., Sun, B., and Cadena, F. (1994). Toxicity of
mixtures of organic chemicals to microorganisms. Water Res. 28,543-551.
Norppa, H. (1981). The in vitro induction of sister chromatid exchanges and chromosome aberrations in human lymphocytes by styrene derivatives. Carcinogenesis 2,237-242.
Oglesby, F.L., Williams, J.L., and Fassett, D.W. (1949). Eighteen-year experience with acetone. In:
American Industrial Hygiene Association Annual Meeting. Detroit, MI.

38

UNEP Publications

OECD SIDSACETONE

Oser, B.L. and Ford, R.A. (1973). Recent progress in the consideration of flavoring ingredients
under the Food Additives amendment. 6. GRAS substances. Food Technol. 27,64-67.
Ott, M.G., Skory, L.K., Holder, B.B., Bronson, J.M., and Williams, P.R. (1983a). Health evaluation of employees occupationally exposed to methylene chloride. General study design andenvironmental considerations. Scand. J. Work Environ. Health 9(Suppl 1),1-7.
Ott, M.G., Skory, L.K., Holder, B.B., Bronson, J.M., and Williams, P.R. (1983b). Health evaluation of employees occupationally exposed to methylene chloride. Mortality. Scand. J. Work
Environ. Health 9(Suppl 1),8-16.
Ott, M.G., Skory, L.K., Holder, B.B., Bronson, J.M., and Williams, P.R. (1983c). Health evaluation of employees occupationally exposed to methylene chloride. Clinical laboratory evaluation.
Scand. J. Work Environ. Health 9(Suppl 1),17-25.
Patrick, R. and Cairns, J. (1968). The relative sensitivity of diatoms, snails, and fish to twenty
common constituents of industrial wastes. Progr. Fish Culturist 30,137-140.
Peden, V.H. (1964). Determination of individual serum "ketone bodies," with normal values in
infants and children. J. Lab. Clin. Med. 63,332-343.
Platen, H. and Schink, B. (1989). Anaerobic degradation of acetone and higher ketones via carboxylation by newly isolated denitrifying bacteria. J. Gen. Microbiol. 135,883-891.
Possanzini, M., Di Palo, V., Petricca, M., Fratarcangeli, R., and Brocco, D. (1996). Measure-mentsof lower carbonyls in Rome ambient air. Atmos. Environ. 30,3757-3764.
Pozzani, U.C., Weil, C.S., and Carpenter, C.P. (1959). The toxicological basis of threshold limit
values: 5. The experimental inhalation of vapor mixtures by rats, with notes upon the relationshipbetween single dose inhalation and single dose oral data. Am. Ind. Hyg. Assoc. J. 20,364-369.
Price, K.S., Waggy, G.T., and Conway, R.A. (1974). Brine shrimp bioassay and seawater BOD ofpetrochemicals. J. Water Pollut. Control Fed. 46,63-77.
Raleigh, R.L. and McGee, W.A. (1972). Effects of short, high-concentration exposures to acetone
as determined by observation in the work area. J. Occup. Med. 14,607-610.
Rathbun, R.E., Stephens, D.W., and Tai, D.Y. (1993). Bacterial degradation of acetone in an outdoor model stream. Environ. Pollut. 79,153-162.
Rayburn, J.R. and Fisher, W.S. (1997). Developmental toxicity of three carrier solvents using
embryos of the grass shrimp, Palaemonetes pugio. Arch. Environ. Contam. Toxicol. 33,217-221.
Reinhartz, A., Lambert, I., Herzberg, M., and Fish, F. (1987). A new, short term, sensitive, bacterial
assay kit for the detection of toxicants. Toxicity Assess. 2,193-206.
Rhim, J.S., Park, D.K., Weisburger, E.K., and Weisburger, J.H. (1974). Evaluation of an in vitro
assay system for carcinogens based on prior infection of rodent cells with nontransforming RNA
tumor virus. J. Natl. Cancer Inst. 52,1167-1173.

UNEP Publications

39

OECD SIDSACETONE

Roberts, D.N., MacGregor, F.B., Robson, A.G., Cocker, J., Rusznac, C., Schroter, R., Davies, R.J.,
and Pride, N.B. (1996). Monitoring of the nasal response to industrial and environmental stimuli.
In: Society of Occupational Medicine Annual Scientific Meeting. Birmingham, United Kingdom.
Rustung, E., Koren, F., and Föyen, A. (1931). Über Aufnahme und von Aceton im Organismus vonKaltblütern. Biochem. Z. 242,366-376 (German).
Sabel, G.V. and Clark, T.P. (1984). Volatile organic compounds as indicators of municipal solid
waste leachate contamination. Waste Manage. Res. 2,119-130.
Sack, T.M., Steele, D.H., Hammerstrom, K., and Remmers, J. (1992). A survey of householdproducts for volatile organic compounds. Atmos. Environ. 26A,1063-1070.
Sanders, P.F. (1995). Calculation of soil cleanup criteria for volatile organic compounds ascontrolled by the soil-to-groundwater pathway: Comparison of four unsaturated soil zone leachingmodels. J. Soil Contam. 4,1-24.
Satoh, T., Omae, K., Nakashima, H., Takebayashi, T., Matsumura, H., Kawai, T., Nakaza, M., andSakurai, H. (1996). Relationship between acetone exposure concentration and health effects inacetate fiber plant workers. Int. Arch. Occup. Environ. Health 68,147-153.
Schubert, U., Wisanowsky, L., and Kull, U. (1995). Determination of phytotoxicity of several
volatile organic compounds by investigating the germination pattern of tobacco pollen. J. Plant
Physiol. 145,514-518.
Seeber, A., Kiesswetter, E., and Blaszkewicz, M. (1992). Correlations between subjective disturbances due to acute exposure to organic solvents and internal dose. Neurotoxicology 13,265-270.
Shepson, P.B., Hastie, D.R., Schiff, H.I., Polizzi, M., Bottenheim, J.W., Anlauf, K., Mackay, G.I.,
and Karecki, D.R. (1991). Atmospheric concentrations and temporal variations of C1-C3 carbonylcompounds at two rural sites in central Ontario. Atmos. Environ. 25A,2001-2015.
Singh, H.B., Kanakidou, M., Crutzen, P.J., and Jacobs, D.J. (1995). High concentrations andphotochemical fate of oxygenated hydrocarbons in the global troposphere. Nature 378,50-54.
Slemr, J., Junkermann, W., and Volz-Thomas, A. (1996). Temporal variations in formaldehyde,
acetaldehyde and acetone and budget of formaldehyde at a rural site in southern Germany. Atmos.
Environ. 30,3667-3676.
Slooff, W., Canton, J.H., and Hermens, J.L.M. (1983). Comparison of the susceptibility of 22
freshwater species to 15 chemical compounds. I. (Sub)acute toxicity tests. Aquatic Toxicol.
4,113-128.
Slooff, W. and Baerselman, R. (1980). Comparison of the usefulness of the Mexican axolotl(Ambystoma mexicanum) and the clawed toad (Xenopus laevis) in toxicological bioassays. Bull.
Environ. Contam. Toxicol. 14,439-443.
Smith, M.S., Francis, A.J., and Duxbury, J.M. (1977). Collection and analysis of organic gases fromnatural ecosystems: Application to poultry manure. Environ. Sci. Technol. 11,51-55.

40

UNEP Publications

OECD SIDSACETONE

Smyth, H.F., Weil, C.S., West, J.S., and Carpenter, C.P. (1969). An exploration of joint toxic
action: Twenty-seven industrial chemicals intubated in rats in all possible pairs. Toxicol. Appl.
Pharmacol. 14,340-347.
Smyth, H.F., Carpenter, C.P., Weil, C.S., Pozzani, U.C., and Striegel, J.A. (1962). Range finding
toxicity data: List VI. Am. Ind. Hyg. Assoc. J. 23,95-107.
Solberg, S., Dye, C., Schmidbauer, N., Herzog, A., and Gehrig, R. (1996). Carbonyls and nonmethane hydrocarbons at rural European sites from the Mediterranean to the Arctic. J. Atmos.
Chem. 25,33-66.
Specht, H., Miller, J.W., and Valaer, P.J. (1939). Acute response of guinea pigs to the inhalation ofdimethyl ketone (acetone) vapor in air. Pub. Health Rep. 52,944-954.
Spicer, C.W., Buxton, B.E., Holden, M.W., Smith, D.L., Kelly, T.J., Rust, S.W., Pate, A.D.,
Sverdrup, G.M., and Chuang, J.C. (1996). Variability of hazardous air pollutants in an urban area.
Atmos. Environ. 30,3443-3456.
Steinberg, S.P. and Kreamer, D.K. (1993). Evaluation of the sorption of volatile organic compounds by unsaturated calcareous soil from southwestern Nevada using inverse gas chromatography. Environ. Sci. Technol. 27,883-888.
Stewart, R.D., Hake, C.L., Wu, A., Graff, S.A., Forster, H.V., Keeler, W.H., Lebrun, A.J., Newton,
P.E., and Soto, R.J. (1975). Acetone: Development of a biologic standard for the industrial worker
by breath analysis. US Dept. of Commerce, Report No. PB82-172917. National Institute for
Occupational Safety and Health. Cincinnati, OH.
Sulway, M.J., Trotter, M.D., Trotter, E., and Malins, J.M. (1971). Acetone in uncontrolled diabetes.
Postgrad. Med. J. 47(Suppl),383-387.
Sunesson, A.-L., Nilsson, C.-A., Andersson, B., and Blomquist, G. (1966). Volatile metabolites
produced by two fungal species cultivated on building materials. Ann. Occup. Hyg. 40,397-410.
Tanii, H., Tsuji, H., and Hashimoto, K. (1986). Structure-toxicity relationship of monoketones.
Toxicol. Lett. 30,13-17.
Taylor, D.G., Trudgill, P.W., Cripps, R.E., and Harris, P.R. (1980). The microbial metabolism ofacetone. J. Gen. Microbiol. 118,159-170.
Tunç, I, Erler, F., Dagli, F., and Çalis, Ö. (1997). Insecticidal activity of acetone vapours. J. Stored
Prod. Res. 33,181-185.
USEPA (1994). US Environmental Protection Agency, Toxic Release Inventory Data for 1992.
National Toxicology Information Program, National Library of Medicine. Bethesda, MD.
Van Duuren, B.L., Loewngart, G., Seidman, I., Smith, A.C., and Melchione, S. (1978). Mouse skincarcinogenicity tests of the flame retardants tris (2,3-dibromopropyl)phosphate, tetrakis(hydroxymethyl)-phosphonium chloride, and polyvinyl bromide. Cancer Res. 38,3236-3240.
Waggy, G.T., Conway, R.A., Hansen, J.L., and Blessing, R.L. (1994). Comparison of 20-d BOD
and OECD closed-bottle biodegradation tests. Environ. Toxicol. Chem. 13,1277-1280.
UNEP Publications

41

OECD SIDSACETONE

Wallen, I.E., Greer, W.C., and Lasater, R. (1957). Toxicity to Gambusia affinis of certain purechemicals in turbid waters. Sewage Ind. Wastes 29,695-711.
Ward, J.M., Quander, R., Devor, D., Wenk, M.L., and Spangler, E.F. (1986). Pathology of aging
female SENCAR mice used as controls in skin two-stage carcinogenesis studies. Environ. Health
Perspec. 68,81-89.
Wieland, O. (1968). Ketogenesis and its regulation. Adv. Metab. Disorders 3,1-47.
Wigaeus, E., Holm, S., and Astrand, I. (1981). Exposure to acetone. Uptake and elimination in man.
Scand. J. Work Environ. Health 7,84-94.
Williamson, D.H. and Whitelaw, E. (1978). Physiological aspects of the regulation of keto-genesis.
Biochem. Soc. Symp. 43,137-161.
Winder, C. and Turner, P.J. (1993). Solvent exposure and related work practices amongst
apprentice spray painters in automotive body repair workshops. Ann. Occup. Hyg. 36,385-394.
Winek, C.L. (1976). Tabulation of therapeutic, toxic, and lethal concentrations of drugs andchemicals in blood. Clin. Chem. 22,832-836.
Wysocki, C.J., Dalton, P., Brody, M., and Lawley, H.J. (1997). Odor and irritation thresholds foracetone in acetone-exposed factory workers and control (occupationally-nonexposed) subjects. Am.
Ind. Hyg. Assoc. J. 58,704-712.
Yocom, J.E., Hein, G.M., and Nelson, H.W. (1956). A study of the effluents from backyard
incinerators. J. Air Pollut. Control Assoc. 6,84-89.
Zakova, N., Zak, F., Froelich, E., and Hess, R. (1985). Evaluation of skin carcinogenicity of technical 2,2-bis-(p-glycidyloxyphenyl)propane in CF1 mice. Food Chem. Toxicol. 23,1081-1089.
Zimmermann, F.K., Mayer, V.W., Scheel, I., and Resnick, M.A. (1985). Acetone, methyl ethyl
ketone, ethyl acetate, acetonitrile and other polar aprotic solvents are strong inducers of aneu-ploidy
in Saccharomyces cerevisiae. Mutat. Res. 149,339-351.
Zweidinger, R.B., Sigsby, J.E., Tajada, S.B., Stump, F.D., Dropkin, D.L., Ray, W.D., and Duncan,
J.W. (1988). Detailed hydrocarbon and aldehyde mobile source emissions from roadway studies.
Environ. Sci. Technol. 22,956-962.

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OECD SIDSACETONEH E D S E T
Data Sheet
CAS-No.:
EINECS-No.:
IUPAC-Name:
1.03

Submitter Identification
Company
StreetDate
Postal Code
Town
Country
Phone
Telefax
Telex N/A

1.04

lead organization
Environmental Protection Agency
Chemical Manufacturers Association
02/20/97
401 M Street, SW
20460
Washington DC
United States
202-260-3749
202-260-8168
N/A
no

Substance Information
Molecular Formula:
Molecular Weight:
Smiles Code:
Substance Type
Physical Status
Purity1.2

Environmental Protection Agency
401 M Street, SW
02/20/97
20460
Washington, DC
United States
202-260-3749
202-260-8168

OECD and Company Information
Type
Name
Partner
Date
StreetPostal Code
Town
Country
Phone
Telefax
Telex
Other Manufacturer

1.1

67-64-1
200-662-2
Acetone

C3H6O
58.08
CC(=O)C
organic
liquid
99.5-99.8% (w/w)

Synonyms
Remark

2-Propanone
Beta-Ketopropane
Acetone
UNEP Publications

43

OECD SIDSACETONE
Dimethyl Ketone
Methyl Ketone
Propanone
Ketone Propane
Ketone, Dimethyl

1.3

Impurities
RemarkRemarkReference

Water, not more than 0.5 wt % (ASTM D1364); acidity (as free aceticacid), not more than 0.002 wt %, equivalent to 0.019 mg of KOH pergram of sample (ASTM D1613); water miscibility, no turbidity or
cloudiness at 1:10 dilution with water (ASTM D1722); alkalinity (asammonia), not more than 0.001 wt % (ASTM D1614); andpermangamate time, color of added KMnO4 must be retained at least
30 min at 25 C in the dark (ASTM D1363).
Other impurities that have been identified include: benzene (0-50ppm), acetaldehyde (0-70 ppm), methanol (0-500 ppm), diacetone
alcohol (0-300 ppm), mesityl oxide (0-10 ppm), formaldehyde (0-1ppm), isopropanol (0-100 ppm).
Kirk-Othmer. 1991. Encyclopedia of Chemical Technology, Fourth
Edition. Volume 1. John Wiley & Sons. New York.
Gerlich, O. (1995). Euclid data sheet: Acetone. Existing SubstanceDossier. Phenolchemie GmbH. Gladbeck, Germany.

1.5

Quantity
Quantity Produced
or Imported
Produced 12 mo
After Regulation
Imported 12 mo
After Regulation
RemarkInformation Source>1,000,000 tons (1993)
yes
yes
11 Producers in United States, global production.
Chemical Manufacturers Association

1.6.1 Labelling
LabellingSpecific Limits
Symbols F
R Phrases
S Phrases
Text

As in Directive 67/548/EEC
no
Nota
11
9-16-23-33
Keep container in a well-ventilated place--Keep away fromsources of ignition--No smoking--Do not breathe vapors-Take precautionary measures against static discharges.
Separate the phrases with '-' and the text for S-phrases with '-'.

1.6.2 Classification
44

UNEP Publications

OECD SIDSClassification
Class of Danger
R Phrases
1.7

1.8

ACETONE
as in Directive 67/548/EEC
highly flammable
11

Use Pattern
Type
Category
Remarkindustrial
chemical industry: used in synthesis
bisphenol-A, isophorone, methyl isobutyl ketone, otherchemical intermediates

Type
Category
Remarkindustrial
basic industry: basic chemicals
major use as solvent for fats, oils, waxes, resins, plastics,
lacquers, paints, inks, varnishes, rubber cements

Type
Category
Remarkindustrial
chemical industry: used in synthesis
methyl methacrylate, methacrylic
methacrylates (33%)

Type
Category
Remarkindustrial
process solvent: used in manufacturingsmokeless gunpowder, cellulose acetate yarn, vitaminintermediates

Type
Category
Remarkindustrial
other
antiseptic solution, cleaning and drying agent, pharmaceutical
aid

acid

and

higher

Occupational Exposure Limit Values
Type of Limit
Value
Country
Reference

8-h TWA PEL (OSHA)
2400 mg/m3 (1000 ppm)
United States
Code of Federal Regulations 41:50-204.50, 1994.

Type of Limit
Value
Country
Remark

8-h TWA
1185 mg/m3 (500 ppm)
Australia
Short-Term Exposure Limit 2400 mg/m3 (1000 ppm)

Type of Limit
Value
Country
Remark8-h MAK (DE)
1200 mg/m3 (500 ppm)
Austria, Germany, Switzerland (DFG-MAK/DFG-Peak)Short-Term Exposure Limit 6000 mg/m3 (2500 ppm)

Type of Limit
Value

8-h TWA TLV1780 mg/m3 (750 ppm)
UNEP Publications

45

OECD SIDSCountry46

ACETONE

RemarkBelgium, Luxembourg: ARAB-TWA/ARAB-STEL Ireland,
Italy: ACGIH-TWA/ACGIH-STEL
Portugal, Spain: ACGIH-TWA/ACGIH-STEL
Short-Term Exposure Limit 2400 mg/m3 (1000 ppm)

Type of Limit
Value
Country
Remark

8-h TWA OEL
800 mg/m3 (330 ppm)
Czechoslovakia
Short-Term Exposure Limit 4000 mg/m3 (1660 ppm)

Type of Limit
Value
Country

8-h TWA (AGSM)
600 mg/m3 (250 ppm)
Denmark

Type of Limit
Value
Country

8-h TWA
200 mg/m3 (84 ppm)
China

Type of Limit
Value
Country
Remark

8-h TWA OEL
1200 mg/m3 (500 ppm)
Finland
Short Term Exposure Limit 1500 mg/m3 (625 ppm)

Type of Limit
Value
Country

8-h TWA OEL
1800 mg/m3 (750 ppm)
FranceType of Limit
Value
Country
Remark

8-h TWA OEL
600 mg/m3 (250 ppm)
Hungary
Short Term Exposure Limit 1200 mg/m3 (500 ppm)

Type of Limit
Value
Country
Remark

8-h TWA OEL
1780 mg/m3 (750 ppm)
India
Short Term Exposure Limit 2375 mg/m3 (1000 ppm)

Type of Limit
Value
Country

MAC (Japan)
470 mg/m3 (200 ppm)
Japan

Type of Limit
Value
Country

MAC (NL) 8-h TWA
1780 mg/m3 (750 ppm)
The Netherlands

Type of Limit
Value
Country

8-h TWA OEL
2400 mg/m3 (1000 ppm)
The Philippines

Type of Limit
Value

8-h TWA OEL
200 mg/m3 (84 ppm)
UNEP Publications

OECD SIDS

1.9

ACETONECountry

PolandType of Limit
Value
Country
Remark

8-h TWA
200 mg/m3 (84 ppm)
RussiaShort Term Exposure Limit 200 mg/m3 (84 ppm)

Type of Limit
Value
Country
Remark

8-h TWA OEL
600 mg/m3 (250 ppm)
SwedenShort Term Exposure Limit 1200 mg/m3 (500 ppm)

Type of Limit
Value
Country

8-h TWA OEL
2400 mg/m3 (1000 ppm)
TurkeyType of Limit
Value
Country
Remark

8-h TWA (EH40)
1780 mg/m3 (750 ppm)
United Kingdom
Short Term Exposure Limit 3560 mg/m3 (1500 ppm)

Type of Limit
Value
Country
RemarkRemark

8-h TLV TWA (ACGIH)
1780 mg/m3 (750 ppm)
United States
Short-Term Exposure Limit 2375 mg/m3 (1000 ppm)
Exposures above the TLV-TWA up to the STEL should not belonger than 15 minutes and should not occur more than fourtimes per day.

Source of Exposure
RemarkAcetone is a product of the photooxidation of some alkane andalkene compounds that are found in urban air and is also a byproduct resulting from oxidation of humic substances. In
addition, natural sources of acetone include by-products fromforest fires, volcanoes, and metabolism of insects and higher
animals.

RemarkAcetone is a normal constituent of human blood and is acomponent of human breath (of metabolic origin).

RemarkAcetone may be released to the environment as stackemissions, fugitive emissions, and in waste water in its
production and use in the manufacture of methacrylates, as asolvent, and as a chemical intermediate in the manufacture of
methyl isobutyl ketone and other chemicals.

RemarkAcetone has also been identified in wastewater from industrial
and municipal treatment plants.

UNEP Publications

47

OECD SIDS
RemarkACETONE
Acetone does not appear to be persistent in the environment
due to its biodegradability, despite its widespread presence inthe environment.

2. Physico-chemical Data
2.1

Melting Point
Value
GLP
Reference

2.2

Boiling Point
Value
GLP
Reference

2.3

2.5

48

0.791 g/mL at 20 °C
no data
Handbook of Chemistry and Physics (1986). R.C. Weast (ed.),67th Ed., p. C51. CRC Press Inc. Boca Raton, FL.

Vapour Pressure
Value
GLP
Reference

182 mm Hg at 20 °C
no data
Kirk-Othmer Encyclopedia of Chemical Technology (1991).
4th Ed. Volume 1. John Wiley & Sons, New York, NY.

Value
MethodGLP
Reference

230 mm Hg at 25 °C
other (calculated)no data
NOMO5 Program. Syracuse Research Corp.,Syracuse, NY.

Partition Coefficient
Value
Type
GLP
Reference

2.6

56.1 °C at 760 mm Hg
no data
Handbook of Chemistry and Physics (1986). R.C. Weast (ed.),67th Ed., p. C51. CRC Press Inc. Boca Raton, FL.

Density
Value
GLP
Reference

2.4-94.6 °Cno data
Handbook of Chemistry and Physics (1986). R.C. Weast (ed.),67th Ed., p. C51. CRC Press Inc. Boca Raton, FL.

-0.24
Log PownoHansch, C. and Leo, A. (1979). Substituent Constants for
Correlation Analysis in Chemistry and Biology, p. 179. John
Wiley & Sons, New York, NY.

Water Solubility

UNEP Publications

OECD SIDS
Description
GLP
RemarkReference

2.7

465 °C (autoignition temperature)
no data
Fire Hazard Properties of Flammable Liquids, Gases, andVolatile Solids (1991). National Fire Protection Association,
NFPA 325M, 10th Ed. Quincy, MA.

Flammability
Result
GLP
Reference

2.10-17 °C
closed cup
no data
Fire Hazard Properties of Flammable Liquids, Gases, andVolatile Solids (1991). National Fire Protection Association,
NFPA 325M, 10th Ed. Quincy, MA.

Auto Flammability
Value
GLP
Reference

2.9

miscibleno data
Miscible with water, alcohol, dimethylformamide, ether.
The Merck Index (1983). M. Windholz (ed.), 10th Ed., p. 57.
Merck & Co., Rahway, NJ.

Flash Point
Value
Type
GLP
Reference

2.8

ACETONEhighly flammable
no data
Fire Hazard Properties of Flammable Liquids, Gases, andVolatile Solids (1991). National Fire Protection Association,
NFPA 325M, 10th Ed. Quincy, MA.

Explosive Properties
Result
GLP
Reference

not explosive
no data
Fire Hazard Properties of Flammable Liquids, Gases, andVolatile Solids (1991). National Fire Protection Association,
NFPA 325M, 10th Ed. Quincy, MA.

3. Environmental Fate and Pathways
3.1

Stability

3.1.1 Photodegradation
Type
Light Source
Light Spect.
Rel. Intens.
Spectrumair
xenon lamp
250-330 nm
Based on intensity of sunlightlambda (max) >295 nm
epsilon (max) 295 nm
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49

OECD SIDS
Concentration
GLP
Test substance
Result

Test condition
Reference

Type
Light Spect.
Rel. Intensity
Spectrum
GLP
Test substance
ResultReference

ACETONE
200 mg/L
no datano data
Quantum yield varied with wavelength from 1.59 to 0.27 forCO2 production. Direct photolysis half-life was 32 days. The
half-life reported is the annual average in the lower
troposphere at 40 degrees northern latitude. Indirect photolysis
rate constant estimated to be 0.00000026 cm3/mol/sec basedon OH sensitizer concentration of 1,180,000 mol/cm3.
Temperature for direct photolysis test equaled room
temperature
Meyrahn, H., Pauly, J., Schneider, W., and Warneck, P.
(1986). Quantum yields for the photodissociation of acetone
in air and an estimate for the lifetime of acetone in the lower
troposphere. J. Atmos. Chem. 4:277-291.
air279-313 nm
based on intensity of sunlightlambda (max) >295 nm
epsilon (max) 295 nm
no datano data
Quantum yield: 0.15 (25 torr); 0.08 (> 400 torr) Photolysis
half-life is 40 days near the earth surface to 10 days at 200
mbar pressure. Attack by hydroxyl radicals with half-life of
20 days near earth surface to 100 days at 200 mbar pressure.
Gardner, E.P. (1984). The primary quantum yields ofphotodecomposition of acetone in air under troposphericconditions. J. Phys. Chem. 88:5069-5076.
Chatfield, R.B., Gardner, E.P., and Calvert, J.G. (1987).
Sources and sinks of acetone in the troposphere: Behavior ofreactive hydrocarbons and a stable product. J. Geophys. Res.
92:4208-4216.

3.2

Monitoring Data (Environment)
Type
Media
RemarkReference

Type
Media
Remark50

background concentration
air
Acetone detected at 1.6-4 part per billion by volume (ppbv),
4.8-12 ppbC, average concentration over a 1-yr period in
Denver, Colorado, USA.
Anderson, L.G., Lanning, J.A., and Wolfe, P. (1994). Acetone
in the urban atmosphere: A case study in Denver, Colorado.
Israel J. Chem. 34:341-353.
background concentrationair
1.6 ppb (4.8 ppbC) and 1.8 ppb (5.4 ppbC) found in two ruralsites in Ontario, Canada, 1988.
UNEP Publications

OECD SIDSACETONE

Reference

Shepson, P.B., Hastie, D.R., Schiff, H.I., Polizzi, M.,
Bottenheim, J.W., Anlauf, K., Mackay, G.I., and Karecki,
D.R. (1991). Atmospheric concentrations and temporalvariations of C1-C3 carbonyl compounds at two rural sites incentral Ontario. Atmos. Environ. 25A:2001-2015.

Type
Media
Remarkbackground concentrationair
12 ppb (36 ppbC) in troposphere above Tucson, Arizona; 2.8
ppb (8.4 ppbC) at two rural sites 40 km away.
Snider, J.R. and Dawson, G.A. (1985). Tropospheric lightalcohols, carbonyls, and acetonitrile: Concentrations in thesouthwestern United States and Henry's Law data. J. Geophys.
Res. 90:3797-3805.

Reference

Type
Media
RemarkReference

background concentration
air
Range of 4.1-94 part per billion by volume (ppbv), 12.3-282
ppbC, at two urban sites in USA. Additionally, a range of19.5-89.6 ppbv, (58.5-268.8 ppbC) was reported in a variety
of work settings, including indoor air.
Kelly, T.J., Callahan, P.J., Piell, J., and Evans, G.F. (1993).
Method development and field measurements for polar
volatile organic compounds in ambient air. Environ. Sci.
Technol. 27:1146-1153.

Type
Media
RemarkReference

background concentration
air
Qualitative detection in volcanic gas from Guatemala.
Stoiber, R.E., Leggett, R.E., Jenkins, T.F., Murrmann, R.P.,
and Rose, W.I. (1971). Organic compounds in volcanic gas
from Santiaguito volcano, Guatemala. Am. Geolog. Soc. Bull.
82:2299-2302.

Type
Media
Remarkcontaminated siteair
Acetone detected at 770-4100 parts per billion by volume(ppbv) 2310-12,300 ppbC, around several different
manufacturing sites.
Hoshitia, Y., Nihei, Y., Muto, G. (1981). Pattern display forcharacterization of trace amounts of odorants discharged fromnine odor sources. Analyst 106:1187-1202.

Reference

Type
Media
RemarkReference

background concentrationair
6.7-32.3 parts per billion as carbon (ppbC) was detected inseven Florida (USA) sites.
Lonneman, W.E., Sella, R.L., and Bufalini, J.J. (1978).
Ambient air hydrocarbon concentrations in Florida. Env. Sci.
Technol. 12:459-463.
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51

OECD SIDS
Type
Media
RemarkReference

Type
Media
RemarkReference

Type
Media
RemarkReference

Type
Media
RemarkReference

Type
Media
RemarkReference

Type
Media
Remark52

ACETONEbackground concentrationair
0.5-20.6 parts per billion as carbon (ppbC) was detected in
USA continental and marine areas.
Duce, R.A., Mohnen, V.A., Zimmerman, P.R., Grosjean, D.,
Cautreels, W., Chatfield, R., Jaenicke, R., Ogren, J.A.,
Pelliari, E.D., and Wallace, G.T. (1983). Organic material in
the global troposphere. Rev. Geophys. Space Phys. 21:921952.
background concentrationair
An average of 470 parts per trillion by volume (pptv) (1410
pptC) of acetone at ground level to 120 pptv (360 pptC) in theupper troposphere was detected.
Arnold, F., Knop, G., and Ziereis, H. (1986). Acetone
measurements in the upper troposphere and lower
stratosphere- implications for hydroxyl radical abundances.
Nature 321:505-507.
background concentrationair
4-52 part per billion as carbon (ppbC) was detected at threesites in the USA.
Arnts, R.R. and Meeks, S.A. (1981). Biogenic hydrocarbon
contribution to the ambient air of selected areas. Atmos.
Environ. 15:1643-1651.
contaminated site
ground water
A concentration of 43,700 µg/L was detected onsite at acontaminated landfill; 0.2-0.7 µg/L acetone was found inwells adjacent to the landfill.
DeWalle, F.B. and Chien, E.S.K. (1981). Detection of traceorganics in well water near a solid waste landfill. J. Am.
Water Works Assoc. 73:206-211.
contaminated siteair
20-250 part per billion by volume (ppbv) (60-750 ppbC) was
detected in a house near a contaminated landfill.
Hodgson, A.T., Garbesi, K., Sextro, R.G., and Daisey, J.M.
(1992). Soil-gas contamination and entry of volatile organic
compounds into a house near a landfill. J. Air Waste Manage.
Assoc. 42:277-283.
other
air
Acetone was detected in seven different product categories.
The percentage of products with acetone at the average
concentration (w/w%) are as follows:
UNEP Publications

OECD SIDS

Reference

Type
Media
RemarkReference

Type
Media
RemarkReference

Type
Media
RemarkReference

Type
Media
RemarkReference

Type
Media
RemarkACETONE
23% automotive - 28.1
11% household cleaners - 0.3
51% paints - 29.3
15% fabric & leather - 12.9
16% electronic equipment - 0.3
5% oils, greases, lubricants - 0.2
24% adhesives - 18.8
Sack, T.M., Steele, D.H., Hammerstrom, K., and Remmers, J.
(1992). A survey of household products for volatile organic
compounds. Atmos. Environ. 26A:1063-1070.
other
air
Acetone was found in the homes of smoking and non-smoking
adults at average concentrations of 71 and 50 µg/m3,
respectively.
Heavner, D.L., Morgan, W.T., and Ogden, M.W. (1996).
Determination of volatile organic compounds and respirable
suspended particulate matter in New Jersey and Pennsylvania
homes and workplaces. Environ. Int. 22:159-183.
other
air
Acetone was emitted from particle board at rate ranging from37- 41 µg/m2/h.
Tichenor, B.A. and Mason, M.A. (1988). Organic emissions
from consumer products and building materials to the indoor
environment. J. Air Pollut Control Assoc. 38:264-268.
other
air
78.8 ppm (236.4 ppmC) found in smoke from polypropylene
burning.
Woolley, W.D. (1982). Smoke and toxic gas production fromburning polymers. J. Macromol. Sci. Chem. A17:1-33.
background concentrationair
14-66 µg/m3 (6-30 ppb) (18-120 ppbC) acetone was detected
in a new office building over a period of one year.
Hodgson, A.T., Daisey, J.M., and Grot, R.A. (1991). Sources
and source strengths of volatile organic compounds in a new
office building. J. Air Waste Manage. Assoc. 41:1461-1468.
contaminated siteair6838-32,500 part per billion by volume (ppbv) (20,514-97,500
ppbC) was detected in the air at municipal landfill sites.

UNEP Publications

53

OECD SIDSACETONE

Reference

Brosseau, J. and Heitz, M. (1994). Trace gas compoundemissions from municipal landfill sanitary sites. Atmos.
Environ. 28:285-293.

Type
Media
Remarkcontaminated site
water
Acetone ranged from 9 ppb influent to 41 ppb effluent in a
textile finishing plant.
Gordon, A.W. and Gordon, M. (1981). Analysis of volatileorganic compounds in a textile finishing plant effluent. Trans.
Ky. Acad. Sci. 42:149-157.

Reference

Type
Media
RemarkReference

Type
Media
RemarkReference

Type
Media
RemarkReference

background concentrationwater
0-41 ng/mL acetone was detected in cloud water at a remotecontinental (USA) site.
Aneja, V.P. (1993). Organic compounds in cloud water andtheir deposition at a remote continental site. J. Air Waste
Manage. Assoc. 43:1239-1244.
background concentrationwater
0-0.052 mg/L acetone was detected in seawater samples from
Florida and the Eastern Mediterranean.
Corwin, J.F. (1969). Volatile oxygen-containing organic
compounds in sea water: Determination. Bull. Marine Sci.
19:504-509.
background concentration
biota
Acetone is a normal endogenous biochemical that can beroutinely detected and measured in body fluids. Detectableamounts of acetone have been found in a variety of biological
specimens including whole blood (fetal through adult),
cerebrospinal fluid, urine, exhaled air, and breast milk.
Dowty, B.J., Laseter, J.L., and Storer, J. (1976). The
transplacental migration and accumulation in blood of volatileorganic compounds. Pediatr. Res. 10:696-701.
Sulway, M.J., Trotter, M.D., Trotter, E., and Malins, J.M.
(1971). Acetone in uncontrolled diabetes. Postgrad. Med. J.
47(Suppl.):383-387.
Zlatkis, A., Bertsch, W., Lichtenstein, H.A., Tishbee, A.,
Shunbo, F., Liebich, H.M., Coscia, A.M., and Fleischer, N.
(1973). Profile of volatile metabolites in urine by gas
chromatography-mass chromatography. Anal. Chem. 45:763767.
Pellizzari, E.D., Hartwell, T.D., Harris, B.S.H., Waddell,R.D., Whitaker, D.A., and Erickson, M.D. (1982). Purgeable

54

UNEP Publications

OECD SIDSACETONE
organic compounds in mother's milk. Bull. Environ. Contam.
Toxicol. 28:322-328.

Type
Media
RemarkReference

background concentration
biota
The normal limit for blood, serum, and plasma acetone in nonfasting adults has been shown to range from 0.8-4.4 mg/L
depending on the analytical method applied. The acetone
concentration in plasma can be 8-11% greater than the level inwhole blood. Infants, pregnant women, and training athletes
can have ketone body levels that are elevated 2 to 20-foldabove normal due to the ketogenesis resulting from theirhigher energy requirements.
Paterson, P., Sheath, J., Taft, P., and Wood, C. (1967).
Maternal and foetal ketone concentration in plasma and urine.
Lancet II:862-865.
Koeslag, J.H., Noakes, T.D., and Sloan, A.W. (1980).
Post-exercise ketosis. J. Physiol. 301:79-90.
Ashley, D.L., Bonin, M.A., Cardinali, F.L. McCraw, J.M., andWooten, J.V. (1994). Blood concentrations of volatile organic
compounds in a nonoccupationally exposed US populationand in groups with suspected exposure. Clin. Chem. 40:14011404.
Trotter, M.D., Sulway, M.J., and Trotter, E. (1971). The rapid
determination of acetone in breath and plasma. Clin. Chem.
Acta 35:137-143.
Kimura, M., Kobayashi, K., Matsuoka, A., Hayashi, K., andKimura, Y. (1985). Head-space gas-chromatographic
determination of 3-hydroxybutyrate in plasma after enzymic
reactions, and the relationship among the three ketone bodies.
Clin. Chem. 31:596-598.
Brega, A., Villa, P., Quadrini, G., Quadri, A., and Lucarelli,C. (1991). High-performance liquid chrom-otographic
determination of acetone in blood and urine in the clinicaldiagnostic laboratory. J. Chromatogr. 553:249-254.
Gavino, V.C., Vinet, B., David, F, Garneau, M., andBrunengraber, H. (1986). Determination of the concen-trationand specific activity of acetone in biological fluids. Anal.
Biochem. 152:256-261.
Wang, G., Maranelli, G., Perbellini, L., Raineri, E., andBrugnone, F. (1994). Blood acetone concentration in "normal
people" and in exposed workers 16 h after the end of theworkshift. Int. Arch. Occup. Environ. Health65:285-289.
UNEP Publications

55

OECD SIDS
Type
Media
RemarkReference

ACETONEbackground concentration
biota
Endogenous acetone concentrations in normal human spot
urine specimens have been shown to range from 0.3-3.0 mg/L.
The urinary concentration of acetone was not found toincrease appreciably when test subjects performed lightphysical exercise. A consistent diurnal trend was observed,
however, with higher urine acetone concentrations found in
the late evening and early morning than during the day.
Brega, A., Villa, P., Quadrini, G., Quadri, A., and Lucarelli,C. (1991). High-performance liquid chrom-atographic
determination of acetone in blood and urine in the clinicaldiagnostic laboratory. J. Chromatogr. 553:249-254.
Kobayashi, K., Okada, M., Yasuda, Y., and Kawai, S. (1983).
A gas chromatographic method for the determination ofacetone and acetoacetic acid in urine. Clin. Chem. Acta
133:223-226.
Levey, S., Balchum, O.J., Medrano, V., and Jung, R. (1964).
Studies of metabolic products in expired air. II. Acetone. J.
Lab. Clin. Med. 63:574-584.
Pezzagno, G., Imbriani, M., Ghittori, S., and Capodaglio, E.
(1988). Urinary concentration, environ-mental concentration,and respiratory uptake of some solvents: Effect of the work
load. Am. Ind. Hyg. Assoc. J. 49:546-552.
Wang, G., Maranelli, G., Perbellini, L., Raineri, E., andBrugnone, F. (1994). Blood acetone concentration in "normal
people" and in exposed workers 16 h after the end of theworkshift. Int. Arch. Occup. Environ. Health 65:285-289.

Type
Media
RemarkReference

background concentration
biota
The normal value for endogenous acetone in expired air
specimens from adult humans was found to average between
0.7-1.6 mg/L, regardless of whether the subjects were fed or
fasted overnight.
Rooth, G. and Tibbling, G. (1968). Free fatty acids, glycerol
and alveolar acetone in obese women during phenformin
treatment. Acta Med. Scand. 184:263-267.
Rooth, G. and Östenson, S. (1966). Acetone in alveolar air,and the control of diabetes. Lancet II:1102-1105.
Levey, S., Balchum, O.J., Medrano, V., and Jung, R. (1964).
Studies of metabolic products in expired air. II. Acetone. J.
Lab. Clin. Med. 63:574-584.

56

UNEP Publications

OECD SIDSACETONE
Crofford, O.B., Mallard, R.E., Winton, R.E., Rogers, N.L.,
Jackson, J.C., and Keller, U. (1977). Acetone in breath andblood. Trans. Am. Clin. Climatol. Assoc. 88:128-139.
Trotter, M.D., Sulway, M.J., and Trotter, E. (1971). The rapid
determination of acetone in breath and plasma. Clin. Chem.
Acta 35:137-143.
Jansson, B.O. and Larsson, B.T. (1969). Analysis of organic
compounds in human breath by gas chromatography-mass
spectrometry. J. Lab. Clin. Med. 74:961-966.
Stewart, R.D. and Boettner, E.A. (1964). Expired-air acetone
in diabetes mellitus. New Eng. J. Med. 270:1035-1038.
Tassopoulos, C.N., Barnett, D., and Fraser, T.R. (1969)
Breath-acetone and blood-sugar measurements in diabetes.
Lancet II:1282-1286.
Phillips, M. and Greenberg, J. (1987). Detection ofendogenous acetone in normal human breath. J. Chromatogr.
422:235-238.
Wang, G., Maranelli, G., Perbellini, L., Raineri, E., andBrugnone, F. (1994). Blood acetone concentration in "normal
people" and in exposed workers 16 h after the end of theworkshift. Int. Arch. Occup. Environ. Health 65:285-289.

Type
Media
RemarkReference

Type
Media
Remarkother
biota
Four workers exposed to 30 ppm (71.1 mg/m3) of acetone for
2 h were found to retain about 80% of the inhaled acetone.
The concentration of acetone in the urine increased fromabout 0.75 mg/L at the beginning of the workshift to about 2.0
mg/L by the end of the shift. The acetone in venous bloodincreased from 1.0 mg/L at the start of the shift to 3.3 mg/L by
the end. Urine and blood acetone levels returned to normal
within 24 h.
Baumann, K. and Angerer, J. (1979). Untersuchungen zur
Frage der beruflichen Lösungsmittelbelastung mit Aceton.
Krebsgefaehrdung Arbeitsplatz Arbeitsmed. 19:403-408.
other
biota
Biological monitoring of styrene exposure in the workplace
was not affected by co-exposures to acetone. Styrene
metabolite concentrations in the urine of 22 workers exposed
to styrene and acetone were not affected by 8-h TWA acetone
exposures that ranged from about 10-210 ppm (25 to 498
mg/m3).
UNEP Publications

57

OECD SIDS
Reference

ACETONE
DeRosa, E., Cellini, M., Sessa, G., Saletti, C., Rausa, G.,
Marcuzzo, G., and Bartolucci, G.B. (1993). Bio-logicalmonitoring of workers exposed to styrene and acetone. Int.
Arch. Occup. Environ. Health 65:S107-S110.

3.3 Transport and Distribution in Environmental Compartments
3.3.1 Transport
Type
Media
MethodResultReference

Type
Media
MethodResultReferencevolatility
water-airmass-transfer coefficients measurement
The liquid film mass-transfer coefficient KL ranged from 0.280.54 m/day.
Rathbun, R.E. and Tai, D.Y. (1982). Volatilization of ketones
from water. Water Air Soil Pollut. 17:281-293.
volatility
water-airacetone measured in model stream
Volatilization coefficient ranged from 82,300-111,000 min-1.
Rathbun, R.E., Stephans, D.W., and Tai, D.Y. (1991). Fate ofacetone in an outdoor model stream with a nitrate supplement,
southern Mississippi, U.S.A. J. Hydrol. 123:225-242.

3.3.2 Distribution
Media
MethodRemarkResultReference

Media
MethodResultReference

Media
MethodResultReference58

water-airother (measurement)
Partition between air and seawater at a variety of temperatures
was measured and calculated.
Partition coefficient K (m/atm) was 14.8-71.3.
Zhou, X. and Mopper, K. (1990). Apparent partition
coefficients of 15 carbonyl compounds between air andseawater and between air and freshwater: Implications for airsea exchange. Environ. Sci. Technol. 24:1864-1869.
water sediment
other (measurement)
200-230 ppm acetone was detected in wastewater; acetone
was not detected in river water or sediment.
Jungclaus, G.A., Lopez-Avila, V., and Hites, R.A. (1978).
Organic compounds in an industrial wastewater: A case studyof their environmental impact. Environ. Sci. Technol.12:8896.
water-airother (measurement)
Henry's law constant was 25.6-27.0 m/atm at 25°C.
Betterton, E.A. (1991). The partitioning of ketones between
the gas and aqueous phases. Atmos. Environ. 25A:1473-1477.
UNEP Publications

OECD SIDS

3.4

ACETONE

Mode of Degradation
RemarkReference

biological oxidation
Rathbun, R.E., Stephens, D.W., and Tai, D.Y. (1993).
Bacterial degradation of acetone in an outdoor model stream.
Environ. Pollut. 79,153-162.
Rathbun, R.E., Stephans, D.W., and Tai, D.Y. (1991). Fate ofacetone in an outdoor model stream with a nitrate supplement,
southern Mississippi, U.S.A. J. Hydrol. 123,225-242.
Taylor, D.G., Trudgill, P.W., Cripps, R.E., and Harris, P.R.
(1980). The microbial metabolism of acetone. J. Gen.
Microbiol. 118,159-170.

3.5

Biodegradation
Type
Inoculum
Degradation
Results
MethodGLPTest substance
Reference

aerobic
activated sludge, domestic
78% after 28 days
readily biodegradable
OECD Guideline 301 D
no datano data
Waggy, G.T., Conway, R.A., Hansen, J.L., and Lessing, R.L.
(1994). Comparison of 20-d BOD and OECD closed-bottle
biodegradation tests. Environ. Toxicol. Chem. 13:1277-1280.

Type
Inoculum
Concentration
Degradation
MethodGLPTest substance
Reference

aerobic
activated sludge, domestic
100 mg/L
42% after 155 hotherno datano data
Urano, K. and Kato, Z. (1986). A method to classify
biodegradabilities of organic compounds. J. Hazard. Materials
3:147-159.

Type
Inoculum
Concentration
Degradation
Results
MethodGLPTest substance
Remarkaerobic
activated sludge, domestic
500 mg/L
0% after 24 h
Under test conditions no biodegradation observed
othernono dataThis study used a quite high substrate concentration for alimited period of time (24 h), when contrasted to more current
methods.
UNEP Publications

59

OECD SIDS60

ACETONE

Reference

Gerhold, R.M. and Malaney, G.W. (1966). Structural
determinants in the oxidation of aliphatic compounds by
activated sludge. J. Water Pollut. Control Fed. 38:562-579.

Type
Inoculum
Concentration
Degradation
Results
MethodGLPTest substance
RemarkReference

aerobic
activated sludge, domestic
2.5 mg/L
78.2%
readily biodegradableothernono dataResults based on BOD.
Lamb, C.B. and Jenkins, G.F. (1952). B.O.D. of syntheticorganic chemicals. Proc. Ind. Waste Conf. 36:326-339.

Type
Inoculum
Concentration
Degradation
Results
MethodGLPTest substance
Reference

aerobic
activated sludge, domestic, adapted
333 mg/L
86% after 8 hreadily biodegradableothernono data
Hatfield, R. (1957). Biological oxidation of some organic
compounds. Ind. Eng. Chem. 49:192.

Type
Inoculum
Degradation
MethodGLPTest substance
RemarkTest concentration
Reference

aerobic
activated sludge, domestic, adapted
47% after 10 daysothernono data
Early study of a wastewater treatment plant.
250-1000 mg/L.
Mills, E.J. and Stack, V.T. (1954). Biological oxidation ofsynthetic organic chemicals. Proc. Ind. Waste. Conf. 38:492517.

Type
Inoculum
Degradation
GLP
Test substance
RemarkTest concentration
Reference

aerobic
activated sludge, domestic, adapted
38% after 5 days
no datano dataResults based on BOD measurement.
0.4-3.2 mg/L
Babeu, L. and Vaishnav, D.D. (1987). Prediction of
biodegradability for selected organic chemicals. J. Ind.
Microbiol. 2:107-115.

Typeanaerobic
UNEP Publications

OECD SIDS
Inoculum
Concentration
Degradation
GLP
Test substance
RemarkRemarkReference

3.6

ACETONE
inoculum from sediment and groundwater
50 mg/L100% after 244 days
no datano data
Test concentration reported as ppm carbon.
Results were comparable in sulfite and nitrate-reducing
systems.
Mormile, M.R., Liu, S., and Suflita, J.M. (1994). Anaerobic
biodegradation of gasoline oxygenates: Extrapolation of
information to multiple sites and redox conditions. Environ.
Sci. Technol. 28:1727-1732.

Type
Inoculum
Concentration
Degradation
GLP
Test substance
RemarkReference

aerobic
activated sludge, domestic
10 mg/L
81% after 20 days
no datano data
BOD/ThOD ratio.
Young, R.H.F., Ryckman, D.W., and Buzzell, J.C. (1968). An
improved tool for measuring biodegradability. J. Water Pollut.
Control Fed. 40:R354-R368.

Type
Inoculum
Concentration
Degradation
GLP
Test substance
RemarkReference

aerobic
activated sludge, domestic
3.2 mg/L
38% after 5 days
no datano dataresults based on BOD.
Vaishnav, D.D., Boethling, R.S., and Babeu, L. (1987).
Quantitative structure-biodegradability relationships foralcohols, ketones and alicyclic compounds. Chemosphere
16:695-703.

Type
Inoculum
Degradation
GLP
Test substance
RemarkConcentration
Reference

aerobic
lab-generated organisms seeded from domestic sludge.
100%
no datano data
Removal rate was 125 mg/L/day after a 5-day lag.
166-500 mg/L.
Chou, W.L., Speece, R.E., and Siddiqi, R.H. (1978).
Acclimation and degradation of petrochemical wastewatercomponents by methane fermentation. In: Biotechnology andBioengineering Symposium No. 8., C.D. Scott, ed., pp. 391414. John Wiley and Sons, New York, NY.

BOD5, COD or BOD5/COD Ratio
UNEP Publications

61

OECD SIDS
Method
Year
BOD5
COD
GLP

other
1979
1.85 g/g
1.92 g/g
no data

BOD5/COD Ratio
MethodConcentrations
Remark

0.96
APHA "Standard Methods" 1989.
3, 7, and 10 mg/L were used.
In additional testing, BOD10, BOD15, and BOD20 were
determined (Birdie et. al., 1979).
ThOD - 2.21 (based on calculation).
BOD10 - 76% of ThOD
BOD15 - 83% of ThOD
BOD20 - 84% of ThOD
COD Method = ASTM D1252-67 (reapproved 1974).
BOD5 Method = APHA Standard Methods No. 219,1971

Test condition

3.7

ACETONE

Reference

Birdie, A.L., Wolff, C.J.M., and Winter, M. (1979). BOD and
COD of some petrochemicals. Water Res. 13:627-630.

BOD5/COD Ratio
BOD5
Concentrations
MethodReferenceno data
56% of ThOD3, 7, 10 mg/L
APHA Standard Methods 1989.
Waggy, G.T., Conway, R.A., Hansen, J.L., and Blessing, R.L.
(1994). Comparison of 20-d BOD and OECD closed-bottle
biodegradation tests. Environ. Toxicol. Chem. 13:1277-1280.

Bioaccumulation
Species
Temperature
BCF
Year
GLP
Test condition
Reference

haddock (adult)
7 °C
0.69
1931
no
staticRustung, E., Koren, F., and Föyen, A. (1931). Über Aufnahmeund von Aceton im Organismus von Kaltblütern. Biochem. Z.
242:366-376.

4. Ecotoxicity
4.1

Acute/Prolonged Toxicity to Fish
Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP

62

flow throughSalvelinus fontinalis
96 h6070 mg/L
no datano data
UNEP Publications

OECD SIDS
Test Substance
RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test Substance
RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test Substance
RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring

ACETONEno data
The exposure process is described in U.S. EPA: Methods for
Acute Toxicity Tests with Fish, Macro-invertebrates, andAmphibians. EPA-660/3-75-009. Committee on Methods for
Toxicity Tests with Aquatic Organisms (1975). The methods
used by Cardwell et.al. (1974) are similar in duration of
exposure, type of test vessel, physical/chemical parameters
monitored, selection of dilution water, and selection of test
species.
Cardwell, R.D., Foreman, D.G., Payne, T.R., and Wilber, D.J.
(1974). Acute and chronic toxicity of four organic chemicals
to fish. Project Report to C.E. Stephen, U.S. EPA,
Environmental Research Laboratory - Duluth. Duluth, MN.
flow throughLepomis macrochirus
96 h7300 mg/L
no datano datano data
Test Method similar to U.S. EPA: Methods for Acute Toxicity
Tests with Fish, Macroinvertebrates, and Amphibians. EPA660/3-75-009. Committee on Methods for Toxicity Tests with
Aquatic Organisms, 1975.
Cardwell, R.D., Foreman, D.G., Payne, T.R., and Wilber, D.J.
(1974). Acute and chronic toxicity of four organic chemicals
to fish. Project Report to C.E. Stephen, U.S. EPA,
Environmental Research Laboratory - Duluth. Duluth, MN.
flow throughPimephales promelas
96 h9100 mg/L
no datano datano data
Test method similar to U.S. EPA: Methods for Acute Toxicity
Tests with Fish, Macroinvertebrates, and Amphibians. EPA660/3-75-009. Committee on Methods for Toxicity Test with
Aquatic Organisms, 1975.
Cardwell, R.D., Foreman, D.G., Payne, T.R., and Wilber,
D.J.(1974). Acute and chronic toxicity of four organic
chemicals to fish. Project Report to C.E. Stephen, U.S. EPA Environmental Research Laboratory - Duluth. Duluth, MN.
staticGambusia affinis
72 h
13,000 mg/L
no data
UNEP Publications

63

OECD SIDS
GLP
Test substance
Results

RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test Substance
RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test Substance
RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
Test method
64

ACETONEno datano data24-h LC50 = 13,500 mg/L
48-h LC50 = 13,000 mg/L
Below 11,500 mg/L, the fish showed no permanent distress.
Method similar to Doudoroff et al., Bioassay methods for theevaluation of acute toxicity of industrial wastes to fish.
Sewage Ind. Wastes 23:1380-1397, 1951.
Wallen, I.E., Greer, W.C., and Lasater, R. (1957). Toxicity to
Gambusia affinis of certain pure chemicals in turbid waters.
Sewage Ind. Wastes 29:695-711.
flow throughPimephales promelas
96 h8120 mg/L
yes
no datano data
Method similar to: Methods for Measuring the Acute Toxicity
of Effluents to Aquatic Organisms. W. Piltier, Bioassay
Subcommittee. EPA Biological Advisory Committee, Ecology
Branch. EPA-600/4-28-012, 1978.
Veith, G. (1983). Structure-toxicity relationships for thefathead minnow, Pimaphales promelas: Narcotic industrial
chemicals. Can. J. Fish Aquat. Sci. 40:743-748.
staticOncorhynchus mykiss
96 h5540 mg/L
no datano dataprescribed by 1.1-1.4
Method similar to: Methods for Measuring the Acute Toxicity
of Effluents to Aquatic Organisms. W. Piltier, Bioassay
Subcommittee. EPA Biological Advisory Committee, Ecology
Branch, EPA-600/4-28-012, 1978.
Johnson, W.W. and Finley, M.T. (1980). Handbook of Acute
Toxicity of Chemicals to Fish and Aquatic Inver-tebrates.
Department of the Interior Fish and Wildlife Service. Resource
Publication 137. Washington, DC.
flow throughPimephales promelas
96 h6210-8120 mg/L
yes
no datano datasimilar to OECD Guideline 204.
UNEP Publications

OECD SIDS
RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
Test method

Reference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkRemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance

ACETONE
Results from 3 test runs (LC50 in mg/L):
24-h: 8830, 9400, 8030
72-h: 8120, 7940, 6400
96-h: 8120, 7280, 6210
Brooke, L.T., Call, D.J., Geiger, D.L., and Northcott, C.E.
(1984). Acute Toxicities of Organic Chemicals to Fathead
Minnows (Pimephales promelas). Center for Lake Superior
Environmental Studies.
staticPoecilia reticulata
14 day6400 mg/L
no datano datano datasimilar to U.S. EPA: Methods for Acute Toxicity Tests with
Fish, Macroinvertebrates, and Amphibians. EPA-660/3-75009. Committee on Methods for Toxicity Tests with Aquatic
Organisms, 1975.
Konemann, H. (1981). Quantitative structure-activity
relationships in fish toxicity studies. Part 1: Relationship for 50
industrial pollutants. Toxicology 9:209-221.
flow throughSalmo gairdneri
24 h6100 mg/L
no datano datano data
Acetone (2930 mg/L) produced an increase in ventilation rate,
reaching a maximum of 158% of controls at 21 hours for theduration of the exposure period.
Method similar to that contained in: Sprague, J.B. (1969).
Measurement of pollutant toxicity to fish. I. Bioassay methods
for acute toxicity. Water Res. 3:793-821.
Majewski, H.S., Klaverkamp, J.F., and Scott, D.P. (1978).
Acute lethality and sub-lethal effects of acetone, ethanol, andpropylene glycol on the cardiovascular and respiratory systemsof rainbow trout (Salmo gairdneri). Water Res. 13:217-221.
staticLepomis macrochirus
96 h8300 mg/L
no datanono data

UNEP Publications

65

OECD SIDS
RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReference

Type
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkResult66

ACETONE
Test method similar to Doudoroff, P. (1951). Bioassay
methods for the evaluation of acute toxicity of industrial
wastes to fish. Sewage Ind. Wastes 23:1380-1397.
Cairns, J. and Scheier, A. (1968). A comparison of the toxicity
of some of the common industrial waste components tested
individually and combined. Progressive Fish Culturist 30:3-8.
staticCarassius auratus
24 h>5000 mg/L
no datano datano data
Method similar to that described in: American Public Health
Association. Review papers on measurement of pollutant
toxicity to fish. Sprague, J.B. (1969). Bioassay methods for
acute toxicity. Water Res. 3:793-821.
Birdie, A.L., Wolff, C.J.M., and Winter, M. (1979). The acutetoxicity of some petrochemicals to goldfish. Water
Res.13:623-626.
staticLeuciscus idus
48 h
7505-11,300 mg/L
no datano datano data
Test method similar to: U.S. EPA: Methods for acute toxicity
tests with fish, macroinvertebrates, and amphibians. EPA660/3-75-009. Committee on methods for toxicity tests withaquatic organisms, 1975.
Juhuke, I. and Luedemann, D. (1978). Results of the study of
200 chemical compounds on acute toxicity using the golden
orfe test. Z. Wasser Abwasser Forsch. 11:161-164.
flow throughPimephales promelas
1h6210-8030 mg/L
yes
no datano data
Test method similar to U.S. EPA: Methods for acute toxicity
test with fish, macroinvertebrates, and amphibians. EPA660/3-75-009. Committee on Methods for Toxicity Test with
Aquatic Organisms, 1975.
Results of 3 test runs are as follows (LC50 in mg/L):
24-h: 8830, 9400, 8030
48-h: 8290, 8880, 7940
UNEP Publications

OECD SIDS

Test substance
Reference

4.2

ACETONE72-h: 8120, 7940, 6400
96-h: 8120, 7280, 6210
minimum purity 90%; analysis of test article in water from fish
exposure tanks.
Brooke, L.T., Call, D.J., Geiger, D.L., and Northcott, C.E.
(1984). Acute toxicities of organic chemicals to fatheadminnows (Pimephales promelas). Center for Lake Superior
Environmental Studies. University of Wisconsin - Superior.
pp. 319.

Acute Toxicity - Aquatic Invertebrates
Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReferenceSpecies
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReferenceSpecies
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReference

Daphnia magna
48 h12,600 & 12,700 mg/L (two laboratories)
no datano datano data
Tests conducted according to a protocol from the Dutch
Standard Institute (Adema, 1978).
Canton, J.H. and Adema, D.M.M. (1978). Repro-ducibility ofshort-term and reproduction toxicity experiments with Daphnia
magna and comparison of the sensitivity of Daphnia magnawith Daphnia pulex and Daphnia cucullata in short-term
experiments. Hydrobiologia 59:135-140.
Daphnia pulex
48 h8800 mg/L
no datano datano data
Tests conducted according to a protocol from the Dutch
Standard Institute (Adema, 1978).
Canton, J.H. and Adema, D.M.M. (1978). Repro-ducibility ofshort-term and reproduction toxicity experiments with Daphnia
magna and comparison of the sensitivity of Daphnia magnawith Daphnia pulex and Daphnia cucullata in short-term
experiments. Hydrobiologia 59:135-140.
Daphnia cucullata
48 h7635 mg/L
no datano datano data
Tests conducted according to a protocol from the Dutch
Standard Institute (Adema, 1978).
Canton, J.H. and Adema, D.M.M. (1978). Repro-ducibility ofshort-term and reproduction toxicity experiments with Daphnia
magna and comparison of the sensitivity of Daphnia magna
UNEP Publications

67

OECD SIDSACETONEwith Daphnia pulex and Daphnia cucullata in short-term
experiments. Hydrobiologia 59:135-140.

Species
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReferenceSpecies
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReferenceSpecies
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReferenceSpecies
Exposure Period
LC50
Analyt. Monitoring
GLP
68

Daphnia magna
48 h13,500 mg/L
no datano datano data
Procedure used individuals 12-hours old. The test water wasfrom a local spring-fed pond with an average hard-ness 154.5
mg/L, pH of 7.7, and temperature of 22°C.
Randall, T.L. and Knopp, P.V. (1980). Detoxification of
specific organic substances by wet oxidation. J. Water Pollut.
Control Fed. 52:2117-2130.
Daphnia magna
24 h>10,000 mg/L
no datano datano data
Procedure used individuals 24-hours old. Test used tap water
free of chlorine, saturated with oxygen, hardness 16 (German),
pH 7.6-7.7, temperature 20-22°C.
Bringmann, V.G. and Kuhn, R. (1977). Results of thedamaging effect of water pollutants on Daphnia magna. Z.
Wasser Abwasser Forsch. 10:161-166.
Daphnia pulex
18 h1550 mg/L
no datano datano data
Test containers selected for compatibility with the size of thetest organism. Duplicate test chambers with 10-12
concentrations. Test duration was 18 hours of which 16 hours
were fluorescent illumination. Water temperature 23°C plus orminus 2°C. No supplemental food or air.
Bowman, M.C., Oller, W.L., and Cairns, T. (1981). Stressedbioassay systems for rapid screening of pesticide residues. Part
I: Evaluation of bioassay systems. Arch. Environ. Contam.
Toxicol. 10:9-24.
Culex restuans (white-dotted mosquito)
18 h7840 mg/L
no datano data
UNEP Publications

OECD SIDS
Test substance
RemarkReferenceSpecies
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReferenceSpecies
Exposure Period
EC50
Analyt. Monitoring
GLP
Test substance
Test method
RemarkResultReferenceSpecies
Exposure Period
LC50

ACETONEno data
Test containers selected for compatibility with the size of thetest organism.
Duplicate test chambers with 10-12
concentrations. Test duration was 18 hours of which 16 hours
were fluorescent illumination. Water temperature was 23°C
plus or minus 2°C. No food or air added.
Bowman, M.C., Oller, W.L., and Cairns, T. (1981). Stressedbioassay systems for rapid screening of pesticide residues. Part
I: Evaluation of bioassays systems. Arch. Environ. Contam.
Toxicol. 10:9-24.
Hyalella azteca
18 h3520 mg/L
no datano datano data
Test containers selected for compatibility with the size of thetest organism. Duplicate test chambers with 10-12
concentrations. Test duration was 18 hours of which 16 hours
were fluorescent illumination. Water temperature was 23°C
plus or minus 2°C. No food or air added.
Bowman, M.C., Oller, W.L., and Cairns, T. (1981). Stressedbioassay systems for rapid screening of pesticide residues. Part
I: Evaluation of bioassay systems. Arch. Environ. Contam.
Toxicol. 10:9-24.
Lithodes antarcticus (southern king crab, larval stage)
120-192 h.
1010-4660 mg/L
no datano dataas prescribed by 1.1-1.4
American Public Health Association for Static Bioassay
Procedures (APHA, AWWA, WPCF) 1976.
The mortality curve of larvae exposed to 7500 mg/L acetone(acetone controls) did not differ from that of seawater controls.
Results as LC50 in mg/L are as follows:
120-h: 4660
144-h: 3880
168-h: 2330
192-h: 1010
Lombardo, R.J., Ferrari, L., and Vinuesa, J.H. (1991). Effects
of lindane and acetone on the development of larvae of thesouthern King Crab (Lithodes antarcticus). Bull. Environ.
Contam. Toxicol. 46:185-192.
Streptocephalus rubricaudatus
24 h64,300 mg/L
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Analyt. Monitoring
GLP
Test substance
RemarkReferenceSpecies
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReference

4.3

no datano datano data
The hatching and 24-h toxicity test procedure used dry-stored
cysts of S. rubricaudatus (originating from Algeria). Hatching
was obtained by hydrating dried cysts in a petri dish in U.S.
EPA freshwater medium (1985). After 18 hours incubation (at25°C), the free-swimming larvae were pipet-transferred into asecond petri dish for a supplemental period of 6 h. The test
endpoint was death, defined by the complete lack of movement
during 10 seconds of observation under a dissection
microscope.
Crisinel, A., Delaunay, L., Rossel, D., and Tanadellas, J.
(1994). Cyst-based ecotoxicological tests using Anostracans:comparison of two species of Streptocephalus. Environ.
Toxicol. Water Qual. 9:317-326.
Daphnia magna
48 h104,712 mol/L
no datano datano dataAge of test organism was less than 2 days; number of test
organisms per group was 25; test volume was 1 L; temperature
was 22°C plus or minus 1°C; hardness was approximately
equal to one.
Hermens, J., Cantor, H., Janssen, P., and DeJong, R. (1984).
Quantitative structure-activity relationships and toxicity
studies of mixtures of chemicals with anesthetic potency: acutelethal and sublethal toxicity to Daphnia magna. Aquatic
Toxicol. 5:143-154.

Toxicity to Aquatic Plants e.g. Algae
Species
Endpoint
Analyt. Monitoring
GLP
Test substance
RemarkMethod70

ACETONE

Chlorella pyrenoidosa
see below
no datano datano data
Also tested was the green algae, Scenedesmus quadricauda.
Photosynthesis was used as the test criterion and wasquantified by monitoring the uptake of 14CO2 from NaH14CO3,
as previously described by Stratton et al. (1980). Acetone
alone was not inhibitory to either S. quadricauda or C.
pyrenoidosa. Photosynthetic activity in these species was
stimulated above 0.2% acetone while stimulatory activity
increased 30-40% at an acetone concentration of 1.0%.
Method similar to: Stratton, G.W. et al. (1980). Bull. Environ.
Contam. Toxicol. 24:562.
UNEP Publications

OECD SIDSACETONE

Reference

Stratton, G.W. and Corke, C.T. (1981). Interactions between
acetone and two pesticides toward unicellular green algae.
Bull. Environ. Contam. Toxicol. 27:13-16.

Species
Endpoint
Exposure Period
EC50
Analyt. Monitoring
GLP
Test substanceExposure Period
RemarkChlorella pyrenoidosa
growth rate
14 day3020 mg/L
no datano datano data
10-14 days.
Growth was monitored by following the increase in opticaldensity over time for 10-14 days using a spectrophotometerequipped with a universal test tube adapter and appropriate
filters. Effects of acetone were assayed against the growth of
C. pyrenoidosa at five to ten concentrations ranging from 0.1%
to 6.0%.
Stratton, W.S. and Smith, T.M. (1988). Interaction of organic
solvents with the green alga Chlorella pyrenoidosa. Bull.
Environ. Contam. Toxicol. 40:736-742.

ReferenceSpecies
Endpoint
Analyt. Monitoring
GLP
Test substance
Remarkeference

Species
Endpoint
Analyt. Monitoring
GLP
Test substance
MethodRemarkChlorella pyrenoidosa
Effects on membrane integrity and cell leakage
no datano datano data
Acetone-induced leakage from C. pyrenoidosa was monitored
by following the loss of carbon compounds from cells using
radioisotopic techniques. The cells were radiolabeled
photosynthetically using 14C-sodium bicarbonate. Significant
leakage occurred at 1.5% and lower (depending on the
exposure period (i.e., 24, 48, or 96 h).
Stratton, G.W. (1989). Effect of the solvent acetone on
membrane integrity in the green alga, Chlorella pyrenoidosa.
Bull. Environ. Contam. Toxicol. 42:754-760.
Anabaena inaequalis
photosynthetic ability
no datano datano data
Cells were incubated for 2 h and harvested by filtration
through 0.45 m membrane filters. Photosynthetic changes
were noted by monitoring the uptake of 14CO2 from
NaH14CO3. The amount of radioactivity incorpor-ated into thecells was determined using a liquid scintillation counter.
Percent inhibition was calculated. Anabaena cylindrica andAnabaena variabilis also examined.
A. inaequalis photosynthetic activity was significantly alteredat acetone concentrations of 1000 mg/L and 4000 mg/L, where
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ReferenceSpecies
Endpoint
Analyt. Monitoring
GLP
Test substance
MethodRemarkReferenceSpecies
Endpoint
Analyt. Monitoring
Year
GLP
Test substance
RemarkResultReferenceSpecies72

ACETONE
stimulation was observed. A. variabilis photosynthesis was
significantly stimulated by acetone concentrations below
10,000 mg/L. No significant stimulation of 14CO2 uptake
occurred with A. cylindrica, although inhibition was observed
above 6000 mg/L acetone. Inhibition was 75% at 8000 mg/L
and 95% at 10,000 mg/L.
Stratton, G.W., Burrell, R.E., Krup, M.L., and Corke, C.T.
(1980). Interactions between the solvent acetone andpyrethroid insecticide permethrin on activities of the bluegreen alga Anabaena. Bull. Environ. Contam. Toxicol. 24:562569.
Anabaena inaequalis
nitrogen fixation ability
no datano datano data
Assayed using the acetylene reduction technique. After the
addition of a 10% atmosphere of acetylene, the cells wereincubated for 5 h and the ethylene produced was assayed bygas chromatography. A. variabilis was not included in thesestudies due to its inability to fix nitrogen. Anabaena cylindricaand Anabaena variabilis were also examined
A. inaequalis activity was stimulated by all acetone
concentrations from 1000 mg/L to 10,000 mg/L. The degree ofstimulation was greater than that observed in photosynthetic
studies. A. cylindrica exhibited significantly increased
acetylene reduction at levels of acetone less than 4000 mg/L
and decreased significantly at levels greater than 5000 mg/L.
Stratton, G.W., Burrell, R.E., Krup, M.L., and Corke, C.T.
(1980). Interactions between the solvent acetone andpyrethroid insecticide permethrin on activities of the bluegreen alga Anabaena. Bull. Environ. Contam. Toxicol. 24:562569.
Skeletonema costatum
growth sensitivity
no data1988
no datano dataS. costatum was cultured in growth medium to achieve theselected density of 100,000 cells/mL. Total cell count and total
cell volume were measured by use of a Coulter counter.
Classified as practically nontoxic (> 100 mg/L).
Cowgill, U.M., Milazzo, D.P., and Landenberger, B.D. (1989).
Toxicity of nine benchmark chemicals to Skeletonema
costatum, a marine diatom. Environ. Toxicol. Chem. 8:451455.
Scenedesmus quadricauda
UNEP Publications

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Endpoint
Analyt. Monitoring
GLP
Test substance
RemarkResultReference

4.4

ACETONE
toxicity thresholdno datano datano data
Additional Species tested was Microcystis aeruginosa. Test
cultures prepared from the dilution series and the control
cultures were kept under standardized conditions for 8 days
with constant lighting at 27 °C. Cultures were shaken daily andthe concentration of the algal suspen-sions of each test culture
was measured turbidimetrically.
The chemical concentration causing the onset of cell
multiplication inhibition was defined as the toxicity threshold.
The toxicity threshold was 7500 mg/L for S. quadricauda and530 mg/L for M. aeruginosa.
Bringmann, G. and Kuhn, R. (1978). Testing of substances fortheir toxicity threshold: model organisms Microcystis(Diplocystis) aeruginosa and Scenedesmus quadricauda. Mitt.
Internat. Verein. Limnol. 21:275-284.

Toxicity to Bacteria
TypeSpecies
Exposure Period
LC50
Analyt. Monitoring
GLP
Test substance
RemarkReference

Type
Species
Endpoint
Exposure Period
Analyt. Monitoring
GLP
Test substance
RemarkResultaquatic
Paramaecium caudatum
4h
6800 mg/L
no datano datano data
Method described in: Stressed bioassay systems for rapid
screening of pesticide residues. I. Evaluation of bioassay
systems. Environ. Contam. Toxicol. 10:9-24. (1981).
Rajini, P.S., Krishnakumare, M.K., and Majunder, S.K. (1989).
Cytotoxicity of certain organic solvents and organophosphorus
insecticides to the ciliated protozoan Paramecium caudatum.
Microbios 59:157-163.
other
Uronema parduzci
toxicity threshold
20 h
no datano datano data
The protozoan test Species was fed with pure inactive culturesof E. coli to avoid metabolism of the test article by thebacteria. The test period for determination of a toxicity
threshold was 20 h. Quantification of bacteria (food) andprotozoa (test species) was done by cell counter. A 5%
difference in protozoan cell count between test article andcontrol was used to determine the toxicity threshold.
Result is given as a toxicity threshold of 1710 mg/L.
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Reference

Bringmann, G. and Kuhn, R. (1980). Determination of theharmful effect of water pollutants on protozoa. II.
Bacteriovorous ciliates. Z. Wasser Abwasser Forsch. 13:26-31.

TypeSpecies
Endpoint
Exposure Period
Analyt. Monitoring
GLP
Test substance
Remarkother
Chilomonas paramecium
toxicity threshold48 hno datano datano data
The flagellate saprozoic protozoan test species was fed pure
inactive cultures of E. coli to avoid metabolism of the test
article by the bacteria. The test period for determination of a
toxicity threshold was 48 h. Quantification of bacteria(food)and protozoa (test species) was by electronic cell counter. A
5% difference in protozoan cell count between test Species andcontrols was used to determine the toxicity threshold.
Result is reported as a toxicity threshold of 3516 mg/L.
Bringmann, G. and Kuhn, R. (1980). Determination of
biological damage from water pollutants to protozoa. III.
Saprozoic flagellates. Z. Wasser Abwasser Forsch. 13:170173.

ResultReference

Type
Species
Exposure Period
Analyt. Monitoring
GLP
Test substance
RemarkResultReference

Type
Species
Endpoint
Analyt. Monitoring
GLP
Test substance74

ACETONEother
Entosiphon sulcatum
72 h
no datano datano data
The protozoan test Species was fed pure inactive cultures of E.
coli to avoid metabolism of the test article by the bacteria. The
test period for determination of a toxicity threshold was 72 h.
Quantification of bacteria (food) and flagellates (test species)
was performed by electronic cell counter. A 5% difference inprotozoan cell count between test species and controls wasused to determine the toxicity threshold.
Result is reported as a toxicity threshold of 28 mg/L.
Bringmann, G. and Kuhn, R. (1978). Determination of thebiological toxicity of water-bound substances towards
protozoa. I. Bacteriovorous flagellates (model organism:
Entosiphon sulcatum). Z. Wasser Abwasser Forsch. 11:210215.
aquatic
Pseudomonas putida
oxygen uptake
no datano dataas prescribed by 1.1-1.4
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RemarkResultReference

Type
Species
Endpoint
Analyt. Monitoring
GLP
Test substance
RemarkResultReference

Type
Species
Exposure Period
IC50
Analyt. Monitoring
GLP
Test substance
RemarkReference

ACETONE
Oxygen uptake was measured over a 10-min. period at 27°C
before, during, and after sample addition. Growth was
determined by inoculating P. putida into medical flats andincubating at 27°C. Thirty minutes before inoculation withacetone, the test cultures were diluted with fresh medium to adensity with an absorption of approximately 0.8 at 600 m
measured spectrophotometrically. The test solutions wereredistributed to medical flats, acetone added, and incubated for6 hours at 27°C. Growth was terminated by formalin addition
and immediately followed by density measurements.
Oxygen uptake over 10 min (EC10) was 1380 mg/L. Growth
inhibition over 7 h (EC10) was 540 mg/L.
Slabbert, J.L. and Grabow, W.O.K. (1986). A rapid water
toxicity screening test based on oxygen uptake of
Pseudomonas putida. Toxicity Assess. 1:13-26.
aquatic
Escherichia coli
minimal inhibitory concentrations (MIC)no datano datano data
Test Species was a mutant strain with enhanced sensitivity to awide spectrum of toxic substances. The assay is based on theability of toxicants to inhibit the de novo synthesis of an
inducible enzyme, e.g., β-galactosidase, by a rough mutant of
E. coli, which is highly sensitive to a wide spectrum of toxic
substances.
The minimal inhibitory concentration (MIC) was 25,000 mg/L
(defined as the concentration causing 20% toxicity).
Reinhartz, A., Lampert, I., Herzberg, M., and Fish, F. (1987).
A new short-term sensitive bacterial assay kit for the detectionof toxicants. Toxicity Assess. 2:193-206.
aquatic
Polytox (proprietary blend of 12 aerobic bacteria strains)
6h48,000 mg/L
no datano datano data
The percent inhibition at different concentrations of acetone
was based on the reduction in oxygen uptake rate of spiked
reactors compared to that of the control reactor. Plottedagainst the respective concentrations, the concentration
causing 50% inhibition or IC50 was determined.
Nirmalakhandan, N., Arulgnanendran, V., Mohsin, M., Sun,B., and Cadena, F. (1994). Toxicity of mixtures or organic
chemicals to microorganisms. Water Res. 28:543-551.

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Type
Species
EC50
Analyt. Monitoring
MethodYear
GLP
Test substance
RemarkResultReference

ACETONEaquatic
activated sludge of a predominantly domestic sewage
77.4 mg/L
no data
ISO 81921991
no dataas prescribed by 1.1-1.4
Activated sludge of a predominantly industrial sewage wasalso tested.
EC50 for the industrial/synthetic sewage was 59.4 mg/L.
Kilroy, A.C. and Gray, N.F. (1992). The toxicity of fourorganic solvents commonly used in the pharmaceuticalindustry to activated sludge. Water Res. 26:887-892.

Type
Species
Exposure Period
EC50
Analyt. Monitoring
MethodGLPTest substance
Reference

aquatic
activated sludge
16 h>5000 mg/L
no data
OECD Guideline 209
no datano data
Alsop, G.M., Waggy, G.T., and Conway, R.A. (1980).
Bacterial growth inhibition test. J. Water Pollut. Control Fed.
52:2452-2456.

Type
Species
Exposure Period
EC50
Analyt. Monitoring
MethodGLPTest substance
Reference

aquatic
activated sludge of a predominantly domestic sewage
3h>1000
no data
OECD Guideline 209
no dataas prescribed by 1.1-1.4
Klecka, G.M. and Landi, L.P. (1985). Evaluation of the OECD
activated sludge respiration inhibition test. Chemosphere
14:1239-1251.

4.5.2 Chronic Toxicity to Aquatic Invertebrates
Species
Endpoint
Exposure
EC50
Analyt. Monitoring
GLP
Test substance
Method76

Lithodes antarcticus
mortality
7 day>0.75 g/L
no datano dataas prescribed by 1.1-1.4
Theexperiments
were
conducted
followingtherecommendations of the APHA, AWWA, WPCF Standard
Methods for the examination of water and wastewater, 14th
UNEP Publications

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RemarkReference

4.6

ACETONEed., Am. Pub. Health Assoc., Washington, D.C. 1976, i.e. 7day, 48-h static renewal. 8°C and 35 parts per thousand
salinity.
Mortality in the seawater controls was lower than 10% during
the first seven days of culture and the acetone controls (0.75g/L) did not show mortality above that of the seawater controls
during this period.
Lombardo, R.J., Ferrari, L., and Vinuesa, J.H. (1991). Effects
of lindane and acetone on the development of larvae of theSouthern King Crab (Lithodes antarcticus Jaquinot). Bull.
Environ. Contam. Toxicol. 46:185-192.

Toxicity to Terrestrial Organisms

4.6.2 Toxicity to Terrestrial Plants
Species
Endpoint
Exposure Period
NOEC
GLP
Test substance
RemarkMethodResultReferenceSpecies
Endpoint
Exposure Period
GLP
Test substance
MethodRemarkRaphanus sativus L. var. Champion 708 (radish)emergence and growth
7 day
100 mg/Lnono data
Also tested were Lactuca sativa L. var. 525 Ithaca M.T.O.
(lettuce) and Lolium perenne L. var. Manhattan (rye grass).
The bioassay was most similar to the blotter-sandwich
technique, and was designed to determine the dose-response
characteristics of acetone on the germination and early growthof three representative terrestrial plants during a 7-day
exposure period.
7-day NOEC for all three Species was 100 mg/L.
Gorsuch, J.W., Kringle, R.O., and Robillard, K.A. Chemical
effects on the germination and early growth of terrestrial plants(1990). In: Plants for Toxicity Assessment, ASTM STP 1091.
W. Wang, J.W. Gorsuch, and W.R. Lower, eds., pp. 49-58.
American Society for Testing and Materials. Philadelphia, PA.
Zea mays L. var. rugosa Bouaf
Total germination and percentage of normal seedlings
5 sec., 0.25, 0.50, 1.0, 2.0, 4.0, or 8.0 h; immersion in 100%
acetone.
no dataas prescribed by 1.1-1.4
The organic solvent infusion technique has been usedsuccessfully to improve germination.
Total germination and percentage of normal seedlings in both
cultivars (Florida Staysweet and Crisp-n-Sweet 710) weresignificantly decreased after 8 h of immersion in acetone.
Average seedling dry weight, however, did not decrease.
Results indicate that acetone could be used as an infusion
agent for fungicides in the seed of some sweet corn cultivars
without compromising seed germination or vigor.
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Reference

Hung, P.E. (1992). Infusion of shrunken-2 sweet corn seedwith organic solvents: effects on germination and vigor.
Horticult. Sci. 27:467-470.

Species
Endpoint
Exposure Period
Year
GLP
Test substance
MethodCucumis sativus (long green cucumber)
active dormancy - breaking factor
various
1993
no dataas prescribed by 1.1-1.4
Dormant and non-dormant seeds were immersed in acetone inglass-stoppered containers at 10°C for various time periods.
After treatment the seeds were allowed to air-dry for 24 h inopen petri dishes and then used in germination experiments.
Acetone was found not only to break the dormancy incucumber seeds, but also to prevent its induction by far-red
light. The data also show that prevention of dorm-ancy
development as well as breakage of dormancy by acetone areaccompanied by a change in the permeability of the cell
membrane of the perisperm-endosperm envelope around theembryo.
Amritphale, D., Dixit, S., and Singh, B. (1993). Effect ofacetone on the induction and breakage of secondary dormancy
in seeds of cucumber. J. Exp. Botany. 44:1621-1626.

RemarkReference

4.6.3

Toxicity Non-Mammalian Terrestrial Species
Species
Endpoint
Exposure Period
LC50
GLP
Test substance
MethodRemarkReference

4.7

Coturnix coturnix japonica
mortality
5 days>20,000 ppm
no dataas prescribed by 1.1-1.4
5-day dietary trial with 14-day old coturnix quail.
Total mortality was 0/45 at 5 days.
Hill, E. F. and Carmardese, M.B. (1986). Lethal dietary
toxicities of environmental contaminants and pesticides to
Coturnix. Patuxent Wildlife Research Center. Laurel, MD. pp.
22-23.

Biological Effects Monitoring
RemarkReference78

ACETONEThe bioaccumulation potential of a chemical in muscle tissue
from rainbow trout has been shown to be related to the octanol
water partition coefficient. The partition coefficient for acetoneof -0.24 indicates a high degree of water solubility and low
potential to bioaccumulate or biomagnify in the environment.
Paterson, S. and Mackay, D. (1989). Correlation of tissue,
blood and air partition coefficients of volatile organic
chemicals. Br. J. Ind. Med. 46:321-328.
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OECD SIDSACETONE
Neely, W.B., Branson, D.R., and Blau, G.E. (1974). Partition
coefficient to measure bioconcentration potential of organic
chemicals in fish. Environ. Sci. Technol. 8:1113-1115.

4.8

Biotransformation and Kinetics
Type
RemarkResultReference

Type
RemarkResultReference

Type
Remarkplant
The objective of the experiment was to determine if acetone
inhibitsthemutagenic
activityofpromutagenic
dimethylnitrosamine (DMN) and methylbutylnitrosamine in ahigher plant, Arabidopsis thaliana. Seeds were immersed for 3
hours at 25°C in 1 mL of acetone mixed with buffer for
pretreatment. They were then immersed for 3 hours at 25°C in
2 mL of the mixture containing the mutagens and acetone fortreatment. Following treatment, the seeds were rinsed for 30
min in distilled water and sown on soil in a greenhouse.
The frequency of mutations and the degree of sterility induced
by DMN was markedly reduced in the presence of acetone.
Gichner, T. and Veleminsky, J. (1986). Organic solvents
inhibit the mutagenicity of promutagens dimethyl-nitrosamineand methylbutylnitrosamine in a higher plant Arabidopsis
thaliana. Mutagenesis 1:107-109.
animal (Daphnia magna)
The hypothesis of constancy of the tissue residues in animals
treated with narcotic organic chemicals was tested bydetermining the effect of body length, time, and ambientconcentration on tissue concentration in Daphnia magna
narcotized by exposure to toxic levels of acetone.
The lower than expected toxicity of acetone may be due to thedegradation of this chemical by Daphnia. Acetone, a simple
organic compound, may be readily metabolized by Daphnia.
As a result, some of the radioactivity in Daphnia tissues would
be associated with accumulated metabolites rather than theoriginal compound, and the narcotizing body burdens ofacetone would be over-estimated. Acetone did not exert asignificant negative influence on the effective internal
concentration. When predicted body burdens for acetone were
calculated using mean body sizes, exposure concentrations,and exposure durations, body burden acetone residues of 115
mmole/kg were more than an order of magnitude from theoverall mean for all narcotics tested.
Pawlisz, A.V. and Peters, R.H. (1993). A test of theequipotency of internal burdens of nine narcotic chemicals
using Daphnia magna. Environ. Sci. Technol. 27:2801-2806.
otherThis paper reports the results of a research program concernedwith the analyses and explanation of differences in sensitivityof species to toxic substances using biological properties of thespecies. The project aims at the development of predictive
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ResultReference

Type
RemarkReference

Type
RemarkReference

4.9

80

ACETONEmodels, which, in analogy to QSARs, are called Quantitative
Species Sensitivity Relationships. The distributions of acutetoxicity data of different Species were studied for 26
chemicals.
Chemicals with a specific mode of action have large sensitivity
ratios whereas inert chemicals with lower toxicity have lower
ratios. Acetone had the lowest ratio of all twenty-six chemicals
studies.
Hoekstra, J.A., Vaal, M.A., Notenboom, J., and Sloof, W.
(1994). Variations in the sensitivity of aquatic species to
toxicants. Bull. Environ. Contam. Toxicol. 53:98-105.
plant (various species)
This paper describes experiments conducted to test the effects
of volatiles including (acetone) on seed deterioration during
seed storage. Seeds tested were lettuce, soybean, sunflower,
carrot, and rice. It has been shown that the yields of volatiles
such as acetone in soybean seeds increase during seeddevelopment and decrease to trace levels after reaching yellow
maturation. The authors showed in a preliminary study that theevolution of volatiles, such as acetone, is a widespread
phenomenon occurring in stored seeds. Many types of dry
seeds that were tested continued to evolve volatiles andaccumulate them during storage. Acetone was found to have
only slight deleterious effects on some species.
Zhang, M., Maeda, Y., Furihata, Y., Nakamaru, Y., and Esashi,
Y. (1994). A mechanism of seed deterioration in relation to thevolatile compounds evolved by dry seeds themselves. Seed
Sci. Res. 4:49-56.
aquatic (Daphnia magna)
This work examines the hypothesis that exposure of Daphnia
magna to sublethal levels of narcotic contam-inants including
acetone may affect subsequent sensitivity of animals. Prior
exposure (24 h) of Daphnia to sublethal levels of acetone had
no effect on their sensitivity to effective levels of thesechemicals. Effective burdens (24-h acute exposure) wereindependent of the sublethal body burdens (24-h sublethal
exposure) and of the sublethal water concentrations (p <0.025). These results imply that animals from polluted sites
should be no more resistant to high body residues of pollutants
than those from clean sites and that the toxicity of narcoticorganic compounds like acetone may be independent of thetime course of uptake.
Pawlisz, A.V. and Peters, R.H. (1995). Effects of sublethal
exposure on lethal body burdens of narcotic organic chemicals
in Daphnia magna. Environ. Sci. Technol. 29:613-621.

Additional Reports

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RemarkReference

RemarkReference

RemarkReference

RemarkReference

RemarkACETONEThe objective of this paper is to compare the usefulness of arepresentative of the Urodela (Ambystoma mexicanum) andAnura (Xenopus laevis) species as biological indicators intoxicological bioassays. Toxicity test conditions were as
follows: static, 1-L size, 20°C plus or minus 1°C, circadianlight and dark schedule, 48-h exposure for acetone. The 48-h
LC50 for A. mexicanum was 20,000 mg/L and the over 48-h
LC50 for A. laevis was 24,000 mg/L.
Sloaff, W. and Baesselman, R. (1980). Comparison of theusefulness of Mexican Axolotl (Ambystoma mexicanum) andthe clawed toad (Xenopus laevis) in toxicological bioassays.
Bull. Environ. Contam. Toxicol. 24:439-443.
The effects of acetone on the growth of four fungi were
determined to be as follows: EC50 for Polyporous hirsutus was
greater than 2.0%, Pestalotia sp. was 1.25%, Sclerotinia
homeocarpa was 0.88%, and Fusarium oxysporum was 1.8%.
It was concluded that acetone was a moderately fungitoxic
compound, but the specific mode of action was not elucidated.
Burrell, R.E. and Corke, C.T. (1980). Interactions of thesolvent acetone with the fungicides benomyl and captan infungal assays. Bull. Environ. Contam. Toxicol. 25:554-561.
This paper provides the 96-h TLm (50% survival) for Lepomis
macrochirus (bluegill sunfish) of 8300 ppm and the 120-h TLm(50% reduction in number of cells produced) for the diatom
Nitzschia linearis (widely distributed in unpolluted soft fresh
waters of the U.S.) of 11,493-11,727 ppm acetone.
Patrick, R., Cairns, J., and Scheir, A. (1968). The relative
sensitivity of diatoms, snails, and fish to twenty common
constituents of industrial wastes. Progressive Fish Culturist
30:137-140.
Acetone is often used as a carrier solvent in aquatic bioassays
at 100 ppm without affecting the evaluation of the test article.
This paper provides comparative chronic data for Daphnia
magna and Pimephales promelas. Endpoints evaluated include:
survival of adults, number of young per adult, primiparous
instar, days to primiparous instar, and total number of broods
for the daphnid. Fish endpoints included: embryo survival,
hatching rate, larval survival, length and weight. Differences
between the solvent control (acetone and dilution water) andcontrol dilution water were minimal.
McCarthy, J.F. and Whitmore, D.K. (1985). Chronic toxicity
of di-n-butyl and di-n-octyl phthalate to Daphnia magna andthe fathead minnow. Environ. Toxicol. Chem. 4:167-179.
Static acute and flow-through toxicity tests were performed
with Daphnia magna. The 48-h LC50 value for acetone was
39,000 µL/L. The maximum acceptable toxicant
concentrations determined during the chronic toxicity test with
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Reference

RemarkReference

RemarkResultReference

Remark82

ACETONE
acetone were between 1400 and 2800 µL/L. Acetone wassufficiently low in toxicity to suggest that the recommended
usage limits for acetone as a co-solvent (500 µL/L during
acute toxicity tests; 100 µL/L during chronic toxicity tests).
LeBlanc, G.A. and Surprenant, D.C. (1983). The acute andchronic toxicity of acetone, dimethylformamide, andtriethylene glycol to Daphnia magna (Straus). Arch. Environ.
Contam. Toxicol. 12:305-310.
A multi-species test procedure was used to measure the acuteaquatic effects of acetone on seven aquatic species
simultaneously: Asellus intermedius (pillbug), Daphnia magna(water flea), Dugesia tigrina (flatworm), Gammarus fasciatus(sideswimmer), Helisoma trivolvis (snail), Lumbriculus
variegatus (segmented worm) and Pimephales promelas(fathead minnow). These species were chosen because of theirecological importance diversity, and amenability to laboratory
culturing. The 96-h static LC50 for all species was > 100 mg/L.
Ewell, W.S., Gorsuch, J.W., Kringle, R.O., Robillard, K.A.,
and Spiegel, R.C. (1986). Simultaneous evolution of the acuteeffects of chemicals on seven aquatic species. Environ.
Toxicol. Chem. 5:831-840.
The test species was Xenopus laevis and the endpoint was theminimum concentration inhibiting growth. The method was thefrog embryo teratogenesis assay Xenopus (FETAX), as
described by Damont et al. (1983). The 96-h bioassay
determines the relative teratogenic potential. The purpose ofthis experiment was to determine whether carrier solvents
interacted with the teratogens t-retinoic acid and 6aminonicotinamide to affect survival, development, andgrowth of Xenopus embryos.
The 96-h minimum concentrations that inhibited growth were:
18,000 mg/L for trial 1, 15,000 mg/L for trial 2, and 10,000
mg/L for trial 3.
Rayburn, J.R. Fort, D.J., McNew, R., and Bantel, J.A. (1991).
Synergism and antagonism induced by three carrier solventswith t-retinoic acid and 6-aminonico-tinamide using FETAX.
Bull Environ. Contam. Toxicol. 46:625-632.
The test species was Xenopus laevis and the endpoint was the
reproduction rate for 12 weeks post-hatch at 0.10% acetone.
The method uses groups of eggs that were put either in 800mL jars or 3-L glass containers and maintained in aerated tap
water at 22°C (plus or minus 1°C) under 16-h photoperiod
conditions. According to the volume of water the eggs werereared in groups of 10 or 25. After hatching, tadpoles were fed
Infusyl tablets. Each jar or tank was covered with a glass platein order to limit evaporation. Water was changed weekly.
Daily monitoring of egg and tadpole mortality was conducted
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ResultReference

ACETONEthroughout the first week of treatment. The metamorphosis
pattern was investigated on surviving tadpoles.
Growth by weight and development were slightly delayed inanimals at the beginning of treatment (premetamor-phosis).
After metamorphosis, the weight of juvenile Xenopus washigher than that of the water controls. It was speculated thatacetone might first delay develop-ment; then because of
feeding habits or other reasons, tadpoles could regain normal
weight gain and even show a tendency for increased growth.
Marchal-Segault, D. and Tamade, F. (1981). The effects oflindane, an insecticide, on hatching and postembryonicdevelopment of Xenopus laevis (Daudin) Anauran Amphibian.
Environ. Res. 24:250-258.

5. Toxicity
5.1

Acute Toxicity

5.1.1 Acute Oral Toxicity
TypeSpecies
Value
GLP
Test substance
ReferenceLD50
rat
ca. 5800 mg/kg
no datano data
Freeman, J.J. and Hayes, E.P. (1985). Acetone potentiation of
acute acetonitrile toxicity in rats. J. Toxicol. Environ. Health
15:609-621.

Type
Species
Value
GLP
Test substance
Reference

LD50
rat
ca. 8400 mg/kg
nono dataSmyth, H.F., Carpenter, C.P., Weil, C.S., Pozzani, U.C., andStriegel, J.A. (1962). Range-finding toxicity data: List VI. Am.
Ind. Hyg. Assoc. J. 23:95-107.

Type
Species
GLP
Test Substance
RemarkLD50
ratnoanalytical grade acetone (ACS specifications).
Groups of 6-12 male and female Sprague-Dawley rats ofvarious ages were intubated with neat acetone. They wereobserved for 1 week. LD50 values in g/kg (95% confidence
limits) were: newborn, 1.7 (1.3-3.0), 14-day-old, 4.4 (3.1-6.3),
young adults [80-160 g], 7.2 (5.4-9.5), older adults [300-470g], 6.7 (6.1-7.3).
Kimura, E.T., Ebert, D.M., and Dodge, P.W. (1971). Acutetoxicity and limits of solvent residue for sixteen organic
solvents. Toxicol. Appl. Pharmacol. 19:699-704.

Reference

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Type
Species
Value
GLP
Test substance
RemarkReference

ACETONELD50
mouse
ca. 5250 mg/kg
no datano data
Male ddY mice weighing 24-27 g were intubated with acetone
following ip injection of 0.16 mL of olive oil/g. LD50 value of5250 mg/kg was reported with a 95% confidence range of3580-7700 mg/kg.
Tanii, H., Tsuji, H., and Hashimoto, K. (1986). Structuretoxicity relationship of monoketones. Toxicol. Lett. 30:13-17.

5.1.2 Acute Inhalation Toxicity
TypeSpecies
Exposure Time
Value
GLP
Test substance
RemarkReference

Type
Species
GLP
Test substance
RemarkReference

LC0
rat
30 minute16,000 ppm
nono data
Female rats were exposed (whole body exposure) to acetone atnominal air concentrations of the following: 6/6 rats died at
32,000 ppm; 1/6 animals exposed to 16,000 ppm acetone for 4
hours also died.
Smyth, H.F., Carpenter, C.P., Weil, C.S., Pozzani, U.C., andStriegel J.A. (1962). Range-finding toxicity data: List VI.
Am. Ind. Hyg. Assoc. J. 23:95-107.
LC50
rat
no
no data
LC50 values with 95% confidence intervals for 4-hr and 8-hr
exposures were 32,000 ppm (27,400-37,200) and 21,000 ppm(17,900-24,800). Exposure was to female Carworth FarmsNelson rats.
Pozzani, U.C., Weil, C.S., and Carpenter, C.P. (1959). The
toxicological basis of threshold limit values: 5. The
experimental inhalation of vapor mixtures by rats, with notes
upon the relationship between single dose inhalation and single
dose oral data. Am. Ind. Hyg. Assoc. J. 20:364-369.

5.1.3 Acute Dermal Toxicity
TypeSpecies
Value
GLP
Test substance84

LD0
rabbit>7400 mg/kg
nono data
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RemarkReference

Type
Species
Value
MethodGLPTest substance
RemarkReference

Type
Species
Value
GLP
Test substance
RemarkReference

5.2.

ACETONE
Exposure time was 24 hours. Both sexes were used; skin wasabraded. Test substance was "practical" grade.
Roudabush, R.L., Terhaar, C.J., Fassett, D.W., and Dziuba,
S.P. (1965). Comparative acute effects of some chemicals on
the skin of rabbits and guinea pigs. Toxicol. Appl. Pharmacol.
7:559-565.
LD0guinea pig> 7400 mg/kg
othernono data
Male Hartley-derived guinea pigs were used; abraded andintact skin was exposed for 24 h to a "practical" grade ofacetone.
Roudabush, R.L., Terhaar, C.J., Fassett, D.W., and Dziuba,
S.P. (1965). Comparative acute effects of some chemicals on
the skin of rabbits and guinea pigs. Toxicol. Appl. Pharmacol.
7:559-565.
LD50
rabbit>15,700 mg/kg
nono data
Exposure was for a 24-h period. The hair was completely
clipped from the trunk of four male albino rabbits. The dose
was injected under an impervious plastic film (method ofDraize et al., J. Pharmacol. Exp. Therap. 82:377, 1944).
Animals were observed for 14 days.
Smyth, H.F., Carpenter, C.P., Weil, C.S. (1962). Rangefinding toxicity data: List VI. Am. Ind. Hyg. Assoc. J. 23:95107.

Corrosiveness and Irritation

5.2.1 Skin Irritation
SpeciesResultClassification
GLP
Test substance
RemarkReference

rabbitnot irritating
not irritatingnono data
Exposure time was 24 h. Acetone, 0.01 mL, was applied to theshaved stomach of 5 rabbits.
Smyth, H.F., Carpenter, C.P., and Weil, C.S. (1962). Rangefinding toxicity data: List VI. Am. Ind. Hyg. Assoc. J. 23:95107.

5.2.2 Eye Irritation
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SpeciesResultClassification
GLP
Test substance
MethodResults

Reference

ACETONErabbithighly irritating
irritatingnono data
20 µL of acetone was added to the center of cornea and the eye
was read 18-24 h later and scored after staining withfluorescein.
The dose administered was 15.8 mg. Acetone was assigned arating of Grade 5 in system with maximum of Grade 10. The
10-grade ordinal series is based upon the degree of corneal
necrosis that results from instillation of various volumes andconcentrations of a chemical. Grade 1 indicates at most a verysmall area of necrosis resulting from 0.5 mL of undiluted
chemical in the eye. Grade 5 indicates a severe burn from0.005 mL, and grade 10 indicates a severe burn from 0.5 mL of
a 1% solution in water or propylene glycol.
Carpenter, C.P. and Smyth, H.F. (1946). Chemical burns of the
rabbit cornea. Am. J. Ophthamol. 29:1363-1372.
Smyth, H.F., Carpenter, C.P., and Weil, C.S. (1962). Rangefinding toxicity data: List VI. Am. Ind. Hyg. Assoc. J. 23:95107.

SpeciesResultClassification
MethodGLPTest substance
RemarkReference

rabbithighly irritating
irritating
Draize Test
no datano data
0.1 mL of acetone was placed in the conjunctival sac and theeye was scored at 24 h. The data from this study indicate that
corneal thickening is directly related to eye irritation anddamage (r=0.86). Acetone eye swelling (215%) was rated assevere. Irritancy ratings for aqueous solutions were: 3, 10, and
30% acetone, mild irritation; 1% acetone, mild/slight irritation;
corneal thickening ratings for 1, 3, 10, and 30% aqueous
acetone solutions were all mild.
Kennah, H.E.. Hignet, S., Laux, P.E., Dorko, J.D., and Barrow,
C.S. (1989). An objective procedure for quantifying eye
irritation based upon changes of corneal thickness. Fund. Appl.
Toxicol. 12:258-268.

5.3 Sensitization
Type
SpeciesResultClassification
GLP
86

Mouse ear swelling test
mouse
not sensitizing
not sensitizing
no data
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Test substance
MethodRemarkResultReference

ACETONEno data
Following removal of hair with clippers, mice are injected
twice intradermally in the test area with Freund's complete
adjuvant. The mice are tape stripped in the application area,
and the chemical or solution (0.1 mL) is applied topically.
Stripping and application of the Test substance is repeated on
three additional consecutive days. Seven days later, 20 µL of
test compound or solution is applied to the left ear and 20 µLof the vehicle (if any) is applied to the right ear. Twenty-fourand 48-h later, the ear thicknesses are measured while theanimals are under light ether anesthesia.
This test was reported to have correctly identified 48/49 known
human sensitizers and 23/23 known human nonsensitizers. The
missed compound was a weak human sensitizer. Acetone wasalso not a sensitizer in a modified MEST that used a patch-testprocedure for the sensitization step.
Acetone was not a sensitizer in a similar mouse ear
sensitization test (Descotes, 1988) or in a modification of theguinea pig maximization test of Magnusson and Kligman(Nakamura et al., 1994).
Gad, S.C., Dunn, B.J., Dobbs, D.W., Reilly, C., and Walsh,
R.D.(1986). Development and validation of an alternative
dermal sensitization test: The mouse ear swelling test (MEST).
Toxicol. Appl. Toxicol. 84:93-114.
Descotes, J. (1988). Identification of contact allergens: The
mouse ear sensitization assay. J. Toxicol. Cutaneous Ocular
Toxicol. 7:262-272.
Nakamura, A., Momma, J., Sekiguchi, H., Noda, T., Yamano,T., Kaniwa, M., Kojima, S., Tsuda, M., and Kurokawa, Y.
(1994). A new protocol and criteria for quantitative
determination of sensitization potencies of chemicals by
guinea pig maximization test. Contact Dermatitis 31:72-85.

5.4

Repeated Dose Toxicity
Species
StrainSex
Route of Administration
Exposure Period
Frequency of Treatment
Post Exposure
Observation Period
Doses

Control Group
Methodmouse
B6C3F1male/female
drinking water
14 days and 13 weeks
ad libitumnone
14 days: 0.5, 1.0, 2.0, 5.0, and 10.0%; 5 mice/sex.
13-week females: 0.25, 0.5, 1.0, 2.0, and 5.0%; 10 mice each.
13-week males: 0.125, 0.25, 0.5, 1.0, and 2.0%; 10 mice each.
YesOECD Guideline 407
OECD Guideline 408 was used for the 13-week studies.
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GLP
Test substance
RemarkRemarkRemarkResultReferenceSpecies
StrainSex
Route of Administration
Exposure Period
Frequency of Treatment
Post Exposure
88

ACETONEyes
as prescribed by 1.1-1.4
NOEL: 1% (males: 14 days, 1579 mg/kg; 13 weeks,
2258 mg/kg; females: 14 days, 3023 mg/kg; 13 weeks,4156 mg/kg.
LOEL: 2% (males: 14 days, 3896 mg/kg; 13 weeks, 4858
mg/kg; females: 14 days, 5481 mg/kg; 13 weeks, 5945 mg/kg.
Mice, 6-7 weeks old at start of the study, were housed
individually. Drinking water containing acetone and NIH 07
feed were provided ad libitum. The time-weighted average
dosages were: 14-day males, 965, 1579, 3896, 6348, 10,314
mg/kg; 14-day females, 1569, 3023, 5481, 8804, 12,725
mg/kg; 13-week males, 380, 611, 1353, 2258, 4858 mg/kg;
13-week females, 892, 2007, 4156, 5945, 11,298 mg/kg. Body
weights were determined weekly and water consumption twice
weekly. At necropsy, liver, right kidney, right testis, heart,
thymus, brain, lungs, and, at 13 weeks only, spleen were taken
for determination of weights and histopathology. Blood
samples were obtained before the 13-week sacrifice formeasurement of hematological indices. Male reproductive
endpoints were assessed and stage and length of the estrous
cycle were evaluated in females.
Water consumption, and thus acetone dose, was reduced atacetone concentrations of 5% and above. There were no
deaths during the studies. Body weight gain was depressed inmice given 10% acetone in the 14-day study only. There wereno treatment-related clinical signs of toxicity. Absolute andrelative liver weights in female mice only were significantly
elevated in the 13-week 5% group; similar increases were seenin the 14-day animals. Hematological changes observed in the
13-week animals were increased hematocrit in 5% females (p< 0.01), increased hemoglobin in 2% (p < 0.05) and 5% (p <0.01) females and 0.5, 1.0, and 2% males (p < 0.05).
Histopathological alterations were seen only in mice during the
14-day studies; these included centrilobular hepatocellular
hypertrophy in 5 of 5 male mice in each of the 2, 5, and 10%groups, 2 of 5 females in the 5% group, and 5 of 5 females in
the 10% group. There were no changes in male or female
reproductive indices.
Dietz, D.D., Leininger, J.R., Rauckman, E.J., Thompson,
M.B., Chapin, R.E., Morrissey, R.L., and Levine, B.S. (1991).
Toxicity studies of acetone administered in the drinking waterof rodents. Fund. Appl. Toxicol. 17:347-360.
rat
Fischer 344
male/female
drinking water
14 days and 13 weeks
ad libitum
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Observation Period
Doses
Control Group
MethodGLPTest substance
RemarkRemarkResultACETONEnone
14-day: 0.5, 1.0, 2.0, 5.0, 10%; 5/sex/dose level.
13-week: 0.25, 0.5, 1.0, 2.0, 5.0%; 10/sex/dose level.
Yes
OECD Guideline 407
OECD Guideline 408 was used for the 13-week studies.
yes
as prescribed by 1.1-1.4
Rats, 6-7 weeks old at start of the study, were housed 5 per
cage. Drinking water containing acetone and NIH 07 feed
were provided ad libitum. The time-weighted average doses
were: 14-day males, 714, 1616, 2559, 4312, and 6942 mg/kg;
14-day females, 751, 1485, 2328, 4350, 8560 mg/kg; 13-weekmales, 200, 400, 900, 1700, and 3400 mg/kg; 13-weekfemales, 300, 600, 1200, 1600, and 3100 mg/kg. Body weights
were determined weekly and water consumption twice weekly.
At necropsy, liver, right kidney, right testis, heart, thymus,
brain, lungs, and, at 13 weeks only, spleen were taken for
determination of weights and histopathology. Blood samples
were obtained before the 13-week sacrifice for measurement ofhematological indices. Male reproductive endpoints wereassessed, and stage and length of the estrous cycle were
evaluated in females.
NOEL was 2% for 14-day (males: 2%, 2559 mg/kg; females:
5%, 4350 mg/kg); 1% for 13-week (males: 1%, 900 mg/kg;
females: 5%, 3100 mg/kg).
LOEL was 5% for 14-day (males: 5%, 4312 mg/kg; females:
10%, 8560 mg/kg); 2% for 13-week (males: 2%, 1700 mg/kg).
No deaths were seen during the study. Water consumption, andthus the acetone dose, was reduced in rats given 5% or greaterlevel of acetone. Body weights were depressed in male andfemale rats given 5 or 10% acetone in both the 14-day and 13week studies. There were no treatment-related clinical toxic
signs during the studies. During the 13-week study, relative
kidney (both sexes), liver (both sexes), and testis weights were
found in the 2 and 5% groups. Similar increases were reported
to have occurred in the 14-day study at the same or lower
doses (numbers not given). Hematological effects included
mild lymphocytosis in male rats at 2% and male and males at
5%, decreased erythrocyte counts and hemoglobin levels at 2
and 5% and reticulocyte counts at 0.5% in male rats, andincreased mean corpuscular hemoglobin and mean cell volume
at 1% and higher in males and in 5% females. Platelet counts
were mildly depressed in males and females in the 5% dosegroups.
Histopathologic lesions included bone marrow
hypoplasia in 5 of 5 male rats given 10% acetone in the 14-day
study. Dose-related increases in the incidence and severity ofnephropathy, similar to that seen in aging rats, were seen inmale rats. Minimal-to-mild splenic pigmentation was seen inmale rats at the 2% and 5% dose levels in the 13-week studies.
Acetone exposure of male rats for 13 weeks resulted in
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ReferenceSpecies
StrainSex
Route of Administration
Exposure Period
Frequency of Treatment
Post Exposure
Observation Period
Doses
MethodGLPTest substance
RemarkResult90

ACETONE
depressed sperm motility, cauda epididymal weight, andepididymal weight and an increased incidence of abnormal
sperm. There was no indication of changes in vaginal cytology
suggestive of changes in the estrous cycle.
Dietz, D.D., Leininger, J.R., Rauckman, E.J., Thompson,
M.B., Chapin, R.E., Morrissey, R.L., and Levine, B.S. (1991).
Toxicity studies of acetone administered in the drinking waterof rodents. Fund. Appl. Toxicol. 17:347-360.
rat
Sprague-Dawley
male/female
gavage93, 94, or 95 days (interim sacrifice at 46 or 47 days)
once/day
1 day
100, 500, 2500 mg/kg; 30 M/30 F per dose levelControl
Groupyes
OECD Guideline 408
yes
as prescribed by 1.1-1.4
Thirty male and 30 female 31-day-old rats were housed
individually. Animals were dosed once/day by oral gavage
with solutions of 0, 1.0, 5.0, or 25% acetone in reagent grade
water. Dosing volumes were adjusted weekly for body-weightchanges. Animals were dosed for 46-47 days (interim
sacrifice) or 93-95 days (final sacrifice). Retroorbital blood
samples and urine were collected prior to interim sacrifice of
10 males and 10 females from each group at 46-47 days and 20
males and 20 females from each group at 94-96 days (one day
after end of dosing period). Ophthalmic examinations wereconducted prior to study termination. Extensive grosspathological examination was performed at necropsy at whichtime organs were removed for determination of weights at final
sacrifice. Approximately 26 organs or tissues and all tissue
masses were removed at final necropsy and prepared forhistological examination.
One control female (day 85), one 100 mg/kg female (day 3),
two 2500 mg/kg males (days 6 and 36), and three 2500 mg/kg
females (days 3, 3, and 56) died during the study; deaths of 5of the 6 were ascribed to dosing errors. No toxicologicallysignificant effects on body weight or food intake were seen.
Clear salivation and clear salivation prior to dosing were seen
in both sexes in the 2500 mg/kg group. Hemoglobin,
hematocrit, and mean cell volume were significantly increasedin males of the 2500 mg/kg group at the interim sacrifice. At
the final sacrifice, hemoglobin, hematocrit, mean cell volume,and mean cell hemoglobin were significantly elevated in 2500
mg/kg males and hemoglobin and hematocrit in 2500 mg/kg
females. Statistically sig-nificant differences at final sacrifice
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ReferenceSpecies
StrainSex
Route of Administration
Exposure Period
Frequency of Treatment
Post Exposure
Observation. Period
Doses
Control Group
GLP
Test substance
RemarkACETONE
included decreased platelet count in 2500 mg/kg males,
increased mean cell volume in 500 mg/kg females, increased
alanine amino-transferase in 2500 mg/kg females at the interim
sacrifice and in males at the final sacrifice, depressed glucose
and potassium levels in 2500 mg/kg males at the final
sacrifice. Other statistically significant and nonsignificant
changes were reported in 2500 mg/kg males and females at the
final sacrifice, but these were not considered toxi-cologicallysignificant. Statistically significant organ weight changes
included increased kidney weights in 500 and 2500 mg/kg
females, increased kidney-to-body and -brain weight ratios formales and females in the 2500 mg/kg group, increased
liver/body weight ratio in 2500 mg/kg males, increased liver
weights, and liver-to-body and -brain ratios in 2500 mg/kg
females, depressed brain weights in 2500 mg/kg males, andincreased heart/brain weight ratio in 2500 mg/kg females.
Histopathological findings included renal proximal tubule
degeneration in control and exposed animals of both sexes andintracyto-plasmic droplets or granules (hyaline droplets ) in theproximal tubular epithelium in control and exposed animals,
predominantly in males. (Kidney lesions are expectedcomponents preceding the development of chronic progressive
glomerulonephtopathy, a common aging syndrome in SpragueDawley rats.) Although the incidence levels for both of theselesions were similar in control and exposed animals, theseverity of distribution was markedly altered with increasing
dose. In male rats, testicular interstitial edema was seen in bothcontrol and test animals with similar incidence and severity.
Reactive hyperplasia of the mesenteric and mandibular lymph
nodes and splenic granular pigmentation was seen morecommonly in 2500 mg/kg male rats; these increases were notstatistically or biologically significant.
Mayhew, D.A. and Morrow, L.D. (1988). Ninety-day gavage
study in albino rats using acetone. United States
Environmental Protection Agency Contract No. 68-01-7075.
American Biogenic Corporation Study 410-2313.
rat
Sprague-Dawleymaleinhalation
2, 4, and 8 weeks
3 h/day, 5 days/wk
2 weeks (following 8-week exposure only)
19,000 ppm; 9 animals (total)/time-of-exposure groupyes
no data
ACS Grade, Instr-Analyzed (J.T. Baker)
Groups of rats were exposed to 19,000 ppm of acetone for 3 h
per day. Exposures were repeated 5 times per week for 2, 4, or
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ResultReference

5.5

8 weeks. At 2, 4, and 8 weeks of exposure and 2 weeks
postexposure, groups of 5 exposed animals and 5 controls were
weighed and anesthetized (pentobarbital), and blood waswithdrawn for deter-mination of serum glutamic-oxaloacetictransaminase (SGOT, lactic dehydrogenase (LDH), and bloodurea nitrogen (BUN). The rats were killed, and the wholebrain, lungs, kidneys, and liver were removed and weighed.
Lungs were also weighed dry to determine fluid content, andtriglyceride was determined in liver. At each time interval, 4exposed rats and 4 controls were killed, and liver, heart, lung,kidney, and brain were taken for histopathologicalexamination.
Body weight gain was slightly, but nonsignificantly (p>0.05),
depressed throughout the exposure period and 2 weeks
postexposure. Brain and kidney weights were depressed during
the exposure period only. Nonsignif-icant increases in SGOT
(AST) were seen at 2, 4, and 8 weeks. No other effects wereseen. Although body, brain, and kidney weights weredepressed and SGOT was slightly elevated, there were no
statistically significant findings with respect to any
toxicological index meas-ured. There were no untoward
histopathological findings.
Bruckner, J.V. and Peterson, R.G. (1981). Evaluation of
toluene and acetone inhalant abuse. II. Model develop-ment
and toxicology. Toxicol. Appl. Pharmacol. 61:302-312.

Genetic Toxicity in Vitro
Type
System of Testing
Concentration
Metabolic Activation
Result
GLPTest substance
RemarkResult92

ACETONE

chromosomal aberration
Chinese hamster lung fibroblast cell line CHL (Cancer
Research Institute: Tokyo)
40 mg/mL
with and without
positiveno datano data
Cells were exposed to chemical for 24 or 48 h. Colcemid
added 2 h before harvesting cells, which were trypsin-ized,
suspended in hypotonic KCl for 13 min, and separated bycentrifuging. The cells were fixed with acetic acid-methanol
and fixed on glass slides, which were air dried. The cells were
stained with Giemsa, and 100 metaphases were scored forpolyploid cells and structural chromosomal aberrations.
Acetone produced 6.0% polyploid cells at 48 h, and 28.0%
cells with structural aberrations were at 24 h. The authors
consider an incidence of less than 4.9% aberrations to be
negative and greater than 10% to be positive. The dose atwhich structural aberrations were detected in 20% of themetaphases observed (D20) was 36.9 mg/mL. The authors
noted that the test was positive at 48 h also, but negative in thepresence of S9 mix. Control and solvent-control (saline,
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Reference

Type
System of Testing
Concentration
Metabolic Activation
Result negative
GLP
Test substance
RemarkResultReference

Type
System of Testing
Concentration
Metabolic Activation
Result negative
GLP
Test substance
RemarkResultACETONE
DMSO, ethanol, sodium carboxymethyl cellulose) incidencesof aberrations were said to be 3% or less.
Ishidate, M., Jr., Sofuni, T., Yoshikawa, K., Hayashi, M.,
Nohmi, T., Sawada, M., and Matsuoka, A. (1984). Primary
mutagenicity screening of food additives currently used inJapan. Food Chem. Toxicol. 22:623-636.
chromosomal aberration
Chinese hamster ovary cells
0.5-5.0 mg/mL
with and without
no dataas prescribed by 1.1-1.4
Cells were exposed to chemical for 8 h, washed to remove thetest chemical, and treated with colcemid for 2.0-2.5 h before
cell harvest. The method of Galloway et al., Environ. Mutagen.
7,1985 was followed except that the total duration of 10-12 h.
The cells were fixed with 3:1 acetic acid-methanol and stainedwith 5% Giemsa on glass slides. Simple, complex, and "other"aberrations were determined on 100-200 cells. Chromatid andchromosome gaps were recorded but were not used in theanalysis.
Acetone produced 0-3.5% simple aberations and 0-2%
complex aberations, and a total percentage of 1.5-4.0% for thethree dose levels tested. The results were equal to or less thanthe values observed with untreated control cells.
Loveday, K.S., Anderson, B.E., Resnick, M.A., and Zeiger, E.
(1990). Chromosome aberration and sister chromatid exchange
tests in Chinese hamster ovary cells in vitro. V: Results with46 chemicals. Environ. Mol. Mutagen. 16:272-303.
sister chromatid exchange
Chinese hamster ovary cells
0.05-5.0 mg/mL
with and without
no dataas prescribed by 1.1-1.4
Cells were exposed to chemical for 2 h before adding
bromodeoxyuridine (BrdUrd), which was incubated for 24 h.
After 26 h fresh medium with BrdUrd and colcemid was added
for an additional 2-2.5 h at 37°C. Cells were examined forsigns of toxicity (confluence in the monolayer) before
harvesting. Cells were separated by centrifugation, fixed with
3:1 acetic acid-methanol, fixed on glass slides, and stainedwith Hoechst 33258 and then 5% Giemsa. Fifty (50) second
division metaphase cells were scored for sister chromatid
exchanges (SCEs).
Acetone produced 8.5-8.7 SCEs per cell when tested without
activation at the three dose levels examined. When tested with
UNEP Publications

93

OECD SIDS

Reference

Type
System of Testing
Concentration.
Metabolic Activation
Result negative
GLP
Test substance
MethodRemarkReference

Type
System of Testing
Concentration.
Metabolic Activation
Result
GLPTest substance
Method94

ACETONEactivation 6.4-7.5 SCEs per cell were observed. The results
were equal to or less than the values observed with untreatedcontrol cells. A postive trend test with at 20% increase inchromatid exchanges with at least one dose was required for apositive response.
Loveday, K.S., Anderson, B.E., Resnick, M.A., and Zeiger, E.
(1990). Chromosome aberration and sister chromatid exchange
tests in Chinese hamster ovary cells in vitro. V: Results with46 chemicals. Environ. Mol. Mutagen. 16:272-303.
two-stage cell transformation assay
BALB/3T3 clone A31-1-1 (JCRB0601)
0.5%
without
no datano data
BALB/3T3 cells in culture were treated with test chem-ical(but not acetone) for 72 h. The chemical was removed, and thecells were grown in medium for 3 days. The promoter 12-Otetradecanoylphorbol 13-acetate (TPA) or 0.5% acetone wasadded. After two weeks, the promoter was removed, and thecells were grown for 3 weeks at which time they werecollected and stained with Giemsa.
Acetone caused no transformation when applied during thepromotion phase to cells treated with DMSO. It is not clearthat cells were treated with acetone alone or with acetone
followed by TPA. TPA was, however, applied to the cells in
acetone solution.
Sakai, A. and Sato, M. (1989). Improvement of carcin-ogenidentification in BALB/3T3 cell transformation by applicationof a 2-stage method. Mutat. Res. 214:285-296.
minimal inhibitory concentration
trp- E. coli, 3 strains: WP2 (wild-type, repair proficient),
WP67 (uvr- polA-), and CM871 (uvrA- recA- lexA-).
Up to 40 mg/wellwith and without
negativeno datano dataSix replicates (rows) of eight twofold dilutions of eachcompound were prepared in Microtiter plates. Three rows werefilled with phosphate-buffered saline and three with S9 mix.
One strain of each of the three bacteria was added to each of
the eight wells in one of the rows. The plates were incubated at
37°C and observed for increases in turbidity or the formationof a pellet of settled cells. Apparently positive results wereconfirmed by subculture on agar plates. Method is liquid
micromethod modification of the rec-assay system with B.
UNEP Publications

OECD SIDS

RemarkReference

ACETONE
subtilis (Kada et al., 1981) and the E. coli system of McCarroll
et al. (1981).
Method results in a minimal inhibitory concentration (MIC).
The MIC for acetone under each condition of strain andactivation (six values) was > 40 mg/well. A ratio between the
MICs in repair-proficient (WP2) and repair-deficient (WP67
and CM871) strains greater than 2 was considered to besignificant in the test. Although these ratios could not be
obtained for acetone (since all values were "> 40 mg"), thevalues suggest that acetone would be an extremely weak DNAdamaging agent if it were positive. The overall accuracy forpredicting car-cinogenicity for the DNA-repair test was 72.4%
for a battery of 75 of the 135 compounds for which clear
carcinogenicity data were available and that included several
compounds reported to be nonmutagenic carcin-ogens or
noncarcinogenic mutagens.
De Flora, S., Zanacchi, P., Camoirano, A., Bennicelli, C., andBadolati, G.S. (1984). Genotoxic activity and potency of 135
compounds in the Ames reversion test and in a bacterial DNArepair test. Mutat. Res. 133:161-198.
Kada, T., Hirano, K., and Shirasu, Y. (1980). Screening ofenvironmental chemical mutagens by the Rec-assay systemwith Bacillus subtilis. In: De Serres, F.J. and Hollaender, A.
(Eds.). Chemical Mutagens, Vol. 6, Plenum, New York, 149173.
McCarroll, N.E., Piper, C.E., and Keech, B.H. (1981). An E.
coli microsuspension assay for the detection of DNA damage
induced by direct-acting agents and promutagens. Environ.
Mutagen. 3:429-444.

Type
System of Testing
Concentration.
GLP
Test substance
RemarkResults
Methodmitotic chromosomal malsegregation, mitotic recombination,and point mutations.
Saccharomyces cerevisiae diploid strain D61.M
6.82-7.83%
no datano data
Chemicals were at least 97%
Positive for aneuploidy; negative for mitotic recombinationand point mutations.
Chemicals were pipetted directly into growing cultures in
peptone-glucose-yeast extract (YEPD) medium and incubatedat 28°C for 4 h, placed in an ice bath for < 16 h, and thenincubated at 28°C on a shaker for 4 h (cold-interruption
procedure). Samples of cultures were plated on a selective
cyclohexamide medium. After 6-7 days, the plates were scoredfor colony color and numbers. Red colonies reflect cumulative
effects of events like point mutations, mitotic recombinations,and deletion of chromosomal fragments. White colonies
UNEP Publications

95

OECD SIDS

RemarkRemarkConcentration.
Metabolic Activation

96

ACETONE
contain presumptive monosomics; these are confirmed byestablishment of a requirement for leucine.
Acetone gave inconsistent results with the original protocol,
which did not have the ice-storage step. The authors found thatstorage in ice for 16 h or more fol-lowing the initial incubation
gave repeatable positive results (Zimmermann et al. 1984).
Most of the cyclohex- amide-resistant colonies were white andalmost all of these were leucine requiring, indicating that thesecolonies were monosomics. Red resistant colonies did notincrease and were not significantly leucine requiring,indicating that acetone did not induce point mutations or
recombinations under the test conditions.
Using the method of Zimmermann et al. (1985), Mayer and
Goins (1994) reported that concentrations of acetone up to 459
mM (2.7%) did not cause chromosome loss or mutations in S.
cerevisiae D61.M. In an interlaboratory comparison of mitotic
chromosome loss in S. cerevisiae, acetone was positive in one
laboratory at levels of ca. 45-55 mg/mL using the coldinterruption procedure of Zimmermann et al. (1985) but
negative in a second lab-oratory. Both laboratories reported
acetone negative using the standard procedure with overnightincubation at 28°C (Whittaker et al., 1989). Acetone waspositive for production of aneuploidy in S. cerevisiae using thecold-interruption procedure of Zimmermann et al. (1985) atlevels > 40 mg/mL. It was negative using the standard
procedure and did not produce other genetic effects (genemutation, mitotic recombination, etc.) with either protocol(Albertini, 1991). The merokinetic effect (multipolarity) of
acetone on chromosome division of human leukocytes wasreported by Kabarity (1969). Acetone caused the formation ofmultiple-spindle apparatus leading to the movement of eachpart of the centrosome to one pole. The author concluded thatlymphoma TK+/- 3.7.2C cells
10-30 mg/mL
without
Resul0 Reference EHRT (1987). Screening of Priority
Chemicals for Reproductive Hazards. Environmental HealthResearch and Testing, Inc. Cincinnati, OH. Project No. ETOX85-

UNEP Publications

OECD SIDSACETONEEXTRACT FROM IRPTC LEGAL FILESUNEP Publications

97

OECD SIDSACETONE

File: 17.01 LEGAL
rn : 3971
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: AUS
type
: REC
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
TLV
|
-------------------------------TWA: 1780MG/M3 (750PPM) STEL: 2375MG/M3 (1000PPM)
entry date: MCH 1985
original : ILO , , , , ,amendment: AOHGN*, APPROVED OCCUPATIONAL HEALTH GUIDE THRESHOLD LIMITVALUES, , , , 1983*******

File: 17.01 LEGAL
rn : 14731
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: BEL
type
: REC
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
TLV
|
-------------------------------TWA: 1780MG/M3 (750PPM); STEL: 2375MG/M3 (1000PPM)
entry date: JUL 1987
original : ILO , , , , ,amendment: TLVBE*, THRESHOLD LIMIT VALUES(TOLERABLE LIMIT VALUES), , , ,1984*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area
: FIN

rn : 15424

rtecs notype

:AL3150000: REC-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MPC
|
-------------------------------TWA: 1200MG/M3 (500PPM) STEL: 1500MG/M3 (625PPM)
entry date: MAY 1989
original : ILO , , , , ,amendment: APWFI*, HTP-ARVOT (LIST OF LIMIT VALUES FOR CONCENTRATIONS OFTOXIC SUBSTANCES KNOWN TO BE HARMFUL TO HEALTH), 25 , , 10 ,98

UNEP Publications

OECD SIDSACETONE1988*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no
area
: HUN
type
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MAC
|
-------------------------------TWA: 200MN/M3; STEL(30 MIN): 1000MG/M3
entry date: MCH 1985

rn : 16007:AL3150000: REG

original : ILO , , , , ,amendment: HSMSZ*, HUNGARIAN STANDARD MSZ NO., 21461-78 , , , 1978*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: ITA-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
TLV
|
-------------------------------1000MG/M3 (420PPM)
entry date: MCH 1985

rn : 16192

rtecs notype

:AL3150000: REC

original : ILO , , , , ,amendment: TLVIT*, VALORI LIMITE PONDERATI(APPRAISED LIMIT VALUES), , ,*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: NLD-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MXL
|
-------------------------------TWA: 1780MG/M3 (750PPM)
entry date: JUN 1987

rn : 16428

rtecs notype

UNEP Publications:AL3150000
: REC

99

OECD SIDSACETONEoriginal : ILO , , , , ,amendment: NMACN*, NATIONALE MAC-LIST(NATIONAL MAC-LIST), , , , 1986*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: POL-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MPC
|
-------------------------------TWA: 200MG/M3
entry date: MCH 1985

rn : 16943

rtecs notype

:AL3150000: REG

original : ILO , , , , ,amendment: OMLWS*, ORDINANCE OF THE MINISTER OF LABOUR, WAGES AND SOCIALAFFAIRS, 22DEC , , , 1982*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area
: ROM

rn : 17169

rtecs notype

:AL3150000: REG-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MPC
|
-------------------------------TWA: 1000MG/M3; CLV: 1500MG/M3
entry date: MCH 1985
original : ILO , , , , ,amendment: OMHRO*, ORDINANCE OF THE MINISTRY OF HEALTH, 60 , , , 1975*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: CHE-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MAK
|
-------------------------------100

rn : 17543

rtecs notype

UNEP Publications:AL3150000: REG

OECD SIDSACETONE

TWA: 1780MG/M3 (750PPM)
entry date: DEC 1987
original : ILO , , , , ,amendment: ZWACH*, ZULAESSIGE WERTE AM ARBEITSPLATZ(PERMITTED VALUES IN
THE WORKPLACE), , , , 1987*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: YUG-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MAC
|
-------------------------------TWA: 800MG/M3 (336PPM)
entry date: MCH 1985

rn : 18086

rtecs notype

:AL3150000: REG

original : ILO , , , , ,amendment: ORYUG*, ORDINANCE, 24-3698/1 , , , 1971*******
File: 17.01 LEGAL
rn : 50877
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: IMO
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AQ
|
EMI
|
PRMT
|
| AQ
|
MARIN
|
PRMT
|
-------------------------------This substance is presently considered to present no harm to humanhealth, marine re sources, amenities or other legitimats uses of the sea
when discharged into the sea from tank cleaning or deballasting
operations
entry date: APR 1993
original : IMODC*, , , , , 1992*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area
: ARG

rn : 100031

rtecs notype

UNEP Publications:AL3150000
: REG

101

OECD SIDSACETONE-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MPC
|
-------------------------------8H-TWA : 1780 MG/M3 (750 PPM), 15MIN-STEL : 2375 MG/M3 (1000 PPM)(MAXIMUM 4 TIMES/DAY WITH INTERVALS OF A LEAST 60 MINUTES)
entry date: OCT 1991
effective date: 29MAY1991
title: LIMIT VALUES FOR CHEMICAL SUBSTANCES IN THE WORKINGENVIRONMENT-RESOLUTION NO. 444/1991 OF THE MINISTRY OF WORK AND SOCIALSECURITY (AMENDING REGULATION DECREE NO. 351/1979 UNDER LAW NO.
19587/1972: HYGIENE AND SAFETY AT WORK)
original : ARGOB*, Boletin Oficial de la Republica Argentina(Argentinian
Official Bulletin), 24170 , I , 1 , 1979
amendment: ARGOB*, Boletin Oficial de la Republica Argentina(Argentinian
Official Bulletin), 27145 , I , 4 , 1991*******

File: 17.01 LEGAL
rn : 300477
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: CAN
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
TLV
|
-------------------------------TWA: 750 PPM, 1,780 MG/M3; STEL: 1,000 PPM, 2,375 MG/M3. PRESCRIBED BY
THE CANADA OCCUPATIONAL SAFETY AND HEALTH REGULATIONS, UNDER THE CANADALABOUR CODE (ADMINISTERED BYTHE DEPARTMENT OF LABOUR). THE REGULATIONSSTATE THAT NO EMPLOYEE SHALL BE EXPOSED TO A CONCENTRATION OF AN
AIRBORNE CHEMICAL AGENT IN EXCESS OF THE VALUE FOR THAT CHEMICAL AGENTADOPTED BY ACGIH (AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL
HYGIENISTS) IN ITSPUBLICATION ENTITLED: "THRESHOLD LIMIT VALUE AND
BIOLOGICAL EXPOSURE INDICES FOR 1985-86".
entry date: MCH 1991
effective date: 13MCH1986
amendment: CAGAAK, Canada Gazette Part II, 120 , 6 , 1105 ,*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: CAN-------------------------------|subject|specification|descriptor||-------+-------------+----------|| TRNSP ||CLASS || LABEL ||RQR|| PACK |||-------------------------------102

rn : 301601

rtecs notype

UNEP Publications:AL3150000: REG

OECD SIDSACETONEPIN (PRODUCT IDENTIFICATION NO.): UN1090. CLASS (3.1): FLAMMABLE LIQUID.
SPECIAL PROVISIONS: 99. PACKING GROUP II, (I=GREAT DANGER, III=MINORDANGER). MAXIMUM AMOUNT PER PACKAGE THAT MAY BE TRANSPORTED ON PASSENGER
AIRCRAFT OR VEHICLE: 5 L. MAXIMUM AMOUNT PER PACKAGE THAT MAY BE
TRANSPORTED ONA CARGO AIRCRAFT: 60 L. PRESCRIBED BY THE TRANSPORTATIONOF DANGEROUS GOODS REGULATIONS, UNDER THE TRANSPORTATION OF DANGEROUS
GOODS ACT (ADMINISTERED BY THE DEPARTMENT OF TRANSPORT). THE ACT AND
REGULATIONS ARE INTENDED TO PROMOTE SAFETY INTHE TRANSPORTATION OFDANGEROUS GOODS IN CANADA, AS WELL AS PROVIDE ONE COMPREHENSIVE SET OF
RULES APPLICABLE TO ALL MODES OF TRANSPORT ACCROSS CANADA. THESE ARE
BASED ONUNITED NATIONS RECOMMENDATIONS. THE ACT AND REGULATIONS SHOULD
BE CONSULTED FOR DETAILS. RECORDS ARE ENTERED UNDER THE PROPER
SHIPPINGNAME FOUND IN THE REGULATIONS; THIS MAY INCLUDE VERY GENERALGROUPS OF CHEMICAL SUBSTANCES.
entry date: OCT 1991
effective date: 06DEC1990
amendment: CAGAAK, Canada Gazette Part II, 124 , 26 , 5523 ,*******
File: 17.01 LEGAL
rn : 302345
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: CAN
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| GOODS |
CONSM
|
RQR
|
| LABEL ||PRO|| SALE |||| IMPRT |||-------------------------------IT IS PROHIBITED TO SELL, ADVERTISE OR IMPORTINTO CANADA ADHESIVES,
CLEANING SOLVENTS, THINNING AGENTS AND DYES CONTAINING ACETONE, WHEN
PACKAGED AS CONSUMER PRODUCTS, UNLESS DETAILED LABELLING REQUIREMENTS
ARE MET. THIS PROHIBITION IS PRESCRIBED BY SCHEDULE I OF THE HAZARDOUS
PRODUCTS ACT (HPA), ADMINISTERED BY THE DEPARTMENT OF CONSUMER AND
CORPORATE AFFAIRS. IT AUTHORIZES THE PROHIBITION OF PRODUCTS THAT ARE
LIKELY TO BEOF DANGER TO THE HEALTH AND SAFETY OF THE PUBLIC.
entry date: MAY 1991
effective date: 01NOV1988
amendment: CAGAAK, Canada Gazette Part II, 122 , 24 , 4625 ,*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: CAN-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| USE
|
OCC
|
RQR
|
| STORE |||| LABEL |||--------------------------------

rn : 302508

rtecs notype

UNEP Publications:AL3150000
: REG

103

OECD SIDSACETONE

INGREDIENT DISCLOSURE LIST CONCENTRATION 1% WEIGHT/WEIGHT. THE WORKPLACE
HAZARDOUS MATERIALS INFORMATION SYSTEM (WHMIS) IS A NATIONAL SYSTEM TOPROVIDE INFORMATION ON HAZARDOUS MATERIALS USED IN THE WORKPLACE. WHMISIS IMPLEMENTED BY THE HAZARDOUS PRODUCTS ACT AND THE CONTROLLED PRODUCTS
REGULATIONS (ADMINISTERED BY THE DEPARTMENT OF CONSUMER AND CORPORATE
AFFAIRS). THE REGULATIONS IMPOSE STANDARDS ON EMPLOYERS FORTHE USE,STORAGE AND HANDLING OF CONTROLLED PRODUCTS AND ADDRESS LABELLING AND
IDENTIFICATION, EMPLOYEE INSTRUCTION AND TRAINING, AS WELL AS THE UPKEEP
OF A MATERIALS SAFETY DATA SHEET (MSDS). THE PRESENCE IN A CONTROLLED
PRODUCT OF AN INGREDIENT IN A CONCENTRATION EQUAL TO OR GREATER THANSPECIFIED IN THE INGREDIENT DISCLOSURE LIST MUST BE DISCLOSED IN THE
SAFETY DATA SHEET.
entry date: APR 1991
effective date: 31DEC1987
amendment: CAGAAK, Canada Gazette Part II, 122 , 2 , 551 ,*******
File: 17.01 LEGAL
rn : 400270
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: CSK
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
AMBI
|
CLASS |-------------------------------THE SUBSTANCE IS CLASSIFIED IN THE FOURTH GROUP OF AIR POLLUTANTS(ORGANIC GASES AND VAPOURS)
entry date: JAN 1992
effective date: 1OCT1991
title: PROVISION OF FEDERAL COMMITTEE FOR ENVIRONMENT TO ACT NO. 309
FROM 9 JULY 1991 ON AIR PROTECTION AGAINST AIR POLLUTANTS
original : SZCSR*, Sbirka Zakonu Ceskoslovenske Socialisticke
Republiky(Collection of the Law of Czechoslovak Socialist
Republic), , 84 , 2061 , 1991*******

File: 17.01 LEGAL
rn : 400406
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: CSK
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| WASTE |INDST|CLASS ||||
RQR|-------------------------------THE SUBSTANCE IS CLASSIFIED AS HAZARDOUS WASTE COMPONENT. IT IS OR CAN
BE DANGEROUS TO HUMAN HEALTH OR ENVIRONMENT. QUANTITY, SPECIFICATION,USE OR DISPOSAL OF THE WASTE MUST BE REPORTED TO AUTHORITIES. TRANSPORT
AND DISPOSAL OF THE WASTE MUST BE PERFORMED IN ACCORDANCE WITH SPECIAL
DIRECTIVE
entry date: JAN 1992
effective date: 1AUG1991
title: PROVISION OF FEDERAL COMMITTEE FOR ENVIRONMENT WHICH DECLARES
104

UNEP Publications

OECD SIDSACETONE

WASTE CLASSIFICATION AND CATALOGUE
original : SZCSR*, Sbirka Zakonu Ceskoslovenske Socialisticke
Republiky(Collection of the Law of Czechoslovak Socialist
Republic), , 69 , 1650 , 1991*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: CSK-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MAC
|
-------------------------------TWA: 800.0MG/M3; CLV: 4000.0MG/M3
entry date: DEC 1991

rn : 400540

rtecs notype

:AL3150000: REG

effective date:

MCH1985

title: DIRECTIVE NO. 46/1978 ON HYGIENIC REQUIREMENTS ON OCCUPATIONALENVIRONMENT
original : HPMZC*, HYGIENICKE PREDPISY MINISTERSTVA ZDRAVOTNICTVICSR(HYGIENIC REGULATIONS OF MINISTRY OF HEALTH OF CSR), 39 ,, , 1978amendment: HPMZC*, HYGIENICKE PREDPISY MINISTERSTVA ZDRAVOTNICTVICSR(HYGIENIC REGULATIONS OF MINISTRY OF HEALTH OF CSR), 58 ,, , 1985*******

File: 17.01 LEGAL
rn : 401111
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: CSK
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| FOOD ||MPC|-------------------------------LIMIT OF ADDITIVE PRESENT DUE TO PRODUCTION, PACKING, TRANSPORT AND
STORAGE OF FOOD PRODUCTS: 5G/KG.
entry date: DEC 1991
effective date: 1JUL1986
title: DIRECTIVE NO. 50/1978 ON FOREIGN SUBSTANCES IN FOODSTUFFS
original : HPMZC*, HYGIENICKE PREDPISY MINISTERSTVA ZDRAVOTNICTVICSR(HYGIENIC REGULATIONS OF MINISTRY OF HEALTH OF CSR), 43 ,, , 1978amendment: HPMZC*, HYGIENICKE PREDPISY MINISTERSTVA ZDRAVOTNICTVICSR(HYGIENIC REGULATIONS OF MINISTRY OF HEALTH OF CSR), 61 ,, , 1986*******UNEP Publications

105

OECD SIDSACETONE

File: 17.01 LEGAL
rn : 500483
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: DEU
type
: REC
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| AQ||
CLASS |
| USE
|
INDST
|
RQR
|
-------------------------------THIS SUBSTANCE IS CLASSIFIED AS IN GENERAL NOT HAZARDOUS TO WATER(WATER-HAZARD CLASS: WGK 0). (THE DIFFERENT CLASSES ARE: WGK 3 = VERYHAZARDOUS; WGK 2 = HAZARDOUS; WGK 1 = SLIGHTLY HAZARDOUS; WGK 0 = IN
GENERAL NOT HAZARDOUS.) THE CLASSIFICATION FORMS THE BASIS FOR
WATER-PROTECTION REQUIREMENTS FOR INDUSTRIAL PLANTS IN WHICH
WATER-HAZARDOUS SUBSTANCES ARE HANDLED.
entry date: DEC 1991
title: ADMINISTRATIVE RULES CONCERNING WATER-HAZARDOUS SUBSTANCES(VERWALTUNGSVORSCHRIFT WASSERGEFAEHRDENDE STOFFE)
original : GMSMA6, Gemeinsames Ministerialblatt. Joint Ministerial
Papers, , 8 , 114 , 1990*******

File: 17.01 LEGAL
rn : 502155
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: DEU
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
EMI
|
MPC
|
-------------------------------THIS SUBSTANCE BELONGS TO CLASS III. THE AIR EMISSIONS OF ORGANICCOMPOUNDS MUST NOT EXCEED (AS THE SUM OF ALL COMPOUNDS IN ONE CLASS) THE
FOLLOWING MASS CONCENTRATIONS: CLASS I - 20 MG/M3 AT A MASS FLOW OF >=0.1 KG/H; CLASS II - 100 MG/M3 AT A MASS FLOW OF >= 2 KG/H; CLASS III 150 MG/M3 AT A MASS FLOW OF >= 3 KG/H. IF COMPOUNDS FROM DIFFERENTCLASSES ARE PRESENT, THE MASS CONCENTRATION MUST NOT EXCEED 150 MG/M3 AT
A TOTAL MASS FLOW OF >= 3 KG/H.
entry date: JAN 1992
effective date: 01MCH1986
title: TECHNICAL GUIDELINES FOR AIR POLLUTION CONTROL (TECHNISCHEANLEITUNG ZUR REINHALTUNG DER LUFT)
original : GMSMA6, Gemeinsames Ministerialblatt. Joint Ministerial
Papers, , 7 , 93 , 1986*******
File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
106

rn : 502438

rtecs noUNEP Publications:AL3150000

OECD SIDSACETONE

area
: DEU
type
: REC
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MAK
|
-------------------------------8H-TWA: 1000 ML/M3 (PPM); 2400 MG/M3 (20C, 101.3 KPA). SUBSTANCEELICITING VERY WEAK EFFECTS. 60MIN-STEL: 2000 ML/M3 (PPM); 4800 MG/M3;
CEILING VALUE; 3X/SHIFT. VAPOUR PRESSURE: 24 KPA AT 20 C.
entry date: JAN 1992
title: MAXIMUM CONCENTRATIONS AT THE WORKPLACE AND BIOLOGICAL TOLERANCEVALUES FOR WORKING MATERIALS (MAXIMALE ARBEITSPLATZKONZENTRATIONEN UND
BIOLOGISCHE ARBEITSSTOFFTOLERANZWERTE)
original : MPGFDF, MITTEILUNG DER SENATSKOMMISSION ZUR PRUEFUNGGESUNDHEITSSCHAEDLICHER ARBEITSSTOFFE (DEUTSCHEFORSCHUNGSGEMEINSCHAFT), XXVII , , 17 , 1991*******

File: 17.01 LEGAL
rn : 510565
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: DEU
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| CLASS ||CLASS || LABEL ||RQR|| PACK ||RQR|-------------------------------CLASSIFICATION AND LABELLING IN GERMANY IS GENERALLY THE SAME AS FOR THE
EEC (SEE OJEC** L180, 1991). HOWEVER, SLIGHT MODIFICATIONS MAY BE
INTRODUCED FOR SOME SUBSTANCES IN THE GERMAN LEGISLATION.
entry date: APR 1992
effective date: 15JUN1991
title: ORDINANCE ON HAZARDOUS SUBSTANCES. (GEFAHRSTOFFVERORDNUNG)
original : BGZBAD, Bundesgesetzblatt (Federal Law Gazette), , I , 1931 ,1991*******

File: 17.01 LEGAL
rn : 612864
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: GBR
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| TRNSP ||CLASS || LABEL ||RQR|-------------------------------LABELLING OF ROAD TANKERS: FLAMMABLE LIQUID. EMERGENCY ACTION CODE:
2(Y)EUNEP Publications

107

OECD SIDSACETONE

entry date: JAN 1983

effective date: 28MCH1979

title: HAZARDOUS SUBSTANCES (LABELLING OF ROAD TANKERS) REGULATIONS 1978
original : GBRSI*, STATUTORY INSTRUMENTS, 1702 , , , 1978*******

File: 17.01 LEGAL
rn : 650642
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: GBR
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| TRNSP |
MARIN
|
RQR
|
| AQ
|
MARIN
|
RQR
|
| AQ
|
EMI
|
RQR
|
-------------------------------CLASSIFIED AS A NON-POLLUTING LIQUID SUBSTANCE. DOCUMENTARY EVIDENCE OF
ASSESSMENT AND APPROVAL REQUIRED BY A CARRIER. DISCHARGE INTO THE SEA IS
NOT PROHIBITED.
entry date:1992
effective date: 06APR1987
title: THE MERCHANT SHIPPING (CONTROL OF POLLUTION BY NOXIOUS LIQUIDSUBSTANCES IN BULK) REGULATIONS 1987, SCHEDULE 2
original : GBRSI*, STATUTORY INSTRUMENTS, 551 , , 15 , 1987
amendment: GBRSI*, STATUTORY INSTRUMENTS, 2604 , , 2 , 1990*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area
: GBR

rn : 665433

rtecs notype

:AL3150000: REG-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
OES
|
-------------------------------8H-TWA: 1780MG/M3 (75PPM); STEL(10MIN-TWA): 3560MG/M3 (3560PPM)
entry date:1992
effective date: 01JAN1992
title: EH40 OCCUPATIONAL EXPOSURE LIMITS FOR USE WITH THE CONTROL OF
SUBSTANCES HAZARDOUS TO HEALTH REGULATIONS
original : GBRSI*, STATUTORY INSTRUMENTS, 1657 , , 10 , 1988
amendment: GNHSE*, GUIDANCE NOTE FROM THE HEALTH AND SAFETY EXECUTIVE,
EH40 , , 11 , 1992*******

File: 17.01 LEGAL
108

rn : 762000
UNEP Publications

OECD SIDSACETONEsystematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: IND
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| MANUF ||RQR|| SAFTY ||RQR|| STORE ||RQR|| IMPRT ||RQR|-------------------------------These rules define the responsabilities of occupiers of any industrial
activity in which this toxic and hazardous substance may be involved.
These responsabilities encompass: (a) assessment of major hazards(causes, occurrence, frequency); (b) measures to prevent accidents andlimit eventual impairment to human health and pollution of theenvironment; (c) provision of relevant factual knowledge and skills toworkers in order to ensure health and environmental safety when handlingequipments and the foregoing chemical; (d) notification of the competentauthorities in case of major accidents; (e) notification of sites to thecompetent authorities 3 months before commencing; (f)preparation of an
on-site emergency plan as to how major accidents should be coped with;(g) provision of competent authorities with information and means to
respond quickly and efficiently to any off-site emergency; (h) provisionof information to persons outside the site, liable to be affected by amajor accident; (i) labelling of containers as to clearly identify
contents, manufacturers, physical, chemical and toxicological data; (j)preparation of a safety data sheet including any significant information
regarding hazard of this substance and submission of safety reports tothe competent authorities; (k) for the import of a hazardous chemical to
India, importers must supply the competent authorities with specified
information regarding the shipment.
entry date: SEP 1992
effective date: 27NOV1989
title: THE MANUFACTURE, STORAGE AND IMPORT OF HAZARDOUS CHEMICALS RULES.
1989
original : GAZIN*, THE GAZETTE OF INDIA, 787 , , , 1989*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: JPN-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MAC
|
-------------------------------TWA: 470MG/M3 (200PPM)
entry date: DEC 1991

rn : 800148

rtecs notype

:AL3150000: REC

title: MAXIMUM ALLOWABLE CONCENTRATIONS RECOMMENDED BY THE JAPANESEASSOCIATION OF INDUSTRIAL HEALTH.
original : SAIGBL, Sangyo Igalu (Japanese Journal of Industrial Health),
33 , 4 , 277-287 , 1991
UNEP Publications

109

OECD SIDSACETONE*******

File: 17.01 LEGAL
rn : 1010048
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: MEX
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MXL
|
-------------------------------AT ANY WORKPLACE WHERE THIS SUBSTANCE IS PRODUCED, STORED OR HANDLED A
MAXIMUM PERMISSIBLE LEVEL OF 2400MG/M3 (1000PPM) MUST BE OBSERVED FOR A
PERIOD OF 8 HOURS OR 3000MG/M3 (1260PPM) FOR 15 MINUTES FOUR TIMES A DAY
WITH INTERVALS OF AT LEAST 1 HOUR.
entry date: DEC 1991
effective date: 28MAY1984
title: INSTRUCTION NO.10 RELATED TO SECURITY AND HYGIENIC CONDITIONS AT
WORKPLACES. (INSTRUCTIVO NO. 10, RELATIVO A LAS CONDICIONES DE SEGURIDADE HIGIENE DE LOS CENTROS DE TRABAJO).
original : DOMEX*, Diario Oficial, , , , 1984
amendment: DOMEX*, Diario Oficial, , , , 1989*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no
area
: RUS
type
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
MAC
|
|
|
|
CLASS |-------------------------------CLV: 200.0MG/M3 (VAPOUR) HAZARD CLASS: IV
entry date: MAY 1990

rn : 1120809:AL3150000: REG

effective date: 01JAN1989

amendment: GOSTS*, GOSUDARSTVENNYI STANDART SSSR(STATE STANDARD OF
USSR), 12.1.005 , , , 1988*******
File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: RUS-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
AMBI
|
MAC
|
-------------------------------110

rn : 1122198

rtecs notype

UNEP Publications:AL3150000: REG

OECD SIDSACETONE

0.35MG/M3 1X/D, 0.35MG/M3 AV/D.
entry date: SEP 1985

effective date:

AUG1984

amendment: PDKAV*, PREDELNO DOPUSTIMYE KONTSENTRATSII (PDK)ZAGRYAZNYAYUSHCHIKH VESHCHESTV V ATMOSFERNOM VOZDUKHENASELENNYKH MEST (MAXIMUM ALLOWABLE CONCENTRATIONS (MAC) OF
CONTAMINANTS IN THE AMBIENT AIR OF RESIDENTIAL AREAS),
3086-84 , , , 1984*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area
: RUS

rn : 1122704

rtecs notype-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AQ
|
SURF
|
MAC
|
|
|
|
CLASS |-------------------------------2.2MG/L HAZARD CLASS: III
entry date: JUL 1990

:AL3150000: REG

effective date:

1JAN1989

amendment: SPNPV*, SANITARNYE PRAVILA I NORMY OKHRANY POVERKHNOSTNYKHVOD OT ZAGRIAZNENIA (HEALTH REGULATION AND STANDARDS OF
SURFACE WATER PROTECTION FROM CONTAMINATION), 4630-88 , , ,1988*******

File: 17.01 LEGAL
rn : 1200096
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: SWE
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
HLV
|
-------------------------------1D-TWA: 600MG/M3 (250PPM). 15MIN-STEL: 1200MG/M3 (500 PPM)
entry date:1992
effective date: 01JUL1991
title: HYGIENIC LIMIT VALUES.
original : AFS***, ARBETARSKYDDSSTYRELSENS FOERFATTNINGSSAMLING, 1990:13, , 5-64 , 1990*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetonern : 1302002

UNEP Publications

111

OECD SIDSACETONE

reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: USA
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| FOOD |
ADDIT
|
RSTR
|
| TRANS ||RSTR|| STORE ||RSTR|| PACK ||RSTR|-------------------------------; Summary - THIS SUBSTANCE IS INCLUDED ON A LIST OF SUBSTANCES USED TO
PREPARE ADHESIVES WHICH MAY BE SAFELY USED AS COMPONENTS OF ARTICLESINTENDED FOR USE IN PACKAGING, TRANSPORTATION, OR HOLDING FOOD INACCORDANCE WITH THE FOLLOWING PRESCRIBED CONDITIONS: SUBSTA NCE MUST BE
SEPARATED FROM THE FOOD BY A FUNCTIONAL BARRIER, MUST NOT EXCEED LIMITSOF GOOD MANUFACTURING PRACTICE USED WITH DRY FOODS, OR NOT EXCEED TRACEAMOUNTS AT SEAMS AND EDGE EXPOSURES WHEN USED WITH FATTY AND AQUEOUS
FOODS. ALSO REGULATED BY SEA M INTEGRITY, LABELING STANDARDS, AND ANYPROVISION UNDER 21 CFR 175
entry date: NOV 1991
effective date:1977
title: SUBSTANCES FOR USE ONLY AS COMPONENTS OF ADHESIVES
original : FEREAC, Federal Register, 42 , , 14534 , 1977
amendment: CFRUS*, Code of Federal Regulations, 21 , 175 , 105 , 1988*******

File: 17.01 LEGAL
rn : 1309525
systematic name:2-Propanone
common name:acetone
reported name :2-PROPANONE
cas no:67-64-1
rtecs no:AL3150000
area
: USA
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| CLASS |
INDST
|
RQR
|
| AIR
|
EMI
|
RQR
|
| AQ
|
EMI
|
RQR
|
-------------------------------5000 (2270); Summary - RELEASES OF THIS HAZARDOUS SUBSTANCE, IN
QUANTITIES EQUAL TO OR GREATER THAN ITS REPORTABLE QUANTITY (RQ),REPORTED AS [LBS (KG)!, ARE SUBJECT TO REPORTING TO THE NATIONALRESPONSE CENTER UNDER THE COMPREHENSIVE ENVIRONMENTAL RESPONSE,
COMPENSATION, AND LIABILITY ACT. (#)- RQ IS SUBJECT TO CHANGE
entry date: SEP 1991
effective date:1990
title: CERCLA: LIST OF HAZARDOUS SUBSTANCES AND REPORTABLE QUANTITIES
original : CFRUS*, Code of Federal Regulations, 40 , 302 , 4 , 1990
amendment: CFRUS*, Code of Federal Regulations, 40 , 302 , 4 , 1990*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE112

rn : 1323003

UNEP Publications

OECD SIDS
cas noarea

ACETONE:67-64-1: USA

rtecs notype

:AL3150000: REG-------------------------------|subject|specification|descriptor||-------+-------------+----------|| CLASS |
PESTI
|
RQR
|
| MANUF |
PESTI
|
PRMT
|
| FOOD |
ADDIT
|
RQR
|
-------------------------------CASE NAME ACETONE; Summary - THIS SUBSTANCE IS INCLUDED ON A LIST OF
ACTIVE INGREDIENTS CONTAINED IN A PRODUCT FIRST REGISTERED BEFORENOVEMBER 1, 1984, FOR WHICH A REGISTRATION STANDARD HAS NOT BEEN ISSUED.
PUBLICATION OF THIS LIST INITIATES AN ACCELERATED REREGISTRATION ANDDATA C ALL-IN FOR PRODUCTS CONTAINING THE LISTED ACTIVE INGREDIENTS.
entry date: JAN 1992
effective date:1989
title: FEDERAL INSECTICIDE, FUNGICIDE, AND RODENTICIDE ACT PESTICIDESREQUIRED TO BE REREGISTERED; LIST D
original : FEREAC, Federal Register, 54 , 204 , 43388 , 1989
amendment: FEREAC, Federal Register, 54 , 204 , 43388 , 1989*******

File: 17.01 LEGAL
rn : 1324017
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: USA
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AQ
|
GRND
|
MONIT |
| AQ
|
GRND
|
MXL
|
-------------------------------; Summary - THIS LIST IS REQUIRED ONLY FOR GROUND-WATER MONITORING AT
RCRA LAND BASED HAZARDOUS WASTE DISPOSAL UNITS. THIS FINAL RULE WILLREQUIRE THAT AN ANALYSIS OF ALL THE CONSTITUENTS OF THIS LIST BE
PERFORMED ON THE GROUND WATER TAKEN FROM WELLS SURROUNDING TH OSE UNITS.
THIS ANALYSIS TAKES PLACE WHEN GROUND-WATER CONTAMINATION IS FIRSTDETECTED, AND THEN AGAIN ONCE PER YEAR 40 CFR 264. WHEN A LISTEDCONSTITUENT IS FOUND TO BE PRESENT A BACKGROUND VALUE MUST BE SET INCOMPLIANCE WITH 40 CFR 264.98(H)(2) UNLE SS OTHERWISE STATED.
entry date: SEP 1991
effective date:1987
title: LIST (PHASE 1) OF HAZARDOUS CONSTITUENTS FOR GROUND-WATERMONITORING FINAL RULE: INCLUDING MAXIMUM CONCENTRATION OF CONSTITUENT:FOR GROUNDWATER PROTECTION.
original : FEREAC, Federal Register, 52 , , 25947 , 1987
amendment: CFRUS*, Code of Federal Regulations, 40 , 264 , , 1990*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE

rn : 1325006

UNEP Publications

113

OECD SIDS
cas noarea

ACETONE:67-64-1: USA

rtecs notype-------------------------------|subject|specification|descriptor||-------+-------------+----------|| SAFTY |
OCC
|
MXL
|
| USE
|
OCC
|
MXL
|
-------------------------------20000 PPM
entry date: OCT 1991

:AL3150000: REC

effective date:

JUN1990

title: POCKET GUIDE TO CHEMICAL HAZARDS
original : XPHPAW, US PUBLIC HEALTH SERVICE PUBLICATION, 90 , 117 , 30 ,1990
amendment: XPHPAW, US PUBLIC HEALTH SERVICE PUBLICATION, 90 , 117 , 30 ,1990*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area
: USA

rn : 1332196

rtecs notype

:AL3150000: REG-------------------------------|subject|specification|descriptor||-------+-------------+----------|| WASTE |INDST|CLASS || STORE ||RQR|| TRNSP |
REMOV
|
RQR
|
-------------------------------IGNITABLE; Summary - THIS CHEMICAL, IF DISCARDED, MUST BE TREATED AS AN
ACUTE HAZARDOUS WASTE. ACUTE HAZARDOUS WASTES REGULATIONS ARE MORE
RESTRICTIVE FOR EXCLUSION. ANY RESIDUE OF THIS CHEMICAL LABELED AS
ACUTELY HAZARDOUS AND REMAINING IN A CONTAINER, OR AN INNER LINER REMOVED FROM A CONTAINER, IS CONSIDERED A HAZARDOUS WASTE IF DISCARDED
UNLESS TRIPLE RINSING OR OTHER CLEANING MEASURES ARE TAKEN (40 CFR
261.33E).
entry date: JAN 1992
effective date:1980
title: RCRA-RESOURCE AND CONSERVATION RECOVERY ACT: DISCARDED COMMERCIAL
CHEMICAL PRODUCTS, OFF-SPECIFICATION SPECIES, CONTAINER RESIDUES, AND
SPILL RESIDUES THEREOF.
original : FEREAC, Federal Register, 45 , , 78541 , 1980
amendment: CFRUS*, Code of Federal Regulations, 40 , 261 , 33 , 1990*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :2-PROPANONE
cas no:67-64-1
area
: USA

114

rn : 1332565

rtecs notype

UNEP Publications:AL3150000: REG

OECD SIDSACETONE-------------------------------|subject|specification|descriptor||-------+-------------+----------|| WASTE |INDST|CLASS || STORE ||RQR|| TRNSP |
REMOV
|
RQR
|
-------------------------------IGNITABLE; Summary - THIS CHEMICAL, IF DISCARDED, MUST BE TREATED AS AN
ACUTE HAZARDOUS WASTE. ACUTE HAZARDOUS WASTES REGULATIONS ARE MORE
RESTRICTIVE FOR EXCLUSION. ANY RESIDUE OF THIS CHEMICAL LABELED AS
ACUTELY HAZARDOUS AND REMAINING IN A CONTAINER, OR AN INNER LINER REMOVED FROM A CONTAINER, IS CONSIDERED A HAZARDOUS WASTE IF DISCARDED
UNLESS TRIPLE RINSING OR OTHER CLEANING MEASURES ARE TAKEN (40 CFR
261.33E).
entry date: JAN 1992
effective date:1980
title: RCRA-RESOURCE AND CONSERVATION RECOVERY ACT: DISCARDED COMMERCIAL
CHEMICAL PRODUCTS, OFF-SPECIFICATION SPECIES, CONTAINER RESIDUES, AND
SPILL RESIDUES THEREOF.
original : FEREAC, Federal Register, 45 , , 78541 , 1980
amendment: CFRUS*, Code of Federal Regulations, 40 , 261 , 33 , 1990*******

File: 17.01 LEGAL
rn : 1334044
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: USA
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| USE
|
|
RQR
|
| PACK ||RQR|-------------------------------THIS SUBSTANCE IS LISTED AS AN ADJUVANT OF RELEASE AGENTS, WAXES, ANDDISPERSANTS.; Summary - THIS SUBSTANCE IS INCLUDED IN A LIST OF RESINOUS
AND POLYMERIC COATINGS WHICH MAY BE USED AS THE FOOD CONTACT SURFACE OF
ARTICLES IF THE COATING IS APPLIED AS A CONTINUOUS FILM PRODUCED FROMANY BASIC OLEFIN POLYMER LISTED IN 21 CFR 177.1520 1988 AND FOR MULATEDFROM OPTIONAL SUBSTANCES WHICH ARE RECOGNIZED AS SAFE FOR USE IN OR ON
FOOD AND FROM SUBSTANCES SUBJECT TO LIMITATIONS AS DESCRIBED HERE.
entry date: NOV 1991
effective date:1977
title: INDIRECT FOOD ADDITIVES: ADHESIVES AND COMPONENTS OF COATINGS FORPOLYOLEFIN FILMS
original : FEREAC, Federal Register, 42 , , 14534 , 1977
amendment: CFRUS*, Code of Federal Regulations, 21 , 175 , 320 , 1988*******

File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :2-PROPANONE
cas no:67-64-1
area
: USA

rn : 1336032

rtecs notype
UNEP Publications:AL3150000
: REG
115

OECD SIDSACETONE-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
EMI
|
RQR
|
| SOIL |
EMI
|
RQR
|
| AQ
|
EMI
|
RQR
|
| MANUF |
EMI
|
RQR
|
-------------------------------; Summary - FACILITIES THAT EXCEEDED A MANUFACTURING, IMPORTATION, OR
PROCESSING THRESHOLD OF 25,000 LBS OR THE USE OF 10,000 LBS FOR THISCHEMICAL MUST REPORT TO EPA ANY RELEASES OF THE CHEMICAL (OR CATEGORYCHEMICAL) TO AIR, LAND, WATER, POTW, UNDERGROUND INJECTIO N, OR OFF SITE
TRANSFER. THIS REGULATION COVERS STANDARD INDUSTRIAL CLASSIFICATION(SIC) CODES 20-39 ONLY).
entry date: OCT 1991
effective date:1987
title: SUPERFUND AMENDMENTS AND REAUTHORIZATION ACT, TITLE III. EPCRASECTION 313 LIST OF TOXIC SUBSTANCES
original : CFRUS*, Code of Federal Regulations, 40 , 372 , 65 , 1988
amendment: CFRUS*, Code of Federal Regulations, 40 , 372 , 65 , 1988*******
File: 17.01 LEGAL
rn : 1340604
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: USA
type
: REC
-------------------------------|subject|specification|descriptor||-------+-------------+----------|
| AIR
|
OCC
|
TLV
|
-------------------------------Time Weighted Avg (TWA) 750 ppm, 1780 MG/M3, skin; Short Term Exposure
Limit (STEL) 1000 ppm, 2380 MG/M3; Summary - THIS THRESHOLD LIMIT VALUEIS INTENDED FOR USE IN THE PRACTICE OF INDUSTRIAL HYGIENE AS A GUIDELINEOR RECOMMENDATION IN THE CONTROL OF POTENTIAL HEALTH HAZARDS.
entry date: DEC 1991
effective date:1989
title: THRESHOLD LIMIT VALUES
original : ACGIH*, Threshold Limit Values and Biological Exposure
Indices, , , 11 , 1989
amendment: ACGIH*, Threshold Limit Values and Biological Exposure
Indices, , , 11 , 1991*******
File: 17.01 LEGAL
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
area: EEC-------------------------------|subject|specification|descriptor||-------+-------------+----------|| FOOD ||RQR|| FOOD ||MXL|| FOOD ||RSTR|-------------------------------116

rn : 1402094

rtecs notype

UNEP Publications:AL3150000: REG

OECD SIDSACETONE

THE SUBSTANCE MAY BE USED FOR THE MANUFACTURE OF REGENERATED CELLULOSE
FILM WHICH IS INTENDED TO OR DOES COME INTO CONTACT WITH FOODSTUFFS. IT
MAY BY USED AS SOLVENT; MAXIMUM TOTAL QUANTITY OF ALL SOLVENTS:
0.6MG/DM2 ON THE SIDE IN CONTACT WITH FOODSTUFFS.
entry date: OCT 1987
effective date: 01APR1987
title: COUNCIL DIRECTIVE OF 25 APRIL 1983 ON THE APPROXIMATION OF THE
LAWS OF THE MEMBER STATES RELATING TO MATERIALS AND ARTICLES MADE OF
REGENERATED CELLULOSE FILM INTENDED TO COME INTO CONTACT WITHFOODSTUFFS. (83/229/EEC).
original : OJEC**, Official Journal of the European (Communities)/Union,
L123 , , 31 , 1983
amendment: OJEC**, Official Journal of the European (Communities)/Union,
L228 , , 32 , 1986*******
File: 17.01 LEGAL
rn : 1402327
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: EEC
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| FOOD |
INDST
|
PRMT
|
-------------------------------THIS SUBSTANCE, PROVIDED IT SATISFIES THE PURITY CRITERIA LAID DOWN, MAY
BE USED AS AN EXTRACTION SOLVENT DURING THE PROCESSING OF RAW MATERIALS,
OF FOODSTUFFS, OF FOOD COMPONENTS, OR OF FOOD INGREDIENTS. IT SHOULD BE
USED IN COMPLIANCE WITH GOOD MANUFACTURING PRACTICE FOR ALL USES: I.E.
ITS USE SHOULD RESULT IN THE PRESENCE OF RESIDUES OR DERIVATIVES INTECHNICALLY UNAVOIDABLE QUANTITIES PRESENTING NO DANGER TO HUMAN HEALTH.
entry date:1991
effective date: 13JUN1991
title: COUNCIL DIRECTIVE OF 13 JUNE 1988 ON THE APPROXIMATION OF THE
LAWS OF THE MEMBER STATES ON EXTRACTION SOLVENTS USED IN THE PRODUCTION
OF FOODSTUFFS AND FOOD INGREDIENTS. (88/344/EEC).
original : OJEC**, Official Journal of the European (Communities)/Union,*******

File: 17.01 LEGAL
rn : 1421907
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: EEC
type
: REG
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| CLASS ||CLASS || LABEL ||RQR|| PACK ||RQR|-------------------------------CLASS: F - HIGHLY FLAMMABLE; HIGHLY FLAMMABLE (R 11). LABEL: F - HIGHLY
FLAMMABLE; HIGHLY FLAMMABLE (R 11); KEEP CONTAINER IN A WELL-VENTILATEDPLACE (S 9); KEEP AWAY FROM SOURCES OF IGNITION - NO SMOKING (S 16); DO
NOT BREATH GAS/FUMES/VAPOUR/SPRAY (APPROPRIATE WORDING TO BE SPECIFIEDUNEP Publications

117

OECD SIDSACETONE

BY THE MANUFACTURER) (S 23); TAKE PRECAUTIONARY MEASURES AGAINST STATICDISCHARGES (S 33).
entry date: APR 1992
effective date: 1JUL1992
title: COUNCIL DIRECTIVE 67/548/EEC OF 27 JUNE 1967 ON THE APROXIMATION
OF THE LAWS, REGULATIONS AND ADMINISTRATIVE PROVISIONS RELATING TO THE
CLASSIFICATION, PACKAGING AND LABELLING OF DANGEROUS SUBSTANCES
original : OJEC**, Official Journal of the European (Communities)/Union,
196 , , 1 , 1967
amendment: OJEC**, Official Journal of the European (Communities)/Union,
L 180 , , 79 , 1991*******

File: 17.01 LEGAL
rn : 1645330
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: IMO
type
: REC
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| TRNSP |MARIN|
CLASS || LABEL |||| PACK |||-------------------------------HAZARD CLASS: 3 = INFLAMMABLE LIQUID. PACKING GROUP: II = MEDIUM DANGER(I=GREAT DANGER - III=MINOR DANGER). UN NO. 1090
entry date: JAN 1991
amendment: !IMCOC*, International Maritime Dangerous Goods Code, , ,10004 , 1990*******

File: 17.01 LEGAL
rn : 1744374
systematic name:2-Propanone
common name:acetone
reported name :ACETONE
cas no:67-64-1
rtecs no:AL3150000
area
: UN
type
: REC
-------------------------------|subject|specification|descriptor||-------+-------------+----------|| TRNSP ||CLASS || LABEL |||| PACK |||-------------------------------HAZARD CLASS: 3 = INFLAMMABLE LIQUID. PACKING GROUP: II = MEDIUM DANGER(I=GREAT DANGER - III=MINOR DANGER). UN NO. 1090
entry date: AUG 1990
amendment: !UNTDG*, UN Transport of Dangerous Goods, Recommendation
prepared by theCommittee of Experts on the Transport ofDangerous Goods, , , 15 , 1989

118

UNEP Publications