Acetone (EHC 207, 1998)

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

ENVIRONMENTAL HEALTH CRITERIA 207

ACETONE

This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.

First draft prepared by Mr D J Reisman, US Environmental Protection
Agency, Cincinnati, USA

Published under the joint sponsorship of the United Nations
Environment Programme, the International Labour Organisation, and the
World Health Organization, and produced within the framework of the
Inter-Organization Programme for the Sound Management of Chemicals.

World Health Organization
Geneva, 1998

The International Programme on Chemical Safety (IPCS),
established in 1980, is a joint venture of the United Nations
Environment Programme (UNEP), the International Labour Organisation
(ILO), and the World Health Organization (WHO). The overall
objectives of the IPCS are to establish the scientific basis for
assessment of the risk to human health and the environment from
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Chemicals (IOMC) was established in 1995 by UNEP, ILO, the Food and
Agriculture Organization of the United Nations, WHO, the United
Nations Industrial Development Organization, the United Nations
Institute for Training and Research, and the Organisation for Economic
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Development to strengthen cooperation and increase coordination in the
field of chemical safety. The purpose of the IOMC is to promote
coordination of the policies and activities pursued by the
Participating Organizations, jointly or separately, to achieve the
sound management of chemicals in relation to human health and the
environment.

WHO Library Cataloguing in Publication Data

Acetone.

(Environmental health criteria; 207)

1. Acetone 2. Environmental exposure
I. International Programme on Chemical Safety II. Series

ISBN 92 4 157207 8 (NLM Classification: QD 305.K2)
ISSN 0250-863X

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CONTENTS

ENVIRONMENTAL HEALTH CRITERIA FOR ACETONE

PREAMBLE

ABBREVIATIONS

1. SUMMARY
1.1. Properties
1.2. Uses and sources of exposure
1.2.1. Production
1.2.2. Uses and emissions into the environment
1.3. Environmental transport, distribution and transformation
1.4. Environmental levels and human exposure
1.5. Kinetics and metabolism
1.6. Effects on laboratory mammals and in vitro systems
1.7. Effects on humans
1.8. Effects on other organisms in the laboratory and field

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL
METHODS
2.1. Chemical identity
2.2. Physical and chemical properties
2.2.1. Physical properties
2.2.2. Chemical properties
2.3. Conversion factors
2.4. Analytical methods
2.4.1. Biological media
2.4.2. Environmental media

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3.1. Natural occurrence
3.2. Anthropogenic sources
3.2.1. Production levels and processes
3.2.2. Uses
3.2.3. Releases
3.2.3.1 Air
3.2.3.2 Water
3.2.3.3 Soil

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION
4.1. Transport and distribution among media
4.1.1. Air
4.1.2. Water
4.1.3. Soil
4.2. Biotransformation
4.2.1. Bioconcentration and biomagnification
4.2.2. Biodegradation
4.2.2.1 Microbial degradation

4.3. Bioavailability from environmental media
4.4. Interaction with other physical, chemical or biological
factors
4.5. Ultimate fate following use

5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1. Environmental levels
5.1.1. Air
5.1.1.1 Indoor air
5.1.2. Water
5.1.3. Soil and sediment
5.1.4. Food
5.1.5. Other environmental levels
5.2. General population exposure
5.3. Occupational exposure

6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS
6.1. Absorption
6.1.1. Inhalation exposure
6.1.1.1 Human studies
6.1.1.2 Experimental animal studies
6.1.2. Oral exposure
6.1.2.1 Human studies
6.1.2.2 Experimental animal studies
6.1.3. Dermal exposure
6.1.3.1 Human studies
6.1.3.2 Experimental animal studies
6.1.4. Absorption summary
6.2. Distribution
6.2.1. Inhalation exposure
6.2.1.1 Human studies
6.2.1.2 Experimental animal studies
6.2.2. Oral exposure
6.2.3. Injection exposure
6.2.4. Distribution summary
6.3. Metabolism
6.3.1. Human studies
6.3.2. Experimental animal studies
6.3.3. Metabolism summary
6.4. Elimination and excretion
6.4.1. Human studies
6.4.1.1 Occupational exposure studies
6.4.2. Experimental animal studies
6.4.3. Elimination/excretion summary
6.4.4. Physiologically based pharmacokinetic model
6.5. Retention and turnover

7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS
7.1. Short-term toxicity
7.1.1. Skin and eye irritation
7.2. Longer-term toxicity
7.3. Reproductive toxicity, embryotoxicity and teratogenicity
7.4. Mutagenicity
7.5. Carcinogenicity
7.6. Immunotoxicity
7.7. Special studies
7.8. Factors modifying toxicity; toxicity of metabolites
7.9. Mechanisms of toxicity - mode of action

8. EFFECTS ON HUMANS
8.1. Effects on humans
8.1.1. Non-occupational exposure
8.1.2. Occupational exposure
8.2. Subpopulations at special risk

9. EFFECT ON OTHER ORGANISMS IN THE LABORATORY AND FIELD
9.1. Aquatic organisms
9.1.1. Acute toxic effects on aquatic fauna
9.1.2. Chronic effects on aquatic fauna
9.1.3. Effects on aquatic plants

9.2. Effects on bacteria and protozoa
9.3. Terrestrial organisms
9.3.1. Effects on fauna
9.3.2. Effects on flora

10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
10.1. Evaluation of human health effects
10.2. Evaluation of effects on the environment

11. FURTHER RESEARCH

12. PREVIOUS EVALUATION BY INTERNATIONAL BODIES

REFERENCES

RÉSUMÉ

RESUMEN

NOTE TO READERS OF THE CRITERIA MONOGRAPHS

Every effort has been made to present information in the criteria
monographs as accurately as possible without unduly delaying their
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Criteria monographs, readers are requested to communicate any errors
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* * *

A detailed data profile and a legal file can be obtained from the
International Register of Potentially Toxic Chemicals, Case postale
356, 1219 Châtelaine, Geneva, Switzerland (telephone no. + 41
22 - 9799111, fax no. + 41 22 - 7973460, E-mail irptc@unep.ch).

* * *

This publication was made possible by grant number
5 U01 ES02617-15 from the National Institute of Environmental Health
Sciences, National Institutes of Health, USA, and by financial support
from the European Commission.

Environmental Health Criteria

PREAMBLE

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* Effects on laboratory mammals and in vitro test systems
* Effects on humans
* Effects on other organisms in the laboratory and field
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JMPR

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WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR ACETONE

Members

Dr D. Anderson, British Industrial Biological Research Association
(BIBRA) Toxicology International, Carshalton, Surrey, United Kingdom

Dr Sin-Eng Chia, Department of Community, Occupational and Family
Medicine, National University of Singapore, Faculty of Medicine,
Singapore

Mr J. Fawell, National Centre for Environmental Toxicology, Medmenham,
United Kingdom

Dr L. Fishbein, Fairfax, Virginia, USA ( Chairman)

Dr H. Hansen, Division of Toxicology, Agency for Toxic
Substances and Disease Registry, Atlanta, Georgia, USA

Mr H. Malcolm, Institute of Terrestrial Ecology, Monks Wood
Experimental Station, Huntingdon, United Kingdom ( Co-Rapporteur)

Dr M.V. Park, Edinburgh Centre for Toxicology, Edinburgh, United
Kingdom

Mr D.J. Reisman, National Center for Environmental Assessment, US
Environmental Protection Agency, Cincinnati, Ohio, USA
( Co-Rapporteur)

Dr A. Wibbertman, Fraunhofer Institute for Toxicology and Aerosol
Research, Hanover, Germany ( Vice-Chairman)

Observers

Dr D. Morgott, Toxicological Sciences Laboratory, Health, Safety and
Environment, Eastman Kodak Company, Rochester, New York, USA
(representing the American Industrial Health Council)

Dr D. Owen, Shell Chemicals Europe Limited, London, United Kingdom
(representing the European Centre for Ecotoxicology and Toxicology of
Chemicals)

Dr P. Montuschi, Department of Pharmacology, Catholic University of
the Sacred Heart, Rome, Italy (representing the International Union of
Pharmacology)

Secretariat

Dr E. Smith, International Programme on Chemical Safety, World Health
Organization, Geneva, Switzerland

WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR ACETONE

A WHO Task Group on Environmental Health Criteria for Acetone met
at the British Industrial Biological Research Association (BIBRA)
Toxicology International, Carshalton, Surrey, United Kingdom, from 1
to 5 December 1997. Dr S. Jaggers opened the meeting and welcomed the
participants on behalf of the host institute. Dr E. Smith, IPCS,
welcomed the participants on behalf of the Director, IPCS, and the
three IPCS cooperating organizations (UNEP/ILO/WHO). The Task Group
reviewed and revised the draft criteria monograph and made an
evaluation of the risks for human health and the environment from
exposure to acetone.

Mr D.J. Reisman, US Environmental Protection Agency, Cincinnati,
USA, prepared the first draft of this monograph. The second draft,
incorporating comments received following the circulation of the first
draft to the IPCS Contact Points for Environmental Health Criteria
monographs, was also prepared by Mr. Reisman.

Dr E.M. Smith and Dr P.G. Jenkins, both of the IPCS Central Unit,
were responsible for the overall scientific content and technical
editing, respectively.

The efforts of all who helped in the preparation and finalization
of the monograph are gratefully acknowledged.

* * *

The US Environmental Protection Agency funded the preparation of
this Environmental Health Criteria monograph, financial support for
the Task Group meeting was provided by the United Kingdom Department
of Health, and the meeting was organized by the British Industrial
Biological Research Association (BIBRA).

ABBREVIATIONS

BOD biochemical oxygen demand
CAS Chemical Abstracts Services
DOT/UN/NA/IMCO Department of Transportation/United Nations/North
America/International Maritime Dangerous Goods Code
EINECS European Inventory of Existing Chemical Substances
EPA Environmental Protection Agency
FID flame ionization detector
GC gas chromatography
HPLC high performance liquid chromatography
HRGC high resolution gas chromatography
HSDB Hazardous Substances Data Bank
IC ion chromatography
LOEL lowest-observed-effect level
MS mass spectrometry
NCI National Cancer Institute
NIOSH National Institute for Occupational Safety and Health
NOEL no-observed-effect level
OHM/TADS Oil and Hazardous Materials/Technical Assistance Data
System
ppbv parts per billion (by volume)
RBC red blood cell
RCRA Resource Conservation and Recovery Act
RGD reduction gas detector
RTECS Registry of Toxic Effects of Chemical Substances
TWA time-weighted average
UV ultraviolet
v/v volume per volume
WBC white blood cell

1. SUMMARY

1.1 Properties

Acetone (relative molecular mass = 58.08) is a clear colourless
flammable liquid (flash point -17°C closed cup, -9°C open cup;
flammability limits in air at 25°C = 2.15-13% v/v). The explosive
limits in air are 2.6-12.8% v/v. It has a high evaporation rate
(vapour pressure 181.72 mmHg at 20°C) and a low viscosity (0.303 cP at
25°C). It is miscible with water and organic solvents.

1.2 Uses and sources of exposure

1.2.1 Production

Acetone is manufactured mainly by the cumene peroxidation or
isopropyl alcohol dehydrogenation processes. The cumene peroxidation
process produces trace quantities of benzene as a by-product.

1.2.2 Uses and emissions into the environment

Acetone is used mainly as a solvent and intermediate in chemical
production. Major uses are in the production of methyl methacrylate,
methacrylic acid and higher methacrylates, bisphenol A, methyl
isobutyl ketone, drug and pharmaceutical applications, and as a
solvent for coatings and for cellulose acetate. There are also food
uses as an extraction solvent for fats and oils, and as a
precipitation agent in sugar and starch purification.

Atmospheric emissions occur from consumer products including nail
polish removers, particle board, carpet backing, some paint removers,
and liquid/paste waxes or polishes. Certain detergents/cleansers,
adhesives, and automobile carburetor and choke cleaners also contain
acetone.

Acetone is released into surface water in wastewater effluents
from a wide range of manufacturing processes and industries, such as
paper, plastic, pharmaceuticals, specialty cleaning and polishing
products, paint and allied products, gum and wood chemicals, cyclic
intermediates, industrial organic chemicals, gypsum products, paper
board products, and energy-related industries, such as
coal-gasification and oil shale processing.

Sources of acetone release into soil include disposal of
agricultural and food waste, animal waste, atmospheric wet deposition,
household septic tank effluents and chemical waste disposal sites.

1.3 Environmental transport, distribution and transformation

Acetone released to the atmosphere is degraded by a combination
of photolysis and reaction with hydroxyl radicals. The average
half-life for acetone degradation in the atmosphere is approximately
30 days. Acetone can be physically removed from air by wet deposition.
The dominant degradation process for acetone in soil and water is
biodegradation, and acetone is readily biodegradable. Volatilization
of acetone from the aquatic environment can be a significant transport
process. Acetone is a volatile compound that will evaporate from dry
surfaces. Since acetone is miscible in water, it can leach readily in
most types of soil. Concurrent biodegradation may diminish the general
significance of leaching if biodegradation occurs fast enough.

1.4 Environmental levels and human exposure

Exposure to acetone results from both natural and anthropogenic
sources. Acetone also occurs as a metabolic component in blood, urine
and human breath. It occurs as a biodegradation product of sewage,
solid wastes and alcohols, and as an oxidation product of humic
substances. Acetone has been detected in a variety of plants and foods
including onions, grapes, cauliflower, tomatoes, morning glory, wild
mustard, milk, beans, peas, cheese and chicken breast. Natural
emissions from a variety of tree species contain acetone vapour. Human
sources of emissions to the aquatic environment include waste-water
discharges from many industries and leaching from industrial and
municipal landfills. A major source of human emission to air is
evaporation of acetone solvent from coating products such as paints,
cleaners, varnishes and inks. Acetone is an emission product from the
combustion of wood, refuse and plastics. It is also emitted in exhaust
from automobile, diesel and turbine engines. Concentrations of acetone
monitored in the atmosphere range from 0.5 to 125.4 µg/m³ (0.2-52.9
ppb).

1.5 Kinetics and metabolism

Acetone is one of three ketone bodies that occur naturally
throughout the body. It can be formed endogenously in the mammalian
body from fatty acid oxidation. Fasting, diabetes mellitus and
strenuous exercise increase endogenous generation of acetone. Under
normal conditions, the production of ketone bodies occurs almost
entirely within the liver and to a smaller extent in the lung and
kidney. The process is continuous, and the three products are excreted
into the blood and transported to all tissues and organs of the body
where they can be used as a source of energy. Two of these ketone
bodies, acetoacetate and ß-hydroxybutyrate, are organic acids that can
cause metabolic acidosis when produced in large amounts, as in
diabetes mellitus. Acetone, in contrast, is non-ionic and is derived
endogenously from the spontaneous and enzymatic breakdown of
acetoacetate. Endogenous acetone is eliminated from the body either by

excretion in urine and exhaled air or by enzymatic metabolism. Under
normal circumstances, metabolism is the predominant route of
elimination and handles 70-80% of the total body burden.

Acetone is rapidly absorbed via the respiratory and
gastrointestinal tracts of humans and laboratory animals, as indicated
by the detection of acetone in blood within 30 min of inhalation
exposure and 20 min of oral administration. Studies of rats indicate
that orally administered acetone is extensively absorbed, whereas
during inhalation exposures humans absorb approximately 50% of the
amount of inhaled acetone. However, lower and higher respiratory
absorption values have been reported. The nasal cavities of humans and
laboratory animals appear to have a limited ability to absorb and
excrete acetone vapour, compared with the remainder of the respiratory
tract.

Acetone is uniformly distributed among non-adipose tissues and
does not accumulate in adipose tissues. In mice, maximum acetone
concentrations in adipose tissues were reported to be about one-third
of those in non-adipose tissues following inhalation exposure. Acetone
is rapidly cleared from the body by metabolism and excretion.
Half-times for acetone in human alveolar air and venous and arterial
blood are -4, 6 and 4 h, respectively. Exhalation is the major route of
elimination for acetone and its terminal metabolite (CO₂) and the
fraction of administered acetone that is exhaled as unchanged acetone
is dose-related. Urinary excretion of acetone and its metabolites
occurs, but this route of elimination is minor compared with
exhalation of acetone and respiratory CO₂.

Exogenously supplied acetone enters into many metabolic reactions
in tissues throughout the body, but the liver appears to be the site
of most extensive metabolism. Carbon from orally administered acetone
has been detected in cholesterol, ammo acids, fatty acids and glycogen
in rat tissues, urea in urine and unchanged acetone and CO₂ in
exhaled breath. Metabolically, acetone is degraded to acetate and
formate; this accounts for the entry of carbon from acetone into
cholesterol, fatty acids, urea and amino acids, and formation of
3-carbon gluconeogenic compounds.

Gluconeogenesis from acetone has been proposed to proceed by two
pathways. The first pathway proceeds through the initial catalytic
action of acetone monooxygenase and acetol monooxygenase, which
convert acetone to acetol and acetol to methylglyoxal, respectively.
Both of these enzymatic activities are induced by acetone and have
been identified as an isozyme of ethanol-inducible, hepatic eytochrome
P-450IIE1. The second gluconeogenic pathway involves the formation of
1,2-propanediol from acetone catalysed by acetone monooxygenase and a
non-characterized enzyme capable of converting acetol to
1,2-propanediol.

1.6 Effects on laboratory mammals and in vitro systems

Oral LD₅₀ values in adult rats are in the range of 5800-7138
mg/kg. The 4-h inhalation LC₅₀ value is 76 000 mg/m³ (32 000 ppm).

Acute exposure to acetone has been found to alter performance in
neurobehavioural tests in laboratory animals at concentrations greater
than 7765 mg/m³ (>3270 ppm).

Experimental animal data characterizing the effects of long-term
oral or inhalation exposure to acetone are not available, due probably
to its low toxicity and its endogenous characteristics.

Prolonged acetone inhalation exposure of rats to 45 100 mg/m³
(19 000 ppm), 3 h/day, 5 days/week for 8 weeks, produced a reversible
decrease in absolute brain weight. No consistent changes were noted in
weights of other organs or the whole body, in blood chemical indices,
in liver triglyceride levels or in the histology of the heart, lung,
kidney, brain or liver.

In a 90-day gavage study of rats, increased blood parameters
(increased haemoglobin, haematocrit) were observed at dose levels
>500 mg/kg per day, and a NOAEL of 500 mg/kg per day was identified.
In a 13-week drinking-water study, toxic effects were noted in male
rats exposed to concentrations >20 g/litre (approx. 1700 mg/kg body
weight per day), namely increased relative organ weights, altered
haematological indices and mild nephropathy. In female rats
administered the highest concentration, 50 g/litre (approx. 3400 mg/kg
body weight per day), the effects were increased organ relative
weights and altered haematological indices. In addition, a 13-week
exposure to 50 g/litre caused altered relative testis weight and
altered sperm motility and morphology in male rats. Female mice given
50 g/litre (approx. 11 298 mg/kg body weight per day) in
drinking-water had altered liver and spleen weights and a marginally
increased incidence of centrilobular hepatocellular hypertrophy. No
toxic effects were observed in male mice administered 20 g/litre (4858
mg/kg body weight per day), the highest acetone level administered to
male mice. Thirteen-week exposures to concentrations < 10 g/litre
(900 mg/kg body weight per day) in drinking-water were associated with
no toxic effects in male rats; concentrations < 20 g/litre were
NOELs for female rats (1600 mg/kg body weight per day) and mice (male
4858 mg/kg body weight per day; female 5945 mg/kg body weight per day)
of both sexes.

In a preliminary 14-day drinking-water study of rats and mice,
dose-related centrilobular hepatocellular hypertrophy was noted in
male mice exposed to concentrations of 20-100 g/litre.

Pretreatraent of rodents with acetone enhances the hepatotoxic
effects of a number of compounds, notably halogenated alkanes, It is
hypothesized that the potentiation of the hepatotoxicity is mediated
by acetone-induced elevations of enzymatic activities (hepatic
mixed-function oxidases) that are responsible for the generation of
toxic intermediates from administered halogenated alkanes.

Acetone has tested negatively for genetic toxicity in numerous
non-mammalian systems, as well as in in vitro and in vivo
mammalian systems. Positive results are restricted to a single test
for aneuploidy in a yeast species exposed to high concentrations of
acetone (6.82%) in its growth medium. Acetone is not considered to be
genotoxic or mutagenic.

In a study of pregnant rats and mice exposed to acetone vapour
during days 6-19 of gestation, slight developmental toxicity was
observed following exposures of rats to 26 100 mg/m³ (11 000 ppm) for
6 h/day (increased percentage of litters with at least one fetal
malformation) and following exposures of mice to 15 670 mg/m³ (6600
ppm) for 6 h/day (small decrease in fetal weight and small increase in
percentage incidence of late resorptions). An atmospheric
concentration of 5200 mg/m³ (2200 ppm) was identified as a NOAEL for
developmental toxicity in both mice and rats. In a gavage study,
treatment at 3500 mg/kg per day during organogenesis impaired
reproduction in a screening test in mice. Negative results in vivo
in two different species, using oral and intraperitoneal routes,
indicated that no mutagenic changes were produced in mammals exposed
to acetone.

Reports of other reproductive effects of acetone include
observations of testicular effects and changes in sperm quality in
rats administered drinking-water containing 50 g acetone/litre for 13
weeks. No investigations of the effect of oral doses of acetone on
fetal development (fetotoxicity and teratogenicity) were available.

Acetone has been used extensively as a solvent vehicle in skin
carcinogenicity studies and is not considered carcinogenic when
applied to the skin.

1.7 Effects on humans

Acetone is relatively less toxic than many other industrial
solvents; however, at high concentrations, acetone vapour can cause
CNS depression, cardiorespiratory failure and death. Acute exposures
of humans to atmospheric concentrations as high as approx. 4750 mg/m³
(approx. 2000 ppm) have been reported to produce either no gross toxic
effects or minor transient effects, such as eye irritation. More
severe transient effects (including vomiting and fainting) were
reported for workers exposed to acetone vapour concentrations >25 500
mg/m³ (>12 000 ppm) for approx. 4 h. Acute exposures to acetone have
also been reported to alter performance in neurobehavioural tests in

humans at 595 mg/m³ (250 ppm). Females exposed to atmospheric
concentrations of 2370 mg/m³ (1000 ppm) were reported to suffer
menstrual irregularities.

1.8 Effects on other organisms in the laboratory and field

For most freshwater and saltwater animal species, 48- and 96-h
LC₅₀ and EC₅₀ values are >5540 mg/litre.

Growth of the alga Chlorella pyrendoidosa exposed to acetone at
257.4 mg/litre for 76 h was inhibited. There was inhibition of growth
of Chlamydomonas eugametos exposed to acetone for 48 h at 790
mg/litre. Photosynthesis was increased in Scendesmus quadricauda and
C. pyrenoidosa exposed to 79.0 and 790 mg/litre.

The 7- to 8-day toxicity thresholds for the green alga
S. quadricauda and the cyanobaeterium (blue-green alga)
Microcystis aeruginosa were 7500 and 530 mg/litre, respectively,
indicating that the green alga was more resistant to the toxic action of
acetone. The diatom Nitzschia linearis also seemed very resistant,
with a 5-day EC₅₀ of 11 493 to 11 727 mg/litre. Similarly, the saltwater
diatom Skeletonema costatum was very resistant with 5-day EC₅₀
values of 11 798 and 14 440 mg/litre.

Bacteria appear more resistant to acetone than protozoans.
Photobacterium phosphoreum, Pseudomonas putida and a mixed
microbial culture had EC₅₀ values of 1700 to 35 540 mg/litre, and the
protozoan Entosehon sulcatum had an EC₅₀ of 28 mg/litre. This may
be related to cell wall differences.

Quails and pheasants had oral 5-day LC₅₀ values > 40 g/kg
diet. Fertile mallard eggs were not affected when immersed in 10%
acetone for 30 seconds; however, immersion in 100% acetone resulted in
decreases in survival, embryonic weight and embryonic length, but it
is not clear if this was due to the toxic or the solvent properties of
acetone. White Leghorn chicken eggs injected with 5 µl acetone did not
appear to have any significant changes in mortality or malformations.

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS

2.1 Chemical identity

Chemical name acetone
Synonym(s) dimethyl ketone; 2-propanone;
beta-ketopropane
Chemical formula C₃H₆O
Chemical structure
O
"
H₃C - C - CH₃

Identification numbers:
CAS registry 67-64-1

NIOSH RTECS AL3150000

EPA Hazardous Waste
(RCRA) U002; F003

OHM/TADS 7216568

DOT/UN/NA/IMCO shipping UN1090

HSDB 41

EINECS 200-662-2

Relative molecular mass 58.08

2.2 Physical and chemical properties

2.2.1 Physical properties

Acetone is a clear and colourless liquid with a strong "fruity"
odour. It is miscible with water and organic solvents such as ether,
methanol, ethanol and esters (Nelson & Webb, 1978). The physical
properties of acetone, such as high evaporation rate, low viscosity
and miscibility, make it suitable for use as a solvent (Krasavage et
al., 1982). The physical properties of acetone are shown in Table 1.

2.2.2 Chemical properties

Acetone shows reactions typical of saturated ketones (SRI, 1996).
These reactions include addition, oxidation-reduction and
condensation, and yield alcohols, ketals, acids and amines (Papa &
Sherman, 1981). The chemical reactivity of acetone is commercially
important for the synthesis of methyl methacrylate, diacetone alcohol,
bisphenol A and other derivatives (SRI, 1996).

Table 1. Physical and chemical properties of acetone

Property Value/description^a Reference

Relative molecular mass 58.08 Riddick et al, (1986)

Colour Clear colourless Sax & Lewis (1987)

Physical state Liquid Sax & Lewis (1987)

Melting point -95.35°C Weast (1987}

Freezing point -94.7°C at 1 atm Riddick et al. (1986)

Boiling point 56.2°C at 1 atm Weast (1987)
(760 torr)

Density:

at 20°C 0.78996 g/ml Riddick et al. (1986)

at 26°C 0.78440 g/ml Riddick et al. (1966)

at 30°C 0.78033 g/ml Riddick et al. (1986)

Odour threshold:

Acetone in water 20 mg/litre Amoore & Hautala
(1983)

Air (absolute) 30-48 mg/m³ Amoore & Hautala
(13-26 ppm (v/v)) (1983)

Air (detection) 9.5 mg/m³ (4 ppm) Wysocki et al. (1997)

100% odour recognition 237-332 mg/m³ Hellman & Small
(100-140 ppm) (1974); Leonardos et
al. (1969)

Table 1 (contd).

Property Value/description^a Reference

Solubility:

Water at 20°C Completely miscible Windholz (1963)

Organic solvent(s) Soluble in organic
solvents Windholz (1983)

Viscosity at 25°C 0.303 cP Riddick et al. (1986)

Partition coefficients:

Log K_ow -0.24 Sangster (1989)
Log K_oc 0.73^b Lyman (1982)
K_B/A 301 ± 22 Dills et al. (1994)

Vapour pressure 181.72 mmHg (at 20°C) Riddick et al. (1986)
231.06 mmHg (at 25°C) Riddick et al. (1986)

Henry's law constant: 4.26 × 10^-5 atm-m³/mol Rathbun & Tai (1987)
at 25°C

Flashpoint (closed cup) -17°C Riddick et al. (1986)
(open cup) -9°C Riddick et al. (1986)

Flammability limits Lower, 2.2%; Clayton & Clayton
in air at 25°C upper, 13.0% (1982)

Minimum ignition 465°C Riddick et al. (1986)
temperature

Explosive limits Lower, 2.6% in air (v/v); Sax & Lewis (1987)
upper, 12.8% in air (v/v) Sax & Lewis (1987)

^a w/v = weight per volume, v/v = volume per volume.
^b Estimated by regression equation 4-13 in Lyman (1982).

2.3 Conversion factors

Conversion factors in air at 25°C:
1 ppm = 2.374 mg/m³
1 mg/m³ = 0.421 ppm

2.4 Analytical methods

A number of analytical methods is available for the detection,
sampling and monitoring of acetone and its metabolites in the various
media. Acetone is a well-studied chemical and is used frequently in
the laboratory. This section is a review of the more established and
standard practices in use today.

2.4.1 Biological media

Methods for determining the presence of acetone in biological
organisms are listed in Table 2. Acetone is found in almost every
tissue and organ in the human body. Acetone and two other chemicals,
beta hydroxybutyrate and acetoacetate, are collectively referred to as
"ketone bodies". In the last 30 years much has been learned of acetone
in biological tissue since the discovery that acetone levels in
diabetes mellitus patients with severe hyperketonaemia may be
significant (Trotter et al., 1971). Higher acetone levels may be found
in the blood levels of individuals or animals after strenuous exercise
or prolonged dieting. Acetone production is also increased in animals
in disease states such as diabetes and anorexia.

The development of biological analytical methods can be done to
measure, but this does not distinguish acetone from either endogenous
and exogenous sources or from acetone in ketone levels in body fluids,
since acetone is produced within the biological system by breaking
down lipids and stored fats. Most of the methods for measuring acetone
in expired air use gas chromatography (GC/FID) and involve the
breakdown of beta-hydoxybutyrate and acetoacetate into acetone, which
is isolated and quantified by any of the techniques listed in Table 2.
The differences between these methods have been mainly concerned with
the nature of the column packing and with the various methods of
sample collection.

The determination of acetone in blood is difficult because it is
a metabolite and the quantity produced depends on storage time, even
when the blood samples are stored at 4°C (Trotter et al., 1971). The
delay between sample collection and analysis could lead to spuriously
elevated acetone concentrations because of the spontaneous
decarboxylation of acetoacetate (Van Stekelenburg & Koorevaar, 1972).
One method for the determination of acetone in the clinical laboratory
involves deproteinizing with acetonitrile and derivitization of the
sample with 2,4-dinitrophenylhydrazine, followed by isolation and
quantification of the hydrazone by high pressure liquid chromatograph

Table 2. Analytical methods for determining acetone in biological media

Sample matrix Preparation method Analytical Sample detection Reference
method limit

Whole blood, urine Centrifuged and deproteinized GC-HPLC 33 µg/ml Gavino et al. (1986)
with acetonitdle and 2,4-DNPH
added

Whole blood Deproteinized with HClO₄ and GC-FID 0.4 µmol/litre Mangani & Ninfali
subjected to purge-and-trap (1988)

Whole blood Purge-and-trap GC-MS 0.2 µg/ml Ashley et al. (1992)

Serum Deproteinized with sodium HRGC-FID <58 µg/ml Smith (1984)
tungstate and cupric sulfate (<1 nmol/litre)

Serum Sample centrifuged and clear GC-FID 5.8 mg/ml Cheung & Lin
filtrate injected (0.1 nmol/ml) (1987)
into GC

Urine Diluted sample derivatized with GC-FID 0.2 µg/ml Kobayashi et al.
pentafiuorobenzyloxyl ammonium (3.45 µmol/ml) (1983)
chloride and extracted with
hexane

Liver perfusate, Reduction to isopropanol using GC-HPLC 33 µmol/ml Gavino et al. (1987)
blood, urine sodium borohydrid and
separation by HPLC

Liver Liver perfusion medium reduced GC-FID 3.78 µg/ml in Holm & Lundgren
with NaBH₄ and an aliquot of perfusate (1984)
reduced solution injected (65 µmol/litre)
into GC

Liver, kidney, lung Purge-and-trap GC-FID No data Holm & Lundgren
and adipose tissue (1984)

Breath Direct injection into GC GC-FID No data Trotter et al. (1971);
Jansson & Larsson (1969)

(HPLC) (Brega et al., 1991). This method prevents acetoacetate, which
is present in plasma, from being thermally degraded to acetone on the
column when using a GC method (Gavino et al., 1987). The HPLC method
can also be used to measure acetone in urine or liver perfusate. This
method can be used in experiments requiring multiple samples and thus
can be used for diabetic patient monitoring, as well as for
occupational exposure monitoring.

2.4.2. Environmental media

Analytical methods for determining acetone in air, water and soil
are presented in Table 3. The commonly used methods are direct GC/MS
of a sample concentrate or HPLC of the 2,4-dinitrophenyl-hydrazine
derivative. In the United Kingdom, the 2,4-dinitrophenyl-hydrazine
HPLC method is applied to the analysis of acetone in water and there
is a standardized validated method (UK SAC, 1988).

When sampling for acetone, the incorrect use of Tedlar bags and
activated carbon may lead to spurious results.

Table 3 Analytical methods for determining acetone in environmental samples

Sample matrix Preparation method Analytical method Sample detection Reference
limit

Air (occupational) Air passed through charcoal and components GC-FID (NIOSH 7 µg/litre NIOSH (1994)
desorbed with CS₂ method 1300)

Air Air passed through a cryogenic trap and the GC-RGD 10 ppt O'Hara & Singh
(ambient) trapped component injected into GC (1988)

Air Air passed through HPLC-UV <3 µg/litre Risner (1995)
(ambient) 2,4-dinitrophenylhydrazine-coated cartridge and eluted reversed-phase
with acetonitrile and tetrahydrofuran column

Air (indoor) Diffusive sampler with silica gel tape impregnated with HPLC-UV 15 µg/litre Brown et al.
2,4-dinitrophenylhydrazine and eluted with acetonitrile (1994)

Air Air passed through a 1% sodium bisulfite solution and Spectrophotometry <0.5 ppm (in Amlathe & Gupta
absorbed acetone reacted with alkaline vanilla solution solution) (1990)

Rural air Air passed through silica gel coated with HPLC-UV No data Shepson et al.
2,4-dinitrophenylhydrazine and eluted with acetonitrile (1991)

Water Sample reacted with alkaline diazotized anthranilic Spectrophotometry 500 µg/litre Rahim & Bashir
acid solution (1981)

Fresh and seawater Sample derivatized with 2,4-dinitrophenylhydrazine HPLC-UV detection 0.5 nmol/litre Kieber & Mopper
passed through a C₁₈ cartridge and absorbed (0.03 µg/litre) (1990)
compound eluted with acetonitrile

Waste water, soil or Sample or sample mixed with reagent water subjected GC-MS 100 µg/litre US EPA (1986b)
sediment to purge-and-trap (EPA method 8240) (water)
100 µg/k9
(sediment and
soil)

Fresh fruit Vacuum distillation followed by solvent extraction HRGC-MS No data Takeoka et al.
of pulp (1988)

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1 Natural occurrence

Acetone occurs as a metabolic component in blood, urine and human
breath (Conkle et al., 1975). Because endogenous acetone formation is
so closely linked with the utilization of stored fats as a source of
energy, background levels can fluctuate depending on an individual's
health, nutrition, and level of activity (Morgott, 1993). The acetone
level in the human body at any instant is reflective of acetoacetate
production and ketogenesis. It occurs naturally as a biodegradation
product of sewage, solid wastes and alcohols and as an oxidation
product of humic substances. Acetone has been detected in a variety of
plants and foods, including onions, grapes, cauliflower, tomatoes,
morning glories, wild mustard, milk, beans, peas, cheese and chicken
breast (Day & Anderson, 1965; Grey & Shrimpton, 1967; Palo & Ilkova,
1970; Lovegren et al., 1979). Natural emissions from a variety of tree
species contain acetone vapour (Isidorov et al., 1985) and another
source is direct emission from the ocean (Zhou & Mopper, i990).

3.2 Anthropogenic sources

There are many anthropogenic sources of acetone, with various
levels and concentrations that cover a broad range. Human sources of
emissions to the aquatic environment include wastewater discharges
from many industries (Perry et al., 1978; NLM, 1992) and leaching from
industrial and municipal landfills (Sabel & Clark, 1984; Brown &
Donnelly, 1988). A major source of emission to the air is from
evaporation of acetone solvent from coating products such as paints,
cleaners, varnishes and inks. Acetone is an emission product from the
combustion of wood, refuse and plastics (Lipari et al., 1984; Graedel
et al., 1986), and is emitted in exhaust from automobile, diesel and
turbine engines (Barber & Lodge, 1963; Lloyd, 1978; Jonsson ct al.,
1985; Graedel et al., 1986; Westerholm et al., 1988; Zweidinger et
al., 1988).

Other important anthropogenic sources of acetone in the air are
chemical manufacture (Graedel et al., 1986), tobacco smoke (Manning et
al., 1983), wood burning and pulping (Lipari et al., 1984; Graedel et
al., 1986; Kleindienst et al., 1986), polyethylene burning (Hodgkin et
al., 1982), refuse combustion (NAS, 1976), petroleum production
(Graedel, 1978), and certain landfill sites (LaRegina et al., 1986;
Militana & Mauch, 1989; Hodgson et al., 1992). Acetone is formed in
the atmosphere from the photochemical oxidation of propane (Singh &
Hanst, 1981; Arnold et al., 1986) and possibly from propylene oxide
and epichlorohydrin (Spicer et al., 1985).

In a US EPA-sponsored survey of household products analysed by
purge-and-trap GC/MS for volatile organic compounds, acetone was found

in 314 of 1005 products (31.2%). Of the eight product categories, the
highest categories were paint-related (51.5% contained acetone),
adhesive-related (24.3%) and automotive (22.7%) products (Sack et al.,
1992).

3.2.1 Production levels and processes

In 1994, world acetone capacity amounted to almost 3.83 million
tonnes (SRI, 1996). Since approximately 80% of acetone is produced as
a co-product of phenol, demand for phenol largely determines acetone
production levels. World production in 1994 was estimated to be 3.22
million tomes, and demand for acetone was expected to grow at an
average annual rate of 3.3% annually from 1994 to 1999 (SRI, 1996).

The USA is the largest producer of acetone. Table 4 depicts the
capacity of the largest manufacturers in the USA in 1995, while Table
5 shows the capacity of other countries. The annual capacity in the
European Union in 1992-1994 was 1.1-1.2 million tonnes.

Most acetone is manufactured by one of two processes, cumene
peroxidation (94% yield) or isopropyl alcohol dehydrogenation (IPA)
(95% yield) (SRI, 1996). In the peroxidation process, cumene is
oxidized to hydroperoxide, which is cleaved to yield acetone and
phenol. In the dehydrogenation process, isopropyl alcohol is
catalytically dehydrogenated to yield acetone and hydrogen (Nelson &
Webb, 1978). The cumene peroxidation process accounts for 96%; IPA
accounts for the other 4%. Production grade acetone is 99.5% acetone,
0.5% water. Fermentation of corn starch and molasses to produce
acetone, using Clostridium acetobutylicium, is utilized in several
countries, including Russia, Egypt, Brazil and India (Sifniades,
1985). Although acetone is more costly to produce by the IPA process,
this process has no benzene contamination. Acetone produced through
the cumene process contains benzene at concentrations < 10 ppm
(SRI, 1996).

Some companies recover acetone as a by-product (SRI, 1996). For
example, in the United Kingdom there is a plant producing 52 000
tonnes per year that recovers acetone as a by-product of acetic acid
manufacture, and two Japanese manufacturers recover acetone from
cresol production.

3.2.2 Uses

Acetone is used primarily as an intermediate in chemical
production and as a solvent (SKI, I996). It is used as a solvent for
resins, paints, inks, varnishes and lacquers and in adhesives,
thinners and clean-up solvents. Pharmaceutical applications of acetone
include use as an intermediate and solvent for drags, vitamins and
cosmetics (Nelson & Webb, 1978). It has uses as an extraction solvent
for fats and oils and a precipitation agent in the purification of
starches and sugars (FAO/WHO, 1971).

Table 4: Major manufacturers of acetone in the USA in 1995^a

Manufacturer Location Annual capacity
(thousands of tonnes)

Allied Signal, Inc, Philadelphia, PA 280
Aristech Chemical Corp. Ironton, OH 180
Dow Chemical USA Oyster Creek, TX 161
Eastman Chemical Co. Kingsport, TN 13
Mt. Vernon Partnership Mount Vernon, IN 191
Georgia Gulf Corp. Pasadena, TX 45
Plaquemine, LA 123
Goodyear Tire & Rubber Co. Bayport, TX 7
JLM Chemicals, Inc. Blue Island, IL 26
Shell Chemical Co. Deer Park, TX 182
Texaco, Inc. El Dorado, KS 26
Union Carbide Corp. Institute, WV 77

Total 1281

^a SRI (1996)

Table 5: Production capacity of acetone in 1995 (excluding the USA)^a

Country Annual capacity
(thousands of tonnes)

Germany 388
Italy 235
France 168
United Kingdom 97
Netherlands 80
Spain 75
Brazil 71
Finland 65
Mexico 22
Argentina 20
Venezuela 10

TOTAL 1185

^a SRI (1996)

In 1995 the USA use pattern for acetone was as follows: acetone
cyanohydrin/methyl methacrylate, methacrylic acid and higher
methacrylates (45%); solvent applications (17%); bisphenol A (18%);
aldol chemicals/methyl isobutyl ketone and others (12%); and
pharmaceutical and other applications (8%) (SKI, 1996).

The largest solvent application for acetone is as a surface
coating, including use as a thinner and wash solvent. In 1995,
greatest use of acetone as a solvent was in automotive coatings, both
original equipment and automotive refinishing (SKI, 1996). The next
greatest use for acetone is the production of acetone cyanohydrin
which is used to produce an acrylic resin monomer, methyl
methacrylate. Bisphenol A is produced from acetone and used in
polycarbonate resins.

Acetone is also used in food processing as an extraction solvent
for oils and fats and as a precipitation agent in the purification of
starches and sugars.

3.2.3 Releases

3.2.3.1 Air

Atmospheric emissions are likely from the many consumer products
containing acetone (US EPA, 1989). Such products include nail polish
removers, particle board (Tichenor & Mason, 1988), carpet backing
(Hodgson et al., 1993), some paint removers, a number of liquid/paste
waxes or polishes, some detergents/cleansers, adhesives (Knöppel &
Schauenburg, 1989; Sack et al., 1992) and carburetor and choke
cleaners (US EPA, 1989).

Atmospheric emissions from the phenol/acetone production process
are approximately 0.44 g per kg of acetone produced (Sifniades, 1985).

3.2.3.2 Water

Acetone is released into surface water as wastewater from certain
chemical manufacturing industries (Jungclaus et al., 1978; Hites &
Lopez-Avila, 1980; Gordon & Gordon, 1981). It is also released in
water from energy-related industries, such as coal-gasification
(Pellizzari et al., 1979; Mohr & King, 1985) and oil shale processing
(Pellizzari et al., 1979; Hawthorne & Sievers, 1984). Acetone was
found in 27 of 63 effluent water samples from a wide range of chemical
industries in the USA (Perry et al., 1979). It has been detected in
effluents from various industrial production processes including
paper, plastic, pharmaceutical, specialty cleaning and polishing
products, paint and allied products, gum and wood chemicals, cyclic
intermediates, industrial organic chemicals, gypsum products, and
paper board products.

Acetone can be released to groundwater as a result of leaching
from municipal and industrial landfills (Gould et al., 1983; Steelman
& Ecker, 1984; Sawhney & Raabe, 1986; Brown & Donnelly, 1988). It may

also leach from solvent cement used in joining polyethylene and other
plastic pipes used in drinking-water distribution and domestic
plumbing (Anselme et al., 1985). One of the sources of acetone in
seawater is the sensitized photoreaction of dissolved organic matter
(Mopper & Stahovec, 1986).

3.2.3.3 Soil

Acetone leaches readily in soil. The US Agency for Toxic
Substances and Disease Registry (ATSDR, 1994) found the amount of
acetone released into soil from landfills in the USA accounted for
approximately 0.1% of the total environmental release of acetone.
Sources of acetone release into soil include disposal of agricultural
and food waste, animal wastes, and atmospheric wet deposition. Acetone
was detected in 43% of the soil from designated waste disposal sites
tested for acetone. Household septic tank effluents are another source
of acetone in soil (DeWalle et al., 1985).

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION

4.1 Transport and distribution among media

Acetone is commonly found in air, water, soil and biological
samples, and these background levels can he from both human-made and
natural sources. Acetone occurs naturally in trees, plants, forest
fires and volcanic gases. When animals and humans catabolize body fat,
acetone is exhaled and metabolized. Human-made sources include tobacco
smoke, combustive engine exhaust and waste incineration. The exchange
of carbonyl compounds (including acetone) between air and natural
waters is governed by the appropriate partition coefficients, in
addition to production and loss processes in both media (Benkelberg et
al., 1995).

4.1.1 Air

The significant environmental fate processes for the degradation
of acetone in the ambient environment are photolysis and reaction with
hydroxyl radicals (Meyrahn et al., 1986; Kerr & Stocker, 1986).
Meyrahn et al. (1986) measured the quantum yields of acetone
photolysis at environmental wavelengths and projected the following
rate constants for the lower troposphere at 40°N latitude: in January,
3.3 × 10^-8/sec; in July, 1.8 × 10^-7/sec; yearly average,
1.0 × 10^-7/sec. These rate constants correspond to half-lives of
243, 45 and 80 days for January, July and the yearly average,
respectively. These rate constants intentionally neglect reaction of
excited acetone molecules with oxygen. Based on the photodecomposition
data of Gairdner et al. (1984), the rate constants of Meyrahn et al.
(1986) would be about twice as great if the neglected reaction were
included. Using this factor of 2, the total yearly average photolysis
half-life (plus reaction of excited acetone molecules) is about 40
days. The rate constant for the reaction of hydroxyl radicals with
acetone at 25°C is in the range of 2.2-2.6 × 10^-13 cm³/molecule-sec
(Kerr & Stocker, 1986; Wallington & Kurylo, 1987). Probable pathways
for the reaction of acetone with hydroxyl radicals in the troposphere
have been postulated, and methyl-glyoxal is the primary product of
this reaction (Altshuller, 1991). The primary products of acetone
photolysis in sunlight are carbon dioxide and acetylperoxynitrate
(Altshuller, 1991). The photochemical oxidation of acetone in the
presence of nitrogen oxides produces small amounts of peroxyacetic
acid and peroxyacetyl nitrate (Hanst & Gay, 1983).

The photolysis lifetimes of acetone under cloudless conditions at
40°N latitude, and at sea level during winter and summer were
estimated to be 83 and 19 days, respectively (Martinez et al., 1992).
Other investigators have estimated that the average atmospheric
lifetime of acetone due to photolysis at 40°N latitude is 80 days/year
and varies from 243 in January to 45 in July (Meyrahn et al., 1986).
Meyrahn et al. (1986) estimated the average lifetime of acetone at

40°N due to combined hydroxyl radical reaction and photolysis to be 32
days/year, corresponding to a half-life of approx. 22 days. The
decomposition rate showed a pronounced dependence on latitude, with
greater losses of acetone occurring near the equator compared to the
poles. In very polluted air, the hydroxyl radical concentration
increased by an order of magnitude, which would lower the half-life by
an order of magnitude.

The complete miscibility of acetone in water suggests that
physical removal from air by wet deposition (rainfall, dissolution in
clouds, etc.) is probable (Aneja, 1993). The reactions of acetone
vapour with nitrogen oxides, hydroxyl radicals (OH), singlet molecular
oxygen (¹ Delta _g), singlet atomic oxygen (O(³P)), and nitrate
radicals have been studied. Given the second order rate constants for
the reactions of acetone with ¹ Delta _g (Datta & Rao, 1979) and O(³P)
(Lee & Timmons, 1977), and the concentrations of singlet molecular and
atomic oxygen in the atmosphere (Graedel, 1978), these reactions are
insignificant in determining the fate of acetone in the atmosphere.
However, Grosjean & Wright (1983) detected acetone in rain, cloud,
mist and fog water that was collected in Southern California, USA. In
certain instances, physical removal by wet deposition may be
environmentally significant, especially since the degradation rate is
not very fast. The reaction of acetone with nitrate radicals in the
atmosphere was also determined to be insignificant (Boyd et al.,
199l). Smog chamber studies with acetone and nitrogen oxides have
shown that acetone has low reactivity in terms of ozone and nitrogen
dioxide formation and that the rate of disappearance of acetone by
this process is low (Altshuller & Cohen, 1963; Dimitriades & Joshi,
1977).

Using 72-h back trajectories, Aneja (1993) studied organic
compounds transported in cloud water whose origin was an industrial
valley. Acetone was found in cloud water at an average of 460 ng/litre
(range 0-4100 ng/litre), in clouds of low pH (2.78).

4.1.2 Water

The miscibility of acetone in water and the estimated low value
of 0.73 for log K_oc (see Table 1) suggests that adsorption of acetone
to sediments and suspended solids is not significant. When water is
not present, acetone vapour adsorbs rather strongly to the clay
component of soil by hydrogen bonding (Goss, 1992; Steinberg &
Kreamer, 1993). The sorption is inversely dependent on relative
humidity, so increasing the humidity decreases sorption drastically.
In water-saturated soil or sediment, K_oc values (organic carbon), and
not hydrogen bonding, may control the sorption of acetone (Steinberg &
Kreamer, 1993). The experimental adsorption studies with Kaolinite,
montmorillonite, and stream sediments showed very little or no loss of
acetone from water to the adsorbents (Rathbun et al., 1982).

The transport of acetone from the water column to the atmosphere
depends on the Henry's law constant. The Henry's law constant for
acetone is 4.26 × 10^-5 atm-m³/mol (see Table 1), which suggests that
volatilization of acetone from water, although not very fast, could be
significant (Thomas, 1982), and likely to be important in determining
the fate of acetone in streams (Rathbun et al., 1982). The
volatilization rate of a chemical depends on the characteristics of
the chemical and the presence of water, and on other ambient
conditions (e.g., water depth, suspended solid concentration, water
current, wind speed, temperature). Based on an estimation method
(Thomas, 1982) and the Henry's law constant value, the volatilization
half-life of acetone from a model river 1 m deep, flowing at a current
of 1 m/second with a wind velocity of 3 m/sec is between 18 and 19 h.
The mean volatilization coefficient for acetone in a model outdoor
stream was found to be in the range of 7.15 × 10^-4 to 14.8 × 10^-4/min
(Rathbun et al., 1989, 1991). Therefore, the volatilization half-life
of acetone from the model stream is in the range of 8-16 h. It was
concluded that volatilization will control the fate of acetone in
water (Rathbun et al., 1989, 1991). Using a computer simulation model
the volatilization half-life from a model pond (2 m deep) was
estimated to be around 9 days.

The average of four experimentally determined rate constants for
the reaction of acetone with hydroxyl radicals in water (pH 6-7) is
1.1 × 10^-8 litres/mol-sec (Buxton et al., 1988). Assuming the
hydroxyl radical concentration in brightly sunlit natural water is 1.0
× 10^-17 mol/litre, the half-life for the reaction is almost 20 years.
Thus, photo-oxidation reactions of acetone in environmental waters do
not appear to be a significant removal process. Also, photolysis of
acetone in water, based on a rate constant for the reaction of acetone
with hydroxyl radicals in water at pH 7 of 5.8-7.7 × 10⁷
litres/mol-sec and a concentration of hydroxyl radicals in eutrophic
waters of 3 × 10^-17 M (Mill & Mabey, 1985), will not be significant.
Rathbun & Tai (1982) measured the mass transfer coefficient (K_L for
acetone in water and reported values ranging from 0.310 to 0.537. When
distilled water or natural water containing acetone was exposed to
sunlight for 2-3 days, no photodecomposition of acetone was observed
(Rathbun et al., 1982). Experimental hydrolysis data for acetone have
not been found in the available literature. However, ketones generally
resist aqueous environmental hydrolysis (Harris, 1982) and hydrolysis
of acetone is not expected to be significant in the environment.

Bacterial degradation of acetone occurs, and the rate is
increased if acclimatization of the bacteria is achieved before higher
concentrations are present (see section 4.2.2.1). Both volatilization
and biodegradation are likely to play a part in the loss of acetone
from surface waters. The most significant process will depend on
particular circumstances, such as depth and amount of aeration.

4.1.3 Soil

The two significant transport properties for acetone in soil are
volatilization and leaching, and acetone is also expected to
biodegrade rapidly. Leaching transports acetone from soil to
groundwater, with the rate of leaching from soil by rainwater
depending on the sorption characteristics of acetone in the various
types of soil. Since acetone may be controlled by K_oc in
water-saturated soil and has a low K_oc value, sorption of acetone
in such soil will be weak. A sorption study with moist clay soils
indicated that aqueous acetone causes swelling in these soils (Green
et al., 1983), and this process may allow the retention of a small
fraction of acetone. Volatilization transports acetone from soil to
the atmosphere. The volatility rate of acetone from soil depends on
the soil characteristics (moisture content, soil porosity, etc.).
Since acetone is weakly sorbed to soil, the volatility depends
primarily on fire moisture content of the soil. In dry soil, the
volatilization rate from soil surfaces is high due to the high vapour
pressure of acetone. In moist soil, the rate of volatilization is
similar to that of acetone in water and depends on the Henry's law
constant. Acetone volatilizes moderately under these conditions. The
detection of acetone at higher concentrations in downwind air of a
landfill site, compared to upwind air (Militana & Mauch, 1989),
indicates that acetone can volatilize from soil.

No data regarding the transport or uptake of acetone from soil to
plants are available.

While acetone is expected to biodegrade readily in soil, no data
are available to suggest that any degradation process in soil, other
than biodegradation, is significant.

Acetone has been detected in leachates from municipal and
industrial landfills (Sabel & Clark, 1984; Sawhney & Kozloski, 1984;
Brown & Donnelly, 1988), demonstrating that leaching through soil can
occur. The presence of other leachate constituents can adversely
affect the biodegradation efficiency of microbes to use acetone.

Acetone has a relatively high vapour pressure (231.06 mmHg at
25°C) (Riddick et al., 1986) and is used as an evaporative solvent in
a variety of applications. Because of its volatile properties, acetone
can be expected to evaporate from dry surfaces, particularly in spills
on the soil surface. Although evaporation from dry surfaces should be
a significant process, sufficient data are not available to predict
the relative significance of evaporation from moist soils, where
biodegradation and leaching will compete with evaporation as a removal
process.

4.2 Biotransformation

4.2.1 Bioconcentration and biomagnification

The very low log K_ow value of -0.24 (see Table 1) suggests that
bioconcentration (a process leading to a higher concentration of a
chemical in an organism relative to that in its environment) of
acetone in either aquatic or terrestrial organisms, and
biomagnification (series of processes in an ecosystem by which higher
concentrations of a chemical are attained in organisms at higher
trophic levels) of acetone from animals of lower to higher trophic
levels is unlikely.

4.2.2 Biodegradation

Many aerobic biodegradation screening studies with mixed
microorganisms from waste-treatment plant effluents, activated sludge,
or sewage have examined the biodegradability of acetone (Lamb &
Jenkins, 1952; Heukelekian & Rand, 1955; Stafford & Northup, 1955;
Ettinger, 1956; Hatfield, 1957; Gaudy et al., 1963; Price et al.,
1974; Thom & Agg, 1975; Bridie et al., 1979; Urano & Kato, 1986a,b;
Babeu & Vaishnav, 1987; Bhattacharya et al., 1990). These strutues
indicate that acetone is easily biodegradable with acclimatized
microorganisms or after a suitable lag period (approx. 1 day) (Urano &
Kato, 1986a,b), as long as the initial concentration of acetone is not
at a toxic level. For example, acetone at a concentration of 500
mg/litre was toxic to microorganisms when biooxidation of acetone by
activated sludge was attempted (Gerhold & Malaney, 1966).
Biodegradation of acetone was similar in seawater and fresh water
(Takemoto et al., 1981 ). The 20-day biochemical oxygen demand (BOD)
for acetone for fresh water and saltwater was 78% and 76%,
respectively (Lamb & Jenkins, 1952; Price et al., 1974). After a
suitable lag period (5 days), acetone biodegraded quantitatively under
anaerobic conditions with anaerobic acetate-enriched culture medium
(Chou et al., 1979). A biodegradation study of acetone in natural
water collected from Lago Lake near Athens, Georgia, determined that
the biodegradation kinetics were multiphasic in nature and depended on
the substrate concentration. The determined rate of degradation was
faster at higher initial concentrations (the maximum concentration
used was 0.5 mg/litre) (Hwang et al., 1989).

In a laboratory experiment with natural stream water and
sediment, no acetone was lost in 338 h under sterile conditions in
closed flasks. However, with non-sterile natural sediment, 100% of the
acetone was lost in 500 h following a lag period of 90 h. (Rathbun et
al., 1982). The authors of this study concluded that biodegradation
was one of the important processes for the loss of acetone in streams.
Rathbun et al. (1982) separated his study into two groups to observe
the effects of pre-exposure acclimatization. One group was pre-treated
with a small concentration of acetone overnight and the other did not
get pre-treatment. The treatment reduce the lag time, and degradation
coefficients were much lower for the pre-treated groups. First-order

rate coefficients for the bacterial degradation of acetone at 25°C
ranged from 0.43-0.9 days^-1 (not pre-treated), giving half-lives of 2
days. Significant loss of acetone due to biodegradation was not
observed in a later study when acetone was injected continuously in an
outdoor model stream (Rathbun et al., 1988, 1989, 1991, 1993).
Attempts to induce biodegradation by adding glucose and a nutrient
solution containing bacteria acclimated to acetone were unsuccessful.
The authors concluded that the residence time of acetone in the model
stream (6 h) was too short for the bacteria to become acclimated in
the water before initiation of biodegradation. However, this
explanation may not be valid if attached bacteria, rather than
free-floating bacteria, dominate the biodegradation process. As an
alternative explanation, the authors indicated that the observed
limitation in the nitrate concentration in the stream may be
responsible for the lack of acetone biodegradation.

4.2.2.1 Microbial degradation

Many aerobic biological screening studies have examined the
biodegradability of acetone and have found it to be readily
biodegradable (Lamb & Jenkins, 1952; Heukelekian & Rand, 1955;
Stafford & Northrup, 1955; Ettinger, 1956; Hatfield, 1957; Ludzack &
Ettinger, 1960; Price et al., 1974; Bridie et al., 1979; Takemoto et
al., 1981; Urano & Kato, 1986a,b; Vaishnav et al., 1987; Hwang et al.,
1989). One of these studies examined acetone biodegradation in a
natural water experiment and found acetone to be readily biodegraded
in Lago Lake water collected near Athens, Georgia, USA (Hwang et al.,
1989).

Platen et al. (1990) studied the enrichment, isolation,
characterization and the stoichiometry of acetone and its degradation.
In their study, acetone was oxidized completely by
Desulfococcus biacutus, a gram negative, anaerobic sulfate-reducing
bacterium using acetone as its sole organic substrate. Enzyme studies
indicated that acetone was metabolized by condensation with carbon
dioxide to a C⁴ compound (possibly free acetoacetate) and moved into
intermediary metabolism as acetoacetyl-coenzyme A. Acetoacetyl-CoA is
cleared by a thiolase reaction to acetyl-CoA which is completely
oxidized by the carbon monoxide dehydrogenase pathway. In
acetone-amended slurries, 76% of the theoretically-expected sulfate
was depleted, and in nitrate-amended slurries > 100% of the
theoretically-expected amounts of nitrate were consumed after 85 days
of incubation. Chou et al. (1979) also showed that acetone can be
degraded by anaerobic biodegradation.

Waggy et al. (1994) compared a USA 20-day biochemical oxygen
demand (BOD) test with the Organization for Economic Cooperation and
Development (OECD) closed bottle biodegradation test (Test 301D)
(OECD, 1981). In the 20-day BOD test, the results were 56, 76, 83 and
84%, at 5, 10, 15 and 20 days, respectively, and in the OECD test were
68, 72 and 78% for 5, 15 and 28 days, respectively, indicating good
correlation (Waggy et al., 1994). These test results classify acetone

as readily biodegradable. In a laboratory study using a microbial
culture from domestic waste water without acclimation, Price et al.
(1974) measured fresh water BODs (% biooxidation) to be 76, 82, 85 and
96% for 5, 19, 15 and 20 days, respectively. In "synthetic" saltwater,
the values for the same periods were 66, 88, 88 and 100%.

4.3 Bioavailability from environmental media

Acetone is expected to be bioavailable.

4.4 Interaction with other physical, chemical or biological factors

The atmospheric degradation of volatile organic compounds (VOCs)
in the presence of nitrogen oxides (NO_x) leads to the production of
ozone. During complete oxidation of the VOCs free radical reactions
occur in the presence of sunlight with acetone (and other ketones),
participating as an intermediate with ozone as a byproduct. One method
of measuring the contribution of acetone is by the reactivity of it
with the hydroxyl radical (OH*).

The degradation of acetone in the lower troposphere may be
initiated by photolysis or reaction with OH* radicals. The reactions
with ozone (OD) or NO_x are too slow to be important under
tropospheric conditions (Johnson & Jenkin, 1991). The rate of the
initiating reaction of OH* with acetone is well established at
2.26 × 10^-13cm³/ molecule per sec (Atkinson, 1985).
Accordingly, the tropospheric lifetime of acetone with respect to
removal by OH radicals is approximately one month; therefore, the loss
of acetone by photooxidation is the major removal process of acetone
in the troposphere (Johnson & Jenkin, 1991).

The mechanism for acetone photodissociation has been reviewed by
Gardner et al. (1984). At 40°C, using the Gardner equations, the
average tropospheric lifetime would be halved to about 15 days, In
summary, the ozone concentrations predicted by the model were not
significantly affected by removal of the acetone emissions (Johnson &
Jenkin, 1991). Chatfield et al. (1987) examined the effect of
atmospheric pressure on the photolytic lifetime of acetone, and then
compared the result with losses caused by hydroxyl radical reactivity.
Reactions with hydroxyl radicals were much higher at ground level than
at increasing altitude where photolysis was more important in
degrading acetone.

The formation of ground-level ozone has become an air pollution
problem, especially in crowded, urban areas. Ozone is formed from the
complex photochemical interaction of some VOCs and NO_x compounds.
Andersson-Sköld et al. (1992) calculated photochemical ozone creation
potentials (POCP) for 75 organic compounds, while Carter (1994)
developed maximum incremental ozone reactivity (MIR) scales to measure
the potential of VOCs to create ozone. Both research groups found that

ketones are weak producers of ozone, with acetone having one of the
lowest ozone formation potentials. Derwent et al. (1996) calculated a
POCP for acetone using a European model, which takes into account the
difference in conditions between European and North American cities;
the MIR model is considered more appropriate for North American
conditions. Andersson-Sköld et al. (1992) found similar values to
Derwent et al. (1966), indicating that acetone has "a remarkably low
POCP". Because of the low POCP, acetone has been suggested as a
potential substitute for high POCP aromatic hydrocarbons or the
chlorine-containing solvents.

4.5 Ultimate fate following use

The environmental fate of acetone can be predicted, since many of
the major fate processes have been investigated. When released to the
atmosphere, acetone will degrade through a combination of photolysis
and reaction with hydroxyl radicals (Meyrahn et al., 1986). Acetone
can be removed from the air by rainfall (wet deposition), as shown by
its detection in rainwater samples (Grosjean & Wright, 1983), but this
does not appear to be a significant route most of the time. In soil,
many studies have shown that acetone is readily biodegradable.
However, leaching may occur, especially if other chemicals are present
that may destroy or hinder microorganisms from degrading acetone.
Acetone can volatilize from water, as well as soil surfaces (Rathbun
et al., 1982). Since acetone is miscible with water and has a low
K_oc, it leaches rather than adsorbs to soil. Where biodegradation is
inhibited or limited, acetone may reach the groundwater as a result of
leaching from spills or landfills (Steelman & Ecker, 1984; Brown &
Donnelly, 1988). Manufacturing and processing facilities may also
release acetone to air and water through discharges, and through other
wastes transported to landfills.

5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

5.1 Environmental levels

5.1.1 Air

Acetone is a commonly found volatile contaminant. It is one of
the more long-lived intermediates that are produced in the oxidation
of light non-methane hydrocarbons (Henderson et al., 1989). Monitoring
data, covering rural, urban, remote and other areas, are available;
values depend upon where the sampling was done, as well as the time of
the year and sampling technique. Examples arc presented in Table 6.

Grosjean et al. (1989) collected samples in three large urban
areas in Brazil (Sao Paulo, Rio de Janeiro, Salvador) with populations
ranging from 2 to 13 million people. In Sao Paulo, acetone levels were
in the range of 0.5-7 µg/m³ (0.2-3 ppb), in Rio 1.2-9 µg/m³ (0.5-3.8
ppb), and in Salvador 0-49.9 µg/m³ (0-21 ppb). In 1975, Brazil
initiated a nationwide programme of production of ethanol from sugar
cane, and by 1988, when these samples were taken, approximately
one-third of the vehicles in use were ethanol-fuelled. Formaldehyde,
acetaldehyde and acetone were the three carbonyls with the highest
values, but these levels were still not higher than levels in other
parts of the world.

Acetone was one of the VOCs identified in the air of the storage
section of a municipal waste truck (Wilkins, 1994). Although the exact
measurement was not given in the study report, the author stated that
the concentration was below 1780 mg/m³ (750 ppm) (the TLV value).
Brosseau & Heitz (1994) measured the gases emitted from a municipal
landfill site and found acetone in two samples: one at 77 µg/m³ (32.5
ppbv) and the other at 16 µg/m³ (6.84 ppbv).

Chatfield et al. (1987) studied the behaviour of acetone in the
troposphere. Over the Atlantic Ocean (35°N), the mean concentration of
acetone in the lower troposphere is approximately 1.2 µg/m³ (0.5
ppb). Chatfield et al. (1987) stated that a significant amount of
carbon appeared to be cycled as acetone, with attack by hydroxyl
radicals and photolysis as the chief loss mechanisms, and that propane
may contribute nearly half of the acetone observed in the upper
atmosphere. Henderson et al. (1989) continued this work by showing
that the effects of surface sources of higher order alkanes, alkenes
and terpenes play a major role in the amount of acetone in the
troposphere.

Granby et al. (1997) measured acetone levels simultaneously in a
busy Copenhagen street (22 000 cars/day) and a semi-rural site 30 km
west and found little difference in mean concentrations (2.4 µg/m³
vs. 2.1 µg/m³; 1 ppb vs. 0.9 ppb). They found very weak correlations
with carbon monoxide and NO_x; indicating sources other than
automobile exhaust, the most likely being oxidation of reactive
hydrocarbons from long-range transport of polluted air masses. Since

Table 6. Environmental air levels in various locations

Sampling Area Concentration^a Sampling dates Reference
µg/m3 ppb

City/Tucson, Arizona, USA 28.5 12 February-September 1982 Snider & Dawson (1985)
Urban/Tulsa, OK, USA 11.4-125.4 4.8-52.8 1978 Arnts & Meeks (1981)
Urban/South and Central America 0.5-49.9 0.2-21 1988 Grosjean et al. (1989)
Rural/Arizona, USA 6.7 2.8 February-September 1982 Snider & Dawson (1985)
Rural/Colorado, USA 12.1-56.3 5.1-23.7 1978 Arnts & Meeks (1981)
Rural/Egbert, Ontario 0.9-8.8 0.39-3.6 1989 Shepson et al. (1991)
9
Rural/Dorset, Ontario 1.5-10.2 0.65-6.3 1989 Shepson et al. (1991)
Forest/Texas, USA 6.9-46 2.9-19.4 January 1978 Seila (1979)
Remote/Alaska 0.7-6.9 0.3-2.9 1967 Cavanagh et al. (1969)
Mountains/Tennessee, USA 5-28.5 2.1-12 1978 Arnts & Meeks (1981)
Mountains/Bavaria, Germany approx. 1.2 0.54^b August 1995 Leibrock & Slemr (1997)
Ocean/Atlantic 35°N 1.2 0.5 Chatfield et al. (1987)

^a Some sampling in the above studies may have been conducted using Tedlar bags that are known to contaminate
air samples with acetone (Henderson et at., 1989). Non-range values are mean values.
^b Measured as propylene equivalents of oxygenated hydrocarbons in ppbC (ppb of carbon).

the acetone concentrations in this study are only slightly higher than
those found in rural, remote and ocean atmospheres, it appears that
the acetone is probably not transported a great distance in the lower
troposphere.

Arnold et al. (1997) measured upper tropospheric concentrations
of acetone at 9000 m over the northeastern Atlantic, near Ireland in
1993. Measured acetone concentration was found to correlate positively
with that of sulfur dioxide (SO₂), reaching a maximum abundance of
approx. 7 µg/m³ (3 ppb). This concentration is markedly higher than
the concentration of 1.2 µg/m³ (0.5 ppb) in the lower troposphere
reported by Chatfield et al. (1987). As the SO₂ level decreased, so
did the acetone concentration. Either the acetone was transported from
direct emissions from the USA, or a photochemical hydrocarbon
conversion had occurred.

In a review of earlier studies, Singh et al. (1994) found acetone
at a range of approx. 0.9-5.2 µg/m³ (approx. 0.4-2.3 ppb), with a
mean of 3.1 µg/m³ (1.14 ppb), in the troposphere. Using a three
dimensional photochemical model, Singh et al. (1994) found that the
greatest source of acetone was the oxidation of precursor hydrocarbons
(51%); other sources were biomass burning (26%), biogenic emissions
(21%) and an anthropogenic emission (approx. 3%). Atmospheric removal
was mainly by photolysis (64%), followed by reaction with OH^*
radicals (24%) and deposition (12%). Other important points were:

* there is substantial variability in atmospheric abundance
* the concentration of acetone appears to vary with altitude
* upper atmospheric transport is possible since the half-life is
>10 days
* acetone appears to be the most abundant non-methane organic
species in the atmosphere
* the geochemical background of acetone appears to be 1.2 µg/m³
(approx. 0.5 ppb)

5.1.1.1 Indoor air

Shah & Singh (1988) reported a concentration of 19 µg/m³ (8 ppb)
in household indoor air. These authors compiled available data to
calculate an average outdoor concentration of 16.4 µg/m³ (6.9 ppb).
Other investigators reported similar results (Jarke et al., 1981).
Tichenor & Mason (1988) measured acetone levels in the range of 37-41
µg/m³ (approx. 15-17 ppb) per hour being emitted from low-density
particle board used in home construction in the USA. The reason for
the higher indoor air concentration was the use of acetone-containing
consumer products inside homes. The potential for intrusion of acetone
present as Soil gas into a house adjacent to a landfill was
characterized by Hodgson et al. (1992), but the measurement was for
only a single house. The average concentration was 47.5 µg/m³ (20
ppb).

Hodgson et al. (1991) collected air samples in a
newly-constructed building at four different times over a period of
14 months. The major source of VOCs was not the new construction
materials, but the liquid-process copiers and plotters where acetone
concentrations ranged from 28.8 to 66.6 µg/m^s (12-28 ppb).

5.1.2 Water

Acetone has been qualitatively detected in drinking-water in
various cities in the USA, including Miami, FL; Ottumwa, IO;
Philadelphia, PA; Cincinnati, OH; Calhoun, GA; Dalton, GA; Gastonia,
NC; Durham, NC; New Orleans, LA; Rome, GA; and Tuscaloosa, AL (Bertsch
et al., 1975; US EPA, 1975; Shackelford & Keith, 1976). In the US EPA
National Organics Reconnaissance Survey (NORS), involving
drinking-water supplies from 10 cities in the USA, acetone was
qualitatively detected in all the cities. An acetone concentration of
1 µg/litre was found in drinking-water samples from Seattle, WA (US
EPA, 1975).

Acetone was detected in 33/204 surface water samples collected
from sites near heavily industrialized areas in the USA during
1975-1976 (Ewing et al., 1977). It was detected in 12.4% of all
groundwater samples analysed from 178 USA hazardous waste (Superfund)
sites as part of a national programme to investigate and remedy
potential problems at these sites (Plumb, 1987).

Acetone is released to water in wastewater discharges from
industry and sewage treatment. It was found in 23/63 effluent waters
from a wide range of chemical manufacturers around the USA at
concentrations ranging from < 10 to 100 µg/litre (Perry et al.,
1978). A comprehensive survey of wastewater from 4000 industrial and
publicly owned treatment works detected acetone in a wide range of
wastewater from industries such as leather tanning, petroleum
refining, nonferrous metals, paint and ink, printing and publishing,
coal mining, organics and plastics, inorganic chemicals, textile
mills, pulp and paper, robber processing, pesticide manufacture,
photographic industries, pharmaceuticals, porcelain/enamels,
mechanical products and transportation equipment. The highest effluent
concentration of acetone from all industries was 37.7 mg/litre, which
was detected in the paint and ink industry; however, the median
acetone level was 0.89 mg/litre (NLM, 1992).

Acetone can be released to groundwater by leaching from municipal
and industrial landfills. Leachate collected from a Minnesota (USA)
municipal landfill contained as much as 13 mg acetone/litre (Sabel &
Clark, 1984). Levels of 2.94.8 mg/litre were detected in leachate
samples collected in the USA from an industrial landfill in
Connecticut in 1982-1983 (Sawhney & Kozloski, 1984) and from one in
Michigan that contained up to 62 mg acetone/litre (Brown & Donnelly,
1988).

Acetone has also been detected at 0.2-0.7 µg/litre in water from
several artesian wells adjacent to a landfill in Wilmington, Delaware,
USA (DeWalle & Chian, 1981). The concentration of acetone was up to 3
mg/litre in a drinking-water well in New Jersey (Burmaster, 1982;
Steelman & Ecker, 1984).

The concentration of acetone in open ocean water (Tongue of the
Ocean, Bahamas) was approx. 0.35 µg/litre (Kieber & Mopper, 1990).
Corwin (1969) measured VOCs in seawater and found acetone levels in
the Florida Straits (USA) of 14-52 µg/litre at depths ranging from 0
to 160 metres at approx. 35% salinity. Similar concentrations were
found in the Mediterranean where the measurements were 18-52 µg/litre
at slightly higher salinity (approx. 39%).

5.1.3 Soil and sediment

There are few data regarding the level of acetone in soil and
sediment. Acetone has been detected in 43% of the soil samples in
designated waste disposal sites in the USA for which acetone
determination has been made (ATSDR, 1994). The maximum concentration
of acetone in soils from Vega Alta Public Supply well sites in Puerto
Rico and the mean concentration of acetone in soil from Summit
National Site, Ohio, was 9.5 mg/kg (ATSDR, 1994). Because of its high
water solubility and low sediment adsorption coefficient, acetone in
an aquatic system is predominantly found in water, rather than in
sediment.

5.1.4 Food

Acetone has been qualitatively detected in blue cheese (Day &
Anderson, 1965), baked potatoes (Coleman et al., 1981), roasted
filbert nuts (Kinlin et al., 1972), chicken breast muscle (Grey &
Shrimpton, 1967) and nectarines (Takeoka et al., 1988). Acetone
concentrations of 795 mg/kg and 11 mg/kg were identified in
Czechoslovakian milk samples and milk cream culture, respectively
(Palo & Ilkova, 1970). Milk samples from Swedish dairy cattle were
found to contain acetone concentrations ranging from 18 to 226
mg/litre (0.32-3.89 µmol/litre) (Andersson & Lundstrom, 1984).
Pellizzari et al. (1982) qualitatively identified acetone in all 8
selected human milk samples collected from volunteers in Bayonne, NJ,
Jersey City, NJ, Bridgeville, PA, and Baton Rouge, LA. A variety of
bean types (common, lima, mung and soy) contained acetone levels
ranging from 260-2000 µg/kg, with a mean level of 880 µg/kg, and
levels of 530 and 230 µg/kg were detected in split peas and lentils,
respectively (Lovegren et al., 1979). Acetone has also been detected
in onions, grapes, cauliflower, tomatoes and wild mustard (NLM, 1992).

5.1.5 Other environmental levels

Acetone is ubiquitous in the environment and is found at a wide
range of concentrations.

5.2 General population exposure

Acetone is readily absorbed from the lung and gastrointestinal
tract following inhalation and ingestion (see chapter 6). It can also
be absorbed through the skin. The low values for K_oc (see Table 1)
and a moderate value for Henry's law constant (Rathbun & Tai, 1987)
suggest that the bioavailability of acetone from contaminated water
and soil as a result of contact may be significant. However,
quantitative data regarding the rate and extent of dermal absorption
of acetone from contaminated water and soil are lacking. The high
water solubility and low K_oc value for acetone suggest that
bioavailability from ingested soil (e.g., children playing at or near
contaminated sites) will be high, but, again, quantitative absorption
data are lacking. Data on bioavailability of acetone from ingested
plant food are not available.

Exposure to acetone occurs from both natural and anthropogenic
sources, and it is endogenously produced by all humans. The general
population is exposed to acetone by inhaling ambient air, ingesting
food, and drinking-water containing acetone. Dermal exposure to
acetone may result from skin contact with consumer products (e.g.,
certain nail polish removers, paint removers, and household cleaning
and waxing products). Assuming concentrations of acetone are 19 µg/m³
(8.0 ppb) in indoor air and 16.4 µg/m³ (6.9 ppb) in outdoor air (Shah
& Singh, 1988) and that an average person inhales 15 m³/day of indoor
air and 5 m³/day of outdoor air daily, the estimated exposure to
acetone by inhalation is 0.37 mg/day. This value is much lower than an
estimate based upon an earlier exposure level found by one of these
researchers. Singh & Hanst (1981) estimated that an acetone
concentration of 0.26 µg/m³ (0.111 ppb) will occur in the lower
troposphere as a result of atmospheric oxidation of naturally
occurring propane, with levels of 35 ng/m³ (15 ppt) in the upper
troposphere and 7 ng/m³ (3 ppt) in the stratosphere. Since the
sampled atmospheric concentrations of acetone are 0.723-127.25 µg/m³
(0.3-52.8 ppb), and maintaining that the average adult human inhales
20 m³ air/day, the average daily exposure of acetone from inhalation
can be estimated to be 14.5-2545.0 µg, or up to 2.5 mg/day.

Wang et al. (1994) measured acetone concentrations in 89
non-occupationally exposed subjects and found acetone mean values of
840 µg/litre in blood, 842 µg/litre in urine, 715 ng/litre in alveolar
air and 154 ng/litre in environmental air. The researchers found no
significant difference in blood levels between smokers (896 µg/litre)
and nonsmokers (792 µg/litre), and likewise between hospital staff
(719 µg/litre) and blood donors (966 µg/litre). The results are
similar to those of Pezzagno et al. (1986) who measured 760 µg
acetone/litre in urine.

The endogenous acetone level in the body at any instant reflects
acetoacetate production (Morgott, 1993). The concentration of acetone
in whole blood does not differ from that in plasma (Gavino et al.,
1986). Even in healthy subjects, the level of acetone in blood or

plasma varies with fasting or non-fasting conditions and depends on
the weight of the subject. Generally, the blood or plasma acetone
concentrations are higher in fasted than non-fasted subjects and
higher in subjects who are not obese, compared to obese subjects (Haff
& Reichard, 1977). It should be noted that normal and abnormal
physiological conditions and disease states may increase ketogenesis
and the body burden of acetone. Acetone levels in athletes and
pregnant women (among many groups) may be elevated because these
groups of people have greater energy requirements. Ashley et al.
(1994) measured blood concentrations in non-occupationally exposed
populations. The mean concentration in a control group in the USA was
3.1 mg/litre. In a group of nine volunteer subjects, the mean blood
concentration before entering a van designed for clinical examinations
for a health survey was 1.9 mg/litre and after 3 h in the van the mean
blood concentration was virtually unchanged at 2 mg/litre, although
the range before entry was 1 3.6 mg/litre and after 3 h was 0.9-5
mg/litre, i.e. the high end of the range was over 1.4 mg/litre higher
when the subjects were tested after breathing the same air for 3 h.

Individuals with uncontrolled diabetes mellitus or diabetic
ketoacidosis may have plasma acetone levels as high as 750 mg/litre
(Trotter et al., 1971). The acetone concentrations in body fluids and
expired air in studies of healthy individuals and diabetic patients
are shown in Table 7. Clinical findings in eases of acute acetone
intoxication suggest that acetone blood levels over 1000 mg/litre are
necessary to cause unconsciousness in humans (Ramu et al., 1978), but
lower levels may interrupt physiological processes in diabetics.

Approximate reference concentrations for human plasma acetone are
< 10 mg/litre for a "healthy" individual, < 100 mg/litre for an
occupationally exposed individual, 100-700 mg/litre for an individual
with diabetic ketoacidosis and > 200 mg/litre for an individual
showing symptoms of "toxic" exposure (Tietz, 1983).

5.3 Occupational exposure

Kiesswetter et al. (1994) investigated occupational acetone
exposure using two groups of eight healthy male workers on nine shift
days. Using personal sampling, exposure was higher in the first half
of the shift (2730 mg/m³) than in the second half (1720 mg/m³).
For monitoring purposes, the researchers studied the relationship of
acetone in air versus three urine parameters: (1) concentration of
acetone in urine; (2) concentration of urine related to creatinine
excretion; and (3) concentration of acetone in urine in relation to
time (sampling period) and excreted urine volume. The concentration of
acetone in urine was moderately correlated to that in air. Some of the
ratings of well-being in the workers con-elated with the acetone
concentrations in the urine but not with the acetone concentrations in
the workplace air.

Table 7. Concentrations of acetone in body fluids and expired air of humans

Medium Subject Concentration Reference

Blood Healthy (non-fasted) 0.93 mg/litre Gavino et al. (1986)

Blood Health (non-fasted) 0.84 mg/litre Brugnone et al. (1994)

Blood Healthy (non-fasted) 1.8 mg/litre (median) Ashley et al. (1994)

Plasma Healthy (3-day fasted) 46.5 mg/litre Haff & Reichard (1977)

Plasma Healthy (non-fasted) 1.74 mg/litre Trotter et al. (1971)

Plasma Obese (3-day fasted) 17.4 mg/litre Haff & Reichard (1977)

Plasma Ketoacidotic 424 mg/titre Trotter et al. (1971)

Plasma Ketoacidotic 290 mg/litre Haff & Reichard (1977)

Urine Healthy 0.23-0.41 mg/litre Kobayashi et al. (1983)

Urine Healthy 0.84 mg/litre Brugnone et al. (1994)

Urine Healthy (endogenous) 0.76 mg/litre Pezzagno et al. (1986)

Urine Diabetic 0.64-9.0 mg/litre Kobayashi et al. (1983)

Expired air Healthy 1.23 µg/litre Jansson & Larsson (1969)

Expired air Healthy 1.16 µg/litre Trotter et al. (1971)

Expired air Healthy 1.3 µg/litre Phillips & Greenberg (1987)

Wang et al. (1994) calculated a blood-air coefficient for acetone
of 146. On average, the blood acetone levels of workers were 56 times
higher than those of subjects only exposed environmentally. These
researchers calculated the half-life of acetone in blood to be 5.8 h
for the interval between the end of one shift and the beginning of the
next (approx. 16 h). Analyses were made of workers before the start of
their shift, and mean acetone levels were 3.5 mg/litre in blood and 13
mg/litre in urine. Wigaeus (1981) calculated the acetone half-life to
be 6.1 h. These values indicate that the 16-h period between
workshifts did not allow for complete elimination of acetone absorbed
from the previous workshift.

In a study of environmental tobacco smoke (ETS) and its
contribution to VOC concentrations, Heavner et al. (1996) measured
acetone levels in smoking and non-smoking workplaces and homes. The
mean levels were: non-smoking workplace, 59.77 µg/m³ (SD 79.78);
smoking workplace, 952.86 µg/m³ (SD 3988.25); non-smoking home, 50.12
µg/m³ (SD 58.5); smoking home, 71.19 µg/m³ (SD 118.17).
Approximately 6% of the acetone found in the air of smoking workplaces
and homes was attributed to ETS.

Workers in industries that manufacture and use acetone can be
exposed to much higher concentrations of acetone than the general
population. For example, the concentrations of acetone in the
breathing zone air in a paint factory, a plastics factory, and an
artificial fibre factory in Italy were > 3.48 mg/m³ (Pezzagno et
al., 1986). The concentration of acetone in a plastic plant in Japan,
where bathtubs were produced, was > 100 mg/m³ (Kawai et al., 1990a).
The inhalation exposure of workers to acetone in a shoe factory in
Finland ranged from 25.4-393.4 mg/m³ (Ahonen & Schimberg, 1988). The
concentration of acetone in the air of a solvent recycling plant was
as high as 42 mg/m³, the mean exposure being 1 mg/m³ (Kupfers