INTOX Home Page




    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
    exposure to chemicals, through international peer review processes, as
    a prerequisite for the promotion of chemical safety, and to provide
    technical assistance in strengthening national capacities for the
    sound management of chemicals.

         The Inter-Organization Programme for the Sound Management of
    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
    Co-operation and Development (Participating Organizations), following
    recommendations made by the 1992 UN Conference on Environment and
    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

    WHO Library Cataloguing in Publication Data


         (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

         The World Health Organization welcomes requests for permission to
    reproduce or translate its publications, in part or in full. 
    Applications and enquiries should be addressed to the Office of
    Publications, World Health Organization, Geneva, Switzerland, which
    will be glad to provide the latest information on any changes made to
    the text, plans for new editions, and reprints and translations
    already available.

    (c) World Health Organization 1998

         Publications of the World Health Organization enjoy copyright
    protection in accordance with the provisions of Protocol 2 of the
    Universal Copyright Convention.  All rights reserved.

         The designations employed and the presentation of the material in
    this publication do not imply the expression of any opinion whatsoever
    on the part of the Secretariat of the World Health Organization
    concerning the legal status of any country, territory, city, or area
    or of its authorities, or concerning the delimitation of its frontiers
    or boundaries.

         The mention of specific companies or of certain manufacturers'
    products does not imply that they are endorsed or recommended by the
    World Health Organization in preference to others of a similar nature
    that are not mentioned. Errors and omissions excepted, the names of
    proprietary products are distinguished by initial capital letters.





    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

         2.1. 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

         3.1. Natural occurrence
         3.2. Anthropogenic sources
              3.2.1. Production levels and processes
              3.2.2. Uses
              3.2.3. Releases

         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
                 Microbial degradation

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

         5.1. Environmental levels
              5.1.1. Air
                 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

         6.1. Absorption
              6.1.1. Inhalation exposure
                 Human studies
                 Experimental animal studies
              6.1.2. Oral exposure
                 Human studies
                 Experimental animal studies
              6.1.3. Dermal exposure
                 Human studies
                 Experimental animal studies
              6.1.4. Absorption summary
         6.2. Distribution
              6.2.1. Inhalation exposure
                 Human studies
                 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
               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

         7.1. 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

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

         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

         10.1. Evaluation of human health effects
         10.2. Evaluation of effects on the environment







         Every effort has been made to present information in the criteria
    monographs as accurately as possible without unduly delaying their
    publication.  In the interest of all users of the Environmental Health
    Criteria monographs, readers are requested to communicate any errors
    that may have occurred to the Director of the International Programme
    on Chemical Safety, World Health Organization, Geneva, Switzerland, in
    order that they may be included in corrigenda.

                                 *     *     *

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

                                 *     *     *

         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



         In 1973 the WHO Environmental Health Criteria Programme was
    initiated with the following objectives:

    (i)   to assess information on the relationship between exposure to
          environmental pollutants and human health, and to provide
          guidelines for setting exposure limits;

    (ii)  to identify new or potential pollutants;

    (iii) to identify gaps in knowledge concerning the health effects of

    (iv)  to promote the harmonization of toxicological and
          epidemiological methods in order to have internationally
          comparable results.

         The first Environmental Health Criteria (EHC) monograph, on
    mercury, was published in 1976 and since that time an ever-increasing
    number of assessments of chemicals and of physical effects have been
    produced.  In addition, many EHC monographs have been devoted to
    evaluating toxicological methodology, e.g., for genetic, neurotoxic,
    teratogenic and nephrotoxic effects.  Other publications have been
    concerned with epidemiological guidelines, evaluation of short-term
    tests for carcinogens, biomarkers, effects on the elderly and so

         Since its inauguration the EHC Programme has widened its scope,
    and the importance of environmental effects, in addition to health
    effects, has been increasingly emphasized in the total evaluation of

         The original impetus for the Programme came from World Health
    Assembly resolutions and the recommendations of the 1972 UN Conference
    on the Human Environment.  Subsequently the work became an integral
    part of the International Programme on Chemical Safety (IPCS), a
    cooperative programme of UNEP, ILO and WHO.  In this manner, with the
    strong support of the new partners, the importance of occupational
    health and environmental effects was fully recognized. The EHC
    monographs have become widely established, used and recognized
    throughout the world.

         The recommendations of the 1992 UN Conference on Environment and
    Development and the subsequent establishment of the Intergovernmental
    Forum on Chemical Safety with the priorities for action in the six

    programme areas of Chapter 19, Agenda 21, all lend further weight to
    the need for EHC assessments of the risks of chemicals.


         The criteria monographs are intended to provide critical reviews
    on the effect on human health and the environment of chemicals and of
    combinations of chemicals and physical and biological agents.  As
    such, they include and review studies that are of direct relevance for
    the evaluation.  However, they do not describe  every study carried
    out.  Worldwide data are used and are quoted from original studies,
    not from abstracts or reviews.  Both published and unpublished reports
    are considered and it is incumbent on the authors to assess all the
    articles cited in the references.  Preference is always given to
    published data.  Unpublished data are only used when relevant
    published data are absent or when they are pivotal to the risk
    assessment.  A detailed policy statement is available that describes
    the procedures used for unpublished proprietary data so that this
    information can be used in the evaluation without compromising its
    confidential nature (WHO (1990) Revised Guidelines for the Preparation
    of Environmental Health Criteria Monographs. PCS/90.69, Geneva, World
    Health Organization).

         In the evaluation of human health risks, sound human data,
    whenever available, are preferred to animal data.  Animal and  in 
     vitro studies provide support and are used mainly to supply evidence
    missing from human studies.  It is mandatory that research on human
    subjects is conducted in full accord with ethical principles,
    including the provisions of the Helsinki Declaration.

         The EHC monographs are intended to assist national and
    international authorities in making risk assessments and subsequent
    risk management decisions.  They represent a thorough evaluation of
    risks and are not, in any sense, recommendations for regulation or
    standard setting.  These latter are the exclusive purview of national
    and regional governments.


         The layout of EHC monographs for chemicals is outlined below.

    *    Summary -- a review of the salient facts and the risk evaluation
         of the chemical
    *    Identity -- physical and chemical properties, analytical methods
    *    Sources of exposure
    *    Environmental transport, distribution and transformation
    *    Environmental levels and human exposure
    *    Kinetics and metabolism in laboratory animals and humans

    *    Effects on laboratory mammals and  in vitro test systems
    *    Effects on humans
    *    Effects on other organisms in the laboratory and field
    *    Evaluation of human health risks and effects on the environment
    *    Conclusions and recommendations for protection of human health
         and the environment
    *    Further research
    *    Previous evaluations by international bodies, e.g., IARC, JECFA,

    Selection of chemicals

         Since the inception of the EHC Programme, the IPCS has organized
    meetings of scientists to establish lists of priority chemicals for
    subsequent evaluation.  Such meetings have been held in: Ispra, Italy,
    1980; Oxford, United Kingdom, 1984; Berlin, Germany, 1987; and North
    Carolina, USA, 1995. The selection of chemicals has been based on the
    following criteria: the existence of scientific evidence that the
    substance presents a hazard to human health and/or the environment;
    the possible use, persistence, accumulation or degradation of the
    substance shows that there may be significant human or environmental 
    exposure; the size and nature of populations at risk (both human and
    other species) and risks for environment; international concern, i.e.
    the substance is of major interest to several countries; adequate data
    on the hazards are available.

         If an EHC monograph is proposed for a chemical not on the
    priority list, the IPCS Secretariat consults with the Cooperating
    Organizations and all the Participating Institutions before embarking
    on the preparation of the monograph.


         The order of procedures that result in the publication of an EHC
    monograph is shown in the flow chart.  A designated staff member of
    IPCS, responsible for the scientific quality of the document, serves
    as Responsible Officer (RO).  The IPCS Editor is responsible for
    layout and language.  The first draft, prepared by consultants or,
    more usually, staff from an IPCS Participating Institution, is based
    initially on data provided from the International Register of
    Potentially Toxic Chemicals, and reference data bases such as Medline
    and Toxline.

         The draft document, when received by the RO, may require an
    initial review by a small panel of experts to determine its scientific
    quality and objectivity.  Once the RO finds the document acceptable as
    a first draft, it is distributed, in its unedited form, to well over
    150 EHC contact points throughout the world who are asked to comment
    on its completeness and accuracy and, where necessary, provide
    additional material.  The contact points, usually designated by
    governments, may be Participating Institutions, IPCS Focal Points, or
    individual scientists known for their particular expertise.  Generally
    some four months are allowed before the comments are considered by the

    RO and author(s).  A second draft incorporating comments received and
    approved by the  Director,  IPCS, is then  distributed to Task Group
    members, who carry out the peer review, at least six weeks before
    their meeting.

         The Task Group members serve as individual scientists, not as
    representatives of any organization, government or industry.  Their
    function is to evaluate the accuracy, significance and relevance of
    the information in the document and to assess the health and
    environmental risks from exposure to the chemical.  A summary and
    recommendations for further research and improved safety aspects are
    also required.  The composition of the Task Group is dictated by the
    range of expertise required for the subject of the meeting and by the
    need for a balanced geographical distribution.

         The three cooperating organizations of the IPCS recognize the
    important role played by nongovernmental organizations.
    Representatives from relevant national and international associations
    may be invited to join the Task Group as observers.  While observers
    may provide a valuable contribution to the process, they can only
    speak at the invitation of the Chairperson. Observers do not
    participate in the final evaluation of the chemical; this is the sole
    responsibility of the Task Group members.  When the Task Group
    considers it to be appropriate, it may meet  in camera.

         All individuals who as authors, consultants or advisers
    participate in the preparation of the EHC monograph must, in addition
    to serving in their personal capacity as scientists, inform the RO if
    at any time a conflict of interest, whether actual or potential, could
    be perceived in their work.  They are required to sign a conflict of
    interest statement. Such a procedure ensures the transparency and
    probity of the process.

         When the Task Group has completed its review and the RO is
    satisfied as to the scientific correctness and completeness of the
    document, it then goes for language editing, reference checking, and
    preparation of camera-ready copy.  After approval by the Director,
    IPCS, the monograph is submitted to the WHO Office of Publications for
    printing.  At this time a copy of the final draft is sent to the
    Chairperson and Rapporteur of the Task Group to check for any errors.

         It is accepted that the following criteria should initiate the
    updating of an EHC monograph: new data are available that would
    substantially change the evaluation; there is public concern for
    health or environmental effects of the agent because of greater
    exposure; an appreciable time period has elapsed since the last

    FIGURE 1

         All Participating Institutions are informed, through the EHC
    progress report, of the authors and institutions proposed for the
    drafting of the documents.  A comprehensive file of all comments
    received on drafts of each EHC monograph is maintained and is
    available on request.  The Chairpersons of Task Groups are briefed
    before each meeting on their role and responsibility in ensuring that
    these rules are followed.



    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,

    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

    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)


    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

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


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


         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).


    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
    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 -17C closed cup, -9C open cup;
    flammability limits in air at 25C = 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 20C) and a low viscosity (0.303 cP at
    25C). 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 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 g/m3 (0.2-52.9

    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 -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

         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

    1.6  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 l acetone did not
    appear to have any significant changes in mortality or malformations.


    2.1  Chemical identity

    Chemical name                 acetone
    Synonym(s)                    dimethyl ketone; 2-propanone;
    Chemical formula              C3H6O
    Chemical structure            
                                  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/descriptiona           Reference

    Relative molecular mass           58.08                        Riddick et al, (1986)

    Colour                            Clear colourless             Sax & Lewis (1987)

    Physical state                    Liquid                       Sax & Lewis (1987)

    Melting point                     -95.35C                     Weast (1987}

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

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


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

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

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

    Odour threshold:

    Acetone in water                  20 mg/litre                  Amoore & Hautala

    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/descriptiona           Reference

    Water at 20C                     Completely miscible          Windholz (1963)

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

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

    Partition coefficients:

    Log Kow                           -0.24                        Sangster (1989)
    Log Koc                           0.73b                        Lyman (1982)
    KB/A                              301  22                     Dills et al. (1994)

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

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

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

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

    Minimum ignition                  465C                        Riddick et al. (1986)

    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 25C:
         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 4C (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 g/ml            Gavino et al. (1986)
                             with acetonitdle and 2,4-DNPH

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

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

    Serum                    Deproteinized with sodium         HRGC-FID           <58 g/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 g/ml            Kobayashi et al.
                             pentafiuorobenzyloxyl ammonium                       (3.45 mol/ml)       (1983)
                             chloride and extracted with

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

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

    Air (occupational)      Air passed through charcoal and components                 GC-FID (NIOSH        7 g/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 g/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 g/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 g/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 g/litre)    (1990)
                            compound eluted with acetonitrile

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

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


    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.,

    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 1995a

    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  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 (Knppel &
    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).  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).  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).


    4.1  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 40N 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 25C 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
    40N 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 40N 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

    40N 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,

         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 Koc (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, Koc 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 (KL 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 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 Koc in
    water-saturated soil and has a low Koc 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
    25C) (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

    4.2  Biotransformation

    4.2.1  Bioconcentration and biomagnification

    The very low log Kow 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 25C
    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.  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.,

         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 (NOx) 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 NOx 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 40C, 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 NOx compounds.
    Andersson-Skld 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-Skld 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
    Koc, 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.


    5.1  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 g/m3 (0.2-3 ppb), in Rio 1.2-9 g/m3 (0.5-3.8
    ppb), and in Salvador 0-49.9 g/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 g/m3 (32.5
    ppbv) and the other at 16 g/m3 (6.84 ppbv).

         Chatfield et al. (1987) studied the behaviour of acetone in the
    troposphere. Over the Atlantic Ocean (35N), the mean concentration of
    acetone in the lower troposphere is approximately 1.2 g/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

         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 g/m3
    vs. 2.1 g/m3; 1 ppb vs. 0.9 ppb). They found very weak correlations
    with carbon monoxide and NOx; 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                     Concentrationa               Sampling dates              Reference
                                      g/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)
    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    0.54b         August 1995                 Leibrock & Slemr (1997)
    Ocean/Atlantic 35N               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

         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 g/m3 (3 ppb). This concentration is markedly higher than
    the concentration of 1.2 g/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 g/m3 (approx. 0.4-2.3 ppb), with a
    mean of 3.1 g/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 g/m3
         (approx. 0.5 ppb)  Indoor air

         Shah & Singh (1988) reported a concentration of 19 g/m3 (8 ppb)
    in household indoor air. These authors compiled available data to
    calculate an average outdoor concentration of 16.4 g/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
    g/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 g/m3 (20

         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 g/ms (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 g/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 g/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,

         Acetone has also been detected at 0.2-0.7 g/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 g/litre (Kieber & Mopper, 1990).
    Corwin (1969) measured VOCs in seawater and found acetone levels in
    the Florida Straits (USA) of 14-52 g/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 g/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

    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 mol/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 g/kg, with a mean level of 880 g/kg, and
    levels of 530 and 230 g/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 Koc (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 Koc 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 g/m3
    (8.0 ppb) in indoor air and 16.4 g/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 g/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 g/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 g, 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 g/litre in blood, 842 g/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 g/litre)
    and nonsmokers (792 g/litre), and likewise between hospital staff
    (719 g/litre) and blood donors (966 g/litre). The results are
    similar to those of Pezzagno et al. (1986) who measured 760 g
    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 g/litre            Jansson & Larsson (1969)

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

    Expired air     Healthy                 1.3 g/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 g/m3 (SD 79.78);
    smoking workplace, 952.86 g/m3 (SD 3988.25); non-smoking home, 50.12
    g/m3 (SD 58.5); smoking home, 71.19 g/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