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 Dr P. Lundberg (National Institute of
    Occupational Health, Sweden), Dr M. Crookes (Building Research
    Establishment, United Kingdom), and Dr S. Dobson and Mr P. Howe
    (Institute of Terrestrial Ecology, Monks Wood, United Kingdom)

    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, 1996

         The International Programme on Chemical Safety (IPCS) is a joint
    venture of the United Nations Environment Programme (UNEP), the
    International Labour Organisation (ILO), and the World Health
    Organization (WHO). The main objective of the IPCS is to carry out and
    disseminate evaluations of the effects of chemicals on human health
    and the quality of the environment. Supporting activities include the
    development of epidemiological, experimental laboratory, and
    risk-assessment methods that could produce internationally comparable
    results, and the development of manpower in the field of toxicology.
    Other activities carried out by the IPCS include the development of
    know-how for coping with chemical accidents, coordination of
    laboratory testing and epidemiological studies, and promotion of
    research on the mechanisms of the biological action 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 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 ; 186)

    1.Ethylbenzene - toxicity  2.Benzene derivatives
    3.Environmental exposure  I.Series

    ISBN 92 4 157186 1                 (NLM Classification: QV 633)
    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 1996

         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

         2.1. Identity
         2.2. Physical and chemical properties
         2.3. Conversion factors
         2.4. Analytical methods
              2.4.1. Ethylbenzene in air
              2.4.2. Ethylbenzene in water
              2.4.3. Ethylbenzene in biological material
              2.4.4. Metabolites of ethylbenzene in urine

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

         4.1. Transport and distribution between media
              4.1.1. Air
              4.1.2. Water
              4.1.3. Soil
              4.1.4. Sediment
         4.2. Transformation
              4.2.1. Biodegradation
             Aerobic degradation
             Anaerobic degradation
              4.2.2. Abiotic degradation
              4.2.3. Bioaccumulation

         5.1. Environmental levels
              5.1.1. Air
              5.1.2. Surface water and sediment
              5.1.3. Groundwater
              5.1.4. Urban run-off, effluent and landfill leachate
              5.1.5. Soil
              5.1.6. Biota
         5.2. General population exposure
              5.2.1. Environmental sources
              5.2.2. Food
              5.2.3. Drinking-water
         5.3. Occupational exposure during manufacture,
              formulation or use
              5.3.1. Biological monitoring

         6.1. Absorption
              6.1.1. Skin absorption
              6.1.2. Absorption via inhalation
              6.1.3. Absorption after oral intake
         6.2. Distribution
         6.3. Metabolic transformation
         6.4. Elimination and excretion

         7.1. Single exposure
         7.2. Short-term exposure
         7.3. Long-term exposure
              7.3.1. Oral exposure
              7.3.2. Inhalation exposure
         7.4. Skin and eye irritation, sensitization
         7.5. Reproductive toxicity, embryotoxicity
              and teratogenicity
         7.6. Mutagenicity and related end-points
         7.7. Carcinogenicity
         7.8. Other special studies
         7.9. Factors modifying toxicity

         8.1. Volunteer studies
         8.2. Occupational exposure

         9.1. Microorganisms
         9.2. Aquatic organisms
         9.3. Terrestrial organisms

         10.1. Evaluation of human health risks
         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 Châtelaine, Geneva, Switzerland (Telephone No. 9799111).

                             *     *     *

         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 14 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

    FIGURE 1

    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

         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, BIBRA Toxicology International, Carshalton, Surrey,
       United Kingdom

    Dr A. Bobra, Environment Canada, Orleans, Ontario, Canada

    Dr K. Hatfield, Division of Standards Development and Technology
       Transfer, National Institute for Occupational Safety and Health,
       Cincinnati, Ohio, USA

    Mr L. Heiskanen, Environmental Health Assessment and Criteria Section,
       Chemical Safety Unit, Department of Human Services and Health,
       Canberra, Australia

    Mr P. Howe, Institute of Terrestrial Ecology, Monks Wood, Abbots 
       Ripton, Huntingdon, Cambridgeshire, United Kingdom

    Dr You-xin Liang, Department of Occupational Health, Shanghai Medical
       University, Shanghai, China

    Professor M. Lotti, Institute of Occupational Medicine, University of
       Padua, Padua, Italy  (Chairman)

    Dr P. Lundberg, Department of Toxicology, National Institute of
       Occupational Health, Solna, Sweden  (Co-rapporteur)

    Dr Vesa Riihimaki, Institute of Occupational Health, Helsinki, Finland

    Dr Leif Simonsen, National Institute of Occupational Health,
       Copenhagen, Denmark

     Representatives of other Organizations

    Dr P. Montuschi, Institute of Pharmacology, Faculty of Medicine and
       Surgery, Catholic University of the Sacred Heart, Rome, Italy
       (representing the International Union of Pharmacology)


    Dr B.H. Chen, International Programme on Chemical Safety, World Health
       Organization, Geneva, Switzerland  (Secretary)


         A WHO Task Group on Environmental Health Criteria for
    Ethylbenzene met at the British Industrial Biological Research
    Association (BIBRA) Toxicology International, Carshalton, Surrey,
    United Kingdom, from 27 February to 2 March 1995.  Dr D. Anderson
    opened the meeting and welcomed the participants on behalf of the host
    institute.  Dr B.H. Chen, 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 ethylbenzene.

         Dr P. Lundberg, National Institute of Occupational Health,
    Sweden, Dr M. Crookes, Building Research Establishment, United Kingdom
    and Dr S. Dobson and Mr P. Howe, Institute of Terrestrial Ecology,
    Monks Wood, United Kingdom, prepared the first draft of this
    monograph.  The second draft was prepared by Dr Lundberg and Mr Howe,
    incorporating comments received following the circulation of the first
    draft to the IPCS Contact Points for Environmental Health Criteria
    monographs.  Dr S. Soliman, College of Agriculture & Veterinary
    Medicine, Saudi Arabia, contributed to the final text of the document.

         Dr B.H. Chen and Dr P.G. Jenkins, both members 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 document are gratefully acknowledged.

                               *    *    *

         Financial support for this Task Group was provided by the United
    Kingdom Department of Health as part of its contributions to the IPCS.


    FID       flame ionization detection

    GC        gas chromatography

    MS        mass spectrometry

    PID       photoionization detection

    VOC       volatile organic compound

    1.  SUMMARY

         Ethylbenzene is an aromatic hydrocarbon manufactured by
    alkylation from benzene and ethylene.  The estimated yearly production
    in the USA is about 5 million tonnes, and in 1983 it was approximately
    3 million tonnes in western Europe.  Ethylbenzene is a colourless
    liquid with a sweet gasoline-like odour.  It is mainly used for the
    production of styrene.  It is also used in technical xylene as a
    solvent in paints and lacquers and in the rubber and chemical
    manufacturing industries.  It is found in crude oils, refined
    petroleum products and combustion products.

         Ethylbenzene is a non-persistent chemical, being degraded
    primarily by photo-oxidation and biodegradation.  Volatilization to
    the atmosphere is rapid.  The photo-oxidation reaction of ethylbenzene
    in the atmosphere may contribute to photochemical smog formation.

         The log octanol-water partition coefficient is 3.13, indicating a
    potential for bioaccumulation.  However, the limited evidence
    available shows that ethylbenzene bioconcentration factors are low for
    fish and molluscs.  Elimination from aquatic organisms appears to be

         Ethylbenzene levels in air at rural sites are generally less than
    2 µg/m3.  Mean levels of ethylbenzene ranging from 0.74 to 100 µg/m3
    have been measured at urban sites.  The levels of ethylbenzene found
    in surface waters are generally less than 0.1 µg/litre in
    non-industrial areas.  In industrial and urban areas ethylbenzene
    concentrations of up to 15 µg/litre have been reported.  Ethylbenzene
    levels in sediments are generally less than 0.5 µg/kg, although levels
    between 1 and 5 µg/kg have been found in sediments from heavily
    industrialized areas. Concentrations in uncontaminated groundwater are
    generally less than 0.1 µg/litre, but are much higher in contaminated

         The acute toxicity of ethylbenzene to algae, aquatic
    invertebrates and fish is moderate.  The lowest acute toxicity values
    are 4.6 mg/litre for the alga  Selenastrum capricornutum (72-h EC50
    based on growth inhibition), 1.8 mg/litre for  Daphnia magna (48-h
    LC50) and 4.2 mg/litre for rainbow trout (96-h LC50).  No information
    is available regarding chronic exposure of aquatic organisms to

         There is limited information regarding the toxicity of
    ethylbenzene to bacteria and earthworms.  There are no data for
    terrestrial plants, birds or wild mammals.

         Human exposure to ethylbenzene occurs mainly by inhalation;
    40-60% of inhaled ethylbenzene is retained in the lung.  Ethylbenzene is
    extensively metabolized, mainly to mandelic and phenylglyoxylic acids. 
    These urinary metabolites can be used to monitor human exposures.

         Ethylbenzene has low acute and chronic toxicity for both animals
    and humans.  It is toxic to the central nervous system and is an
    irritant of mucous membranes and the eyes.  The threshold for these
    effects in humans after short single exposures was estimated to be
    about 430-860 mg/m3 (100-200 ppm).

         Inhalation of ethylbenzene for 13 weeks by rats and mice at
    concentrations up to 4300 mg/m3 (1000 ppm) did not lead to
    histopathological lesions.  The no-observed-effect level, based on
    increased liver weight in rats, was 2150 mg/m3 (500 ppm).

         Ethylbenzene is an inducer of liver microsomal enzymes.  It is
    not mutagenic or teratogenic in rats and rabbits.  No information is
    available on reproductive toxicity or carcinogenicity of ethylbenzene.

         A guidance value of 22 mg/m3 (5 ppm) has been calculated from
    animal studies.  The estimated exposure of the general population
    (even in the worst case situation) is below this guidance value. 
    Long-term occupational exposure to ethylbenzene concentrations
    estimated to be of this order of magnitude did not cause adverse
    health effects in workers.


    2.1  Identity

    Empirical formula:            C8H10

    Chemical structure:


    Chemical name:                Ethylbenzene

    Synonyms:                     Phenylethane, EB, Ethylbenzol

    Relative molecular mass:      106.16

    CAS registry number:          100-41-4

    RTECS registry number:        DA 07000000

    EEC number:                   601-023-00-4

    2.2  Physical and chemical properties

         Some physical and chemical properties of ethylbenzene are given
    in Table 1.

         The solubility of ethylbenzene in water is 152 mg/litre at 20°C
    and 101.3 kPa (DEC, 1992) and 138 mg/litre at 15°C (Heilbron et al.,
    1946).  Ethylbenzene is soluble in ethanol, diethylether and most
    other organic solvents (ECETOC, 1986; DEC, 1992).  At room temperature
    ethylbenzene is a colourless liquid with a sweet, gasoline-like odour
    (Windholz, 1983).

         The odour threshold concentration in air is about 2 mg/m3 and in
    water about 0.1 mg/litre (temperature not stated) (Anon, 1987; DEC,
    1992).  Ethylbenzene floats on water and, because of its significant
    vapour pressure and low water solubility, it will disperse in the
    atmosphere (ECETOC, 1986).

    Table 1.  Some physical and chemical properties of ethylbenzenea


    Physical state (20°C; 101.3 kPa)                        liquid
    Colour                                                  colourless
    Boiling point (°C) (101.3 kPa)                          136.2
    Melting point (°C)                                      -94.95
    Density (25°C; g/cm3)                                   0.866
    Vapour pressure (kPa at 20°C)                           1.24
    Flash point (°C)                                        12.8
    Refractive index (15°C, D line)                         1.49857
    Saturation % in air (20°C; 101.3 kPa)                   1.2
    Explosion limits (20°C; 101.3 kPa)                      1-7.8
    Log octanol/water partition coefficient (Log Kow)       3.13
    Henry's Law Constant (Pa m3/mol)                        887
    Log Sorption Partition Coefficient (Log Koc)            1.98-3.04
    Water Solubility (20°C; 101.3 kPa; mg/L)                152

    a    From:  Heilbron et al. (1946); Sax (1979); Verschueren (1983);
                Ullman (1983); Anon (1987); Weast (1988); ATSDR (1990); 
                Cavender (1993); DEC (1992); Mackay et al. (1992)

    2.3  Conversion factors

         1 ppm = 4.3 mg/m3 at 20°C and 101.3 kPa
         1 mg/m3 = 0.23 ppm at 20°C and 101.3 kPa

    2.4  Analytical methods

    2.4.1  Ethylbenzene in air

         Ethylbenzene in air can be analysed according to NIOSH (1984). 
    The air is sampled on a solid sorbent (coconut shell charcoal) and
    desorbed with carbon disulfide.  Aliquots are analysed by gas
    chromatography (GC) with flame ionization detection (FID).  With a
    desorption volume of 0.5 ml, 2.17-8.62 mg can be measured.  The
    detection limit is about 0.1 mg/m3 for a 10-litre sample.  Other
    volatile organic solvents are possible interferences (NIOSH, 1984).

         To avoid the use of carbon disulfide, sampling on montmorillonite
    clays (minerals consisting of a three-layer aluminosilicate lattice)
    and thermal desorption have been used (Harper & Purnell, 1990).  This
    method has not, however, yet been fully evaluated under actual
    sampling conditions in the field.

         A method using photoionization detection (PID) for GC, instead of
    FID, has been described.  PID is one to two orders of magnitude more
    sensitive to most aromatics than is FID (Hester & Meyer, 1979).  In an
    evaluation of sampling and analytical methods for monitoring several
    volatile organic compounds in air, sampling in a stainless steel
    canister was shown to be the best.  Using cryogenic pre-concentration
    followed by gas-liquid chromatography (GLC) equipped with a selective
    detector, ethylbenzene could be analysed at the ppb level (Jayanty,

         The sensitivity of the GC/FID method for analysing ethylbenzene
    and other volatile organic compounds can be improved by using wide
    bore capillary columns (0.4-0.75 mm internal diameter).  By this
    means, ethylbenzene can be separated from the C8 isomers even in
    complex mixtures (Frank et al., 1990).  Several kinds of Bentones with
    structures similar to that of Bentone 34 have been tested and compared
    for the purpose of improving the resolution of ethylbenzene and xylene
    isomers by GC.  Bentone SD-3 was found to have higher selectivity
    toward these close-boiling compounds than the well-known stationary
    phase Bentone 34 (Zlatkis & Jiao, 1991).

         Ultraviolet-spectrometry has also been used for analysis
    (Yamamoto & Cook, 1968).  Commercial detection tubes are available
    with a detection range of 132.3-1764.0 mg/m3 (DEC, 1992) and of
    4.41-220 µg (Gentry & Walsh, 1987).

    2.4.2  Ethylbenzene in water

         Determination of ethylbenzene in water has been performed by
    using the "head-space" technique coupled to GLC, in combination with
    mass spectrometry (MS) or infrared detection (Rosen et al., 1963;
    Burnham et al., 1972; Kleopfer & Fairless, 1972; Grob, 1973).  A
    purge-and-trap method has been developed for determination of four
    pollutants, including ethylbenzene, in aqueous samples.  Water samples
    are purged at 50°C with helium and the analytes are trapped on Tenax
    GC.  The trap is thermally desorbed directly into a gas chromatograph
    equipped with FID.  The method is laboratory validated for the range
    of 20-500 ppb using a 5 g aqueous sample (Warner & Beasley, 1984).

         Zhang & Pawliszyn (1993) developed a headspace solid phase
    microextraction technique to determine ethylbenzene and other volatile
    organic compounds (VOC) in water.  The detection limit was found to be
    at the ng/litre level.

    2.4.3  Ethylbenzene in biological material

         The head-space technique can also be used for measurements of
    ethylbenzene in blood.  The detection limit has been reported to be
    0.01 mg/litre (Radzikowska-Kintzi & Jakubowski, 1981).  The head-space

    methodology must, however, be optimized specifically for blood rather
    than using parameters derived from head-space experiments with aqueous
    media (Dills et al., 1991).

         An analytical method has been developed that enables the
    determination of ethylbenzene and other volatile organic compounds in
    10 ml of blood samples at the ng/litre level.  The method depends on
    purge-and-trap GC/MS and shows excellent reproducibility and recovery
    even at ultra-trace levels (Ashley et al., 1992).

         A method for analysing ethylbenzene in subcutaneous fat was
    described by Wolff et al. (1977).  Fat biopsies are obtained by using
    a 30 cm3 silanized glass syringe and a size 16 G needle.  The fat
    globules are washed from the syringe and needle by saline.  The fat-
    saline suspension is frozen and thawed to 0°C prior to analysis.  Fat
    globules are weighed and aliquots of CS2 are added. The solution is
    analysed by GC with dual flame ionization detectors.

         A method for the determination of ethylbenzene and other
    alkylbenzenes in plant foliage was developed by Keymeulen et al.
    (1991).  Using a gas chromatograph-quadrupole mass spectrometer in 
    the selected-ion monitoring mode, calibration graphs and detection
    limits for these hydrocarbons were determined.  Extraction was
    performed with dichloromethane and the optimum extraction time was
    found to be 6 h.

         Murray & Lockhart (1981) prepared fish muscle for analysis by
    extraction with dichloromethane and clean up on a florisil column. 
    Samples were analysed using GC with a FID.  A detection limit of
    5 µg/g was achieved with 98-102% recovery.  A procedure to identify and
    quantify ethylbenzene in fish samples by GC/MS using a fused-silica
    capillary column (FSCC) and vacuum extraction has been developed
    (Hiatt 1981, 1983; Dreisch & Munson 1983).  Improved resolution and
    detection limits at the ng/g level have been achieved with this

    2.4.4  Metabolites of ethylbenzene in urine

         One of the biomarkers of human exposure to ethylbenzene is the
    urinary concentration of mandelic acid.  Mandelic acid is also a
    metabolite of styrene.  Methods to monitor mandelic acid in urine were
    initially developed in order to evaluate exposure to styrene.

         In the GC method, mandelic acid is determined after extraction
    from urine by diethyl ether (Engström & Rantanen, 1974; Gromiec &
    Piotrowski, 1984).  The detection limit for mandelic acid by this
    method was 1.0 mg/litre.  Gas chromato-graphic methods require
    derivatization of the acid with diazomethane or silyl reagent before
    analysis.  This is not necessary for the HPLC or the ITP methods
    (Sollenberg, 1991). Urinary samples extracted by diethyl ether can

    also be determined by isotachophoresis (ITP) with a detection limit of
    0.04 mmol/litre  (Sollenberg, 1991).  This method is comparable to a
    high-performance liquid chromatographic (HPLC) method first described
    in 1977, with a detection limit of 0.01 mmol/litre (Ogata et al.,
    1977; Sollenberg, 1991).

         Determination of another major metabolite of ethylbenzene,
    phenylglyoxylic acid, in the urine of occupationally exposed people
    has been carried out by HPLC methods.  The limit of determination is
    0.1 mg/litre (Inoue et al., 1995).

         HPLC and ITP techniques can also be used for the simultaneous
    determination of mandelic and phenylglyoxylic acids in the urine of
    rats (Sollenberg et al., 1985).

         GC methods have been developed for analysis of other metabolic
    products of ethylbenzene.  Simultaneous determination of several 
    minor metabolites in urine from man and rats (e.g., acetophenone,
    1-phenylethanol, omega-hydroxyacetophenone, 4-ethylphenol,
    2,4-dimethylphenol and 3-methylbenzylalcohol) can be achieved with one
    method (Engström, 1984a).


    3.1  Natural occurrence

         Ethylbenzene is present in crude oil (Wiesenburg et al., 1981).

    3.2  Anthropogenic sources

         Ethylbenzene is present in refined products (Korte & Boedefeld,
    1978).  It is produced by incomplete combustion of natural materials,
    making it a component of forest fires and cigarette smoke.

    3.2.1  Production processes

         About 90% of all ethylbenzene used in the chemical industry is
    produced via the classic Friedel-Crafts alkylation of benzene with
    ethylene using soluble aluminium chloride catalyst.  These
    liquid-phase processes generally involve ethyl chloride or
    occasionally hydrogen chloride as a catalyst promoter.  In a variation
    on this method, dry benzene plus ethylene, catalyst and promoter are
    fed continuously to the alkylation reactor (Lewis et al., 1983;
    Fishbein, 1985).

         Other procedures which have been employed to a much lesser extent
    for the preparation of ethylbenzene include fractionation of petroleum
    and ultra-fractionation from a mixed xylene stream (Seader, 1982;
    Fishbein, 1985).  It is not, however, economical to isolate
    ethylbenzene from the catalytic raffinate (Fishbein, 1985;  ECETOC,

         An interesting approach for the preparation of ethylbenzene has
    been developed by Levesque & Dao (1989).  In this method the
    alkylation of benzene to produce ethylbenzene was performed
    successfully using an aqueous solution of ethanol of concentration
    similar to a fermentation broth.

    3.2.2  Production levels

         In the USA, the production of ethylbenzene in 1982 and 1983 was
    3.0 and 3.6 million tonnes, respectively (Webber, 1984).  According to
    Fishbein (1985), the annual capacity for the production of
    ethylbenzene was estimated to be about 4.6 million tonnes in the USA
    in 1983.  In 1986, production in the USA was reported to be
    approximately 4.1 million tonnes (US ITC, 1987).  The estimated annual
    production for ethylbenzene was 5.3 and 5.1 million tonnes for 1993
    and 1992, respectively, in the USA.  Ethylbenzene was the 19th in 1993
    and the 18th in 1992 chemical out of the top 50 chemicals in the USA
    (US Chemical Industry, 1994).  In 1983 the production of ethylbenzene
    in western Europe was around 3 million tonnes (ECETOC, 1986).

    3.2.3  Uses

         About 95% of ethylbenzene produced is employed for the production
    of styrene.  Ethylbenzene is a constituent (15-20%) of commercial
    xylene ("mixed xylenes"), and hence used as a component of solvents,
    as a diluent in paints and lacquers, and as a solvent in the rubber
    and chemical manufacturing industries.

         Ethylbenzene ("mixed xylenes") can also be added to motor fuels. 
    A typical ethylbenzene content of a reformate is about 4% (by volume)
    (Fishbein, 1985).


    4.1  Transport and distribution between media

         The majority of ethylbenzene released into the environment passes
    directly into the atmosphere or into surface water.

    4.1.1  Air

         It can be predicted from physico-chemical properties that, when
    ethylbenzene is released into air, the major part remains in the
    atmosphere and only small amounts are found in water, soil and
    sediment.  If it is assumed that all ethylbenzene is continuously
    released to the atmosphere, the Level III generic fugacity model
    consisting of homogeneous compartments of air, water, soil and
    sediment predicts that over 99% of ethylbenzene would be distributed
    in the atmosphere at steady state.  Ethylbenzene discharged to the
    atmosphere has very little potential for entering other media. 
    Precipitation from the atmosphere can occur.  The key processes
    determining overall fate are reaction in the air and advection (Mackay
    et al., 1992).

         Ethylbenzene has a low water solubility (152 mg/litre at 20°C)
    and a relatively high vapour pressure (1.24 kPa at 20°C).  This means
    that only a very small proportion of ethylbenzene in the atmosphere is
    likely to be removed by precipitation.  This is shown by the fact that
    it has been detected only at low levels in rain water samples (see
    section 5, Table 3).  Ethylbenzene may adsorb to atmospheric
    particulates and be removed along with the particles by precipitation
    or dry deposition.

    4.1.2  Water

         Transport and distribution of a substance in the aquatic
    environment are dependent on its solubility, movement of the water,
    exchanges at the air-water interfaces, adsorption to sediment and
    particulate matter, and bioconcentration in aquatic organisms.  The
    residence time in water is also dependent upon the type of
    environmental conditions encountered, such as temperature, wind speed,
    currents, ice cover, etc.

         For ethylbenzene, the half-life at 20°C in a river 1 m deep,
    flowing at 1 m/sec and with a wind velocity of 3 m/sec, calculated
    according to the method described by Thomas (1982) for high volatility
    compounds, is 3.1 h.  The half-lives in a marine mesocosm were 20 days
    at 8-16°C in the spring, 2.1 days at 20-22°C in the summer and 13 days
    at 3-7°C in the winter (Wakeham et al., 1983).  Volatilization was a
    dominant factor.  The increased turnover time during summer was also
    probably due to biodegradation.  The seasonal variations between
    winter and spring may have largely been due to changes in hydrodynamic
    conditions as a result of changes in wind-driven turbulence.

         If it is assumed that ethylbenzene is continuously released only
    into the water compartment, the Level III generic fugacity model
    predicts that approximately 93% of ethylbenzene would be distributed
    into the water at steady state, 4.5% into the atmosphere, 2.5% into
    the sediment and 1% into the soil.  The key processes determining
    overall fate are reaction in water and evaporation (Mackay et al.,

         It has been estimated (Callahan, 1979) from a computed Henry's
    Law constant of 6.44 × 10-3 atmos.m3.mol-1 that the volatility of
    ethylbenzene from water will be very similar to that of toluene
    (Henry's Law constant = 6.68 × 10-3 atmos.m3.mol-1).  Thus,
    ethylbenzene can be expected to have a half-life for volatilization
    from still water at a depth of 1 m of about 5 to 6 h (Mackay &
    Leinonen, 1975).  A measured value of the Henry's Law constant of 
    8.43 × 10-3 atmos.m3.mol-1 (Mackay et al., 1979) supports this

    4.1.3  Soil

         If it is assumed that ethylbenzene is only released to the soil
    compartment, the Level III generic fugacity model indicates that
    approximately 1% of ethylbenzene should be distributed into water,
    4.9% into the atmosphere, 94.7% into the soil and >1% into the
    sediment.  The soil acts only as a reservoir.  The soil concentration
    is controlled almost entirely by the rate at which it can evaporate
    (Mackay et al., 1992).

         In a study by Jaynes & Boyd (1991), the sorption isotherms of
    ethylbenzene and some other volatile organic compounds on organo-clays
    indicated that sorption occurred by partition interactions with the
    hexadecyltrimethylammonium (HDTMA)-derived organic phase.
    Mineral-charge effects on sorption of ethylbenzene were evident. 
    Greater sorption of ethylbenzene and other alkylbenzenes by high-
    charge HDTMA clays was attributed to the ability of the large basal
    spacings to accommodate larger solute molecules (Jaynes & Boyd, 1991).

         Several studies of soil-water partitioning for ethylbenzene have
    been reported.  In one study a value of 1.01 (log value) was found for
    the soil-water partition coefficient (Kp) for a soil of 4.02
    (± 0.06)% organic carbon content (Vowles & Mantoura, 1987).  Pussemier
    et al. (1990) reported a soil organic carbon-water partition
    coefficient (Koc) of 2.41 (log value).  Roy & Griffin (1985)
    estimated log Koc values of 2.60 and 2.87 derived from equations
    using solubility and Kow data, respectively.  The soil organic
    matter-water partition coefficient (Kom) was measured as 1.98 (log
    value) for a soil containing 1.9% organic matter (Chiou et al., 1983).
    Lee et al. (1989) reported log Kom values ranging from 1.73 to 1.97
    for untreated soil and from 2.37 to 3.23 for soil treated with organic
    cations.  It is likely that ethylbenzene will be adsorbed to soil to
    some extent.  Roy & Griffin (1985) predicted that ethylbenzene would

    have low mobility in water-saturated soil, based on the predicted Koc
    values.  However, Howard (1989) stated that the range of soil-water
    partition coefficients suggests that ethylbenzene is adsorbed
    moderately by soil and will probably leach through soil.  The presence
    of ethylbenzene in bank infiltrate water suggests that there is a high
    probability of it leaching through soil.  Other factors influencing
    the movement of ethylbenzene through soil to groundwater include soil
    type, soil porosity, amount of rainfall, depth of groundwater and
    extent of degradation.

         The competitive adsorption of ethylbenzene and water on bentonite
    was studied by Rhue et al. (1989) using a technique that allowed the
    amount of adsorbed water and the alkylbenzene to be measured
    independently.  Results indicated that ethylbenzene adsorption on the
    clay was not affected by water at relative humidities near 0.23 but
    was reduced significantly at values near 0.5.

         Laboratory studies indicate that volatilization of ethylbenzene
    occurs rapidly from sludge-treated soil (100% removal of an initial
    concentration of 50 mg/kg occurred within 6 days) (Water Pollution
    Control, 1989).

         It has been reported that sorption isotherms of ethylbenzene and
    some other nonionic organic compounds by maize  (Zea mays) residues
    and soil are linear.  Sorption coefficients of the corn residues were
    from 35 to 60 times greater than for surface soil (1.9% organic
    matter), demonstrating the high sorptive capability of these residues
    (Boyd et al., 1990).

         Annable et al. (1993) studied the reduction of gasoline component
    (including ethylbenzene) leaching potential by soil venting.  Results
    from columns vented for different periods of time showed vented soil
    to be effective at reducing constituent concentrations in leachate
    ultimately to about 1 µg/litre.

         Clapp et al. (1994) compared the performance of activated sludge
    (AS) and fixed-film processes with biological aerated filter (BAF)
    fermenters for removal of priority pollutants, including ethylbenzene. 
    They found that the AS and BAF fermenters achieved comparable VOC
    removal, and stripping rates were slightly higher for the AS
    fermenters;  degradation rates were slightly higher for the BAF

    4.1.4  Sediment

         The physical-chemical properties of ethylbenzene indicate that
    only small amounts should be found in sediment.

    4.2  Transformation

    4.2.1  Biodegradation  Aerobic degradation

         Ethylbenzene has been shown to be biodegradable in aquatic
    systems.  In simulations of spring and summer conditions in a coastal
    bay, half-lives of 20 days and 2.1 days, respectively, were obtained
    for ethylbenzene.  Both volatilization and biodegradation were
    responsible for removal (Wakeham et al., 1983).  The reduction in
    half-life in the summer was thought to represent an increase in
    microbial degradation.  An adaptation period was found to be important
    for microbial degradation to take place.  It was concluded that
    microbial degradation becomes important under warm conditions, with
    high biological activity, for the removal of ethylbenzene from the
    aquatic environment.  Howard (1991) report a half-life for aqueous
    biodegradation, in an unacclimated system, of 3 to 10 days.

         In an inherent biodegradability test (OECD 302 C), ethylbenzene
    was degraded by 81 to 126% biological oxygen demand (BOD) in 2 weeks
    (CITI, 1992).  In another biodegradability test, ECETOC (1986)
    reported that the BOD of ethylbenzene was determined after 6, 9 and 20
    days and that biodegradation corresponding to 32, 36 and 45% of the
    theoretical oxygen demand (TOD) was found.  Pitter & Chudoba (1990)
    reported a BOD5/TOD ratio of 0.29 for ethylbenzene.

         Ethylbenzene, as part of the water-soluble fraction of gas oil,
    has been shown to be degraded to 1-phenylethanol by the autochthonous
    microflora of clean groundwater.  After an initial lag phase of 3 to 4
    days, complete disappearance of ethylbenzene (from an initial
    concentration of 45 µg/litre) occurred within 12 days at 10°C
    (Kappeler & Wuhrmann, 1978a,b).

         Ethylbenzene was shown to be removed in core samples from an area
    that had been previously contaminated with unleaded gasoline. 
    Complete degradation occurred within three weeks on incubation of
    ethylbenzene in core samples that had previously had hydrogen peroxide
    added, whereas a small amount of ethylbenzene remained after three
    weeks in the previously gasoline-contaminated and uncontaminated core
    samples (Thomas et al., 1990).

         In static experiments, where ethylbenzene was incubated in the
    dark for 7 days with settled domestic wastewater as microbial
    inoculum, followed by 3 weekly subcultures from the medium,
    ethylbenzene was shown to be 100% degraded within 7 days in the
    initial inoculum and the three subsequent subcultures when the initial
    ethylbenzene concentration was 5 mg/litre.  At an initial ethylbenzene
    concentration of 10 mg/litre, 69% degradation of ethylbenzene occurred

    within 7 days in the initial culture, rising to 100% degradation
    within 7 days in the third subculture, indicating that gradual
    adaptation was needed for degradation of the higher concentration
    (Tabak et al., 1981).

         Soil bacteria have been shown to be capable of using ethylbenzene
    as a sole carbon source.  Microbial oxidative degradation has been
    shown to proceed via hydroxylation of the aromatic ring to give
    2,3-dihydroxy-1-ethylbenzene (Gibson et al., 1973).  A similar
    intermediate has been postulated in the degradation of ethylbenzene by
     Pseudomonas sp. NCIB 10643 cultures.  The 2,3-dihydroxy intermediate
    was suggested to undergo further degradation by meta cleavage of the
    aromatic ring (Smith & Ratledge, 1989).

          Nocardia tartaricans has been shown to be capable of converting
    ethylbenzene to 1-phenylethanol and acetophenone in a shake flask
    culture using hexadecane as the source of carbon and energy (Cox &
    Goldsmith, 1979).

         Bestetti & Galli (1984) showed that  Pseudomonas fluorescens can
    utilize ethylbenzene as sole carbon source.  Degradation appeared to
    occur by meta cleavage of the ring, with formation of the semi-
    aldehyde.  Utkin et al. (1991) have also recently shown that a species
    of  Pseudomonas is capable of growing on ethylbenzene as the
    sole source of carbon.  Products observed included 1-phenylethanol,
    2-phenylethanol, phenylacetate, salicylate, 2-hydroxyphenylacetate and
    mandelate.  Anaerobic degradation

         In a study to simulate the anaerobic degradation of landfill
    leachate on aquifer material that was known to support methanogenesis,
    no significant degradation of ethylbenzene was observed over the first
    20 weeks of the experiment.  However after 40 weeks the concentration
    of ethylbenzene was found to be 26% of the original value, and after
    120 weeks the concentration was < 1% of the original value (Wilson et
    al., 1986).

         Ethylbenzene, at a concentration of 500 mg/litre, was not found
    to be metabolized by or toxic to enriched methane-producing cultures
    (Chou et al., 1978).

         Ethylbenzene has been shown to undergo anaerobic degradation by
    aquifer microorganisms under denitrifying conditions in the presence
    of nitrate.  A lag period of around 30 days was observed before
    biodegradation of ethylbenzene occurred, but total removal of
    ethylbenzene occurred within the 56-day test period.  Using aquifer
    material that had been previously contaminated with jet fuel, little
    degradation of ethylbenzene occurred over the 180-day test period, but
    this was enhanced by addition of nitrate (Hutchins et al., 1991a,b). 
    Kuhn et al. (1988) also studied the degradation of ethylbenzene under

    denitrifying conditions using nitrate as the sole electron acceptor. 
    In their experiment an aquifer column was used which was capable of
    degrading  m-xylene.  The concentration of ethylbenzene was only
    slightly reduced during passage through the column, and the authors
    concluded that microbial mineralization of ethylbenzene was unlikely
    under denitrifying conditions.  However, they did point out that the
    experiment was only carried out for 6 days.  A longer experimental
    period might have allowed another microbial population to grow within
    the column that could have been capable of degrading ethylbenzene. 
    Ethylbenzene, as a component of crude oil contamination of anoxic
    groundwater, has been found to be degraded in the anoxic region, but
    the rate of disappearance was found to increase significantly in the
    more oxygenated parts of the aquifer (Cozzarelli et al., 1990).

    4.2.2  Abiotic degradation  Photolysis

         Ethylbenzene does not absorb UV-visible radiation appreciably at
    wavelengths longer than 290 nm.  This means that it is unlikely to be
    directly photolysed in the troposphere or in solution, as the earth's
    ozone layer absorbs radiation at wavelengths less than 290 nm (Crookes
    & Howe, 1992).  Mabey et al. (1982) stated that direct photolysis of
    ethylbenzene is not environmentally significant.  Photo-oxidation

         Atmospheric oxidation of ethylbenzene is rapid and proceeds via
    free-radical chain processes.  The most important oxidant is the
    hydroxyl radical, but ethylbenzene is also reactive with other species
    found in the atmosphere, such as alkoxy radicals, peroxy radicals,
    ozone and nitrogen oxides.  Estimates for the half-life of
    ethylbenzene in the atmosphere have been made from smog chamber
    experiments and from knowledge of the reaction rate constant for
    reaction with hydroxyl radicals.  Atkinson (1985) reviewed the
    available hydroxyl radical reaction rate constant data and recommended
    a kOH value of 7.5 × 10-12 molecule-1.cm3.sec-1 at 25°C for
    reaction with ethylbenzene.

         A study by Callahan (1979) produced an atmospheric half-life of
    around 15 h for ethylbenzene.  Another report gave a figure of 51%
    loss of ethylbenzene due to reaction with hydroxyl radicals in one day
    (12 sunlight hours) (Singh et al., 1981, 1983).  An atmospheric
    lifetime of 14 sunlight hours has been quoted based on a value of kOH
    (Singh et al., 1986).  An important point when considering these data
    is that the half-life calculated depends on several factors, including
    temperature and also the actual concentration of hydroxyl radicals in
    the atmosphere.  It is known that the concentration of hydroxyl
    radicals depends greatly on the amount of sunlight available; thus a
    typical figure is around 2 × 106 molecules/cm3 in summer months,

    falling by a factor of approximately 2 in winter months (Singh et al.,
    1986).  At night the concentration of hydroxyl radicals is negligible. 
    Even so, it can be seen that ethylbenzene is removed from the
    atmosphere quite readily by reaction with hydroxyl radicals.  It is
    also possible that ethylbenzene will be removed from aquatic systems
    by similar types of reactions, as hydroxyl radicals are known to exist
    in aquatic systems.  Hydrolysis

         It is considered unlikely that ethylbenzene will hydrolyse under
    typical conditions found in the environment.

    4.2.3  Bioaccumulation

         Ethylbenzene has an octanol-water partition coefficient of 3.13
    (log value), which indicates that bioaccumulation of ethylbenzene
    could take place. Using this partition coefficient, an estimated
    bioconcentration factor (BCF) of 2.16 (log value) can be calculated
    (Bysshe, 1982).

         In goldfish, a measured BCF of 1.19 (log value) has been reported
    (Ogata et al., 1984).  No details of exposure concentrations or length
    of exposure were given.

         When the manila clam  (Tapes semidecussata) was exposed to
    ethylbenzene at a concentration of 0.08 mg/litre in water containing
    other petroleum hydrocarbons, the concentration found in the tissue
    was 0.37 mg/kg after 8 days.  Depuration occurred rapidly after
    exposure ceased, tissue concentrations being below the limit of
    detection (< 0.13 mg/kg) after 15 days (Nunes & Benville, 1979).

         The low measured BCF values indicate that biomagnification of
    ethylbenzene through the aquatic food chain is unlikely.  No aquatic
    food chain magnification was predicted from the model calculations and
    empirical observations by Thomann (1989).


    5.1  Environmental levels

    5.1.1  Air

         Measured levels of ethylbenzene in air are presented in Table 2. 
    Mean levels of ethylbenzene ranging from 0.74 to 100 µg/m3 have been
    measured at urban sites.  Industrial releases and vehicle emissions
    are the principal sources of ethylbenzene.  Levels found at rural
    sites are generally < 2 µg/m3.

         Ethylbenzene levels for indoor air are included in section 5.2.1.

    5.1.2  Surface water and sediment

         The levels of ethylbenzene found in surface water are shown in
    Table 3.  These are generally less than 0.1 µg/litre in non-industrial
    areas.  In industrial and urban areas ethylbenzene concentrations of
    up to 15 µg/litre have been reported.

         In 1985, 21 water samples and 21 bottom sediment samples were
    collected at 7 sites in Japan and were analysed for the presence of
    ethylbenzene.  None of the water samples contained ethylbenzene; 3 of
    the sediment samples from one site contained ethylbenzene
    concentrations of 0.9 to 2.7 µg/kg dry weight.  The detection limit
    was 0.02 µg/litre for water and 0.8 µg/kg dry weight for bottom
    sediment.  In 1986, ethylbenzene was detected in 7 out of 133 samples
    of surface water at 5 out of 46 sites (0.03-1.1 µg/litre) and in 
    28 out of 120 samples of bottom sediment at 15 out of 40 sites
    (0.5-28 µg/kg dry weight).  The detection limit was 0.03 µg/litre for 
    water and 0.5 µg/kg dry weight for sediment (EAJ, 1989).

         Staples et al. (1985) reviewed the US EPA's STORET water quality
    database and reported that median levels of ethylbenzene in ambient
    surface water were less than 5.0 µg/litre between 1980 and 1982. 
    Ethylbenzene was detected in 10% of the 1101 samples collected during
    this period.  The median ethylbenzene concentration in sediment was
    5.0 µg/kg dry weight, the compound being detected in 11% of the 350

         In a study of the Tees Estuary, United Kingdom, levels of
    ethylbenzene between 1 and 5 µg/kg were found in river sediment from a
    heavily industrialized area (Whitby et al., 1982).

        Table 2.  Concentrations of ethylbenzene in air


    Sampling source               Concentration (µg/m3)       References

    Rural                         0.23-1.6 (range of means)   Petersson (1982), Clark et al. (1984b), Jüttner (1988), Lanzerstorfer 
                                                              & Puxbaum (1990), Kawata & Fujeda (1993)

    Urban                         0.74-100 (range of means)   Grob & Grob (1971), Bos et al. (1977), Louw et al. (1977), Singh et 
                                  (maximum value, 360)        al. (1981; 1982; 1986), Nelson & Quigley (1982), Harkov et al. (1983), 
                                                              De Bortoli et al. (1984), Clark et al. (1984a), Guicherit & Schulting
                                                              (1985), Jonsson et al. (1985), Hunt et al. (1986),  Bruckmann et al.
                                                              (1988), Lanzerstorfer & Puxbaum (1990), Chan et al. (1991a), Derwent
                                                              (personal communication to the IPCS, 1991),

    Industrial/residential site   22.0 (annual mean)          Bruckmann et al. (1988)
    near a rubber factory

    Industrial site near          10.8 (annual mean)          Bruckmann et al. (1988)
    refineries producing
    lubricating oil

    Industrial site               94 (mean)                   Kroneld (1989)
    near automotive               52 (< 1.6 km away)          Sexton & Westberg (1980)
    painting plant                11.5 (6.4 km away)
                                  5 (17.6 km away)

    Near to car plant             86                          Petersson (1982)
                                  27.8 (1 km away)

    Road tunnels                  2.1-48.2                    Bos et al. (1977), Hampton et al. (1983), Dannecker et al. (1990)

    Motorway                      147 (mean)                  Thorburn & Colenutt (1979)

    Table 3.  Concentrations of ethylbenzene in water


    Sampling source                   Concentration       Reference

    Surface waters

       Non-industrial river sites     < 0.1               Waggott (1981), McFall et al. (1985), SAC (1989)

       Industrial/urban river sites   1.9-15              Gomez-Belinchon et al. (1991)
                                      (range of means)

       Estuary (industrial area)      ND-1.8              Whitby et al. (1982)

       Seawater                       0.0018-0.026        Gschwend et al. (1982), Gomez-Belinchon
                                      (range of means)    et al. (1991)

       Sea near offshore oil          0.07                Sauer (1981)

    Rainwater                         0.0006-0.009        Kawamura & Kaplan (1983), Pankow et al. (1984)


       Uncontaminated                 NDb-0.07            Kenrick et al. (1985)

       Contaminated                   30-2000             Tester & Harker (1981), Van Duijvenbooden &
                                                          Kooper (1981), Stuermer et al. (1982), Rao et al.

       Water-table at a solvent       up to 28 000        Cline & Viste (1985)
       recovery facility

    Table 3.  (Cont'd)


    Sampling source                   Concentration       Reference


       Effluent from wastewater/      NDc-14              Kennicutt et al. (1984);  Namkung & Rittmann
       sewage treatment works                             (1987); Feiler et al. (1979); Michael et al.
                                                          (1991);  Gossett et al. (1983)

    Landfill leachate                 1.7-2310            Först et al. (1984);  Reinhard et al. (1984);
                                                          Van Duijvenbooden & Kooper (1981);  Cline &
                                                          Viste (1985)

    a   ND = not detected
    b   detection limit = 0.01 µg/litre
    c   detection limit not stated
             A sludge characterization study for a slip containing wastewater
    sludge situated in Baltimore Harbour, USA, was performed.  The slip
    contained an estimated 14 100 m3 of sludge, which averaged 20% solids
    (by weight).  Organic compounds were found to be the primary
    constituents in the sludge, the highest concentrations being
    represented by benzene, ethylbenzene, toluene and xylenes (Mott &
    Romanow, 1991/1992).

    5.1.3  Groundwater

         The levels of ethylbenzene in groundwater are summarized in Table

         Ethylbenzene levels in uncontaminated groundwater are generally
    < 0.1 µg/litre.  However, much higher levels have been reported for
    groundwater contaminated via waste disposal, fuel spillage and
    industrial facilities.  At a solvent recovery facility, ethylbenzene
    concentrations of up to 28 000 µg/litre were measured.

         Lesage et al. (1990) detected ethylbenzene in 3% of anoxic
    groundwater samples at a concentration of 2 µg/litre.  Goodenkauf &
    Atkinson (1986) analysed 63 wells and detected ethylbenzene in only
    one at a concentration of 0.99 µg/litre; the detection limit was 
    0.5 µg/litre.  Ethylbenzene was found in 3 out of 466 groundwater 
    samples collected in the USA in 1982. The maximum concentration was 
    1.1 µg/litre and the detection limit 0.5 µg/litre (Cotruvo, 1985).

    5.1.4  Urban run-off, effluent and landfill leachate

         The levels of ethylbenzene in effluent from wastewater/sewage
    treatment plants and landfill leachate are summarized in Table 3.

         When Perry et al. (1979) analysed a range of industrial effluent
    samples, 19 contained < 10 µg/litre, 4 contained 10-100 µg/litre and
    2 contained > 100 µg/litre.  Staples et al. (1985) reported that
    ethylbenzene was detected in 7.4% of 1368 industrial effluent samples
    collected between 1980 and 1983, the median concentration being less
    than 3.0 µg/litre.

         Cole et al. (1984) detected ethylbenzene in 4% of urban run-off
    samples.  Concentrations ranged from 1-2 µg/litre; however, no
    detection limits were stated.

    5.1.5  Soil

         ATSDR (1990) reported that ethylbenzene was detected in 9.22%
    soil samples from 1177 sites.  The geometric mean of these samples was
    697 µg/kg.

    5.1.6  Biota

         Several species of aquatic organisms have been analysed for
    ethylbenzene (Table 4).

    Table 4.  Levels of ethylbenzene in aquatic species (Gossett et al., 1983)


                        Species                          Ethylbenzene level
                                                         µg/kg wet weight

    Pacific sanddab (Citharichthys xanthostigma) (liver)       <0.3

    scorpion fish (Scorpaena guttata) (liver)                  <0.3

    Dover sole (Microstomus pacificus) (liver)                  0.3

    white croaker (Genyonemus lineatus) (liver)                4

    shrimp (muscle)                                            <0.3

    invertebrate (whole body)                                  <0.3

    NOTE: No detection limits were stated; organisms were collected from an
    area near to the discharge zone of a waste treatment plant; ethylbenzene
    levels of 14 µg/litre in effluent and 0.5 µg/kg (dryweight) in sediment
    were measured in the area at the time of sampling.

         In 1986, ethylbenzene was detected in 43 out of 138 fish samples
    at 16 out of 42 sites in Japan, the concentrations ranging from 1.0 to
    9.8 µg/kg wet weight.  The detection limit was 1 µg/kg wet weight
    (EAJ, 1989).

         Staples et al. (1985) reviewed the US EPA's STORET water quality
    database and reported that ethylbenzene was not detected in 97 biota
    samples (detection limit, 0.025 mg/kg wet weight).

         Lockhart et al. (1992) reported data on ethylbenzene levels in
    freshwater fish sampled in the Canadian Arctic in 1985 and 1986.  Mean
    ethylbenzene concentrations ranged from 2.45 to 49.6 µg/kg in muscle
    tissue and from 1.81 to 46.3 µg/kg in liver tissue for burbot.  In
    whitefish muscle tissue samples, mean ethylbenzene concentrations
    ranged from 7.46 to 104 µg/kg.

    5.2  General population exposure

    5.2.1  Environmental sources

         The magnitude of natural releases into the environment has not
    been established.

         Although ethylbenzene is ubiquitous in rural and urban
    atmospheres, levels in urban areas are elevated due to vehicular and
    industrial emissions.  Ethylbenzene was not detectable in some rural
    samples, while those taken on busy urban streets contained levels up
    to 99 µg/m3 (23.1 ppb) (ATSDR, 1990).

         The Environmental Protection Agency (USA) conducted a study of
    ethylbenzene levels in public access buildings and found that
    concentration, which was 387 µg/m3 (90 ppb) at the time construction
    was completed, declined to 39 µg/m3 (9 ppb) following several months
    of occupation of the building.  This indicated that building materials
    and/or finishings, such as paints, carpets and adhesives, were likely
    sources of emissions (Pellizzari et al., 1984).  Subsequent emission
    studies using inhalation chambers revealed that ethylbenzene was
    emitted from glued carpet at a mean level of 6.4 (± 3.2) µg/m3,
    corresponding to an emission rate of 77 (± 39) ng/min per m2 (Wallace
    et al., 1987c).  Hodgson et al. (1991) studied the emissions of
    volatile organic compounds in a new office building over a period of
    14 months.  Ethylbenzene levels in the building ranged from 7.0 to
    11.8 µg/m3, as compared to 1.8 µg/m3 in the outdoor air.  The
    authors suggested that motor vehicles in the underground carpark of
    the building were one of the major sources of ethylbenzene, but this
    area was not specifically monitored.

         Wallace et al. (1987a,b) monitored ethylbenzene in breathing-zone
    air, exhaled air and ambient air samples taken from some of the home
    backyards of 400 residents of an industrial/chemical manufacturing
    area (the cities of Bayonne and Elizabeth, New Jersey, USA).  Median
    levels of ethylbenzene ranged from 4.6 to 7.1 µg/m3 for breathing-
    zone air, 1.3 to 2.9 µg/m3 for exhaled air and 2.2 to 4.0 µg/m3
    for backyard air.  Personal air monitoring conducted at home
    yielded high ethylbenzene levels, believed to be due to the presence
    of the chemical in tobacco smoke.  The maximum geometric mean
    ethylbenzene exposure of people living in homes with smokers (13
    µg/m3) was approximately 1.5 times the geometric mean of people
    living in homes without smokers (8 µg/m3).  Wallace et al. (1987a)
    found the geometric mean level of ethylbenzene in the expired air of
    smokers (n=200) to be 2 to 3 times higher than in that of non-smokers
    (n=322).  Wallace et al. (1987a) estimated that the total amount of
    ethylbenzene in the mainstream smoke of a single cigarette, containing
    16 mg of tar and nicotine, was 8 µg.

         In another study, the blood concentration of ethylbenzene was
    measured in 13 non-smokers and 14 cigarette smokers, all living in an
    urban area.  The concentration of ethylbenzene in blood ranged from
    175 to 2284 ng/litre and 378 to 2697 ng/litre, respectively
    (Hajimiragha et al., 1989).

         Fellin & Otson (1993)  monitored indoor air for ethylbenzene in
    754 randomly selected Canadian residences in 1986.  Mean ethylbenzene
    concentrations were 6.46 µg/m3 in winter, 8.15 µg/m3 in spring, 4.35
    µg/m3 in summer and 13.97 µg/m3 in autumn.

         Wallace et al. (1989) carried out a study on seven volunteers who
    performed 25 common activities thought to increase personal exposure
    to volatile organic compounds during a 3-month period.  Monitoring
    personal, indoor and outdoor air levels, as well as exhaled breath,
    revealed that painting and using a carburettor cleaner resulted in an
    80-fold increase in ethylbenzene exposure.  Combustion sources
    (including cigarette smoke), gasoline vapours and consumer products
    containing ethylbenzene increased exposures by up to 6 times over the
    background level.

         Chan et al. (1991b) studied exposure of commuters in Boston, USA
    to ethylbenzene.  These individuals spent 1.3 to 1.7 h per day (5% to
    7% of the day) commuting and this contributed 10-20% of their total
    daily ethylbenzene exposure.  The results showed that the highest
    exposures were associated with commuting by car (5.8 µg/m3) and that
    the use of car heaters resulted in even higher in-vehicle levels of
    ethylbenzene.  Heater use resulted in a passenger compartment mean
    ethylbenzene level of 8 µg/m3, whereas non-use resulted in 3.7
    µg/m3.  The authors postulated that heaters can increase influx of
    both the vehicle's own exhaust and general roadway exhaust.

         Coal-fired power stations have been found to emit ethylbenzene
    along with other volatile organic compounds (Garcia, 1992).

         Bevan et al. (1991) monitored exposure to vehicle emissions while
    commuting by bicycle on urban roads in Southampton, United Kingdom and
    compared it with ethylbenzene exposure for a typical suburban area. 
    Mean ethylbenzene levels on urban roads were 30.3 µg/m3 compared with
    15.1 µg/m3 for suburban areas.  The authors reported that 2 metres
    from the exhaust of a stationary idling vehicle the mean ethylbenzene
    level was  137 µg/m3.

         Ashley et al. (1994) analysed the blood ethylbenzene
    concentration of 631 non-occupationally exposed people in the USA. 
    The mean and median levels were 0.11 and 0.06 µg/litre, respectively,
    and the detection limit was 0.02 µg/litre.

         Kawai et al. (1992) evaluated urinalysis and blood analysis as
    means of detecting human exposure to ethylbenzene and some other
    volatile organic compounds, using 143 exposed and 20 non-exposed
    workers.  They found that both solvent concentration in blood and
    metabolite concentration in urine correlated significantly with the
    concentration of the solvent in air.

         Pellizzari et al. (1982) analysed volatile organic compounds in
    human milk samples taken from lactating women living in urban areas of
    the USA and found ethylbenzene in all eight samples.  Ethylbenzene has
    also been detected in human axillary volatiles (Labows et al., 1979). 
    However, both these studies were based solely on qualitative scans of
    the mass spectra peaks from GC/MS analysis; no detection limits were

    5.2.2  Food

         Ethylbenzene has been detected in several types of dried legumes. 
    Levels of between 0 and 11 µg/kg (mean 5 µg/kg) in beans, 13 µg/kg in
    split peas and 5 µg/kg in lentils were measured (Lovegren et al.,

         Although ethylbenzene has been detected in the skin of roasted
    guinea hens (at a level of 2 µg/kg) by Noleau & Toulemonde (1988), the
    authors did not state whether the source of the ethylbenzene was
    directly from the skin or the cooking process.

    5.2.3  Drinking-water

         Otson et al. (1982) found that ethylbenzene levels in Canadian
    treated potable water ranged from <1 to 10 µg/litre.  Westrick et al.
    (1984) reported that ethylbenzene was detected in 8 out of 945 samples
    of finished (undefined) water from groundwater supplies.  The levels
    ranged from 0.74 to 12 µg/litre.  Coleman et al. (1984) analysed
    drinking-water from Cincinnati, USA and found an  ethylbenzene level
    of 0.036 µg/litre.

         Durst & Laperle (1990) studied the migration of ethylbenzene from
    polystyrene containers into stored deionized water.  The water samples
    were stored for up to 90 days at temperatures ranging from 24 to 66°C. 
    Migration of ethylbenzene increased with time and storage temperature. 
    The levels in the water samples ranged from 16 µg/litre on day 1 to 41
    µg/litre at 24°C, 48 µg/litre at 38°C and 107 µg/litre at 52°C. 
    Ethylbenzene levels of up to 209 µg/litre were detected on day 8 at

    5.3  Occupational exposure during manufacture, formulation or use

         Occupational exposure to ethylbenzene alone is rare. 
    Simultaneous exposure to other organic solvents usually occurs.

         The following ethylbenzene exposure levels have been reported
    from various occupational settings: exposure to gasoline, mean
    concentration of less than 0.08 mg/m3 (Rappaport et al., 1987);
    exposure to jet fuel, mean concentrations of 0.02 mg/m3 (4 h) and
    0.07 mg/m3 (15 min) and maximum concentrations of 1.3 mg/m3 (4 h)
    and 8.0 mg/m3 (15 min) (Holm et al., 1987); exposure in petroleum and
    chemical factories, mean concentration of 7.7 mg/m3 (Inoue et al.,
    1995); exposure while varnishing vehicles, average concentration of 17
    mg/m3 (Angerer & Wulf, 1985); exposure during paint-rolling and
    brushing, maximum concentration of 3.2 mg/m3 (Verhoeff et al.,
    1988); exposure in a petroleum company and a pharmaceutical factory,
    concentration range of 0.05-23 mg/m3 (Lu & Zhen, 1989).

         During painting operations, ethylbenzene and some other volatile
    organic compounds were detected in the working atmosphere at
    concentrations ranging from 0.1 to 69.1 ppm (Vincent et al., 1994).

    5.3.1  Biological monitoring

         Determination of mandelic acid in urine has been recommended as a
    biomarker of exposure to ethylbenzene.  In studies by Bardodej &
    Bardodejová (1970) and by Gromieck &  Piotrowski (1984), exposure to
    ethylbenzene at 430 mg/m3 (100 ppm) for 8 h resulted in 13 mmol/litre
    and 7.8 mmol/litre, respectively, of mandelic acid in the
    end-of-exposure urine samples.  A value of 1.5 g mandelic acid per g
    creatinine (about 10 mmol/litre) in the post-shift urine has been
    proposed as a Biological Exposure Index (ACGIH, 1985-1986).

         In specific analysis (e.g., by gas chromatography), the urinary
    level of mandelic acid is negligible (less than 0.2 mmol/litre) in the
    general population.  However, certain drugs may be metabolized to
    mandelic acid (Aitio et al., 1994).

         Monitoring of personal exposure has shown that low ethylbenzene
    concentrations of approximately 8.6 mg/m3 (2 ppm) correlate
    significantly (correlation coefficients of 0.6-0.7) with urinary
    phenylglyoxylic acid concentration, suggesting that measurements of
    this acid in the urine could be used for biomonitoring (Inoue et al.,


    6.1  Absorption

    6.1.1  Skin absorption

         One human subject was exposed for 2 h to ethylbenzene vapour at
    concentrations ranging from 650 to 1300 mg/m3 in an exposure chamber. 
    The exposed skin accounted for 90-95% of the total skin area.  Clean
    breathing air was provided by means of a gas-tight respirator.  The
    mandelic acid concentration in urine, before, during and up to 6 h
    after exposure, was within physiological limits (approximately 2.7
    mg/litre).  The authors concluded that the skin is not a relevant
    route of entry into the body for ethylbenzene vapours (Gromiec &
    Piotrowski, 1984).

         The possible absorption of liquid ethylbenzene across human sin
    has also been studied (Dutkiewicz & Tyras, 1967).  Ethylbenzene
    (0.2 ml=174 mg) was applied in a watch glass tightly fixed on the
    forearm.  The exposed skin area was 17.3 cm2.  After 10-15 min the
    contents of the watch glass space was extracted with ethanol and the
    recovered amount of ethylbenzene determined spectrophotometrically. 
    On the basis of the quantity of ethylbenzene not recovered, the mean
    absorption rate for seven people was calculated to be 28 mg/cm2 per
    hour (range 22-33 mg cm2 per hour).

         The penetration rate of ethylbenzene through excised rat skin has
    been determined in a penetration chamber.  One ml of ethylbenzene was
    applied to 2.55 cm2 skin.  After a 6-h application period, the
    penetration rate was found to be about 0.99 nmoles/cm2 per min 
    (6 µg/cm2 per hour (Tsuruta, 1982).

         Percutaneous absorption of ethylbenzene has been studied in
    hairless mice (11 animals) (Susten et al., 1990). 14C-ring-labelled
    ethylbenzene (in a volume of 5 µl) was injected into a chamber glued
    onto the back skin (0.8 cm2), and the animals were housed in
    metabolism cages for 4 h.  During that period exhaled breath samples
    were collected.  At the end of 4 h, the animals were killed and the
    absorbed dose was measured in the excreta and carcass.  A total of
    95.2 (± 1)% of the nominal dose was recovered.  The absorption rate
    was calculated to be 0.037 (± 0.0315) mg/cm2 per min (2.2 ± 1.9
    mg/cm2 per hour).

         Dermal absorption of volatile organic chemicals from aqueous
    solutions has been studied in male Fischer-344 rats.  For 24 h the
    rats were exposed (3.1 cm2 dorsal shaved skin) to 2 ml (in a glass
    exposure cell) of one-third saturated, two-thirds saturated, or a
    fully saturated solution of ethylbenzene.  Blood samples were obtained
    at 0, 0.5, 1, 2, 4, 8, 12 and 24 h.  The peak blood level (exposure to
    neat ethylbenzene) was 5.6 mg/litre.  The level reached a maximum 

    within 4 h and then either remained at about the same level for the
    duration of the exposure or decreased.  The blood levels were directly
    related to the exposure concentrations (Morgan et al., 1991).

         The data concerning skin permeability of ethylbenzene in humans
    (Dutkievicz and Tyras, 1967) is not consistent with the animal data. 
    The reliability of the estimated fluxes of ethylbenzene through human
    skin must be questioned because they are many times higher than the
    measured fluxes through rat skin, whereas from studies of  in vitro
    percutaneous absorption it is known that rat skin is more permeable
    than human skin (mean ratio about 3) for several chemicals (Barber et
    al., 1992).

    6.1.2  Absorption via inhalation

         When volunteers (number not given) were exposed to 99, 185, 198
    or 365 mg/m3 (23, 43, 46 or 85 ppm) ethylbenzene for 8 h, 64% of the
    inhaled ethylbenzene was taken up by the respiratory tract (Bardodej &
    Bardodejova, 1966).  In another study, six volunteers were exposed
    under controlled conditions for 8 h to 18, 34, 80, 150 or 200 mg/m3. 
    The retention of ethylbenzene in the lungs (difference in
    concentration between inhaled and exhaled air) was 49% (± 5%)
    independent of the exposure concentration (Gromiec & Piotrowski,

         When volunteers were exposed to 430 mg/m3 or 870 mg/m3 of
    "industrial xylene" (containing 40% ethylbenzene and 60% xylenes) for
    2 h, about 60% was taken up, independent of concentration.  If the
    workload increased during exposure, the retention dropped to 50%
    (Ĺstrand et al., 1978).

         In a study by Chin et al. (1980a), rats (male, Harlan-Wistar)
    were exposed to 14C-labelled ethylbenzene at a concentration of 1000
    mg/m3 for 6 h.  Assuming a ventilation rate of 100 ml/min, each rat
    had an estimated intake of 36 mg ethylbenzene, of which 44% was

    6.1.3  Absorption after oral intake

         Toxicity studies in various animal species show indirectly that
    ethylbenzene is absorbed after oral administration (Wolf et al., 1956,
    NTP, 1992).  Moreover, in one study, ethylbenzene appeared to be
    rapidly and well absorbed from the gastro-intestinal tract since more
    than 80% of the administered radioactively labelled compound was
    recovered in urine within 48 h (Climie et al., 1983).

    6.2  Distribution

         When volunteers (n=12) were exposed for 2 h to 100 or 200 ppm
    "industrial xylene", the amount of ethylbenzene taken up correlated
    with the amount of body fat ("industrial xylene" consisted of 40.4%
    ethylbenzene, 49.4%  m-xylene, 8.8%  o-xylene and 1.4%  p-xylene). 
    The concentration of ethylbenzene ranged from 4 to 8 mg/kg in
    subcutaneous adipose tissue 30 min after exposure.  There was,
    however, a negative correlation between the concentration in the
    adipose tissue and the estimated relative amount of fat (Engström &
    Bjurström, 1978).

         The ethylbenzene concentration in the subcutaneous fat of workers
    in a styrene polymerization plant was less than 0.8 mg/kg.  The level
    of exposure to ethylbenzene was reported to be below 17 mg/m3 (4
    ppm).  The 25 workers were exposed to a variety of other chemicals as
    well (Wolff et al., 1977).

         When rats were exposed to 1000 mg/m3 14C-ring-labelled
    ethylbenzene for 6 h, 0.2% of this radioactivity was found 42 h later
    in the tissues, mainly in the liver, gastrointestinal tract, fat and
    the carcass (Chin et al., 1980a).

         In a study by Engström et al., (1985), male Wistar rats (n = 20)
    were exposed to 215, 1290 or 2580 mg ethylbenzene/m3 (50, 300 or 600
    ppm) for 6 h/day, and 5 days/week for up to 16 weeks.  The
    concentration of ethylbenzene in perirenal fat was measured in weeks
    2, 5 and 9.  There were no consistent changes in ethylbenzene levels
    during the course of exposure.  After 16 weeks the amount of
    ethylbenzene in perirenal fat was 8.5, 167.7 and 262.2 mg/kg fat at
    the three exposure levels, respectively.

    6.3  Metabolic transformation

         Metabolic pathways of ethylbenzene based on urinary metabolites
    have been proposed for humans (Fig. 1) and for rats (Fig. 2).  The
    main metabolic pathway is oxidation of the side chain, both in humans
    and in animals.  However, it has been demonstrated that there are both
    qualitative and quantitative inter-species differences in the
    metabolites produced (Engström et al., 1984; Engström 1984b).  In
    humans, the main metabolites of ethylbenzene are mandelic and
    phenylglyoxylic acids. In several animal species the metabolic
    transformation continues to benzoic acid, leading to excretion of
    hippuric acid after conjugation with glycine.  This conjugate is
    generally one of the main urinary metabolites, together with mandelic
    acid, in rats and dogs (Chin et al., 1980b).  Hydroxylation of the
    aromatic nucleus is a minor pathway.  In the rabbit this phenolic
    pathway accounts for less than 2% of the ethylbenzene absorbed (Kiese
    & Lenk, 1974).

    FIGURE 2

    FIGURE 3

         Ethylbenzene is metabolized by the microsomal cytochrome P-450
    enzyme system.  Although specific isozymes have not been unequivocally
    identified, enzyme induction studies suggest that CYP2B1/2, CYP1A1/2
    and CYP2E1 may be involved (see section 7.8).

         Four male volunteers were exposed to 655 mg/m3 (150 ppm)
    ethylbenzene for 4 h and urine was collected for 24 h.  Mandelic acid
    (71.5%) and phenylglyoxylic acid (19.1%) were the main metabolites,
    but smaller amounts of 1-phenylethanol,  p-hydroxyacetophenone,
     m-hydroxyacetophenone, 1-phenyl-1,2-ethandiol, 4-ethylphenol,
    omega-hydroxyacetophenone and acetophenone were also found.  Ring
    oxidation accounted for 4.0%.  Simultaneous exposure to 150 ppm
     m-xylene did not alter the urinary metabolite pattern, but it
    delayed excretion and decreased the amounts of metabolites excreted 
    (Engström et al., 1984).  Mandelic acid (64%) and phenylglyoxylic aid
    (25%) were found to be the main urinary excretion products in
    volunteers after an 8-h exposure to 99-365 mg/m3 (23-85 ppm)
    ethylbenzene (Bardodej & Bardodejová, 1970).

         When two volunteers were exposed by inhalation to 430 mg/m3 (100
    ppm) ethylbenzene for 4 h, most of the mandelic acid was excreted as
    the R-enantiomer (Drummond et al., 1989).

         In a study by Korn et al. (1992), urinary samples from workers
    exposed to ethylbenzene, toluene and xylenes were analysed.  The
    average urinary concentration of phenylglyoxylic acid was 50.1
    mg/litre.  The concentration of mandelic acids was 135.2 mg/litre, of
    which 127.8 mg/litre was R-mandelic acid and 7.3 mg/litre was
    S-mandelic acid.  The R/S ratio was independent of the air
    concentration of ethylbenzene, which varied between 6.4 and 142 mg/m3
    (1.5 and 33 ppm).

         Four female histology laboratory assistants were exposed to a
    mixture of xylenes (75%) and ethylbenzene (25%). The air concentration
    of the solvent was 160-179 mg/m3, and the concentration of
    ethylbenzene in blood collected at the end of the working day was
    reported to be 0.5 to 0.8 mg/litre. The 24-h excretion of
    2-ethylphenol in urine varied between 4.4 and 6.0 mg corresponding to
    1 to 1.5% of the retained ethylbenzene (Angerer & Lehnert, 1979).  The
    findings by Angerer & Lehnert (1979) that ethylbenzene is metabolized
    to 2-ethylphenol could not be verified by Engström et al. (1984).

         Male Wistar rats (6 per group) were exposed for 6 h to
    ethylbenzene at 1290 or 2580 mg/m3 (300 or 600 ppm).  The urine was
    collected for 48 h from the onset of exposure.  Altogether, 14
    different metabolites from ethylbenzene were identified.  The main
    metabolites were 1-phenylethanol, mandelic acid and benzoic acid, each
    of which accounted for about 25%.  Only 13% (low dose) and 6% (high 

    dose) of the estimated absorbed doses were eliminated during the 6-h
    exposure.  Over the 48-h period, the corresponding values were 83% and
    59%, respectively.  The metabolic pattern was similar, irrespective of
    the exposure level (Engström, 1984b).

         In another study, male Wistar rats (20 per group) were exposed to
    215, 1290 or 2580 mg ethylbenzene/m3 (50, 300 or 600 ppm) for 6
    h/day, 5 days/week, for up to 16 weeks.  Urinary excretion of some of
    the metabolites was measured in weeks 2, 5 and 9.  A significant
    dose-related percentage decrease of phenylglyoxylic acid and hippuric
    acid plus benzoic acid was found.  A corresponding increase of
    1-phenylethanol and omega-hydroxyacetophenone excretion was also
    noted. The total amount of metabolites in urine collected during the
    24 h after onset of exposure remained, however, constant at each
    exposure level throughout the study (Engström et al., 1985).

         When a single oral dose of 318 mg ethylbenzene/kg body weight was
    administered to rabbits, the main urinary metabolites found were
    hippuric acid and methylphenylglucuronic acid, which together
    represented 60-70% of the dose, while mandelic acid and phenaceturic
    acid were minor metabolites (El Masry et al., 1956).

         It has been established in  in vivo studies that experimental
    animals convert ethylbenzene mainly to the R-enantiomer of mandelic
    acid (Drummond et al., 1990).  In an  in vitro study it was found
    that ethylbenzene is hydroxylated by cytochrome P-450cam (from
     Escherichera coli) almost exclusively at the secondary ethyl carbon
    with about a 2:1 ratio of R:S products (Filipovic et al., 1992).

         The rates of metabolism of ethylbenzene have been studied  in
     vitro in rabbit liver and lung.  Organs from five female animals
    were used, but details of the experimental procedures were not
    reported.  For the liver (mean weight 76 g) the rate of metabolism was
    453 nmol/g tissue per 10 min (34.4 µmol per liver per 10 min or 11.7
    nmol per nmol cytochrome P-450 per 10 min).  The corresponding figures
    for lung (mean weight 7.7 g), were 680 nmol, 5.3µmol and 200.1 nmol,
    respectively. Thus, lung tissue may significantly contribute to the
    body clearance of ethylbenzene in rabbits (Sato & Nakajima, 1987).

    6.4  Elimination and excretion

         In humans, ethylbenzene is mainly excreted in the urine as
    mandelic and phenylglyoxylic acids (Bardodej & Bardodejová, 1970;
    Ĺstrand et al., 1978; Engström et al., 1984; Gromiec & Piotrowski,
    1984).  Only up to 5% of retained ethylbenzene is estimated to be
    exhaled without transformation (Ĺstrand et al., 1978).  The
    elimination half-lives of ethylbenzene in exhaled air and urine have
    been estimated to be 0.5-3 h and 8 h, respectively (Wolff, 1976).  In
    human volunteers exposed to 100 or 200 ppm "industrial xylene" for
    2 h, there was no decline in the concentration of xylenes plus 

    ethylbenzene in the gluteal subcutaneous adipose tissue between 30 min
    and 22 h after exposure (Engström & Bjurström, 1978).  The elimination
    of mandelic acid has been found to be biphasic, with half-lives of 3.1
    and 24.5 h (Gromiec & Piotrowski, 1984).

         The elimination kinetics for 10 volatile organic compounds, 
    including ethylbenzene, has been studied in human volunteers exposed
    to a variety of consumer products.  Breath samples were collected
    post-exposure and analysed by GC/MS.  The half-lives for the 10
    chemicals varied from a few hours to 1-2 days.  The authors concluded
    that volatile organic compounds exhibit relatively short residence
    times in the body (Pellizzari et al., 1992).

         Male Harlan-Wistar rats exposed to 14C-ring-labelled
    ethylbenzene (1000 mg/m3) for 6 h excreted 82% of the radioactivity
    in the urine, 8.2% in expired air (0.03% as CO2) and 0.7% in faeces. 
    After 42 h, 0.2% remained in the tissues. The remaining 8.3% could not
    be accounted for (Chin et al., 1980a).


    7.1  Single exposure

         Single high exposures to ethylbenzene cause irritation of the
    mucous membranes and central nervous system effects. The results from
    single exposure  in vivo studies are summarized in Table 5.

        Table 5.  Single exposure of animals to ethylbenzenea


    Species   Route         Dose                        Parameter         Reference

    Rat       oral          3.5 g/kg                    LD50              Wolf et al. (1956)

    Rat       oral          4.7 g/kg                    LD50              Smyth et al. (1962)

    Rat       inhalation    9.37 g/m3 (2180 ppm)        Minimum           Molnár et al. (1986)
                                                        narcotic conc.

    Rat       inhalation    17.2 g/m3 (4000 ppm) 1 h    LC10              Smyth et al. (1962)

    Rat       inhalation    17.2 g/m3 (4000 ppm) 4 h    LC50              Smyth et al. (1962)

    Rat       inhalation    34.4 g/m3 (8000 ppm) 1 h    LC100             Smyth et al. (1962)

    Rabbit    dermal        77.4 g/kg                   LD50              Smyth et al. (1962)

    a    Additional information is given in the following reviews: DFG (1985), ECETOC (1986).
    7.2  Short-term exposure

         In a short-term study, six male rats (Sprague Dawley) were
    exposed for 6 h/day during 3 consecutive days to 8.6 g/m3 (2000 ppm)
    ethylbenzene.  The animals were killed 16-18 h after the last
    exposure. Small increases in dopamine and noradrenaline levels and
    turnover in various parts of the hypothalamus and the median eminence
    were reported.  Ethylbenzene was also found to produce selective
    reduction in prolactin and corticosterone secretion and selective
    increase in dopamine turnover within the dopamine-cholecystokinin-8-
    immuno-reactive nerve terminals of the nucleus accumbens (posterior
    part) (Andersson et al., 1981).

         When eight male rabbits (New Zealand) were exposed 12 h daily for
    7 days to 3.22 g/m3 (750 ppm) ethylbenzene, there was a marked
    (p<0.05) depletion of striatal and tuberoinfundibular dopamine.  Such
    an effect was also caused by intraperitoneal dosing of rabbits (eight
    per group) with mandelic or phenylglyoxylic acid (4 mmol/kg per day
    for 3 days) in saline (Romanelli et al., 1986).

         In a 4-week inhalation study Fischer-344 rats (five of each sex
    per group) were exposed to ethylbenzene for 6 h/day, 5 days per week,
    at exposure levels of 0, 426, 1643 or 3363 mg/m3 (0, 99, 382 or 782
    ppm).  At the two highest exposure levels, sporadic lacrimation and
    salivation, as well as significantly (p<0.05) increased liver
    weights, were seen.  At the highest exposure level, there was a small
    increase in leukocyte counts and, in males, a marginal increase in
    platelet counts (Cragg et al., 1989).

         In the same study, mice (B6C3F1) of both sexes were similarly
    exposed.  At 1643 and 3363 mg ethylbenzene/m3, females showed
    significantly (p<0.01) increased absolute and relative liver weights. 
    In males a significantly (p<0.05) increased relative liver-to-brain
    weight ratio was seen.  Male and female rabbits (New Zealand White)
    were also used in this study.  The exposure levels were 0, 1643, 3363
    and 6923 mg/m3 (0, 382, 782 and 1610 ppm).  At the highest exposure
    level females gained weight more slowly than controls but neither sex
    exhibited gross or microscopic organ changes (Cragg et al., 1989).

         No changes in mortality pattern were seen in the three species. 
    There were no changes in clinical chemistry parameters in rats or
    rabbits.  Mice were not subjected to clinical chemistry or 
    haematological examinations due to the small volume of blood that
    could be collected.  For similar reasons, urinalyses were performed
    for rats (no change) but not for mice.  Rabbits were excluded from
    urinalysis for logistical reasons.  No changes in gross or microscopic
    pathology were noted in any of over 30 tissues from each of the three
    species when the animals were exposed at the highest concentration
    (Cragg et al., 1989).

    7.3  Long-term exposure

    7.3.1  Oral exposure

         Matched groups of 10 Wistar female rats were given daily
    ethylbenzene doses of 0, 13.6, 136, 408 or 680 mg/kg by stomach tube
    5 days a week for 6 months.  The two highest dosages induced slight
    increases in liver and kidney weights and slight cloudy swelling of
    parenchymal liver cells and of the tubular epithelium in the kidney
    (Wolf et al., 1956).

    7.3.2  Inhalation exposure

         In a 13-week National Toxicology Program study, groups of 10 rats
    (F-344/N) and 10 mice (B6C3F1) of each sex were exposed for 6 h (plus
    10 min to reach 90% of the target chamber concentration) per day,
    5 days per week for 92 (female rats), 93 (male rats), 97 (female mice)
    or 98 (male mice) days, at ethylbenzene concen-trations of 0, 430,
    1075, 2150, 3225 or 4300 mg/m3 (0, 100, 250, 500, 750 or 1000 ppm). 
    Blood for clinical chemistry and haematological examination was
    collected on study days 4 and 23 and again at week 13 from both male
    and female rats.  Dose-related increases in absolute liver weight were
    seen in both sexes of mice exposed to the two highest dose levels, and
    the relative kidney weight of female mice exposed to 4300 mg/m3 was
    greater than that of the controls.  Increased absolute and relative
    liver and kidney weights were seen in male rats exposed to the two
    highest dose levels.  Increased absolute liver and kidney weights were
    seen in female rats exposed to the three highest dose levels, but no
    increased relative liver and kidney weights were seen.  No chemically
    related histopathological changes were observed in any rat or mouse
    tissues.  Clinical chemistry results were negative (NTP, 1992).

         In another study, groups of five male rats (Wistar) were exposed
    for 6 h/day, 5 days/week to ethylbenzene concentrations of 0, 215,
    1290 or 2580 mg/m3 (0, 50, 300 or 600 ppm) and sacrificed after 2, 5,
    9 or 16 weeks of exposure.  At 2580 mg/m3 liver cells showed a slight
    proliferation of smooth endoplasmic reticulum, slight degranulation
    and splitting of rough endoplasmic reticulum, and enlarged
    mitochondria.  At the same dose level, liver microsomal protein, but
    not cytochrome P-450, concentration was slightly increased.  There was
    also an increase in NADPH-cytochrome  c reductase, 7-ethoxycoumarin-
     O-deethylase and UDPG-transferase activities in the liver.  In the
    kidney only the two latter enzymes showed dose-related increases. 
    Urinary excretion of thioethers was measured to ascertain the
    generation of electrophilic intermediates during ethylbenzene
    metabolism.  Excretion of thioethers increased in a dose-dependent
    manner, with some fluctuation over the course of 7 weeks, reaching
    about eight times the control level at 2580 mg ethylbenzene/m3. 
    However, there was no decrease in hepatic or renal levels of
    glutathione (GSH), indicating that the cells were able to maintain the
    intra-cellular homeostasis of GSH during exposure (Elovaara et al.,

         In inhalation experiments, matched groups of 10-25 male and
    female Wistar rats, 5-10 guinea-pigs, 1-2 rabbits and 1-2 rhesus
    monkeys of either sex or both sexes were all exposed 7 h/day, 5
    days/week, for up to 6 months.  The exposure levels were 0, 1720 and
    2580 mg/m3 (0, 400 and 600 ppm) for 186 days, 5375 mg/m3 (1250 ppm)
    for 214 days (no monkeys) or 9460 mg/m3 (2200 ppm) for 144 days (rats
    only).  Slight effects were seen in rats: increased liver and kidney 

    weights at 1720 mg/m3; increased liver and kidney weights at 2580
    mg/m3; and small histopathological changes (cloudy swelling) in liver
    and kidney at 5375 and 9460 mg/m3 (Wolf et al. 1956).

         In guinea-pigs and monkeys slightly increased liver weights were
    noted in the 2580 mg/m3 group only.  At the same exposure level,
    small histopathological effects in the testes, described as
    degeneration of the germinal epithelium, were seen in rabbits and
    monkeys.  At 5375 mg/m3 a slight growth depression was noted in
    guinea-pigs.  The no-observed-effect level (all four species) was
    considered to be about 860 mg/m3 (200 ppm) (Wolf et al., 1956).  It
    should be noted, however, that Cragg et al. (1989) found no
    histopathological effects in the testes of rats and rabbits exposed to
    up to 3363 mg/m3 (782 ppm) for 4 weeks, and the lack of toxicity was
    confirmed by NTP (1992).

    7.4  Skin and eye irritation, sensitization

         Inhalation for 3 min of ethylbenzene at a concentration of 4300
    mg/m3 caused slight nasal irritation in guinea-pigs, and an 8-min
    exposure caused eye irritation as well.  At 8600 mg/m3 a 1-min
    exposure was enough to cause both effects (Cavender, 1993).

         Two drops of undiluted ethylbenzene placed in the eyes of rabbits
    resulted in slight conjunctival irritation but no effects on the
    cornea (Wolf et al., 1956).  A slight conjunctival irritation with
    some reversible corneal injury was reported in rabbits in a study by
    Smyth et al. 1962.

         Undiluted ethylbenzene has been shown to produce moderate
    irritation when applied to the uncovered skin of rabbits (Smyth et
    al., 1962).  The application of undiluted ethylbenzene to the ear and
    to the shaved abdomen of rabbits up to 20 times during a 4-week period
    resulted in moderate irritation.  There was erythema and oedema with
    superficial necrosis and exfoliation of large patches of skin (Wolf et
    al., 1956).

         No animal sensitization studies have been reported.

    7.5  Reproductive toxicity, embryotoxicity and teratogenicity

         In an inhalation study, rats (Wistar or Sprague-Dawley) and
    rabbits (New Zealand White) were exposed to 430 or 4300 mg/m3 (100 or
    1000 ppm) ethylbenzene for 6 to 7 h/day on gestation days 1 to 19
    (rats) or 1 to 24 (rabbits).  All pregnant animals were sacrificed on
    the day before term (day 21 for rats, day 30 for rabbits).  The
    rabbits had a significantly (p<0.05) reduced number of live pups per
    litter at both exposure levels, but the number of implantations per
    litter and the number of dead or resorbed fetuses per litter did not
    differ from those of the controls.  Maternal toxicity in rats exposed 

    to 4300 mg/m3 was reflected in increased liver, kidney and spleen
    weights.  There was a significant (p<0.05) increase in the incidence
    of extra ribs in both of the exposed rat groups (Hardin et al., 1981).

         In a further study, rats (CFY) were exposed to ethylbenzene
    concentrations of 600, 1200 or 2400 mg/m3 continuously (24 h/day)
    from day 7 to day 15 of pregnancy.  They were then killed on day 21. 
    Mice (CFLP) were exposed for three periods of 4 h per day to 500
    mg/m3 on days 6-15 of pregnancy and killed on day 18.  Rabbits (New
    Zealand White) were exposed continuously on days 7-20 of gestation to
    500 or 1000 mg/m3 and were killed at day 30.  The maternal toxic
    effects (not specified) in mice and rats were moderate and
    dose-dependent.  In both species ethylbenzene caused skeletal growth
    retardation, extra ribs and reduced fetal growth rate at the highest
    concentration.  In rabbits, the highest dose concentration caused mild
    maternal toxic effects (decreased weight gain) and reduction in the
    number of fetuses due to abortion (Ungváry & Tátrai, 1985).

         When rats (F-344/N) and mice (B6C3F1) were exposed to
    ethylbenzene at concentrations of 0, 430, 2150 and 4300 mg/m3 (0,
    100, 500 and 1000 ppm), 6 h per day, 5 days per week, for 13 weeks,
    there were no changes in sperm or vaginal cytology (NTP, 1992).

         Rat embryos were explanted on day 9 of gestation and cultured in
    rat serum with added xylene (containing 18% ethylbenzene) at
    concentrations up to 1.0 ml/litre serum.  Dose-dependent retardation
    of growth and development was seen but there were no observable
    teratogenic effects (Brown-Woodman et al., 1991).

         No multigeneration and reproductive studies on ethylbenzene have
    been reported.

    7.6  Mutagenicity and related end-points

         In a National Toxicology Program study, ethylbenzene was not
    mutagenic in Salmonella tests and did not induce chromosomal
    aberrations or sister chromatid exchange in Chinese hamster ovary
    (CHO) cells  in vitro, although it did induce trifluorothymidine
    resistance in mouse lymphoma cells at the highest concentration tested
    (80 mg/litre).  There was no increase of micronuclei in the peripheral
    blood of mice exposed to ethylbenzene (NTP, 1992).

         In several other studies ethylbenzene did not induce point
    mutations (with or without added metabolic activation system).  In
    addition, it did not cause an increase in the spontaneous
    recessive-lethal frequency in the Drosophila recessive-lethal test,
    nor had it any chromosomal effects  in vitro (Donner et al., 1980; 
    Florin et al., 1980; Dean et al., 1985).  Ethylbenzene had a marginal
    effect on sister chromatid exchange in human lymphocytes  in vitro
    when a high (10 mmol/litre) concentration was used (Norppa & Vainio, 

    1983).  In addition, in the TK+/- test in mouse lymphoma cells there
    was a slight effect at a high concentration (80 mg/litre) (McGregor et
    al., 1988).  This study is obviously the same as the one subsequently
    reported by NTP (1992).

         No excess of chromosomal aberrations in bone marrow cells was
    seen in rats after up to 18 weeks of exposure (6 h/day, 5 days/week)
    to 300 ppm of a xylene mixture containing 18.3% ethylbenzene (Donner
    et al., 1980).

    7.7  Carcinogenicity

         In a carcinogenicity study, rats (Sprague-Dawley) were exposed to
    one of several aromatic hydrocarbons, including ethylbenzene.  Groups
    of rats (40 of each sex) were exposed to 500 mg ethylbenzene (in olive
    oil) per kg body weight by gavage, 4 or 5 days per week for 104 weeks. 
    Results were determined after 141 weeks.  The first malignant tumour,
    a nephroblastoma, was observed after 33 weeks.  The total number of
    malignant tumours was 31 in the 77 animals of the exposed group alive
    at 33 weeks compared with an incidence of 23 of 94 animals in the
    control group.  The authors concluded that ethylbenzene caused an
    increase in the incidence of total malignant tumours, although there
    was no increase in the incidence of any specific type of tumour
    (Maltoni et al., 1985).  It is difficult to draw any firm conclusion
    from this study because of inadequate reporting.

    7.8  Other special studies

         Ethylbenzene was found to have low acute cytotoxicity  in vitro
    on Ehrlich ascites cells (Holmberg & Malmfors, 1974).

         The effects of ethylbenzene have been studied in four  in vitro
    test systems: decreased cell growth in Ascites sarcoma BP 8 cells;
    decreased oxidative metabolism in hamster brown fat cells; cell
    membrane damage of human embryonic lung fibroblasts; and inhibition of
    ciliary activity in chicken embryo trachea.  On a 0-9 point scale
    (equivalent to 0-100%) the activity of these four systems scored 4, 6,
    8 and 8, respectively (Curvall et al., 1984).

         The activity of cytochrome CYP2E1 can be monitored in microsomal
    preparations by  p-nitrophenol hydroxylation.  When rabbit (white
    male New Zealand) liver microsomes were treated with up to 0.25 mM
    ethylbenzene an inhibition of  p-nitrophenol hydroxylation was seen
    (Koop & Laethem, 1992).

         In a study by Pyykkö et al. (1987), Sprague-Dawley male rats were
    given ethylbenzene dissolved in corn oil intraperitoneally in a single
    dose of 5 mmol/kg (530 mg/kg body weight).  The rats were killed 24 h
    later and the livers and lungs removed.  In the liver 7-ethoxycoumarin-
     0-deethylase (a marker of CYP2B1/2) was induced 4-fold; no induction

    was found in the lung.  Ethylbenzene also induced 7-ethoxyresorufin-
     0-deethylase (a marker of CYP1A1/2) both in the liver (4-fold)
    and the lung (2.5 fold).  These findings are common to many aromatic

         Alterations in the levels of specific cytochrome P-450 isozymes
    were measured by Western immunoblotting techniques using rabbit
    anti-rat polyclonal antibodies for cytochrome CYP1A1, CYP2B1 and
    CYP2E1 on rat liver microsomes.  The rats, male and female Holtzman
    rats, were given 10 mmoles ethylbenzene per kg body weight for 3 days
    and killed 24 h after the last injection.  Ethylbenzene was shown to
    induce CYP2B1/2B2 to a greater extent in male rats, while cytochrome
    CYP2E1 was only induced in female rats.  The level of cytochrome
    CYP1A1 was not affected by ethylbenzene (Sequeira et al., 1992).

         In another study (Gut et al., 1993), Wistar male rats were
    exposed in a dynamic inhalation apparatus to 4 mg ethylbenzene/litre
    air, 20 h per day, for 4 days.  The rats were then killed and liver
    microsomes prepared.  By use of Western immunoblotting techniques it
    was shown that cytochrome CYP2B1 was induced and the cytochrome CYP2E1
    levels were decreased.

         In a sensory irritation test, groups of four male mice
    (Swiss-Webster) were exposed for 30 min to ethylbenzene at
    concentrations of 1.76, 3.7, 8.06, 17.07 or 41.45 g/m3 (410, 860,
    1875, 3970 or 9640 ppm).  The RD50 value, i.e. the concentration
    necessary to depress the respiratory rate by 50%, was calculated to be
    17.46 g/m3 (4060 ppm) (95% confidence interval 10.6-28.6 g/m3;
    2480-6660 ppm).  The respiratory rate decreased due to sensory
    irritation of the upper respiratory tract (Damgĺrd Nielsen & Alarie,
    1982).  In a similar test male mice (Swiss F1) were exposed for about
    5 min to different concentrations of ethylbenzene.  At least four
    different concentrations were used and there were six mice for each
    concentration.  In this study the RD50 value was calculated to be
    6.16 g/m3 (1432 ppm) (De Ceaurriz et al., 1981).

    7.9  Factors modifying toxicity

         Rats (Sprague-Dawley) were exposed for 2 h to 774 mg/m3 (180
    ppm) ethylbenzene.  One of two corresponding animals received 20 mmol
    ethanol/kg body weight in physiological saline intraperitoneally
    before exposure to ethylbenzene.  Ethanol enhanced significantly (1.4
    fold) the blood levels of inhaled ethylbenzene (Römer et al., 1986).


    8.1  Volunteer studies

         A dermal maximization test conducted on 25 volunteers at a
    concentration of 10% ethylbenzene in petrolatum produced no skin
    sensitization reaction (ECETOC, 1986).

         In a review of studies from the 1930s, it was stated that
    exposure to 21.5 g/m3 (5000 ppm) ethylbenzene for a few seconds gives
    intolerable irritation of nose, eyes and throat.  A few seconds of
    exposure to 4.3 g/m3 (1000 ppm) initially gives eye irritation which
    diminishes after a few minutes of exposure (Damgĺrd Nielsen & Alarie,

         In a study on ethylbenzene metabolism in man it was incidentally
    reported that, when the exposure was above the occupational limit
    value (8 h; 430 mg/m3,100 ppm), complaints of fatigue, sleepiness,
    headache and irritation of the eyes and respiratory tract were
    reported (Bardodej & Bardodejová, 1970).

         Healthy male subjects were exposed to technical xylene
    (containing 20.7% ethylbenzene) for 2 h with or without a 100-watt
    workload on an ergometer cycle.  The air concentration of technical
    xylene was 435 or 1300 mg/m3.  During work at the higher exposure
    level, evidence of performance decrement was observed in three of the
    five performance tests: reaction time addition test (p<0.05),
    short-term memory (p<0.05) and choice reaction time (p<0.10)
    (Gamberale et al., 1978).

    8.2  Occupational exposure

         A number of epidemiological studies have been carried out on
    groups occupationally exposed to mixtures of solvents, including
    ethylbenzene.  In these studies it is difficult to attribute the
    effects to ethylbenzene or any other single chemical present. 
    Ethylbenzene occurs in mixed xylenes (at up to 30%) and effects of
    occupational exposure to mixed xylenes are usually presented as
    effects of xylenes and not of ethylbenzene.

         A cross-sectional epidemiological study showed no strong evidence
    of adverse neurobehavioural effects in 105 house painters when
    compared with 53 workers from various professions (non-painters).  The
    concentration of ethylbenzene at the workplace was up to 12.9 mg/m3
    (3 ppm).  Other solvents present were ethyl acetate, toluene, butyl
    acetate, methyl isobutyl ketone and xylene.  In two neurobehavioural
    tests significant differences were found between painters and controls

    (the tests were "change of personality" and "short-term memory
    capacity").  In a subgroup of painters with repeated prenarcotic
    symptoms at the workplace, the differences were more pronounced
    (Triebig et al., 1988).

         In a study involving 35 spray painters, employed for between 2
    and 26 years, erythrocyte and haemoglobin levels were slightly (but
    not statistically significantly) lower than those of the controls. 
    The concentration of ethylbenzene was 17.2 mg/m3 (4 ppm) (Angerer &
    Wulf, 1985).

         In a medical surveillance report of some 200 ethylbenzene-
    production workers, mandelic acid concentrations in urine were 
    measured twice a year for 20 years.  Mandelic acid concentration
    in the samples never exceeded 3.25 mmol/litre (=497 mg/litre), and the
    mean value was 0.20-0.30 mmol/litre.  According to the authors, a
    post-shift urine mandelic acid concentration of 6.25 mmol/litre is
    equivalent to an air concentration of 200 mg/m3.  Therefore, the
    measured maximum and mean mandelic acid values were considered to be
    equivalent to air ethylbenzene concentrations of about 86 and 8.6
    mg/m3 (20 and 2 ppm), respectively.  None of the workers examined
    over the last 10 years showed any effects on the levels of
    haemoglobin, leucocytes or platelets, nor did they have a changed
    haematocrit or alanine aminotransferase activity (Bardodej & Círek,

         Minor changes in evoked potential and nerve conduction velocity
    were found in 22 workers exposed to ethylbenzene at concentrations of
    0.43-17.2 mg/m3 (0.1-4 ppm) for 4-20 years.  They were also exposed
    to styrene (about 1.5 ppm) (Lu & Zhen, 1989).


    9.1  Microorganisms

         Ethylbenzene has been shown to inhibit the respiration of sewage
    sludge utilizing biogenic substrates.  Two screening tests were used,
    RIKA and OECD 209.  The concentration of ethylbenzene used was at the
    limit of solubility in the medium (approximately 150 mg/litre), and
    inhibitions of the respiration rate of 30% (ACCEDE 209) and 100%
    (RIKA) were observed (Volskay & Grady, 1990).

         Bringmann & Kühn (1980) studied the effect of ethylbenzene on
    bacteria. A toxicity threshold of 12 mg/litre for  Pseudomonas putida
    was obtained in a cell multiplication inhibition test.

    9.2  Aquatic organisms

         Numerous acute toxicity tests have been carried out on
    ethylbenzene.  Organisms that have been studied include protozoans
    (Bringmann & Kühn, 1980), algae (US EPA, 1978; Bringmann & Kühn, 1980;
    Galassi et al., 1988; Masten et al. 1994), water fleas (LeBlanc, 1980;
    Bringmann & Kühn, 1982; Abernethy et al., 1986; Galassi et al., 1988; 
    Vigano, 1993), diatoms (US EPA, 1978; Masten et al., 1994), copepods,
    grass shrimp (Potera, 1975), bay shrimps (Benville & Korn, 1977),
    mysid shrimps (US EPA, 1978; Masten et al., 1994), Dungeness crabs
    (Caldwell et al., 1976) and Pacific oysters (LeGore, 1974).  Fish that
    have been studied include rainbow trout (Mayer & Ellersieck, 1986;
    Galassi et al., 1988), guppy (Pickering & Henderson, 1966; Galassi et
    al., 1988), bluegill (Pickering & Henderson, 1966; Buccafusco et al.,
    1981), fathead minnow, goldfish (Pickering & Henderson, 1966), channel
    catfish (Mayer & Ellersieck, 1986), Atlantic silverside (Masten et
    al., 1994), striped bass (Benville & Korn, 1977) and sheepshead minnow
    (US EPA, 1978; Heitmuller et al., 1981).

         Many of the test results are not comparable, owing to
    inconsistent exposure conditions, resulting from emulsions, open
    static systems and systems with large air spaces.  Aquatic toxicity
    results from consistent exposure conditions, which are comparable, are
    shown in Table 6.

         No information regarding chronic exposure of aquatic organisms to
    ethylbenzene has been reported.

        Table 6.  Toxicity of ethylbenzene to aquatic organisms


    Species              Age/size    Stat/flowa   Temperature   Salinity   pH   Parameterc  Concentration    Reference
                                                  (°C)          (0/00)                      (mg/litre)d

    Alga                             stat                                       72-h EC50   4.6              Galassi et al. (1988)
    (Selenastrum                     stat         19-21                         48-h EC50   7.2 (3.4-15.1)   Masten et al. (1994)
    capricornutum)                   stat         19-21                         96-h EC50   3.6 (1.7-7.6)    Masten et al. (1994)

    Water flea           < 24 h      statb                                      24-h LC50   2.2              Galassi et al. (1988)
    (Daphnia magna)                  statb        21-25                         48-h LC50   2.1e             Abernethy et al. (1986)

                         < 24 h      statb                                      48-h LC50   1.81-2.38        Viganň (1993)

    (Skeletonema                     statb        19-21                         48-h EC50   7.5 (5.0-11.2)   Masten et al. (1994)
    costatum)                        statb        19-21                         72-h EC50   4.9 (2.4-9.8)    Masten et al. (1994)
                                     statb        19-21                         96-h EC50   7.7 (5.9-10.0)   Masten et al. (1994)

    Mysid shrimp         < 24 h      flow         24-26         20         8.0  48-h LC50   >5.2             Masten et al. (1994)
    (Mysidopsis          < 24 h      flow         24-26         20         8.0  96-h LC50   2.6 (2.0-3.3)    Masten et al. (1994)

    Rainbow trout                    stat                                       96-h LC50   4.2              Galassi et al. (1988)

    Guppy                            stat                                       96-h LC50   9.2              Galassi et al. (1988)

    Table 6.  (Cont'd)


    Species              Age/size    Stat/flowa   Temperature   Salinity   pH   Parameterc  Concentration    Reference
                                                  (°C)          (0/00)                      (mg/litre)d

    Atlantic silverside  3-15 mg     flow         21-23         20              48-h LC50   6.4 (5.8-7.5)    Masten et al. (1994)
    (Menidia menidia)    3-15 mg     flow         21-23         20              96-h LC50   5.1 (4.4-5.7)    Masten et al. (1994)


    a    in all cases a closed system was used; stat = static conditions (water unchanged for the duration of the test);
         flow = flow-through conditions (ethylbenzene concentration in water continously maintained)
    b    air space was eliminated
    c    the EC50 for algae was based on growth inhibition
    d    test concentrations were measured, unless stated otherwise
    e    nominal test concentration;

    9.3  Terrestrial organisms

         An LC50 value of 47 µg per cm2 of contact area was obtained for
    earthworms exposed to ethylbenzene adsorbed on filter paper in glass
    vials (Neuhauser et al., 1986).  Callahan et al. (1994) reported a
    2-day LC50 value of 4.93 µg/kg for  Eisenia foetida in a contact
    toxicity test.

         No toxicity data on plants, birds and wild mammals have been


    10.1  Evaluation of human health risks

         The acute and chronic toxicities of ethylbenzene are low.  The
    toxic effects in humans and animals relate to depression of the
    central nervous system (CNS) and to irritation of the mucous membranes
    and eyes.  No data concerning carcinogenic or reproductive effects
    have been reported.  Ethylbenzene does not have significant mutagenic
    properties or teratogenic effects.

         Exposure to more than 430 mg/m3 (100 ppm) causes symptoms of CNS
    depression and irritation in humans.

         A 20-year medical surveillance study of 200 workers showed no
    indications of effects in routine blood tests.  The maximum exposure,
    estimated from the urinary concentration of mandelic acid, was less
    than about 86 mg/m3 (20 ppm) and the mean value about 8.6 mg/m3
    (2 ppm).

         In a 13-week animal study, increased liver weight was the only
    dose-related biological finding in male rats.  This was seen at a
    concentration of 3225 mg/m3 (750 ppm) or more.

         The definition and aim of the use of a guidance value for the
    general population have been described by IPCS (1994).

         On the basis of biological significance criteria cited above, a
    no-observed-effect level (NOEL) of 2150 mg/m3 (500 ppm) was defined. 
    The no-observed-adverse-effect level would be higher than 4300 mg/m3
    (1000 ppm) (highest concentration used), since the increase in liver
    weight was not associated with any histopathological findings.  A NOEL
    of 2150 mg/m3 (500 ppm) was used as the basis for determining the
    guidance value.  The following uncertainty factors were used: 10 for
    interspecies variability; 5 for intraspecies variability (effect seen
    in males only); and 2 for lack of chronic toxicity data.  This gives a
    guidance value of 22 mg/m3 (5 ppm).

         From the medical surveillance study the NOEL could be estimated
    to be between 8.6 mg/m3 (2 ppm) (mean value) and 86 mg/m3 (20 ppm)
    (maximum value).  However, since no dose-response relationship was
    derived, this study is not suitable for the estimation of a guidance
    value.  Furthermore, no effects would be expected at this exposure
    level, which is almost the same as the guidance value.

         Humans are exposed to ethylbenzene principally by inhalation,
    where the substance is rapidly absorbed into the body.  Exposure by
    skin absorption or ingestion may also occur.  Ethylbenzene is not
    considered to bioaccumulate.

         Table 7 gives the estimated weekly ethylbenzene dose resulting
    from different types of exposure.  A guidance value of 22 mg/m3
    (5 ppm) ethylbenzene is approximately equivalent to a weekly ethyl-
    benzene dose of 2000 mg.  This is 100 times higher than the worst
    exposure situation of the general population.

        Table 7.  Estimated weekly ethylbenzene dose from different types of exposures


    Type of exposure              Reported concentration   Weekly total amount   Dose mg/week
                                  in media                 inhaled, ingested
                                                           or smoked

    General population

      Inhalation (means)b         0.74-100 µg/m3           140 m3                0.07-10c

      Ingestion (food)            13 µg/kgd                7 kg                  0.1

      Drinking- or groundwaterb   0.07-1.1 µg/litree       14 litres             0.01

                                  30.0 µg/litref                                 0.42


      Inhalation (mean)g          10 mg/m3                                       300c

      Inhalation (max)g           100 mg/m3                50 m3                 3000c

      Inhalationh                 430 mg/m3                                      12700c

    Smokers                       8 µg/cigarettei          140 cigarettes/week   1.1

    a    Based on a breathing rate of 20 m3/day
    b    Values from Tables 2 and 3
    c    Retention 60%
    d    Lovegren et al. (1979) (highest reported value)
    e    Highest reported values of uncontaminated groundwater
    f    Lowest reported value of contaminated groundwater
    g    Bardodej & Círek (1988)
    h    Corresponds to occupational exposure limits in several countries
    i    Wallace et al. (1987a)
         A 2-year carcinogenicity study has been performed by the National
    Toxicology Program (USA) but the results are not yet available.

    10.2  Evaluation of effects on the environment

         Ethylbenzene is found in air, water, soil, sediment, biota and
    groundwater.  It is released primarily into air and water from various
    natural and anthropogenic sources.  The atmosphere is the major sink
    for ethylbenzene.  Ethylbenzene is rapidly photo-oxidized in the
    atmosphere and this may contribute to photo-chemical smog formation. 
    In water, the key processes determining overall fate are
    volatilization and biodegradation.

         The log octanol/water partition coefficient is 3.13, indicating a
    potential for bioaccumulation.  However, the limited evidence 
    available shows that ethylbenzene bioconcentration factors are low for
    fish and molluscs.  Elimination from aquatic organisms appears to be
    rapid.  Biomagnification through the food chain is unlikely.

         Mean levels of ethylbenzene in air ranging from 0.74 to 100
    µg/m3 have been measured at urban sites.  Industrial releases and
    vehicle emissions are the principal sources of ethylbenzene.  Levels
    found at rural sites are generally <2 µg/m3.  The levels of
    ethylbenzene in surface water are generally less than 0.1 µg/litre in
    non-industrial areas.  In industrial and urban areas ethylbenzene
    concentrations of up to 15 µg/litre have been reported.  Urban
    run-off, effluent and landfill leachate are sources of local
    contamination.  Ethylbenzene levels in sediment are generally < 0.5
    µg/kg.  Levels of ethylbenzene between 1 and 5 µg/kg have been found
    in sediments from heavily industrialized areas.  Ethylbenzene levels
    in uncontaminated groundwater are generally < 0.1 µg/litre.  However,
    much higher levels have been reported for groundwater contaminated via
    waste disposal, fuel spillage and industrial facilities.

         Acute toxicity studies on aquatic organisms show ethylbenzene to
    be of moderate toxicity.  The lowest acute toxicity values are 4.6
    mg/litre for algae (72-h EC50), 1.8 mg/litre for daphnids (48-h LC50)
    and 4.2 mg/litre for fish (96-h LC50).  There are no chronic toxicity
    studies on aquatic organisms.

         There is limited information regarding the toxicity of
    ethylbenzene to bacteria and earthworms.  There are no data for
    terrestrial plants, birds or wild mammals.

         On the basis of available data, it is concluded that ethylbenzene
    is unlikely to be found at levels in the environment that will cause
    adverse effects on aquatic and terrestrial ecosystems, except in cases
    of spills or point-source emissions.


         Ethylbenzene has low toxicity.  Its vapour irritates the mucous
    membranes to a limited extent and causes prenarcotic effects on the
    central nervous system.

         With respect to the general population, a tentative guidance
    value of 22 mg/m3 (5 ppm) for ethylbenzene in inhaled air has been
    derived, although information on certain important toxicity end-points
    are unavailable.  This value would correspond to a weekly absorbed
    dose (daily ventilation of 20 m3 with 60% retention) of about 2000
    mg.  It is at least 200 times higher than the dose received in the
    most polluted living environment reported.  Hence, no harmful effects
    on the general population would be expected.  However, it should be
    noted that the guidance value of 22 mg/m3 (5 ppm) is about 10 times
    higher than the odour threshold (about 2.2 mg/m3; 0.5 ppm), and so
    exposure at that level may cause annoyance.  On the other hand, odour
    detection may be considered to be a safeguard against excessive

         Ethylbenzene is a non-persistent chemical and is degraded
    primarily by photooxidation and biodegradation.  Volatilization to the
    atmosphere is rapid.  Photooxidation reactions of ethylbenzene may
    contribute to photochemical smog formation.

         Limited evidence suggests that bioaccumulation is low in aquatic
    organisms.  Ethylbenzene is unlikely to cause adverse effects in
    aquatic or terrestrial ecosystems except in cases of spills or
    point-source emissions.


    a)   To fill the data gaps that currently limit the toxicological
         evaluation of ethylbenzene, an appropriate rodent carcinogenicity
         study and a reproductive toxicity study are needed.  (The former
         study has been conducted but the study report has not yet been

    b)   There is little information on the long-term effects of
         ethylbenzene in humans and, in particular, no dose-response or
         dose-effect data are at hand.  Epidemiological studies of
         populations occupationally exposed to ethylbenzene should be
         encouraged.  In this context, the use of ethylbenzene metabolites
         in urine as a marker of exposure can be of special value because
         the method determines the internal doses that individuals receive
         via all routes of exposure.  Because ethylbenzene is a central
         nervous system depressant, and because some studies suggest that
         high doses of the substance or its metabolites may affect the
         metabolism of some neurotransmitters in the brain, epidemiological
         studies should address the central nervous system as a potential
         target organ.  Moreover, since ethylbenzene is almost invariably
         only one of the components in solvent mixtures at the workplace,
         study designs that address possible interactions between
         ethylbenzene and other solvents are desirable.

    c)   Further mechanistic studies are needed.


         A guideline value of 300 µg/litre for ethylbenzene in
    drinking-water was recommended by WHO in 1993.


    Abernethy S, Bobra AM, Shiu WY, Wells PG, & Mackay D (1986) Acute
    lethal toxicity of hydrocarbons and chlorinated hydrocarbons to two
    planktonic crustaceans: The key role of organism-water partitioning.
    Aquat Toxicol, 8: 163-174.

    ACGIH (1985-1986) Threshold limit values and biological exposure
    indices. Cincinnati, Ohio, American Conference of Governmental
    Industrial Hygienists.

    Aitio A, Riihimäki V, Liesivuori J, Järvisalo J, & Hernberg S (1994)
    Biological monitoring. In: Zenz C, Dickerson OB, & Horvath EP Jr ed.
    Occupational medicine, 3rd ed. Saint Louis, Missouri, C.V. Mosby &
    Co., pp 132-158.

    Andersson K, Fuxe K, Nilsen OG, Toftgĺrd R, Eneroth P, & Gustafsson JĹ
    (1981) Production of discrete changes in dopamine and noradrenaline
    levels and turnover in various parts of the rat brain following
    exposure to xylene,  ortho-, meta-, and  para-xylene, and
    ethylbenzene. Toxicol Appl Pharmacol, 60: 535-548.

    Angerer J & Lehnert G (1979) Occupational chronic exposure to organic
    solvents. VIII. Phenolic compounds-metabolites of alkylbenzenes in
    man. Simultaneous exposure to ethylbenzene and xylenes. Int Arch Occup
    Environ Health, 43: 145-150.

    Angerer J & Wulf H (1985) Occupational chronic exposure to organic
    solvents. XI. Alkylbenzene exposure of varnish workers: effects on
    hematopoietic system. Int Arch Occup Environ Health, 56: 307-321.

    Annable MD, Wallace RB, Hayden NJ, & Voice TC (1993) Reduction of
    gasoline component leaching potential by soil venting. J Contam
    Hydrol, 12(1-2): 151-170.

    Anon (1987) Chemical review: ethylbenzene. Danger Prop Ind Mater Rep,
    7: 13-35.

    Ashley DL, Bonin MA, Cardinali FL, McCraw JM, Holler JS, Needham LL, &
    Patterson DG Jr (1992) Determining volatile organic compounds in human
    blood from a large sample production by using purge and trap gas
    chromatography and mass spectrometry. Anal Chem, 64(9): 1021-1029.

    Ashley DL, Bonin MA, Cardinali FL, McCraw JM, & Wooten JV (1994) Blood
    concentrations of volatile organic compounds in a non occupationally
    exposed US population and in groups with suspected exposure. Clin
    Chem, 40(7): 1401-1404.

    Ĺstrand I, Engström J, & Övrum P (1978) Exposure to xylene and
    ethylbenzene. I. Uptake, distribution and elimination in man. Scand J
    Work Environ Health, 4: 185-194.

    Atkinson R (1985) Kinetics and mechanisms of the gas-phase reactions
    of the hydroxyl radical with organic compounds under atmospheric
    conditions. Chem Rev, 85: 69-201.

    ATSDR (1990) Toxicological profile for ethylbenzene. Atlanta, Georgia,
    Agency for Toxic Substances and Disease Registry (ATSDR/TP/-90-15).

    Barber ED, Teetsel NM, Kolberg KF, & Guest D (1992) A comparative
    study of the rates of  in vitro percutaneous absorption of eight
    chemicals using rat and human skin. Fundam Appl Toxicol, 19: 493-497.

    Bardodej Z & Bardodejová E (1970) Biotransformation of ethylbenzene,
    styrene, and  alpha-methylstyrene in man. Am Ind Hyg Assoc J, 31:

    Bardodej Z & Círek A (1988) Long-term study on workers occupationally
    exposed to ethylbenzene. J Hyg Epidemiol Microbiol Immunol, 32: 1-5.

    Benville PE Jr & Korn S (1977) The acute toxicity of six monocyclic
    aromatic crude oil components to striped bass  (Morone saxatilis) and
    bay shrimp  (Crago franciscorum). Calif Fish Game, 63: 204-209.

    Bestetti G & Galli E (1984) Plasmid-coded degradation of ethylbenzene
    and 1-phenylethanol in  Pseudomonas fluorescens. FEMS Microbiol Lett,
    21: 165-168.

    Bevan MAJ, Proctor CJ, Baker-Rogers J, & Warren ND (1991) Exposure to
    carbon monoxide, respirable suspended particulates and volatile
    organic compounds while commuting by bicycle. Environ Sci Technol, 
    25: 788-791.

    Bos R, Guicherit R, & Hoogeveen A (1977) Distribution of some
    hydrocarbons in ambient air near Delft and the influence on the
    formation of secondary air pollutants. Sci Total Environ, 7: 269-281.

    Boyd SA, Xiangcan J, & Lee JF (1990) Sorption of nonionic organic
    compounds by corn residues from a no-tillage field. J Environ Qual,
    19(4): 734-738.

    Bringmann G & Kühn R (1980) Comparison of the toxicity thresholds of
    water pollutants to bacteria, algae and protozoa in the cell
    multiplication inhibition test. Water Res, 14: 231-241.

    Bringmann G & Kühn R (1982) [Findings concerning the harmful effect
    of water pollutants on  Daphnia magna in a further developed
    standardized test procedure.] Z Wasser/Abwasser Forsch, 15(1): 1 (in

    Brown-Woodman PDC, Webster WS, Picher K, & Ritchie HE (1991)
    Embryotoxicity of xylene and toluene: an  in vitro study. Ind Health,
    29: 139-152.

    Bruckmann P, Kersten W, Funcke W, Balfanz E, König J, Theisen J, Ball
    M, & Päpke O (1988) The occurrence of chlorinated and other trace
    compounds in urban air. Chemosphere, 17: 2363-2380.

    Buccafusco RJ, Ells SJ, & LeBlanc GA (1981) Acute toxicity of priority
    pollutants to bluegill  (Lepomis macrochirus). Bull Environ Contam
    Toxicol, 26: 446-452.

    Burghardt E & Jeltes R (1975) Gas chromatographic determination of
    aromatic hydrocarbons in air using a semi-automatic preconcentration
    method. Atmos Environ, 9: 935-940.

    Burnham AK, Calder GV, Fritz JS, Junk GA, Svec HJ, & Willis R (1972) 
    Identification and estimation of neutral organic contaminants in
    potable water. Anal Chem, 44: 139-142.

    Bysshe SE (1982) Bioconcentration factors in aquatic organisms. In:
    Lyan WJ, Reehl WF, & Rosenblatt DH ed. Handbook of chemical property
    estimation methods - Environmental behaviour of organic compounds. New
    York, McGraw-Hill Book Company, pp 5/1-5/30.

    Caldwell RS, Caldarone EM, & Mallon MH (1976) Effects of a seawater-
    soluble fraction of Cook Inlet crude oil and its major aromatic
    components on larval stages of the Dungeness crab,  Cancer
     magister dana. In: Fate and effects of petroleum hydrocarbon in
    marine organisms and ecosystems. Oxford, New York, Pergamon Press, pp

    Callahan CA, Shirazi MA, & Neuhauser EF (1994) Comparative toxicity of
    chemicals to earthworms. Environ Toxicol Chem, 13(2): 291-298.

    Callahan MA (1979) Water related environmental fate of 129 priority
    pollutants.  Washington, DC, US Environmental Protection Agency (EPA

    Cavender F (1993) Aromatic hydrocarbons. In: Clayton GD & Clayton FE
    ed.  Patty's industrial hygiene and toxicology, 4th revis ed. New
    York, John Wiley and Sons, vol 2B, pp 1267-1442.

    Chan CC, Özkaynak H, Spengler JD, & Sheldon L (1991a) Driver exposure
    to volatile organic compounds, CO, ozone and NO2 under different
    driving conditions. Environ Sci Technol, 25: 964-972.

    Chan CC, Spengler JD, Özkaynak H, & Lefkopoulou M (1991b) Commuter
    exposures to VOCs in Boston, Massachusetts. J Air Waste Manage Assoc,
    41(12): 1594-1600.

    Chin BH, McKelvey JA, Tyler TR, Calisti LJ, Kozbelt SJ, & Sullivan LJ
    (1980a)  Absorption, distribution, and excretion of ethylbenzene,
    ethylcyclohexane and methylethylbenzene isomers in rats. Bull Environ
    Contam Toxicol, 24: 477-483.

    Chin BH, McKelvey JA, Calisti LJ, Kozbelt SJ, & Sullivan LJ (1980b) A
    comparison of  in vivo and  in vitro (tissue explant) techniques:
    metabolic profile of ethylbenzene in the rat and the dog. Bull Environ
    Contam Toxicol, 25: 241-245.

    Chiou CT, Porter PE, & Schmedding DW (1983) Partition equilibria of
    non-ionic organic compounds between soil organic matter and water.
    Environ Sci Technol, 17: 227-231.

    Chou WL, Speece RE, & Siddiqi RH (1978) Acclimation and degradation of
    petrochemical wastewater components by methane fermentation.
    Biotechnol Bioeng Symp, 8: 391-414.

    CITI (1992) Biodegradation and bioaccumulation data on existing
    chemicals based on the CSCL Japan. Tokyo, Chemicals Inspection and
    Testing Institute, pp 3-9.

    Clapp LW, Talarczyk MR, Park JK, & Boyle WC (1994) Performance
    comparison between activated sludge and fixed-film processes for
    priority pollutant removals. Water Environ Res, 66(2): 153-160.

    Clark AI, McIntyre AE, Perry R, & Lester JN (1984a) Monitoring and
    assessment of ambient atmospheric concentrations of aromatic and
    halogenated hydrocarbons at urban, rural and motorway locations.
    Environ Pollut, B7: 141-158.

    Clark AI, McIntyre AE, Lester JN, & Perry R (1984b) Ambient air
    measurements of aromatic and halogenated hydrocarbons at urban, rural
    and motorway locations. Sci Total Environ, 39: 265-279.

    Climie IJG, Hutson DH, & Stoydin G (1983) The metabolism of
    ethylbenzene hydroperoxide in the rat. Xenobiotica, 13: 611-618.

    Cline PV & Viste DR (1985) Migration and degradation patterns of
    volatile organic compounds. Waste Manage Res, 3: 351-360.

    Cole RH, Frederick RE, Healy RP, & Rolan RG (1984)  Preliminary
    findings of the priority pollutant monitoring project of the
    nationwide urban runoff program.  J Water Pollut Control Fed,
    56: 898-908.

    Coleman WE, Munch JW, Streicher RP, Ringhand HP, & Kopfler FC (1984)
    Identification and measurement of components in gasoline, kerosene and
    No.2 fuel oil that partition into the aqueous phase after mixing. Arch
    Environ Contam Toxicol, 13: 171-178.

    Cotruvo JA (1985) Organic micropollutants in drinking water: An
    overview. Sci Total Environ, 47: 7-26.

    Cox DP & Goldsmith CD (1979) Microbial conversion of ethylbenzene to
    1-phenylethanol and acetophenone by  Nocardia tartaricans ATCC 31190.
    Appl Environ Microbiol, 38: 514-520.

    Cozzarelli IM, Eganhouse RP, & Baedecker MJ (1990) Transformation of
    monoaromatic hydrocarbons to organic acids in anoxic groundwater
    environment. Environ Geol Water Sci, 16: 135-141.

    Cragg ST, Clarke EA, Daly IW, Miller RR, Terrill JB, & Ouellette RE
    (1989) Subchronic inhalation toxicity of ethylbenzene in mice, rats,
    and rabbits.  Fundam Appl Toxicol, 13: 399-408.

    Crookes MJ & Howe PD (1992) Environmental hazard assessment:
    Ethylbenzene. Garston, United Kingdom, Department of the Environment,
    Directorate for Air, Climate and Toxic Substances, Toxic Substances
    Division, Public Building Research Establishment, 40 pp (TSD/7).

    Curvall M, Enzell CR, & Pettersson B (1984) An evaluation of the
    utility of four  in vitro short term tests for predicting the
    cytotoxicity of individual compounds derived from tobacco smoke. Cell
    Biol Toxicol, 1: 173-193.

    Damgĺrd Nielsen GD & Alarie Y (1982) Sensory irritation, pulmonary
    irritation and respiratory stimulation by airborne benzene and
    alkylbenzenes: Prediction of safe industrial exposure levels and
    correlation with their thermodynamic properties. Toxicol Appl
    Pharmacol, 65: 459-477.

    Dannecker W, Schröder B, & Stechmann H (1990) Organic and inorganic
    substances in highway tunnel exhaust air. Sci Total Environ, 93:

    Dean BJ, Brooks TM, Hodson-Walker G, & Hutson DH (1985) Genetic
    toxicology testing of 41 industrial chemicals. Mutat Res, 153: 57-77.

    De Bortoli M, Knöppel H, Pecchio E, Peil A, Rogora L, Schauenburg H,
    Schlitt H, & Vissers H (1984) Integrating 'real life' measurements of
    organic pollution in indoor and outdoor air of homes in Northern
    Italy. In: Proceedings of the 3rd International Conference on Indoor
    Air Quality and Climate. Stockholm, Swedish Council for Building
    Research, vol 4, pp 21-26.

    DEC (1992) Health-based recommended occupational exposure limit for
    ethylbenzene. The Hague, Directorate-General of Labour.

    De Ceaurriz JC, Micillino JC, Bonnet P, & Guenier JP (1981) Sensory
    irritation caused by various industrial airborne chemicals. Toxicol
    Lett, 9: 137-143.

    DFG (German Research Council) (1985) [Materials hazardous to health.
    Justification of MAC values in terms of toxicology and occupational
    medicine], 11th ed. Weinheim, VCH Publishers (in German).

    Dills RL, Kent SD, Checkoway H, & Kalman DA (1991) Quantification of
    volatile solvents in blood by static headspace analysis. Talanta,
    38: 365-374.

    Donner M, Mäki-Paakkanen J, Norppa H, Sorsa M, & Vainio H (1980)
    Genetic toxicology of xylenes. Mutat Res, 74: 171-172.

    Dreisch FA & Munson TO (1983) Purge-and-trap analysis using fused
    silica capillary column GC/MS. J Chromatogr Sci, 21: 111-118.

    Drummond L, Caldwell J, & Wilson HK (1989) The metabolism of
    ethylbenzene and styrene to mandelic acid: stereo chemical
    considerations. Xenobiotica, 19: 199-207.

    Drummond L, Caldwell J, & Wilson HK (1990) The stereo selectivity of
    1,2-phenylethanediol and mandelic acid metabolism and disposition in
    the rat. Xenobiotica, 20: 159-168.

    Durst GL & Laperle EA (1990) Styrene monomer migration as monitored by
    purge and trap gas chromatography and sensory analysis for polystyrene
    containers. J Food Sci, 55(2): 522-524.

    Dutkiewicz T & Tyras H (1967) A study of the skin absorption of
    ethylbenzene in man. Br J Ind Med, 24: 330-332.

    EAJ (1989) Chemicals in the environment. Tokyo, Environment Agency of

    ECETOC (1986) Joint assessment of commodity chemicals No.7: 
    Ethylbenzene.  Brussels, European Chemical Industry Ecology and
    Toxicology Centre.

    El Masry AM, Smith JN, & Williams RT (1956) Studies in detoxication.
    69. The metabolism of alkylbenzenes:  n-propylbenzene and
     n-butylbenzene with further observations on ethylbenzene. Biochem J,
    64: 50-56.

    Elovaara E, Engström K, Nickels J, Aitio A, & Vainio H (1985)
    Biochemical and morphological effects of long-term inhalation exposure
    of rats to ethylbenzene. Xenobiotica, 15: 299-308.

    Engström KM (1984a) Urinalysis of minor metabolites of ethylbenzene
    and  m-xylene. Scand J Work Environ Health, 10: 75-81.

    Engström KM (1984b) Metabolism of inhaled ethylbenzene in rats. Scand
    J Work Environ Health, 10: 83-87.

    Engström J & Bjurström R (1978) Exposure to xylene and ethylbenzene.
    II. Concentration in subcutaneous adipose tissue. Scand J Work Environ
    Health, 4: 195-203.

    Engström KM & Rantanen J (1974) A new gas chromatographic method for
    determination of mandelic acid in urine. Int Arch Arbeitsmed,
    33: 163-167.

    Engström KM, Riihimäki V, & Laine A (1984) Urinary disposition of
    ethylbenzene and  m-xylene in man following separate and combined
    exposure. Int Arch Occup Environ Health, 54: 355-363.

    Engström KM, Elovaara E, & Aitio A (1985) Metabolism of ethylbenzene
    in the rat during long-term intermittent inhalation exposure.
    Xenobiotica, 15: 281-286.

    Feiler HD, Vernick AS, & Storch PJ (1979) Fate of priority pollutants
    in POTW's. In: Proceedings of the 8th National Conference on Municipal
    Sludge Management, pp 72-81.

    Fellin P & Otson R (1993) Seasonal trends of volatile organic
    compounds (VOCs) in Canadian homes. In: Proceedings of the 6th
    Conference on Indoor Air Quality and Climate, Helsinki, 1993, vol 2,
    pp 117-122.

    Filipovic D, Paulsen MD, Loida PJ, Sligar SG, & Ornstein RL (1992) 
    Ethylbenzene hydroxylation by cytochrome P450cam. Biochem Biophys Res
    Commun, 189: 488-495.

    Fishbein L (1985) An overview of environmental and toxicological
    aspects of aromatic hydrocarbons. IV. Ethylbenzene. Sci Total Environ,
    44: 269-287.

    Florin I, Rutberg L, Curvall M, & Enzell CR (1980) Screening of
    tobacco smoke constituents for mutagenicity using the Ames' test.
    Toxicology, 15: 219-232.

    Först C, Stieglitz L, Roth W, & Kuhnmünch S (1984) Quantitative
    analysis of volatile organic compounds in landfill leachates. Int J
    Environ Anal Chem, 37: 287-293.

    Frank H, Senf L, & Welsch T (1990) Some application of wide bore
    capillary gas chromatography in occupational medicine. Z Gesamte Hyg
    Grenzgeb, 36(12): 668-671.

    Gamberale F, Annwall G, & Hultengren M (1978) Exposure to xylene and
    ethylbenzene. III. Effects on central nervous functions. Scand J Work
    Environ Health, 4: 204-211.

    Galassi S, Mingazzini M, Vigano L, Cesareo D, & Tosato ML (1988)
    Approaches to modelling toxic responses of aquatic organisms to
    aromatic hydrocarbons. Ecotoxicol Environ Saf, 16: 158-169.

    Garcia JP, Beyne-Masclet S, Mouvier G, & Masclet P (1992) Emissions of
    volatile organic compounds by coal-fire power stations. Atmos Environ,
    A26(9): 1589-1597.

    Gentry SJ & Walsh PT (1987) Eight-hour TWA personal monitoring using a
    diffusive sampler and short-term stain tube. Am Ind Hyg Assoc J,
    48: 287-292.

    Gibson DT, Gschwendt B, Yeh WK, & Kobal VM (1973) Initial reactions in
    the oxidation of ethylbenzene by  Pseudomonas putida. Biochemistry,
    12: 1520-1528.

    Gomez-Belinchon JI, Grimalt JO, & Abaigčs J (1991) Volatile organic
    compounds in two polluted rivers in Barcelona (Catalonia, Spain).
    Water Res, 25: 577-589.

    Goodenkauf O & Atkinson JC (1986) Occurrence of volatile organic
    chemicals in Nebraska ground water. Ground Water, 24: 231-233.

    Gossett RW, Brown DA, & Young DR (1983) Predicting the bioaccumulation
    of organic compounds in marine organisms using octanol/water partition
    coefficients. Mar Pollut Bull, 14: 387-392.

    Grob K (1973) Organic substances in potable water and in its
    precursor. Part 1. Methods for their determination by gas-liquid
    chromatography. J Chromatogr, 84: 255-273.

    Grob K & Grob G (1971) Gas-liquid chromatographic-mass spectrometric
    investigation of C6-C20 organic compounds in an urban atmosphere
    - An application of ultra trace analysis on capillary columns. J
    Chromatogr, 62: 1-13.

    Gromiec JP & & Piotrowski JK (1984) Urinary mandelic acid as an
    exposure test for ethylbenzene. Int Arch Occup Environ Health,
    55: 61-72.

    Gschwend PM, Zafiriou OC, Mantoura RFC, Schwarzenbach RP, & Gagosian
    RB (1982)  Volatile organic compounds at a coastal site. I. Seasonal
    variations. Environ Sci Technol, 16: 31-38.

    Guicherit R & Schulting FL (1985) The occurrence of organic chemicals
    in the atmosphere of the Netherlands. Sci Total Environ, 43: 193-219.

    Gut I, Terelius Y, Frantik E, Linhart I, Soucek P, Filipcová B, &
    Klucková H (1993) Exposure to various benzene derivatives
    differentially induces cytochromes P450 2B1 and P450 2E1 in rat liver.
    Arch Toxicol, 67: 237-243.

    Hajimiragha H, Ewers U, Brockhaus A, & Boettger A (1989) Levels of
    benzene and other volatile aromatic compounds in the blood of
    non-smokers and smokers. Int Arch Occup Environ Health, 61: 513-518.

    Hampton CV, Pierson WR, Schuetzle D, & Harvey TM (1983) Hydrocarbon
    gases emitted from vehicles on the road. 2. Determination of emission
    rates from diesel and spark-ignition vehicles. Environ Sci Technol,
    17: 699-708.

    Hardin BD, Bond GP, Sikov MR, Andrew FD, Beliles RP, & Niemeier RW
    (1981)  Testing of selected workplace chemicals for teratogenic
    potential. Scand J Work Environ Health, 7(Suppl 4): 66-75.

    Harkov R, Kebbekus B, Bozzelli JW, & Lioy PJ (1983) Measurement of
    selected volatile organic compounds at three locations in New Jersey
    during the summer season. J Air Pollut Control Assoc, 33: 1177-1183.

    Harper M & Purnell CJ (1990) Alkylammonium montmorillonites as
    adsorbents for organic vapors from air. Environ Sci Technol,
    24: 55-62.

    Heilbron I, Bunbury HM, & Jones WE ed. (1946) Dictionary of organic
    compounds. London, vol II, p 20.

    Heitmuller PT, Hollister TA, & Parrish PR (1981) Acute toxicity of 54
    industrial chemicals to sheepshead minnows  (Cyprinodon variegatus).
    Bull Environ Contam Toxicol, 27: 596-604.

    Herman DC, Inniss WE, & Mayfield CI (1990) Impact of volatile aromatic
    hydrocarbon, alone or in combination, on growth of the freshwater alga
     Selenastrum capriocornutum. Aquat Toxicol, 18(2): 87-100.

    Hester NE & Meyer RA (1979) A sensitive technique for measurement of
    benzene and alkylbenzenes in air. Environ Sci Technol, 13: 107-109.

    Hiatt MH (1981) Analysis of fish and sediment for volatile priority
    pollutants.  Anal Chem, 53: 1541-1543.

    Hiatt MH (1983) Determination of volatile organic compounds in fish
    samples by vacuum distillation and fused silica capillary gas
    chromatography-mass spectrometry. Anal Chem, 55: 506-516.

    Hodgson AT, Daisey JM, & Grot RA (1991) Sources and source strengths
    of volatile organic compounds in a new office building. J Air Waste
    Manage Assoc, 41(11): 1461-1468.

    Holm S, Norbäck D, Frenning B, & Göthe CJ (1987) Hydrocarbon exposure
    from handling jet fuel of some Swedish aircraft units. Scand J Work
    Environ Health, 13: 438-444.

    Holmberg B & Malmfors T (1974) The cytotoxicity of some organic
    solvents. Environ Res, 7: 183-192.

    Howard PH (1989) Handbook of environmental fate and exposure data for
    organic chemicals. Volume 1: Large production and priority pollutants.
    Chelsea, Michigan, Lewis Publishers, Inc.

    Howard PH (1991) Handbook of environmental degradation rates. Chelsea,
    Michigan, Lewis Publishers, Inc., pp 340-341.

    Hunt WF Jr, Faoro RB, & Freas W (1986) Report of the interim data base
    for state and local air toxic volatile organic chemical measurements.
    Washington, DC, US Environmental Protection Agency (EPA 450/4-86-012).

    Hutchins SR, Sewell GW, Kovacs DA, & Smith GA (1991a) Biodegradation
    of aromatic hydrocarbons by aquifer microorganisms under denitrifying
    conditions. Environ Sci Technol, 25: 68-76.

    Hutchins SR, Downs WC, Wilson JT, Smith GB, Kovacs DA, Fine DD,
    Douglass RH, & Hendrix DJ (1991b) Effect of nitrate addition on
    biotransformation of fuel-contaminated aquifer: Field demonstration.
    Ground Water, 29(4): 571-580.

    Inoue O, Seiji K, Kudo S, Jin C, Cai SX, Liu SJ, Watanabe T, Nakatsuka
    H, & Ikeda M (1995) Urinary phenylglyoxylic acid excretion after
    exposure to ethylbenzene among exposed Chinese workers. Int J Occup
    Environ Health, 1: 1-8.

    IPCS (International Programme on Chemical Safety) (1994) Environmental
    health criteria 170: Assessing human health risks of chemicals:
    Derivation of guidance values for health-based exposure limits.
    Geneva, World Health Organization, 73 pp.

    Jayanty RKM (1989) Evaluation of sampling and analytical methods for
    monitoring toxic organics in air. Atmos Environ, 23: 777-782.

    Jaynes WF & Boyd SA (1991) Clay mineral type and organic compound
    sorption by hexadecyltrine-thylammonium-exchanged clays. Soil Sci Soc
    Am J, 55(1): 43-48.

    Jonsson A, Persson KA, & Grigoriadis V (1985) Measurements of some low
    molecular weight oxygenated, aromatic and chlorinated hydrocarbons in
    ambient air and in vehicle emissions. Environ Int, 11: 383-392.

    Jüttner F (1988) Quantitative analysis of monoterpenes and volatile
    organic pollution products (VOC) in forest air of the Southern Black
    Forest. Chemosphere, 17: 309-317.

    Kappeler T & Wuhrmann K (1978a) Microbial degradation of the
    water-soluble fraction of gas oil, I. Water Res, 12: 327-333.

    Kappeler T & Wuhrmann K (1978b) Microbial degradation of the
    water-soluble fraction of gas oil. II. Bioassays with pure strains.
    Water Res, 12: 335-342.

    Kawai T, Yasugi T, Mizunuma K, Horiguchi S. Iguchi H, Uchida Y, Iwami
    O, & Ikeda M (1992) Comparative evaluation of urinalysis and blood
    analysis as means of detecting exposure to organic solvents at low
    concentrations. Int Arch Occup Environ Health, 64(4): 223-234.

    Kawamura K & Kaplan IR (1983) Organic compounds in the rainwater of
    Los Angeles. Environ Sci Technol, 17: 497-501.

    Kawata K & Fujeda Y (1993) Volatile aromatic hydrocarbons in ambient
    air. Jpn J Toxicol Environ Health, 39(1): 37-43.

    Kennicutt MC II, Brooks JM, & McDonald TJ (1984) Volatile organic
    inputs from an ocean outfall near Barceloneta, Puerto Rico.
    Chemosphere, 13: 535-548.

    Kenrick MAP, Clark L, Baxter KM, Fleet M, Jones HA, Gibson TM, &
    Turrell MB (1985) Trace organics in British aquifers - a baseline
    survey. Water Research Centre, Environment (TR No. 223).

    Keymeulen R, Van-Langenhove H, & Schamp N (1991) Determination of
    monocyclic aromatic hydrocarbons in plant cuticles by gas
    chromatography-mass spectrometry. J Chromatogr, 541(1-2): 83-88.

    Kiese M & Lenk W (1974) Hydroxyacetophenones: urinary metabolites of
    ethylbenzene and acetophenone in the rabbit. Xenobiotica, 4: 337-343.

    Kleopfer RD & Fairless BJ (1972) Characterization of organic
    components in a municipal water supply. Environ Sci Technol,
    6: 1036-1037.

    Koop DR & Laethem CL (1992) Inhibition of rabbit microsomal cytochrome
    P-450 2E1-dependent p-nitrophenol hydroxylation by substituted benzene
    derivatives. Drug Metab Dispos, 20: 775-777.

    Korn M, Gfrörer W, Herz R, Wodarz I, & Wodarz R (1992)
    Stereometabolism of ethylbenzene in man: gas chromatographic
    determination of urinary excreted mandelic acid enantiomers and
    phenylglyoxylic acid and their relation to the height of occupational
    exposure. Int Arch Occup Environ Health, 64: 75-78.

    Korte F & Boedefeld E (1978) Ecotoxicological review of the global
    impact of the petroleum industry and its products. Ecotoxicol Environ
    Saf, 2: 55-103.

    Kroneld R (1989) Volatile pollutants in suburban and industrial air.
    Bull  Environ Contam Toxicol, 42: 868-872.

    Kuhn EP, Zeyer J, Eicher P, & Schwarzenbach RP (1988) Anaerobic
    degradation of alkylated benzenes in denitrifying laboratory aquifer
    columns. Appl Environ Microbiol, 54: 490-496.

    Labows J, Preti G, Hoelzle E, Leyden J, & Klingman A (1979) Analysis
    of human axillary volatiles: Compounds of exogenous origin. J
    Chromatogr, 163: 294-299.

    Lanzerstorfer CH & Puxbaum H (1990) Volatile hydrocarbons in and
    around Vienna, Austria. Water Air Soil Pollut, 51: 345-355.

    LeBlanc GA (1980) Acute toxicity of priority pollutants to water flea
     (Daphnia magna). Bull Environ Contam Toxicol, 24: 684-691.

    Lee JF, Crum JR, & Boyd SA (1989) Enhanced retention of organic
    contaminants by soils exchanged with organic cations. Environ Sci
    Technol, 23: 1365-1372.

    LeGore RS (1974) The effect of Alaskan crude oil and selected
    hydrocarbon compounds on embryonic development of the pacific oyster,
     Crassostrea gigas. Doctoral Thesis, University of Washington. Diss
    Abstr, B35: 3168.

    Lesage S, Jackson RE, Priddle MW, & Riemann PG (1990) Occurrence and
    fate of organic solvent residues in anoxic groundwater at the
    Gloucester Landfill, Canada. Environ Sci Technol, 24: 559-566.

    Levesque P & Dao LH (1989) Alkylation of benzene using an aqueous
    solution of ethanol. Appl Catal, 53(2-3): 157-167.

    Lewis PJ, Hagopian C, & Koch P (1983) Styrene. In: Kirk RE & Othmer DF
    ed. Encyclopedia of chemical technology, 3rd ed. New York, Wiley
    Interscience, vol 21, pp 770-801.

    Lockhart WL, Wagemann R, Tracey B, Sutherland D, & Thomas DJ (1992)
    Presence and implications of chemical contaminants in the freshwaters
    of the Canadian Arctic. Sci Total Environ, 122(1/2): 165-243

    Louw CW, Richards JF, & Faure PK (1977) Determination of volatile
    organic compounds in city air by gas chromatography combined with
    standard addition, selective subtraction, infra red spectrometry and
    mass spectrometry. Atmos Environ, 11: 703-717.

    Lovegren NV, Fisher GS, Legendre MG, & Schuller WH (1979) Volatile
    constituents of dried legumes. J Agric Food Chem, 27: 851-853.

    Lu BQ & Zhen ZH (1989) [Health standards for ethylbenzene in the air
    of workplaces.] Beijing, Chinese Academy of Preventive Medicine,
    Institute of Occupational Medicine (in Chinese).

    Mabey W, Smith JH, Podoll, RT, Johnson HL, Mill T, Chou TW, Gate J,
    Waight-Partridge I, Jaber H, & Vandenberg D (1982) Aquatic fate
    process for organic priority pollutants. Washington, DC, US
    Environmental Protection Agency (EPA 440/481-14).

    McFall JA, Antoine SR, & DeLeon IR (1985) Organics in the water column
    of Lake Pontchartrain. Chemosphere, 14: 1253-1265.

    McGregor DB, Brown A, Cattanach P, Edwards I, McBride D, Riach C, &
    Caspary WJ (1988) Responses of the L5178Y tk+/tk- mouse lymphoma
    cell forward mutation assay: III. 72 coded chemicals. Environ Mol
    Mutagen, 12: 85-154.

    Mackay D & Leinonen PJ (1975) Rate of evaporation of low-solubility
    contaminants from water bodies to atmosphere. Environ Sci Technol,
    9: 1178-1180.

    Mackay D, Shiu WY, & Sutherland RP (1979) Determination of air-water
    Henry's law constants for hydrophobic pollutants. Environ Sci Technol,
    13: 333-337.

    Mackay D, Shiu WY, & Ma KC (1992) The illustrated handbook of
    physical-chemical properties and environmental fate for organic
    chemicals. Volume 1. Monoaromatic hydrocarbons, chlorobenzenes and
    polychlorinated biphenyls. Chelsea, Michigan, Lewis Publishers, Inc.

    MacLeod G & Ames JM (1987) Effect of water on the production of cooked
    beef aroma compounds. J Food Sci, 52: 42-45.

    Maltoni C, Conti B, Cotti G, & Belpoggi F (1985) Experimental studies
    on benzene carcinogenicity at the Bologna Institute of Oncology:
    Current results and ongoing research. Am J Ind Med, 7: 415-446.

    Masten LW, Boeri RL & Walker JD (1994) Strategies employed to
    determine the acute aquatic toxicity of ethyl benzene, a
    highly-volatile, poorly water-soluble chemical. Ecotoxicol Environ
    Saf, 27: 335-348.

    Mayer FL & Ellersieck MR (1986) Manual of acute toxicity:
    Interpretation and data base for 410 chemicals and 66 species of
    freshwater animals. Washington, DC, US Department of the Interior,
    Fish and Wildlife Service, p 460 (Resource Publication No. 160).

    Michael LC, Pellizzari ED, & Norwood DL (1991) Application of the
    master analytical scheme to the determination of volatile organics in
    wastewater influent and effluents. Environ Sci Technol, 25: 150-155

    Molnár J, Paksy KA, & Náray M (1986) Changes in the rat's motor
    behaviour during 4-hour inhalation exposure to prenarcotic
    concentrations of benzene and its derivatives. Acta Physiol Hung,
    67: 349-354.

    Morgan DL, Cooper SW, Carlock DL, Sykora JJ, Sutton B, Mattie DR, &
    McDougal JN (1991) Dermal absorption of neat and aqueous volatile
    organic chemicals in the Fischer 344 rat. Environ Res, 55: 51-63.

    Mott JG & Romanow S (1991/1992) Sludge characterization, removal and
    dewatering. J Hazard Mater, 29(1): 127-140.

    Murray DAJ & Lockhart WL (1981) Microextraction and gas chromatographic
    analysis of selected petroleum hydrocarbons in water and fish tissue.
    J Chromatogr, 212: 305-311.

    Namkung E & Rittmann BE (1987) Estimating volatile organic compound
    emissions from publicly owned treatment works. J Water Pollut Control
    Fed, 59: 670-678.

    Nelson PF & Quigley SM (1982) Non-methane hydrocarbons in the
    atmosphere of Sydney, Australia. Environ Sci Technol, 16: 650-655.

    Neuhauser EF, Loehr RC, & Malecki MR (1986) Contact and artificial
    soil tests using earthworms to evaluate the impact of wastes in soil.
    In: Petros JK, Lacy WJ, & Conway RA end. Hazardous and industrial
    solid waste testing: Fourth symposium. Philadelphia, Pennsylvania,
    American Society for Testing and Materials, pp 192-203 (ASTM STP 886).

    NIOSH (1984) Method 1501. In: Manual of analytical methods, 3rd ed.
    Cincinnati, Ohio, National Institute for Occupational Safety and
    Health, vol 2.

    Noleau I & Toulemonde B (1988) Volatile components of roasted guinea
    hen. Lebensm.Wiss Technol, 21: 195-197.

    Norppa H & Vainio H (1983) Induction of sister-chromatid exchanges by
    styrene analogues in cultured human lymphocytes. Mutat Res,
    116: 379-387.

    NTP (1992) Toxicity studies of ethylbenzene in F344/N rats and B6C3F1
    mice (inhalation studies). Research Triangle Park, North Carolina, US
    Department of Health and Human Services, National Toxicology Program
    (NIH Publication No. 92-3129).

    Nunes P & Benville PE Jr (1979) Uptake and depuration of petroleum
    hydrocarbons in the Manila clam,  Tapes semidecussata Reeve. Bull
    Environ Contam Toxicol, 21:719-726.

    Ogata M, Sugihara R, & Kira S (1977) Quantitative determination of
    urinary hippuric acid and  m- or  p-methylhippuric acid as indices
    of toluene and  m- or  p-xylene exposure by high performance liquid
    chromatography. Int Arch Occup Environ Health, 39: 199-206.

    Ogata M, Fujisawa K, Ogino Y, & Mano E (1984) Partition coefficients
    as a measure of bioconcentration potential of crude oil compounds in
    fish and shellfish. Bull Environ Contam Toxicol, 33: 561-567.

    Otson R, Williams DT, & Bothwell PD (1982) Volatile organic compounds
    in water at thirty Canadian potable water treatment facilities. J
    Assoc Off Anal Chem, 65: 1370-1374.

    Pankow JF, Isabelle LM, & Asher WE (1984) Trace organic compounds in
    rain. I. Sampler design and analysis by adsorption/thermal desorption
    (ATD). Environ Sci Technol, 18: 310-318.

    Pellizzari ED, Hartwell TD, Harris BSH, Waddell RD, Whitaker DA, &
    Erickson MD (1982) Purgeable organic compounds in mother's milk. Bull
    Environ Contam Toxicol, 28: 322-328.

    Pellizzari ED, Sheldon L, Sparacino C, Bursey J, Wallace L, & Bromberg
    S (1984) Volatile organic levels in indoor air. In: Berglund B,
    Lindvall T, & Sundell J ed. Indoor air, chemical characterization and
    personal exposure. Stockholm, Swedish Council for Building Research,
    vol 4, pp 21-26.

    Pellizzari ED, Wallace LA, & Gordon SM (1992) Elimination kinetics of
    volatile organics in humans using breath measurements. J Expo Anal
    Environ Epidemiol, 2: 341-355.

    Perry DL, Chuang CC, Jungclaus GA, & Warner JS (1979) Identification
    of organic compounds in industrial effluent discharges. Washington,
    DC, US Environmental Protection Agency (EPA 600/4-79-016).

    Petersson G (1982) Ambient hydrocarbons from motor-car assembly plants
    in Scandinavia. Environ Pollut, B4: 207-217.

    Pickering QH & Henderson C (1966) Acute toxicity of some important
    petrochemicals to fish. J Water Pollut Control Fed, 38: 1419-1429.

    Pitter P & Chudoba J (1990) Biodegradability of organic substances in
    the aquatic environment. Boca Raton, Florida, CRC Press, Inc., p 269.

    Potera FT (1975) The effects of benzene, toluene and ethylbenzene on
    several important members of the estuarine ecosystem. Lehigh
    University (Ph.D. dissertation).

    Pussemier L, Szabó G, & Bulman RA (1990) Prediction of the soil
    adsorption coefficient Koc for aromatic pollutants. Chemosphere 
    21: 1199-1212.

    Pyykkö K, Paavilainen S, Metsä-Ketelä T, & Laustiola K (1987) The
    increasing and decreasing effects of aromatic hydrocarbon solvents on
    pulmonary and hepatic cytochrome P-450 in the rat. Pharmacol Toxicol,
    60: 288-293.

    Radzikowska-Kintzi H & Jakubowski M (1981) Internal standardization in
    the head space analysis of organic solvents in blood. Int Arch Occup
    Environ Health, 49: 115-123.

    Rao PSC, Hornsby AG, & Jessup RE (1985) Indices for ranking the
    potential for pesticide contamination of groundwater. Soil Crop Sci
    Soc Proc, 44: 1-8.

    Rappaport SM, Selvin S, & Waters MA (1987) Exposures to hydrocarbon
    components of gasoline in the petroleum industry. Appl Ind Hyg, 
    2: 148-154.

    Reinhard M, Goodman NL, & Barker JF (1984) Occurrence and distribution
    of organic chemicals in two landfill leachate plumes. Environ Sci
    Technol, 18: 953-961.

    Rhue RD, Pennell KD, Rao PS, & Reve WH (1989) Competitive adsorption
    of alkylbenzene and water vapors on predominantly mineral surfaces.
    Chemosphere, 18(9-10): 1971-1986.

    Romanelli A, Falzoi M, Mutti A, Bergamaschi E, & Franchini I (1986)
    Effects of some monocyclic aromatic solvents and their metabolites on
    brain dopamine in rabbits. J Appl Toxicol, 6: 431-435.

    Römer KG, Federsel RJ, & Freundt KJ (1986) Rise of inhaled toluene,
    ethyl benzene,  m-xylene, or mesitylene in rat blood after treatment
    with ethanol. Bull Environ Contam Toxicol, 37: 874-876.

    Rosen AA, Skeel RJ, & Ettinger MB (1963) Relationship of river water
    odour to specific organic contaminants. J Water Pollut Control Fed,
    35: 777-782.

    Roy WR & Griffin RA (1985) Mobility of organic solvents in
    water-saturated soil material. Environ Geol Water Sci, 7: 241-247.

    SAC (1989) Analysis of potentially dangerous substances in UK 
    waters. Bedford, United Kingdom, SAC Scientific (DOE Reference 
    No. PECD-7/7/306).

    Sato A & Nakajima T (1987) Pharmacokinetics of organic solvent vapors
    in relation to their toxicity. Scand J Work Environ Health, 13: 81-93.

    Sauer TC Jr (1981) Volatile liquid hydrocarbon characterization of
    underwater hydrocarbon vents and formation waters from offshore
    production operations. Environ Sci Technol, 15: 917-923.

    Sax NI (1979) Dangerous properties of industrial chemicals, 5th ed.
    New York, Van Nostrand Reinhold Co.

    Seader JD (1982) Separation systems synthesis. In: Kirk RE & Othmer DF
    ed. Encyclopedia of chemical technology, 3rd ed. New York, Wiley
    Interscience, vol 20, pp 710-711.

    Sequeira DJ, Eyer CS, Cawley GF, Nick TG, & Backes WL (1992)
    Ethylbenzene-mediated induction of cytochrome P450 isozymes in male
    and female rats. Biochem Pharmacol, 44: 1171-1182.

    Sexton K & Westberg H (1980) Ambient hydrocarbon and ozone
    measurements downwind of a large automotive painting plant. Environ
    Sci Technol, 14: 329-332.

    Singh HB, Salas LJ, Smith AJ, & Shigeishi H (1981) Measurements of
    some potentially hazardous organic chemicals in urban environments.
    Atmos Environ, 15: 601-612.

    Singh HB, Salas LJ, & Stiles RE (1982) Distribution of selected
    gaseous organic mutagens and suspect carcinogens in ambient air.
    Environ Sci Technol, 16: 872-880.

    Singh HB, Salas LJ, Stiles R, & Shigeishi H (1983) Measurements of
    hazardous organic chemicals in the ambient atmosphere. Washington, DC,
    US Environmental Protection Agency (EPA 600/3-83-002).

    Singh HB, Ferek RJ, Salas LJ, & Nitz KC (1986) Toxic chemicals in the
    environment: A program of field measurements. Washington, DC, US
    Environmental Protection Agency (EPA 600/3-86/047).

    Smith MR & Ratledge C (1989) Catabolism of alkylbenzenes by
     Pseudomonas sp. NCIB 10643. Appl Microbiol Biotechnol, 32: 68-75.

    Smyth HF Jr, Carpenter CP, Weil CS, Pozzani UC, & Striegel JA (1962)
    Range-finding toxicity data: List VI. Am Ind Hyg Assoc J, 23: 95-107.

    Sollenberg J (1991) Analytical isotachophoresis in biological
    monitoring of exposure to industrial chemicals. J Chromatogr,
    545: 369-374.

    Sollenberg J, Smallwood AW, & Lowry LK (1985) Determination of
    mandelic and phenylglyoxylic acids in rat urine by high-performance
    liquid chromatography and by isotachophoresis. J Chromatogr,
    343: 175-178.

    Staples CA, Werner AF, & Hoogheem TJ (1985) Assessment of priority
    pollutant concentrations in the United States using STORET database.
    Environ Toxicol Chem, 4(2): 131-142.

    Stuermer DH, Ng DJ, & Morris CJ (1982) Organic contaminants in
    groundwater near to an underground coal gasification site in
    North-Eastern Wyoming. Environ Sci Technol, 16: 582-587.

    Susten AS, Niemeier RW, & Simon SD (1990)  In vivo percutaneous
    absorption studies of volatile organic solvents in hairless mice. II.
    Toluene, ethylbenzene and aniline. J Appl Toxicol, 10: 217-225.

    Tabak HH, Quave SA, Mashni CI, & Barth EF (1981) Biodegradability
    studies with organic priority pollutant compounds. J Water Pollut
    Control Fed, 53: 1503-1518.

    Tester DJ & Harker RJ (1981) Groundwater pollution investigations in
    the Great Ouse basin. Water Pollut Control, 80: 614-631.

    Thomann RV (1989) Bioaccumulation model of organic chemical
    distribution in aquatic food chains. Environ Sci Technol,
    23(6): 699-707.

    Thomas JM, Gordy VR, Fiorenza S, & Ward CH (1990) Biodegradation of
    BTEX in subsurface materials contaminated with gasoline: Granger,
    Indiana. Water Sci Technol, 22: 53-62.

    Thomas RG (1982) Volatilization. In: Lyman WJ, Reehl WF, & Rosenblatt
    DH ed. Handbook of chemical properties: Estimation methods. New York,
    McGraw-Hill Book Co.

    Thorburn S & Colenutt BA (1979) A gas chromatographic comparison of
    volatile organic compounds in urban and rural atmospheres. Int J
    Environ Stud, 13: 265-271.

    Triebig G, Claus D, Csuzda I, Druschky KF, Holler P, Kinzel W, Lehrl
    S, Reichwein P, Weidenhammer W, Weitbrecht WU, Weltle D, Schaller KH,
    & Valentin H (1988) Cross-sectional epidemiological study on
    neurotoxicity of solvents in paints and lacquers. Int Arch Occup
    Environ Health, 60: 233-241.

    Tsuruta H (1982) Percutaneous absorption of organic solvents. III. On
    the penetration rates of hydrophobic solvents through the excised rat
    skin. Ind Health, 20: 335-345.

    Ullman (1983) [Encyclopaedia of chemical technology.] Weinheim, Verlag
    Chemie, vol 24, pp 525-544 (in German).

    Ungváry G & Tátrai E (1985) On the embryotoxic effects of benzene and
    its alkyl derivatives in mice, rats, and rabbits. Arch Toxicol,
    8(suppl): 425-430.

    US Chemical Industry (1994) Facts and figures for the chemical
    industry. Chem Eng News, July 4: 28-33.

    US EPA (1978) In-depth studies on health and environmental impacts of
    selected water pollutants. Washington, DC, US Environmental Protection
    Agency (Contract No. 68-01-4646).

    US ITC (1987) Synthetic organic chemicals: United States production
    and sales, 1986. Washington, DC, US International Trade Commission.

    Utkin IB, Yakimov MM, Matveeva LN, Kozlyak EI, Rogozhin IS, Solomon
    ZG, & Bezborodov AM (1991) Degradation of styrene and ethylbenzene by
     Pseudomonas species Y2. Microbiol Lett, 77: 237-242.

    Van Duijvenbooden W & Kooper WF (1981) Effects on groundwater flow and
    groundwater quality of a waste disposal site in Noordwijk, The
    Netherlands. Sci Total Environ, 21: 85-92.

    Verhoeff AP, Suk J, & Van Wijnen JH (1988) Residential indoor air
    contamination by screen printing plants. Int Arch Occup Environ
    Health, 60: 201-209.

    Verschueren K (1983) Handbook of environmental data on organic
    chemicals, 2nd ed. New York, Van Nostrand Reinhold Co., pp 628-630.

    Viganň L (1993) Reproductive strategy of  Daphnia magna and toxicity
    of organic compounds. Water Res, 27: 903-909.

    Vincent R, Poirot P, Sabra I, Rieger B, & Cicolella A (1994)
    Occupational exposure to organic solvents during paint stripping and
    painting operations in the aeronautical industry. Int Arch Occup
    Environ Health, 65(6): 377-380.

    Volskay VT Jr & Grady CPL Jr (1990) Respiration inhibition kinetic
    analysis. Water Res, 24: 863-874.

    Vowles PD & Mantoura RFC (1987) Sediment-water partition coefficients
    and HPLC retention factors of aromatic hydrocarbons. Chemosphere, 
    16: 109-116.

    Waggott A (1981) Trace organic substances in the River Lee. In:
    Chemistry in water reuse. Ann Arbor, Michigan, Ann Arbor Science
    Publishers, Inc., vol 2, pp 55-99.

    Wakeham SG, Davis AC, & Karas JL (1983) Mesocosm experiments to
    determine the fate and persistence of volatile organic compounds in
    coastal seawater. Environ Sci Technol, 17: 611-617.

    Wallace LA, Pellizzari E, Hartwell TD, Perritt R, & Ziegenfus R
    (1987a) Exposures to benzene and other volatile compounds from active
    and passive smoking. Arch Environ Health, 42(5): 272-279.

    Wallace LA, Pellizzari E, Hartwell TD, Sparacino C, Withmore R,
    Sheldon L, Zelon H, & Perritt R (1987b) The TEAM study: Personal
    exposures to toxic substances in air, drinking water, and breath of
    400 residents of New Jersey, North Carolina, and North Dakota. Environ
    Res, 43: 290-307.

    Wallace LA, Pellizzari E, Leaderer B, Zelon H, & Sheldon L (1987c)
    Emissions of volatile organic compounds from building materials and
    consumer products. Atmos Environ, 21(2): 385-393.

    Wallace LA, Pellizzari ED, Hartwell TD, Davis V, Michael LC, &
    Whitmore RW (1989) The influence of personal activities on exposure to
    volatile organic compounds. Environ Res, 50(1): 37-55.

    Warner JM & Beasley RK (1984) Purge and trap chromatographic method
    for the determination of acrylonitrile, chlorobenzene,
    1,2-dichloroethane and ethylbenzene in aqueous samples. Anal Chem,
    56: 1953-1956.

    Water Pollution Control (1989) Fate of organics on land-applied
    sludges. Water Pollut Control, 127: 12.

    Weast RC ed (1988) Handbook of chemistry and physics, 69th ed. Boca
    Raton, Florida, CRC Press, Inc.

    Webber D (1984) Top 50 chemical products. Chem Eng News, May 7: 8-10.

    Westrick JJ, Mello JW, & Thomas RF (1984) The groundwater supply
    survey. J Am Water Works Assoc, 76: 52-59.

    Whitby FJ, Harland BJ, & Comber MHI (1982) Aromatic hydrocarbons in
    the Tees Estuary. London, Department of Health (DOE Contract

    WHO (1993) Guidelines for drinking-water quality. Volume 1:
    Recommendations, 2nd ed. Geneva, World Health Organization.

    Wiesenburg DA, Bodennec G, & Brooks JM (1981) Volatile liquid
    hydrocarbons around a production platform in the northwest Gulf of
    Mexico. Bull Environ Contam Toxicol, 27: 167-174.

    Wilson BH, Smith GB, & Rees JF (1986) Biotransformation of selected
    alkylbenzenes and halogenated aliphatic hydrocarbons in methanogenic
    aquifer material: A microcosm study. Environ Sci Technol, 20:

    Windholz M ed (1983) The Merck index: An encyclopedia of chemicals,
    drugs and biologicals, 10th ed. Rahway, New Jersey, Merck & Co., Inc.

    Wolf MA, Rowe VK, McCollister DD, Hollingsworth RL, & Oyen F (1956) 
    Toxicological studies of certain alkylated benzenes and benzene. Arch
    Ind Health, 14: 387-398.

    Wolff MS (1976) Evidence for existence in human tissues of monomers
    for plastics and rubber manufacture. Environ Health Perspect,
    17: 183-187.

    Wolff MS, Daum SM, Lorimer WV, Selikoff IJ, & Aubrey BB (1977) Styrene
    and related hydrocarbons in subcutaneous fat from polymerization
    workers.  J Toxicol Environ Health, 2: 997-1005.

    Yamamoto RK & Cook WA (1968) Determination of ethyl benzene and
    styrene in air by ultraviolet spectrophotometry. Am Ind Hyg Assoc J,
    29: 238-241.

    Zhang Z & Pawliszyn J (1993) Headspace solid-phase microextraction.
    Anal Chem, 65(14): 1843-1852.

    Zlatkis A & Jiao J (1991) Evaluation of new organoclay stationary
    phases for the separation of ethylbenzene and xylene isomers.
    Chromatographia, 31(9-10): 457-464.

    1.  RESUME

         L'éthylbenzčne est un hydrocarbure aromatique qui s'obtient par
    une réaction d'alkylation mettant en jeu le benzčne et l'éthylčne. 
    Aux Etats-Unis, on estime sa production annuelle ŕ environ 5 millions
    de tonnes.  En 1983, l'Europe occidentale en a produit environ 3
    millions de tonnes.  Il se présente sous la forme d'un liquide
    incolore dégageant une odeur douceâtre qui rappelle l'essence.  On
    l'utilise principalement pour la production de styrčne.  Ajouté ŕ du
    xylčne technique, il sert également de solvant pour les peintures et
    les vernis et on l'emploie aussi dans l'industrie chimique et dans
    celle du caoutchouc.  Il est présent dans le pétrole brut, les
    produits raffinés dérivés du pétrole et dans leurs produits de

         L'éthylbenzčne n'est pas persistant car il se décompose dans
    l'environnement, principalement par photo-oxydation et par dégradation
    biologique.  Il est possible que la photo-oxydation de l'éthylbenzčne
    dans l'atmosphčre contribue ŕ la formation du smog photochimique.

         Le logarithme du coéfficient de partage entre l'octanol et l'eau
    est égal ŕ 3,13, ce qui indique que le composé se pręte ŕ une
    bioaccumulation.  Cependant, les données limitées dont on dispose
    montrent que le facteur de bioaccumulation de l'éthylbenzčne est
    faible pour les mollusques et les poissons.  Apparemment, il est vite
    éliminé par les organismes aquatiques.

         A la campagne, la concentration d'éthylbenzčne dans l'air est
    généralement inférieure ŕ 2 µg/m3. Sur des sites urbains, on a
    trouvé des teneurs moyennes allant de 0,74 ŕ 100 µg/m3. La
    concentration d'éthylbenzčne présente dans les eaux superficielles 
    est généralement inférieure ŕ 0,1 µg/litre dans les zones non
    industrialisées.  En revanche, dans les zones urbaines ou
    industrialisées, la concentration peut atteindre 15 µg/litre.  Dans
    les sédiments, la concentration est en général inférieure ŕ
    0,5 µg/litre, encore que l'on ait signalé des valeurs comprises entre
    1 et 5 µg/litre dans des sédiments provenant de régions fortement
    industrialisées.  Dans les eaux souterraines non contaminées, la
    concentration est habituellement inférieure ŕ 0,1 µg/litre, mais elle
    est beaucoup plus élevée dans les eaux contaminées.

         L'éthylbenzčne présente une toxicité aiguë modérée pour les
    algues, les invertébrés aquatiques et les poissons.  La valeur de la
    CE50 ŕ 72 h est de 4,6 mg/litre pour l'algue Selenastrum
     capricornutum, la CL50 ŕ 48 h est de 1,8 mg/litre pour  Daphnia
     magna, et on a une CL50 ŕ 96 h de 4,2 mg/litre pour la truite
    arc-en-ciel.  On ne possčde aucune donnée sur l'exposition chronique
    des organismes aquatiques ŕ l'éthylbenzčne.

         En ce qui concerne les bactéries et les lombrics, les données
    toxicologiques sont limitées.  Il n'en n'existe aucune sur les
    végétaux terrestres, les oiseaux ou les mammifčres sauvages.

         Chez l'homme, l'exposition ŕ l'éthylbenzčne se produit
    principalement par inhalation; 40 ŕ 60% du composé sont retenus dans
    les poumons.  L'éthylbenzčne est fortement métabolisé, principalement
    en acides mandélique et phénylglyoxylique.  On peut utiliser les
    métabolites présents dans les urines pour surveiller l'exposition

         Qu'elle soit aiguë ou chronique, la toxicité de l'éthylbenzčne
    est faible pour l'homme et les animaux.  Il exerce des effets toxiques
    sur le systčme nerveux central et il est irritant pour les muqueuses
    et les yeux.  Le seuil de concentration pour ces effets chez l'homme a
    été estimé ŕ environ 430-860 mg/m3 (100-200 ppm) lors d'une seule
    exposition de courte durée.

         Des rats et des souris ŕ qui on avait fait inhaler pendant 13
    semaines de l'éthylbenzčne ŕ des concentrations allant jusqu'ŕ 4300
    mg/m3, n'ont présenté aucune lésion histopathologique. La dose sans
    effet observable (critčre retenu: l'augmentation du poids du foie) a
    été estimée ŕ 2150 mg/m3 (500 ppm).

         L'éthylbenzčne stimule les enzymes des microsomes hépatiques.  Il
    n'est ni mutagčne ni tératogčne pour le rat ou le lapin. On ne dispose
    d'aucune donnée au sujet de ses effets toxiques éventuels sur
    l'appareil reproducteur ni sur son pouvoir cancérogčne.

         Une valeur-guide de 22 mg/litre (5 ppm) a été calculée ŕ partir
    des résultats fournis par les études sur l'animal.  On estime que la
    population générale est exposée ŕ des concentrations inférieures ŕ
    cette valeur, męme dans les cas les plus graves.  On a constaté qu'une
    exposition de longue durée en milieu professionnel, ŕ des concentration
    de cet ordre, n'avait aucun effet nocif sur la santé des travailleurs


         El etilbenceno es un hidrocarburo aromático que se obtiene por
    alkilación del benceno y del etileno.  La producción estimada en los
    Estados Unidos de América es de unos cinco millones de toneladas por
    ańo, y en Europa occidental fue de aproximadamente tres millones de
    toneladas en 1983.  El etilbenceno es un líquido incoloro de olor
    dulce semejante al de la gasolina.  Se utiliza principalmente para la
    producción de estireno.  También se utiliza en el xileno técnico como
    disolvente de pinturas y lacas, así como en la industria del caucho y
    en la fabricación de sustancias químicas.  Se encuentra en el petróleo
    crudo, en los productos de petróleo refinados y en productos de

         El etilbenceno es una sustancia química no persistente, que se
    degrada principalmente por fotooxidación y biodegradación.  Su
    volatilización en la atmósfera es rápida.  La reacción de foto-
    oxidación del etilbenceno en la atmósfera puede contribuir a la
    formación de niebla fotoquímica.

         El logaritmo del coeficiente de reparto octanol-agua es 3,13, lo
    que indica posibilidad de bioacumulación.  Sin embargo, los limitados
    indicios disponibles muestran que los factores de bioconcentración del
    etilbenceno son bajos para peces y moluscos.  La eliminación por los
    organismos acuáticos parece ser rápida.

         Los niveles de etilbenceno en el aire en puntos rurales son
    generalmente inferiores a 2 µg/m3.  En puntos urbanos se han
    registrado niveles medios de etilbenceno que oscilan entre 0,74 y 100
    µg/m3.  Los niveles de etilbenceno detectados en las aguas
    superficiales son generalmente inferiores a 0,1 µg/litro en zonas no
    industriales.  Se han comunicado concentraciones de etilbenceno de
    hasta 15 µg/litro en zonas industriales y urbanas.  Los niveles de
    etilbenceno en sedimentos son generalmente inferiores a 0,5 µg/kg,
    aunque en sedimentos de zonas muy industrializadas se han encontrado
    niveles de 1 a 5 µg/kg.  Las concentraciones en aguas subterráneas no
    contaminadas son generalmente inferiores a 0,1 µg/litro, pero son
    mucho más elevadas en aguas subterráneas contaminadas.

         La toxicidad aguda del etilbenceno para las algas, los
    invertebrados acuáticos y los peces es moderada.  Los valores de
    toxicidad aguda más bajos son de 4,6 mg/litro para el alga
     Selenastrum capricornutum (CE50 a las 72 horas, sobre la base de la
    inhibición del crecimiento), 1,8 mg/litro para  Daphnia magna (CL50
    a las 48 horas) y 4,2 mg/litro para la trucha irisada (CL50 a las 96
    horas).  No se dispone de información sobre la exposición crónica de
    los organismos acuáticos al etilbenceno.

         Hay información limitada sobre la toxicidad del etilbenceno para
    las bacterias y para las lombrices.  No hay datos relativos a las
    plantas terrestres, las aves y los mamíferos silvestres.

         La exposición humana al etilbenceno se produce principalmente por
    inhalación; el 40-60% del etilbenceno inhalado se retiene en los
    pulmones.  El etilbenceno se metaboliza extensamente, transformándose
    sobre todo en ácidos mandélico y fenilglioxílico.  Estos metabolitos
    urinarios pueden utilizarse para vigilar la exposición humana.

         El etilbenceno tiene una toxicidad aguda y crónica baja tanto
    para los animales como para el hombre.  Es tóxico para el sistema
    nervioso central e irrita las mucosas y los ojos.  El umbral para esos
    efectos en el ser humano después de exposiciones únicas breves se
    estimó en aproximadamente 430-860 mg/m3 (100-200 ppm).

         La inhalación de etilbenceno por ratas y ratones durante 13
    semanas en concentraciones de hasta 4300 mg/m3 (1000 ppm) no dio
    lugar a lesiones histopatológicas.  El nivel sin efectos observados,
    sobre la base de un aumento del peso del hígado en las ratas, fue de
    2150 mg/m3 (500 ppm).

         El etilbenceno es un inductor de las enzimas microsómicas
    hepáticas.  No es mutagénico ni teratogénico en ratas y conejos.  No
    se dispone de información sobre la toxicidad reproductiva ni la
    carcinogenicidad del etilbenceno.

         Se ha calculado un valor de orientación de 22 mg/m3 (5 ppm) a
    partir de estudios realizados en animales.  La exposición estimada de
    la población general (incluso en la peor de las situaciones) es
    inferior a ese valor de orientación.  La exposición ocupacional a
    largo plazo a concentraciones de etilbenceno estimadas en este orden
    de magnitud no ocasionaron efectos adversos en la salud de los

    See Also:
       Toxicological Abbreviations
       Ethylbenzene (ICSC)
       Ethylbenzene  (IARC Summary & Evaluation, Volume 77, 2000)