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.

    Published under the joint sponsorship of
    the United Nations Environment Programme,
    the International Labour Organisation,
    and the World Health Organization

    First draft prepared by Dr S. Dobson,
    (Institute of Terrestrial Ecology, United Kingdom)
    and Dr A.A. Jensen (Danish Technological Institute)

    World Health Orgnization
    Geneva, 1990

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    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

    WHO Library Cataloguing in Publication Data


        (Environmental health criteria ; 136)

        1.Trichloroethanes - adverse effects 2.Trichloroethanes - toxicity
        3.Environmental exposure 4.Environmental pollutants 

        ISBN 92 4 157136 5        (NLM Classification: QV 633)
        ISSN 0250-863X

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    1.   SUMMARY


         2.1   Identity
         2.2   Physical and chemical properties
               2.2.1   Physical characteristics
               2.2.2   Chemical reactivity
               2.2.3   Commercial products
         2.3   Conversion factors
         2.4   Analytical methods


         3.1   Production processes
         3.2   Production levels
         3.3   Uses


         4.1   Distribution and transport between media
               4.1.1   Atmospheric transport
               4.1.2   Transport in water
               4.1.3   Transport in soil
         4.2   Degradation and transformation
               4.2.1   Abiotic degradation
                In the atmosphere
                In water
               4.2.2   Biodegradation
         4.3   Bioaccumulation


         5.1   Environmental levels
               5.1.1   Air
               5.1.2   Water
               5.1.3   Sediment and soil
               5.1.4   Biota
         5.2   General population exposure
               5.2.1   Food
               5.2.2   Drinking-water
               5.2.3   Air
               5.2.4   Consumer products and cosmetics

         5.3   Occupational exposure


         6.1   Absorption
               6.1.1   Animal studies
                Oral absorption
                Skin absorption
               6.1.2   Human studies
                Skin contact
         6.2   Distribution and retention
               6.2.1   Animal studies
               6.2.2   Human studies
         6.3   Metabolic transformation
               6.3.1   Animal studies
               6.3.2   Human studies
               6.3.3   Metabolic interactions
         6.4   Elimination
               6.4.1   Animal studies
               6.4.2   Human studies
         6.5   Biological monitoring
         6.6   Bioaccumulation


         7.1   Acute toxicity
               7.1.1   Irritation
               7.1.2   Short-term exposure
                Oral administration
         7.2   Long-term exposure
         7.3   Reproductive toxicity, embryotoxicity, and
         7.4   Mutagenicity
         7.5   Carcinogenicity
               7.5.1   Oral administration
               7.5.2   Inhalation
         7.6   Immunotoxicity and sensitization
         7.7   Interactions
         7.8   Mechanisms of action


         8.1   Controlled human studies
               8.1.1   Single exposure period
               8.1.2   Repeated exposure

         8.2   Accidental exposure
               8.2.1   Confined spaces at workplaces
               8.2.2   Solvent abuse
               8.2.3   Medical use
               8.2.4   Ingestion
               8.2.5   Drinking-water contamination
         8.3   Effects on the skin and eyes
         8.4   Long-term occupational exposure
         8.5   Interactions


         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









    Dr L.A. Albert, Consultores Ambientales Asociados, Xalapa, Veracruz,
       Mexico  (Vice-Chairman)

    Dr A.H. El-Sebae, Faculty of Agriculture, Alexandria University,
       Alexandria, Egypt

    Dr S. Fairhurst, Medical Division, Health and Safety Executive,
       Bootle, Merseyside, United Kingdom  (Chairman)

    Dr B. Gilbert, Technology Development Company (CODETEC), Cidade
       Universitaria, Campinas, Brazil

    Dr A.A. Jensen, Danish Technological Institute, Taastrup, Denmark

    Dr T. Kawamoto, Department of Environmental Health, University of
       Occupational and Environmental Health, Japan School of Medicine,
       Kitakyushu City, Japan

    Ms I.R. Nielsen, Environment Section, Organic Materials Division,
       Building Research Establishment, Garston, Watford, United Kingdom

    Dr B. Wahlstrom, Department of Science and Technology, National
       Chemicals Inspectorate, Solna, Sweden

    Mr R. Walentowicz, Exposure Assessment Group, US Environmental
       Protection Agency, Washington, DC, USA

    Mrs G. Wood, Criteria Section, Bureau of Chemical Hazards,
       Environmental Health Directorate, Health Protection Branch, Health
       & Welfare, Tunney's Pasture, Ottawa, Canada


    Dr M.A. Collins, ICI Chemicals & Polymers, Occupational Health,
       Runcorn, Cheshire, United Kingdom

    Dr C. De Rooij, Solvay, Brussels, Belgium


    Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
       Experimental Station, Abbots Ripton, Huntingdon, Cambridgeshire,
       United Kingdom  (Rapporteur)

    Dr M. Gilbert, International Programme on Chemical Safety, World
       Health Organization, Geneva, Switzerland  (Secretary)

    Mr P.D. Howe, Institute of Terrestrial Ecology, Monks Wood
       Experimental Station, Abbots Ripton, Huntingdon, Cambridgeshire,
       United Kingdom  (Temporary Adviser)


       Every effort has been made to present information in the criteria
    documents as accurately as possible without unduly delaying their
    publication.  In the interest of all users of the Environmental Health
    Criteria documents, readers are kindly 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, Palais des
    Nations, 1211 Geneva 10, Switzerland (Telephone No. 7988400 or


       A WHO Task Group on Environmental Health Criteria for
    1,1,1-Trichloroethane met at the Institute of Terrestrial Ecology
    (ITE), Monks Wood, United Kingdom, from 20 to 24 May 1991.  Dr M.
    Roberts, Director, ITE, welcomed the participants on behalf of the
    host institution and Dr M. Gilbert opened the meeting on behalf of the
    three cooperating organizations of the IPCS (UNEP/ILO/WHO). The Task
    Group reviewed and revised the draft criteria document and made an
    evaluation of the risks for human health and the environment from
    exposure to 1,1,1-trichloroethane.

       The first draft of this document was prepared by Dr S. Dobson (ITE)
    and Dr A.A. Jensen (Danish Technological Institute). Dr M. Gilbert and
    Dr P.G. Jenkins, both members of the IPCS Central Unit, were
    responsible for the technical development and editing, respectively.

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


    cAMP        cyclic adenosine monophosphate

    cGMP        cyclic guanosine monophosphate

    CNS         central nervous system

    NOAEL       no-observed-adverse-effect level

    NOEL        no-observed-effect level

    OECD        Organization for Economic Cooperation and Development

    ppt         parts per trillion

    1.  SUMMARY

         1,1,1-Trichloroethane is a chlorinated hydrocarbon which is
    manufactured from vinyl chloride or vinylidene chloride by
    chlorination.  The world production was approximately 680 000 tonnes
    in 1988.  It is a colourless, volatile liquid with a characteristic
    odour, and its vapour is more dense than air. It is mainly used in
    metal degreasing and as a solvent in many industrial and consumer
    products, including adhesives, spot removers, and aerosol cans.  It is
    also a chemical intermediate.  Technical trichloroethane usually
    contains 3-8% stabilizers to prevent degradation and the formation of
    hydrochloric acid; this protects metal parts from corrosion.  It is
    non-flammable under normal conditions, but the vapour burns at high
    temperatures and, during welding operations, its degradation products
    include the poisonous gas phosgene.  Contact with aluminium,
    magnesium, and their alloys may result in very violent reactions.

         1,1,1-Trichloroethane reaches the environment readily.  Owing to
    its long residence time in the troposphere (about 6 years) and low
    biodegradability, it is now ubiquitous in the environment, even far
    from industrial areas. Concentrations of up to 86 µg/m3 (16 ppb,
    w/w) have been determined in air sampled near industries producing or
    handling the compound.

         Trichloroethane is mobile in soils and reaches the ground water. 
    Concentrations of up to 1600 µg/litre have been found in ground or
    surface waters.  This may be a source of contamination for
    drinking-water supplies.

         It is estimated that 15% of the annual release of
    1,1,1-trichloroethane is transported to the stratosphere where it
    causes ozone depletion by liberating chlorine atoms.

         Acute toxic effects have been observed in bioassays with
    crustaceans and fish at concentrations above 7 mg/litre.  Limited
    information suggests that bioaccumulation in aquatic organisms is low. 
    The small amount of data makes it difficult to evaluate any effects on
    terrestrial organisms.

         Humans are exposed to 1,1,1-trichloroethane principally by
    inhalation, and the substance is then rapidly absorbed into the body. 
    Exposure by skin contact or ingestion may also occur.  Trichloroethane
    is distributed widely in body tissues and crosses the blood-brain and
    placental barriers.  It has also been found in human breast milk, but
    is not thought to be bioaccumulated.  The main route of elimination is
    exhalation of unchanged compound.

         The acute and chronic toxicities of 1,1,1-trichloroethane are
    relatively low, but, under conditions of high exposure, there is a
    risk of toxic effects.  Such conditions may occur in cases of

    occupational exposures, solvent abuse or accidents.  Since the solvent
    is volatile and the vapour is much more dense than air, unexpectedly
    high and dangerous concentrations may occur in confined spaces such as
    "empty" storage tanks.  This has caused several fatal and near-fatal
    poisonings at workplaces and elsewhere.

         The critical effect in humans is on the central nervous system. 
    Observable effects range from slight behavioural changes (accompanied
    by mild eye irritation) at 1.9 g/m3 (350 ppm) to unconsciousness and
    respiratory arrest at higher concentrations.  However, fatal cardiac
    anomalies may also occur.  Trichloroethane is less toxic to the liver
    than are most other organochlorine solvents.  The no-observed-effect
    level (NOEL) for humans appears to be in the region of 1.35 g/m3
    (250 ppm).

         No adequate study of human carcinogenic effects has been
    published. However, a long-term inhalation study on rats and mice
    exposed to 8.1 g/m3 (1500 ppm) gave no evidence of any carcinogenic
    effect.  1,1,1-Trichloroethane does not have significant genotoxic

         Developmental toxicity, but not teratogenicity, has been observed
    in rats and rabbits at concentrations that were toxic to the mother
    animals. The limited epidemiological evidence on reproductive effects
    is inconclusive.


    2.1  Identity

         1,1,1-Trichloroethane is an organochlorine solvent belonging to
    the family of chlorinated alkanes.

    Chemical structure:

                                   Cl     H
                                   |      |
                            Cl --  C  --  C  --  H
                                   |      |
                                   Cl     H

    Empirical formula:       C2H3Cl3

    Relative molecular
    mass:                    133.4

    IUPAC name:              1,1,1-trichloroethane

    CAS name:                ethane, 1,1,1-trichloro-

    Some common
     synonyms:               methylchloroform, MC, 1,1,1-TCE

    Some common
     trade names:            Chlorothene, Aerothene TT, Alpha-T,
                             Genklene, Inhibisol

    CAS registry
     number:                 71-55-6

    EEC identity
     number:                 602-013-00-2

    RTECS number:            KJ2975000

    2.2  Physical and chemical properties

    2.2.1  Physical characteristics

         In its pure state, 1,1,1-trichloroethane is a colourless,
    volatile liquid with a characteristic chloroform-like odour.  The
    odour threshold is reported to be around 540 mg/m3 (100 ppm)
    (Stewart, 1968).

         Trichloroethane has two structural isomers.  The
    1,1,2-trichloroethane isomer can be an impurity in the manufacture of
    1,1,1-trichloroethane and it is known to have a different spectrum of

         Some physical and chemical properties of pure 1,1,1-
    trichloroethane are listed in Table 1.

    2.2.2  Chemical reactivity

         1,1,1-Trichloroethane has no recorded flash point and is
    therefore sometimes considered as non-flammable.  However, it
    decomposes and/or oxidizes at high temperatures (> 300 °C) to
    hydrochloric acid and dichloroethene, together with some phosgene
    (Hardie, 1964).  When catalysed by metal salts, especially aluminium
    compounds, degradation occurs at lower temperatures (Dreher, 1989) and
    decomposition in air to hydrogen chloride, carbon dioxide, and traces
    of chlorine occurs slowly at ambient temperatures (Pearson &
    McConnell, 1975).  The formation of phosgene by the photooxidation of
    1,1,1-trichloroethane during welding operations may be considerable
    (Dahlberg et al., 1973).  1,1,1-Trichloroethane can burn in the vapour
    state (de Nevers, 1986) and in admixture with air forms explosive
    mixtures (Wrightson & Santon, 1988; Bretherick, 1989).  Contact with
    aluminium, magnesium, and their alloys may result in very violent
    reactions (Bretherick, 1981).  Trichloroethane reacts slowly with
    water, but more rapidly with alkaline solutions such as an aqueous
    suspension of calcium hydroxide, forming 1,1-dichloroethene
    (vinylidene chloride) (Hardie, 1964).  Hydrolysis, which is very slow
    at 20 °C but rapid at 80 °C (see Table 7), occurs in the presence of
    water or aqueous acids, yielding hydrochloric and acetic acids
    (Gerkens & Franklin, 1989).

    2.2.3  Commercial products

         Analytical grade 1,1,1-trichloroethane has a purity of > 99.0%
    and contains no added stabilizers (Fluka, 1988).

         Commercially available technical and solvent grade products have
    a purity of 90-95% and usually contain 3-8% stabilizers, mainly to
    prevent the generation of hydrochloric acid and to avoid corrosion of
    metal parts (Fluka, 1988).  The stabilizers used are chemical
    compounds, such as nitromethane,  N-methyl pyrrole, 1,4-dioxane,
    butylene oxide, 1,3-dioxolane, nitroethane, toluene, diisopropylamine,
    methyl ethyl ketone, isobutyl alcohol, and 2-butanol (IARC, 1979;
    Clayton & Clayton, 1981; US EPA, 1984; CEC, 1986).

        Table 1.  Physical and chemical properties of 1,1,1-trichloroethane

    Melting point                    -30.4 °C                        Weast (1986)

    Boiling point (at 760 mmHg)      74.1 °C                         Weast (1986)

    Density                          1.3390                          Weast (1986)

    Vapour density (air = 1)         4.6                             US EPA (1984)

    Vapour pressure (at 20 °C)       13.3 kPa (100 mmHg)             Weast (1986)

    Refractive index (at 20 °C)      1.4379                          Weast (1986)

    Concentration in                 16.7%                           Clayton &
     saturated air                                                   Clayton (1981)

    Solubility in water              0.3 g/litre at 25 °Ca           IARC (1979)
                                     0.95 g/litre at 20 °C           Archer (1979)
                                     0.480 g/litre at 20 °C          Pearson (1982)

    Soluble in                       acetone, benzene, chloroform,   Windholz (1983)
                                     methanol, ether, ethanol,       Weast (1986)
                                     carbon disulfide, carbon        CEC (1986)

    Partition coefficients                                           Veith et al.
     octanol/water (log Pow)         2.47 (measured)                 (1980)
     water/air (at 20 °C)            0.71                            Pearson (1982)
     blood/air (at 37 °C)            3.3                             US EPA (1984)

    Flammability                     nonflammable under normal       CEC (1986)
                                     conditions, vapour burns
                                     at high temperature

    Auto-ignition temperature        537 °C                          Archer (1979)

    Explosive limits in air          8.0-10.5 vol %                  Archer (1979)
     at 25 °C

    a   US EPA (1984) reported a water solubility of 4.4 g/litre at 25 °C.
         Twenty-two samples of stabilized technical 1,1,1-trichloroethane
    were shown to contain potential mutagens or carcinogens such as
    vinylidene chloride, dichloroethane, and 1,2-epoxybutane (Henschler et
    al., 1980).

    2.3  Conversion factors

              1 ppm = 5.40 mg/m3
              1 mg/m3 = 0.185 ppm

    2.4 Analytical methods

         The first step of an analytical method for routine measurements
    of trichloroethane in air is sampling either on activated charcoal
    (tubes or diffusion samplers) filters and extraction by a solvent
    (e.g., carbon disulfide) or on a polymer trap and desorption by
    heating.  This is followed by determination by gas chromatography (GC)
    combined with either electron capture detector (ECD), flame ionization
    detector (FID) or mass spectrometry (MS). GC is also used for the
    determination of trichloroethane in other types of samples (water,
    sediment, blood, etc.) by, for example, headspace analysis.

         Indicator tubes may be used for preliminary surveys of air
    levels.  The detection limit is about 270 mg/m3 (50 ppm)
    (Drägerwerk, 1986).

         Some examples of analytical methods are summarized in Table 2.

        Table 2.  Analytical methods

    Medium    Specification    Sampling method                 Analytical method  Detection limit             Reference

    Air                        trap on charcoal extract               GC-FID      300 ng/sample               Niosh (1977)
                               with carbon disulfide                                                          Otson & Chan (1987)

    Air                                                               GC-ECD      125 mg/m3                   Henschler (1978)
                                                                                  (10 litres air)

    Air                        trap on Porapak-N, desorb              GC-ECD      160 mg/m3                   Russell & Shadoff (1977)
                               at 200 °C, dry over MgSO4              GC-MS       (30 ppt)

    Water                      sparge with helium, trap               GC-MS                                   Coleman et al. (1976)
                               on Tenax GC, desorb by heat

    Water                      direct injection of headspace          GC-ECD      0.05 µg/litre               Piet et al. (1978)

    Water                      headspace air, trap on Tenax           GC                                      Pereira & Hughes (1980)

    Water     drinking-water   trap on XAD-2                          GC-MS       0.1 µg/litre                Otson (1987)

    Blood     rat arterial     headspace gas collected over           GC-FID      0.5 µg (6.4 µg/g            Westerberg & Larsson (1982)
                               75-150 µl at 75 °C, direct                         blood)

    Blood     human                                                   GC-ECD      0.05 mg/litre               Henschler (1978)

    Blood     human            extraction with hexane                 GC-ECD      < 0.07 µmol/litre           Pekari & Aitio (1985)

    Brain     rat              headspace gas collected                            0.5 µg (2.5 µg/g tissue)    Westerberg & Larsson (1982)



          1,1,1-Trichloroethane is a man-made chemical; there are no
     natural sources.  In 1988, world-wide production was approximately
     680 000 tonnes per year.  However, the annual production level is
     expected to decline progressively due to international agreements on
     the control of ozone-depleting substances.  It is used mainly in
     metal degreasing and as a solvent in many consumer products, but also
     finds use as an intermediate in the production of other chemicals.

    3.1  Production processes

         All 1,1,1-trichloroethane in the environment is anthropogenic in
    origin, since it does not occur naturally.  It is usually produced by
    the hydrochlorination of vinyl chloride to 1,1-dichloroethane,
    followed by thermal chlorination to 1,1,1-trichloroethane (Fishbein,
    1979).  1,1-Dichloroethene (vinylidene chloride) can also be directly
    hydrochlorinated to 1,1,1-trichloroethane, and direct chlorination of
    ethane or chloroethane can be used.  However, the latter methods may
    generate other halogenated hydrocarbons as by-products (Fishbein,

    3.2  Production levels

         The estimated world production capacity of 1,1,1-    
    trichloroethane was 480 000 tonnes/year in 1973 (McConnell et al.,
    1975) and 680 000 tonnes/year in 1988 (Midgley, 1989).  About half the
    production is in the USA and 100 000 tonnes is produced in Japan
    annually.  The production of 1,1,1-trichloroethane in Japan more than
    doubled in the period from 1979 to 1989.  The production in the
    European Economic Community in 1979 was estimated to be 140 000
    tonnes/year (Torslov, 1988).  Production capacity is about 100 000
    tonnes in Germany, while in 1973 the United Kingdom and France
    produced 20 000 and 11 000 tonnes, respectively.  The annual
    production in eastern Europe is estimated to be less than 1000 tonnes.

         The western European consumption of 1,1,1-trichloroethane in 1985
    was estimated to be 173 000 tonnes, the worldwide value being about
    500 000 tonnes.

         Information prepared by the European Chemical Industry Federation
    (CEFIC, 1986) suggested that consumption of 1,1,1-trichloroethane in
    western Europe increased during the 1970s but stabilized during the

         The estimated annual worldwide production of
    1,1,1-trichloroethane is shown in Table 3.

    Table 3.  Production and sales of 1,1,1-trichloroethane (tonnes/year)

    Year      Worldwide     W. European     W. European    USA           Japanese
              productiona   productionb     salesc         productiond   productione

    1970         155
    1971         175
    1972         227
    1973         279                                         245
    1974         314                           92
    1975         307                           86
    1976         407                           99
    1977         480                           109           289
    1978         524                           120           292
    1979         506                           147                          77
    1980         552                           144           315            86
    1981         549                           146           274            88
    1982         514                           142                          89
    1983         541                           140           226            96
    1984         600                           144                          111
    1985         588                           150           394            120
    1986         609            205            138           291            128
    1987         627            203            130           314            131
    1988         678            218            129           340            139
    1989                        222            130                          164
    1990                        229            122           338

    a Midgley (1989)
    b CEFIC (1991)
    c CEFIC (1986)
    d NIOSH (1979); Midgley (1989); CMR (1991)
    e MITI (1990)

         Midgley (1989) examined the annual sales of 1,1,1-trichloroethane
    and grouped uses into three categories: those that result in emissions
    for less than 6 months, for 1 year, and for more than one year.  He
    found that applications, such as solvent cleaning, that lead to rapid
    emission, account for 95 to 97% of the annual reported production of
    1,1,1-trichloroethane.  A geographical breakdown of the emission data
    into global regions revealed that during the period 1980-1988 between
    90% and 94% of the total production of 1,1,1-trichloroethane was sold
    to the industrial north, i.e. above latitude 30°N.

         Under the agreement of the London Conference of the Montreal
    Protocol (June, 1990), use of 1,1,1-trichloroethane will be

    3.3  Uses

         1,1,1-Trichloroethane is used mainly in metal cleaning/
    degreasing and as a solvent in various formulations, including
    adhesives, paints, varnishes, inks, dry cleaning agents, and
    typewriter correction fluids.  It is also utilized as a solvent in
    aerosols, and it can be used as an additive to raise the flash point
    of many flammable solvents.  1,1,1-Trichloroethane also finds uses as
    a coolant and lubricant in metal cutting oils, as a solvent in textile
    dyeing, for cleaning plastic moulds, and as a developer for printed
    circuit boards.

         Formerly, 1,1,1-trichloroethane was used as a solvent for various
    insecticides, and, together with ethylene gas, for degreasing citrus
    fruits and post-harvest fumigation of strawberries.

         1,1,1-Trichloroethane is also a chemical intermediate in the
    production of vinylidene chloride.  In the USA, this accounts for 23%
    of the total consumption of 1,1,1-trichloroethane, but this use 
    appears to represent only 5-10% of the production elsewhere.



         1,1,1-Trichloroethane has a residence time of about 6 years in
     the troposphere, where it is oxidized to trichloroacetaldehyde and
     trichloroacetic acid.  It reaches the stratosphere in significant
     amounts, which results in ozone depletion through the liberation of
     reactive chlorine atoms.  The ozone-depleting potential of
     1,1,1-trichloroethane is ten times lower than that of
     trichlorofluoromethane (CFC-11), and the global-warming potential is
     about 40 times lower.

         In water, 1,1,1-trichloroethane is slowly dehydrochlorinated to
     1,1-dichloroethene and hydrolysed to ethanoic acid, the former
     process being favoured by alkalinity.  1,1,1-Trichloroethane does not
     bind to soil particles and thus leaches readily into ground water.

         Biodegradation to 1,1-dichloroethane and chloroethane has been
     reported to occur under anaerobic conditions.

         1,1,1-Trichloroethane does not appear to bioaccumulate.

    4.1  Distribution and transport between media

         1,1,1-Trichloroethane enters the environment primarily via
    evaporation to the atmosphere, although some is discharged in
    industrial effluents.  McConnell et al. (1975) reported rapid transfer
    of 1,1,1-trichloroethane from water to air and concluded that,
    irrespective of whether 1,1,1-trichloroethane enters the environment
    via water or air, a wide distribution of the chemical is likely.

         Neely (1982) used the vapour pressure, water solubility, and
    relative molecular mass of 1,1,1-trichloroethane to assess its
    partitioning between major environmental compartments.  The
    partitioning pattern was estimated to be 99.92% in air, 0.08% in
    water, and zero in either benthic sediments or ground.  Torslov (1988)
    obtained similar results using a computer model based on the
    principles of the "fugacity" model of Mackay and predicted an
    environmental distribution of 99.29% in air, 0.7% in water, 0.01% in
    soil, sediment and aquatic biota, and zero in suspended aquatic

         In 1978 it was estimated that 97.3% of the 1,1,1-trichloroethane
    used in the USA was released to the environment.  Of this, 86% was
    released to the air, 1% to water, and about 10% was disposed of as
    waste (Fischer et al., 1982).  It was also estimated that only about
    6% of the 1,1,1-trichloroethane produced is emitted to the air or
    waste water during production, the remainder being released during
    use. The global-warming potential of 1,1,1-trichloroethane, an effect
    which results from its accumulation in the atmosphere, is about 40

    times lower than that of trichlorofluoromethane (CFC-11) and 14 times
    lower than that of carbon tetrachloride.

    4.1.1  Atmospheric transport

         Atmospheric transport is the major route by which
    1,1,1-trichloroethane is transported in the environment.  Hence, it
    has been measured in air at remote locations (see section 5.1.1) and
    in rainfall (see section 5.1.2).

         The ratio between concentrations of 1,1,1-trichloroethane in the
    northern and southern hemispheres is decreasing (Khalil & Rasmussen,
    1984).  Lower levels are found at mid latitudes during the summer
    because of greater removal by hydroxyl radicals (see section 4.2).

         In a study of a whole range of halocarbons, Edwards et al. (1982)
    estimated that, of the chlorine in the troposphere, 45% originated
    from industry and 55% from natural or non-industrial sources of methyl
    chloride.  Of the anthropogenic chlorine, 13% derived from the release
    of 1,1,1-trichloroethane.

         In the troposphere, 1,1,1-trichloroethane is predominantly
    degraded by oxidation, but some is rained out and some is transferred
    to the stratosphere.  Prior to 1977 the residence time in the
    troposphere was estimated to be 1 to 2  years (NRC, 1976), but the use
    of more reliable estimates of globally averaged levels has led to a
    calculated residence time of 5-7 years (Khalil & Rasmussen, 1984;
    Prinn et al., 1987; Midgley, 1989).

         1,1,1-Trichloroethane has a long enough atmospheric lifetime for
    a certain portion to reach the stratosphere.  In the early 1970s, it
    was calculated that approximately 12% of 1,1,1-trichloroethane
    reaching the troposphere would be transferred to the stratosphere. 
    Revised figures have calculated that nearer to 15% is transferred
    (McConnell & Schiff, 1978; Singh et al., 1982).

         In the stratosphere, 1,1,1-trichloroethane is degraded by
    photochemical processes, forming chlorine atoms and thence chlorine
    radicals that have the potential to deplete stratospheric ozone (see
    section 4.2.1).

    4.1.2  Transport in water

         In aquatic systems, volatilization is the major route for
    1,1,1-trichloroethane removal.  Oxidation and hydrolysis do not appear
    to play an important part in the aquatic fate of 1,1,1-trichloroethane
    (Dilling et al., 1975).  Dilling et al. (1975) found
    1,1,1-trichloroethane to be rapidly evaporated from water.  At 25 °C,
    90% evaporation occurred within 60-80 min from an aqueous solution
    containing 1 mg 1,1,1-trichloroethane/litre, the half-life being 20
    min.  The rate of disappearance was examined in the presence of

    various natural and added "contaminants", such as clays, limestone,
    peat, and other chemicals.  None of these contaminants affected the
    disappearance rate by more than a factor of 2.  It was concluded that
    no adsorption onto sediment or solids had taken place.

    4.1.3  Transport in soil

         The adsorption of 1,1,1-trichloroethane to soil is proportional
    to the organic carbon content of the soil (Urano, 1985).  It has a low
    adsorption to silt loam (Chiou et al., 1979).  These authors presented
    data which show that adsorption by soil organic matter occurs via a
    partitioning process rather than by physical adsorption.

         In a dissertation report, Drake (1987) studied the fate in
    aerobic unsaturated soils.  1,1,1-Trichloroethane was applied to
    columns containing sandy or sandy loam soils (organic carbon contents
    of 0.69% and 3.76%, respectively), and mass balances were carried out
    to determine the fate of the compound.  The processes studied were
    volatilization, transport, biodegradation, and sorption.  There was no
    indication of biodegradation, but volatilization appeared to play a
    major role in the mass balance.  Approximately 90% and 45% of the
    1,1,1-trichloroethane applied to the sandy and sandy loam soils,
    respectively, were estimated to be lost via volatilization. 
    Breakthrough of 1,1,1-trichloroethane was documented in both soils,
    and effluent levels of up to 10% of the 1 mg/litre influent level were
    observed after 25 days (Drake,1987).

    4.2 Degradation and transformation

    4.2.1  Abiotic degradation  In the atmosphere

         Using a concentration of 0.44 % (w/v) 1,1,1-trichloroethane in
    air in an enclosed flask exposed to external solar diurnal and
    climatic variations of incident radiation and temperature, Pearson &
    McConnell (1975) estimated the half-life to be 26 weeks.  This is
    similar to the values found for dichloromethane and chloroform, and is
    much slower than most other chlorohydrocarbons.  The authors also
    exposed 1,1,1-trichloroethane in the flasks to air in the presence of
    xenon arc radiation above 290 nm (which resembles sunlight) and
    monitored the degradation products.  They identified carbon dioxide,
    hydrochloric acid, and a trace amount of chlorine.  Traces of ozone,
    chlorine or nitrogen dioxide, gases that are known to occur in the
    atmosphere, were found to influence the product composition.  Thus, if
    a minor amount of chlorine was initially present during the
    photo-oxidation of 1,1,1-trichloroethane, then rather more chlorine
    was found at the end of the experiment.

         When 1,1,1-trichloroethane enters the troposphere, it is oxidized
    by reaction with the free hydroxyl radicals produced by the action of

    solar UV light to form trichloroacetaldehyde, which is further
    oxidized to  trichloroacetic acid.  The half-life for oxidation of
    1,1,1-trichloroethane has been estimated to range from 2 to 5.5 years,
    corresponding to residence times of 5 to 7 years (Yung et al., 1975;
    McConnell & Schiff, 1978; Pearson, 1982).  Slightly wider ranges of
    residence times have been recorded by other authors (Prinn et al.,
    1987; Fisher et al., 1990a), but the global average value generally
    used is around 6 years.  As suggested in section 4.1.1, calculations
    indicate that 15% of 1,1,1-trichloroethane is transported to the
    stratosphere.  There it is degraded by photochemical processes,
    induced by shorter wavelength higher energy solar radiation which does
    not occur at the tropospheric level, liberating chlorine atoms:

              CH3CCl3  ->  CH3CCl2 + ClÊ

    Free radical chlorine atoms (ClÊ) destroy ozone and are regenerated to
    repeat the process.

              ClÊ + O3  ->  ClOÊ + O2

              ClOÊ + OÊ  ->  ClÊ + O2

              ClOÊ + NO  ->  ClÊ + NO2

         The ozone-depleting effect of 1,1,1-trichloroethane is estimated
    to be 0.11 that of the chlorofluorocarbon CFC-11 (US EPA, 1980a; UNEP,
    1989).  In water

         Two parallel reactions result in the degradation of
    1,1,1-trichloroethane in water: (a) dehydrochlorination to
    hydrochloric acid and 1,1-dichloroethene; (b) hydrolysis to
    hydrochloric and ethanoic acids (see section 2.2.2) (Gerkens &
    Franklin,1989).  These reactions are influenced to a different degree
    by temperature and alkalinity (Pearson, 1982; CEFIC, 1986; Gerkens &
    Franklin, 1989).  Thus the calculated half-life at 10 °C in initially
    neutral demineralized water is 9.3 years and the observed half-life at
    20 °C is 1.7 years (Gerkens & Franklin, 1989).  The half-life of
    1,1,1-trichloroethane in water at varying temperatures is summarized
    in Table 4.  Pearson & McConnell (1975) determined a half-life of 39
    weeks at 10 °C in sea water at pH 8.  These authors stated that it is
    the dehydrochlorination reaction which is very pH dependent.  In
    artificial sea water containing salts at a concentration of
    33 g/litre, the degradation rate was identical to that in
    demineralized water.  At 25 °C, hydrolysis under neutral conditions
    was approximately 2.7 times faster than dehydrochlorination. 
    Half-lives at higher temperatures have been reported by Haag & Mill
    (1988) and Gerkens & Franklin (1989).

    Table 4.  Half-life of 1,1,1-trichloroethane in water at varying 

    Temperature (°C)       Half-life               Reference

          10               0.75 years        Pearson & McConnell (1975)
                           9.3 yearsb        Gerkens & Franklin (1989)

          20               1.7 years         Gerkens & Franklin (1989)
                           > 2.8 years       Vogel & McCarty (1987)

          25               0.5 years         Dilling et al. (1975)
                           0.8 years         Gerkens & Franklin (1989)
                           1 year            Haag & Mill (1988)

          40               24 days           Haag et al. (1986)
                           28 days           Gerkens & Franklin (1989)

          55               3.6 days          Gerkens & Franklin (1989)
                           4.1 days          Mabey et al. (1983)

          60               1.9 days          Walraevens et al. (1974)
                           1.9 days          Gerkens & Franklin (1989)
                           2.2 days          Haag et al. (1986)

          65               0.9 days          Walraevens et al. (1974)
                           1 day             Gerkens & Franklin (1989)

          80               2.8 h             Archer & Stevens (1977)
                           4.1 h             Gerkens & Franklin (1989)
                           5.1 h             Haag & Mill (1988)
                           5.3 h             Mabey et al. (1983)

    a  From: Gerkens & Franklin (1989)
    b  Extrapolation outside the temperature range investigated
         Since the chemical degradation rates are so slow, evaporation
    turns out to be the most important mechanism of loss from water
    (Dilling et al., 1975).  These authors found a chemical degradation
    half-life in water containing 8.3 ppm oxygen at 25 °C of 6.9 months in
    natural sunlight.  The same half-life was found in the dark, showing
    that photodegradation is negligible at the earth's surface.

    4.2.2  Biodegradation  Anaerobic

         In batch bacterial cultures, under methanogenic conditions at 
    35 °C in the dark, 1,1,1-trichloroethane at an initial concentration 
    of 100 µg/litre was almost completely degraded within 8 weeks, the 
    final concentration being 0.3 µg/litre.  No degradation occurred in the 
    sterile controls.  In a separate experiment, 1,1,1-trichloroethane 
    (160 µg/litre) was added to a continuous-flow methanogenic fixed-film 
    laboratory-scale column containing a bacterial inoculum.  As with the 
    batch experiment, 1,1,1-trichloroethane was almost completely degraded 
    within 10 weeks (Bouwer & McCarty, 1983a).  The degradation products of 
    1,1,1-trichloroethane were not identified. 

         In a study by Gossett (1985), 1,1,1-trichloroethane (initial
    concentration, 1.13 mg/litre) was degraded to 1,1-dichloroethane,
    without a lag phase, in a bath inoculated with activated sludge under
    methanogenic conditions.  All had been degraded within 6 days and 40%
    was degraded to 1,1-dichloroethane.  The fate of the other 60% is
    unknown; some leakage occurred but not enough to account for the rest
    of the loss.

         Bouwer & McCarty (1983b) found no degradation of
    1,1,1-trichloroethane, at an initial nominal concentration of 60
    µg/litre, after 8 weeks of incubation under anaerobic conditions in
    the presence of batch cultures of denitrifying bacteria.

         Klecka et al. (1990) reported that 1,1,1-trichloroethane was
    readily degraded in both methanogenic and sulfate-reducing microbial
    cultures and that there was no lag period before the onset of
    degradation.  Transformation products included 1,1-dichloroethane,
    chloroethane, and 1,1-dichloroethene.  The latter was shown to be the
    product of abiotic breakdown, since it also occurred in microbial
    cultures poisoned by mercuric chloride.

         Parsons & Lage (1985) found that 1,1,1-trichloroethane was
    biodegraded under anaerobic conditions in sediment.  All of the added
    1,1,1-trichloroethane (4-5 µg/ml) had disappeared within 4 to 5
    months, the major degradation product being 1,1-dichloroethane. 
    Parsons et al. (1985) reported that 16 weeks after the addition of
    1,1,1-trichloroethane at a concentration of 3.6 mg/litre, 880 µg/litre
    of dichloroethane had been formed.

         Wilson & White (1986) found no degradation of
    1,1,1-trichloroethane (added at a concentration of 765 µg/litre) in
    sand columns that were continuously supplied with propane for 21 days.

         Boyer et al. (1987) demonstrated microbial degradation of
    1,1,1-trichloroethane, added at a level of 5 or 20 mg/litre, in a
    packed bed (soil and activated carbon) laboratory reactor, which
    simulated an  in situ decontamination system.  The authors stated
    that biodegradation occurs under anaerobic conditions if a preferred
    substrate such as ethanol is present.  After 43 days, no
    1,1,1-trichloroethane was detectable in the reactor effluent 
    (< 20 µg/litre).  No chlorinated metabolic intermediates were 
    observed.  Aerobic

         Wilson et al. (1983) found no aerobic degradation of
    1,1,1-trichloroethane, at a concentration of 1 mg/litre, in soil
    samples collected from just above and below the groundwater table. 
    The samples were incubated in the dark for 9 or 27 weeks.

    4.3  Bioaccumulation

         A bioconcentration factor of 9, comparable to that of other
    chlorinated solvents, has been reported for the bluegill sunfish
    (Veith et al., 1980).  This is much lower than that predicted from the
    measured octanol/water partition coefficient of 2.47.  The same
    authors also measured the loss of 1,1,1-trichloroethane from the
    bluegill sunfish following exposure for 28 days to a mean water
    concentration of 73 µg/litre.  The half-life of 1,1,1-trichloroethane,
    as measured by the loss from the tissues of half the residue
    concentration attained at equilibrium, was found to be less than 24 h.



         As a consequence of release during its production and use,
     1,1,1-trichloroethane is found in water, soil, biota, and,
     especially, in air. The background levels of 1,1,1-trichloroethane in
     air have increased over recent decades, although the rate of increase
     seems to be declining.  Levels in industrial and urban areas tend to
     be higher than those in rural areas.

         For the general population, air is the major source of exposure. 
     In some cases, indoor air may contain higher levels than outdoor air. 
     Under normal conditions, food and drinking-water are minor sources.
     1,1,1-Trichloroethane has been found in breast milk.  The use and
     abuse of consumer products and cosmetics containing 1,1,1-
     trichloroethane as a solvent may lead to considerable exposure.

         Workers who use 1,1,1-trichloroethane, especially for degreasing
     or dry-cleaning operations, are particularly exposed to this solvent,
     although some exposure is likely in its manufacture.  In the
     workplace, air is the major source of exposure but dermal exposure
     may also occur.

    5.1  Environmental levels

    5.1.1  Air

         Rasmussen et al. (1981) monitored atmospheric concentrations of
    1,1,1-trichloroethane in the Antarctic and the north Pacific coastal
    region of the USA between 1975 and 1980.  They found that
    trichloroethane levels increased annually by over 20% during the
    period 1975-1978, then dropped below 10% during the period 1978-1980
    in the Antarctic and reaching 0.55 µg/m3 (102 ppt) by 1980.  In the
    Pacific north-west, a level of 0.84 µg/m3 (156 ppt) was reached by

         It has been estimated that the annual global increase in the rate
    of emission of trichloroethane was 17% between the years 1956 and 1973
    but only 8% per annum between 1975 and 1980 (Khalil & Rasmussen,
    1981).  This decline in turn resulted in a diminution of the
    differences in atmospheric levels between the northern and southern
    hemispheres (Khalil & Rasmussen, 1984).

         Grimsrud & Rasmussen (1975) measured mean 1,1,1-trichloroethane
    concentrations of 0.54 µg/m3 (100 ppt) in the atmosphere over the
    rural north-west of the USA (Washington State) between December 1974
    and February 1975, and Rasmussen & Khalil (1983) found 0.947 µg/m3
    (175 ppt) in the lower troposphere over the Arctic in 1982.  Average
    concentrations of 1,1,1-trichloroethane in air over Hokkaido, Japan,
    increased slightly between 1979 and 1988 and were of the order of

    0.54-0.65 µg/m3 (100-120 ppt) (personal communication by T. Tominaga
    & Y. Makiide to the IPCS, 1990).

         Pearson & McConnell (1975) analysed air samples from various
    locations in the United Kingdom.  The highest levels of
    1,1,1-trichloroethane, approximately 86 µg/m3 (16 ppb by mass), were
    found near an organochlorine manufacturing plant at Runcorn, Cheshire,
    and levels of 33.5-59.4 µg/m3 (6.2-11 ppb by mass) were found at
    Runcorn Heath.  In suburban areas of the cities of Liverpool and
    Manchester, the concentrations ranged from 0.54 to 32.4 µg/m3
    (< 0.1 to 6 ppb by mass).

         Levels of 1,1,1-trichloroethane in air are summarized in Table 5.

         Fischer et al. (1982) stated that, in relatively non-polluted
    areas, average concentrations of 1,1,1-trichloroethane could be
    assumed to be 0.54 µg/m3 (100 ppt) and in polluted areas levels of
    2.7-5.4 µg/m3 (500-1000 ppt) could be expected.  They also reported
    that near to large manufacturers or consumers concentrations could be
    as high as 540 µg/m3 (100 000 ppt).  Lillian et al. (1975) monitored
    air samples for 1,1,1-trichloroethane at various locations in the USA
    and found mean levels ranging from 0.52 µg/m3 (0.097 ppb) at a rural
    site in Wilmington, Ohio, to 8.6 µg/m3 (1.59 ppb) in an urban area
    of Bayonne, New Jersey.

         Air samples collected in the North Atlantic between 1982 and
    1985, in the region of the Westerlies and the North-East trade winds,
    contained 1.08 µg/m3 (200 ppt).  Above the trade winds (at 1800 m
    above sea level) a lower concentration of 0.84 µg/m3 (155 ppt) was
    found.  An equivalent concentration was found at sea level in the
    region of the intertropical convergence.  Baseline levels of
    1,1,1-trichloroethane in 1985 in the South Atlantic were about 0.76
    µg/m3 (140 ppt) (Class & Ballschmiter, 1986).  Rasmussen & Khalil
    (1982) calculated that average concentrations of 1,1,1-trichloroethane
    in 1978 were 0.632 µg/m3 (117 ppt) in the northern hemisphere and
    0.486 µg/m3 (90 ppt) in the southern hemisphere.

    Table 5.  1,1,1-Trichloroethane concentrations in air

    Type of        Locality                      Year             Concentration          Reference
    location                                                           (ppt)

    Industrial     Runcorn, UK                   1973             approx. 16 000         Pearson & McConnell (1975)
                   Bayonne, NJ, USA              1973                75-14 400           Lillian et al. (1975)

    Urban          Los Angeles, USA              1972                130-2300            Simmonds et al. (1974)
                   Liverpool-Manchester, UK      1973               < 100-6000           Pearson & McConnell (1975)
                   New York, USA                 1974                100-1600            Lillian et al. (1975)
                   Bochum, Germany               1978                18-1610a            Bauer (1981)
                   Lyon, France                                     < 840-2010           Correia et al. (1977)
                   Denver, USA                   1980                171-2699            Singh et al. (1982)
                   Various sites, Japan        1982-1985              20-340             Magara & Furnichi (1986)

    Rural          California, USA               1972                  10-50             Simmonds et al. (1974)
                   Various sites, UK             1973                1000-4000           Pearson & McConnell (1975)
                   Various sites, USA            1974                 30-350             Lillian et al. (1975)
                   Hengelo, Netherlands                                20-50             Correia et al. (1977)
                   Oregon, USA                 1975-1985     121 (1975) - 158 (1985)b    Prinn et al. (1987)

                   Tasmania, Australia         1978-1985      66 (1978) - 116 (1985)b    Prinn et al. (1987)
                   Hokkaido, Japan             1979-1980              100-120            Personal communication by
                                                                                         T. Tominaga & Y.
                                                                                         Makiide to the IPCS (1990)

    Oceanic        Hawaii, Pacific             1980-1982      111 (1980) - 125 (1982)    Khalil & Rasmussen (1984)
                   Samoa, Pacific              1978-1982      75 (1978) - 104 (1982)     Khalil & Rasmussen (1984)
                   Various sites, Atlantic       1982                132-214c            Class & Ballschmiter (1986)
                   Barbados, Atlantic          1978-1985      93 (1978) - 144 (1985)     Prinn et al. (1987)

    Table 5 (contd).

    Type of        Locality                      Year             Concentration          Reference
    location                                                           (ppt)

    Polar          Near Barrow, Arctic         1979-1982      117 (1979) - 143 (1982)    Khalil & Rasmussen (1984)
                   South Pole, Antarctic       1975-1980      45 (1975) - 102 (1980)     Khalil & Rasmussen (1984)

    a   The concentrations varied with wind direction and increased in the afternoon.
    b   These are minimum and maximum monthly mean mixing ratios and differ slightly from the original data
        published by Khalil & Rasmussen (1984).
    c   Northern hemisphere levels were consistently higher than southern hemisphere values.

    5.1.2  Water

         1,1,1-Trichloroethane has been reported to occur in ground water
    in many countries.  Background levels tend to be low, but high levels
    of contamination are possible as a result of industrial activity and
    waste disposal.

         Levels of 1,1,1-trichloroethane in water are summarized in 
    Table 6.

         Relatively high levels observed in rain water at Runcorn, United
    Kingdom (Pearson & McConnell, 1975), in the river Rhine, Germany
    (Fischer et al., 1982), in a canal in Modena, Italy (Aggazzotti &
    Predieri, 1986), in rivers that flow through industrial or large
    cities in Japan (Goto, 1979), in the inshore waters of Liverpool bay,
    United Kingdom (Correira et al., 1977), in ground water in Birmingham,
    United Kingdom (Rivett et al., 1990), and in Maryland, USA (Dever,
    1986) all appear to be derived from nearby industrial activities where
    1,1,1-trichloroethane is either manufactured or used.

         Background levels in snow (Pearson, 1982) and in the open ocean
    (Pearson, 1982; Fischer et al., 1982) are usually very low, although
    levels up to 0.97 µg/m3 (0.18 ppb) have been found by Fischer et al.
    (1982) in the eastern Atlantic ocean.

    5.1.3  Sediment and soil

         Gossett et al. (1983) found 1,1,1-trichloroethane levels of
    < 0.5 µg/kg (dry weight) in marine sediment collected from the
    vicinity of a Los Angeles waste water treatment plant, the effluent
    from which contained 31 µg/litre.

         Fischer et al. (1982) analysed soil samples from an industrial
    area of West Germany and found that 1,1,1-trichloroethane
    concentrations in soil interstitial water and soil particles were near
    to or less than the detection limits (0.1 µg/litre and 0.1 µg/kg,
    respectively).  Samples of soil air contained 1,1,1-trichloroethane
    levels ranging from 0.2 to 10 µg/m3.  In the same study, soil air
    samples from over 1000 bore holes in various locations were analysed. 
    1,1,1-Trichloroethane concentrations ranged from 1 µg/m3 in a rural
    area to over 2.2 µg/m3 in agricultural and forest soils near
    industrial sources and to 9 µg/m3 in urban areas.

         Pearson & McConnell (1975) measured a combined concentration of
    1,1,1-trichloroethane and carbon tetrachloride in sediments of
    Liverpool Bay, United Kingdom, of 5.5 µg/kg (5.5 ppb).

        Table 6.  1,1,1-Trichloroethane levels in water

    Type of water     Locality                Characteristics              Year       Concentration              Reference

    Rain water        Runcorn, UK             near manufacturing site                 0.09                       Pearson & McConnell
                      Japan                   urban                        1975       none detected              Goto (1979)
                      Various sites           rain                                    0.005-0.09                 Pearson (1982)
                      Various sites           snow                                    0.001-0.03                 Pearson (1982)

    Rivers & canals   Rhine, Germany          river                                   0.01-3300                  Fischer et al. (1982)
                      Netherlands             canals                     1972-1976    0.07-0.3 w/w               Correia et al. (1977)
                      R. Durance, France      river                      1972-1976    none detected              Correia et al. (1977)
                      Modena, Italy           canal                                   10-40                      Aggazzotti & Predieri
                      Japan                   river, industrial            1975       approx. = 5.1              Goto (1979)
                      Japan                   river, large city            1975       approx. = 2.5             Goto (1979)
                      Japan                   river, smaller cities        1975       approx. = 0.1-0.81         Goto (1979)

    Sea               Not defined             inshore waters                          0.15                       Pearson (1982)
                      Liverpool Bay, UK       inshore water              1972-1976    < 0.25-3.3                 Correia et al. (1977)
                      East Atlantic           open ocean                              0.05-0.18                  Fischer et al. (1982)
                      "Typical sites"         open ocean                              0.01-0.03                  Pearson (1982);
                                                                                                                 Fischer et al. (1982)

    Wells & ground
    waters in

                      Zurich, Switzerland     ground water                 1977       0.02-2.8                   Giger et al. (1978)
                      Japan                   urban, shallow               1982       0.2-1600                   Magara & Furuichi
                                              urban, deep                  1982       0.2-70

    Table 6 (contd).

    Type of water     Locality                Characteristics              Year       Concentration              Reference

    Wells & ground
    waters in

                      Emilia-Romagna, Italy   "ground water"                          < 1                        Aggazzotti & Predieri
                      Various sites           underground water                       0.2 (typical), 5 (high)    Pearson (1982)
                      Various sites, UK                                    1983       0.48 (average)             Kenrick (1983)
                      Birmingham, UK          industrial, ground water   1986-1988    > 0.2-780 (46% of sample)  Rivett et al. (1990)
                      Maryland, USA           near electronic plant                   up to 1600                 Dever (1986)


                      Emilia-Romagna, Italy   chlorinated water                       0.1-0.5                    Aggazzotti & Predieri

    5.1.4  Biota

         Table 7 gives the ranges of 1,1,1-trichloroethane concentrations
    found in various marine biota collected in United Kingdom estuaries
    (Liverpool Bay, Firth of Forth, and Thames Estuary) by Pearson (1982)
    and Pearson & McConnell (1975).

         Dickson & Riley (1976) analysed various fish species and a
    mollusc species from Port Erin, Isle of Man, United Kingdom, and found
    trichloroethane (isomer not stated) concentrations of 2 and 9 µg/kg
    dry weight, respectively, in gill and brain tissue of the eel  Conger
     conger.  Analysis of cod  (Gadus morhua) revealed trichloroethane
    levels ranging from 5 µg/kg in muscle and liver tissue to 16 µg/kg in
    brain tissue.  Muscle tissue of coalfish  (Pollachius birens)
    contained 6 µg/kg, and a level of 4 µg/kg was found in the digestive
    tissue of the mollusc  Modiolus modiolus.

         Gossett et al. (1983) collected various marine biota from the
    vicinity of the Los Angeles County, USA, waste water treatment plant. 
    1,1,1-Trichloroethane concentrations of 4 µg/kg wet weight were found
    in whole invertebrate samples and < 0.3 µg/kg wet weight in shrimp
    muscle.  Levels ranged from < 0.3 to 7 µg/kg wet weight in the liver
    of various fish species.

    5.2  General population exposure

    5.2.1  Food

         A study of the average daily intake of trichloroethane in Germany
    showed that 10%, i.e. 3.6 µg/day, originated from foodstuffs (Duszeln
    et al., 1982).  Uhler & Diachenko (1987) found levels of
    1,1,1-trichloroethane in nine foodstuffs (mainly cheeses and ice
    cream), sampled in the USA, at levels of between 1 and 37 µg/kg. 
    These levels were thought to arise from contamination either by air
    contact with fugitive emission of cleaning solvent or by contact with
    packaging materials containing 1,1,1-trichloroethane.

    Table 7.  Concentration of 1,1,1-trichloroethane in various marine

         Organism                   Concentration (µg/kg)
         Plankton                         0.03-10.7
         Marine algae                       10-25
         Molluscs                         0.05-10
         Crustaceans                       0.7-34
         Fish, flesh                       0.7-5
         Fish, liver                         1-15
         Sea-birds, eggs                     3-30
         Sea-birds, liver                    1-4
         Seal, liver                       0.2-4
         Seal, blubber                       8-24

    a  From: Pearson (1982)

         Entz & Diachenko (1988) surveyed 52 margarines and spread
    products from supermarkets in the Washington, D.C. metropolitan area
    between 1980 and 1982 and a further 18 products in 1984.  In addition,
    19 margarines were examined at manufacturing plants in 1982.  The
    following levels were found:

                              Number of store     Number of manufacturing
                              shelf samples       plant samples 

         Not detecteda              11                    1
         Trace levelsa              12                    1
         < 50 µg/kg                 35                   15
         50-100 µg/kg                7                    2
         > 100-500 µg/kg             5                    -


    a  Trace levels of 1,1,1-trichloroethane represented < 5 µg/kg; the
         detection limit was  about a third of the trace level.

         Miller & Uhler (1988) similarly studied 46 butter samples and
    reported levels of from 10 µg/kg to more than 100 µg/kg.  In one
    sample containing 7500 µg/kg, the source was traced to a packing

         Pfannhauser et al. (1988) found that levels of
    1,1,1-trichloroethane were mostly below 10 µg/kg in samples of
    Austrian olive oil, cheese, and chocolate; only one sample of olive
    oil contained over 100 µg/kg.  The authors suggested that cleaning

    solvents in production areas and packaging materials were possible
    sources for the contamination.

         Pellizari et al. (1982) analysed breast milk for
    1,1,1-trichloroethane in four urban areas of Pennsylvania, New Jersey,
    and Los Angeles, USA.  They sampled up to 12 women at each site, and
    eight samples out of 42 were analysed manually by experienced
    spectroscopists.  1,1,1-Trichloroethane was identified in all of the
    samples, but no actual levels were reported.  Travis et al. (1988)
    also suggested contamination of human breast milk based on
    pharmacokinetic modelling.

          Table 8 summarizes data on the concentrations of
    1,1,1-trichloroethane reported in foods.

    5.2.2  Drinking-water

         An investigation of drinking-water from 100 cities in Germany
    showed a range of trichloroethane concentrations from < 0.1 to 1.7
    µg/litre (Bauer, 1981).

         A study of the daily average intake of trichloroethane in Germany
    revealed that 0.6%, i.e. 0.2 µg/day, of the intake came from
    drinking-water.  These calculations were based on a daily intake of 1
    litre of drinking-water containing 0.2 µg trichloroethane/litre of
    water (Düszeln et al., 1982).

         In the USA, 23 wells out of 1611 tested contained
    1,1,1-trichloroethane.  Another investigation in the USA showed
    detectable concentrations in 835 of 1071 samples, with a maximum value
    of 607.8 µg/litre and a 90th percentile of 6.1 µg/litre (Fischer et
    al., 1982).

         Pearson (1982) reported a value of 0.1 µg/litre as a typical
    level of 1,1,1-trichloroethane in drinking-water.  Fielding et al.
    (1981) surveyed 14 drinking-water sources in the United Kingdom over
    a period of 9 months in 1976.  1,1,1-Trichloroethane was found at 3
    out of 14 sites and, although no actual levels were reported, it was
    implied that concentrations were less than or equal to 1 µg/litre.

         Dever (1986) reported levels of 1,1,1-trichloroethane in a
    contaminated water supply in Montgomery County, Maryland, USA.  Both
    raw and treated potable water samples were analysed, and
    1,1,1-trichloroethane levels of 180 µg/litre and 30 µg/litre,
    respectively, were found.

    Table 8.  Concentrations of 1,1,1-trichloroethane (µg/kg) in various foodstuffsa

    Foodstuff                 Mean content     Range             Reference                 
    Dairy products                             0.1-10            Pearson (1982)
                                                0-0.6            Bauer (1981)

    Meat                                         3-6             McConnell et al. (1975)
                                                                 Pearson (1982)

    Vegetable oils                             0.5-10            Pearson (1982)
                                             < 1 - > 100         Pfannhauser et al. (1988)

    Margarine                     45         n.d. - 500          Entz et al. (1982)
                                                                 Entz & Diachenko (1988)

    Butter                        16           10-7500           Entz et al. (1982)
                                                                 Miller & Uhler (1988)

    Ice cream                      2                             Entz et al. (1982)

    Cheese                                       7-9             Entz et al. (1982)
                                              < 1 - 100          Pfannhauser et al. (1988)

    Bread                          2                             McConnell et al. (1975)
                                                                 Pearson (1982)

    Potatoes                                     1-4             McConnell et al. (1975)

    Fruit and vegetables                         2-3             McConnell et al. (1975)
                                                                 Pearson (1982)

    Fish flesh                                  0.7-5            McConnell et al. (1975)
                                                                 Pearson (1982)

    Table 8 (contd).


    Foodstuff                 Mean content     Range             Reference

    Fish (cod) liver,
     muscle, stomach                            5-7b             Dickson & Riley (1976)

    Tea (packet)                   7                             McConnell et al. (1975)

    Rolled oats                  770c                            Daft (1988)

    Popcorn                        5                             Daft (1988)

    Pinto beans                    5                             Daft (1988)

    Chocolate products                        < 1 - 100          Pfannhauser et al. (1988)

    Fatty foods                                <1 - 10           Pfannhauser et al. (1988)


    a  Fresh (wet) weight, unless specified otherwise; n.d. = not detected
    b  Dry weight
    c  Possibly from fumigant contamination

         Wallace et al. (1987) measured low levels of
    1,1,1-trichloroethane in drinking-water collected in 3 states in the
    USA during 1981/1982.  The average levels in New Jersey were 0.2-0.6
    ng/litre (maximum levels were 1.6-5.3 ng/litre), and in North Carolina
    and North Dakota they were lower still, i.e. 0.03 ng/litre and 0.04
    ng/litre, respectively.

         An environmental monitoring study carried out near
    1,1,1-trichloroethane production plants and user facilities in
    1976/1977 yielded the following 1,1,1-trichloroethane levels in hotel
    tap water (US EPA, 1977):

         Freeport, Texas (industrial area): 17 µg/litre; Lake Charles,
    Louisiana (industrial area): 0.3 µg/litre; Helena, Arkansas (rural
    area): 0.4 µg/litre.

         Concentrations of 1,1,1-trichloroethane in Japanese tap water
    (Osaka City) were reported to range from 0.078 to 0.212 µg/litre
    (Kajino & Yagi, 1980).

    5.2.3  Air

         In relatively non-polluted areas, the average concentration of
    1,1,1-trichloroethane in air can be assumed to be around 540 ng/m3
    (100 ppt), increasing to 2700-5400 ng/m3 (500-1000 ppt) in
    industrialized areas (Bouwer & McCarty, 1983a,b).  In Germany, the
    average air concentration was found to be about 2 µg/m3 (Düszeln &
    Thiemann, 1985).

         In a monitoring study conducted in 1981 on 350 residents of New
    Jersey, USA, Wallace et al. (1986) found median indoor air
    concentrations of 17 µg/m3 both at night and during the day. 
    Concentration ranged from 0.16 to 333 000 µg/m3.  The median outdoor
    air level was 4.5 µg/m3, the range being 0.05 to 470 µg/m3. 
    Analyses conducted on the breath of these individuals showed median
    levels of 6.6 µg/m3 (ranging from 0.06 to 520 µg/m3).

         A study of the average daily intake of trichloroethane in Germany
    estimated that 89%, i.e. 32 µg of the daily intake of 35.8 µg, came
    from the air.  This calculation was based on a daily inhalation of 20
    m3 air containing 1.6 µg trichloroethane/m3 (300 ppt) (Düszeln et
    al., 1982).

         In Japan, 15 sites of Yokohama City and Kawasaki City were
    sampled from July 1985 to July 1986.  Mean (of 5) concentrations of
    14.6, 12.4, and 8.6 µg/m3 were measured in industrial, commercial,
    and residential areas, respectively (Urano et al., 1988).  The
    calculated average intake (µg/day) by inhalation in each area was 135,
    114, and 81, respectively.

         It can be concluded that, in general, inhalation is the most
    important source of human exposure to trichloroethane.

    5.2.4  Consumer products and cosmetics

         Trichloroethane is used as a solvent in aerosol and non-aerosol
    consumer products, and the concentration may be anywhere in the range
    10-100% (IARC, 1979).  In aerosol cans for cosmetics, a concentration
    of up to 35% is allowed in countries of the Economic European
    Community (EEC).  Consumer use and abuse of such products may lead to
    considerable exposure to trichloroethane, which can be much higher
    than from other sources.

         In a study by Otson et al. (1984), two fabric protectors (450 g
    of each) containing 75% and 97% 1,1,1-trichloroethane, respectively,
    were sprayed onto a sofa in a room with a volume of 28 m3.  Initial
    concentrations were as high as 1800 mg/m3.  Concentrations dropped
    rapidly to less than 150 mg/m3 when the room was ventilated, but
    under unventilated conditions they remained above 1000 mg/m3 for at
    least one hour and dropped below 500 mg/m3 only after more than 2 h.

    5.3  Occupational exposure

         In general, exposure levels of trichloroethane at the workplace
    are much lower than established limit values for workplace air.  The
    8-h time-weighted average (TWA) concentrations measured in the United
    Kingdom in vapour-degreasing baths were typically 10.8-270 mg/m3
    (2-50 ppm) (HSE, 1990).

         In addition to workers engaged in the manufacturing and
    production of trichloroethane and trichloroethane-containing products,
    the workers most likely to be exposed to trichloroethane are those
    engaged in dry-cleaning or degreasing processes in the metallic and
    electronic industries.  It was estimated that about 2.23 million
    workers were potentially exposed to trichloroethane in the USA (NIOSH
    Survey, 1983).

         During the period 1983 to 1986, the Danish Labour Inspection
    Service made 476 measurements of trichloroethane at workplaces in
    Denmark (AMI, 1988).  In 6% of the samples the levels were found to
    exceed the Occupational Limit Value of 540 mg/m3 (100 ppm).



         1,1,1-Trichloroethane is rapidly absorbed through the lungs. 
     Absorption through the gastrointestinal tract and skin also occurs,
     but is of less importance than the inhalation route.  In humans, the
     absorption from the lungs is about 25 to 40% of the inhaled dose over
     6 to 8 h.  1,1,1-Trichloroethane is distributed widely to body
     tissues, especially to those with a high lipid content, e.g., brain
     and adipose tissue.  It crosses the blood-brain and placental
     barriers.  Less than 7% of an absorbed dose is metabolized. 
     Metabolism appears to be saturable.  Excretion by exhalation of
     unchanged compound accounts for > 90% of the absorbed dose.  Less
     than 1% of 1,1,1-trichloro-ethane remains in the human body after 9

    6.1  Absorption

         1,1,1-Trichloroethane is rapidly absorbed through the lungs and
    the gastrointestinal tract.  Absorption through skin also occurs, but
    is of minor importance compared to uptake via inhalation.

    6.1.1  Animal studies  Inhalation

         The absorption in the lungs of rats exposed to 270 or 2700 mg
    1,1,1-trichloroethane/m3 (50 or 500 ppm) has been shown to be
    time-dependent.  The initial uptake was more than 80% of the dose. 
    During the first hour the absorption decreased to around 50%, the
    decrease being greater in the high-dose group (Dallas et al., 1989). 
    Because 1,1,1-trichloroethane is poorly metabolized (see section 6.3),
    absorption is expected to be low as steady state is approached.

         In dogs exposed to 4.05, 8.1 or 10.8 g/m3 (750, 1500 or 2000
    ppm) for one hour by inhalation, the cumulative uptake was 27, 45, and
    71 mg/kg, respectively.  This represented about 14% of inhaled
    amounts.  Concentrations in arterial and venous blood did not attain
    a steady state during this period (Hobara et al., 1982).  Oral absorption

         Oral toxicity data (see section 7.1, Table 10) suggest that
    1,1,1-trichloroethane is readily taken up from the gastrointestinal
    tract (Reitz et al., 1988).  Skin absorption

         The percutaneous penetration of 1,1,1-trichloroethane was studied
    in guinea-pigs by applying the solvent in a skin depot (a glass ring

    attached to the skin and covered with glass).  Absorption  was found
    to be rapid and to result in blood levels of 1.9 mg/litre during the
    first 30 min.  These levels were higher than those found for carbon
    tetrachloride and perchloroethylene (1.1 mg/litre in both cases) in
    the same study (Jakobson et al., 1980, 1982).  HSE (1984) calculated
    a rate of absorption through the skin of 6 µg/min per cm2 from this

         Compared to methylene dichloride, chloroform, carbon
    tetrachloride, and 1,1,2-trichloroethane, the skin penetration of
    1,1,1-trichloroethane in mice was found to be lower.  The penetration
    rate of these solvents increased with the degree of water solubility
    (Tsuruta, 1975).

    6.1.2  Human studies

         The absorption of trichloroethane in humans has been studied
    following exposure by inhalation and by skin contact.  No studies have
    so far been carried out using the oral route, but reports of
    intoxication following oral ingestion indicate that the chemical can
    be absorbed by this route (Stewart & Andrews, 1966, 1971).  Inhalation 

         The absorption of 1,1,1-trichloroethane in the lungs is lower
    than that of most other chlorinated solvents.  This is due to the
    relatively low blood/air partition coefficient of 3.3 (US EPA, 1984).

         Studies with human volunteers (males), exposed by inhalation to
    1,1,1-trichloroethane at concentrations from around 200 mg/m3 (35
    ppm) to 2000 mg/m3 (350 ppm) for 6-8 h, showed that about 25-40% of
    the trichloroethane inhaled was absorbed by the lungs, depending on
    its concentration in the inhaled air, duration of exposure, body
    weight and amount of adipose tissue, blood circulation, and other
    factors (Astrand et al., 1973; Humbert & Fernandez 1977; Monster et
    al., 1979; Nolan et al., 1984).  The amount absorbed increased with
    increasing work-load, due presumably to an increase in breathing rate
    (Monster et al., 1979).  Skin contact

         Percutaneous absorption of 1,1,1-trichloroethane has been
    measured in human subjects.  Following the immersion for a few minutes
    of a thumb or a hand in liquid 1,1,1-trichloroethane, it is possible
    to detect the solvent in the breath (Stewart & Dodd, 1964).

         The absorption of trichloroethane through the skin is slower than
    for aromatic solvents and perchloroethylene, and is, in general,
    considered of minor importance compared to the more rapid uptake via
    the lungs (Humbert & Fernandez, 1977).  Dermal application to human
    volunteers of 15 ml 1,1,1-trichloroethane under occlusion resulted in

    16.2-27 mg/m3 (3-5 ppm) of the solvent in the exhaled air.  This
    corresponded to a 2-h inhalation exposure of 54-108 mg/m3 (10-20
    ppm) (Nakaaki et al., 1980).

         Trichloroethane vapour can also be absorbed through the intact
    skin, but the amount absorbed in the body has been estimated to be a
    thousand times less than the amount absorbed by inhalation (Riihimaki
    & Pfaffli, 1978).

    6.2  Distribution and retention

         Compared with many other chlorinated hydrocarbon solvents,
    1,1,1-trichloroethane has a high lipid/blood partition coefficient
    (108 at 37 °C).  It would therefore be expected to distribute widely
    into body tissues, especially into those, such as brain and adipose
    tissue, with high lipid content (US EPA, 1984; CEC, 1986).

         Blood and exhaled breath concentrations of 1,1,1-trichloroethane
    in rats increased rapidly after inhalation exposure, approaching, but
    not reaching, steady state after a 2-h exposure (Dallas et al., 1989).

    6.2.1  Animal studies

         When rats were exposed to 2700 mg/m3 (500 ppm) (6 h per day for
    4 days), only trace amounts of 1,1,1-trichloroethane could be detected
    in the liver, brain, and blood 17 h after the end of the exposure
    period.  A higher concentration remained in adipose tissue, but this
    represented only about 5% of the concentration immediately after
    exposure (Savolainen et al., 1977). These data indicate that
    1,1,1-trichloroethane does not accumulate in the tissues.  This is
    supported by the observation that no significant tissue accumulation
    occurred in rats exposed to 8100 mg/m3 (1500 ppm), 6 h per day, 5
    days per week, for 16 months (Schumann et al., 1982).

         In a study by Danielsson et al. (1986), pregnant mice were
    exposed to 14C-labelled 1,1,1-trichloroethane by inhalation for 10
    min on days 11, 14 or 17 of gestation.  Radioactivity was detected in
    the brain, lungs, liver, and kidney of the maternal mouse immediately
    after exposure, the concentrations being approximately the same in all
    tissues.  The fetal and placental uptake was measured at all stages of
    gestation studied.  Although the fetal uptake was low compared with
    uptake to the maternal brain, the authors stated that
    1,1,1-trichloroethane passes as easily through the placental barrier
    as through the blood-brain barrier.  After exposure,
    1,1,1-trichloroethane disappeared from both maternal and fetal bodies
    within 24 h.  A small amount of non-volatile radioactivity was present
    in both the mother and fetus.

         Concentrations of 1,1,1-trichloroethane in exhaled air from dogs
    exposed to 3780, 8100 or 10 800 mg/m3 (700, 1500 or 2000 ppm)
    increased rapidly for one hour, approaching steady-state levels at 80

    to 90% of inhaled air concentrations.  After one hour's recovery, 66
    to 71% of the total uptake had been excreted through the lungs (Hobara
    et al., 1982).

    6.2.2  Human studies

         In a fatal case of 1,1,1-trichloroethane intoxication, residues
    of the solvent were determined in the bile, blood, brain, kidney,
    liver, and lung.  The concentration was highest in the brain, followed
    by the kidney (Caplan et al., 1976).  This indicates that
    1,1,1-trichloroethane can also cross the blood-brain barrier in

         Samples of kidney, lung, and muscle tissues taken from hospital
    patients in Finland contained small amounts of 1,1,1-trichloroethane
    (0.1 to 0.4 µg/kg) (Kroneld, 1989).  In human samples from the German
    Ruhr district, levels of 1.8 to 5.6 µg/kg (fresh weight) were found in
    the same tissues.  In addition, 2.1 µg/kg was found in fat tissue and
    1.9 µg/kg in liver tissue (Bauer, 1981).

    6.3  Metabolic transformation

         1,1,1-Trichloroethane is a fairly stable molecule, which is
    metabolized in mammals to a lesser degree than other trichlorinated
    solvents (Ikeda & Ohtsuji, 1972).  As shown in Fig. 1, the principal
    metabolites are 2,2,2-trichloroethanol and trichloroacetic acid
    (Humbert & Fernandez, 1977).  These metabolites are formed in the
    liver by microsomal oxidases (cytochrome P-450) (Ivanetich & Honert,
    1981; US EPA, 1984).  Trichloroethanol is conjugated with glucuronic
    acid before excretion in the urine.

    6.3.1  Animal studies

         In an early study in rats, less than 3% of a single
    intraperitoneal injected dose of about 700 mg 1,1,1-trichloroethane/kg
    body weight was metabolized within 25 h; the rest was expired
    unchanged.  The metabolites identified, accounting for 1.6% of the
    dose, were the glucuronide of 2,2,2-trichloroethanol in the urine
    (53%) and 14CO2 in the expired air (30%) (Hake et al., 1960).

         When 1,1,1-trichloroethane (143 mg/kg) was administered in the
    drinking-water to rats over an 8-h period, the percentage of the dose
    recovered as metabolites within 56 h was 6%, of which 37% was excreted
    in the urine and 37% as 14CO2 in the expired air (Reitz et al.,
    1988).  Following repeated administration by gavage for 4 weeks, the
    percentage of the administered dose recovered as metabolites in male
    rats within 48 h was 4.2%.  Under similar experimental conditions in
    mice, 6.1% of the administrated dose was recovered as metabolites
    (Mitoma et al., 1985).  A single inhalation exposure for 4 h at a
    concentration of 1188 or 2376 mg/m3 (220 or 440 ppm) resulted in,
    respectively, urine metabolite concentrations of 0.58 and 0.97 mg/kg

    FIGURE 1

    body weight.  Both trichloroethanol and trichloroacetic acid were
    identified as metabolites in the urine, trichloroethanol being
    excreted (as the glucuronide) much faster than trichloroacetic acid
    (Eben & Kimberle 1974).

         Following a single inhalation exposure of rats to 810 and 
    8100 mg/m3 (150 and 1500 ppm), only a 2-4 times increase in excreted
    metabolites was found between the two doses, suggesting metabolic
    saturation.  Repeated exposure to 8100 mg/m3 over 16 months did not
    change the amount of 1,1,1-trichloroethane metabolites.  Similar
    results were obtained in mice.  In both rats and mice, urine
    metabolites accounted for 40-70% of the total amount metabolized. 
    Overall, mice were found to biotransform approximately 5 times more
    1,1,1-trichloroethane (per kg body weight) than rats.  In rats and
    mice an age-related increase in the amount metabolized was observed in
    aged animals as opposed to young adults (Schumann et al., 1982).

    6.3.2  Human studies

         The average amount of metabolites excreted in the urine of humans
    (workers or volunteers) exposed to 1,1,1-trichloroethane in the air
    (22-1890 mg/m3, 4-350 ppm) was variable, but was typically between
    3 and 7% of the absorbed dose.  The ratio of the metabolites
    trichloroethanol glucuronide and trichloroacetic acid was about 2 to
    1, but this increased with increasing exposure concentration (Seki et
    al., 1975; Humbert & Fernandez, 1977; Monster et al., 1979; Nolan et
    al., 1984).

    6.3.3  Metabolic interactions

         Simultaneous exposure to other solvents tends to increase the
    retention and decrease the metabolism of 1,1,1-trichloroethane
    (Savolainen et al., 1981).  1,1,1-Trichloroethane metabolism was
    accelerated in rats pre-treated with ethanol because of the induction
    of metabolic enzymes (Sato et al., 1980).

    6.4  Elimination

         Regardless of the route of administration, the main excretory
    route for 1,1,1-trichloroethane is exhalation via the lungs.  This may
    be explained by the relatively low solubility in blood.

    6.4.1  Animal studies

         In rats and mice, 55% to 98% of the 1,1,1-trichloroethane was
    excreted unchanged in expired air after oral or intraperitoneal
    exposure (Hake et al., 1960; Reitz et al., 1988).

         Following inhalation exposure, 94-98% of the absorbed
    1,1,1-trichloroethane was excreted unchanged in the expired air of
    rats during 72 h.  In mice, the corresponding figure was 87-97%.  The

    rate of elimination was somewhat higher in mice; 85% was eliminated
    during the first 3 h compared to 65% in rats (Schumann et al., 1982).

         A total of about 1-8% of an absorbed dose in rodents is excreted
    in the urine (Hake et al., 1960; Schumann et al., 1982).

         After exposure to 1,1,1-trichloroethane vapour, the level in
    blood plasma decreases rapidly in a diphasic or triphasic manner,
    depending on the exposure level.  Following exposure to 810 mg/m3
    (150 ppm), the half-lives were 10 and 139 min, whereas with 8100
    mg/m3 (1500 ppm), the half-lives were 36 and 238 min.  In mice the
    half-lives were a little shorter (Schumann et al., 1982).

    6.4.2  Human studies

         Studies with human volunteers show that over 90% of the absorbed
    trichloroethane is excreted unchanged in the expired air.  Only minor
    parts (5-7%) of the absorbed solvent are excreted in the urine (as
    trichloroethanol glucuronide and trichloroacetic acid) (Stewart et
    al., 1969; Humbert & Fernadez, 1977; Nolan et al., 1984).  The main
    product was found to be 2,2,2-trichloroethanol glucuronide, the
    excretion of which was completed within 8 days.  The secondary product
    was trichloroacetic acid; its excretion occurred somewhat later and
    was completed within 12 days (Humbert & Fernandez, 1977).

         The elimination of 1,1,1-trichloroethane, measured as plasma
    concentration and concentration in expired air, in six human
    volunteers exposed to 191 or 1911 mg/m3 (35 or 350 ppm) for 6 h
    could be described by a three-compartment model with estimated
    half-lives of 44 min, 5.7 h, and 53 h, respectively.  Less than 1%
    remained in the body after 9 days (Nolan et al., 1984).

         In a study by Nolan et al. (1984), the trichloroethane
    concentrations in blood and expired air were proportional to the
    exposure concentration after 6 h of exposure and indicated that about
    25% of the 1,1,1-trichloroethane inhaled during the exposure was

    6.5  Biological monitoring

         Several options exist for the biological monitoring of exposure
    to 1,1,1-trichloroethane (Monster 1986).  These include the
    determination of:

    Ê    the unchanged solvent in blood or alveolar air;

    Ê    the metabolite trichloroethanol in blood, alveolar air or urine;

    Ê    the metabolite trichloroacetic acid in blood and urine.

         Table 9 indicates the mean concentrations of these parameters as
    a result of exposure of subjects for 8 h/day (5 days/week) to a
    time-weighted average (TWA) concentration of 270 mg/m3 (50 ppm)
    (Monster, 1986).

    Table 9.  Mean concentrations of 1,1,1-trichloroethane,
              trichloroethanol, and trichloroacetic acid in blood,
              alveolar air, and urinea

                                                 Time after exposure of sampling
    Test                            End of       5-15 min       16 h         64 h

    Blood (mg/litre)
     1,1,1-trichloroethane                          0.9                      0.07
     trichloroethanol                              0.16                        -
     trichloroacetic acid              2.3                       1.6

    Alveolar air (mg/m3)
     1,1,1-trichloroethaneb                      210 (39)     13 (2.4)      8 (1.5)
     trichloroethanol                              0.014        0.007          -

    Urine (mg/g creatinine)
     trichloroacetic acid              4.9                       2.5          0.9
     trichloroethanol                  2.5                       1.8          1.5

    a  From: Monster (1986)
    b  Values in parentheses are in ppm
         Trichloroethane concentrations in blood measured after work on a
    Friday seem to be the best single parameter for estimation of the
    TWA-week exposure (Monster, 1986).  For one-day exposure, the
    trichloroethane level in blood and urine is most useful (Monster,

         Droz et al. (1989) suggested a physiological model for describing
    variability in the biological monitoring of solvent exposure. 
    Standard statistical distributions are used to simulate variability in
    exposure concentration, physical workload, body fluid, liver function,
    and renal clearance.  For groups of workers exposed daily, the model
    calculates air monitoring indicators and biological monitoring
    results, including levels in expired air, blood, and urine.  The
    calculated results obtained are discussed and compared with measured
    data for physiological and toxicokinetic parameters for six solvents
    including 1,1,1-trichloroethane and their metabolites.  It is

    suggested that such mathematical models are applicable for prediction
    and management studies.

    6.6  Bioaccumulation

         Inhalation exposure of rats to 2700 mg/m3 (500 ppm) for 4 days,
    6 h per day, led to an accumulation of 1,1,1-trichloroethane in the
    fat 17 h after the last exposure.  Further exposure on the 5th day
    increased brain, liver, lung, and blood levels (Savolainen et al.,

         A study by Travis et al. (1988) indicated that bioaccumulation of
    organic chemicals, including 1,1,1-trichloroethane, perchloroethane,
    trichloroethylene, and dichloromethane, in human adipose tissues was
    positively correlated with their octanol-water partition coefficients. 
    The information presented, however, was based on data from a human
    pharmacokinetic model.



         1,1,1-Trichloroethane administered by various routes has low
     acute toxicity for laboratory animals.  The acute toxicity pattern is
     characterised by central nervous system depression and respiratory
     arrest at lethal levels.  1,1,1-Trichloroethane is a moderate skin
     and mild eye irritant.

         Short-term inhalation exposure of rats to 4320-5400 mg/m3
     (800-1000 ppm) or more produced an increase in liver weight.  At
     similar concentrations in mice, the liver changes were more marked
     and included fatty infiltration and single cell necrosis.  Minor
     cytoplasmic alterations were seen in mice exposed to 1350 mg/m3
     (250 ppm).  Studies on Mongolian gerbils using 1,1,1-trichloroethane
     concentrations down to 378 mg/m3  (70 ppm) revealed effects on DNA
     concentrations and other biochemical effects in several regions of
     the brain.  The significance of these findings is uncertain.  The
     no-observed-effect level (NOEL) for rats is about 2700 mg/m3  (500

         In long-term toxicity studies, 1,1,1-trichloroethane
     administration led to reduced weight gain in both rats and mice. 
     Slight microscopic hepatic effects were seen, but only at the highest
     concentration of 8100 mg/m3  (1500 ppm).  There was no evidence of
     carcinogenic potential in oral and inhalation studies on rats and
     mice.  One study reported increased incidence of leukaemia but this
     study is considered inadequate.

         1,1,1-Trichloroethane has been shown to have low genotoxic
     potential in a range of in vitro and in vivo studies.

         In a multigeneration study on mice, there was no evidence of
     adverse reproductive effects (including effects on fertility) caused
     by 1,1,1-trichloroethane in drinking-water at concentrations up to
     1000 mg/kg body weight.  Inhalation studies on female rats and mice
     at 4590 mg/m3  (850 ppm) showed no evidence of teratogenic or
     fetotoxic effects.  However, in rats exposed to 11 340 mg/m3 (2100
     ppm), there was some evidence of fetotoxicity.

         The data available are inadequate to assess the immunotoxic
     potential of 1,1,1-trichloroethane.

         Enhanced toxicity of 1,1,1-trichloroethane was observed when
     exposure was combined with exposure to ethanol.

    7.1  Acute toxicity

         1,1,1-Trichloroethane has a very low acute toxicity in laboratory
    animals dosed by various routes of administration.  Selected LD50
    and LC50 values are given in Tables 10 and 11.

         The toxicological pattern of acute trichloroethane poisoning is
    central nervous system (CNS) depression, eventually culminating in
    respiratory arrest or cardiac failure at lethal exposure levels
    (Stewart, 1968).

         The findings of rapid and shallow breathing in a dog following
    inhalation of 0.9% (by volume) 1,1,1-trichloroethane (corresponding to
    48 600 mg/m3 or 9000 ppm) may be related to an increase in the
    activity of the lung stretch receptor in the vagus nerve (Kobayashi et
    al., 1986).  A level of 1.3% increased the heart rate but 2.8%
    decreased it (Kobayashi et al., 1987).

         Non-lethal acute toxicity has also been investigated (see Table
    12).  In a study on rats, 50% of the experimental group showed loss of
    coordination (ataxia) after inhalation of 20 400 mg/m3 (3780 ppm)
    for 4 h, and loss of righting-reflex was observed at 45 800 mg/m3
    (8480 ppm).  Tremors and death were observed at 64 800 mg/m3 (12 000
    ppm) within one hour of exposure (Mullin & Krivanek, 1982).

         Cardiac sensitization to adrenaline was reported in dogs exposed
    to 37 800 mg/m3 (range: 21 600 to 59 400 mg/m3) for 5 min (Clark
    & Tinston, 1982).  An increase in concentration (range: 37 300 to 373
    000 mg/m3) and inhalation period (0.5 to 20 min) was accompanied by
    a decrease in the amount of adrenaline that induced arrhythmia
    (Kobayashi et al., 1982).

         Reinhardt et al. (1973) reported that 1,1,1-trichloroethane
    caused cardiac sensitization to adrenaline in dogs at and above the
    0.5% (v/v) level.  The marked response was associated with ventricular
    fibrillation following the challenge dose of adrenaline.  At this
    level, the solvent was also associated with excitement and struggling
    in the animals.  Histopathological examination of samples from the
    dogs that developed fatal arrhythmias did not show any gross or
    microscopic abnormalities.

    Table 10.  Acute toxicity (LD50) of 1,1,1-trichloroethane in experimental animals

    Species             Sex               Route           LD50 (mg/kg        Reference
                                                          body weight)

    Rat                male                oral              14 300      Torkelson et al. (1958)
    Rat               female               oral              11 000      Torkelson et al. (1958)
    Mouse             female               oral                9700      Torkelson et al. (1958)
    Guinea-pig     male & female           oral                8600      Torkelson et al. (1958)
    Rabbit         male & female           oral              10 500      Torkelson et al. (1958)
    Rabbit         male & female           skin              15 800      Torkelson et al. (1958)
    Mouse             female          intraperitoneal          3700      Gradiski et al. (1974)
    Mouse              male           intraperitoneal          5080      Klaassen & Plaa (1966)
    Dog                male           intraperitoneal          4140      Klaassen & Plaa (1967)

    Table 11.  Acute toxicity by inhalation (LC50) of 1,1,1-trichloroethane
               in experimental animals

    Species           Sex                 LC50           Exposure          Reference
                                  (g/m3)      (ppm)      duration

    Rat         male & female       97.2      18 000         3 h       Adams et al. (1950)
    Rat         male & female       76.9      14 250         7 h       Adams et al. (1950)
    Rat             male            99.4      18 400         4 h       Siegel et al. (1971)
    Rat             male            55.6      10 300         6 h       Bonnet et al. (1981)
    Rat         male & female      205        38 000       15 min      Clark & Tinston (1982)
    Mouse           male           120        22 240       30 min      Woolverton & Balster (1981)
    Mouse          female           72.4      13 410         6 h       Gradiski et al. (1978)
    Mouse           male            21.1        3910         2 h       Horiguchi & Horiguchi (1971)
    Mouse           male            99.1      18 358         1 h       Moser & Balster (1985)
    Mouse           male           111        20 616       30 min      Moser & Balster (1985)
    Mouse           male           159        29 492       10 min      Moser & Balster (1985)

    Table 12.  Non-lethal acute toxicity in experimental animals
               exposed to 1,1,1-trichloroethane by inhalation

    Species    Exposure      Exposure      Effects                  Reference
               level         duration

    Rat        45 800           4 h        loss of righting         Mullin & Krivanek (1982)
                                           reflex (EC50)

    Rat        20 400           4 h        loss of coordination     Mullin & Krivanek (1982)

    Mouse      31 000           1 h        inverted screen test     Moser & Balster (1985)
                                           performance (EC50)

    Dog        37 800          5 min       cardiac sensitization    Clark & Tinston (1982)
                                           to adrenaline

    Dog        21 600        a few min     decrease in blood        Kobayashi et al. (1983)

         The effect of 1,1,1-trichloroethane on liver enzyme activity in
    the serum of experimental animals has been investigated.  An almost
    lethal intraperitoneal dose of 1,1,1-trichloroethane (0.87 ml/kg body
    weight) caused a significant elevation of ALAT (alanine
    aminotransferase) in dogs (Klaassen & Plaa, 1967), and one eighth of
    a lethal intraperitoneal dose caused a significant elevation in SDH
    (sorbitol dehydrogenase) (Lundberg et al., 1986).  In both studies,
    the hepatotoxicity of 1,1,1-trichloroethane was relatively small
    compared to that of other organic solvents, e.g., chloroform, carbon
    tetrachloride, dimethylformamide (Lundberg et al., 1986),
    dichloromethane, 1,1,2-trichloroethane, and trichloroethylene
    (Klaassen & Plaa, 1967).

    7.1.1  Irritation

         Trichloroethane has been shown to produce "mild" skin irritation
    in rabbits when repeatedly applied topically under an occlusive
    dressing.  Redness was noted and the skin became scaly, but the effect
    was transient, the skin rapidly returned to normal (Torkelson et al.,

         After guinea-pigs had been exposed to 1 ml of
    1,1,1-trichloroethane via a skin depot (a glass ring attached to the
    skin and covered with glass), for 15 min, oedema was observed. 
    Prolonged exposure for several hours led to more severe inflammatory
    reactions in the upper part of the dermis, and histological
    examination at 15 min and 1, 4, and 16 h showed a number of changes to
    the epidermis.  The extent of these changes increased with duration of
    exposure (Kronevi et al., 1981).

         Repeated topical application of trichloroethane to abraded and
    non-abraded rabbit skin for up to 90 days resulted in slight,
    reversible irritation (Torkelson et al., 1958).  The same study showed
    that when trichloroethane was applied soaked in a cotton wool pad and
    bandaged to the shaven belly of a rabbit slight reddening and
    scaliness occurred, but this only increased slightly with repeated

         The application of 0.5 ml trichloroethane to the shaven skin of
    rabbits under an occlusive dressing for 24 h, resulted in moderate
    skin irritation (Duprat et al., 1976).  In a recent study of OECD
    methods (4-h exposure under semi-occlusive dressing) trichloro-ethane
    was reported to be a skin irritant (van Beek, 1990).

         Trichloroethane is a "mild" eye irritant.  Slight to moderate
    pain and slight conjunctival irritation, but no corneal damage, was
    reported following a single application of 100 µl trichloroethane to
    the eyes of rabbits (Torkelson et al., 1958).  Duprat et al. (1976)
    also found that instillation of 0.1 ml trichloroethane to the eyes of
    rabbits produced slight irritation.

    7.1.2  Short-term exposure  Inhalation

         When groups of rats, guinea-pigs, rabbits, dogs, and squirrel
    monkeys were exposed to 1,1,1-trichloroethane (11 880 mg/m3, 2200
    ppm) for 8 h/day, 5 days/week for 6 weeks, the only sign of toxicity
    was reduced body weight gain in rabbits and dogs.  There were no
    effects on haematological parameters or serum urea nitrogen and no
    histopathological changes were observed (Prendergast et al., 1967).

         In a study by Adams et al. (1950), rats were exposed to 0 or 27
    000 mg/m3 (0 or 5000 ppm) for 7 h/day on 32 out of 45 days and
    guinea-pigs received 20 to 65 7-h exposures to 0, 3510, 8100, 16 200
    or 27 000 mg/m3 (0, 650, 1500, 3000 or 5000 ppm) for a period of 1-3
    months.  Body weight gain was reduced in both species at all exposure
    levels used, but there were no other signs of toxicity and no effects
    were observed on blood urea nitrogen.  The only 1,1,1-trichloroethane-
    related effect observed on histopathological examination was fatty
    degeneration, without necrosis, in the liver of guinea-pigs at 16 200
    and 27 000 mg/m3.

         Rats exposed to 2700 mg/m3 (500 ppm), 6 h/day for 5 days,
    showed no behavioural effects.  However, there was a slight decrease
    in brain RNA content relative to controls (Savolainen et al., 1977). 
    Inhalation of 1750 mg/m3 (320 ppm) for 30 days had no effects on the
    composition of brain lipids in rats (Kyrklund et al., 1988).

         When rats were given 4320 mg/m3 (800 ppm) by inhalation 6
    h/day, 5 days/week for 4 weeks, absolute and relative liver weights
    were increased but there was no induction of liver microsomal
    cytochrome P-450 (Toftgaard et al., 1981).  A 1-h daily exposure to 54
    000 mg/m3 (10 000 ppm) for 3 months resulted in a narcotic effect
    (sedation and transient sleep) and in an increase of relative liver
    weight in rats, but there was no evidence of organ damage (Torkelson
    et al., 1958).

         When rats were exposed continuously for 100 days to 1350 or  5400
    mg/m3 (250 or 1000 ppm), no effects were observed in the low-dose
    group but an increase in relative liver weight was seen in the
    high-dose group (McEwen & Vernot, 1974).  No toxicity was observed in
    similar experiments with dogs and monkeys (McEwen & Vernot 1974).

         Exposure of mice to 5400 mg/m3 (1000 ppm) continuously for 14
    weeks resulted in marked liver changes (elevated relative liver
    weight, moderate liver triglyceride accumulation, and necrosis of
    individual hepatocytes).  Electron microscopy showed extensive
    cytoplasmic modifications consisting of vesiculation of the rough
    endoplasmic reticulum with loss of attached polyribosomes, increased
    smooth endoplasmic reticulum, microbodies (peroxisomes), and
    triglyceride droplets.  The observed toxic effects were similar to,

    but much less severe than, those produced by carbon tetrachloride. 
    Only minor cytoplasmic alterations were seen in mice exposed to 1350
    mg/m3 (250 ppm) (McNutt et al., 1975).

         No signs of toxicity were observed in rats, rabbits, guinea-pigs,
    dogs or monkeys exposed to 2730 mg/m3 (500 ppm) 7 h/day, 5 days/week
    for 6 months (Torkelson et al., 1958).

         In a study by Prendergast et al. (1967), rats, rabbits,
    guinea-pigs, dogs, and monkeys were exposed continuously to 754 or
    2059 mg/m3 for 90 days.  At the higher dose level, there were no
    deaths in any species after 90 days, and the authors stated that no
    visible toxic signs were observed.  However, at the lower dose level,
    some deaths occurred (2 out of 15 rats and 1 out of 3 rabbits). 
    Varying degrees of lung congestion were noted in the surviving
    animals.  In view of this and the deaths at the lowest dose tested,
    the authors stated that no positive conclusion could be drawn as to
    whether the effects were associated with the exposure.

         No adverse effects were seen in male Wistar rats exposed to 1100
    mg/m3 (204 ppm) 8 h/day, 5 days/week for 14 weeks (Eben & Kimmerle,

         When young adult Mongolian gerbils (Meriones ungiculatus) were
    continuously exposed to 378, 1134 or 5400 mg/m3 (70, 210 or 1000
    ppm) for 3 months, followed by a 4-month period without exposure,
    increased glial fibrillary acidic protein (GFA) was found in the
    cerebral cortex at the two highest exposure levels, indicating
    astrogliosis in this region of the brain (Rosengren et al., 1985).  In
    a similar study by Karlsson et al. (1987), the DNA concentrations in
    several brain regions were decreased in animals exposed to 378 mg/m3
    (70 ppm), the only exposure concentration used.

         Table 13 summarizes data from short-term inhalation studies.  Oral administration

         When rats were dosed orally with 1,1,1-trichloroethane in corn
    oil, 5 days/week for 6 weeks, a dosage of 3.2 g/kg body weight per day
    had no adverse effects.  However, total doses of 5.6 g/kg body weight
    in females and 10 g/kg body weight in males induced 40% mortality and
    decreased the body weight of survivors (NCI, 1977).  In mice no
    mortality was seen with a dose of 5.6 g/kg body weight.  Thus,
    trichloroethane has low toxicity in rats and mice following repeated
    exposure by the oral route.

        Table 13.  Short-term toxicity (exposure-effect relationships) in
               experimental animals exposed to 1,1,1-trichloroethane by
    Species      Exposure      Exposure       Effects                  Reference
                 level         duration

    Rat             5400        100 days      increased relative       McEwen & Vernot
                                              liver weight             (1974)

    Rat             1100        14 weeks,     NOAEL                    Eben & Kimberle
                                8 h/day,                               (1974)
                               5 days/week

    Gerbil          5400        3 months      reduced brain weight     Rosengren et al.

    Gerbil           380        3 months      biochemical changes      Karlsson et al.
                                              in the brain             (1987)

    Mouse           5400        14 weeks      liver necrosis           McNutt et al.

    Mouse           1350        14 weeks      minor liver effects      McNutt et al.

    Rat, dog,       2700        6 months,     NOAEL                    Torkelson et al.
    rabbit,                     7 h/day,                               (1958)
    monkey,                    5 days/week

    Rat, dog,       2000         90 days      NOAEL                    Prendergast et al.
    rabbit,                                                            (1967)

    7.2  Long-term exposure

         In the NCI (1977) carcinogenesis study (see section 7.5.1 for
    details of doses), reduced weight gain was noted in both rats and mice
    during the exposure period at all dose levels.  Furthermore, bloody
    discharge and crusting around the eyes of some rats was observed
    during the second year (NCI, 1977).

         In an oncogenicity inhalation study, female rats exposed to the
    highest concentration (8100 mg/m3, 1500 ppm) of 1,1,1-
    trichloroethane exhibited a significant decrease in body weight, and
    both females and males showed very slight microscopic hepatic effects
    at 6, 12, and 18 months.  At lower concentrations and in male rats and
    mice of both sex, no toxicity was observable (Quast et al., 1988).

    7.3  Reproductive toxicity, embryotoxicity, and teratogenicity

         Inhalation studies in female rats and mice gave no evidence of
    any teratogenic or fetotoxic effects followed exposure to
    1,1,1-trichloroethane at a concentration of 4700 mg/m3 (875 ppm) for
    7 h/day on days 6-15 of gestation (Leong et al., 1975).  No signs of
    maternal toxicity were noted.

         In a study of female rats exposed to a higher
    1,1,1-trichloroethane concentration (11 340 mg/m3, 2100 ppm, 6
    h/day, 5 days/week) for 2 weeks before mating and/or during 20 days of
    gestation (6 h/day, 7 days/week), there was some evidence of
    fetotoxicity.  This consisted of reduced fetal weight in the group
    exposed during pregnancy only and minor visceral and skeletal
    abnormalities, such as delayed ossification, in the group exposed
    before and during pregnancy (York et al., 1982).  No signs of maternal
    toxicity were observed.

         In a two-generation fertility study incorporating teratogenicity
    and dominant lethal elements, mice received 0, 100, 300 or 1000 mg
    1,1,1-trichloroethane/kg daily in the drinking-water (Lane et al.,
    1982).  Two or three litters were produced from each of the two
    generations, and the parental animals and offspring were used
    variously to investigate fertility, developmental toxicity, and
    dominant lethal effects.  No adverse effects on any aspect of
    reproduction were evident in this study.  The level of
    1,1,1-trichloroethane in the drinking-water in this study was reported
    to be up to 6000 mg/litre but was not actually measured.  In a further
    study, rats exhibited slight aversion to 30 mg/litre in drinking-water
    (George et al. 1989).

         Rats (Sprague-Dawley) and rabbits (New Zealand White) were
    exposed on days 6-15 and 6-18 of gestation, respectively, to 0, 5400,
    16 200 or 32 400 mg/m3 (0, 1000, 3000 or 6000 ppm) for 6 h/day. 
    1,1,1-Trichloroethane was found to be developmentally toxic to both
    rats and rabbits at the highest dose level, producing an increase in

    unossified and poorly ossified cervical centra, decreased female fetal
    body weight, an increase in non-viable implantations in rats, and an
    increase in the frequency of bilateral extra 13th rib in rabbits. 
    Both rats and rabbits showed a NOEL of 16 200 mg/m3 for
    developmental toxicity.  For both species, the developmental toxicity
    was seen in the presence of maternal tox-icity (Personal communication
    by E.Z. Francis to S. Ells, US EPA, Test Rules Development Branch,
    Existing Chemical Assessment Division.  Review of Developmental
    Toxicity Studies on 1,1,1-Trichloroethane (TCE). OHEA, ORD. Sept. 28,

         Dapson et al. (1984) reported that exposure to 10 mg
    1,1,1-trichloroethane per litre drinking-water caused cardiac
    anomalies in developing Sprague-Dawley rats.  The repeatability of
    this preliminary study was investigated by George et al. (1989), who
    exposed male and female CD rats to 3, 10 or 30 mg of 97% pure
    1,1,1-trichloroethane per litre drinking-water using 0.05% Tween 80 as
    an emulsifying agent.  The animals were exposed for a period of 14
    days before and at least 13 days after co-habitation.  Sperm-positive
    females continued to be exposed during pregnancy and lactation until
    postnatal day 21.  No significant effects were noted concerning the
    reproductive competence of the parental animals or the postnatal
    growth and development of the offspring (fertility, length of
    gestation period, litter size, pup body weight, and pup survival were
    all investigated).  In addition, there was no increase in the
    incidence of any cardiac malformations or other anomalies.  Thus the
    finding of Dapson et al. (1984) was not confirmed using a different
    strain of rats and a 3-fold higher concentration of

    7.4  Mutagenicity


         1,1,1-Trichloroethane has been tested extensively for
     mutagenicity, both in vitro  and in vivo,  and the principal studies
     are summarized in Table 14.  The results of most of the studies were
     clearly negative.  The positive results seen in some in vitro tests
     give rise to some concern, but may well have been due to the presence
     of stabilizers and/or impurities.  Some of the studies yielding
     negative results were of insufficient sensitivity.  All of the in
     vivo tests gave negative results.  Overall, it appears that
     1,1,1-trichloroethane does not have significant mutagenic potential.

        Table 14.  Mutagenicity studies

    Test method       Organism                 Test conditions      Result                        References

    In vitro studies on microorganisms

    Baterial           Salmonella typhimurium    many studies, using  mostly negative; some         Simmon et al. (1977), Snow et al. (1979),
     mutagenicity     or  Escherichia coli       liquid or vapour,    positive results attributed   Nestmann et al. (1980), Gocke et al. (1981),
                                                 with and without S9  to stabilizers or impurities  Rowland & Severn (1981), McDonald (1981),
                                                 activation                                         Nagao & Takahashi (1981), Richold & Jones
                                                                                                    (1981), Simmon & Shepherd (1981),
                                                                                                    Ichinotsubo et al. (1981), de Serres &
                                                                                                    Ashby (1981), HSE (1984), Shimada et al.

    Bacterial DNA      E. coli or Bacillus       several studies      mainly negative;              Kada (1981), Ichinotsubo et al. (1981),
     damage/repair     subtilis                                       occasionally equivocal        Green (1981), Tweats (1981), Rosenkranz
     tests                                                            results                       et al. (1981), de Serres & Ashby (1981)

    Yeasts,            Saccharomyces             numerous studies     negative                      HSE (1984), de Serres & Ashby (1981),
     gene mutation,    cerevisiae
     gene conversion   Schizosaccharomyces

                       S. cerevisiae and mice    5000 mg/kg           negative                      Loprieno et al. (1979)
                      (host-mediated assay)      intraperitoneal

    Table 14 (contd).

    Test method       Organism                 Test conditions      Result                        References

    In vitro mammalian cell studies

    Chromosome        CHO cells                ± S9 activation      clear positive without S9;    Galloway et al. (1987)
     aberrations                                                    equivocal with S9

    Gene mutation     L5178Y mouse             ± S9                 equivocal with S9;            Myhr & Caspary (1988)
                      lymphoma cells                                negative without S9

    Unscheduled       rat, mouse hepatocytes;  ± S9                 negative                      Althaus et al. (1982), Martin &
     DNA synthesis    HeLa cells                                                                  McDermid (1981)

    DNA repair        rat hepatocytes          ± S9                 mainly negative; some         Williams (1983), Shimada et al. (1985)
                                                                    positive results attributed
                                                                    to presence of stabilizers
                                                                    or impurities

    Sister chromatid  CHO cells                ± S9                 negative                      Perry & Thomson (1981)
     exchange                                                       equivocal                     Galloway et al. (1987)

    Cell              various cell types       ± S9                 both positive and             Daniel & Dehnel (1981), Styles (1981),
     transformation                                                 negative results              Price et al. (1978), Hatch et al. (1983)
                                                                                                  Tu et al. (1985), HSE (1984)

    Drosophila studies

    Sex-linked                                 25 nM                negative                      Gocke et al. (1981)

    Table 14 (contd).

    Test method       Organism                 Test conditions      Result                        References

    In vivo mammalian studies

    Chromosome        rats                     875 or 1750 ppm      negative                      Quast et al. (1978)
     aberrations                               6 h/day, 52 weeks
     (bone marrow)

    Micronucleus      mice                     34-67 mg/kg          negative                      Salamone et al. (1981)

    Micronucleus      mice                     11-42 mg/kg          negative                      Tsuchimoto & Matter (1981)

    Micronucleus      mice                     266-2000 mg/kg       negative                      Gocke et al. (1981)

    Dominant          mice                     100-1000 mg/kg per   negative                      Lane et al. (1982)
     lethal                                    day oral

    Sperm             mice                     130-2680 mg/kg per   negative                      Topham (1980)
     morphology                                day intraperitoneal

    DNA binding       rats and mice                                 low binding                   Prodi et al. (1988)

    7.5  Carcinogenicity

         1,1,1-Trichloroethane has been investigated for carcinogenic
    effects in life-time bioassays on both rats and mice by oral
    administration or inhalation.

    7.5.1  Oral administration

         In a US National Cancer Institute (NCI) assay, 7 week-old
    Osborne-Mendel rats were fed by gavage a 75% solution of technical
    grade 1,1,1-trichloroethane in corn oil, 5 days/week for 78 weeks. 
    The daily doses were calculated to be 750 or 1500 mg/kg body weight,
    and the study was terminated after 110 weeks.  The number of animals
    in each treated group was 50 of each sex, and the control groups
    consisted of 20 animals of each sex, which were not vehicle dosed.  No
    increased tumour incidence was found (NCI, 1977).  However, because of
    an unusually high mortality both among treated and control animals
    (only 6 out of 240 animals survived the 110 weeks to the end of the
    experiment), this study was considered insufficient by US EPA (1984)
    and placed in class D (not applicable to assess human

         In another NCI study with 5-week-old B6C3F1 mice, technical grade
    trichloroethane containing 3% 1,4-dioxane was given by gavage as a
    40-60% solution in corn oil at two dose levels (average daily doses:
    2807 and 5615 mg/kg body weight) 5 days/week for 78 weeks.  The same
    number of animals was used as in the NCI rat study reported above. 
    All surviving animals were killed after 90 weeks of study.  A variety
    of neoplasms was observed in the treated groups, but the incidence was
    not statistically significantly different from that of the control
    groups (NCI, 1977).  Again the mortality rate was very high in both
    treated and control animals, although it was a little lower than in
    the rat study. Nevertheless this study was also considered
    insufficient (US EPA 1984).

         In a study by Maltoni et al. (1986), groups of male and female
    rats were given 1,1,1-trichloroethane (500 mg/kg body weight) in olive
    oil by gavage (4 to 5 days/week for 104 weeks).  The
    1,1,1-trichloroethane contained about 4% 1,4-dioxane and 1% of other
    impurities.  An increased incidence of "leukaemias" was detected in
    the exposed group.  However, data were not evaluated statistically nor
    were any data for historical controls supplied.

    7.5.2  Inhalation

         In an inhalation study carried out by the Dow Chemical Co.,
    1-month-old Sprague-Dawley rats were exposed to technical
    1,1,1-trichloroethane (6 h/day, 5 days/week for 12 months) and
    observed 18 months later, before the survivors were killed.  Each dose
    group consisted of 96 rats of each sex.  The unexposed control group
    consisted of the same number of rats as the two exposed groups

    together.  The two exposure concentrations used were 4778 mg/m3 (875
    ppm) and 9555 mg/m3 (1750 ppm).  The treatment had no significant
    effect on mortality, and the tumour incidence in the treated animals
    was similar to that of the controls (Rampy et al., 1977).  The purity
    of the 1,1,1-trichloroethane used was 96%, and the stabilizers were 3%
    1,4-dioxane, 0.4% nitromethane, and 0.5% butylene oxide.  In the
    validation of this study, it was pointed out that the exposure period
    was only 12 months and not lifelong, that no subchronic range-finding
    test had been done, and that the exposure concentration could have
    been too low (US EPA, 1984).

         A more recent long-term inhalation study, this time on both rats
    and mice, has been carried out by the Dow Chemical Co. (Quast et al.,
    1988).  Groups of male and female 4- to 6-week-old Fischer-344 rats
    and 5- to 6-week-old B6C3F1 mice (80 of each sex per group) were
    exposed to 1,1,1-trichloroethane (technical formulation) vapour
    concentrations of 0 mg/m3, 820 mg/m3 (150 ppm), 2730 mg/m3 (500
    ppm), 8190 mg/m3 (1500 ppm) 6 h/day, 5 days/week for 2 years.  Ten
    animals of each sex from each group were predesignated for interim
    sacrifices after 6, 12, and 18 months of exposure.  The purity of the
    formulation was 94% (by volume) 1,1,1-trichloroethane, 5% stabilizers
    (butylene oxide,  tert-amyl alcohol, methyl butynol, nitroethane, and
    nitromethane) and < 1% minor impurities.  In none of the treated
    animal groups, did the tumour incidence differ significantly from that
    of the controls.

         The early studies with mice and rats were evaluated at IARC
    (International Agency for Research on Cancer) and considered
    inadequate (IARC, 1979; IARC, 1987).

    7.6  Immunotoxicity and sensitization

         Shmuter (1977) exposed rabbits to 1,1,1-trichloroethane
    concentrations of 2 mg/m3 (0.4 ppm), 10 mg/m3 (1.8 ppm), and 100
    mg/m3 (18 ppm) by inhalation 3 h/day, 6 days/week for 8-10 months. 
    At week 6,  Salmonella typhimurium was injected subcutaneously to
    investigate the immune response over an 8-month period.  The antibody
    response was depressed at both 10 mg/m3 and 100 mg/m3.  This
    reduction in immune response was followed by an increased
    electrophoretic mobility of the antibodies toward alpha- and
    ß-globulin fractions and also by a significant drop in the level of
    normal haemolysins to the Forsman's antigen of the sheep erythrocytes
    occuring during treatment.

    7.7  Interactions

         Interaction between 1,1,1-trichloroethane and ethanol was studied
    in mice given ethanol (0-2 g/kg body weight) by gavage 30 min before
    exposure to up to 120 000 mg trichloroethane/m3 (22 200 ppm) by
    inhalation.  Different combinations of exposure to the solvents
    enhanced the toxicity of trichloroethane in the animals previous

    exposed to ethanol.  The observed behavioural and lethal effects were
    dose related for each compound and additive (Woolverton & Balster,

         When dogs anaesthetized with either pentobarbital sodium or
    chloralose plus pentobarbital sodium were acutely exposed to a
    commercial spot remover containing 1,1,1-trichloroethane, there was a
    dose-dependent biphasic decline in arterial pressure with an initial
    increase in the heart rate.  A similar effect was obtained when
    1,1,1-trichloroethane (99.5% by volume) was used instead of the
    commercial spot remover.  It was found that the type of anaesthetic
    contributed in part to the effect.  The authors reported that, in
    addition to the peripheral vascular effects, significant alterations
    in myocardial function occurred, and they concluded that the solvent
    acts by inhibiting myocardial contractility (Herd et al., 1974).

    7.8  Mechanisms of action

         1,1,1-Trichloroethane given to mice intraperitoneally or by short
    inhalation exposure has been shown to reduce the cyclic guanosine
    monophosphate (cGMP) content in the cerebellum, cerebral cortex, and
    brain stem.  This was attributed to an increased rate of cGMP
    hydrolysis (Nilsson, 1986a).  The cyclic adenosine monophosphate
    (cAMP) content in the brain stem of mice was increased in a
    dose-related and time-dependant manner. This might be mediated by
    adrenoceptor interaction stimulating the catalytic unit of adenylate
    cyclase (Nilsson, 1986b).

         A study on isolated mouse brain synaptosomes exposed  in vivo
    and  in vitro showed that 1,1,1-trichloroethane increases calcium
    influx in the brain stem but not in the cerebellum and cerebral
    cortex.  The data indicated that 1,1,1-trichloroethane may influence
    voltage-dependant calcium channels in brain stem nerve endings
    (Nilsson, 1987).

         1,1,1-Trichloroethane suppressed the uptake of ovabain
    taurocholate and 2-aminoisobutyric acid, but not of cadmium chloride
    or 3- O-methyl-D-glucose, into isolated rat hepatocytes.  Both the
    cellular ATP level and ATP-ase activities in isolated membrane
    fractions were also decreased.  It was suggested that energy-dependant
    transport functions are disrupted, owing to decreased ATP levels
    and/or inhibition of membrane ATP-ases (Kukongviriyapan et al., 1990).



         Both acute and long-term inhalation exposure to
     1,1,1-trichloroethane can produce CNS effects ranging from slight
     behavioural changes to unconsciousness.  Death may follow from
     respiratory failure or cardiac arrest.  There is also the possibility
     of hepatic alterations and cardiac damage.

         Ingestion and dermal exposure do not appear to be serious
     concerns, although skin irritation may occur.

         1,1,1-Trichloroethane has properties (see chapter 2) that make it
     a dangerous compound in poorly ventilated areas and confined spaces
     such as tanks and vaults.  The vapour is five times more dense than
     air, which may result in non-uniform distribution, and very high
     levels can occur in certain areas such as the bottom of empty tanks
     and container vessels.  The combination of these properties has been
     the cause of some serious accidents, including fatalities.  Solvent
     abuse has also produced a large number of fatalities.

         There are insufficient studies to permit any conclusion
     concerning the reproductive and carcinogenic effects of this compound
     on humans.

         Exposure to 1,1,1-trichloroethane may increase sensitivity to
     other compounds, e.g., anaesthetics.

         The NOEL for humans appears to be in the region of 1350 mg/m3
     (250 ppm).

         Table 15 summarizes the toxic effects of 1,1,1-trichloroethane
     after inhalation exposure.

    8.1  Controlled human studies

         Several studies on volunteers under controlled conditions have
    investigated the effects of 1,1,1-trichloroethane on the CNS as
    measured by performance in certain behavioural tests.  These studies
    have usually been conducted using the technical grade of
    1,1,1-trichloroethane containing stabilizers, since this is the type
    of exposure that occurs most frequently.

        Table 15.  Toxic effects in humans related to inhalation exposure to 1,1,1-trichloroethane

     Exposure concentration        Duration of exposure         Effect                                    Reference
    (mg/m3)            (ppm)

     378 000          70 000            a few min               death                                     Northfield (1981)

      54 000          10 000              2 min                 general anaesthesia when given            Dornette & Jones (1960)
                                                                together with nitrous oxide (N2O)

    > 27 000          > 5000             10 min                 death                                     Kleinfeld & Feiner (1966)

      27 000            5000              5 min                 marked incoordination                     Stewart (1968)

      10 260            1900              5 min                 disturbance of equilibrium                Torkelson et al. (1958)

        5400            1000           short-term               mild eye and nasal discomfort,            Stewart (1968)
                                                                impairment of coordination

        5000             920            70-75 min               CNS disturbances (lightheadedness),       Torkelson et al. (1958)
                                                                slight eye irritation

        4860             900             73 min                 impaired performance in Romberg's         Stewart et al. (1961)
                                                                test, mild eye irritation

        2700             500          6-7 h/day for             impaired performance in Romberg's         Stewart et al. (1969)
                                         5 days                                                           test after 1 h of exposure, mild
                                                                eye irritation, drowsiness, headaches

        2700             500           90-450 min               no CNS disturbances                       Torkelson et al. (1958)

        2430             450             30 min                 dizziness, mild eye irritation            Salvini et al. (1971)

        2430             450             30 min                 reduced reaction time and                 Gamberale & Hultengren (1973)
                                                                perceptual speed

    Table 15 (contd).

     Exposure concentration        Duration of exposure         Effect                                    Reference
    (mg/m3)            (ppm)

        1890             350             30 min                 reduced perceptual speed                  Gamberale & Hultengren (1973)

        1900             350              3.5 h                 reduced psychomotor performance           Mackay et al. (1987)

      < 1860           < 345            6.7 years               NOEL                                      Maroni et al. (1977)

      < 1350           < 250            1-6 years               NOEL                                      Kramer et al. (1978)

        1350             250             30 min                 NOEL                                      Gamberale & Hultengren (1973)

         950             175              3.5 h                 reduced reaction time                     MacKay et al. (1987)

         540             100                                    odour threshold                           Stewart (1968)

    8.1.1  Single exposure period

         In a study by Torkelson et al. (1958), four volunteers were
    exposed in an inhalation chamber to average trichloroethane levels of
    4968 mg/m3 (920 ppm) for 70-75 min.  Symptoms of slight CNS
    disturbances (lightheadedness) were noted in three of the  four
    subjects and slight eye irritation was noted in one individual.  Two
    volunteers reported a strong odour during the experiment. 
    Concentrations in the range of 2700-2970 mg/m3 (500-550 ppm) for
    90-450 min apparently produced no symptoms of CNS disturbance, but
    exposure to 10 260 mg/m3 (1900 ppm) for 5 min produced a very
    noticeable odour and obvious disturbances in equilibrium. 
    Unfortunately, full details of this study are not available.

         Exposure to about 2700 mg/m3 (500 ppm) trichloroethane for
    78-186 min did not result in CNS toxicity or other effects (Stewart et
    al., 1961).  However, exposure to about 4860 mg/m3 (900 ppm) for up
    to 73 min resulted in CNS disturbances (light-headedness and impaired
    Romberg test performance) in approximately half of the subjects.  Mild
    eye irritation was also observed.  In another experiment in this
    series, the volunteers were exposed to increasing concentrations in
    the range of 0-14 310 mg/m3 (0-2650 ppm) over a 15-min period. 
    Signs of mild eye irritation were noted in six out of seven subjects
    when the concentration reached about 5400 mg/m3 (1000 ppm), and
    there was a rapid increase in CNS symptoms, principally dizziness. 
    Throat irritation was experienced by six out of seven subjects at
    about 10 800 mg/m3 (2000 ppm).  Severe CNS disturbances (imbalance,
    light-headedness) occurred at the end of the exposure period, when the
    concentration had reached 14 310 mg/m3.  In addition, minor effects
    on liver and kidney function were seen.  The authors considered that
    all the effects were reversible.

         The effect on young men of exposure to a mean trichloroethane
    level of 2430 mg/m3 (450 ppm) for two periods of 4 h (separated by
    a lunch break of 1´ h) was investigated by Salvini et al. (1971).  The
    volunteers experienced dizziness and slight excitation, but only
    during the first 30 min of exposure, and mild eye irritation was
    noted.  No significant change in performance in any of the behavioural
    tests was seen.

         In a study by Gamberale & Hultengren (1973), 12 male volunteers
    were exposed to 1350 mg/m3 (250 ppm) for 30 min, followed by 1890
    mg/m3 (350 ppm) for the next 30 min, and 2430 mg/m3 (450 ppm) and
    2970 mg/m3 (550 ppm) for subsequent 30-min periods.  At 2430
    mg/m3, the reaction time, perceptual speed, and manual dexterity
    were reduced, and at 1890 mg/m3 the perceptual speed was reduced. 
    The NOEL was 1350 mg/m3.

         Mackay et al. (1987) reported the results of an exposure chamber
    study in which volunteers were exposed to 950 mg/m3 (175 ppm) and
    1990 mg/m3 (350 ppm) for 3 to 5 h.  Several human psychomotor

    behavioural tests were employed, including two new ones.  One was
    concerned with distraction of attention and concentration (the Stroop
    test) and the other with analysing grammatical statements (the
    syntactic reasoning test).  Performance deficits in the psychomotor
    behavioural tests were recorded in volunteers exposed to
    1,1,1-trichloroethane; these depended on the time of exposure and the
    blood levels.  The performance changes were rapid and occurred in some
    cases within 20 min.  However, different effects were found.  In the
    Stroop test, enhanced performance was observed following exposure,
    whereas the syntactic reasoning test was found not to respond to
    1,1,1-trichloroethane exposure effects.  Measures of short-term
    subjective well-being were not affected by exposure.  Other
    parameters, such as simple reaction time and four-choice reaction time
    were increased.

         The effect of exposure to trichloroethane on performance in a
    very extensive range of behavioural tests was investigated by
    Savolainen et al. (1981, 1982a, 1982b).  Nine healthy male students
    (aged 20-25) were exposed in an inhalation chamber to 1080 and 2160 mg
    trichloroethane/m3 (200 and 400 ppm) for 4 h, with a 6-day interval
    between exposure at the two levels.  There was no clear indication of
    any effects on the CNS, although some minor changes were noted in
    body-sway measurements when the subjects had their eyes closed.

    8.1.2  Repeated exposure

         The effect of repeated exposure of male volunteers to 2700
    mg/m3 (500 ppm), 7 h/day for 5 days, was studied in an inhalation
    chamber (Stewart et al., 1969).  Several subjective symptoms were
    noted, e.g., drowsiness, headaches, lightheadedness, and eye and nose
    irritation, but the absence of a control group made it difficult to
    assess the significance.  No performance impairment in behavioural
    tests (modified Romberg test) was noted, apart from the inability of
    two subjects to perform the balance test on two occasions.

    8.2  Accidental exposure

         Respiratory system symptoms, such as cough, breathlessness, and
    chest tightness, are common in cases of acute poisoning (Boyer et al.,

         Since 1,1,1-trichloroethane is a very volatile solvent with a
    saturated vapour concentration of 864 g/m3 (160 000 ppm) at 25 °C,
    there is a potential for very high air concentrations in confined
    spaces, such as tanks and vaults.  Furthermore, its  vapour is five
    times more dense than air.  This may result in non-uniform
    distribution in the workplace air and very high levels in certain
    areas such as  just above degreasing vessels and at the bottom of
    empty tanks, even though levels elsewhere are low and safe.  This
    property has been the cause  of some serious accidents and fatalities.

         A near-fatal childhood intoxication was described by Gerace
    (1981).  A 4-year-old boy was playing under his bed covers with a
    flower-making kit which contained a 30-cm3 container of
    1,1,1-trichloroethane.  Because of some unusual noises heard by a
    sibling, the child was quickly discovered.  However, he was not
    breathing at this point.  He was resuscitated on the way to the
    hospital but remained comatose for about 12 min after arrival.  The
    author suggested that the child was rendered unconscious by the
    1,1,1-trichloroethane and that the noises heard were seizures caused
    by hypoxia.  The child was released 48 h after admission.  According
    to the author, clinical investigation during the child's hospital stay
    demonstrated some hepatic abnormalities with alteration in liver

         Caplan et al. (1976) reported the death of a woman due to
    accidental exposure while cleaning a paint spill using a paint thinner
    in a poorly ventilated room.  Autopsy results showed "mild fatty
    changes" in the liver and acute oedema and congestion of the lungs. 
    The concentrations of 1,1,1-trichloroethane in the brain, kidney,
    liver, and blood were 36, 12, 5, and 2 mg/100 ml, respectively.

    8.2.1  Confined spaces at workplaces

         A man who had spent 10 min in a vault, where the concentration of
    1,1,1-trichloroethane was estimated to be well in excess of 27 g/m3
    (5000 ppm), collapsed and died shortly after leaving the vault
    (Kleinfeld & Feiner, 1966).

         Seven fatalities from using trichloroethane to clean equipment on
    naval ships or aircraft tanks have been reported (Stahl et al., 1969;
    Hatfield & Maykoski, 1970).  The exposure level in one of these cases
    was estimated to be in the order of 270 g/m3 (50 000 ppm).  In all
    cases the most significant pathological finding was pulmonary oedema. 
    Liver damage was not seen.

         Other case histories with accidental death due to
    1,1,1-trichloroethane exposure in confined spaces have been reported
    (Stewart 1968; Bonventre et al.,  1977).

         During the period 1961-1980, the Factory Inspectorate in the
    United Kingdom revealed 52 incidents due to trichloroethane (McCarthy
    & Jones, 1983).  Loss of consciousness was reported in 26 cases and
    death in three cases, all involving very young workers.  In one case
    the worker died after leaning over an open tank of trichloroethane,
    apparently to wash his hands in the solvent.  He was found unconscious
    slumped over the side of the tank, and the solvent concentration in
    his breathing zone was later estimated to be about 378 g/m3 (70 000
    ppm) (Northfield, 1981).  In a second case, a worker was using
    trichloroethane for cleaning purposes in a closed room (Jones &
    Winter, 1983).  He was found on the floor with chemical burns on the
    head and neck, which was consistent with prolonged skin absorption

    from spills of solvent on the floor.  The third case was a teenage
    worker who cleaned the interior of a car with a cloth soaked in the
    solvent (Jones & Winter, 1983).  Death was presumed to be from
    1,1,1-tri-chloroethane intoxication and simultaneous inhalation of

    8.2.2  Solvent abuse

         During the 1960s, 110 cases of sudden death from solvent abuse
    were reported in the USA.  Of these, spot remover containing
    1,1,1-trichloroethane was identified as responsible for 29 cases
    (Bass, 1970).  Death frequently occurred immediately following
    stressful activity.  Where autopsies were performed, no abnormalities
    could be detected, and it was suggested that deaths was due to cardiac

         Over the period 1971-1981, 140 deaths from solvent abuse were
    reported in the United Kingdom; 20 of them were believed to be due to
    1,1,1-trichloroethane, mainly in dry-cleaning fluid, domestic cleaners
    or plaster remover (Anderson et al., 1982).

         In the case of a fatality due to the abuse of cleaning solvent
    containing 1,1,1-trichloroethane, very minor hepatic changes were seen
    (Hall & Hine, 1966).  In four cases of deaths caused by inhalation of
    typewriter correction fluid containing 1,1,1-trichloroethane and
    trichloroethylene, the autopsies showed no evidence of kidney or liver
    damage (King et al., 1985).

         According to Marjot & McLeod (1989), toluene and the chlorinated
    hydrocarbons 1,1,1-trichloroethane and trichloroethylene can cause
    permanent damage to the kidney, liver, heart, and lung in certain
    volatile substance abusers.

    8.2.3  Medical use

         Trichloroethane has been used as an anaesthetic on an
    experimental basis.  General anaesthesia in humans has been rapidly
    induced by 2 min of exposure to 54 000 mg/m3 (10 000 ppm) given with
    a mixture of nitrous oxide (N2O) and oxygen (80:20).  Cardiovascular
    side effects (slight to severe hypotension, cardiac arrhythmias, and,
    in one case, cardiac arrest) were observed in several of the patients
    during anaesthesia.  In view of these effects, the experimental use of
    1,1,1-trichloroethane as an anaesthetic was discontinued (Dornette &
    Jones, 1960).

         In the USA, after aerosol drug products containing
    1,1,1-trichloroethane had been implicated in 21 deaths from their
    abuse or misuse, the Food and Drug Administration (FDA) removed the
    products from the market (US Food and Drug Administration, 1973).  The
    medical products were mainly used as cough suppressants and contained
    1,1,1-trichloroethane as a solvent for the active ingredients and to

    reduce the vapour pressure of the propellants.  The FDA found lack of
    general recognition by qualified experts of the safety or
    effectiveness of 1,1,1-trichloroethane in aerosol drug products
    intended for inhalation.

         Under 1977 rules from the FDA, it was stated that
    1,1,1-trichloroethane is potentially toxic to the cardiovascular
    system by sensitizing the heart to adrenaline (Food and Drug
    Administration, 1977).

    8.2.4  Ingestion

         In a case of accidental ingestion of about 600 mg
    trichloroethane/kg, signs of severe gastrointestinal irritation
    (vomiting, diarrhoea) were evident shortly after the ingestion.  There
    was no evidence of any CNS disturbance or any liver or kidney
    dysfunction (Stewart & Andrews, 1966).

         Ingestion of about 30 ml trichloroethane has been found to cause
    severe vomiting and diarrhoea (CEC, 1986).

    8.2.5  Drinking-water contamination

         In December 1981, a water well in Santa Clara County, California,
    USA, was removed from service after contamination with
    1,1,1-trichloroethane and other solvents was detected.  A
    1,1,1-trichloroethane level of 1.7 mg/litre was detected at the well
    head, but the level of the other contaminants (dichloroethylene,
    isopropyl alcohol, and freon) was not reported.  Subsequently
    suspicion of a cluster of spontaneous abortions and congenital heart
    anomalies from pregnancies conceived during 1980-1981 was reported by
    the local community.  Epidemiological studies indicated that a cluster
    did exist, that the odds ratio for spontaneous abortion was 2.3 and
    the relative risk for congenital malformations was 3.1, but they were
    unable to draw a direct link between the ingestion of the contaminated
    water and these effects (Goldberg et al., 1990).

    8.3  Effects on the skin and eyes

         Prolonged or repeated skin contact with 1,1,1-trichloroethane may
    lead to dermatitis, due to its defatting action.  However, despite its
    wide use only a few cases of skin irritancy have been reported
    (Torkelson et al., 1958).

         Immersion of a hand in liquid 1,1,1-trichloroethane for 30 min
    resulted in mild erythema, which persisted for one hour (Stewart &
    Dodd, 1964).

         Splashed in the eye, the compound may produce conjunctivitis
    (Stewart, 1968).  However, accidental eye contact has been reported to
    produce only transient irritation (Savolainen et al., 1982a,b).

    Exposure to a vapour concentration of 2700 mg/m3 (500 ppm) may
    produce mild eye irritation (see section 8.1).

    8.4  Long-term occupational exposure

         A case study described a patient with liver cirrhosis after
    several years of heavy exposure to trichloroethylene followed by 3
    months of work that frequently involved using aerosolized degreaser
    containing trichloroethane (Thiele et al., 1982).

         An investigation of the neurotoxicity of trichloroethane was
    carried out on a group of 22 female workers exposed to the solvent for
    an average period of 6.7 years.  The group was subdivided into three
    exposure groups (mean levels: 594 mg/m3 (110 ppm), 756-864 mg/m3
    (140-160 ppm), and 1080-1863 mg/m3 (200-345 ppm)).  Each woman had
    a general physical examination, and information about symptoms was
    obtained from a questionnaire.  The measurement of nerve conduction
    velocity and psychometric functions indicated no differences between
    the exposed workers and an unexposed control group of 7 workers
    (Maroni et al., 1977).

         Hodgson et al. (1989) reported that four out of ten clinical
    cases of fatty liver disease were associated with occupational
    exposure to 1,1,1-trichloroethane.

         A matching-pair study of 151 pairs of workers at textile plants,
    with and without daily exposure to trichloroethane levels of up to
    1365 mg/m3 (250 ppm), found no toxic effect among the exposed
    workers, the majority of whom were exposed to less than 810 mg/m3
    (150 ppm) for a period of 1-6 years (Kramer et al., 1978).

         In a case-control study of the effect of occupational exposure to
    various solvents on spontaneous abortion rates in Finland (1973-1983),
    a statistically significant elevation in relative risk was found for
    exposure to organic solvents in general.  However, there were very few
    cases related specifically to 1,1,1-trichloroethane.  The low
    statistical power, therefore, precludes any conclusion as to whether
    the data show an effect or not for 1,1,1-trichloroethane (Lindbohm et
    al., 1990)

         There are no adequate epidemiological studies available
    concerning long-term exposure to 1,1,1-trichloroethane and

    8.5  Interactions

         Chronic cardiac arrhythmia developed in two cases, after routine
    halothane anaesthesia, in subjects with previous repeated long-term
    exposure to 1,1,1-trichloroethane (in one case, occupational and in
    the other, due to solvent abuse).  The effects involved myocardiac
    damage with either ventricular arrhythmia or deterioration of left

    ventricular function.  In one of the cases, the pathologist suggested
    a subacute myocarditis superimposed on long-standing damage.  The
    authors postulated that the interaction between the two chemicals may
    have caused the cardiac deterioration and concluded that cardiac
    damage sustained after long-term exposure to 1,1,1-trichloroethane may
    be severe, life-threatening, and irreversible (McLeod et al.,1987)

         Marjot & McLeod (1989) reported two cases, a 14-year-old boy
    exposed to 1,1,1-trichloroethane via solvent abuse and a 54-year-old
    man exposed occupationally, where the cardiac toxicity of
    1,1,1-trichloroethane may have been increased by exposure to halothane
    (2-bromo-2-chloro-1,1,1-trifluoroethane) as an anaesthetic.



         1,1,1-Trichloroethane is not likely to be a significant hazard to
     non-target organisms in the environment.  For example, 96-h LC50
     values for fish ranged from 33 mg/litre for dabs to 105 mg/litre for
     fathead minnows.  The 48-h LC50  for Daphnia was around 60 mg/litre. 
     The EC50  for carbon dioxide incorporation into algae was 5

    9.1  Microorganisms

         A toxic threshold of 93 mg 1,1,1-trichloroethane/litre has been
    estimated for the inhibition of cell multiplication in the bacterium
    Pseudomonas putida (Bringmann & Kuhn, 1977).  The 3-h EC50 values,
    for inhibition of photosynthesis (measured by monitoring the uptake of
    14CO2), for the green algae  Chlamydomonas angulosa (at a cell
    concentration of 5 x 104 cells/ml) and  Chlorella vulgaris (at a
    cell concentration of 20 x 104 cells/ml) were 280 mg/litre and 153
    mg/litre, respectively, under static conditions (Hutchinson et al.,
    1980).  Bringmann & Kuhn (1978) calculated toxic thresholds of 350
    mg/litre and 430 mg/litre, respectively, for inhibition of cell
    multiplication, over an 8-day period, of the cyano bacterium
    (blue-green alga)  Microcystis aeruginosa and the green alga
     Scenedesmus quadricauda.  The 96-h EC50 for chlorophyll a and cell
    number in the green alga  Selenastrum capricornutum was > 669
    mg/litre (US EPA, 1980a,b). Pearson & McConnell (1975) assessed the
    toxicity of 1,1,1-trichloroethane to the unicellular alga
    Phaeodactylum tricornutum by measuring changes in the uptake of
    carbon, from 14CO2, during photosynthesis, and obtained an EC50
    of 5 mg/litre.

    9.2  Aquatic organisms

         The acute toxicity of 1,1,1-trichloroethane to aquatic organisms
    is summarized in Table 16.

         Flow-through tests gave much lower LC50 values than static
    tests, suggesting that some loss via evaporation may be occurring. 
    The 48-h LC50 for aquatic invertebrates ranges from 7.5 mg/litre for
    barnacles in a flow-through test to > 530 mg/litre for daphnids in a
    static test.  The 96-h LC50 for fish ranges from 33 mg/litre for the
    dab  (Limanda limanda) in flow-through tests to 105 mg/litre for the
    fathead minnow  (Pimephales promelas) in static tests.

    Table 16.  Acute toxicity of 1,1,1-trichloroethane to aquatic organisms


    Organism                     Age/      Stat/   Temperature   Hardnessc     pH        Duration       LC50e        Reference
                                 size      flowa                   (°C)                     (h)      (mg/litre)


    Mysid shrimp                           stat                                             96         31.2 n        US EPA (1980b)
      (Mysidopsis bahia)

    Barnacle                    nauplii    stat                                             48          7.5 n        Pearson & McConnell (1975)
      (Eliminius modestus)

    Water flea                  < 24 h     stat       21-23         72         6.7-8.1      48         > 530 n       LeBlanc (1980)
      (Daphnia magna)           4-6 day    stat       21-25                                 48          59.6         Abernethy et al. (1986)
                                4-6 day    stat                                             48          57.6         Bobra et al. (1984)


    Dab                        15-20 cm    flow                                             96          33 m         Pearson & McConnell (1975)
      (Limanda limanda)

    Sheepshead minnow           8-15 mm    stat       25-31       10-31d                    96      71 (60-81) n     Heitmuller et al. (1981)
      (Cyprinodon variegatus)

    Bluegill                  0.32-1.2 g   stat       21-23        32-48       6.7-7.8      24          110 n        Buccafusco et al. (1981)
      (Lepomis macrochirus)   0.32-1.2 g   stat       21-23        32-48       6.7-7.8      96      72 (57-90) n     Buccafusco et al. (1981)
                                           stat                                             96         69.7 n        US EPA (1980b)

    Fathead minnow                1 g      stat        12                      7.8-8.0      96     105 (91-126) n    Alexander et al. (1978)
      (Pimephales promelas)       1 g      flow        12                      7.8-8.0      96   52.8 (43.7-77.7) m  Alexander et al. (1978)

    Table 16 (contd).
    Organism                     Age/      Stat/   Temperature   Hardnessc     pH        Duration       LC50e        Reference
                                 size      flowa                   (°C)                     (h)      (mg/litre)
    Fish (contd)

    Guppy                      2-3 month   statb                                            168          133         Konemann (1981)
      (Poecilia reticulata)

    a  stat = static conditions (water unchanged for the duration of the test) unless stated otherwise; flow = flow-through conditions
       (1,1,1-trichloroethane concentration continuously maintained)
    b  static conditions but water renewed daily
    c  hardness expressed as mg CaCO3 per litre
    d  value refers to salinity (%), not hardness
    e  n = nominal; m = measured

         LeBlanc (1980) exposed the water flea  Daphnia magna to
    1,1,1-trichloroethane for 48 h under static conditions.  At the
    highest concentration of 530 mg/litre, no discernible effect was
    observed.  A no-observed-effect level (NOEL) of 43 mg/litre was
    estimated by Heitmuller et al. (1981) after exposing the sheepshead
    minnow  (Cyprinodon variegatus) to 1,1,1-trichloroethane for 96 h.

         When Thompson & Carmichael (1989) exposed the water flea  Daphnia
     magna to 1,1,1-trichloroethane concentrations of between 1.3 and 23
    mg/litre for 17 days under semistatic conditions (water renewed every
    2 days), no effect on mortality or reproduction (as measured by number
    of offspring per parent) was observed at 1.3 mg/litre.  However, the
    mortality increased with increasing concentration of
    1,1,1-trichloroethane from 30% at 2.4 mg/litre to 100% at 23 mg/litre. 
    The number of offspring per parent was significantly reduced at
    concentrations of 2.4 mg/litre or more.

         Thompson & Carmichael (1989) also exposed the mirror carp
     Cyprinus carpio to 1,1,1-trichloroethane concentrations ranging from
    1.4 to 30 mg/litre for 14 days under flow-through conditions.  There
    was no mortality at any of the concentrations, but at the highest
    concentration the fish showed surfacing behaviour, loss of balance and
    coughing, and their mean weight decreased.  The authors considered,
    therefore, that the NOEL was the next highest concentration, i.e. 7.7

         Alexander et al. (1978) observed fathead minnows  (Pimephales
     promelas), during exposure to 1,1,1-trichloroethane for up to 96 h,
    for the following effects: loss of equilibrium, melanization,
    narcosis, and swollen, haemorrhaging gills.  The concentration
    producing one or more of these observable effects in 50% of the fish
    (EC50) was 11.1 mg/litre.

    9.3  Terrestrial organisms

         Thompson & Carmichael (1989) exposed emergent seedlings of crop
    sorghum  (Sorghum bicolor) and oil seed rape  (Brassica napus) to
    1,1,1-trichloroethane in the gaseous phase at nominal concentrations
    of between 3.2 and 320 mg/litre (g/m3) for a period of 14 days (the
    test material was replenished after 7 days in a sealed vessel).  Mean
    measured concentrations ranged from 58% to 75% of the nominal
    concentration, reflecting the decline of 1,1,1-trichloroethane in the
    gas phase concentration during the 7-day periods between toxicant
    renewal.  In the case of  Sorghum bicolor, the 14-day EC50 (based
    on mean plant weight and a mean measured 1,1,1-trichloroethane
    concentration) was 48 mg/litre; the NOEL being 19 mg/litre.  For
     Brassica napus, the 14-day EC50 was 19 mg/litre and the NOEL 6.9
    mg/litre, both values being based on mean measured concentrations.

         Rajendran (1990) exposed 1- to 2-day-old pupae of the red flour
    beetle  (Tribolium castaneum) to 1,1,1-trichloroethane in fumigation
    chambers.  An LC50 of 208.4 mg/litre was estimated after a 24-h
    exposure and a 20-day post-fumigation observation period.  When pupae
    were exposed to a mixture of 1,1,1-trichloroethane and methyl bromide
    at a concentration of 2.5 mg/litre or 3.0 mg/litre, the toxicity was
    similar to that of the individual components.

         In a contact toxicity test, red earthworms  (Eisenia foetida)
    were exposed to 1,1,1-trichloroethane via filter paper in glass vials. 
    An LC50 of 83 µg/cm2 was estimated (Neuhauser et al., 1986).

         Elovaara et al. (1979) injected 1,1,1-trichloroethane, at
    concentrations ranging from 5 to 100 µmol/egg, into the air space of
    fertilized chicken eggs at 3 or 6 days of incubation, and the
    embryotoxicity was evaluated after 14 days of incubation.  A clear
    dose-response relationship with respect to survival was found,
    irrespective of whether the eggs were injected after 3 or 6 days of
    incubation.  The approximate LD50 for 1,1,1-trichloroethane was
    between 50 and 100 µmol/egg.


    10.1  Evaluation of human health risks

         Humans are exposed to 1,1,1-trichloroethane principally by
    inhalation, where the substance is rapidly absorbed into the body.
    Exposure by skin absorption or ingestion may also occur but, compared
    to inhalation, is of lesser concern.  1,1,1-Trichloroethane is
    considered not to bioaccumulate.  The acute and chronic toxicities are
    fairly low.  Under conditions of high exposure there is a risk of
    toxic effects; such conditions may occur in occupational exposures,
    solvent abuse or accidents.  Since 1,1,1-trichloroethane is volatile
    and the vapour is much more dense than air, toxic and explosive
    concentrations may occur unexpectedly in confined spaces.  This has
    caused several fatal and near-fatal accident at workplaces and
    elsewhere.  The critical effect in humans relates to the central
    nervous system, leading to unconsciousness and respiratory arrest at
    high concentrations.  1,1,1-Trichloroethane is less toxic to the liver
    than most other organochlorine solvents.  The no-observed-effect level
    for humans appears to be in the region of 1350 mg/m3 (250 ppm). 
    Although one study suggested effects at a lower level, the
    interpretation of the results was unclear.

         Studies on Mongolian gerbils involving 1,1,1-trichloroethane
    levels down to 378 mg/m3 (70 ppm) revealed effects on DNA
    concentrations and other biochemical effects in several brain regions. 
    If these findings are validated and confirmed, this may be of
    significant concern.

         No adequate study of carcinogenic effects on humans has been
    published.  A long-term inhalation study on rats and mice exposed to
    8100 mg/m3 (1500 ppm) gave no evidence of any carcinogenic effects. 
    One study recorded increases numbers of "leukaemias", but it was
    performed under non-standard protocol.  It gave no statistical
    evaluation and is, therefore, considered inadequate.  It is unlikely
    that 1,1,1-trichloroethane itself presents a significant risk of
    genotoxic or carcinogenic effects in humans.

         1,1,1-Trichloroethane is not teratogenic and elicits no
    developmental effects at doses that are not maternally toxic.  The
    limited epidemiological evidence on reproductive effects is
    inconclusive due to the low statistical power of the study.

    10.2  Evaluation of effects on the environment

         1,1,1-Trichloroethane is released in large quantities to the
    environment.  Due to its volatility and general stability it is a
    ubiquitous environmental contaminant.

         Although the ozone-depleting and global-warming potentials of
    1,1,1-trichloroethane are lower than those of many

    chlorofluorocarbons, the large-scale release of the compound into the
    atmosphere merits serious concern in these respects.

         As a result of its widespread use and disposal and its mobility
    in soil, persistent 1,1,1-trichloroethane contamination of ground
    water, including deep aquifers, occurs.

         Conditions under which 1,1,1-trichloroethane causes
    ecotoxicological effects are not found in the environment except after


    a)   Emissions of 1,1,1-trichloroethane should be reduced as far as  
         is practicable in order to minimize exposure of workers and of  
         the general population.
    b)   The release of 1,1,1-trichloroethane into the environment must  
         be reduced to the greatest extent possible in order to avoid  
         damage to the ozone layer.

    c)   Contamination of ground water by 1,1,1-trichloroethane from  
         spills and waste disposal should be avoided.

    d)   Safe substitutes for 1,1,1-trichloroethane should be identified.


    a)   More study is needed to clarify the possible effects of
         1,1,1-trichloroethane on the biochemistry of the central nervous
         system and their significance.

    b)   More study is necessary to clarify the possible interaction  
         between 1,1,1-trichloroethane and ethanol in humans.

    c)   An adequate subchronic or long-term oral study is needed to  
         assess the hepatotoxicity of 1,1,1-trichloroethane.

    d)   Further epidemiological studies on reproductive effects are  


         IARC (International Agency for Research on Cancer) working groups
    have evaluated 1,1,1-trichloroethane and concluded that the evidence
    for genotoxicity is limited (IARC, 1979, 1987).


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         Le 1,1,1-trichloréthane est un hydrocarbure chloré produit par
    chloration du chlorure de vinyle ou du chlorure de vinylidène.  En
    1988, la production mondiale était d'environ 680 000 tonnes.  C'est un
    liquide incolore et volatil à l'odeur caractéristique dont la vapeur
    est plus dense que l'air.  On l'utilise essentiellement pour le
    dégraissage des surfaces métalliques et comme solvant dans un grand
    nombre de produits industriels et de produits de consom-mation,
    notamment des adhésifs, des détachants et des bombes aérosols.  Il
    sert également d'intermédiaire en synthèse chimique.  Le
    trichloréthane technique contient généralement 3 à 8% de stabilisants
    destinés à empêcher sa décomposition et la formation d'acide
    chlorhydrique;  les parties métalliques sont ainsi protégées de la
    corrosion.  Il est ininflammable dans les conditions normales mais la
    vapeur s'enflamme à haute température et, au cours du soudage, elle
    peut se décomposer en libérant du phosgène, un gaz toxique.  Des
    réactions extrêmement violentes peuvent se produire en cas de contact
    avec de l'aluminium, du magnésium ou leurs alliages.

         Le 1,1,1-trichloréthane pénètre facilement dans l'environne-ment. 
    Comme il séjourne longtemps dans la troposphère (environ six ans) et
    qu'il n'est que lentement biodégradable, on le retrouve maintenant
    partout dans l'environnement, même à grande distance des zones
    industrielles.  A proximité d'installations industrielles où ce
    composé est produit ou manipulé, on a trouvé du 1,1,1-trichloréthane
    à des concentrations atteignant 86 µg/m3 (16 000 ppm, p/p) dans des
    échantillons d'air.

         Le trichloréthane se déplace dans le sol et parvient jusqu'aux
    eaux souterraines.  On en a trouvé à des concentrations atteignant
    1600 µg/litre dans les eaux souterraines ou les eaux de surface.  Ce
    phénomène peut être à l'origine de la contamination des réserves d'eau

         On estime que 15% des émissions annuelles de
    1,1,1-trichloré-thane sont entraînées dans la stratosphère où elles
    peuvent endommager la couche d'ozone par libération d'atomes de

         Des essais biologiques sur des crustacés et des poissons à des
    concentrations supérieures à 7 mg/litre ont révélé des effets toxiques
    aigus.  On possède quelques données selon lesquelles le composé ne
    s'accumulerait que faiblement chez les organismes aquatiques.  En
    raison du caractère limité des données disponibles, il est difficile
    d'évaluer les effets qu'il peut avoir sur les organismes terrestres.

         L'exposition humaine au 1,1,1-trichloréthane est due
    principalement à l'inhalation de ce composé qui est ensuite rapidement
    résorbé par l'organisme.  Il peut y avoir également exposition par
    contact cutané ou ingestion.  Le trichloréthane se répartit largement

    dans les tissus de l'organisme et il traverse la barrière
    hématoencéphalique et placentaire.  On le retrouve également dans le
    lait humain mais il ne semble pas qu'il s'accumule dans les tissus. 
    Sa principale voie d'élimination est l'exhalation du composé non

         La toxicité aiguë et chronique du 1,1,1-trichloréthane est
    relativement faible mais en cas de forte exposition, le risque
    d'intoxication est réel.  Cela peut se produire en cas d'exposition
    professionnelle, d'accidents ou encore de toxicomanie aux solvants. 
    Comme il s'agit d'un solvant volatil dont la vapeur est beaucoup plus
    dense que l'air, il peut se trouver à des concentrations
    inhabituellement fortes et dangereuses dans des espaces confinés comme
    les réservoirs "vides".  Ce genre de situation a donné lieu à
    plusieurs intoxications mortelles ou qui auraient pu l'être sur les
    lieux de travail ou ailleurs.

         Chez l'homme, l'effet critique s'exerce au niveau du système
    nerveux central.  On observe des effets qui vont de légers troubles du
    comportement (accompagnés d'une légère irritation occulaire) à la dose
    de  1,9 g/m3 (350 ppm), jusqu'à l'inconscience et à l'arrêt
    respiratoire lorsque la concentration est élevée.  Dans certains cas,
    des anomalies cardiaques mortelles peuvent se produire.  Le
    trichloréthane est moins toxique pour le foie que la plupart des
    autres solvants organiques chlorés.  La dose sans effet observable
    pour l'homme se situe autour de 1,35 g/m3 (250 ppm).

         Aucune étude satisfaisante n'a été publiée sur les effets
    cancérogènes de ce solvant chez l'homme.  Toutefois une étude par
    inhalation de longue durée sur des rats et des souris exposés à 8,1
    g/m3 (1500 ppm) n'a pas révélé le moindre effet cancérogène.  Le
    1,1,1-trichloréthane ne présente pas d'activité génotoxique

         Chez des rats et des lapins exposés au trichloréthane à des
    concentrations qui étaient toxiques pour les femelles gestantes, on
    n'a pas noté d'effets tératogènes, malgré la présence d'effets
    toxiques sur le développement.  Les données épidémiologiques relatives
    à ces effets sur la reproduction sont trop limitées pour permettre
    d'en tirer une conclusion.


         El 1,1,1-tricloroetano es un hidrocarburo clorado que se fabrica
    a partir del cloruro de vinilo o del cloruro de vinilideno por
    cloración.  En 1988 la producción mundial fue de unas 680 000
    toneladas.  Es un líquido volátil e incoloro con un olor
    característico, y su vapor es más denso que el aire.  Se utiliza
    principalmente en el desengrasado de metales y como disolvente en
    muchos productos industriales y de consumo, como adhesivos,
    quitamanchas y envases de aerosoles.  Es también un producto químico
    intermediario.  El tricloroetano de calidad técnica suele contener del
    3% al 8% de estabilizadores que impiden la degradación y la formación
    de ácido clorhídrico a fin de proteger las partes metálicas de la
    corrosión.  En condiciones normales no es inflamable, pero su vapor
    arde a altas temperaturas y, durante las operaciones de soldadura, su
    degradación produce fosgeno, un gas tóxico.  Cuando entra en contacto
    con el aluminio, el magnesio y sus aleaciones puede provocar
    reacciones muy violentas.

         El 1,1,1-tricloroetano llega fácilmente al medio ambiente. Su
    prolongada permanencia en la troposfera (unos seis años) y baja
    biodegradabilidad son razón de su actual omnipresencia en el medio
    ambiente, incluso lejos de las zonas industriales.  En muestras de
    aire de zonas próximas a industrias que lo fabrican o lo manipulan se
    han detectado concentraciones de hasta 86 µg/m3 (16 ppb, peso/peso).

         El tricloroetano se desplaza en los suelos y alcanza las aguas
    subterráneas.  Se han encontrado concentraciones de hasta 1600
    µg/litro en aguas subterráneas o superficiales.  Esta puede ser una
    fuente de contaminación para suministros de agua potable.

         Se estima que el 15% del volumen anual liberado llega a la
    estratosfera, donde libera átomos de cloro que contribuyen a la
    destrucción del ozono.

         En bioensayos con crustáceos y peces se han observado efectos
    tóxicos agudos con concentraciones superiores a 7 mg/litro.  Limitada
    información limitada disponible parece indicar que la bioacumulación
    en los organismos acuáticos es baja.  La escasez de datos dificulta la
    evaluación de los posibles efectos en los organismos terrestres.

         El ser humano está expuesto al 1,1,1-tricloroetano principalmente
    por inhalación, y luego el organismo absorbe rápidamente la sustancia. 
    También se puede dar la exposición por contacto cutáneo o ingestión. 
    El tricloroetano se distribuye ampliamente por los tejidos y atraviesa
    las barreras hematoencefálica y placentaria.  Aunque también se ha
    encontrado en la leche humana, no parece que se produzca
    bioacumulación.  La principal vía de eliminación es la exhalación del
    compuesto inalterado.

         Las toxicidades aguda y crónica del 1,1,1-tricloroetano son
    relativamente bajas, pero en condiciones de exposición intensa pueden
    producirse efectos tóxicos.  Estas condiciones se pueden presentar en
    casos de exposición profesional, de abuso del disolvente o de
    accidentes.  Dado que el disolvente es volátil y el vapor es mucho más
    denso que el aire, se pueden producir concentraciones inesperadamente
    elevadas y peligrosas en espacios reducidos, como depósitos de
    almacenamiento "vacíos".  Así, se han producido algunas intoxicaciones
    mortales y casi mortales en lugares de trabajo y otros.

         El efecto más importante en el ser humano se produce en el
    sistema nervioso central.  Los efectos observables van desde ligeros
    cambios de comportamiento (acompañados de una leve irritación ocular)
    con 1,9 g/m3 (350 ppm) hasta la pérdida del conocimiento y el paro
    respiratorio con concentraciones más elevadas.  Sin embargo, también
    se pueden producir anomalías cardíacas fatales.  La toxicidad hepática
    del tricloroetano es inferior a la de la mayoría de los disolventes
    organoclorados.  El nivel sin efecto observado (NOEL) para la especie
    humana parece ser del orden de 1,35 g/m3 (250 ppm).

         No se han publicado estudios adecuados sobre los efectos
    carcinogénicos en la especie humana.  Sin embargo, en los estudios de
    inhalación prolongada en ratas y ratones expuestos a 8,1 g/m3 (1500
    ppm) no se obtuvieron pruebas de ningún efecto carcinogénico.  El
    1,1,1-tricloroetano no tiene un potencial genotóxico importante.

         En ratas y conejos se ha observado toxicidad en la fase de
    crecimiento, pero no teratogenicidad, con concentraciones que fueron
    tóxicas para las madres.  Las escasas pruebas epidemiológicas en
    relación con sus efectos sobre la reproducción no son concluyentes.

    See Also:
       Toxicological Abbreviations
       Trichloroethane, 1,1,1- (WHO Food Additives Series 16)
       Trichloroethane, 1,1,1- (PIM 540)
       Trichloroethane, 1,1,1- (IARC Summary & Evaluation, Volume 71, 1999)