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    1,1,1-TRICHLOROETHANE




    Maeve McParland

    National Poisons Information Service (London Centre)
    Medical Toxicology Unit
    Guy's & St Thomas' Hospital Trust
    Avonley Road
    London
    SE14 5ER
    UK


    This monograph has been produced by staff of a National Poisons
    Information Service Centre in the United Kingdom.  The work was
    commissioned and funded by the UK Departments of Health, and was
    designed as a source of detailed information for use by poisons
    information centres.

    Peer review group: Directors of the UK National Poisons Information
    Service.


    1  SUBSTANCE/PRODUCT NAME

    1.1  Origin of substance

    1,1,1-Trichloroethane is a synthetic chemical. There are no natural
    sources, however it is a common environmental contaminant. It was
    first prepared in 1840 by the action of chlorine on
    1,1-dichloroethane, and first produced commercially in 1946. It is now
    produced commercially by chlorination of ethane, or hydrochlorination
    of 1,1-dichloroethylene or, more commonly, via hydrochlorination of
    vinyl chloride (IARC Monograph, 1979; Durrans, 1971; ILO, 1983; Mark
    et al, 1979).

    1.2  Name

    1.2.1  Brand/trade name

    Tipp-ex, Tipp-ex Thinners (Tippex GmbH), Liquid Paper (Point GmbH).

    1.2.2  Generic name

    1,1,1-Trichloroethane

    1.2.3  Synonyms

    Methyl chloroform, alpha-trichloroethane, methyl trichloromethane,
    1,1,1-Trichloroethan (German), 1,1,1-Trichloorethaan (Dutch),
    1,1,1-Tricloroetano (Italian), 1,1,1-Trichloroethane (French).

    1.2.4  Common names/street names

    Genklene, Inhibisol, Chlorothene.

    1.3  Chemical group/family

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

    1.4  Substance identifier and/or classification by use

    1.5  Reference numbers

         CAS                 71-55-6
         RTECS               KJ 2975000
         EINECS              2007563
         UN                  831
         EEC identity no     602-013-00-2

    1.6  Manufacturer

         Name           Tipp-ex GmbH and Co. KG
         Address        Rossertstrasse 6, D-65835 Leiderbach.
         Telephone      06196-6003-0
         Fax            Not known

         Name           Point GmbH
         Address        Vienna.
         Telephone      Not known
         Fax            Not known

    1.7  Supplier/importer/agent/ licence holder

         Name           Tipp-ex Ltd
         Address        Camberley, Surrey GU15 3DT

         Name           Gillette UK Ltd (Liquid Paper)
         Address        London

    1.8  Presentation

    1.8.1  Form

    Various.

    1.8.2  Formulation details

    Various.

    1.8.3  Pack sizes available

    Various. Tipp-ex and Tipp-ex thinnners are available in 30ml bottles.
    Liquid Paper is available in 20ml bottles.

    1.8.4  Packaging

    Various. Tipp-ex and Liquid Paper are both available in white plastic
    screw top bottles with black and red labelling.

    1.9  Physico-chemical properties

    Chemical structure
         1,1,1-trichloroethane
         Molecular Weight = 133.42
         CH3CCL3

    Physical state
         Liquid (non-viscous)

    Colour
         Colourless

    Odour
         Sweetish odour similar to that of chloroform or carbon
         tetrachloride. The odour of 1,1,1-trichloroethane is considered
         distinctive or powerful enough to provide satisfactory warning of
         exposure, however, it is usually noticeable at about 100ppm which
         is below the level required to cause acute toxic effects (Clayton
         and Clayton,  1981).

    pH
         No information available.

    Solubility in water and organic solvents
         It is slightly soluble in water, soluble in chloroform, ethanol,
         ethyl ether, acetone, methanol, benzene, carbon disulphide, and
         carbon tetrachloride. Solubility in water = 0.95g/L at 20C.

    Important chemical interactions
         A mixture of 1,1,1-trichloroethane and  potassium may explode on
         light impact.

         Violent decomposition with evolution of hydrogen chloride may
         occur when 1,1,1-trichloroethane comes into contact with
          aluminium, magnesium or their alloys (Bretherick, 1981).

         It reacts violently with  dinitrogen tetroxide, oxygen, liquid 
          oxygen, sodium, sodium hydroxide and  sodium potassium alloy 
         (Sax, 1984).

         Phosgene is produced when 1,1,1-trichloroethane comes into
         contact with  iron, copper, zinc or  aluminium at high
         temperatures (Carchman et al, 1984).

         Analytical grade 1,1,1-trichloroethane has a purity of >99.0%
         and contains no added stabilizers. Commercially available
         technical and solvent grade 1,1,1-trichloroethane has a purity of
         90-95% and usually contains 3-8% of stabilizers, mainly to
         prevent the generation of hydrochloric acid and to avoid
         corrosion of metal parts. The stabilizers (usually a mixture) are
         nitromethane, N-methyl pyrole, 1,4-dioxane, butylene oxide,
         1,3-dioxolane, nitroethane, toluene, di-isopropylamine, methyl
         ethyl ketone, iso-butyl alcohol and 2-butanol (IARC Monograph
         1979; Carchman et al, 1984; Fielder et al, 1984).

    Major products of combustion/pyrolysis
         A considerable amount of energy is required for ignition and it
         will not sustain combustion (Clayton and Clayton, 1981).

    Explosion limits
         In air at 25C = 8.0-10.5 vol %

    Flammability
         Nonflammable under normal conditions, vapour burns at high
         temperatures (>360C)

    Boiling point
         74.1 C

    Density
         1.3249 (26/4C)

    Vapour pressure
         13.3 Kpa (100mmHg) at 20C

    Relative vapour density
         4.6 (air =1)

    Flash point
         None

    Reactivity
         A mixture of 1,1,1-trichloroethane and potassium may explode on
         light impact.

         Violent decomposition with evolution of hydrogen chloride may
         occur when 1,1,1-trichloroethane comes into contact with
         aluminium, magnesium or their alloys (Bretherick, 1981).

         It reacts violently with dinitrogen tetroxide, oxygen, liquid
         oxygen, sodium, sodium hydroxide and sodium potassium alloy (Sax,
         1984).

         Phosgene is produced when 1,1,1-trichloroethane comes into
         contact with iron, copper, zinc or aluminium at high temperatures
         (Carchman et al, 1984).

    1.10  Hazard/risk classification

    1.11  Uses

    1,1,1-Trichloroethane is used industrially and domestically as a
    degreaser, dry cleaning agent, and solvent in paints, glues and
    aerosol products. A common source is typewriter correction fluid, and
    correction fluid thinners, in commercial products such as Tipp-ex(TM)
    and Liquid paper(TM).

    1,1,1-Trichloroethane has rapid anaesthetic action and was used for
    this purpose medically but was abandoned with the advent of safer
    agents.

    It is an important chemical intermediate, and is used as an additive
    to raise the flash point of many flammable solvents.

    1.12 Toxicokinetics

    1.12.1  Absorption

    1,1,1-Trichloroethane is rapidly absorbed through the lungs and the
    gastrointestinal tract. Absorption through skin also occurs (Stewart
    and Dodd, 1964), but is of minor significance compared to uptake via
    inhalation.

    1,1,1-Trichloroethane has a relatively low blood/air partition
    coefficient, therefore steady state tissue levels are attained slowly
    and the vapour is eliminated relatively rapidly in expired air after
    exposure.

    Studies with human volunteers (males), exposed by inhalation to
    1,1,1-trichloroethane at concentrations from around 35ppm to 350ppm
    for 6 hours demonstrated that about 25-40 % of the trichloroethane
    inhaled was absorbed by the lungs. The amount varied depending on the
    1,1,1-trichloroethane concentration in the inhaled air, duration of
    exposure, body weight and amount of adipose tissue, blood circulation
    and other factors (Astrand et al, 1973; Monster et al, 1979; Nolan et
    al, 1984). Uptake from inhalation increases with physical activity.

    1.12.2  Distribution

    1,1,1-Trichloroethane has a high lipid/blood partition coefficient and
    is therefore expected to distribute widely into body tissues,
    particularly into those with high lipid content such as the brain and
    adipose tissue. It passes readily through the human blood-brain
    barrier and is also believed to cross the placental barrier to the
    foetus. In one postmortem examination following an acute lethal
    exposure, 1,1,1-trichloroethane was detected in the blood, brain and
    liver (D'Costa and Gunasekera, 1990).

    1.12.3  Metabolism

    1,1,1-Trichloroethane is mainly (90%) excreted unchanged through the
    lungs (Nolan et al, 1984). 60%-80% of an absorbed dose is exhaled
    within one week, however traces may be found in the post-exposure
    expired breath for as long as one month (Baselt and Cravey, 1989).
    Small amounts of 1,1,1-trichloroethane are slowly metabolized by
    oxidation to trichloroethanol, which is conjugated with glucuronic
    acid before excretion in the urine. This accounts for only about 2% of
    an absorbed dose. Trichloroacetic acid is formed from trichloroethanol
    as a further oxidation product and is also found in the urine to the
    extent of about 1.5% of a dose (Monster et al, 1979). Simultaneous
    exposure to other solvents tends to increase the retention and
    decrease the metabolism of 1,1,1-trichloroethane (Savolainen et al,
    1981).

    1.12.4  Elimination

    Regardless of the route of administration, the main excretary route
    for 1,1,1-trichloroethane is exhalation via the lungs. Initial
    excretion is fairly rapid (70% reduction of the level in expired air
    within 2 hours (Monster et al, 1977), but this is followed by slower
    elimination, with small amounts being detected in the breath for up to
    several days post-exposure.

    Studies with human volunteers show that over 90% of the absorbed
    1,1,1-trichloroethane is excreted unchanged in the expired air. Only
    minor quantities (5-6%) of the absorbed solvent are excreted in the
    urine (as trichloroethanol glucuronide and trichloroacetic acid)
    (Monster et al, 1979). Less than 1% of an absorbed dose remained in
    the body after 9 days (Nolan et al, 1984).

    1.12.5  Half-life

    At or below TLV of 350 ppm elimination (in expired air) was reported
    to be triexponential (Nolan et al, 1984):
    Initial phase = 44 minutes,
    Intermediate phase = 5-7 hours,
    Terminal phase = 53 hours.

    The half lives of the metabolites in urine were:
    2,2,2-Trichloroethanol = 13 hours,
    Trichloroacetic acid = 51 hours.
    Urinary excretion rate of the two metabolites is very variable and
    provides only a rough estimate of exposure (Nolan et al, 1984).

    1.12.6  Special populations

    Simultaneous exposure to other solvents tends to increase the
    retention and decrease the metabolism of 1,1,1-trichloroethane
    (Savolainen et al, 1981), so occupational exposure to mixed solvents
    may put workers at greater risk of 1,1,1-trichloroethane toxicity.

    2  SUMMARY

    3  EPIDEMIOLOGY OF POISONING

    Most cases of poisoning with 1,1,1-trichloroethane result from
    accidental occupational exposure or intentional abuse, commonly
    referred to as volatile solvent abuse (VSA). Accidents involving the
    accumulation of high concentrations are rare, the highest risk group
    are intentional abusers.

    Occupational Exposure

    A review of industrial accidents noted to the Factory Inspectorate in
    the UK during the period 1961-1980, and involving certain halogenated
    hydrocarbon solvents revealed 52 incidents due to
    1,1,1-trichloroethane (McCarthy and Jones, 1983).

    Volatile Substance abuse

     Modes of abuse: Techniques vary depending on the product but all
    involve deep breathing through the nose and mouth and not just
    sniffing as the term 'glue sniffing' implies. Terms of abuse used are
    'huffing' and 'bagging', and are methods used with the intention of
    maximising the concentration of solvent in inhaled air:

     Huffing:- The solvent (liquids - dry cleaning fluids and typewriter
    correction fluids) is poured onto a piece of cloth and held to the
    nose or mouth.

     Bagging:- A small amount of the solvent (viscous products - usually
    glue) is poured into a polythene bag and the open end placed over the
    nose and mouth, the vapour released is rebreathed until the desired
    effect is achieved.

    The packaging and container size of typewriter correction fluids also
    enables them to be inhaled directly from the bottle.

     Products abused: The source for 1,1,1-Trichloroethane abuse is
    commonly typewriter correction fluids (Tipp-ex(TM) and Liquid
    Paper(TM)). Factors contributing to its popularity are: low cost,
    availability and easy concealment.

     Morbidity and Mortality: Bass (1970) first drew attention to the
    increase in deaths attributable to VSA in the United States during the
    1960s. In this review spot remover containing 1,1,1-trichloroethane
    was identified as being responsible for 29 out of 110 (26%) cases of
    sudden death. Death was from cardiac arrhythmias, leading to
    fibrillation and cardiac arrest due to the combined effect of
    hypercapnia (from repeated inhalation from a bag) and catecholamine
    release (due to stress), on the myocardium that had been sensitized to
    these agents by the volatile solvent.

    Watson (1979) reported the first substantial study of VSA deaths in
    Britain. She reported 45 cases of sudden death and showed a doubling
    in the number of deaths between the time periods of 1970-1973 and
    1974-1975. Anderson et al (1985), stated that deaths from VSA were
    about 100 per annum, occurring most frequently in males under 20 years
    of age.

    In the United Kingdom between 3.5% and 10% of young people have at
    least experimented with VSA and current users comprise 0.5-1% of the
    secondary school population (Ramsey et al, 1989). There is a trend
    towards the misuse of products containing gases, predominantly butane
    (Esmail et al, 1992).

     Prevention: In England and Wales the Intoxicating Substances
    (Supply) Act (1985) makes it an offence to sell, or to offer for sale,
    substances to children under the age of 18 years if the vendor has
    grounds for believing that those substances are likely to be inhaled
    to achieve intoxication.

    In an attempt to address the problem of solvent abuse the German
    company manufacturing Tipp-ex(TM) (Tipp-ex GmbH and Co) introduced a
    water based correction fluid in addition to the older version
    containing 1,1,1-trichloroethane. In 1984 the manufacturer of Liquid
    Paper(TM) added mustard oil to the product in an attempt to discourage
    abuse, and strengthened the wording of its product warning label.

    4  MECHANISM OF ACTION/TOXICITY

    1,1,1-Trichloroethane sensitizes the heart to catecholamines, is a
    central nervous system and respiratory system depressant, and a skin
    and mucous membrane irritant.

    1,1,1-Trichloroethane is less toxic than other chlorinated
    hydrocarbons which may be explained in part by its lesser degree of
    metabolism, the majority of an inhaled dose being excreted via the
    lungs. It is weakly anaesthetic when compared to other chlorinated
    hydrocarbons (Kelafant et al, 1994).

    Acute intoxication with 1,1,1-trichloroethane causes initial
    excitement and euphoria followed by depression of the central nervous
    system with dizziness, drowsiness, ataxia and headache, progressing to
    coma and death from respiratory depression in severe cases. Death also
    occurs from ventricular arrhythmias as at high concentrations the
    solvent sensitizes the myocardium to adrenaline and other
    catecholamines.

    The vapour and liquid are irritating to the skin and mucous membranes.
    Nausea, vomiting and diarrhoea have all been reported following
    ingestion.

    1,1,1-Trichloroethane causes minimal hepatic dysfunction, except in
    high concentrations, and animal livers are relatively resistant to all
    except lethal levels of 1,1,1-trichloroethane (Stewart,1971).

    5  FEATURES OF POISONING

    5.1  Acute

    5.1.1  Ingestion

    Ingestion of 1,1,1-trichloroethane causes irritation to the
    gastrointestinal tract with subsequent nausea, vomiting, abdominal
    pain and diarrhoea. Symptoms have been noted within 30 minutes of
    ingestion (Gerace, 1981).

    It is well absorbed by ingestion (Gerace, 1981) and causes central
    nervous system depression with dizziness, drowsiness, headache and
    ataxia, progressing to coma and death from respiratory depression in
    severe cases (Stewart, 1968). Convulsions may occur.

    Sensitization of the myocardium to adrenaline and other catecholamines
    may occur causing potentially fatal arrhythmias (Hall and Hine, 1966;
    Bass, 1970; Stewart, 1971; Reinhardt et al, 1973; Travers, 1974).

    The irritant effect of 1,1,1-trichloroethane on the gastrointestinal
    tract with concurrent decrease in conscious level presents the risk of
    gastric aspiration.

    In a report of accidental ingestion of 1 oz (approx. 28ml) of
    1,1,1-trichloroethane, severe gastrointestinal irritation developed
    shortly after ingestion requiring hospital admission, where a gastric
    lavage was performed. No CNS disturbance or neurological abnormalities
    were observed on investigation 4 hours post-exposure (Stewart and
    Andrews, 1966).

    5.1.2  Inhalation

    1,1,1-Trichloroethane vapours are irritating to the eyes and mucous
    membranes causing coughing and chest tightness as the concentration
    increases (Environmental Health Criteria 136, 1992). It has a
    depressant action on the central nervous system and is narcotic at
    high concentrations.

    With intentional abuse an initial excitatory phase occurs which may be
    followed by depression and a hangover effect (similar although less
    severe than that caused by alcohol) (Watson, 1982). This initial
    euphoria may progress to confusion, disorientation, dizziness,
    headache, incoordination, drowsiness, hallucinations and aggressive
    behaviour while continued exposure will lead to coma, convulsions,
    respiratory depression, cardiovascular collapse and death (Stewart,
    1971).

    Recovery from 1,1,1-trichloroethane induced narcosis is usually
    complete with no serious sequelae (Torkelson et al, 1958; McCarthy and
    Jones, 1983)

    Vomiting can occur with the risk of aspiration of stomach contents
    (Hall and Hine, 1966).

    Sensitization of the myocardium to adrenaline and other catecholamines
    may occur causing potentially fatal arrhythmias (Hall and Hine, 1966;
    Bass, 1970; Stewart 1971; Reinhardt et al, 1973; Travers, 1974).

    5.1.3  Dermal

    Like many solvents 1,1,1-trichloroethane will defat the skin.
    Absorption through the skin can occur but it is not a significant
    route of exposure. Despite its widespread use only a few cases of skin
    irritancy have been reported.

    Skin vesication and erythema may occur with prolongued contact (Jones
    and Winter, 1983).

    In a volunteer study, immersion of a hand in liquid
    1,1,1-trichloroethane for 30 minutes resulted in mild erythema, which
    persisted for one hour (Stewart and Dodd, 1964).

    Allergic contact dermatitis presenting as severe eczema has been
    reported following exposure to 1,1,1-trichloroethane (Ingber, 1991).

    5.1.4  Ocular

    When 1,1,1-trichloroethane comes into contact with the eye only
    superficial and transient eye irritation occurs. 1,1,1-Trichloroethane
    tested by drop application to rabbit eyes caused slight conjunctival
    irritation and no corneal damage (Grant and Schuman, 1993).

    5.1.5  Other routes

    Intraperitoneal

    The intraperitoneal LD50 value has been reported to be 5.1g/kg in
    the rat, and values in the range 2.6-4.9g/kg have been obtained in
    mice. In all cases the compound was given as a solution in vegetable
    oil. Much higher toxicity was reported when 1,1,1-trichloroethane was
    given in dimethylsulphoxide (DMSO), the LD50 in this case being
    84mg/kg in the mouse. This was presumably due to more rapid uptake
    from the peritoneal cavity using this route. This study did not give
    any indication of toxic effects other than lethality (Fielder et al,
    1984).

    In another intraperitoneal study using mice, liver damage was noted 24
    hours after a dose of 3.7g/kg. The damage consisted of slight
    necrosis, hepatocyte enlargement and vacuolation. A slight rise in
    serum aminotransferase was also noted (Klassen and Plaa, 1966).

    5.2  Chronic toxicity

    5.2.1  Ingestion

    There is no human data.

    5.2.2  Inhalation

    A Japanese study on women chronically exposed to levels of up to about
    350ppm (established TLV) gave no evidence of any disturbances in the
    central or peripheral nervous system (HSE Toxicity Review 9, 1984).

    Kelafant et al (1994) studied 28 workers with long term repetitive
    high exposures to 1,1,1-trichloroethane (exposure levels were not
    known but thought to be very high as environmental controls were poor
    and subjects frequently complained of mild neurological symptoms while
    working). They were evaluated for complaints of short term memory
    loss, moodiness, disequilibrium, irritability and decreased ability to
    concentrate. As a group they had significant deficits on
    neuropsychological testing and platform posturography demonstrated
    deficits in vestibular, somatosensory and occular components of
    balance. They concluded that the encephalopathic picture in these
    subjects is similar to reported with other solvents.

    House et al (1994), report a case of peripheral neuropathy occurring
    possibly as a result of daily exposure to 1,1,1-trichloroethane.

    5.2.3  Dermal

    Prolonged or repeated skin contact with 1,1,1-trichloroethane may lead
    to dermatitis, due to its defatting action. Despite its widespread use
    only a few cases of skin irritancy have been reported. Skin vesication
    and erythema may occur with prolonged contact (Jones and Winter,
    1983).

    Allergic contact dermatitis presenting as severe eczema has been
    reported following exposure to 1,1,1-trichloroethane (Ingber, 1991).

    Liss (1988), described two cases of peripheral neuropathy among
    workers who immersed their hands in 1,1,1-trichloroethane while using
    it as a degreaser.

    Repeated topical application of 1,1,1-trichloroethane to abraded and
    non-abraded rabbit skin for up to 90 days, resulted in slight
    reversible irritation (Torkelson et al, 1957).

    5.2.4  Ocular

    Repeated daily application of about 50l of 1,1,1-trichloroethane to
    eyes of rabbits (5 days a week for 2 weeks) led to the development of
    a mild inflammatory reaction. The reaction disappeared within 48 hours
    of the last application (Fielder et al, 1984).

    5.2.5  Other routes

    No data.

    5.3  Systematic description of clinical effects

    5.3.1  Cardiovascular

     Acute effects

    Hypotension may be noted following acute exposure and cardiovascular
    collapse has been reported after large, single exposures.

    Sensitization of the myocardium to adrenaline and other catecholamines
    may occur causing potentially fatal arrhythmias (Hall and Hine, 1966;
    Bass, 1970; Stewart 1971; Reinhardt et al, 1973; Travers, 1974).

     Chronic effects

    Banathy and Chan (1983) described the postmortem findings in a 14 year
    old Liquid Paper(TM) abuser who died suddenly which revealed
    myocardial degenerative changes including interfibrillary oedema,
    swollen and ruptured myofibrils (see case 12, section 7).
    Wright and Strobl (1984) reported a case of prolonged cardiac
    arrhythmias in a 45 year old man, after low level exposure to
    1,1,1-trichloroethane. The patient was previously well with no history
    of cardiovascular disease. He experienced almost continuous inhalation

    and dermal exposure to 1,1,1-trichloroethane in his occupation. An
    irregular heart beat was discovered on routine physical examination
    and 24 hour monitoring revealed multiple ventricular ectopic beats,
    episodes of ventricular bigeminy, trigeminy and ventricular
    fibrillation. The arrhythmias continued for 2 weeks after cessation of
    exposure and resolved completely after one month.
    McCleod et al (1987) suggest an adverse interaction between
    1,1,1-trichloroethane and halothane. The authors report on two
    patients with repeated exposure to 1,1,1-trichloroethane who
    experienced cardiac deterioration with halothane anaesthesia. They
    proposed the possibility of chronic cardiac toxicity induced by
    repeated exposure to 1,1,1-trichloroethane followed by a toxic
    interaction with halothane.

    5.3.2  Respiration

    Respiratory system symptoms such as cough, breathlessness and chest
    tightness are common in cases of acute poisoning (Boyer et al, 1987).
    Respiratory depression may occur following acute exposure.

    Woo et al (1983), reported a case of hypoxemia and chest pain
    following inhalation of a 1,1,1-trichloroethane aerosol product. The
    solvent was combined with a surface active agent in the product. The
    combined formulation increased the water solubility of
    1,1,1-trichloroethane and enhanced disposition in the upper airway
    thus causing considerable respiratory distress. The authors concluded
    that the symptoms could not be attributed to the propellant, surface
    active agent or 1,1,1-trichloroethane alone.

    5.3.3  Neurological

     Acute effects

    1,1,1-Trichloroethane causes central nervous system depression, the
    severity of symptoms depending on the concentration and exposure time.

     Initial mild effects: dizziness, headache, ataxia, incoordination,
    fainting.
     As concentration increases: collapse, coma.

    A 15 year old boy suffered intense cerebral oedema with tonsillar
    herniation following acute exposure (suspected abuse) to 1,1,1-
    trichloroethane in typewriter correction fluid and subsequently died
    (D'Costa and Gunaskera, 1990).

     Chronic effects

    A Japanese study on women chronically exposed to levels of up to about
    350ppm (established TLV) gave no evidence of any disturbances in the
    central or peripheral nervous system (HSE Toxicity Review 9, 1984).

    Kelafant et al (1994) studied 28 workers with long term repetitive
    high exposures to 1,1,1-trichloroethane (exposure levels were not
    known but thought to be very high as environmental controls were poor
    and subjects frequently complained of mild neurological symptoms while
    working). They were evaluated for complaints of short term memory
    loss, moodiness, disequilibrium, irritability and decreased ability to
    concentrate. As a group they had significant deficits on
    neuropsychological testing and platform posturography demonstrated
    deficits in vestibular, somatosensory and occular components of
    balance. They concluded that the encephalopathic picture in these
    subjects is similar to reported with other solvents.

    Liss (1988), described two cases of peripheral neuropathy among
    workers who immersed their hands in 1,1,1-trichloroethane while using
    it as a degreaser. House et al (1994) report a case of peripheral
    neuropathy occurring possibly as a result of daily exposure to
    1,1,1-trichloroethane.

    5.3.4  Gastrointestinal

    Nausea, vomiting and diarrhoea occur. Gastrointestinal symptoms may
    predominate shortly after ingestion, with the later features
    resembling those expected following inhalation exposure.

    In a case of accidental ingestion of approximately 600mg of
    1,1,1-trichloroethane/kg, signs of severe gastrointestional irritation
    (vomiting, diarrhoea) were evident shortly after the ingestion
    (Stewart and Andrews, 1966).

    5.3.5  Hepatic

    1,1,1-Trichloroethane causes minimal hepatic dysfunction, except in
    high concentrations. In humans transient rises in liver enzymes have
    been reported (Gerace, 1981).

    Halevy et al (1980) report a case of liver damage following acute
    occupational exposure to 1,1,1-trichloroethane, although this may have
    been due to an individual hypersensitivity reaction (see case 6,
    section 7).

    In a study of long term occupationally exposed workers to
    1,1,1-Trichloroethane for neurological deficits, hepatic function was
    also monitored and was normal in all cases (Kelafant et al, 1994). In
    a matched pair study under controlled conditions to 500ppm (7 hours a
    day) for five days, volunteers showed evidence of mild CNS
    disturbance, but there was no evidence of any liver or kidney
    dysfunction from clinical chemistry studies at the end of the exposure
    period (Stewart et al, 1969).

    Thiele et al (1982) report a case of hepatic cirrhosis after several
    years of heavy exposure to trichloroethylene followed by 3 months of
    work that involved using an aerosolized degreaser containing
    1,1,1-trichloroethane. They suggest that an individual suffering

    hepatic injury from a chlorinated hydrocarbon may be at risk of
    further progression of the disease upon subsequent exposure to even a
    relatively non-toxic member of this family of organic solvents (in
    this case 1,1,1-trichloroethane).

    Animal livers are relatively resistant to all except lethal levels of
    1,1,1-trichloroethane (Stewart, 1971).

    5.3.6  Urinary

    In a matched pair study under controlled conditions to 500ppm (7 hours
    a day) for five days, volunteers showed evidence of mild CNS
    disturbance. There was no evidence of any liver or kidney dysfunction
    from clinical chemistry studies at the end of the exposure period
    (Stewart et al, 1969).

    5.3.7  Endocrine and reproductive system

    No human data available.

    5.3.8  Dermatological

    Absorption through the skin can occur but is not a significant route
    of exposure (ACGIH 1986). Skin vesication and erythema may occur with
    prolongued contact (Jones and Winter, 1983).

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

    Allergic contact dermatitis presenting as severe eczema has been
    reported following chronic exposure to 1,1,1-trichloroethane (Ingber,
    1991).

    5.3.9  Eye, ears, nose and throat

    1,1,1-Trichloroethane vapours are irritating to the eyes and mucous
    membranes. Contact with the eyes will cause transient, superficial
    irritation only.

    No systemic toxic effects on the human eye occur from exposure to
    1,1,1-Trichloroethane. 1,1,1-Trichloroethane tested by drop
    application to rabbit eyes caused slight conjunctival irritation and
    no corneal damage (Grant and Schuman, 1993).

    5.3.10  Haematological

    No abnormalities reported.

    5.3.11  Immunological

    No abnormalities reported.

    5.3.12  Metabolic

    5.3.12.1  Acid-base disturbances

    No abnormalities reported.

    5.3.12.2  Fluid and electrolyte distrurbances

    No abnormalities reported.

    5.3.12.3  Other

    None.

    5.3.13  Allergic reactions

    Halevy et al (1980) report a case of liver damage following acute
    occupational exposure to 1,1,1-trichloroethane, although this was
    thought to have been due to an individual hypersensitivity reaction
    (see case 6, section 7).

    5.3.14  Other clinical effects

    None.

    5.4  At risk groups

    5.4.1  Elderly

    No data.

    5.4.2  Pregnancy

    No data.

    5.4.3  Children

    Gallagher (1990) recommends caution in the use of some adhesive tape
    remover products in intensive care nurseries. 1,1,1-Trichloroethane is
    a component of some commercially available tape remover pads that are
    used in intensive care to lessen the skin trauma from removal of
    adhesive tape. The simulated use of 2 different pads in an infant
    incubator produced detectable levels of 1,1,1-trichloroethene for
    several minutes. Since the risk to a neonate is unknown, the author
    recommends that these pads should not be used on the skin of neonates
    in incubators.

    5.4.4  Enzyme deficiencies

    No data.

    5.4.5  Enzyme induced

    No data.

    5.4.6  Occupations

    Mainly used as a metal degreaser therefore at risk occupations are:
    heavy equipment mechanics and cleaners, automechanics, machine
    operatives, assemblers, printers, garage workers, tool and dye makers.
    Industrial chemists using it as an intermediate and dry cleaners are
    also at risk.

    Thiele et al (1982) suggested that pre-exposure to other chlorinated
    hydrocarbons may increase the potential for hepatic damage from
    1,1,1-trichloroethane.

    5.4.7  Others

    Adolescents are particularly susceptible to volatile substance abuse,
    including the abuse of 1,1,1-trichloroethane.

    Exposure to 1,1,1-trichloroethane may increase sensitivity to other
    compounds, e.g. anaesthetics (McCleod et al, 1987).

    6  MANAGEMENT

    6.1  Decontamination

    Following inhalation of 1,1,1-Trichloroethane patients should be
    removed from the source of exposure. Maintain respiration and cardiac
    output. Seek medical advice as soon as possible. First aiders should
    wear protective clothing to prevent secondary contamination.

    Contaminated clothing should be removed and exposed skin irrigated
    immediately with copious amounts of water.

    Eyes should be irrigated for at least 15 minutes with water or normal
    saline. They should then be examined with fluorescein, referral to an
    ophthalmologist may be necessary.

    Although no evidence could be found to suggest that
    1,1,1-trichloroethane is an aspiration hazard itself, the irritant
    effect of 1,1,1-trichloroethane on the gastrointestinal tract with
    concurrent CNS depression increases the risk of aspiration of stomach
    contents. Thus emesis is contraindicated and gastric lavage with a
    cuffed ET tube if necessary, is the preferred method of gastric
    decontamination.

    The use and efficacy of activated charcoal has not been studied, nor
    the optimum timing for gastric lavage following ingestion, however a
    abdominal x-ray (1,1,1-trichloroethane is radio-opaque) may aid the
    decision.

    6.2  Supportive care

    Treatment is primarily symptomatic, with support of the cardiovascular
    and respiratory systems. Use of adrenaline or related sympathomimetic
    stimulants are contraindicated due to the risk of inducing ventricular
    fibrillation.

    6.3  Monitoring

    Level of consciousness, ECG, respiratory rate function should all be
    monitored, along with liver and kidney function in severe cases.

    A chest x-ray is indicated in patients with respiratory symptoms and
    in cases of suspected aspiration.

    6.4  Antidotes

    There is no specific antidote for 1,1,1-trichloroethane intoxication.

    6.5  Elimination techniques

    The efficacy of enhanced elimination techniques (e.g. haemodialysis,
    haemoperfusion, etc) has not been established.

    6.6  Investigations

    1,1,1-Trichloroethane is radio-opaque and following acute
    intoxications, abdominal x-ray examinations may be useful for
    diagnosis. Furthermore, they may provide evidence for the
    effectiveness of gastric lavage (Dally et al, 1986).

    Typewriter correction fluid contains titanium dioxide and the presence
    of white particulate matter in the nose and/or on hands maybe a clue
    to diagnosis.

    1,1,1-Trichloroethane is present in expired breath in significant
    concentrations to allow specific identification if this technique is
    available (Gerace, 1981).

    Blood and urine toxicological analysis may be useful in confirming
    exposure.

    6.7  Management controversies

    Although little evidence could be found to suggest that
    1,1,1-trichloroethane is an aspiration hazard itself, the irritant
    effect of 1,1,1-trichloroethane on the gastrointestinal tract with
    concurrent CNS depression increases the risk of aspiration of stomach
    contents. Thus emesis is contraindicated and gastric lavage with a
    cuffed ET tube if required, is the preferred method of gastric
    decontamination.

    Dickerson and Biesemer (1982 - see section 9.10) from studies in rats,
    concluded that 1,1,1-trichloroethane was capable of lung injury and
    posed an aspiration risk from aspiration of the volatile hydrocarbon
    itself. Travers (1974) references Hall and and Hine (1966) in claiming
    one of the causes of death with 1,1,1-trichloroethane is aspiration of
    the solvent.

    Woo et al (1983), reported a case of hypoxemia and chest pain
    following inhalation of a 1,1,1-trichloroethane aerosol product. The
    solvent was combined with a surface active agent in the product. The
    combined formulation increased the water solubility of
    1,1,1-trichloroethane and enhanced deposition in the upper airway thus
    causing considerable respiratory distress. The authors concluded that
    the symptoms could not be attributed to the propellant, surface active
    agent or 1,1,1-trichloroethane alone.

    7  CASE DATA

    CASES FROM THE LITERATURE

    Case 1: Accidental in a child

    Shortly after being put to bed by his parents, a previously well 4
    year old boy was heard to be making unusual noises. He was found under
    the bed clothes limp and apnoeic. While an ambulance was called his
    father administered mouth to mouth resuscitation. En route to hospital
    ventilatory support was continued. On arrival at hospital he was pale,
    comatose and unresponsive to painful stimuli. An erythematous,
    blistered area was noted on the right cheek. Vital signs were as
    follows: pulse 120 beats/minute; blood pressure 100/70 mmHg;
    respirations 24/minute. The child was monitored and oxygen by mask and
    intravenous fluids were given. Twelve minutes after arrival in the
    emergency department the patient started to move spontaneously and
    then awoke and became alert and orientated. The stomach was emptied
    and activated charcoal and magnesium sulphate administered.
    Investigations revealed normal electrolytes, glucose, BUN, blood
    count, and chest x-ray. A toxicology screen was also normal. Later in
    the day however, alkaline phosphatase, LDH and SGOT were noted to be
    raised. The child was discharged well 48 hours after admission and 6
    month follow up revealed the child to being well with no long term
    sequelae.

    The child was thought to have attempted to play with a sibling's toy
    flower making kit which contained a 30ml container of
    1,1,1-trichloroethane. As this had been forbidden to him he had taken
    it to play with under the covers. The fumes probably rendered him
    unconscious at which time the 1,1,1-trichloroethane spilled onto the
    bed. He fell with his cheek into the compound and continued to inhale
    the fumes. The unusual noise heard may have been a seizure secondary
    to hypoxia or airway compromise with a decreased level of
    consciousness (Gerace, 1981).

    Case 2: Fatal accidental occupational

    A 15 year old male died 6 weeks after starting his first job. His
    duties involved using 1,1,1-trichloroethane in a centrifuge to
    degrease small metal parts. The process involved supporting the parts
    on perforated trays, which rested across the top of a tank of cold
    1,1,1-trichloroethane, and scooping up the solvent in cans and running
    it over the parts. The open top of the tank measured approximately
    0.9m by 0.6m and stood 0.75m above floor level by the doorway, it was
    not fitted with extract ventilation.

    The body of the deceased was found at about midday slumped over the
    edge of the tank. It is thought he may have decided to wash his hands
    in the solvent before going to lunch, and been over come by the vapour
    while bending over the edge of the tank. Death was certified as being
    due to cardiorespiratory failure due to 1,1,1-trichloroethane vapour
    (Northfield, 1981).

    Case 3: Fatal accidental occupational

    A 20 year old apprentice electrician was found dead on the floor of a
    fume filled room, where he had earlier been using
    1,1,1-trichloroethane as a degreasing solvent from an open bowl. The
    exact circumstances of the solvent's use leading to the incident are
    not known, although an upright, half-full can of solvent was on the
    workbench and there was evidence of some spillage on the floor. The
    man had been seen 2 hours previously by a colleague and had appeared
    well.

    At postmortem the deceased had blistering and second degree burns on
    his face and neck, the skin changes being in line with the folds of
    his clothing, and consistent with prolonged contact of the solvent
    with the body. There was oedema and congestion of the brain and lungs,
    and small serous effusions in both pleural cavities. The stomach
    showed mucosal congestion and a few scattered petechial haemorrhages.
    The blood concentration of 1,1,1-trichloroethane was 4.2mg/100ml, and
    the brain concentration was 123mg/100g and it was detected in the
    liver. At inquest it was concluded that death resulted from
    suppression of the respiratory centre secondary to severe central
    nervous system depression (Jones and Winter, 1983).

    Case 4: Fatal accidental occupational

    A 27 year old radiator and metal tank repairman was dicovered by
    colleagues in the tail portion of a 450-gallon aircraft tip with only
    his legs protruding from the upper end of the tank. He was
    unresponsive, cyanotic and apnoeic. Artificial resuscitation was begun
    immediately upon removal and then continued with a respiration device
    by an occupational nurse. An ambulance was summoned and artificial
    respiration continued until the worker arrived at the industrial
    dispensary where he was pronounced dead by the duty physician.

    Environmental measurements obtained approximately one hour and twenty
    minutes after the accident revealed a a 1,1,1-trichloroethane
    concentration of 500 ppm within the tank. At autopsy the diagnoses
    were coronary artery sclerosis and acute passive congestion of the
    vicera and petechial haemorrhages in the lung and brain. Toxicological
    analysis indicated a blood 1,1,1-trichloroethane concentration of
    6mg/100ml (Hatfield and Maykoski, 1970).

    Case 5: Fatal accidental occupational

    An 18 year old male was found with his head submerged in a bath of
    1,1,1-trichloroethane. There was respiratory and cardiac arrest with
    fixed, dilated pupils. Artificial respiration and cardiac massage were
    initiated about 15 minutes after his discovery and he was intubated
    and ventilated. Spontaneous respiration was resumed but he did not
    regain consciousness. Cerebral atrophy was evident on a CAT scan
    carried out 2 months after the accident, and the protective eye reflex
    was absent on both sides suggesting a lesion of the occipital cortex,
    while the pupils remained dilated and inactive to light. There was
    restlessness and jerking of the limbs and trunk and fixed flexion of
    all four limbs developed. There were recurrent urinary infections and
    the patient died 39 months after the accident.

    At autopsy the brain showed symmetrical infarction of the lenticular
    nuclei and of the occipital cortex, these changes possibly being the
    cause of the neurological manifestations during life. The authors
    noted that the pattern of cerebral hypoxia was similar, although not
    identical to that found in carbon monoxide poisoning and suggested it
    may be specific for 1,1,1-trichloroethane poisoning (Gresham and
    Treip, 1983).

    Case 6: Accidental occupational causing short term liver
    damage (possibly individual hypersensitivity reaction)

    A 55 year old male was spraying with 1,1,1-trichloroethane in a small
    room with limited ventilation. Several hours after the exposure he
    felt dizzy with headache, nausea, cramping abdominal pain and passed a
    few watery stools. At 48 hours post-exposure his sclerae were noticed
    to be yellow and he developed coughing and a temperature of 40C.
    Although the past medical history showed a previous episode of
    hepatitis A during childhood, there had been no evidence of consequent
    liver damage. On admission at 48 hours post-exposure, serum bilirubin
    was 3.6mg/100ml of which 2.7mg/100ml was conjugated; SGOT 89iu; LDH
    280iu; alkaline phosphatase 287 iu (normal 80). Creatinine in blood
    was 1.55mg/100ml, and urinalysis showed a proteinuria with 2.9g in 24
    hour urine collection. Liver function tests showed a continuing
    deterioration until the 6th day post exposure, peak levels being
    4.9mg/100ml total bilirubin (most of it conjugated), SGOT 287iu; LDH
    328iu, and alkaline phosphatase 287iu. Liver function then began to
    improve but not until 38 days post-exposure did it become normal. A
    percutaneous liver biopsy taken 14 days after exposure to
    1,1,1-trichloroethane, while the liver function was still grossly

    deranged, showed preservation of the lobular structure with
    infiltration of the portal spaces by lymphocytes, histocytes,
    neutrophils, and eosinophils and cholestasis. At follow up at one year
    after the intoxication there was no evidence of disturbed liver or
    kidney function.

    Other significant findings were an urticarial rash developing on day
    9, eosinophilic infiltration was found in the liver, and a MIF
    (migration inhibition factor) test following stimulation of the
    patient's lymphocytes was positive for 1,1,1-trichloroethane. These
    findings, along with the minimal neurological symptoms experienced,
    suggest the possibility of an individual hypersensitivity reaction
    (Halevy et al, 1980).

    Case 7: Fatal intentional abuse

    A 13 year old male was witnessed inhaling Tipp-ex(TM)
    (1,1,1-trichloroethane) from a polythene bag in the early evening. He
    returned home later and appeared well, and subsequently went to his
    bedroom to inhale some more. Shortly after this he collapsed and died.
    Resuscitation was attempted after rapid transfer to hospital but was
    unsuccessful.

    At autopsy, internal examination revealed mild venous congestion and
    oedema of both lungs. The air passages contained blood stained fluid
    along with sticky mucous and the mucosal lining was slightly reddened.
    Toxicological analysis revealed a 1,1,1-trichloroethane blood
    concentration of 0.003 g/g (MacDougal et al, 1987).

    Case 8: Fatal intentional abuse

    A 15 year old boy became ataxic and disorientated after inhaling
    Tipp-ex(TM) (1,1,1-trichloroethane) thinning fluid and was dead on
    arrival at the casualty department less than 6 minutes later. The
    deceased had been previously well and had never to his parents
    knowledge abused solvents before.

    Postmortem examination showed intense congestion and oedema of both
    lungs, and frothy fluid in the main air passages. Toxicological
    analysis revealed a blood 1,1,1-trichloroethane concentration of 0.2
    g/g (MacDougal et al, 1987).

    Case 9: Fatal intentional abuse

    A 18 year old apprentice seaman collapsed on the deck of his ship. A
    bottle of 1,1,1-trichloroethane along with a rag soaked in the solvent
    was found in his bunk. He received mouth to mouth resuscitation then
    was moved to a dispensary where he was intubated and ventilated.
    Ventricular fibrillation was observed and external cardiac massage was
    started. Defibrillation was required numerous times and bicarbonate,
    calcium, atropine, isoprenaline, lignocaine, noradrenaline, phenytoin
    and intracardiac adrenaline were all administered. He was transferred

    to a naval hospital, 6 hours after collapsing. At this stage he was
    cyanotic, his blood pressure was 80/60, with a regular pulse of
    160/minute, and he responded only to painful stimuli. A chest x-ray
    showed bilateral pulmonary infiltrates and an ECG showed wide QRS
    complexes along with ventricular tachycardia. Biochemistry was as
    follows: serum sodium 154mEq/L; potassium 2.8mEq/L; chloride 87mEq/L;
    CO2 32mEq/L; Blood urea nitrogen 18mg/100ml; glucose 410mg/100ml;
    serum osmolality 344mOsm/L; haemoglobin 16.9 g/100ml; haematocrit 50.6
    volumes per cent; white blood cell count 31,400mm3 . The SGOT was 160
    IU, the alkaline phosphatase 27 IU, lactic dehydrogenase 1500 IU, with
    a total bilirubin of 0.35mg/100ml. Arterial blood gas analysis while
    the patient was breathing 5 litres of oxygen/minute via an
    endotracheal tube revealed: pH 7.61; pO2 26mm Hg; haemoglobin
    saturation 57%. There was adequate urine output but with gross
    haematuria.

    The patient was given steroids, antibiotics and potassium and
    continued to be ventilated. Progressive hypotension and bradycardia,
    unresponsive to isoprenaline and noradrenaline, and several episodes
    of cardiac arrest eventuated in his death 24 hours after collapse.

    Autopsy showed heavy and congested lungs but no evidence of pulmonary
    oedema or aspiration pneumonitis. The heart showed right atrial
    dilatation and circumferential left ventricular subendocardial
    haemorrhage and microscopically there was widespread recent
    infarction. This was probably due to a prolonged period of hypoxaemia
    and hypotension followed by intensive resuscitation efforts. Except
    for mild congestion of the vicera, cerebral oedema and Purkinje cell
    chromatolysis, the remaining organs were grossly and microscopically
    normal. The clinically described gross haematuria had no anatomic
    counterpart in the kidneys and was probably due to traumatic insertion
    of an indwelling catheter.

    Postmortem tissue concentrations of 1,1,1-trichloroethane could not be
    detected in the liver, kidney, blood or brain and the analyses for
    other drugs (opiates, barbiturates, amphetamines) were negative with
    only lignocaine present in tissues in detectable concentrations
    (Travers, 1974).

    Case 10: Fatal intentional abuse

    A previously well 13 year old male was playing with a friend outdoors
    when he suddenly got up and ran along a nearby path shouting and then
    fell to the ground apparently lifeless. His friend said he thought he
    had broken his neck on collapsing. An adult arrived on the scene and
    as he could find no pulse attempted cardiopulmonary resuscitation
    while an ambulance was called. The boy however was dead on arrival at
    hospital. This was the only available clinical information prior to
    autopsy.

    Postmortem examination revealed no evidence of any significant bodily
    injury, no evidence of head or neck injury and the brain appeared
    normal. There was some congestion of the mucosa of the trachea and
    major bronchi but no evidence of inhalation of any foreign material or
    of gastric contents. The stomach contained partly digested food
    material only, with no evidence of recent ingestion of tablets. The
    heart appeared anatomically normal and showed no macroscopic
    pathology. The remainder of the postmortem examination and subsequent
    histological examination of body tissues showed no evidence of natural
    disease, and in the absence of any significant macroscopic pathology
    the cause of death was thought to be due to a cardiac arrhythmia.

    During external examination of the body however, some white material
    was noticed around the nail beds, and this along with venous blood and
    lung tissue were taken for toxicological analysis. Results revealed
    the presence of 1,1,1-trichloroethane in the blood and lung tissue and
    the white material from the nails showed traces of titanium dioxide.
    In view of the findings and subsequent police investigations the cause
    of death was concluded to be acute ventricular dysrhythmia due to
    inhalation of trichloroethane. The police investigations revealed that
    the boy had started inhaling typewriter correction fluid vapour about
    5 months prior to his death. He did this about three times a week and
    during each of these occasions would use up to two bottles of fluid a
    time. Numerous empty bottles of typwriter correction fluid were found
    in his bedroom. The type of correction fluid used contained
    1,1,1-trichloroethane as its solvent and the white particulate base
    contained titanium dioxide (Ranson and Berry, 1986).

    Case 11: Fatal intentional abuse

    A previously healthy 15 year old boy retired to his bedroom early one
    evening and 2 hours later appeared in the sitting room complaining of
    double vision and hallucinations, he subsequently collapsed.
    Resuscitation was commenced by ambulance men who arrived immediately
    and was continued in hospital but was unsuccessful. A bottle of
    Tipp-ex(TM) was later discovered in his room.

    Postmortem examination showed a grossly oedematous brain and marked
    tonsillar herniation and uncal grooving. Oedema was also present in
    the lungs, liver and gut. The heart was normal. Toxicological analysis
    revealed a blood 1,1,1-trichloroethane concentration of 1.7mg/L and
    the solvent was also detected in the brain and liver. The rest of the
    toxicology screen was negative and no alcohol was detected (D'Costa
    and Gunaskera, 1990).

    Case 12: Fatal Intentional abuse

    A 14 year old boy had been sniffing Liquid Paper(TM) correction fluid
    with friends and on leaving a house collapsed at the front gate and
    died. Police enquiries revealed that he had been inhaling the
    substance on an irregular basis for a few months.

    Autopsy showed cerebral oedema with anoxic-hypoxic changes in the
    cortex and medulla; yellowish to dark red areas in the septal and left
    anterior regions of the myocardium; very congested lungs with
    inhalation of gastric contents and intra-alveolar haemorrhages on
    microscopy; and marked irritation of the airways with small
    haemorrhagic areas. Microscopic examination of the myocardium revealed
    degenerative changes including interfibrillary oedema, swollen and
    ruptured myofibrils, and a wavy, fibrillar pattern.

    Routine toxicological examinations performed on specimens of the
    vicera, blood and urine, failed to detect the presence of any common
    drugs or alcohols. Headspace gas chromatography with electron captive
    detection was used to detect volatile substances. The presence of
    1,1,1-trichloroethane was detected in each of the specimens although
    concentrations were not measured (Banathy & Chan, 1983).

    INTERNAL CASES NPIS (LONDON)

    Accidental ingestion in children

    Of 20 cases of accidental ingestion referred to the National Poisons
    Information Service (London), 15 remained asymptomatic. In most cases
    the amount ingested was given as either unknown (although very little)
    or as a mouthful, although one 2 year old male was reported to have
    taken 50ml. In the children showing clinical effects, these were
    nausea and vomiting (2/5), drowsiness (3/5) and buccal irritation
    (1/5). Of the twenty children, 5 were not admitted to hospital care,
    14 were observed (3 of which were also given ipecac) and discharged
    well within 24 hours of ingestion. The 2 year old male with a history
    of ingestion of 50ml was x-rayed (1,1,1-trichloroethane is
    radio-opaque, Dally et al, 1987) and although this was slightly more
    opaque than usual it was not considered helpful in acertaining the
    severity of exposure. He was discharged well after 3 days.

    Fatal inhalation (intentional abuse)

    A 15 year old boy suffered cardiorespiratory arrest at home after
    inhaling Tipp-ex(TM). The amount of solvent or period of inhalation
    was not known, but an episode of violent activity was reported prior
    to his collapse. On arrival at hospital he was in asystole, and full
    cardiopulmonary resuscitation was attempted but was unsuccessful (NPIS
    (London) 84/22696).

    Accidental ingestion (adult)

    A 27 year old female accidentally ingested a small amount of
    1,1,1-trichloroethane while syphoning. She developed dry mouth, mild
    retrosternal burning, headache and slight drowsiness. She was observed
    only and was discharged well after 3 hours (NPIS (London) 82/17087).

    Skin exposure

    A 19 year old male attended a burns unit having sustained a chemical
    burn to the left forearm while at work. He had been working with a
    cleaning fluid containing 1,1,1-trichloroethane. He was treated with
    irrigation and dressings were applied and he attended regularly as an
    out-patient for monitoring of the wound. The extent of necrosis
    progressed and his forearm became swollen, inflamed and painful at 6
    days. With arm elevation and co-fluampicil the swelling settled, and
    the patient was discharged with arrangements for out-patient
    dressings.

    On day 30 the patient returned complaining that pain and swelling had
    returned the previous day. Examination revealed minimal separation of
    extensive eschar on the dorsum of the right forearm but moderate local
    erythema and swelling. The wound was pus discharging and a swab of
    this grew  Staphylococcus aureus, which was treated with
    flucloxacillin. At this stage surgical excision and a split skin graft
    was carried out. There was good take of the graft and only minimal
    scarring at 4 month follow up (NPIS (London) 87/8962).

    The exposure was thought to be from 1,1,1-trichloroethane only,
    however it is unlikely that 1,1,1-trichloroethane alone would have
    caused such a severe reaction.

    8  ANALYSIS

    8.1  Agent/toxin/metabolite

    1,1,1-Trichloroethane is stable in blood if sample precautions are
    taken (see below). In fatal cases, analysis of tissues (particularly
    brain) may show high concentrations of 1,1,1-trichloroethane even if
    little is detectable in blood.

    Analysis of expired air by direct mass spectrometry can detect many
    solvents several days after an exposure but the technique is limited
    to cooperative, conscious patients (Flanagan et al, 1990).

    Urinary metabolites (trichloroethanol and trichloroacetic acid) serve
    as a qualitative index of exposure only.

    8.2  Sample containers to be used

    A glass container with an anticoagulant (lithium heparin, ethylene
    diamine tetra-acetic acid), preferably with a cap lined with metal
    foil should be used. The tube should be as full as possible and should
    only be opened when required for analysis and then only when cold
    (4C). If sample volume is limited, a container to match the available
    volume should be selected to ensure minimal headspace (Flanagan et al,
    1990).

    8.3  Optimum storage conditions

    Between -5C and 4C.

    8.4  Transport of samples

    Biological specimens should be packaged separately from any products
    thought to have been abused to prevent chemical cross contamination.

    8.5  Interpretation of data

    Blood 1,1,1-trichloroethane concentrations were measured by headspace
    chromatography in samples from 48 patients referred to the London
    Poisons Unit during 1980-1986 and data from a further 18
    1,1,1-trichloroethane related VSA (volatile substance abuse) deaths
    were also obtained. Blood 1,1,1-trichloroethane concentrations ranged
    from 0.1-60mg/L and although there was a broad relationship between
    blood concentration and severity of poisoning, there were large
    variations within each patient group. The absence of a good
    correlation between blood concentration and clinical features was
    thought to be due to rapid initial changes in tisssue distribution,
    and in addition, in many non fatal cases, other compounds were
    present, further complicating any interpretation of a dose response
    relationship (Meredith et al, 1989).

    8.6  Conversion factors

    1mg/L = 183 ppm (approx.) at 25C, 76mmHg
    1ppm = 5.46 mg/m3 (approx.) at 25C, 76mmHg

    8.7  Other recommendations

    None.

    9  OTHER TOXICOLOGICAL DATA

    9.1  Carcinogenicity

    There are no adequate epidemiological studies available concerning
    long term exposure to 1,1,1-trichloroethane and carcinogenicity. The
    International Agency for Research on Cancer concluded that an
    evaluation on human carcinogenicity of 1,1,1-trichloroethane could not
    be made (IARC, 1979).

    In a carcinogenicity study, rats and mice were orally administered
    1,1,1-trichloroethane in two different dose levels, 5 days a week for
    78 weeks. Both male and female test animals exhibited early mortality
    compared with untreated controls, and a variety of neoplasms were
    found in both treated animals and controls. Although rats of both
    sexes demonstrated a positive dose-related trend, no relationship was
    established between the dosage group and the species, sex, type of
    neoplasm or sites of occurrence (National Cancer Institute, 1977).

    9.2  Genotoxicity

    No relevent data on human genotoxicity.

    9.3  Mutagenicity

    The mutagenicity of 1,1,1-trichloroethane has been studied extensively
    in bacterial systems, however no data has been published on its
    ability to produce mutations in mammalian cells in culture. There is
    no evidence from the available data to indicate that the compound
    itself has mutagenic potential but, in view of the limitations, no
    conclusions can be drawn (Toxicity Review 9, HSE, 1984).

    9.4  Reprotoxicity

    No relevant data on human reprotoxicity.

    9.5  Teratogenicity

    No relevant data on human teratogenicity.

    Suspicion of a cluster of spontaneous abortions and congenital heart
    anomalies from pregnancies during a period of water contamination,
    occurred in the US in 1981. A 1,1,1-trichloroethane level of 1.7mg/L
    was detected in the well, along with other solvent contaminants
    (dichloroethylene, isopropyl alcohol and freon - levels of these not
    reported). Epidemiological studies indicated that a cluster did exist,
    and that the odds ratio for spontaneous abortion was 2.3, and the
    relative risk for congenital malformations was 3.1. A direct link
    between the ingestion of the contaminated water and these effects,
    however, could not be established (Goldberg et al, 1990).

    Schwetz et al (1975), studied the teratogenicity of
    1,1,1-trichloroethane in mice and rats, in which mean litter data only
    was reported. At inhalation levels of 875ppm daily (7 hours/day on
    days 6-15 of pregnancy), no evidence of embryolethality, fetotoxicity
    or teratogenicity was found.

    York et al (1982) reported no persistent detrimental effects in female
    rats exposed to 1,1,1-trichloroethane before mating and or during
    pregnancy. Levels of exposure were 2100  200ppm.

    9.6  ADI

    9.7  MRL

    9.8  AOEL

    Long term exposure limit 350ppm (1900mg m-3).
    Short term exposure limit 450ppm (2450 mg m-3).

    9.9  TLV

    Air: 350ppm (1900mg/m3)

    9.10  Relevant animal data

    In a study by Dickerson and Biesemeier (1982) forced aspiration of
    1,1,1-trichloroethane resulted in death for 50% of the test animals
    (male adult Sprague-Dawley albino rats) in less than 10 minutes. Death
    appeared due to pulmonary haemorrhage and/or cardiac arrest. The
    authors therefore concluded that use of a cuffed endotracheal tube
    should be considered in cases of 1,1,1-trichloroethane ingestion.

    Reinhardt et al (1973) reported that 1,1,1-trichloroethane caused
    cardiac sensitation 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.

    9.11  Relevant  in vitro data

    None.

    10  ENVIRONMENTAL DATA

    All the environmental data below was obtained from Environmental
    Health Criteria 136 (WHO, 1992). The primary reference sources are
    also listed in the reference section of this document.

    10.1  Ecotoxicological data

    Solubility in water

    In water 1,1,1-trichloroethane is slowly dehydrochlorinated to
    1,1-dichloroethane and hydrolysed to ethanoic acid, the former process
    being favoured by alkalinity. McConnell et al (1975) reported rapid
    transfer of 1,1,1-trichloroethane from water to air.

    Volatilisation

    In aquatic systems volatilization is the major route for
    1,1,1-trichloroethane removal. Dilling et al (1975) found
    1,1,1-trichloroethane to be rapidly evaporated from water. At 25C,
    90% evaporation occurred within 60-80 minutes from an aqueous solution
    containing 1mg of 1,1,1-trichloroethane/litre, the half life being 20
    minutes.

    LC50

    In rats after 4 hours = 18400ppm
    In mice after 30 minutes = 22240ppm
    In mice after 6 hours = 10300ppm

    10.2  Behaviour

    Adsorption onto soil

    1,1,1-trichloroethane does not bind to soil particles. Urano (1985)
    and Chiou et al (1979) presented data which show that adsorption by
    soil organic matter occurs via a partitioning process rather than a
    physical process.

    Mobility/leaching data

    1,1,1-Trichloroethane leaches readily into ground water.

    10.3  Biodegradation

    Environmental fate

    1,1,1-trichloroethane enters the environment primarily via
    evapouration 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.

    In 1978, it was estimated that 97.3% of the 1,1,1-trichloroethane used
    in the USA was released into the environment. Of this 86% was released
    into 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 as waste or waste
    water during production, the remainder being released during use.

    1,1,1-Trichloroethane has a residence time of about 6 years in the
    troposphere (Khalil & Ramussen, 1984; Prinn et al, 1987; Midgley,
    1989) 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 trifluoromethane
    (CFC-11), and the global warming potential is about 40 times lower.

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

    Abiotic transformation

     Atmospheric:-
    In the troposphere 1,1,1-trichloroethane is initially oxidized to
    trichloroacetaldehyde and then further to trichloroacetic acid. In the

    stratosphere it is degraded by photochemical processes and liberates
    chlorine atoms.

     In Water:-
    In water degradation of 1,1,1-tricloroethane occurs by a)
    dehydrochlorination to hydrochloric acid and 1,1-dichloroethene and b)
    hydrolysis to hydrochloric and ethanoic acids.

    Aerobic/anaerobic

    Biodegradation to 1,1-dichloroethane and chloroethane has been
    reported to occur under anaerobic conditions (Klecka et al, 1990).
    Wilson et al (1983) found no aerobic degradation of trichloroethane,
    at a concentration of 1mg/L, in soil samples collected from just above
    and below the ground water table.

    Microbial

    Not known.

    Photolysis

    In the stratosphere, 1,1,1-trichloroethane is degraded by
    photochemical processes, forming chlorine atoms, and therefore,
    chlorine free radicals that have the potential to deplete
    stratospheric ozone. In sunlight it forms 1,1,1,2-tetrachloroethane
    with some penta- and hexachloroethane. Calculations indicate that 15%
    of 1,1,1-trichloroethane is transferred to the stratosphere (McConnell
    and Schiff, 1978; Singh et al, 1982). The ozone depleting effect of
    1,1,1-trichloroethane is estimated to be 0.11 that of the
    chlorofluorocarbon CFC-11 (UNEP, 1989).

    Hydrolysis

    Two parallel reactions result in the degradation of
    1,1,1-trichloroethane in water;
    a) degradation to hydrochloric acid and 1,1-dichloroethane,
    b) hydrolysis to hydrochloric and ethanoic acids.
    The reaction rates are influenced by temperature and alkalinity
    (Gerkins and Franklin, 1989; CEFIC, 1986; Pearson, 1982).

    Reduction and oxidation

    1,1,1-Trichloroethane enters the troposphere and is oxidized (by free
    hydroxyl radicals) to form trichloroacetaldehyde, which is further
    oxidized to trichloroacetic acid. The half-life for oxidation is
    estimated in the range of 2-5.5 years (Yung et al,1975; McConnell and
    Schiff, 1978; Pearson, 1982).

    Half-life in water, soil and vegetation

     In water:-
    In water containing 8.3ppm oxygen at 25C = 6.9 months in natural
    sunlight or in darkness.

     In air:-
    In air the half-life of oxidation ranges from 2-5.5 years.

     In vegetation:-
    Not known.

    10.4  Environmentally important metabolites

    1,1,1-Trichloroethane liberates reactive chlorine atoms in the
    stratosphere, resulting in ozone depletion.

    10.5  Hazard warnings

    10.5.1  Aquatic life

    10.5.2  Bees

    10.5.3  Birds

    10.5.4  Mammals

    10.5.5  Plants

    10.5.6  Protected species

    10.6  Waste disposal data

    Liquid spills can be treated in several ways:
    a) If small, absorb on paper towels and evaporate in a fume cupboard
    or remove outside for evaporation or subsequent disposal by another
    method.
    b) If large, absorb on sand or vermiculite, shovel into a covered
    container and remove outside.
    c) Any spillage up to about 2.5 litres can be treated by adding a
    non-flammable dispersing agent and working it into an emulsion with
    brush and water. About one volume dispersing agent is needed for every
    two volumes of flammable water-insoluble liquid spilt (less with
    non-flammable water-insoluble liquids) together with 10 volumes of
    water. The emulsion can then be run to waste with large quantities of
    water. With these proportions there is no danger of a flammable vapour
    mixture developing in the drainage system. Advice should be obtained
    from the water authority before this method of disposal is used.

    Subsequent disposal of small amounts not run to waste can be dealt
    with by evaporation in the open air. Larger amounts should be disposed
    of by burial in a licenced site or by incineration in an approved
    incinerator.

    Following removal of the material from the site of the spillage, the
    area should be ventilated to remove any residual vapour, and/or washed
    with water and soap or detergent to remove any traces of material. Any
    contaminated personal or protective clothing should be thoroughly
    cleaned to remove all traces of contaminant. (Luxon, 1992).

    Author

    Maeve McParland

    National Poisons Information Service (London Centre)
    Medical Toxicology Unit
    Guy's & St Thomas' Hospital Trust
    Avonley Road
    London
    SE14 5ER
    UK

    This monograph was produced by the staff of the London Centre of the
    National Poisons Information Service in the United Kingdom. The work
    was commissioned and funded by the UK Departments of Health, and was
    designed as a source of detailed information for use by poisons
    information centres.

    Peer review was undertaken by the Directors of the UK National Poisons
    Information Service.

    December 1995

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