Henrietta Wheeler

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

    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


    1.1  Origin of substance

    Tetrachloroethylene is a synthetic chemical with no natural sources
    (Ware, 1988).

    1.2  Name

    1.2.1  Brand/trade name

    Ankilostin; Antisal 1; Dee-Solv; Didakeno; Dowclean EC; Dow-per; ENT
    1860; Fedal-Un; Nema; Perawin; Perclene; Percosolv; Perklone; PerSec;
    Perwin; Tetlen; Tetracap; Tetralax; Tetraleno; Tetravec; Tetroguer;

    1.2.2  Generic name


    1.2.3  Synonyms

    Carbon bichloride, carbon dichloride, ethylene tetrachloride, PCE,
    per, perc, perchlor, perchlorethylene, perchloroethylene, percosolve,
    perk, tetrachlorethylene, tetrachloroethylene,
    1,1,2,2-tetrachloroethylene, tetrachloroelthylenum.

    1.2.4  Common names/street names

    1.3  Chemical group/family

    Halogenated aliphatic hydrocarbon.

    1.4  Substance identifier and/or classification by use

    Halogenated aliphatic hydrocarbon.

    1.5  Reference numbers

         CAS                 127-18-4
         RTECS/NIOSH         KX 3850000
         EINECS              2048259
         UN                  1897

    1.6  Manufacturer

    Not applicable.

    1.7  Supplier/importer/agent/ licence holder

    Not applicable.

    1.8  Presentation

    1.8.1  Form

    Halogenated aliphatic hydrocarbon.

    1.8.2  Formulation details

    1.8.3  Pack sizes available

    1.8.4  Packaging

    The European Economic Commission regulations state that the label
    should read that tetrachloroethylene is harmful if inhaled or
    swallowed, and should be kept out of reach of children. Contact with
    the eyes must be avoided (WHO, 1984).

    1.9  Physico-chemical properties

    Chemical structure       C2Cl4
    Physical state           liquid
    Colour                   Clear and colourless
    Odour                    ether-like odour at 50 ppm. Odour threshold
                             0.3 ppm in water; 1.0 ppm in air.


    Water at 25°C 150 mg/L. Organic solvents: miscible with alcohol,
    ethyl, ether, chloroform benzene, solvent hexane, and most of the
    fixed and volatile oils.

    Autoignition temperature      No data available

    Important chemical interactions

    Mixtures of tetrachloroethylene and dinitrogen tetroxide are explosive
    when subject to shock (Commission of the European Communities, 1986).
    tetrachloroethylene reacts violently or explosively with certain
    alkali or alkaline earth metals. Granular barium in contact with
    tetrachloroethylene is susceptible to detonation. A mixture of lithium
    shavings and tetrachloroethylene is impact-sensitive and will explode,
    possibly violently. When heated together, potassium and
    tetrachloroethylene explode at 97-99°C. A tetrachloroethylene sodium
    mixture does not explode under similar conditions (Commission of the
    European Communities, 1986; Sax, 1984).

    Major products of combustion/pyrolysis

    Tetrachloroethylene is slowly decomposed by light and by various
    metals in the presence of moisture (Commission of the European
    Communities, 1986; Reynolds, 1993). Tetrachloroethylene decomposes
    upon heating above 150°C forming phosgene and hydrochloric acid. 

    Trichloroacetyl chloride is described as a major degradation product
    and phosgene a lesser one (Commission of the European Communities,

    Explosion limits         No data
    Flammability             non-flammable
    Boiling point            121.2°C
    Density                  1.6227 g/ml (at 20°C)
    Vapour pressure          18.47 mmHg (at 25°C)
    Relative vapour density  5.83
    Flash point              None

    1.10  Hazard/risk classification

    1.11  Uses

    Tetrachloroethylene was first commercially produced in USA in 1925.

    Tetrachloroethylene has been the solvent of choice in the dry cleaning
    industry since the 1950s (Blair et al, 1979) and is used extensively
    in textile processing as a scouring solvent to remove the oil from the
    fabrics (Ellenhorn and Barceloux, 1988; Sax, 1984; Torkelson, 1994;
    Ware, 1988). It is used in manufacturing fluorocarbons, as a drying
    agent for metals and some other solids, as a fumigant for insects and
    rodents (Gehring et al, 1991), as a heat transfer medium, and as a
    degreasing solvent (Sax, 1984; Torkelson, 1994). It is also used in
    aerosol cleaners, ignition wire driers, spot removers, fabric and wood
    cleaners (Ellenhorn and Barceloux, 1988; Finkel et al, 1983; Sax,
    1984; Torkelson, 1994). An unfortunate number of deaths from
    tetrachloroethylene have been from sleeping bags that have not been
    properly cleaned of the dry cleaning chemical prior to use (Finkel et
    al, 1983).

    Tetrachloroethylene is active against hookworms ( Ancylostoma and
     Necator), its use of was prevalent in the 1920s and 1930s in India
    and the Pacific Islands (Ware, 1988). Tetrachloroethylene may still be
    used in endemic areas although it has generally been superseded by
    drugs that are less toxic and easier to administer (Reynolds, 1993).
    It has also been used in the treatment of fasciolopsiasis (Reynolds,

    1.12  Toxicokinetics

    1.12.1  Absorption

    Pulmonary absorption is the primary route of entry of
    tetrachloroethylene under industrial conditions (Baselt and Cravey,

    Human volunteers at rest absorbed about 25% of tetrachloroethylene
    administered by inhalation exposure at 72 or 144 ppm over a 4 hour
    period. At first the compound was absorbed rapidly, but uptake
    decreased as exposure continued. The uptake was influenced more by 

    (lean) body mass than by respiratory minute volume or adipose tissue
    (Monster and Houtkooper, 1979). During work the uptake and minute
    volume increased to 3 fold the value at rest. In the post-exposure
    period the quotient of the blood concentrations and exhaled air
    concentrations of tetrachloroethylene remained at nearly 23. Following
    exposure about 80 to 100% of the uptake was excreted unchanged by the
    lungs, whereas 70 hours after exposure the amount of trichloroacetyl
    chloride (TCA) excreted in urine represented about 1% of the uptake
    (Monster et al, 1979; Monster and Houtkooper, 1979; Monster, 1979).

    Dermal absorption was rapid in both mice and guinea-pigs, peak
    concentrations of tetrachloroethylene in the blood of guinea-pigs
    being reached 30 minutes after application. The level of
    tetrachloroethylene in the blood of rats reached a maximum 1 hour
    after oral ingestion, or immediately after 6 hour inhalation (WHO,
    1984; Pegg et al, 1979).

    1.12.2  Distribution

    The deposition of tetrachloroethylene in man is poorly understood
    (Baselt and Cravey, 1990).

    Tetrachloroethylene is lipophilic and accumulates in the liver, brain,
    kidney, lung and adipose tissue, with gradual redistribution
    (Lukaszewski, 1979; Ware, 1988). It crosses the blood-brain barrier
    (Ware, 1988).

    In human tissue at autopsy, ratios of fat-to-liver concentrations are
    greater than 6:1 (McConnell et al, 1975). The fat-to-blood ratio is
    about 90:1 and the half-life for saturation of the fat to 50% of its
    equilibrium concentration is about 25 hour (Monster, 1979).

    Tetrachloroethylene has an estimated volume of distribution of 8.2
    L/kg after an oral dose of 400 mg.

    A postmortem after a fatal tetrachloroethylene exposure revealed an
    eight times greater concentration in the brain compared to the blood
    (Lukaszewski, 1979), whereas in another postmortem the liver contained
    the highest tetrachloroethylene levels (Levine, 1981).

    1.12.3  Metabolism

    Less than 4% of the estimated absorbed dose of tetrachloroethylene is
    metabolised and excreted as trichloroacetic acid in humans (Fernandez
    et al, 1979; Ferroni et al, 1992).

    Tetrachloroethylene is stored in the fat and adipose tissue and slowly
    metabolised with the loss of chlorine (Gosselin et al, 1984). Once
    absorbed, the highest concentrations of tetrachloroethylene are found
    in the adipose tissue, reflecting its high lipid solubility (Ware,
    1988). The principle site of metabolism is the hepatic microsomal
    cytochrome P450 mixed-function oxidase system in a dose-dependent
    manner (Gehring et al, 1991; Torkelson, 1994).

    Tetrachloroethylene is probably transformed by oxidation to
    perchloroethylene oxide and subsequently by rearrangement to
    trichloroacetyl chloride and then by hydrolysis to trichloroacetic
    acid (TCA) (Lukaszewski, 1979; Yllner, 1961). Metabolism takes place
    mainly in the liver. The maximum concentration of TCA is reached at 20
    hours after exposure (Monster, 1979).

    The major urinary metabolite seems to be trichloroacetic acid, over
    half appears as the acid and its conjugate. Much smaller amounts of
    oxalic acid, trichloroethanol, dichloroacetic acid and
    N-trichloroacetyaminoethanol or its conjugate are excreted (Commission
    of the European Communities, 1986; Skender et al, 1991; Torkelson,

    Tetrachloroethylene may give rise to reactive intermediate metabolites
    that may impair the tubero-infundibular dopaminergic system (Ferroni
    et al, 1992). This mechanism may involve neuroendocrine changes
    accounting for gynaecological disturbances eg oligo-menorrhoea and
    reduced fertility (Zielhuis et al, 1989) and spontaneous abortion or
    perinatal death (Olsen et al, 1990).

    1.12.4  Elimination

    There seems to be no apparent difference in elimination pathways or
    metabolism in animals exposed by oral or inhalation routes. The major
    determinant of metabolism and tissue distribution is body burden (Pegg
    et al, 1979).

    The majority of tetrachloroethylene (about 80%) is eventually excreted
    unchanged in expired air; initial elimination is rapid but a
    proportion may be retained and excreted slowly (Baselt and Cravey,
    1990; Reynolds, 1993; Skender et al, 1991). 15% of an inhaled dose is
    eliminated unchanged within 1 hour, 3% is metabolised and excreted via
    the urine over a 67 hour period (Baselt and Cravey, 1990; Commission
    of the European Communities, 1986; Koppel et al, 1985).

    Approximately 25% of an inhaled dose is excreted unchanged in the
    breath over 40 hours following exposure (Baselt and Cravey, 1990).

    Elimination is then slow due to the release from the fat store,
    repeated daily exposures leads to accumulation of tetrachloroethylene
    in man (Ellenhorn and Barceloux, 1988).

    Alveolar breath concentrations of tetrachloroethylene approach 50% of
    the atmospheric concentration of the chemical during constant exposure
    (Baselt and Cravey, 1990). In subjects exposed to 100 ppm of the
    vapour, breath concentrations averaged 15 ppm during the first hour
    after exposure, 8 ppm after 15 hours and 4.5 ppm after 71 hours
    (Stewart et al, 1970).

    Chlorinated metabolites of tetrachloroethylene generally do not exceed
    concentrations of 100mg/L in urine workers exposed to the vapor at air
    concentrations of up to 400 ppm (Ikeda et al, 1972).

    1.12.5  Half-life

    The biological half-life of tetrachloroethylene on inhalation has been
    estimated from pulmonary excretion data as between 3 and 72 hours
    (Baselt and Cravey, 1990).

    Trichloroacetic acid, as a metabolite of tetrachloroethylene, is
    eliminated with a half-life of 144 hour via the urine (Ware, 1988).

    The biological half-life of tetrachloroethylene appears to be 144
    hours following ingestion (Gosselin et al, 1984; Ikeda, 1977; Koppel
    et al, 1985; Lukaszewski, 1979).

    1.12.6  Special populations

    No data.

    2  SUMMARY


    Tetrachloroethylene was introduced in to the dry cleaning industry in
    the late 1930s, but did not replace other synthetic solvents until
    shortly after the second world war. By 1977, about 74% of dry cleaning
    outlets used tetrachloroethylene (Brown and Kaplan, 1987). At least
    1.6 million workers in US are potentially exposed to
    tetrachloroethylene annually (Brown and Kaplan, 1987).


    4.1  Mechanism

    Systemic toxicity after acute overexposure to tetrachloroethylene
    vapour is characterised by central nervous system depression,
    hypotension, cardiac arrhythmias, hepatic and renal injury; death may
    be due to respiratory failure. The major response to
    tetrachloroethylene at high concentrations is CNS depression. It is
    not, however, sufficiently effective to be considered a useful
    anaesthetic (Torkelson, 1994).

    Tetrachloroethylene may sensitise the myocardium to adrenaline and
    other catecholamines at high levels of exposure (Hathaway et al, 1991;
    Torkelson, 1994).

    The vapour and liquid are irritating to the skin and mucous membranes.
    There may be nausea and gastrointestinal upset at high concentrations.
    Changes in the liver and kidneys may be seen following excessive
    exposure; however the effects are not as severe or striking as they
    are with other hydrocarbons, e.g. carbon tetrachloride (Ellenhorn and
    Barceloux, 1988; Torkelson, 1994).

    Dependence may follow habitual inhalation of small quantities of
    tetrachloroethylene vapour.

        4.2  Toxic dose



    Dose     Exposure       Symptoms                Comments                Reference
    (ppm)    time

    50       8 hours        No physiological        Odour threshold         Commision of the 
                            effects                 (very faint) to         European 
                                                    unacclimatised          Communities, 1986

    216      45 mins-       Respiratory                                     Rowe et al, 1952
             2 hours        irritation

    275      3 hours        Coma for 1 hour.        Concentration of        Hathaway et al, 1991
    then     then           Deranged LFTs           tetrachloroethylene 
    100      30 minutes     for 2-3 weeks           in expired air, 
                            post-exposure           diminished slowly
                                                    over 2 weeks

    400      2 hours        Eye irritation,         Odour strong, but       Commision of the 
                            slight nasal            tolerable               European Communities,
                            irritation, ataxia                              1986

    600      10 minutes     Numb mouth, dizzy,      Odour very              Commision of the 
                            ataxic for 10           strong but              European Communities, 
                            minutes post-           tolerable               1986

    1,060    1-2 minutes    Not tolerated for       Exposed in              Rowe et al, 1952
                            more than 2 minutes     chamber

    1,500    30 minutes     'Gagging', irritation   Odour almost            Commision of the 
                            of eyes and             intolerable             European Communities, 
                            respiratory tract                               1986
                            (almost intolerable),
                            loss of consiousness


    Dose     Exposure       Symptoms                Comments                Reference
    (ppm)    time
    5,000    6 minutes      Vertigo, nausea and                             Hathaway et al, 1991
                            confusion for 10 
                            minutes post-

    Two adults who died shortly after massive exposure of
    tetrachloroethylene fumes in dry cleaning establishments were found to
    have the following concentrations (mg/L or mg/kg) of
    tetrachlorethylene (Baselt and Cravey, 1990):

    Patient       Blood     Brain    Lung    Liver    Kidney
    Patient 1     44        360      3       -        -
    Patient 2     4.5       69       30      240      71

    Chronic inhalation:

    Twenty dry cleaning workers exposed for an average of 7.5 years to
    concentrations of 1-40 ppm had altered electrodiagnostic and
    neurological rating scores (Hathaway et al, 1991). Abnormal EEG
    readings were found in 4 out of 16 factory employees exposed to
    concentrations ranging from 60-450 ppm for 2 to 20 years (WHO, 1984).


    A 6 year old boy ingested 8-10 ml of tetrachloroethylene and became
    comatose. He developed a peak blood level of 22 mg/L but survived
    (Koppel et al, 1985).


    5.1  Acute

    5.1.1  Ingestion

    Ingestion of tetrachloroethylene may cause gastric irritation with
    nausea and vomiting. It may cause CNS depression, dizziness,
    inebriation, lightheadedness, mental dullness and incoordination
    (Hathaway et al, 1991; Stewart et al, 1970). CNS depression may range
    form mild narcosis to coma with respiratory depression or death
    (Hathaway et al, 1991).

    Respiratory effects include coughing, wheezing, pulmonary oedema and
    increasing cyanosis. These may occur due to aspiration or following
    large inhalation exposure. Full recovery may be seen if exposure is

    Tetrachloroethylene is thought to sensitise the myocardium to
    endogenous catecholamines which may cause arrhythmias and sudden death
    after massive acute exposures.

    Ingestion of tetrachloroethylene has been associated with the
    development of toxic epidermal necrolysis (Potter, 1960).

    5.1.2  Inhalation

    Tetrachloroethylene vapours are irritant to nasal, ocular and
    respiratory mucosa (Rowe et al, 1952). Headache, fatigue, ataxia,
    dizziness, nausea, vomiting, hypotension, mental confusion and
    temporary blurred vision have been reported after inhalation (Baselt
    and Cravey, 1990; Clement International Corporation, 1993; Rowe et al,
    1952). Tetrachloroethylene is a CNS depressant and causes drowsiness
    that can lead to coma or death.

    Tetrachloroethylene is thought to sensitise the myocardium to
    endogenous catecholamines which may cause arrhythmias and sudden death
    after massive acute exposures.

    Short-term exposure tests prove that the visual system is one of the
    target organs of acute tetrachloroethylene toxicity.

    5.1.3  Dermal

    Tetrachloroethylene is irritant to the skin. It may cause dry, scaly
    skin, blisters and dermal burns (Baselt and Cravey, 1990; Finkel et
    al, 1983). Erythema and a severe burning sensation may occur if
    tetrachloroethylene is left on the skin for 40 minutes or longer
    (Hathaway et al, 1991). Dermatitis is caused by defatting of the skin
    (Torkelson, 1994).

    5.1.4  Ocular

    Tetrachloroethylene vapours are irritating to eyes at high
    concentrations (Ellenhorn and Barceloux, 1988; Grant and Schuman,
    1993; Torkelson, 1994). An ocular splash exposure is expected to cause
    lacrimation and burning but no permanent damage (Rowe et al, 1952;
    Torkelson, 1994).

    Spraying rabbits in the eyes with tetrachloroethylene caused immediate
    blepharospasm and pain. The corneal epithelium became granular and
    optically irregular patches of epithelium were lose, both eyes
    recovered completely within 2 days (Grant and Schuman, 1993).

    5.1.5  Other routes

    Tetrachloroethylene has been found to be weakly nephrotoxic and
    hepatotoxic following subcutaneous injection in mice.

    Dogs were killed by intravenous doses of 85 mg/kg; the few that
    received 75 mg/kg or less survived (Gehring et al, 1991).

    5.2  Chronic toxicity

    5.2.1  Ingestion

    When tetrachloroethylene was administered in drinking water for 90
    days to mice, body weight was decreased and there were suggestions of 

    liver effects but no clear evidence of injury at 1400 mg/kg/day
    (Gehring et al, 1991; Torkelson, 1994).

    There is no human data available.

    5.2.2  Inhalation

    Since tetrachloroethylene is minimally metabolised, slowly excreted,
    and presumed to be accumulative, chronic exposure to a lower vapour
    concentration could conceivably result in human injury or organ
    dysfunction (Monster and Houtkooper, 1979; Stewart, 1969; Stewart et
    al, 1970).

    In a chronic overexposure, post-mortem findings included haemorrhagic
    pneumonitis and pulmonary oedema (Trense and Zimmerman, 1969).

    Tetrachloroethylene is thought to sensitise the myocardium to
    endogenous catecholamines which may cause arrhythmias and sudden death
    after massive acute or chronic exposures. Chronic occupational
    exposure has been known to produce multiple ventricular premature
    beats (Abedin et al, 1980).

    Odour tolerance seems to be exhibited in chronically exposed humans.
    Sixteen subjects were exposed to 100 ppm over a 7 hour period,
    initially 100% were able to detect a faint odour; by the end of
    exposure only 40% were still able to detect the odour of the solvent.
    Subjects exposed for 5 consecutive days reported that their ability to
    perceive the odour progressively diminished during the course of the
    week. Although initially the odour was detected on entering the
    chamber upon the second day, within two hours only three were able to
    smell tetrachloroethylene (Stewart et al, 1970).

    Chronic occupational exposure of three years resulted in peripheral
    neuropathy, hepatitis, confusion, disorientation, muscle cramps,
    fatigue, agitation and damage to liver, kidney and spleen (Baselt and
    Cravey, 1990). One case of fatal chronic poisoning showed lobular
    necrosis of the liver at postmortem (Trense and Zimmerman, 1989).

    Liver enlargement was still present 6 months after cessation of
    exposure in one chronic occupational poisoning (Meckler and Phelps,

    A connective tissue disorder characterised by Reynauld's phenomenon,
    alopecia, myositis and strongly positive antinuclear antibodies in
    patients chronically exposed to tetrachloroethylene has been described
    by Sporrow in 1977 (Baselt and Cravey, 1990).

    Tetrachloroethylene may give rise to reactive intermediate metabolites
    that may impair the tubero-infundibular dopaminergic system (Ferroni
    et al, 1992). This mechanism may involve neuroendocrine changes
    accounting for gynaecological disturbances eg oligo-menorrhoea and
    reduced fertility (Zielhuis et al, 1989) and spontaneous abortion or
    perinatal death (Olsen et al, 1990).

    Chronic low level exposures of tetrachloroethylene may effect colour
    vision although the pathogenesis is unclear (Cavalleri et al, 1994).
    The effect does not seem to be rapidly reversible.

    Chronic low levels of tetrachloroethylene may significantly impair
    performance and affect pituitary function, thus causing increased
    levels of the dopaminergic modulation of prolactin (Olsen et al,

    5.2.3  Dermal

    Chronic skin exposure may cause reddening and chapping of the skin.
    Dry, scaly and fissured dermatitis may also occur from repeated skin

    5.2.4  Ocular

    Chronic low level exposures of tetrachloroethylene may affect colour
    vision although the pathogenesis is unclear (Cavalleri et al, 1994).
    The effect does not seem to be rapidly reversible.

    5.2.5  Other routes

    No human data available.

    5.3  Systematic description of clinical effects

    5.3.1  Cardiovascular

    Tetrachloroethylene may sensitise the myocardium to adrenaline and
    other catecholamines. However, in dogs exposed to highly anaesthetic
    levels of tetrachloroethylene (5000 to 10,000 ppm) cardiac arrhythmias
    were not detected (Hathaway et al, 1991). The significance of these
    findings for humans exposed to allowable concentrations is very
    questionable (Torkelson, 1994).

    Multiple ventricular premature beats occurred in a worker with chronic
    exposure and tetrachloroethylene was detected in the blood. No
    arrhythmia was noted one month after the exposure was discontinued
    (Abedin et al, 1980).

    5.3.2  Respiration

    Upper respiratory tract irritation may occur with exposure to high
    concentrations of airborne tetrachloroethylene (Clement International
    Corporation, 1993; Finkel et al, 1983; Torkelson, 1994). Respiratory
    failure may occur in massive overexposure (Rowe et al, 1952).

    In a chronic overexposure, postmortem findings included haemorrhagic
    pneumonitis and pulmonary oedema (Trense and Zimmerman, 1969).

    5.3.3   Neurological

    Ingestion or inhalation of tetrachloroethylene causes CNS depression,
    dizziness, headache, inebriation, slurred speech, lightheadedness,
    mental dullness and incoordination (Hathaway et al, 1991; Stewart,
    1969; Stewart et al, 1970). CNS depression may range form mild
    narcosis to coma with respiratory depression or death (Hathaway et al,

    A 62 year old man presented with inebriation following exposure to 500
    ppm. He recovered within 6 hours (McMullen, 1976).

    19 volunteers exposed to tetrachloroethylene vapor concentrations of
    20, 100 and 1,500 ppm for 1 month (5 days/week). EEG changes were
    recorded in 7 out of 19 subjects during 100 ppm exposure. The EEG
    changes were characterised by a reduction in overall wave amplitude
    and frequency, most evident in the occipital leads. The altered EEG
    pattern was similar to that seen in healthy adults during drowsiness,
    light sleep and first stages of anaesthesia (Stewart et al 1981).

    In 4 volunteers exposed acutely to 1,000-1,500 ppm dizziness for less
    that 2 hours suffered mood changes, ataxia, dizziness and faintness.
    Following exposure to 2,000 ppm for 7.5 minutes, subjects experienced
    a sensation of impending collapse (Carpenter, 1937). Long exposures
    have resulted in collapse, coma and seizures (Hake and Stewart, 1977).

    Chronic low levels of tetrachloroethylene affects attention and
    executive function, and mood functions thought to be mediated by the
    frontal and limbic system of the brain (Echeverria et al, 1995).

    Peripheral neuropathy has been described following chronic exposure
    (Hathaway et al, 1991).

    5.3.4  Gastrointestinal

    Nausea and vomiting occur following exposure by inhalation or
    ingestion (Baselt and Cravey, 1990; Torkelson, 1994).

    5.3.5  Hepatic

    Liver damage may result from chronic or severe acute exposure
    (Hathaway et al, 1991; Reynolds, 1993; Stewart, 1969; Stewart et al,

    The liver is a target organ in humans, particularly in those
    accidentally exposed to high concentrations. Hepatocellular damage was
    documented by biopsy in a case study of a women exposed occupationally
    to tetrachloroethylene fumes (Meckler and Phelps, 1966). Liver damage
    also has been diagnosed by the presence of hepatomegaly, icterus and
    elevations of serum biomarkers of liver dysfunctions (Hake and
    Stewart, 1977; Meckler and Phelps, 1966).

    In a chronic exposure liver enlargement was still present 6 months
    after cessation of exposure to tetrachloroethylene (Meckler and
    Phelps, 1966).

    Chronic occupational exposure has resulted in hepatitis, muscle cramps
    and agitation (Baselt and Cravey, 1990).

    5.3.6  Urinary

    Proteinuria and haematuria has occurred following massive acute
    exposure. Proteinuria lasted 20 days in a 60 year old man found lying
    in a pool of tetrachloroethylene. Oliguric renal failure has occurred
    from inhalation exposure from a self-service dry-cleaning machine
    (Hake and Stewart, 1977).

    5.3.7  Endocrine and reproductive system

    A small scale study on menstral disorders in dry cleaning workers was
    carried out by Zielhuis et al (1989). Although there were limitations
    upon the study, the results indicated that menstral disorders
    (dysmenorrhoea, unusual cycle length, menorrhagia and premenstrual
    syndrome) were higher than in the control group.

    Several recent case-control studies in dry cleaning workers suggest
    that women have an increased risk of spontaneous abortion (Clement
    International Corporation, 1993; Kyyrönen et al, 1989).

    Eskenazi et al (1991) found that the sperm of male dry cleaning
    workers exposed to tetrachloroethylene had more amplitude of lateral
    head displacement (ALH) and less linearity in their sperm swimming
    paths compared to a control group. Although their semen was considered
    to be within normal limits the quality was diminished. As exposure to
    tetrachloroethylene increased, men were found to have fewer narrow
    sperm but more round sperm. Infertility has been reported in men with
    mostly round headed sperm. These sperm lack an acrosome and are unable
    to penetrate the ovum. Although proportions of round sperm are
    increased and dose-related in tetrachloroethylene exposed men, these
    proportions are considerably lower than those noted in a group of
    infertile men.

    Tetrachloroethylene may give rise to reactive intermediate metabolites
    that may impair the tubero-infundibular dopaminergic system (Ferroni
    et al, 1992). This mechanism may involve neuroendocrine changes
    accounting for gynaecological disturbances eg oligo-menorrhoea and
    reduced fertility (Zielhuis et al, 1989) and spontaneous abortion or
    perinatal death (Olsen et al, 1990).

    A six-week old, breast-fed infant suffered an enlarged liver and
    obstructive jaundice under conditions where the mother's milk was
    found to contain up to 1 mg tetrachloroethylene per 100 ml caused by
    her occupational exposure (Commision of the European Communities,

    Rabbits exposed to 15 mg/L, one hour daily for 15 days developed
    gradual increases in the plasma and urine concentrations of
    corticosteroids, adrenaline, noradrenaline and
    3-methyl-1-hydroxymandelic acid. These effects lasted for 30 days
    following cessation of exposure (Maxxa and Brancaccio, 1971). Similar
    effects have not been reported in exposed humans.

    An increase number of resorption delayed skull, ossifications,
    subcutaneous oedema, and sternal malformations were found in the
    offspring of rats exposed to 300 ppm tetrachloroethylene for 7 hours
    as day on days 6 to 15 of pregnancy (Hathaway et al, 1991).

    5.3.8  Dermatological

    Tetrachloroethylene is irritant to the skin. It may cause dry, scaly
    skin, blisters and dermal burns (Baselt and Cravey, 1990; Finkel et
    al, 1983). Erythema and severe burning sensation may occur if
    tetrachloroethylene is left on the skin for 40 minutes or longer
    (Hathaway et al, 1991). Dermatitis is caused by defatting of the skin
    (Torkelson, 1994).

    Symptoms of coldness, stiffness, burning pain and discolouration of
    hands on exposure reported following tetrachloroethylene exposure
    (Rowell, 1977).

    Ingestion of tetrachloroethylene was associated with the development
    of toxic epidermal necrolysis (Potter, 1960).

    5.3.9  Eye, ears, nose and throat

    Ocular splash exposure is expected to cause lacrimation and burning,
    but no permanent damage (Rowe et al, 1952; Torkelson, 1994).

    The vapour is irritating to the eyes, nose and throat at high
    concentrations (Ellenhorn and Barceloux, 1988; Grant and Schuman,
    1993; Torkelson, 1994).

    5.3.10  Haematological

    A 13 month old male with sickle cell trait exhibited evidence of
    intravascular haemolysis within 24 hours of ingestion and aspiration
    of tetrachloroethylene (Algren and Rogers, 1992).

    A father and son who were exposed to organic solvents including
    tetrachloroethylene was reported to have polycythemia vera, a
    proliferative disorder of bone marrow pluripotent stem cells. The son
    had 22 years exposure history, including transient exposure above 300
    ppm for 5 minutes out of 3 hours (Ratnoff and Gress, 1980). Because
    genetic and other environmental factors may predispose a person to
    develop polycythemia vera, this condition cannot be related
    specifically to tetrachloroethylene exposure.

    5.3.11  Immunological

    No human data available.

    5.3.12  Metabolic  Acid-base disturbances

    No data.  Fluid and electrolyte disturbances

    No data.  Other

    No data available.

    5.3.13  Allergic reactions

    No human data available.

    5.3.14  Other clinical effects

    Individuals who live close to dry cleaning facilities using
    tetrachloroethylene have been found to have appreciable amounts of
    this agent in their exhaled breath (Finkel et al, 1983).

    5.4  At risk groups

    5.4.1  Elderly

    The elderly with declining organ function may be at increased risk
    from tetrachloroethylene exposure.

    5.4.2  Pregnancy

    Exposure to high concentrations of tetrachloroethylene during
    pregnancy has been associated with spontaneous abortion in a case
    control study of dry cleaner and laundry workers (Kyyrönen et al,

    Tetrachloroethylene is excreted in breast milk and has been associated
    with obstructive jaundice in breast fed new born babies (Bagnell and
    Ellenberger, 1977).

    5.4.3  Children

    No data available.

    5.4.4  Enzyme deficiencies

    No data available.

    5.4.5  Enzyme induced

    No data available.

    5.4.6  Occupations

    Most exposures to tetrachloroethylene are occupational, workers most
    at risk are those working in the dry cleaning and textile industries.

    5.4.7  Others

    No data available.


    6.1  Decontamination


    Emesis is not recommended due to the risk of aspiration. Clear fluids
    should be encouraged. Gastric lavage with a cuffed endo-tracheal tube,
    to ensure the airway is protected as the aspiration risk is high,
    should be considered. Data on humans are too limited to predict with
    confidence a quantity at which gastric lavage should be carried out.
    The use and efficacy of activated charcoal has not been studied
    (Ellenhorn and Barceloux, 1988).


    Following inhalation patients should be removed from the source with
    care so as not to contaminate the rescuers and monitored for signs of
    respiratory distress.


    Exposed skin should be flushed immediately with copious amounts of


    Eyes should be irrigated for at least 15 minutes with water of normal
    saline. The eye should be examined with fluorescein, an
    ophthalmological referral may be necessary.

    6.2  Supportive care

    The most important management principles are decontamination,
    monitoring the level of consciousness and respiration, ECG, renal and
    liver function. Treatment is symptomatic and supportive.

    An emetic must not be given due to the risk of aspiration;
    sympathomimetic agents must not be given due to the risk of
    sensitisation of the myocardium to catecholamines.

    6.3  Monitoring

    Monitor liver function, renal function and perform urinalysis for
    patients with a significant exposure. Daily urinalysis for proteinuria
    and haematuria may be useful after massive exposures (Torkelson,

    Monitor the level of consciousness and respiratory function. Oxygen
    should be administered if breathing difficulties occur, ventilate if
    necessary. A chest X-ray is advised for patients with persistent
    respiratory symptoms due to the risk of pulmonary oedema.

    Monitoring the urinary concentrations of chlorinated metabolites of
    tetrachloroethylene is of only limited use, because saturation of the
    metabolic pathways occurs at air concentrations greater than 50 ppm
    and there is no correlation between concentration of urinary
    metabolites and exposure at higher air concentrations (Baselt and
    Cravey, 1990).

    6.4  Antidotes

    There are no known antidotes.

    6.5  Elimination techniques

    Koppel et al (1985) demonstrated in a child who ingested 8-10 ml that
    controlled hyperventilation enhanced pulmonary elimination of
    tetrachloroethylene. Under this treatment, the clinical condition of
    the patient improved considerably. Under hyperventilation the
    half-life was reduced to 30 minutes and about 1% of the ingested dose
    was excreted via the urine in the first three days with the bulk of
    the dose being eliminated via the lungs (Koppel et al, 1985).

    This has not been demonstrated elsewhere.

    6.6  Investigations

    Measured breath tetrachloroethylene concentrations after cessation of
    exposure correlate well with the amount absorbed and with the blood
    levels (Baselt and Cravey, 1990). This may also be of use in
    monitoring workers with chronic exposure (Torkelson, 1994).

    Blood tetrachloroethylene concentrations have generally not proved
    useful if exposure is known, but may be of use for diagnosis. However,
    Skender et al (1991) believes the most reliable indicator of
    tetrachloroethylene appears to be in blood.

    Tetrachloroethylene is radiopaque  in vitro and an X-ray may be of
    use in confirming ingestion.

    6.7  Management controversies

    Following large inhalation or oral exposure the patient must be kept
    at complete bed rest, in a quiet environment, on an ECG monitor for at
    least 12 hours post-exposure. The use of catecholamines (eg
    adrenaline) must be avoided.

    Koppel et al (1985) demonstrated that controlled hyperventilation
    enhanced pulmonary elimination of tetrachloroethylene. This has not
    been demonstrated elsewhere, but may be considered in cases of severe

    7  CASE DATA


    1) A 13 month old black male, developed pneumonia and respiratory
    failure following the ingestion and aspiration of a dry cleaning fluid
    containing tetrachloroethylene. Immediately following the ingestion,
    he became unconscious and had a brief generalised convulsion. Upon
    arrival at hospital, he was intubated and stabilised with mechanical
    ventilation. During the next 24 hours, the serum haemoglobin
    concentration fell to 3.5 g/100ml, prompting further investigation to
    determine the etiology of the marked decrease in haemoglobin. During
    this time, the patient had not experienced any cardiovascular
    instability, and his overall condition had improved. The possibility
    of occult blood loss was considered but could not be substantiated. A
    sickle cell screen was positive. Haemoglobin electrophoresis
    subsequently demonstrated haemoglobin AS, consistent with sickle cell
    trait. No further haemolysis was observed, and transfusion was not
    necessary. The patient was weaned from mechanical ventilation on the
    fourth day and recovered without further complications (Algren and
    Rodgers, 1992).

    2) A 6 year old boy drank 8-10 ml of tetrachloroethylene and one hour
    later was admitted to hospital with deterioration of his conscious
    state to coma. In order to prevent aspiration, the child was
    intubated, and a gastric lavage with paraffin oil was performed. The
    initial tetrachloroethylene blood level was 21.5 mg/ml;
    hyperventilation therapy was instigated 2 hours after ingestion. The
    patient received 6000 U/24 hours of heparin to prevent coagulation
    with intravenous infusion therapy. Under this treatment, the clinical
    condition of the patient improved considerably. Under hyperventilation
    the half-life was reduced to 30 minutes and about 1% of the ingested
    dose was excreted via the urine in the first three days with the bulk
    of the dose being eliminated via the lungs. Hyperventilation was
    terminated on day five. However, extubation was not possible because
    of a marked stridor, which necessitated intubation for a further 24
    hours. On the ninth day the boy was discharged with no signs of liver
    or kidney damage (Koppel et al, 1985).


    3)A 33 year old man was found unconscious after performing work on a
    plugged line in a commercial dry cleaning establishment. He had been
    left alone to work on the dry-cleaning machine for approximately 20
    minutes before being found. He died on the way to hospital. The blood
    concentrations of tetrachloroethylene was 44 mg/L, brain tissue levels
    were 360 mg/L and in the lungs 3 mg/L was detected. Tests for alcohol
    and other drugs proved negative. The lack of metabolites in the urine
    was consistent with the short time interval between initial exposure
    and death. Absence of tetrachloroethylene in the stomach contents
    eliminated ingestion as the route of absorption. The level of
    tetrachloroethylene in the lungs, although low in comparison with the
    blood, does not indicate the method of absorption since
    tetrachloroethylene is both absorbed and excreted via the lungs.
    Distribution of tetrachloroethylene was consistent with its lipophilic
    properties, being highest in the brain and lowest in the lung tissue
    (Lukaszewski, 1979).

    4) A 24 year old white male was admitted to hospital with a six month
    history of "skipping of heart beats", dizziness and headache. These
    symptoms became progressively worse in the two to three months prior
    to admission. There was no history of dyspnoea, angina pectoris,
    diabetes, blackouts, chest pain, hypertension, Raynaud's phenomenon or
    drug abuse. Seven months prior to admission the patient had begun
    working in a dry cleaning facility where he was responsible for the
    treatment of clothes with tetrachloroethylene. On examination he was
    alert, orientated and apyrexial with an irregular pulse of 70/minute,
    and a blood pressure within normal limits. On examination nothing
    remarkable was found. ECG on admission demonstrated sinus rhythm and
    multiple ventricular premature beats (VPB). All other findings were
    normal. The VPBs on admission did not respond to lignocaine.
    Continuous 24 hour ECG monitoring revealed multiple unifocal VPBs, but
    on the second day after admission, without any further treatment, the
    VPBs became less frequent. By the fourth day the patient was free from
    headache, dizziness and VPBs. On the fifth day he was discharged with
    a plasma tetrachloroethylene level of 0.15 ppm. A few days later the
    patient returned to work and soon began to become symptomatic again.
    Two weeks later he returned to hospital, physical examination was
    normal but resting ECG revealed frequent VPB and plasma
    tetrachloroethylene levels were 3.8 ppm. The patient was advised to
    leave his present employment; one month after exposure stopped the
    patient was free from neurological symptoms and cardiac arrhythmias
    (Abedin et al, 1980).

    Internally extracted data on cases

    Of 14 cases of tetrachloroethylene exposure reported, 2 were
    asymptomatic and all the other cases recovered within 5 days
    post-exposure. Clinical effects that were reported were nausea,
    vomiting, slurred speech, ataxia, drowsiness, disorientation,
    confusion, euphoria, restlessness, shortness of breath, nystagmus,
    hypotonia, tachypnoea and coma.

    One adult aged 20 years ingested 20 ml of tetrachloroethylene.
    Initially he was unconscious; he then became disorientated and
    aggressive and developed oculogyric crisis and a disturbance in his
    liver function. He received a gastric lavage, intravenous fluids and
    acetylcysteine. The patient was well after 3 days and was discharged.

    A 2“ year old boy ingested an unknown quantity of tetrachloroethylene.
    He developed ataxia, vomiting, drowsiness and then became unconscious.
    He had nystagmus, hypotonia and was tachypnoeic. ECG was normal and
    chest X-ray showed mild shadowing. He was discharged well 2 days post-


    8.1  Agent/toxin/metabolite

    8.2  Sample containers to be used

    8.3  Optimum storage conditions

    8.4  Transport of samples

    8.5  Interpretation of data

    The biological tolerance of tetrachloroethylene in blood 16 hours
    after exposure (TVL = 50 ppm) is 6.0µmol/L (Skender et al, 1991).
    Tetrachloroethylene concentrations averaged 1.2 mg/L in 26 workers
    exposed to an average air concentration of 21 ppm for 30 minutes.
    Blood concentrations in 6 subjects reached an average peak level of
    194 ppm of vapour (Baselt and Cravey, 199o); the compound was rapidly
    cleared from the blood when exposure ended and was not detectable (at
    sensitivity limit of 1mg/L) after 30 minutes. Blood concentrations
    were found to correlate with the atmospheric tetrachloroethylene
    concentrations as well as degree of physical activity of an individual
    (Monster et al, 1979).

    8.6  Conversion factors

    1 mg/L = 0.00289 mmol/L (blood)
    1 mg/L = 147.4 ppm (air)
    1 ppm = 6.78 mg/m3 at 25°C, 760 torr

    8.7  Other recommendations


    9.1  Carcinogenicity

    Increased incidence of hepatocellular carcinomas in mice given
    tetrachloroethylene in doses of 500 to 1000 mg/kg for 78 days have
    been noted (Baselt and Cravey, 1990; Ellenhorn and Barceloux, 1988;
    Hathaway et al, 1991; Pegg et al, 1979). An increase in mononuclear

    cell leukaemia in rats inhaling doses of 200 to 400 ppm for 2 years
    has also been reported (Hathaway et al, 1991).

    Two limited epidemiological studies on the mortality of individuals
    with occupational tetrachloroethylene exposure in dry-cleaning and
    laundering operations have indicated an increase in liver cancer
    (Blair et al, 1979). However, these studies are not satisfactory for
    reaching definite conclusions about the potential for
    tetrachloroethylene carcinogenicity in humans (Hathaway et al, 1991).
    A 1987 cohort mortality study of dry-cleaning workers with exposure to
    tetrachloroethylene as well as other petroleum-based solvents detected
    an increased incidence of urinary tract cancers (Brown and Kaplen,

    A study in Massachusetts was carried out after tetrachloroethylene was
    found to have been in the drinking water for 20 years. There seemed to
    be an increase in leukaemia and bladder cancer in the individuals
    exposed, which was associated with chronic exposure (Aschengrau et al,

    Other cohort and proportionate mortality studies have variously
    reported excesses of leukaemias, lymphosarcomas and cancer of skin,
    cervix, oesphagus, kidney, colon, lung, liver and pancreas (Clement
    international Corporation, 1993; Hathaway et al, 1991).

    However, there have been also been a number of studies (as reviewed in
    Clement International Corporation, 1993) that have demonstrated that
    there is not enough human data or evidence to connect high
    concentrations of tetrachloroethylene to cancer. But this chemical is
    suspected as being a human carcinogen and handled as such (Hathaway et
    al, 1991).

    9.2  Genotoxicity

    Assays of clastogenic effects in humans following occupational
    exposure to tetrachloroethylene show inconsistent results. Increases
    in chromosome aberrations and sister chromatid exchanges were not
    detected in lymphocytes from 10 workers exposed to tetrachloroethylene
    (Ikeda et al, 1980).

    9.3  Mutagenicity

    Tetrachloroethylene is a weak mutagen, yielding positive results in
    bacterial assays, but baseline responses in mammalian systems did not
    find increased sister chromatid exchanges or chromosomal aberrations
    in lymphocytes of workers exposed to tetrachloroethylene (Ikeda et al,

    9.4  Reprotoxicity

    Pregnant rats exposed to 300 ppm tetrachloroethylene for 7 hours a
    day, on days 6 through 15 of gestation had 4 to 5% reduced in body
    weight and twice the number of per implantation compared with controls
    (Ware, 1988).

    9.5  Teratogenicity

    An increased number of resorption delayed skull, ossifications,
    subcutaneous oedema, and sternal malformations were found in the
    offspring of rats exposed to 300 ppm tetrachloroethylene for 7 hours a
    day on days 6 to 15 of pregnancy (Hathaway et al, 1991).

    No reports of teratogenicity associated with tetrachloroethylene were
    found in humans.

    9.6  ADI

    9.7  MRL

    0.6 ppm (Clement International Corporation, 1993).

    9.8  AOEL

    9.9 TLV

    50 ppm (COSHH, 1995; Ferroni et al, 1992).

    9.10  Relevant animal data

    Experimental rats were unconscious in minutes following exposure to
    concentrations of 6,000 ppm or more, several hours at 3,000 ppm but
    not at 2,000 ppm (Rowe et al, 1952).

    In rats exposed via inhalation, tetrachloroethylene levels rise more
    or less continuously with duration of exposure in brain, lungs, and
    fat, but they tend to level off in blood and liver after a 3 hour
    exposure. Brain cerebrum concentrations of tetrachloroethylene exceed
    blood levels by about four-fold and brain cerebellum levels by
    three-fold, independent of the duration of exposure (Savolainen et al,

    Rats were exposed to tetrachloroethylene vapour levels of 70, 230 and
    470 ppm for 7 months. Occasionally the rats were exposed to higher
    concentrations (averaging 7,000 ppm) and became slightly ataxic which
    disappeared within a few minutes post-exposure. It is thought that
    they developed tolerance to high concentrations. All concentrations
    above 2,750 ppm produce anaesthesia during acute exposure. However,
    after 6 exposures to concentrations of 2,750 ppm it was found that the
    rats did not become anaethetised even above a concentration of 10,000
    ppm (Carpenter, 1937).

    When fed to laboratory mice, an LD50 of 8850 mg/kg was determined.
    Dogs and cats have survived doses of 4000 mg/kg and rabbits 5000
    mg/kg. However, dogs were killed by intravenous doses of 85 mg/kg; the
    few that received 75 mg/kg or less survived (Gehring et al, 1991).

    Single oral doses of [36Cl] tetrachloroethylene were absorbed
    completely when administered to rats at 189 mg/kg (Daniel, 1963), as
    were doses of [14C] tetrachloroethylene dissolved in corn oil
    administered to mice at 500 mg/L (Schumann et al, 1980).

    Several mutagenicity studies have been performed on
    tetrachloroethylene which employ the Ames  Salmonella/microsomes test
    or modifications of this test. Most tests reveal little or no evidence
    of mutagenic activity, except at concentrations that resulted in
    greater than 90% bacterial toxicity (Ware, 1988).

    9.11  Relevant  in vitro data

    No data


    10.1  Ecotoxicological data

    Solubility in water

    Municipal drinking-water in the UK contains an average of 1.3 mg/L of
    tetrachloroethylene and the total daily food intake is about 160 mg
    per day (WHO, 1984).

    WHO drinking water guidance level based on a carcinogenic endpoint in
    10µ/L (Clement International Corporation, 1993).

    In ground water where volatilisation does not occur,
    tetrachloroethylene remains for months or years.

    In 1988, in the US, it was estimasted that 23,000 pounds of
    tetrachloroethylene was released to water from manufacturing and
    processing facilities.


    Volatilisation seems to be the major way in which tetrachloroethylene
    is lost from water.


    Tetrachloroethylene is ubiquitous in air, with levels in the ppt to
    ppb range.

    Tetrachloroethylene has been detected in dairy products (milk, cheese
    and butter) at 0.3-13 µg/kg, meat at 0.9-1.0 µg/kg, oils and fats at
    0.01-7 µg/kg, beverages at 2-3 µg/kg, fruits and vegetables at 0.7-2
    µg/kg and fresh bread at 1 µg/kg (Clement International Corporation,

    The log octanol/water partition coefficient is 2.86.

    10.2  Behaviour

    Adsorption onto soil

    Contamination of soil can occur via leachate from landfill sites. It
    is very mobile in soil and readily migrates to ground water.

    10.3  Biodegradation

    Environmental fate

    About 85% of tetrachloroethylene used annually in the USA is lost to
    the atmosphere, and the world-wide emission of tetrachloroethylene has
    been estimated to be about 450 kilotonnes per year (WHO, 1984). In the
    United Kingdom, estimates for air samples range from 1-9 ppt from over
    the Atlantic Ocean near Lands End, 8-57 ppt on Exmoor, and 15-40 ppb
    at a Northern England industrial area (Commision of the European
    Communities, 1986).

    Atmospheric emissions occur from metal degreasing uses, production of
    fluorocarbons and other chemicals, textile industry uses, and
    miscellaneous solvent-associated applications. Annual mean levels of 6
    ppb and 10 ppb were detected downwind of a chemical laundry and a
    rubber factory, respectively, in Hamburg, Germany (Bruckmann et al,
    1987). Emissions also occur at landfill sites containing the chemical.
    Levels of 0.7 ppb and 0.9 ppb were detected 1.5 and 0.5 metres above
    landfill soil near the city of Bielefeld, Germany (Clement
    International Corporation, 1993).

    In 1988 it was estimated that a total of 32.3 million pounds of
    tetrachloroethylene was released to the air from manufacturing and
    processing facilities in the US (Clement International Corporation,

    Releases of tetrachloroethylene to surface water appear to be minor in
    comparison to atmospheric releases (Clement International Corporation,
    1993). Release to water through aqueous waste account for 1% or less
    of the total releases of tetrachloroethylene to the environment
    (Clement International Corporation, 1993). Aeration processes at waste
    treatment facilities strip much of the tetrachloroethylene from the
    water and release it into the atmosphere as a result of the high
    volatility of this chemical.

    There are many processes of recycling tetrachloroethylene, which
    generate tetrachloroethylene-containing sludges and dirty filters that
    have been landfilled in the past. Contamination of soil can occur
    through leaching of tetrachloroethylene from these disposal sites. In
    1988, 106,000 pounds of tetrachloroethylene was thought to be released
    to land from manufacturing and processing facilites in the US (Clement
    International Corporation, 1993).


    Tetrachloroethylene can be transformed by reduction dehalogenation to
    trichloroethylene, dichloroethylene and vinyl chloride under anaerobic
    conditions. It has also been suggested that there is a potential that
    tetrachloroethylene completely mineralises to carbon monoxide in soil
    and aquifer systems and in biological treatment processes (Vogel and
    McCarty, 1985).



    Benignus et al (1985) (as cited in Commission of the European
    Commmunities, 1986) state that tetrachloroethylene undergoes
    photochemical degredation in the troposphere. Trichloroacetyl chloride
    is described as a major degredation product and phosgene a lesser one.
    tetrachloroethylene exists in the troposphere for one year or less.


    Tetrachloroethylene in the atmosphere is hydrolysed to trichloroacetic
    acid and then decomposes to carbon dioxide and chloride ions (Pearson
    and McConnell, 1975).

    Half-life in water, soil and vegetation

    Zoeteman et al (1980) estimated the half-life of tetrachloroethylene
    to be 3-30 days for river water and 30-300 days for lake- and ground-

    10.4  Environmentally important metabolites

    Tetrachloroethylene in the atmosphere is hydrolysed to trichloroacetic
    acid and then decomposes to carbon dioxide and chloride ions (Pearson
    and McConnell, 1975). Under certain conditions, tetrachloroethylene in
    ground water has been reported to degrade to and then to
    dichloroethylene and vinyl chloride.

    10.5  Hazard warnings

    10.5.1  Aquatic life

    Concentrations of tetrachloroethylene detected in fish in the Irish
    Sea ranged from below detection limits to 43 ng/g (dry weight), which
    was only 2-25 times greater thatn levels found in seawater. Levels of
    0.3-43 µg/g (wet weight) were found in 15 species of fish collected
    off the coast of Great Britain (Clement International Corporation,

    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

    One method of disposal involves absorption by vermiculite, dry sand,
    earth, or a similar material and then burial in a secured sanitary
    landfill. A second method involves incineration after mixing with
    another combustible fuel. With the latter method, combustion must be
    complete to prevent the formation of phosgene, and an acid scrubber
    must be used to remove the haloacids produced (Clement International
    Corporation, 1993).


    Henrietta Wheeler

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

    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.

    March 1996


    Abedin Z, Cook R and Milberg RM. 1980
    Cardiac toxicity of perchloroethylene (a dry cleaning agent).
    South Med J 73 (8):1081-1083

    Algren JT and Rodgers GC. 1992
    Intravascular hemolysis associated with hydrocarbon poisoning
    Pediatr Emerg Care 8 (1):34-35

    Aschengrau A, Ozonoff D, Paulu C, Coogan P, Vezina R, Heeren T and
    Zhang Y. 1993
    Cancer risk and tetrachloroethylene-contaminated drinking water in
    Arch Environ Hlth 48 (5):284-292

    Bagnell PC and Ellenberger HA. 1977
    Obstructive jaundice due to a chlorinated hydrocarbon in breast milk.
    Can Med Assoc J 117:1047-8

    Baselt RC and Cravey RH. 1990
    Disposition of Toxic Drugs and Chemicals in Man, 3rd Ed.
    Year Book Medical Publishers pp 775-777

    Benignus V, Chao W, Chen et al. 1985
    Health assessment document for tetrachloroethylene.
    US Environmental Protection Agency
    Research Triangle Park NC
    EPA/600/8-82/005f Final report

    Blair A, Decoufle P and Grsumsn D. 1979
    Causes of death among laundry and dry cleaning workers.
    AJPH 69(5):508-511

    Brown DP and Kaplen SD. 1987
    Retrospective cohort mortality study of dry cleaning workers using
    J Occup Med 29 (6):535-541

    Bruckmann P, Kersten W, Funcke W et al. 1988
    The occurrence of chlorinated and other organic trace compounds in
    urban air
    Chemosphere 17:2363-2380

    Carpenter CP. 1937
    The chronic toxicity of tetrachloroethylene.
    J Ind Hyg Toxicol 19:323-337

    Cavalleri A, Godda F, Pattrinieri M, Fantuzzi G, Righi E and
    Aggazzotti G. 1994
    Perchloroethylene exposure can induce colour vision loss
    Neuroscience 179:162-166

    Clement International Corporation. 1993
    Toxicological profile for tetrachloroethylene, US Department of Health
    and Human Services.
    Prepared by: Clement International Corporation

    Commission of the European Communities. 1986
    Organo-chloride Solvents. Health risks to workers.
    Royal Society of Chemistry.

    COSHH. 1995
    EH40/95 Occupational Exposure Limits 1995

    Daniel JW. 1963
    The metabolism of 36Cl-labelled trichloroethylene and
    tetrachloroethylene in the rat
    Biochem Pharmacol 12:795-802

    Echeverria D, White RF, Sampaio C. 1995
    A behaviorial evaluation of tetrachloroethylene exposure in patients
    and dry cleaners: Apossible relationship between clinical and
    preclinical effects
    JOEM 37(6):667-680

    Ellenhorn MJ and Barceloux DG. 1988
    Medical Toxicology: Diagnosis and Treatment of Human Poisoning.
    Elsevier pp986-987

    Eskenazi B, Wyrobek AJ, Fenster L, Katz DF, Sadler M, Lee J, Hudes M
    and Rempel DM. 1991
    A study of the effect of perchloroethylene exposure on semen quality
    in dry cleaning workers.
    Am J Ind Med 20:575-591

    Fernandez J, Guberan E and Caperos J. 1976
    Experimental human exposures to tetrachloroethylene vapour and
    elimination in breath after inhalation
    Am Ind Hyg Assoc J 37:143-150

    Ferroni C, Mutti A, Folli D, Bergamaschi E and Fanchin I. 1992
    Neurobehavioral and neuroendocrine effects of occupational exposure to
    Neurotoxicology 13:243-248

    Finkel JA, Hamilton A and Hardy HC. 1983
    Hamilton and Hardy's Industrial Toxicology, 4th Ed.
    John Wright pp236-237

    Gehring PJ, Nolan RJ, Watanabe PG and Schumann AM. 1991
    Solvents, Fumigants, and Related Compounds.
    In Hayes WJ and Laws ER (eds).
    Handbook of Pesticide Toxicology, Vol 2.
    Academic Press Inc. pp696-702

    Gosselin RE, Smith RP and Hodge HC. 1984
    Clinical Toxicology of Commercial Products, 5th ed.
    Williams and Wilkins p374

    Grant WM and Schuman JS. 1993
    Toxicology of the Eye, 4th Ed.
    Charles C Thomas

    Hake Cl and Stewart RD. 1977
    Human exposure to tetrachloroethylene: inhalation and skin contact
    Environ Hlth Perspect 21 (12):231-238

    Hathaway GJ, Proctor NH, Hughes JP and Fischman ML (eds). 1991
    Proctor and Hughes' Chemical Hazards of the Workplace, 3rd ed.
    Van Nostrand Reinhold pp464-466

    Ikeda M, Ohtsuji H, Imamura T and Komoike Y. 1972
    Urinary excretion of total trichloro-compounds, trichloroethanol, and
    trichloroacetic acid as a measure of exposure to trichloroethylene and
    Brit J Ind Med 29:328-333

    Ikeda M, Koizumi A, Watanabe T, Endo A and Sato K. 1980
    Cytogenetic and cytokinetic investigations on lymphocytes from workers
    occupationally exposed to tetrachloroethylene.
    Toxicol Lett 5:251-256

    Ikeda M. 1977
    Metabolism of trichloroethylene and tetrachloroethylene in human
    Environ Hlth Perspect 21(12):239-245

    Koppel C, Arendt U and Koeppe P. 1985
    Acute tetrachloroethylene poisoning - blood elimination kinetics
    during hyperventilation therapy.
    Clin Toxicol 23 (2-3):103-115

    Kyyrönen P. 1989
    Spontaneous abortions and congenital malformations among women exposed
    to tetrachloroethylene in dry cleaning.
    J Ep Com Hlth 43:346-351

    Levine B, Fierro MF, Goza SW and Valentour JC. 1981
    A tetrachloroethylene fatality
    J Forens Sci 26:206

    Lukaszewski T. 1979
    Acute tetrachloroethylene fatality.
    Clin Toxicol 15 (4):411-415

    Mazza V and Brancaccio A. 1971
    Adrenal cortical and medullar hormones in experimental
    tetrachloroethylene poisoning.
    Folia Medical (Naples) 54:204-207

    McConnell G, Ferguson DM, Pearson CR. 1975
    Chlorinated hydrocarbons and the environment
    Endeavor 34: 13-18

    McMullen JK. 1976
    Perchloroethylene intoxication
    Br Med J 2:1563-1564

    Meckler LC and Phelps DK. 1966
    Liver disease secondary to tetrachloroethylene exposure.
    JAMA 197 (8):662-663

    Monster AC, Boersma G and Steenweg H. 1979
    Kinetics of tetrachloroethylene in volunteers; influence of exposure
    concentration and work load.
    Int Arch Occup Environ Health 42:303-2309

    Monster AC. 1979
    Difference in uptake, elimination, and metabolism in exposure to
    trichloroethylene, 1,1,1-trichloroethane and tetrachloroethylene.
    Int Arch Occup Environ Health 42:311-317

    Monster AC and Houtkooper JM. 1979
    Estimation of individual uptake of Trichloroethylene,
    1,1,1-trichloroethane and tetrachloroethylene from biological
    Int Arch Occup Environ Health 42:319-323

    Olsen J, Hemmink K, Ahlborg G, Bjerkedal T, Kjjronen P, Taskinan H,
    Lindbohm ML et al. 1990
    Low birth weight, congenital malformation and spontaneous abortion
    among dry-cleaner workers in Scandinavia
    Scand J Work Environ Health 15:238

    Pearson CR and McConnell G. 1975
    Chlorinated C1 and C2 hydrocarbons in the marine environment.
    Proc R Soc Lond B 189: 305-332

    Pegg DG, Zempel JA, Braun WH and Watanabe PG. 1979
    Disposition of tetrachloro(14C)ethylene following oral and inhalation
    exposure in rats.
    Toxicol Appl Pharmacol 51:465-474

    Potter B et al. 1960
    Tetrachloroethylene (perchloroethylene).
    Arch Dermatol 82:903

    Ratnoff WC and Grass RE. 1980
    The familial occurrence of polycythemia vera: report of a father and a
    son, with consideration of the possible atiologic role of exposure to
    organic solvents, including tetrachloroethylene
    Blood 56:233-236

    Reynolds JEF (ed). 1993
    Martindale: The Extra Pharmacopoeia 30th Ed.
    The Pharmaceutical Press

    Rowe VK, McCollister DD, Spencer HC, Adams EM and Irish DD. 1952
    Vapour toxicity of tetrachloroethylene for laboratory animals and
    human subjects.
    Am Arch Indust Hyg Occup Med 5:566-579

    Rowell N. 1977
    Renal function in experimental tetrachloroethylene poisoning.
    Practitioner 219:820

    Savolainen H, Pfaffli P, Tengen M and Vainio H. 1977
    Biochemical and behavioral effects of inhalation exposure to
    tetrachloroethylene and dichloromethane
    J Neuropathol Exp Neurol 36(6):941-949

    Sax NI. 1984
    Dangerous properties of industrial materials, 6th ed.
    Van Nostrand Reinhold Co p2517

    Schumann AM, Quast JF and Watanabe PG .1980
    The pharmacokinetics and macromolececular interactions of
    perchloroethylene in mice and rats as related to oncologenicity
    Toxicol Appl Pharmacol 55:207-219

    Skender LJ, Karacic V and Prpic-Majic D. 1991
    Comparative study of human levels of trichloroethylene and
    tetrachloroethylene after occupational exposure.
    Arch Environ Health 46 (3):174-178

    Stewart RD. 1969
    Acute tetrachloroethylene intoxication.
    JAMA 208 (8):1490-1452

    Stewart RD, Baretta ED, Dodd HC and Torkelson TR. 1970
    Experimental human exposure to tetrachloroethylene.
    Arch Environ Health 20 (2):224-229

    Torkelson TR. 1994
    Halogenated aliphatic hydrocarbons containing chlorine, bromine and
    In Clayton GD and Clayton FE (eds).
    Patty's Industrial Hygiene and Toxicology 4th Ed. Vol II, Part E

    Trense E and Zimmerman H. 1969
    Lethal inhalation poisoning due to the chronic effects of
    tetrachloroethylene vapors.
    Zentralblatt fur Arbeitsmedizin und Arbeitsshutz 19:131-137

    Vogal TM and McCarty PL. 1985
    Biotransformation of tetrachloroethylene to trichloroethylene, vinyl
    chlide, and carbon dioxide under methanogenic conditions
    Appl Environ Microbiol 49 (5):1080-1083

    Ware GW (ed). 1988
    In Reviews of Environmental Contamination and Toxicology.
    Vol 106
    Springer-Verlag pp175-188

    WHO. 1984
    Environmental Health Criteria 31.

    Yllner S. 1961
    Urinary metabolites of 14C-tetrachloroethylene in mice.
    Nature 191 (8):820

    Zielhuis GA, Gijsen R and van der Gulden JWJ. 1989
    Menstrual disorders amongst dry-cleaning workers
    Scand J Work Environ Health 15:238

    Zoeteman BCJ, Harmsen K, Linders JBHJ, Morra CFH and Slooff W. 1980
    Persistent organic pollutants in river water and groundwater of the
    Chemosphere 9: 231-249