The evaluations contained in this document were prepared by the
    Joint FAO/WHO Expert Committee on Food Additives*
    Rome, 21-29 April 1976

    Food and Agriculture Organization of the United Nations

    World Health Organization

    *Twentieth Report of the Joint FAO/WHO Expert Committee on Food
    Additives, Geneva, 1976, WHO Technical Report Series No. 599, FAO Food
    and Nutrition Series No. 1.



         1,1,2-Trichloroethylene has been evaluated for acceptable daily
    intake for man by the Joint FAO/WHO Expert Committee on Food Additives
    in 1970 (see Annex I, Ref. 23, p. 121).

         Since the previous evaluation, additional data have become
    available and are summarized and discussed in the following monograph.
    Previously published monograph has been expanded and is reproduced in
    its entirety below.


    Biochemical Aspects

    Absorption, distribution and excretion

         Probably between 71-76% of inhaled trilene is rapidly absorbed
    through the lungs. In man most absorption occurs within the first few
    minutes of exposure and then decreases to an equilibrium between
    air/blood concentrations. Moderate absorption can occur through intact
    skin and from the gastrointestinal mucosa after ingestion (von
    Oettingen, 1955).

         In the rat, rabbit and dog absorbed trilene is distributed among
    all organs and tissues but concentrates mostly in fat and brain and
    least in skeletal muscle; lung and liver also retain low levels
    (Barrett et al., 1939; Clayton & Parkhouse, 1962; von Oettingen,
    1955). Similar organ concentrations were found in guinea-pigs but high
    levels were also found in ovaries and adrenals (Fabre & Truhaut,
    1952). In the rat trilene and tri-chloracetic acid may be selectively
    bound to erythrocytes hence giving high spleen levels (Fabre &
    Truhaut, 1952) but plasma proteins may also be involved (Soucek &
    Vlachová, 1960). In man trilene is detectable in the blood within 30
    minutes of inhalation (Stewart et al., 1962).


         Trilene is metabolized slowly to chloralhydrate (via an epoxide)
    and then rapidly to 2,2,2-trichloracetic acid (CCl3COOH) and
    2,2,2-trichlorethanol (CCl3CH2OH), which latter two metabolites are
    excreted as urinary glucuronides (e.g. trichlorethanol glucusiduronic
    acid) very little unchanged trilene appearing in the urine (Powell,
    1945; Butler, 1949; Uhl & Haag, 1958; Williams, 1959; Smith, 1966).
    Dogs excrete 5-8% of absorbed trilene as trichloracetic acid and
    15-20% as trichlorethanol up to 4 days after exposure (Barrett et al.,

    1939; Barrett & Johnston, 1939; von Oettingen, 1955). The lung and
    spleen, less so the liver, are probably the main sites of metabolism
    (Fabre & Truhaut, 1952; Defalgue, 1961). Rats excrete about 4% of
    inhaled trilene as trichloracetic acid, the lung and spleen being the
    main sites of metabolism in vitro and in vivo, the liver being
    less important (Fabre & Truhaut, 1952).

         Male rats (250-300 g body wt) were dosed with 0.5 ml of a 20%
    solution of trichloroethylene (TCE) in olive oil. Urine was analysed
    daily for a 7 day period. Maximal excretion of the metabolites
    occurred 24-48 hrs after dosing. 24 hrs following administration
    of the TCE in olive oil, 0.82% of the dose was excreted as
    trichloroacetic acid, 0.12% as trichlorethanol and 11.3% as the
    trichlorethanol glucuronide. During the 7 day period the metabolites
    in urine accounted for 16.44% of the administered dose (2.14% as
    trichloracetic acid, 0.82% as free trichlorethanol and 13.8% as
    trichlorethanol glucuronide). Free TCE was not detected in urine or a
    24 expired air sample. No metabolites of TCE were detected in the
    faeces. When rats were given a single oral dose of TCE (0.25 or
    0.5 ml), urinary metabolites accounted for 18% of the administered
    dose (Daniel, 1957a). 36Cl labelled trilene was given to rats by
    gavage. 10-20% was excreted in the urine as trichloracetic acid (1-5%)
    and trichlorethanol(10-15%), 0-0.5% in the faeces and 72.85% probably
    as trilene in the expired air. The metabolites were formed by intra-
    molecular rearrangement. Radioactivity was excreted for up to 18 days
    after single dosing (Daniel, 1963). In vitro-studies on rat liver
    microsomes showed conversion of trilene to chloral (Byington &
    Leibman, 1965). Rabbits excrete 0.5% of absorbed trilene as
    trichloracetic acid (Fabre & Truhaut, 1952; Defalgue, 1961) and after
    oral dosing by gavage no significant effects were seen on urobilin,
    blood, glucose level or serum cholesterol (Dervilleé et al., 1938).
    Guinea-pigs show presence of trichloracetic acid in their urine after
    inhalation (Fabre & Truhaut, 1952). Calves similarly metabolize orally
    administered trilene to trichloracetic acid (1%) and trichlorethanol
    (13-25%) appearing in their urine together with a trace of trilene.
    The balance is probably exhaled or excreted in the faeces (Seto &
    Schultze, 1955).

         Man excretes 6-16% of inhaled trilene as trichloracetic acid
    (Ahlmark & Forssman, 1951); others found 7-27% of retained trilene
    being excreted as trichloracetic acid (Powell, 1945; Soucek et al.,
    1952) as well as trichlorethanol, monochloracetic acid and chloroform
    (Soucek et al., 1952; Defalgue, 1961). Small amounts of trichloracetic
    acid may continue to be excreted in the urine for up to 12 days after
    single exposure (von Oettingen, 1955). Five human subjects exposed for
    5 hours to trilene excreted 4% of the retained dose as monochloracetic
    acid, 19% as trichloracetic acid and 50% as trichlorethanol over the
    next 14 days (Soucek & Vlachová, 1960; Defalgue, 1961). In another
    experiment 8 subjects inhaled trilene for 5 hours, 51-64% of the

    inhaled trilene was retained the rest exhaled unchanged. Of the
    retained trilene 38-50% was excreted as urinary trichlorethanol and
    27-36% as urinary trichloracetic acid. 8.4% of trichloracetic acid and
    trichlorethanol was excreted in the faeces. Sweat and saliva contained
    also both metabolites (Bartonicek, 1962). In all species most of the
    trichloracetic and trichlorethanol is excreted in the first 2 days
    after exposure but excretion may go on up to 53 days. Some 2-4 hours
    elapse after single exposure before trichloracetic acid appears in the
    blood reaching a maximum in 20-50 hours (Ahlmark & Forssman, 1951;
    Defalgue, 1961). Trichlorethanol appears to be the main metabolite and
    is much more toxic (Bartonicek & Teisinger, 1962). Disulfiram
    decreases the excretion of trichloracetic acid and trichlorethanol by
    acting either on converting enzymes or on trilene release from fat
    depots (Bartonicek & Teisinger, 1962) while glucose and insulin
    increase production (Soucek & Vlachová, 1960).

         Chronic exposure may cause disturbance of protein metabolism by
    an increase in the ß-globulin to 16-21% (normal 10-14%) and in fat
    metabolism by an increase in unsaturated fatty acids (Guyot-Jeannin &
    Van Steenkiste, 1958). Repeated inhalation or oral ingestion by rats
    causes transitory elevation of SGOT levels for 24 hours after the last
    exposure, the SGPT levels remaining normal. SGOT levels return to
    normal within 9 days after exposure. No such transitory effects are
    seen in rabbits (Tolot et al., 1966; Viallier & Casanova, 1965).
    Previous ingestion of ethanol potentiates trilene toxicity in rats as
    shown by a rise in SGOT, SGPT and SICD (isocitric dehydrogenase) and
    wide-spread degenerative lipid infiltration as well as early
    centrilobular necrosis of the liver (Cornish & Adefuin, 1966).

         The biological half life (T1/2) of the urinary metabolites of TCE
    was studied in factory workers between 20 and 50 years old (24 males
    and 6 females). The mean T1/2 of total trichloro-compounds was
    approximately 41 hr (Ikeda & Imamura, 1973).

         In a study in which rats and hamsters were exposed to
    trichloroethylene vapor with or without pretreatment with
    phenobarbital. Pretreatment with phenobarbital resulted in a marked
    increase in rate of urinary excretion of trichloro-compounds. Liver
    preparations from rats treated with phenobarbital showed a marked
    increase in the rate of trichloroethylene metabolism compared to
    untreated rats. Pretreatment of rats with trichloroethylene failed to
    induce this enzyme (Ikeda & Imamura, 1973).

         Single exposure of mice to the inhalation LD50 of trilene showed
    some hepatotoxicity as evidenced by a rise in SGPT (Gehring, 1968).

         Trilene passes readily through the placenta and occurs in foetal
    blood in higher concentrations (Helliwell & Hutton, 1950). Orally
    administered trilene has no effect on rat liver glutathione levels
    (Johnson, 1965).


    Special studies on carcinogenicity

         Groups each of 100 weanling (45 day old) mice (C57BL/C3H strain)
    equally divided by sex, were dosed daily, 5 days per week with TCE
    dissolved in corn oil. Initial dosage levels were 1000 and 2000 mg/kg
    for males and 700 and 1400 mg/kg for females. These doses were
    increased once to 1200 and 2400 mg/kg for males and 900 and 1800 mg/kg
    for females. Control mice (40) received an equivalent amount of corn
    oil. At week 36 of the study the mice were placed on a regime of no
    dosing for one week, followed by 4 weeks of dosing. At weeks 78 dosing
    was stopped on the mice maintained until the study was terminated at
    week 90. The time weighted average intakes were calculated to be 1169
    and 2339 mg/kg for males and 869 and 1739 mg/kg for females. During
    the course of the study the mice were housed in cages of solid
    polypropylene without filters. Ten mice were housed in each cage.
    Mice in this study were maintained in a room housing mice on other
    studies receiving the following compounds, trichloroethylene,
    1,1,2,2-tetrachloroethane, chloroform, 3-chloropropene, chloropicrin,
    dibromochloropropane (DBCP), ethylene dibromide, 1,1-dichloroethane, 
    sulfolene, iodoform, methyl chloroform, 1,1,2-trichloroethane,
    tetrachloroethylene, hexachloroethane, carbon disulfide,
    trichlorofluoromethane, and carbon tetrachloride. 27/50 and 14/48 and
    12/20 of high, low and control groups male mice and 8/47 and 8/50 and
    0/50 of high, low and control groups female mice died during the
    course of the study. Histopathology of a variety of neoplastic and
    non-neoplastic lesions showed primary liver tumors (hepatocellular
    carcinoma in 1/20 control males, 26/50 low dose males, 31/48 high dose
    males, 0/20 control females, 4/50 low dose and 11/47 high dose
    females). Metastasis of the hepatocellular carcinoma to the lung
    occurred in 4/26 low dose males and 3/31 high dose males. Malignant
    lymphoid tumors (e.g. reticulum-cell sarcoma, lymphosarcoma and
    malignant lymphoma) were recognized in 1/20 control males, 4/50 low
    dose males, 2/48 high dose males, 1/20 control females, 5/50 low dose
    females and 6/47 high dose females. Other tumors observed in various
    animals included benign fibrous tumors, adenoma of the Harderian
    gland, endometrial adenocarcinoma, ovarian granulosa-cell carcinoma
    and mammary adenocarcinoma (Weatherholtz et al., 1975).

    Special inhalation studies

         Observations in animals exposed for varying periods up to 10
    months show disturbed coordination and hyperexcitability but no
    effects on liver or kidney or blood chemistry. Only the CNS showed
    some oedema and ganglion cell degeneration (Browning, 1965). Rats,
    guinea-pigs, squirrel monkeys, rabbits and dogs were exposed to
    3825 mg/m3 for 6 weeks without significant adverse effects. Exposure
    to 189 mg/m3 for 90 days also revealed no significant pathological

    changes (Prendergast et al., 1967). Groups of 20 mice were exposed for
    1-8 weeks to 200 or 1600 ppm daily for 4 hours. Only slight transient
    fatty hepatic degeneration and no renal effects were seen (Kylin et
    al., 1965).

         Guinea-pigs were exposed to vapour of trilene for 2-1/2 to 4
    months without adverse effects on bodyweight, haematological findings
    or urinalysis results but there was slight evidence of hepatic
    parenchymal degeneration and renal glomerular and tubular degeneration
    (Lande et al., 1939). Rabbits given for 1-5 months 0.074 g/kg trilene
    showed little adverse effect on bodyweight, haematological finding,
    urinary analysis but some hepatic and renal lesions were seen (Lande
    et al., 1939). Dogs were exposed to 150-750 ppm daily for 2-8 weeks.
    Hepatic injury as evidence by BSP excretion, glycogen depletion and
    parenchymal degeneration as well as weight loss, lethargy and
    diarrhoea occurred but cleared on stopping exposure (Seifter, 1944).

    Special studies on pharmacological effects

         Trilene exerts a variety of pharmacological effects. It depresses
    the CNS with predominant narcotic action but needs relatively high
    dosage (Defalgue, 1961). In the CNS there is a variable effect on
    blood pressure. Cardiac arrhythmias are frequent with anaesthetic use
    (Defalgue, 1961) and bradycardia, ectopic beats and other arrhythmias
    have been seen in dogs and rabbits. Possibly some vasoconstriction in
    the capillary bed may occur (von Oettingen, 1955). In the R.S. the
    most common reaction is tachypnoea, especially in young children
    (Defalgue, 1961). Little effects occur in the G.I. tract (Defalgue,
    1961) nor were any effects seen on basal metabolic rate, liver or
    kidney function (von Oettingen, 1955). Trilene absorbed through the
    skin appears in the alveolar air (Stewart & Dodd, 1961).

    Special studies on reproduction

         Eight males and 16 female rats were fed on a diet containing 0%
    or 5% of instant decaffeinated coffee solids extracted with trilene
    (equivalent to a residue of 0.5 ppm trilene). Two generations were
    studied as regards paternal and filial mortality, conception rate,
    resorption, litter size, growth and survival of litter. Organ weights,
    blood chemistry, urinalysis and histopathology of the F2 generation
    were normal (Zeitlin, 1967).

    Special studies on teratogenicity

         A teratogenicity study in rats fed 5% of trilene extracted
    instant decaffeinated coffee solids (equivalent to 0.5 ppm trilene)
    was done for 2 weeks before mating until the 20th day of the 2nd
    pregnancy. Foetuses were examined and resorption sites counted. No
    significant deformities were noted in the test groups nor was there
    any excessive resorption. Alizarin staining revealed no foetal
    skeletal abnormalities (Zeitlin, 1966).

    Special studies on toxic factor

         Soyabean meal extracted with trilene but not with hexane or
    carbon tetrachloride has caused fatal refractory haemorrhagic aplastic
    anaemia in cattle (Stockman, 1916; Picken et al., 1955). The toxic
    factor was shown to be associated with the protein fraction (Picken &
    Biester, 1957; Seto et al., 1958). Similar effects were produced
    by trilene-extracted meat scrap (Rehfeld et al., 1958). However,
    chicks fed trilene-extracted meat scraps showed improved growth
    (Balloun et al., 1955). The toxic factor has been identified as
    S-trans-(dichlorovinyl)-L-cysteine, a reaction product of trilene and
    protein which becomes freed on protein hydrolysis (McKinney et al.,
    1957). Using radio labelled trilene it has been shown that this
    reaction is unlikely to occur when extracting coffee (Brandenberger et
    al., 1969).
        Acute toxicity


    Animal       Route            ml/kg
                                  bodyweight     LD100                    Reference

    Mouse        inhalation         -            7 900 ppm (2 hrs)        von Oettingen, 1955
                 s.c.              11.0          -                        Plaa et al., 1958
                 i.p.               2.2          -                        Klaassen & Plaa, 1966

    Rat          oral               4.92         -                        Smyth et al., 1969
                 inhalation         -            20 000 ppm               Adams et al., 1951

    Guinea-pig   inhalation         -            37 000 ppm (40 min)      von Oettingen, 1955

    Rabbit       s.c.               -            1 800 mg/kg              Barsoum & Saad, 1934
                 inhalation         -            11 000 ppm               Bernardi et al., 1956
                 percutaneous     >20            -                        Smyth et al., 1969

    Dog          i.v.               -            150 mg/kg                Barsoum & Saad, 1934
                 i.p.               1.9          -                        Klaassen & Plaa, 1967
         Mice, rats, guinea-pigs and rabbits dying acutely from
    inhalation, show no toxic effects on the tissues, liver or kidney nor
    after s.c. or i.v. administration (Browning, 1965). I.p. injection of
    2.5 ml/kg trilene into mice had no effect on PSP excretion and
    produced no proteinuria or glycosuria, nor histological renal changes
    (Plaa & Larson, 1965). Oral doses of 3-4 ml/kg bodyweight were fatal
    to rats, mice and guinea-pigs with signs of gastro-intestinal
    irritation (von Oettingen, 1955). Chronic oral poisoning has caused
    some liver and renal damage in dogs and rabbits (von Oettingen, 1955).

         Trilene is a local irritant on the skin, causing blisters and
    necrosis in man and desquamation with ulceration in rabbits (von
    Oettingen, 1955).

    Short-term studies


         Groups each of 10 mice (C57BL/C3H strain) equally divided by sex
    were dosed by intubation for five consecutive days/week for 6 weeks,
    with TCE at a level equivalent to 0, 1000, 1780, 3160, 5620 or
    10 000 mg/kg body wt. The mice were then maintained for two weeks
    under control conditions. Body wt gains in all surviving groups were
    not significantly affected in a dose related manner. All mice at the
    high dose level died during the first week of the study, and only
    1/5 survived the next highest dose level. There were no deaths at
    3160 mg/kg body wt dose or lower. No gross lesions were observed at
    the termination of the study (Weatherholtz et al., 1975).


         Groups each of 10 rats (Osborne Mendel) equally divided by sex
    were dosed by intubation for five consecutive days/week for 6 weeks,
    with TCE at a level equivalent to 0, 562, 1000, 1780, 3160 or
    5620 mg/kg body wt. The rats were then maintained for a further two
    weeks without administration of TCE. At the high dose level all rats
    died by week 6. Body weight gains of all treated groups were less than
    control. Effects noted in animals at the highest dose range included
    hunching, urine stains, alopecia and labored respiration. Gross
    necropsy findings at week 6 of the study included dilation of kidney
    of one male, and redness of one kidney of male, both in the 1780 ppm
    group, and large abscessed areas in all lobes of the lungs of the
    animals. No other lesions were reported (Weatherholtz et al., 1975).

    Long-term studies


         (See special studies on carcinogenicity)


         Groups of 20 male and female rats were fed instant decaffeinated
    coffee solid extracted with trilene for 2 years at 0% or 5% of their
    diet (equivalent to a residue of 0.5 ppm trilene) without deleterious
    effects on survival, behaviour, growth, food consumption, urinalysis, 
    haematology, organ weights and histopathological findings (Zeitlin,

         Groups each of 100 weanling rats (Random Bred, Osborne-Mendel)    
    equally divided by sex were dosed daily, 5 days per week, with TCE
    dissolved in corn oil at initial dosage levels 1300 and 650 mg/kg.
    These dosages were adjusted downward at week 7 and again at week 16.
    Control mice (40) received an equivalent amount of corn oil. At week
    36 of the study the mice were placed on a regime of no dosing for one
    week, followed by 4 weeks of dosing. At week 78 dosing was stopped
    and the animals maintained until week 110. The time weighted average
    intakes were calculated to be 1097 and 549 mg/kg body weight. During
    the course of this study the rats were maintained in a room housing
    rats on other studies and receiving the following compounds,
    trichloroethylene, dibromochloropropane, ethylene dichloride,
    1,1,-dichloroethane, and carbon disulfide. All rats in this room were
    housed in hanging galvanized steel cages without air filters.
    Individual bodyweights and food consumption were recorded at weekly
    intervals for the first ten weeks and at monthly intervals thereafter.
    Treated rats showed a decreased total weight gain during the period of
    growth, and survivors at the end of the study showed a lower
    bodyweight than controls. 47/50, 42/50 and 17/20 of the high, low and
    control male rats, and 37/50, 35/49 and 12/20 of the high, low and
    control female rats died before the termination of the study.
    Statistical analyses of the results indicated that the probability of
    survival was decreased by exposure to TCE. Histopathology of the
    various lesions in the test animals indicated a variety of neoplastic
    and non-neoplastic lesions in control, low dose and high dose rats.
    None of these lesions appeared to be compound related. The only drug
    related lesion was a slight to moderate degenerative and regenerative
    tubular alterations, primarily affecting proximal tubular epithelium
    which was observed in low and high dose males and females, but not in
    controls (Weatherholtz et al., 1975).

    Observations in man

         There is much experience from safe use of trilene as an
    anaesthetic for man and from various other analgesic inhalation
    treatments now abandoned e.g. trigeminal neuralgia, migraine, angina
    (von Oettingen, 1955). Some authorities recognize a syndrome of
    chronic intoxication (Moeschlin, 1956) others admit only to a
    transient neurasthenic symptom complex (Anderssen, 1957). Fumes or
    the liquid can cause skin burns. No evidence exists of serious
    haematological effects. Neurological disturbances are similar to
    neurasthenic conditions with rarely apparent cardiac disturbances.
    Trigeminal palsies and optic nerve involvement may have been due to
    impurities but have not been seen with pure material. Irritation of
    the lungs and gastrointestinal symptoms have been reported after
    industrial over-exposure. Addiction has been reported (Bardodej &
    Vyskocil, 1956; Browning, 1965; Patty, 1958; Defalgue, 1961; Milby,
    1968; Mitchell & Parsons-Smith, 1969). Psychomotor performance is not
    affected by exposure to 100 ppm but there is a decline in performance
    at higher inhalation levels (Stops & McLaughlin, 1967).

         Eight males were exposed to 0, 100, 300 or 1000 ppm in air for 2
    hours. At 1000 ppm visual perception and motor skills were adversely
    affected (Vernon & Ferguson, 1969). In another experiment leucocyte
    alkaline phosphatase levels in peripheral leucocytes were elevated
    after prolonged exposure. This effect is reversible (Friborská, 1969).

         Acute human poisoning cases have recovered without hepatic or
    renal sequelae. After ingestion there is some burning of the oral
    mucosa, later nausea and vomiting with vertigo, ataxia, somnolence,
    confusion, delirium and coma (Browning, 1965). Excessive inhalation
    has been blamed for hepato-nephritis but the incidence is very low and
    it is possible that liver and renal involvement are the result of
    underlying previous disease (Roche et al., 1958). Untoward effects on
    the circulation, cardiac irregularities and excessive capillary oozing
    with tachypnoea but no adverse hepatic effects have been reported
    after anaesthetic use (von Oettingen, 1955). Ingestion of 60 ml
    appears to be fatal in man (Pebay-Peyroula et al., 1966). At elevated
    temperatures trilene reacts with soda lime to form dichloracetylene
    and this reacts further to generate phosgene carbonylchloride and
    various acids which are all toxic (Defalgue, 1961). The TLV is 100 ppm
    (Amer. Conf. Gov. Ind. Hyg., 1969).


         Metabolic data from studies conducted in rats indicate a rapid
    excretion of TCE or its oxidation products, trichloracetic acid,
    trichlorethanol or trichlorethanol glucuronide. Pretreatment with
    phenobarbital induces a marked increase in urinary metabolites.
    However, urinary excretion represents less than 20% of the ingested
    dose and none is detectable in the feces.

         In short-term range finding studies mice were found to be more
    resistant than rats challenged with similar dosage on an mg/kg basis.

         Data from lifetime gavage studies in rats and mice are
    compromised by the presence of other halogenated substances in the
    rooms where the animals were kept. This may in part explain the life-
    shortening seen in the control rats as well as the fed rats. However,
    even at these high doses there was no increased incidence of tumors in
    treated rats as compared to their controls.

         In the mouse study survival to 90 weeks was adequate for all
    groups and the tumors noted in the treated groups were generally
    absent in the controls. Thus regardless of the presence of other
    halogenated solvents in the same quarters as the TCE treated mice,
    there is a definite dose related increase in the incidence of
    hapatocellular carcinoma in the treated mice. Therefore, based on the
    data from the 90-week mouse intubation study, TCE must tentatively be
    considered a carcinogen. However, for a more definitive statement as
    to the carcinogenesis of TCE, the mouse study should be repeated
    without the uncontrolled multifactorial effects of stimulation,
    suppression, synergism, etc., that may have been caused by the
    presence of other halogenated solvents.


         Trichloroethylene has been shown to be a carcinogen in a long-
    term gavage study with mice. Pending resolution of some uncertainties
    in the manner in which the study was carried out the earlier tentative
    approval for TCE as a solvent is withdrawn.

    Further work (before an ADI can be allocated)

         Well-controlled lifetime oral exposure studies in two species.


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    See Also:
       Toxicological Abbreviations
       Trichloroethylene (EHC 50, 1985)
       Trichloroethylene (ICSC)
       Trichloroethylene (FAO/PL:1968/M/9/1)
       Trichloroethylene (IARC Summary & Evaluation, Volume 63, 1995)