March 31, 1987

                                  Health Advisory
                              Office of Drinking Water
                        U.S. Environmental Protection Agency
        The Health Advisory (HA) Program,  sponsored by the Office of Drinking
   Water (ODW),  provides information on the health effects, analytical method-
   ology and treatment technology that would be useful in dealing with the
   contamination of drinking water.  Health Advisories describe nonregulatory
   concentrations of drinking, water contaminants at which adverse health effects
   would not be anticipated to occur over specific exposure durations.  Health
   Advisories contain a margin of safety to protect sensitive members of the

        Health Advisories serve as informal technical guidance to assist Federal,
   State and local officials responsible for protecting public health when
   emergency spills or contamination situations occur.  They are not to be
   construed as legally enforceable Federal standards.  The HAs are subject to
   change as new information becomes available.

        Health Advisories are developed for One-day, Ten-day, Longer-term
   (approximately 7 years, or 10% of an individual's lifetime) and Lifetime
   exposures based on data describing noncarcinogenic end points of toxicity.
   Health Advisories do not quantitatively incorporate any potential carcinogenic
   risk from such exposure.  For those substances that are known or probable
   human carcinogens, according to the Agency classification scheme (Group A or
   B), Lifetime HAs are not recommended.  The chemical concentration values for
   Group A or B carcinogens are correlated with carcinogenic risk estimates by
   employing a cancer potency (unit risk)  value together with assumptions for
   lifetime exposure and the consumption of drinking water.  The cancer unit
   risk is usually derived from the linear multistage model with 95% upper
   confidence limits.  This provides a low-dose estimate of cancer risk to
   humans that is considered unlikely to pose a carcinogenic risk in excess
   of the stated values.  Excess cancer risk estimates may also be calculated
   using the One-hit, Weibull, Logit or Probit models.  There is no current
   understanding of the biological mechanisms involved in cancer to suggest that
   any one of these models is able to predict risk more accurately than another.
   Because each model is based on differing assumptions, the estimates that are
   derived can differ by several orders of magnitude.

    Trichloroethylene                                             March 31, 1987


         This Health Advisory is based upon information presented in the Office
    of Drinking Water'.s Health Effects Criteria Document (CD) for Trichloroethylene
    (U.S. EPA, 1985a).  The HA and CD formats are similar for easy reference.
    Individuals desiring further information on the toxicological data base or
    rationale for risk characterization should consult the CD.  The CD is available
    for review at each EPA Regional Office of Drinking Water counterpart (e.g.,
    Water Supply Branch or Drinking Water Branch), or for a fee from the National
    Technical Information Service, U.S. Department of Commerce, 5285 Port Royal
    Rd., Springfield, VA 22161, PB # 86-118106/AS.  The toll free number is (800)
    336-4700; in Washington, D.C. area:  (703) 487-4650.


    CAS No.   79-01-6

    Structural Formula




            TCE, trichloroethene, acetylene trichloride, Tri, Trilene


            Industrial solvent and degreaser for metal components

    Properties  (Torkelson and Rowe, 1981; Windholtz, 1983)

            Chemical Formula                  C2HC13
            Molecular Weight                  131.40
            Physical State                    Colorless liquid
            Boiling Point                     86.7°C
            Vapor Pressure                    77 mm (25°C)
            Density at 25°C                   1.4 g/mL
            Water Solubility                  0.1 g/1 00 mL (20-C)
            Odor Threshold (water)            0.5 mg/L
            Odor Threshold (air)              2.5-900 mg/m3
            Organoleptic Threshold (water)    0.31 mg/L (Amoore and Hautala, 1983)
            Conversion Factor                 1 ppm » 5.46 mg/m3


         0  Trichloroethylene  (TCE) is a synthetic chemical with no natural

         *. Production of,,TCE was 200 million ,lbs in.1982 (U.S. ITC, 1983).
                                      '   -      . .  „   ?" VJ
         0  The major sourjce'of TCE released to the- environment is from its use
            'as a metal degreaser.  Since TCE is'nojb consumed during this use, the
            .majority of all TCE production is.,released to the environment.  Most

     Trichloroethylene                               March  31, 1987

                 .  '                       -3-                  '

             of  the releases occur to the atmosphere by evaporation.  However, TCE
             which is not lost to evaporation becomes heavily contaminated with
             grease and oil and has been disposed of by burial in landfills, dumping
             on  the ground or into sewers.   Because metal working operations are
             performed nationwide, TCE releases occur in all industrialized areas.
             Releases of TCE during production and other uses are relatively minor.

           0  Trichloroethylene released to the air is degraded in a matter of a few
             days.  Trichloroethylene released to surface waters migrates to the
             atmosphere in a few days or weeks where it also degrades.   Photo-
             oxidation appears to be the predominant fate of this compound  (U.S.
             EPA,  1979).  Trichloroethylene  which is released to the  land does not
             degrade rapidly, migrates readily to ground water and remains in
             ground water for months to years.  Under certain conditions, TCE in
             groundwater appears to degrade  to dichloroethylene and vinyl chloride.
             Trichloroethylene also may be formed in ground water by  the degradation
             of  tetrachloroethylene  (Parsons et al., 1984;  Vogel and  McCarty,
             1985).  Trichloroethylene, unlike other chlorinated compounds, does not
             bioaccumulate in individual animals or food chains.

           8  Because of the large and dispersed releases, TCE occurs widely in the
             environment.  Trichloroethylene is ubiquitous  in the air with levels
             in  the ppt to ppb range.  Trichloroethylene is a common contaminant
             in  ground and surface waters with higher levels found in ground
             water.  Surveys of drinking water supplies have found that  3% of all
             public systems derived -from well water contain TCE at levels of 0.5
             ug/L or higher.  A small number of systems (0.04%) have  levels higher
             than  100 ug/L.  Public systems  derived from surface water also have
             been  found to contain TCE but at lower levels. Trichloroethylene has
             been  reported to occur in some  foods in the ppm range.

           0  The major sources of exposure to TCE are from  contaminated  water and
             to  a  lesser extent air; food is only a minor source of TCE  exposure
              (U.S. EPA, 1983).



           0  Data on absorption of ingested  TCE are limited.  When a dose of 200
             mgA9 of 14C-TCE in corn oil was administered  to rats, 97%  of the
             dose was recovered during 72 hours after dosing (DeKant  et  al., 1984).


	°  Doses of 0, 10, 100 or 1,000 mg TCE/kg/day were administered by gavage
              to rats  five days/week  for six weeks  (Zenick et al.,  1984).  Marginal
              increases  in TCE tissue  levels were detected in the 10 mg/kg/day and
              100 mgAg/day dose groups.  Compared  to  controls, a marked increase
              in TCE levels in most tissues was observed in  the highest dose  group.
              Trichloroethylene was distributed in  all tissues examined with  the
              highest  concentrations  in the fat, kidney, lung, adrenals, vas
              deferens,  epididymis, brain and  liver.

    Trichloroethylene                                             March 31,  1987

         0  Studies indicate that TCE is metabolized to trichloroethylene oxide,
            trichloracetaldehyde, trichloroacetic acid, monochloroacetic acid,
            trichloroethanol and trichloroethanol glucuronide (U.S. EPA, 1985a).


         0  Trichloroethylene and its metabolites are excreted in urine, by
            exhalation and, to a lesser degree, in sweat, feces and saliva
            (Soucek and Vlachova, 1959).



    Short-term Exposure                                            .

         0  Oral exposure of humans to 15 to 25 ml (21 to 35 g) quantities of TCE
            resulted in vomiting and abdominal pain, followed by transient uncon-
            sciousness (Stephana, 1945).

    Long-term Exposure

         0  Studies of humans exposed occupationally have shown an increase in
            serum transaminases, which indicates damage to the liver parenchyma
            (Lachnit, 1971).  Quantitative exposure levels were not available.

    Short-term Exposure

         0  The acute oral LDso of TCE in rats is 4.92 g/kg
            (NIOSH, 1980).

    Long-term Exposure

         0  Rats exposed to 300 mg/m3 (55 ppm) TCE five days/week for 14 weeks
            had elevated liver weights (Kimmerle and Eben, 1973).

    Reproductive Effects

         0  No data were available on the reproductive effects of TCE.

    Developmental Effects
         0  No data were available on the developmental effects of TCE.


         0  Trichloroethylene was mutagenic in Salmonella typhimurium and in the
            B. coli K-12 strain, utilizing liver microsomes for activation (Greim
            et al., 1975, 1977).

   Trichloroethylene                                             March 31,  1987



        0  Technical TCE (containing epichlorohydrin and other compounds) was
           found to induce a hepatocellular carcinogenic response in B6C3F-J  mice
           (NCI, 1976).   Under the conditions  of  this experiment, a carcinogenic
           response was  not observed in Osborne-Mendel rats.   The "time-weighted"
           average doses were 549 and 1,097 mg/kg for both male and female  rats.
           The time-weighted average daily doses  were 1,169 and 2,339 mgA9  f°r
           male mice and 869 and  1,739 mg/kg for  female mice.

        0  Epichlorohydrin-free TCE was reported  to be carcinogenic in B6C3F!|
           mice when administered in corn oil  at  1,000 mg/kg/day, 5 days/wk, for
           103 weeks (NTP, 1982).  It was not  found to be carcinogenic in female
           Fischer 344 rats when  administered  in  corn oil at  500 or 1,000 mg/kg/day,
           5 days/wk, for 103 weeks.  The experiment with male rats was considered
           to be inadequate since these rats received doses of TCE that exceeded
           the maximum tolerated  dose.

        0  TCE has been  shown to  be carcinogenic  in mice utilizing the inhalation
           as well as the oral route of exposure.  The National Cancer Institute
           (1976) and the National Toxicology  Program (1982)  each conducted  an
           oral gavage study with TCE, one contaminated with  epichlorohydrin and
           the other free of epichlorohydrin,  respectively.  In these studies,
           as described  above,  B6C3Fi mice were used, and the  results were
           unequivocally positive, showing liver  neoplasms.

        0  In an inhalation study, Henschler et al. (1980) reported dose-related
           malignant lymphomas in female mice  exposed to 100  or 500 ppm TCE  vapor
           6 hrs/day, 5  days/wk,  for 18 months (HANtNMRI strain).  However,  the
           authors downplayed the significance of this observation, indicating
           that this strain of mice has a high incidence of spontaneous lymphomas.

        0  Fukuda et al. (1983) found pulmonary adenocarcinomas in female ICR
           mice on exposure to TCE vapor*

        0  Henschler et  al. (1984) tested Swiss (ICR/HA) mice  and reported that
           when the animals were  treated by gavage with TCE in corn oil, no
           statistical differences were observed  in the incidence of cancers.
           The results of this study can be questioned because the dose schedule
           was often interrupted  even with half of the original dose.  Therefore,
           it is very difficult to assess the  exposure.  A slight increase in
           tumors was found in all groups treated with TCE but did not approach
           statistical significance.

        0  The Van Duuren study (1979) with skin  applications  of TCE in ICR/HA
           mice does not negate the positive findings with other strains of  mice
           and other routes of exposure.


        Health Advisories (HAs) are generally  determined for  One-day, Ten-day,
   Longer-term (approximately 7 years) and Lifetime exposures  if adequate data

Trichloroethylene                                             March'31, 1987a

are available that identify a sensitive noncarcinogenic end point of toxicity.
Ihe HAs for noncarcinogenic toxicants are derived using the following formula:

              HA = JNOAEL or LOAEL) x (BW) „ 	mg n (	ug/L)
                      (UF) x (	L/day)


        NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level
                         in mg/kg bw/day.

                    BW = assumed body weight of a child (10 kg) or
                         an adult (70 kg).

                    UF =» uncertainty factor (10, 100 or 1,000), in
                         accordance with NAS/ODW guidelines.

             	 L/day = assumed daily water consumption of a child
                         (1 L/day) or an adult  (2 L/day).

One-day and Ten-day Health Advisory

     Suitable data were not available to estimate One-day and Ten-day Health

Longer-term Health Advisory

     No suitable data are available from which  to calculate a Longer-term
Health Advisory.

Lifetime Health Advisory

     The Lifetime HA  represents  that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure.  The Lifetime HA
is derived in a three step process.  Step 1 determines the.Reference Dose
(RfD), formerly called the Acceptable Daily Intake  (ADI).  The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious  effects over a  lifetime, and is derived from
the NOAEL  (or LOAEL), identified from a .chronic (or subchronic) study, divided
by an uncertainty factor(s).  From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2).  A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level,  assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of  the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult*—She Lif-etime-HA—ia determined in Step 3 by  factoring in other sources
of exposure, the relative source contribution (RSC).  The RSC from drinking
water is based on actual exposure data or, if data  are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals.  If the contaminant is classified as a
Group A or B carcinogen, according to the Agency's  classification scheme of
carcinogenic potential  (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.

Trichloroethylene                                             March 31, 1987a

     Trichloroethylene may be classified in Group Bi Probable Human Carcinogen,
according to EPA's weight-of-evidence scheme for the classification of carcino-
genic potential (U.S. EPA, 1986).  Because of this, caution must be exercised
in making a decision on how to deal with possible lifetime exposure to this
substance.  The risk manager must balance this assessment of carcinogenic
potential against the likelihood of occurrence of health effects related to
non-carcinogenic end-points of toxicity.  In order to assist the risk manager
in this process, drinking water concentrations associated with estimated
excess lifetime cancer risks over the range of one in ten thousand to one
in a million for the 70 kg adult, drinking 2 liters of water per day, are
provided in the following section.  In addition, in this section, a Drinking
Water Equivalent Level .(DWEL) is derived. A DWEL is defined as the medium-
specific (in this case, drinking water) exposure which is interpreted to be
protective for non-carcinogenic end-points of toxicity over a lifetime of
exposure.  The DWEL is determined for the 70 kg adult, ingesting 2 liters of
water per day.  Also provided is an estimate of the excess cancer risk that
would result if exposure were to occur at the DWEL over a lifetime.

     Neither the risk estimates nor the DWEL take relative source contribution
into account.  The risk manager should do this on a case-by-case basis,
considering the circumstances of the specific contamination incident that.has

     The study by Kimmerle and Eben (1973)is the most appropriate from which
to derive the DWEL. evaluated the subacute exposure to trichloro-
ethylene via inhalation by adult rats for some 14 weeks following, exposure to
55 ppm (300 mg/m^), five days a week.  Indices of toxicity include hemato-
logical investigation, liver and renal function tests, blood glucose and organ/
body weight ratios.  Liver weights were shown to be elevated while other test
values were not different from controls.  The elevated liver weights could be
interpreted to be the result of hydropic changes or fatty accumulation.  The
no-observed-effect level was not identified since only a single concentration
was administered.  From these results, a LOAEL of 55 ppm (300 mg/m3) was
identified.  Ifeing the LOAEL, the DWEL is derived as follows:

Step 1:   Determination of the Total Absorbed Dose (TAD)

          TAD - OOP mg/m3) (8 m3/dav) (5/7) (0.3) ,7,35 mg/kg/day
                             (70 kg )


        300 mg/m3 « LQAEL for liver effects in rats

        8 m3/day  = Volume of air inhaled during the exposure period

           5/7    » Conversion factor for adjusting from 5 days/week exposure
                    to a daily dose

           0.3    « Ratio of the dose absorbed.

          70 kg   » Assumed weight of adult.

Trichloroethylene                                             March 31, 1987


Step 2:  Determination of the Reference Dose (RfD)

                   RfD « 7.35 mg/kg/day = 0.00735 mg/kg/day
                            (100)  (10)              y/ y/  *


        7.35 mg/kg/day » TAD.

             1,000     = uncertainty factor, chosen in accordance with NAS/ODW
                         guidelines for use with a LOAEL from an animal study.

Step 3:  Determination of the Drinking Water Equivalent Level (DWEL)

           DWEL = (0*00735 mg/kg/day)(70 kg) _ 0%26 mg/L (260 ug/L)
                           2 L/day

        0.00735 mg/kg/day = RfD.

                    70 kg = assumed body weight of an adult.

                  2 L/day = assumed daily water consumptiion of an adult.

     The estimated excess cancer risk associated with lifetime exposure to
drinking water containing TCE at 260 ug/L is approximately 1 X 10~4.  This
estimate represents the upper 95% confidence limit from extrapolations prepared
by EPA's Carcinogen Assessment Group using the linearized, multistage model.
The actual risk is unlikely to exceed this value, but there is considerable
uncertainty as to the accuracy of risks calculated by this methodology.

Evaluation of Carcinogenic Potential

     0  IARC (1982) has classified TCE in Group 3.

     0  Trichloroethylene has been classified in Group B2:  Probable Human
        Carcinogen.  This classification for carcinogenicity was determined
        by a technical panel of EPA's Risk Assessment Forum using the EPA
        risk assessment guidelines for carcinogens (U.S. EPA, 1986).  This
        category is used for agents for which there is "sufficient evidence*
        for human carcinogenicity from animal studies and for which there is
        "inadequate evidence" or "no data" from human studies.

     0  Using the improved multistage linearized model, it can be estimated
        that water with TCE concentrations of 280 ug/L» 28 ug/L or 2.8 ug/L
        may increase the risk of one excess cancer per 1 04, 105 or 106 people
        exposed, respectively.  These estimates were calculated from the 1976
        NCI bioassay data, which utilized TCE contaminated with epichlorohydrin.
        Since then, an NTP  (1982) bioassay utilizing epichlorohydrin-free TCE
        has become available; the data from this bioassay have been reviewed
        and evaluated for carcinogenicity, and epichlorohydrin-free TCE has
        been reported to be carcinogenic in mice.

      Trichloroethylene                                             March 31, 1987

           0  ACGIH (1984) has recommended a threshold limit value (TLV) of 50 ppm
                  270 mg/m3) and a short-term exposure limit (STEL) of 150 ppm
           0  The HAS (1980) recommended One- and Seven-day SNARLS of 105 and 15 mg/L,
              respectively .

           0  The WHO ( 1 981 ) recommended a drinking water guidance level of 30 ug/L
              based on a carcinogenic end point.

           0  The EPA (U.S. EPA, 1980) recommended a water quality criterion of
              6.77 mg/L for effects other than cancer.

           0  The EPA (U.S. EPA, 1985d) has promulgated a Recommended Maximum
              Contaminant Level (RMCL) of zero based upon its classification as a
              known or probable human carcinogen and has proposed a Maximum Contami-
              nant Level (MCL) of 0.005 mg/L based on its RMCL and appropriate
              feasibility studies.
              Analysis of TCE is .by a purge-and-trap gas chromatographic procedure
              used for the determination of volatile organohalides in drinking water
              (U.S. EPA,  1985b).  This method calls for the bubbling of an inert
              gas through the sample and trapping TCE on an adsorbant material.
              The adsorbant material is heated to drive off the TCE onto a gas
              chromatographic column.  This method is applicable to the measurement
              of TCE over a concentration range of 0.01 to 1500 ug/L.  Confirmatory
              analysis for TCE is  by mass spectrometry (U.S. EPA, 1985c).  The
              detection limit for  confirmation by mass spectrometry is 0.2 ug/L.
           0  Treatment technologies  which  will remove  TCE from water include
              granular activated carbon (GAG)  adsorption,  aeration and boiling.

           0  Dobbs and Cohen (1980)  developed adsorption  isotherms for several
              organic chemicals  including TCE.  It was  reported that Pibrasorb®
              300 carbon exhibited  adsorptive  capacities of 7 mg,  1.6 mg and 0.4 mg
              TCE/gm carbon at equilibrium  concentrations  of 100,  10 and 1  mg/L,
              respectively.  USEPA-DWRD installed  pilot-scale adsorption columns
              at different sites in New England and Pennsylvania.   In New England,
              contaminated well  water with  TCE concentrations ranging from 0.4 to
              177 mg/L was passed through GAG  columns until a breakthrough concen-
              tration of 0.1  mg/L was achieved with empty  bed contact time (EBCT)
              of 18 and 9 minutes,  respectively (Love and  Eilers,  1982).  In
              Pennsylvania,  TCE  concentrations ranging  from 20 to  130 mg/L were
              reduced to 4.5 mg/L by  GAG after 2 months of continuous operation
            .  (ESE, 1985).

Trichloroethylene                                              March 31, 1987

        TCE is amenable to aeration on the basis of its Henry's Law Constant
        of 550 atm  (Kavanaugh and Trussell, 1980).  In a full plant-scale
        (3.78 MGD) redwood slat tray aeration column, a removal efficiency of
        50-60% was achieved from TCE initial concentrations of 8.3-39.5 mg/L
        at an air-to-water ratio of 30:1 (Hess et al., 1981).  In another
        full plant-scale (6.0 MGD) multiple tray aeration column study, TCE
        removal of 52% was achieved from 150 mg/L (Hess et al., 1981).  A
        full plant-scale packed tower aeration column removed 97-99% of TCE
        from 1,500-2,000 mg/L contaminated groundwater at air-to-water ratio
        of 25:1 (ESE, 1985).

        Boiling also is- effective in eliminating TCE from water on a short-term,
        emergency; basis.  Studies have shown 5 minutes of vigorous boiling
        will remove 95% of TCE originally present (Love and Eilers, 1982).
                 r '
        Air stripping is an effective, simple and relatively inexpensive process
        for removing TCE and other volatile organics from water.  However, use
        of this process then transfers the contaminant directly to the air
        stream.  When considering use of air stripping as a treatment process,
        it is suggested that careful consideration be given to the overall
        environmental occurrence, fate, route of exposure and various other
        hazards associated with the chemical.

    Trichloroethylene                                              March 31, 1987



    ACGIH.  1984.  American Conference of Governmental Industrial Hygienists.
         Documentation of the threshold limit values.  4th ed.  1980-1984 Supplement.
         pp. 406-408.

    Amoore,  J.E., and E.  Hautala.  1983.  Odor as an aid to chemical safety:
         Odor thresholds compared with threshold limit values and volatilities
         for 214 industrial chemicals in air and water dilution.  J. Appl. Tox.

    deKant,  W. Metzderm and 0. Henschler.  1984.  Novel metabolites of trichloro-
         ethylene through dechlorination reactions in rats, mice and humans.
         Biochem. Fharmacol.  33:2021-2027.

    Dobbs, R.A., and J.M. Cohen.  1980.  Carbon adsorption isotherms for toxic
         organics.  EPA 600/8-80-023, Office of Research and Development, MERL,
         Wastewater Treatment Division, Cincinnati, Ohio.

    ESE.  1985.  Environmental Science and Engineering.  Draft technologies and
         costs for the removal of volatile organic chemicals from potable water
         supplies.  ESE No. 84-912-0300 prepared for U.S. EPA, Science and Technology
         Branch, CSD, ODW, Washington, D.C.

    Fukuda,  K., K. Takemoto and H. Tsuruta.   1983. Inhalation carcinogenicity of
         trichloroethylene in mice and rats.  Ind. Health.  21:243-254.

    Greim, H., D. Bimboes, G. Egert, W. Giggelmann and M. Kramer.  1977.  Muta-
         genicity and chromosomal aberrations as an analytical tool for in vitro
         detection of mammalian enzyme-mediated formation of reactive metabolites.
         Arch. Toxicol.  39:159.

    Greim, H., G. Bonse,  Z. Radwan, D. Reichert and D. Henschler.  1975.  Muta-
         genicity ^n vitro and potential carcinogenicity of chlorinated ethylenes
         as a function of metabolic oxirane formation.  Biochem. Pharmacol.

    Henschler, D., W. Romen, H.M. Elsasser,  D. Reichert, E.Eder and Z. Radwan.
         1980.  Carcinogenicity study of trichloroethylene by long-term inhalation
         in the animal species.  Arch. Toxicol.  43:237-248.

    Henschler, D., H. Elsasser, W. Romen and E. Eder.  1984.  Carcinogenicity
         study of trichloroethylene, with and without epoxide stabilizers, in
         mice.  J. Cancer Res. Clin. Oncol.  104:149-156.

    Hess, A.F., J.E. Dyksen and G.C. Cline.  1981.  Case study involving removal
         of organic chemical compounds from ground water.  Presented at Annual
         American Water Works Association Conference, St. Louis, Missouri.

    IARC.  1982.  IARC monographs on the evaluation of the carcinogenic risk of
 ' '•      chemicals to humans.  Supplement 4, Lyon, France..

Trichloroethylene                                              March 31, 1987

Kavanaugh, M.C., and R.R. Trussell.  1980.  Design of aeration towers to
     strip volatile contaminants from drinking water.  JAWWA.  December.

Kimmerle, G., and A. Eben.  1973.  Metabolism, excretion and toxicology of
     trichloroethylene after inhalation*  1.  Experimental exposure on rats.
     Arch. Toxicol.  30:115.

Lachnit, V.  1971.  Halogenated hydrocarbons and the liver.  Wien. Klin.
     Wochenschr.  83(41 ):734.

Love, O.T., Jr., and R.G. Eilers.  1982.  Treatment of drinking water containing
     trichloroethylene and related industrial solvents.  JAWWA.  August.

MAS. 1980. National Academy of Sciences.  Drinking Water and Health. Volume 3.
     National Academy Press. Washington, DC.

NCI.  1976.  National Cancer Institute.  Carcinogenesis bioassay of trichloro-
     ethylene.  U.S. Department of Health, Education and Welfare, Public
     Health Service, CAS No. 79-01-6, February.

NIOSH.  1980.  Registry of Toxic Effects of Chemical Substances.  U.S. Depart-
     ment of Health and Human Services.  DHHS (NIOSH) 81-116.

NTP. 1982.  National Toxicology Program.  Carcinogenesis bioassay for tri-
     chloroethylene.  CAS # 79-01-6.  No. 82-1799. (Draft).

Parsons, P., P.R. Wood and J. DeMarco.  1984.  Transformation of.tetrachloro-
     ethene and trichloroethene in microcosms and groundwater.  JAWWA,

Soucek, B., and D. Vlachova.  1959.  Metabolites of trichloroethylene excreted
     in the urine by man.  Pracoc. Lek.  11:457.

Stephens, C.A.  1945.  Poisoning by accidental drinking of trichloroethylene.
     Brit. Med. J.  2:218.

Torkelson, T.R., and V.K. Rowe.  1981.  Halogenated aliphatic hydrocarbons.
     Ini  Industrial Hygiene and Toxicology.  3rd ed.  Vol. 2B.  John Wiley
     and Sons, New York.  p. 3553.

U.S. EPA.  1979.  U.S. Environmental Protection Agency.  Water Related Environ-
     mental Fate of 129 Priority Pollutants, Office of Water Planning and
     Standards, EPA-440/4-79-029.

U.S. EPA.  1980.  U.S. Environmental Protection Agency.  Ambient water quality
     criteria document for trichloroethylene.  Office of Water Research and
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