March  31,  1987
                             TETRACHLOROETHYLENE (PCE)

                                  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.

    Tetrachloroethyiene                                        March 31,  1987


         This Health Advisory (HA) is based on information presented in the
    Office of Health and Environmental Assessment Criteria Document (CD)  for
    Tetrachloroethyiene (U.S. EPA, I985a).  Individuals desiring further  informa-
    tion on the toxicological data base or rationale for risk characterization
    should consult the CD.  The CD is available for a fee from the National
    Technical Information Service, U.S. Department of Commerce, 5285 Port Royal
    Rd., Springfield, VA, 22161.  The toll-free number is (800) 336-4700; in the
    Washington, D.C. areas (703) 487-4650.


    CAS No.  127-18-4

    Structural Formula

                                          Cl - C = C - Cl
                                               I    I
                                               Cl  Cl

    Synonyms^  •

            PCE, Perchloroethylene, 1,1,2,2-Tetrachloroethylene, Perc


            Solvent for many organic substances
            In drycleaning processes
            Metal degreaser
            Intermediate in the synthesis of certain fluorocarbons
            In the textile industry  (Fuller, 1976)

    Properties  (Verschueren, 1977; Torkelsen and Rowe, 1981; Windholz, 1983)
            Chemical Formula
            Molecular Weight              165.85
            Physical State                liquid
            Boiling Point                 121.2°C
            Melting Point
            Density                       —
            Vapor Pressure                19 mm Hg
            Specific Gravity              1.623
            Water Solubility              150 mg/L (258C)
            Log Octanol/Water Partition   2.86
            Taste Threshold               —
            Odor Threshold (water)        300 ug/L
            1 ppm in air                  6.78
            Conversion Factor             —

     Tetrachloroethylene                                        March 31, 1987



          0  Tetrachloroethylene (PCE) is a synthetic chemical with no natural sources.

          0  Production of PCE was 550 million pounds in 1982  (U.S. ITC, 1983).

          0  The majority of PCE is not consumed during its various uses, but is
             released directly to the atmosphere.  Tetrachloroethylene that does
             not evaporate during use becomes heavily contaminated with grease and oil
             and is disposed of in the forms of solid and liquid wastes.  During
             disposal,  PCE is dischrarged directly to land and surface water.
             Because metal and fabric cleaning industries are widely dispersed,
             PCE releases occur nationwide.

          0  PCE released to air degrades in a matter of days or weeks.  PCE
             released to water degrades slowly; volatilization appears to be the
             major transport process for removal of PCE from aquatic systems (U.S.
             EPA, 1979).  It is very mobile in soil and readily migrates to ground
             water.  In ground water, where volatilization does not occur, PCE
             remains for months or years.  Under certain conditions, PCE in ground
             water has  been reported to degrade to trichloroethylene and then to
             dichloroethylene and vinyl chloride (Parsons et al.,  1984; Vogel and
             McCarty, 1985).

          0  Tetrachloroethylene is ubiquitdus in the air with levels in the ppt
             to ppb range.  It is also 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 PCE levels of 0.5 ug/L or higher.   A small
             number of  systems (0.7%) have levels higher than 5 ug/L.  Public
             systems derived from surface water have also been found to contain
             tetrachlorethylene but at lower levels.

          0  The major  sources of exposure to tetrachloroethylene  are from contami-
             nated water and to a lesser extent air.  Tetrachloroethylene has been
             reported to occur in some foods in the ppm range, but food is considered
             only a minor source of exposure (U.S. EPA,  1983).

             Single oral doses of (36d)-pcE were absorbed completely  when admini-
             stered to rats at a concentration of 189 mg/kg (Daniel,  1963) as  were
             doses of (14c)-PCE administered to mice at a dose of  500  mg/kg (Schu-
             mann et al.,  1980).

           - Human volunteers at rest absorbed about 25 percent of PCE admini-
             stered by inhalation exposure at 72 or 144 ppm over a four-hour
             period.  The compound initially was absorbed rapidly, with  decreasing
             uptake as exposure continued.  Absorption was determined  by measuring
             PCE and its metabolites (trichloroethanol,  trichloroacetic  acid)  in
             exhaled air,  blood and urine  (Monster,  1979;  Monster  et al.,  1979;
             Monster and Houtkooper,  1979).

    Tetrachloroethylene                                        March 31,  1987



         0  Once in the bloodstream,  PCE tends to distribute to body fat.  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 and the half-life for saturation of the fat to 50% of its
            equilibrium concentration is about 25 hours  (Monster,  1979).

         0  In rats exposed via inhalation, PCE levels rise more or less  continu-
            ously with duration of exposure in brain,  lungs,  and fat,  but tend to
            level off in blood and liver after a 3-hour  exposure.   Brain cerebrum
            concentrations of PCE exceed blood levels by about four-fold, and
            brain cerebellum by about three-fold,  independent of the duration of
            exposure (Savolainen et al., 1977).


         0  Only small amounts of PCE (less than 4% of the estimated absorbed dose)
            are metabolized and excreted as trichloroacetic acid in humans (Ogata
            et al., 1971; Fernandez et al., 1976).

         0  Oxidative metabolism is proposed to proceed  via an epoxide intermediate
            which can lead to the major metabolite,  trichloroacetic acid.  (U.S.
            EPA, 1985a).  In humans,  PCE is metabolized  to trichloroethanol,
            trichloroacetic acid and unidentified chlorinated products (Ikeda and
            Ohtsuji, 1972; Ikeda, 1977).

         0  Workers exposed occupationally reached a plateau rate  of urinary
            metabolite excretion (measured as total trichloro-compounds)  when the
            workplace air concentrations of PCE approached 100 ppm.  Metabolite
            excretion did not increase when air concentrations rose to 400 ppm
            (Ikeda et al., 1972).
            PCE itself is eliminated primarily via the lungs.   The respiratory
            half-life for PCE elimination has  been estimated at 65 to 70 hours
            (Stewart et al.,  1970;  Ikeda and Imamura,  1973).

            Trichloroacetic acid, as a metabolite of PCE,  is eliminated with a
            half-life of 144  hours  via the urine (Ikeda and Imamura,  1973).
            Liver, kidney, and CNS effects have been observed in humans occupationally
            exposed to tetrachloroethylene (U.S. EPA, 1985a).

            Hookworm treatment with oral PCE was prevalent in the 1920s and 1930s
            in India and the Pacific Islands.  Thousands of individuals received
            oral doses of approximately 0.15 mL/kg (Kendrtck, 1929)  or a total
            dose of about 4 mL for adults (Fernando et al., 1939).  No-effect
            levels for oral exposure cannot be derived from these clinical reports,

Tetrachloroethylene                                        March 31,  1987


        although they suggest that PCE Is relatively nontoxic by the  oral
        route at these doses.

     0  Stewart et al. (1974) exposed 19 volunteers to PCE (20 to 150 ppm) for a
        5-week period and noted deleterious effects (decreased odor perception,
        diminished response on the modified Romberg test)  at 100 ppm  but not
        at 20 ppm.


Short-term Exposure

     0  In mice, the 24-hour LD50s/LC5os are:   8.8 to 10.8 gAg by the oral
        route (Wenzel and Gibson,  1951), 5,200 ppm with 4 hours inhalation
        exposure (Friberg et al.,  1953) and 4.7 gAg intraperitoneal  (Klaassen
        and Plaa, 1966).

     0  In rats, the 24-hour LD50s/LC5os are 13 gAg oral (Smyth et al., 1969)
        and 4,000 ppm with four hours inhalation exposure (Carpenter  et al.,

     0  Single oral gavage doses of 2,158 mgAg pCE to rabbits resulted in a
        50% increase in serum lipoprotein levels and mild transient elevations
        of serum enzymes (alkaline phosphatase, SCOT, SGPT) which were indica-
        tive of liver damage (Fujii, 1975).

     0  A dose-response related increase in fatty infiltration of the livers
        of mice was observed after four hours of exposure to 200 to 3,000 ppm
        (1400 to 20,000 mg/m3) via inhalation (Kylin et al., 1963).  Decreased
        hepatic ATP and increased total lipid and triglyceride levels were
        observed in mice exposed to 800 ppm PCE in air for three hours (Ogata
        et al., 1968).

     0  Schumann, et al. (1980) administered tetrachloroethylene in corn oil
        to rats and mice via gavage for 11 consecutive days at does of 100,
        250, 500 and 1000 mgAg-  F°r mice, histopathological changes (centrilobu-
        lar swelling) were observed at all dose levels and increased  body weight/
        liver weight ratios were observed at doses of 250 mgAg/day and higher.
        Rats were more resistant with toxicity (increased liver weight and
        serum enzyme levels) apparent only at the highest dose.  A LOAEL of
        100 mgAg/dav was identified based on histopathological changes in

Longer-term Exposure

     8  Rats were exposed to 70, 230 or 470 ppm PCE  (470, 1600, or 3200 mg/m3)
        by inhalation 8 hours/day, 5 days/week for 150 days.  No significant
        changes were observed at 70 ppm; renal and liver congestion and swelling
        were observed at 230 and 470 ppm (Carpenter, 1937).

     0  Rats, rabbits and monkeys were exposed via inhalation to PCE at 400 ppm
        (2700 mg/m3) 7 hours/day, 5 days/week for up to 179 days (Rowe, et
        al., 1952). . Histopathological examination of the liver, kidney and spleen
        revealed no significant changes at this exposure level.

Tetrachioroethylene                                        March 31,  1987

     0  Guinea pigs showed a dose dependent increase in liver weight and
        fatty infiltration of the liver when exposed to 100, 200 or 400 ppm
        (680, 1400, or 2700 mg/m3) for up to 169 exposures over 236 days
        (Rowe et al., 1952).

     0  Kylin et al. (1965) observed fatty infiltration in livers of mice
        exposed to 200 ppm (1400 mg/m3), 4 hours/day, 5 days/week for 8 months.

     0  In a study by Buben and O1Flaherty (1985), male Swiss-Cox mice were
        exposed to tetrachloroethylene in corn oil via gavage at doses of 0,
        20, 100, 200, 500, 1000, 1500, and 2000 mg/kg» 5 days/week for 6 weeks.
        Liver toxicity was evaluated by several parameters including liver weight
        /body weight ratio, hepatic triglyceride concentrations, DNA content,
        histopathological evaluation and serum enzyme levels.  Increased
        liver triglycerides were first observed in mice treated with 100 mg/kg.
        Liver weight/body weight ratios  were significantly higher than controls
        for th 100 mg/kg group, and slightly higher than controls in the 20
        mg/kg group.  A NOAEL of 20 mg/kg/<3ay was identified based on the
        absence of hepatotoxic effects.

     0  Toxic nephropathy was observed in mice exposed to 386 and 1072 mg/kg
        in corn oil via gavage, 5 days/week, for 78 weeks (NCI, 1977).

Reproductive Effects

     0  Rabbits showed liver enzyme changes and renal function alterations
        following 200 to 300 ppm exposures (1400 to 20,000 mg/m3), 4 hours/day,
        5 days/week for 9 weeks (Brancaccio et al., 1971; Mazza, 1972).

     0  Pregnant rats exposed to 300 ppm PCE (20,000 mg/m3) for 7 hours/day,
        on days 6 through 15 of gestation had 4 to 5% reduction in body weight
        and twice the number of resoprtions per implantation compared with
        controls (Schwetz et al. (1975).

Developmental Effects

     0  Schwetz et al. (1975) assayed for reproductive and developmental
        effects in rats and mice exposed to 300 ppm PCE (20,000 mg/m3) by
        inhalation for 7 hours/day on gestational days 6 through 15.  Pregnant
        mice exhibited a significant increase in the mean relative liver
        weights and their fetuses weighed significantly less than controls.
        In the mouse pups, significant subcutaneous edema, delayed skull
        ossification and ^he presence of split sternebrae were observed.

     0  Offspring of rats exposed to PCE (900 ppm  [6100 mg/m3], days 7-13
        of gestation; 900 ppm, days 14-20 of gestation; 100 ppm  [680 mg/m3],
        days 14-20 of gestation) were evaluated with respect to brain histo-
        pathoiogy and biochemistry and several behavioral parameters.  No
        significant differences were found between controls and the 100 ppm
        dose group.  Differences in neurotransmitter levels and some altera-
        tions on behavioral tests were noted in the 900 ppm dose groups.

   Tetrachloroethylene                                        March 31,  1987



        0  Several mutagenicity studies have been performed on PCE which -employ
           the Ames Salmonella/microsome test or modifications of this test.
           Most tests  reveal little or no evidence of mutagenic activity by PCE
           except at concentrations which result in greater than 90% bacterial
           toxicity (U.S.  EPA,  1985a).


        8  PCE containing  stabilizers  was concluded by NCI (1977) to be a  liver
           carcinogen  in B6C3F-] mice administered 386 to 1,072 mgAg by  gavage
           for 78 weeks.  No conclusion concerning the effects on Osborne-Mendel
           rats administered 471 to 949 mg/kg by gavage could be made because of
           high mortality  rates (median survival for treated animals was less than
           68 weeks compared to greater than 88 weeks for controls).

        0  In the NTP  (1985) inhalation bioassay, rats and mice of both  sexes
           were exposed to 0,  200 and  400 ppm (rats) and 0, 100 and 200 ppm
           (mice) tetrachloroethylene.  Male rats exhibited a significantly
           increased incidence of mononuclear cell leukemia,  and an increased
           incidence of renal tubular  adenomas/carcinomas (combined).  PCE
           induced hepatocellular carcinomas in male and female mice at  both
           doses.  Classification of PCE as carcinogenic in the rat is contro-
           versial.  The Science Advisory Board's Halogenated Organics Subcommittee
           (U.S. EPA,  1987)  has questioned the relevance of mononuclear leukemia
           to man, a species not susceptible to this type of leukemia, and the
           validity of combining renal adenomas/carcinomas to achieve statistical
           significance to the results.


        Health Advisories  (HAs) are generally determined for One-day, Ten-day,
   Longer-term (approximately 7 years) and Lifetime exposures if adequate  data
   are available that identify a sensitive noncarcinogenic end point of  toxicity.
   The HAs for noncarcinogenic toxicants are derived using the following formula:

                 HA = (NOAEL or LOAEL) x (BW) = 	   /L (	   /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

Tetrachloroethylene                                        March 31, 1987


One-day Health Advisory

     The available studies were not considered sufficient for derivation of a
One-day HA.  It is recommended that the value for the Ten-Day HA, 2 mg/1, be
used at this time as a conservative estimate for the One-Day HA.

Ten-day Health Advisory

     Hepatotoxicity in mice exposed to tetrachloroethylene was selected as the
basis for calculating the Ten-day HA value.  Schumann et al. (1980) administered
PCE in corn oil to rats and mice via gavage for 11  consecutive days at doses
of 0, 100, 250, 500 and 1000 mg/kg.  For mice, histopathological changes
(centrilobular hepatocellular swelling) were observed in all treated animals,
and increased liver weight/body weight ratios were  observed in animals exposed
to doses of 250 mg/kg and higher.  The lowest dose,  100 mg/kg/day,  represents
the LOAEL for the study.  This value is consistent  with the estimated LOAEL
(based on altered hepatic lipid and triglyceride content) of 160 mg/kg/day
for mice exposed to 200 ppm for 4 hours (Kylin et al, 1963; see appendix),
and could be used as the basis for the Ten-Day Health Advisory with the
application of an uncertainty factor of 1000.  This  uncertainty factor is in
accordance with NAS/ODW guidelines for derivation of the HA based on a LOAEL
from an animal study.  Data from longer-term studies indicates that an uncer-
tainty factor of 1000 may be overly conservative in this case.

   Buben and 0"Flaherty (1985) treated mice with doses ranging from 20 to
2000 mg/kg, 5 days/week for 6 weeks and observed a  slight increase in liver
weight in mice treated with 20 mg/kg; at 100 mg/kg,  increases were significantly
different from controls.  From this study, a dose of 20 mg/kg was identified as
a NOAEL and 100 mg/kg was identified as a LOAEL. Basing the Ten-day HA on the
NOAEL of 20 mg/kg with an uncertainty factor of 100 is consistent with the
protection of humans from the CNS effects observed  by Stewart et al. (1980)
at 100 ppm for 7 hours (approximately 20 mg/kg, see appendix).

The value was calculated as follows:

     Ten-day HA = (20 mgAg/day) (10 kg) = 2.0 mg/L  = 2,000 ug/L
           y         (100) (1 L/day)
        20 mgAg/day = NOAEL based on the absence of effects on liver weight
                       of mice exposed to tetrachloroethylene via gavage.

               10 kg = assumed body weight of child.

                 100 = uncertainty factor, chosen in accordance with NAS/ODW
                       guidelines for use of a NOAEL from an animal study.
             1 L/day = assumed daily water consumption for a child.

Tetrachloroethylene                                        March 31, 1987


Longer-term Health Advisory

     The study by Buben and 0'Flaherty was also selected as the basis for the
longer-term HA.  Lifetime carcinogenicity bioassays did not provide an indication
of toxicity at the low dose range (NCI, 1977; NTP, 1985).  The NOAEL of
20 mg/kg/day and the LOAEL of 100 mg/kg/day identified in the study by Buben
and O'Flaherty are consistent with estimates of LOAELs from inhalation studies.
A LOAEL of 63 mg/kg/day (based on increased liver weight and fatty infiltration
of the liver) was estimated from chronic exposure of guinea pigs to 100 ppm
for 7 hours/day (Rowe et al., 1952;  see appendix), and a LOAEL of 160 mg/kg/day
(based on fatty infiltration of the  liver) from mice exposed to 200 ppm for 4
hours (Kylin et al,  1965).  The Longer-term HA value for a 10-kg child was
calculated as follows:

  Longer-term HA       =  (20 mg/kg/day)(5/7)(10 kg)  =  , >4   /L = ,,400   /L
                               (100) (1 L/day)
       20 mg/kg/day  =  NOAEL based on the absence of effects on liver weight
                        for mice exposed to tetrachloroethylene via gavage.

       5/7           =  factor to convert 5 day/week exposure to daily exposure.

       10 kg         =  assumed weight of child.

       100           =  uncertainty factor chosen in accordance with NAS/ODW
                        guidelines for used of a NOAEL from an animal study.

       1 L/day       =  assumed water consumption for a 10 kg child.

     The Longer-term HA value for a 70-kg adult was calculated as follows:

    Longer-term       =  (20 mg/kg/day)(5/7)(70 kg)  =  5>0   /L  =  5 000   /L
                             (100) (2 L/day)                                y
        20 mg/kg/day = NOAEL based on the absence of  effects  on liver  weight
                       for mice exposed to tetrachloroethylene  via gavage.

                 5/7 = factor to convert 5 day/week exposure  to daily  exposure.

                 100 = uncertainty factor,  chosen in  accordance with NAS/ODW
                       guidelines for use of a NOAEL  from an  animal study.

               70 kg = assumed weight of adult.

             2 L/day = assumed water consumption for  70 kg adult.

Tetrachloroethylene                                        March 31, 1987


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-
uidLe of d 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.  The Lifetime HA is 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.

     No suitable chronic oral or lifetime oral studies were located in the
literature to serve as the basis for the Lifetime HA value.  NOAELs were not
identified in the NCI (1977) study in which LOAELs were identified at high
doses (386 ragAg/day, mice, 471 mgAg/day, rats).  The NTP (1983) study in
which lower doses were tested has not been validated.

   Approximate NOAELs and LOAELs calculated from chronic and lifetime inhalation
studies give less conservative estimates of toxic doses than the six-week
oral study of Buben and O'Flaherty (1985).  LOAEL estimates of 63 mgAg/day
for guinea pigs exposed to 100 ppm, 7 hrs/day (Rowe et al., 1952),  400 mgAg/day
for rats exposed to 475 ppm for 7 hr/day (Carpenter,  1937) and 160 mgAg/day
for mice exposed to 100 ppm for 6 hr/day (NTP, 1985)  are consistent with the
NOAEL of 20 mgAg/day and LOAEL of 100 mgAg/day identified in the study by
Buben and O'Flaherty.  In this study, mice were treated with doses of 20 to
2000 mgAg/day, 5 days/week for 6 weeks.  A slight increase in liver weight
was observed at 20 mgAg» at 100 mgAgr liver weight and hepatic triglyceride
levels were significantly increased over controls.  Using the NOAEL of 20
mgAg/day and an uncertainty factor of 1000 consistent with the use of data
from less than lifetime studies, the Reference dose and DWEL were calculated
as follows:

Step 1:  Determination of the Reference Dose (RfD)

     Reference Dose = (20 mgAg/day) (5/7) =  Q.0143

     20 mgAg/day = NOAEL based on the absence of effects in liver weight
                    for mice exposed to tetrachloroethylene via gavage.

Tetrachloroethylene                                        March 31, 1987


              S/7 = factor to convert 5 day/week exposure to daily exposure.

             1000 = uncertainty factor, chosen in accordance with NAS/ODW
                    guidelines for use with a NOAEL from an animal study of
                    less-than-lifetime duration.

Step 2:  Determination of the Drinking Water Equivalent Level (DWEL)

      DWEL  =  (0.0143 mg/kg/day) (70 kg)   =  0>5 mg/L  =  500 ug/L
                      (2 L/day)


      0.0143 mg/kg/day = RfD.

                 70 kg = assumed body weight of an adult.

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

Step 3:  Determination of the Lifetime Health Advisory

     A lifetime HA is not recommended for PCE because of its classification as
group B2:  probable human carcinogen (US EPA, 1986).  The estimated excess
cancer risk associated with lifetime exposure to drinking water containing
tetrachloroethylene at 500 ug/L is approximately 1 x 10~^.  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.

     Controversy surrounds the classification of PCE.  The Science Advisory
Board, Halogenated Organics Subcommittee has recommended a classification of
Group C:  possible human carcinogen (U.S. EPA, 1987).  This committee
concluded that the animal evidence of carcinogenicity was limited and
questioned grouping rat renal adenomas/carcinomas for statistical analysis
and extrapolating  mouse mononuclear cell leukemia to man, a species which is
not susceptible to this type of leukemia.  In contrast to group B2 carcinogens
for which no lifetime HA values are recommended, lifetime HA values are
calculated for group C carcinogens as follows:

       Lifetime HA  =  500 ug/L x 20%  =  10 ug/L

              500 ug/L = DWEL.

                   20% = assumed relative source contribution from water.

                    10 = additional uncertainty factor per ODW policy to
                         account for possible carcinogenicity.

     Tetrachloroethylene                                         March  31,  1987


     Evaluation of Carcinogenic  Potential

          0  The National  Academy of  Sciences  (NAS,  1977,  1980)  and  EPA's Carcinogen
            Assessment Group (Anderson,  1983) have  calculated  drinking water  con-
            centrations that would be  estimated  to  increase  the risk by one excess
            cancer per million  (10~®)  and  per one hundred thousand  (10~5).  Assuming
            consumption of  2 liters  of water/day by a  70  kg  adult over a 70 year
            lifetime,  NAS calculated drinking water concentrations  of  3.5  ug/L and
            35 ug/L for 10~6 and 10~5  risks, respectively.   CAG calculated concen-
            trations of 66,  6.6  and  0.7  ug/L for 10~4,  10~5  and 10~6 risks, respec-
            tively.  Each group  employed the linearized,  non-threshold multistage
            model,  extrapolating from  data obtained in the 1977 NCI bioassay  in

          0  The linear multistage model  is only  one method of  estimating carcino-
            genic  risk.  It is possible  to estimate carcinogenic risk  with the
            probit, logit or Weibull models, but for PCE  the data are  inadequate
            for calculating reasonable risk estimates  using  these techniques.
            While  recognized as  statistically alternative approaches,  the  range of
            risks  described by using any of these modelling  approaches has little
            biological significance  unless data  can be used  to  support the selection
            of one model  over another.  In the interest of consistency of  approach
            and in providing an  upper  bound on the  potential cancer risk,  the
            Agency has recommended use of  the linearized  multistage approach.

          0  IARC (1979) stated that  there  is limited evidence  to conclude  that it
            is a carcinogen in mice, and placed  it  in  Group  3.

          0  The US EPA Carcinogen Assessment Group  (CAG)  classified tetrachloroethylene
            in Group B2:  Probable human  carcinogen  (U.S.  EPA,  1986).   This classifica-
            tion has been questioned by  the Science Advisory Board, Halogenated Orgar) < < •
            Subcommittee, which  has  recommended  a classification of Group  C:
            Possible human  carcinogen  (U.S. EPA, 1987).


          0   The World Health Organization has recommended a tentative guideline
             value of 10  ug/L for PCE  in drinking water,  based  on carcinogenic
             properties (WHO, 1984).

          0   The National Academy of Sciences  (NAS, 1980) calculated 24-hour  and
             7-day SNARLS.   The  24-hour  SNARL was 172  mg/L,  based on a 490 mg/kg
             LOAEL following i.p. administration, a 100-fold uncertainty factor,
             and a 70 kg  adult drinking  2  L/day  of  drinking  water.  A  7-day SNARL
             of 24.5 mg/liter was calculated by  dividing  the 24-hour SNARL by  seven*


          0   Analysis of  tetrachloroethylene is  by  a purge-and-trap gas chromato-
             graphic procedure used  for  the determination of volatile  organohalides
             in drinking  water  (U.S. EPA,  1985b).   This method  calls for the

March 31, 1987
              bubbling of an inert gas through the sample and trapping tetrachloro-
              ethylene on an adsorbant material.  The adsorbant material is heated
              to drive off the tetrachloroethylene onto a gas chromatographic
              column.  This method is applicable to the measurement of tetrachloro-
              ethylene over a concentration range of 0.03 to 1500 ug/L.  Confirmatory
              analysis for tetrachloroethylene is by mass spectrometry (U.S. EPA,
              1985c).  The detection limit for confirmation by mass spectrometry is
              0.3 ug/L.
              Treatment technologies which will remove tetrachloroethylene from
              water include granular activated carbon adsorption (GAG),  aeration
              and boiling.

              Dobbs and Cohen (1980) developed adsorption curves for several organic
              chemicals including PCE.  It was reported' that Filtrasorb® 300 carbon
              exhibited adsorptive capacities of 51  mg, 14 mg, 3.9 mg and 1.1  mg
              PCE/gm carbon at equilibrium concentration  of 1,000,  100,  10 and 1
              mg/L respectively.   USEPA-DV7RD installed pilot-scale adsorptiion
              columns in New Jersey and Rhode Island.  In Rhode Island,  a Filtrasorb®
              400 GAC column maintained a concentration of PCE below 0.1 mg/L for
              11 weeks of operation and below for 20 weeks of operation  in the
              effluent, given an  influent concentration that ranged from 600 to
              2,500 mg/L (Love and Eilers, 1982).  In New Jersey,  PCE concentration
              ranging from 60 to  205 mg/L were reduced to less than 0.1  mg/L by
              GAC over a 58-week  study period (Love and Eilers, 1982).

              PCE is amenable to  aeration on the basis of its Henry's Law Constant
              of 1,100 atm (Kavanaugh and Trussell,  1980).  In a pilot-scale packed
              tower aeration study, removal efficiencies  of 72 to 99.8%  for PCE
              were achieved using air-to-water ratios of  5-80, respectively (ESE,

              In diffused-air aeration pilot-scale studies using either  spiked
              Cincinnati tap water (17-1,025 mg/L PCE) or actual PCE contaminated
              New Jersey groundwater (94 mg/L PCE),  diffused aeration removed  90%
              of PCE at an air-to-water ratio of 4 for the latter and 98+% for the
              Cincinnati water at air-to-water ratios of  8, 16 and 20 (Love and
              Eilers, 1982).

              Air stripping is an effective, simple  and relatively inexpensive
              process for removing PCE 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 treat-
              ment 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.

    Tetrachloroethylene                                        March 31,  1987



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Tetrachloroethylene                                        March 31, 1987


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March 31, 1987
           Estimation of absorbed dose based on inhalation exposure



Approx .



minute vol.




Time of

. 4


Stewart et al, 1977
Rowe et al, 1952

Savolainen et al, 1977
Savolainen et al, 1977
Carpenter, 1937
Carpenter, 1937
NTP, 1985
NTP, 1985
Kylin, 1963, 1965
aDose =  [PCE(mg/D] [min. vol. (L/hr) ] [Time (hr/day) ] [50% absorption]/[bw(kg)]

         [PCE(mg/L]        =  [PCE(ppm)] x (6.78 mg/m3 - ppm) x (1 L/1000 m3)
         [min. vol.(L/hr)] =  [min. vol.(L/min)] x  (60 min/hr)