EPA-540/1-86-041
                                                                 Off'ce-of Research and Development
                                                                 Office of Health and Environmental
                                                                 Assessment
                                                                 Environmental Criteria and
                                                                 Assessment Office
                                                                 Cincinnati OH 45268
                      Superfund
vvEPA
                       HEALTH EFFECTS ASSESSMENT
                       FOR  1,2-t-DICHLOROETHYLENE

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                                           EPA/540/1-86-041
                                           September  1984
       HEALTH EFFECTS  ASSESSMENT
       FOR 1.2-T-DICHLOROETHYLENE
    U.S. Environmental  Protection Agency
     Office of Research and Development
Office of  Health and Environmental Assessment
Environmental Criteria  and Assessment Office
            Cincinnati, OH  45268
    U.S. Environmental  Protection Agency
  Office of  Emergency and Remedial Response
Office of Solid Waste and Emergency Response
            Washington, DC  20460

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                                  DISCLAIMER

    This  report  has  been  funded  wholly  or  In  part by  the  United  States
Environmental  Protection  Agency under  Contract  No.  68-03-3112  to  Syracuse
Research Corporation.  It has been  subject  to  the Agency's peer and adminis-
trative review, and  It has  been  approved  for  publication as an EPA document.
Mention of  trade  names or  commercial  products  does  not  constitute  endorse-
ment or recommendation for use.
                                      11

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                                   PREFACE


    This report  summarizes  and  evaluates Information relevant  to  a prelimi-
nary  Interim  assessment  of adverse  health effects  associated with  1.2-t-
dlchloroethylene.   All   estimates  of  acceptable  Intakes  and  carcinogenic
potency presented  1n  this document should  be  considered as  preliminary  and
reflect limited  resources  allocated  to  this project.   Pertinent toxlcologlc
and environmental  data  were located  through  on-Hne literature  searches  of
the Chemical  Abstracts,  TOXLINE,  CANCERLINE  and  the  CHEMFATE/DATALOG  data
bases.  The basic  literature searched  supporting this document  1s  current  up
to September, 1984.   Secondary  sources of Information  have also been  relied
upon  1n  the  preparation of  this  report  and  represent large-scale  health
assessment  efforts  that  entail   extensive  peer  and   Agency  review.   The
following Office  of  Health  and  Environmental  Assessment  (OHEA)  sources  have
been extensively utilized:


    U.S. EPA.   1980a.   Ambient  Water  Quality  Criteria for Dlchloroethy-
    lenes.  Environmental  Criteria Assessment  Office,   Cincinnati,  OH.
    EPA 440/5-80-041.  NTIS PB 83-117525.

    U.S.  EPA.   1982.   Reportable Quantity  for  1,2-D1chloroethylene.
    Prepared  by  the  Environmental   Criteria  and  Assessment  Office,
    Cincinnati,   OH,  OHEA for the  Office of  Solid Waste and Emergency
    Response,  Washington, DC.

    U.S.  EPA.   1983b.   Hazard  Profile  for  trans-1,2-D1chloroethylene.
    Prepared  by  the  Environmental   Criteria  and  Assessment  Office,
    Cincinnati,   OH,  OHEA for the  Office of  Solid Waste and Emergency
    Response,  Washington, DC.

    The Intent  1n  these  assessments Is to  suggest  acceptable  exposure  levels
whenever sufficient  data  were available.  Values were  not  derived or  larger
uncertainty factors  were employed when   the  variable  data  were  limited  1n
scope  tending to generate conservative (I.e.,  protective) estimates.  Never-
theless, the  Interim values presented reflect the relative degree of  hazard
associated with exposure or risk to the chemlcal(s) addressed.

    Whenever possible,  two  categories  of  values  have  been estimated for  sys-
temic  toxicants  (toxicants  for  which  cancer Is  not the  endpolnt of concern).
The  first,  the  AIS  or  acceptable  Intake  subchronlc,  Is  an  estimate of  an
exposure  level   that  would  not be expected  to cause  adverse  effects  when
exposure occurs  during  a limited  time Interval  (I.e.,   for an  Interval  that
does  not  constitute  a  significant portion of  the Hfespan).   This type  of
exposure  estimate has  not  been extensively used  or  rigorously  defined,  as
previous  risk  assessment  efforts  have  been  primarily  directed  towards
exposures from  toxicants  In ambient  air  or water  where lifetime exposure  1s
assumed.   Animal  data  used for  AIS  estimates  generally  Include exposures
with  durations  of 30-90 days.   Subchronlc human data are rarely available.
                                      111

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Reported exposures are usually  from  chronic  occupational  exposure situations
or from reports of acute  accidental  exposure.

    The AIC,  acceptable   Intake  chronic,  1s  similar 1n  concept  to  the  ADI
(acceptable  dally  Intake).   It 1s  an  estimate  of an  exposure level  that
would  not  be expected to cause adverse effects  when  exposure occurs  for  a
significant portion  of  the Hfespan  [see  U.S.  EPA  (1980b)  for  a discussion
of  this  concept].   The  AIC  1s  route specific   and  estimates  acceptable
exposure  for  a given  route with  the  Implicit  assumption that  exposure  by
other routes Is Insignificant.

    Composite  scores  (CSs)  for  noncardnogens  have  also  been  calculated
where data  permitted.  These  values  are used for  ranking  reportable quanti-
ties; the methodology for their development 1s explained  1n U.S.  EPA (1983a).

    For compounds for which there  1s  sufficient  evidence  of  carclnogenlcHy,
AIS  and, AIC values  are   not derived.   For  a  discussion  of risk assessment
methodology  for  carcinogens refer to  U.S.  EPA  (1980b).   Since  cancer  1s  a
process that  1s  not characterized by  a threshold,  any exposure  contributes
an Increment of  risk.   Consequently,  derivation of  AIS and  AIC  values would
be Inappropriate.   For  carcinogens,   q-|*s  have been  computed  based  on  oral
and Inhalation data 1f available.
                                      1v

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                                   ABSTRACT


    In order  to  place the risk  assessment 1n proper context,  the  reader  Is
referred to the  preface  of  this document.  The preface  outlines  limitations
applicable to all documents of  this  series  as  well  as  the appropriate Inter-
pretation and use of the quantitative estimates.

    Information concerning toxlcologlcal  consequences  of 1,2-t-dlchloroethy-
lene exposure 1s extremely limited.   Data  were  Inadequate to  estimate an AIS
or AIC  for  either  the oral or  Inhalation  routes.   A CS  of 10.5  was  derived
based on  hlstopathologlcal  changes  1n  the liver  and  lungs of rats  exposed
via Inhalation.  This compound  has not  been tested  for  carc1nogen1dty.   The
limited mutagenldty data are negative.

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                               ACKNOWLEDGEMENTS


    The  Initial  draft  of  this   report  was  prepared  by  Syracuse  Research
Corporation under  Contract No.  68-03-3112  for EPA's  Environmental  Criteria
and  Assessment  Office,  Cincinnati,  OH.   Dr.  Christopher  DeRosa and  Karen
Blackburn were the Technical Project Monitors  and  Helen Ball  was the Project
Officer.  The final documents  In  this  series  were  prepared for the Office of
Emergency and Remedial Response,  Washington, DC.

    Scientists from  the  following U.S. EPA offices  provided  review  comments
for this document series:

         Environmental Criteria and Assessment Office, Cincinnati, OH
         Carcinogen Assessment Group
         Office of A1r Quality Planning and Standards
         Office of Solid Waste
         Office of Toxic Substances
         Office of Drinking Water

Editorial review for the document series was provided by:

    Judith Olsen and Erma Durden
    Environmental Criteria and Assessment Office
    Cincinnati, OH

Technical support services for the document series  was provided by:

    Bette Zwayer, Pat Daunt, Karen Mann and Jacky Bohanon
    Environmental Criteria and Assessment Office'
    Cincinnati, OH
                                      v1

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TABLE OF CONTENTS

1.
2.


3.










4.








5.


ENVIRONMENTAL CHEMISTRY AND FATE 	
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . .
2.1.
2.2.
ORAL 	
INHALATION 	
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS 	
3.1.


3.2.


3.3.


3.4.
SUBCHRONIC 	
3.1.1. Oral 	
3.1.2. Inhalation 	
CHRONIC 	
3.2.1. Oral 	
3.2.2. Inhalation 	
TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS. . . .
3.3.1. Oral 	
3.3.2. Inhalation 	
TOXICANT INTERACTIONS 	
CARCINOGENICITY 	 '. 	
4.1.


4.2.


4.3.
4.4.
HUMAN DATA 	
4.1.1. Oral 	
4.1.2. Inhalation 	
BIOASSAYS 	
4.2.1. Oral 	
4.2.2. Inhalation 	
OTHER RELEVANT DATA 	
WEIGHT OF EVIDENCE 	
REGULATORY STANDARDS AND CRITERIA 	
Page
1
. . . ' 3
. . . 3
3
4
4
. . . 4
4
4
. . . 4
. . . 4
. . . 5
. . . 5
. . . 5
5
6
. . . 6
. . . 6
. . , 6
. . . 6
. . . 6
6
. . . 6
6
. . . 8

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                          TABLE OF  CONTENTS  (cont.)

RISK
6.1.


6.2.


6.3.



ASSESSMENT 	
ACCEPTABLE INTAKE SUBCHRONIC (AIS) 	
6.1.1. Oral 	
6.1.2. Inhalation 	
ACCEPTABLE INTAKE CHRONIC (AIC) 	
6.2.1. Oral 	
6.2.2. Inhalation 	
CARCINOGENIC POTENCY (q^*) 	
6.3.1. Oral 	
6.3.2. Inhalation 	
REFERENCES 	
Page
	 9
	 9
	 9
	 9
	 9
	 9
	 10
	 10
	 10
	 10
	 11
APPENDIX: Summary Table for 1,2-t-01chloroethylene	    15

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                            LIST OF ABBREVIATIONS
ADI                     Acceptable  dally Intake
AIC                     Acceptable  Intake chronic
AIS                     Acceptable  Intake subchronlc
BCF                     B1oconcentrat1on factor
CAS                     Chemical  abstract service
CS                      Composite score
l.p.                    IntraperHoneal
ppm                     Parts  per million
STEL                    Short-term  exposure limit
TLV                     Threshold limit value
                                      1x

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                     1. ENVIRONMENTAL CHEMISTRY AND FATE
    The relevant physical  and  chemical  properties and environmental  fate  of
l,2-t-d1chloroethylene  (CAS No.  156-60-5)  are as  follows:

     Chemical  class:                 halogenated aliphatic  hydrocarbon
     Molecular weight:               96.95
     Vapor pressure at  25°C:        324  mm Hg (Torkelson  and Rowe,  1981)
     Water solubility at 20°C:       6300 mg/8. (Torkelson  and Rowe,  1981)
     Octanol/water
     partition coefficient:         3 (estimated)
     BCF:                            0.5  (estimated)
     Half-lives In
       A1r:                         2.1  days (Hendry and  Kenley,  1979)
       Water:                        1-6  days (estimated)

    The octanol/water  partition coefficient  value  has  been estimated  from
the equation  of  Kenaga and Goring  (1980)  and the value  of  water  solubility
data.   Similarly, the value for  the  BCF has  been  estimated from the equation
of Velth et al.  (1979)  and the  estimated  octanol/water partition coefficient
value.
    The half-lives of  1,2-t-d1chloroethylene,  due to  Us  volatilization  from
aquatic media, have  been  estimated  from the  reaction rate ratio (0.601)  and
the oxygen reaeratlon rate of 0.19-0.96  day~  (Mabey et  al., 1981).
    Pertinent  data  regarding   the  fate  of  1,2-t-d1chloroethylene  1n  soil
could  not  be  located 1n the available  literature.  Based on the behavior  of
this  compound  In aquatic   media, evaporation  1s  expected  to  be  the predomi-
nant  loss  process from  the soil  surface.   In subsurface  soil, blodegradatlon
of  this  compound 1s likely  to  be  a slow  process  (Tabak  et  al.,  1981),  and
the compound  1s  not  likely to be sorbed strongly to  soil  because  of Us  low
                                    -1-

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octanol/water partition coefflcent value.  Therefore, the compound  1s  expec-



ted to_Jeach from subsurface  soil  Into  groundwater.   Page (1981)  reported



1,2-t-d1chloroethylene 1n  groundwaters  from New Jersey at  a  frequency of  51%.
                                    -2-

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           2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
2.1.   ORAL
    Pertinent data  regarding the  oral  absorption  of  1,2-t-d1chloroethylene
could  not  be  located  In  the  available  literature.  The  U.S.  EPA  (1980a)
estimates  that   "virtually   100  percent  of  ingested  OCE  may  be  absorbed
systemlcally,"  based  on  the studies  of Daniel  (1963)  and  Monster et  al.
(1976) using trlchloroethylene.
2.2.   INHALATION
    Pertinent data  regarding the  absorption  of  1,2-t-d1chloroethylene  from
the respiratory tract could  not be  located  In the available literature.   The  '
U.S.  EPA  (1980a) estimates  that   "35-50  percent of  inhaled DCE	may  be
absorbed systemically," based on the  studies  of  Daniel  (1963)  and Monster et
al. (1976)  using trlchloroethylene.
                                    -3-

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                3.  TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1.   SUBCHRONIC
3.1.1.   Oral.    Springer  (1965)  administered   a   mixture  of   1,2-c-and
l,2-t-d1chloroethylene to  rats  for  7  weeks (0.05,  0.25,  0.5 or  1.0  g/kg).
It was not clear from the  review  1f  these were dally, weekly or  total  doses.
No adverse effects were  reported  at  any  dose.  Pertinent  data  regarding the
subchronlc oral  toxldty  of  pure 1,2-t-d1chloroethylene were not  located  In
the available literature.
3.1.2.   Inhalation.    In   an  unpublished  study,   Torkelson  (1965)  exposed
rats, rabbits,  guinea pigs and dogs  to  atmospheres  containing 60% 1,2-c- and
40% l,2-t-d1chloroethylene (500 or 1000 ppm)  7 hours/day,  5  days/week  for  6
months.   No  adverse  effects  were  observed  on  growth,  mortality,   organ
weights,  body  weight,  hematology,  clinical  chemistry,  gross  pathology  or
hlstopathology.
    Freundt et al.  (1977)  exposed groups of six  female  Wlstar  rats  to  atmo-
spheres containing  200  ppm  1,2-t-d1chloroethylene  8 hours/day,  5 days/week
for 1,  2,  8  or  16 weeks.   The  liver and  lungs were  examined hlstologlcally
at  the  end of  each  of these  time periods.  Progressive damage to the  lungs
and  fatty  changes  1n  the liver  were  observed.   By 16  weeks,  3/6  animals
developed  "severe"  fatty  changes  1n the  liver,  and 2/6  developed  "slight"
fatty changes.
3.2.   CHRONIC
3.2.1.   Oral.    Pertinent  data   regarding  the  chronic  oral   toxlclty  of
1,2-td1chloroethylene were not located 1n the  available literature.
3.2.2. Inhalation.   Pertinent data regarding the  chronic  Inhalation  toxldty
of 1,2-t-dlchloroethylene were not located In  the  available literature.
                                    -4-

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3.3.   TERATOGENICITY AND OTHER REPRODUCTIVE  EFFECTS
3.3.1.   Oral.   Pertinent data  regarding  the  teratogenlcHy  or other  repro-
ductive  effects   of   l,2-t-d1chloroethylene  could  not  be  located  In  the
available literature.
3.3.2.   Inhalation.   Pertinent  data  regarding the  teratogenlcHy or  other
reproductive effects  of  1,2-t-d1chloroethylene could  not  be located  1n  the
available literature.
3.4.   TOXICANT INTERACTIONS
    Pertinent data regarding  the Interaction of  1,2-t-dlchloroethylene with
other toxicants could not be located 1n the available literature.
                                    -5-

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                              4. CARCINOGENICITY
4.1.   HUMAN DATA
4.1.1.   Oral.   Pertinent  data  regarding  the  cardnogenlcHy  of  orally
administered  1,2-t-d1chloroethylene  1n humans  could not  be  located  1n  the
available literature.
4.1.2.   Inhalation.   Pertinent   data   regarding  the  cardnogenlcHy   of
Inhaled  1,2-t-dlchloroethylene  1n  humans  could  not  be  located  1n  the
available literature.
4.2.   BIOASSAYS
4.2.1.   Oral.   Pertinent  data  regarding  the  carclnogenlclty  of  orally
administered  1,2-t-d1chloroethylene   1n  experimental  animals  could  not  be
located In the available literature.
4.2.2.   Inhalation.   Pertinent   data   regarding  the  carclnogenlclty   of
Inhaled 1,2-t-dlchloroethylene  1n  experimental  animals could not  be located
1n the available literature.
4.3.   OTHER RELEVANT DATA
    Grelm et  al.  (1975)  reported  negative  results for 1,2-t-d1chloroethylene
using  Escherchla  coll K12  as  the Indicator organism.   Cerna   and  Kypenova
(1977) ^.found  1,2-t-d1chloroethylene  to be nonmutagenlc  1n  Salmonella  tester
strains, and  this compound  failed  to  Induce  chromosomal  aberrations  as Indi-
cated  by  cytogenic  analysis of bone  marrow  cells  1n  mice  following repeated
1.p. Injections.
4.4.   WEIGHT OF EVIDENCE
    Pertinent  data  regarding  the  carclnogenlclty of  1,2-t-d1chloroethylene
1n  humans  or  animals  could  not  be  located  1n  the available  literature.
Using  the  criteria  for  evaluating the overall  weight  of evidence  for  car-
clnogenlclty  to  humans proposed  by  the Carcinogen  Assessment  Group  of  the
                                    -6-

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U.S. EPA  (Federal  Register,  1984), 1,2-t-d1chloroethylene  is  most  approprl
ately designated a Group D - Not Classified chemical.
                                    -7-

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                     5.   REGULATORY  STANDARDS AND  CRITERIA
    The ACGIH  (1980, 1981)  has  established a  TLV of  200 ppm  (-790  mg/m3)
and a  STEL of  250  ppm  (-1000 mg/m3),  based upon  the unpublished  study  by
Torkelson  (1965).   This  standard does  not distinguish  between  the c1s  and
trans  Isomers.
                                    -8-

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                             6.   RISK ASSESSMENT
6.1.   ACCEPTABLE INTAKE SUBCHRONIC (AIS)
6.1.1.   Oral.  The available  data were  Inadequate  for  the derivation  of  a
subchronlc oral AIS for 1,2-t-dlchloroethylene.
6.1.2.   Inhalation.   Two  studies  (Torkelson,  1965; Freundt  et al.,  1977)
were  located  1n  which 1,2-d1chloroethylene was administered  to experimental
animals.   Torkelson  (1965)  observed  no  effects of  subchronlc  Inhalation
exposure to 1000  ppm  of a mixture  of 1,2-d1chloroethylene  Isomers  (-400 ppm
of  the  trans  Isomer)  for  6  months.   In  contrast, Freundt  et al.  (1977)
reported fatty changes  In the  liver  and  minor  changes  In the lungs  following
exposure to 200  ppm  1,2-t-dlchloroethylene for  16 weeks.  Because  of  these
contradictions, the data  are not  considered  suitable  for  the  derivation  of
an AIS.
    A  CS  was  calculated  for  the  effects   of  fatty  liver  changes  and
progressive pulmonary hlstopathologlcal   lesions  observed  by Freundt et al.
(1977)  1n  rats  exposed  to  200  ppm 1,2-t-dlchloroethylene  8  hours/day,  5
days/week for  16 weeks.   A human  MED was  obtained by expanding to continuous
exposure and  applying the assumptions that  the human Inhalation rate  1s  20
m3  of  air/day   with  an  absorption  factor  of   0.5.    Additionally,  an
uncertainty factor of  10  was applied because  the  Freundt et al. (1977)  study
was  subchronlc In duration.   The resulting human MED  of  189  mg/day  corre-
sponds  to  an  RV.  of 2.1.   The   hlstopathologlc  changes   In  the liver  and
lungs  were rated  an  RVg of  5.   A CS  of  10.5,  the  product  of  RVd  and
RV  , was derived.
6.2.   ACCEPTABLE INTAKE CHRONIC (AIC)
6.2.1.   Oral.  The available  data were   Inadequate  for  the derivation  of  an
oral AIC 1,2-t-dlchloroethylene.
                                    -9-

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6.2.2.   Inhalation.   The available data were  Inadequate  for the  derivation
of a chronic Inhalation AIC  for  l,2-t-d1chloroethylene.
6.3.   CARCINOGENIC POTENCY  (q^)
6.3.1.   Oral.     Pertinent   data    regarding   the   cardnogenlclty    of
1,2-t-dlchloroethylene following  oral  exposure could not  be located  1n  the
available literature.   Therefore,  no q^* could  be  derived.
6.3.2.   Inhalation.      Pertinent    data     regarding     the     Inhalation
cardnogenlclty  of  1 t2-t-d1chloroethylene  could  not   be  located  1n  the
available literature.   Therefore,  no q   could  be  derived.
                                    -10-

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                                7. REFERENCES



ACGIH  (American  Conference  of  Governmental  Industrial  Hyg1en1sts).   1980.

Documentation of the Threshold  Limit  Values for Substances 1n Workrook  A1r,

4th ed.  Cincinnati,  OH.   p.  130-131.   (Cited in U.S.  EPA,  1983b)



ACGIH  (American  Conference  of  Governmental  Industrial  Hyg1en1sts).   1981.

Documentation of the  TLV.   p. 130-131.   (Cited  1n U.S.  EPA,  1982)



Cerna,  M.  and  H.  Kypenova.   1977.   Mutagenlc  activity  of  choroethylenes

analyzed by  screening  system tests.   Mutat. Res.   46: 214.   (CHed  1n  U.S.

EPA, 1983b)


                                          oc
Daniel,  J.W.   1963.   The  metabolism of    C1-labeled  trichloroethylene  and

tetrachloroethylene  In  the  rat.  Blochem.  Pharmacol.   12: 795-802.   (CHed

1n U.S. EPA,  1980a)



Federal  Register.  1984.   Environmental  Protection Agency.   Proposed  guide-

lines for carcinogenic  risk assessment.   Federal Register   49:46294-46299.



Freundt, K.J., G.P.  Llebaldt and E. Lleberwlrth.   1977.  Toxldty  studies  on

trans-1.2-d1chloroethylene.  Toxicology.   7: 141-153.   (Cited 1n U.S.  EPA,

1982)



Grelm, H., G.  Bonse, Z.  Radwan, D.  Relchert and  D. Henschler.   1975.   Muta-

genldty jjn  vitro  and  potential cardnogenlclty of chlorinated  ethylenes  as

a   function   of   metabolic  oxlran  formation.    Blochem.  Pharmacol.    24:

2013-2017.  (Cited In U.S.  EPA,  1980a,  1983b)


                                    -11-

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Hendry,  D.G.  and  R.A.  Kenley.   1979.    Atmospheric  reaction  products  of



organic compounds.   U.S.  EPA,  Office  of  Chemical  Control,  Office of  Toxic



Substances, Washington, DC.   EPA 560/12-79-001.







Kenaga,  E.E.  and  C.A.J.  Goring.   1980.   Relationship  between  water  solu-



bility,  soil   sorptlon,  octanol-water  partitioning  and  concentration  of



chemicals  1n  biota.   In:  Aquatic Toxicology, ASTM  STP707,  J.G. Eaton,  P.R.



Parrlsh and A.C. HendMcks, Ed.  American  Society for  Testing  and  Materials,



Philadelphia,  PA.  p. 78-115.







Mabey,  W.R.,  J.  H.   Smith  and  R.T.  Podoll,  et  al.   1981.   Aquatic  Fate



Process  Data  for  Organic  Priority  Pollutants.   U.S. EPA,  Office of  Water



Regulations and  Standards, Monitoring  and  Data Support D1v.,  Washington, DC.



EPA 440/4-81-014.







Monster,  A.C.,   G.  Boersma  and  W.C.  Duba.    1976.   Pharmacok1net1cs  of



tMchloroethylene  1n  volunteers,  Influence of workload  and  exposure  concen-



tration.   Ind.  Arch.  Occup.  Environ.  Health.   38:  87-102.   (Cited  1n  U.S.



EPA, 1980a)







Page,  G.W.  1981.  Comparison of groundwater and surface water  for  patterns



and  levels of  contamination   by  toxic substances.   Environ.  Sc1.  Techno!.



15: 1475-1481.







Tabak,  H.H.,  S.A.  Quare,  C.T.  Mashnl and  E.F.  Broth.  1981.   Blodegrad-



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