TECHNICAL REPORT DATA
                            ffleate read Instructions on tht rtveru before completing)
 1. REPORT NO.
  EPA/600/8-88/023
                              2.
              3. RECIPIENTS ACCESSION NO.
                  PB88-179486/AS
 4. TITLE AND SUBTITLE
              5. REPORT DATE
   Health Effects Assessment for  bis(2-Chloroethyl)ether
                                                           «. PERFORMING ORGANIZATION CODE
 7. AUTHOR(S)
                                                           8. PERFORMING ORGANIZATION REPORT NO
 9. PERFORMING ORGANIZATION NAME ANO ADDRESS
                                                           10. PROGRAM ELEMENT NO.
                                                           11. CONTRACT/GRANT NO.
 12. SPONSORING AGENCY NAME ANO ADDRESS
 Environmental  Criteria and Assessment  Office
 Office  of Research and Development
 U.S.  Environmental Protection Agency
 Cincinnati.  OH  45268	
              13. TYPE OF REPORT AND PERIOD COVERED
              14. SPONSORING AGENCY CODE

                 EPA/600/22
 15. SUPPLEMENTARY NOTES
 6. ABSTRACT
   This  report summarizes and evaluates  information relevant to a  preliminary interim
 assessment  of adverse health effects  associated with specific chemicals  or compounds.
 The  Office  of Emergency and Remedial  Response (Superfund) uses these  documents in
 preparing cost-benefit analyses under Executive Order 32991 for decision-making under
 CERCLA.  All  estimates of acceptable  intakes  and carcinogenic potency presented in
 this document should be considered as preliminary and reflect limited resources
 allocated to  this project.  The intent  in  these assessments is to suggest acceptable
 exposure levels  whenever sufficient data are  available.   The interim  values presented
 reflect the relative degree of hazard associated with exposure or risk to the
 chemical(s) addressed.  Whenever possible,  two  categories of values have been
 estimated for systemic toxicants (toxicants for which cancer is not the  endpoint of
 concern).   The first, RfD$ or subchronic reference dose, is an estimate  of an exposure
 level that  would not be expected to cause  adverse effects when exposure  occurs during
 a limited time interval.  The RfD is  an estimate of an exposure level  that would not
 be expected to cause adverse effects  when  exposure occurs for a significant portion
 of the lifespan.   For compounds for which  there is sufficient evidence of
 carcinogenic!ty,  qi*s have been computed,  if  appropriate, based on oral  and
 inhalation  data  if available.
                               KEY WORDS AND DOCUMENT ANALYSIS
                  DESCRIPTORS
6.IDENTIFIERS/OPEN ENDED TERMS  C. COSATI Field/Croup
 8. DISTRIBUTION STATEMENT

  Public
19. SECURITY CLASS (This Report I

  Unclassified
21. NO. of PAGES
                                             20. SECURITY CLASS (This page I
                                                Unclassified
                           22. PRICE
EPA fmnt 2220-1 (R»». 4-77)   PREVIOUS KOITION is OMOLCTC
                                                                                 /SO

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                                            EPA/600/8-88/023
                                            Hay, 1987
          HEALTH EFFECTS ASSESSMENT
         FOR BIS(2-CHLOROETHYL)ETHER
ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL  ASSESSMENT
      OFFICE OF RESEARCH AND DEVELOPMENT
    U.S. ENVIRONMENTAL PROTECTION AGENCY
            CINCINNATI, OH 45268

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                                  DISCLAIMER


    This   document   has   been  reviewed   1n  accordance   with   the   U.S.
Environmental  Protection  Agency's  peer  and  administrative review policies
and approved for publication.  Mention of  trade names  or  commercial products
does not constitute endorsement 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  b1s(2-
chloroethyl)ether.    All  estimates   of   acceptable  Intake  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  TOXLINE   and  the  CHEMFATE/OATALOG   data  bases.  The  basic  literature
searched  supporting  this document  1s current  up  to May,  1986.   Secondary
sources  of information  have also been relied upon  In  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  Document  for
    Chloroalkyl  Ethers.   Prepared  by the Office of Health and  Environ-
    mental  Assessment,   Environmental  Criteria  and Assessment  Office,
    Cincinnati,  OH  for the Office  of Water Regulations and  Standards,
    Washington,  DC.    EPA 440/5-80-030.   NTIS  PB  81-117418.

    U.S.  EPA.   1980b.    Hazard  Profile  for   B1s(2-chloroethyl )ether.
    Prepared  by  the  Office  of  Health   and  Environmental   Assessment,
    Environmental Criteria  and Assessment  Office,  Cincinnati, OH  for
    the Office of Solid Waste  and  Emergency  Response,  Washington,  DC.

    The  Intent 1n these assessments  1s 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.
Nevertheless, 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
systemic  toxicants   (toxicants  for  which  cancer   1s  not  the  endpolnt  of
concern).  The first,  RfD$  (formerly AIS)  or  subchronlc reference  dose,  1s
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  llfespan).
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  1n  ambient  air  or water  where  lifetime
exposure  1s  assumed.    Animal  data  used  for   RFD$   estimates   generally
Include  exposures with  durations  of 30-90  days.   Subchronlc  human  data  are
rarely  available.  Reported exposures  are usually  from  chronic occupational
exposure  situations  or  from  reports  of acute  accidental  exposure.   These
values   are   developed  for  both   Inhalation   (RfD$j)   and   oral   (RfD$Q)
exposures.
                                     111

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    The  RfO  (formerly  AIC)  1s  similar  1n  concept  and  addresses  chronic
exposure.   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 llfespan  [see  U.S.  EPA  (1980c)  for  a discussion  of  this  concept].   The
RfD  1s  route-specific  and  estimates  acceptable  exposure  for  either  oral
(RfOg)  or  Inhalation  (RfOj)  with  the   Implicit  assumption  that  exposure
by other routes 1s Insignificant.

    Composite  scores  (CSs)   for  noncarclnogens  have  also  been  calculated
where  data permitted.   These  values  are  used  for  Identifying  reportable
quantities  and  the methodology  for  their development  1s  explained  1n  U.S.
EPA (1983).

    For compounds  for which  there Is sufficient evidence  of  carclnogenlclty
RfD$  and  RfD  values  are  not derived.   For  a  discussion of  risk  assessment
methodology for  carcinogens  refer  to  U.S.  EPA  (1980c).   Since  cancer  1s  a
process that  Is  not  characterized by a  threshold,  any  exposure  contributes
an Increment  of  risk.  For  carcinogens,  q-|*s  have  been computed,  If appro-
priate, based  on oral and Inhalation data  1f  available.
                                     1v

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                                   ABSTRACT


    In  order  to  place the  risk  assessment  evaluation  In  proper  context,
refer  to  the preface  of  this  document.   The  preface  outlines  limitations
applicable  to  all  documents  of   this  series  as  well  as  the  appropriate
Interpretation and use of  the quantitative estimates  presented.

    B1s(2-chloroethyl)ether   was   carcinogenic   1n   orally   exposed   mice,
associated  with an  Increased  Incidence of  hepatomas.   The EPA  weight  of
evidence  classification  for  cardnogenlclty  1s  Group  82  because of  strong
response  1n mice and supporting mutagenlcHy findings.  The  U.S.  EPA (1980a)
derived  a  q-|*  of  1.1  (mg/kg/day)"1   from  the  study  1n  mice.   This  q-|*
1s  adopted  for  the  purposes  of this  document.   Because  the  chemical  Is  a
carcinogen In animals,  H  1s  Inappropriate to  derive  RfD$  and RfO values.

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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.   Or.  Christopher  DeRosa and  Karen
Blackburn  were  the  Technical  Project  Monitors  and  John  Helms  (Office  of
Toxic  Substances)  was  the Project  Officer.   The  final  documents   1n  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 Air 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 the following:

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

Technical  support  services  for  the document  series  was  provided  by  the
following:

    Bette Zwayer,  Jacky Bohanon and Kim  Davidson
    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 	
HEIGHT OF EVIDENCE 	
REGULATORY STANDARDS AND CRITERIA 	
Page
. . . 1
. , . 3
. . . 3
. . . 3
. . . 4
. . . 4
. . . 4
4
4
. . . 4
4
4
. . . 4
. . . 4
. . . 5
6
. . . 6
. . . 6
6
6
. . . 6
. . . 6
. . . 8
. . . 8
. . . 10

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                           TABLE OF CONTENTS (cont.)

                                                                        Page
 6.  RISK ASSESSMENT	   11

     6.1.   SUBCHRONIC REFERENCE DOSE (RfOs) 	   11

            6.1.1.   Oral (RfDso)	   11
            6.1.2.   Inhalation (RfD$i)	   11

     6.2.   REFERENCE DOSE (RfD)	   11

            6.2.1.   Oral (RfD0)	   11
            6.2.2.   Inhalation (RfDi) 	   11

     6.3.   CARCINOGENIC POTENCY (q-|*)	   11

            6.3.1.   Oral	   11
            6.3.2.   Inhalation	   11

 7.  REFERENCES	   13

APPENDIX: Oral Summary Table for B1s(2-chloroethyl )ether 1n
          Male C57B1/6xC3H/Anf Mice	   17
                                     V111

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                            LIST OF ABBREVIATIONS
CS                      Composite  score
ppm                     Parts  per  million
STEL                    Short-term exposed level
RfD                     Reference  dose
RfDj                    Inhalation  reference dose
RfDg                    Oral  reference dose
RfDgj                   Subchronlc  Inhalation reference dose
RfD$o                   Subchronlc  oral reference dose
TLV                     Threshold  limit value
TWA                     Time-weighted  average
                                      1x

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                      1.  ENVIRONMENTAL CHEMISTRY AND FATE

    The  relevant  physical  and chemical  properties  and environmental  fate of
b1s(2-chloroethyl)ether  are  presented  In  Table 1-1.   Synonyms  for  b1s-
(2-chloroethyl )ether  are:   sym-dkhloroethyl  ether;  1,1' -oxyb1s(2-ch!oro-
ethane); B,Q'-d1chloroethyl ether; OCEE and Chlorex.
    In   the  atmosphere,   b1s(2-chloroethylJether   Is   expected   to  exist
primarily  1n  the  vapor  phase.   The atmospheric half-life listed 1n Table 1-1
1s  the  half-life  for the  reaction  of  gaseous  b1s(2-chloroethyl)ether  with
photochemlcally  generated  hydroxyl  radicals.   Based  on  a rate  constant  of
1.79X10-11   cmVmolecule-sec   at  25°C  and   an   ambient  hydroxyl  radical
concentration  of  8.0x10*   molecules/cm3,  a  half-life  of  13.44   hours  has
been  calculated   (U.S.  EPA,  1986a).   Considering  Us  relatively  high  water
solubility   (1.74x10*  mg/s.   at   20°C),   b1s(2-chloroethyl)  ether  also  1s
Hkely to be removed by wet deposition from the atmosphere.
    The  half-life  of  b1s(2-chloroethyl)ether  In  aqueous  and  soil  systems
could  not  be  located  1n   the  available  literature.    In  aqueous  systems,
volatilization and  hydrolysis  may be  Important  removal  mechanisms, although
the former  process  1s expected  to be much faster  than  the latter (Callahan
et  al.,  1979).   Based  on   the  bloconcentratlon factor  and  soil  adsorption
coefficient,  bloaccumulatlon  1n  aquatic  organisms  and  adsorption  to  sus-
pended solids  and  sediments  should  not be  significant.   In  soils with  low
sorptlon constant,  b1s(2-chloroethylJether  should  be  mobile  and groundwater
contamination may  occur  below  solid  waste landfills  (Wilson et  al.,  1981;
DeWalle and Chlan,  1981).  Based  on  Us  vapor  pressure (0.75  mm Hg at 20°C),
b1s(2-chloroethyl)ether   should  volatilize relatively  rapidly from dry  soil
surfaces.
0086h                               -1-                              01/22/87

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                                  TABLE 1-1    .

         Selected Physical and Chemical  Properties and Half-Lives for
                            B1s(2-Chloroethyl)Ether
        Property
        Value
      Reference
CAS number:

Chemical class:

Molecular weight:



Chemical Structure:



Freezing point:

Boiling point:

Vapor pressure:

Water solubility:
Log octanol/water
partition coefficient:

B1oconcentrat1on factor
Soil adsorption:
coefficient
111-44-4

aliphatic haloether

143.01

    Cl  H       H   Cl
    II       II
H-C-C-0-C-C-H
    II       II
    H   H       H   H

-50°C

178.5°C

0.75  mm Hg (20°C)

1.74xl04 mg/8. (20°C)
1.02x10* mg/l (temp-
erature unspecified)


1.29

11, blueglll sunflsh
(Lepomls macrochlrus)

80, fine sand
ACGIH, 1986

ACGIH, 1986

Weber et al.
1981
Velth et al., 1980
Callahan et al., 1979
Hansch and Leo, 1985

Velth et al., 1980


Wilson et al., 1981
Half-lives:
  Air
  Water
  Soil
-13 hours
NA
NA
U.S. EPA, 1986a
NA = Not available
0086h
       -2-
             01/22/87

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           2.  ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS



 2.1.   ORAL



    B1s(2-ch1oroethy1)ether  appears  to  be  nearly completely  absorbed from



 the  gastrointestinal  tract of  rats.   Llngg et al.  (1982)  administered a 40



 mg/kg  dose  of  l4C-b1s(2-chloroethyl )ether  1n  corn oil  by gavage  to adult



 male  Sprague-Dawley  rats  and   measured   the  radioactivity  1n  expired  air



 excreta,  carcass  and  cage wash  at  48  hours  posttreatment.   Only 2.4X of the



 administered  dose  of  radioactivity  was  located 1n the feces.  Total recovery



 accounted  for  80.9/4  of  the  administered  dose.   These  data  suggest  that



 gastrointestinal absorption was  nearly complete.



 2.2.   INHALATION



    Limited  data  concerning the  Inhalation  absorption  of b1s(2-chloroethyl)



 ether were available.  Schrenk  et  al.  (1933) reported  that  exposure  to bis



 (2-chloroethyl)ether  In  guinea  pigs was  assolcated with  brain,  liver  and



 kidney  congestion  as  well  as  lung  congestion.   These   results  suggest some



 absorption by the  respiratory tract.
0086h                               -3-                              09/05/86

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                3.  TOXICITY  IN HUMANS AND EXPERIMENTAL ANIMALS
3.1.   SUBCHRONIC
3.1.1.   Oral.   Pertinent  data  regarding  the  oral   subchronlc  toxlclty  of
b1s(2-chloroethyl)ether could not be located  1n  the available  literature.
3.1.2.   Inhalation.    Pertinent  data  regarding  the  Inhalation   subchronlc
toxldty of  b1s(2-chloroethyl )ether could not  be located  1n the  available
literature.
3.2.   CHRONIC
3.2.1.   Oral.   Welsburger  et al.  (1981) gave groups  of  26 male  and  26
female  Charles   River  CD  rats  25  or  50  mg/kg  b1s(2-chlorethyl)ether  by
gavage,  twice  weekly  for  18 months,  followed   by  a  6-month   observation
period.  Negative  and  vehicle  controls  were  also  maintained.    High-dose
females had a higher mortality rate than negative  or  pooled  vehicle controls
and  survival  was  unaffected  1n males.  Mean  body  weights   were  lower  In
treated females  and high-dose males  than In the  corresponding  controls.
3.2.2.   Inhalation.    Pertinent   data  regarding   the  chronic   Inhalation
toxldty of  b1s(2-chlorethyl )ether  could  not  be  located  1n the  available
literature.
3.3.   TERATOGENICITY AND  OTHER REPRODUCTIVE  EFFECTS
3.3.1.   Oral.   Pertinent  data  regarding the  teratogenlc  and reproductive
effects  after oral  administration  of  b1s(2-chlorethy i Jether could  not  be
located 1n  the available  literature.
3.3.2.   Inhalation.   Pertinent  data  regarding  the   teratogenlc  and repro-
ductive  effects  after  Inhalation   exposure  to  b1s(2-chlorethyl)ether  could
not be located 1n the available IHeratue.
0086h                               -4-                              09/05/86

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 3.4.    TOXICANT  INTERACTIONS
     Pertinent  data  regarding  the  toxicant  Interactions  of  b1s(2-chloro-
 ethyl)ether  with  other  chemicals  could  not  be  located  In  the available
 literature.
0086h                               -5-                              09/05/86

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                             4.  CARCINOGENICITY
4.1.   :HUMAN DATA
4.1.1.   Oral.   Pertinent  data regarding  the carclnogenlcHy  to humans  of
b1s(2-ch1oroethyl)ether  from  oral  exposure  could  not  be  located  1n  the
available literature.
4.1.2.   Inhalation.    Pertinent  data   regarding   the  carclnogenlcHy   to
humans of  b1s(2-chloroethyl)ether  from  Inhalation could not  be located  In
the available literature.
4.2.   BIOASSAYS
4.2.1.   Oral.   Innes  et al.  (1969)  gave  groups  of  18 male  and 18  female
mice of  two  different  cross  strains  100 mg/kg of  b1s(2-chloroethyl)ether  by
stomach  tube  from age  7-28  days  and  thereafter In the diet at  300  ppm  until
week 80.   The Incidence  of hepatomas  1n  males  of both  strains  and females  of
one strain  were statistically higher  than  controls.   Details   are  presented
1n Table  4-1.
    Helsburger et al.  (1981) obtained negative results  In  an   oral  carclno-
genlcHy  assay  1n  which  Charles Liver  CD  rats of both  sexes  were given  25
and  50  mg/kg/day  of   b1s(2-chloroethyl )ether  twice  weekly  for  18  months,
followed  by  a  6-month  observation  period.   Although  the  authors  suggested
that  the doses  for  males   were  not  sufficient   to  elicit a  carcinogenic
response, they  nonetheless   concluded  that  b1s(2-chloroethylJether  was  not
carcinogenic In  rats.
4.2.2.   Inhalation.    Pertinent  data   regarding   the  carclnogenlcHy   to
animals  of  b1s(2-chloroethyl)ether  from Inhalation could  not  be located  In
the available literature.
0086h                               -6-                              09/05/86

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                                   TABLE  4-1

        Incidence of Hepatomas In Two Strains of Mice Given Oral Doses
                  of B1s(2-chloroethyl)ether for -18 months3
Strain Sex
Controls0
C57Bl/6xC3H/Anf M
Controls0
C57Bl/6xC3H/Anf F
Controls0
C57B1/6xAKR M
Doseb
(mg/kg/day)
0
39
0
39
0
39
Tumor Incidence
(p value)
8/79
14/16 (p<0.01)
0/87
4/18 (p<0.01)
5/90
9/17 (p<0.01)
aSource: Innes et al., 1969

bDose  as  calculated  by  U.S.  EPA  (1980a)  based  on  dietary consumption  of
 300 ppm and assuming a mouse consumes 13% of Us body weight as food/day.

°Pooled  control  data  were  used  because  statistical  tests revealed  Uttle
 heterogeneity among groups.
0086h                               -7-                              09/05/86

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4.3.   OTHER RELEVANT INFORMATION
    B1s(2-chloroethy1)ether  was  negative  1n  qualitative tests.   Van  Duuren
et  al.  (1972)  observed  no  Initiating  activity  1n  the  2-stage  mouse  skin
assay  using phorbol  myrlstate  acetate  as  a  promoter.  Weekly  subcutaneous
Injections  of  1   mg  b1s(2-ch1oroethyl)ether  showed  a  borderline  Increase
(p>0.05)  1n  the   Incidence  of   Injection  site  sarcomas  In  exposed  female
ICR/Ha  Swiss  mice  (Van  Duuren  et  al.,  1972).   No  tumors  were detected  at
sites  distant  from the  Injection  site.   Male  mice  Injected  1ntraper1toneally
with  b1s(2-chloroethyl)ether did   not  exhibit  a   pulmonary  tumor  response
significantly different from that of controls  (Thless et  al.,  1973).
    B1s(2-chloroethyl )ether was positive  In mlcroblal  mutagenlcHy tests  and
negative  In  mammalian  test  systems.   Using  different  tester   strains  of
Escherlchla coll.  Salmonella typhlmuMum  and  Bacillus subtlUs.  Shlrasu  et
al.  (1975)  found   b1s(2-chloroethyl)ether  to  be   a  direct-acting  mutagen.
Positive  results  were obtained  In  S. typhlmuMum  strain  TA100 with  b1s(2-
chloroethyl)ether  vapors   (Simmon  et al.,  1977).    Jorgenson  et  al.  (1977)
obtained negative results  In mice using the heritable translocatlon test.
4.4.   WEIGHT OF EVIDENCE
    The  degree  of  evidence on carclnogenlclty  of  b1s(2-chloroethyl)ether  1n
humans 1s considered Inadequate because  of the  lack  of human  case  reports  or
epidemiologies  studies.   The degree  of evidence  1n  animals 1s  considered
sufficient; although b1s(2-chloroethylJether was not carcinogenic  In  rats  by
the  oral route  (Welsburger  et  al., 1981),  1t elicited  hepatomas  1n  mice
after  oral  exposure (Innes et al.,  1969).   Two limitations of  the  Innes  et
al.  (1969)  study   are  noted.   First,  an  Increased  tumor   Incidence  was
observed  In a  tumor   type  (hepatoma)  that  often  occurs  spontaneously  1n
0086h                               -8-                              05/26/87

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 mice.   Second,  hepatomas  In  mice are  difficult  to  classify.   In  the  rat
 study    It   Is   difficult    to    evaluate    carcinogenic    potential   of
 b1s(2-chloroethylJether because the exposure was less than a lifetime.
    These  limitations  and negative  results  obtained  In qualitative  tests
 (Van Duuren  et  al.,  1972;  Thless  et al., 1973)  suggested that the quality of
 evidence   for   b1s(2-chloroethyl)ether   was   more   appropriately  viewed  as
 limited;   however,  assigning  this  chemical  to   Group   82,  probable  human
 carcinogen,  Is  appropriate because  the  Incidences observed  1n  the  Innes et
 al.   (1969)    study   were   very   high   (53-88%)   and   were   statistically
 significantly  greater  than controls.   The  supporting details of  this  study
 together   with   the  positive  mutagenlcHy   findings  do  not   warrant  a
 downgrading    of    the   mouse    liver    tumor     response.     Therefore,
 b1s(2-chloroethyl)ether   1s   assigned  to  EPA  Group   B2:   probable  human
 carcinogen (U.S. EPA, 1986b).
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                     5.   REGULATORY STANDARDS AND CRITERIA

    U.S.  EPA (1980a)  derived the  criteria of  0.003,  0.030  and 0.30  vq/i
at  risk  levels  of  10~7,   10~6  and   10~5,   respectively,   based   on  the
Incidence  of  hepatomas  1n  strain   (C57Bl/6xC3H/Anf)F.   male  mice  orally
exposed for 80 weeks.   In deriving these criteria, a bloconcentratlon factor
of  6.9  was  applied  and dally  consumption  of  2 l  water  and  6.5 g  of  fish
was  assumed.   NAS   (1980)  estimated  that  at  a concentration   of  1  yg/l,
the risk  of cancer  for both sexes was  8.1xlO~7.   The  upper  95% confidence
estimate was 1.2xlO~«.
    ACGIH (1986)  recommended  a  TLV-TWA of  5  ppm (-30  mg/m3)  and  a  TLV-STEL
of  10  ppm   (-60  mg/m3)  and noted  that  skin  exposure  may  contribute  to
overall exposure.   OSHA (1985)  adopted  a  celling of 15  ppm  (90  mg/m3)  and
also noted that  b1s(2-chloroethyl)ether  may  be  absorbed  through the skin.
0086h                               -10-                             03/10/87

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                              6.  RISK ASSESSMENT



 6.1.    SUBCHRONIC  REFERENCE  DOSE  (RfDc)
                                      O


 6.1.1.    Oral  (RfDSQ).   It  1s   Inappropriate  to  derive  an  RfDSQ  because



 b1s(2-chloroethyl )ether  1s  a  carcinogen.
 6.1.2.    Inhalation   (RfDSI).    It   1s   Inappropriate   to  derive  an     ..



 because  b1s(2-chloroethyl )ether  Is a carcinogen.



 6.2.   REFERENCE DOSE  (RfD)



 6.2.1.    Oral   (RfDQ).    It  1s   Inappropriate  to  derive  an  RfD_  because


 b1s(2-ch1oroethyl )ether  1s a carcinogen.



 6.2.2.    Inhalation   (RfD,).    It  Is   Inappropriate   to  derive  an   RfD.


 because  b1s(2-chloroethyl jether  1s a carcinogen.


 6.3.   CARCINOGENIC POTENCY (q.,*)



 6.3.1.    Oral.   U.S.   EPA  (1980a) used  the  linearized  multistage model  to



 derive   a  q *  of   1.1  (mg/kg/day)'1.   The  q *  was   based   on   a  hepatoma



 Incidence  of  14/16 (p<0.01) 1n  male  mice (strain  C57Bl/6xC3H/Anf )  given 39



 mg/kg/day  b1s(2-chloroethyl )ether for 80  weeks,  compared with  an Incidence



 of  8/79   In  controls.   The data  used  1n  the  derivation  of  this q  *  are



 presented  In  Table 6-1.  Although  some  of the assumptions and  calculations



 applied  In this  derivation  vary  slightly from  current  methodology (U.S. EPA,



 1980c),  the   q  *  of  1.1  (mg/kg/day)'1  Is  adopted as   the  q *  for  orally


 exposed  humans for  the purposes of this document.


 6.3.2.    Inhalation.  Data were Insufficient  for deriving an Inhalation q *
0086h                               -11-                             05/07/87

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                                   TABLE 6-1
                   Cancer Data Sheet for Derivation of a q-|*

Compound:  b1s(2-chloroethyl)ether
Reference:  Innes et al., 1969
Specles/straln/sex:  C5781/6xC3H/Anf male mice
Route/vehicle:  oral: gavage  followed by diet
Length of exposure (le) = 560 days
Length of experiment (Le) = 560 days
Llfespan of animal (L) = 560  days
Body weight = 0.03 kg (assumed)
Tumor site and type:  hepatomas
Exposure
(ppm)
0
300
Transformed Dose
(mg/kg/day)
0
39
Incidence
No. Responding/No.
8/79
14/16
Tested

Unadjusted q-i* = 8.6xlO"2 (mg/kg/day)"1
Human q-j* = 1.1 (mg/kg/day)'1
0086h                               -12-                             03/10/87

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                                7.  REFERENCES







ACGIH  (American Conference  of Governmental  Industrial  Hyg1en1sts).   1986.



Documentation of the  Threshold  Limit  Values  and  Biological  Exposure  Indices,



5th ed.  Cincinnati, OH.  p. 186.







Callahan, M.A., M.W.  Sllmak,  N.W. Gabel, et al.  1979.  Water-Related  Envi-



ronmental Fate  of  129 Priority Pollutants,  Vol.  II.   U.S.  EPA,  Washington,



DC.  EPA 440/4-79-0298.







Dewalle, F.B. and  E.S.K.  Chlan.  1981.  Detection of trace  organlcs  In well



water near a solid waste landfill.  J. Am.  Water  Works  Assoc.  73:  206-211.







Hansch,  C.  and   Leo, A.J.   1985.    Medchem  Project  Issue  No.  26.   Pomona



College, Claremont, CA.







Innes,  J.R.M.,  B.M.  inland,  M.G.  Valevlo,  et al.  1969.   Bloassay of  pesti-



cides  and  Industrial  chemicals  for  tumor1gen1dty  1n  mice:  A  preliminary



note.  J. Natl.  Cancer Inst.   42:  1101.







Jorgenson, T.A., C.J. Rushbrook,  G.W.  Newell and  R.G. Tardlff.   1977.   Study



of the  mutagenlc potential of  b1s-(2-chloroethyl) and  b1s-(2-chlor1sopropyl)



ethers   In  mice   by   the  heritable   translocatlon  test.   Toxlcol.   Appl.



Pharmacol.  41:  196-197.
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L1ngg, R.D., W.H. Kaylor,  S.M.  Pyle, M.M.  Domino,  C.C.  Smith  and G.F.  Wolfe.



1982.  Metabolism  of b1s(2-chloroethyl)ether and  b1s(2-chlor1sopropyl)ether



1n the rat.  Arch.  Environ. Contam.  Toxlcol.   11(2):  173-183.







NAS  (National   Academy   of  Sciences).    1980.    Drinking  Water  and  Health.



Volume VI. Organic  Solvents,  p. 710-713.







OSHA  (Occupational  Safety  and  Health  Administration).   1985.   OSHA  Safety



and Health Standards.  Code of Federal  Regulations.   29,  1910.1000.







Schrenk,   H.H.,  F.A.  Patty  and  W.P.  Yant.   1933.   Acute  response  of  guinea



pigs to vapors  of some new  commercial  organic compounds.  VII.  Dlchloroethyl



ether.  Pub. Health Rep.   48:  1389.







Shlrasu,   Y., M.  MoMya,  K.  Kato and T. Kada.   1975.   Mutagenlclty  screening



of pesticides In mlcroblal systems.   Mutat.  Res.   31:  268-269.







Simmon, V.F.,  K. Kauhanen  and  R.G.  Tardlff.   1977.   Mutagenlc activity  of



chemicals   Identified  In  drinking  water.   Dev.  Toxlcol. Environ.  Sd.   2:



249-258.







Thless, A.M.,  W. Hey and H.  Zeller.   1973.   Zur Tox1kolog1e von  D1chlord1-



methylather-Verdacht   auf  Kanzerogene  Wlrkung   auch   belm  Menschen.    Zbl.



Arbeltsmed.  23: 97.   (Cited 1n  U.S.  EPA,  1980a)
0086h                               -14-                              01/22/87

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 U.S.  EPA.   1980a.   Ambient  Hater Quality Criteria  Document  for Chloroalkyl
                        i
 Ethers.   Prepared  by  the  Office  of Health  and  Environmental  Assessment,
 Environmental  Criteria and Assessment Office, Cincinnati,  OH  for the Office
 of Water Regulations and Standards,  Washington,  DC.  EPA 440/5-80-030.  NTIS
 PB81-117418.

 U.S.  EPA.   19805.   Hazard Profile  for  B1s(2-chloroethyl)ether.   Prepared by
 the  Office  of  Health  and  Environmental  Assessment,  Environmental  Criteria
 and  Assessment  Office,  Cincinnati,  OH   for  the   Office  of  Solid  Waste,
 Washington, DC.

 U.S.  EPA.   1980c.   Guidelines  and  Methodology  Used  1n  the Preparation  of
 Health  Effect  Assessment Chapters   of  the  Consent  Decree  Water  Criteria
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 Environmental   Criteria  and  Assessment  Office,  Cincinnati,   OH.   Federal
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 U.S.  EPA.    1983.   Methododology  and  Guidelines   for  Reportable  Quantity
 Determinations  Based on Chronic  Tox1c1ty  Data.   Prepared  by  the  Office  of
 Health  and  Environmental Assessment,  Environmental Criteria and Assessment
 Office,  Cincinnati,  OH,  for  the  Office  of  Solid  Waste  and  Emergency
 Response, Washington, DC.

U.S. EPA.   1986a.   Graphical Exposure Modeling  System (GEMS)  Fate  of  Atmo-
 spheric Pollutants (FAP).  OTS,  Washington, DC.
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U.S.  EPA.   19866.    Guidelines  for  Carcinogen  Risk  Assessment.   Federal
Register.  51(185):  33993-34003.

Van DQuren, B.L., C.  Katz, B.M. Goldschmldt, K. Frankel and A. S1vak.  1972.
CardnogenlcHy  of   halo-ethers.   II.  Structure-activity  relationships  of
analogs of bls(chloromethyl)  ether.   J.  Natl. Cancer Inst.   48: 1431.

Velth. G.D., K.J. Macek, S.R. Petrocell and J.  Carrol.  1980.  An evaluation
of  using  partition  coefficients and  water  solubility  to estimate bloconcen-
tratlon  factors  for  organic  chemicals  1n  fish.   Aquat.  Toxlcol.  Am.  Soc.
Test.  Mater,  p.  116-129.

Weber, R.C., P.A. Parker  and  M.  Bowser.  1981.  Vapor Pressure Distribution
of Selected Organic  Chemicals.   U.S.  EPA,  Cincinnati, OH.   EPA 600/2-81-021.

Welsburger E.K.,  B.M. Ulland,  J-M. Nam,  J.J. Gart and  J.H. Welsburger.  1981.
CardnogenlcHy tests of certain environmental  and Industrial chemicals.  J.
Natl.  Cancer Inst.   67(1):  75-88.

Wilson, J.T.,  C.G.  Enfleld,  W.J.  Dunlap,   R.L.  Crosby,  D.A. Foster  and L.B.
Baskln.  1981.   Transport  and fate of selected  organic pollutants In a sandy
soil.   J. Environ.  Qua!.   10:  501-506.
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