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0089H
-13-
12/10/86

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    In reviewing studies of  the  reproductive  effects  of dietary endrln, U.S.
EPA  (1985a)  concluded that  at  high gavage  doses endrln was  teratogenlc  In
mice and hamsters but not  In rats.   They also concluded that endrln given to
pregnant animals was  associated  with behavioral changes  1n  the offspring  1n
all three species.
3.3.2.   Inhalation.  No  data concerning  possible reproductive  or  terato-
genlc  effects  of   endrln  from  Inhalation  exposures  were  located  1n  the
available literature.
3.4.   TOXICANT INTERACTIONS
    There 1s  relatively  little  Information available concerning Interaction
of  endrln  with  other pesticides.   KepHnger  and  Delchmann  (1967)  studied
acute  oral   toxlclty  of  combinations   of  pesticides,  and  found  that  LD,.-
values  were  lower   than  expected  (I.e.,  suggestive  of some  antagonistic
effect)  for  mixtures  of   endrln  with  parathlon,  DOT  or Delnav.   Additive
effects were  Indicated when  endrln  was  administered  with dlazlnon, toxaphene
or  malathlon.   Endrln plus  aldrln  showed a  more than  additive  effect,  and
endrln  plus   chlordecone  exerted   a   potentiating   effect.   Ludke  (1976)
reported that  endrln was  more  toxic  to  birds  1f they already had a body
burden of other organochlorlne compounds.
0089h                               -14-                             12/10/86

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                             4.  CARCINOGENICITY
4.1.   HUMAN DATA
4.1.1.   Oral.   Pertinent  data  regarding  cardnogenlclty  of   endrln   1n
humans by oral exposure could not be located 1n the available literature.
4.1.2.   Inhalation.   Studies  of workers  occupatlonally exposed  to  endrln
have not demonstrated  any  association  between  exposure and  Incidence  of  any
type  of  cancer  (IARC,  1974).    Jager  (1970)  and  Jager  and Versteeg  (1973)
studied 233 workers  employed  1n the manufacture of endrln  and  other organo-
chloMne Insecticides  In a  plant  1n the  Netherlands.   Lengths of  exposure
were  4-13.2  years.   No  cases  of cancer  attributable  to pesticide  exposure
were found.
4.2.   BIOASSAYS
4.2.1.   Oral.   Several  long-term  studies 1n which  endrln  was  administered
orally to animals were summarized 1n Table 3-2.
    The first  study  of endrln  cardnogenlclty  was conducted by  Treon  et  al.
(1955).   Endrln  was  administered   to   28-day-old  rats,   20  males  and  20
females/group, In doses  of 0,  1, 5,  25,  50 or  100 ppm endrln In the feed  for
106  weeks.   Doses  >25 ppm  for  females  and  >50 ppm  for  males resulted  In
significant mortality  by  106  weeks so  that  few  animals   remained  at these
higher  doses  for pathological  examination.  The  authors   reported  that  the
Incidence of  neoplasla was no  greater  among experimental animals  than among
controls In the  tissues  studied  (liver,  kidney,  brain,  heart,  adrenal  gland,
spleen,  skin,  lung  and  other  unidentified tissues).   No   primary  data  were
presented.  Subsequent Independent  assessment  of  hlstologlcal  specimens  led
to  the  report (Reuber,  1979)  that  one  animal  Ingesting 25  ppm  had  a  carci-
noma  of  the  pituitary and one  Ingesting 50 ppm  a  bronchogenlc carcinoma.
0089h                               -15-                             12/10/86

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No  malignancies  were  originally  reported  In  untreated rats  although these
(and  endr.ln-treated  animals) were  later  reported  to have  developed benign
tumors of the breast and retlculum sarcomas.
    Delchmann et al.  (1970)  fed diets  containing 0,  2, 6 or 12 ppm endrln to
groups of  50 male and  50  female  Osborne-Mendel  rats.   Male animals treated
with  2,  6  or 12 ppm  showed  15, 9 and  24 Incidences,  respectively, of malig-
nant  tumors  compared  with  18% In  controls.   In females  the corresponding
Incidence of  malignancies  were 21,  11  and 22% with  24% 1n control animals.
The  predominant  tumor  type  1n  both   sexes  for  all  groups  was  malignant
lymphoma.  The  authors  concluded  that endrln  fed  for  a  lifetime to albino
rats was neither tumorlgenlc nor carcinogenic.
    NCI  (1979)   conducted   chronic  bloassays  with  Osborne-Mendel  rats  and
B6C3F1 mice  (50/sex/group).  Matched  controls  consisted of 10  rats  or  mice
of  each  sex.   Pooled controls that  were  used for  statistical  evaluations
consisted of matched  controls plus  40  untreated male and 40 untreated female
rats  or  50  untreated male  and 50 untreated  female  mice from similar studies
of other chemicals.   Dietary levels were 2.5 or  5 ppm for  male  rats, 3  or 6
ppm for  female  rats, 1.6 or 3.2 ppm for male mice and  2.5  or 5 ppm for fe-
male  mice.   Rats  were exposed for 80  weeks  and sacrificed at  111-114 weeks.
Extensive hlstopathology was  conducted of all  the major organs  In the rats.
Comparing  Incidences  of malignant  tumor  formation  1n  Individual  tissues
between  control  and  treated animals,  the authors concluded that  endrln was
not carcinogenic  1n  either  sex of  rat.  Mice  wre  exposed for  80 weeks and
all surviving  mice  were sacrificed after  90  or 91  weeks.   Because  of the
high mortality In the  treated groups,  hlstologlcal  examination of tissue was
limited  to  the  liver  only.   However,  a  significant  Incidence of  tumors was
not observed  for any  site  1n either  sex.   NCI  (1979)  concluded  that under
the conditions of this bloassay endrln  was not carcinogenic for B6C3F1 mice.

0089h                                -16-                             03/05/87

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    In a lifetime study described by Reuber  (1978),  groups  of  24 male and 24
female 22-day-old Osborne-Mendel  rats  were  fed  diets  containing 0,  0.1,  1,
5, 10 or  25  ppm endrln.  Because 50% of  the rats at 26 ppm died within the
first week, this group was restarted with  32-day-old rats.   Survival  did not
appear  to  be  affected by  treatment.   The  highest Incidence  of  malignant
tumors  1n  male and  female  rats  occurred  at 0.1  ppm,  but  the  malignancies
were  not  dose-related.  Treated  male  rats  had  a higher Incidence of  renal
disease than controls,  but  this was not dose-related,  and  the  threshold for
this effect appeared to be 1  ppm.
    Reuber (1979) reviewed two  unpublished studies  on mice.  In  one study, a
group of 50  male  and 50 female C3HF mice were fed  a diet  containing  2.5 ppm
endrln, while  a control group of 75 males  and  75 females were  fed a normal
diet  for  104 weeks.  The 2.5  ppm level  was apparently  toxic  to  these mice,
causing decreased  survival  compared  with controls.  This  study  was deter-
mined to  be  Inadequate for assessing  cardnogenldty.   In the  second mouse
study,  groups  of  100 C57B1/6J  or  C3D2F1/3  strain  mice  were  fed  diets
containing 0,  0.3 or  3 ppm endrln.   A few mice at the highest  dose level
Initially  had  convulsions   but  recovered.   Treated   female   mice  had  an
Increased  Incidence of  liver   carcinomas,  which  developed  earlier  than 1n
controls,  but   these  results   are of questionable  significance  because the
high  tumor Incidence  normally seen  1n  untreated  mice  makes  these  strains
unsuitable  for  carc1nogen1c1ty  testing  (Reuber,   1979).   Furthermore,  no
dose-related trends 1n tumor Incidence were apparent.
    On  the basis of  these  and  other  studies,  Reuber  (1979)  concluded that
endrln was carcinogenic  In  rats and probably In  mice and  dogs;  however, the
absence of a dose-related trend  1n  Incidence  of any type of  tumor  In  these
studies or 1n  the  Delchmann  et  al.  (1970) or  Treon  et al.  (1955)  studies
makes this conclusion  questionable.

0089h                               -17-                              12/10/86

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    Reuber  (1979)  also  examined  data  from  the  NCI  (1979)  bloassay  using
rats.   By combining  the  Incidence  of  benign and  malignant  tumors  or  by
combining  the  Incidence of  carcinomas and  sarcomas  regardless  of site  of
origin,  Reuber  (1979)  concluded  that  endrln  was  carcinogenic  In rats  and
that female  rats  appeared  to be  more  susceptible  than male  rats  at  various
target sites.  The U.S. EPA  (1979b) noted  that  tumor Incidence  data reported
by Reuber  (1979)  was  subject to Interpretation since  two  other  pathologlsts
did not concur with his analysis.  U.S.  EPA  (1979b)  concluded that endrln Is
"unlikely  to  be   a   human   carcinogen."   In  reviewing  the  Reuber   (1979)
results,  the U.S.  EPA  (1985a) noted that his  criteria  for  assessing cardno-
genlclty  are  different from other  Investigators,  and therefore  until  those
differences are resolved  1t 1s  difficult  to  draw any conclusions from  his
findings.
4.2.2.   Inhalation.    Pertinent  data   regarding   the  carc1nogen1c1ty   of
endrln  1n  experimental  animals  by Inhalation  exposure could not  be  located
In the available literature.
4.3.   OTHER RELEVANT DATA
    U.S.  EPA  (1985a)  reviewed  the available data  concerning  mutagenldty of
endrln  In  various  assay  systems,  and  found that  endrln  generally  gave
negative  results  In  mlcroblal   systems  with  or without metabolic  activation
1n  DrosophHa.  and  1n  jji   vitro  mammalian systems.   A  positive  result  was
reported  by Dlkshlth  and Datta  (1973)  who found that  Intratestlcular  Injec-
tions of  0.25 mg  endrln caused  chromosomal aberrations 1n  germinal tissue of
rats.
0089h                               -18-                             12/10/86

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4.4.   HEIGHT OF EVIDENCE
    According to U.S. EPA  (1986), endrln  Is  most  appropriately classified as
a  Group  E  chemical.  I.e.,  chemicals  for  which  there  1s  no evidence  of
carclnogenlclty  for  humans.   This  classification  Is  based on  the  negative
results from  four  animal  studies  Including the NCI  (1979)  bloassay.   Endrln
has not  been classified  by  IARC  (1979);  however,  the U.S. EPA  (1985c)  has
also reported a Group E classification for endrVn.
0089h                               -19-                             03/05/87

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                     5.   REGULATORY STANDARDS AND CRITERIA

    The U.S. EPA (1980a, 1985b) has  recommended  several  criteria  for  endrln.
U.S. EPA  (1980a)  derived an RfD  of  0.001 mg/kg/day  based  on a  rat  and  dog
NOEL of 1  ppm  In  the diet from the Treon et al. (1955)  studies.   Using this
RfD, U.S.  EPA  (1980a)  derived a  water  quality  criterion  of  2.5 wg/i  for
the  protection of   human  health;   however,  U.S.  EPA  (1980a)  decided  to
recommend  1 yg/i  as  the ambient   water  criterion  to  be  consistent  with
the existing drinking water standard  of 1 yg/l.
    U.S.  EPA  (1985a,c)  derived a  RfD of 0.0016 mg/l based the  dog  dietary
NOEL of  1  ppm (0.045 mg/kg/day)  reported by  Treon et al.  (1955).  U.S.  EPA
(1985a)  used  the dose  of  0.2 mg/kg/day  from  the  Revzln  (1968) study  to
calculate  1-day  HAs of  0.070  and  0.020  mg/l  for adults  and  children,
respectively.   U.S.   EPA  (1985a) used the level of  1  ppm endrln  1n the diet,
equivalent  to   0.05   mg/kg/day  from  the  Nelson  et   al.   (1956)  study,  to
calculate  10-day  HAs of  0.018  and 0.005  mg/l  for adults  and  children,
respectively.
    U.S.  EPA  (1985b) has  recommended  an  RfD of  0.0002 mg/kg/day which  Is
based on  a dog NOEL  of  0.02 mg/kg/day.  ACGIH  (1986) recommended a  TLV-THA
of 0.1  mg/m3  for  occupational atmospheric  exposure to  endrln, which  1s  the
same as the OSHA (1983)  standard.
0089h                               -20-                             12/10/86

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                             6.  RISK ASSESSMENT
6.1.   SUBCHRONIC REFERENCE DOSE (RfD$)
6.1.1.   Oral   (RfO§_).    Although   the   carclnogenldty   of   endrln   Is
questionable  (see  Chapter 4),  the U.S.  EPA (1985a,c)  has  not performed  a
quantitative  cardnogenlclty risk  assessment for  endrln.   U.S. EPA  (1979b)
concluded that endrln Is  "unlikely to be  a  human  carcinogen."   Therefore,  U
Is appropriate to derive RfDSQ  and  RfOQ  values.
    The  18-month  dog  study   by   Treon   et  al.  (1955)  provides   the  most
appropriate  basis  for an  RfDSQ.   In  this  study,  growth of beagle dogs  was
affected at  4 ppm endrln 1n the diet,  and  dogs fed 3  ppm  (0.12-0.25  mg/kg/
day)  experienced  Increased relative  kidney and  heart  weights.  No  adverse
effects were  observed  1n  four  dogs receiving 1 ppm  (0.045-0.120 mg/kg/day).
Since U.S.  EPA (1985a)  used the lower  end  of  this range to derive an AAOI,
the  same  procedure will  be used  to  derive an RfDgQ-   Therefore,  dividing
the NOEL  of 0.045 mg/kg/day by an uncertainty  factor  of 100  to account  for
1nterspec1es   extrapolation  and   Intraspecles  variations   In  sensitivity
results  In  an RfDso  of   0.00045  mg/kg/day,  or   0.03  mg/day  for  a  70  kg
human.  The CBI files contain  no data  to dispute this RfDSQ.
6.1.2.   Inhalation   (RfO.,).   The   available   data   are   Inadequate   for
calculation of an RfDSI value  for  Inhalation exposure.
6.2.   REFERENCE DOSE (RfO)
6.2.1.   Oral   (RfDQ).    A   review  of    the   literature,    Including   an
unpublished  study  from  the CBI files concerning  endrln and the various  RfD
values  that  have been promulgated by the different branches  of the  Agency,
has  Indicated that the  CBI  1s the most  appropriate basis  for an RfO.   In
this  2-year  dog study, beagle  dogs  (7/sex/group) received  diets  containing
0, 0.1, 0.5,  1.0,  2.0 or  4.0 ppm  endrln for >2 years.   Interim sacrifices (2
0089h                               -21 -                             07/09/87

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dogs/sex/group)  were  performed  at  6  and 12  months.   Parameters  monitored
Included  growth,  food  consumption,  behavior,  serum  and  urine  chemistry,
organ weights  and hlstopathology of  all major  organs.   Animals  treated  at
the  2  and  4  ppm dose levels  experienced convulsions,  slight  Increase  1n
relative  liver  weights,  and mild hlstopathologlcal  changes In  liver  cells.
Because of the effects observed  In  the  dogs  consuming  diets containing 2 ppm
endrln  (0.05  mg/kg/day),  this  level  was considered  the  LOAEL.   No  adverse
effects  were  observed  In  dogs  receiving diets  containing <1   ppm  endrln.
Therefore, 1 ppm (0.025 mg/kg/day)  was  considered the NOEL.   An uncertainty
factor  of  100  was  applied  to  this   NOEL  to  derive  an  RfDQ of  0.00025
mg/kg/day.  No uncertainty factor for  use of  subchronlc  data  was applied 1n
this  case because  several  chronic  studies  also  Indicated thresholds  near
this  level.    Therefore,   the   RfOQ of  0.00025  mg/kg/day  Is  recommended.
This value 1s equivalent to 0.02 mg/day  for a 70 kg human.
    There  1s  a  large amount  of long-term oral  toxldty data  available for
endrln  that  can.  be used to  calculate  CSs.  Effects associated  with  chronic
oral exposure  to  endrln Include  CNS signs, decreased  survival,  altered organ
weights and minor hlstopathologlcal alteration, and developmental  toxldty.
Treon et  al. (1955) reported decreased  survival  In  rats  fed diets containing
50  ppm  endrln  for  2  years.   Decreased  survival  In mice was  observed  In  a
2-year  study by  Reuber  (1979)  at 2.5  ppm 1n  the  diet and by  NCI  (1979)  at
3.2 ppm In the diet for 80 weeks.   Mice are  clearly more sensitive than rats
to  the  life-shortening effects  of  endrln.   Although  altered  organ  weights
and minor hlstopathologlcal  lesions were  observed In rats  at  2 ppm  1n the
diet  (Delchmann  et al.,  1970)   and dogs at  1 ppm  (Reuber,  1979),  the RV&
associated with  these effects Is not sufficient  to  generate CSs greater than
those associated  with  reduced  survival  1n mice  at  slightly higher  doses.


0089h                               -22-                             07/09/87

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Similarly, CNS  signs  such  as  hyperexcHabllHy and tremors observed  In  rats
at 2.5  ppm 1n  the diet  and In mice at  1.6  ppm (NCI, 1979),  If  assigned  an
RV   of  7,  would not  be  associated with a CS  greater than  those associated
with reduced  survival.  The CBI files  contained   a  3-generat1on reproduction
study  In   rats  1n which  3  ppm endrln  In  the  diet  resulted In  Increased
mortality  1n   the   F^    and   F-    generations.   Table  6-1   contains   CSs
derived  for   decreased  survival 1n  mice.  CNS  signs   In  mice  and  decreased
survival In  rats  In  a 3-generat1on  reproductive  study.   The  maximum CS was
obtained  using  data  provided  by  Reuber  (1979)   which  showed  decreased
survival  1n  C3HF  mice fed  2.5 ppm  endrln  In  the  diet  for 2  years.   These
data resulted 1n a CS of  52 (see Table 6-1).
6.2.2.   Inhalation  (RfO,).   The  only  available  long-term Inhalation  data
were provided by  Treon  et  al. (1955);  however,  only one  concentration was
used  (-5.4 mg/m3),  and   this  was  lethal  .to  some  of the  mice  and  rabbits
tested.   Therefore,  no   RfO.   can   be  calculated.   It   1s   possible  to
calculate a CS, however,  and this  Is  presented 1n  Table 6-1.
0089h                               -23-                             07/09/87

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                                7.   REFERENCES

ACGIH  (American  Conference  of  Governmental  Industrial  Hyg1en1sts).   1986.
Documentation  of  the  Threshold  Limit  Values,  5th  ed.   Cincinnati,  OH.
p. 231.

Bedford,  C.T.,   R.K.  Harrod,  E.G.   Hoadley  and  O.H.  Huston.   1975.   The
metabolic fate of endrln 1n the rabbit.   Xenoblotlca.   5(8):  485-500.

CBI  (Confidential  Business   Information).    1986.    Confidential   Business
Information File pertaining to endrln.   U.S. EPA,  Washington,  DC.

Chernoff, N. and  R.J.  Kavlock.   1982.   An Jji  vivo  teratology  screen  utiliz-
ing pregnant mice.  J. Toxlcol. Environ.  Health.  10(4-5):  541-550.

Chernoff, N., R.3.  Kavlock,  R.C.  Hanlsch,  et  al.   1979.   Perinatal  toxlclty
of endrln  In rodents.  Fetotoxlc effects  of prenatal exposure  In  hamsters.
Toxicology.  13: 155-156.

Delchmann, H.B.,  H.E.  MacOonald,  E. Blum,  et al.  1970.  TumorIgenlclty of
aldrln,  dleldrln  and  endrln In the  albino  rat.   Ind.  Med.  Surcj.   39(10):
426-434.

DlkshHh, T.S.S.  and  K.K.  Oatta.   1973.   Endrln  Induced  cytologlcal  changes
1n albino rats.  Bull. Environ. Contain.  Toxlcol.  9: 65-69.
0089h                               -25-                             12/10/86

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Good, E.E. and G.W. Ware.  1969.  Effects of  Insecticides  on  reproduction  In
the  laboratory mouse.   IV. Endrln and  dleldMn.   Toxlcol. Appl.  Pharmacol.
14: 201-203.

Gray, I.E.,  Jr.  and R.J.  Kavlock.   1984.   An  extended  evaluation of an  In
vivo  teratology   screen  utilizing  postnatal   growth  and  viability  1n  the
mouse.  Teratog.  Cardnog.  Mutagen.   4(5):  403-426.

Gray,  I.E.,  R.J.  Kavlock, N.  Chernoff,  J.A.  Gray  and  J.  HcLamb.  1981.
Perinatal  toxldty  of  endMn  1n  rodents.    III.  Alterations  of  behavioral
ontogeny.  Toxicology.   21(3):  187-202.

Green,  V.A.   1969.   Effects  of  pesticides   on  rat  and  chick  embryo.  Iri:
Trace  Substances  In  Environmental  Health.   III.  Proc.  Univ.  Missouri  3rd
Ann. Conf. Trace  Subst.  Environ.  Health,   p. 183-209.

Hoogendam, I., J.P.J.  Versteeg and  M.  deVHeger.  1962.   Electroencephalo-
grams 1n Insecticide toxldty.   Arch.  Environ. Health  4:  86-94.

IARC  (International Agency for  Research  on Cancer).  1974.   IARC  Monographs
on  the  Evaluation  of  the Carcinogenic Risk of  Chemicals  to Man.   WHO, IARC,
Lyons, France.   Vol. 5,  p.  151-170.

IARC  (International Agency for  Research  on Cancer).  1979.   IARC  Monographs
on  the  Evaluation of the  Carcinogenic  Risk  of Chemicals to Man.   Chemical
and  Industrial  process  associated with  cancer  In  humans.   Supplement  1.
WHO, IARC, Lyon,  France.


0089h                               -26-                              12/10/86

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Jager,  K.H.   1970.   AldMn,  DleldMn,  Endrln  and  Telodrln.    Elsevler
Publishing Co.,  New York.   p.  78-224.

Jager, K.U. and  J.P.J.  Versteeg.   1973.   Long-term occupational exposure  to
the Insecticides aldrln,  dieldrin,  endrln,  and telodrln.   Br.  0.  Ind.  Med.
30(2): 201-202.

Kavlock,  R.J., M.  Chernoff, R.C.  Hanlsch,  G.  Gray, E. Rogers and I.E.  Gray.
1981.   Perinatal  toxlclty of  endrln  1n  rodents.   II.  Fetotoxlc  effects  of
prenatal  exposure 1n rats  and  mice.   Toxicology.   21(2): 141-150.

Kepllnger, M.L.  and W.B.   Delchmann.   1967.   Acute toxldty of combinations
of pesticides.  Toxlcol. Appl. Pharmacol.   10:  586-595.

Ludke,  J.L.   1976.   Qrganochlorlne  pesticide   residues   associated   with
mortality:  Addltlvlty  of  chlordane   and  endrln.   Bull.  Environ.   Contam.
Toxlcol.   16:  253-260.

Lyman, U.J.,  W.F.  Reehl  and  D.H. Rosenblatt.  1982.   Handbook of  Chemical
Property Estimation Methods.  McGraw H111  Book  Co., New York.  p. 4-9.

Morris, R.D.  1968.   Effects  of  endrln feeding on survival  and reproduction
1n the deer mouse, Peroroyscus  manlculatus.   Can.  3. Zool.   46(5): 951-958.

NCI  (National Cancer  Institute).  1979.   Bloassay  of  endrln for  possible
carc1nogen1c1ty.    NCI  Cardnogenesls  Tech.   Rep.   Ser.   No.  12.   (Also
published as NTIS PB-288461)


0089h                               -27-                             12/10/86

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Nelson, S.C.,  T.L.  Bahler, W.V.  Hartwell,  O.A.  Greenwood  and L.H.  Harris.
1956.   Serum  alkaline  phosphatase  levels,  weight  changes,  and  mortality
rates of rats fed endrln.   Agrlc.  Food Chem.  4: 696-700.

OSHA  (Occupational  Safety and  Health Administration).   1983.  OSHA  Safety
and Health Standards,   29  CFR 1910.1000.

Ottolenghl, A.Q., 3.K.  Haseman  and F. Suggs.   1974.  Teratogenlc  effects  of
aldrln, dleldrln, and  endrln 1n hamsters  and mice.  Teratology.  9: 11-16.

Reuber,  M.D.   1978.   Carcinomas,  sarcomas  and  other  lesions  1n  Osborne-
Hendel rats Ingesting  endrln.  Exp. Cell. B1ol.  46(3):  129-145.

Reuber, M.D.   1979.  Carc1nogen1c1ty  of  endrln.   Sc1.  Total  Environ.   12(2):
101-135.

Revzln,  A.M.   1968.    Effects  of  chronic   endrln   administration on  brain
electrical activity In the squirrel monkey.   Fed. Proc.   27:  297.

Speck,  L.B.  and C.A.  Maaske.   1958.   The  effects  of chronic  and  acute
exposure of rats  to endrln.  Am. Ned.  Assoc. Arch. Ind.  Health.  18:  268-272.

Treon,  J.F.,  F.P.  Cleveland  and  J.  Cappel.   1955.   Toxldty of  endrln  for
laboratory animals.   Agrlc. Food Chem.  3:  842-848.

U.S. EPA.   1979a.  Reviews of  the  Environmental  Effects  of  Pollutants:  XIII.
Endrln.  Prepared by the  Health Effects  Research Laboratory,  Cincinnati,  OH.
EPA 600-1-79-005.

0089h                               -28-                             12/10/86

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U.S.  EPA.   1979b.  Endrln:  Position Document  4.   EPA/SPRO-80/39.   NTIS  P8
81-109480.  82 p.

U.S.  EPA.   1980a.   Ambient Water Quality  Criteria  for Endrln.   Prepared  by
the  Office  of Health  and Environmental  Assessment,   Environmental  Criteria
and  Assessment  Office,  Cincinnati,  OH  for the  Office of Hater  Regulations
and Standards, Washington, DC.  EPA 440/5-80-047.  NTIS PB 81-117582.

U.S.  EPA.   1980b.  Hazard  Profile  for  Endrln.  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
Documents.  Federal Register.  45(231): 49347-49357.

U.S.  EPA.   1984.   Methodology and Guidelines  for Reportable  Quantity Deter-
minations Based  on  Chronic  Toxlclty  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.  1985a.   Drinking  Water Criteria  Document for  Endrln.   Prepared by
the  Office  of Health  and Environmental  Assessment,   Environmental  Criteria
and  Assessment Office,  Cincinnati,  OH  for  the Office  of Drinking Water,
Washington, DC.  EPA/600/X-84/176.  NTIS PB86-117967.
0089h                               -29-                             07/09/87

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U.S. EPA.  1985b.  Acceptable Dally  Intakes  for  Organic  Chemicals,  Inorganic
Chemicals,  and   Synthetic  Organic   Chemicals.    Criteria   and   Standards
Division, Office of Drinking Water, Washington, DC.

U.S. EPA.   1985c.  National  Primary  Drinking  Water Regulations;  Synthetic
Organic Chemicals, Inorganic Chemicals,  and  Microorganisms;  Proposed  Rule 40
CFR Part 141.   Federal Register.  50(219): 46396-47025.

U.S.  EPA.   1986.   Guidelines   for  Carcinogen  Risk  Assessment.    Federal
Register.  51(185): 33992-34003.

Wolfe,  H.R., W.F.  Durham and J.F.  Armstrong.   1963.  Health  hazards  of  the
pesticides endrln and dleldrln.   Arch. Environ. Health.   14:  622-633.
0089h                               -30-                             03/05/87

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