ENDRIN
Ambient Water Quality Criteria
              Criteria and Standards Division
              Office of Water Planning and Standards
              U.S. Environmental Protection Agency
              Washington, B.C.

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                         CRITERION  DOCUMENT



                               ENDRIN




 CRITERION



                            Aquatic Life



      For endrin  the criterion  to  protect freshwater aquatic life




 as derived using the Guidelines  is 0.0020 ug/1  as a 24-hour




 average and  the  concentration  should not exceed 0.10 ug/1 at  any




 time.



      For endrin  the criterion  to  protect saltwater aquatic life




 as derived using the Guidelines  is 0.0047 ug/1  as a 24-hour



 average and  the  concentration  should not exceed 0.031 ug/1 at any




 time.



                            Human Health "



    For the protection of human health from the toxic properties



of endrin ingested through water and contaminated aquatic  organisms>



the ambient v/ater criterion is determined to be 1 ug/1.

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Inter oduct ion
     Endrin is the common name of one member of the cyclodiene
group of pesticides.  It is a cyclic hydrocarbon having
a chlorine-substituted methano bridge structure.  Endrin
was introduced into the United States in 1951.  The endrin
sold in the United States is a technical grade product/
containing not less than 95 percent active ingredient, available
in a variety of diluted formulations.  Jarvinen and Tyo
(1978)  found the solubility of endrin to be about 200 /ig/1.
     Known uses of endrin in the United States are as an
avicide/ rodenticide, and insecticide, the latter being
the most prevalent.  The largest single use of endrin domesti-
cally is for the control of lepidopteron larvae attacking
cotton crops in the southeastern and Mississippi delta states.
Its persistence in soil led to its discontinuation for control
of tobacco worms.  Thus, endrin enters the environment pri-
marily as a result of direct applications to soil and crops.
Waste material discharge from endrin manufacturing and formu-
lating plants and disposal of empty containers also contribute
significantly to observed residue levels.  In the past several
years, endrin utilization has been increasingly restricted
and production has continued to decline.  In 1978, endrin
production was approximately 400,000 Ibs. (U.S. EPA, 1978).
     In the aquatic environment endrin is acutely toxic
to carp at 0.046/ag/l (lyatomi, et al. 1958) and to the
pink shrimp at 0.037 jug/1 (Schimmel, et al. 1975).  It is
chronically toxic to the fathead minnow at 0.187 /ig/1  (Jarvinen
and Tyo, In Press) and at .038 /ig/1 to the grass shrimp
                              A-l

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(Tyler-Schroeder, In Press).  Endrin has been reported to
bioconcentrate by factors as high as 15,000 in freshwater
fish (Hermanutz, 1978) and 6,400 in marine fish  (Hansen,
et al.  1977).
     Endrin is toxic to mammals, but a no-effect level of
1 mg/kg for the .rat and the dog has been established by
Brooks (1974).  Quantitative data on endrin toxicity to
humans are not available.
                               A-2

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                          REFERENCES







Brooks, G.T. 1974.  Chlorinated insecticides. Vol. II: Bio-



logical and environmental aspects.  CRC Press, Cleveland,



Ohio.







Hansen, D.J., et al. 1977.  Endrin: Effects on the entire



life-cycle of saltwater fish, Cyprinodon variegatus.  Jour.



Toxicol. Environ. Health 3: 721.








Hermanutz, R. 1978.  Endrin and malathion toxicity to flagfish,



Jordanella floridae.  Arch. Environ. Contain. Toxicol. 7:



159.







lyatomi, K.T., et al. 1958.  Toxicity of endrin to fish.



Prog. Fish. Cult. 20: 155.








Jarvinen, A.W., and R.M. Tyo.  Toxicity of fathead minnows



of endrin in food and water.  Arch. Environ. Contain. Toxicol.



7: 1  (In press).








Schimmel, S.C, et al. 1975.  Endrin:  Effects on  several



estuarine organisms.  Proc. 28th Annu. Conf. S.E. Assoc.



Game  and Fish Comm., 1974. p. 187.
                                A-3

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Tyler-Schroeder, D.B.  Use of grass shrimp, Palaemonetes



pugio, in a life-cycle toxicity test.  In Proceedings of



a Symposium on Aquatic Toxicology and Hazard Evaluation.



L.L. Marking and R.A. Kimerle, eds. Am. Soc. Testing and



Materials (ASTM), October 31-November 1, 1977.  (in press)







U.S. EPA. 1978.  Endrin-Position Document 2/3.  Special



Pesticide Review Division.  Office of Pesticide Programs,



Washington, D.C.
                                A-4

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AQUATIC LIFE TOXICOLOGY*

                      FRESHWATER ORGANISMS

Introduction

     Endrin is one of a group of chlorinated  hydrocarbon

pesticides developed after the broad scale  use  of  DDT  and  its use

grew during the 1950s.  Perhaps because  endrin  has a high  acute
                           /
toxicity to aquatic organisms, it was more  frequently  tested  in

aquatic toxicity tests than related  insecticides such  as

chlordane, heptachlor and aldrin.

     Since it is a broad spectrum pesticide/  endrin was  used  to

control many pests including termites, mice,  and army  worms.   In

the latter 1960's it was extensively used  for cotton boll  worm

control.  Its persistence in soil, while good for  termite

control, led to its discontinuation  for  tobacco worms.   Early

testing identified its high toxicity to  mammals.

     Endrin is very insoluble in water.  Recently, Jarvinen and

Tyo (1978) used a saturator in their toxicity tests and  found the

solubility in water to be about 200  ug/1.   Nearly  all  of  the
*The reader is referred to the Guidelines  for  Deriving Water

Quality Criteria or the Protection of Aquatic  life [43 FR 21506

(May 18, 1978) and 43 FR 29028  (July 5,  1978)]  in order to better

understand the following discussion and  recommendation.   The

following tables contain the appropriate data  that were found in

the literature, and at the bottom of each  table are the calcula-

tions for deriving various measures of  toxicity as described in

the Guidelines.
                               B-l

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early work with endrin  and  aquatic  animals  used  acetone or some



other solvent and  in  those  few  tests where  concentrations  were



measured; the actual  concentrations may  have  been considerably



lower than the calculated ones.   Some workers  used  a  wetting



agent such as Triton  X-100  in the acetone-endrin solution  to



improve dispersion  in the test  water.



     Because only  acetone was used  in many  of  the tests and



because concentrations  were  not measured, the  toxicity data



reported most probably  underestimate the true  toxicity. There is



no way to quantify  this effect  but  the adjustment factors  for



unmeasured concentrations as described in the  Guidelines are



the best estimates  that can  be  made at this time.



     Because of the difficulty  of dissolving  endrin in water,



data from the flow-through  tests  that have  been  conducted  in



which concentrations  were not measured may  be  less  reliable than



data from good static tests.  Recent as  well  as  some  earlier



studies used measured concentrations and these data provide a



reference point from  which  to evaluate other  data.



     Ferguson and  co-workers at Mississippi State University  have



published numerous  articles  on  endrin resistance that developed



in populations of  aquatic organisms exposed to high water



concentrations of  endrin as  a result of  its use  for cotton.



Nearly all of their work used static, unmeasured test procedures



and the data, at best,  can  be used  for relative  toxicity



purposes.  Clearly, they did demonstrate a  marked increase in



tolerance to endrin of  a variety  of species.   None  of the  data on
                               B-2      i

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resistant populations has been included since the criterion  is



expected to protect unacclimated populations as well as others.



Acute Toxicity



     Table 1 lists 41 data points for acute toxicity of endrin  to



freshwater fish.  Only seven of these data from four different



papers were based on measured concentrations and flow-through



procedures.  Of the nine data points for fathead minnows,  three



were derived from static tests with unmeasured concentrations.



The adjusted values are closer to the flow-through, measured



values than the unadjusted values suggesting the appropriateness



of the adjustments.  No tests on other species with measured



concentrations have been reported.  This is- due in part to the



limited use of gas chromatography during the earlier work  and  the



high toxicity which required very low detection limits which were



not achievable until analytical procedures were improved.



     With a few notable exceptions, especially lyatomi et  al.



(1958), most of the adjusted LC50 values are between 0.2 and 1.0



ug/1 suggesting a relatively narrow range of species sensitivity.



lyatomi, et al. (1958) reported a 3,100 times range  in LC50  value



for carp depending on age.  No other workers have found such



differences due to age.  By excluding that work, all other values



are within a range of about 75 times.  When the geometric  mean  of



all data is divided by the species sensitivity factor  (3.9), the



Final Fish Acute Value of 0.10 ug/1 is obtained as an estimate  of
                              B-3

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the concentration needed  to be equal  to or  less  than  the  LC50
value for 95 percent of all species.  Four  of  the  41  adjusted
values are lower than 0.10 ug/1 and two of  those are  from the
paper by lyatomi, et al.  (1958) that  was discussed  above.   The
use of the sensitivity factor, therefore, seems  reasonable.
     Twenty-five LC50 values have been reported  for invertebrate
species but 17 species have been tested.  None of  the 25  data
were based on measured concentrations and only two  are  based on
flow-through procedures.  Most of the species  tested  are
substantially more tolerant than fish with  few exceptions.
Glass shrimp and stoneflies are comparable  to  fishes  in
sensitivity.  Daphnia magna is among  the more  tolerant.   The
generally higher tolerance of the insects and  related groups  is
unexpected since endrin is such an effective insecticide.
     When the geometric mean LC50 value is  divided  by the species
sensitivity factor  (21),  the Final Invertebrate  Value (0.30 ug/1)
is higher than only  3 of  the 25 in the table,  suggesting  an
appropriate adjustment.
     The Final Acute Value is based upon  the Final  Fish Acute
Value of 0.1 ug/1.
Chronic Toxicity
     Life-cycle chronic tests have been completed  with fathead
minnows and flagfish giving chronic values  of  0.187 and 0.257
ug/1/ respectively  (Table 3).  Mount  (1962), working  with the
bluntnose minnow, a  species closely related to the  fathead
minnow, found a no  observed effect concentration between  0.1
                               B-4

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and 0.4 ug/1 (Table 6).  Spawning did not occur  in  this  test  but



the test extended for 291 days and the results are  consistent



with those for the fathead minnow.



     Endrin seems to enter the body rapidly as indicated  by  the



short time for the tissues to reach equilibrium  with  the  water



(Jarvinen and Tyo, 1978).  The short biological  half-life, as



observed by Jackson (1976) (Table 6), demonstrates  that  endrin is



different from related pesticides such as DDT.   Jarvinen  and  Tyo



(1978) observed metabolites of endrin in the  tissues  of  their



test fish suggesting an important rate of degradation as  well as



elimination.



     Jarvinen and Tyo (1978) also demonstrated that:   (1) when



food is contaminated with endrin, the toxicity of endrin  in  the



water is greater than when uncontaminated food is fed;  (2) the



contribution of endrin to the body burden by  food is  only 10  to



15 percent of that contributed by water; and  (3) residues contri-



buted by food were additive to those contributed by water.



Unfortunately, the existing data base is not  sufficient  to make  a



precise allowance for exposure through both routes  for various



species.



     The difference between the concentrations in water  that



cause acute and chronic effects is small.  Mount (1962)  cited a



reference in which the difference between acute  and chronic



effect levels for pheasants was small as was  true with  the



bluntnose minnows.  In Table 3, one can see the  same  indication
                               B-5

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as shown by the large geometric.mean application  factor  (0.37).



     When the geometric mean chronic value  is divided  by  the



species sensitivity factor  (6.7),  the 95 percent  value is  0.033



ug/1 which is about 30 percent of  the estimate  of  the  chronic



value (0.09 ug/D using the application factor  and the Final Fish



Acute Value.



     No chronic data for  invertebrate species were found.   This



deficiency may not be serious, since, based  upon  the acute data



in Tables 1 and 2, invertebrate  species are  less  sensitive than



fish.



Plant Effects



     Data on the toxicity of endrin to five  species of algae are



listed in Table 4.  Apparently,  algae are  not sensitive  to



endrin, and the lowest value is  475 ug/1 for growth inhibition of



Anacystis nidularas.



Residues



     Steady-state bioconcentration factors  (BCF)  have  been



measured for nine species of organisms including  algae,  mussels,



and  fish.  The geometric  mean of these factors  is  1,200.   Table  5



also shows effect levels  from feeding endrin residues  to  various



organisms.  The lowest effect level is the  FDA  guideline  (0.03



mg/kg) for animal feed.   Therefore, the Residue Limited  Toxicant



Concentration  is 0.03 mg/kg divided by the  highest BCF for a fish



species of 15,000 or 0.0020 ug/1.



Miscellaneous



     Table 6,  containing  data for other effects not listed in  the



first five tables, does not indicate any significant effect levels



that would alter the conclusions discussed previously.
                               B-6

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CRITERION FORMULATION



                     Freshwater Aquatic Life



Summary of Available Data



     The concentrations below have been rounded to  two  significant



figures.



     Final Fish Acute Value - 0.10 ug/1



     Final Invertebrate Acute Value = 0.30 ug/1



          Final Acute Value = 0.10 ug/1



     Final Fish Chronic Value = 0.033 ug/1



     Final Invertebrate Chronic Value = not available



     Final Plant Value = 480 U9/1



     Residue Limited Toxicant Concentration = 0.0020 ug/1



          Final Chronic Value = 0.0020 ug/1



          0.44 x Final Acute Value = 0.044 ug/1



The maximum concentration of endrin is the Final Acute  Value  of



0.10 ug/1 and the "24-hour average concentration is  the  Final



Chronic Value of 0.0020 ug/1.  No important adverse effects on



freshwater aquatic organisms have been reported to  be caused  by



concentrations lower than the 24-hour average concentration.



     CRITERION:  For endrin the criterion to protect freshwater



aquatic life as derived using the Guidelines is 0.0020  ug/1 as a



24-hour average and the concentration should not exceed 0.10  ug/1



at any time.
                              B-7

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                        Table  1.   Freshwater fish acute values for endrln
co
         Or gar)
                                         Adjusted
Bioaesay  Test      Time      LC50       LC50
Method*   Cone.**   Ihre)      (ug/lL     (ug/1)     reference
Coho salmon,
Oncorhynchus kisutch
Coho salmon,
Oncorhynchus kisutch
Coho salmon,
Oncorhynchus kisutch
Chinook salmon.
Qncorhynchus tshawytscha
Chinook salmon,
Oncorhynchus tshawytacha
Cutthroat trout,
Salmo clarki
Cutthroat trout.
Salmo clarki
Rainbow trout,
Salmo gairdneri
Rainbow trout,
Salmo gairdneri
Rainbow trout.
Salmo gairdneri
Rainbow trout,
Salmo -gairdneri
Brook trout.
Salvelinus fontinalis
Brook trout,
Salvollnus fontinalis
Goldfish,
Carnssius auratus
Goldfish,
S

S

S

S

S

S

S

S

S

S

S

S

S

S

S
U

U

U

U

U

U

U

U

U

U

U

U

U

U

U
96

96

96

96

96

96

96

96

96

96

96

96

96

48

96
0.

0.

0.

1.

0.

0.

0.

0.

1.

0.

0.

0.

0.

2.

2.
51

27

76

2

92

113

192

405

1

58

9

355

59

0

1
0.

0.

0.

0.

0.

0.

0.

0.

0.

0.

0.

0.

0.

0.

1.
28

15

42

66

50

06

11

22

60

32

49

19

32

89

15
Katz

Katz

Post

Katz

Katz

Post

Post

Post

, 1961

& Chadwick,

& Schroeder

, 1961

& Chadwick,

tt Schroeder

& Schroeder

& Schroeder



1961

, 1971



1961

, 1971

, 1971

, 1971

Macek, et al. 1969

Katz

Katz

Post

Post


. 1961

& Chadwick,

& Schroeder

& Schroeder

lyatomi, et al.





1961-

, 1971

, 1971

1958

Henderson, et al. 195!
         Carassius auratus

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               Table  1.    (Continued)
                                                                 Adjusted
Organism
Carp.
Cyprinus carpio
Carp.
Cyprinus carpio
Carp,
Cyprinus carpio
Carp (egg) .
Cyprinus carpio
Carp (fry).
Cyprinus carpio
03 Carp (fry) ,
' Cyprinus carpio
Carp (fry),
Cyprinus carpto
Carp (fry).
Cyprinus carpio
Carp (fry).
Cyprinus carpio
Carp (fry).
Cyprinus carpio
Bluntnose minnow,
Pimcphales notatus
Bluntnose minnow,
I'iiuephales notatus
Bluntnose minnow,
Pimcphales notatus
Fathead minnow.
Bioassay
Method*
S
S
S
S
S
S
S
S
S
S
FT
FT
FT
FT
Cone **
U
U
U
U
U
U
U
U
U
U
U
U
U
M
Time
iiilS)
48
48
48
24
. 24
24
24
24
24
24
96
96
96
96
LC50
140.00
6.0
5.0
19.9
8.5
10.7
4.9
4.2
0.061
0.046
0.27
0.29
0.47
0.50
LC50
fuq/l)
61.99
2.66
2.21
7.18
3.07
3.86
1.77
1.52
0.022
0.017
0.21
0.22
0.36
0.50
keterer.ce
lyatomi, et
lyatomi, et
lyatomi, et
lyatomi, et
lyatomi, et
lyatomi, et
lyatomi, et
lyatomi, et
lyatomi, et
lyatomi. et
Mount, 1962
Mount, 1962
Mount, 1962
Brungs & Bal
Pimephales promelas

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               Table   1.   (Continued)
                                                                 Adjusted
Bioassay
Organism Method*
Fathead minnow, FT
Pimephalea promelaa




03
1
o


Fathead minnow,
Pimophalea promelaa
Fathead minnow,
Pimephales promelaa
Fathead minnow,
Pimophalea promelaa
Fachead minnow,
Piniephalea promelaa
Fachead minnow,
Pimephales promelaa
Fathead minnow,
Pimcphalea promelaa
Fathead minnow,
Piniephalea promelaa
Flagfish.
Jordanella floridae
Mosquitofish,
Gamhusia affinia
Guppy.
Lebistes reticulatua
Guppy,
I.ehisCes reticulatus
Threespine stickleback,
Gasterosteus aculeacua
Largemouth bass.
FT
FT
FT
S
S
S
FT
FT
S
S
S
S
S
Test . Time
ConCi* thrsl
M 96
M
M
M
U
U
U
M
M
U
U
U
U
U
96
96
48
48
96
96
96
96
96
96
96
96
48
LCSO
Jug/1)
0.49
0.
0.
0.
0.
1.
1.
0.
0.
0.
0.
1.
0.
0.
40
45
57
77
1
4
26
85
75
9
6
44
27
LCSO
JUCI/1)
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
49
40
45
46
34
60
77
26
85
410
492
875
241
097
Keterer.ce
Brunga & Bailey,
Brunga & Bailey,
Brunga & Bailey,
Lincer, et al.
Lincer. et al.
Henderson, et al
Henderson, et al
1966
1966
1966
1970
1970
. 1959
. 1959
Solon, et al. 1969
Hermanutz, In press
Katz £, Chadwick, 1961
Katz & Chadwick, 1961
Henderson, et al. 1959
Katz, 1961
Fabacher, 1976
Micropterua salmoides

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                         Table  1.   (Continued)
CO
I
          Organism
Blueglll,
I.epomis macrochirus

Blucgill.
Lcpomia macrochirus

Bluegill.
Lepomis macrochirus

Bluegill.
LepomLs macrochirus

Bluegill.
Lepomts macrochtrus

Bluegill.
I.epomis macrochirus

Bluegill.
Lepomi-s macrochtrus

Bluegill.
I.epomis macrochirua

Bluegill.
Lepomls macrochirus

Bluegill.
Lepomts macrochirus

Bluegill.
Lepomis roacrochtrus

Bluegill.
I.epomis macrochirus

BlueKill.
Lepomis macrochirus
                        Bioassay  Test      Time
                        Method*   Conct**    Ihra)
                                     Adjusted
                           LC50      LC50
                            (uq/1)    Jnq/iL _ Heterei.ee
S


S


S


S


S


S


S


S


S


S


FT


S
U


U


U


U


U


U


U


U


U


U


U


U.


U
96


96


96


96


96


96


96


96


96


96


96


24


96
0.6


8.25


5.5


2.4


1.65


0.86


0.33


0.61


0.41


0.37


0.66


2.0


0.61
0.33     Katz & Chadwick, 1961


4.51   " Katz & Chadwick. 1961  .


3.00     Katz & Chadwick. 1961


1.31     Katz & Chadwick. 1961  -


0.90     Katz a, Chadwick. 1961-


0.47     Katz & Chadwick, 1961


0.18     Katz & Chadwick. 1961


0.33     Macek, et al.   1969


0.22     Macek, et al.   1969


0.20     Macek. et ai.   1969


0.36     Henderson, et al.  1959


l.54     Bennett & Day.  1970


3.34     Sanders,  1972
          *  S = static, FT =• flow-through
          ** U = unmeasured, M =• measured                       0. 389
             Geometric mean of adjusted  values - 0.389 yg/1      3.9  "0.10 iig/1
             Lowest value from a flow-through test with measured  concentrations = 0.26 Mg/1

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               Table   2.     Freshwater Invertebrate acute values for endrin
biodssay
Organism Meinou*











CO
1
I-1
to















Clam.
Eupcra slngleyi
Snail..
Physa gyrina
Cladoceran,
Slmocephalus serrulatus
Cladoceran,
Slmocephalus serrulatus
Cladoceran.
Daphnla magna
Copcpod,
Cyclopold

Sou/bug,
Ascllus brevicaudus
Scud.
Gainmarus fasciatus
Scud.
Canuuarus fasciatus
Scud,
Gainmarus fasciatus
Scud ,
Ganunarus lacustris
Scud.
Gainmarus lacustris
Glass shrimp,
Palacmonetes kadiakensis
Glass shrimp,
Palacmonetes kadiakensis
Glass shrimp,
S

S

S

S

S

S


S

S

S

FT

S

S

S

FT

S
Test
Time
LC50
Adjusted
LCbO
Cone.** (niai (»i
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                               Table  2.   (Continued)
CD
I
(-•
U)
                               Bioassay  Test      Time
                               Method*   Cone. **   (t\ta)
                                                                 Adjusted
                                                       LCSO      LCSO
                                                       (ug/11     (ug/l>     Reterence
Crayfish, S
Orconectea nais
Crayfish. S
Orconectea nais
Mayfly. S
llexagenia bilineata
Mayfly. S
Ephemerella grand! s
Stonefly. S
Acroneuria pacifica
Stonefly, S
Ptcronarcys californica
Sconefly. S
Ptcronarcys californica
Stonefly, S
Pteronarcella badia
Sconefly, S
Claassenia aabulosa
Damselfly, S
Ischnura verticalus

U 96

U 96

U 96

U 96

U 96

U 96

U 96

U 96

U 96

U 96

320

3.2

64

4.7

0.32

2.4

0.25

0.54

0.76

1.8

271.0

2.71

54.2

3.98

0.27

2.03

0.21

0.46

0.64

1.53

Sanders, 1972

Sanders, 1972

Sanders, 1972

Gaufin, et al.

Jensen & Gaufin

Jensen & Gaufin

Sanders & Cope,

Sanders & Cope,

Sanders & Cope,

Sanders , 1972







1965

. 1966

, 1966

1968

1968

1968



*  S =• static, FT - flow- through

** U = unmeasured

   Geometric mean of adjusted  values  =  6.22  pg/1
                                                                . 0.30 ug/1

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                    Table 3.   Freshwater fish chronic values'for endrln
      Organism
Test*
                                             Limits
Chronic
Value
(uq/11
                                                                      Reference
      Fathead  minnow,
      Pitnephales  promclas

      Flagfish.
      Jordanclla  floridae
 LC     0.14-0.25    0.187
 LC     0.22-0.3
 0.257
               Jarvinen & Tyo, 1978
Hermanutz, 1978
     *   LC «»  life cycle  or  partial  life  cycle
                                                         0  219
         Geometric mean of chronic values -  0.219  pg/1    ^ i   -  0.033  pg/1

         Lowest  chronic value  ° 0.187  pg/1
CD
I
                                      Application  Factor  Values
96-hr LC50
Species (MR/!)
Fathead minnow, 0.409*
Ptmephales promelas
Flagfish. 0.85
Jordanella floridae

MATC
(tig/1) AF Reference
0.187 0.46 Jarvinen & Tyo, 1978

0.257 0.30 Hermanutz. 1978

         Geometric mean AF = 0.37
                         Geometric mean LC50 -0.59 pg/1
                                   0.37   VO.l x  0.59 -  0.09  pg/1
        *  Since Jarvinen and Tyo  (1978) did not provide a :%-hr LC50 value,  the
           geometric mean of six 96-hr LC50 values  (for  flow  through tests -with measured
           concentrations) was used as an estimate  of  the LC50  for  calculating an  AF for
           fathead minnows.

-------
                        Table   4.   -Freshwater plant effects  for endrin


                                                  Concentration
Organism
Alga.
Anacystls nldularas
Alga,
Mtcrocystis aeruginosa
Alga.
Anabaena cylindrlca
Alga.
Sccnedesmua quadricauda
Alga.
Ocdogonium sp.
Effect
growth
growth
growth
growth
growth
(uq/1) Reference
475 Batterton, 1971
> 1.000 •'. Vance & Drummond, 1969
<5,000
>15,000 Vance & Drummond. 1969
>20,000 Vance & Drummond , 1969
> 20 ,000 Vance & Drummond, 1969
03
I
Lowest plant value - 475 i'g/1

-------
               Table  S.   Freshwater residues for endrin




CD
1
I-1
Ol


Organ Jem
Alga.
Microcyatts aeruginosa
Alga. .
Anabaena cylindrica
Alga.
Scenedesmus quadricauda
Alga.
Ocdogonlum sp.
Mussels,
(Mixed species)
Fathead minnow,
Pimephales promelaa
Fathead minnow,
Pimephalea promelas
Channel catfish,
Ictalurus punctatus
Flagfish.
Jordanclla floridae
Organism
Man
Domestic animals
Rainbow trout,
Salmo gairdneri
fioldfish,
Car ass ins auratus
Bioconcentration Factor (days)
200
222
156
140
3,000
10.000
7,000
2,000
1,640
15,000
Maximum Permissible Tissue
Action Level or Effect
edible fish and shellfish
animal feed
osmoregulation
growth inhibition
7
7
7
7
21
47
300
41
55
65
Concentration
Concentration
(mg/kf>)
0.3
0.03
0.725
0.43
Heference
Vance & Drummond, 1969
Vance & Drummond, 1969
Vance & Drummond, 1969
Vance & Drummond, 1969
Jarvinen & Tyo, 1978
Mount & Putnicki, 1966
Jarvinen & Tyo, 1978
Argyle, et al. 1973
llermanutz, 1978
Reference
U.S. FDA Admin. Guideline
7420.09, 1973
U.S. FDA Admin. Guideline
7426.04, 1974
Grant & Mehrie, 1973
Grant & Mehrie, 1970
Fathead minnow,
I'iiucpliales promo las
reduced survival
0.63
Jarvinen & Tyo,  1978

-------
CO
I
                       Table  5.   (Continued)
        Geometric mean  bloconcentration factor for all species = 1,200


        Highest bloconcentration  factor for  a single  fish species - 15,000
        For FDA animal  feed:   °'"g  g§    =  0.0000020 mg/kg or 0.0020 pg/1
        For effect on wildlife:       " **  °-00036  mE/kS or 0.36 Mg/-l

-------
                    Table 6.  Other freshwater data  for  endrin
Ornanism
Test
purgtipn.  Etfect
Result
jug/11    petereiictj
Rainbow trout,
Salmo pairdneri
Golden shiner,
Notemi ftonua crysoleucas
Bluntnose minnow,
Plmcphales notatus
Channel catfish,
Ictalurus punctatus
Yellow bullhead.
Ictalurus natalls
DO
1 Black bullhead,
*-* Ictalurua mclas
Mosquitofish,
fiambusla afflnis
Largemouth bass,
Micropterus salmoides
Blucglll.
I.epomis macrochirus
Stonefly,
Pteronarcys californica
Stonefly,
Acroneurla pacifica

15 rain
36 hrs
291 days
12 days
36 hrs
36 hrs
36 hrs
20 days
30 days
30 days
ATPase inhibition :
LC50
Growth inhibition
Half life of residue
LC50
LC50
LC50
LC20
Weak inhibition of Mg2
and Na+-Kf ATPase
LC50
LC50
10.-"
molar
2.0
0.4
1.25
0.37
1.0
0.1
*
. 41.7 MM
1.2
0.035
Davis, et al. 1972
Ludke. et al. 1968
Mount, 1962
Jackson, 1976
Ferguson :& Blngharo, 1966
Ferguson, et al. 1965
Ferguson, et al. 1966
Fabacher, 1976
Cutkomp, et al. 1971
Jensen &.-iGaufin, 1966
Jensen & Gaufin, 1966
Lowest value = 0.035 |ig/l

-------
                       SALTWATER ORGANISMS



Introduction



     The acute toxicity of endrin to saltwater organisms  has  been



relatively well studied particularly in the 1960's, probably



because it has been used widely and has proven to be  one  of the



most acutely toxic insecticides.  Data on bioaccumulation of



endrin and its chronic toxicity have been available only  recently.



Although the criterion for endrin is based on its bioconcentra-



tion, acute and chronic toxicity to invertebrate species  is only



slightly above the Final Chronic Value.  The similarity of these



values is significant because only slight excursions  above an



acceptable concentration of endrin in water may  result  in acute



toxicity or unacceptable accumulation in seafood consumed by  man.



Acute Toxicity



     Acute toxicity tests have been conducted with seventeen



species of saltwater fishes and sensitivity varies considerably



(Table 7).  Adjusted LC50 values ranged from 0.026 ug/1 for



chinook salmon (Schoettger, 1970) to 1.7 ug/1 for northern puffer



(Eisler, 1970b).  Only two, usually tolerant, species,  the sheep-



shead minnow (Hansen, et al. 1977) and the sailfin molly



(Schimmel, et al. 1975) have been tested for 96-hours in  flow-



through tests with measured endrin concentrations.  Sheepshead



minnow fry, juveniles, and adults did not differ in their sensi-



tivity to acute exposure to endrin (Hansen, et al. 1977)„ Fifteen



species of freshwater fishes, excluding carp, were as sensitive as



saltwater fishes; adjusted LC50 values ranged from 0.06 to 4.51



ug/1 (Table 1).
                              B-19

-------
     Acute toxicity tests with saltwater invertebrate  species  also
demonstrate that endrin  is very toxic  (Table 8).  The  variability
in adjusted LC50 or EC50 values is greater than  that for  fishes,
ranging from 0.037 to 670 ug/l«  Unlike most insecticides,  the
sensitivity of arthropods to endrin is not much  different  from the
sensitivity of fishes.   The penaeid shrimp were  the most  sensitive
species tested, with adjusted LC50 values from 0.037 to 0.099  ug/1
(Schimmel, et al. 1975;  Lowe, unpublished; and Butler, 1963).
Adjusted LC50 values of  five other arthropod species ranged  from
0.23 ug/1 for Korean shrimp (Schoettger, 1970) to 8.3  ug/1  for
blue crabs (Butler, 1963).  The sensitivity of different  life-
stages of grass shrimp is similar, differing by  only a factor  of
3.4 (Tyler-Schroeder, In press).  American oysters were less
sensitive than arthropods, with adjusted EC50 values,  based  on
decreased shell deposition or abnormal development of  larvae,
ranging from 14.2 to 670 U9/1 (Table 8).  The toxicity of  endrin
to oysters may be directly related to water temperature.   The
range in adjusted LC50 values for 17 species of  freshwater  mol-
lusks and arthropods (0.20 to 298 ug/1; Table 2) was almost  as
great as the range for saltwater species but none was  as  sensitive
as penaeid shrimp.
     Data on LC50 values for fishes and invertebrate species  in
acute toxicity tests with endrin support the hypothesis that  the
acute toxicity of endrin is underestimated by static tests  and  by
not measuring concentrations of endrin in test water.  Therefore,
LC50 values must be adjusted for test  conditions if relative
                               B-20

-------
species sensitivity is to be understood.  For the same tests,  LC50



or EC50 values based on nominal concentrations for sheepshead  min-



nows (0.40 ug/D i sailfin mollies (0.79 u.g/1)/ grass shrimp  (0.73



ug/1)/ pink shrimp (0.049 ug/Dt and American oysters  (19.1  ug/1)



were higher than LC50 or EC50 values for measured concentrations



(Table 7; Schimmel, et al. 1975).  Additionally, LC50 values based



on static tests were greater than LC50 values for flowthrough



tests of the same duration for shiner perch, dwarf perch, Korean



shrimp, and grass shrimp (Earnest and Benville, 1972; Schoettger,



1970; Tyler-Schroeder, In press; Schimmel, et al. 1975;  Eisler,



1969).  The greater variability in sensitivity of invertebrate



species to endrin than was observed for fishes supports  the  need



for a higher species sensitivity factor for invertebrate  species.



     The Final Acute Values of fish and invertebrate species are



similar.  The Final Fish Acute Value, obtained by dividing the



geometric mean of the adjusted LC50 values  (0.209 ug/1)  by the



species sensitivity factor (3.7), is 0.056 ug/1.  The Final  Inver-



tebrate Acute Value, obtained by dividing the geometric  mean of



the adjusted LC50 values for invertebrate species (1.5 ug/D by



the species sensitivity factor  (49), is 0.031 ug/1.  The  species



sensitivity factors for fish and invertebrate species seem appro-



priate because the adjusted LC50 values of one of 17 fishes  was



less than the Final Fish Acute Value and the Final Invertebrate



Acute Value was slightly less than adjusted LC50 values  of the



most sensitive of the nine species tested.  The Final Acute  Value



is 0.031 ug/1.
                              B-21

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Chronic Toxicity



     Sheepshead minnows  (Schimmel,  et  al.  1975;  Hansen,  et  al.



1977), spot (Lowe, 1965),  and muiranichog  (Eisler,  1970a)  have  been



exposed chronically to endrin for 10 days  or  longer  (Tables 9 and



12).  Only the life-cycle  exposure  of  sheepshead  minnows (Hansen,



et al. 1977) is suitable  for obtaining a Final Fish  Chronic Value.



In this test, embryos exposed to 0.31  and  0.72 ug/1  hatched early;



all fry exposed to 0.72 ug/1/ and about one-half  exposed to 0.31



ug/1/ died.  Females died  during spawning,  fewer  eggs were



fertile, and survival of  exposed progeny decreased  in 0.31  ug/1.



No significant effects were observed on survival, growth, or



reproduction at an exposure concentration  of  0.12 ug/1.   The  MATC



limits, 0.12 to 0.31 ug/1/ were not much less than  the  96-hour



LC50, 0.34 ug/1/  indicating that there is  little  difference be-



tween endrin concentrations that produce acute effects  and  ones



that produce no effect in  chronic tests.   Life-  cycle tests with



the freshwater fish, fathead minnow and flagfish  also show  little



difference between acute  and chronic toxicity of  endrin (Table 3).



The saltwater Final Fish  Chronic Value for endrin is obtained by



dividing the chronic value (0.19 ug/1) by  the species sensitivity



factor  (6.7) and  is 0.028  ug/1.



     An embryo-larval test with sheepshead minnows  (Schimmel, et



al. 1975) was not used to  obtain a  chronic value  because only



LC50 values and nominal observed no-effect concentrations were



reported (Table 12).  However, results were similar  to  those  re-



ported  in the life cycle  test.  The LC50 value based on measured
                               B-22

-------
concentrations for fry on the 33rd day of the experiment was  0.158



ug/l«  Although fish exposed to a nominal concentration of  0.21



ug/1 had no significant mortality, they were visibly  affected by



endrin.



     Fifty-seven percent of the juvenile spot were  exposed  to



endrin at a concentration of 0,075 ug/1 within 19 days.  Spot



exposed to 0.05 ug/1 were apparently not affected  (Lowe, 1966).



Fish exposed to 0.05 ug/1 exhibited no signs of poisoning and



survival, length and weight did not differ  from those of control



organisms.  The nominal,, no observed effect concentration of  0.05



ug/1 was 0.21 of the adjusted LC50 of 0023  v.q/1, and  this also



supports the hypothesis of a minimal difference between the acute



and the chronic toxicity of endrin to fish.



     The only other datum on chronic effects of endrin on a salt-



water fish (Fundulus heteroclitus) show a 10-day LC50 based on



nominal concentrations of 0.33 ug/1 (Eisler, 1970a)f  which  is



little different from the unadjusted 96-hour LC50 values of 0.6



and 1.5 ug/1 (Eisler, 1970b).



     One saltwater invertebrate species, grass shrimp, has  been



exposed to endrin in a partial life-cycle toxicity  test (Tyler-



Schroeder, In press).  Survival of the parental generation  was



reduced by exposure to 0.11 ug/l«  Onset and duration of spawning



were significantly delayed and lengthened for female  grass  shrimp



at all exposure concentrations (0.03 to 0.79 ug/l)« The number of



females depositing eggs was less  than that  of controls, but egg
                              B-23

-------
production and hatching  success apparently were not  affected.
Larval mortality increased,  time  to metamorphosis  increased,  and
growth of juvenile shrimp was decreased by endrin  concentrations
of 0.11 ug/1 and higher.
     The Final Invertebrate  Chronic Value was obtained  for  endrin
(Table 10), even though  all  tested concentrations  significantly
impaired some life-cycle function.  A lower MATC limit  of 0.03
ug/1 was selected because the only effect was a delay  in onset of
spawning of about one week.  A delay of one week probably would
not affect natural populations.   The upper MATC limit of 0.05 ug/1
was set on decrease  in number of  ovigerous females and  delay  in
spawning of 3 to 4 weeks.  The Final Invertebrate  Chronic Value of
0.075 ug/1 is obtained by dividing the chronic value (0.038)  by
the species sensitivity  factor  (5.1).  The species sensitivity
factor is needed because grass shrimp are intermediate  in their
sensitivity to acute exposure to  endrin, compared  to other  salt-
water invertebrate species.
Plant Effects
     Three published studies on five species of phytoplankton and
a natural phytoplankton  community (Table 11) indicate  that  effects
of endrin on phytoplankton are unlikely at concentrations protec-
tive of acute effects on most invertebrate and fish  species.
Menzel, et al. (1970) in tests with four phytoplankton  species
found effects at concentrations greater than 1 ug/l»  Productivity
of natural phytoplankton communities was reduced by  46  percent  in
                               B-24

-------
1,000 ug/1 (Butler, 1963).  Growth rate of Agmenellum guadrupli-
catum was reduced in as little as 0.2 ug/1 (Batterton, et al.
1971).
Residues
     The bioconcentration of endrin from water into  the  tissues
of saltwater organisms has been well studied  (Table  12 and  13).
Probable steady-state bioconcentration factors (BCF) are available
from studies with American oysters (Mason and Rowe,  1976; Wilson,
1966); grass shrimp (Tyler-Schroeder, In press); sheepshead min-
nows (Hansen, et al. 1977); and spot (Lowe, 1966).   Additional BCF
data (Table 13) are available from 96-hour exposures of  oysters,
grass shrimp, pink shrimp, sheepshead minnows, and sailfin  mol-
lies, to endrin (Schimmel, et al. 1975).
     Bioconcentration factors (Table 12) for  endrin  in American
oysters exposed for seven days ranged from 1,670 to  2,780  (Mason
and Rowe, 1976).  Endrin accumulated rapidly, reaching steady-
state after about 48 hours of exposure.  Oysters placed  in  endrin-
free water depurated endrin at a rate of 0.005 ug/g  h~"l, result-
ing in a biological half-life of 67 hours.  Based on this experi-
ment, the oysters exposed to endrin in a flow-through test  by
Wilson (1966) were probably at steady-state and had  a BCF of
1,000, based on a nominal water concentration.  Oysters  exposed
for only 96 hours had an average BCF of 1,200 (Schimmel, et al.
1975) .
     Bioconcentration factors for endrin in grass shrimp in two
experiments averaged 1,490 and 1,600 (Tyler-Schroeder> In press).
                              B-25

-------
In the first experiment,  steady-state was reached  after  2.5 days
of a 21-day exposure.  Ninety percent of the endrin was  depurated
within 4.2 days.   In  the  second experiment, the  average  BCF of
endrin was 1,600  in parental generation shrimp from a partial
life-cycle exposure lasting 5 months.  Average bioconcentration
factors after a 96-hour exposure were 830 for grass shrimp and 980
for pink shrimp (Schimmel, et al. 1975).
     Bioconcentration data for two of three species of saltwater
fish differs little from  those for invertebrate  species.  Biocon-
centration factors calculated from nominal water concentrations
were 1,340 for spot exposed for 8 months and 1,560 for spot ex-
posed for 5 months (Lowe, 1966).  The average BCF  for juvenile
sheepshead minnows exposed for 28 days was 2,500,  for adults ex-
posed for 147 to  161  days the BCF was 6,400 (Hansen, et  al. 1977)
and for juveniles  exposed 4 days the BCF was 2,600 (Schimmel, et
al. 1975).  Sailfin mollies exposed to endrin for  four days had an
average BCF of 2,400  (Schimmel, et al. 1975).
     The use of data  on the bioconcentration of  endrin (Table 12)
and on the FDA limit  of 0.03 mg/kg for animal feed results in a
Residue Limited Toxicant  Concentration (RLTC) for  endrin of 0.047
ug/1.  This value  is  lower than the Final Fish or  Invertebrate
Chronic Values and the Final Plant Value and therefore the RLTC
becomes the Final  Chronic Value.
Miscellaneous
     Other data included  in the tables but not yet discussed, do
not contribute significantly to the derivation of  a criterion for
endrin.
                               B-26

-------
CRITERION FORMULATION



                      Saltwater Aquatic-Life



Summary of Available Data



     The concentrations below have been rounded  to  two  significant



figures



     Final Fish Acute Value = 0.056 ug/1



     Final Invertebrate Acute Value = 0.031 ug/1



          Final Acute Value = 0.031 ug/1



     Final Fish Chronic Value = 0.028 ug/1



     Final Invertebrate Chronic Value = 0.0075 ug/1



     Final Plant Value = 0.2 ug/1



     Residue Limited Toxicant Concentration = 0.0047  ug/1



          Final Chronic Value = 0.0047 ug/1



          0.44 x Final Acute Value = 0.014 ug/1



     The maximum concentration of endrin  is the  Final Acute  Value



of 0.031 ug/1 and the 24-hour average concentration  is  the Final



Chronic Value of 0.0047 ug/l«  No important adverse  effects  on



saltwater aquatic organisms have been reported to be  caused  by



concentrations lower than the 24-hour average concentration.



     CRITERION:  For endrin the criterion to protect  saltwater



aquatic life as derived using the Guidelines is  0.0047  ug/1  as  a



24-hour average and the concentration should not exceed 0.031 ug/1



at any time.
                              B-27

-------
              Table  7.    Marine fish acute values for endrin
                         Bioasaay   Teat       Time
                         Method*    cone.**    Ihrs)
          Adjusted
LC50      LC50
(uq/U     (ug/1)    Reference











CD
1
fO
00
















• g iinriiai fc— «
American eel.
Anguilla roatrata
Gulf menhaden,
Brevortia patronus
Chinook salmon,
Oncorhynchus tshawytscha
Sheepshead minnow (fry) ,
Cyprinodon variegatus
Sheepshead minnow
(juvenile).
Cyprinodon vartegatus
Sheepshead minnow (adult).
Cyprinodon variegatus

Sheepshead minnow
(juvenile) ,
Cyprinodon vartegatus
Sheepshead minnow,
Cyprinodon variegatus
Mummichog,
Fundulus heteroclitus
Mununi cliog ,
Fundulus heteroclitus
Striped killifish.
Fundulus malalis
Longnose killifish.
Fundulus similis
Longnose killifish.
Fundulus similis
Sailfin molly.
S

FT

S

FT

FT


FT


FT


FT

S

S

S

FT

FT

FT
U

U

U

M

M


M


M


U

U

U

U

U

U

M
!*•••*
96

24

96

96

96


96


96


24

96

96

96

24

48

96
0.6
i
0.80

0.048

0.37

0.34


0.36


0.38


0.32

0.6

1.5

0.3

0.23

0.3

0.63
0.32

0.41

0.026

0.37

0.34


0.36


0.38


0.16

0.33

0.82

0.16

0.12

0.19

0.63
Eialer, 1970b

Lowe, 1966

Schoettger, 1970

Hansen, et al.

Hansen, et al.


Hansen, et al.


Schimmel, et al.


Lowe, 1966

Eialer, 1970b

Eisler, 1970b

Eialer, 1970b

Lowe, 1966

Butler. 1963

Schimmel, et al.






1977

1977


1977


1975














1975
Poecilia laciplnna

-------
                          Table  7.  (Continued)
                                                                            Adjusted
DO
I
N)
VO
E
Organism £
Atlantic silverside.
Mcnidia menidia
Threespine stickleback,
Gastcrosteus aculeatus
Threespine stickleback,
Gasterosteus aculeatus
Threespine stickleback,
Gasterosteus aculeatus
Threespine stickleback,
Gas Coros Lens aculeatus
Threespine stickleback,
Gasterosteus aculeatus
Threespine stickleback,
Gasterosteus aculeatus
Threespine stickleback,
Gasterosteus aculeatus
Striped bass,
Morone saxtilis
Spot.
Leiostomus xanthurus '
Shiner perch,
Cymatogaster aggregate
Shiner perch,
CyinatQRaster aggregate
Dwarf perch.
Micromctrus minimus
Dwarf perch,
Micrometrus minimus
Blue-head.
iioassay
lethod*
S
S
S
S
S
S
S
S
FT
FT
S
•
FT
S
FT
S
Test
Cone,**
U
U
U
U
U
U
U
U
U
U
U
U
U
U
U
Time
(hfs)
96
96
96
96
96
96
96
96
96
24
96
96
96
96
96
LC50
Juq/i)
0.05
I
1.65
1.50
1.20
1.57
1.57
0.44
0.50
0.094
0.45
0.8
0.12
0.6
0.13
O.I
LC50
(uci/U
0.027
0.90
0.82
0.66
0.86
0.86
0.24
0.27
0.072
0.23
0.44
0.09
0.33
0.10
0.055
Katz & Chadwick, 1961


Katz & Chadwick. 1961


Katz, 1961


Katz, 1961
           Tlialassoma bifasciatum
                                                                                      Earnest & Benvilie, 1972


                                                                                      Earnest & Benville. 1972


                                                                                      Earnest & Benville, 1972


                                                                                      Earnest & Benville, 1972


                                                                                      Eisler, 1970b

-------
              Table  7.   (Continued)
                                                      LC50
Organism
Adjusted
LC50
Jug/ilKeterei.ce




Striped mullet,
Mugtl cephalus
Striped mullet,
Mugil cephalus
Striped mullet,
Mugtl cephalus
Northern puffer,
Sphaeroidcs maculatus

S U
FT U
FT U
S U
96 0.3 0.16 Eisler, 1970b
24 2.6 1.3 Lowe, 1966
48 0.4 0.25 Lowe, data sheets
96 3.1 1.7 Eisler. 1970b
* S - static. FT - flow through
CD
1
** u B unmeasured, M =
measured

                                                        0 209
   Geometric mean of adjusted  values • 0.209 ug/i     —y -t   - 0.056 ug/1

   Lowest value from .a flow-through test with measured concentrations - 0.34 Mg/1

-------
                       Table   8.   Marine invertebrate acute values for endrin
         QliianiSJD
Uiodssay  Test      Time
MsLUiiiirL  Cone.**   (ins) .
                                                                LC50
                                                                          Adjusted
                                                                          L0!>0
                                                                                    heterence
03
I
u>
American oyster (embryo),  S        U        48
Crassostrea virginica

American oyster,           FT       M        96
Crassostrea virginica

American oyster,           FT       U        96
Crassostrea virgintca

American oyster,           FT       U        96
Crassostrea virgintca

Blue crab,                 FT       U        48
Callinectes saptdus

Sand shrimp,               S        U        96
Cragon soptemspinosa

Hermit crab,               S        U        96
Pagurus longicarpus

Korean shrimp.             S        U        96
Palaemon macrodactylua

Korean shrimp,             FT       U        96
Palaemon macrodactylus

Crass shrimp (larva).      FT       M        96
Palacmonetes pugio

Grass shrimp (juvenile),   FT       M        96
Palaemonetea pugto

Grass shrimp (adult).      FT       M        96
Palaemonetes pugto

Grass shrimp,              FT       M        96
Palaemonetes pugio

Crass shrimp,              FT       U        48
Palaemonetes pugio.
                                                                790***    670


                                                               14.2***   14.2


                                                                 33***   25.4


                                                                AGO***    308


                                                                 25
                              1.7


                               12


                              4.7


                              0.3


                              1.2


                              0.35


                              0.69


                              0.63


                              0.8
8.3


1.4


 10


4.0


0.23


1.2


0.35


0.69


0.63


0.26
                                                  Davia & Hidu, 1969
                                                  Schimmel, et al.  1975
                                                  Butler, 1963
                                                  Lowe, data sheets
                                                  Butler, 1963
                                                                                    Eisler,  1969
                                                                                    Eisler,  1969
                                                                                    Schoettger,  1970
                                                                                    Schoettger,  1970
                                                                                   Tyler-Schroeder,  In press
                                                                                   Tyler-Schroeder,  In press
                                                                                   Tyler-Schroeder,  In press
                                                                                    Schimmel,  et  al.   1975
                                                                                   Lowe,  data  sheets

-------
Organism
                        Table  8.  (Continued)
Bioassay  Teat      Time
Method*   Cone.**   (his)
          Adjusted
LC50      LC50
(ug/1)     (ug/H     Reterence
00
U)
fO
Grass shrimp, S U
Palaemonetes vulgaris
Pink shrimp, FT M
Pcnaeus duorarum
Pink shrimp. FT U
Penacus duorarum
Brown shrimp, FT U
Penaeus aztecus

* S = static, FT «• flow- through
** U •* unmeasured, M = measured
*** Abnormal development of oyster larvae;
of brown shrimp or blue crabs.
96 1.8 1.5 Eisler, 1969
96 0.037 0.037 Schimmel, et al. 1975
48 0.2 . 0.066 Lowe, data sheets
48 0.3*** 0.099 Butler, 1963
decreased growth of oyster; or loss of equilibrium
     Geometric mean of adjusted  values = 1.5  Mg/1     —TK— - 0.031  wg/1

     Lowest value from a flow-through test with measured concentrations • 0.037 iig/1

-------
              Table   9.  Marine  fish  chronic  values  for  endrln .


                                                 Chronic
                                       Limits    Value
Organism                     Test*      (ug/i)     tug/1)         Reference


Shcepshead minnow,            LC      0.12-0.31   0.19          Hanaen. et  al.   1977
Cyprtnodon vartegatus


* LC «• life cycle or partial life cycle

       Geometric mean chronic values 6

       Lowest chronic value - 0.19 Mg/1
                                              0 19
Geometric mean chronic values •» 0.19 yg/1      ; 2  - 0.028  ng/1
                              Application Factor Values
03
U)
Species
Sheepshead
Cyprtnodon
minnow,
varlegatus
96-hr LC50
(MR/1)
0.34
MATC
lilB/li
0.12-9.31
Geometric mean AF - 0.56
AF
0.56
Reference
Hansen, et al.
Geometric mean LC50 » 0.
1977
34 ug/1
                                   0.56 I/IK34 iig/1 x 0.056 ug/1 - 0.077 gg/1

-------
                     Table  10.  Marine invertebrate chronic values  for endrln  (Tyler-Schroeder, In press)


                                                             Chronic
                                                  Limits     Value
           Organlam                     Teat*      (ug/11     (ug/ll


           Grass shrimp,                 LC      0.03-0.05*   0.038
           Palaemonetes pugto



           *  LC - life cycle or partial life cycle

           ** Onset of spawning was delayed about one week in shrimp exposed  to 0.03  ng/1.   Because
              a delay of one week would probably not affect natural populations, MATC limits were
              set on decreases in number of ovigerous females and  delayed spawning of 3-4 weeks  in
              0.05 wg/1 of endrin.

              Geometric mean of chronic values - 0.038 iig/1     PiPrD.. »» 0.0075 \ig/l

              Lowest chronic value - 0.039 pg/1
CO
I
to

-------
                          Table  11.  Marine plane effects  for endrin
CD
I
CO
Ul
Organism
Alga.
Agmcnellum
quadruplicatum
Alga.
Dunaliella
tertiotecta
Alga.
Skeletonema costatura
Alga.
Skeletonema costatum
Alga.
Coccolithus huxlegi
Alga.
Coccolithus huxlegi
Alga.
Cyclotella nana
Alga,
Cyclotella nana
Natural phytoplankton
communities
Concentration
Effect (uq/lj
Growth rate 0.2. 19, 95
inhibited 475, 950
No effect on 1,000
'••C or cell
division
lkC uptake >10
reduced
Growth reduced 100
first 5 days of
test
ll*C uptake >10
reduced
Growth reduced 100
'"•C uptake >1.0
Growth reduced 100
467. decrease in 1,000
productivity;
Reference
Batterton, et
Menzel, et al
Menzel, et al
Menzel. et al
Menzel, et al
Menzel. et al
Menzel, et al
Menzel, et al
Butler, 1963
al. 1971
. 1970
. . 1970
. 1970
. 1970
. 1970
. 1970
. 1970
            Lowest plant value =  0.2 Mg/1

-------
               Table  12.   Marine residues for endrin














CO
1
OJ
en








Organism
American oyster.
Crassostrea virginica
American oyster,
Crassostrea virginica
Crass shrimp,
Palacmonetes pugio
Grass shrimp.
Palaemonetes pugio
Sheepshead minnow,
Cyprinodon variegatua
Sheepshead minnow.
Cyprinodon variegatus
Spot.
Leiostomus xanthurus



Organism
Man

Domestic animals


Time
fiioconcentration Factor (days)
1.670-2,780

1.000

1,490

1,600

2,500

6.400

1,450


Maximum Permissible Tissue

Action Level or Effect
edible fish and shellfish

animal feed

7

10

21

145

28

147-161

5 to 10
months

Concentration
Concentration
(mg/kg)
0.3

0.03


Keterence


Mason & Rowe, 1976

Wilson, 1966

Tyler-Schroeder
press
Tyler-Schroeder
press
Hansen, et al.

Hansen. et al.

Lowe, 1966




Reference
U.S. FDA Admin.
7420.09. 1973
U.S. FDA Admin.
7426.04, 1977



, In

, I"

1977

1977







Guideline •

Guideline •

Highest bioconcentrstion factor for a single fish species - 6,400
Lowest residue concentration - 0.03 rag/kg
       0.0000007 mg/kg or 0.0047 ng/1

-------
                    Table   13.    Other marine data for endrin
                         Test
Orqanism
                                   Ettect
                          Result
                          (ug/11     Ref ereii
American oyster,
Crassostrea virginica
Grass shrimp,
Palaemonetes pugio
Grass shrimp,
Palaemonetes pugio
Pink shrimp,
Penaeus duorarum
Sheepshead minnow,
Cyprinodon varicgatus
Sheepshead minnow,
Cyprinodon variegatus
00
^ Sheepshead minnow,
-J Cyprinodon variegatus
Sheepshead minnow
(embryo- juvenile) ,
Cyprinodon variegatus
Sheepshead minnow
(embryo-juvenile) ,
Cyprinodon vartegatus
Mummichog,
Fundulus heteroclitis
Sailfin molly,
Poccilia latipina
Spot.
I.eiostoinus xanthurus
Spot,
Leiostomus xanthurus
Northern puffer.
4 days
4 days
1.5 hrs.
4 days
4 days
1.5 hrs.
1.5 hrs.
33 days
33 days
10 days
4 days
8 mos.
8 mos.
4 days
Bioconcentration
factor = 1,200
Bioconcentration
factor •» 830
No avoidance
Bioconcentration
factor - 980
Bioconcentration
factor = 2,600
Avoidance
No avoidance
LC50
Bioconcentration
factor 3,300 to 4.800
LC50
Bioconcentration
factor - 2.400
Death
No effect
Abnormal liver
Schimmel, et al.
Schimmel, et al.
0.1, 1.0, llansen, et al.
10
Schimmel, et al.
Schimmel, et al.
0.1, 1.0 llansen. 1969
0.01. 10 Hansen. 1969
0.16 Schimmel, et al.
Schimmel, et al.
0.33 Eisler, 1970a
Schimmel, et al.
0.075 Lowe. 196&
0.05 Lowe. 196 &
0.05 Eisler & Edmunds
1975
1975
1973
1975
1975

1975
1975
1975
. 1966
Sphacroides maculatus
function

-------
                            ENDRIN



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Bull. Environ. Contain. Toxicol.  6: 589.







Bennett, H.J., and J.W. Day, Jr.  1970.  Absorption of endrin



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Brungs, W.A., and G.W. Bailey.  1966.  Influence of suspended



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Inter. Fish Wildl. Circ.  167: 11.







Cutkomp, L.K., et al.  1971.  ATPase activity in fish tissue



homogenates and inhibitory effects of DDT and related compounds,



Chem. Biol. Int.  3: 439.
                               B-38

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Davis, H.C., and H. Hidu.  1969.  Effects of pesticides



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Fish. Bull.  67: 393.







Davis, P.W., et al.  1972.  Organochlorine insecticide,



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Earnest, R.D., and P.E. Benville, Jr.  1972.  Acute toxici-



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Eisler, R.  1969.  Acute toxicities of insecticides to marine



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Eisler, R.  1970a.  Factors affecting pesticide-induced



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Eisler, R.  1970b.  Acute toxicities of organochlorine and



organophosphorous insecticides to estuarine fishes.  Tech.



Pap. 46.  Bur. Sport Fish. Wildl. U.S. Dep. Inter.







Eisler, R., and P.H. Edmunds.  1966.  Effects of endrin



on blood and tissue chemistry of a marine fish.  Trans.



Am. Fish. Soc.  95: 153.
                               B-39

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Fabacher, D.L.  1976.  Toxicity of endrin and an endrinmethyl
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Ferguson, D.E., et al.  1965.  Tolerance of five chlorinated
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Ferguson, D.E., and C.R. Bingham.  1966.  Endrin resistance
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Ferguson, D.E., et al.  1966.  Dynamics of endrin uptake
and release by resistant and susceptible strains of mosquito-
fish.  Trans. Am. Fish. Soc.  95: 335.

Gaufin, A.R., et al.  1965.  The toxicity of ten organic
insecticides  to various aquatic invertebrates.  Water Sewage
Works 12: 276.

Grant, B.F.,  and P.M. Mehrle.  1970.  Chronic endrin poisoning
in goldfish,  Carassius auratus.  Jour. Fish. Res. Board
Can.  27: 2225.

Grant, B.F.,  and P.M. Mehrle.  1973.  Endrin toxicosis in
rainbow  trout, Salmo  gairdneri.  Jour. Fish. Res. Bpard
Can.  30: 31.
                               B-40

-------
Hansen, D.J.  1969.  Avoidance of pesticides by untrained
sheepshead minnows.  Trans. Am. Fish. Soc.  98: 426.

Hansen, D.J., et al.  1973.  Avoidance of pesticides by
grass shrimp, Palaemonetes pugio.  Bull. Environ. Contam.
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Hansen, D.J., et al.  1977.  Endrin:  Effects on the entire
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Henderson, C., et al.  1959.  Relative toxicity of ten chlori-
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Hermanutz, R.  1978.  Endrin and malathion toxicity to flag-
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lyatomi, K.T., et al.  1958.  Toxicity of endrin to fish.
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Jackson, G.A.  1976.  Biologic half-life of. endrin in channel
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Jarvinen, A.W., and R.M. Tyo.  1978.  Toxicity of fathead minnows
of ejpdrin in food and water.  Arch. Environ. Contam. Toxicol.
7: 1.
                               B-41

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Jensen, L.D., and A.R. Gaufin.  1966.  Acute and long-term
effects of organic insecticides on two species of stonefly
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Katz, M.  1961.  Acute toxicity of some organic insecticides
to three species of salmonids and the threespine stickleback.
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Katz, M., and G.G. Chadwick.  1961.  Toxicity of endrin
to some Pacific Northwest fishes.  Trans. Am. Fish. Soc.
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Korn, S., and R. Earnest.  1974.  Acute toxicity of 20
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Lincer, J.L., et al.  1970.  DDT and endrin fish toxicity
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Am. Fish. Soc.  99: 13.

Lowe, J.I.  1966.  Some effects of endrin on estuarine fishes,
Proc. Am. Conf. S.E. Assoc. Game and Fish Comm.

Lowe, J.I.  Results of toxicity tests with fishes and macroin-
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                               B-42

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Ludke, J.L., et al.  1968.  Some endrin relationships in
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Notemigonus crysoleucas.  Trans. Am. Fish. Soc.  97: 260.

Macek, K.J., et al.  1969.  Effects of temperature on the
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Mason, J.W., and D.R. Rowe.  1976.  Accumulation and loss
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                               B-43

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                               B-44

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                              B-45

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Mammalian Toxicology and Human Health Effects
                           Summary
     Endrin is the common name of one member of the cyclo-
diene group of pesticides.  It is a cyclic hydrocarbon having
a chlorine-substituted methano bridge structure.  Endrin
was introduced into the United States in 1951 and is manufac-
tured domestically by the Velsicol Chemical Corporation.
The endrin sold in the United States is a technical grade
product, containing not less than 95 percent active ingred-
ient, available in a variety of diluted formulations.
     Known uses of endrin in the United States are as an
avicide, rodenticide, and insecticide, the latter being
the most prevalent.  The largest single use of endrin domesti-
cally is for the control of lepidopteron larvae attacking
cotton crops in the southeastern and Mississippi delta states.
Thus, endrin enters the environment primarily as a result
of direct applications to soil and crops.  Waste material
discharge from endrin manufacturing and formulating plants
and disposal of empty containers also contribute significant-
ly to observed residue levels. In the past several years,
endrin utilization has been increasingly restricted, and
production has continued to decline.  In 1978, endrin produc-
tion was approximately 400,000 Ibs  (U.S. EPA, 1978).
     Wild and domestic mammals are exposed to endrin primar-
ily through ingestion of treated foliage, although dermal
contact and inhalation also occur.  Endrin shows little
tendency to accumulate in tissues other than adipose tissue;
levels of up to 23.7 ^ag/g have been detected both in internal
and external fat of a variety of species following ingestion

                              C-l

-------
of endrin-contaminated feed (Long, et al. 1961).
     Metabolism of endrin has been studied extensively in
rats. Endrin is readily metabolized in the liver and excreted
as hydrophilic metabolites. However, certain toxic metabo-
lites such as 12-ketoendrin (also known as 9-ketoendrin)
can be retained for longer periods of time.  Rats excrete
endrin and its metabolites primarily in the feces; in rabbits,
excretion is primarily via the urine.
     Endrin is highly toxic to all animals regardless of
the route of exposure (Treon, et al. 1955). The primary
toxic effect of acute exposure is on the central nervous
system. When lethal concentrations are administered to experi-
mental animals, convulsions may occur as soon as 30 minutes
after exposure, and may culminate in death through respira-
tory failure in about 48 hours.  The dose lethal to 50 percent
of the experimental animals ranges from 3 mg/kg for the
monkey to 50 mg/kg for the goat.
     Many cases of mammalian fatalities have been reported
outside the laboratory. For example, field application of
endrin at rates of 0.55 to 2.75 kg/ha resulted in the death
of 33 to 100 percent of various species of wild mice inhabit-
ing the target area  (Dana and Shaw, 1958).
     The chronic toxicity of endrin to mammals is greater
than that of other organochlorine pesticides.  Sublethal
effects in wild animals manifest primarily as behavioral
and reproductive disorders, i.e., improper maternal care,
temporary loss of normal activity, increased vulnerability
to predators, reduced reproductive potential, increased
post-natal mortality and fetal death.  Chronic exposure

                               C-2

-------
to endrin may also be fatal.  Five to eight mg/kg in the
diet was fatal to dogs in 18 to 44 days.  Twelve mg/kg in
the diet for life decreased the survival time for mice.
Deer mice succumbed to a diet which contained only 2 mg/kg
endrin.
     No malignancies attributable to endrin exposure have
been reported in the literature; however, endrin has been
found to cause chromosomal aberrations in rats following
intratesticular injection. Teratogenesis, growth retardation
and increases in fetal mortality have been observed in mice
and hamsters following endrin administration.
     Human exposure to endrin occurs through the diet, from
inhalation, and through dermal contact.  The average dietary
intake in the United States in 1973 was 0.033 jag/day  (0.0005
yg/kg/day) for a 69.1 kg man.  This is far below the maximum
daily intake of 138.2 jig/day (2 ug/kg/day) established by
the World Health Organization.  Respiratory and/or dermal
exposure to endrin occur during manufacture and distribution
but are more likely to result from agricultural uses.
     Outbreaks of human poisoning have resulted from acci-
dental contamination of foods and have been traced to doses
as low as 0.2 mg/kg body weight.  Endrin toxicity seems
to result primarily from the effects of endrin and its metabo-
lites on the central nervous system.  Symptoms usually observ-
ed in victims of endrin poisoning were convulsions, vomiting,
abdominal pain, nausea, dizziness, and headache. Respiratory
failure was the most common cause of death.  Significantly
increased activity of the hepatic microsomal drug-metaboliz-
                              C-3

-------
ing enzymes has occurred  in  individuals employed  in  the
manufacture of endrin. No irreversible adverse effects of
occupational exposure  to  endrin have been reported in the
literature so far.
     Food contamination by endrin still occurs, but  to a
constantly decreasing  extent.  At present, levels are approxi-
mately 4,000 times lower  than those acceptable to the World
Health Organization. Background concentrations in the atmos-
phere, hydrosphere, and lithosphere, far removed  from agricul-
tural areas where endrin  is  used and industrialized  areas
where endrin is manufactured, are generally below the levels
of detection.
     The adverse effects  of  endrin on fish and wildlife
inevitably spread to man.  The most direct consequence of
endrin applied to the  environment is contamination of the
human food supply. Humans ingest endrin-treated agricultural
produce as well as meat from domesticated and wild animals
and fish which feed on contaminated vegetation.   Ingestion
of 20 mg endrin per day by cows resulted in levels of up
to 0.25 pg/g of endrin in milk. Aquatic invertebrates and
fish bioconcentrate considerable quantities of endrin from
water and pass it on to predatory birds.  This contaminated
fowl  (or the fish themselves) may, in turn, be ingested
by humans.
     In animals, chronic  exposure to endrin may result in
damage to the liver, kidneys, heart, brain, lung, adrenal
glands, and spleen. Effects  secondary to central  nervous
system disorders have  also been observed following chronic
                             C-4

-------
exposure of mammals to sublethal doses of endrin.  These
include behavioral abnormalities, changes in carbohydrate
metabolism, and changes in the composition of the blood.
Although no malignancies attributable to endrin have been
reported, chromosomal abnormalities and teratogenesis have
been induced by endrin in several mammalian species.
                             C-5

-------
                           EXPOSURE
Ingestion from Water
     Occasionally, groundwater may contain more than  0.1 ug/1
of endrin, but levels as high as 3 ug/1 have been correlated
with precipitation and run-off following endrin applications
(U.S. EPA, 1978). Drinking water from Franklin, Louisiana,
an area of high endrin usage, was found to contain a  maximum
of 23 ng/1 (Laner, et al. 1966).
     In a study conducted between March 1964 and June 1967,
more than 500 grab samples of finished drinking water and
corresponding raw water were collected from ten selected
municipal water treatment plants whose source was either
the Mississippi or the Missouri Rivers.  Of the 458 finished
water samples assayed, 156  (34 percent), contained detec-
table concentrations of endrin.  However, the number  of
finished water samples containing concentrations of endrin
in excess of 0.1 ug/1 decreased from 23  (ten percent), in
the period 1964-1965, to zero, in the period 1966-1967  (Schafer,
et al. 1969).
     The most recent study of endrin contamination of drink-
ing water was conducted by the U.S. Environmental Protection
Agency  (1974). Endrin was detected in the finished water
from the Carrollton Water Plant in New Orleans, Louisiana.
The highest concentration measured from all samples was
only 4 ng/1.
Ingestion from Foods
     The general population has little exposure to endrin
in the diet.  In a series of analyses of total diets  deter-
                             C-6

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mined from "market basket" samples in five regions of  the
United States, the total average intake from food ranged
from approximately 0.009 jug/kg body weight per day in  1965
to 0.0005 ^ig/kg body weight per day in 1970  (Table 1)  (Duggan   >
and Lipscomb, 1969; Duggan and Corneliussen, 1972). The
six year average intake was 0.005 jug/kg body weight per
day.  A market basket consisted of 117 food  items grouped
into 12 composites required for the 14-day diet for a  16-
to 19-year-old male.  All foods were treated normally  before
analysis, i.e., meats were cooked, etc.  The average daily
intake remained at trace levels throughout the period  1965-
1970; however, the frequency of occurrence decreased somewhat
(Table 1).  The breakdown of endrin levels by food class
is given in Table 2.
     Processing of some foods before human consumption signif-
icantly changed endrin residues.  Endrin increased in  soy-
bean oils (0.28 ppm) relative to whole crop  levels  (0.07
ppm) by the extraction process  (Hill, 1970;  USDA Plant Pest
Control Division, 1968). Storage above 12 weeks decreased
endrin residues in Irish and sweet potatoes  by 20 percent
(Solar, et al. 1971). Heat processing and freezing further
lowered potato residues 65 and 52 percent, respectively.
Studies on turnips  (Wheeler, et al. 1969) and carrots  (Hermanson,
et al. 1970)  identified 50 to 80 percent of  the endrin in
the peels.
     Endrin disappearance from growing and harvested crop
is so variable that "half-life" data for endrin persistence
on food plants should be viewed with skepticism  (Hill  1970).
                             C-7

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                                TABLE 1

              Average Incidence and Daily Intake of Endrin
                     (Duggan and Corneliussen, 1972)
Year
Percent positive
   composites
Daily intake.
   (mg)
mg/kg/body wt/day
1965
1966
1967
1968
1969
1970
2.8
2.0
1.7
1.1
3.3
1.4
Ta
T
T
0.001
T
T
0.000009
0.000004
0.000004
0.00001
0.000004
0.0000005
aT = Trace, 0.001 mg
                            C-8

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                                     TABLE 2

            Calculated Daily. Intake of Endrin by Food Class  (mg/day)
                         (Duggan and Corneliussen, 1972)
      Meat, fish,           Leafy
Year and poultry Potatoes vegetables
  Root     Garden
vegetables fruit
Oils, fats,
shortening

1965
1966
1967
1968
1969 T
1970 	
K
Tb
T
T
T
T
T

T 	 	
	 T T
T T 	
	 _ 	 	
	 	 T
T T

	
T
	
0.001
	
— — —
 No detectable levels were found in dairy products, grains and  cereals,
 legume vegetables, fruits, sugars and adjuncts, or beverages.

3T=Trace, <0.001 mg/day
                                   C-9

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The loss of endrin depends on the sum of many factors,  includ-
ing temperature, volatilization, metabolism, and dislodgement
by wind and rain.  Since generalizations cannot be made
that endrin on a given crop will always "disappear" at  the
same rate, only residue analyses on harvested crops can
be ascertained as to potential hazard to humans.
     A bioconcentration factor (BCF) relates the concentration
of a chemical in water to the concentration in aquatic organ-
isms, but BCF's are not available for the edible portions
of all four major groups of aquatic organisms consumed  in
the United States.  Since data indicate that the BCF for
lipid-soluble compounds is proportional to percent lipids,
BCF's can be adjusted to edible portions using data on per-
cent lipids and the amounts of various species consumed
by Americans.  A recent survey on fish and shellfish consump-
tion in the United States  (Cordle, et al. 1978) found that
the per capita consumption is 18.7 g/day.  From the data
on the nineteen major species identified in the survey  and
data on the fat content of the edible portion of these  species
(Sidwell, et al. 1974) , the relative consumption of the
four major groups and the weighted average percent lipids
for each group can be calculated:
                          Consumption       Weighted Average
        Group              (Percent)         Percent Lipids
Freshwater  fishes              12                   4.8
Saltwater fishes               61                   2.3
Saltwater molluscs             9                   1.2
Saltwater decapods             18                   1.2
Using the percentages  for  consumption and  lipids  for each
of these groups, the weighted  average percent  lipids is
2.3  for consumed fish  and  shellfish.
                              C-10

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     Measured steady-state bioconcentration factors were
obtained for endrin using six species:
 Organisms
      Percent Adjusted
BCF   Lipids    BCF
                                                    Reference
American oyster,     1,670-2,780   1.5  3,303
Crassostrea virginica
American oyster,         1,000
Crassostrea virginica
Grass shrimp,            1,490
Palaemonetes pugio
Grass shrimp,            1,600
Palaemonetes pugio
Sheepshead minnow,       2,500
Cyprinodon variegatus
Sheepshead minnow,       6,400
Cyprinodon variegatus
Spot,                    1,450
Leiostomus xanthurus
Fathead minnow,         10,000
Pimephales promelas
Fathead minnow,          7,000
Pimephales promelas
Channel catfish,         2,000
Ictalurus punctatus      1,640
                                   1.5  1,533

                                   1.1  3,115

                                   1.1  3,345

                                   5.0  1,150

                                   5.0  2,944

                                   3.1  1,076

                                   8.0  2,875

                                   8.0  2,012

                                   3.2  1,302
                        Mason  & Rowe,
                        1976
                        Wilson, 1966
                        Tyler-Schroeder,
                        In press
                        Tyler-Schroeder,
                        In press
                        Hansen, et  al.
                        1977
                        Hansen, et  al.
                        1977
                        Lowe,  1966
                        Mount  &  Putnicki,
                        1966
                        Jarvinen &  Tyo,
                        1978
                        Argyle,  et  al.
                        1973
Each of these measured BCF's was adjusted  from  the  percent
lipids of the test species to  the  2.3 percent lipids that
is the weighted average for consumed fish  and shellfish.
The geometric mean was obtained for each species, and then
for all species. Thus, the mean bioconcentration  factor  for
endrin and the edible portion  of all aquatic organisms con-
sumed by Americans is calculated to be  1,900.
                              C-ll

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     Because of the dynamic  state of endrin  in  the  biological
tissues of lower animals  (Mount/ et al.   1966),  the bioac-
cumulation is short-lived, and  tissue burdens diminish  rapidly
once the environmental  source is removed.   (Toxic endrin
metabolites, such as 12-ketoendrin, may'persist  for longer
periods of time). Commercial catfish from Arkansas  and  Missis-
sippi were reported to  contain  average  residues  ranging
from 0.01 to 0.41 jag/g.   Four percent of  the samples exceeded
the FDA action level for  maximum permissable endrin concentra-
tion of 0.3 jag/g in the edible  portion  of fish  (Hawthorne,
et al. 1974; Crockett,  et al. 1975).
     Humans may also be exposed to endrin in cow milk and
steer, lamb, and hog meat, however, endrin  is so rapidly
metabolized and excreted  that tissue levels  are  usually
at or below the dietary concentrations  of endrin.   Residue
levels in excess of 0.25  ug/g on a fat  basis were detected
in the milk of 40 Wisconsin  dairy herds between  1964 and
1967  (Moubry, et al. 1968).  Endrin was  presumably retained
in the milk fat for up  to four  weeks.   However,  the quanti-
ties of endrin ingested during  that period were  not control-
led.  Williams and Mills  (1964) studied the  appearance  of
endrin in cow's milk under controlled feeding conditions.
Endrin .concentrations in  the milk increased  progressively
during the first few days of feeding until  they  plateaued
at 13 to 15 days. When  ingestion of endrin ceased,  residues
in milk declined sharply  and following  20 days  on an endrin-
free diet, detectable  (greater  than 0.001 /ig/g)  levels  were
present only in milk samples from cows  fed  the  highest  levels
of endrin  (0.3 mg/kg).  Endrin  is apparently excreted in

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milk in higher concentrations when fed as a residue  on  hay
than when fed dissolved in soybean oil  (Ely, et  al.  1957).
However, in general, a total daily endrin intake of  greater
than 20 mg as a residue sprayed in forage is necessary  for
excretion of measurable quantities of endrin in  milk.   In
another study (Saha, 1969), the ratio of residue in  milk
to feed was 0.07.
     Studies by Brooks (1969) demonstrated that  steers,
lambs, and hogs receiving 0.1 mg/kg endrin in  the diet  for
12 weeks showed little tendency to deposit endrin in body
tissues.  Continuous feeding of up to 2 mg/kg  resulted  in
a maximum body fat content of 1 pg/g.  Long, et  al.  (1961)
reported high levels of storage (23.7 /ig/g) in the adipose
tissue of lambs. Higher levels were detected in  the  internal
fat surrounding the stomach and thoracic cavity  than in
external fat deposits.  After the lambs were transferred
to untreated pasture, endrin levels in fat decreased somewhat,
but levels of approximately 6.4 to 13.8 >ig/g were still
retained in fat.  Pigs receiving 510 mg endrin over  30  days
had fat endrin levels of no more than 2 /ig/g,  and no endrin
was detected in any other tissue (Brooks, 1974).
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Inhalation
     Agricultural workers, home gardeners, and those  involved
in manufacture or distribution of endrin might thus become
exposed through inhalation.  Respiratory exposure during
periods of orchard spraying may generally be expected to
reach 0.01 mg/hour (Wolfe, et al. 1963; Wolfe, et al.  1967).
     Wolfe, et al. (1963) reported that spraying of potatoes
with a one percent solution of endrin dust produced levels
of 0.41 mg/hour for respiratory exposure. During the  spraying
of raw crops the respiratory exposure rate was below  the
limits of detection of the analytical method employed (Jegier,
1964).
     Another possible means of inhalation exposure to endrin
is from the residues on  tobacco plants used for smoking.
Bowery, et al.  (1959) found that tobacco retained an  average
of 0.2 pg of endrin per  commercial cigarettes. Forty  percent
of the residual endrin disappears during the curing process,
but the remainder persists throughout the cigarette manufac-
turing process.  Endrin  residues in pipe tobacco increased
approximately three-fold from 1969  (0.05 /ag/g) to 1971 (0.114
 /ag/g). Residues of endrin in cigars remained at approximately
0.06 pg/g from 1969 to 1972.  Endrin residues in cigarettes
decreased from 0.18 /ig/g to 0.09 yug/g from 1969 to 1971
(Bowery, et al. 1959; Domanski and Guthrie, 1974).
     According to data compiled by the U.S. Environmental
Protection Agency, exposure of the general populace to endrin
via the air decreased from a maximum level in 1971 at Greeley,
Colorado, of 25.6 /ug/m   to a maximum in 1975 of 0.5/ig/m
at Jackson, Mississippi. None of the monitoring data  contain-
ed endrin levels consistently near the threshold limit value
                              C-14

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of 100 jag/m  suggested by the American Conference of Govern-
mental Industrial Hygienists for 1971.
Dermal
     The most significant occupational dermal exposure  to
endrin occurs during field applications. During dusting
or spray-machine operations, dermal exposure is almost  always
greater than respiratory exposure. Dermal exposure during
orchard spraying is likely to range up to 3 mg/body/hour,
for workers wearing standard protective clothing in which
       2
3.15 ft  of the body is exposed. Potentially, and probably,
the greatest hazard associated with the use of endrin,  however,
occurs during measuring and pouring the emulsifiable concen-
trate solution  (Wolfe, et al. 1963, 1967).
     Of the situations tested, higher levels of exposure
occurred during dusting of potatoes with a one percent  endrin
dust. Levels of up to 18.5 mg/hour for dermal exposure  were
found (Wolfe, et al. 1963) . During the application of endrin
to row crops, a dermal exposure of 0.15 mg/hour was noted
(Jegier, 1964).
                       PHARMACOKINETICS
Absorption
     Endrin is known to be absorbed through the skin, the
membraneous areas of the lungs, and through the lining  of
the gut, however, the literature reveals no data on the
rates of absorption.
Distribution
     Humans do not tend to store endrin in significant  quanti-
ties.  No residues were detected in plasma, adipose tissue,
or urine of workers occupationally exposed to endrin  (Hayes
                              C-15

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and Curley,  1968). Measurable  levels  of  endrin  have  not
been detected  in  human  subcutaneous fat  or  blood,  even in
those areas  where it  is used extensively,  such  as  India
or the lower Mississippi delta area  (Brooks,  1974).  Despite
its high acute toxicity, endrin is a  relatively nonpersistent
pesticide  in humans.  Endrin residues  have  only  been  detected
in the body  tissues of  humans  immediately  after an acute
exposure.  However, little is known concerning the  persistence
and toxicity of endrin  metabolites.
     As a  result  of acute endrin poisoning, high levels
of endrin  have been observed in both  blood and  urine but
no endrin  has  been detected in cerebral  spinal  fluid accord-
ing to Cobel,  et  al.  (1967). Endrin-poisoned  humans  have
been reported  as  having an endrin content  as  high  as 400
jug/9 in fat  tissue and  10 pg/g in other  tissues (Coble,
et al.  1967).  However, the 400 /ig/g  value was  obtained
using a bioassay  technique presently  regarded as unreliable
(Curley, et  al. 1970).   The 10 pg/g value  was determined
from a patient who died from repeated exposures to endrin.
Much lower values of  endrin were obtained  from  an  autopsy
of body tissues of victims poisoned by eating endrin-contamin-
ated bread in  Saudi-Arabia (Table 3).  Blood and urine samples
taken from patients 29  to 31 days after  the outbreak were
uniformly  negative for  endrin  (Curley, et  al. 1970). Low
blood levels were detected in  three humans who  recovered
after accidental  ingestion of  endrin.  In one  case, the concen-
tration of endrin in  the blood 30 minutes  after convulsions
occurred was 0.053 jug/g and 20 hours  past  convulsions it
was recorded at 0.038 jug/g. This same patient excreted 0.02
                              C-16

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                      TABLE 3
       Endrin  Concentrations Found in Victims
        of  Endrin Poisoning in Saudi Arabia.
               (Curley, et al. 1970)
Sample                  Endrin concentrations  (;ug/l)

Blood                         0.007-0.032
Urine                         0.004-0.007
Vomitas                       5.24
Tissues (autopsy) from:
     Stomach                  0.16
     Liver                    0.685
     Kidney                   0.116
                   017

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/!g/9  endrin  via the urine during the following 24 hours
 (Coble,  et al.  1967).
      Richardson,  et al. (1967)  fed endrin to nine-month
 old dogs for 128  consecutive days at a level of 0.1 mg/kg
 body  weight  per day.   Blood concentrations during the experi-
 ment  ranged  from 0.002 to 0./008 jug/g.  At the termination
 of the  experiment,  concentrations in the adipose tissue
 ranged  from  0.3 to 0.8 jug/g; heart, pancreas and muscle
 were  at  the  lower end  of this range, while the concentration
 in the  hepatic  tissues was 0.077 to 0.085 pg/g. The kidneys
 and lungs had similar  concentrations.
      The amounts  of endrin detected from the tissues of
 dogs  that survived after being  fed for approximately six
 months  on diets containing endrin in concentrations of 4
 to 8  mg/kg were as follows: 1 /ag/g in the fat; 1 jig/g in
 the liver; and  0.5 pg/g in the  kidneys (Treon, et al. 1955).
 Metabolism
      Endrin  is  metabolized and  excreted more rapidly than
 other chlorinated hydrocarbon insecticides (Jager, 1970).
 There is good evidence that endrin is quickly metabolized
 in mammals  (probably in the liver) and excreted as a hydro-
 philic  metabolite.
      In vitro studies  appear to support the hepatic metabo-
 lism  of  endrin. A metabolite behaving as a mono-hydroxy
 derivative was  produced when endrin was incubated at 30°C
 for several  hours with both rat liver and pig liver microso-
 mes and NADPH  (Brooks, 1969). Formation of the derivative
 was suppressed  by sesamex, an inhibitor of microsomal oxi-
 dations.
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     Information regarding the metabolic fate of endrin
in vivo is conflicting. Baldwin, et al.  (1970) found that
endrin is metabolized in the rat to at least three metabo-
lites.  One is 9-ketoendrin, which is found in the urine.
The other two metabolites are excreted in the feces and
have not been found in body tissues. The acute oral LD50
of ketoendrin to rats (62 mg/kg) is higher than that of
endrin (25 mg/kg), and the rearrangement would appear to
be a detoxication reaction (Brooks, 1969). Oxidation without
skeletal rearrangement has been indicated to preponderate
in mammals although details remain to be worked out  (Brooks,
1974).
     However, Bedford, et al. (1975) studied LDeg values
based on ten day mortalities for endrin and three of its
mammalian metabolites (anti-12-hydroxyendrin, syn-12-hydroxy-
endrin, and 12-ketoendrin) in rats. The metabolites were
all more toxic than the parent compound LDcn values. Rapidity
of intoxication, sex differences, and analysis of the brains
of rats dosed with the various compounds indicated that
12-ketoendrin may be the acute toxicant in each case. Thus,
the oxidative metabolism of endrin may be responsible for
its acute toxicity.
     Jager (1970) found, in feeding experiments with rats,
that females metabolize endrin more slowly than males. When
carbon-14 labeled endrin was fed to male and female rats,
the males excreted 60 percent of it in the feces within
the first 24 hours and the females only 39 percent. Less
than one percent was excreted in the urine.  Of the total
                             C-19

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radioactivity excreted  in  the  feces,  70 to 75 percent occur-
red in the form of hydrophilic metabolites; the remainder
was in unchanged endrin. Twenty-four  hours after  the last
dose, only hydrophilic  metabolites were excreted.
     Sex differences  in the rate of endrin metabolism in
rats were also found  by Hutson, et alo  (1975). Although
the major metabolite  in both sexes was anti-12-hydroxyendrin,
excreted via the bile as the glucuronide, male rats produced
the metabolite at a higher rate than  did females.  A minor
metabolite was trans-4,5-dihydroisodrin-4,5-diol.  There
was a sex difference  in the production and excretion of
12-ketoendrin, which  was observed as  a urinary metabolite
in male rats.  The major urinary metabolite in female rats
was anti-12-hydroxyendrin-o-sulfate.  These authors also
found the formation of  12-ketoendrin  to be directly related
to the acute toxicity of endrin.
Excretion
     At high dosage levels, excretion of endrin appears
to be slower. Body content of  endrin  declines fairly rapidly
after a single dose or  when a  continuous feeding  experiment
is terminated.  When  the exposure to  endrin ceases, the
concentration in the  tissues diminishes rapidly  (Brooks,
1969) .
     Endrin  is primarily excreted with the feces, much of
it by way of the bile.  The liver has  been  identified as
the major excretory organ  for  endrin  in the rat.  The amount
of radioactivity in the feces  of the  rat,  from intravenously
administered carbon-14  labeled endrin, reflects the amount
of radioactivity entering  the  gastrointestinal tract via
                             C-20

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the bile (Cole, et al. 1968).
     The major metabolite in both male and female rats was
anti-12-hydroxyendrin, which was excreted via the bile as
the glucuronide (Hutson, et al. 1975), trans-4,5-dihydroiso-
drin-4,5-diol was a minor biliary metabolite. 12-ketoendrin
was observed as the primary urinary metabolite in the male
rat; the major urinary metabolite in female rats was anti-
12-hydroxyendrin-o-sulfate. Syn-12-hydroxyendrin was not
detected.
     Cole,  et al. (1968) also studied rates of excretion
of radio carbon-labeled endrih in whole rats, bile-fistulated
rats, and isolated perfused rat livers. Over 90 percent
of the excreted radioactivity was found in the feces of
the intact animals and in the bile of the fistulated animals.
Fifty percent of the radioactive endrin was excreted within
the first 24 hours. In the fistulated animals, 50 percent
of the endrin radioactivity was excreted in the bile in
approximately one hour in the perfused experiments  (Cole,
et al. 1968).
     With the exception of endosulfan, endrin is the least
persistent of any of the chlorinated hydrocarbon pesticides
in mammals. It is rapidly metabolized and eliminated from
vertebrate tissues. Excretion occurs through the milk as
well as through the urine and the feces (Brooks, 1974).
Endrin metabolites, one of which is known to be several
times more toxic than endrin itself, may persist for longer
periods of time.
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                           EFFECTS
Acute, Sub-acute/ and Chronic Toxicity
     Endrin is classified as "very highly hazardous", meaning
that any contact with very small amounts of the substance
may result in severe systemic toxicity or death  (Thompson,
1971). Endrin is the most acutely toxic of the cyclodiene
insecticides and yet, except for endosulfan,  is least persis-
tent in mammals  (Brooks, 1974). Endrin toxicity can be elicited
from any route of exposure.  When ingested in one dose by
rats, endrin is about three times as toxic as aldrin and
about 15 times as toxic as DDT  (Treon, et al. 1955).  Upon
intravenous administration to mice, endrin was five times
as toxic as dieldrin  (Walsh and Fink, 1972).
     The onset of endrin toxicity symptoms is rapid. The
return to normal among those who survive is also rapid.
The recovery from endrin intoxication is faster than from
other cyclodiene pesticides  (Brooks, 1974).
     Symptoms of acute endrin poisoning in mammals clearly
indicate that endrin  is a neurotoxicant. The  first indica-
tion of acute endrin poisoning  is usually central nervous
system excitation as evidenced  by hypersensitivity to external
stimuli associated  with generalized tremors and followed
by severe tonic-clonic convulsions  (Brooks, 1974). These
convulsions may  occur as early  as 30 minutes  after acute
endrin exposure  (Brooks, 1974).  Convulsions  can culminate
in death from respiratory failure  (Brooks, 1974). In the
range of the acute  oral LD    (17 to 43 mg/kg), death of
rats may result  after 48 hours  (Boyd and Stefec, 1969).
                              C-22

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     Other symptoms of acute endrin poisoning include brady-
cardia (slowed heartbeat),  increase in blood pressure, saliva-
tion, and body temperature, leukocytosis (increase in number
of white blood cells), increased hemoconcentration, decreased
blood pH, increased cerebrospinal fluid pressure and cerebral
venous pressure, increased  renal vascular resistance with
decreased renal blood flow  and glomerular filtration rate,
decrease in catecholamine concentration of the adrenals,
and increased levels of circulating epinephrine and norepine-
phrine (Emerson, et al. 1964; Reins, et al.  1966). Pathologi-
cal observations of rats from autopsy reveal signs of a
stress reaction, degenerative changes in kidneys,  liver
and brain capillaries and venous congestion, and loss of
weight and dehydration of some organs (Boyd and Stefec,
1969) .
     The symptoms in man include headache, dizziness, abdomi-
nal disturbances, nausea, vomiting, mental confusion, muscle
twitching, and epileptiform convulsions which may  occur
suddenly and without prior  warning  (Brooks, 1974).
     Mammalian susceptibility to endrin toxicity varies
greatly with age, sex, and species as shown in Table 4.
The LD5Q values range from 1.37 to 43 mg/kg.  Apparently,
mice and monkeys are most sensitive, and guinea pigs are
more resistant. Rabbits seem to be somewhat more resistant
than monkeys to a single dose of endrin.  The acute toxicity
of endrin is, however, high for all these species.
                             C-23

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                      TABLE 4
      Acute  Oral Toxicity of Endrin to Mammals

     Animal  (age, sex)   LD
     Mouse                    1.37a
     Rats (6 months, M)         43b
     Rats (6 months, F)          7
     Rats (30 days, M)          30b
     Rats (30 days, F)          17
     Rat                         3a
     Rabbits (F)              7-10b
     Hamster                    10a
     Guinea pigs  (F)            16
     Guinea pigs  (M)            36
     Monkey                      3
aNIOSH, 1977
bTreon, et al. 1955
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     In rats and guinea pigs, females are more susceptible
than males.  The greater susceptibility of female rats six
months of age, than that of younger female rats is the reverse
of the more normal relationship between age and suscepti-
bility found in males..
     When endrin was maintained in contact, as a dry 100-
mesh, powder, with either intact or abraded skin of female
rabbits for 24 hours, the minimum lethal dosage was found
to be greater than 60 and less than 94 mg/kg. Poisoned ani-
mals had convulsions, but neither gross nor microscopic
evidence of damage to the skin was found. Degeneration of
the cells in the central zones of the lobules of the livers
of rabbits was observed  (Treon, et al. 1955).
     Graves and Bradley  (1965) determined an LDcn of 5.6
mg/kg for endrin injected into the peritoneal cavity of
Swiss albino mice. An intravenous LDcg of 2.3 mg/kg was
determined by Walsh and Fink  (1972) for adult male mice.
Endrin injected into dogs intravenously at a dosage of 3
mg/kg resulted in death in approximately 75 percent of the
animals (Hinshaw, et al. 1966).
     Target organs found in acute experiments are not always
the same as those following repeated exposure over long
periods of time. The central nervous system is the target
of acute endrin poisoning. When an animal is repeatedly
exposed to low doses (0.8 to 3.5 mg/kg/day) of endrin, it
can often make compensatory adjustments to cope with the
initial nervous system injury until damage to liver or other
organs intervenes. However, Chernoff, et al. (1979) found
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that the threshold level for convulsions in hamsters was
10 mg endrin/kg body weight. This convulsive dose was approxi-
mately twice that  required for the production of teratogenic
effects.
     After exposure of rats, rabbits, guinea pigs, cats,
dogs, and monkeys to varying doses, routes, and frequencies
of administration, diffuse degenerative changes were observed
in the livers, kidneys, and brains of all fatally poisoned
animals. Tissue alterations were also observed in some of
the surviving animals  (Treon, et al. 1955). Rabbits subjected
to multiple dermal applications (20 to 44 mg/kg) exhibited
severe fatty degeneration of the liver (Treon, et al. 1955).
A series of 50 oral doses of 1 to 5 mg/kg/day in a rabbit
caused diffuse degeneration and fatty vacuolization of the
hepatic and renal cells and degeneration of heart tissue.
Rabbits that survived  118 periods of inhalation of 0.36
ppm endrin developed a granulomatous type of pneumonitis
(Treon, et al. 1955).
     Revin (1968) found that chronic administration of endrin
can lead to convulsions. He administered endrin to squirrel
monkeys at a minimum rate of 0.2 mg/kg/day, which caused
a characteristic change in the electroencephalogram  (EEC)
from relatively small  doses — 0.5 to 1.0 mg/kg. At total
doses of 5 to 10 mg/kg, electrographic seizures develop-
ed.  Endrin administration was stopped after seizures, but
after three weeks, EEC's and behavior were still abnormal.
Recurrence of seizures, under stress conditions, months
after termination of endrin administration demonstrated
that even small amounts of endrin stored in the body after
                             C-26

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exposure cannot be regarded as toxicologically inert. Endrin,
mobilized by stress, may cause toxic responses in  the brain.
If concentrations in the fat of these monkeys  (approximately
25 jug/g after four months)  were sufficient to cause  seizures,
the same stress to an animal storing 2.5 jug/g may  induce
EEC and, possibly, behavioral changes  (Revin, 1968).
     The chronic toxicity of endrin is greater than  that
of other organochlorine pesticides. In prolonged feeding
experiments, rats can consume diets containing approximately
three times as much aldrin and 12 times as much DDT  as  endrin
without increase in relative weights of specific organs.
Dogs are at least 10 times as susceptible to the toxic  effects
of endrin as to those of DDT  (Treon, et al. 1955).   Species
and sex differences exist in susceptibility to chronic  endrin
toxicity. Females are generally more susceptible than males.
Rabbits and dogs are more susceptible  than rats  (Treon,
et al. 1955).
     Mammalian species appear to be sensitive to the toxic
effects of endrin at low levels in their diet. Significant
mortality during a seven month period  appeared in  deer  mice
when fed 2 mg/kg endrin in the diet (Morris, 1968).  The
deer mice exhibited symptoms of hypertension, uncoordination,
muscle tremors, and convulsions which  increased in intensity
until death occurred.
     Endrin fed throughout the life to Osborne-Mendel rats
at 12 mg/kg in the diet decreased viability. Mean  survival
time fell from 19.7 months to 17.6 months for males  and
from 19.5 months to 18.2 months for females. The endrin-
fed rats experienced moderate increases in incidence of
                                027

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congestion and focal hemorrhages of  the lung;  slight  enlarge-
ment, congestion and mottling of the liver;  slight  enlarge-
ment, discoloration or congestion of the kidneys  (Deichmann,
et al. 1970).
     Dogs can tolerate only about half as much endrin in
their diet as rats. Dogs, which died when fed  toxic concentra-
tions (5 mg/kg or more) of endrin for 18 to  44 days,  regurgi-
tated their food, became  lethargic,  salivated, and  subsequent-
ly refused to eat. These  dogs became emaciated and  developed
respiratory distress and  signs of irritation of the central
nervous system. Dogs fed  a diet containing endrin  (8  mg/kg
for six weeks) exhibited  enlargement of the  liver,  kidneys,
and brain and reduction in the deposition of free peritoneal
             i
and omental fat. After 19 months on  diets containing  3 mg/kg
endrin, dogs had significantly enlarged kidneys and hearts
(Treon, et al. 1955).
     Fatally poisoned dogs exhibited diffuse degenerative
lesions in the brain, heart, liver,  and kidneys, plus pulmon-
ary hyperemia and edema.  Severe renal damage was apparent
characterized by diffuse  degeneration and necrosis  of the
convoluted tubules.  The  liver had diffuse degeneration
and fatty vacuolization and, in some cases,  necrosis  of
the liver cells  (Treon, et al. 1955).
                                C-28

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Synergism and/or Antagonism
     The acute oral toxicity (LD,-Q) of equitoxic doses of
combinations of 15 pesticides was examined by Keplinger
and Deichmann (1967).  The results are presented in Table
5. Endrin plus diazinon, endrin plus toxaphene, and endrin
plus malathion showed additive effects; while endrin plus
parathion, endrin plus ODT and, particularly, endrin plus
delnav showed lower than expected LDj-g's, suggestive of antago-
nistic effects.  Joint administration of endrin and its
closely related compound aldrin showed a more than additive
effect, and endrin plus chlordane was found to exert a poten-
tating effect.

                           TABLE 5
         Expected and observed oral LD^Q'S of Endrin
                plus  other  Pesticides  rn  Mice.
                (Keplinger and Deichmann, 1967)
Other
Pesticides
Chlordane
Aldrin
Dieldrin
Diazinon
Malathion
Toxaphene
Parathion
DDT
Delnav
Expected
LD50
(mg/*g)
473
63
63
93
703
63
12
213
87
Observed
LD50
(mg/fcS)
211
34
50
93
820
77
18
400
195
Ratio
E/0
2.22
1.83
1.25
1.00
0.85
0.81
0.65
0.53
0.44
     No other information is available on synergistic and/or
antagonistic effects of endrin.
                             C-29

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Teratogenicity
     Rats and mice were given 0.58 mg endrin/kg body weight
four times weekly for a month, and then after a week or more
without endrin treatment, the animals were allowed to become
pregnant  (Nodu, e't al. 1972) . A reduced survival rate was
found in both species.  Nine mouse fetuses with club foot
were found in the treated group of 177, while only one fetus
with club foot was in the control group of 303.
     Endrin exerted embryocidal and teratogenic effects
on pregnant hamsters. Both soft and skeletal tissue malforma-
tions were produced. Single  oral doses of endrin  (5 mg/kg)
administered to pregnant Syrian golden hamsters on day seven,
eight, or nine of gestation  caused a high incidence of fetal
death, congenital abnormalities and growth retardation.
Thirty-two percent of the implantations resulted  in fetal
mortalities.  Teratogenic effects were observed in 28 percent
of the fetuses from hamsters treated on day eight. Open
eye occurred in 22 percent,  webbed foot in 16 percent, cleft
palate in 5 percent, cleft lip in 1 percent, and  fused
ribs in 8 percent  (Ottolenghi, et al. 1974).
     Ottolenghi, et al.  (1974) also found endrin  to be terato-
genic in mice, but frequency and gravity of the defects
produced were less pronounced than in the hamsters when
a single dose  (2.5 mg/kg in  mice and 5 mg/kg in hamsters)
of half the LDcQ was administered. Abnormalities  in the
mice included open eye and cleft palate.
     Golden hamsters, intubated with endrin  (0.75 and 1.5
mg/kg) on days 5 to 14 of gestation had less reactive loco-
motor activity than controls during gestation but not at
                              C-30

-------
weaning (Gray, et al. 1979).  The offspring of these dams
were tested in open field at 15, 20, 27, 34, and 44 days
of age.  Fifteen-day-old pups at the 1.5 mg/kg dose were
approximately 90 percent more active than controls but this
difference disappeared by day 34. Prenatal endrin exposure
appeared to have behavioral effects in hamsters and their
offspring.
     Chernoff, et al. (1979)  found that a single dose of
endrin administered on pregnancy, day eight, produced meningoen-
cephaloceles at doses above 1.5 mg/kg and fused ribs at
doses above 5.0 mg/kg. Open eyes, cleft palates, and webbed
feet were not noted. It was suggested that a teratogenic
level of endrin in humans could be lower than the levels
estimated to cause human convulsions since the conclusive
dose in hamsters was approximately twice that required for
the induction of terata.
Mutagenicity
     Endrin, as well as aldrin and dieldrin, can cause chromo-
some damage (Grant, 1973). Symptoms of cellular degeneration
have been observed in germinal tissue of male albino rats
treated with 0.25 mg endrin administered intratesticularly
(Dikshith and Datta, 1972). The most conspicuous effects
were chromosomal aberrations, including stickiness, bizarre
configurations, formation of chromosome fragments, and abnor-
mal restitution of chromosomes.  Formation of single and
double bridges with acentric fragments was very common,
disturbing the normal disjunction of chromosomes and even-
tually affecting the chromosome complements of the division

                              C-31

-------
products  (Dikshith and Datta, 1973).  Unequal distribution
of chromosomes at anaphase was also observed. Severe cell
damage resulted in liquefication and transformation of the
chromatin mass into an amorphous lump  (Dikshith and Datta,
1972) . These were the only instances reported of mutagenicity
related to endrin.
     However, chlorinated cyclopentadienes, such as endrin,
were suggested to undergo metabolic conversion forming acylat-
ing and possibly mutagenic tetrachlorocyclopentadienone.
Using mouse liver microsomes for metabolic activation and
!_.. coli K12 (343/113) to detect mutagenicity, tetrachlorocyclo-
pentadiene and pentachlorocyclopentadiene were highly muta-
genic after metabolic activation, wheras hexachlorocylcopenta-
diene was not  (Goggelman, et al. 1978).
Carcinogenicity
     No malignancies attributed to endrin exposure have
been reported. Endrin fed to weanling Osborne-Mendel rats
for a lifetime at dietary levels of 2, 6, or 12 mg/kg was
neither tumorigenic nor carcinogenic  (Deichmann, et al.
1970; Deichmann and MacDonald, 1971; Deichmann, 1972).
     A recently completed National Cancer Institute bioassay
for possible endrin carcinogenicity concluded that endrin
was not carcinogenic for Osborne-Mendel rats or for B6C3F1
mice (U.S. Dept. Health, Education, and Welfare, 1979).
                              C-32

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                           CRITERION FORMULATION


Existing Guidelines and Standards


     In 1965, maximum permissable levels were assigned to each of the


organochlorine compounds based on the "maximum acceptable concentrations"


suggested on July 9, 1965, by the subcommittee on Toxicology to the Public


Health Service Advisory Committee on Drinking Water Standards (Schafer,  et


al. 1969).  This concentration for endrin was 0.001 ppn.  In 1967, the


"maximum reasonable stream allowance" for endrin of 0.1 ppb was suggested


by Ettinger and Mount (1967) and was accepted as a guideline.


     A maximum acceptable level of 0;002 mg/kg body weight/day was established


by a Joint FAO/WHO Meeting on Pesticide Residues in Food held in Rome,


November, 1972 (FAO, 1973).

                                        B
     A threshold limit value of 100 ug/m  was set for atmospheric levels


of endirn by the American Conference of Governmental Industrial Hygienists


for 1971 (Yobs, et al. 1972).  A threshold limit value of 100 ug/m3 for an


eight hour time-weighted average occupational exposure has also been estab-


lished by the Occupational Safety and Health Administration  (U.S. Code of


Federal Regulations, 1972).


     Toxic pollutant effluent standards (40 CFR Part 129.102) were promulgated


by the U.S.E.P.A.  These allowed an effluent concentration of 1.5 ug/1 per


average working day calculated over a period of one month, not to exceed


7.5 ug/1 in any sample representing one working day's effluent.  In addition,


discharge is not to exceed .0006 kg per 1,000 kg of production.


Current Levels of Exposure


     While no recent data are available on levels of exposure of humans  to


endrin it appears that the risk of exposure is decreasing because of the


decreased usage of the pesticide.,


     In a survey of over 500 drinking water samples, the number of samples con-


taining concentrations of endrin in excess of 0.1 ug/1, which has been estab-


lished as a maximum reasonable stream allowance, decreased from 23 in the period

                                     C-33

-------
1964-1965 to 0 in the period 1966-1967  (Schafer, et al.
1969). The most recent study found only 4 ng/1 in contami-
nated drinking water  (U.S. EPA, 1974).
     In a series of analyses of total diets, the average
daily intake of endrin remained at trace levels  «0.001
mg) during the period 1965-1970, but the frequency of occur-
ance decreased considerably  (Duggan and Lipscomb, 1969;
Duggan and Corneliussen, 1972).
     Exposure of the general populace to endrin  in the air
decreased from a maximum level of 25.6 jug/m  in  1971 at
Greeley, Colorado, to a maximum of 0.5 jjg/m  in  1975 in
Jackson, Mississippi,  (U.S.EPA, 1971).
Special Groups at Risk
     Agricultural workers, home gardeners, and those involved
in endrin manufacture and distribution  are the most likely
to be exposed to endrin.  They may be exposed through inhala-
tion or dermal exposure. The most significant occupational
exposure comes during spraying of fields, and dermal exposure
is almost always greater than  respiratory exposure.  Probably
the greatest hazard associated with the use of endrin occurs
when measuring and pouring the emulsifiable concentrate
material. Because endrin has been shown to cause teratogenic
effects, pregnant women, particularly those whose diets
may contain large amounts of fish, must also be  considered
a  special group at risk. Evidence that  endrin may cause
chromosomal damage in germinal tissue suggests that men
and women of child-bearing intent may also be a  special
risk group.
                              C-34

-------
     Endrin concentrations are highest in the atmospheres
over agricultural areas and probably reach their peak levels
during the pesticide use season.  Of all urban communities,
those surrounded by farm lands run the highest risk of atmos-
pheric contamination.  Endrin absorbed to particulates could
not be detected in the air over representative communities
but may perhaps be present at very low concentrations in
the vapor phase.  Urban communities far removed from agricul-
tural areas are unlikely to experience significant contamina-
tion.  The homes of occupationally exposed workers have
higher levels of atmospheric contamination than do those
of the general populace.
Basis and Derivation of Criterion
     The limited teratogenic and mutagenic studies on endrin
suggest that effects are induced with high endrin doses.
However, an unusual administration route was used in these
studies.  Such levels do not occur in water supplies under
normal circumstances, therefore, the results of these studies
were not used as the basis for the criterion.  More toxico-
logical data must be gathered about these potential effects
of endrin before a final conclusion can be reached.  The
available data do not indicate that endrin is carcinogenic.
     On the basis of long-term dietary studies in mammals
and occupational exposures in man, a realistic drinking
water criterion may be proposed. Maximum no-effect dietary
levels of endrin reported for experimental animals are:
                             C-35

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Species       Dose  level  (Duration)                     Reference
Mouse     1 mg/kg  (lifetime)                       U.S.  EPA.  1973
Rat       1 mg/kg  (2 Years)                        Treon,  et  al. 1955
Rat       1 mg/kg  (established  no-effect  level)    Brooks,  1974
Hamster   1.5 mg/kg (no effect  level)  (one  day)    Chernoff,  et al.
                                                   1979
Dog       0.1 mg/kg (128  days)                     Richardson, et  al.
                                                     1967
Dog       1 mg/kg  (established  no-effect  level)    Brooks,  1974
     Extrapolation of  the  0.1  mg/kg  no-effect  dietary  level
for the dog to man is  reasonable.  Since  experimental studies
of chronic human  ingestion are not available  (but  acute
exposure data are),  and  valid  long-term  animal feeding studies
have been done  in more than one species,  an uncertainty
factor of 100 may be used  in the absence of any indication
of carcinogenicity in  arriving at  a  water criterion. In
deriving a water  quality criterion,  human exposure to  endrin
was assumed to come  from daily ingestion of 2  1 of water
and 18.7 g of fish with  a  bioconcentration factor  of 1900
for endrin. Using a  no-effect  dose level of 0.1 mg/kg, the
total allowable  intake for a 70-kg man  is:
     0.1 mg endrlnA,  x  70  Rg  =
                                         factor)
The criterion  for  endrin is thus:
     x = 70 jug/day               _  ,  R7    ,,       ,  Q
         2/1 I (0.0187 kg x 1900)'  1'87  ^g/1  -~  1'9
                              C-36

-------
     This approximates closely the 1 jug/1 maximum allowable

concentration for endrin proposed by the Public Health Service

for drinking water.  It is therefore, recommended that the

endrin criterion be established at 1 jug endrin/1 of ambient

water  (1 ppb).

     This calculation assumes that 100 percent of man's

exposure is assigned to the ambient water pathway.  Although

it is desirable to establish a criterion based upon total

exposure potential, the data for other exposure conditions

have not been factored into this analysis.

     In summary, based upon the use of toxicologic data

for dogs, and an uncertainty factor of 100, the initial

level for endrin corresponding to daily intake of 70 jug/day,

is Iv9 jug/1.  Since the existing 1 >ug/l allowable concentration

in the drinking water standards is reasonably close to 1.9

jug/1, it is recommended that 1.0 >ug/l be used as the criterion

with notation that there are special groups at risk.   Drinking
 If endrin was present in waters from which edible  fish
were located and if these fish concentrate endrin by  a factor
of 1900, this criterion may not be sufficient to protect
a special high risk group(i.e., pregnant women who  consume
a single dose of endrin contaminated fish) .  Given  the biocon-
centration factor, fish in water at the maximum recommended
concentration of 1 jug/1, may contain 1.9 ;ug/g endrin. A
250/g portion of fish would contain approximately 0.5 mg
endrin.(or 0.01 mg/kg for a 50/kg female).  This dose provides
a margin of safety of only 150 over the NOEL of 1.5 mg/kg
for teratogenicity in the hamster  (Chernoff, et al. 1979).
The adequacy of this margin of safety is highly questionable,
especially given the likelihood of consumption of more than
250/g of fish at a given time. The recommended water  quality
criterion of 1 jug/1 was based on a chronic exposure study,
teratologic outcomes are more likely to occur with  acute
exposures at critical times in gestation.
                               C-37

-------
water contributes five percent of the assumed exposure while



eating contaminated fish products accounts for 95 percent.



     The criterion level for endrin can alternatively be



expressed as 1.1 jug/1 if exposure is assumed to be from



the consumption of fish and shellfish alone.
                               C-38

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