Aspects of Pesticidal Use
of Endrin
on Man and the Environment
Environmental Protection Agency
November 1973
-------
Prepared for the Office of Pesticide Programs,
Environmental Protection Agency by:
Special Pesticide Review Group
Scientific Committee:
Homer E. Fairchild, Ph.D., Chairman
Lamar B. Dale, Jr., Ph.D., Executive Secretary
Ronald L. Baron, Ph.D.
Thomas C. Carver
Joseph G. Cummings
Allen Duvall
John Kolojeski
Calvin M. Menzie
Orville E. Paynter, Ph.D.
Lessel L. Ramsey
Paul H. Schwartz, Ph.D.
Clara H. Williams, Ph.D.
Anne R. Yobs, M.D.
Special Working Group on Endrin
Chapter I William V. Hartwell, Ph.D.
Chapter II Padma R. Datta, Ph.D.
Chapter III Merle Markley
Chapter IV Raymond E. Landolt
Chapter VI Samuel C. Billings
Chapter VII Samuel C. Billings
Edited by: William V. Hartwell, Ph.D. (Team Leader)
Library Assistance Of:
Mr. Robert Ceder
Mrs. Claudia Lewis
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Aspects of Pesticidal Use of Endrin on Man and the Environment
Table of Contents
Chapter I.
Chapter II.
Chapter III,
Chapter IV.
Chapter VI.
Chapter VII.
Chemistry and Methodology of Endrin
Pharmacology, Toxicology, Epidemiology . . . .
Toxicity, Fate, and Significance of Endrin
in the Environment
Residues in Crops and Food Items .......
The Use of Endrin in Relation to the Hazards
of Safety of Continued Use
General Discussion of the Hazards of Endrin in
Relation to Use Patterns
7
25
85
246
283
299
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Introduction
Endrin is the most acutely toxic member of the groups of cyclodiene
insecticides which includes aldrin, dieldrin, isodrin, and telodrin.
Endrin has been used as an agricultural pesticide for more than
20 years to control a variety of chewing and sucking insect pests which
inhabit the soil and infest crops. It is also used to control mice
populations in deciduous orchards, as an avicide, and as a rodent
repellent in the reseeding'of forest.
Endrin is highly toxic, it is persistent, and residues in the soil,
water and animal tissues have resulted from uses to control insects, birds,
and rodents. Records show substantial reductions in populations of non-
target species in some areas where endrin has been used. These factors
have aroused serious concern among various groups of conservationists.
Prior to 1965, when large quantities of endrin were used on sugar
cane and cotton, substantial fish kills in the lower Mississippi River
were attributed to endrin contamination from industrial effluent and by
runoff and drift from nearby agricultural uses.
Since 1965 the number of registered uses for endrin have declined
probably due in part to the high toxicity, the lack of tolerances greater
than zero and the development of insect resistance to the pesticide.
However, since the cancellation of the use of DDT on cotton, the cotton
use of endrin has increased 2.5 times during the past year. Large fish
and bird kills have been associated with this increase in use on cotton.
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Summary
Endrin is the common name for the insecticide which contains at
least 92 percent 1, 2, 3, 4, 10, 10-hexachloro-6,7-epoxy-l, 4, 4a, 5,
6, 7, 8, 8a-octahydro-l, 4, 5, 8 endo endo-dimethanonaphthalene. Endrin
was first synthesized in the 1940's and has been used as an insecticide
since 1951.
During the 1970-1971 growing season, endrin was registered for foliar
and soil applications as an insecticide oh cotton, corn, small grains,
sugar cane, potatoes, sorghum, and sugar beets. Other uses included
seed treatment, post-harvest use in orchards as a ground spray for orchard
mouse control, as an avicide, and for use on ornamentals in greenhouses
and nurseries. The uses on corn, potatoes, sorghum and sugar beets have
subsequently been cancelled because of lack of tolerances.
The quantities of endrin used in 1970-1971 were 43 percent of that used
in 1966 with 34 percent of the total used on cotton, 14 percent on corn, 16
percent on small grain and 28 percent for control of the orchard mouse.
During 1971-1972, the amount used was more than twice that used during the
prior year; the use on cotton accounted for this increase.
Endrin is the most acutely toxic of the cyclodiene pesticides in use
today, having an acute oral LDgg in rats of approximately 7.5 mg/kg and
an acute dermal toxicity in the same species of 15 mg/kg. However, unlike
the other cyclodienes, endrin is rapidly metabolized and excreted and
neither endrin or its metabolites appear to be accumulating in adipose
tissue of the general population or in occupationally exposed workers.
2
-------
The pharmacological action of endrin is similar no that of the other
cyclodienes with central nervous stimulation being the predominant effect.
In laboratory animals, there appears to be a latent period of about one
hour before the onset of convulsions, regardless of the amount of endrin
ingested. Hepatic enzyme induction has been noted in long-term feeding
studies in the rat.
Pathologic findings associated with life-span feeding of high levels
(25-100 ppm) of endrin in the diet were diffuse degeneration of the brain,
liver, kidneys and adrenal glands. No significant toxicological effects
were associated with levels of 1 ppm or less. The dogs are approximately
twice as sensitive to the toxic effects of endrin as the rat. No increase in
the incidence of malignant tumors in the test groups was noted over the
control animals of either species. In a three generation reproduction
study in rats, levels of endrin up to 2.0 ppm had no effect on fertility,
gestation, viability, and lactation indices. While no teratogenic studies,
per se, have been carried out on endrin, no teratogenic effects were
noted in the reproduction studies cited above. However, this can not be
taken as conclusive evidence of the lack of teratogenic potential of
endrin. No mutagenic studies on endrin have been reported.
Endrin has been included in most of the surveys of chlorinated
insecticide levels in adipose tissue and blood. Even in those areas
where endrin is most extensively used (e.g., India and the Lower
Mississippi area) endrin was not found in human subcutaneous fat
or in blood from the general population at a limit of detection of
0.03 ppm and lower. Levels of the 9-keto metabolites of endrin in
3
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four human fat samples were all less than 0.0004 ppm. Studies carried
out on occupationally exposed workers have revealed harmful physio-
logical effects only in those instances where absorption of endrin
has occurred from careless handling.
The Joint Expert Committee on pesticide residues has determined the
FAO/WHO "no effect" levels for endrin in the rat and the dog to be 1 ppm.
This is equivalent to 0.05 mg/kg body weight/day for the rat and 0.025
mg/kg body weight/day for the dog. The acceptable daily intake for man
(ADI) has been estimated to be 0.0002 mg/kg body-weight.
Adequate methodology has been developed for monitoring endrin in
food, water, air, and wildlife. During the period from 1964-1969, 111,296
samples of domestic food were examined for endrin residues. No residues
of endrin were found in finished or crude corn oil or cottonseed oil,
milk, dairy products, or baby foods. However, there was an increase in
the percentage of endrin residues found in samples of small fruits, root
vegetables meat, poultry, and grains for animal use during this period.
The highest incidence of endrin residues were found in domestic samples
of crude soybean oil followed by fish and root vegetables.
The average dietary intake of endrin for the period of 1964-1970
g/kg body weight/
day). The average daily intake of 0.0011 mg/kg body weight was reported
for all chlorinated organic pesticides for the same period. The maximum
dietary intake of endrin from a well-balanced-diet was approximately
0.001 mg/day (7 percent of the ADI). This was attributed to levels found
in meat, poultry, potatoes, leafy vegetables, and garden fruit for the
-------
period June 1968 to April 1969. During the period Jui.e 1969 to April 1970
similar amounts of endrin were ingested in the balanced diet, but the
highest levels of contamination were found in potatoes, root vegetables,
and garden fruits.
Volatilization is considered to be a major factor in the
disappearance of endrin from treated soil. Although endrin has
not been identified as an air contaminater from distant sources,
detectable amounts have been measured as drift following spraying
and dusting operations. A recent fish-kill in Alabama was attributed
to drift from applications to cotton by aircraft.
Occurrence of endrin in water has been related to agricultural
uses on adjacent soil and to industrial contamination from chemical
plants. Endrin has not been detected in water from the major drainage
basins since 1968, but the detection of endrin in fish taken from these
waterways suggest periodic contamination from point sources particularly
in the Mississippi, Arkansas, and White Rivers of the Southern States.
Results of intensive studies indicate that the major portion of water
burden of endrin is from that absorbed on suspended microparticulates which
possibly result from agricultural run-off.
Endrin is less persistent than dieldrin, but detectable amounts
may remain through several growing seasons. Endrin is lost from soil
through erosion by water and wind, volatilization from soil surfaces,
direct uptake by plant roots and biological conversion. Residues in
agricultural soils have not been detected below 12 inches. Endrin
degrades rapidly in flooded soils with high organic matter. Endrin
-------
ketone, endrin aldehyde and an unidentified hydrophilic product have
been detected in soil.
•r
Amounts of endrin which is translocated into growing plants is
v.
directly related to amounts in the soil. Residues have been detected
in stems on leaves of cereal grains but none have been reported in the
grain or seed portion. Amounts detected in grasses, alfalfa, root crops,
peanuts and soybeans were greater than the amounts in the soil in which
the crops were grown.
Effects of endrin on fishes and other wildlife/is related to high
V,
toxicity of this pesticide. Several fish kills have resulted from
run-off following treatment of sugar beets and cotton. The LC5Q for
most fish is within the range 0.05-3.1 ppb. Levels of 5 ppb in water
caused embryonic death during the gastrula and blastula stages. In
some species 0.0001 ppb induce changes in behavior patterns which inter-
feres with courtship fertilization processes. Reported c-Kanges in
values and bioaccumulation by lower members of the aquatic food web at
rates 920-2800 times the level found in water indicates the development
of resistance to endrin. Results of field and laboratory testing indicate
that endrin is the most toxic chlorinated hydrocarbon pesticide to wild.
mammals and birds. Trace amounts detected in fat of game animals are not
considered a dietary hazard for humans. Dietary levels of 1 ppm are lethal
for several species of birds, and < 0.1 ppm caused cessation of egg
production.
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CHAPTER I
Chemistry and Methodology of Endrin
I.A. Introduction
Endrin was first synthesized in the 1940's and has been used
as an insecticide since 1951. It is one of a series of chlorinated
cyclodienes which has insecticidal properties. In an attempt to
determine the chemical nature of the toxic moiety, Soloway (1965)
examined 106 cyclodienes. He found high insecticidal action only in
those compounds in which there were two electronegative centers, close
to each other, and on a plane of symmetry defined by the dimethano-
bridge. In this respect there appears to be remarkably little
difference in the insecticides aldrin, dieldrin, endrin and telodrin.
The similar effects caused by these substances on the central nervous
system suggest that they act on similar sites. The electron-rich
sites of these molecules which are not believed to be chemically
active, are considered likely locations for strong electrostatic
Interaction---possibly on nerve cell membrane (Benson, 1969). The
epoxi'des -ire believed to be the active compounds since only those
compounds in which the double bond on the nonchlorinated side of the
molecule is readily epoxidized, display insecticidal activity. The
rigid case configuration with the electronegative centers of the
chlorine atoms of these lipid-soluble substances is thought to be
important to the passage across membranes and to their molecular
action (Hathaway, 1965). Because of the similarity in structure
of the molecules, and similarity of clinical effects from acute
-------
exposure in most animals and man, it is likely that the toxicological
action occurs on similar, if not the same sites, in the central nervous
system.
I.B. General Chemistry
Endrin is the common name for the insecticide which contains at
least 92 per cent 1,2,3,4,10,10-hexachloro-6,7-epoxy-l,4,4a,5,6,7,8,8a-
octahydro-1,4,5,8 endo endo-dimethanonaphthalene (Jager, 1970). The
empirical formula C,pIL,Cl,0, is described by the following graphic
and spacial presentations p-.
Cl
Cl ,2
JC
cilj?
H '0 H ,
4a
Cl
I.B.I. P_hy_s.:Lc'lLj3_r5PJ:3LtieJ: Crystalline and technical endrin are stable to
light and air.
Endrin is a sterioisomer of dieldrin; a fact/borne out by the
wide differences in melting points of the two substances—dieldrin
L50°C, F.ndrin 235°C. In the convention of the American Chemical
.Society, Endrin has the endo, endo configuration with respect to the
two mnthano moities of the molecule. The chlorinated "left" side
which represents about 75 percent of the mass of the molecule is
identical in aldrin,dieldrin,isodrin, telodrin, heptachlor and
,O
chlordane. Solubility of endrin (Kirk-Othmer, 1963) isjdifferent
solvents is presented in Table I.B.I. ^
8
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Table I.B.I.
Solubility of Endrin
Solvent Solubility in % by
Weight at 25°C
Acetone 28
Amylacetate 24
Benzene 37
Butyl Alcohol 7
Carbon Tetrachloride 24
Cyclohexanone 44
Diesel Oil 11
Ethyl Alcohol 4
Ethylene Dichloride 41
Fuel Oil 11
Heavy Aromatic Naphthalene 32
Isopropyl Alcohol 4
Kerosene 6
Methyl Alcohol 3
Methyl Cellosolve 10
Methyl Ethyl Ketone 33
Mineral Spirits 9
Toluene 46
Trichloroethylene 41
Turpentine 19
Velsicol AR-50 35
Xylene "~) 3.9
Water ^ >0.1 ppm
/
Other physical properties of endrin (Martin, 1961; Terriere, 1964;
Richardson and Miller, 1960) are presented in Table I.E.2.
Table I.E.2.
Physical Properties of Endrin
Molecular weight 380.93
Physical Stnte Pure: white crystalline solid
powder.
Technical •- light tan flowable
Vapor pressure Technical: 2.7 X 10-7 mm Hg
at 25°C
FlammabLlity Non-flammable
Mel tin;', point 235° C decomposes
Bulk density (Ib/ft3) 55-60
Specific gravity 1.70 20°C
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I.E.2. Available forms
The following preparations are available commercially:
I.C.
Wettable powders
Dust Concentrates
Field strength dusts
Eraulsible concentrates
Granules
Contain 25-50 percent active ingredient. .
Contain 20-75 percent active ingredient to
be diluted with inert filler prior to field
use.
Contain 0.5 - 1.0 percent active ingredient.
Contain 15-48 percent active ingredient to
be mixed with water before use.
Contain 2-5 percent active ingredient
ready for field use.
Combinations with organic - As emulsible concentrates to be diluted
phosphates
with water before use.
Endrin is manufactured by the following procedure (Shell, Velsicol,
1970):
(1) Hexachlorocyclopentadiene (?') is adducted with vinyl chloride
(££) by the Diels-Alder process to yield the hexachlorocyclo-
pentadiene-vinyl chloride adduct (iii) (1,2,3,4,5,7,7-heptachloro-
bicyclo[2.2.1]hept-2-ene).
(2) The adduct (Hi) is dehydrohalogenated with alcoholic base to
yield 1,2,3,4,7,7,--hexachlorobicyclo[2.2.l]hepta-2,5-diene (iv).
(3) The chlorinated bicycloheptadiene is adducted with cyclopentadiene
(y) to yield isodrin (vi) (1,2,3,4,10,10-hexachloro-l,4,4a.,5.,8,8a--
hexahyd ro~erido--endo-l ,4 :5,8--dimethanonaphthalene).
(4) Isodrin is treated with peracetic acid to yield endrin (vii).
This nrocess of synthesis may be represented symbolically as
follows:
-------
f]) Adduction:
Cl
H Cl
C
Cl
i.-Cl HCH
c ci
i
^^
(2) Dehydrohalogenation:
Cl
Cl
citci""" H Base
Cl
Cl
^^^
(3) Adduction:
Cl
ci
Cl
C1—C1
ci
^v
(4) Epoxidation:
v^ oxidation
Cl
Cl
Cl
Cl ' \
Cl
H
:'- Cl
I;
I- H
H
Cl
Cl •
Cl
Cl
^ H
Cl-r Cl
Cl
iv
Cl
CI~
Cl
ci-ci H--I-H;
H
H
ci
vi
Cl
Cl
\ "*>*
i. H'LH I '
H "v-, H
H
I.D. Chemical reactions
Crystalline and technical grade preparations of endrin are stable
to light and air. However under biological conditions, or by exposure
to sunlight, ultraviolet light, Lewis acids, or heat, products shown
in Figure I.D. may.be formed.
-------
Cl
Cl
Cl,.
(i) Endrin
-7
(iii~) Endrin Aldehyde
Endrin Half Cage Keton
( A Ketom
rf
Figure I.D. Degradation products of Endrin
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I.D.I. Derijaatives
During analysis by GLC on conventional support media endrin
tends to tail and decompose (MacDonell, 1968). After suitable
support media and operating conditions had been determined, elution
patterns from known preparations and preparations from experimental
sources suggested that the molecule was changed prior to extraction
/" "'
/ of during cleanup. Heat induces formations of I.D. (iv~) (Benson,
1969). Treatment with concentrated sulfuric acid for 10-15 minutes
at room temperature causes isomerization of endrin to I.D. (Hi) and
I.D. (iv) (Chou and Cochrane, 1969). Treatment with zinc chloride in
hydrochloric acid converted endrin to I.D. (iv) without other by-
products (Weincke, 1969). When treated with aqueous solutions of
chromous chloride endrin is converted to I.D. (V) (Chou and Cochrane,
1971)..
I.D.2. Photochemistry
Endrin in hexane and cyclohexane was converted by irradiation
at 253.7 mm, 300 mm and sunlight to I.D. (y) in yields up to 80 per-
cent (Zabik, 1971). This product which is highly resistant to
oxidation reduction procedures has been detected in fields where
endrin has been used. When applied to growing bean leaves, which
were subsequently exposed to sunlight for 1 hour, rotenone enhanced
photoconver.sion of endrin to the aldehyde and ketone isomers (Ivie,
1970. Exposure to ultraviolet light induces formation I.D. (iv)
(Benson, 1969).
I.D.3. Degradation Products
Endrin is converted to more hydrophilic substances by plants,
animals and bacteria. The A ketone I.D. (iv~) and the alcohol I.D. (ii)
-------
have been recovered from soybean plants which were grown in soil
treated with ' C-endrin (Nash and Beall, 1971). Within four weeks
14
following foliar application of C-endrin to white cabbage two
hydrophilic metabolites and unaltered endrin were found in plant
tissue and soil, one metabolite was tentatively identified as I.D.
(iv) (Weisgerber, 1969). Five conversion products were found in
soil and plant tissue 12 weeks after topical application of endrin
to collard plants. One group of these was slightly more hydro-
philic than endrin, and the other two products were strongly hydro-
philic. Two of the first group had GLC retention times similar to
endrin ketone: one of these had chlorine structure similar to endrin
but a higher molecular weight (Bayless e_^ al., 1970). Of 150 micro-
bial isolates from various soil samples, 25 degraded endrin. At
least 7 metabolites were isolated from a mass culture of Pseudomonas.
Most of the metabolites were ketones and aldehydes with 5 or 6
chlorine atoms.
One metabolite which occurred in all samples was I.D. (u)
(Matsurma et al_. , 1971) .- Twenty microbial cultures such as Trichoderma
sp., Pseudomonas sp. and Bacillus sp., capable of degrading dieldrin,
degraded endrin to keto-endrins (Patil et al., 1971).
Two unidentified compounds and I.D. (ii), I.D. (Hi), and I.D.
(£?>) have been identified in tissue and feces from rats dosed orally
14
with C-endrin (Richardson, 1970). Compound I.D. (iv) has been
recovered from human and animal tissue (Schultz, 1964).
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I.E. Methods for Analysis
• Ouantiti.es of endrin have been determined hy biological and
chemical methods. Biological methods are relatively insensitive
and nonspecific and have been replaced by faster more specific
chemical procedures. Chemical procedures include analysis of
chlorine, infra red and visible spectrophotometric measurement,
and separation and quantitation by thin layer and gas chromatography.
Samples submitted for analysis are extracted with solvents such
as benzene, toluene, and mixtures of benzene, toluene, hexane, or
pentane which contain alcohols or acetone. Treatment of the ex-
tracts include concentration and cleanup by solvent fractionation
or chromatography on flurosil, celite, aluminum or "David-dow"
columns. The type of material in the sample, and the method used
for detection indicate the solvent mixture to be used for extraction
and the degree of cleanup required prior to analysis. The following
is a brief description of accepted methods of analysis.
I.E.I. Dioassay - Living populations of insects or crustaceans such as
DrosophiMa • sp. , house flies, cray. fish, daphnia and aphids, were
exposed for predetermined periods of time to extracts from samples
suspected of containing endrin. Mortality of text organisms
caused by unknown concentrations of endrin was compared with
mortality produced by known amounts. Although this method was
used widely before more accurate methods were developed, it lacks
specificity and sensitivity. Greatest value of bioassay is at low
residue levels, provided sample history is known and contamination
with other insecticides can be excluded (Tew and Sillibourne, 1961,
1961a; lleusman, 1961- ^uedemann) and Neuman, 1961; Bringmann and
-------
and Kiihn, 1960; McDonald, 1962: Sun and Sanjean, 1961).
I.E.2. Total Chlorine - Organic chlorine (White, 1961) is reduced to
inorganic chloride by such means as sodium alcohol reduction,
sodium-bip.henyl reagent, quartz tube or Parr bomb combustion.
Inorganic chloride is then determined by several methods such
as Volhard titration, potentiometric or amphrometic titration.
Specificity of this method depends on effective separation of
the substance to be analyzed from interfering substances.
I.E. 3. Spactrophotometric Methods - Several colorimetric methods are
available for residue analysis.
I.E.3.a. After cleanup, the sample is reacted with phenylazide. The re-
sulting dehydrophenyltriazole derivative is coupled with a diazotized
amine to form a colored complex (White, 1961; Shell, 1957). Endrin
must be reduced with sodium alcohol before it will react with phenyl-
azide. The method is slow and reagents are unstable.
I.E.3.b. Infra red method - This method is based on the comparisons of the
heights of absorption bands at 11.4 - 11.8 microns of an unknown
with a calibration curve prepared from materials of known purity
(White, 1961). Since dieldrin has similar absorbance, careful
cleanup is required for this method. This rapid, versatile method
is used extensively for quality control, but initial expense for
instrumentation, maintenance of instrument and training are high.
I.E.4. Chromatographic methods
I.E.4.a. Thin-layer chromatography - Extract of samples is reduced in
volume and purified, either by chromatography or florisil, magnesium
oxide or aluminum oxide (activated at 270°C for 3 hours) or by solvent
portioning. After concentration a portion of the extract is applied
-------
to a restricted area of a plate containing an inert adsorbent and
developed with a suitable solvent. In one instance endrin in alfalfa
hay was measured with silica Gel H; benzene was developing solvent,
and detection was with standard indophenal blue spray (Archer, 1968).
TLC has been used to detect metabolites of endrin and as a
preparative procedure for GLC. Solvent systems and Rf values for
alumina thin layer chromatography of hydroxychlordane and some
endrin metabolites are presented in Table I.E.I. (Nash and Beall, 1971).
Table I.E.I.
Solvent systems and Rf values for alumina thin layer
chromatography of hydroxychlordene, endrin delta
keton, endrin aldehyde, and endrin alcohol
Solvent Systems
(1) Heptane-acetone
(80 + 20)
Hydroxy- Endrin Endrin Endrin
chlordene Ketone Aldehyde Alcohol
0.21+O.Qia 0.49+0.04 0.17+0.03 0.22+0.01
(2) Ilexane-ethylacetate- 0.59+0.05 0.74+0.07 0.38+0.04 0.50+0.03
acetic acid
(70 -30+2)
(3) Kthyl acetate
(4) llexane-acetone-
methanol
(80 - 10 + 10)
(5) Acetone
0.47+0.03 0.76+0.02 0.37+0.02 0.41+0.02
0.55+0.04 0.72+0.02 0.41+0.03 0.36+0.04
0.87+0.02 0.93+0.01 0.66+0.05 0.87+0.03
•-i
Mean and standard deviation of 4 replications.
I.E.4.b. Gas 1iquid chromatography
GLC is the presently preferred analytical method. The technique
permits measurements with greater than 100 times the sensitivity of
other methods. This procedure requires extensive cleanup but permits
-------
the quantitation of multiple components in each sample. Different
types of samples are extracted with polar solvents and purified by
column chromatoeraphy on florisil or oxides of magnesium and alumi-
num. Micro-liter quantities of concentrates are. introduced into
chromatographic systems which consist of an inert gas flowing at a
constant rate in one direction over a stationary phase maintained
under predetermined temperature conditions. Components are separated
by their relative afinities for the solid phase and are elicited
and at characteristic time intervals after addition to the system.
Quantitation is obtained with highly sensitive electronic devices
which monitor and record changes in the characteristics of the gas
as it leaves the column. Types of samples and differences in com-
ponents to be measured determine type of solid phase used in the
column (Dale et_ aJ. , 1966; Sessions et_ auL., 1968: Woodhamet__al. ,
1970: Taylor, 1970; Nash and Beall, 1971).
Retention times on different stationary phases relative to
aldrin of some organochlorine pesticides are presented in Table I.E.2.
(Sessions e_t aJL. , 1968) .
Table I.E.2.
Retention Data for Three Types of Stationary Phase
Pesticide
Lindane
Heptachlor
Aldrin
Heptachlor epoxide
Fndosulfan A
Dieldrin
p,p'-DDE
Undrin (major peak)
Endosulfan B
/;,p'--DDT
p,p'-WE
SE30
0.44
0.78
1.00
1.30
1.67
2.01
2.15
2.27
2.33
2.89
3.74
Stationary phase
QFi
0.85
0.9
(5') 1.00 (4')
1.90
2.59
3.10
2.06
>6
4.77
2.72
4.33
XE60
1.32
0.95
1.00(2-1/2')
2.33
2.60
3.60
2.97
4.05
7.65
4.03
7.13
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When electron capture detectors are used.it is essential to
determine the linear response range of each individual pesticide
because of the characteristics of each detection. Detection limits
and linear resonse ranges v?ith one electron capture detector are
presented in Table I.E.3. (Sessions et al., 1968).
Table I.E.3.
Linear Dynamic Range of Pesticides
Pesticide
Lindane
Aldrin
Heptachlor
Heptachlor
Dieldrin
Endosulfan A
Endosulfan B
p,p'-DDE
Endrin
p,p'-DDT
p,p'-DDT
epoxide
A
B
Detection
limit* (ng)
0.0007
0.0013
0.0012
0.0015
0.002
0.002
0.0025
0.003
0.015
0.015
0.015
Linear response range (ng^
min.
0.003
0.005
0.005
" 0.006
0.008
0.008
0.01
0.01
0.05
0.05
0.05
studied max.
0.5
0.75
0.6
0.7
2.5
0.7
1.0
1.5
3.5
5.0
5.0
* Equivalent to a peak of height 2% fsd on attenuation setting
1x4 (1.2 X 10-9 A full scale)
Retention times on several solid phases of different degradation
products of cndrin and hydroxychlordene recovered from soybean leaves
and stems, relative to retention time of aldrin, are presented in
Table I.E.3. (Nash and Beall, 1971).
-------
Gas-liquid chromatographic identification of degradation products in
extracts from leaves and stems of soybeans p.rown in endrin- and hepta-
chlor-treated soil
Standard
or
Cleanup
Fraction
15% OF-1-10% DC-200
3% OV-17
1.5% OV-17-2% QF-1
5% SF.-30
standard
fraction
chloroform
standard
fraction
chloroform
standard
fraction
chloroform
standard
fraction
chloroform
(c)
(d)
(c)
(d)
(c)
(d)
(c)
(d)
Endrin Endrin
Endrin Alcohol Aldehyde
2.
2.
46
46
none
2.
2.
95
95
none
2.
2.
98
98
none
2.
2.
28
28
none
3.33
3.33
none
4.89
4.89
none
4.77
4.77
none
2.51
2.51
none
3.80
3.80
none
4.45
none
none
4.82
none
none
2.28
none
none
Endrin
Ketone
5
5
5
7
7
7
7
7
7
3
3
3
.80
.80
.80
.64
.64
.64
.85
.85
.85
.42
.42
.42
Hydroxy-
chlorden
1.12
1.12
—
1.25
1.25
—
1.24
1.24
..._
—
—
The GLC method is highly sensitive and may be used to corroborate
TLC measurements. Instrumentation and maintenance are expensive and
highly trained technicians are needed for successful analysis.
-------
CHAPTER T
BIBLIOGRAPHY
Archer, I.E. (1968) Location, Extraction and Removal of Endrin Residue
on Alfalfa Hay. J. Dairy Science 51,j.O: 1606-1611.
Bayless, A., Weisgerber, I., Klein, W. and Korte, F. (1970) Contribution
to ecological chemistry, XXV. Conversion and residue behavior of
14,,-endrin in cotton. Tetrahedron 26(3): 775-778.
\j ™~
Benson, W.R. (1969) The chemistry of pesticides. Ann. New York Acad.
Sci. 160 Art. 1.: 7-29.
Bringmann, G. and Kiihn, R. (1960) The water-toxicological detection of
insecticides. Gesundh. Ing. 81: 243-234 from Chemical Abstracts
54: 35523° 1960.
Chou, A.S.Y., Cochrane, P.W. (1969) Cyclodiene Chemistry, II. Derivative
Formation for identification of Heptachlor, Heptachlor Epoxide, cis-
Chlordane, Trans-chlordane, Dieldrin and Endrin by gas chromatography.
J.A.O.A.C. 52 No 6: 1220-1227.
Chou, A.S.Y. and Cochrane, W.P. (1971) Derivative formation for simultaneous
identification of Heptachlor and Endrin pesticide residues by Gas
Chromatography. J.A.O.A.C. 54 No 5: 1124-1131.
Dale. W.K., Curby, A., and Cueto, C., Jr. (1966) Hexane extractable
chlorinated insecticides in human blood. Life Sciences _5_: 47-54.
Hathaway, D.K. (1965) The biochemistry of dieldrin and telodrin. Arch.
Environ. Health 11: 380-388.
Heu.sman, H. (1961) Characterization of chlorinated hydrocarbons in the
DrosoDhila test. L. Angew. Zool. 48: 1-29 from Chemical Abstracts
57: 2629h 1962.
'•! 1
-------
fUchardfinn. L.T. and Miller, D.M. (I960) Funp.i toxic! Ly of Chlorinated
hydrocarbon insecticides in relation to water solubility and vapor
pressure. Can. J. Botany 38; 163-75.
Richardson, A., Robinson, J., and Baldwin, M.T. (1970) Metabolism of
Endrin in the Rat. Chem. and Ind. 15: 502-503.
Schultz, D.R. and DeVries, D.M. (1964) The determination of Endrin and
its Metabolite in Animal tissue. Abs. paper. Am, Chem. Soc. 148 -
Aug-Sept 27A. Paper #65.
Sessions, D.J., Telling, G.M., Usher, C.D. (1968) A rapid sensitive
procedure for the routine determination of organo-chlorine pesticide
residues in vegetables. J. Chromat. 33, 3-4: 435-49.
Shell Chemical Co. (1957) A Review of Residue Analysis for the determination
of Aldrin, Dieldrin, Endrin and Phosdrin insecticides.
Shell-Velsicol, private communication (Pet No. l-F-1060 Nov 16, 1970)
Soloway, S. (1965) Correlations between biological activity and molecular
structure of cyclodiene insecticides. Advances in pest Control
research 6:85-126.
Sun, Y.P. and Sanjean (1961) Specificity of bioassay of insecticide
residues with special reference to phosdrin. J. Econ. Entomol.
54: 841-846.
Taylor, T.S. (1970) Design of a Column for gas chromatographic anlysis
of chlorinated hydrocarbon pesticides. J. Chromatog _5_2: 141-144.
Terriere, L.C. (1964) Endrin, In: Zweig, G., ed: Analytical Methods.
Pesticides, Plant Growth regulators and Food Additives, Vol II.
Insecticide, New York Academic Press p 209-22.
-------
Tew, R.P. and Sillibourne, J.M. (1961) Pesticide Residue on fruit, I.
Micro-bioassay of pesticides using the vinegarfly, Drosophilia
melanogaster, J. Sci. Food Agr. 12: 618-23.
Tew, R.P. and Sillibourne, J.M., (1961a) Pesticide residue on fruit, II.
Determination of aldrin, dieldrin, and endrin residues by the organic
chlorine and phenylazide methods and by microbioassay. J. Sci.
Food Agr. 12_: 618-623.
Weisgerher, I., Klein, W., Djirsarai, A. and Korte, F. (1968) Insecticides
in Metabolism 15, Distribution and Metabolism of 14 -Endrin in White
(^
Cabbage. Ann. Chem. 713: 175-179.
Weisberger, I., Klein, W., and Korte, F. (1969) Insecticide Metabolism
XVII. Residue behavior and Metabolism of endrin-[14-C] in tobacco.
Ann. Chem. 729: 193-197.
White, T.T. and McKinley, G.G. (1961) Determination of Aldrin, Dieldrin
or Endrin in formulations, Aas. Offie. Canal. Chem. J. ^4»3: 591-595.
Weincke, W. W., Burke, J.A. (1969) Derivatization of Dieldrin and Endrin
for Conformation of Residue Identity. J.A.O.A.C. 52 No 6: 1277-1280.
Woodham, D.W.,Loftis, C.D., and Collier, C.W. (1970) Identification of
gas chromatographic dieldrin and aldrin peaks by Chemical Conversion.
Abstr. papers Am. Chem. Soc. Joint Conf. Pest, paper 65.
Zabik, M.J., Schultz, R.D. Burton, W.L., Pope, R.E. (1971) Photochemistry
of bioactive compounds - Studies of a mjaor photolytic product of
Endrin. J. Agr. Food Chem. 19(2): 308-313.
-------
Ivie, G.W. and Casida, J.E. (1970) Enhancement of photoalteration of
Cyclodiene Insecticide Chemical Residues by Rotenone. Science
67: 1620-1621.
Jager, K.W. (1970) Aldrin, Dieldrin, Endrin, and Telodrin. p 44.
Eluevier Publishing Co. Amsterdam, London, New York.
Kirk-Othmer (1963) Encyclopedia of Chemical Technology Second edition
Vol. 5, p 245.
Liiedemann, D. and Neuman, H. (1961) The use of Artemia solina as test
animal for detection of contact insecticides. L. Angew. Zool. 58:
325-332 from Chemical Abstracts 5_7_: 12957d 1962.
llacDonell, H.L. and Eaton, D.L. (1968) Thermal Decomposition of Endrin
as a Measure of Surface Activity of Gas Chromatographic Support
Media. Analytical Chemistry _4_0: 1453-1455.
McDonald, S. (1962) Rapid detection of chlorinated insecticides in aqueous
suspension with Gammaru lacustris lacustris. Can. J. Zool. 40:
719-723 from Chemical Abstracts 58: 889C 1963.
Martin, H. (1961) Guide to the Chemicals used in crop Protection Ottawa,
Queens Printer and Controler of Stationery, pp 185-6.
Matsurma, F., Khanvilhau, V.G., Patil, K.C. and Boush, G.M. (1971)
Metabolism of Endrin by Certain soil microorganisms. J. Agr. Food
Chem. 1_9_0.): 27-31.
Nash, R.G., Beall, L.M., Jr.(1971) Extraction and identification of
endri.n and heptachlor degradation products. J.A.O.A.C. j>4_(4) : 959-963.
Patil, K.C., Matsumuva, F., Boush, G.M. (1970) Degradation of Endrin,
Aldrin, and DDT by soil microorganisms. Appl. Microbiol. 19(5) :
879-881.
-------
Chapter II
Pharmacology, Toxicology, and Epidemiology
Endrin is the most acutely toxic of the cyclodiene pesticides in
,^*-
use today. However, unlike the other cyclodienes, endrin isxrapidly
metabolized and excreted and neither endrin or its metabolities appear
to be accumulating in the adipose tissues of the general population or
in occupationally exposed workers.
II.A. Pharmacology of Endrin
As with the other cyclodienes, the principal pharmacological action
of endrin is that of central stimulation. The rate of metabolism and
excretion of endrin is rapid when compared to that of its stereoisomer
dieldrin, or other chlorinated hydrocarbons.
-------
II.A.I. Absorption, Distribution, and Excretion
The pertinent literature on the absorption, distribution, and
excretion of endrin, when fed or exposed to various laboratory animals
has been reviewed.
II.A.f(b)) Absorption
In-^the toxicity section, it is noted that endrin is toxic to all
animals regardless of route of exposure. It may, therefore, be
concluded that endrin is absorbed through all the various routes.
Endrin is virtually non-soluble in water and readily soluble in lipids.
This differential solubility is a factor determining endrin's
absorption by different routes. As shown in Table I!. 1, the
absorption by the dermal route, the liquid formulation is more toxic
than are the powdered forms of endrin. A comparison of LD5Q values for
the various routes of administration may give an indication of their
relative efficiencies as a route of absorption. The possible N.
biotransformation to a non-toxic or more toxic compound than the parent
compound must be, however, considered in such LDgQ values with dermal
LDgQ values for identical formulations of endrin do not show any
striking differences. The inhalation data is inadequate; but it^js^
suggestive that complete absorption could occur via this route. There
is very little information regarding either the amount of the rate of
absorption of endrin through different routes of entry to the organism.
-------
TABLE I I.I. ACUTE DERMAL TOXICITY OF ENDRIN
SPECIES
Rat
Rat
Rat
Rat
Rabbitt
Peanut oil solution
19.2% (w/u) emu!sifiable
concentrate containing
xylenes
Xylene Solution
20% emu!sifiable
concentrate in xylene
Dry crystalline powder
20% emulsifiable
concentrate'contai ni ng
xylenes.
5.6
11.3
15.0
60 male, 120 female
100
Worden, A. N..e_t al_., (1958)
Worden, A. N. et al., (1958)
Gaines, T. B. TT96¥)
Lade, B. I., (1960)
Newell, G.'W. (1960)
Newell, G. W. (1960)
Letter to Shell Bulletin (1960)
50
-------
5
II.A.l(b) Distribution and Storage
Endrin, like other chlorinated pesticides, when fed to animals, C
\)-^
is partly stored unchanged in the tissues, particularly in the adipose7'..
!•*
,',.,/
tissues (Kiigemagi et il. , 1958; Street et al., 1957; Terriere et al., •
/ I '
hSJM-fof
1958, 1959, and Treon et al., 1955). When fed aVfiigh levels, endrin
4—
is excreted in milk and eggs (Ely et. a]_., 1957; Street et_ al_., 1957,
and Terriere je_t ^1_., 1958). The ratio of the level In fatty tissue tcK r
v *'
the dietary level has been estimated at 0.5-2.0, depending upon the
dietary level (Kiigemagi et al_., 1958; Terriere. et al-. 1958, and
Treon et a]_., 1955).
Unlike the situation with its stereoisomer, dieldrin, the extent
of storage of endrin is relatively small, and the compound is
eliminated more quickly, due probably to its rapid biliary excretion
(Cole et. al_., 1970). Levels of the 9-keto metabolite of endrin in
four human fat samples were all less than 0.0004 ppm (•^-0.4 ppb),
(Richardson, 1970).
The maximum concentration of endrin in various tissues of animals
maintained on experimental diets are summarized in Table II. 2.
Korte et.il., (1970) reported that when endrin was given orally
to rats at a daily dose corresponding to 0.4 ppm in the diet, a steady
state of storage was reached after about six days for male and female
rats. The storage level for females (27 percent) is about twice as
high as for the males (14 percent). These figures are based on the
total amount of radioactivity administered. Four days after cessation
-------
TABLE II. 2
MAXIMUM CONCENTRATION OF ENDRIN IN TISSUES OF ANIMALS MAINTAINED ON DIETS CONTAINING ENDRIN
Animal
Dog!/
II
L. /
CattleH/
II *
tl
n
11
II
Sheep
M
n
n
ii
H
• /
HogsH/
M
II
Chickens^/
ti
M
M
Endrin in
Diet, ppm
3
1
5.0
2.5
2.0
0.75
0.25
0.10
5.0
2.0
2.5
0.75
0.25
0.10
0.75
0.25
0.10
2.25
0.75
0.25
0.10
MAXIMUM ENDRIN CONTENT OF TISSUE AT END OF FEEDING PERIOD, ppm
Body Fat
3.4
3.5
2.5
1.3
1.0
0.4
0.2
0.1
1.2
1.5
2.8
0.5
0.1
0.1
0.1
0.1
0.1
18.0
4.0
1.0
0.6
Liver
1.2
1.2
0.2
0.2
0.1
0.1
0.1
0.1
0.1
0.1
0.1
0.1
Kidney
0.3
1.1
0.1
0.1
0.1
0.1
0.1
0.1
0.1
0.1
0.1
0.1
Muscle Heart Brain
1.5 3.0
1.5 2.0
1
0.3 0.1 0.1
0.1 0.1 0.1
0.1 0.1 - 0.1
0.1 0.1 0.1
0.1
0.1
0.1
0.1
0.1
0.1
0.3
0.1
0.1 .
Spleen Reference
1.6 Treon, J. F. (1956).
1.3 Treon, J. F. (1956),
Claborn, H. V. et al . , (1960).
Claborn, H. V. et al., (I960)
Terriere, L. C. et al.,(1958),
and Kiigemagi et al.,(1958).
Terriere, L. C. et al.,(1958),
and Kiigemagi et al.,(1958).
Terriere, L. C. et al_. ,(1958),
and Kiigemagi et al.,(1958).
Terriere, L. C. et. al.. ,(1958),
and Kiigemagi et al.,(1958).
Claborn, H. V. et al., (1960).
Claborn, H. V. et al., (1960).
Street, J. C. et al . , (1964),
Terriere, L. C. et al.,(1958)b
and Kiigemati et al~, (1958).
Terriere, L.C. et al.,(1958),
and Ki'gemagi et al., (1958).
Terriere, L.C. e_t al_. ,(1958),
and Kiigemagi et al.,{1958).
Terriere, L.C. et al.,(1958),
Terriere, L.C. et af. ,(1958).
Terriere, L.C. et a!., (1958).
Terriere, L.C. et al., 1959 .
Terriere, L.C. £l al. , 1959 .
Terriere, L.C. e_L al. , 1959 .
Terriere, L.C. et al.,(1959).
a/Feeding period for dogs was 18 months.
b/Feeding period for cattle, sheep and hogs was 12 weeks.
c/Feeding period for chickens was 6 weeks.
Phenylazlde method of analysis—sensitive to 0.1 ppm. [Terriere et al_., 1958 and K11gemag1 et al., 1958] ,
-------
of dosing, the males contained only 5.3 percent', and females, 15 percent
of the administered radioactivity. The biological half-life of endrin
in male rats, at the storage level investigated, is 2-3 days; in females,
>
it is approximately 4 days. The radioactivity was mainly excreted in
the feces, which contained during the first 24 hours after oral
administration, 70 to 75 percent of the radioactivity as hydrophilic
metabolites. After the first 24 hours, only metabolites were present
in the feces. Following intravenous injection of 200 ug ^C endrin/kg
bodyweight in two doses, male rats retained 5.2 percent and females 12.1
percent of the administered radioactivity after 24 hours.
Walsh (1971) reported the distribution patterns of endrin or
dieldrin in brain, liver, fat, and blood after an i.v. injection of
an LDgQ of endrin in male CF#1 mice. He found that endrin equilibrates
sooner in liver, fat and blood, while dieldrin equilibrates sooner in
brain tissues. The rate of accumulation of dieldrin and endrin in the
brain did not correlate with the onset and development of .the convulsive
seizure pattern,
II.A.l(c) Excretion
A male rat was fed a dietary level of 30 ppm of ^C-labelled endrin
for eight days (Ludwig, 1965 and 1966). About 60-70 percent excretion
was noted from the first day, and after three days the feces contained
more than 80 percent of the administered radioactivity. On day 9, 84
percent had been excreted; and, there appeared to be a level of
saturation after 6-7 days of feeding. The feces contained about 75-80
-------
8
percent metabolites, of which there were at least two different
compounds. The fatty tissue stored 3-4 ppm of endrin, giving a storage
ratio of about 10:1. Compared to 84 percent excretion in the feces,
only about 0.5 percent was found in the urine.
Korte £t aj_., (1970) measured the excretion rate of ^C-endrin
after oral administration. The biological half-life after a dose of
16 or 64 ug/kg body weight was one to two days. However, at a dose
of 128 ug/kg, the half-life increased to approximately six days,
indicating a decreased excretion at higher dosage levels.
The rapid rate of metabolism and excretion of endrin compared
to that of other chlorinated hydrocarbon insecticides has been
confirmed by a study on rats, with and without bile/r6stula, and on
vW--y
isolated perfused rat liver (Cole et al_., 1970; Altmefer^t ^1_., 1969).
In rats receiving a daily oral administration of 32 ug/kg, the storage
reached a state of equilibrium after 5-6 days. Under these conditions,
the half-life was three days in male rats and four days in female rats,
(Klein and Drefahl, 1970).
Klevay (1970) studied the excretion of endrin by the isolated
perfused liver of male and female rats. The excretion of the radio-
activity by the bile duct of the male livers was significantly greater
than the female livers. The ' C-endrin appeared two to twelve time
more rapidly in the bile of the male livers than in that of the female
livers and the author thought that this explained the lesser toxicity
and lesser adipose tissue storage of endrin in male rats.
-------
9
II.A. 2 Biotransformation (Metabolism)
There is considerable indirect evidence that endrin degrades to a
less toxic derivative. It has also been assumed that endrin either is
metabolized and stored in a chemical form not detected by analytical
methods or is rapidly metabolized and excreted.
The information available on the metabolism of endrin up to 1967
have been reviewed previously (Soto and Deichmann, 1967; Brooks, 1969).
The following experimental data summarizes the pertinent information
leading to the current knowledge on the metabolism of endrin (see
Figure II. 1).
In rats, Klein etaQ.., (1968) and Richardson et. ^1.., (1970)
found that endrin is rapidly metabolized and excreted, principally in
the feces. The feces contain two metabolites as well as endrin itself.
Baldwin .et _aJL , (1970) found that the major fecal metabolite is a
secondary alcohol formed by substituting a hydroxyl group for one of
the hydrogens of the methano-bridge of endrin (II). The other fecal
metabolite is also an alcohol. Three days after a single oral dose of
^C-labelled endrin, approximately half of the ^C radioactivity remained
in the bodies of the rats. This material was principally one metabolite
which was identified as 9-keto endrin (I), an oxidation product of the
secondary alcohol found in feces.
When 14C-labelled endrin was administered orally to rabbits at
0.5 mg/kg body-weight at three and four day intervals, four metabolites
were isolated from the urine which appear to have the following chemical
'12
-------
Metabolite III
(minor fecal
metabolite)
a inono-
hydroxylated
endrin.
X
Cl
Metabolite II
(major fecal metabolite)
Cl
(dclta-keto-endrin ,
not found as a metal-
in rats)r
^Cl
Metabolite I
(in tissues)
9-keto derivative
Figure II. 1
-------
10
natures: k (40 percent of excreted radioactivity) is a conjugate
compound of a hydroxy derivative of endrin; B^ (12 percent) is a
monohydroxy derivative of an unbridged endrin isomeric ketone; £ (40
percent) is the 4a-hydroxyendrin; £ (8 percent) has a molecular weight
of 420 and the C-C double bond intact in the chlorinated ring. None
of these compounds is the delta-keto endrin (Korte and Porter, 1970).
The acute oral 1050 for delta-keto 153, a metabolite of endrin
formed in plants, has been found to be 62.1 mg/kg and 23.6 mg/kg for
male rats and mice, respectively (Newell, 1964). For the aldehyde,
the acute oral 1050 in male mice is 500 mg/kg (Newell, 1964). The
lethal dose of delta-keto 153 for three routes of administration has
been reported by Witherup (1964); the results are summarized in
Table II. 3.
TABLE II. 3
LETHAL DOSES OF DELTA-KETO ENDRIN FOR VARIOUS ROUTES OF ADMINISTRATION
Animal
Rabbits
Rats
Route of
Administration
Intravenous
oral (acute)
Vehicle
Peanut oil
ii
Lethal dose mg/kg
5
M 120-280
F 10-36
Rats cutaneous " >• 940 in M and F*
* At dosages of 180-940 mg/kg applied to the skin and washed off
6 hours later; all rats survived and exhibited no ill effects,
except transient losses in body weight.
-------
12
11.A. 3 Effect on Enzymes and other Biochemical Paramfeters
In monkeys which had received exposure to an unspecified quantity
of endrin, there were significant changes in the enzymes serum glutamic-
oxaloace_tic_t_ransaminase and serum glutamic-pyruvic transaminase
dearth, 1967b
Elevation of serum alkaline phosphatase has been observed in rats
fed 25 ppm, and possibly in rats fed 5 or 1 ppm of endrin for 16 weeks
(Nelson et _al_., 1956), but not in dogs feed 4 ppm of endrin for two
years (Jolley et al_., 1969), nor in human subjects occupationally
exposed to unspecified levels of endrin (Shell, 1965).
Weil and Russells (1940) have reported a decrease in alkaline
phosphatase in rats after eight hours fasting; these observations
indicate some degree of enzymatic abnormality and functional liver
damage. Hart (1964) has noted a stimulatory effect of chlorinated
hydrocarbons resulting in increased hepatic drug enzyme activity, and
this suggests a possible biochemicaV^te-r%tip.n/involving liver.
Daugherty crt a]_. , (1963) reported that there was no effect of
endrin on substrate-linked phosphorylation, and Weikel e_t al_., (1968)
noted no effect from endrin on the phosphate exchange rate.
Nelson et aj_., (1956) showed that endrin, unlike aldrin, dieldrin, and
DOT, does not inhibit the phosphate exchange rate in whole blood.
There are no specific studies on hepatic enzyme induction, however,
enhancement of enzyme(s) are indicated in the long-term feeding studies
of rats (Nelson ert al_. , 1956; Treon ejt al_., 1955) and dogs (Treon et a!.,
1955; Richardson et_ jil_., 1967). Based on these data, a 1 ppm dietary
If)
-------
13
level of endrin may be regarded as the "no effect" level in the rat
and the dog. This no-effect level can also be applicable to the
enzyme induction level in the rat and the dog.
II.A. 4 Pharmacodynann'cs
Reins ert a]_., (1964) noted an increase in peripheral blood
pressure and in renal vascular resistance after intravenous infusion
of endrin in dogs. Adrenalectomy partially offset the marked drop in
renal blood flow after endrin infusion, although systemic hypertension
was unaffected. It was suggested that endrin stimulates the sympatho-
adrenal system accounting for the increased peripheral vasoconstriction.
.The results were by no means conclusive, however, and considerable work
involving the effect of endrin on the kidney remains to be done.
Emerson jet aj_., (1963) have reported a possible scheme of the
mechanism of action of acute endrin intoxication (See Figure II. 2).
While most of the effects of endrin appear to be caused by direct action
on the central nervous system, some may result secondarily from altered
cerebral hemodynamics.
Speck and Maaske (1958) noted a latent period of 45-60 minutes
before the appearance of convulsions in rats, regardless of the amount
of endrin dose. It was shown that injections of trypan blue sufficient
to color the choroid plexus prevented the convulsions which was
interpreted to be an indication the "blood-brain barrier" permeability
was increased by endrin. The validity of this interpretation is
questionable.
-------
PERIPHERAL
ACTION
V
v
CENTRAL
KERVOUS
ACTION
L..
INCREASED
.CAPILLARY
i'[FISSURE OR
PERMEABILITY
EMi'ERATUKE
EXCITABILITY
CONVULSIONS
INCREASED
LEUKOCYTE
CONCENTRATION
CERECRAL j
ARTEiMOLAK j
DILATATION1
HEMOCOI-ICENTRATION
INCREASE!.
CEREURAL
VENOUS
PRESSURE -.
PAUA-
ri .'iF / v 1 i HJ 11C
DISCHARGE
ART;-:KIOLAR
CONSTRICTION
INCREASED
IKTRACRANIAL
PRESSURE
IBRADYCAFUIA
I LXCESSIV
Uj SALIVATIO
\ /
\
X
\
INCREASE
:D
REGIONAL
CAPILLARY
PRESSURE
/
SPLE
GONT1UC
/
Figure II.2. A j'Oj;SJBLE _SC!:r.MA OF_. ACTTOjI_ OF 1'^DRTN.
-------
15
Electroencephalograms made after the administration of large doses
of endrin showed irregular slowing, irregular spikes, and frequent
convulsive discharges. Severe chronic convulsions could be produced
by auditory or tactile stimulation of the rats. It was noted that a
tolerance appeared to develop during subacute exposure to endrin in
long-term feeding period, the electroencephalograms appeared normal
although convulsions were produced (Speck and Maaske, 1958).
Degenerative changes, which were not described, have been noted
in the brain after lethal intoxication by endrin, but there is no
record of any lesion in the peripheral neural tissues (Treon et al.,
1955).
Intravenous injections of endrin in anesthetized pigeons, produced
a number of changes in telencephalic neuronal functions (Revizin, 1966).
Emerson et al., (1964) observed that dogs treated with a lethal
dose of endrin followed the usual pattern of symptoms and that their
tolerance for barbiturates increased greatly during intoxication even
though the barbiturates decreased the arterial blood pressure. Emerson
(1965) reported that endrin administered to beagle dogs produced
cardiovascular alterations such as hypertension and severe bradycardia.
Decreased glomerular filtration rate and renal blood flow with
c
hypertension and bradycardia were observed by Reins et aj_., (1964).
Endrin caused an increase in the venous return and corresponding
elevation of cardiac output with no change in peripheral resistance
(Reins et a]_., 1966).
-------
16
A noticeable rise ir/cardi a/flow coincided with a steady drop in
\^"^
resistance (Hinshaw £t jil_., 1966); the left arterial pressure increased
strikingly within 15 minutes after treatment with endrin, but the right
arterial pressure held steady. Gourdey ejt jal_., 1954, reported that the
chlorinated hydrocarbon insecticides exerted their effects through
central rather than peripheral stimulation. Convulsions apparently
originate from a direct action of endrin on the central nervous system.
Sowell et al., (1968) summarized the physiological changes produced by
endrin as shown in Figure II. 3.
Effect on Liver, Kidney and Other Organs
There have been reports of possible impairment in liver (Nelson
et, aj_., 1956) and kidney function (Reins jet aj_., 1964). An increased
serum alkaline phosphatase level due to ingestion of endrin indicates
impaired liver function, but the data used to arrive at this
conclusion is statistically insignificant and, therefore, open to
criticism. The impairment of kidney function, particularly the
decreased glomerular filtration rate, is indicated to result secondarily
from alteration in peripheral hemodyn'amics.
Diets containing endrin in the concentration of 8 ppm, when fed
for almost six months, did produce enlargement of the liver, kidneys
and brain of dogs. After 19 months of feeding diets containing 3 ppm
of endrin, the kidneys and hearts of dogs were significantly enlarged.
Other viscera were unaffected at the 3 ppm level and no visceral weight
changes were noted at the feeding level of 1 ppm (Treon ^t al_., 1955;
Treon et al_. , 1966) unpublished report of Kettering Laboratory,
May 9, 1955).
-------
ENIJKJN'
INJECTION
CNS
LE7T VENTRI
\
N
s
•
:
/
i
RVES
INCREASED
VE
RE
:ous
I URN
\
CONVUL
MUSCL
" ^' V
ADRENALS PARASYMPATHETIC
1 NERVES V
4* . 1 HEART FAILUi
MARKED
INCREASE V
IN P
,A,SMA EXCESSIVE SALIVATION
CATl-:Cl!Oi,AMlNES ^
(POT EN
HATED BY DECREASED
AC1DOSIS) . CARDIAC
f
SIGNS
ES)
RELE
OF METAB
DECREASE IN
VASCULAR
RESJCJ'AKCE >
OUTPUT
DECREASE IN
>' ni-l'LLilv ii GASEOUS
TRANSPORT IN LUNGS
<\SE
3LITES 1—^. HYPOXIA
ACIDOSIS
Figure II.3. PliYSlOLOCICAL CHANGES PRODUCED BY ENDRIN
-------
18
Male rats showed a significant enlargement of their livers i.n
relation to total body weight after two years of feeding endrin at
levels of 25 ppm and 5 ppm. This phenomenon was not noted in female
rats nor in male rats fed levels of 1 ppm endrin. Female rats which
were fed a diet containing 5 ppm of endrin showed an increase in the
weight of the kidneys as compared to body weight. This was not noted
in males nor at other feeding levels in females. No other changes in
the weight of viscera were noted (Treon ejt a.l_., 1955).
II. B. Toxicology
Endrin has the highest acute toxicity by all routes of exposure
to mammals of all of the chlorinated hydrocarbon pesticides in use
today. Dermal absorption is apparently rapid and complete. However,
endrin is rapidly metabolized and excreted and adipose storage does
not present a problem. The level of endrin causing no toxicological
effects for the rat is 1 ppm in the diet, equivalent to 0.05 mg/kg
body weight/day; for the dog is 1 ppm in the diet, equivalent to
0.025 mg/kg body weight/day. The FAO/WHO estimate of acceptable daily
intake for man is 0.0002 mg/kg body weight.
II. B. 1 Acute Toxicity
Acute oral, dermal, and inhalation toxicity studies have been
out for endrin.
-------
19
II. B. l(a) Acute Oral Toxlcity
The acute LDg0 toxicity (single dose) of 4-dimethanonaphthalenes
(aldn'n, isodrin, dieldn'n and endrin), when given orally to non-fasted
rats or rabbits, has been shown to be more closely related to the
spatial configuration than to the empirical composition of these compounds,
Isodrin or endrin having the endo, endo configuration are more
toxic than those which have the endo, exo configuration (aldrin,
dieldrin). The LD5Q values of acute oral toxicity in various species
of laboratory animals are summarized in Table II. 4.
The laboratory animals that absorbed endrin at a lethal oral dose
exhibited the following pattern of toxic symptoms: stimulation,
hyperexcitability, hyperactivity, uncoordination and exaggerated body
movements, ultimately leading to convulsions, depression, and death.
It was also noted that there is an interval of up to an hour or so
following oral dosing before the onset of lethargy prefacing the tremors
(Speck and Maaske, 1958 and Zavon 1961).
The LDgQ values shown in Table II. 4 for cats, rabbits, monkeys
and guinea pigs are less accurate than those for rats, because of
smaller numbers of animals used. It is apparent, in general, monkeys
and cats are more susceptible than of rats and guinea pigs are more
resistant. Rabbits, are also somewhat more resistant.
-------
TABLE II. 4
ACUTE ORAL TOXICITY OF ENDRIN
Strain or
SPECIES Breed
Rat Carworth
Rat Carworth
Rat
Cat Tabby
Rabbit Dutch
Guinea Pig Albino
Dog
Monkey
Monkey
Goat
Dosage
Number of Form
Animals O.lto 1.0% LD50 (mg/kg)
Used W/V in
Age M
29-31 10
days
6 mos. 10
6 mos.
Adult 1
Adult
Adult 2
Adult 2
Adult
Adult
£ Peanut Oil M
10 Solution 28.8
(27.8-28.8)
10 Solution 43.4
(42.1-43,4)
—
1 Solution 5
4 Solution —
2 Solution 36
(24-36)
Water- 10
Suspension
2 Solution 1-3
12
96% Technical
£
16
(16.4-16.8)
7.3
(7.3-11.7)
40-43
5
(7-10)
16
(10-16)
1-3
12
25-50
Reference
Treon et al . , 1955.
Treon et al., 1955.
Speck and Macke, 195
Treon et al . , 1955.
do
do
Kettering, 1955,
Shell Document K-55-1
Treon et al .., 1955;
Barth, 1967
Tucker, 1970.
-------
21
Adult female rats (6 months of age) are more susceptible to the
toxic effects of endrin than are younger immature female rats. The
difference in susceptibility of guinea pigs, in relation to sex,
appears to be similar to that of rats. Females are more susceptible
than males.
The acute toxicity of endrin appears to be influenced by the diet.
Three groups, each comprising about 100 male rats, were fed for 28 days
either a normal diet, a normal protein diet containing protein only as
casein, or a low protein diet. The acute toxicity to endrin was then
determined by a single oral administration of the pesticide. The LDgQ
values were 27, 17, and 7 mg/kg for the animals fed the respective diets,
indicating an approximately fourfold increase in toxicity between the
normal and low protein diet as well as an effect due to the type of
protein fed (Boyd and Stefec, 1969).
II.B. l(b) Acute Dermal Toxicity
The acute toxicity of endrin upon application to the intact or
abraded skin of female rabbits for 24 hours according to the sleeve
method of Draize, Woodard and Calvery (1944) are summarized in Table II. 5.
The minimum lethal dose was found to be greater than 60 mg and less than
94 mg per kg. body weight. Neither gross nor microscopic evidence of
damage to the skin of these animals was found (Treon et_ al_., 1955).
-------
TABLE II. 5 22
IMMEDIATE TOXICITY OF ENDRIN MAINTAINED IN CONTACT WITH INTACT
SKIN OF FEMALE RABBITS BY METHOD OF DRAIZE, WOODARD AND CALVERY
(APPLIED AS RECRYSTALLIZED DRY POWDER THAT PASSED 100-MESH SCREEN
MAINTAINED UNDER RUBBERSLEEVE FOR 24 HOURS)
No. of Animals
That Died/No, of
Dosage, G./Kg. Animals Given Dose
0.25-3.6 8/8
0.16 2/3
0.125 1/3
0.094 1/3
0.060 0/3
Treon e_t aT_., (1955) also reported the effects of the intermittent
cutaneous contact of endrin to intact skin of rabbits and their findings
are summarized in Table II. 6.
These data indicate endrin is rapidly and completely absorbed from
intact skin.
II. B. l(c) Acute Inhalation Toxicity
Treon ejt a/L , (1955), exposed several species of animals to air
containing the sublimed vapor of endrin in the concentration of 5.44
Mgrams per liter (0.36 ppm). The results are summarized in the
Table II. 7. The endrin concentration of the air in the inhalation
chambers was determined 4 times daily.
-------
TABLE II. 6
EFFECTS OF ENDRIN ADMINISTERED UPON SKIN OF FEMALE RABBITS FOR
2 HOURS ON EACH OF 5 DAYS PER WEEK OVER SEVERAL DAYS.*
No. of Doses
Applied
19-25
40-70
25-45
G.
0.150
0.075
0.075
Daily Dosage
G./Kg.
0.067-0.091
0.020-0.042
0.027-0.044
Condition
of Skin
Intact
Intact
Abraded
No. That Died/No.
Given Material
3/3
1/3
1/4
* Treon et a]_. (1955)
ro
CO
-------
TABLE II. 7
FATE OF ANIMALS EXPOSED INTERMITTENTLY TO VAPOR OF ENDRIN IN AIR
(EXPOSED FOR 7 HOURS PER DAY 5 DAYS PER WEEK. CONCENTRATION, 5.44 Mgrams/liter, i.e., 0.36 ppm)
Species
Cat
Guinea pig
Hamster
Rat
Rabbit1/
-------
25
II. B. 2 Subacute Toxicity
Worden (1969) reported the mortalities of rats during the first
37 days of feeding diets containing various levels of endrin. The
data are summarized in Table II. 8. He found that there were no
further deaths among the groups of survivor rats at 37 days when those
rats were transferred from an experimental to a control diet. One of
the males continuing to receive the experimental diet of 25 ppm of endrin
died on day 50. The symptoms induced by endrin included: hypersensitivity,
audiogenic seizures (which occurred frequently during the cleaning of
the room), swelling of the subcutaneous tissues of the head, staring eyes,
bloody incrustations over the eyelids, sporadic mild convulsions lasting
over 30 seconds, and, in fatal cases, violent convulsions resulting in
death. The symptoms were more marked during the earlier stages of the
study and were less severe in animals that survived. This may have
reflected loss of more susceptible animals, but may also have been due
to tolerance.
Groups consisting of five male and five female rats were fed
dietary levels of 0, 1, 5, 25, 50 or 100 ppm of endrin for up to 16 weeks.
All of the group fed 100 ppm died within the first two weeks and only
two rats fed 50 ppm and three fed 25 ppm survived. Three males fed
5 ppm also died; the other animals were continued on the test diet for
the full 16 weeks. Weight loss was roughly dose related but was
evident in all test groups, as was hypersensitivity to tactile stimuli.
-------
TABLE II. 8
MORTALITY DURING 37 DAYS OF SUBACUTE
ADMINISTRATION OF ENDRIN TO RATS.*
26
7
Endrin 25
35
50
100
2/5
5/5
5/5
5/5
.3/5
4/5
5/5
5/5
1
1
1
1
F,1M,3F
FJF.3F
F,1F,1M
F.1F.1M
,4F,4M
,3M,4M
,1M,3F
,2F,2F
,5M.,5M,6F,6M
,3M,3MS4F,6F,6M
,2M,3F,3M,4M,4M
* Worden (1969)
-------
27
There was an initial drop in serum alkaline phosphatase during the first
three to eight weeks; feeding, which was then followed by an increase at
all dose levels. At the end of the 16 weeks, the phosphatase level was
elevated above the controls in all the test groups, the levels being
highest in the groups fed 25 and 50 ppm (Nelson et al_., 1956). However,
other statisticians have considered that the elevation of serum alkaline
phosphatase was not significant in the groups fed 1 and 5 ppm of endrin
(Williams, 1966).
In a series of experiments by Treon ^t aj_., (1955), dogs were fed
diets containing from 1 to 50 ppm endrin along with control groups for
periods of time up to 47 days.
Two of the four dogs fed diets containing 8 ppm and the one fed 5
ppm died. The data are shown in Table II. 9.
The two surviving dogs on 8 ppm were kept on the diet for about
six months and then sacrificed; increased organ to body-weight ratios
for the liver, kidney and brain were found (See Table II. 10), and
histopathological examination showed degeneration of kidney tissue.
Three of the four dogs on 4 ppm of endrin survived and there were no
symptoms in dogs fed 1 or 3 ppm.
Cattle and sheep were not affected by 5 ppm of endrin their diet
for 112 days (Radeleff, 1956).
Groups of 20 seven-day old chicks each were unaffected by feeding
diets for 12 weeks containing 0, 1.5 or 3 ppm of endrin. When the
concentration was increased to 6 or 12 ppm, the birds became highly
excitable, failed to gain as much weight as the controls, and the
50
-------
TABLE II. 9
FATE OF DOGS GIVEN ENDRIN IN DIET*
(Insecticide introduced into diet 6 days of each week)
Daily Dosage in Relation to
Food Body weight,
ppm mg./kg.
10
8
2) b/
8)
5
4
3
1
0 b/
0.49-0.81
0.29-0.62
0.09-0.17
0.31-0.65
0.20-0.27
0.15-0.21
0.12-0.25
0.045-0.12
0
Sex and
(no. of dogs)
Duration of Period
of Feeding on Diet
Containing Endrin, Months
Fate
50
25
5) I/
20)
2.50-4.00
1.21-2.20
0.25-0.36)
0.97-1.27)
M(l) FM)
F(2)
F(D
18-20 days.
18-30 days
4.7
Both died.
Both died.
Died.
i>\ i)
M(l), F(2)
M(2), F(2)
24-44 days
5.7
9.9
47 days
5.7
18.7
18.7
18.7
Both died.
One died.
One died.
Died.
All survived.
All survived.
All survived.
All survived.
a/ Smaller dosage given during first portion (2.9 months) of feeding period,
larger dosage during remainder of period.
b/ Three additional control dogs survived 5.7 months.
* Treon et al_. , (1955)
ro
CO
-------
TABLE II. 10
Endrin in
Diet, ppm
8
4
0
RATIO OF WEIGHT
n
3
3
3
OF FAT AND
6 MONTHS ON
ORGANS TO BODY WEIGHT OF DOGS FED ALMOST
DIETS CONTAINING ENDRIN
Grams per 100
Liver Kidneys
3.16
3.06
2.66
0.52
0.36
0.37
Grams Body Weight
Brain
1.16
0.92
0.85
Fat
0.20
0.30
0.43
* Treon et al. (1955)
ro
vo
-------
30
survival rates over a 12 week period were 85 and 5 percent,
respectively, compared to 100 percent in the control (Sherman and
Rosenberg, 1954).
Groups of 40 quail, each were fed dietary levels of 0, 0.5, 1,
5, 10, 20 or 50 ppm endrin in their diet, starting when one day old.
Survival was adversely affected in all the test groups, and there
were no survivors beyond two weeks in the birds fed 10 ppm or more.
Food consumption was abnormally low. Symptoms involved lack of
muscular coordination, tremors, bedraggeled appearance and rigidity
with occasional convulsive movement (DeWitt, 1956).
Day-old pheasants, in groups of 40, did not survive beyond
eight days when fed dietary levels of 5 or 20 ppm endrin. Reduced
food consumption occurred, and the symptoms were the ?ame as those
seen in quail (DeWitt, 1956).
II. B. 3 Chronic Toxicity
The pathologic findings associated with the life-span feeding
of endrin to rats at various dosage levels are show!) in Table II. 11.
In a two-year experiment, groups of 20 male and 20 female rats
each were fed diets containing 0, 1, 5, 25, 50 and 100 ppm of endrin.
Concentrations of 50 and 100 ppm were lethal within a few weeks. The
concentration of 25 ppm increased the mortality rate of the females
(See Table II. 12). Non-survivors at the three higher levels exhibited
diffuse degeneration of the brain, liver, kidneys and adrenal glands.
3
-------
TABLE 11.11 PATHOLOGIC FINDINGS ASSOCIATED WITH THE INCORPORATION
OF ENDRIN IN THE DIETS OF RATS*
Level of
Exposure, ppm
Time (maximum),
years
Pathologic Findings
100
50
25
5
1
2
2
Diffuse degeneration of brain, liver
and kidney; 6 rats with diffuse degen
eration and necrossis of proximal and
distal convoluted tubules.
Diffuse degeneration of brain, liver,
kidneys and adrenals; no specific
renal lesions; slight fatty vacuoli-
zation of hepatic cells in two
animals.
Diffuse degeneration of brain, liver,
kidneys and adrenals; remainder of
viscera normal.
Normal viscera.
Normal viscera.
* Treon et al_. 91955)
ro
-------
TABLE 11.12
MORTALITY AMONG GROUPS OF CONTROL RATS AND RATS FED 2 YEARS
ON DIETS CONTAINING ENDRIN*
No. That Died/No. Fed on Diet
P. P.M.
100
50
25
5
1
0
a/ P. Z. 0.01.
b/ This value is
c/ P. 0.05-0.01.
MALES
80 weeks
18/20 a/
13/20 W
5/20
5/20
5/20
7/20
only slightly above 0.05.
106 weeks
18/20
16/20
9/20
13/20
9/19
12/20
FEMALES
80 weeks
18/20 a/
19/20 a/
12/20£/
7/20
4/20
5/20
106 week
19/20 a/
20/20 a/
15/20
12/20
9/20
13/20
Treon, et.a]_. (1955)
U)
CO
-------
33
The survivors in the two higher levels showed degenerative changes in
the liver only, while those fed at the lower levels had normal viscera.
At a level of 5 ppm or higher, an increase in lever to body-weight
ratio in males was observed. (See Table II. 13). This effect was not
observed in males fed 1 ppm or in females fed at either 1 or 5 ppm
endrin. Too few observations were made upon other groups to provide
statistically significant data. Treon et al., (1955) concluded from
the results of this experiment that the "no effect" level of endrin is
at the level of 1 ppm in diet.
A total of 1600 mice in equal numbers of each sex, consisting
of one inbred and one hybrid strain, were divided into four groups,
two of which were fed a control diet and the other two fed 0.3 or 3.0
ppm of endrin. Feeding of the test diet was started at five weeks of
age and continued throughout their normal lifespan, or until sacrifice.
Because of an early high incidence of fibroadenomas occurring in both
control and test groups in the hybrid strain, all the females of that
strain were sacrificed after 72 weeks for pathological examination.
A few of the mice, fed 3.0 ppm only, displayed convulsions in the
early stages of feeding but recovered and survived. Mortality was not
adversely affected by endrin, nor was body-weight or food intake.
?Jo hematological abnormalities Were evident in two males in the hybrid
group fed 0.3 ppm, which had severe leukemia. In either sex, the total
number of neoplasms was not influenced by the endrin content of the
diet, except in the case of hepatomas in the females of the hybrid strain,
which were significantly higher than the controls in the mice of the group
fi
-------
TABLE 11.13
RATIO OF WEIGHT OF LIVER TO BODY WEIGHT OF RATS FED 2 YEARS
Endrin in Diet
ppm
100
~J 50
25
5
1
0
25
5
1
0
Sex
M
M
M
M
M
M
F
F
F
F
ON DIETS. CONTAINING
n
2
4
n
7
10
8
5
8
n
7
ENDRIN*
Ratio of
Weight of
Liver to Body
Weight
G./100 G. P
3.26 a/
3.08 a/
3.03 0.02-0.01
3.14 0.05-0.01
2.82 > 0.05
2.66 ...
3.43 a/
3.22 ->0.05
3.08 ^0.05
0 IVI <£
3.01 . . . **
^/ Too few for statistical determination.
-------
fed 3.0 ppm, and sacrificed between weeks 53 and 60 of the feeding
period. Because of a relatively high incidence of hepatomas in one
group of controls of this strain, the increase at the 3.0 ppm level was
considered not due to endrin. It was noted that in no animals of
either sex were there any metastases of the hepatomas into the lungs
(Mitherup et al., 1970).
In an experiment of about 19 months' duration, groups comprising
two male and two female dogs were placed on diets containing 0, 1 or
3 ppm of endrin. All dogs on 3 ppm had increased organ to body-weight
ratios for the kidneys and heart. On the other hand, the ratios of
the weights of the livers, brains, spleens and fat to body-weight of
dogs fed either 3 or 1 ppm were not significantly different from
those of control beagles (See Table II. 14). Some female dogs fed
1 or 3 ppm of endrin had a renal abnormality characterized by a
slight tubular vacuolation; this change was also observed in the
female control dog. Male dogs in both control and test groups had
normal viscera.
From these series of experiments, Treon et al. (1955), summarized
the dog experimental results as follows:
(1) Dogs can consume safely about one-half the concentration of
endrin in their diets that rats can tolerate, if comparison is made
on the basis of comparably prolonged periods of time.
(2) Dogs are at least ten times as susceptible to the toxic
effects of endrin as to those of DDT, if judged by the histopathological
findings in certain organs of these animals, when fed upon diets
containing endrin or DDT in comparable concentrations.
-------
Groups comprising seven male and seven female dogs were fed
dietary levels of 0, 0.1, 0.5, 1.0, 2.0 or 4.0 ppm of endrin for two
years. Scheduled autopsies were performed on two dogs of each sex
from the 0, 1.0 and 4.0 ppm groups at six and 12 months. There were
no deaths due to the treatment nor were there any differences in body-
weight increase or food consumption between the group. The only
clinical abnormalities noted were in one female and two male dogs fed
4.0 ppm, and one female fed 2.0 ppm. These animals showed evidence of,
or were observed having, convulsions; the earliest incidence was
observed in a male dog after five months on 4.0 ppm. The only change
in organ weights were occasional slight increases in liver or liver-
to-body-weight ratios in the dogs fed 2.0 and 4.0 ppm. After two years.
histopathological examination showed slight vacuolation of hepatic cells
in the females and diffuse pigmentation of the hepatic cells in one
male and all females. At 4.0 ppm, vascular degeneration and diffuse
brown pigment in the hepatic cells was evident in all dogs, without any
sex differentiation. In two of the dogs, which had convulsions,
autopsies revealed some pathological changes in the brain. All other
organs in the dogs fed 2.0 or 4.0 ppm and all organs in the dogs fed
1.0 ppm or less, showed no morphological changes which were considered
to be attributable to feeding endrin. There were no significant changes
in the blood picture or in the chemical or physical characteristics of
the urine attributable to endrin. After two years, levels of liver
enzymes, prothrombin time, bromsulphthalein clearance, serum protein
-------
electrophorosis, glucose, urea nitrogen, cholesterol, calcium,
inorganic phosphorus, total bilirubin or uric acid showed no changes
attributable to endrin feeding (Jolley et al., 1969).
II. B. 4 Carcinogenic Studies
In the chronic studies carried out in mice, rats, and dogs, endrin
was not reported to cause an increase in the occurrence of malignant
tumors over that of the control animals. Similar results were used
by Diechmann, et al., (1970) in the study reported below.
Beginning with weanling rats, varying numbers of rats of both
sexes were fed dietary levels of 0, 2, 6, or 12 ppm of endrin throughout
their lifetime. No primary malignant hepatic tumors were found in any
animals upon histological examination. Two benign hepatic tumors
(haemangiomas) were found in one male control rat and the other in a
female fed 6 ppm of endrin. Tumor incidence in other tissues also
was not significantly different between the control and experimental
animals (Diechmann et al., 1970).
SO
-------
TABLE II. 14
RATIO OF WEIGHT OF FAT AND ORGANS TO BODY WEIGHT OF DOGS FED
ALMOST 19 MONTHS ON DIETS CONTAINING ENDRIN*
Endrin in
Diet, ppm n
3 4
1 4
0 6^-/
a/ P. 0.05 - 0.01
b/ Includes 2 addi
older and also
Grams per 100 Grams Body Weight
Liver
2.
3.
2.
92
07
86
tional male
eligible for
Ki dneys
0.
0.
0.
52^7
39
42
Brain
0.91
0.91
0.92
Fat Heart
0
0
0
.45 0.84-5/
.45 0.76
.52 0.67
beagles and 2 additional female beagles
AKC registration, employed as controls
Spleen
0.41
0.33
0.30
, less than 2
in overlappi
months
ng experiments
* Treon, et al., (1955)
OJ
VO
-------
40
II.B. 5. Reproduction Studies
Groups of male and female mice were fed endrin at dietary levels
of 0 or 5 ppm for 30 days. Test and control mice were than randomly
paired and continued on the test diet for a further 90 days, there
being a total of 101 pairs in the group fed endrin. The first litters
from test animals were significantly smaller than those from the
control group. The time taken to produce the first litter was not
significantly different between the two groups (Good and Ware, 1969).
Five groups, each comprised of 13-14 pairs of Saskatchewan deer
mice (Peromyscus manicalatus) of varying ages, were fed dietary levels
of 0, 1, 2, 4, or 7 ppm of endrin over intermitten periods between
which times the animals were either fed a normal diet or were
subjected to 48 hours starvation. The animals were sacrificed by
exposing them to cold stress at -16°C, and the time of death recorded.
During feeding, parental mortality increased in proportion to the
level of endrin. Young animals were more susceptible than old.
Starvation increased mortality in all test groups but not in the
controls; this effect was more evident with increasing dose levels.
Litter production frequency and mean litter size before and during
experimental feed were similar. However, post-natal mortality prior
to weaning increased in the young from parents fed 4 or 7 ppm.
Endrin adversely affected the survival time during cold stress in the
females but not in the males (Morris, 1968).
-------
41
Groups of ten male and 20 female rats were fed dietary levels
of 0, 0.1, 1.0 and 2.0 ppm of endrin over a period of three generations.
The Fg generation was mated after 79 days on the test diets, and the
males were rotated. The young from the first litter were discarded at
weaning and the parents mated again after ten days to form the F-]b
generation. Young from this generation were mated when 100 days old,
and this protocol was followed for three generations, using the second
litter in all cases. The size of the litter in the F3 generation from
the 2.0 ppm group was significantly larger than that from the controls.
Mortality was high in the controls which resulted in a greater
percentage survival in the F3a litter in the 0.1 ppm group and in all
F3b litters in the test groups. The weights of weanlings were
comparable to the controls except in the F3 a litters from the 0.1
ppm, which were significantly less due probably to1 the larger litter
sizes in.that group. Examination of the F3b weanlings revealed no
differences in organ to body-weight ratios. It was stated that were
no histological abnormalities, but details of the pathology were not
available. Fertility, gestation, viability and lactation indices did
not indicate that endrin affected any of these parameters (Mine et al.,
1968).
No eggs were produced from quail which received 1 ppm of endrin
in their diet either as winter maintenance or during the reproductive
period (DeWitt, 1955).
-------
42
There was reduced egg production in pheasants, fed 10 ppm of \
enuri.. I".- "^ *t 2 ppm or less. Survival of the chicks to two or-'
six weeks was also markedly reduced at 10 ppm but not at lower doses
V(DeWitt, J965). ...... —•"""'
rk-"", eqgs were injected with 0.5 or 5 mg of endrin per egg. The
hatching rate was 40 or 20 percent, respectively (Dunachie and
f'.fctchsr, 1966).
When 0.2 or 2.0 mg of endrin was injected into the yolk of
fertile eggs incubated for seven days, the hatchability was 40 and
6.9 percent, respectively (Smith e_t a]_., 1970).
The reproduction studies with endrin in various mammalian and
aviari vertebrate species, including chicken egg injection
hatchability data, indicate that endrin had no influence on
maturation but fetal and postnatal mortality were increased.
II. B. 6. Teratogenic Studies
No teratogen.ic studies, per se_, have been carried out on endrin.
No teratogenic effects were noted in the reproduction studies cited
above Urwpver, this can not be taken as conclusive evidence of the
lack of teratogenic potential of endrin.
II. B. 7. Special Studies on the Photoisomerizatton Product of Endrin
''.'hon endrin is irradiated with short wavelength ultraviolet
light, the delta-keto compound is formed in 37 percent yield as well
as an aldehyde in 9 percent yeld. Under the influence of sunlight,
only the ketone is formed. The ketone is about a quarter as toxic
to rats as endrin and, like endrin, is more toxic to the male than
.•c t^e female (Soto and Diechmann, 1970).
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43
II. C. Human Toxicity
II. C.I. Signs and Symptoms of Poisoning
The major clinical manifestation of endrin intoxication in man
are convulsive seizures of several minutes duration followed by semi-
consciousness. More serious symptoms are continuous convulsions,
high fever, and decerebrate rigidity prior to death. Mild symptoms
of poisoning include dizziness, weakness of the legs, abdominal
discomfort, and nausea. Temporary deafness and insomnia may also
occur. It has been estimated, based upon reports of outbreaks of
poisoning, that 0.2-0.25 mg/kg bodyweight will produce a single
convulsion in man, and that repeated convulsions will result from
1 mg/kg (Hayes, 1963).
II. C.2. Treatment and Prognosis of Intoxication
First aid in the case of accidental skin contamination should
consist of immediate removal of all contaminated clothes, including
underwear, and washing of the contaminated skin and hair with soap
and water. All contaminated clothing should be changed and laundered
before re-use.
In the case of ingestion, vomiting should be induced and the
stomach emptied as quickly as possible.
If the patient is unconscious, a free airway should be ensured.
If respiration has stopped, aritficial respiration should be employed.
Medical treatment is largely symptomatic and supportive and
directed against convulsions and anoxemia. Carbonadsorbens may be
given. Sodium sulphate may be administered as a laxative. Oily
laxatives or milk should not be given. Morphine, epinephrine, and
-------
44
noradrenaline are contra-indicated .
An unobstructed airway must be maintained. When needed, oxygen
and/or artificial respiration must be given.
If prompt and adequate treatment is given, then death can be
prevented and even the severest intoxication will recover completely
within some weeks (Princi, 1957). Furthermore, EEG's will return to
a normal pattern within months (Princi, 1957; Hoogendam ejt a]_., 1962
and 1965).
Administration of phenobarbitone may both control prodromal
symptoms and prevent convulsions. When convulsions do occur
barbiturates should be given by slow intravenous infusion, e.g.,
thiopentone sodium, 10 mg/kg, with a maximum of 750 mg for an adult.
The administered dose should be sufficient to control convulsions.
II. C. 3. Observation of Intoxication in Man
In one incident 59 people became ill from the ingestion of bread
accidentally containing up to 150 ppm of endrin, but there were no
fatalities (Davies and Lewis, 1956). Calculations based on the
amount of bread consumed suggested that an intake of 0.2-0.25 mg/kg
could produce a convulsion (Hayes, 1963), whereas the maximum amount
consumed was estimated to have been 1 mg/kg body weight (Zavon, 1961).
Data on the pathology of 60 fetal cases of endrin poisoning, 41
of which involved suicide, have been published by Reddy et al.,
(1966). No specific histopathological organ changes were observed.
These data do not include any reference to the size of the doses
ingested. However, the toxic doses of endrin were estimated to be 5-50
mg/kg by the oral route; the lethal dose of endrin was estimated to
be about 6 grams (Reddy et, aj_., 1966).
G r»
-------
45
Endrin has been found at concentrations of up to 400 mg/kg in the
fat and up to 10 mg/kg in other tissues of people who have been
fatally poisoned poisoned. Hates (1963 and 1966).
Van Raalte (1965) extracted from the world literature all cases
of fatal endrin poisoning known at the time. A total of 97 cases
were reviewed of which 69 cases were suicide, 24 accidental ingestion,
4 occupational cases from endrin spraying. No fatalities were reported
as a result of endrin manufacture and formulation.
Coble ejt aj_., (1967) reported 3 cases of non-fatal convulsive
endrin poisoning in the United Arab Republic resulting from the
consumption of bread made from endrin-contaminated flour. In the
first case, the serum endrin level was 0.053 ug/ml; 30 minutes after
the convulsion endrin could not be detected («^~ 0.004 ug/ml) in
samples of the cerebrospinal fluid. Twenty hours after the onset of
convulsions, the serum endrin level had fallen to 0.038 ug/ml; 10 hours
later, it was 0.021 ug/ml. In cases 2 and 3, no endrin was detected
in the blood 8-1/2 and 19 hours, respectively, after convulsions.
A total of 874 persons were hospitalized, and there were 26 deaths
in several outbreaks of poisoning in Saudi Arabia in 1967 due to
consumption of bread containing endrin. Approximate average levels in
the bread in various outbreaks were 48, 1500, or 400 ppm, corresponding
to a percentage of fatalities of 1.4, 9.5, and 0.4, respectively, among
those poisoned. Blood from patients contained 0.007-0.032 ug/ml endrin.
Signs and symptoms were typical of central nervous system stimulation,
and all survivors rapidly returned to normal (Weeks, 1967).
-------
46
II.C. 4. Symptomatology. Treatment, and Prognosis of Intoxication
Frequently, the first indication of acute endrin poisoning is a
sudden epileptiform convulsions, occurring from 30 minutes to up to 10
hours after exposure (Weeks, 1967). The convulsions last for several
minutes and are usually followed by a semi-conscious state for 1/4-1
hour (Coble £t al_., 1967). Death or permanent brain damage may
ultimately occur resulting from anoxemia due to prolonged convulsions
(Jacobziner £t aU, 1959, Coble ie_t a\_., 1967). In less severe cases
of endrin poisoning, the primary complaints are headache, dizziness,
abdominal discomfort, nausea, vomiting, insomnia, agressiveness and,
rarely, slight mental confusion (Coble £t aK , 1967; Week, 1967).
The prognosis is good if cerebral damage by prolonged anoxemia is
avoided. Recovery to full normal health in such cases is rapid and
usually complete within a few days (Davies e^a]_., 1956). No
specific findings from acute endrin poisoning have been reported at
autopsy (Reddy et al_., 1966; Coble ejt al_., 1967; Weeks, 1967). The
rapidity of the onset of signs and symptoms, predominantly of central
nervous system stimulation, and the rapid return to normal among those
who survive is typical for an intoxication with an organochlorine
insecticide (Weeks, 1967). The recovery from an endrin intoxication
is quicker than that from the other cyclodiene insecticides.
Studies in human subjects experiencing intoxication from endrin
(Coble et al., 1967; Weeks, 1967) and from occupational workers
(Hayes and Curley, 1968; Jager, 1970) have demonstrated that endrin
SB
-------
47
rapidly disappears from the blood in cases of acute intoxication and
cannot be detected in the fat or blood of people exposed to endrin
unless symptoms of intoxication are evident.
II.D. Epidemiology
Endrin has been included in most of the surveys of chlorinated
insecticide levels in adipose tissue and blood. Even in those areas
where endrin is most extensively used (e.g., India and Lower Mississippi
area) endrin could not be found in human subcutaneous fat or in blood
from the general population at the limit of detection of 0.03 mg/kg and
lower (Kunze e_t al_., 1953; Hoffman et. al_., 1964; Dale ejb a]_., 1965;
Zavon e_t aj_., 1965; Novak e_t a]_., 1965; Robinson e_t al_., 1965;
Wiswesser, 1965; Hayes et. al_., 1965; Brown 1967; Hayes, 1967;
Wasserman et al_., 1968; Hayes et al_., 1968; Robinson, 1969). Levels
of the 9-keto metabolite of endrin in four human fat samples were all
less than 0.0004 ppm (Richardson, 1970).
II.D.I. Surveillance Studies of Occupational1y Exposed Workers
In Treon's review of the toxicology of endrin (1956) he states:
"These studies (on workers handling endrin) reveal that harmful
physiological effects to workers are found only in those instances
where excessive absorption has occurred either in the form of an acute
dose or subacute doses from unusually careless handling. No established
cases of chronic illness from exposure to endrin are on record".
In a manufacturing plant in the U.S.A., medical supervision of
workers exposed for a period of 1-19 years (average 12 years) failed
to reveal any unreasonable adverse effects (Hayes et al., 1967).
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48
In these occupationally exposed workers no endrin could be found in the
subcutaneous fat.
Van Dijk (1968) examined serum alkaline phosphatase levels of 15
endrin operators in November 1964, July 1965 and February 1966
respectively. Some of these operators had been working in the endrin
plant for periods up to 8 years. No significant change in the
alkaline phosphatase was found.
Among workers in a plant manufacturing endrin and a number of
other pesticides, no detectable amounts of endrin were found in
samples of plasma, fat, or urine. Exposure was for an average time of
2,106 hours. Based upon the limit of detection, the levels of endrin
were below 0.0030 ppm in plasma, 0.03 ppm in fat and 0.0016 ppm in
urine. Endrin has, however, been detected in the serum and urine of
people who received amounts sufficient to produce intoxication
(Hayes and Curley, 1968).
Serum alkaline phosphatase was determined in 30 workers who had
been exposed to endrin for periods from six weeks to eight years.
There was no difference in the levels found in the exposed group and
those found in a group comprising nine unexposed individuals, nor was
there any relationship detected between the phosphatase levels and
the duration of exposure of the workers (Shell, 1965).
In 45 operators of the endrin plant, of Shell International Ltd.,
blood concentrations have been determined at least once a year since
1964. Endrin has/neveTr\been found in the blood at a detection level
n
I
-------
49
of 0.0 1 ug/ml (since December 1965, 0.005 ug/ml. No worker has ever
been transferred because of an elevated endrin level in blood
(Jager, 1970).
Jager (1970) reported the occurrence of endrin in the blood of
formulators handling endrin.
Twenty percent endrin was accidentally splashed with emu! si fi able
concentrate on the hand of a worker filling a drum. He immediately
took a shower with soap and water and changed clothes. A blood sample
taken one hour after the accident contained: endrin, 0.09 ug/ml;
dieldrin and telodrin below detection level. This man developed no
signs or symptoms of intoxication. Five days later the endrin level
in his blood was ^ 0.005 ug/ml.
A formulator handled technical endrin powder carelessly, producing
a lot of dust, disobeying instructions to wear a dust mask. After
having worked for 4 hours he sustained a convulsive seizure which was
treated with phenobarbital , 60 mg every 3 hours for one day. Afterwards,
he complained of headache only. The next day, he felt well. The
following blood levels of pesticides were found:
Directly after the convulsive seizure: 0.08 ug/ml endrin,
0.11 ug/ml dieldrin;
24 hours later: 0.02 ug/ml endrin,
0.11 ug/ml dieldrin;
4 days after the 2nd samples: -^- 0.005 ug/ml endrin,
0.10 ug/ml dieldrin.
71
-------
50
Four colleagues working next to the worker cited above, but who had
been wearing dust-masks were examined at the same time and showed endrin
levels in the blood of 0.01, 0.01, 0.005, and -^0.005 ug/ml, respectively.
None of these workers had signs or symptoms of intoxication, notwith-
standing the fact that one of them had in addition to 0.01 ug/ml endrin,
a dieldrin level of 0.18 ug/ml in the blood.
An operator was accidentally splashed with 20% endrin emulsifiable
concentrate. He showered and changed clothes 10 minutes after the
accident. Treatment consisted of prophylactic oral doses of phenobarbital
60 mg every 4 hours for 24 hours and close observation. No signs or
symptoms of intoxication were noted. The following blood levels were
found: 40 minutes after the accident: 0.027 ug/ml endrin, 0.01 ug/ml
dieldrin; 12 hours after the accident: 0.025 ug/ml endrin, 0.01 ug/ml
dieldrin.
The endrin blood levels probably peaked between the first and
second samples , i.e., twtween one and twelve hours after the accident.
It is estimated that the blood level of endrin below which no
signs or symptoms of intoxication occurs, is in the range of 0.05 -
0.100 ug/ml. Measurable blood levels (detection level 0.005 ug/ml)
occur only after gross overexposure. The half-life of endrin appears
to be approximately 24 hours. Medical control of a group of workers
exposed over periods up to 13 years has failed to show any effects of
long-term exposure. The blood picture, results of urinalysis, SGOT
and S6PT, alkaline phosphatase and lactic dehydrogenase remained all
72
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51
within normal limits. Electroencephalographic changes which were
occasionally noted returned to normal. Absenteesism due to disease
or accidents was comparable to that of a control group. Because of
the short half-life of endrin, it is (unlike dieldrin) impossible to
calculate the average level of exposure of the workers to endrin
(Jager, 1970).
II.D.2. Steroid Hormonal Metabolism of Endrin Workers
6-B-Hydroxycortisol Excretion in Urine
Many drugs and chemicals may stimulate the hydroxylation of
steroids in the body, amongst them phenobarbital, diphenylhydantoin,
phynylbutazone, and N-phenylbarbital (Werk e_t a1_., 1964; Burstein
et_ a]_., 1965; Kuntzman e£ al_., 1966; Conney, 1967; Kuntzman et a_1.,
1968).
The studies of these investigators suggest that the measurement
of the urin ary excretion of 6-B-hydroxycortisol, a metabolite of
cortisol, compared with the excretion of total 17-hydroxycorticosteroids,
which is not changed by the inducers, might be a useful index for the
induction of hydroxylase in liver microsomes in man. Kuntzman et al.,
(1968) found that 6-B-OH-cortisol excretion in man is normally below
400 ug/day, whereas in situations in enzyme induction, such as in
N-phenylbarbital treated human volunteers, excretions exceeding 400
ug/day were found.
For this study, excretion of 6-B-OH-cortisol and 17-OH-cortico-
steroids were determined in 20 non-insecticide exposed four-shift workers.
-------
52
All urine samples were collected between 8 a.m. and 11 a.m. on the last
day of the morning shift. Hormone determinations were made by Searle
Scientific Services, Lane Road, High Wycombe, Buck, U.K., who also
added their own .control group of 10 men. By determining the ratio
between the excretion of 6-B-hydroxycortisol and 17-OH-corticosteroids,
the factor of diuresis is eliminated and there is no need for examining
24 hour urine samples. Therefore, this method is convenient for use in
healthy workers.
The results of these determinations are summarized in the Figure II.4.
From this it is clear that geometric means and ranges of the ratio in
aldrin-dieldrin workers do not differ from those in tha control groups.
In this group of 13 aldrin-dieldrin workers the range of p, p'DDE in the
blood was 0.006-0.042 ug/ml with an arithmetic mean of 0.015 ug/ml,
which is in the same range as in the general population. Dieldrin levels
in the blood of these 13 workers ranged from 0.018-0.VI0 ug/ml with an
arithmetic-mean of 0.051 ug/ml. In these workers, who had reached a
steady state level as far as dieldrin is concerned, the mean leave
corresponds, according to the formula of Hunter and Robinson (1969), to
an average equivalent oral daily intake of 593 ug/man/day, which is at
least 85 times the intake of the general population in the U.K. and the
U.S.A. for this insecticide. But even the man with highest dieldrin
level in this group-/0.h!0) ug/ml, or 183 times the present blood level
of the general population—showed, apart from a p,p"DDE level of 0.014
ug/ml, a 6-B-hydroxycortisol ratio of 166 29.6, both values being
5.6
-------
Control Group (Searle)
•
Control Group (Shell)
Aldrin-dieldrin workers
Sndrin workers
.V-
10 -
'20 -
13 -
'
8 -
t
1
5 (
-
Ratio
N* = Number of workers.
Figure II. 4. Rat-in _ &-&-cortisol in u?Jl
1
8
10
!
i
i
}
i
t
i1 •
i
i
I • i
i
2
0
3
0
40
r
i
•
I
(
|
60
1
T ~]
8
D
1
1
100
i
!
' 1
!
!
20'Ci
6-B-OH-cortisol in nc/1
17-OH-corticosteroidV :j.n mg/1
in urine.
_
,- .1 —
_._
17-OK-corticosteroids in
limits of this mean and of all observations).
-------
54
quite normal in comparison with the control groups.
The ratio between the excretion of 6-B-OH-cortisol and 17-OH-
corticosteroids was also determined in 8 endrin workers.
It was found that the range and the geometric mean of this ratio,
was significantly higher when compared iwth those of the control groups
and the aldrin-dieldrin workers. The 6-B-OH-cortisol levels in urine
were higher in this group, whereas 17-OH-corticosteroids and 17-keto-
steroids did not show marked differences between groups. Of course,
these levels expressed in mg/1 are dependent on the total urine
production per day.
r» «•••
/h
-------
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-------
Morris, R. D. Effects of endrin feeding on survival and reproduction
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-------
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-------
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-------
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Chapter III , ~\-- - A«^V*
Toxicity, Fate, and Significance of Endrin in the Environment
III.A. Intrpduction - Endrin is the most toxic chlorinated hydrocarbon
pesticide'T It is persistent and residues in soil, water and animal
tissue have resulted from uses to control insects, birds and rodents.
Records show substantial reductions in populations of non-target species
in some areas where endrin has been used. These factors have aroused
serious concern among various groups of conservationists and other
interested individuals lest some non-target wildlife populations become
decimated or extirpated.
III.B. Toxicity to Fish - Acute toxic effects observed under field
conditions generally have resulted from careless application, disposal,
or accidental spillage (Johnson, 1968). Environmental variables su
as the types pH and temperature of soil or the mineral and oxygen content,
turbidity and pH of water influence persistence in soil and the acute
toxicity threshold of fishes.
Pesticides have been used in such quantities that they have become
pollutants of terrestrial and aquatic environments which ranks second
in importance to all other industrial wastes. Surveys of fish kills
carried out by the U.S. Public Health Service (1960, 1961, 1962),demon-
strated that pesticides were the cause of 32 percent of all fish kills
in 1960, 21 percent in 1961, and 18 percent in 1962. Numerous fish kills
have been reported in some areas of the Mississippi Delta adjacent to
lands where, on^a—1-0-year average, 10 Ib. endrin per acre were applied
each year (Tarigwell, 1965)./Thus, fish killed by pesticides exceeded
in number those killed by refinery, paper mill, or plating wastes.
-------
III.B.I. Acute Studies - Results of laboratory studies are usually
reported as LC^Q or TLm values for exposure periods of 1, 2, 3, or 4
days. Tests by lyatomi, et_ a^., (1958) were conducted on young carp;
(Cyprinus^ carpio), and goldfish., (Carassius auratus). LC5Q values
for carp exposed for 48 hours varied from 0.004 to 0.008 ppm at
17-28°C and 0.002 ppm for goldfish, at 27-28°C. Endrin becomes less"
toxic to fish as water temperature is lowered, and fish, eggs and
^
larvae are more resistant than adults. Lethal concentrations determined
by Henderson, et^ a.^., (.1959) were 0.006 ppm for bluegill (Lepomis macrochirus)
and 0.00196 ppm for goldfish at 96-hour exposure.
Static 96-hour bioassays with 12 insecticides were conducted at
24°/00 salinity, 20°C and pH8 with the following seven species of
estuarine teleosts (American eel, Anguilla rostrata; mummichog,
Fundulus heteroclitus; striped killifish, Fundulus majalis; bluehead,
Thalassoma bifasciatum; striped mullet, Mugil cephalus; Atlantic
silverside, Menidia menidia; and northern puffer, Sphaeroides
maculatus. Endrin was consistently the most toxic compound tested.
The LCrQ values of each species in 96 hour tests with endrin is shown
in Table III.B.I. ranged from 0.05 to 3.1 micrograms per liter. JPhe
^
range In LC25 (96 hrs.) and LCy5 (96 hrs.) for endrin in seven species
of estuarine teleosts in ppb were: LC25-0.03 to 1.9; and 1075-0.08
to 4.5. When the relative toxicity of organochlorine insecticides
to marine organisms were compared, it was concluded that teleosts
were less resistant than mollusks and about equal in sensitivity to
decapod crustaceans (Eisler, 1970b).
Rfi
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Table III.B.I.
ACUTE TOXICITY OF ENDRIN TO ESTUARINE FISHES*
SPECIES
Atlantic silverside
Bluehead
Striped killifish
Striped mullet
American eel
Hummichog
Northern Puffer
TOTAL NUMBER
FISH
50
25
60
40
70
49
60
LC5Q in Micrograms Per Liter (ppb)
Active Ingredients At —
24 hr.
0.5
0.6
1.8
0.7
1.1
1.8
3.1
48 hr.
0.08
0.5
0.7
0.3
0.6
0.7
3.1
96 hr.
0.05
0.10
0.30
0.30
0.60
0.60
3.10
*Data from Eisler, 1970b
-------
Toxicities of endrin J:o spjring chinook (Oncorhynchus tshawtscha)
and cohoHOncorhynchus kisutch.) salmon, rainbow trout (Salmo gairdneri) ,
bluegill, mosquitofish (Gambusia affinis), guppies (Lebistes reticulatus),
and marine threespine sticklebacks (Gasterosteus aculeatus) were reported
by Katz and Chadwick (1961). Coho salmon were the most sensitive with
•*-**"" s£** "V ~"~~~—N
a 96-hour TLm of 0.27 ppb;/rainbow trout were 0.90',) chinook salmon,
0.92; guppies, 0.90; bluegills, 0.60; and stickleback, 0.75 ^LJ^pjJb) .
re/ j)»fnv f'jf ^"^ -~
u Screenivasan and Natarajan (1962) tested endrin as a fish toxicant
to eliminate undesirable species. Their data showed«the following
LC^Q values for 24-hours: Tilapia mossambica, O.Olvto 0.013 ppm; Channa
spp., 0.01 to 0.08; Barbus spp., 0.008 to 0.01J; Danio acquipinnatus,
?
0.006 to 0.008; Rasbora daniconius, 0.006 to 0.009; mosquitofish, 0.01£)'
?
to 0.012; and carp, 0.008 to 0.11. •
The toxicity of some insecticides to the Indian catfish, Heteropneustes
fossilis, was studied by Saxena and Aggarwal (1970). This species died
within 5 hours in an aqueous solution containing 0.12 ppm endrin. At
a concentration of 0.014 ppm, fish, could survive only for 12 to 16 hours,
while exposure to 0.00598 ppm caused death within 24 hours. The greatest
concentration at which the fish could survive was 0.00578 ppm.
The effect of potential mosquito larvae control chemicals upon
mosquitofish, a natural predator, was evaluated by Mulla (1963). When
applied at rates of 0.1 Ib./acre, endrin produced a complete kill for
2-3 days, and moderate mortality up to a week post-treatment. Endrin
applied at 0.5 Ib/acre produced 100% mortality up to 20 days after
treatment.
-------
A major obstacle in insecticide use for rice Borer control in paddy
fields is the high, toxlclty of many insecticides to fish growing in paddy
fields under natural or artifical conditions. The Department of Agriculture,
Malaya, studied the toxicity of various insecticides to fish and found that
exposure for 20 hours to 0.45 ppb endrin was lethal for young Ophicephaius
striatus. These results support an earlier opinion that endrin is too
toxic for use at the normal rate of application (1/2-1 pound per acre).
Endrin was found, from tests in Selangor, to be highly toxic to ducks as
well as to fish. The solvent oil also appeared to be a contributing factor
in the toxicity of insecticides (Anon, 1957). With marine species, spot
(Leiostomus xanthurus), the lethal concentration of endrin was 0.1 ppb
after 5 days exposure (Lowe, et^ al_., 1966).
Brungs and Bailey (1966) studied the influence of suspended solids
on the acute toxicity of endrin to fathead minnows (Pimephales promelas).
TLm values for controls (clear water) ranged from 0.47 to 0.52 ug/1.;
while those containing clay in suspension were 0.37 to 0.50 ug/1.
Similar work by Ferguson, et al., (1965) indicates that little of the
endrin associated with bottom sediments becomes available to fish within
a short time.
lilood levels of endrin in gizzard shad (Dorosoma cepedianum) and
channel catfish (Ictalurus punctatus) were studied to determine threshold
levels of acute toxicity. The blood from dead shad had endrin levels
greater than 0.14 ug/g (av. 0.24) blood from live fish contained less
than 0.10 ug/g (av. 0.06). Two gizzard shad with levels above 0.10 ug/g
-------
survived. Similar results were observed in shad exposed tinder field
conditions (Brungs and Mount, 19.66). Results obtained when channel
catfish were exposed to continuously renewed water containing endrin
indicated blood threshold at approximately 0.30 ;ig/g, with minimal over-
lap between living and dead fish (Mount, et_ aiU, 1966). A continuous
flow laboratory system, where pesticide concentrations were kept constant,
was used by Mount and Putnickl (1966) to examine accumulation of endrin
by fathead minnows. Fish exposed to water containing 0.000015 ppm endrin
had total body concentrations 10,000 times those in the water. These
authors also verified the presence of endrin in concentrations from 2
to 4 ug/g in approximately 40 muscle samples of dying channel catfish.
Blood samples taken from dying channel catfish in the 1963 Mississippi
River fish-kill area ranged from 0.40 to 0.56 ug/g (Annpn., 1964).
Endrin toxicity to resistant and susceptible mosquitofish was
assessed by Burke and Ferguson (1960) in both static and flowing
solutions. Resistant fish were obtained from cotton field drainage
ditches while susceptible ones came from insecticide-free ponds. The
Jfv-'
toxicity of a given concentration of endrin was greater togm constantly
renewed solutions than under static conditions. In flowing-water* rate^
of mortality of susceptible specimens exposed at 2.0 ppb was roughly
comparable rates in the resistant forms exposed to 200.0 ppb.
Relative toxicity of endrin to four salmonid species was tested
by Post and Schroeder (1971) . Species used included brook trout
(Salvelinus fontinalis), rainbow trout, cutthroat trout (Salmo
clarki), and coho salmon. TLm figures in ppb were: brook trout
-------
0.355 to 0.59; cutthroat" t-rout, 0.113 to 0.192; rainbow trout, 0.405;
,"' /
and coho salmon, 0./77./The two values each, given for brook and cut-
/ f •
/ S
throat trout showed, the effects of different average body weights.
/ *° j
/ / q-
Endrin was 66% more toxic to 1.15 'brook trout than to 2.04 g brook
/ ' ^
trout and 70% more toxic to 0.37 g cutthroat trout than to 1.25 g fish.
Earnest and Benville (1972) provided data on acute toxicity of
endrin to two surf fishes from the estuarine region of San Francisco Bay.
With the shiner perch (Cymatogaster aggregata) , 96-hour TLmtjQ was 0.8
ug/1 in static and 0.12 in intermittent flow bioassays. Comparable data
for the dwarf perch (Micrometrus minimus) were 0.6 ug/1 for static and
0.13 for intermittent flow tests.
Another study compared results of simultaneous static and dynamic
bioassays of endrin in Pimephales promelas (fathead minnow) which were
acclimated to the laboratory for one month before test ing .^Endrin was
used at concentrations of 1.0, 0.5, 0.34, and 0.22 ppb. The LC5Q (48 hour,
18°C) for endrin was 0.77 ppb (static) and 0.5 ppb (dynamicXor 0.74 times
_ _.
greater for dynamic as compared with static conditions. The LCcQ (96-hour)
for endrin was 0.77 ppb (static) and 0.39 (dyanamic) . LC^Q'jfrom static
C-tests were slightly higher than those from dynamic tests (Lincer, et al.,
1970>-
,
Carp eggs, stripped and fertilized in vitro, were subjected to
a commercial formulation of endrin at concentrations of 0.001, 0.01,
0.10, 1.0, 5.0, and 10.0 ppm active ingredient. Embryo viability was
not signficantly affected at concentrations less than 1 ppm. However,
embryo death at the gastrula and blastula stages resulted at concentrations
of 5 and 10 ppra, respectively CMalone and Blaylock, 1970) .
-------
Lowe (1966) measured 24-hour LCrg's in flowing seawater for spot,
striped mullet (Mugil cephalus), menhaden (Brevoortia patronus),
longnose killifish (Fundulus similis), and sheepshead minnows
(Cyprinidon variegatus). Acute toxicities for these five species
in ppb were: striped mullet, 2.6; spot, 0.45; menhaden, 0.80;
sheepshead minnow, 0.32; and longnose killifish, 0.23. The 24-hour
TLm for previously non-exposed bluegills from Louisiana showed
u^
2.0 + 0.27 ppb, and 2.0 ppb was reported as the/lethal exposure
concentration) (Bennett and Day, 1970). ^ ty-tanf '
Ferguson, et_ al^., (1965) measured TLm values to endrin were for
black bullheads (Ictalurus melas) and mosquitofish in the Mississippi
River. Values for four populations of mosquitofish varied from less
than 0.5 to 120 ppb and for the black bullhead from 0.37 to 2.5 ppb.
The acute 36-hour TLm values were measured by Ferguson and Benghari
(1966) for yellow bullheads (Ictalurus natalis) taken from sprayed
and unsprayed areas in Mississippi. The results show a 60-fold endrin
resistance in fish from treated areas but both levels are well within
the established "highly toxic range" (up to 1.0 ppm) uses as a "rule
of thumb" in pesticide label cautions.
Monthly insecticide tests on two Yazoo-Mississippi Delta oxbow
lakes were made by Bingham (1970). Varying adjacent agricultural
use patterns resulted in high pesticide levels in one lake and much
lower levels in the other. Thirty-six hour bluegill bioassays in
endrin showed TLm values of Wolf Lake fish 20-fold greater than Mossy
Lake fish, or 300 ppb and 15 ppb, respectively.
-------
Butler (1969) discussed the significance of residues in estuarine
fauna. He stated that test procedures showed that 48-hour TLm5Q values
for endrin for various species of crustaceans and fishes were usually
1 ug/g or less within normal ranges of environmental salinity and
temperature.
Adult northern puffers, Sphaeroides maculatus;, were exposed to
graded concentrations of endrin. All fish subjected to 10.0 ppb of
endrin died within 24 hours. At concentrations of 1.0 ppb or lower,
no mortality occurred within 96 hours (Eisler and Edmunds, 1966).
Eight extensive fish kills occurred in agricultural drains of the
Sacramento Valley in July, August and September, 1963. Field investi-
gations revealed that five kills were associated with using endrin in
apple pomace bait to control cutworms in sugar beets. Growers applied
the endrin bait and then irrigated the field to force cutworms to the
t>
sil surface where they could find the bait. Heavy fish losses were
A
attributed to water draining from the field. In one of the five reported
endrin-related kills, as many as 30,000 fishjaay- have been killed (Hunt,
A
1964) .
III.B.2. Chronic Studies - Effects of endrin on aquatic animals and fish
eggs exposed for long periods has been studied. Lowe, et_ al^., (1966)
observed spot, Leiostomus xanthurus) which were reared to sexual maturity
in sea water containing sublethal concentrationgjof 0.05 ppb. These fish
showed no symptoms of poisoning during 8 months exposure. No pathology
was found at this exposure level. In contrast, a 3-week exposure to a
-------
'1
'
near-lethal concentration Cca 0.075 ppb) produced systemic lesions to
the brain, spinal cord, liver, kidneys, and stomach. Test fish sur-
viving long-term exposure to endrin were not affected by subsequent
stress situations, such as rapid salinity change or periods of starvation.
Separate groups of spot were exposed to several concentrations of endrin
for periods up to 19 days. After five days exposure, all fish were dead
in concentrations of 0.1 ppb and above. A lower concentration of 0.075
ppb killed no fish until the ninth day of exposure and 19 days were
required to kill 57% of the population. The 0.05 ppb concentration was
sublethal (Lowe, 1966).
Effects of endrin on egg hatching of the longnose killifish (Fundulus
similis) were studied by placing fertilized eggs in petri dishes containing
0.001 and 0.0001 ppm endrin with daily changes in solution. Hatching
started 15 days after fertilization and continued for 1 week. Hatching
rates were 40 and 45% of the control at these concentrations while
mortality of fry was 6% for each group.
Static bioassays with endrin were conducted on mummichogs Fundulus
heteroclitus, at 24°/oo salinity, 20°C and ph 8.0. Most mummichogs that
survived high LCyc, 24 hr.) levels of organochlorine insecticides for
more than 120 minutes died by day 21 post-exposure. Shorter exposures
produced fewer deaths. In holding studies, mortality was high during
a 240-hour observation period following 96-hour exposure (Eisler, 1970a).
Temperature, salinity, and pH of the medium all influence pesticide-
induced mortality. Toxicity of organochlorine insecticides to mummichogs
-------
was greatest at intermediate temperatures (20°- 25 C.)> and least at
intermediate pH. (7-8) within the ranges tested. Salinity of the medium
had little or no measurable effect on toxicity. Concentrations of endrin
fatal to 50 percent of mummichogs at 96 and at 240 hours were 0.60 and
0.33 ppb, respectively. The LC5Q ratio (96 hrs./240 hrs.) was 1.8.
Mortality of mummichogs following sublethal exposure to endrin showed a
ratio of LCso (96 hrs.) to 1059 (9(6hrs./240 hrs. post-treatment) of
V -c \_ --- '
1.09. wft.c/
A study was made on effects of short-term immersion in high concen-
trations of pesticides. The organochlorine compounds tested produced
similar mprtality patterns by day 21 post-exposure. These consisted of
high survival when exposure was less than 120 minutes, partial survival
when exposed between 120 and about 360 minutes, and few or no survivors
at exposures of 720 minutes and greater. Loss in toxicity occurred with
several insecticides after the test medium had been aerated for 96 hours
before adding fish. However, this treatment caused endrin to be more toxic
t o mummi cho gs .
Mummichogs survived immersion in high (LC75, 24 hrs.) concentrations
of various pesticides without apparent effects, when exposure did not
exceed 120 minutes for organochlorine compounds. Animals that survive
exposure to various concentrations of different toxicants with no signs
of external damage frequently exhibit abnormal rates of growth, repro-
duction, or death during the post-exposure period. These observations
suggest that in areas of extensive tidal flushing, aerial spraying
immediately before very high tides could be accomplished with relatively
minor consequences to non-target species (Eisler, 1970a) .
-------
Chronic endrin poisoning in goldfish, was examined by Grant and
Mehrle (1970). They found that endrin incorporated into the diet of male
goldfish for 3-4 months affected growth, thyroid activity, serum
characteristics, body fat, gonad development, behavior and mortality.
Response to endrin dosage differed according to concentration. Low doses
(4.3 - 43 ;ig/kg body weight/day) either caused no discernible effect or
stimulated growth rate and higher body fat content. Highest doses (143
and 430 ug/kg) caused mortality, decreased growth, and other chronic
symptoms of endrin intoxication.
Bennett and Day (1970) investigated the absorption at sublethal
concentrations of endrin by bluegills which were obtained from a
non-agricultural area and probably had no prior exposure to endrin.
Absorption was measured for the entire body, skeletal muscle and liver.
Initial exposure showed a sharp increase in endrin levels followed/at J
;
t '7 to 8 hours by a decline to a low at 12 hours. Later the concen-
tration in body tissue increased to a high at 24 hours. The decrease
between 7-12 hours suggests that the fish were metabolizing and/or
excreting endrin. atAJ^ -f^t llrl^J^. • -&fjjj^" «
The effects of endrin upon reproduction of a fresh water fish, the
medaka (Oryzias latipes), were studied by Johnson (1967) . Sexually mature
fish were exposed continuously for 23-45 days to renewed solutions
containing 0.04-1.32 ug/1 endrin. Concentrations of 0.6 ug/1 were lethal
to most adult fish. Concentrations of 0.3 pg/1 and lower had no apparent
effect on adults, and survival, growth and spawning activity corresponded
-------
to that of the controls. Medaka affected at higher concentrations displayed
behavior patterns that made courtship and fertilization impossible.
Spawning behavior was not affected at lower concentrations but endrin
accumulated in the eggs. Resulting mortalities affected reproduction"
as completely as disruption of behavior of the adults. ^Depending upon
the concentration to which the parent was exposed, fry died or failed to
develop normally. Eggs from non-exposed parents were incubated directly
in endrin solutions. Massive doses of endrin (10 mg/1 and greater) in
the water had no apparent effect on embryo development until the 8th
or 9th day when they were about to hatch. Embryos developed tremors,
convulsed within the chorion and usually died before hatching. Eggs
incubated in solutions containing 15 ug/1 or greater suffered severe
endrin toxicity at hatching. Concentrations of 10 ug and less causec'
hyperactivity and erratic behavior in the hatching fry.
In an experiment with stickleback, the eggs absorb endrin in
proportion to the concentrations to which they are exposed, but to.. '
a lesser degree than fish. YThe concentrations in eggs were directly
related to effects on hatching fry. Concentration in the egg of
1.8 mg/kg caused erratic fry behavior; 7.8 mg/kg or greater caused
severe muscle tetanus.
The chronic toxicity of endrin to bluntnose minnows (Pimephales
notatus) and guppies was studied intensively by Mount (1962). Neither
species could withstand concentrations greater than 0,5 ppb in water
for more than a few of the 29 days of the tests. Less than 50% of the
-------
test fish could live in 0.5 ppb more than 30 days. At the level of
0.4 ppb, about 65% of the fish, could survive for more than 30 days.
Little mortality was detected at levels of 0.25 and 0*1 ppb in the
water. Cumulative effects or tissue damage did not occur in fish which
survived in water containing endrin. Fish seemed to recover completely
from a single exposure. However, increased activity caused by very
low endrin concentrations could be very damaging to fishes in natural
waters. This could disrupt spawning and make-fish more vulnerable to
predation and other decimating factors.
Grant and Mehrle (1973) studied the effect of sub-lethal doses of
endrin on rainbow trout (Saline- gairdneri). The authors concluded that
endrin caused dysfunction of physiologic processes critical to survival.
Mature trout receiving sublethal doses of endrin (4.3 - 145 mg/kg body
wt./day in 0.215-7.25 mg/kg of food) were then forced to swim for 1
•^
hour. The insecticide affected serum electrolytes, osmolatily, total^
protein, cholesterol, cortisol, lactate, glucose, liver glycogen, and
growth. Forced swimming alone altered 9 of 16 serum parameters examined.j
Growth was inhibited appreciably by 145 mg/kg but not by lower doses.
Visceral fat accumulated 4.8-8.7 mg endrin/g tissue in the 43 and 145
mg/kg exposures.
III.B.3. Special Studies;
III.B.3.a. Residue - Frost (1969), in discussing the contamination of the
world environment by stable pesticides, mentioned that a British study
of refined cod liver oil from fish caught close to or north of the
-------
Arctic Circle showed the presence of 0.09 ppm BHC, 0.02 ppm heptachlor,
0.16 ppm dieldrin, 1.65 ppm DDT and derivatives and 0.03 ppm endrin.'
The spread of pesticide contamination can be partially explained by
transfer of the poisonous compounds by river and ocean currents as well
as by migratory animals.
Spot (Leiostomus xanthurus) that survived an eight-month exposure
to 0.05 ppb endrin were analyzed for residue accumulation. Whole-body
analyses showed a residue to 67.0 ppb. Samples subjected to 5-month.
exposure to the same concentration gave 78.0 ppb residues. No endrin
could be detected in fish from this chronic exposure after being
replaced for 13 days in uncontaminated water (Lowe, 1966).
The extreme toxicity of endrin to fish causes conjecture as to
what the specific action of the toxicant might be. Symptoms appearing
during poisoning indicate that the effect is mediated through the nervous
system. Mount (1962) attempted to determine the point of entry and
the movement of endrin through the body by exposing carp to concentrations
of 2.5 to 10 ppb endrin for periods of 2.5 to 28 days. The digestive tract,
liver, heart-spleen-blood, and kidney contained the highest accumulations.
Maximum concentrations were approximately 160 times greater than in the
test solutions. The heart-spleen of a carp exposed 28 days to 2.5 ppb
contained endrin residues of 400 ppb. Muscle tissue was low in endrin
content. Gills were low or negative. Since the digestive tract was
consistently high, Mount concluded that the endrin probably entered
the body through the intestine.
-------
Crab and seven species of edible marine fish in the Pacific Northwest
were monitored for pesticide levels CStout, 1968). Endrin levels detected
were considered to be an occasional sample contained 0.006 ppm.
Chlorinated hydrocarbon residues were reported for eight representative
species of fishes of the lower Colorado River Basin of southern Arizona
(Johnson and Lew, 1970). The estimated 345,000 acres of cotton land in
the drainage in 1965 received average an application of 1.2 Ib./acre of
?
x f
endrin. Despite this usage only trace amounts of endrin were recovered
as fish residues. Much higher levels of other chlorinated hydrocarbons
A preliminary report on pesticide monitoring in Louisiana was given
by Epps, et^ al_. , (1967) . Extensive sampling occurred in five separate
drainage basins each distinguished by a different type of farming. The
areas were: (1) Six Mile Creek, a forested area never cultivated, which
served as the control; (2) Tensas River, a large cotton and soybean
producing area of the Mississippi Delta with heavy usage; (3) Mermentau
River, a rice growing area in Southwest Louisiana; (4) Bayou Chevreuil,
an area with heavy usage where sugarcane is the only crop; and (5)
Bayou Courtableau, an intensely farmed area in the south-central part
of the State where cotton, sugarcane, and rice are grown. Amounts of
endrin found in 22 samples of bluegills, 17 shad and 27 catfish are
presented in Table III.B.2. In a given stream, variation of residue
levels in fish was not wide. No pesticides were used in the Six Mile
area. Usage was heavy in the Tensas and Courtableau areas. Endrin
was used more extensively in the Chevreuil area; consequently, levels
in fish from this area were relatively higher.
-------
Table I1I.B.2.
Endrin Residues, in Fresh Water Fish from Different Drainage Basins in
Louisiana (ppm),,*
^—N •-" > -, S~\
BG /
\Shad
c4t \
/T -,v
/BG\ ^
j\ .
Angola
P
N
0.05 ^
Blue^
/
>• Chevreuil
P
0.87
0.31
ilTx Lepomis
\
Cour tableau
0.03
0.04
0.06
macrochirus
Mermentaus'
N
N
N
\
v_
Six
Mile
N
N
N
^
Ten
P
P
0.01
C/at
P
N
Gizzard Shad, Dorosoma cepedianum
Channel Catfish, Ictalurus punctatus
•
Present at minimum level of detection
Not detected
( C(lr\
A monitoring program was inaugurated at the Tule and Lower
Klamath Lake Wildlife Refuges in Northeastern California because of
pesticide poisoning of fish-eating birds. This contamination presumably
resulted from irrigation return flow, run-off or leaching of pesticides
from adjoining agricultural lands. Samples were collected over a
two-year period and endrin occurred frequently. Tui chubs (Siphateles
bicolor) accumulated up to 198 ppb. Largemouth bass (Micropterus
salmoides) exposed to live-boxes for periods ranging from 80 to 209 days
accumulated 15.3 to 107.0 ppb endrin residues. The lower figure was in
January when pesticide runoff was at a minimum. The maximum figure occurred /
in September near the end of the pesticide use season (Godsil and Johnson^'*
1968). V. .
\
\
1 n i
-------
Pesticide residues from an estuary near Pensacola, Florida were
monitored for about'1.5 years. Residues in fish from the estuary rarely
exceeded 0.1 ppm. Endrin was found in some samples up to 0.02 ppm
(Hansen and Wilson, 1970).
A national pesticide monitoring program sampled residues in fishes
from 50 stations located in the Great Lakes and in major river basins
throughout the United States. Endrin was reported consistently in
samples from only three stations: Luling, Louisiana (Mississippi River);
Pine Bluff, Arkansas (Arkansas River); and De Vails Bluff, Arkansas
(White River). Thirty of the 50 collection sites recorded endrin-
\ s^ ' \ /
contaminated fish b)it levels we£e generally in the 0.01 - 0.10 ppm
range. A few higher values recorded were: 1.5 ppm for carp from the
Susquehanna River, Maryland; 0.27 ppm for spotted sucker (Minytrema
melanops) from Apalachicola River, Florida; 0.14 ppm for striped mullet
and also channel catfish from the Mississippi River, Louisiana; 0.11 ppm
for smallmouth buffalo (Ictiobus bubalus) and flathead catfish (Pylodictis
olivaris) from the Arkansas River, Arkansas; and 0.71 ppm for channel
catfish from a Colorado River reservoir in Arizona (Henderson, et al.,
1969). <
s~ ~"k
Sriead "j[1970) presented a preliminary report on pesticide residues
in commercially produced catfish. Edible portions of the catfish from
147 commercial catfish farms in Mississippi and Arkansas also were
analyzed. Pesticide residues were found in small amounts in virtually
all fish samples. Endrin residues were detected in 70.6 percent of the
-------
fish from Arkansas and 61.0 from Mississippi. Average endrin residue
levels in catfish were .0265 ppm for Arkansas and .0266 from Mississippi.
The percentage of endrin residues greater than or equal to the 0.3 ppm
level was 2.1 for Arkansas and 1.3 for Mississippi.
Pesticide influence in channel catfish culture in 4 southern states
was reported by Grant (1970). Problems in the culture of catfish included
reproductive failure, excessive mortality, and abnormal growth and
morphogenesis. In a general agricultural area with extensive history
of organic chlorine pesticide use, widespread mortalities of both immature
and adult fish followed an unseasonable, two-week duration of sub-freezing
weather in December. Terminal symptoms were similar to those of pesticide
intoxication.
Fish, fish food, and mud were contaminated with endrin, dieldrin and
DDT (plus its breakdown products). Endrin concentrations ranged from
trace amounts to 0.2 .ug/kg, and DDT levels were about 1 jag/kg, based on
whole fish weight. Mud contained trace amounts of insecticide, but all
three toxicants were found in about 75 % of the diets sampled. Observations
of spring spawning revealed high mortality of embryos before hatching,
and malformed axial skeletons in hatchlings. Skeletal structure was
aberrant - most terata were "tailless," and some had lordosis or scoliosis.
The only other conditions known to produce scoliosis in fishes are vitamin
C deficiency and maintenance in total darkness. The total body endrin
residues in pond-reared channel catfish from 18 sources was within the
range < 0.005, 1.01 ug/g (av. 0.13). Contamination of channel catfish
\
-------
food from 7 sources was < 0.005-0.14 ug/g (av. 0.03). Average value of
endrin residues in fat and ovaries of mature channel catfish, were, fat—
0.5 ug/g CO.1-1.0) in eight samples and ovaries - 0.02 ug/g (ND-0.08)
in five samples.
III.B.4. Resistance - The sensitivity to pesticides in three generations
of sheepshead minnows was examined by Holland and Coppage (1970). The
purpose was to determine whether succeeding generations exposed to DDT
could develop resistance to DDT, and "cross-resistance" to endrin.
Experimental fish were offspring of survivors of exposures to concentrations
of DDT that killed 70% or more of the fish in the previous generation.
Control fish were offspring of unexposed fish. Among controls, and the
F-j_ generation of fish freshly treated with DDT, mortality was 100 percent
following exposure to 1 ppb endrin, but only 5% of an equal number in the
?2 generation succumbed. When fish with long history of exposure to DDT
received similar treatment with endrin 80 fish from the F, generation
died, as opposed to a loss of 40 from 70 tested from the F^ generation.
The authors suggest that lipid metabolism and maturation of ova were
greatest when parent fish were exposed and that incorporation of insecti-
cides into the ova may be the factor that increased sensitivity.
The susceptibility and resistance of mosquitofish to several
insecticides were studied by Boyd and Ferguson (1964). Approximate LD
values for ODD, endrin, aldrin, dieldrin, toxaphene, heptachlor, and
lindane were determined for four populations of mosquitofish, Gambusia
affinis. Results showed resistance and cross-resistance in populations
-------
having past exposure to insecticides. Evidence favoring a genetic basis
for resistance was presented wherein toxlcity levels remained constant in
progeny of resistant fish reared in the absence of insecticides.
Thirty-six hour U^Q values (ppm active ingredient) for endrin
to four populations of mosquitofish are presented in Table III.B.3.
In these trials 50 fish were used on each level tested.
Table III.B.3.
36-Hour LD values (ppm) for endrin in four populations of mosquitofish
Locality
2 miles
State South State
Insecticide College College Indianola Sidon
Endrin LD50 0.001 0.008 0.006 0.12
(ppm)
These values indicate a stong correlation between past exposure to
insecticides and decreased susceptibility to the test compounds. The
values for the untreated State College fish were within the range of those
reported for other species of fish (Rudd and Genelly, 1956) .
The observed resistance resulting from the selective action of
insecticides is probably genetic. Toxicity values for fish at least one
and perhaps as many as three generations removed from exposure to insecti-
cides remained essentially unchanged from those of the original selected
parental population.
« 0 f
DC:
-------
Resistance to endrin in"three species of freshwater fish was
S^~ ' ~^>
investigated by Eerguson, Culley,/ et^ al_., (19-64). Mosquitofish CGambusia
affinis) from cotton producing areas in the Mississippi Delta were
previously found resistant to most commonly used chlorinated hydrocarbon
insecticides. As much as 300-fold resistance persisted among the first
few generation of resistant fish reared in insecticide-free environments.
Continuing concern prompted additional investigation to determine whether
resistance was peculiar to mosquitofish, or an adaptation also possessed
by other fishes living in heavily treated areas. Tolerances of Mississippi
Delta golden shiners (Notemigonus crysoleucas), bluegill sunfish (Lepomis
macrochirus), and green sunfish (Lepomis cyanellus) were determined for
endrin. Delta fish were obtained from Twin Bayou near Indianola, Sunflower
County, Mississippi which is bordered for several miles by large cotton
plantations and subject to insecticide contamination by runoff, drift,
and possibly some direct application. Comparative dosage-mortality data
were collected for fish with minimal prior exposure to insecticides from
non-agricultural areas near State College, Oktibbeha County, Mississippi.
Tests conducted in March and April indicated much higher tolerances
than those of June and July. A change was most apparent in tolerances of
green sunfish to endrin where the 36-hour TLm declined from 575 ppb to
160 ppb. The fish community at Twin Bayou apparently consisted of 7
species, some .of which were represented by incredibly large numbers of
individuals, e.g., mosquitofish. During nearly 100 hours of collecting,
no upper trophic level carnivores such as largemouthed bass or crappie
were observed. This may be the result of biological magnification of
-------
insecticides having a. more severe effect on animals occupying a position
at the top of a food chain.
Comparative toxicity of endrin to resistant (Twin Bayou) and non-
resistant (State College) populations of three species of freshwater fish
is presented in Table III.B.4.
Table III.B.4.
36-hour TLm values to endrin (ppb) observed in resistant and non-resistant
fish
Golden
State
College
3.0
Shiners
Twin
Bayou
310
Bluegills
State
College
1.5
Twin
Bayou
300
Green
State
College
3.4
Sunfish
Twin
Bayou
160
Patterns of insecticide resistance in mosquitof ish, (GambusiaL/af f inis^i
A y
were evaluated by Culley and Ferguson (1969) . The extent of insecticide
resistance in a resistant population from Belzoni, Mississippi, was compared
with that of a susceptible population from State College, Mississippi,
using 28 insecticides from five major groups. Spray records for the
Belzoni area and insecticide characteristics such as stability and
toxicity were used to evaluate patterns in the resistant population.
Comparative 48-hour LC5Q values with endrin from resistant (Belzoni)"-^
and susceptible (State College) populations of mosquitof ish were 0.6
ppb for the State College sample and 314.0 ppb for the Belzoni group .^
T - ~~
or a 523X difference. Resistance was observed with pesticideSrelated
to toxaphene and endrin with patterns of resistance similar to those in
arthropods.
'07
-------
Resistant raosquitofish tolerate as much, as 214./28/ppm endrin in
their tissues, and one such, fish is able to release sufficient endrin
into 10 liters of tapwater to kill five susceptible mosquitofish and
still survive (Ferguson, Ludke,/gJ^ al_., 1966). Resistant green sunfish
vT ^' "'-1 ^~
^ ""' J
survived after each consumed a live mosquitofish containing 24.93 ppm
endrin, but susceptible sunfish died in 15.5 hours. Many green sunfish
regurgitated the endrin-contaminated mosquitofish but died later. Most
- -•—"""" —~^S5- -
regurgitated Gambusia showed nq,e"ffects of digestion; an indication that
endrin was ab'sorbed superficially as suggested by Ferguson and Bingham (1966a)
<==^ -' y . .ffif^H^?
The first report of resistance in a natural population involved DDT-
resistant mosquitofish from an intensively-sprayed cotton-producing area
(Vinson, et^ al^, 1963). Since then, resistance to various organochlorine
toxicants has been recorded in at least seven other species.
Results of 36-hour TLm measurements and gas chromatographic analyses
showed that mosquitofish in waters near heavily-treated cotton fields
and from an uncontaminated site removed endrin from static test solutions
/*.'' \
at the same rate. In susceptible fish/with a 500 ppb endrin solution
\J
'.".love
f r ^ "\ • — t.ierc. j/i n IJHJ* i
aused' 32% mortality in 25 minutes, but Miours were required in resistant
• "**'
fish. Relative mortality of fed and starved fish in endrin solutions
and the rate of endrin uptake discounted swallowing as a primary route
of entry. Six times as much endrin was taken up by the exposed head
region as by the general body surfaces. Oxygen demands of the two
populations were similar, but increased for susceptible fish at low
endrin concentrations and for resistant fish at high concentrations
coincident v/ith the appearance of endrin poisoning symptoms. The
-------
authors conclude that the. mechanism of resistance is physicological
^<
toleration of massive endrin accumulations CF&rgxison, Ludke,.' et al.,
1966).
It was previously stated that resistance to endrin has been observed
in yellow bullheads. Specimens of this fish from contaminated waters
bs
had.36-hour TLm values of 75 ppb, whereas specimens from an unpolluted
source were extremely sensitive - 1.25 ppb. This indicates a 60-fold
endrin resistance in fish in waters subjected to cotton field drainage
(Ferguson, Bingham, 1966). j,^ ti!wM~c*
Possible selective mechanisms in the development of insecticide
resistant fish were evaluated by Finley, et ,al., (1970). Resistant
V ^
and susceptible green surifish populations fed endrin-exposed resistant
mosquitofish had a 45X difference in endrin tolerances. Susceptible
and resistant green sunfish each consumed one mosquitofish, all susceptible
green sunfish died in 6.25 to 21.50 hours (an average of 11.75 hours) and
all resistant and control fish survived the 96-hour test. Results of
bioassays and gas chromatographic analyses showed that insecticide-resistant
fish ]iving near heavily treated cotton fields at Belzoni, Mississippi
were subjected to relatively brief, irregular periods of exposure after
rains. Runoff from cotton fields increased mortality among caged susceptible
and native resistant fish. Feeding of endrin-exposed and field-collected
resistant mosquitofish ((^amfrusiax^finis.) to resistant and susceptible green
\r^/~^~'
sunfish (LepojaaQa cya'ftellus) showed that selective pressure from residues in
~^/^ ^^-v
the food chain among resistant consumers was minimal compared with direct
exposure. No insecticide stratification in the water was indicated by
live-cage bioassays conducted at top and bottom depths.
? MO
*•
-------
Susceptible fish, showed symptoms of poisoning (e-g-> hyperactivity)
soon after consuming the mosquitof ish, and .36 of 40 regurgitated the
mosquitof ish prior to death without apparent correlation between predator
weight and survival time. Resistant green sunfish exhibited no symptoms
of poisoning, and all retained the ingested mosquitof ish. Three samples
(10 whole mosquitofish each) from the group that were consumed contained
^no^4???Wl,Wl
an average of 180 ppm" endrin. *
Residues in whole body samples of individual susceptible green sunfish
that died^efwa continuous diet of field-collected resistant mosquitofish
/I
(1966-1967) showed 0.28, 0.10 and 0.312 ppm endrin. Monthly residue analyses
of pooled samples (about 2 g) of native resistant mosquitofish from the
Belzoni caging area (1966-1967) had endrin residues of 0.54, 0.40 and
0.058 ppm.
These observations suggest that insecticide contamination resulting
from relatively brief period of runoff from adjacent cotton fields consti-
tutes the principal selective mechanism in the development of resistant
fish populations in adjacent waters. Both residue analyses and mortality
of caged fish reflect the increase in pesticide content of streams after
rains .
Succinic dehydrogenase activity on resistant and susceptible mosquito-
fish was investigated (Yarbrough and Wells, 1971). In perfusion studies
no difference in enzymic activity was observed between susceptible and
resistant brains, but with liver homogenates higher enzymic activity was
observed in material from susceptible fish. The higher fat content of
1 Hi
-------
the resistant liver homogenatea probably explains the lower values observed
with resistant fisb. Endrin inhibition of succinic dehydrogenase was
reported in homogenized brains of susceptible fish, whereas varying
degrees of stimulation were observed in resistant brain homogenates.
Similar results were obtained with liver mitochondria from resistant
and susceptible fish. Comparisons of results of liver and brain in
which the mitochondria preparations had been disrupted showed endrin
inhibition at every level tested in both resistant and susceptible samples.
ce.
This study suggests that vertebrate resistant involves a cellular membrane
barrier since inhibition of succinic dehydrogenase activity in resistant
tissue was demonstrated only after mitochondrial membrane was disrupted.
IS'
In a later paper Wells and Yarbrough (1972) compared the in vivo
and in vitro binding patterns of endrin - C in susceptible and resistant
mosquitofish brain and liver cellular fractions. Cell membrane fractions
A"'
or^resistant fish bind more endrin than susceptible fish, while the
resistant mitochondria binds less endrin than susceptible fish mito-
chondria. Differences between endrin uptake in susceptible and resistant
fish, retention of endrin by brain cell membranes, a blood-brain barrier,
and a structural difference in myelin could account for endrin resistance
in mosquitofish.
Oxygen consumption of endrin-resistant mosquitofish was significantly
lower (26%) than that of a susceptible strain. Susceptible fish had an
increased oxygen uptake at the onset of poisoning symptoms, and a decrease
prior to death. Resistant fish, showed no consistent change. At higher
\ I 1
-------
concentrations of exposure (20 and 75 ppb endrtn), total oxygen consumed
by susceptible fish decreased significantly from controls (Mclngvale,
et_ al., (1968).
Ludke, et^ al^., (1968) checked endrin resistance in resistant and
susceptible populations of golden shiners. A 1,000 ppb endrin solution
killed 50°susceptible fish in 75 minutes but only 40 of 50 resistant
shiners in 40 hours. Endrin residues in whole bodies of resistant shiners
killed in endrin-treated water were as much as 82 times those of susceptible
shiners. Endrin concentrations in the blood of living resistant shiners
were as much as 64 times greater than those of endrin-killed susceptible
shiners. ..
Day (1968) found that the longnose killifish exhibits an apparent tidal
rhythm of susceptibility to endrin and sodium chloride. Fish were more
resistant to the chemicals at high tide. The tidal rhythm was not evidenced
after three days. It is possible that the rhythm of susceptibility is
endogenous and is phased by an external tidal factor.
Ferguson (1967) concluded that pesticide-resistant fishes and vertebrates
may pose a major hazard to natural ecosystems. Although selection of a
resistant fishery may permit exposed populations to survive, it may eventually
t
produce a biological component dangerous to all consumers, including man
(Ferguson, Ludk^fe, et^ a^., 1967).
, III.H.3.C. Biological Magnification - All fish and wildlife are part of
the food chain or web which may start with lower lifeforms which concentrate
persistent pesticides in their bodies. When the lower forms are consumed,
-------
a higher dosage is passed on to predatory fish and thence to fish-eating
birds and mammals* Food chains in the aquatic environment are especially
vulnerable since they maybe exposed to pesticides in runoff as well as
to pesticides applied directly to water (Anon., 1964).
Bridges Q.961) reported fish kill in Colorado caused by runoff of
endrin applied to sugar beets. A field adjacent to the affected pond
was sprayed at 6 ounces of active ingredient per acre, and four days
later numbers of dead yellow perch (Perca flavescens), pumpkinseed
\ 7
(Lepomis-^gibbosus), bluegill, black cacppie (Promoxis nigromaculatus),
-—^ • I J ~f
largemouth bass and carp were observed. Pond water contained 0.04 ppm
a month later. Vegetation residues reached a maximum of 0.55 ppm 15
days post-treatment. Residues in the bluegill were 1.00 ppm nearly^
\j
two months later. Endrin disappeared from the water about a month
after application, six weeks in vegetation, two months in bottom mud
and less than 3 months in fishes.
/->
Johnson (1967), in his report on the effects of endrin on the/me'dalca,
gave some data on residue concentrations in adult fish. After 28 days
._-,__ *&4^?
exposure these were approximately .pfoportional to the concentration to
which they were exposed. Calculated accumulation factors showed fish
concentrated endrin in their body from approximately ,177000 to 26,000 ^
~^~- - • \
times the concentration in the water.
The food chain of protozoa to Crustacea to fish was studied by
Priester (.1966) after the toxicity of endrin to each organism had
been determined. Each species was treated with a sublethal dose, and
-------
Crustacea were fed to fish.. Endrin which, was concentrated 920 times
by Daphnia during a 14-day exposure was not detected in fish, after
ingestion of treated daphnia and was not detected in protozoa following
a 7-day exposure to 50 ppb.
The toxicity of endrin-resistant mosquitofish to natural predators
was ascertained by Rosato and Ferguson 0-968). These resistant specimens
were exposed to 2 ppm endrin for 7 days. A single survivor was force-fed
to each of several carnivorous fish, including red fin pickerel (Esox
a. verraiculatus), largemouth bass and bluegills. Mortality of all
w
predator species was 100 percent within 7.1 ana 12.6 hours. Resistant
mosquitofish accumulate endrin residues sufficient to kill potential
predators several hundred times their own weight.
The mass death of fish in the lower Mississippi River in 1963 led
to speculation concerning the accumulation of insecticide residues in
the environment and rumors of increasing concentration of endrin in the
fauna of the food chain. Buildup of endrin in soil and water was postu-
?>
late. However high concentration or time ordered changes in endrin
A
concentrations were observed in twelve successive monthly samplings of
representative fish, shellfish, mud and water from the lower Mississippi
River. Oysters and shrimp were negative throughout. Catfish yielded
0.01, 0.02, and 0.01 ppm of endrin in July 1964; and one reading of
^
0.01 ppm in each of August and October 1964 and June 1965. Bream yielded
one reading of 0.01 ppm in each of July and October 1964 and February
1965. Mud and water were negative throughout apart from two readings
-------
of 0.01 ppm in July 1964 and one of 0.01 ppm in each, of February and June
1965 (Novak and Rao, 1965).
III.B.S.d. Other Studies of Pathological or Physiological Effects - A
study was initiated to determine the pathway of entry into exposed fish.
A comparison was made of mortality rates of normal black bullheads and
others rendered incapable of swallowing endrin. In one group the gut
was tied off in the region of the upper esophagus. A second group was
subjected to the same operation with thread in place but omitting the
ligature. These constituted a sham-operated control. A third group
served as unimpaired controls. In every test, all fish from all three
groups were dead after a 23-hour exposure to 50 ppb endrin. Mortality
rates were nearly identical. These results showed that fish unable.to
swallow endrin died as rapidly as those free to swallow (Ferguson and
Good year, 1967).
The effects of endrin on the oxygen consumption of the bluegill
sunfish, ^epojujrs macVpchirusj,/ were studied by Huner, et^ a!U , (1967).
Katz (1961) and Henderson, et^ aJU , (1959) found endrin to be the most
toxic insecticide tested on various fishes. Effects of sublethal
(0.1 ppb) and lethal (1.0 ppb) endrin concentrations on oxygen consumption
were measured. Increase in oxygen consumption occurred within 5-hour and
24-hour exposures to 0.1 ppb while at 1.0 ppb oxygen consumption was less.
Exercise had no significant effect on oxygen consumption at either concen-
tration but it did affect mucus production and hastened death.
Adult northern puffers, Sphaeroid^es maculatus, were exposed to various
concentrations of endrin and blood and/tissue samples from fish surviving
-------
a %-hour exposure were studied. Mean hemoglobin content and relative
liver size of puffers exposed to 1.0 and 0.05 ppb differed littled from
controls. Concentrations of sodium, potassium, calciun and cholesterol
in serum were consistently higher in exposed fish, but amounts of magnesium
and zinc in the livers of test animals were consistently lower. Exposure
to sublethal concentrations of endrin impaired liver function has shown
elevation in serum content of major cations and cholesterol (Eisler and
Edmunds, 1966). Serum cholinesterase was 2-8 percent of normal were
reported in carp exposed to lethal concentration CO.05 to 0.005 ppm) of
endrin (Hayama and Kuwabara, 1962; together with changes in serum Trans-
aminase Lue-Hurg, 1966) . '
Inhibition by endrin of succinate dehydrogenase and cytochrome oxidase,
two enzymes involved in mitochondria! electron transport in the catfish,
Ictalurus melas, was shown by Colvin and Phillips (1968). Extent of
inhibition depended upon ednrin concentration and the specific activity
of the enzyme preparation. No appreciable effect of endrin on acetyl-
«c*i'?
cholinesterase or NADH - cytochrome-c-reductase was reported. Binding to
lipoprotein components essential for mitochondrial oxidation was proposed
as a logical site for endrin action.
The effect of endrin on uptake of phospholipids, neutral lipids, and
cholesterol by embryos of steelhead trout (Saliao Gairdeiieri) was checked
by Grajcer (1968) . Pathways by which endrin is distributed between the
egg yolk and the developing embryo were studied. In one. trial, fertilized
•>
and unfertilized eggs were'^cocharged with endrin. Another involved
; i P
-------
exposing hatching steelhead eggs to 10 ppb endrin. Exposure stopped
after hatching but endrin assay of of both embryos, yolk sacs and young
continued to 25 days after hatching when the last specimens expired.
In a third experiment, eggs and alevins were continuously" exposed to
endrin.
A small but steady uptake and accumulation of endrin occurred
in all eggs. Fertilized eggs accumulated more endrin (9-40 ug/day)
than the unfertilized eggs CO.30 ug/day). Major uptake occurred with-
in a 24-hour period of hatching during which time alevins increased
their endrin content up to 40 times. Initially most of the endrin
was stored in the yolk. Results of assays indicated an irregular
accumulation of endrin in the embryos. The challenged alevins expired
by the 13th day after hatching. At this time, endrin content in alevins
increased but the uptake of endrin shifted from materials in the extracted
dry weight and phospholipids to the fraction containing neutral lipids
and cholesterol.
Histopathological lesions in cutthroat trout chronically exposed
to endrin were described by Eller (1971). Pathological conditions were
found in the gill, liver, pancreas, brain and gonads. Edema, hemorrhage,
and possibly intracapillary congestion characterized gill damage after
exposure to highest concentrations of 0.04 mg/1 water. Hepatic lesions
in young trout were similar to those preceding the development of
hepatomas in nutritionally deficient fish. Increased incidence and
severity of hepatic degenerative changes in fish exposed to high endrin
levels suggested nutritional difficiency. Marked hyperplasia of pan-
creatic islets and irregular, atypical oocytes were observed after
exposure to high endrin levels.
• 1
* I
-------
III.C. Toxic Effects on Wildlife - Extensive data from laboratory tests
corroborate hazards to birds and mammals resulting from agricultural use
of endrin. Losses among populations of/non-target birds, mammals and
_ t
fish have been caused from registered uses sucfr^as for orchard mouse
control. Resrdue"s~in""m6derVte amounts may accumulate in animal tissues
and may reach toxic levels in aquatic birds. Residues of endrin in
^
animal tissues recede ,£u**hef than DDT, dieldrin or heptachlor epoxide
/t
under withdrawal conditions.
III.C.I. Acute Toxicity - Extensive data from both laboratory tests and
field studies substantiate the highly toxic effects of endrin on both
mammals and birds. Even some registered uses for rodent control have
created losses among non-target bird and mammal species. Residue
accumulation in animal tissues is moderate, but may reach toxic levels
in aquatic birds. Bioaccumulation has been demonstrated.
The acute oral LD50 toxicity of endrin tabulated by Schafer (1972)
was 2.4 mg/kg for red-winged blackbirds (Agelaius phoeniceus) and the
same for starlings (Sturnus vulgaris), 5.6 mg/kg for the common grackle
(QuiscatEus xjuisciila), 5.6 for the common pigeon (Columba livia) ; and
1.8 for the house sparrow (Passer domesticus) . DeWitt, et_ al_., (1960)
listed the approximate U^Q of endrin to bobwhite quail as 5.0, and to
ring-necked pheasants -- 14.0.
' ^ ^
Arasan (thra'amX - endrin-coated pine seed is used to repel birds
and rodents for direct seeding to reestablish confiers. Hamrick (1969)
determined the lethal dosage of treated seeds to several species. Force-
feeding of one treated slash pine seed each to 10 bobwhite quail (Colinus
-------
virginianus) resulted in 100% mortality. Of seven gray squirrels CSciurus
carolinensis) offered a known number of treated seed, five died; these
five gnawed an average of 85 seeds. If completely consumed, this meant
ingestion of 29.7 mg. endrin. Of two others given a mixture of treated
and untreated seed, one died and the other exhibited symptoms of poisoning.
One chipmunk (Tamias striatus), offered treated seed, was found dead
twelve hours later. Possible maximum endrin intake was 1.4 mg. Wild
cotton rats (Sigmodon hispidus) had access to treated seed spilled under
cages. One was observed in severe tremors a day after treated seed
became available. No spilled seeds were touched after the third night.
Twelve pen-reared wildstock turkeys (Meleagris gallapavo) also were
tested. Of 10 turkey hens force fed treated seed, 3 died. Two that
died received 30 seeds (about 2.5 mg/kg of endrin) and the other 36.
The average treated slash pine seed containing 0.35 mg endrin. For
an average-sized adult quail, this would be a dosagevdn excess of the
estimated 1.5 mg/kg 11)50 value. —•"
Luckens and Davis (1965) measured acute toxicity figures for the
big brown bat (Eptesicus fuscus). Endrin administered in the feed induced
mortality at dosses- as low as 4 mg/kg. The'LD^Q^ was 12 mg/kg although
there was one survivor at 20 mg/kg. Results indicated an approximate
LD5Q of 5-8 mg/kg.
In laboratory studies on Japanese quail (Coturnix c. japonica made
by Bakos, £t_ al_., (1968), the lethal dose of endrin was 0.02 ^ig/ml per g
live weight. The authors cautioned that at rates, used for rodent control
jafforded an imminent danger to feathered game.
-------
Treon, et_ al^., (1955) reported acute oral LDrn values (mg/kg) as
follows: monkey - 3; 6-month old rats - 7.5 (F) - 43.4 (M); cats -
Vfninimum'LD5Q\less than 5; 26-31 day old rats - 28.8 (M) and 16.8 (F);
and guinea pigs - 16 (F) and 36 (M) . ^
Negherbon (1959) listed acute^'oral toxicities for endrin in mg/kg
as follows: female rabbit (MfB) - 5 to 7; female guinea pig (MLD) -
10 to 16; male guinea pig (MLD) - 24 to 36; monkey (both sexes) - MLD
of 1 to 3; and the LDrQ for a 7-day old chick as 3.5. . - '
.^^ Toxicity of endrin determined by Tucker and Crabtree (1970) gave
\-'
S \an acute oral LDsg figure of 5.64 mg/kg for 10-13 month old female
^
mallard ducks. Young female ring-necked pheasants (3-4 mo.) were 1.78
mg/kg. Pigeons, of both sexes were 2-5 mg/kg. Four-year old sharptailed
grouse were highly sensitive at 0.75 - 1.5 mg/kg-r — -f&t'T ^ ™i 4 *-«w^-'
5
In a study of the effects of endrin on the pigeon, Revzin (1966)
found the i.v. LD^g was 1.5 mg/kg. The slope of the dose-response curve
was very steep; 1.2 mg/kg was an LD whereas 2.0 mg/kg approximated an
LD
10f). .
Rudd and Genelly (1956) found the LDtjQ for adult female pheasants
to lie between 3.6 (LD2c) and 5.6 (LDgg) mg/kg.
Allard (1971) described wildlife poisoning resulting from an
approved pesticide use. Death of chukar partridges was attributed
to consumption of endrin treated wheat used in a rodent control
program in an orchard. Results of tissue analysis are presented
in Table III. C.I.
-------
Table III.C.I.
Endrin in Tissues
Bird No. Tissue
1 Fat
Liver
Muscle
2 Fat
Liver
Muscle
3 Fat
Liver
Muscle
from Chukar Partridges
(ppm)
Total DDT
1.01
0.50
N.D.
1.15
0.26
N.D.
0.08
0.39
N.D.
Endrin
4.58
0.84
0.05
1.79
0.88
0.06
6.24
1.28
0.04
Waterfowl were selected for acute toxicity tests because they
frequent alfalfa fields in winter when mice are controlled with endrin
(Keith, et al., 1962). Four cackling geese. administered single -oral—
-- V /
^ — jcf. naini
doses of 5 to 10 mg/kg of endrin died, while two others subjected to
c
•
2.5 mg/kg were alive after 9 days.
Results of single, oral doses of endrin given to eight widgeon
showed 3 birds at 5, 2 birds at 10, and 1 bird at 20 mg/kg succumbed.
Two others at 2.5 mg/kg were alive after 9 days. In a,.-chxoniG feeding
trial scheduled for five days, widgeon given daily doses of 1.0, 2.0
5>e^ft?' '
and 2.5 mg/kg' died before the fifth day. Similar results were obtained
fbr J-*1 ?
with white-fronted geese wherein 4 birds given 5 to 10 mg/kg "died while
two others receiving 2J.5 mg/kg were alive after 9 days.
-------
The effect of age on sensitivity (acute oral toxicity) of pesticides
to mallard ducks was recorded by Hudson, et^ alU , (1972). Acute LDcn
values determined on mallards 36 hr., 7 days, 30 days and 6 months after
KatdWr
>bath.iitg-"are presented in Table III.C.2. Central nervous system stimu-
lants produced LD j-g values that decreased from 36 hr. to 7 or 30-day
old birds, and increased from birds aged 7 or 30 days to 6 months.
The results of these tests show that young animals are not always
more susceptible to pesticides than adults and age-susceptibility
factors should be considered important in developing standardized
toxicologic protocols.
Table III.C.2.
Acute Oral I^Q (mg/kg) of Endrin to Mallards of Various Ages
Age
Chemical 36 + hr. 7 + 1 Days 30+3 Days 6 Mo. +3 Days
Endrin 22.3 3.37 2.90 5.33
(9.88-50.3) (2.36-4.80) (2.17-3.88) (3.67-7.73)
.III.C.2. Chronic Toxicity - Chronic toxicity to quail and pheasants
A- ,.'
of endrin was studied by DeWitt (1956). Inclusion of 1 ppm endrin
in diets fed growing quail resulted in hi'gh mortality rates. Young
pheasants failed to survive on diets containing 5 ppm endrin. No ill
effects were noted among quail fed winter diets containing 1 ppm endrin.
Egg production, fertility, and hatchability were relatively unaffected
-------
by inclusion of insecticides/in diets fed breeding quail, but their
chicks showed high mortality rates even when reared on insecticide-free
diets. Hatchability of pheasant eggs and viability of chicks were
adversely affected by endrin in the reproduction diets.
Comparative dietary toxicities of 89 pesticides to birds were
examined by Heath, et^ al^., (1972). Toxicity was expressed as the
LC^Q of active chemical in 5-day ad libitum diet followed by 3
days on untreated diet. Endrin, consistently the most toxic chemical
tested, gave LC values of: bobwhite - 14; Japanese quail - 18;
IV /
pheasant - 14; and mallard -.22 mjgj^cg-, •pn/r? •
/^-/Hl '" k^10}* .._—•-
Hamrick (196%) reported on chronic tests of endrin-coated conifer
seed on wildlife. Six turkeys force-fed sublethal dosages of treated
seed and surviving
-------
(1968) made analyses of renal fat from 45 antelope (Antilocapra americana)
collected in South Dakota. Combined chlorinated insecticide residues
were only 0.08 ppm. No samples had endrin above 0.03 ppm.
Pesticide analyses were run on 21 whitetail deer (Odoco Ileus
virginianus) from the Mississippi Delta Region (Cotton and Herring,
1971) . Only six deer from one collection point contained trace amounts
endrin residues in the fat.
Pesticide residue concentrations in Colorado mule deer COdocoileus
hemionus) were studied by Jewell (1966) . In muscle tissues from nine
deer, endrin residues ranged from none. •determined to 0.072 ppm. In the
adipose tissues of two deer, endrin residues were trace and 0.059 ppm.
Wilson (1967) mentioned pesticide residues from two dead porpoises.
These aquatic mammals represent one of the top trophic levels in a marine
food chain. More than 200 ppm of DDT and its metabolites were found in
i i^ *^
ha rH -
the blubber of both animals, and 0.05 to 2.0 ppm of endrin and dieldrin
. A
residues.
Snyder (1963) obtained endrin residue data on vole ffiicrotus
jq vtM»-\i'l',!""i
pennsylvanicus) .reproduction. Voles which consumed from 5.4 to 126.0
mg/kg endrin in the laboratory contained from 0.16 to 1.92 ppm in their
tissues. Endrin applied at 0.6 Ib/acre did not produce residues in
resident meadow mice while from less than 0.15 to 0.73 ppm was detected
in 11 of 17 animals taken 2 months after treatment with 2.0 Ib/acre.
—•
Mean concentration was 0.34 ppm. Difference in. reproductive rates
between females of endrin-treated and control groups varied only 0.25
or less for corpora lutea, implantation sites, and viable embryos.
t :'#
-------
Harrison (1966) pointed out that endrin was used in Great Britain
to a much lesser extent than aldrin, dieldrin, DDT or BHC. When endrin
was present in avian tissue and eggs in Great Britain, the ratio of
endrin residue to pp'-DDE seldom exceeded 1 to 500, and of endrin to
dieldrin 1 to 100. The following observations from birds at the top
of aquatic or terrestrial food chains are endrin residues in eggs (ppm):
hen harrier (Circus cyaneus) - 0.01; merlin (Falco columbarius)- 0.32;
heron (Ardea cinerea) - 0.03; cormorant (Phalacrocorax carbo) - 0.01;
shag (Phalacrocorax aristotelis) - 0.01; peregrine (Falco peregrinus)-
0.09; osprey (Pandion haliaetus) - 0.002; and sparrow hawk (Accipiter
nisus) - 0.003 - 0.04. Liver samples from the kingfisher (Alcedo atthis)
were 0.24 and from the kestrel (Falco tinnunculus) - 0.13.
A British study by Jefferies and Prestt (1966) mentioned finding
residues of 0.01 ppm endrin in organs of the mallard (Anas platyrhynchos),
a prey species of the lanner (Falco biarmicus).
Other studies in eight British species of adult birds were conducted
^-x—- f of >\ rct-l'S?-
by Gramp and Olney (196y). Forty-five analyses were positive for endrin
in mixed viscera (liver, hear, spleen and gut). Highest amounts found were
6.4 ppm in greenfinch (Carduelis chloris), 2.4 ppm in red-legged
partridge (Alectoris rufa), and 1.53 ppm from a rood' (Corvus
frugilegus).
Koeman and van Genderen (1966) published on pesticide residues
of birds found dead or dying in a coastal Netherlands habitat. The
spoonbill (Platalea leucorodia) showed 0.6, 2.0 and 3.0 ppm for liver
f ''.H:
•r : !
-------
and 0.4 and 0.5 for breast muscle. The oystercatcher Qte-ematopus
ostralegus) had trace and 0.3 for liver. Liver tissue from the sandwich
tern (Sterna sandvicensis) ranged from 0.4 to 0.9 ppm. The common tern
(Sterna hirundo) gave values of present, 0.5 and 3.0 ppm for liver; 0.9
and 3.9 for breast muscle; 2.6 and 7.9 for kidney; and 1.2 and 1.5 for
brain. Spoonbills, oystercatchers, and terns feed predominantly on
crustaceans, mollusks and fish, respectively.
Later Koeman, et^ a!U, (1967) reported upon endrin residues in livers
of sandwich terns found dead in the Dutch Wadden Sea.. Mean values of 2
groups each (33 bird total) were chicks - 0.42 to 0.47 ppm; juveniles -
0.12 to 0.43; and adults - 0.29 to 0.67. Residues in the eggs of several
tern species from the Netherlands, Great Britain, Ireland and Germany
(total 69 eggs) ranged from not detectable (Ireland), 0.03 in only 1 of
5 eggs from Great Britain, 0.08 to 0.24 in Germany, and 0.17 to 0.20 in
the Netherlands. Significant endrin residues were confined to the Dutch
and adjacent German Coasts. Very likely the contamination originated at
least in part from factory effluent.
Numerous birds of prey, owls and other birds were reported dead
in the Netherlands in the winter of 1968-1969 (Koeman, et_ al., 1969).
Onset of mortality coincided with sowing winter cereals, which, owing
to unfavorable weather, occurred late in 1968 and early in 1969. Birds
possibly were poisoned by pesticides used in seed-dressing practice.
Only dieldrin was present in lethal concentrations in the tissues.
However, endrin residues were recorded from liver and kidney tissue
the buzzard (Buteo buteo) - 0.16 ppm, and the long-eared owl (Asio
otus) - 0.13 ppm.
-------
•I > ~-x .
Reichel, et al., (1969) found residues of less anfl 0.1 and) 0.1
" /V '
ppm in carcass, liver and brain of a bald eagle (Haliaeetus Leucocephalus)
u>
from Florida.
Risebrough, et^ al^ , (1968a), in their study of residues among various
raptorial and fish eating birds, found several positive endrin analyses.
Two eggs Craveri's murrelet (Endomychura craveri) from Baja California,
Mexico, contained 0.17 ppm endrin (lipid weight). Three brown pelican
^
(Pelecanus occidentalis) eggs collected from the Gulf of Panama contained
0.06, 0.07 and 1.13 ppm endrin (lipid weight). Two brown booby eggs
(Sula leucogaster), also collected off Panama, had endrin residues of
0.06 and 0.011 ppm (lipid weight). One osprey egg (Pandion haliaetus)
collected in the Gulf of California showed an endrin residue of 0.25 ppm.
South Dakota pheasants (Phasianus colchicus), was described by Linder
and Dahlgren (1970), showed less than 0.03 endrin in brain tissue and crop
^uj o./->o.-;;€-f^/
contents of 14 juveniles and similar levels in adults. Pheasants and sharp-
tailed grouse (Pedioecetes phasianellus campestris) of South Dakota were
analysed by Greichus, et^ al_. , (1968). Endrin residues in the fat were not
found above 0.05 ppm.
The Bureau of Sport Fisheries and Wildlife, United States Department
of the Interior, reported on "Pesticide Residues in Whooping Crane Specimens",
in 1964). Analyses were made for residues in tissues, eggs, and food supplied
to captive birds. Low levels of pesticidal residues were found in all
whooping crane samples examined. Endrin was found only in two eggs at
0.509 and 0.611 ppm. Concentrations of 0.283 and 0.087 ppm were found in
diet samples.
-------
Residues in insects and birds found in Louisiana cotton fields were
recorded by El Saved, et^ al^., (1967) . They found 0.46 ppm endrin in
mayflies but no endrin in six species of birds.
Recommended control for cutworm in Colorado wheatlands has been 3-4
oz. endrin/acre. Bird Census begun in 1969 showed little effect on numbers
the first two weeks after spraying. From 16 to 70-80 days post-spray birds
declined significantly. Twelve dead birds were found in sprayed fields,
none in unsprayed. Sick and dead black-tailed and white-tailed jackrabbits
were observed on sprayed fields as well as three dead cottontails, two
prairie voles and one deer mouse. Three or more domestic sheep ewes and
a lamb died with toxic symptoms after accidentally grazing sprayed areas
at least twice within a two-week period. Residues in cutworms collected
1-16 days post-spray averaged 2.5 ppm and ranged from 0.2 to 10.8 ppm.
Birds found dead and most collected alive around treated fields up to
several weeks post-spray had from less than 0.1 to 0.4 ppm whole carcass
residues (McEwen and Blomberg, 1970).
Organochlorine residues in 21 aquatic bird species from 31 locations
in Alberta, Saskatchewan and Manitoba were determined by Vermeer and
Reynolds (1970). Endrin was among the compounds screened but not detected.
Forty-five bald and 21 golden eagles found sick or dead in 18 states
and Canada during 1964-1965 were analysed for pesticide residues (Reichel,
et_ aJ^., 1969). Endrin residues were detected only in six bald eagles.
Median residue values in ppm were: carcass - 0.09; liver - 0.09; and
brain - trace.
-------
Keith, et_ al^., (1962) examined endrin residues in heart, kidney,
liver, brain and breast muscle tissues from experimental birds and from
those found dead in alfalfa fields in central California treated for mouse
control. Artificial exposure of caged birds to alfalfa treated with
0.8 Ib/acre of endrin resulted in some mortality. Residues in 4 cackling
geese ranged from 1.8 to 2.4 ppm. A ring-necked pheasant (gave 2.8 ppm.
V. . .
These were from birds found dead on a treated field. Dead cackling
geese (4) from another treated field showed residues of 1.7 to 4.1
ppm. Liver birds (4) had residues of 0.8 to 2.4 after 7 days.
Pesticide residues in the common egret (Casmerodius albus) in
California were reported by Faber, et^ al^, (1972). Five specimens
found dead or moribund had endrin residues in the brain of less than
0.10 to 0.28 ppm. Endrin residues were not recovered from liver or
breast muscle.
Wildlife lossess in the field in California were reported by Hunt
(1964). Several small birds observed falling from trees and dying at
the Cotton Research Station in Shafter, Kern County, included doves,
finches, sparrows and mocking birds. Endrin had been applied to cotton
for control of cabbage looper the previous day. The birds apparently
\
had been feeding on cabbage looper larvae that were abundant in the
sprayed plots.
1 /
V\ Endrin residue was found in a composite sample of three birds /
at levels of 1.29 ppm in flesh and 1.45 ppm in the gizzards. The
recommended rate for cabbage looper control was 0.5 pounds endrin/acre.
-------
Residues found indicate that endrin was probably responsible for the
bird die-off.
III.C.3.b. Bioaccumulation and Reproductive Effects - Cramp and Olney
(1967) related the occurrence of up to 6.4 ppm endrin residues in British
birds, and that worms and slugs from an endrin-sprayed field contained
10.3 ppm, indicating'route by which some birds could receive relatively
/ f f \ / /f / /
large amounts. — tyW^ci/fn. C KJ b{ b(i fi^-dr^ 'HI-^ [
Bioaccumulation of endrin from natural food sources in the
bobwhite quail, (Colinus virginianus), was discussed by Gregory (1969)
r~<^
in a simplified food chain situation involving soybeans, Glycimr Max, j
Mexican bean beetles, Epilachna varivestis, and bobwhite quail. One /
group of quail exposed to acute and chronic endrin^concentrations1 was
force-fed contaminated beetles at 1 mg endrin/kg/bird-.-\ Another test
group exposed to acute and chronic dosages was force-fad contaminated
beans at 0.015 mg endrin/kg/bird. Two days following treatment, all
birds were sacrificed. Fat, liver, and gonadal tissues, from both^acute
and chronic dosages, involving beans and beetles, consistently contained
endrin residues. Fat tissue from acute dosage involving beetles contained
0.682 ppm endrin, while the same tissue from chronic dosage contained
0.421. Liver and gonadal tissues from acute dosage utilizing beetles
contained 0.145 and 0.113 ppm endrin, respectively, while those from
chronic dosage contained 0.201 and 0.245 ppm, respectively. Fat tissue
from acute dosage utilizing beans contained 0.014 ppm endrin, while the
same tissue from chronic dosage contained 0.01°ppm. Liver tissue from
I'll)
-------
the acute test averaged 0.004 ppm endrin, and from the chronic phase -
contained 0.007 ppm. Gonadal tissue contained endrin only in trace
amounts.
Analyses of whole birds, from all tests, revealed retention of
approximately 16% of the total acute dose, and 21% of the total chronic
dose. Apparently the compound was not metabolized by any component of
the food chain, but accumulated and was transferred in the original form.
The effects of endrin on parental survival and fertility, litter
size, and young survival to weaning of field-captured deer mice
(Peromyscus maniculatus) were evaluated by Morris (1968). Endrin was
fed at intervals over a 7-month period with standard pellets containing
0, 1, 2, 4 and 7 ppm endrin. Adult mortality during feeding, starvation
and cold stress periods was directly proportional to endrin levels in the
food. Within each group, litter production frequency and mean litter
size before and during experimental feeding were similar. Mortality of
~y
young before weaning .apparently occurred at higher endrin levels. Post-
^4 _- -' ;
natal mortality of young up to weaning may be the main effect of endrin
on reproductive performance.
Morris (1970) later studied the effects of endrin on unenclosed field
populations of meadow voles and deer mice. Treated area was sprayed at
0.5 Ib/acre. Immediate and significant post-spray declines in meadow voles
occurred but no long-term toxicological effect was demonstrated. Population
on the treated area recovered rapidly, eventually exceeding pre-spray
f
numbers in two years. The experimental vole population seemingly responded
to endrin as it would to local depopulation by removal trapping.
Hi
-------
: o ^ ^ '
Although, deer mice were more abundant on the sprayed than on the
control area before endrin application, their numbers were significantly
/*
reduced after spraying and neveY did recover. Recruitment by immigration or
MjH • ^-^
breeding did not occur. All individuals captured on the spray plot the
following two years remained there for only one trapping period. A long-
term toxicological effect on deer mice seemed evident. This showed a /''s-;vX
/7no/<,..,
differential response of the two small mammal populations to endrin./ (: I
Intravenous injection of endrin in the anesthetized pigeon induced
changes in telencephalic neuronal function. Dosages of 4 mg/kg or more
caused seizure activity throughout the telencephalon. At 2-3 mg/kg, endrin
caused seizure activity largely limited to the ectostriatum, a telencephalic
visual projection area. At 0.5-2.0 mg/kg, endrin caused a specific increase
of potentials evoked in the ectostriatum by stimulation of the nucleus
rotundus, a diencephalic visual projection area. Reticular formation
functions tested were little affected. Relatively low brain levels of
endrin may impair visual function in birds. Visual impairment could be
a major factor underlying the well known sensitivity of birds toward endrin
(Revzin, 1966).
III.C.3.C. Endrin as a Ground Spray for Rodent Control - Endrin has
been used both here and abroad for limited agricultural and forestry
purposes in control of various rodents, particularly mice or voles.
Damage may consist of girdling or gnawing the bark of lower limbs,
trunk or roots of forest platings, fruit trees and ornamentals, damage
to forage crops, or by consuming the seed of forest trees.
-------
Endrin is a compound of choice because of its greater toxicity and
apparent effectiveness against rodents. However, opinion has been divided
upon the risk to humans, domestic animals ;and wildlife. Thus, in some
i\
European countries such as Denmark, West Germany and Czechoslovakia,
endrin may be used for vole control without restriction, whereas in
others such as the U.S.S.R., Belgium and the Netherlands, its use is
not permitted for this purpose.
Cook (1964) reports that only limited experiments have been made
in Great Britain for vole control with endrin. Vole populations there
may fluctuate widely from one year to another and many years may pass
before a population reaches a harmful density. When this occurs, damage
in fruit orchards and forest plantations may be heavy. The author did
j
not comment on the efficacy of the compound.
A unique situation prevails in Switzerland regarding use patterns
(Schneider, 1966). There, endrin is forbidden as an insecticide because
of its high toxicity and persistence. On the other hand, it may be
employed under restricted conditions and close supervision for the
destruction of voles (Arvicola terrestris) at a rate of 400 g/hectare.
An emulsion is sprayed on short-cut grass under the trees from mid-October
to mid-November. Only young enclosed orchards are treated. The following
year, 1.9 ppm endrin was found in grass cut for the first time, and 0.27
ppra in the third cutting (Hurter, 1965). Therefore, the use of this grass
was not permitted for fodder.
Areas treated must be enclosed for 5 months by a wire netting-fence
at least 1.2 m high and with a mesh no greater than 5 cm. This precaution
-------
was taken to prevent the poisoning of humans, domestic animals and game.
Schneider further indicates that cats and hares have been poisoned in
cases where this regulation was disobeyed.
Field voles (Microtus agrestis) created considerable concern in
Germany during the period of reforestation following World War II. They
caused serious damage to tree bark in extensive plantations and also in
naturally regenerated forests. B.epellents at stem bases proved impractical
over large areas. Field voles only occasionally accepted poisoned grain,
and coumarin (warfarin) preparations failed entirely. Little was achieved
wvvVVL
with other bait materials. Failure of traditional control methods led to
experiments with chlorinated hydrocarbons starting in 1954 (Schindler,
i
i
1956). Toxaphene and endrin proved effective in these tests. However,
a five-fold dose was used as compared with the rate commonly used for
insects. Dead voles and ones showing affected movements were found only
a few hours after application and two or three days later the areas were
considered free from field voles. The most effective method was spraying
grasses and other surface growth with 1.0 to 1.7 kg of 30 percent endrin
emulsion in 400 to 600 liters of water per hectare. This method was
recommended originally only for fenced areas free of wild game. However,
this restriction was later removed when no injury to game, birds or
domestic livestock was observed.
The control of orchard mice (voles) in the United States has been
studied most intensively over many years by personnel of the Fish and
Wildlife Service, U.S. Department of the Interior, and with endrin,
-------
specifically, by Horsfall and associates of the Virginia Polytechnic
Institute, Blacksburg, Virginia. Studies by both groups started in the
early 1950's. Horsfall's first recorded studies with endrin were published
in 1954 wherein he reported that rates of 2.5 Ib/acre required precautions
and that ground spray rodenticides were hazardous to animals but gave no
data.
Personnel of the Bureau of Sport Fisheries and Wildlife and predecessor
agencies, meanwhile, worked on a wide array of potential orchard mouse
rodenticides between 1934 and the present time. Studies of endrin
apparently were conducted only during the period of 1955-56 and some
reservations were made on this use because of potential hazards to man
and other non-target species. The U.S. Department of Interior now does .
not advocate continued use of chlorinated hydrocarbons nor does it permit
their use on lands under its jurisdiction.
During the period 1949-1969, Horsfall and his co-workers published
more than 40 articles related to orchard mouse control. Those published
since 1955 dealt almost entirely with endrin as a control agent. Rates
used experimentally or operationally varied from 1.2 to 2.7 Ib/acre.
There was a rapid decline in mouse activity to near zero levels in 6 days
or less in 1954. For 1953, 3 to 6 weeks were required for a similar
reaction, apparently associated with differences in moisture conditions
(Horsfall, 1956). Little or no evident deleterious effects were noted on
men or game animals but no quantitative data were presented.
States bordering the Atlantic Seaboard from New England to Georgia
plus Tennessee, Kentucky and Ohio have commercial apple orchards subject
-------
to attack by two species of voles, the meadow" mouse (Microtus spp.) and
the pine mouse (Pitymys pinetorum). Elsewhere in the fruit growing sections
of northern and western states most damage problems are associated with
Microtus alone. This latter species, being primarily a surface feeder,
can generally be effectively controlled with poisoned baits placed in
runways and burrows. However, the subterranean dwelling pine vole damages
orchard trees by gnawing and girdling tree roots at sites where baits
presumably are more difficult to place or are less effective. The pine
vole is the principle apple orchard pest from North Carolina northward to
the southern New England states. Endrin ground sprays at currently recom-
mended rates evidently help control both meadow and pine voles but are
predominately designed to control the latter species.
In his various reports, Horsfall found that endrin reduced mouse
activity in orchards generally, at times suddenly, sometimes gradually,
and occasionally a failure occurred. His "signs of activity" index to
vole numbers was used to demonstrate endrin effectiveness under some
conditions. However, as pointed out by Hayne (1970), this method is
inadequate for exploring why endrin sometimes fails, or for comparing
other candidate control methods with endrin on a quantitative basis.
A research program should develop laboratory and field methods adequate
to support quantitative studies. Such methods already exist for some
small mammals. It should be determined how endrin controls the pine
vole, and why treatments sometimes fail. Then the relative effectiveness
can be appraised for candidate methods to replace endrin. Concurrently,
-------
there is need for accurate before^ and after-treatment wildlife censuses
on treated areas plus residue analyses of dead or dying animals to deter-
mine precisely what caused their demise. Endrin is extremely toxic to
birds, mammals and.fish yet documentation on non-target losses from endrin
orchard spray operations is practically non-existent. Rollins and Horsfall
(1956, 1961), in observing many orchard sprayings, mentioned that some
quail and rabbits had been killed. However, most orchards had only an
occasional dead animal and many had none. Wolfe (1957) recommended 1.2
to 1.4 pounds actual endrin per acre for orchard Microtus control in the
State of Washington. He stated that possibly an occasional quail or
pheasant is killed by endrin sprays, but noted little evidence of such
deaths the previous three years. Fitzwater (1953) recommended against the
use of ground sprays in Michigan due to uncertainty of effectiveness,
especially against pine mice, and danger to wildlife and domestic animals.
Effects of endrin applications on three Fairfield County, Ohio
orchards were observed by Beck (1957). One 100-acre orchard containing
a pond was treated at about 3 Ib/acre. Six hundred walleye pike
averaging 1 Ib. each were stocked in the pond 1 month after spraying
and all apparently died within 3 days. None of the previous resident
fish (minnows, bluegills) were found the following summer. Frogs still
occurred but the tadpoles reportedly died. Terrestrial forms found dead
on the three orchards included rabbits, birds, woodchucks, cats and a
dog.
Forbes (1968) discouraged orchard use of endrin in New York
because of danger to wildlife and the development of resistant mice in
V.I7
-------
the Hudson Valley. Webb and Horsfall (1967) also reported upon a laboratory
study of endrln resistance in pine mice. Wild pine mice with a history of
treatment with endrin from a Berryville, Virginia orchard showed a 12-fold
greater tolerance to the pesticide than did mice from an untreated orchard
near Hagerstown, Maryland. Pooled data indicated LD^Q values of 2.97 and
36.12 mg/kg in this study. Horsfall and Webb (1966) pointed out that a
poison with a median lethal dose of 30 mg/kg should still provide adequate
control if properly exposed. Hayne (1970) cited Tietjen (19^0) that in
1968 in New York orchards, the acut^aT oral LDcQ for pine mice from an
orchard where endrin had been applied for 11 consecutive years at 3.2 Ib/acre
was 5.4 mg/kg, as compared with 1.84 mg/kg where endrin had not been used.
Excretion of C-endrin and its metabolites in endrin susceptible and
resistant pine mice (Microtus pinetorum) was studied by Petrella and Webb
(1973).
It was hypothesized that endrin metabolism may partially contribute
to the greater protection of resistant (R)animals from the toxic effects
of endrin as opposed to susceptible (S) animals. F-^ offspring born of
endrin resistant and susceptible parents, and having LD^Q'S of 18.97 +
1.78 mft/kg and 2.56 + 0.23 mg/kg, respectively, were dosed for 9 days
v/ith 0.51 mg/kg/j,^C-endrin (specific activity 2.19 mCi/mrnole) and feces
tj'
and urine were collected. R animals excreted 71% of the administered
radioactivity (18% in urine, 53% in feces), whereas S animals excreted
51% of the dose (23% in urine, 27% in feces). Fecal metabolite (s),
expressed as percent of the dose, were compared for the two strains.
-------
An approximate 2-fold greater amount was observed in the R animals.
The increased rates of excretion and metabolism may play a part in the
mechanism of resistance observed in these animals.
MacNay (1965) discussed the control of mice, rabbits and deer in
the orchards of Ontario and Quebec. He listed a number of possible
control methods but indicated that ground sprays of DDT, toxaphene or
endrin should be used only as a last resort.
Effects of endrin on vole (Microtus pennsylvanicus) reproduction
in blue grass meadows was studied by Snyder (1963). Endrin spray was
applied at rates of 0.6, 0.9, 1.3 and 2.0 Ib/acre. Censusing was done
2 to 4 months after application. The 0.6 Ib/acre application caused
no population decline. Applications at 0.9, 1.3 and 2.0 Ib/acre caused
reductions of 95, 92 and 71 percent, respectively. Application of 0.6
and 2.0 Ib/acre caused a reduction in the number of litters.
A hazard related to endrin ground cover spray use involves fish
losses due to runoff into farm ponds or adjacent stream drainages.
Such incidents may be related to heavy rains immediately following
application, or spraying of endrin on frozen ground where penetration
is adequate. Studholme (1958) contacted owners of 15 farm ponds in
Pennsylvania orchard spray areas and found that 6 had experienced partial
- "J 5p€/'Vf
or complete loss of fish. A 1959 news release (N.H.F. & G. Dept.) states
that the first fish kill in Pennsylvania attributed to water pollution
by endrin employed to control mice occurred on Yellow Breeches Creek in
Cumberland County. The stream kill appeared to be complete and included
-------
suckers, chubs and minnows. Some endrin had accidentally b.een spilled
while being mixed in a sprayer alongside the stream. Tarzwell (1958)
commented on apparent endrin contamination of a spring used as a
domestic water supply. The source was in a drainage area in Menallen
Township, Pennyslvania planted to fruit trees. Bioassay studies showed
a complete kill of fathead minnows in 4 hours, indicating a concentration
of 10 ppb.
The North Carolina Water Quality Division (1971) issued a report of
a fish kill in Lake Tunaluska, Haywood County. This loss resulted from
endrin used for rodent control by apple growers in the lake drainage
basin just a few days prior to the kill. Endrin residues were washed into
an inlet stream by a heavy rain on November 20. Fish mortalities occurred
from November 21, 1970 to the latter part of March, 1971. Endrin concen-
tration in the water (less than 0.001 mg/1) was less than the TLm value
for carp. However, the long exposure time created by confinement to the
lake permitted accumulation of sufficient endrin to cause death.
estimated 15,776 fish of 8 species perished. Up to 0.66 ppra endrin was
found in bottom mud. One fish contained 3.3 ppm endrin in the liver,
while another showed endrin residues of 1.62 ppm for flesh and 1.10 ppm
for kidney tissue.
Rogers (1972) gave data on water samples from 8 ponds located near
Hancock, Maryland orchards where endrin was applied. Five of these
proved negative while the other contained 0.32, 0.21 and 2.90 ppb.
Wolfe, et^ al^., (1963) reported upon the possible health hazards
of agricultural uses of endrin in the Pacific Northwest. Analyses of
-------
residues on 17 samples of windfall apples ranged from 0.3 to 1.2 ppm.
This average residue of 0.6 ppra would appear to present little hazard
to Children or others. Endrin residues on sprayed orchard grass and
itT~~'-'k
/
fescue were/very"'J>ersistent,
A study was undertaken during 1957 to determine the most effective
method of controlling meadow mice (Microtus sp.) that were girdling trees
in a 140-acre commercial holly grove in Santa Cruz County, California
(Dana and Shaw, 1958). A small one-quarter acre test plot was treated in
June with endrin at a rate of 2 Ib/acre. Subsequent trapping and visual
observation showed that this treatment kept the area free of mice for
about 58 days. Another test in October at the same rate gave protection
for 71 days.
Alfalfa is a major crop in the southern Sacramento Valley, California
and fields are frequently plagued with irruptions of meadow mice (Hunt
and Keith, 1962). Tests were made to determine the efficacy of endrin
for mouse control in dormant alfalfa. This area is also an important
wintering stie for migratory ducks and geese, and contains an abundant
pheasant population. Alfalfa is one of the few sources of green feed
available to these birds in winter. Sites treated for mouse control were
observed to determine if treatments resulted in wildlife mortality. Four
dead cackling geese, a dying house cat, a dead jack rabbit, a dead killdeer
and a dead long-eared owl were found on or near a 30-acre treated area.
A dead pheasant, a dying pheasant and a dead cackling goose were found on
other treated areas.
-------
.
/
Tests were begun to find if birds suffered mortality while held
/
j
on treated fields. Eight cackling geese, seven pintails, seven widgeon
and ten pheasants were placed in cages on a field treated with 0.8 Ib/acre
of endrin. Within one week, four geese, two pintails and one widgeon had
died, while birds held under similar conditions on untreated fields all
survived. Endrin residues on alfalfa during this test ranged from 23 to
120 ppm.
These data were also reported upon by Keith, et al., (1962). Laboratory
studies showed this chemical to be apparently equally toxic to widgeon,
cackling geese and white-fronted geese. The acute oral LD5Q of endrin to
these species is between 2.5 and 5.0 mg/kg. Residues extracted from birds
found dead on alfalfa fields treated with endrin showed 1.8, 2.0,. 2.4 and
) I ' . ff:,ff
2.4 ppm for cackling geese and 2.8 ppm for ring-neck pheasant. &*]"• /• 'J s
l&l-^CM -
Hunt and Keith (1962) also reported upon residue analyses of cackling
geese exposed to endrin on a plot treated for mouse control. Four wild
birds found dead contained from 1.8 to 2.4 ppm, four captive birds dying
after exposure in cages contained 1.7 to 4.1 ppm, and four captive birds
surviving exposure in cages showed 0.8 to 2.4 ppm. All analyses were based
upon composite samples of heart, liver, brain, kidney and muscle.
These authors reported upon effects to wildlife of another endrin use.
S^ Q
Seven valley quail, submitted for examination from the Watsonville area,
were found dead on berry fields sprayed with endrin at 0.3 Ib/acre for
blackfly control. Residue analysis of a composite of seven quail livers
showed 3.35 ppm endrin and 4.30 ppm dieldrin.
-------
Two reports of pheasant mortality were received from farmers in the
Tule Lake area. Two dead pheasant chicks were found in one potato field,
and 20 dead hens and 10 dead chicks in a second field. Both fields had
been treated with 9 ounces of endrin/acre for the control of aphids just
before the losses occurred.
Ferrel (1963) reported that an investigation was made of a die-off of
jackrabbits and cottontail rabbits near San Lucas, Monterery County, California.
By actual count, 147 jackrabbits and 18 cottontails were found dead in the
vicinity of a 92-acre alfalfa field. Endrin was applied to this field for
the control of cutworm at 0.8 Ib/acre just prior to the die-off. Endrin
residues of 1.6 ppm were present in the composite sample of liver and
kidney tissue of one affected jackrabbit, thus implicating endrin as the
cause of this die-off.
To recapitulate the data dn mouse control with endrin in orchards,
an account by Krestensen (1972) gives a brief synopsis of difficulties
encountered with pine mice. He mentioned the experimental use of a
24-acre block in a 300-acre abandonedxprchard near Hancock, Maryland.
The area had been abandoned 4 years previously. Endrin was applied in
the fall of 1967 to bring a heavy population of mice under control. Since
1968, approximately 35 trees were lost due \p damage occurring between
abandonment and the 1967 application of endrin. No endrin was applied
after 1967 and now. approximately 80 percent of Vhe remaining orchard is
dead with most dead trees showing mouse damage. \This may be an extreme
case but shows that some orchardists would be placed at a severe financial
-------
disadvantage if endrin Vas, Tianned for use in mouse control. It is claimed
by most orchardtsts withiri the pine mouse range that endrin may provide
effective if not complete control of pine voles under proper soil and
weather conditions, although fsiilure do occur. Withdrawal of this
endrin use could well create a crisis in pine mouse control since
other baits or ground sprays generally prove less effective. It
\
may be well to consider a limited extension of this endrin use pending
completion of trials on an anti-coagulan\ chemical which poses less
\
hazard from the standpoint of acute toxicifcy. This compound shows
\
some promise in preliminary testing and is being used under experimental
permit. To our knowledge, no other adequate substitute is currently
available for this specialized use.
Attempts at substitute methods of orchard mouse control were reported
by Tietjen (1969). in the search for new poisons, Gophacide,^ •'an experi-
mental organophosphate coded DRC-714, was first investigated in 1961.
Gophacide has a potential for broad use against many agricultural pests
including meadow mice and pine mice. In laboratory tests it was effective
against both with an LD^Q of 3.6 mg/kg for meadow mice and approximately
10.0 mg/kg for pine mice. In field tests conducted against meadow mice
in Colorado, Gophacide in an oat groat bait at a concentration of 0.08
percent, gave better than a 90 percent reduction in activity one week after
treatment.
With the pine mouse, he failed to come up with a grain well enough
accepted to be used as a bait. An additive was found to make grain bait t
more palatable. A fruit extract, DRC-470, proved effective. When 0.2
percent of this material was added to Gophacide-treated oat groat baits
-------
acceptance increased four-^fold Cfrom a mean of 0.23 g/animal/day to 0.97
g/animal/day), no mice refused the baits, and all died. During November \
1968, two large-scale field tests were conducted in Ohio with the trail- j
builder and the oat groat bait plus additive. Pre- and post-treatment ,;
trapping periods were 3 days each with post-treatment trapping commencing /
7 days after treatment. These tests resulted in a 91 and 94 percent reduction ^
in activity of mixed populations of meadow and pine mice. I •'
Hazards to men and wildlife must be ascertained before Gophacide ca
be registered for operational use in orchards.
III.C.3.d. Use of Endrin-coated Conifer Seeds in Reforestation - For about
the past 15 years, endrin-coated conifer seeds have been used to reestablish
forests on burned-over or clear-cut areas. The method is used extensively
for fir, pine and redwood reforestation in the Pacific Coast States and also
for pine regeneration in the Southeast. As pointed out in Chapter VIII,
there are numerous published reports that seed-eating rodents or birds may
consume large quantities of conifer seed and adversely affect reforestation
efforts. White-footed mice, chipmunks, ground squirrels, shrews and certain
seed-eating song birds all have significant effects on reseeding.
It is now common practice to protect conifer seed from such destruction
by coating seeds with endrin at a concentration of 1 Ib. actual endrin per
100 Ib. conifer seed. Endrin is used in conjunction with Arasan (thiram)
?/brJa latex-like adhesive to bind the endrin to the seed. Also a dye or
'^.'S
aluminum powder coating is added in an attempt to make the seed less
attractive to birds.
-------
Morton (1967) reported upon the effects of aerial distribution of
endrin-coated Douglas fir seeds upon the aquatic life of an Oregon coastal
stream. A forest fire destroyed or damaged 46,000 acres of timber in the
upper Smith River drainage, a Pacific coastal stream located in west
central Oregon. Federal and State agencies were concerned over the possible
effects of endrin-coated seed on trout and salmon in streams of the treated
Oxbow Burn area. Earlier study had shown that each treated seed carried
about 0.11 milligram endrin per seed. In the laboratory aquarium, under
static conditions, it was found that six treated seeds placed in 15 1
water at 55 F. would kill half the rainbow trout in 2 days and all of
them in 3 days.
Results of field observations and analyses of samples of live-boxed
and wild salmon, trout and other native species showed no mortality or
residue deposition in tissues over a 6-week period following application.
Seeds were applied at a rate of 3/4 Ib/acre of 1 percent formulation
endrin coating. This gave a calculated rate of 0.0075 pounds actual endrin
per acre, or 4.8 Ib. per square mile. Analyses of 4 water samples taken
1-10 days after seeding gave 2 readings of less than 0.04 ppb endrin, one
of 0.05 ppb and one of 0.556 ppb. The only fish with endrin in their tissues
were red-sided shiners (Richardsonius balteatus) which showed 30 ppb.
Residues of 25 ppb also were found in Pacific crayfish (Astacus trowbridgi).
While this study indicated no serious threat to game fish, it was suggested
that every effort be made to keep treated seed out of streams.
Marston, et^ al^., (1969) described the reseeding of a 175-acre "clear-
cut" watershed in the headwaters of the Alsea River, Oregon. This followed
-------
the conventional practice of aerially broadcasting endrin-coated Douglas
fir seed. Seeding produced measurable amounts of endrin in the streamflow
for 2 hours after seeding started and again during the peak flow of a winter
freshet 6 days after seeding. Total endrin detected during these two
runoff periods amounted to only 0.12 percent of that theoretically applied
to the entire watershed. This was much lower than laboratory results
(11.3 percent) from soaking endrin-treated seed in distilled water for
32 days. No data were given on wildlife effects.
Hooven (1957) reported upon a field test of endrin-treated Douglas
fir seed. The experiment sought to check the effectiveness of endrin for
the control of seed-eating mammals. The experiment utilized three 10-acre
plots, broadcast seeded at the rate of 0.5 Ib. Douglas fir seed an acre.
Two plots were covered with endrin-treated (1 percent) seed and one with
.untreated seed. Plots were located in the Tillamook burn of northwestern
Oregon.
A census of small animals through live trapping and marking was
taken prior to seeding. Two species of mice (Peromyscus sp. and Microtus
'
thomasi) and one of shrews (Sorex sp.) were captured. Trapping, prior
to seed application, showed 47 and 19 small mammals on endrin-treated plots
and 26 on the control. Seeding was in January with post-treatment census
in May. Only 2 mammals were captured on one treated plot and none on the
other. Six deer mice and nine shrews were caught on the control area.
An examination of each plot for seedlings was made in June. Of
100 mil-acre samples per experimental plot, an average of 51 percent were
stocked on treated areas and only 13 percent on the control.
-------
Reseeding on the north coast area of California covered 2,200 acres
in 1965-66 and 7,613 acres in 1966-67. Three-fourths to one pound per
acre of Monterey pine or Douglas fir seed was applied per acre.
Most was treated with 1 percent endrin although part received only 0.5 \
percent (Hunt, 1967) . There was concern over possible harm to anadromous
Y' fisheries and wildlife resources.
Bioassay with 1 percent endrin-treated seeds and rainbow trout showed
\ that two or more endrin-treated seed in a 5-gallon aquarium were fatal
(5 fish—66 hour LC^QQ ). Residue levels in flesh and in fat at various
exposures are given in Table III.C.5. Tests were also made on California
valley quail. A single seed with a calculated 0.219 mg endrin content
produced 73 percent mortality. Two seeds (0.438 mg) gave 100 percent kill.
Post-treatment collections of birds and mammals were made in 1966 on
two reseeded areas. Six of 15 samples positive for endrin residues are
shown in Table III.C.3.
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Table III.C.3.
Endrin Residues
Species
Blue Jay
Mountain Quail
Varied Thrush
Valley Quail
Chickaree
Gray Squirrel
Gray Squirrel
in Wildlife from
Tissue Analyzed
Intestine
Intestine
Intestine
Intestine
Intestine
Stomach
Intestine
Ingesting Treated
No. In
Sample
2
1
4
1
1
1
Conifer Seeds
Endrin
ppm
3.18
1.24
.78
.79
.56
1.17
1.55
In 1967, collections were made subsequent to reseeding treatments.
Residue checks were made also on two mountain and three valley quail taken
miles from any source of endrin. No background levels of endrin were found
in these birds. From treated areas, whole body analysis of Steller's Jay
and flicker showed .13 ppm endrin and another jay—.15 ppm. Other checks
on three jays showed .03 ppm and on five miscellaneous small birds—.47 ppm.
A study was made to determine the toxicity of endrin treated seed to
steelhead fingerlings placed in live cars of a small creek (.45 cfs). Endrin
treated pine seeds were put in cheese cloth bags and placed in the stream
above each live car. Results are shown in Table III.C.4.
-------
Table III.C.4.
Endrin Residues from Treated Seed in Steelhead Fingerlings
Live Car
Number
1
2
3
4
5
6
*Composite
Lbs. seed/cfs
cumulative total
0
.32
1.0
1.8
3.2
5.6
of 10 fingerlings.
Endrin
whole fish*
.001
.013
.036
.051
.102
.156
Residue
fat
.045
.64
3.05
2.00
7.39
8.76
rfj.._.,
(ppm)
water
ND
.000016
.000041
.000039
.000243
.000208
Total amount of seed used above was more than 26 times the theoretical
amount that would result from the prescribed application rate of .75 Ib/acre,
indicating little hazard from acute effects.
In an earlier paper on the same studies, Hunt (1966) gave the data
in Table III.C.5 on fish from bioassay. Levels of endrin residue found in
control fish and water make these data somewhat questionable."
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Table III.C.5.
Endrin Residues
Fish Exposed to
No. of Seeds
0
1
2
4
16
32
64
in Rainbow Trout Exposed to Treated
Endrin
Whole fish
1.5
1.9
1.6
1.9
2.6
2.9
2.8
Seeds in Water
(ppm) Based on
fat content
98.8
139.0
93.2
192.0
290.0
408.0
327.0
Another more recent report from the California Division of Fish
and Game (1968) discusses studies related to endrin-treated conifer
seedings on 20 different areas in Humboldt County. A pine seed
reforestation project was treated with endrin-coated seed on
January 15, 1968. On February 5, 41 dead varied thrush and 2 dead
-J>erc!
Oregon junco were found. On February 8-9, another field search
revealed 37 varied thrush, 2 juncos, 1 valley .quail, 1 hairy woodpecker
and an affected flying squirrel.
Samples checked gave endrin residues as shown in Table III.C.6.
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Table III.C.6.
Endrin Residues in Animals Exposed to Field Application of
Conifer Seed
Species
Varied thrush
II M
Varied thrush
n n
n n
Oregon junco
Varied thrush
Varied thrush
M M
n n
n n
ii n
n n
Flying Squirrel
(sick)
Varied thrush
n M
M II
Oregon junco
Steller Jay
Varied thrush
Oregon junco
Jay
Black-backed three-
toed woodpecker
Varied thrush
Brown headed-
cowbird
No. In
Sample*
10*
tt
10
10
6
n
2
8
"
1
1
1
1
1
1
1
1
1
1
1
1
1
1*
3*.
1*
1**
1*
1**
1**
Tissue
Digestive tract
gizzard
Digestive tract
n n
gizzard
whole
flesh
fat
Digestive tract
n M
Brain
n
Fat
"
Flesh
"
Stomach & Intestine
Whole bird
n n
n n
M n
Whole bird
ii n
n n
n n
n n
n n
n n
Treated
Residues In
ppm Endrin
11.0
134.0
16.5
8.6
10.2
18.8
1.397
0.32
1.71
71.5
85.8
0.081 Mf
0.59K ycai
8.17
6.08
3.82
7.50
0.30
3.6
1.1
N.D.
0.572
0.44
2.08
2.26
0.006
N.D.
1.5
N.D.
-------
Table III.C.6 (continued)
Species
Sparrow
H. thrush
Oregon junco
A=Found dead
**=Shot
No. In
Sample* Tissue
1** " "
2** " "
3** " "
Residues in
ppm Endrin
.0084
N.D.
N.D.
Cotton and Herring (1972) discussed another incident of wildlife
losses from reforestation efforts. Five bobwhite quail were found
dead in clear-cut area in Stone County, Mississippi directly treated
with endrin-coated longleaf pine seeds. Contents of three quail crops
from treated areas showed 14.4 percent pine seed by weight. GLC analyses
of pine seeds from these crops showed:
Endrin 48.906 ppm
A - keto endrin 18.920 ppm
Total endrin 67.826 ppm
dieldrin 0.453 ppm
Contents of crops from 3 quail collected several weeks later from
treated areas, one-third pine seed by weight, analyzed 37.84 ppm endrin
and 16.58 A-keto endrin or 54.42 ppm total endrin. Soybeans composed
100 percent of two quail crops from an untreated area. No endrin residues
were found in the crop contents or gut but brain tissue showed 0.3 ppm
endrin.
-------
Studies by Hamrick (1969) are reported in greater detail under the
wildlife acute studies section. However, it should be mentioned here
that he found that the force-feeding of one endrin-treated;slash pine
seed each to 10 bobwhite quail resulted in 100 percent mortality within
60 hours.
These data demonstrate that, on occasion, the aerial distribution
of endrin-coated conifer seed can have a deleterious effect on seed-
eating birds. One might consider this a hazard to "non-target" species
sinceTforest-dwelling rodents are evidently responsible for a major part
• —f—
of seed losses.
Concern over wildlife losses must be tempered by the fact that,
prior to the use of endrin, direct seeding attempts generally failed.
7
Hazards related to endrin seed treatment are minimized by the low total
poundage used, low application rate per acre, and infrequent use on
managed forests where the harvest cycle may extend from 30 to 100 years
or more.
Some alternative compounds are being tested as potential replace-
ments Cor this endrin use. At present, there are no/registered substitute^) ^u-
materials available. Substitution with a control agent of lower acute^
oral toxicity would be desirable. —-"" Cn
The loss of Douglas fir (Pseudotsuga menziesii) seed to small
mammals is a major obstacle to the success of natural and artificial
seeding. Baiting with 1080 and treating seed with endrin have been
used to prevent lossess but these materials are now subject to Federal
and State restrictions. Pank and Matschke (1972) reported on tKe"
I
-------
UT ,
-\G v \
deeliae—«ad—Eeinjiaaian_ixf deer mouse populations after baiting Douglas
fir clear-cuts with 6-aminonicotinamide. Oat groats treated with 1.0%
active ingredient by weight were broadcast at 1/2 Ib/acre on three
40-acre clear-cuttings. Livetrapping one week after baiting indicated
a 100% reduction of resident deer mouse populations. After one month
reinvasion had brought enough population to justify rebaiting according
to the criterion of five mice captured per 100 trap nights. Laboratory
tests showed good acceptance and effectiveness with 12 species (new
and old world mice, rats, nutria, pocket gophers and jack rabbit).
Initital studies indicated no secondary poisoning hazard.
Deer mice (Peromyscus maniculatus) have long been considered a
major problem in conifer forest replacement, especially where direct
seeding methods are employed. Over the past several decades strychnine,
thallium sulfate, endrin and sodium fluoroacetate (1080) have been used
for control. However, these are highly toxic and there is need for a
safer rodenticide. Howard, eti_ al^., (1970) found this species susceptible
to diphacinone, an anticoagulant. Consumption of 0.01% diphacinone-treated
crimped oat groat bait for at least 3 days was fatal to 80% of the mice.
Longer exposures frequently produced 100% mortality. When the 0.01%
bait was broadcast at 2 Ib/acre in field tests, no deer mice tagged
prior to treatment were recaptured. The susceptibility of deer mice
to diphacinone suggests that it might become a satisfactory substitute
, , ;
for endrin in control of conifer seed damage.r~\^fylf 7V«t ^ '
III.C.4.a. Toxicity to Domestic Animals - There has been an increased
need for determining toxicity to poultry and livestock for pesticides
-------
X
used on forage crops or for parasite control,/ In 1953, Sherman and
( /
Rosenberg checked the oral toxicity of 96%x endrin to New Hampshire
chicks at 7, 21, 45 and 64 days old. The U^g for 7-day old chicks
was 3.5 mg/kg. Older birds were more resistant. At 4.3 rag/kg, there
was 50% mortality among 21-day old birds, 40% mortality at 45 days, and . 'JL
10% mortality at 64 days. !v/4'^
The subchronic toxicity of endrin to New Hampshire chfcks was
investigated by Sherman and Rosenberg (1954). Endrin added to a
starter chick ration at rates of 12, 6, 3 and 1.5 ppm for week-old chicks
was continued on test for 42 days. Death occurred rapidly in lots fed
endrin at higher levels, the majority succumbing during the first week.
The two highest endrin dosages caused chicks to become highly excitable
during the first week. Slight disturbances produced flightiness, nervous
chirping and convulsion. Effects on mortality or growth of chicks to
7 weeks old showed 95% mortality with 12 ppm endrin, 3.5% mortality at
6 ppm and no losses at lower exposure levels. Significantly lower
weight gains were made by female survivors of treatments containing
12 and 6 ppm endrin. Among male survivors, lower weight gains resulted
from feeding rations containing 6 ppm endrin.
Phillips (1973) discussed a case of suspected endrin poisoning in
poultry. The ration was fed to a group of day-old chicks and also to
28-week-old hens. All day-old chicks died within 72 hours of initial
exposure. One hen died in 13 days, and two others in 20 days. Analysis
showed 21 ppm endrin in the diet; 3.9 to 4.9 ppm in carcasses; and/tissues
0.7 to 2.5 ppm. These concentrations were considered sufficient to have
caused the observed clinical signs and deaths.
-------
( '
Toxicity data for 21 pesticides, obtained by the chick embryo I /,n>
/ P
V— -
technique, were compared with acute oral LD5Q values obtained with rats.
A rank correlation was established between these two sets of data. Endrin
toxicity to the chick embryo correlated well with the rat data (Marliac,
e_t al., 1965).
Accidental endrin poisoning was encountered in seven commercial
chicken flocks in the Ottawa Valley, Quebec (Morin, et^ al.., 1970).
Both endrin contaminated feeds and endrin compounded rations proved
toxic for chickens. Losses of 74, 80 and 90% occurred in flocks f-e'd"
rations contaminated with 19, 32 and 35 ppm endrin, respectively. Effect
of rations containing known levels of endrin showed losses on the seventh
day in groups fed '30 ppm or more endrin, leading to 100% mortality in 21
days. In a group fed a ration containing 15 ppm endrin, losses occurred
later and totaled 62.5%. The LD5Q for broiler chickens, 5 weeks of age,
?1
was between 2 and 4 mg/kg. . _v ^
Tucker and Crabtree (1970) indicated the acute oral toxicity/of )
1-2 year old domestic goats to be 25-50 mg/kg. The reference test
"Garner's Veterinary Toxicology," revised by Clarke and Clarke (1967),
states that endrin has been found effective as a systemic acaricide in
cattle. However, at a dose rate of 10 mg/kg of body weight administered
subcutaneously, it was toxic to the host.
Steers, lambs and hogs fed endrin at dietary levels of 0.1 ppm
for 12 weeks showed little tendency to deposit endrin in body tissues//)
After 12 weeks of endrin feeding at 0.25 ppm, the endrin content of
the fat of these animals was not higher than 0.2 ppm. Other tissues
-------
showed no detectable endrin at this intake level. At the 2.0 ppm level,
steers showed 0.9 ppm in both, body and renal fat at 12 weeks. These
residues dropped to 0.3 ppm at 18 weeks (Terriere, et^ aJL , 1958).
Radeleff (1964) recorded results of various feeding levels of
insecticides to cattle and sheep for various times, and maximum fat
residues resulting from such dosages. Endrin fed at 2.5 ppm in the
diet for 16 weeks resulted in a maximum fat residue of 1.6 ppm for
cattle and 3.2 ppm for sheep. Feeding at 5.0 ppm produced maximum fat
residues of 2.4 ppm in cattle and 2.2 ppm in sheep.
Endrin was recommended in 1958 for sugarcane borer control.
A few growers grazed sheep in their fields for grass control. Studies
were made on endrin residues found in lamb fat from animals allowed to
graze for 55 days on endrin-treated pasture. One-fourth pound endrin,
was applied to a 0.5 acre pasture at intervals of roughly 1 week apart
for a total application of 0.75 Ib/acre. On removal, 2 animals showed
residues of 18.3-23.4 ppm endrin for internal fat and 11.5 to 14.0 ppm
for external fat. Two animals sacrificed at 14 days after removal had
20.3 - 23.7 internal and 14.6 - 20.1 ppm endrin in external fat. Final
figurer; after 42 days on untreated pasture were 8.9 - 13.8 ppm internal
and 6.4 - 11.0 ppm endrin residues in external fat. Appreciable endrin
residues were still present in lamb fat 42 days after removal from the
treated pasture (Long, et^ a^L., 1961).
Endrin was administered to bred ewes in order to determine toxicant
storage by the ewe and transferral to the lamb from various dietary intakes,
-------
Treatments were at zero, 0.75 and 2.0 ppm of the roughage consumed. The
toxicant feeding period was 12 weeks, at which time one ewe on each treat-
ment level was slaughtered. Remaining sheep were carried an additional
6 weeks on the same ration without endrin added. The only source of
toxicant to the lamb was through the ewe's milk. Lambs were slaughtered
when approximately 40 days old. Milk samples were collected at 2, 7,
20 and 40 days post-partum.
Ewes sacrificed after 12 - weeks exposure showed from 0.2 to 1.5 ppm
endrin in the fat. All samples had less than 0.1 ppm in flesh. Fat
content of endrin in lambs whose dams received endrin showed 0.3 to 0.5 ppm.
Milk samples from ewes receiving endrin gave values of 0.2, 0.4, 0.13 and
0.21 ppm at 2 days. Figures for 7 days were 0.6, 0.7, 0.12 and 0.18 ppm.
Residues in milk 20 days after birth were 2 samples less than 0.01, 2 at
0.01, and 1 at 0.08 ppm. Finally, the data at 40 days showed one sample
at less than 0.01, 1 at 0.02, 2 at 0.03 and 1 at 0.05 ppm (Street, et al.,
I /., . +-\? "
1957).
Chlorinated hydrocarbon insecticides are fat soluble and when
sprayed on cattle and sheep to control parasites may be absorbed through
Studies were made at Kerrville, Texas over a 6-year period to
5^ ''Olf- "A b*lci \
determine whether or not similar dosage.ss used in feed would lead to meat
and milk contamination and how long residues might persist (Claborn, 1956).
Fat samples were obtained by biopsy, and the data are presented in Table
III.C.5.
""•, t";
-------
Table III.C.7.
;::PK of Endrln Stored in cha ?at of Domestic Animals
Dosage Animal Weeks After Continuous Feeding
(ppm) 4 8 12 16
5 Steer 1.4 - 2.5 1.9
2.2
Heifer 1.2 - 2.4 1.3
0.8 - 3.6
Av. 1.3 1.5 2.4 2.3
Wether 1.9 - 0.5 3.5
1.5 1.4
Ewe 1.1 - 1.2 1.7
2.4 -
2.5 Steer 0.9 - 0.4 1.6
2.8 - 1.0
2.5 Heifer ' 1.6 - ,1.3 0
2.3 - 0.6
Wether 3.4 - 2.8 0.9
. - 1.8 - 0.3
- - 1.6
3.1 - 1.8 2.7
-------
Ely, «&£—ajrry (1957) reported upon endrin found in milk of cows fed
endrin-sprayed alfalfa and technical endrin. Hay made during 2 seasons
from alfalfa sprayed with 2.7, 6.6 and 7.8 oz. endrin/acre, harvested
one week after spraying and stored dry in bales for 6 months, had 2.8,
3.7 and 1.9'ppm endrin, respectively, when fed to dairy cattle. Cows
receiving hay containing endrin residues of 1.9, 2.8 and 3.7 ppm produced
milk with less than 0.15, 0.14 and 0.15 ppm endrin, respectively. When
feeding endrin dissolved in soybean oil to milking cows, higher intakes
were required to detect endrin in the milk than when feeding endrin residues
on alfalfa hay. Toxic symptoms were noted in two cows receiving more than
1.5 mg/kg of endrin in soybean oil.
Dairy cows were given daily doses of endrin ranging from 0.1 to 2.0
total .dietary concentration for 12 weeks. Milk samples were analyzed for
endrin residues during and after the endrin intake period. Various tissue
samples were also analyzed for endrin content at the end of the 12-week
period. Small amounts of endrin (less than 0.01 to 0.10 ppm) were detected
in milk at all levels of intake. Concentrations of endrin up to 1.0 ppm
were found in the body fat (Kiigemagi, et^ al_., 1958).
Residues in milk cows fed rations containing low concentrations of
J &1
five chlorinated hydrocarbon pesticides were studied by Williams ajad^MiirHr"
(1964). The study Involved 16 lactating dairy cows in which mixtures of
five pesticides were fed at approximately 0.05, 0.15 and 0.30 ppm of each
pesticide. The study included 2-week prefeeding, 5-week pesticide-treated
feeding, and 3-week postfeeding periods. Heptachlor epoxide and dieldrin
transferred in the milk in the highest concentration with endrin next in
order. Plateau endrin residue concentrations in milk for the three feeding
-------
levels were 0.004, 0.010 and 0.018 ppm, respectively. This study showed
that very low endrin feeding levels will result in measurable residues in
*
cow's milk. .
In the period 1964 through 1967, various chlorinated hydrocarbon
residues were detected above the actionable level in milk production of
40 Wisconsin dairy herds. Endrin was detected in milk produced by one
•c?
herd. The herd had been treated with an old .formulation of rotenone
for louse control. Shortly after application, three animals went into
convulsions and one eventually died. Approximately 30% endrin was detected
in a small dust sample. Endrin detected in extracted milk fat at 3 intervals
over a 5-week period was 6.76, 0.81 and 0.13 ppm (Moubry, et^ aJU, 1968).
Endrin and four other organochlorine pesticides were fed. in combination
at low levels (0.05, 0.15 and 0.45 ppm) to hens. Residues were determined
in abdominal fat, breast muscle and livers. Tissue samples, taken from
birds at each feeding level and a control at regular;intervals during a
•** ' irtH'/Mi^ •-. -ft-
5-month period, included 2 weeks 'pre-f Gratification, 14 weeks'on the J&w=£
-f-4ed~feed, and 1 month withdrawal. Endrin levels in fat ranged from
about 0.3 to 3.0 ppm and correlated directly with levels in the diet.
Residues in breast muscle all were very low-below 0.03 ppm. Residue
~ Tc4l
plateau levels in livers after 14 weeks of fortified diet were 0.1, 0.2
and 0.35 for the 3 levels fed (Cummings, et^ aj^., 1967).
D
' '* •
A companion study by Cummings, et^al., (1967a), recorded residues
in chicken eggs from low level feeding of five insecticides. Sixty
laying hens were carried for a 20-week period to show residue levels "
it
in eggs from birds maintained on feed containing 0.05, 0.15 or 0.45 ppm
-------
of linden-, heptachlor epoxide, dieldrin, endrin and DDT in combination.
The rate of decline of residue in eggs also was measured over a one-month
withdrawal period. While dieldrin and heptachlor epoxide showed greatest
storage in eggs, endrin was third among five compounds. The "background"
or prefeeding levels of endrin were less than 0.01 ppm. Within 3 days
after feeding pesticide-fortified rations higher levels were observed.
There was a direct relation between the plateau level and the level of
pesticide in the feed. All endrin residues were found in the yolk. Peak
residues after 96 days on treated feed were nearly 0.03 ppm at the 0.05
ppm feeding level; about 0.09 at 0.15 ppm dosage; and 0.03 at the 0.45
.ppm treatment rate. In the latter case residues dropped about 45 percent
after a 30-day return to the uncontaminated diet.
Effects of endrin on the cardiovascular system of the dog were examined!
by Hinshaw, et^ aJL , (1966). Experiments were carried out on anesthetized
dogs administered endrin (3 mg/kg b.wt., i.v.). A marked and progressive
increase in venous return (cardiac output) occurred within 30 minutes
following administration. Total peripheral resistance fell significantly
and remained low. No changes in pulmonary vascular resistance were observed.
Endrin appeared to exert a toxic action on the left ventricle; left heart
failure shown by elevated left arterial pressure regularly occurred.
Animals given endrin exhibited large increases in blood catecholamine
. 5(4A/p£4to'e .
concentration. Adrenalectomy significantly decreased catecholamine which,
however, remained elevated above pre-endrin values.
III.C.5."b. Effects on Eggs and Embryos - Analysis of egg yolk and poultry
tissues for chlorinated hydrocarbon residues was conducted by Stemp, et al.,
(1964). Recovery of endrin from egg yolk varied from 80 to 84 percent while
that from chicken fat was 84 to 86 percent.
-------
Leghorn laying hens were orally administered endrin at three levels
by capsule. Hens were later slaughtered, and abdominal fat samples
collected. Both carcasses and fat were pressure cooked in an autoclave
for 3 hours at 15 p.s.i. Over 95 percent of the insecticide residues
were rendered from the body tissues within one hour and detected in the
fat drippings. Only a trace of residue remained in both white and dark
meat at 2 and 3 hours of processing. Continued heating of fat drippings
produced some destruction of endrin (Stemp, et^ al^., 1965).
Known quantities of various pesticides were injected directly into
the yolk of incubating eggs. Most compounds tested at 10 ppm had little
effect except endrin which showed only a 40 percent hatch. At 100 ppm
the hatching rate for endrin-treated eggs was only 20 percent (Dunachie
and Fletcher, 1966).
The extraction efficiencies, based on the amount of endrin removed
by an exhaustive extraction of four procedures, were compared for
effectiveness in removal of residues incurred in eggs from hens fed
endrin (Wessel, 1969). Endrin residues in eggs from the various samples
and methods tested gave readings of 0.01, 0.02-0.03, 0.09, and 0.18 -
0.20 ppm.
Twenty-five insecticides were tested for their toxicity to hen
embryos at various concentrations, using an egg injection technique.
Most organochlorines did not harm the embryo at high dosages (up to
i
500 ppm), with notable exceptions to this among the cyclodienes. Results
expressed as percent endrin-treated eggs hatching compared with a control
group were 30 percent at 100 ppm; 39 percent at 50 ppm; 23 at 25 ppm:
-------
103 at 10 ppm; and 109 at 5 ppm. Endrin did show inconsistent results.
The terminal stage of incunation was the most susceptible. Effects of
time of~a3ministration of 100 ppm on the hatching of hen's eggs, expressed
as percentage of survival compared with the control were at da^ 5-4;/ at
day 8-75; and at day 10-100 percent? A delay of 8 and 10 days in injecting
greatly reduced the toxicity. In a st^vation experimehtT~at a dose of
5 ppm all chicks were dead by the fifth day; with the same dose and _.-•;
J '
feeding, there was complete survival (Dunachie and Fletcher, 1969) .
The effect of injection of chlorinated hydrocarbon pesticides
on hatchability to eggs also was studied by Smith, et^ al^ , 1970.
Injection of 0.2 mg of endrin into fertile eggs after 7 days of incubation
decreased hatchability to 40 percent. Higher levels were very toxic and
resulted in as low as 1.8 percent hatchability. The concentrations of
endrin used were 0, 0.2, 0.4, 0.8, 1.6 and 2.0 mg/egg.
-------
I I f.!). Toxicity to Other Organisms of Land and Water
III.D.I. Toxicity to Microflora - Vance and Drummond (1969) reported the
biological concentration of pesticides by algae. Algae, the base consti-
tuents of the aquatic food web, concentrate pesticides many fold and
generally are more resistant to toxic effects than higher members of
the food chain. Unialgal culture of two blue-green algae, (Microcystis
aeruginosa and Anabaena cylindrica, and two green algae, (Scenedesmus
quadricauda and Oedogonium sp., were grown under continuous florescent
lighting in aqueous solutions of endrin dissolved in acetone. Comparative
LCiQQ values for the four species listed above were < 5, > 15, > 20, and
> 20 ug/ml respectively. Concentration factors of pesticide residues
extracted after 7 days exposure were in the order 200, 222, 156 and
1AOX, respectively.
Some chlorinated hydrocarbon pesticides can be converted in natural
environments to forms more stable and sometimes more toxic than the
parent compounds which have been called "terminal residues," (Eagan, 1969).
Batterton, (1971) tested the effects of endrin and metabolites on the
growth rates of .two bacteria-free, blue-green algal species, Anacystis
nidulans a fresh water species and Agmenellum quadruplicatum a marine
species. Both species were tolerant to ketoendrin than endrin. Growth
rate of marine species was inhibited by all endrin concentrations tested
(0.2, 19, 95, 475 and 950 ppb) whereas the fresh water form was affected
only at high concentrations. In fresh water algal cultures with 950 ppb
/•—~ -^-pi
insecticide-lag in growth rate was observed for as much as 12 hour^ pre-J f
*S
ceeding exponential growth. The marine form was generally more tolerant
than the freshwater species.
-------
111.1).2. Toxicity to Microfauna and Miscellaneous Invertebrates - Residues
of chlorinated cyclodiene insecticides, as a result of their extensive use
and high stability, may remain in the soil for extended periods. Evidence
has been found, however, to indicate that some micro-organisms from soil
are capable of degrading even the highly persistent pesticides. Matsumura,
et al., (1971) studied the ability to degrade endrin of about 150 isolates
from various soil samples. Of all cultures tested, 25 degraded endrin and
ketoendrin, called metabolite IV was formed by all 25 with mass cultures
of Pseudomonas sp. Major metabolites were designated as III, IV and V
and minor metabolites II and VI.
Bollen and Tu (1971) studied the effects on the activity of soil
organisms of endrin applied at rates used with Douglas fir seeds. In
commom practice 0.5 - 1 Ib. of pine seeds that have been treated with
1-4 grams of endrin per pound acre are applied per acre. At this rate
of application 1 seed occurs in each 2-4 square foot with a maximum appli-
cation of endrin at 3-6 ppm per cubic inch of soil under each seed.
Endrin applied to soil at more than three times the maximum that might
be expected from application of endrin-treated tree seed exerted no
appreciable effect on numbers of soil microbes or on ammonification,
nitrification, or sulfur oxidation.
Drake, e_t al. , (1971) studied the effects of insecticides on soil
arthropods at Tucson, Arizona. Invertebrates were removed from soil
samples in an irrigated pasture treated two years previously at 4 Ib/acre
endrin. Residue in soil at the time of sampling was 0.60 ppm endrin.
Mites and Collembola represented 63 and 31 percent, respectively, of
-------
the invertebrates collected from 15 test plots treated with various
insecticides. Analysis of variance xnaicated no significant differences
between plots in total counts of mites and Collembola. There were
differences among the treatment means for the other arthropods. Eighty
to ,90 percent of the mites in the plot treated with endrin were oribatids.
Ground pearl crawlers (Margarodes sp.) occurred in samples from each test
plot except one treated with DDT-Strobane. Insecticidal residue remaining
in the soil apparently had no significant effect on total numbers and
kinds of invertebrates in the soil community. Homoptera were greatly
decreased in all insecticidal plots. There were no significant differences
in numbers and kinds of soil invertebrates from control plots with those
treated with endrin two years previously.
Bottom organisms were collected from a drainage stream located adjacent
to a commercial orchard which had been treated with endrin for rodent control
in Wisconsin (Moubry, et^ £l_. » 1968). Organisms containing endrin residues
included alder fly larvae (Sialis sp.) — 0.009 ppm; caddis fly larvae
(Limnephilus rhombicus) — 0.003 ppm; and freshwater shrimp (Gammarus sp.)
— 0.013 and 0.025 ppm.
Sanders and Cope (1968) determined the relative toxicity of various
pesticides to naiads of three species of stoneflies Pteronarcys californica,
Pteronarcella badia, and Claassenia sabulosa collected from Colorado mountain
streams, were used. Toxicity of endrin measured for 24-, 48-, and 96-hour
exposures at 15.5°C are presented in Table III.D.I.
-------
Table III.D.I.
LC Values for Stonefly Naiads to Endrin (ppb)
Exposure Time
Species 24-hr. 48-hr. 96-hr.
£. californica 4.0 0.96 0.25
P_. badia 2.8 1.7 0.54
C. sabulosa 3.2 0.84 0.76
Two species of stonefly naiads, Pteronarcys californica and Acroneuria
pacifica also were investigated by Jensen and Gaufin (1966) to evaluate
acute and long-term effects of organic insecticides. The two species were
exposed to concentrations of insecticides equal to or less than their
4-day TLm. Comparative 4-day TLm values for the two test organisms showed
0.32 ppb for for A. pacifica and 2.4 ppb for £. californica. A progressive
reduction of TLm figures occurred for both species exposed to endrin for
30 days. The 30-day TLm for Pteronarcys naiads exposed to endrin was
approximately one-half the value for static, 4-day exposures. The 30-day
TLm values of Acroneuria naiads represented concentrations more than 10
times less than those of the 4-day static values. Results indicate that
endrin has a cumulative effect, and that a relatively large application
factor would be necessary when using static 4-day bioassay results for
estimating safe concentrations over extended periods.
Tolerances of selected freshwater invertebrates to pesticides were
examined by Naqvi and Ferguson (1969). In 48-hour exposures, six species
-------
of cyclopoid copepods from a pesticide contaminated ditch near
Nelzoni, Mississippi, were resistant to high concentrations of nine
pesticides than the same species from areas of minimal pesticide contami-
nation near State College, Mississippi. Similarly, a clam Eupera
singleyi, and a snail, Physa gyrina, from the Belzoni locality had higher
tolerances to endrin than the same species from State College. High
concentrations of 20 insecticides which killed fish within 3 minutes
failed to kill the worm, Tubifex tubifex, from Belzoni in 72-hour tests.
The potential hazard of increased tolerances in these invertebrate species
is the increase in amount of pesticide residues available to higher trophic
levels.
III.D.3. Earthworms - A comprehensive literature review on the effects of
chemicals on earthworms was prepared by Davey (1963) which showed that
these animals may accumulate persistent pesticides in quantities sufficient
to cause toxic effects in predators that feed upon them. Pesticide
concentration by animals in terrestrial situations has not been
demonstrated as frequently as for the aquatic environment. However,
Barker (1958) found that earthworms from areas treated for control
of Dutch elm disease contained amounts of DDT that would be fatal
to robins. Cramp and Olney (1967) reported that a sample of worms and
slugs from an endrin sprayed field contained 10.3 ppm endrin and from
this source some birds could receive relatively large exposures.
Earthworms are surprisingly resistant to different pesticide
formulations. Endrin dust tested in pot experiments at 5 Ib/acre
produced no mortality among Eisenia foetida after 2 months exposure
!70
-------
t/M
(Hopkins and Kirk, 1957) and t'1024 1'b/acre of endrin gave erratic
v
results. Endrin applied as a 0.01 percent emulsion of about 27 Ib/acre
successfully controlled earthworms in tobacco seed beds in India
(Patil, 1960).
Slugs and earthworms in a cotton field accumulated 18 and 11 times
the soil residues of organochlorines. Slugs contained 53 ppm DDT and
its metabolites, 0.4 ppm dieldrin and 1 ppm endrin. Earthworms contained
32 ppm DDT complex residues and traces of dieldrin and endrin (Dustman
and Stickel, 1969).
Soil and earthworms and other soil invertebrates were collected
from 67 agricultural fields in 8 states. Total organochlorine residues
in soils averaged 1.5 ppm, and in earthworms, 13.8 ppm. Amounts of
insecticides in earthworms varied directly with amounts in the soils.
Nearly 24 percent of all soil samples contained endrin, but the amount
exceeded 0.1 ppm in only 6. Endrin occurred in 39 percent of the
earthworm samples. Twenty percent of the samples exceeded 0.1 ppm
endrin. Perhaps the most dramatic biomagnification was shown by
endrin residue data from a Maryland apple orchard. Endrin ppm values
were: soil, 3.47; earthworms, 11.04; slugs, 95.81 - 134.06; and snails,
2.72. Earthworms from another Maryland orchard contained 5.13 ppm
endrin. Presumably the endrin was applied for orchard mouse control.
Earthworms in this study were represented by four genera: Allolobophora,
Diplocardia Helodrilus, and Lumbricus. The amount of residues found in
worms from 15 fields was within the range found to kill birds in short-term
feeding studies. However, this assumption was based upon invertebrate
-------
residues of DDT and metabolites. The effect of reported endrin levels
on animals higher in the food chain is a possible matter of concern, but
remains to be adequately evaluated (Gish, 1970).
The effects of endrin on the numbers and biomass of earthworms were
studied after application to trefoil pasture which had not been previously
treated with herbicides or insecticides for at least five years. Endrin
treatment was made at the rate of 1 Ib. ai/acre. Numbers and biomass
of earthworms three weeks after 20 quadrats were treated ranged from
1 to 17 in numbers and 132.2 gms total biomass. The biomass in treated
plots was less than 50 percent that in untreated plots. Endrin lessened
numbers in the treated quadrats by 52 percent (Thompson, 1971).
III.D.4. Plankton — Results from experiments at Woods Hole, Massachusetts
cited by Vogt (1970) emphasized the dangers of chlorinated hydrocarbon
pollution to the balance of marine life. Some varieties of marine phyto-
plankton were highly sensitive to some chlorinated hydrocarbon pesticides,
but the green flagellate Dunaliella tertiolecta was not sensitive to
1000 ppb endrin. The carbon uptake of Skeletonema costatum and Coccolithus
huxleyi was significantly inhibited with 10 ppb endrin. More than 100 ppb
DDT blocked cell division in S_. costatum after two or three divisions, but
had no influence on £. huxleyi. The /reverse^ of these effects was observed
„- a, uJa&f ,
with endrin. The carbon uptake of Cycloteira nana, the most sensitive, was
inhibited with as little as 1 ppb endrin. Endrin stopped cell division
completely. High concentrations of pesticides could affect the regeneration
of phytoplankton and their subsequent domination by a single species.
The species assayed above by Menzel, et al., (1970) were obtained from
diverse sources. S. costatum is a coastal centric diatom isolated from
-------
Long Island Sound. The naked green flagellate I}, tertiolecta is typical
of tide pools and estuaries. The other two species, £. huxleyi, and the
ccentric diatom C^. nana both were obtained from the Sargasso Sea. Sensitivity
and response to environmental pollutants may vary considerably among species
of marine planktonic algae as shown by the above data. The greater resistance
of one estuarine species, in comparison with the susceptibility of coastal
and open ocean forms may reflect the need for adaptability. Chlorinated
hydrocarbons may not be universally toxic to all species, but may exert a
dramatic influence on the succession and dominance of certain forms.
The metabolic transformation of endrin by marine microorganisms was
p£p£.l icv Vqr- ! CfT
studied by Patil, et ji^L. , (1972). Samples of sea water, bottom sediments
from both ocean and estuaries, surface films, algae and marine plankton
were collected and treated with radioactive insecticides and incubated for
30 days in the laboratory. Seventeen samples were exposed directly to
radioactive endrin. Ketoendrin is known to form by either photochemical
reaction or microbial actions. Although no photolytic reaction could be
observed in control tubes illuminated in the absence of microorganisms, a
photosensitizing substance possibly was present among the microbial products
and the reaction may have been of a photochemical-biochemical nature. The
only water sample which showed degradation was from Hawaiian fish ponds,
which contained algae populations. Fish pond water formed 35.5 percent of
an unknown metabolite of endrin while an algae collection from a stagnant
.fish pond formed 24.4 percent ketoendrin.
Stickel (1968) pointed out that aquatic animals can be adversely
affected by a reduction in their food supply. Phytoplankton communities
-------
are an important food base in aquatic environments whose productivity
can be seriously affected by exposure to small amounts of pesticides.
In controlled 4-hour exposure to 1.0 ppm of endrin, lindane and mirex,
phytoplankton productivity was reduced 28 to 46 percent (Butler, 1963).
III.D.5. Bees and other Pollinating Insects - Twenty chemical treatments
were tested for aphid control in red clover raised for seed in eastern
Washington (Johansen, 1960). Predators and parasites of the clover aphid
in the control plot were sampled after the applications. During the
first six days after application, endrin was the least destructive to
beneficial insects. This material reduced predator-parasite populations
38 percent as compared with checks. However, percent honey bee mortalities
from treatments on red clover at 0.4 Ibs. endrin/acre were 64 percent in one
hour, 80 percent in three hours, and 100 percent in ten hours.
Sixty-one pesticides were tested against 5 parasitic hymenopterans
and 6 predatory coccinellids. Data served as guides in selecting the best
materials for destroying pests without undue harm to natural enemies
(Bartlett, 1963). Single dosages applied were those commonly used on
J
orchard crops. The data suggest that the effect of each pesticide upon
most adult parasitic hymenoptera may be anticipated with a high degree of
-^ A"
reliability. The effect upon predatory coccinellids was much less predictable.
At the high dosage used, many materials were broadly toxic to most
entomophagous species tested. Among these was endrin applied as a 50 percent
wettable powder at 0.5 lb/100 gal. water. Rate of deposition was 6.44 jig/sq.
cm. Toxicity ratings were high for 9 and medium for 2 of the 11 species
tested. High toxicity was expressed as an LTrn of less than 24 hours.
-------
Medium toxicity was delineated as an LT^Q of greater than 24 but less than
100 hours, -v __
Endrin used at low concentration (.0447 percent) represented the
dilution customarily applied to orchard crops as a complete coverage spray.
The high concentration was 10-fold that of the low to simulate possible
dehydration of a 10 percent honey bait applied in a water spray.
Toxicity data were presented as H (high) -50 percent mortality within
1 day or less of first exposure; M (medium)-LDrQ between 1 and 4 days;
L (low) -appreciable, but less than 50 percent kill after 4 days; and
(O)-no detectable mortality in 4 days. At the lower concentration, endr in-
treated bait showed acceptance of 61 and 35 percent for the 2 coccinellid
predators with toxicity of 0-L for both. The parasitic hymenoptera
showed 45 and 56 percent acceptance and toxicities of L and L-M.
At high dosage level acceptance was lower and toxicities rated
higher. For coccinellids, these were 6 and 10 percent acceptance and
L and M toxicity. Comparable data for hymenoptera were 17 and 29 percent
acceptance with high toxicity in both instances. Stomach poison activity
of the chlorinated hydrocarbon group was peculiar. With the exception of
endrin, methoxychlor and lindane, which killed certain species, chlorinated
hydrocarbons were not generally potent stomach poisons (Bartlett, 1966).
Comparative field studies on the toxicity of pesticides to honey bees
(Apis mellifera) were begun by Anderson and Atkins (1967) in 1952 in
California and continued to the time of publication. They rated endrin in
the moderately toxic group which included compounds having LDcn values of
2 to 10 micrograms per bee. Field tests were mainly on alfalfa, cotton,
citrus, ladino clover and sweet corn.
-------
Atkins and Anderson (1967) also issued another paper dealing
exclusively with laboratory tests. Again they referred to endrin
as being moderately toxic. It ranked 58th among 217 compounds tested.
The endrin LD5Q in jig/bee was 2.018.
III.D.6. Crustaceans - A study was designed to determine relative
toxicities of several widely used pesticides to the scud, Gammarus
lacustris, a crustacean commonly found in small streams and ponds of
western United States. Toxic effects were measured by median lethal
concentration (LC,-n ) for 24-, 48-, and 96-hour exposures at 70°F. In
static bioassays at 70°F, estimated LC™ values in micrograms per liter
for endrin were 24-hour, 6.4; 48-hour, 4.7; and 96-hour, 3.0 (Sanders,
1969): kffV-> 1 f \
_/ f) 1^
The activity in water of 14 pesticides used in Utah was determined
by a^modified bioassay method using (5. lacustris as a test animal.
Concentrations (ppm in water) for 96-hour LDt-x values for endrin were
u$fi-P^y •\o--jr 'ft\fvfTQuT
0.0115 (Nebeker and" Gaufin, 1963-64).
Reduction in shell growth, loss of equilibrium, and death are used
as criteria of toxicity in oysters, shrimp, and fish, respectively. Since
insecticides are designed to kill terrestrial arthropods, there is much
concern about the effects of these chemicals on marine crustaceans which
have commercial value such as crabs and shrimp. These animals spend much
time in shallow estuarine waters occasionally polluted with insecticides.
In laboratory studies performed with continuously flowing sea water a
TTpercentageof juvenile brown shrimp, Penaeus aztecus, tolerated a
v|ry low concentration (0.025 ppb) of endrin for 60 days; shrimp survive
11}
ll
-------
only a few days at endrin concentrations greater than 0.05 ppb (Lowe, 1966).
In Korean shrimp (Palaemon macrodactylus) at temperatures ranging between
13 and 18 degrees C, the 96-hour TL^Q values (ug/1) for endrin were 4.7
for static bioassays and 0.12 for intermittent-flow bioassays (Earnest, 1970)
Massive fish kills occurred in the lower Mississippi and Atchafalaya
Rivers and the Gulf of Mexico, in the fall and winter months after 1960,
and were particularly severe in the winter of 1963-64. In fresh waters,
primarily bottom-feeding fish were affected, while in brackish waters
bottom and surface-feeding species were involved. Analysis of fish revealed
that endrin was consistently found in all tissue extracts examined. Endrin
was present in lethal amounts in the blood of dead fish taken from the
Mississippi River. Specimens of dead or moribund catfish collected from
the Mississippi River at Baton Rouge in December 1963 were found to be
toxic to mice. In similar tests oysters taken in good condition from
Grand, Quarantine, American Bays and other shellfish growing areas were
not found to be toxic. Living shrimp collected from the delta of the
Atchafalaya River were found to contain 360 ppb endrin as well as other
insecticides (U.S. Dept. of H.E.W., Publ. Health Ser., 1964). ' ,
,?*•<"
In 24-hour bioassays, fresh-water shrimp, Palaemonetes Kadiakensis,
from 3 areas of intensive pesticide use in the Mississippi delta were
1 to 25 times more resistant to 7 organochlorine, 3 organophosphorus,
and 1 carbamate insecticides than shrimp from Noxubee National Wildlife
Refuge (Bluff Lake). Toxicity, ranked in descending order, was: most
toxic-endrin, DDT, methyl parathion, parathion; medium toxicity-guthion,
lindane, toxaphene, strobane; least toxic-chlordane, sevin and heptachlor.
5 '"''
•
-------
The mortality of susceptible shrimp caged in a canal near cotton fields,
was 66 percent greater than resistant shrimp (Naqvi and Ferguson, 1970).
' / '~\
The importance of daphnids as part of the fresh-water biota, and \
their sensitivity to toxic substances, stimulated many investigators
to use then/as assay organisms. The acute toxicity of endrin to
Daphnia magna, as indicated by 96-hour bioassays and expressed as TLm, /
was 0.332 ppm (Anderson, 1959). Organophosphates generally were more '
toxic than chlorinated hydrocarbons to Daphnia pulex and Simocephalus
serrulatus. Toxicity of hydrocarbons to D. pulex varied greatly with
-^
48-hour EC values ranging from 0.36 to 460 ppb. Estimated 48-hour
50 JU
EC5Q immobilization values, in micrograms per liter, for daphnids exposed
to endrin were: (1) S^. serrulatus -2.6 ug/1 at 60°F and 45 at 70°F; and
for ID. pulejx -20 ug/1 at 60°F. Endrin was 9(6-14) times more toxic
than dieldrin to jS. serrulatus, while IK pulex showed endrin 12 (8-19)
\ ; ••
times more toxic than dieldrin (Sanders and Cope, 1966).
' t
Toxicities of jpesticide ingredients to some fresh water organisms
were reported by Nishiuchi and Hashimoto (1967). Their TLm values for
3 hours exposure to two fresh water daphnids were listed as greater than
10 ppm for both Daphnia pulex and Moina macrocopa. This was a relatively
short exposure period. Fresh water fish and daphnids are clearly different
in susceptibility to pesticides. It is impossible to presume the suscepti-
bility of the fish to pesticides from that of daphnids and vice versa. A
high correlation was recognized between the susceptibilities of the two
daphnids.
Specimens of Daphnia magna, killed by extremely small quantities
of pesticides also were killed by small amounts of extracts.of common
plants, such as lettuce, radishes, and beets. Even following rigorous
17R
-------
cleanup, these plant extracts were toxic enough to the test organism
to mask any mortality caused by pesticide residues. Although D_. magna
is extremely sensitive to many pesticides, its sensitivity to certain
plant extracts and possibly to other ingredients in commercial insecticide
formulations make its use as a bioassay organism of doubtful value.
Gas chromatographs equipped with electron capture detectors had an equal
or better sensitivity to the insecticides tested, and gave more repro-
ducible and more accurate results on field-treated samples of carrot tops
(Frear and Kawar, 1967).
Fish and invertebrates frequenting coastal areas are especially
vulnerable to chemical insecticides which tend to diffuse in drainage
systems and to concentrate in estuaries (Butler, 1966). Several studies
on the effects of insecticides on marine organisms demonstrate that
concentrations which are not sufficient to control many species of
pestiferous insects, including several species of salt-marsh mosquitoes,
can kill eggs and larvae of bivalve mollusks (Davis, 1961) and alter the
tissue chemistry of clams (Eisler and Weinstein, 1967). Acute eradrin
toxicity tests to sand shrimp, (LC in >ig/l) was 2.8 for 24 hours, 1.8
for 48 hours and 1.7 for 96 hours.
For grass shrimp LC^Q'S for endrin were 10.3 ug/1 at 24 hours, 4.3
at 48 hours and 1.8 for 96 hours. Endrin was the most toxic of all
organochlorines tested on this species. LC^'s of endrin to the hermit
crab were 27 }ig/l at 24 hours, 18 at 48 hours and 12 at 96 hours. Lindane,
p,p'-DDT and methoxychlor were more toxic among the organochlorines
(Eisler, 1969).
-------
Red crawfish, Procambarus clarki, collected at Baton Rouge, Louisiana
were exposed to endrin for periods of 24-, 48-, and 96 hours. TLm values
were 0.4 ppm for 24 hours, 0.3 ppm for 48 hours and 0.3 ppm for 96-hour
exposure. Endrin was the most toxic organochlorine compound checked
(Muncy and Oliver, 1963).
III.D.7. Mollusks - A nationwide program was initiated in 1965 to monitor
residues of chlorinated hydrocarbon pesticides in estuarine shellfish.
About 160 stations were established and samples were collected at thirty-
day intervals. Despite the wide array of persistent pesticides used in
Z-
the United States, only DDT, dieldrin, and endrin occurred/most frequently
in monitored samples. Estuarine mollusks were collected at monitoring
stations in five states in 1967. Endrin residues were detected in samples
taken from Texas and California; the maximal level detected was 19 ug/kg.
The Gulf Breeze, Florida laboratory accumulated data on relative toxicity
of commonly used pesticides when exposed to estuarine test animals for one
to four days. In such tests ..48-hour XL™ values for various crustacean
J4r2'
species usually were 1 ug/flcgjor less within normal ranges of environmental
salinity and temperature (Butler, 1969).
Residues of chlorinated hydrocarbon insecticides in the North Sea ' Jr
of «/•*,
environment were studied by Koeman, et^ al_. , (1967-1968). In 1964,'-residues
were detected in Sandwich terns and spoonbills seen dying or found dead
at Texel in the Dutch Wadden Sea (Koeman and van Genderen, 1966). The
symptoms, tremors and convulsions, suggested poisoning, probably by
neurotoxic compounds. Distribution of insecticides in the Dutch and
-------
West Germany coastal environment war. studied further by using the
mussell (Mytilus edulis) as an indicator organism. Mollusks concentrate
chlorinated hydrocarbon insecticides as a consequence at their filter-feeding
habit. In August 1965, mussels were collect at 20 places along the Dutch
coast. Highest residues of chlorinated hydrocarbons were found near the
mouth of the Rhine, and at sites to the northeast. This corresponds with
the outflow of river water as it moves along the Dutch coast and enters the
Wadden Sea. Residues of chlorinated hydrocarbon insecticides in sprat
(Clupea sprattus), juvenile herring (Clupea harengus), and sand eel
(Ammodytes lanceolatus), captured in the Dutch Wadden Sea in 1965 and 1966
are shown in Table III.D.2.
Table III.D.2.
Endrin in Fishes from The Wadden Sea
Number Residue in ppra of body weight
of fishes (geometric mean and ranges)
Year Endrin
1965 103 0.14
(11 samples) (0.07-0.45)
1966 37 0.09
(28 samples) (0.01-0.29)
-------
1
'L'he samples contained telodrin, an insecticide not used in Europe
which was manufactured by a chemical industry near the mouth of the
Rhine. It is likely that some endrin was discharged in the effluents
from the plant. Residues of endrin in mussel (Mytilus edulis) samples
along the Dutch and West German Coast, and at one place on the British
Coast during the summer, 1966 are shown in Table III.D.3.
Table III.D.3.
Endrin in Mytilus edulis taken near Holland
Sampling Residue in ppm of body weight
Place Endrin
Scheveningen 0.36
Katwijk 0.07
/ IJmuiden 0.19
Den Helder 0.05
Griend 0.02
Mellum 0.02
Oldeoog 0.01
Scolt Head (< 0.01
-------
Residues of endrin in mussels (Mytilus edulis) sampled at Scheveningen
between 1965 and 1967 are shown in Table III.D.4.
1
Table III.D.4.
Endrin in Mytilus edulis taken at Different Times of the Year
Date Residue in ppm of Body Weight
Endrin
August 1965 0.05
January 1966 0.20
August 1966 0.36
January 1967 0.26
August 1967 0.04
Chlorinated hydrocarbon pesticide residues in California bays and
estuaries were studied as a part of a nationwide monitoring program.,
Endrin was found only at West Island in the Sacramento-San Joaquin
estuary. It was reported during three different months at this site.
Analyses of clams revealed endrin at 10 ppb or less for the Asiatic
clam, Corbicula fluminea. All samples were screened for 10 organo-
chlorine pesticides but only DDT, DDD, and DDE were routinely found.
Significantly higher pesticide pollution occurred in estuaries receiving
runoff from large agricultural and urban areas than in other estuaries
(Modin, 1969).
The effects of pesticides on oyster growth and presence of residues
as a public health problem were studied. Growth rate of oysters was
-------
reduced 35 to 100 percent following exposure to 0.1 mg/1 endrin. A
residue of 0.033 mg/1 endrin in sea water caused 50 percent reduction
in oyster shell growth. In a 1965 progress report, a Gulf Coast research
center indicated 90 oyster samples positive for chlorinated hydrocarbons.
Residues in water from which oysters were taken ranged from 0.01 to 0.07
mg/1 for endrin. In another study, six oyster samples were taken from
Indian River, Brevard County, Florida. Sampling stations coincided with
commercial fishing sites and within flowing streams considered highly
subject to pesticide runoff. For endrin, the range in water was 0.0013-
0.005 mg/1 which was below that which inhibit oyster growth (Mason and
Rowe, 1969).
Monthly sampling and analyses for endrin residues of mud and water,
top-water fish (bream), bottom-water fish (catfish), shrimp, and oysters
from the lower Mississippi River were carried out for 1 year. Oysters
and shrimp contained less than 0.005 ppm (Novak and Rao, 1965).
Samples of oysters, water, and bottom sediment were collected from
the lower Mississippi River region and southern Barataria Bay. Highest
endrin concentrations found in water and bottom sediment samples were
less than 0.001 and 0.01 ppm, respectively. No endrin residues were
reported from oysters (Hammerstrom, e_t al_. , 1967).
f MolUl'e
S-
water and 65 of bottom sediment were collected from sites where shell-
fish were growing. Median residue levels of endrin in positive oyster
bottom sediment samples were <0.01 and < 0.001 ppm, respectively. Median
In a similar studjy Molule Bay, Alabama, 82 samples of oyster, of
-V
-------
pesticide concentration in positive water samples 0.001 ppm for all
chlorinated pesticides (Hanunerstrom, et^ al_. , 1969).
Wilson (1966) studied the amount of residual pesticides found in
oysters under laboratory conditions at Gulf Breeze, Florida. After
exposure for 10 days in water containing 1.0 ppm had accumulated in
oyster tissue. This indicates a biological magnification of 1000X.
Oysters collected from estuarine areas in South Carolina, Georgia,
Florida, Mississippi, Louisiana and Texas were analyzed for pesticide
residues. Chlorinated pesticides generally were either not detected
or found at relatively low levels in Atlantic and Gulf Coast area
samples. Endrin was detected in 27 of 115 oyster samples within the
range < 0.01 to 0.07 ppm (Bugg, et_ al . , 1967).
Studies were made to determine endrin concentrations in water,
bottom sediment, and oysters in a Louisiana estuarine area, and to
determine interaction with bottom sediment. The species concerned was
the Eastern oyster, (Crassostrea virginica . The study area was near
Barataria Bay, located some 40 miles south of New Orleans. A total
of 111 samples were collected on a bi-monthly basis for eight months in 1968
and 1969, in Grand Bayou, Hackberry Bay and Creole Bay. Endrin was
- luti^ev.
-------
1964-1966 and 1965-1966 indicated that pesticide influx into the study
area had decreased. The 1968-1969 maximum endrin concentration was 29
times less than in 1965-1966 (Rowe, et^ a^. , 1971).
The teneency for molluscs to accumulate aquatic pollutants is well
known. This results from their method of feeding which involves filtration
of large amounts of water. For this reason, Ryan, et^ al_., (1972) studied
use of the mussel Hyridella australis as a biological monitor of endrin
in fresh water from a creek in Victoria, Australia. The mussels carried
less than 0.01 ppm endrin when collected. Caged specimens were subjected
to endrin in the stream. Water samples did not contain more than trace
amounts (< 0.01 ppm), but mussels reached a tissue concentration of 0.38
ppm endrin after 24 days. Residue levels later decreased to 0.05 ppm
at 68 days. Mussels in an experimental tank with 0.5 ppm endrin in solution
reached a tissue residue level of 3.44 ppm in 3 days, a seven-fold increase.
When experimental and control mussels were placed together in fresh water,
the experimental group quickly lost endrin while the control group took
up some of the excreted residues.
Indigenous of coastal areas are especially vulnerable to chemical
insecticides which tend to accumulate in estuaries and inshore environments.
Mollusks are considerably more resistant to insecticides than either teleosts
or decapod crustaceans according to results of 96-hour bioassays with
selected groups of marine fauna (Eisler, 1969 and 1970). Test animals were
adult quahaug clams (Mercenaria mercenaria), and mud snails (Nassa
obsoleta) collected from Sandy Hook Bay, New Jersey. All mollusks
-------
were held 14 days prior to testing in aquaria containing 1,000 liters
of sea water. All clams survived for 133 days following exposure for
96 hours to concentrations up to 10 mg/1 of the four organochlorine
insecticides, including endrin. No deaths occurred among snails during
96-hour exposure to any concentration of endrin or during the remainder
of the 33-day observation period. However, gastropods initially exposed
to 0.1 mg/1 and higher of endrin exhibited a marked reduction in egg
case deposition when compared to controls.
Detoxification of pesticidal residues in fish and shellfish was
studied by Hallab (1968). The objective was to determine detoxification
agents in vivo and in vitro that would lessen or minimize toxicity
of chlorinated pesticides with special reference to shellfish. Oysters
and shrimp were used as experimental animals. Aminopyrine, orinase, and
pyralgin used in 1 and 10 ppm concentrations as detoxification agents
were applied to experimental animals with sublethal doses of chlorinated
pesticides. Orinase at 1 and 10 ppm Showed most promise in degrading
"^r-Trr: - V^
pesticides in oysters and shrimp. m£.
-------
applied at 0.1 and 0.5 Ib/acre. With 0.1 Ib. endrin/acre a 50 percent
mortality occurred at 24 hours and 90 percent loss after 48 hours. Appli-
cation of 0.5 Ib/acre caused 100 percent mortality in 24 hours (Mulla, 1963).
Relative toxicities of several halogenated hydrocarbon insecticides
was measured for grass 'frogs (Rana pipiens) immersed in contaminated solutions.
Endrin concentrations of 0.015 and 0.02 ppm showed no lethal effect after
30 days exposure, while 6 of 20 frogs were dead after 30 days at 0.03 ppm.
Those immersed at the highest concentration changed skin color and became
grayish. Neuro-muscular changes were characteristically produced with 0.03
ppm. Endrin was more toxic than similar amounts of dieldrin, aldrin, chlordane,
toxaphene, methoxychlor or BHC (Kaplan and Overpeck, 1964).
Ferguson and Gilbert (1967) tested cricket frogs and Fowler's toads
from several localities with differing degrees of insecticide contamination
with endrin. The approximate 36-hour TL-- values (Mg/ml) for several
populations were: northern cricket frog (Acris crepitans) —0.4 to 0.6
ppm, southern cricket frog (Acris gryllus)—0.02 to 0.045 ppm, and for
Fowler's toad (Bufo w. fowleri)—0.03 to 0.095 ppm. Anuran populations
captured near treated cotton fields showed up to 200-fold resistance compared
with populations from pesticide-fee areas. Toads were generally more tolerant
than cricket frogs.
i
Mulla (1962) used insecticides to control excessive populations of
frogs and toads in California. Endrin was found to be highly toxic to
tadpoles of the bullfrog. A complete kill occurred at 0.1 Ib/acre^ -^
t
Static bioassays were conducted to determine the relative acute
toxicities of various pesticides to week-old tadpoles of the western
-------
chorus frog (Pseudacris triseriata) and five-week-old tadpoles of Fowler's
toad (Bufo w. fowleri). Endrin was the most toxic to Pseudacris tadpoles,
and the second most toxic to Bufo tadpoles. TLm values in mg/1 at 15 C
for the chorus frog were: 24 hours-0.29; 48 hours-0.29; and 96 hours-
0.18 and for Fowler's toad 0.57, 0.46 and 0.12 at 24, 48, and 96 hours,
respectively (Sanders, 1970).
-------
III.E. Fate in Air - Environmental pollution has received great public
concern but little research has been done on atmospheric pollution by
pesticides. In 1961, Harris and Lichtenstein showed that volatilization
of aldrin, dieldrin, heptachlor and lindane was a major factor in their
disappearance from treated soils. Movement and distribution of pesticides
have been attributed to both atmospheric and hydrospheric currents. The
limited literature available suggests air contamination by evaporation
or codistillation of chlorinated hydrocarbons with water and verified
by occurrence in atmospheric dust, and rainwater. Riseabrough, et al.,
A
(1968) detected chlorinated hydrocarbons, primarily dieldrin, DDT and
fs&&p#4&ii=^-~
DDE'in dust borne by trade winds from European-African land mass to
Barbados, West India. The amounts detected, < 1-164 ppb, suggest that
movement on contaminated dust particles may contribute to contamination
of water and land far distant from sites of use. A study of airborne
particulate pesticides in urban atmospheres was conducted in 1963 and
1964 (Tabor, 1965). Aldrin was detected in measurable amounts in only
one location. No traces of endrin, commonly used in combination with
other pesticides, were found in any samples. Similar observations were
made by Abbott, et^ ajU , (1965, 1966) in dust samples taken in central London
and its suburbs which contained traces of BHC, DDT, DDE, TDE and dieldrin
but not endrin.
In a pilot study designed to measure atmospheric contamination by
19 pesticides air samples were obtained from 9 urban and agricultural
areas in the United States. Most pesticides present in the atmosphere
were particulates. Only DDT was detected at all localities. Twenty-five
samples taken at Stoneville, Mississippi were positive for endrin with
a maximum level of 58.5 ng/cubic meter (Stanley, et^ al_., (1971).
-------
Attempts to use a "balance-sheet" approach to pesticide persistence
have been unsuccessful. Large amounts remained unaccounted for even
in carefully controlled studies. Volatilization losses to the atmosphere
may partially explain such discrepancies.
Volatilization accounted for a significant net loss of 2 percent
endrin applied at 2 Ib. ai/acre to sugar cane. Half was applied to the
cane and half to the soil surface. Mean atmospheric concentration of
endrin reached 540 ng/cubic meter during the 3-day period after application
and decreased asymptotically to 30 ng/cubic meter 77 days later (Willis,
e_t al., 1969).
Jegier (1965) studied the hazards of insecticide applications in
Quebec. A field survey of spraying was conducted to measure respiratory
and dermal exposure of spray operators during application of insecticides
to orchards, small fruits, vegetables and grain. The mean concentration
of endrin in air determined in air inside aircraft to which pilots were
exposed during spraying, was 0.01-0.05 mg per cubic meter. Respiratory
exposures were determined by checking filters of respirators worn by
observers sitting beside spray operators on tractors. Mean respiratory
and dermal exposures of 3 subjects to endrin were 2.4 and 0.15 mg per
man hour. Mean dermal exposure to endrin during aircraft spraying was
1.1 mg per hour, but under high pressure ground spraying conditions,
0.15 mg per hour. The latter value was attributed to the direct injection
of endrin into the ground.
Reports of humidity on residue persistence are meager. Kalkal, et al.,
(1961) found that the fumigant action of some insecticide residues increased
significantly under similar temperature between 55 and 80 percent relative
-------
humidity. Under high humidity, there was a rapid change of insecticide
into the vapor phase and in amounts high enough to account for the fumigant
effect. Heptachlor epoxide loss was approximately 2 times greater at the
higher humidity. Lyon and Davidson (1965) measured residue losses under
high and low humidity conditions. Test conditions were 80+2 F. and
relative humidity at 8+5 and 80+5 percent. Heptachlor epoxide again
showed residue losses two times greater under high humidity. However,
both endrin and coumaphos showed a greater loss at low humidity. Endrin
weight loss was 2.0 mg at 8 percent relative humidity but only 1.1 mg at
80 percent. The exact cause of this variation is unknown.
Organochlorine pesticides were measured in rainwater collected
continuously during 12 months at 7 widely distributed.sites in the
British Isles (Tarrant and Tatton, 1968). BHC, lindane, dieldrin, DDT,
and DDE and TDE were found at all sites throughout the year, but endrin
~
was not detected.
Vaporization of chlorinated hydrocarbon insecticides from soil
surfaces may be an important source of plant contamination. Aerial plant
parts were contaminated by insecticide volatilization from soil surfaces
as well as by root absorption and translocation. These included tests
on soybeans with four pesticides, including endrin. With all chemicals
tested, seeds always showed the lowest residue concentrations (Anon., 1970).
Investigations of climatic effects on insecticide toxicity were
conducted in Texas by Mistric and Gaines (1953). High temperatures and
humidities, rainfall, dew and sunlight proved important in reducing the
-------
toxicity of certain insecticides. Tests also were conducted to determine
effects of wind and other climatic factors. The boll weevil, cotton
leafworm and salt-marsh caterpillar were used as test insects.
Field cage toxicity tests for boll weevil control indicated that
normal climatic factors reduce endrin toxicity when applied at 0.33 Ib.
ai/acre. Temperature range was from 64° to 95 F., and relative humidity
from 28 to 74%. Toxicity (% mortality) decreased to 84.7% immediately
after release, 64.5% after 24 hours, and 43.2% after 48 hours.
In a laboratory study on residual toxicity conducted under assimilated
normal climatic conditions no appreciable loss of mortality from endrin
was observed after 48 hours. Simulated rain applied immediately after
treatment with endrin caused no appreciable reduction in endrin toxicity
to boll weevils. Percent mortality with "no rain" controls was 95.7,
while those subjected to rain showed 93.6. Similar results were obtained
with cotton leafworm.
High and low temperatures had minimal effects on endrin toxicity to
boll weevil. Mortality caused after residues were treated at low temperatures
for 24-hours was 98 percent and 100 percent after similar delay at high
temperatures. Movement of air at 5.9 m.p.h. produced by an electric fan
caused reduction in toxicity to cotton leafworm of endrin applied at 0.1
Ib/acre.
/^1£<
III.F. Fate in Water - The chief Hazard :of pesticide residues in aquatic
•' . _. _ ^^~~ ^
environments is^biological accumulation in the food chain. Organochlorine
insecticides may be absorbed selectively by plankton which are later
consumed by small fish which, in turn, are eaten by larger fish. Biological
» o o
< Jo
-------
I
accumulation does not appear to be an immediate problem with human food
but some evidence indicates possible harmful effects in fish, birds and
marine mammals at the higher trophic levels.
Trace amounts of endrin and other organochlorine compounds can be
removed from waters by treatment with large amounts of activated carbon
(Chesters and Konrad, 1971). Quantities associated with low level chronic
contamination are difficult to remove and available evidence suggests that
current water treatment practices are inadequate to avoid long-term, low-
level contamination (Mrak, 1969) .
Lichtenberg, ej^ jil. > (1969) summarized five annual surveys (1964
through 1968) for chlorinated hydrocarbon pesticides in surface waters of
the United States. Data collected at 110 stations on all major drainages
showed widespread occurrence of these compounds. The reduction of endrin
occurrences from nearly 50% in 1964 to zero in 1968 was considered significant
in light of its association with major fish kills in the lower Mississippi
prior to 1964. It ranked fourth in occurrence after dieldrin, DDT and
£W
DDD. Highest recorded levels for each year in ug/1 were: Potomac-0.094~~ 5°
and Rio Grande-0.067 in 1964; Mississippi (Arkansas) -0.116 and Atchafalaya
(Louisiana)-0.019 in 1965; Hudson-0.069 and South Platte (Colorado) -0.063
in 1966; Kansas-0.133 and Maumee (Ohio)-0.036 in 1967, and none recorded
for the entire country in 1968.
In another program, fish were collected from 50 sampling stations
located in Great Lakes and in major river basins throughout the United States.
wAa/f/W
Endrin was reported consistently in/isamples from only three stations — one
on the Mississippi River in Louisiana, and the Arkansas and White Rivers
-------
in Arkansas. These were all at relatively low levels ( <0.1 ppm). Scattered
higher values were reported from other stations such as the Susquehanna River,
Maryland, Roanoke River, North Carolina, Savannah River, Georgia, Apalachiocola
River, Florida, Lake Ontario, New York, Missouri River, North Dakota, Green
River, Utah, Colorado River, Arizona and The Sacramento River, California.
This constitutes presumptive evidence of widespread contamination of water
/or/aquatic food organisms with endrin (Henderson, et al., 1969).
^/ ~~
Microparticulates suspended in Lake Erie water were collected by
continuous centrifugation and were examined directly or placed on a
sucrose density gradients. Residues were examined by both gas and
thin-layer chromatography. Endrin was shown by both methods to be
associated with microparticles contained in the various fractions of
the gradient. The first gradient fraction of one sample contained
endrin equilavent to 0.69 nanograms/1 of lake water (Pfister, et al. ,
1969).
Pesticide monitoring of the aquatic biota of Tule Lake National
Wildlife Refuge was established because of pesticide poisoning of
fish-eating birds (Godsil and Johnson, 1968). Endrin found regularly
in samples of both water and aquatic biota presumably resulted from
irrigation return flow, runoff or leaching from crop lands. Water
contained a maximum 0.1 ppb endrin in 1965 while tui chubs accumulated
up to 198 ppb the same year.
Effects of pesticide applications in the Houston, Texas area were
measured on shellfish and shellfish-growing waters of Galveston Bay.
Pesticide levels in both water and oysters were low at all times. All
-------
oyster samples contained trace amounts of endrin, but no endrin was
detected in water samples. The occurrence in oysters indicated presence
in water at some previous date (Casper, 1967')"T^ /]6T) *\ f^t"' '*>/ '
Endrin content of marine fish of the northeast Pacific was generally
insignificant—up to 0.006 ppm '(Stout, 1968). Larger pesticide residues
occurred infish taken at the mouth of the Columbia River than in those
from Hecate Strait, British Columbia, where no major river enters the
ocean. Agricultural runoff was considered to be a factor causing higher
residues in the former sample.
The effects of aerial distribution of endrin-coated Douglas fir seeds
on the aquatic life of Oregon coastal streams were studied. Morton (1967)
evaluated effects on game fish of re-seeding a burned-over area in the
Smith River basin. In laboratory tests six treated seeds placed in 15
liters of water at 55 |F. killed half the rainbow trout in an aquarium
/ /
-------
detected in the stream flow for 2 hours after seeding started and again
during the high flow of a winter freshet the sixth day after seeding.
Total amounts of endrin detected during these two runoff periods amounted
to only 0.12% of that theoretically applied to the entire watershed.
Endrin leached off a subsample of seed, covered with distilled water for
32 days, was 28.2 ppb, or 11.3% of the total calculated endrin seed
coating (Marston, et^ al. , 1969).
Samples of a water-suspended sediment mixture from 11 streams in
western United States were analyzed monthly in 1965 and 1966 (Brown and
Nishioka, 1967). A total of 12 insecticides was detected. ^Slightly more
than 50 percent of the positive samples contained 5 ppt or less total
pesticides. Positive occurrences were most frequent from February
through May. Of 165 positive results, only 7 contained endrin which
occurred in samples from the Missouri# Colorado, Rio Grande and Snake
Rivers within the range 5-40 ppt. In a follow-up study the network
was increased to 20 sampling stations during the October, 1966 to 1968
period (Manigold and Schulze, 1969). Of 235 positive samples, four
contained endrin; these were from stations on the Brazoa, Colorado
and Gila Rivers at concentrations of .02, .07, .01, and .01 ppb.
Pesticides in water and sediments of the lower Mississippi River
and its tributaries were analyzed by Barthel, et_ al_.'» (1969). Pesticide
residues were detected from both agricultural and non-agricultural sources.
There was no indication of a general buildup>of chlorinated hydrocarbon
pesticide residues in stream sediments from farm use. Significantly
higher residues in water and sediment were found in tributary streams
-------
near manufacturing or formulating plants in Tennessee and Mississippi.
Water samples from Wolf River and Cypress Creek near Memphis, Tennessee
contained 0.25-2.03 ppb endrin and 5.04-6.5 ppb ketoendrin. No contami-
nation was found in 1966 in Mississippi River sediments upstream from
the confluence with Wolf River which suggests that manufacturing wastes
were the source of pollution. Traces of some of these pollutants were
found in sediments 500 miles downstream near Baton Rouge, Louisiana.
These findings are related to a summary report of the 1963 Mississippi
fish kill which led to the announcement that endrin was the cause of
1963-65 fish losses in the lower Mississippi River (Mount and Putnicki,
1966). Beginning in November, 1960, large numbers of. dying fish were
observed in the Mississippi and Atchafalaya Rivers and associated
bayous. There were few mortalities in 1961 and 1962, but a heavy kill
occurred again in 1963. Fresh, brackish water and marine fish species
were affected. Lethal threshold concentrations of endrin in the blood
were determined from dying bullheads, buffalo and gizzard shad. Blood
samples of these species were well above the lethal level measured
in the laboratory. Water concentrations of endrin in the Mississippi
River varied from 0.1 to 0.2 ug/1 at West Memphis and New Orleans. This
concentration was acutely lethal in laboratory tests on channel catfish,
largemouth buffalo and gizzard shad. It may be difficult to understand
that such minute quantities of endrin such as 0.1 ppb could be acutely
toxic to fish. However, in 2 hours the blood of a catfish has attained
an endrin concentration more than 1,000 times that of the surrounding
-------
water, and fathead minnows exposed to .015 ug/1 had total body concentrations
1,000 that of the water.
A creek flowing into Lake Erie and a controlled drainage system
(the water of which is pumped into Lake Erie) were monitored for
insecticide residues during 1970 (Miles and Harris, 1971). Residues
in water, mud, and fish were most pronounced in the more abundant
DDT complex and dieldrin. Endrin was determined in chubs and suckers
(10-18 ppb) although it was not detectable in the water or mud.
Samples of oysters, sediment and water were checked^ from an
'70m^r-/!jf
estuarine area of Louisiana (Rowe, e_t al^. , 1971). Water samples
from all stations on every sampling date contained less than 1 ppb
of endrin. However, samples of sediment and oysters showed a
chain buildup to levels five times as great. Oysters, water and bottom
sediments were checked for endrin from the lower Mississippi River region
and southern Barataria Bay. Collections were made during three separate
6-8 month periods between 1964 and 1966. Highest endrin concentrations
in water were less than 0.001 ppm with median values being the same.
Bottom sediments were less than 0.01 ppm and oysters had a similar
median value (Hammerstrom, et al., 1967).
The ecological distribution of pesticides in Lake Poinsett,
South Dakota was studied by Hannon, e_t ai_., (1970). DDT and metabolites
were found at all trophic levels and heptachlor, aldrin, dieldrin and
lindane were present in most sample types. Endrin was not detected above
analytical confidence limits in any sample.
-------
After accidental spillage of the agricultural pesticides nabam and
endrin into Mill River, Prince Edward Island, there were extensive
mortalities among brook trout and juvenile Atlantic salmon. Abnormal
behavior including unseasonal downstream movements in summer and unusual
response to an electric field were observed among surviving trout and
salmon (Saunders, 1969).
Sparr and Appleby (1966) determined the concentration of endrin
in waterways, fish and mud from a cotton field treated three times with
endrin at 0.3 Ib. per acre. Endrin in the soil did not exceed 0.04 ppm,
even after subsequent sprayings. Traces of endrin were found in fish
but not in mud. Pvunoff water from the cotton field showed only 0.05 ppm
after the last spraying. Pesticides in drinking water from 10 selected
municipal water supplies whose source was either the Missouri or
Mississippi River was assayed by Schafer, et^ al_. , (1969). Over 500
. grab samples of finished drinking water were checked for 10 chlorinated
pfarn.
pesticides and about 1/3 of the samples contained endrin.'v t)fcf >::f !\ _
Studies were conducted in Louisiana to assess methodology of
S
measurement and to determine the extent and duration of surface water
contamination by endrin used in sugar cane culture. .In 1961, up to
,j 1
W«^ '
360 ppt of endrin was recovered from water. Endrin was recovered from
each of six streams sampled, three of which were at sites of fish kills
attributed to endrin. In 1964 with more efficient sampling techniques
700-820 ppt were detected. Surface runoff was the main source of endrin
contamination (Lauer, e_£ a.L. , 1966).
-------
Average annual applications of/7.5 from repeated applications at
0.03 Ib/acre had been made to cotton fields near Greenville, Mississippi
since 1956. During 1965, endrin residues in soil averaged 0.3 ppm in the
spring and 0.32 ppm in the fall. Water accumulating in a nearby slough
was sampled 19 times between April and February. Measurable endrin
residues were detected on only 6 sampling dates in amounts ranging from
0.07 to 1.A9 ppm. Samples of slough sediment showed endrin residues on
3 of 19 collection dates, ranging from 0.27 to 0.91 ppm (Iverson, 1967).
Effects of pesticides on raw waste water were studied by Canter,
et al., (1969). Reagent grade endrin in concentrations up to 50 mg/1
had no effect on the B.O.D. of sewage. Commercial endrin caused an „ taw
/*
increase in chemical oxygen demand (C.O.D.) of 20 mg/1 per mg of endrin<
Escherichia coli cultures could grow "on nutrient agar containing commercial
endrin in concentrations up to 500 mg/1. E^. coli suspensions did not show
viability after 1 hour exposure to 3000 mg. per 1. endrin.
III.G. Fate in Plants - Amounts of endrin taken up by soybean, wheat, corn,
alfalfa, bromegrass and cucumber seedlings from five soils treated with
0.5 or 5.0 ppm C-14 labeled insecticide were determined in greenhouse
experiments (Beall and Nash, 1969). Residue concentrations in plants
usually were well below soil treatment rates, although endrin residues
in alfalfa and bromegrass exceeded the treatment rate of some soils. Mean
concentrations of residues taken up (regardless of soils) showed endrin
second only to heptachlor among insecticides tested. Data suggested
linearity of residue uptake with soil concentration at low soil treatment
rates. Silt negatively affected endrin uptake. No degradation products
-------
of endrin were detected. Persistence in soil was positively correlated
with organic matter.
The persistence of endrin in sassafras loam soil in New Jersey and
translocation into potatoes were determined. Test plots were treated
at 3 and 6 Ib/acre of 2% endrin granules. Damage to the tuber from
wireworm decreased as the endrin residue increased. Residues were
detected in potatoes from the first two plantings but none from the third.
Potatoes grown the first year after treatment (1963) contained endrin
residues at 84-117 ppb in soil treated with 3 Ib/acre and 100-133 ppb
at 6 Ib/acre. The following year (1964) 17 ppb endrin was found at
3 Ib. treatment and 12-17 ppb at 6 lbsc(Winnett and Reed, 1968).
Residues of cyclodienes were found in the foliage of wheat grown
in soil treated with aldrin and endrin, but no residues were found in
the grain (Saha and McDonald, 1967).
Field and laboratory studies determined contamination of several
commercially important crops grown in soil containing known concentrations
of endrin was investigated by a regional committee in six states, Florida,
Mississippi, North and South Carolina, Texas and Virginia. Problems
of low residues were associated with soybeans grown in soils containing
relatively high levels of endrin in turnips and in green tobacco leaves.
Since the tolerance for endrin is zero in turnip greens, the small amounts
detected were illegal. The low residues of endrin found in green tobacco
leaves presented no food residue problems (Van Middelem, 1969).
Forty-nine fields of peanuts, potatoes and carrots were monitored
for chlorinated hydrocarbon pesticides in soil and root crops in seven
-------
Eastern states (Seal, et_ aJL. , 1967). With methods of detection sensitive
to 0.01 ppm endrin was found in the soil from about one-fifth of the
fields, but no residues of endrin were identified in crop samples.
Samples of soil and turnips grown in Florida in fine, loamy sand
soils fortified with 1,2 and 4 Ib/acre endrin were analyzed for endrin.
Soil samples were taken within 24 hours after planting and on the day
of harvest. Levels of endrin in planting soils .treated with 0,1,2 and
4 Ib/acre were 0.01, 0.64, 0.74, and 1.98 respectively and at harvest
soil levels were 0.03, 0.77, 1.59 and 3.71 ppm. Endrin was translocated
from soil into the turnip plant to only a limited extent. At rates of
4 Ib/acre turnip peel contained the highest insecticide level (0.12 ppm)
and peeled turnips and turnip greens contained 0.04 and 0.02 ppm. Above
ground plant parts could have been contaminated by vaporization, co-
distillation and splashing or blowing of contaminated soil onto' the
leaves and stems (Wheeler, et^ aJL. , 1969).
•'•;'ft><)i ~.y
Soybeans grown in Mississippi soils fortified with 2,4 and 8 Ib/acre
of endrin were analyzed to determine possible crop contamination
(lta.rren.tlne and Cain, 196y) . Follow:! ng applications at 0,2,4, and 8 Ib/acre,
^ ivite*?/>,<£.jI&A £t*-e^b.-# (kty 4@iv*),^ I
levels of endrin in planting soil were 0, 0.59, 1.20 and 1.49 ppm respectively,
and 0, 0.34, 1.04 and 1.79 ppm in htirvest soil. Endrin levels in soybeans ^"^i-
o/i -
wore 0.01, 0.04, 0.08 and 0.12 ppm for the respective application levels?'' •
Peanuts and soybeans grown in Texas soilg^fortifled at planting with
endrin were analyzed to determine crop contamination (Dorough and Randolph,
1969). F.ndrin residues in peanut planting soil treated with 0, 1, 2, and
-------
4 Ib/acre were 0.15, 0.32, 0.90 and 2.08 ppm, respectively; harvest soil
contained 0.13, 0.23, 0.51 and 0.60 ppm and harvested peanuts contained
0.00, 0.02, 0.07 and 0.10 ppm. Soybean planting soil treated .similarly
contained 0.18, 0.47, 1.11 and 1.49 ppm, harvest soil contained 0.12,
0.17, 0.49 and 0.48 ppm, and harvested soybeans contained 0.00, 0.00,
0.02, and 0.03 ppm, respectively.
Absorption of insecticides by soybeans through the roots and through
the aerial portion of the plant from vaporized soil application was studied.
Surface and subsurface soils were separated by a sealed disk with no part
of the plant above soil touching the surface-treated soil. Treated surface
^4W fe* l^ff ? '.• "
and subsurface layer (250 and 1500 g., respectively) soils contained 0.5
„ /jjrw ncci.tfo'kct •et^/'-'h '
mcc of C-14 labeled endrin'l Plants were allowed to grow for 53 days,
harvested, and separated into upper leaves, stem and lower leaves and
stem, pods and seeds. In subsurface studies, larger amounts of endrin
residues transmitted by root sorption were found in the lower stem. In
surface treatment studies, lower leaves contained most residues with upper
leaves containing the next largest amounts. Residues of endrin resulted
from root uptake and translocation, and to a lesser degree from vapori-
zation from soil surfaces (Nash and Beall, 1970).
The action of endrin on the bean stem miner, a destructive pest on
young soybeans in Formosa was studied by Lee (1962) in connection with its
translocation in soybean plants. Summer plants, 8-11 days old were
completely protected for 15 days with foliar spray applied at relatively
low dosages such as 90 g. ai/hectare. Endrin emulsion showed some degree
of repellency to ovipositing flies, but its persistent effect caused the
-------
kill of newly hatched larvae through translocation into the post-treatment
growth of plants in which the eggs x^ere laid.
In. 1966, comparative samples of soil and soybean seed and plants
were collected for analysis from Greenville, Mississippi and Mobile,
A.lahama, and from 27 sites in 3 other Southern states and 3 Midwestern
states. Endrin residues were found in about three-fourths of the
samples from Arkansas and Mississippi. Endrin had been used extensively
for cotton insect control at the Greenville, Mississippi study area prior
to planting soybeans. Soybean seed, plants and soil sampled from 10
blocks totaling 219 acres, contained an average of 0.38 ppm, 0.28 ppm,
and 0.07 ppm, respectively. Endrin residues which appeared in soybean
samples collected in Mississippi and Arkansas and were apparently related
to the use of endrin for cotton insect control. When endrin soil concen-
trations ranged from 0.10 ppm to 0.20 ppm, residues frequently were detected
in soybeans grown in such soil. This contamination may have resulted partly
from translocation from the soil and partly from drift or inadvertent
overspray (U.S. Dept. of Agriculture, 1968).
Information was obtained on pesticide levels in crops and soils over
a '.5-yc:ar period on approximately 1 square mile study areas at Grand Forks,
North Dakota; Yuma, Arizona; and Mob Me, Alabama. Endrin found in about
'
^ .
ha. IT i. he- s'ii'1 samples, averaged 0.26 pprnT Actual soil residue levels
changed little during the 3-year period. Endrin was found in 13% of the
small grain, corn and sorghum samples at an average of 0.08 ppm. Endrin
residues averaged 0.23 ppm in 17% of the samples from soils where alfalfa
and grass wore grown. An average of O.U7 ppm endrin was found in 15% of
the forage samples (Sand, 1968).
-------
Knutson, et_ al., (1971) measured insecticide residues in corn planted
in an irrigated area in Kansas. At harvest, levels from 0.06 to 2.43
ppm endrin were detected in foliage following foliar applications in early
August. No residues were found in the grain following either soil or
foliage application.
A study was conducted in Colorado by Jewell (1966) to determine whether
pesticides sprayed in or around orchards might cause contamination of/transect
vegetation. ^Samples of willow, bigtoothed sage, antelope bitterbrush, orchard
x
grass, a'lfalfa, clover, serviceberry, mountain mahogany, rabbitsbrush,
chokecherry, apple, rose and scrub oak were tested for endrin.
Endrin was used to control voles in orchards of Switzerland' (Schneider,
1966). An emulsion was sprayed"' on shortcut grass under the trees in October
and November. The following year, 1.9 ppm endrin was traceable to grass of
the first cutting, and 0.27 ppm in the third cut. For this reason use of
such grass was not permitted for domestic animal fodder.
Organochlorine insecticide soils from southwestern Ontario were analyzed
for organochlorine pesticides to determine if residues were sufficient to
cau.se unacceptable residues in crops used for animal feed. Alfalfa, oats,
corn, suj'.ar beets, potatoes, and carrots were planted in soil containing
insecticide residues. Soil B, a fine sandy loam soil (1.4% organic matter)
contained 0.76 ppm cyclodiene insecticides, with the predominant material
being dieldrin. Soil D, a muck soil (66.5% organic matter) contained
10.44 ppm cyclodiene insecticides. In soils B and D, small amounts of
endrin were detected in most crops tested (Harris and Sans, 1969).
-------
Fourteen Ib. endrin/acre incorporated 4 to 6 inches into a sandy
loam soil at Riverside, California resulted in 2.3 to 4.7 mcg/g of
^'
0-6 inch soil layer. Nine carrot varieties, Daucus carota, were compared
for uptake of endrin residues. This varied from 1 to 4 ppm of apparent
endrin among the varieties studied. Most endrin residue occurred in
carrot skin (Hermanson, i •» <•»
•
-------
weekly over 38 consecutive days. Fifty-gram butterfat samples were used
for the following analyses: (1) 11 samples from the control cows, (2)
11 samples from animals on the endrin-treated plot, and (3) 11 samples
of control butterfat fortified with 2 ppm endrin. The absorbance values
of the 11 samples from (2) were not greater than the values for the
corresponding control samples (Johnsen, et_ al., 1961).
AFter foliar applications to white cabbage, C-14 endrin partially
evaporated from the surfaces and was also partially taken up by the plant
and released in a few weeks via transpiration. Two to four weeks after
application unaltered endrin and two hydrophilous metabolites A and B,
were found in both plants and soil. Metabolite B was identical to
endrin-ketone (Weisgerber, ejt^ al^. , 1968).
14
Cotton plants treated with C endrin, were analyzed to determine
distribution and behavior of residues. Upper surfaces of leaves from
cotton plants grown in the greenhouse were treated 3 times with 600
ul of a solution of 17 mg 14-C endrin (1.85 mCi/niM) and 313 mg unlabeled
r^-endrin in 50 ml acetone. Plants were harvested 12 weeks after the last
application and separated into samples of leaf, stem, roots, seed pod,
seed fiber and seed. One-third of the radioactivity applied was recovered
in the combined plant and soil samples. Of total activity: 30.5% (36.6
ppm) was found in and on living leaves, 49.2% (201.2 ppm) in and on dead
leaves, 0.27% (0.33 ppm) in stems, 0.06% (4.9 ppm) in seed pods, 0.003%
(0.36 ppm) and trace amounts in fibers, seeds, and the soil. No activity
was detected in root samples. Five conversion products detected represented
24% of the total endrin recovered. One group of three was only slightly
-------
more hydrophilic than endrin and the other two products were strongly
hydrophilic. Two conversion products of the first group had retention
times identical with endrin ketone. One was later positively identified
as endrin ketone. The ohter had a slightly higher molecular weight and
had the chlorine structure of endrin (Bayless, et^ ad., 1970).
The effects of cultivation conditions on residues and metabolism
of C-14 labeled endrin were tested with tobacco (Weisgerber, et al.,
1969). After 6 weeks, 32 to 47 percent of the topically applied endrin
remained on tobacco leaves in the plants. One extremely hydrophilic
degradation product was found in plants and on the soil but was not
characterized because of low concentration. This substance which differed
from photodegradation products was similar in chromatographic behavior
to the metabolite earlier reported for white cabbage. The percentage of
metabolites increases with better cultivation conditions, lower endrin
dosage, and increases with time after treatment.
o
Experiments with endrin - H on cotton were made by Korte, et al.,
(1970). Low amounts of the keto-rearrangement product were detected on
the leaf; surfaces, but no penetration was detected. This keto-compound
probably was formed by JV rearrangement of endrin on the leaf surface.
Later these authors observed uptake and metabolism of endrin by cabbage,
tobacco, carrots and wheat germ buds. After application of endrin
C in acetone to leaf surfaces or to the soil, material from leaves,
roots, stalks, and soil was extracted at various intervals.
In a greenhouse experiment with cabbage four weeks after application
0.8 percent o.f the applied radioactivity was found on the leaf surfaces,
" •' 5 Q
-------
.4.4 percent in the plants, and 0.2% in stalks and roots. Hydrophilic
metabolites were found at an increasing rate from leaves to soil.
A disappearance of residues by transpiration, corresponding to that
of the cabbage experiments, was also found in carrots and tobacco. Four
weeks after application of -^C endrin to tobacco leaves, 29 percent of
the applied radioactivity remained present on leaf surfaces, and 7% in
the plants. The slower disappearance of residues from tobacco probably
is due to a lower rate of transpiration. Metabolic rates on carrots
strongly depended upon the form of application. Three weeks after
application of C endrin into the soil, the metabolic rate, based upon
recovered radioactivity, was 12 percent after injection into the roots
and 32 percent after application on the leaves near the vegetation point.
Four different treatments of endrin ground spray were applied on
Virginia orchards of two varieties of apples during two different seasons.
Application rates were at 2 and 41b/acre. Both picked and dropped
fruits from the succeeding apple crop were analyzed for endrin. Amounts
of endrin detected in picked apples was U—.005 ppm and 0.028 ppm in the
dropped fruits (Horsfall, et al., 1970).
A
Health hazards of endrin in some agricultural uses in the Pacific
Northwest were examined by Wolfe, et^ aJ., (1963). Each fall, many
orchardists in that area spray their orchard cover crops with 1.2-1.4
Ibs. endrin per acre for control of meadow mice (Microtus). Residues/
on windfall apples in endrin-sprayed orchard cover crops were obtained
on 17 Scimples taken soon after spraying. Endrin residues ranged from
0.3 to 1.2 ppm with an average of 0.6 ppm. This average value agrees
1! .10
-------
quite closely with residue tests reported by Wolfe (1957) where residues
on windfall apples following endrin spraying ranged from 0.3 to 0.5 ppm.
Orchard grass and fescue samples contained 60, 240 ppm endrin during the
first month after application. From 25 to 100 ppm was still present at
the end of the fifth month. Gyrisco and Huddleston (1961) noted similar
persistence and variability for endrin residues following a single
application on an alfalfa-brome grass mixture.
The morphological and somatic chromosomal aberrations induced by
pesticides in barley were examined by Wuu and Grant (1966). The percentage
germination of barley seeds treated with solutions of endrin containing
500, 1000, and 1500 ppm for 6, 12 and 24 hours was evaluated. In general,
germination of seeds treated with endrin for 24 hours was 55 percent of the
treated for 6 hours. Chromosome aberrations induced by endrin in root tip
cells of C, seedlings were 6.01 to 9.05 percent greater than abnormal
seedlings. The most common cytological aberration observed was chromosome
breakage. Occurrence of these chromosome irregularities and malformations
suggest that hereditary constitution of seeds of some plants may be changed
if the plants are subjected to chance pesticide treatment.
ITT.II. Fate in Soil - The fate of pesticides in soil is influenced by
environmental processes (1) adsorption and degradation (2) leaching into
lower soil strata (3) direct uptake by plant roots (4) evaporation or
volatilization from soil surface and (5) erosion of the soil by water
or wind.
Insufficient monitoring data are presently available to assess the
extent of endrin contamination of soils. It is not well known whether
contamination is confined to areas where endrin is used extensively.
11
-------
The organochlorine insecticide content of 40 mineral soils and
16 organic soils and sediments was determined from random samples collected
from Wisconsin and eight states west of the Mississippi River. Approximately
half the samples contained no detectible residues. None of the soil samples
examined contained endrin. It is not known whether this was due to relatively
rapid degradation or simply to lack of use on the soils sampled (Trautmann,
f ' J
et al. , 1968). -^U^^"' ~ '
A comprehensive review paper was presented on insecticide residues
in soils by Edwards (1966). According toxESwards, Foster, et_ al_. , (1956),
^dfiU/i^
-------
Menzie (1972) in his paper on the fates of pesticides in the environ-
ment listed the approximate "half-life" of Isodrin/endrin in the soil as
4-8 years. The persistence and fate of endrin in soil is dependent both
-~L (A ?-
uponxc1remicair,ana a variety of environmental factors. The above range
merely indicates that half the endrin may have volatilized or degraded
within that period.
From 1953 to 1957, annual applications of endrin at rates of 4.9
to 5.4 Ib/acre were applied to Holtville sandy clay soil in California
,J- wtlCTT-IW '
•^ Lx-" ' '
(Hermanson, e_t al_. , 1971). Measurable/endur-i-ng soil insecticide/residues
occurred in soils receiving endrin at 5 Ib/acre/year. A rank of decreasing
persistence (a persistency index:1.00=no degradation or disappearance
during the first year) over an 11-year period listed endrin as 0.20.
Consequences derived from regression analysis showed that endrin had
a persistence "half-life" of 4 years.
The percentage of technical endrin remaining in Congaree sandy
//
loam soil after 1^4 years was 41. Treatments and maintenance of the
soils were such that leaching, volatilization, photodecomposition,
mechanical removal and probably biological decomposition (because of
high initial application rate) were at a minimum. This value may
approach an upper limit of endrin persistence in soil (Nash and Woolson,
1967).
The 38 cm profile distribution in 1966 of several chlorinated
insecticides in cultivated Congaree sandy loam soil was recorded by
Nash and Woolson (1968). Tests were made 13 years after the last
applications in 1953. Test areas had received accumulations of
-------
pc-Htloidcs of 73 or 146 kg/ha from frequently repeated foliar appli-
cations during three growing seasons (1951-53). Endrin was found
throughout the soil profile. Eighty percent of the total endrin
residues were concentrated in the upper 23 cm of soil, which probably
corresponds to the cultivated layer. The quantity of insecticide in
the top 7.6 cm of soil was less than the mean quantity between 7.6
A
and 23 cm depths. This inciaates that volatility and photodecomposition
may play an,important part in dissipation. The degree of persistence
/5 nidrGfocf
-can "be "v±-SHal-i«e$ by the fact that, 12 years after application, 28
percent of the foliar applications and 44 percent of the soil-incorporated
endrin remained in the soil of test plots.
Insecticides were used extensively on shadegrown tobacco crops in
the Florida-Georgia area for many years. Experimental work was undertaken
to determine: (1) amounts of chlorinated hydrocarbon insecticides which may
accumulate in soil without apparent detriment to tobacco; (2) their rate
of disappearance under shade conditions; and (3) the amounts of organic
chlorine which had accumulated in the soil of commercial fields (Kincaid,
•
et al., 1960).
Kndrin at 15 and 75 pounds.emulsifiable concentrate, was applied )
March 6, 1953, to triplicate plots. Data on insecticide residues were
given. The major portion of each insecticide disappeared during the
test period of 5-2/3 years. Calculated from linear equations best
fitted to the data, the percentage of endrin which disappeared during
any one year was 11%. /
-------
Commercially grown onions and the soils on which they were grown
were evaluated in 10 major onion-producing states for pesticide residues.
It was found that soil from 15.5 % of the sites contained endrin. Soil
residues in ppm ranged from 0.01 to 2.05 but averaged only 0.06. No
residues were detected in onion samples (Wiersma, et^ a.1^ , 1972).
Forty-one agricultural soil samples from 21 vegetable farms in
Saskatchewan were analyzed for insecticide residues. All but 2 of
41 samples had more than 0.01 ppm of total organochlorine pesticide
residues. However, endrin was present in only one sample at 0.48 ppm
(Saha and Sumner, 1971).
Soil samples were collected on 31 farms located throughout southwestern
Ontario. The soil types ranged from sand to muck. Endrin was detected at
a concentration of 3.8 ppm in 1' samples', and trace amounts in 2 other samples.
Highest organochlorine residues occurred in tobacco, vegetable and orchard
soils. Development of cyclodiene resistance by soil insects in southwestern
Ontario can be correlated with levels of cyclodiene residues in the soil
(Harris, et_ al. , 1966).
A unique opportunity to study insecticide usage and resulting residue
was provided by creation of a new irrigation district in central Kansas.
During the period 1960-1969, this site developed from dry- land farming
with little use of insecticides to intensified crop production and
pesticide usage. Endrin foliar sprays were applied in early August to
corn at silking time. Endrin levels on foliage collected soon after
spraying were 0.9-6 ppm. Endrin residues at harvest ranged from 0.06 to
2.43 ppm. No endrin residues were detected in corn grain sampled at
-------
harvest. Capped wells, from 13 to 71 feet deep, contained no residues
at the 0.1 ppb level. Vertical penetration of other soil-applied pesti-
cides did not exceed 12 inches, nor was there evidence of lateral
contamination of ground water from adjacent lands. Surface waters from
the adjoining reservoir and river contained no residues at the 0.1 ppb
level. Endrin was detected in surface waters at trace levels ( <0.1 ppb)
(Knutson, et_ al., 1971).
Mullins, et^ aJ., (1971) studied the presence and persistence of
organochlorine insecticide in Colorado soils. Fifty samples of orchard
and cultivated soils were collected from eleven sites which had a history
of endrin use. Endrin residues were detected in trace amounts from only
two sites.
Organochlorine insecticide residues in agricultural soil and legume
crops were measured in northeastern Saskatchewan by Saha, et_ al_., (1968).
Soil samples from 20 fields were analyzed. Endrin was present in 15
percept of the fields at 0.01 to 0.02 ppm. Residues of endrin in legume
crops were either undetectible or present in only trace amounts.
Soil samples from 67 fields in 22 counties of 8 states in the
South and Midwest were analyzed for organochlorine pesticide residue.
Total organochlorine insecticides in soils averaged 1.5 ppm. Nearly
24% of the samples contained endrin, but only in six samples contained
more than 0.1 ppm. Samples positive for endrin were obtained from
cotton fields in Alabama, Arkansas, Louisiana and Mississippi. Other
crop areas with endrin soil residues were sugar cane fields in Louisiana,
-------
corn fielclH in Illinois and apple and peach orchards in Maryland. Maximum
readings on cotton land_were in Alabama (0.11 ppm) , while Maryland orchard
0.2$-^^^ ..... ,
soils contained ir^Wn1- ppm) (Gish, 1970). ' ?htf wuc0i < * f
A%=— ^
Results from bioassay and gas chromatographic techniques indicated
that amounts of endrin lethal to fish occurred in bottom muds from a
Leflore County, Mississippi bayou. Cotton fields adjacent to these
waters had been treated with endrin. Aerial applications in 1963 totaled
Mt-tf?
14 Ibs. endrin/ac.' and for 1964, 4.8 Ib/acre. Several mud samples from
this locality contained 6.1-48.2 ppb endrin. Acetone extracts from such
muds killed test fish (Ferguson ,/tudke), et al. , 1965^' Wl
-------
Several insecticides, including endrin, were applied to Pullman clay
loam soil in Texas at 1.6 Ib/acre. Chlorinated hydrocarbons gave satis-
factory control of wireworm and grubs for five years after treatment. Neither
-'1 ,•'••?
grain sorghum or wheat yields were affected by the insecticides (Daniel,,X ^ >^ "/'
.-/ C^ * V
1966). Endrin residues in the soil varied from 0.06 ppm in the upper six
inch layer to 0.009 ppm at 12 inches.
In another study of pesticide residues in soils and crops in
Southwestern Ontario, Harris and Sans (1969) reported endrin values of
¥\
0.14 ppm before planting and 0.11 ppm after harvest on dandy loam soil.
However, comparable figures on muck soils were much greater, being
5.94 and 5.80 ppA /respectively.
Monitoring for chlorinated hydrocarbon pesticide residues was
conducted in seven Eastern states by Seal, e£ al_. , (1967). Endrin
occurred in the soil of about one-fifth of 49 fields checked. Range of
amounts detected in carrots and potaotes was 0.05-0.50 ppm. , /• / • /^^ ''
.'f!/e, 3•• C"-<:";C-' '-' -
Wiersma, et al., (1971) reported on a later phase of the national
soils monitoring program. Endrin was not detectedT^but results of -
their analyses of 242 cropland and 117 non-cropland samples from 6
states indicated widespread in occurrence of several other organo-
chlorlne pesticides.
The effect of 29 pesticides, including endrin, on the production of
C02 and nitrification by soil microorganisms was determined. A few
compounds were stable but without significant effect in soil. Some
(including cyclodienes) persisted and depressed respiration and nitri-
fication, and oi-.hers displayed toxicity but were transformed by soil
"
-------
microorganisms (Bartha, et al., 1967). C09 production in soil containing
r"' ' . ^
endrin 250 and 2500 ppm endrin was inhibited 20 percent but these
treatment levels had no effect on soil fortified with glucose.
It was apparent that endrin did not influence nitrification.
/r^>, u^-lA^-4.
At the 250 ppm soil treatment level, NOo - production for endrin-treated
v.
soils was 15.7 mg at 6 days, 47.2 mg at 12 days, and 70.5 mg at 18 days:
The persistence and moderate toxicity of the cyclodiene compounds
in soil, described by others, also was observed in these studies. No
indication of microbial degradation was obtained. Biological epoxidation
of endrin would not have been detected by the analytical methods employed.
-------
Chapter III
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-------
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o*
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-------
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-------
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-------
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*
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-------
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* •
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-------
V.Y'U: , '!, }'. . , .'in-i Y. irl.orour.ii, .1. 1). Vi-rU-hrat
-------
>im::,ii, .J. :•. '-id I.'. ; •. -, i. i . '•.'."•i.i'br.-il e ii::;'c.t ir.uU: TO:;I s:|..-;:ico:
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Chapter IV
Residues in Crops and Food Items
IV.A. Introduction - Residues of endrin in food and feed crops may
result from the direct application of the pesticide to the crop,
translocation to growing plants from contaminated soils, or by drift
from application to adjacent areas. Foliar application of endrin may
dissipate by weathering; but limited absorption and translocation can
occur in some plants. Soil applications are more likely to persist
from one growing season to the next depending on the type of soil and
the amount of material applied. The occurrence of residues in certain
crops such as soybeans, vegetables and peanuts may be contingent upon
crop rotation practices and prior pesticide usages.
Some endrin residues are removed from human food by processing
prior to consumption. Substantial quantities of endrin have not been
reported in commercially processed vegetable oils. However, the seed
meal formed by removal of the crude oil may contain pesticide residues
which appear as contaminants in meat, milk and eggs following use of
the meal as animal feed. Endrin residues in tobacco are not removed
by curing or by subsequent manufacture of tobacco products. Endrin
residues occur in sediment or lees after fermentation of wines, but
none has been reported in the wine. The processing of crops for human
consumption may affect the removal of endrin residues depending on the
type of crop, the location of the residue in the plant and the severity
of the procedure used. During the commercial processing of oil seed
products, endrin is not detected in the refined oil of any of the oil
') f
-------
seed crops. However, the residue content in the oil seed meal is
important because of its general use in animal feeds. Endrin residues
in tobacco were not significantly reduced.
Endrin in contaminated food and feed is deposited in fatty tissue
of animals or excreted in milk and eggs in amounts proportional to
levels of intake. Following withdrawal of contamination, the levels
of endrin in the fatty tissue and in eggs and milk dissipated over a
period of time related to amounts detected and types of fatty tissue
involved.
IV.B. Tolerances - Tolerances are established to control the amount
of pesticide residue that may remain in or on food so that pesticides
can be used effectively in the production of food without harm to the
consumer. The presence of some pesticide residue in selected foodstuffs
is allowed in amounts demonstrated to be no higher than those resulting
from "good agricultural practice" provided that the final amount of
residue in the daily food is no greater than the amount accepted as safe
for long-term consumption for man.
In establishing safe limits for chemicals used in post-harvest
treatment of raw agricultural products, numerical tolerances are
established by the Environmental Protection Agency for regulatory
purposes. These are listed in Table IV.B.I for endrin on raw agri-
cultural commodities. The regulations provide that processed foods
prepared from raw foods containing residues within legal tolerances
will not be illegal if the residues have been removed to the extent
possible in good manufacturing practices and if the remaining residue
< \ I m
'
-------
cloea not exceed the tolerances on the raw product. These tolerances
are at levels that permit the use without danger of excessive residue
occurring. A summary of recommendations of FAO/WHO for tolerances and
practical residue limits as applied to raw agricultural products moving
in commerce are presented in Table IV.B.2. The figures include the sum
of endrin and delta-kito endrin (FAO/WHO, 1971).
•»'-fl
-------
Table IV.B.I.
TOLERANCES FOR ENDRIN ON RAW AGRICULTURAL COMMODITIES
TOLERANCES
COMMODITY
Soybeans
Cottonseed
0.2 (proposed)
0.1 (proposed)
Eggs and the fat
of cattle, goats,
hogs, horses, milk,
poultry and sheep 0.05 (proposed)
Apples, sugarcane
grain of barley, oats
rye and wheat 0.02 (proposed)
Crude soybean oil 0.5 (proposed)
Broccoli, brussels 0.0
sprouts, cabbage,
cauliflower,
cottonseed, cucumbers,
eggplant, peppers,
potaotes, sugarbeet
tops, summer squash
and tomatoes
ANALYTICAL
METHOD
REFERENCE
gas chromatographic
procedure with an
electron capture
detector.
FR Feb. 5, 1971
FR Jan. 1, 1972
-------
Table IV.B.2.1
Recommendations for Endrin Concerning Acceptable Daily
Intakes, Tolerances, and Practical Residue Limits, as of November 1971 (FAQ/WHO)
Maximum Acceptable
Daily Intake
(mg/kg body wt.)
0.0002
Tolerances and Guideline Levels
Commodity ppm
Cottonseed
Crude Cottonseed 0.1
oil
Edible cottonseed
Maize oil 0.02
Apples, Wheat,
Barley, Sorghum,
rice (husk
and/or polished) 0.02
Practical Limit
Commodity ppm
Milk and Milk
products (fat
(basis 0.02
Eggs
(shell-free) 0.2
o - p
. MJ
-------
Policy Consideration for Residues - With recent advances in analytical
methodology, more sensitive and sophisticated procedures have been
developed for detecting presticide residues in levels as low as parts
per billion. The President's Science Advisory Committee recommended in
a report, "Use of Pesticides", dated May 15, 1963, that the accretion of
residues in the environment be controlled by an orderly reduction in the
use of persistent pesticides. Tolerances for those insecticides were to
represent residual amounts resulting from recommended operational pro-
cedures which were considered to be without hazard when consumed in the
daily diet. In addition, tolerances should be rescinded for those crops
on which there are no registered uses and on those crops which may result
in residues in other commodities for which tolerances are not established.
Acceptable Daily Intake - The daily dosage of a chemical which during an
entire lifetime appears to be without appreciable risk on the basis of
all facts known at this time. Without appreciable risk is taken to mean
the practical certainty that injury will not result even after a lifetime
of exposure. The maximal acceptable daily intake of endrin for man is
estimated to be 0.0002 mg/kg of body weight. This value was derived from
minimal daily dosage which caused no detectable changes in experimental
animals. In rats, the 1.0 ppm level of endrin in the daily diet is
equivalent to 0.05 mg/kg of body-weight was determined as causing no
significant toxicological effect.
-------
In dogs, the 1.0 ppm of endrin in the daily diet is equivalent to
0.025 mg/kg of body-weight was determined as causing no significant
toxicological effect (FAO/WHO, 1970); For calculation of tolerances,
the ADI must be considered in relation to the acutal quantities of food
items containing the economic posion which, are being eaten by a given
population.
IV.B.I. Monitoring Programs - The Food and Drug Administration, Department
of Health, Education, and Welfare, monitors pesticide residues in the
Nation's food supply through two programs. One program, commonly known
as the "total diet program" involves the examination of food ready to
be eaten. The total diet samples are purchased from retail stores,
bimonthly, in five regions of the United States. The food items and
proportion used represent a two-week diet of high consumption level for
a 16-19-year-old male which was constructed with the advice and assistance
of U.S. Department of Agriculture. The average intake is based on
consumtion of 4 kg food/day, which is almost twice that consumed by
the "average" man. The foods are prepared for consumption and composited
into 12 classes of similar foods.
The purpose of the second program is to determine the compliance
with tolerances of residues on raw agricultural products shipped in
interstate commerce and imported into the United States. The Consumer
and Marketing Service of the U.S. Department of Agriculture obtains and
monitors meat and poultry samples from animals and poultry slaughtered
in all federally inspected establishments and from shipments imported
into the United States.
-------
During the five-year period from 1964 to 1969, 111,296 samples of
domestic foods were examined for residues. A summation of the rates
of endrin residues in various commodities is presented in Table IV.B.3.
No endrin residues were found in finished or crude corn oil or cotton-
seed oil, milk, dairy products or baby foods. However, there appears
to be an increase in the percentage of endrin residue found in samples
of small fruits, root vegetables, meat, poultry and grains for animal
use during the 1964 to 1969 period. An average of the incidence and
levels of endrin found in domestic and imported commodities is presented
in Table IV.B.4. The highest incidence of endrin residues were found
in domestic samples of crude soybean oil followed by fish and root
vegetables. The highest incidence of endrin residue was in imported
samples of large fruit followed by vine and ear vegetables and small
fruit. The highest incidence of endrin residue in meal composite sample
occurred in potaotes (Duggan, R,E., 1971).
-------
Table IV.B.3.
Percent of Commodities with Endrin Residue, 1964-1969
Domestic
Large Fruits
Small Fruits
Grain and
Cereals for
human us e
Vegetables
Leaf and Stem
Vine and Ear
Root
Beans
Fluid Milk
Dairy products
Meat
Poultry
Eggs
Fish
Shellfish
Grain-animal
use (1966-69)
Baby Food
Tree Nuts
1964-67
1.37
0.52
0.20
4.56
3.25
5.17
0.31
(1965-67
0.10)
—
1.15
8.20
3.47
(1966-67
0.43)
0.81
1968 1969
4.02 1.30
1.75 6.01
0.90 0.34
3.84 1.46
5.07 3.54
4.39 10.23
—
—
0.77 1.54
3.28 8.57
0.60 0.50
3.97 4.79
0.60
0.28 0.96
—
Imported
1964-67 1968
32.50 20.86
1.37 10.34
1.09
2.46
9.52 9.33
0.28
1.17
(1965-67
0.79) 0.24
—
— •
2.67 4.92
1.53
(1966-67
— )
_ — __
1969
—
—
—
5.00
—
4.17
3.61
—
—
2.20
15.88
—
__ —
-------
Peanut Oil
Crude
Meal
Refined
Table IV.B.3 (Cont'd)
Percent of Commodities with Endrin Residue, 1964-1969
Domestic . Imported
1964-69 1967 1968 1969 1964-66 1967
2.78
Cotton Seed Oil
Crude
Meal
Refined
Soybean Oil
Crude
Meal
Refined
Corn Oil
Crude
Meal
Refined
6.12
1968
1969
6.56
29.41
1.72
3.12
-------
Table IV.B.4
Incidence of Endrin Residues for 1964-1969
Domestic
Incidence Ave.
% ppm
Fluid Milk (fat)
Dairy Products
(fat)
Meat (fat)
Poultry
0.4
Imported
Incidence Ave.
% ppm
Meal Composite
Incidence Ave.
% ppm
Large Fruit
Small Fruit
Grain and
Cereals
Vegetables
Leaf and Stem
Vine and Ear
Root
Potatoes
Beans
2.0
1.5
0.3
4.0
3.5
5.5
0.3
T
T
T
T
T
T
T
30.6
4.4
1.0
2.0
8.8
1.5
1.4
0.01
T
T 1.5 TT
T 3.7 0.001
T 3.0 TT
T 2.2 TT
14.2 0.001
T — —
1.0
(1968-1969)
Eggs
Fish
Shellfish
Grain (animal)
(1966-1969)
Tree nuts
Baby Food
4.4
0.9
5.7
2.5
0.4
0.7
T
T
T
T
T
—
—
2.9 T
2.4 T
—
T
1.5
TT
-------
Table IV.B.4. (cont'd)
Peanut Oil
Crude 2.4 0.007
Meal Cake —
Refined --
Cotton Seed Oil
Crude —
Meal Cake 1.4 TT
Refined
Soybean Oil
crude
Meal Cake
Refined
Corn Oil
crude
Refined
. 9.3
0.8
0.028
TT
T = 0.005 ppm
TT = 0.001 ppm
-------
The average dietary intake of endrin for the period of 1964-1970
was calculated to be 2.5 percent of the ADI (0.000005 rag/kg body weight/
day). The average daily intake of 0.0011 mg/kg body weight was reported
for all chlorinated organic pesticides for the period of 1964-1970. Dairy
products, meat, fish and poultry classes comprise the source of approxi-
mately half of the intake of total chlorinated residues while grains,
fruits and garden fruits account for about 40% of the intake of chlorinated
hydrocarbon insecticides. The maximum dietary intake of endrin from a well-
balanced diet was approximately 0.001 mg/day (7 percent of the ADI). This
was attributed to levels found in meat, poultry, potaotes, leafy vegetables
and garden fruit for the period of June 1968 to April 1969. During the
period of June 1969 to April 1970, similar amounts of endrin were ingested
in the balanced diet, but highest levels of contamination were found in
potaotes, root vegetables and garden fruits (Duggan, R.E., 1972).
The incidence and daily intake in milligrams of endrin found in the
total diet for the five-year period of 1964 to 1969 are presented in Table
IV.B.5 (Duggan, R.E., et^ al., 1971), and Table IV.B.6 summarizes a
distribution of the level of endrin residues found in domestic samples
for the period of 1963 to 1966 (Duggan, R.E., 1969).
IV.C. Residues in Crops from Direct Application - Maturing cabbage was
treated with endrin at the rate of 0.8, 0.5, and 0.25 pounds of actual
pesticide per acre. Residue levels were determined at intervals of
0, 1, 3, 5, 7, 10, 14, and 21 days after application by gas chromatography.
The residue levels of endrin for the 0.8 pound per acre application were
reported as 4.17 ppm on the day of application followed by a decrease
-------
Table IV.B.5.
Average Incident and Daily Intake of Endrin
1964-1965
Positive
Composites
2.8
Range
(ppm) :
(
1965-1966
T=< 0.001 mg)
1966-1967
Daily % Daily %
Intake Positive Intake Positive
Mg. Compo- Mg. Compo-
sites sites
T 2.0 T
Percent of Endrin in
T-0.03 0.04-0.10 0.11-0
1.7
Table IV. B.
Domestic Food
.50 0.51-1.0
Daily
Intake
Mg.
T
6
Samples for
1.01-1.50
1967-1968 1968-1969
% Daily % Daily
Positive Intake Positive Intake
Compo- Mg. Compo- Mg.
sites sites
1.1 0.001 3.3 T
1963-1966
Number
Above Excessive of
1.51-2.0 2.01 Residues Residues
72.0 20.1
7.5
0.2
0.2
29.8 1,212
-------
to 0.81, 0.30, and 0.13 ppm by the 7th, 14th, and 21st day, respectively.
The residue levels of endrin for the 0.5 pounds per acre application were
reported as 2.26 ppm on the day of application followed by decrease to
0.32, 0.17, and 0.10 by the 7th, 14th, and 21st day, respectively. The
residue levels of endrin for the 0.25 pound per acre application were
as 0.21, 0.09, and 0.004 for the 7th, 14th, and 21st day, respectively,
after application. Residue values of endrin were not reported for the
initial 0.25 pound per acre sample (Mattick, L.R., 1963).
Tomatoes, snapbeans, and collards were dusted with a two percent endrin
formulation at the rate of 30 pounds per acre. Residue levels were
determined by the phenyl azide colorimetric method from samples taken
immediately after treatment and daily thereafter. Endrin residues in
tomatoes were reported as 0.31 ppm on the day of application and were
not detected on the first day after application. Endrin residues on
snapbeans were reported as 0.48 ppm on the day of application and were
not detected on the third day after application. Endrin residues on
collards were reported as 17.3 ppm on the day of application and were
not detected on the fourth day after application (C.H. Brett, 1958).
Emulsifiable concentrates of aldrin, dieldrin and endrin were applied
to alfalfa at the rate of four ounces per acre to determine their relative
persistence on fresh forage. The resulting endrin residue on the green
samples were determined photometricly at 0, 7, 14, 21, and 28 days
following application. Endrin residues were reported as 63.3 ppm on the
day of application followed by a decrease to 7.1, 3.43?-0.25 and <, 0.11
-------
ppm by the 7th., 14th, and 21st and 28th. day respectively. Endrin residues
were usually at about the limits of the level of detection in 28 days on the
fresh alfalfa. The author concludes that endrin residues were more
persistent than those of aldrin but somewhat less than dieldrin residues
(G.G. Gyrisco, 1961).
The foliar application to apple trees of 0.05 percent endrin resulted
in an initial deposit of 104 ppm with 13 percent of the initial deposit
remaining after one week and 2 percent after 7 weeks. Endrin residues
were determined by gas-liquid chromatography from apple leaf samples
taken prior to spraying, one hour after spraying and at 1, 3, 7, and
11 weeks afterward. The ketone isomer of endrin was detected after one
week, but not in later samples. The aldehyde isomer was present to the
extent of 15 percent of the total residue on the leaves in the sample
taken after 7 weeks, but it was not detected in the samples taken 4 weeks
later (Harrison, R.B., et al., 1967).
Residues of endrin on windfall apples and orchard cover crops were
determined following a single October application of 1.2 pounds endrin
per acre for mouse control. After spraying, the endrin residues on wind-
fall apples were reported to range from 0.3 to 1.2 ppm with an average
of 0.6 ppm. During the first month after application, the endrin residues
on orchard grass and fescue ranged from 60 to 240 ppm. At the end of the
fifth month, the endrin residues on orchard grass and fescue were 100 ppm.
The authors conclude that there is little residue deterioration on orchard
grass during the cool conditions encountered in the fall and winter months
(Wolfe, H.R., 1963).
o
-------
Two ground spray applications of endrin were applied to apple
orchards for mouse control. The first application was made during
the fall after harvest and the second in spring of the following
year when the leaves and fruit were forming. Endrin was applied
at two and four pounds per acre to the width of limb-end to limb-
end ground strip for the length of the tree line of two separate
orchards. Residues were determined by gas-liquid chromatography
from samples of both dropped and hand-picked fruit taken from the
treated and control areas. The neighboring control orchards had
never been ground sprayed with endrin. Traces of endrin> 0.0005
ppm were reported in samples of the neighboring control orchards.
Dropped apples from the spring spraying of 2 and 4 pounds endrin
per acre showed a residue range of 0.005 to 0.028 ppm. The quantities
of endrin on picked fruit from spring application of either 2 or 4
pounds per acre were trace 0.005 ppm of endrin. The authors conclude
that as judged by the permissible residue standard of 0.04 ppm action-
able level, no significant endrin residue persisted in either picked
or dropped fruits harvested from any of the ground sprayed plots
(Horsfall, at al., 1970).
The foliar application of 12.6 mg of l^C-labeled endrin to the
leaf surfaces of cotton plants resulted in a recovery of 33 percent
of the labeled material 12 weeks after the last application. Twenty-
six percent of the labeled material was found in the leaves with the
remainder found in the stalks, pods, fibers, seed and oil. The recovered
-------
activity consists of endrin and at least, five conversion products, one
of which, is identical with the keto-rearrangement product of endrin
(Bayless, A., et al., 1970).
Tobacco plants grown under covered conditions so to protect the
14
plants from rain were treated with 2.08 mg of C-labeled endrin per
plant. Six weeks after the foliar application, a residue of 32 to
47 percent of the initial deposit of endrin remained on the tobacco
leaves and in the plant. In addition to the unchanged endrin, at
least one hydrophilic degradation product was reported in the plants
and soil. It was not identical with the photodegradation products
of endrin (Weisgerber, I., et_ a^., 1969).
TDE and endrin were reported as the major organic insecticides
used on flue cured tobacco for the control of the tobacco hornworm.
The modified Schechtor-Hallor method was used for DDT and the dechlori-
nation sulfanilic acid-phenyl azide method was used to determine the
endrin residue on tobacco. TDE and endrin residues on green tobacco
during priming time were reported above 50 and 10 ppm, respectively.
These residues are dissipated about 45 percent during processing.
Auction market tobacco contains approximately 37 ppm of TDE and
1.8 ppm of endrin. An average of 13 ug of TDE and 0.2yg of endrin are
found per commercial cigarette (T.G. Bowery, 1959).
IV.D. Residues after Processing - Crude soybean and cottonseed oil
were spiked with 1.0 ppm endrin and processed by stimulated commercial
-------
processing procedures. Samples of crude oil and products were analyzed
by gas-liquid chromatography. The unit processes in edible oil manu-
facture are alkali-refining bleaching, hydrogenation and deodorization.
Neither alkali-refining or bleaching reduce the endrin contamination.
Endrin is eliminated from the edible oil by either hydrogenation or
deodorization or by both procedures. The presence of rearrangement
or unknown breakdown products of endrin were not detected in the
hydrogenated oil. The data indicates that endrin or its isomerization
products appear to be removed from the neutral oil during deodorization
by forced volatilization. The authors conclude that normal commercial
processing of crude vegetable oils for human consumption effectively
removes any chlorinated pesticides which may be present in crude oils
(Smith, K.J., et al., 1968).
Endrin residues in vegetable oil seeds and products of soybeans,
cotton, peanut, and corn were reported for the fiscal period 1964 to
1966. Endrin residues were reported in the raw products of soybeans,
peanut and corn, but none in cottonseed. Of the three commodities
containing residues in the raw products, only soybeans and peanuts
were reported to contain endrin in the crude oil. Only soybean meals
or cakes were reported to contain endrin residue. Endrin was not
detected in the refined oil of any of the four oil seed crops (Duggan,
R.E., 1968).
Endrin residues in sugarbeets and processing products were deter-
mined by gas chromatography from sugarbeets grown in endrin treated soil.
The soil surface was sprayed with an endrin emulsion applied at the rate
-------
o£ five pounds actual per acre and double-disced within three hours of
application. The treated and control area was seeded on the following
day and the sugarbeets grown to maturity. The resulting endrin residues
were reported as 2.790 ppm in soil (at harvest), 0.244 ppm in raw sugar-
beets, 0.195 ppm in cossettes (sliced sugarbeet prior to extraction),
1.621 in dried pulp, 0.360 ppm in carbonation mud, 0.008 in raw juice
and 0.004 ppm in first carbonation juice. The dried pulp contained the
major portion of endrin that was found in the processing method. The
processing did not include the molassess and sugar product. Sugarbeets
grown in soil of this test area are generally considered to contain an
average of 14 percent crude sugar (.sugar plus molasses). The endrin
content of the treated soil at the time of harvest was reported as
5.06 pounds per acre (K..C. Walker, 1965).
To determine the distribution of endrin through the preparation
of wines, 1.0 ppm of endrin was added to the grape musts. The samples
of musts lees, wines and distillates were analyzed by paper chromatography
for endrin residues. At this level of endrin contamination there was
no measurable effect on fermentation. None of the endrin residues was
detected in the finished wine or distillate of the lees. Endrin was
reported in the sediments or lees removed after fermentation at 0.9 ppm
(Painter, R.R., e_t al., 1963).
Irish and sweet potatoes were spiked with 100 ppm of endrin. The
effects of irradiation, storage, potato type and processing on the
residue content of endrin in potatoes was determined by gas-liquid
chromatograph. The two methods of processing were: (1) heat processing,
-------
with and without water; and (2) frozen, blanched and unblanched. Irradi-
ation did not significantly affect the quantity of the endrin residue.
Storage for 6 weeks did not significantly decrease the endrin residual
level while storage for 12 weeks did significantly decrease level of
endrin. The decrease in pesticide residue from processing was dependent
on the potato type. Residues of endrin from processing were reduced
49.75 percent in sweet potatoes and 65.12 percent in Irish potatoes.
Heat processing effectively reduced the endrin residue content by 27.0
percent. Endrin was affected to a greater extent by heat processing
with water than heat processing alone. Blanching significantly reduced
the endrin residue levels in the potatoes (J.M. Solar, 1971).
Field-cured alfalfa hay samples were contaminated with endrin and
subjected to various extraction techniques for the removal of endrin
residues. By analysis, the contaminated hay contained a residue of
900 ppb of endrin. Residues were determined by thin-layer chromatography
and gas-liquid chromatography. Endrin residues were not removed by
washing with hot or cold water. Oven heat removed approximately 35% of
the residue. The residue removal was increased to 73% when the hay was
saturated with water and heated. The residue was not loosely deposited
nor chemically bound to the plant materials. It was found mainly in the
wax-like material of the plant cuticle. Endrin was 93 percent removed
by vapor washing with common solvents such as benzene or water. The
author concludes that the vapor treatment of contaminated hay with steam
before dehydration may have some practical application for pesticide
removal (Archer, I.E., 1968).
-------
The concentration of endrin in commercial tobacco in 1956 was barely
detectable with, the methods available. Levels as high as 1.3 ppm were
reported by 1964. During harvesting of the tobacco leaves, applications
of insecticides are recommended immediately after priming to provide
a maximal period of seven days between application and priming. Endrin
residues from 5 to 13 ppm were reported on the green leaf after weathering
for 7 days. Forty percent of the chlorinated hydrocarbon residues are
lossed during the flue-curing process. Storage or aging of tobacco had
little effect on the residue content of organochlorine residue in tobacco.
In experimental cigarettes impregnated with, endrin approximately 20% of
the applied insecticide appeared in the mainstream of smoke with approxi-
mately 80% endrin dissipated during the smoking process.
Residues were measured in flue-cured tobacco, the principal ingredient
of cigarettes, which was obtained from the auction markets in North Carolina,
South Carolina, Georgia and Florida. Residues in cigar wrapper tobacco
in Florida and residues in manufactured tobacco products on the 1962 retail
market were also determined. All samples were analyzed by electron capture
, gas chromatograph. High residues of endrin were found on some of the samples
of flue-cured tobacco in North Carolina as well as the cigar wrapper tobacco
in Florida. All of the cigarette samples contained endrin, with half
containing 1 ppm or more. The maximum residue of 2 ppm endrin found in
one filter brand was 7 times greater than the maximum found in cigarettes
in 1957. Endrin was detected in 7 of the 9 samples of pipe tobacco and
snuff, with one sample of snuff running as high as 2 ppm (Lawson, F.R.,
et al., 1964) .
-------
Representative samples of six brands of cigarettes were purchased
on the retail market during 1966 and 1967. The tobacco was analyzed by
electron-capture gas chromatography. In tobacco samples taken in 1966, endrin
was reported in concentrations of 0.49-1.57 ppm. In 1967, the concentration
of endrin in the same brands of cigarettes was reduced to 0.31 to 1.20 ppm.
The average level of endrin in 1967 was only 61% of that reported in 1966
(Sheets, T.J., 1968).
King-sized cigarettes of a standard brand were purchased on the open
market and separated from the paper. Residues were determined by electron-
capture gas chromatographic method. Tobacco from a commercial cigarette
was shown to contain 43 ppm DDT-TDE and no endrin residues (Skrentry, R.F.,
e^_al., 1971).
Cigarette tobacco from Japanese, German and American brands were
analyzed for chlorinated hydrocarbon pesticide residues by gas
chromatography. The average pesticide contents for the three Japanese
brands were as follows: ex -BHC 0.1 ppm; 3-BHC 0.2 ppm; y-BHC (lindane)
0.1 ppm;5 -BHC 0.1 ppm; p,p'-DDT 0.4 ppm; aldrin 0.1 ppm; dieldrin
0.2 ppm; endrin 0.5 ppm. The West German and American cigarettes, similar
in pesticide content, showed no detectable contamination with 3 -BHC,
<5-BHC or aldrin. They contained average quantities of 0.02 ppm a-BHC,
0.1 ppm Y-BHC, 5 ppm p,p'-DDT, 0.2 ppm dieldrin and 1.5 ppm endrin
(Karvahara, T., et_ a.L., 1971).
IV.E. Residues in Animals from Direct Application - Milk samples containing
endrin were taken from dairy animals dusted with a rotenone formulation
-------
contaminated with, approximately 30 percent endrin. Endrin residues were
determined by gas-liquid chromatography. Shortly after application, three
cows went into convulsions, and one animal died. Endrin was detected in
extracted fat of the initial milk samples at 6.76 ppm. This level of
endrin was reduced to 0.81 ppm in 14 days followed by a further reduction
to 0.13 ppm in 36 days after the initial sample was taken. The authors
conclude that the retention time of chlorinated hydrocarbons in milk
follow the order of dieldrin> DDT and its analogues> BHC> lindane> endrin>
methoxychlor (Moubry, R.J., 1968).
IV.F. Residues in Animals from Feed Contamination - Feed contaminated
with endrin at the levels of 2.5 and 5.0 ppm were fed to cattle for
16 weeks. Tissue samples of fat were taken from both groups at 4,8,
12, and 16 weeks during the feeding period. Levels of endrin in the
fatty tissue of cattle fed the 2.5 ppm level averaged 1.2, 2.6, 0.8,
and 0.8 ppm at 4,8,12, and 16 weeks respectively. Levels of endrin
in the fatty tissue of cattle fed 5.0 ppm 1.3, 1.5, 2.4 and 2.3 ppm at
4,8,12, and 16 weeks respectively. Endrin was not reported in the
tissue samples taken four weeks after the last feeding of either dosage
level. In comparing endrin to other pesticide contaminates likely to
occur in the feed of cattle and sheep the authors report the order of
storage in fat as follows: aldrin > dieldrin > heptachlor epoxide>
BHC > DDT > chlordane > lindane> endrin> heptachlor > toxaphene,
(Claborn, et_ al. , 1960).
The cumulative results of several studies on the propensities
of various organochlorine insecticides to be excreted in the milk of
-------
cows fed known amounts of contaminated feed were reported by J.G. Sana
(1969) in the order of heptachlor epoxide > aldrin > dieldrin > kelthane >
endrin > y-BHC> DDT > heptachlor > toxaphene > chlordane> methaxychlor.
Endrin residue in milk per ppm residue in feed was reported in the ratio
of 0.07 ppm to one. The author concludes that the relative rate of
detoxification of these insecticides should follow the reverse order,
methoxychlor being most readily detoxified and heptachlor epoxide the
least readily detoxified. Similar order has been found to prevail for
storage in body fat (Ganon, e£ al., 1959).
Lactating dairy cows received an average daily dose of endrin from
0.06 to 0.11 mg per kilogram of body weight gave average concentrations
of endrin in the milk of approximately 0.1 to 0.2 ppm. Alfalfa sprayed
with 2.7, 6.6, and 7.8 ounces of endrin per acre was harvested one week
after spraying and stored for six months. The hay treated at 2.7 and
6.6 ounces per acre was fed for 48 days while the hay treated with 7.8
ounces per acre was fed for 63 days. Residues of endrin in milk and
hay were determined by the amperometric silver nitrate titration method.
Hay made from the alfalfa plots sprayed with 2.7, 6.6, and 7.8 ounces
of endrin per acre had an average endrin residue of 2.8, 3.7, and 1.9
ppm, respectively, at the time of feeding. The average endrin content
of the milk of cows receiving hay contaminated with 1.9, 2.8, and 3.7
ppm was 0.05, 0.14, and 0.15 ppm, respectively. A daily intake of
approximately 0.05 mg per kilogram of body weight of endrin and below
did not result in the excretion of measurable amounts of endrin into
the milk (Ely, R.E., et al., 1957).
-------
A mixture of five pesticides (heptachlor epoxide, dieldrin, endrin,
lindane and DDT) were added to the grain rations of lactating dairy cows
at the levels of 0.05, 0.15, and 0.30 ppm. All samples were examined
by the electron-capture gas chromatographic method. Residues of endrin
and lindane were found in the milk at all three feeding levels, although
at lower concentrations than heptachlor epoxide and dieldrin. No endrin
or lindane was found in the milk of the control animals. The residue of
endrin in milk reached a maximum at the end of the 35-day feeding period
for all three dosage levels. The plateau concentrations of endrin residue
in milk were 0.004, 0.010, and 0.018 ppm for the three respective feeding
levels. During the three week withdrawal period the residue level of
endrin in the milk samples returned to baseline values in approximately
8, 17, and 23 days after the last exposure to the three respective feeding
levels. Feed consumption and milk production were very uniform for the
entire duration of this study (Williams, S., et_ al_., 1964).
Endrin was fed to steers, lambs and hogs at 0.1, 0.25, and 0.75 ppm
in their diet for 12 weeks to determine the extent of tissue residue likely
to result from feeding contaminated forage crops to livestock. All tissue
samples were analyzed for endrin by the spectrophotometric method. The
general appearance and weight gains were considered normal for both the
treated and control animals. Only endrin residue levels of 0.25 ppm or
higher were present in amounts that could be consistently detected by the
analytical method. Steeds accumulated the highest level and hogs showed
the least tendency to store endrin in the fatty tissue. Residues of endrin
-------
in the fatty tissue of hogs and lambs were reduced below the level of
detectability within six weeks after the last exposure. The endrin content
of the fat of steers was reduced 60 percent within six weeks of the last
exposure. There was no decrease in the endrin content of the meat as the
result of cooking (Terriere, L.C., et al., 1958).
Lactating dairy cows were fed daily doses of 0.1, 0.25, 0.75, and
2.0 ppm of endrin in their grain ration for 12 weeks. All of the milk
and body tissue samples were analyzed for endrin by the spectrophotometric
method. The lower levels of endrin fed were of the same order of magni-
tude as those expected from actual field use of endrin on forage crops.
The general appearance, weight gained and milk production were considered
normal for the treated and control animals. Endrin residues in the milk
were reported for those animals receiving endrin at 0.25 ppm and above.
These residues were apparent in the milk within the first week and except
for the 2.0 ppm level had disappeared from the milk within one month
after the feeding had ceased. The endrin residue in milk reached a plateau
within a month and remained at this level for the remainder of the exposure.
Endrin residues in fat were reported at the 0.25 ppm level and above the
maximum concentration being 1.0 ppm. These residues had disappeared within
one month after the feeding had ceased. This study indicates that in dairy
cows the ratio of storage in body fat to intake is about 1 to 2 for all
levels tested (Kiigemagi, Ulo, est_ al., 1958).
To demonstrate the relationship between the low level pesticide
residue commonly found in commercial poultry feed and the resultant
residues in eggs, lindane, heptachlor, dieldrin, endrin and DDT were
-------
fed in combination at levels of 0.05, 0.15 and 0.45 ppm to hens for a
14-week period. Residues were determined in eggs by the electron-capture
gas chromatography method of analysis. The level of storage in eggs
approached a plateau at the end of the 14-week period. Endrin residues
in eggs were reported in the range of 0.03 to 0.3 ppm for the the three
dosage levels. The plateau level of endrih residue in eggs is proportional
to the level of pesticide in the feed for all pesticides except DDT.
Endrin residues in eggs slowly declined but were still present at the
end of the month withdrawal period. The distribution of pesticides
between egg yolk and white were reported in the following ratios in
yolk to white; lindane 90/10; p,p'-DDT 93/7; DDE 95/5; heptachlor epoxide
99/1; dieldrin 99/1 and endrin 100/0. The average egg production was
approximately 60 percent (Cuinmings, J.G., 1966).
To demonstrate the relationship between low level pesticide residues
commonly found in commercial poultry feeds and the resultant residues in
poultry tissue, lindane, heptachlor, dieldrin, endrin and DDT were fed
in combination at the levels of 0.05, 0.15, and 0.45 ppm to hens for a
14-week period. Residues were determined in abdominal fat, breast muscle
and liver by electron-capture gas chromatography. The tendencies of the
pesticides to store in the abdominal fat and eggs were in the order of
dieldrin
-------
of DDT, the residue plateau levels in the fat were proportional to the
feeding levels. The plateau residues in the abdominal fat were about
10 times greater for each pesticide than the respective amounts found
in eggs. The endrin residues in breast tissue were reported in the
range of 0.01 to 0.03 ppm. Endrin residues in fatty tissue were reported
in the range of 0.035 to 3.5 ppm for the three dosage levels. Lindane
residue showed the greatest decline rate while endrin residues were still
evident during the one-month withdrawal period (Cummings, J.G., et al.,
1967).
Laying pullets and broiler chickens were fed doses of 0.1, 0.25,
0.75, and 2.25 ppm of endrin in their daily diet for periods of six to
eight weeks. Tissues and eggs were examined for endrin residues using
a specific spectrophotometric method of analysis sensitive to 0.1 ppm.
Weight gain, egg production, feed consumption and mortality appeared
normal. The results indicate that a dietary level of 0.10 ppm endrin
fed for 8 weeks will be deposited in the fat without danger of contami-
nating the eggs with endrin. At 0.25 ppm level and above, definite
deposition of endrin in egg tissue occurs after 2 to 4 weeks and it is
evident for about a month after exposure to endrin is stopped. Endrin
residues in the eggs of pullets were reported as 0.2 and 0.3 for the
0.25 and 0.75 ppm dietary level at the end of the eight weeks feeding.
Four weeks after the feeding ceased, the residue in eggs for the 0.25
and 0.75 ppm dietary level had decreased to < 0.01 and 0.2 ppm respectively.
Four weeks after the feeding had ceased the residue in fat for the 0.25
and 0.75 ppm dietary level were reported at 0.3 and 1.1 ppm respectively.
-------
Wlii:n broilers received 0.75 ppm In their diet for six weeks, endrin
residues were reported in fat at 3.1 ppm in breast tissue at 0.2 ppm
and in drumstick at 0.3 ppm. Feeding of 2.25 ppm of endrin resulted
in residues of 17 and 18 ppm in fatty tissue. Cooking failed to
eliminate the residues (Terriere, L.C., 1959).
Tissue levels of endrin were reported- in the fat of lambs 42 days
after the last exposure to an endrin-treated pasture. Six lambs were
grazed on a 0.5 acre of endrin-treated pasture for 55 days and then
removed to graze on the untreated pasture for 42 days. On the day the
animals entered the test area, two percent granules were applied at
0.5 Ib. actual endrin to the treated pasture. This rate of application
was repeated for a total of six applications over a six-week period. No
toxic symptoms were observed during the experimental period. No signi-
ficant difference in average weight increase was reported between the
two groups. Endrin residues in the fat were determined by the chromato-
graphic dechlorination phenyl azide method from samples obtained at 0,
14, and 42 days after the last exposure. The calculated average levels
of endrin residue in the fatty tissue at 0, 14, and 42 days were 16.8,
19.7, and 10.0 ppm, respectively. The author concludes that there was
apparently no measurable loss of endrin from fat 14 days after lambs
were transferred from the treated to the untreated pasture although
there is an indication of some loss from fat after 42 days (Long, W.H.,
et al., 1961).
Feed contaminated with endrin at the levels of 2.5 and 5.0 ppm
were fed to sheep for 16 weeks. Tissue samples of fat were taken
-------
from both groups at 4,8,12 and 16 weeks during the feeding period.
Levels of endrin, in the fatty tissue of sheep fed the 2.5 and 5.0 ppm
level averaged 3.2, 1.8, 2.3, and 1.4 ppm and 1.5, 2.0, 0.8 and 2.2
ppm, respectively. Endrin was not reported in the tissue samples
taken four weeks after the last feeding of either dosage level. In
comparing endrin to other pesticide contaminates likely to occur in the
feed of cattle and sheep, the authors report the order of storage in fat
as follows: aldrin > dieldrin > heptachlor epoxide > BHC > DDT > chlordane >
lindane > endrin >heptachlor > toxaphene (Claborn, et al., 1960).
Pregnant ewes were dosed with gelatine capsules containing a one
percent endrin dust formulation at the levels of 0.75 and 2.0 ppm for
12 weeks as shown in Table IV.F.I. Samples were analyzed by the
phenylazide spectrophotometric method for endrin. Most lambs were
born during the first and second week of feeding. Fat samples were
taken from lambs slaughtered at 6 to 8 weeks of age. The only source
of toxicant to the lambs was that contained in the mother's milk.
The meat samples were reported to contain 0.1 ppm endrin.
Table IV.F.I.
ENDRIN RESIDUES IN FATTY TISSUE OF SHEEP AND IAMBS (ppm)
Dosage Ewes at Ewes at Lambs at
Level 12 weeks 18 weeks 6 weeks
0 0.1 0.4 0.1
0.75 0.5 0.4 0.5
2.00 1.5 0.2 0.3
-------
The excretion of endrin once stored in body tissues appears to be
a rather slow process. Endrin concentrations in the fat samples taken
from lambs at 6 to 8 weeks of age were nearly as great as those found
in the fat tissue of the parent. Appreciable amounts of endrin were
found in the fat of ewes after 12 weeks of treatment. After withholding
the toxicant for six weeks, the endrin content of the fatty tissue of
the ewes was lower but still present in significant amounts (Street,
J.C., e_t a^., 1957).
Residue in Animal Products Processing - The effects of processing and
storage on endrin residues in dairy products was determined by either
adding the pesticide prior to processing the milk or by adding endrin
to the daily diet of cows until the resulting residues in the milk
reached 0.6 to 0.8 ppm endrin. The contaminated milk was then processed
into butter, ice cream, Swiss-type cheese, condensed milk and dry
whole powdered milk. After separation of the whole milk, endrin was
found only in the cream and none was detected in the skim milk.
Endrin was not affected by condensing. Some loss of endrin was reported
during the spray and drum drying process. No significant changes were
observed in the structure or amount of endrin during storage of butter,
cheese, ice cream, and sterilized milk (Langlois, B.E., 1965).
The effects of processing and preparation methods on pesticide
residues was determined on contaminated chicken tissue. Lindane,
endrin, heptachlor, dieldrin and aldrin were fed at 10 ppm to broilers
throughout an eight week growing period. The determinations for tissue
residues were made by electron-capture gas chromatographic method.
-------
Weights of birds receiving endrin and aldrin were lower than the other
groups. Several birds died in the endrin group indicating that the
level of endrin fed was near the maximum amount of residue which, could
be tolerated by the bird. Tissues from these birds were cooked by
baking, frying or steaming in closed containers for 30, 60 and 90
minutes. Residues calculated on a dry matter basis were lowered
during cooking but the reduction in concentration was not significant
in most cases. Lindane concentration was reduced considerably when
tissues were heated in closed containers. Heptachlor epoxide residues
were reduced during heating in closed containers. Heating had no
effect on the residues of endrin, dieldrin, or aldrin. Any loss
which occurred in the cooked samples of endrin, dieldrin and aldrin
was apparently through leaching of fat and water (Ritchey, S.J.
et al., (1972).
-------
BIBLIOGRAPHY
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Alfalfa Hay'1 J. Dairy Science 51(10): 1606-1611 (1968).
Barrentine, B.F.; J.D. Cain "Residue of Endrin and DDT in Soybean Grown
on Soil Treated with. These Compounds. Pest Monit. 3C2): 77-79 (1969).
Bayless, A.; I. Weisgerber: W. Klein; and F. Korte. "Conversion and
Residue Behavior of ^C Endrin in Cotton. Tetrahedron 26: 775-8
(1970).
Beall, M.L. and R.G. Nash. "Cup Seedling Uptake of DDT, Dieldrin, Endrin,
and Heptachlor from Soil" Agronomy Journal 61(4): 571-575 (1969).
Bowery, T.G.; W.R. Evens; F.E. Guthrie; and R.L. Rabb "Insecticide
Residues on Tobacco" J. Agri. Food Chem. 7(10): 693-702 (1959).
Brett, C. H. and T.G. Bowery. "Insecticide Residue on Vegetables. J.Econ.
Entomol. 51(6): 818-821 (1958).
Claborn, H.V.; R.D. Radeleff; and N.C. Bushland. "Pesticide Residue in
Meat and Milk" USDA/ARS 33-63, Dec. 1960.
Cummings, J.G.; K.T. Zee; V. Turner; F. Quinn. "Residues in Eggs from
low level feeding of Five chlorinated Hydrocarbon insecticides to
Hens" Journal of AOAC 49(2): 354-364 (1966).
Cummings, J.G.; M. Eidelman; V. Turner; D. Reed and K. T. Zee. "Residues
in Poultry Tissue from Low Level Feeding of Five Chlorinated Hydrocarbon
Insecticides to Hens. Journal of AOAC 50(2): 418-425 (1967).
Cyrisco, G.G. and E.W. Huddleston. "The Persistence of 'Aldrin, Dieldrin,
and Endrin Residues on Fresh Forage and on Hay Under Various Conditions
of Curing" J. Econ. Entomol 54(4): 718-719 (1961).
Dorough, H.W. and N.M Randolph. "Residues of DDT and Endrin in Peanuts and
Soybeans Grown in Soil Containing these Pesticides" Pest. Monit.
3(2): 90-93 (1969).
Duggan, R.E. "Pesticide Residue in Vegetable Oil Seeds, Oils and By-products"
Pest. Monit. 1(4): 2-7 (1968).
Duggan, R.E. "Pesticide Residue in Foods" Annals of N.Y. Acad. of Sci.,
Vol. 160, Oct. 1, 173-182 (1969).
Duggan, R.E. and P.E. Corneliussen "Dietary Intake of Pesticide Chemicals
in the United States" Pest. Monit. 5(4): 331-341 (1972).
-------
Duggan, R.E.; G.Q. Lipscomb; E.L. Cox; R.E. Hestwole; and R.C. Kling
"Residue in Food and Feed" Pest. Monit. 5(2): 73-212 (1971).
Dupree, Minter and C.M. Beckham "Residues of DDT and Endrin in Soil and
in Vegetables Grown on Land following Insecticide Treated Cotton"
Journal of the Georgia Entomol. Soc. 3(4): 141-146 (1968).
Ely, R.E.; L.A. Moore; R.H. Carter; and B.A. App "Excretion of Endrin in
the Milk of Cows Fed Endrin - Sprayed Alfalfa and Technical Endrin"
Journal Econ. Entomol. 50: 348-349 (1957).
FAO/WHO Minograph AGP: 1970/M/12/1 "Evaluations of Some Pesticide
Residues in Food 1970"
FAO/WHO World Health Organization Tech. Report No. 502 "Pesticide Residue
in Food" FAO Agricultural Studies No. 88 Report of the 1971 Joint
FAO/WHO Meeting.
Guthrie, F.E. and T.G. Bowery "Pesticide Residues on Tobacco" Residue
Review No. 19, 31-56 (1967).
Harris, C.R. and W.W. sans "Absorption of Organochlorine Insecticide
Residues from Agricultural Soils by Crops Used for Animal Feed.
Pest. Monit. 3(3): 182-185 (1969).
Harrison, R.B.; D.C. Holmes; J. Roburn; and J. O'G Tatton "The Fate of
Some Organochlorine Pesticides on Leaves" J. Sci. Food Agri. 18:
10-15 (1967).
Hermanson, H.P.; L.D. Anderson; and F.A. Gunther "Effects of Variety and
Maturity of Carrots Upon Uptake of Endrin Residues from Soil" Jo
Econ. Entomol. 63(5): 1651-1654 (1970).
Horsfall, Frank, Jr.; R.F. Webb, N. 0. Price; and R.W. Young "Residue
in Apples Subsequent to Ground Sprays of Endrin. J. Agri. Food Chem.
18(2): 221-223 (1970).
Kawahara, T.; M. Moku; and H. Nakamura "Chlorinated Hydrocarbon Pesticide
Residues in Marketed Cigarettes" Bull. Agri. Chem. Insp. Sta. (Jap)
11(10): 59-60 (1971).
Kiigemagi, Ulo; R.G. Sprowls; L.C. Terriere "Endrin Content of Milk and
Body Tissue of Dairy Cows Receiving Endrin Daily in Their Diet" J.
Agri. and Food Chem. (6)7: 518-521 (1958).
Terriere, L.C "Endrin Content of Eggs and Body Tissue of Poultry Receiving
Endrin in Their Daily Diet" J. Am. Food Chem. 7(7): 502-4 (1959).
Langlois, B.E.; B.J. Liska, and D.L. Hill "The Effects of Processing and
Storage of Dairy Products on Chlorinated Insecticide Residues II.
Endrin, Dieldrin and Heptachlor" J. Milk and Food Termol. 28(1):
9-11 (1965).
-------
Lawson, F.R.; Calvin Corley, and Milton S. Schuhter "Insecticide Residues
on Tobacco During 1962" Tobacco Sci. 8: 110-112 (1964).
Long, W.H.; L.D. Newsom and A.M. Mullins "Endrin Residues in the Fat of
Lambs Grazed on Endrin-Treated Pasture" J. Econ. Entomol. 54(3):
605-606 (1961).
Mattick, L.R.; D.L. Berry; F.M. Antenucci and A.W. Avens "The Disappearance
of Endrin Residue on Cabbage" J. Agrl. Food Chem. 11: 54-5 (1963).
Moubry, R.J.; Myrdal and A. Sturges "Rate of Decline of Chlorinated Hydro-
carbon Pesticides in Dairy Milk" Pest. Monit. (2)2: 72-79 (1968).
Painter, R.R. and W.W. Kilgore "Distribution of Pesticides In Fermentation
Products Obtained from Artifically Fortified Grape Must" Food Research
28: 342-346 (1963).
Ritchey, S.J.; R.W. Young and E.O. Essary "Effects of Heating and Cooking
Method on Chlorinated Hydrocarbon Residues in Chicken Tissue" J. Agri.
Food Chem. 20(2): 291-293 (1972).
Sana, J.G. "Res. Rev. 26, p.89-126 (1969).
Saha, J.G. and H. McDonald "Insecticide Residue in Wheat Grown in Soil Treated
with Aldrin and Endrin" J. Agri. Food Chem. 15(2): 205-207 (1967).
Sheets, T.J.; J.W. Smith and M.D. Jackson "Insecticide Residues in Cigarettes
Tobacco Sci. 12: 66-69 (1968).
Skrentny, R.F. and H.W. Dorough "Efficiencies of Several Extraction
Procedures in Removing Organochlorine Insecticides from Tobacco"
Tobacco Sci. 15: 111-113 (1971).
Smith, K.J.; P.B. Polen, D.M. Devries and F.B. Coon "Removal of Chlorinated
Pesticides from Crude Vegetable Oils by Simulated Commercial Processing
Procedures" J. Am. Oil Chem. Soc. 45(12): 866-869 (1968).
Solar, J.M.; J.A. Luizzo; and A.F. Novak "Removal of Aldrin, Heptachlor
and Endrin from Potatoes during Processing" J. Agri. Food Chem.
19(5): 1008-1010 (1971).
Street, J.C.; J.E. Butcher; R.J. Raleigh;, and D.C. Clanton "Tissue
Storage and Transferred to the Lamb of Aldrin, Dieldrin, and Endrin
when Fed to Bred Ewes" Proc. Ann. Meeting, Amer. Soc. of Animal
Production No. 8 1957, paper 46.
Terriere, L.C.; Ulo Kiigemagi; and D.C. England "Endrin Content of Body
Tissues of Steers, Lambs, and Hogs Receiving Endrin in Their Daily
Diet" J. Agri. Food Chem. 6(7): 516-518 (1958).
-------
U.S. Uept. of Agriculture, Plant Pest Control Division, Agriculture Res.
Serv. Pest. Monit. 2(1): 58-67 (.1968).
Walker, K.C.; J.C. Maitten; J.A. Onsager; D.M. Powell; and L.I. Butler
"The Fate of Aldrin, Dieldrin, and Endrin Residues During the
Processing of Raw Sugarheets" USDA 33-107 (1965).
Nash, R.G. "Plant Absorption of Dieldrin, DDT and Endrin from Soils"
Agron. J. 60: 217-219 (1968).
Weisgerber, I.; W. Klein and F. Korte "Disappearance of Residues and
Metabolism of Endrin~14C in Tobacco" Liebigs Ann. Chem. 729:
193-197 (1969).
Wheeler, W.B.; H.A. Mogej'C.H. Van Middelem; N.P. Thompson; and W.B. Tappan
"Residues of Endrin and DDT in Turnips Grown in Soil Containing These
Compounds" Pest. Monit. 3(2): 72-76 (1969).
Williams, S.; and P.A. Mills "Residues in Milk of Cows Fed Rations Containing
Low Concentrations of Five chlorinated Hydrocarbon Pesticides" J. of
The AOAC 47(6): 1124-1128 (1964).
Winnett, G. and J.P. Reed "Aldrin, Dieldrin, and Chlordane Persistence -
a 3-year study" Pest. Monit. 3(3): 133-136 (1968).
Wolfe, H.R.; W.F. Durham; J.F. Armstrong, Jr. "Health Hazards of the
Pesticide Endrin and Dieldrin" Archives of Environmental Health
6: 458-464 (1963).
'• 'to
-------
Chapter VI
The use of Endrin in Relation to the Hazards or Safety of Continued Use
Endrin is a synthetic chlorinated hydrocarbon which has been
used as a pesticide (economic poison) for more than 15 years to
control a variety of chewing and sucking insect pests which inhabit
soil and infest crops. It is also used to control mice populations
in deciduous orchards as an avicide, and as a rodent repellent in the
reseeding of forests. Prior to 1965, when the largest quantities of
this pesticide were used, especially on sugar cane and cotton, large
fish kills in the lower Mississippi River were attributed by some
to endrin contamination from industrial effluent and by runoff and
drift from nearby agricultural uses. However, periodic fish which
A
have resulted from a number of complex factors have been reported in
the Mississippi River over many decades. Several additional factors,
including industrial pollution could easily have been involved in these
unfortunate events.
Since 1966 the number of registered uses for endrin have declined
probably due in part to its relatively high tbxicity, the lack of
tolerances greater than zero and the development of resistance to
endrin.
Relative amounts of endrin used since 1970 are presented in
Table VI.A. by insect pests. During the 1970-1971 season, amounts
of endrin used was approximately one-third of the amount used in
1966. Inspite of the cancellation of endrin on corn and other food
-------
crops, amount level during 1971-1972 season was over twice the amount
during the prior season with the increase attributed solely to use on
cotton. Registered uses, rates of application, limitations and registered
alternates are presented in Table VI.B. Registered uses of endrin for
which there is no registered alternate or for which registered alternates
are not as effective as endtin are presented in Table VI.C. Insects
from different areas known to be resistant to endrin are presented in
Table VI.D.
tf '.I '
>'
-------
TABLE VI A
Relative Quantities of Endrin Used During 1970 - 1972.**
1970 - 1971* 1971 - 1972
Field Crop (%) (%)
Cotton 34.1 82.14
Corn 14.9 Cancelled
Small Grain 16.0 6.4
Sugar Cane 2.2 0.009
Seed Treatment 2.1 0.008
Potatoes 0.5 Cancelled
Sorgum, Sugar Beets 0.9 . Cancelled
Orchard (deciduous)
Mouse Control 28.6 11.44
Other
Greenhouse, nursery, bird control 0.7 0.003
*For these uses 132 labels were registered by Shell Chemical Co and Vilsicol Chemical Corp.
**Amount used in 1971 was 43 percent of that used in 1966. In 1971 amount used on cotton
was 18.7 percent of the amount used in 1966S and in 1972 82 percent of the amount used
in 1966. Quantities used for orchard mouse control have increased seven fold since 1966.
-------
TABLE VI B
Summary of Registered Endrin Uses and Alternates
Crop or'Use
Tolerance
(ppm)
Extended
Dosage
( IDS. a/A)
0.25
Limitations
Single application.
Do not apply within
45 days of harvest
or of feeding. Do
not graze livestock
on treated forage.
Do not feed thresh-
ings to livestock.
Pests
Armyworm
Chinch bugs
Cutworms
Fall armyworm
Pale western
cutworm
Possible
Substitutes
Carbaryl
Chlordane
Malathion
Methyl
parathion
Parathion
Toxaphene
Trichlorfon
Parathion
Toxaphene
Toxaphene
Thiodan
Trichlorfon
Parathion
Toxaphene
Toxaphene
Thiodan
Trichlorfon
-------
-2-
Crop or Use
Cotton
Tolerance
0
Extended
Dosage
0.7
Limitations
CO
0.5
Apply for
cutworms.
graze dai
or animal
finished
slaughter
ed fields
entering
in 5 days
treatment
protected
control of
Do not
ry animals
s being
for
on treat-
Workers
fields with-
after
shoul'd be
Do not graze dairy
animals or animals
being finished for
slaughter on treat-
ed fields. Workers
entered fields within
5 days after treat-
ment should be
protected.
Pests
Cutworms
Boll weevil
Substitutes
Carbaryl
Strobane
Toxaphene
Trichlorfon
Azodrin
Carbaryl
Chlordane
EPN
Guthion
Ma lathion
Methyl
parathion
Methyl
trithion
Strobane
Toxaphene
-------
Crop or Use Tolerance Dosage
Cotton (cont.)
-3-
Limitations
Pests
Brown cotton
1eafworm
Cabbage "looper
CO
Cotton
fleahopper
Substitutes
Guthion
Malathion
Parathion
Azodrin
Bacillus
thuringiens-
Methyl
parathion
Thiodan
Bidrin
Carbaryl
Chlordane
Guthion
Malathion
Methyl
parathion
Methyl
trithion
Phosphamidon
Strobane
Thiodan
Toxaphene
Trichlorfon
-------
Crop or Use Tolerance Dosage
Cotton (cont.)
-4-
Limitations
Pests
Cotton leaf
perforator
Cotton leafworm
-co
CD
Garden webworm
Substitutes
Bidrin
Carbaryl
Malathion
Methyl
parathion
Methyl
trithion
Parathion
Trichlorfon
Carbaryl
Guthion
Maithion
Methyl
parathion
Methyl
trithion
Parathion
Trichlorfon
Carbaryl
Guthion
Malathion
Methyl
parathion
Strobane
Toxaphene
-------
Crop or Use Tolerance Dosage
Cotton (cont.)
-5-
Limitations
re
Pests
Greenhouse
leaf tier
Grasshoppers
Fal1 armyworm
False wireworms
(adults)
Substitutes
Carbaryl
Chlordane
Malathion
Methyl
parathion
Strobane
Toxaphene
Carbaryl
Methyl
parathion
Strobane
Toxaphene
Carbaryl
Field crickets
Dieldrin
-------
Crop or Use Tolerance Dosage
Cotton (cont.)
-6-
Limitations
t w
s*
/Salepmarsh
'' caiberpillar
Substitutes
Bidrin
Carbaryl
Chlordane
Guthlon
Malathion
Methyl
parathion
Phosphamidon
Strobane
Toxaphene
Trichlorfon
Bidrin
Diazinon
Methyl
parathion
Parathion
Trichlorfon
-------
Crop or Use Tolerance
Cotton (cont.)
Dosage
-7-
Limitations
Pests
Tarnished plant
bug
Thrips
Substitutes
Bidrin
Carbaryl
Chlordane
Guthion
Malathion
Methyl
parath ion
Phosphamidon
Strobane
Toxaphene
Trichlorfon
Bidrin
Carbaryl
Chlordane
Guthion
Malathion
Methyl
parathion
Methyl
trithion
Parathion
Phosphamidon
Strobane
Toxaphene
-------
Crop or Use Tolerance
Cotton (cont.)
Dosage
2 oz./lOO Ib.
seed
Deciduous Fruits: Extended
Apples
Apricots
Cherries
Nectarines
Peaches
Pears
Plums
Prunes
2.4
-8-
Limitations
Seed treatment
Do not use as food
or feed.
Postharvest application
to orchard floor in Oct.
or Nov. Apply to 500
psi pressure. Do not
cultivate prior to
application or within
2 months thereafter.
Do not treat areas
where^runoff will -.
Pests
Celery leaf
tier
Rapid plant
bug
Crickets
Darkling ground
beetles
False wireworms
Wi reworms
Mouse control
Substitutes
Aldrin
Guthion
Heptachlor
Aldrin
Chlordane
Heptachlor
Toxaphene
Aldrin
Dieldrin
Lindane
Aldrin
Dieldrin
Lindane
-------
Crop or Use
Cotton (cont.)
Deciduous fruits:
(cont.)
Quinces
Apples only
Tolerance
Dosage
Sugarcane
Extended
0.25
(granular)
-9-
Limitations
Pests
Substitutes
contaminate streams,
ponds, or domestic
water supplies. Do not
graze orchards, cut
forage for hay, or
allow drop fruit to be
utilized for any purpose.
Post or otherwise pre-
vent entry to treated
area within 30 days after
treatment.
45 days. 4-8 appli-
cations at 14-day
intervals. 2.0%
granular formulation
only. Do not feed
bagasse or field
trimmings to livestock.
.OR
Sugarcane borer
Carbaryl
Guthion
Thiodan
-------
Crop or Use
Tolerance
Sugarcane (cont.) 0.5
Reforestation
Seed Treatment,
Direct Seeding
Avian Control
Buildings
Ornamentals and
Nursery Stock
Foliage
-10-
Dpsage Limitations Pests
45 days. 4 aplications
at 21 day intervals. Do
not feed bagasse to live-
stock.
0.5 Apply to seed pieces in
open row. Sugarcane beetle
NF
NF
NF
Birds and Mammals
(Repellent
Pest Birds
(Contact Poison)
Cicadas
Cyclamen mite
Substitutes
Aldrin
Fenthion
Carbaryl
Diazinon
Thiodan
Spittlebugs
Methoxychlor
-------
Table VI.C.
Regis; 1:creel use of endrin for which there is no registered
alternate or registered alternate is not as effective as
endrin.
J°_r Use Pest Registered Alternate
deciduous fruit meadow mouse * None
(prii'.i.-irily apples and
peaches)
pine mouse *none
t
Cotton , leaf perforator none satis factory;;
forest seed bird arid rodents none
small grains cutworms none satisfactory
^'Experimental permits have been issued for diaphacinone and
chlorophacinone, however, no data is available as yet on the efficacy
of these compounds.
-------
Tali lc. VI . I).
IV:,t l;.iii)'./n I ii In- i c:; i:. I .ml In Individual. j.n:.(:c I J c i dc in one or
mure nn-nii of tin.- UnUi'd Slater;.
Band-wing white fly
Beet army worm
Boll weevil
Bollworm
Cabbage looper
Cotton aphid
Cotton flcahoppcr
Cotton leaf perforator
Cotton leafworm
Lygus bug
Methyl parathion
organochlorine compounds
organochlorine compounds
DDT
EndrJ.n
Carbaryl
Methyl parathion
TDE
DDT
Organochlorine compounds
Endrin and toxaphcne
Organophosphorous
compounds
benzene
Organochlorine compounds
Organochlorine compounds
DDT
Organophosphorous compounds
organoch]orine compounds
organochlorine compounds
trichlorfon monocratophos
Din-
La.
Ariz. Ark. Cal. Miss.
Ala., Ark., Ga., La.,
Miss., N.C., Okla.,
S.C., Tenn., Texas.
Ala., Ark., Ariz.^ Cal.
Ga., La., Miss., Mo.,
Okla., Tenn. , N.C'jI ,
Texas
Ark., La., Miss.,
Okla., Tenn.
Ariz., La., Okla.
Ark., Okla.
Texas
Ariz., Ga., Tenn.,
Texas
Ala. , Ark-,, Cal. , La. ,
Miss., Okla.
Ariz.
Ark.
Ark., A]a. , Ga., La.,
Miss.,, Tenri.
Texas
Cal.
Army
Cal.
Ark., La., Texas
Cal.
Cal.
Ariz.
Of
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Table VI.D. (cont'cl)
Pest
Pink bollworm
Salt-marsh caterpillar
Southern garden leaf-hopper
Spider mites
J?J• Dl1 LY^li' 1£ t:nrkc:
Pacificus
T. urticae
T_. Pacif icus
Stink bug
Thrips
Frankliniella (mixture
Z • Q cc_Ld o n tolls
T_. YabacT" "
Tobacco budworm
InsccticidcA State-
DDT
Toxaphenc, DDT, Endrin Ariz., Cal.
DDT Cal.
organophosphorous compounds Ala., Cal.
exec.])l: phoratc seed or soil
treatment
I
organophosphorous compounds Ala., Ariz., Cal.'
Except phorate seed or soil Texas
treatment
I
organophosphorous compounds Ala., Ark., Cal.,
except phorate seed or soil La., Miss., N.C. l
treatment .. j \
dicofol ' , Cal.
organochlorine compounds Cal.
dieldrin
endrin
Tox a plicae
organqtb/Lorine compounds
organochlorine compounds
Carbaryl
DDT
Endrin
Strobane plus DDT
TDE
Toxaphcne plus DDT
Cal.
Texas
Texas
La., Texas
Ala., Ga., La., Miss,
N.C., Texas, Ark.
La., Miss., Texas,
Texas. ,
Texas
La., Miss., Texas
organophosphorous compounds Texas, La.
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. CHAPTER VII
General Discussion of the Hazards of Endrin in Relation to
• Use Patterns
Endrin is a relatively persistent snythetic chlorinated
..<
hydrocarbon pesticide with a high acute to'xicity. When ingested
or absorbed into a mammalian organism, it tends to accumulate in "J
fatty tissues. There are zero tolerances on thirteen specific t
i
food crops that are covered by registration; other registrations. r
have also been issued. The principal formulations are granular
products, baits, wettable powders, and emulsifiable concentrates.
Dust formulations are not common and are difficult to handle i
because of drift factors. The following is a summary of benefit/ '
risk relationships pertaining to the principal registered patterns
of use.
1. Foliage Treatments (Small Grains)
The pesticidal benefits from uses to control cutworms and
fV C
armyworms are relatively high since most of the effective alternates r
^^. '
such as aldrin, chlordane and heptachlor are under review for
cancellation. Other alternates tend to be less effective and more
costly. Relatively low dosages and early season usage are required.
The application of spray and granular proportions affords moderate
to low risk to the applicator and low risk of environmental pollution.
The principal risks involved are feed and forage contamination, hazards
to wildlife in the treated fields and in field margins, and possible
contamination of water from run off. Container disposal may also be
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a problem in many cases. There are no residue tolerances on food
and feed crops.
2. Foliage Application (Cotton) but also including Seed Treatment
The benefits of this use are relatively low to moderate since
substitute pesticides are for the most part readily available. However,
these substitutes which include methyl parathion, azinphos methyl, EPN
and monocrotophos (Azodrin) are more costly. Mixtures of endrin and
methyl parathion are widely used; no antidote has been proposed for
this mixture. Human health hazards from endrin spray applications
are low to moderate and low for granular application. Hazards related
\
to environmental pollution are moderate. Moderate hazards are involved
in the treatment site and field margins so far as fish and wildlife are
concerned. There is a zero tolerance on cotton seed which can easily
be violated. Container disposal problems can be serious. Seed treat--
ments have low to moderate benefits; application and environmental
risks are low.
3. Soil and Foliar Applications (Sugarcane)
The pesticidal benefits involved are quite low at this time,
since reasonably adequate substitutes are now available. However,
the environmental and application risks also appear quite low with
spray and granular formulations except with respect to exposed fish
and wildlife. There are, of course, no tolerances in sugar and
related products. Container disposal problems also may be serious.
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4. Seed Treatment (Forest).
The pesticidal benefits involved in this use are quite high
because of rodent feeding on treated seeds. The dosages are
quite low and the seeds are usually broadcast over large uninhabited
areas by aircraft. The risks of these treatments to applicators flying
the aircraft or regulating the treatment from the ground appear to be
quite minimal since all of these applications are on a professional
basis usually by State or Federal official agencies or by large lumber
companies. Environmental pollution may be a factor to some extent
but is probably minimal because of low dosage and the infrequency of
repeated applications. This use affords a substantial danger to
selected types of wildlife since the purpose of the treatment is to
kill various rodents and birds which would otherwise eat the treated
seed. The seeds also are treated to some extent to make them at
least partially repellent to seed-eating birds. Container disposal
may also be somewhat of a problem.
5. Deciduous Orchards (Mouse Control)
The pesticidal benefits from orchard treatments for mouse control
are high since there is no registered substitute. Some promising
alternates are being investigated. Substantial dangers are involved
with this use especially from the standpoint of environmental pollution
and hazards to fish and wildlife in or near the treatment area. There
are no tolerances for residues of endrin on deciduous fruit. Applicator
hazards are relatively low to moderate. Container disposal problems
involve a relatively high risk since large dosages are involved and a
number of containers require disposition.
•'* 01
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6. Foliage Application (Nursery Stock and Ornamentals)
The pesticidal benefits involved are low to moderate since
there are a number of substitutes that are equally effective and
not necessarily expensive. The risk from this use of endrin is
low to moderate. No food commodities are 'involved and environmental
pollution problems do not appear to be serious. Container disposal
could be a problem.
7. Perch Solution (Bird Control)
The benefits from use are moderate to high. Fenthion as a
registered alternate has a high degree of acute toxicity and is
subject to about the same benefit/risk relationship as endrin.
However, present data suggest that fenthion may not be as effective
as endrin under all conditions of use. The risks of application are
relatively low and risks of environmental pollution are moderate as
are the risks to wildlife especially songbirds and other nonpest
birds. Container disposal and disposal of the used perches can be
a relatively serious problem.
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