ORNL
Oak Ridge
National
Laboratory
Operated by
Union Carbide Corporation for the
Department of Energy
Oak Ridge, Tennessee 37830
ORNL/EIS-131
EPA
United States
Environmental Protection
Agency
Office of Research and Development
Health Effects Research Laboratory
Cincinnati, Ohio 45268
EPA-600/1 -79-005
REVIEWS OF THE ENVIRONMENTAL
EFFECTS OF POLLUTANTS:
XIII. Endrin
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RESEARCH REPORTING SERIES
Research reports of the Office of Research and Development, U.S. Environmental
Protection Agency, have been grouped into nine series. These nine broad categories
were established to facilitate further development and application of environmental
technology. Elimination of traditional grouping was consciously planned to foster
technology transfer and a maximum interface in related fields. The nine series are:
1. Environmental Health Effects Research
2. Environmental Protection Technology
3. Ecological Research
4. Environmental Monitoring
5. Socioeconomic Environmental Studies
6. Scientific and Technical Assessment Reports (STAR)
7. Interagency Energy-Environment Research and Development
8. “Special” Reports
9. Miscellaneous Reports
This report has been assigned to the ENVIRONMENTAL HEALTH EFFECTS
RESEARCH series. This series describes projects and studies relating to the tolerances
of man for unhealthful substances or conditions. This work Is generally assessed from a
medical viewpoint, including physiological or psychological studies. In addition to
toxicology and other medical specialities, study areas include biomedical instrumenta-
tion and health research techniques utilizing animals — but always with intended
application to human health measures.
This document is available to the public through the National Technical Information
Service, Springfield, Virginia 22161.
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ORNL/EIS-131
EPA-600/1-79-005
August 1979
REVIEWS OF THE ENVIRONMENTAL EFECTS OF POLLUTANTS: XIII. ENDRIN
Report prepared by
J. Donoso, J. Dorigan, B. Fuller, J. Gordon, M. Kornreich,
S. Saari, L. Thomas, and P. Walker
MITRE Corporation
Westgate Research Park
McLean, Virginia 22101
under Contract No. E(40-l)-4993
with the Department of Energy for
Information Center Complex
Information Division
OAK RIDGE NATIONAL LABORATORY
Oak Ridge, Tennessee 37830
operated by
UNION CARBIDE CORPORATION
for the
DEPARTMENT OF ENERGY
Contract No. W-7405-eng-26
Reviewer and Assessment Chapter Author
Frederick W. Oehme
Kansas State University
Manhattan, Kansas 66506
Interagency Agreement No. D5-0403
Project Officer
Jerry F. Stara
Office of Program Operations
Health Effects Research Laboratory
Cincinnati, Ohio 45268
August 1979
Prepared for
HEALTH EFFECTS RESEARCH LABORATORY
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
CINCINNATI, OHIO 45268
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This report was prepared as an account of work sponsored by an
agency of the United States Government. Neither the United States
Government nor any agency thereof, nor any of their employees, con-
tractors, subcontractors, or their employees, makes any warranty,
express or implied, nor assumes any legal liability or responsibility
for any third party’s use or the results of such use of any information,
apparatus, product or process disclosed in this report, nor represents
that its use by such third party would not infringe privately owned
rights.
This report has been reviewed by the Health Effects Research
Laboratory, U.S. Environmental Protection Agency, and approved for
publication. Approval does not signify that the contents necessarily
reflect the views and policies of the U.S. Environmental Protection
Agency, nor does mention of trade names or commercial products con-
stitute endorsement or recommendation for use.
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Figures.
Tables
Foreword
Acknowledgments
Abstract
1. Executive Summary
1.1 Major Findings
1.2 Major Conclusions
2. Physical and Chemical Properties and Analysis
2.1 Summary
2,2 Nomenclature, Structure, and Synthesis
2.3 Physical and Chemical Properties
2.4 Implications of Chemical and Physical Properties f
Behavior of Endrin in Organisms, Media, Storage,
Agriculture
2.5 Methods of Analysis
2.6 References
3. Biological Aspects in Microorganisms
3.1 Summary
3.2 Bacteria
3.2.1 Metabolism
3.2.2 Effects
3.3 Protozoa and Plankton
3.4 References
4. Biological Aspects in Plants
4.1 Summary
4.2 Nonvascular Plants
4.2.1 Metabolism of Endrin
4.2.2 Effects of Endrin
4.3 Vascular Plants
4.3.1 Metabolism of Endrin
4.3.2 Effects of Endrin
4.4 References
5. Biological Aspects in Animals
5.1 Summary
5.2 Aquatic Animals
5.2.1 Invertebrates
5.2.2 Fish
5.3 Birds
5.3.1 MetabolIsm
5.3.2 Effects of Endrin
5.4 Insects
5.4.1 Metabolism
5.4.2 Effects
5.5 Mammals
5.5.1 Domestic
5.5.2 Wild Mammals
5.6 References . . . . . . . . 122
CONTENTS
vii
xi
xvii
xix
xxi
1
1
9
11
11
11
15
or
and
• . . 18
22
27
34
34
• . . 34
• . . 34
39
39
• . . 43
46
46
48
48
49
49
49
• . . 65
• . . 71
• . . 75
75
76
• . . 76
82
93
93
97
• . 107
• . • 107
• . . 109
112
• . 112
117
111
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iv
7.3.2
7.3.3
7.3.4
7.4 Endrin
7.4.1
7.4.2
7.4.3
134
134
135
135
135
137
140
140
142
144
147
148
149
158
164
164
166
167
167
168
180
184
185
185
186
223
225
225
225
229
242
260
269
269
270
274
280
285
302
312
312
312
312
312
312
313
313
315
6. Biological Aspects in Humans
6.1 Summary
6.2 Metabolism
6.2.1 Exposure
6.2.2 Distribution and Accumulation .
6.2.3 Biotransformation and Elimination
6.3 Effects
6.3.1 Human Exposure
6.3.2 Acute Toxicity
6.3.3 Chronic and Subchronic Toxicity
6.3.4 Carcinogenesis and Mutagenesis
6.3.5 Reproduction and Teratogenesis
6.3.6 Physiological Effects
6.4 References
7. Media Distribution, Transformation, and Transport
7.1 Summary
7.2 Production and Use
7.3 Endrin in the Atmosphere
7.3.1 Introduction
Sources of Endrin in the Atmosphere
Monitoring for Endrin in the Atmosphere
Mechanisms for Removal of Endrin from the Atmosphere
in the Hydrosphere
Introduction
Sources of Endrin in the Hydrosphere and Sediment
Monitoring for Endrin in the Hydrosphere and
203
Sediment
7.4.4 Mechanisms for Removal of Endrin from the
Hydrosphere and Sediment
7.5 Endrin in the Lithosphere
7.5.1 Introduction
7.5.2 Sources of Endrin in the Lithosphere
7.5.3 Monitoring for Endrin in the Lithosphere
7.5.4 Persistence of Endrin in the Lithosphere
7.6 References
8. Environmental Interactions and Their Consequences
8.1 Sitmm ry
8.2 Environmental Cycling of Endrin
8.2.1 Endrin in Food
8.2.2 Terrestrial Ecosystems
8.2.3 Aquatic Ecosystems
8.3 References
9. Environmental Assessment
9.1 Production, Consumption, and Uses
9.1.1 Production and Consumption
9.1.2 Uses
9.2 Biological Effects in the Environment
9.2.1 Microorganisms
9.2.2 Vascular Plants
9.2.3 Aquatic and Higher Animals
9.3 Effects on Human Health
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V
9.3.1 Toxicity . 315
9.3.2 Carcinogenesis, Mutagenesis, and Teratogenesis . . . 315
9.3.3 Potential Health Hazards 315
9.4 Sources of Persistence in the Environment 316
9.4.1 Lithosphere 316
9.4.2 Hydrosphere 317
9.4.3 Atmosphere 317
9.4.4 Detection and Analysis 318
9.5 Standards and Regulations 318
9.6 Environmental Impact 319
9.7 References 319
Bibliography 323
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FIGURES
2.1 Stereochemical structure of endrin, using the von Baeyer—IUPAC
notation 12
2.2 Synthesis of endrin 14
2.3 Synthesis of isodrin 14
2.4 Synthesis of 1,2,3,4,7,7—hexachlorobicyclo—(2.2.l)—2,5—
heptadiene 14
2.5 Schematics of some chemical reactions of endrin 17
2.6 Some thermal and photochemical degradation products of endrin . 19
2.7 Photochemical isomerization of endrin 21
2.8 Photochemical isomerization of endrin 21
3.1 Microbial degradation of endrin 35
3. 2 Anaerobic transformations of hexachloronorbornene by
Clostridiwn butyricum 38
3.3 Effect of endrin and one of its degradation products,
ketoendrin, on two species of blue—green algae, after
36hr 41
3.4 Effect of endrin on Cylindrospermun sp 42
3.5 Uptake of endrin by phytoplankton at various concentrations
over 24 hr and growth rates of same species in 100 ppb
endrin over seven days 43
5.1 Endrin concentration in mussel tissues after exposure to
0.5 ppm endrin and transfer to fresh water 78
5.2 Effects of endrin concentration and exposure time on two
stonefly naiad species so
5.3 Blood levels of endrin in channel catfish exposed to 0.1 ppb
endrin 83
5.4 Mortality of mummichogs to various durations of endrin
treatment 91
5.5 Residual levels of endrin found in breast and fat tissues . . . 94
5.6 Generalized model of the ways in which a biocide may affect a
small—mammal population 121
vii
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viii
6.1 Structures of the metabolites I and II, endrin, ketoendrin,
and dieldrin 138
6.2 Suggested schema for physiological changes produced by endrin . 151
7.1 Atmospheric concentration of endrin 4 ft above ground level
in a sugarcane field and cumulative recovery 169
7.2 Endrin residues remaining in rice plants as determined from
mortality of Corcyra cepholonica larvae 170
7.3 Results from endrin pollution study of the Bayou Yokely
watershed in Louisiana during 1961 187
7.4 Occurrence of endrin in water and biota at pump B 196
7.5 Concentrations of endrin in water from subsamples of Douglas
fir seed soaked for different lengths of time 199
7.6 Percent occurrence of endrin in CAM samples, 1958-65, and in
grab samples, 1964—65 211
7.7 Historical occurrence of endrin in the Mississippi River main
stem, CAN samples from water years 1958—65 212
7.8 Occurrence of endrin in river basins throughout the United
States 213
7.9 Farm production regions 227
7.10 Persistence of endrin in Congaree sandy—loam soil 255
7.11 Distribution of endrin in a 38—cm Congaree sandy—loam soil
profile 13 years after the last foliar application 257
7.12 Loss of endrin from surface of the soil as determined by
bioassay procedure against eye gnats and mosquito larvae . . 259
8.1 Possible routes of endrin into the environment 271
8.2 Movement of endrin through the environment 273
8.3 Transport of vaporized endrin 274
8.4 Food web module 281
8.5 Generalized standing—crop and energy—flow pyramids 288
8.6 Endrin accumulation in clams 289
8.7 Endrin concentration in mussel tissues and rainfall during
ten—day periods of study 290
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ix
8.8 Endrin accumulation in largemouth bass . 292
8.9 Effect of temperature on toxicity of endrin to mummichogs . . . 294
8.10 Compartment model of an aquatic ecosystem 299
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TABLES
2.1 Chemical composition of technical endrin 15
2.2 Physical and chemical properties of endrin 16
2.3 Endrin photoproduct formed vs sun’s intensity 20
3.1 Percent distrubition of endrin and its solvent—extractable
metabolites dur to microorganisms 36
3.2 Concentration of endrin under different soil conditions . . . . 37
3.3 Effects of endrin on bacterial growth 40
4.1 Absorption of endrin from soil by plants 51
4.2 Plant uptake of endrin from soils 55
4.3 Distribution of endrin and its metabolites in plants following
foliar application of 1 C—endrin 56
4.4 Distribution and transformation of endrin 12 weeks after
application of 12.6 mg ‘ C—endrin to leaves of cotton . . . . 59
4.5 Concentration, distribution, and transformation of endrin
as measured four weeks after application of 60 ppm
endrin to leaves of cabbage 60
4.6 Distribution of radioactivity after application of 5 ppm
14 C—endrin to leaves of cabbage 61
4.7 Distribution and metabolism of 1 C—endrin after application
to upper surfaces of leaves of tobacco 63
4.8 Sorption of endrin by soybean from soil and from air 64
4.9 Effect on barley seeds of soaking in endrin solutions 67
4.10 Effect of soil endrin on aboveground portions of corn and
bean 70
5.1 Endrin accumulation factors in aquatic invertebrates 77
5.2 Endrin LC 50 values for aquatic invertebrates 79
5.3 Effects of endrin on survival and growth of oyster larvae and
eggs 82
5.4 Endrin toxicity to some fish as measured by LC 50 87
xi
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xii
96
98
100
101
102
102
104
105
• 108
114
• 115
• 116
• 119
• 120
poisoning in
136
143
146
170
172
5.5 Endrin content of eggs and adipose tissue from white
leghorns
5.6 Comparative dietary toxicity of endrin to birds
5.,7 Toxicity of endrin to adult quail and pheasants
5.8 Toxicity of endrin to juvenile quail and pheasants
5.9 Toxicity of endrin to juvenile quail; intermittent feeding,
28 days between tests
5.10 Toxicity of endrin to New Hampshire chicks of various ages
5.11 Effects of endrin upon reproduction
5.12 Hatchability of hens’ eggs after endrin injection
5.13 Quantity of 1 C—endrin in S and R larvae of Heliothis virescens
central nervous system extracted with n—hexane and
chloroform—methanol
5.14 Endrin residues in cow milk after feeding .
5.15 Endrin lethal toxicity to mammals
5.16 Endrin toxicity in domestic mammals — sublethal
5.17 Applications of endrin in field to kill mice
5.18 Endrine toxicity on wild mammals — sublethal
6.1 Endrin concentrations found in victims of endrin
Saudi Arabia
6.2 Acute oral toxity of endrin to mammals .
6.3 Mortality among groups of control rats and rats
on diets containing endrin
7.1 Disappearance of endrin residues from cabbage
7.2 Persistence and behavior of dieldrin and endrin
types of soil at 45°C
fed two years
in various
7.3 Effects of moisture on persistence and behavior of dieldrin
and endrin in four types of soils exposed at 45°C for
4days
7.4 Effects of humidity on the persistence and behavior of dieldrin
and endrin in four types of soils exposed at 45°C for
4days
173
175
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xiii
7.5 Endrin residues on tomatoes, snap beans, and collards 176
7.6 Concentration of residues found in soybean plants exposed to
topsoil treated with 1 C—endrin 177
7,7 Endrin residues in ambient air 1970 and 1971 181
7.8 Concentrations of endrin collected on ethylene—glycol—
saturated screens 183
7.9 Rainfall, runoff, and endrin loss in runoff from sugarcane
plots following a single endrin application 189
7.10 Concentration of endrin in soil 190
7.11 Effect of time interval between endrin application and rainfall
on endrin concentration in runoff and soil 191
7.12 Concentration of endrin in a drainage slough in Greenville,
Mississippi, and in surface runoff 192
7.13 Residues in water from spraying a cotton field with 0.4
lb/acre endrin 193
7.14 Pump B water and biota analyses 197
7.15 Concentrations of endrin in water from samples of Douglas fir
seed soaked for different lengths of time 198
7.16 Endrin analysis of water samples, Needle Branch Watershed,
January 23—29, 1967 200
7.17 Endrin remaining on 200 repellent—coated seeds after different
periods of exposure 201
7.18 Occurrence of positive and presumptive endrin determinations
in carbon adsorption method and in grab samples 205
7.19 Top ten locations at which highest levels of endrin were
observed 210
7.,20 Endrin residues in whole—water samples and bottom deposits
in drainage basins of the United States and Puerto Rico . . . 214
7.21 Endrin in bottom sediments of Louisiana waterways — 1975 . . . 217
7.22 Endrin concentrations in selected western streams 1965—71 . . . 217
7.23 Concentration of endrin recovered by the carbon adsorption
method from the Franklin Municipal Treatment Plant on
Bayou Tech, Louisiana, 1961—62 218
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xiv
7.24 Endrin in drinking water and associated river water 220
7.25 Endrin concentration in water and bottom mud from three streams
in Ontario, Canada — 1971 221
7.26 Quantities of endrin used on specified crops and number of
acres treated 226
7.27 Quantities of endrin used on all crops and number of acres
treated 227
7.28 Endrin in soil as a function of soil type, crop, and mode of
application 228
7.29 National Soils Monitoring Program for endrin residues:
cropland soil FY 1969 and FY 1970 230
7.30 Summary of endrin residues in cropland soil by cropping region,
F? 1969 and FY 1970 235
7.31 States where endrin was used in F? 1969 and/or FY 1970 . . . . 236
7.32 Endrin in cropland soil by crop — FY 1970 237
7.33 Endrin in cotton—belt soils: 1969—1973 238
7.34 Endrin residues in urban soils 1969—1973 240
7.35 Residues of endrin found in agricultural soils on 16 farms in
southwestern Ontario in 1964, 1966, and 1969 241
7.36 Effect of ultraviolet radiation on the loss of endrin from
petri dishes treated with 100 pg of sample 244
7.37 Influence of treatment depth and one soybean crop on endrin
residues in Lakeland sandy loam 246
7.38 Influence of soil moisture on endrin treatment of Lakeland
sandy loam 247
7.39 Elution characteristics of endrin on various types of soil as
determined by percolation with hexane and distilled water . . 249
7.40 Recovery of endrin from soil at various depths after one year;
initial concentration was 25 ppm 251
7.41 Soils tested for their ability to degrade endrin 253
7.42 Endrin residues found in Pullman clay loam soil 5 and 11 years
after application 253
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xv
7.43. Accumulation of endrin in soil following repeated foliar
application 256
7.44 Loss of endrin activity from the surface of soil in the field
as tested against Hippelates colluson and Culex
quinquefasciatus larvae 258
8.1 Disposal methods used by farmers 272
8.2 Average incidence and daily intake of endrin 275
8.3 Relative composition of diet by food class 276
8.4 Calculated daily intake of endrin by food class 277
8.5 Recommendations for endrin concerning acceptable daily intakes,
tolerances, and practical residue limits as of November 1972 278
8.6 Exposure of workers to endrin 279
8.7 U.S. Environmental Protection Agency worker protection
standards for agricultural use of endrin 279
8.8 Endrin residues from two anastomosing creeks in Wisconsin . . . 289
8.9 Temperature—toxicity relationships for endrin in rainbow trout
and bluegills 293
8.10 36—hr LC 50 values for field fish from endrin—polluted and
nonpolluted areas in Mississippi 295
8.11 Effect of force—feeding one endrin—resistant mosquito fish
to a predator 296
8.12 Distribution of endrin in some components of a model ecosystem 301
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FOREWORD
A vast amount of published material is accumulating as numerous
research investigations are conducted to develop a data base on the
adverse effects of environmental pollution. As this information is
amassed, it becomes continually more critical to focus on pertinent,
well—designed studies. Research data must be summarized and interpreted
in order to adequately evaluate the potential hazards of these substances
to ecosystems and ultimately to public health. The Reviews of the Environ-
mental Effects of Pollutants CREEPs) series represents an extensive com-
pilation of relevant research and forms an up—to—date compendium of the
environmental effect data on selected pollutants.
Reviews of the Environmental Effects of Pollutants: XIII. Endrin
includes information on chemical and physical properties; pertinent
analytical techniques; transport processes to the environment and sub-
sequent distribution and deposition; impact on microorganisms, plants,
and wildlife; toxicologic data in experimental animals including metabo-
lism, toxicity, mutagenicity, teratogenicity, and carcinogenicity; and an
assessment of its health effects in man. The large volume of factual
information presented in this document is summarized and interpreted in
the final chapter, “Environmental Assessment,” which presents an overall
evaluation of the potential hazard resulting from present concentrations
of endrin in the environment. This final chapter represents a major
contribution by Frederick Oehme from Kansas State University.
The REEPs are intended to serve various technical and administrative
personnel within the Agency in the decision—making processes, i.e., in
the development of criteria documents and environmental standards, and
for other regulatory actions. The breadth of these documents makes them
a useful resource for public health personnel, environmental specialists,
and control officers. Upon request these documents will be made available
to any interested individuals or firms, both in and out of the government.
Depending on the supply, the document can be obtained directly by writing
to:
Dr. Jerry F. Stara
U.S. Environmental Protection Agency
Health Effects Research Laboratory
26 W. St. Clair Street
Cincinnati, Ohio 45268
R. J. Garner
Director
Health Effects Research Laboratory
xvi I
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ACKNOWLEDGMENT S
The authors gratefully acknowledge the advice and support of Gerald U.
Ulrikson, Manager, Information Center Complex, Information Division, Oak
Ridge National Laboratory, and Jerry F. Stara, EPA Project Officer. The
cooperation of the Toxicology Information Response Center, the Environ-
mental Mutagen Information Center, and the Environmental Resource Center
of the Information Center Complex is also appreciated.
Appreciation is also expressed to Bonita M. Smith, Karen L. Blackburn,
and Donna J. Sivulka for EPA in-house reviews and editing and for coordi-
nating contractual arrangements. The efforts of Allan Susten and Rosa
Raskin in coordinating early processing of the reviews were important in
laying the groundwork for document preparation. The advice of Walter E.
Grube was valuable in preparation of manuscript drafts. The support of
R. John Garner, Director of Health Effects Research Laboratory, is much
appreciated. Thanks are also expressed to Carol A. Raynes and Peggy J.
Bowman for typing correspondence and corrected reviews.
xix
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ABSTRACT
This study is a comprehensive, multidisciplinary review of the
health and environmental effects of endrin (l,2,3,4,lO,l0—hexachloro—6,7—
epoxy—l,4,4a,5,6,7,8,8a—octahydro—l,4—endo,endo—5,8—dimethanonapthalene).
More than 600 references are cited.
Endrin is used chiefly as an insecticide, particularly for the con-
trol of lepidopterous larvae that infest cotton crops. In 1971, total
U.S. consumption of endrin exceeded 600,000 kg. Of this amount, 75% was
applied to cotton crops, and 99% of the total usage occurred in the south-
eastern and delta states.
Endrin is highly toxic to mammals, birds, fish, and insects, but is
generally nontoxic to plants. Acute exposure of mammals to endrin typi-
cally results in central nervous disorders, with convulsions leading to
death through respiratory failure within two days. Symptoms of acute
endrin exposure in humans include convulsions, vomiting, abdominal pain,
nausea, dizziness, and headaches. Chronic exposure of mammals to endrin
may result in damage to the liver, kidney, heart, brain, lung, adrenal
gland, and spleen. Behavorial abnormalities, reproductive disorders,
changes in carbohydrate metabolism, changes in blood composition, and
other effects secondary to central nervous system disorders have also
been observed following chronic exposure of mammals to sublethal doses
of endrin.
No malignancies attributable to endrin have been reported, but chro—
mosomal abnormalities and teratogenesis have been induced in several
mammalian species by endrin.
Endrin is dissipated from the environment by photochemical and ther-
mal decomposition and by microbial degradation. Relatively few bacteria
can degrade endrin, but many species of algae and fungi exhibit this
ability. The major product of endrin decomposition under natural condi-
tions is ketoendrin.
Environmental contamination by endrin appears to be restricted to
areas where the compound is used intensively; background concentrations
in the atmosphere, hydrosphere, and lithosphere at locations distant from
areas of heavy use are generally below the levels of detection.
xxi
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1. EXECUTIVE SUMMARY
1.1 MAJOR FINDINGS
Endrin (l,2,3,4,lO,1O—hexachloro—6,7—epoxy—l,4,4a,5,6,7,8,8a—
octahydro—l,4—endo, endo—5,8—dimethanonapthalene), the common name for
one member of the cyclodiene group of insecticides, is a cyclic hydro-
carbon having a chlorine—substituted methano bridge structure (Sect. 2.2).
Endrin was introduced in the United States in 1951 and is manufactured
domestically by the Velsicol Chemical Corporation and in the Netherlands
by Shell Nederland Chemie. The endrin sold in the United States is a
technical—grade product containing not less than 95% active ingredient.
It is available in a variety of diluted formulations (Sect. 7.2).
The only known uses of endrin are as an avicide, rodenticide, and
insecticide, the last of these being the most prevalent. The largest
single use of endrin is for the control of lepidopterous larvae attacking
cotton crops in the southeastern and delta states. In 1971 (the last
year for which data are available), 75% of all endrin used (total usage
6.438 x lO kg) was applied to cotton, while 99% of the total usage was
confined to the southeastern and delta states (Sect. 7.5.2).
A variety of analytical techniques are available for the qualita-
tive and quantitative determination of endrin in environmental samples.
Included among these are biological assays, colorimetric methods, thin—
layer chromatography, determination of total chlorine, and infrared
spectroscopy (Sect. 2.5). The method of choice, however, is gas—liquid
chromatography (GLC) using an electron—capture detector. GLC methods
are rapid, simple, and highly sensitive, permitting detection of nano-
gram quantities of endrin residues. Unequivocal confirmation may be
achieved by mass spectrometry. Chemical ionization mass spectrometry
of endrin results in a less complex spectrum than does the electron
impact counterpart and is therefore useful for the identification of
endrin in crude extracts (Sect. 2.5).
Endrin enters the environment primarily as a result of direct
applications to soil and crops. Discharge of waste materials from
endrin manufacturing and formulating plants and disposal of empty con-
tainers also contribute significantly to observed residue levels (Sects.
7.4.2.3 and 8.2). Environmental contamination appears, for the most
part, to be restricted to those areas where endrin is used extensively.
Concentrations as high as 0.64 ppm were observed in Mississippi soils
during 1972, while maximum concentrations in Arkansas and Louisiana
soils during 1973 were 0.24 and 0.48 ppm respectively (Sect. 7.5.3).
Monitoring of the surface waters of United States river basins
between 1957 and 1966 revealed consistent contamination by endrin only
in the lower Mississippi basin. In addition, the highest concentrations
recorded during the six consecutive years from 1960 to 1965 were all
from this area. While residue levels reported between 1970 and 1975
1
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2
were significant (20 ppt), they did not approach the maximum of 214 ppt
present in 1963, when numerous endrin—related fish kills occurred (Sect.
7.4.3). The major source of endrin in rivers and other freshwater bodies
is surface runoff from fields and crops following application (Sect. 7.4.2).
The large—scale use of endrin in the agricultural lands surrounding
the Mississippi River basin prior to 1964 was reflected in the levels of
the pesticide detected in bottom deposits (10,000 ppt) in that year.
The highest concentration of endrin in the sediment of any river basin
between 1970 and 1975 (6700 ppt) was also found in the lower Mississippi
(Sect. 7.4.3).
Extensive monitoring for endrin in the atmosphere has not been
conducted. The highest concentration reported to date was 58.5 ng/m 3
in Stoneville, Mississippi, in 1971 (Sect. 7.3.3). Vaporization of
endrin from treated soils and crops is believed to represent the major
source of atmospheric contamination.
Background concentrations in the atmosphere, hydrosphere, and
lithosphere, far removed from agricultural areas where endrin is applied
and industrial areas where endrin is manufactured, are generally below
the limits of detection (Sects. 7.3.3, 7.4.3, 7.5.3). However, the
structural, chemical, and toxicological similarities between endrin
and related compounds which have been observed at great distances from
their points of application suggest that transport of endrin to remote
areas is not unlikely (Sect. 7). Transport to remote areas and to the
open ocean is expected to occur primarily via the atmosphere (Sect. 7.3).
Most established mechanisms for removal of endrin from the atmo-
sphere, hydrosphere, or lithosphere do not remove it from the environ-
ment, but rather relocate it to other environmental compartments (Sects.
7.3.4, 7.4.4, 7.5.4). Included among those mechanisms which result in
actual dissipation of endrin from the environment are (1) microbial
degradation (Sect. 3.2.1), (2) thermal decomposition (Sect. 2.4), and
(3) photodecomposition (Sect. 2.4). The major product of these reactions
is ketoendrin, which, while more persistent than endrin itself, is sig-
nificantly less toxic to mammals (Sect. 6.2.3).
Relatively few bacteria (2 to 17%) isolated from soil are capable
of degrading endrin. When degradation does occur, ketoendrin is the
predominant metabolite, although other products, including endrin aide—
hyde and endrin alcohol, have also been detected. Anaerobic conditions
generally favor microbial degradation; bacterial transformation increases
with increasing depth of field soil and when soils are flooded (Sect.
3.2.1).
Toxicity of endrin to bacteria manifests as growth inhibition.
However, endrin does not appear to be highly toxic to most species of
bacteria. A correlation between bacterial sensitivity to endrin and
gram response appears to exist. Gram—negative and gram—variable bacteria
grown on solid medium were not affected by surface films of 0.5 mg of
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3
endrin per milliliter; but 50% of gram—positive cultures experienced
growth inhibition under identical conditions (Sect. 3.2.2).
Endrin is degraded to ketoendrin and other metabolites by many
species of algae and fungi as well (Sects. 3.3 and 4.2). The extent to
which degradation occurs varies considerably among the different organisms.
Over 70% of radiocarbon—labeled endrin was recovered unchanged from cul-
tures of Aspergillus niger, while an unidentified yeast culture metabolized
80.6% of the added endrin to ketoendrin (Sect. 4.2). Blue—green algae
bioconcentrate endrin manyf old; however, the degree of bioconcentration
appears to increase with decreasing exposure levels. A bioconcentration
factor of 4500 was observed in Qedogonium spp. following exposure to
only 2.5 ppb.
Both endrin and ketoendrin were found to inhibit growth in the blue—
green alga Anacystis nidulans at concentrations as low as 10 ppb. Growth
inhibition was also observed in two species of nitrogen—fixing blue—green
algae. Inhibition was observed to increase with increasing endrin concen-
tration (Sect. 3.3). Reduction in radiocarbon uptake and inhibition of
cell division in marine phytoplankton occur following exposure to endrin.
Both effects were observed in a particularly sensitive species, Cyclotella
nana, at concentrations as low as 0.01 ppb (Sect. 3.3).
Vascular plants absorb, translocate, and metabolize endrin (Sect.
4.3.1). Absorption through the roots occurs in both root crops and other
types of plants. The quantity of endrin absorbed depends upon endrin con-
centration and soil type and varies considerably with plant species.
Carrots usually absorb more endrin than do other root crops.
The detection of endrin residues in aerial plant parts constitutes
evidence for translocation following root uptake from endrin—containing
soil. Foliar absorption of endrin and its subsequent translocation within
the plant have also been demonstrated. Following application of 1 C—
labeled endrin to the leaves of cotton plants, 20% of the recovered radio-
activity was found in the stalks, pods, fibers, and soil, with traces
observed in the roots and seeds.
As many as five different metabolites have been recovered from
plants, the major metabolite consisting of an endrin alcohol. Ketoendrin,
however, is the only degradation product which has been conclusively
identified (Sect. 4.3.1).
Endrin is generally nontoxic to plants; there are exceptions, however.
The ability of barley (Hordeum vulgare) seeds to germinate is reduced by
exposure to endrin, the extent of reduction being a function of both
endrin concentration and duration of exposure. Cytological studies of
the root—tip cells of the resultant seedlings revealed chromosomal aber-
rations, although obvious morphological effects were not apparent in the
roots themselves. Chromosomal abnormalities were transmitted to the C—2
generation following exposure of seeds to 1000 ppm endrin for 12 hr. A
threefold increase over the spontaneous mutation rate resulted. Meiotic
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4
cells of seedlings sprayed with a 500—ppm solution of endrin exhibited
chromosomal abnormalities at a frequency of 0.98% (Sect. 4.3.2).
The uptake of soil constituents by plants is affected by endrin
contamination of the soil. Abnormalities in uptake of calcium and iron
have been observed in several species. In addition, the quantities of
certain plant constituents are altered when plants are grown in endrin—
containing soil. Variations in amino acid composition as well as in
the levels of both macro— and microelements were observed in the aerial
portions of corn (Zea maya) (Sect. 4.3.2).
Aquatic mollusks and arthropods are exposed to endrin in the water,
sediment, and food sources. These invertebrates extract endrin from
their surroundings, continually exchanging residues between water and
body fluids until an equilibrium is attained. The equilibrium concen-
tration will depend upon both the concentration of endrin in the water
and the species involved. Bioaccumulation factors as high as 49,000
have been observed in snails (Physa sp.), with tissue concentration
reaching 492 ppm. Approximately 17% of 1 C—labe1ed endrin was recovered
from snails in the form of metabolites, indicating that biodegradation
does occur to some extent. Flushing with uncontaminated water results
in rapid elimination of endrin residues from several species of aquatic
invertebrates (Sect. 5.2.1.1).
Endrin is more toxic to aquatic arthropods than to mollusks. Clams
(Mercenaria mercenaria) and mud snails (Nessa obso Zeta) survive at levels
1000 times greater than concentrations (less than 10 ppb) lethal to
several species of marine shrimp. In some species, small changes in
concentration can make the difference between no effect and lethality.
Effective lethal concentrations depend upon factors such as temperature,
duration of exposure, and stage of development.
Other adverse effects noted in aquatic invertebrates include inhi-
bition of shell growth, abnormalities of the nervous system, and repro-
ductive dysfunction (Sect. 5.2.1.2).
Fish are exposed to endrin through the same mechanisms as are
aquatic invertebrates. The primary means of entry into the fish body
is absorption through gill surfaces, and uptake from water far exceeds
that from food. For example, in channel catfish (Ictalur us punctatus),
bioconcentration from water is 2000 times higher than from food. Endrin
Is rapidly eliminated from fish when exposure to contaminated water or
food is terminated.
Mosquito fish (Garribusia affinis) biodegrade approximately 25% of
absorbed endrin, and one metabolite has been tentatively identified as
9—hydroxy endrin. No evidence for biotransformation is available for
other species of fish (Sect. 5.2.2).
Endrin is the most toxic to fish of the common organochlorine
insecticides. The concentration lethal to 50% of experimental fish
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5
(LC 50 ) following 96 hr of exposure is below 1 ppb in many species; 24—hr
LC 50 values of less than 1 ppb are not uncommon. The margin of safety
for lethality in fish exposed to endrin is also exceedingly narrow. Spot
(Leiostomus xanthurus) flourish at 0.05 ppb, but a concentration of
0.1 ppb causes 100% mortality in five days. The primary effect of
endrin in fish is on the nervous system. The brains and nervous tissue
of endrin—resistant mosquito fish absorb three to four times less endrin
than do those of endrin—sensitive fish. Cell membrane fractions from
brains of endrin—resistant fish bind twice as much endrin as those from
susceptible fish, thus reducing the amount of endrin entering the cell.
The increased binding of endrin to myelin tissue in the brain observed
in fish which succumb to endrin toxicity probably results in interference
with nerve transmission. Other effects on fish include reproductive
abnormalities, decreased growth, impaired liver function, pathological
changes in the gills and pancreas, enzyme inhibition, and increased
whole—body lipid.
Birds are exposed to endrin primarily through ingestion of contami-
nated aquatic organisms and water. Endrin is absorbed by the gut and
transported to various body tissues where accumulation occurs. Adipose
tissue contains the highest levels of endrin, while brain tissue contains
the lowest. Accumulation of endrin is proportional to the quantity
ingested. Endrin ingested by laying hens is also transmitted to their
eggs, and a direct relationship between dosage and accumulation exists.
No evidence for biotransformation of endrin by avians has been
found (Sect. 5.3.1).
Lethality is the most frequently observed toxic effect in birds.
Of 89 chemicals tested, endrin proved most toxic to all of four avian
species studied (bobwhites, mallards, pheasants, and Japanese quail).
Concentrations of endrin in feed ranging from 14 to 22 ppm produced 50%
mortality in each species after eight days (five days of exposure to
contaminated feed followed by three days of noricontaminated feed).
The lowest daily oral dose for mallards which produced one or two deaths
in 30 days was 0.125 ppm. Juvenile birds appear more susceptible to the
toxicity of endrin than do adults; males succumb more readily than do
females (Sect. 5.3.2).
Endrin appears to affect the central nervous system prior to death.
Symptoms such as nervousness, tremors, muscular incoordination, and con-
vulsions have been observed in a variety of species (Sect. 5.3.2).
Effects on reproduction have also been observed. Egg production,
hatchability, and viability of chicks were significantly reduced in
pheasants receiving 10 ppm endrin in their feed during the reproductive
period. Reduced chick viability was also observed in quail following
ingestion of feed containing 1.0 ppm endrin (Sect. 5.3.2).
The metabolism, distribution, storage, and excretion of endrin have
been studied extensively in only one type of insect, the larvae of tobacco
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6
budworin (Heliothis virescens fabrieius). Following topical application
of radioactive endrin, the distribution and extent of accumulation in
various tissues were identical in both endrin—resistant and —sensitive
strains. The rate of cuticular penetration was, however, greater in
sensitive strains. Both strains metabolized endrin to ketoendrin and
endrin aldehyde, but two additional metabolites were also produced by
the resistant larvae. Most of the radioactivity excreted by both strains
consisted of unchanged endrin (Sect. 5.4.1).
The basis of endrin toxicity to insects has not yet been experi—
mentally determined; however, it is known that endrin affects the
central nervous system, and the ganglia are believed to be the site of
action (Sect. 5.4.2).
Sublethal concentrations of endrin were not mutagenic in the fruit
fly (Drosophila melanogaster), nor did they affect reproduction or sur-
vival of progeny in lady beetles (Colcomegillar macuZata De Geer) and
red cotton bugs (Dysdercus koenigii). The only other sublethal effect
observed has been inhibition of acid and alkaline phosphatases in the
coccid (Dactylopus confusas) (Sect. 5.4.2).
Wild and domestic mammals are exposed to endrin primarily through
ingestion of treated foliage, although dermal contact and inhalation
also occur. Endrin shows little tendency to accumulate in tissues other
than adipose tissue; levels ranging from 0.01 ppm (in cows) to 23.7 ppm
(in lambs) have been detected in both internal and external fat of a
variety of species following ingestion of endrin—fortified food. Endrin
residues have been detected in milk from endrin—fed cows under natural
as well as experimental feeding conditions. Levels found were propor-
tional to both quantity and duration of endrin ingestion (Sects. 5.5.1
and 5.5.2).
Metabolism of endrin has been studied extensively in the rat (Sect.
6.2.3). Endrin is rapidly metabolized in the liver and excreted as hydro—
philic inetabolites. The biological half—life in male rats receiving
0.4 ppm in the diet is two to three days. In female rats, which metabo-
lize endrin more slowly, the half—life is four days. In rats, both
endrin and its metabolites are excreted primarily in the feces; in
rabbits, excretion is primarily via the urine.
Endrin is highly toxic to all mammals regardless of route of expo-
sure (Sect. 6.3.2). However, it is also rapidly eliminated, so the
return to normal among those that survive is also rapid. The primary
effect of acute exposure is on the central nervous system. When lethal
concentrations are administered, convulsions may occur as soon as 30 mm
after exposure; convulsions can culminate in death through respiratory
failure in about 48 hr. The dose lethal to 50% of experimental animals
ranges from 0.3 mg/kg for the monkey to 50 mg/kg for the goat (Sects.
6.3.2 and 5.5.1).
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7
Many instances of mammalian fatalities have been reported outside
the laboratory. Field application of endrin at rates of 0.55 to 2.75 kg/ha
resulted in the death of 33 to 100% of various species of wild mice.
Forty—two percent of a herd of cows accidentally died after being sprayed
for flies with a 0.34% solution of endrin (Sects. 5.5.1 and 5.5.2).
The chronic toxicity of endrin to mammals is greater than that of
other organochiorine pesticides (Sect. 6.3.3). Sublethal effects in wild
animals manifest primarily as disorders of behavior and reproduction;
improper maternal care, temporary loss of normal activity, and increased
vulnerability to predators are examples of the former, while reduced
reproductive potential, increased postnatal mortality, and fetal death
typify the latter (Sect. 5.5.2).
Laboratory studies have revealed an extensive array of adverse
effects in mammals following chronic exposure to endrin (Sect. 6.3.3).
Endrin can affect the central nervous system at doses substantially below
lethal or convulsive levels. For example, electroencephalogram changes
were observed in squirrel monkeys which received a total endrin dose of
1 mg/kg; seizures were not observed until 10 mg/kg. Exposure of a variety
of species to various doses of endrin via several routes produced diffuse
degenerative changes in one or more of the following organs: liver,
kidney, heart, brain, lung, adrenal glands, and spleen. Inhalation of
0.36 ppm for 118 seven—hour periods was sufficient to produce pneumonitis
in rabbits. Ingestion of 3 ppm for 19 months resulted in enlargement of
the kidneys and heart in dogs, while 5 ppm for two years produced increases
in liver weight in rats (Sect. 6.3.3). Additional effects included blind-
ness, hypertension, bradycardia, changes in carbohydrate metabolism,
abnormalities of electron transport, abnormal trace—metal mobilization,
changes in blood composition, lethargy, avoidance of food, weight loss,
vomiting, and others (Sect. 6.3.3).
No malignancies attributable to endrin exposure have been reported
in the literature; however, endrin has been found to cause chromosomal
aberrations in rats following intratesticular injection (Sect. 6.3.4).
Teratogenesis, growth retardation, and increases in fetal and postnatal
mortality have been observed in rats and hamsters following ingestion
of endrin (Sects. 6.3.4 and 6.3.5).
Chronic exposure to endrin may also be fatal. Five to eight ppm in
the diet was fatal to dogs in 18 to 44 days. Twelve ppm in the diet for
life decreased the survival time for rats. Deer mice succumbed to a diet
which contained only 2 ppm endrin (Sect. 6.3.3).
Development of endrin resistance has been observed in pine mice
(Pityrnys pinetoriuin). Resistance was shown to be hereditary as well as
acquired (Sect. 5.5.2).
Human exposure to endrin occurs through the diet, through inhalation,
and through dermal contact. The average dietary intake in the United
States in 1973 was 0.033 iig/day for a 69.1—kg man. This level is far
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8
below the maximum acceptable daily intake of 138.2 .ig/day established
by the World Health Organization (Sect. 8.3.1). Respiratory and dermal
exposure to endrin is possible during manufacture and distribution, but
is more likely to result, directly or indirectly, from agricultural uses
(Sect. 6.2.1).
Humans do not tend to store endrin in significant quantities, and
residues are only detected in human tissue immediately after an acute
exposure. Humans fatally poisoned by endrin have been reported to have
an endrin content as high as 400 ppm in fat and 10 ppm in other tissues
(Sect. 6.2.2).
Outbreaks of human poisoning have resulted from accidental containi—
nation of foods and have been traced to doses as low as 0.2 mg/kg body
weight. The toxicity of endrin appears to result primarily from the
effects of endrin on the central nervous system. Symptoms usually
observed in victims of endrin poisoning were convulsions, vomiting,
abdominal pain, nausea, dizziness, and headache. When death occurred,
respiratory failure was the most common cause. Sixty fatalities resulted
following ingestion of 5 to 50 mg/kg during a poisoning episode in India.
Men employed in the manufacture of endrin show significantly
increased activity of hepatic microsomal enzymes. No other adverse
effects of occupational exposure to endrin have been reported (Sect.
6.3.1).
Due to the interdependency of all compartments of the ecosphere,
the adverse effects of endrin on fish and wildlife inevitably spread to
man. The most direct consequence of release of endrin into the environ-
ment is contamination of the human food supply. Humans ingest endrin—
treated agricultural produce as well as meat from steers, lambs, and
hogs that feed on contaminated vegetation. Ingestion of 20 mg endrin
per day by cows results in detectable quantities of endrin in milk;
levels of 0.25 ppm endrin in milk on a fat basis have been observed.
Aquatic invertebrates and fish may bioconcentrate considerable quanti-
ties of endrin from water and pass the endrin onto predator birds. The
contaminated fowl (or the fish themselves) may, in turn, be ingested by
humans (Sect. 8.3).
Although contamination of food by endrin still occurs to some extent,
it is apparently decreasing. The frequency of endrin occurrence in food
in 1973 (0.3%) was considerably less than the average frequency of occur-
rence over the six—year period 1965 to 1970 (2.05%). At present, levels
are 4000 times lower than those acceptable to the World Health Organization.
Endrin therefore does not pose a hazard to the general population, and
concern over the possible occurrence of levels capable of threatening
human health is needed only in the geographical locations where the pesti-
cide is used extensively.
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9
1.2 MAJOR CONCLUSIONS
1. The use of endrin is confined, primarily, to the southeastern and
delta states of the United States.
2. Environmental contamination by endrin appears, for the most part,
to be restricted to those areas where endrin is used intensively.
3. Background concentrations in the atmosphere, hydrosphere, and
lithosphere, far removed from agricultural areas where endrin is
applied and industrial areas where endrin is manufactured, are
generally below the levels of detection.
4. Transport of endrin to remote areas and to the open ocean is
expected to occur primarily via the atmosphere.
5. Monitoring data for endrin in the atmosphere are limited due to
the difficulties inherent in ambient air sampling.
6. Endrin is dissipated from the environment by photochemical and
thermal decomposition and by microbial degradation.
7. The major product of endrin decomposition under most natural
conditions is ketoendrin.
8. Relatively few bacteria are capable of degrading endrin, and
degradation occurs most readily under anaerobic conditions.
9. Many species of algae and fungi are capable of endrin degradation.
10. Bioaccumulation of endrin has been observed in blue—green algae,
and growth inhibition has been observed in various species of
algae and phytoplankton following exposure to endrin.
11. Vascular plants absorb, translocate, and metabolize endrin.
12. Endrin generally is nontoxic to plants.
13. Aquatic invertebrates and fish bioconcentrate significant quanti-
ties of endrin from the water.
14. Endrin is more toxic to aquatic arthropods than to mollusks and
is the most toxic to fish of all the commonly used organochiorine
insecticides.
15. The primary effects of endrin on fish are disorders of the central
nervous system, culminating in death.
16. Avians are exposed to endrin primarily through ingestion of con-
taminated aquatic organisms and water.
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10
17. Endrin is extremely toxic to birds, and lethality is the most
frequently observed effect.
18. The basis of endrin toxicity in insects has not yet been determined,
but the central nervous system is believed to be the site of action.
19. Endrin is highly toxic to all mammals regardless of the route of
exposure.
20. Endrin does not persist in mammals, since it is rapidly degraded
and eliminated.
21. Acute exposure of mammals results in central nervous system dis-
orders, with convulsions leading to death through respiratory
failure within two days.
22. Chronic exposure may result in damage to the liver, kidneys, heart,
brain, lung, adrenal glands, and spleen.
23. Behavioral abnormalities, reproductive disorders, changes in carbo-
hydrate metabolism, changes in blood composition, and other effects
secondary to central nervous system disorders have been observed
following chronic exposure of mammals to sublethal doses of endrin.
24. While no malignancies attributable to endrin have been reported,
chromosomal abnormalities and teratogenesis have been induced by
endrin in several mammalian species.
25. Endrin residues have only been detected in human tissue immediately
after an acute exposure.
26. Symptoms of acute endrin exposure in humans include convulsions,
vomiting, abdominal pain, nausea, dizziness, and headache, with
death resulting from respiratory failure.
27. The effects of chronic endrin exposure in humans remain speculative.
28. Human exposure to endrin from ingestion of contaminated food is
decreasing.
29. The possibility of the food supply being contaminated to an extent
that it poses a threat to human health exists only in those areas
where endrin is used extensively.
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2. PHYSICAL AND CHEMICAL PROPERTIES AND ANALYSIS
2.1 SIThINARY
Endrin, a member of the cyclodiene insecticides, is a cyclic
hydrocarbon having a chlorine—substituted methanobridge structure. It
is synthesized by the oxidation of isodrin at temperatures below 100°C.
The product is then normally stabilized by the addition of hexamethylene
tetramine to remove traces of acid, which are responsible for spontaneous
exothermic conversions.
Technical—grade endrin is a light tan powder, which is stable in the
presence of oxidizing agents and alkaline reagents. However, exposure to
acids or sufficient heat can catalyze molecular rearrangement.
Since the only methods for removal of endrin from the environment
appear to be microbial degradation, photodecomposition, and thermal
decomposition, the last two physical liabilities of endrin are quite
significant to environmental distribution and longevity.
Many techniques for endrin determination have been reported, including
bioassay, total chlorine content, silylation, acetylation, spectro—
photometry, and colorimetry. The most sensitive qualitative and
quantitative methods available involve variations in gas chromatography.
2.2 NOMENCLATURE, STRUCTURE, AND SYNTHESIS
Endrin (l,2,3,4,lO,l0—hexachloro—6,7—epoxy—l,4,4a,5,6, 7,8,8a—
octahydro—l,4—endo, endo—5,8—dimethanonapthalene) is the common name
for one member of the cyclodiene group of insecticides (Shell Chemical
Company, 1959). The cyclodiene insecticides are cyclic hydrocarbons
having a chlorine—substituted methanobridge structure.
Endrin contains at least 92% of the endo—endo stereoisomer of
dieldrin or the epoxide of isodrin. Compound 269 and Mendrin are
two additional names given to endrin; the former was used by the Hyman
Company during its developmental stages, and the latter is the trade
name used in South America and India (Shell Chemical Corporation
Handbook, 1959).
The two most common technical systems used in naming endrin are the
British and American. In the British system the prefixes exo and endo
are applied to the methanobridges according to positioning outside or
inside the bent cage structure as a whole. The first prefix that appears
in the name refers to the methanobridge of the lowest numbered nucleus
(1 through 4), while the second prefix applied to the methanobridge is the
highest numbered nucleus (5 through 8). Thus, following the British system
of nomenclature, the chemical name of endrin is 1, 2 ,3,4,lO,lO—hexachloro—
6, 7—epoxy—l, 4, 4a ,5,6,7,8, 8a—octahydro—exo—l—4 , exo—5 , 8—dimethanonaphthalene.
11
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12
In the American system the terms exo and endo indicate which pairs of
exo or endo bonds of each of the norbornene nuclei are used to fuse the
two ring systems together; each prefix, therefore, defines the stereo-
chemistry of the norbornene nucleus to which it applies (Soloway, 1955).
Accordingly, the chemical name for endrin is l,2,3,4,lO,1O—hexachloro—6,7-
epoxy—l,4, 4a,5, 6,7,8, 8a—octahydro—l, 4—endo endo—5, 8—dimethanonaphthalene.
Both of these systems of nomenclature name endrin as a derivative of
octahydro—dimethanonaphthalene. The structural differences between endrin
and other members of the cyclopentadienes are indicated by the use of the
terms exo and endo (relative position of methanobridges in each compound).
Benson (1969), recognizing that none of the compounds of the cyclopentadiene
series was aromatic, recommended the use of the von Baeyer system, which is
widely used and endorsed by the International Union of Pure and Applied
Chemistry (IUPAC) in naming the polycyclic aliphatic compounds. According
to the von Baeyer—IUPAC system, endrin is named as a derivative of
2,3,7,6—endo—2,1—7,8—endo tetracyclo (6.2.13,6.02,7) dodeca—9—ene, which
reflects the fact that it originally received its name because the two
fused norbornene ring systems present were endo—endo with respect to one
another. Therefore, Bedford (1974), using the von Baeyer—IUPAC system for
numbering and naming polycyclic aliphatic compounds, named endrin as the
l,8,9,1O,ll,ll—hexachloro—4,5—exoepoxy—2,3,7,6,—endo—2,l,7,8—endo tetra—
cyclo (6.2.13,6.02,7) dodec—9—ene, which corresponds to the structure
shown in Fig. 2.1.
ORNL—DWG 79—8438
H
Fig. 2.1. Stereochemical structure of endrin, using the von Baeyer—
IUPAC notation (1 ,8,9,10,11,11 —hexachloro—4, 5—exoepoxy—2, 3,7, 6—endo—2, 1,
7,8—endo tetracyclo [ 6.2.13,6 dodec—9—ene).
C I
H
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13
For the purpose of this review, the American system of nomenclature
will be used.
The chlorinated component (left side) of the endrin molecule, which
represents 75% of its mass, is structurally identical to the other
members of the cyclodiene group, including alodan, aldrin, dieldrin,
isodrin, heptachlor, chiordane, and isobenzan.
Roll et al. (1969) applied the nuclear quadrupole resonance (NQR)
technique in order to determine the structure of endrin. The NQR spectrum
of endrin was found to exhibit five major resonance frequencies. The
resonance of both vinylic chlorine atoms appeared at 37.7 MHz, the bridge
dichloromethylene chlorine atom resonances occurred at 36.3 and 37.0 MHz,
and the remaining bridgehead chlorine atom resonances were found at 35.9
and 361 MHz.
The endo—endo characteristics of endrin were substantiated by the
work of Keith (1971), who, in an effort to study the degradation reactions
of some pesticides, implemented the use of paramagnetic resonance spectro—
scopy (PMR), which employs a chemical—shift reagent Eu(DPM) 3 , tris(dipi—
valomethanato europium). Previously, Keith and co—workers (1970) found
that the special feature of the PMR spectra of endrin was the splitting of
the H 2 , H 7 signal into a pair of doublets due to the coupling of H 2 with
H 3 and H 6 and the coupling of H 7 with H 6 and H 3 . However, this charac-
teristic of the endo—endo ring fusion was obscured by the overlap of the
H 2 , 7 and the Ht , 5 signals of endrin in CC1 . The addition of Eu(DPM) 3 to
the endrin solution shifted both the H 2 and H 1 , 5 signals down field in
such a way that the H , 5 shift was much’greater in magnitude than that
of the H 2 , 7 . By separating these two signals, the splitting of the H 2 ,
H 7 signal at the 250 H 2 sweep width is easily observed.
The application of 13 C nuclear magnetic resonance (natural abundance,
Fourier transform spectroscopy) as a means of establishing the complete
molecular configuration of endrin (including the chlorinated section of
the molecule) was undertaken by Roberts et al. (1974). The confirmation
of the resonance positions of the different carbon atoms in the NMR spectra
was successfully attained by the use of the chemical—shift reagent
tris(l,1,l,2,2,3,3—heptafluoro—7, 7—dimethyl—4,6—octanedionate)
europlum(III), Eu(FOD) 3 , as suggested by Rondeau and Sievens (1971).
Endrin is produced by the oxidation of isodrin, with hydrogen peroxide
in acetic acid, at the lowest temperature possible (Fig. 2.2). At 100°C,
isodrin rearranges to a ketone that has no insecticidal effect (Melnikow,
1971).
The precursor of endrin, isodrin, is prepared by the condensation of
cyclopentadiene with 1,2,3,4,7, 7—hexachlorobicyclo— (2.2. l)—2 , 5—heptadiene
according to the reaction shown in Fig. 2.3, whereas the 1,2,3,4,7,7—
hexachlorobicyclo—(2.2.l)—2,5—heptadiene is produced by reacting
hexachloropentadiene with vinyl chloride, followed by dehydrochlorination
with an inorganic base (Fig. 2.4).
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14
ORNL—DWG 79—8139
ISODRIN (4) ÷ ACETIC ACID—HYDROGEN PEROXIDE—’ENDRIN
CI H CI H
H
0
+ CH 3 — —oOH
CI
H 2 02
CI
Fig. 2.2. Synthesis of endrin.
4,2,3,4, 7, 7— HEXACHLOROBICYCLO—(2.2.4)—2,5—HEPTADIENE +
CYCLOPENTADIENE ISODRIN
CI
ORNL—DWG 79—8140
Fig. 2.3. Synthesis of isodrin.
ORNL—DWG 79—8144
4 1 2,3,4,5,7,7—HEPTACHLOROBICYCLO—(2.2.1)-HEPT—2—ENE +
INORGANIC BASE — 4, 2,3,4,71 7—HEXACHLOROBICYCLO—(2.2.l)—
2, 5—HEPTADIENE
CI
c . N.. H
I I I _____
Ilcic c i I
ci 4 ,,2 H 2
CI
Fig. 2.4. Synthesis of 1,2,3,4,7,7—hexachlorobicyclo—(2 ,.2.1)—2,5_
h eptadiene.
BASE
CI
CI
CI
CI H
CI I-I
CI
CI H
-------
15
The endo—endo isomers, like endrin, are less stable than the endo—exo
isomers such as dieldrin. Therefore, endrin formulations are stabilized
by the addition of small amounts of hexamethylene tetraamine (Shell
Chemical Corporation, 1959), inorganic or organic nitrites, epichlorohydrin
and glycidyl ethers (Bellin, 1956), or various alkaline—metal carbonates
(urea, etc.) to remove traces of acid that are responsible for spontaneous
exothermic conversions.
The composition of a typical production batch of endrin as reported
by Shell Chemical Corporation (1959) is shown in Table 2.1.
Table 2.1. Chemical composition of technical endrin
Compound Percent (wt)
Endrin 96.6
Dieldrin 0.42
Aldrin 0.03
Isodrin 0.73
1,2,3,4,7, 7—Hexachloro—l,4—dihydro—l, 4—xnethanobenzine 0.03
l,2,3,4,5,7,7—Heptach loro—1,4,5,6—tetrahydro—l,4—
methanobenzene (heptachloronorbornadiene) 0.08
1,2,3,4,5—Pentachloro—7—oxo—l,4,5,6—tetrahydro—l,4—
methanobenzene (heptachloronorbornene) 0.09
Endrin half—cage ketone (L —ketoendrin; C 12 H 8 C1 5 O) 1.57
Endrin aldehyde (C 12 H 8 C1 6 0) <0.05
Acidity (calculated as HC1) 0.18
Unidentified components 0.12
Source: Shell Chemical Corporation, 1959.
2.3 PHYSICAL AND CHENICAL PROPERTIES
Chemically pure endrin is a white crystalline solid, while technical—
grade endrin is a light tan powder (Brooks, l974a). Endrin is described
as being insoluble in water, only 0.19 ppm (Robeck et al., 1965),
sparingly soluble in methanol, of relatively low solubility in aliphatic
hydrocarbons (0.3 lb/gal), and quite soluble in aromatic solvents
(3.0 lb/gal) (Brooks, l974a).
Technical—quality endrin, as well as the purified cyclodiene, is
stable in the presence of wetting agents, emulsifiers, alkaline oxidizing
agents, and basic reagents. However, the endo—endoconfiguration is
vulnerable to molecular rearrangement catalyzed by acids or heat. Endrin
will melt with this consequent decomposition at 200°C. Therefore, endrin
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16
is susceptible to some carriers used in synthesis, and this decomposition
mechanism is deactivated by the addition of hexamethylenetetramine.
Chemically pure endrin is stable upon exposure to either light or air.
However, exposure to Lewis acids, heat, or ultraviolet radiation induces
the formation of aldehydes, alcohols, or ketones.
Endrin is nonflammable (Robeck et al., 1965), and it has a vapor
pressure of 2 x l0 mm Hg at 25°C. A specific gravity of 1.7 at 20°C
is also typical of the compound (Brooks, 1974a).
The chlorine content of endrin accounts for between 55 and 57% of its
molecular weight, which is 380.9. Endrin contains less than 0.1 wt %
water and less than 0. 4 wt % free acid (calculated as acetic acid). Less
than 0.5% of endrin remains as an insoluble residue after solubilizing in
xylene (Brooks, l974a).
Table 2.2 contains a compilation of the physical and chemical
properties of endrin.
Table 2.2. Physical and chemical properties of endrin
Color White (purified grade)
Light tan (technical grade)
Physical state Crystalline solid (purified grade)
Powder (technical grade)
Melting point 200°C (decomposition)
Vapor pressure 2.7 x i0 nun Hg at 25°C
Specific gravity 1.7 at 20°C
Chlorine content 55 to 57 wt %
Water content 0.1 Vt %
Free acid content 0.4 wt % (acetic acid)
Solubility 31 g/lOO ml acetone at 25°C
28 g/l00 ml amylacetate
51 g/l00 ml benzene
51 g/l00 ml carbon tetrachloride
10 g/lOO ml diesel oil
3 g/100 ml ethanol
87 g/lOO ml ethylene dichioride
10 g/100 ml fuel oil
3 g/lOO ml isopropano].
5 g/100 ml kerosene
2 g/l00 ml methano’.
40 g/lOO ml methyl ethyl ketone
74 g/lOO ml toluene
21 g/l00 ml turpentine
55 g/100 ml xylene
Source: Reprinted with permission from C. T. Brooks, Chlorinated
Insecticides, Vol. 1, Technology and Application, 1974. Copyright
The Chemical Rubber Co., CRC Press, Inc.
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17
Endrin reacts to give products of simple ring opening with both neutral
and acidic agents (Lidov et al., 1950). Soloway et al. (1960) obtained
a significant product of endrin rearrangement by ref luxing for 23 hr
(with vigorous stirring) a mixture of 25 g endrin, 100 ml butyl ether,
and 100 g concentrated hydrochloric acid. The new compound, a pentacyclic
ketone (Fig. 2.5, structure 10), was also obtained by heating 2 g endrin in
a test tube at 150°C. The exothermic reaction occurred when the tempera-
ture rose to 278°C. In the acid—catalyzed rearrangement, the conjugate
acid of endrin was said to undergo ring opening of the oxirane group with
the formation of a bond between carbons 4 and 10. The extra charge left
on carbon 9 is stabilized by a hydride shift from carbon 5 and a loss
of a proton from oxygen to give the pentacyclic ketone.
Skerrett and Baker (1959) treated endrin with boron trifluoride in
benzene solutions and obtained two separate compounds, the half—cage ketone
(Fig. 2.5, structure 3) and the pentacyclic aldehyde (Fig. 2.5, structure
2). On the other hand, Weineke and Burke (1969) showed that treatment
of endrin with zinc chloride in hydrochloric acid converted endrin to the
half—cage ketone without any other by—products (Fig. 2.5, structure 3).
ORNL—DWG 79—8134
CAGE
ALCOHOL
HALF — CAGE
KETONE
PENTACYCLIC
ALOE HYDE
C I H
CI
CI
CI
C I
D(v), c,m
CI
CI CH O
me
CI
CI
Fig. 2.5.
Schematics of some chemical reactions of endrin.
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18
Further treatment of the ketone with lithium aluminum hydride produced
the cage alcohol as shown in Fig. 2.5, structure 4. Brooks (1974a),
utilizing the results of Adams and Mackenzie (1969), suggested that
endrin was reductively dechlorinated with sodium methoxide in
methanol—dimethylsulfoxide in order to give analogues in which one of
the chlorine atoms in the methanobridge was replaced by hydrogen (Fig. 2.5,
structure 9); presumably, this conversion occurred without skeletal
rearrangement.
In connection with derivative formation for identification of endrin
residues by gas chromatography, Chau and Cochrane (1969) found that
treatment with concentrated sulfuric acid at room temperature for 10 to
15 mm caused the isomnerization of endrin to an aldehyde and a ketone
(Fig. 2.5, structures 2 and 3). Further investigations into derivative
formation (Chau and Cochrane, 1971) produced the reduction of endrin by
chromous chloride to yield a pentachioro derivative whose elemental
analysis, IR and NMR spectroscopy, suggested structure 7, Fig. 2.5, but
treatment of endrin with chromous acetate under acidic conditions
produced small amounts of the isonieric ketone (Fig. 2.5, structure 8)
(Chau, 1972). Endrin also reacts with bromine to form the 4,5—dibromide,
which, in turn, reacts with sodium sulfide enneahydrate to form the
4,5—episulfido compound, producing the sulfoxide upon oxidation (Metcalf,
1955).
The electrochemnical reduction of endrin was studied by Bukowsky and
Cisak (1968). Their results indicated that the il—endo chlorine was
first to be replaced followed by both chiorines in positions 9 and 10.
The bridgehead chlorines (positions 1 and 8), which are equivalent, were
the last to be replaced.
2.4 INPLICATIONS OF CHEMICAL AND PHYSICAL PROPERTIES FOR BEHAVIOR
OF ENDRIN IN ORGANISMS, MEDIA, STORAGE, AND AGRICULTURE
In order to determine the chemical nature of toxicity, Soloway (1965)
examined the insecticidal action of 106 cyclodienes. High insecticidal
activity was found only in those compounds with two centers of electro—
negativity placed close to each other and situated in the plane of
symmetry as defined by the dimethanobridge. Consequently, there were
very small differences in insecticidal action among aldrin, dieldrin, endrin,
and telodrin. The similarities in biological effects caused by these
pesticides on the central nervous systems suggest that all of them act
on the same sites. According to Benson (1969), the electron—rich sites
of these molecules, which were not believed to be chemically active, are
most likely locations for strong electrostatic interaction possible on
nerve cell membranes.
Further results of Soloway (1965) suggested that the epoxides were the
active compounds, while only those other compounds in which the double bond
of the nonchlorjnated side of the molecule is readily epoxidized display
insecticidal activity. The rigid—cage configuration of the cyclodiene
compounds possessing electronegative centers in their chlorine atoms and
their lipid—soluble characteristics is believed to be important to their
passage across membranes as well as their molecular action (Hathway, 1965).
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19
The major products resulting from the photochemical and thermochemical
isomerization of endrin have been identified, and their structures, along
with that of the parent compound, are presented in Fig. 2.6. Since these
two processes and microbial decomposition are the only means of endrin
degradation, they are significant parameters for environmental distribution.
ORNL—DWG 79—8135
I ENDRIN
C I
CI
UENDRIN KETONE
V DECHLORIATED ENDRIN KETONE
Fig. 2.6. Some thermal and photochemical degradation products of
endrin. Source: modified from Plimmer, 1971.
Photolysis of solid endrin (I) by exposure to a germicidal lamp gave
a 37% yield of endrin ketone (II) and a 9% yield of the aldehyde (III).
These compounds together with a small quantity of the “bird—cage” alcohol
(IV) have also been identified following the thermal isomerization of
endrin (Plimmer, 1971). Photolysis of endrin in hexane gives a
monodechiorinated ketonic compound (V). The dechlorinated endrin isomer
has been identified in the field as well (Klein and Korte, 1967).
Mitchell (1962) and Roburn (1963) accomplished the photochemical
isomerization of endrin by exposing samples of the pesticide to ultraviolet
CI
C,
CI
CI
in ENDRIN ALDEHYDE
CI
H
I ENDRIN ALCOHOL
-------
20
light. Rosen et al. (1966), extending Roburn’s work, found that exposure of
endrin to a 2537—A germicidal lamp for 48 hr yielded 37% ketone and 9%
aldehyde. The infrared spectra of these two isomers were identical to
those published by Phillips et al. (1962). The mechanism of isomerization
of these two carbonyl compounds from endrin involves either a hydride
shift or hydrogen abstraction of an epoxy hydrogen, while photosensitizers
such as rotenone appear to enhance the photochem ca1 alteration (Ivie
and Casida, 1970). Zabik et al. (1971), using a somewhat different
approach, studied the photolytic decomposition of endrin in solution.
Hexane and cyclohexane solutions of endrin were exposed to uv sources
(253.7 to 300 nun) and sunlight. The extent of the reactions were followed
by both gas chromatography and IR spectroscopy. Irradiation of hexane
solutions of endrin gave essentially the same results as those obtained
with cyclohexane. The photolysis of endrin, using uv light or sunlight,
proceeded with the formation of a half—cage ketone compound 1,8—exo—
9,ll,ll—pentachloro—pentacyclo—(6.2. 1.1. 3,6.02 ,7.0 ,10) dodec—5—one.
This photoproduct of endrin was found to be highly resistant to the usual
oxidation and reduction processes (Fig. 2.5, structure 5). However, the
only significant reaction of the molecule was that of a trans—annular
enolizarion (homoenolization) in the presence of bases to give the
pentachioro—cage alcohol. Its suggested structure based on IR, uv, and
NMR spectroscopy is shown in Fig. 2.5, structure 6.
The rate of photoconversion of endrin in the solid state to its
isomerides on exposure to natural sunlight was studied by Burton and Pollard
(1974). Individual glass planchets containing 10 mg endrin were exposed to
natural sunlight. At intervals, samples were removed from the sunlight
and analyzed for the disappearance of endrin and for the appearance of
ketoendrin by infrared spectroscopy. The experiment was conducted
once in June and once in October in order to assess the effects of sunlight
intensity of the reaction rate. The results for both trials are presented
in Table 2.3 and in Figs. 2.7 and 2.8. The intensity of the sunlight is
apparently a very important factor in determining the rate of isomerization,
since the disappearance of endrin and the conversion to ketoendrin were
considerably more rapid in June than in October. The change in the slope
of the curves in Fig. 2.7 after nine days is also indicative of a
decreasing rate of isoinerization and probably reflects the diminishing
intensity of the October sunlight toward the end of the month.
Table 2.3. Endrin photoproduct formed vs sun’s intensity
Days exposed
I4onth
Isomeric
(II) form
ketone
ed (%)
5
October
14
5
June
46
12
October
30
12
June
65
Source: W. B. Burton and G. E. Pollard, Bull. Environ. Contain.
Toxicol. 13(1): 113—116 (1974). Copyright 1974 by Springer-Verlag.
-------
Li
ORNL-DWG 79-8436
10
8
6
4
2
0
20
Fig. 2.7. Photochetnical isomerization of endrin. Source:
W. B. Burton and G. E. Pollard, Bull. Environ. Contain. Toxicol.
13(1): 113—116 (1974). Copyright 1974 by Springer-Verlag.
ORNL-DWG 79-8137
fO
8
6
4
2
0
30
Fig. 2.8. Photochemical isomerization of endrin. Source:
W. B. Burton and G. E. Pollard, Bull. Environ. Contain. Toxicol.
13(1): 113—116 (1974). Copyright 1974 by Springer-Verlag.
LU
z
LU
C)
LU
0
U)
0
z
0
z
LU
U-
0
E
0 5 10 f5
DAYS EXPOSED TO JUNE SUNLIGHT
LU
z
0
F-
LU
C)
U i
0
U)
c
0
0
z
LU
U-
0
0
E
0 6 12 18 24
DAYS EXPOSED TO OCTOBER SUNLIGHT
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22
Phillips et al. (1962), in studying the gas chromatographic behavior
of endrin at 230°C, found that this compound gave two peaks of almost equal
size and that neither one of the two peaks was due to endrin. In order
to evaluate this finding, endrin was placed in a potassium bromide dish
and heated to 240°C. Infrared spectra, as well as gas chromatographic
analysis of the reaction products, showed that the two peaks found in the
gas chromatographic analysis of endrin corresponded to two different
compounds, namely, a ketone and an aldehyde (Fig. 2.5, structures 2 and 3).
The isomerization of endrin to ketoendrin over a five—year dark
storage period at room temperature was reported by Barlow (1965).
Apparently, the isomerization process at room temperature was triggered
by impurities present in the endrin sample. Later studies carried out
by Graham and Kenner (1969) showed that heat—induced decomposition of
endrin in KBr dishes or in the open followed the same route, regardless of
temperature, to give a large excess of the ketone isomer over the aldehyde
isomer. This finding led to the recommendation that endrin standards
should be stored in opaque bottles below room temperature, and that
standards should be evaluated for composition before use.
2.5 METHODS OF ANALYSIS
The preparation of samples prior to endrin extraction varies according
to the type of material to be analyzed. In general, pulverized or dust
formulations require min:imal preparation, whereas human, animal, or plant
tissues are minced or blended into homogenates. Appropriate sample
aliquots are then extracted with solvents such as acetone, benzene,
toluene, hexane, petroleum, ether, pentane, or any combination of these
polar—nonpolar solvents (Chau, l972b; Reinke et al., 1973; Bontoyan and
Jung, 1972; Stalling et al., 1972; Young and Burke, 1972; Ali et al.,
1969; Goodwin et al., 1961).
Endrin extraction is accomplished by either maceration of the samples,
exhaustive extraction in a Soxhlet apparatus, or dynamic equilibration
(shaking) for a predetermined period of time. Elution of the sample
through a chromatographic column is also used and recommended in some
analytical procedures; however, the extraction procedure used is
dependent upon the type of material to be analyzed. Fibrous materials
such as plant tissues require longer contact with the extracting solvent
than do powders or dust formulations.
The treatment of the extract for qualitative or quantitative
measurement of endrin is determined by the nature of the extract, the
method of detection, and the desired accuracy. In a few cases it is
possible to use an analytical method in which there is little or no
interference from impurities (Biros et al., 1972; Dougherty et al.,
1972). In most cases, however, some degree of purification is necessary,
and the cleanup procedures include distillation, evaporation, solvent
fractionation, and partition chromatography through florisil, celite,
silica gel, or aluminum oxide columns.
Partition of pesticide extracts between immiscible solvents is often
used to give partition cleanup before florisil chromatography. Seven of
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23
these liquid—liquid partition techniques are fully described in the Food
and Drug Administration pesticide manual (1971).
A partitioning method for sample cleanup prior to gas—liquid
chromatography (GLC) determination of common organochlorine pesticide resi-
dues in biological samples was described by Kadoum (1969). Plant or animal
tissue hexane extracts are partitioned four consecutive times with 95%
aqueous acetonitrile solutions. The total recovery of endrin, measured
by peak height in the chromatograxn, amounted to 95% of that added to
the biological extract. Young and Burke (1972) used a microscale alkali
treatment on biological sample extract prior to endrin determination
by GLC. Endrin extracts were ref luxed with alcoholic potassium hydroxide
in the steam bath for a predetermined length of time and partitioned into
hexane. Recoveries of unchanged aidrin, dieldrin, and endrin range from
70 to 90%. Young suggested that the high recovery following alkali
treatment be used in the identity confirmation of these pesticides.
The troublesome lipid removal from fish extracts prior to GLC was
successfully accomplished by gel permeation chromatography. Using
cyclohexane and Bio Beans SX2, Stalling et al. (1972) obtained 100%
recoveries of 1 C—endrjn with less than 0.5% of the original lipid
present in the endrin fraction. In the case of fish extracts containing
endrin at concentrations below 0.1 ppm, additional cleanup with florisil
was recommended.
The analytical methods used for quantitative or qualitative
determination of endrin fall into two categories. The first consists in
using the ability of living organisms to withstand the toxicological effects
of powders, dust formulations, emulsifiable liquids, and extracts of endrin.
These techniques are classified as biological methods or bioassays. The
second category utilizes one or more physicochemical properties of endrin
as well as any available analytical instrumentation designed for the
measurement of those properties. These methods are classed as chemical
methods.
Biological methods using fish, insect larvae, aphids, and daphnia have
been described in the literature by Ali et al. (1969, 1973), Tew and
Sillibourne (1961a, 196lb), McDonald (1962), and Sun and Sanjean (1961).
All of these methods use either percent mortality or LD 50 data obtained
by submitting the test organisms to unknown concentrations of purified
or nonpurified endrin extracts. The results obtained are quantified by
comparison with mortality or LD 50 data produced by known concentrations
of endrin under the same experimental conditions. Although these methods
are convenient and relatively inexpensive, they lack sensitivity,
specificity, and, in some cases, reproducibility.
The determination of total chlorine is one of the most common chemical
methods for analysis of chlorinated pesticides. An application of this
technique to endrin analysis is described by Porter (1964). There are
many modifications to this technique, but the usual Stephanov’s procedure
involves three stages: (1) ref luxing the sample for half an hour with
metallic sodium in 99% isopropyl alcohol, (2) elimination of excess sodium,
and (3) titration of chlorine by the classical Volhart method.
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24
As an alternative to the sodium reduction procedure, the Association
of Official Analytical Chemists (AOAC) methods book (1975) uses sodium
diphenyl to liberate chlorine ions from endrin samples. In a still
different analytical procedure, endrin is treated with H 2 SO to form a
ketone derivative which possesses a definite and identifiable retention
time in the GLC (Chau and Cochrane, 1969). Similarly, HBr, Cr0 3 , and
HC1 under various conditions have been utilized for the positive identif i—
cation of endrin found in soil, vegetables, forage crops, and fat extracts
(Chau and Cochrane, 1971). An alternative confirmation test for endrin
utilizes preferential reductive dechlorination of endrin with CrCl 2 in
order to yield the pentachloroketone. This derivative has a different
retention time from the conmion organochiorine pesticides (Chau, 1970).
Woodham et al. (1972) found that endrin will form derivatives when
reacted with 10% BC1 3 —2—chloroethanol solution. The new derivative delta—
ketoendrin produced a characteristic GLC peak with longer retention time,
while the reaction time required for this conversion was only 10 mm. On
the other hand, Chau’s (1974) simplified procedure for the acid—catalyzed
isomerization of endrin uses acidified alumina microcolumns as the solid
matrix for the reaction to occur. Yields of 75% ketone I isomer were
obtained in approximately 1—1/2 hr contact time, and no interference
from chlorinated pesticide residues other than dieldrin was found to
occur. This procedure is sensitive to 1 mg endrin.
Silylation and acetylation reactions for the identification and
confirmation of the photoproducts of endrin by GLC were defined by Chau
(1972b), Ketones I and II are converted to alcohols under biphenyl
reduction for many chlorine—containing pesticides, and Lakshimarayana
(1974) proposed the Beckman (1963) method of liberating origanically
bound chlorine (ref luxing sample in a hydrocarbon solvent with a boiling
point above 100°C) with subsequent electrometric chlorine determination
based on the procedure described by Northrup (1948).
The combustion or quartz tube method and the classical Parr bomb method
initially used in composition analysis of endrin and other chlorinated
pesticides are no longer considered definitive (Gunther and Blinn, 1955).
The total chlorine method as applied to technical endrin is a
nonspecific method; that is, it determines all of the chlorinated compounds
present in the sample. However, this technique is widely used as a plant
control procedure for formulation of technical chlorinated pesticides or in
situations where the pesticide formulations or extracts are devoid of
any other chlorine—containing ingredients.
The spectrophotometric method used for the determination of endrin
and its technical formulations Is outlined in the Chemical Specialties
Manufacturers Associations chemical analysis test methods (1972) and the
AOAC methods book (1975). This method uses the absorption of endrin in the
infrared region of the spectra and employs the absorption peak at 11.76 mm
with a baseline drawn between 11.5 and 11.97 mm. The measurements are most
commonly made in chloroform or carbon tetrachloride, and recommendations
for the removal of any interfering absorption must be observed.
-------
25
A relatively new technique which generates the mass spectra of a
material, chemical ionization (CI) mass spectrometry, was described by
Munson and Field (1966). The characteristic ionization spectra of the
material in question are produced by ionic reactions rather than by
electron impact (Damico et al., 1968). The ionic reactions take place
in methane or mixtures of methane with small concentrations of other
compounds at pressures up to 2 torr within the source of the mass
spectrometer. The presence of small amounts of certain substances
produces very marked changes in the relative concentration of the ions
formed from the methane. These changes are the result of rapid reactions
between the product ions of methane and the added material. The newly
formed ions, in turn, produce a spectrum which is characteristic of each
of the substances added.
The application of CI mass spectrometry as an analytical tool for the
determination of chlorinated cyclodienes was reported by Biros et al.
(1972) and Dougherty et al. (1972). These investigators, using methane
as the reacting gas, were able to show that the CI mass spectra of
endrin were less complex than the electron impact counterpart. The
authors examined the positive and negative CI spectra of ten other poly—
chlorinated cyclodienes and pointed out the usefulness of this technique
for the determination of endrin and its degradation products. It was
also suggested that because of the simplicity of the spectra, CI mass
spectra could be applied to the direct examination of crude residue
extracts for both identity and quality.
The application of mass spectrometry coupled with gas chromatography
for endrin determination at the nanogram level was reported by Abrahamson
(1972). Although the instrumentation used iS often beyond the economic
capabilities of many analytical laboratories, the technique offers
(1) relatively uniform, high sensitivity for all materials which volati-
lize, (2) excellent selectivity from interfering materials (use of
specific ion detector or high resolution), (3) freedom from false positive
results, and (4) the ability to identify unexpected materials easily.
Colorimetric methods have been employed for residue rather than for
composition analysis. However, Terriere (1964) described a method
involving the reaction of endrin with phenyl azide to form a phenyldihydro—
triazole derivative. The triazole is dissolved in ethanol and treated
with hydrochloric acid. The resulting secondary amine Is coupled with
diazotized dinitroaniline to form an intense red color. The method is
sensitive, but requires high dilution leading to a decrease in precision.
Tewari and Sharma (1977) also reported a specific color reaction f or
endrin sensitive up to 0.05 mg endrin per 100 g of tissue.
Visweswariah and Jayaram (1971) described a semiquantitative
colorimetric procedure using acetone solutions of endrin, among other
chlorinated pesticides, hydrolyzed with monoethylamine and heat. The
hydrolyzed solutions are then treated with silver nitrate to produce a
white gelatinous turbid suspension characteristic of endrin. The procedure
can be made quantitative by comparison with predetermined turbidity
charts.
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26
Thin—layer chromatographic (TLC) techniques are regarded as simple,
quick, inexpensive, and easily reproducible. This method has been used
for the determination of endrin in commercial formulation as well as
for residue analysis. The procedure requires glass plates varying in
size from 20 x 20 cm (Bontoyan and Jung, 1972) to microslides 2.5 to 7.5 cm
(Visweswariah et al., 1971). The plates are usually covered with a
pure silica gel or an aluminum oxide layer with or without silver nitrate
(Visweswariah et al., 1971; Reinke et al., 1973; Bontoyan and Jung, 1972;
Lakshimarayana and Menon, 1971; Sherina and Bloomer, 1977). Thin-layer
chrotnatographic testing has been recommended as a confirmatory test or
for the isolation of endrin prior to its GLC determination. The TLC
procedure has also been used as a qualitative or quantitative analytical
tool. The sensitivity of the method varies between 0.1 g (GLC) to 1.0 g
endrin (visual).
The GLC methods used in the determination of endrin in commercial
formulations and residue extracts lack some precision, but are rapid,
simple, sensitive, and highly specific. The ability of the gas chroma—
tographic procedures to measure extraordinarily low levels of endrin,
from nanogram (10—s g) quantities to picogram (10—12 g) quantities, has
encouraged several scientists to look more closely to GLC methodology
for the determination and quantification of endrin in biological specimens,
environmental samples, and agricultural commodities.
In 1962, Phillips et al. developed a chromatographic technique using
710 silicone oil on GC—22 supersupport as a chromatographic column. The
two peaks found at a column temperature of 270°C were believed to be the
catalytic product of endrin isomerization due to impurities present in the
analyzed extract or the lack of cleanup procedures. Direct GLC deterinina—
tions of endrin in agricultural, atmospheric, and industrial samples were
obtained by using electron—capture—ionization detectors. Goodwin et al.
(1961) reported 95% recoveries from crop extracts (apples, broccoli,
cabbage, carrots, lettuce, etc.) containing 0.1 to 0.25 ppm endrin. The
quickness of the method, the elimination of sample cleanup, and the
versatility of the electron—capture GLC technique were emphasized by
these researchers.
Recognizing that the most vital component of the GLC technique is the
chromatographic column itself, Chau and Wilkinson (l972a) found that a
combination of OV—1O1 and OV—210 silicon oils on Chromosorb—W columns
not only provided a means of separating photoendrin (half—cage ketone)
from endrin but also retained good separation properties for the routine
analysis of other organochlorine pesticides. The retention times of
endrin and its photoproduct, using 2—1/2 SE—30 columns, were nearly
identical (Zabik et al., 1971). Hastings and Aue (1974) studied the
advantages of using chromatographic columns consisting of Carbowax
20—N modified celite covered with a 3% load of Apiezon L (Applied Science
Laboratory, State College, Pennsylvania). The presence of an ultrathin,
nonextractable film of Carbowax 20—N in a support used in typical GLC
exerts a strong effect on the state of deactivation, but does not
significantly influence the separation pattern prescribed by the liquid
-------
27
phase; furthermore, the quality of the chromatographic separation of
aidrin, dieldrin, endrin, and heptachlorepoxide was much superior when
Carbowax 20 modified celite columns rather than bare celite columns were
used.
Burke and Holswade (1964, 1966) found that during the residue
determinations of polycyclodiene insecticides by electron—capture GLC,
interferences occurred not only from peak overlap of the various pesticides
themselves, but also from extraneous contamination, for example, the
laboratory, the technique, or naturally occurring components coextracted
from the sample. The use of confirmatory procedures for the positive
identification of endrin has been suggested by several investigators
(Bowman and Beroza, 1965; Schutzmann et al., 1966; Fahey and Schechter,
1961; Bann et al., 1958; Woodham et al., 1972; Wiencke and Burke, 1969;
Chau and Cochrane, 1969, 1971 among others). These procedures involve
either of two well—known principles: (1) acid—catalyzed isomerization
or (2) derivative formation by reacting endrin with an appropriate
reagent.
Lidov et al. (1950) and Soloway et al. (1960) treated endrin with
mineral or Lewis acids and obtained the half—cage pentacycloketone
alkaline conditions, and the alcohols are silylated or acetylated. The
GLC retention times of silyl esters or acetates are different from that of
endrin. Thus, this procedure makes it possible to differentiate between
unreacted endrin and its photodegradation products.
2.6 REFERENCES
Abrahamson, F. P. 1972. Applications of Mass Spectrometry to Trace
Determination of Environmental Toxic Materials. Anal. Chem. 44(14):
28A— 35A.
Adams, C. H. M., and K. Mackenzie. 1969. Dehalogenation of Isodrin and
Aidrin with Alkoxide Bases. J. Chem. Soc. (London): 480—486.
Au, K. A., N. M. Das, and M. R. G. K. Nair. 1969. Bioassay of Insecticide
Residues on Crops. I. Persistence of Endrin Residues on Paddy. Agric.
Res. J. Kerala 7(2): 107—109.
Au, K. A., and M. R. G. K. Nair. 1973. Microbioassay of Endrin Residues
on Rice. 2. Determination of Residues on Rice Plants. Madras Agric. J.
60(7): 439—440.
Association of Official Analytical Chemists. 1975. Official Methods of
Analysis Book. AOAC, Washington, D.C.
Bairn, J. N., S. C. Lau, J. Potter, H. W. Johnson, Jr., and A. E. O’Donnell.
1958. Determination of Endrin in Agricultural Products and Animal Tissues.
J. Agric. Food Chem. 6(3): 196—202.
-------
28
Barlow, F. 1965. Spontaneous Decomposition of a Sample of Pure Endrin.
In: Ministry of Overseas Development, Tropical Pesticides Research Unit,
Portion Report No. 314.
Beckman, H. F. 1963. Analytical Methods for Pesticide, Plant Growth,
Regulators, and Food Additives. Vol. I. Academic Press, New York, p. 269.
Bedford, C. T. 1974. VonBaeyer/IUPAC Names and Abbreviated Chemical
Names of Metabolites and Artifacts of Aidrin (}IIIDN), Dieldrin (HEOD) and
Endrin. Pestic. Sci. 5(4): 473—489.
Benson, W. R. 1969. Note on Nomenclature of Dieldrin and Related
Compounds. J. Assoc. Of f. Anal. Chem. 52(5): 1109—1111.
Bellin, R. H. 1956. Endrin Stabilization Using Inorganic and Organic
Nitrite Salts. U.S. Patent No. 2,768,178. Washington, D.C.
Biros, F. J., R. C. Dougherty, and J. Dalton. 1972. Positive Chemical
Ionization Mass Spectra of Polycyclic Chlorinated Pesticides. Org. Mass
Spectrom. 6(11): 1161—1169.
Bontoyan, W. R., and P. D. Jung. 1972. Thin—Layer Chromatographic
Detection of Chlorinated Hydrocarbons as Cross—Contaminants in Pesticide
Formulations. J. Assoc. Of f. Anal. Chem. 55(4): 851—856.
Bowman, M. C., and M. Beroza. 1965. Extraction p—Values of Pesticides
and Related Compounds in Six Binary Solvent Systems. J. Assoc. Of f. Anal.
them. 48(5): 943—952.
Brooks, G. T. 1974a. Chlorinated Insecticides. Vol. 1: Technology
and Application. CRC Press. Cleveland, Ohio.
Bukowski, J. A., and A. Cisak. 1968. Structure Investigation of
Chlorinated Dimethanonaphthalene (Dieldrin and Endrin) Derivatives by the
PHR Method. Rocz. Chem. 42(7—8): 1339—1349.
Burke, J., and W. Holswade. 1964. Gas Chromatography with Microcoulometric
Detection for Pesticide Residue Analysis. J. Assoc. Of f. Anal. them.
47(5): 845—859.
Burke, J. A, and W. Holswade. 1966. A Gas Chromatographic Column for
Pesticide Residue Analysis: Retention Times and Response Data. J. Assoc.
Of f. Anal. them. 49(2): 374—385.
Burton, W. B., and C. E. Pollard. 1974. Rate of Photochemical
Isomerization of Endrin in Sunlight. Bull. Environ. Contain. Toxicol.
12(1): 113—116.
Chau, A. S. Y. 1970. Chromous Chloride Reductions. IV. Reaction of
Endrin with Chroinous Chloride Solution. Bull. Environ. Contam. Toxicol.
5(5): 435—439.
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29
Chau, A. S. Y. 1972a. Confirmation of Pesticide Residue Identity
(Part III) — Derivative Formation in Solid Matrix for the Confirmation
of Endrin by Gas Chromatograph. Bull. Environ. Contam. Toxicol. 8(3):
169—176.
Chau, A. S. Y. 1972b. Confirmation of Pesticide Residue Identity. I.
Derivative Formation for the Confirmation of Photoproducts of Endrin:
Hexachioro— and Pentachioro—Ketone Pesticide Residues by Gas Chromatography.
.J. Assoc. Off. Anal. Chem. 55(3): 519—525.
Chau, A. S. Y. 1974. Confirmation of Pesticide Residue Identity. VII.
Solid Matrix Derivation Procedure f or the Simultaneous Confirmation of
Heptachlor and Endrin Residues in the Presence of Large Quantities of
Polychiorinated Biphenyls. J. Assoc. Of f. Anal. Chem. 57(3): 585—591.
Chau, A. S. Y., and W. P. Cochrane. 1969. Cyclodiene Chemistry. III.
Derivative Formation for the Identification of Heptachior, Heptachlor
Epoxide, cis—Chiordane, trans—Chiordane, Dieldrin, and Endrin Pesticide
Residues by Gas Chromatography. J. Assoc. Of f. Anal. Chem. 52(6):
1220—1226.
Chau, A. S. Y., and W. P. Cochrane. 1971. Chromous Chloride Reductions.
VI. Derivative Formation for the Simultaneous Identification of Heptachlor
and Endrin Pesticide Residues by Gas Chromatography. J. Assoc. Of f. Anal.
Chem. 54(5): 1124—1131.
Chau, A. S. Y., and R. J. Wilkinson. 1972a. Some Separation
Characteristics of an OV—lol/OV—21O Column for Organochlorinated Pesticides
with Particular Reference to the Separation of Photoendrin and Endrin.
Bull. Environ. Contam. Toxicol. 7(2): 93—104.
Chau, A. S. Y., and R. J. Wilkinson. 1972b. Chromous Chloride Reduction.
VII. Stereochemistry and Structure of the Major Product Employed in the
Confirmation of Endrin Residues. Bull. Environ. Contam. Toxicol. 8(2):
105—108.
Chemical Specialties Manufacturers Association. 1972. Chemical Analysis
Test Methods Book — Soap and Cosmetics Chemical Specialties Blue Book.
CSMA, Washington, D.C., pp. 152—198.
Damico, J. N., R. P. Barron, and J. N. Ruth. 1968. Mass Spectra of Some
Chlorinated Pesticidal Compounds. Org. Mass Spectrom. (London) 1(2):
331—342.
Dougherty, R. C., J. Dalton, and F. J. Biros. 1972. Negative Chemical
Ionization Mass Spectra of Polycyclic Chlorinated Insecticides. Org.
Mass Spectrom. (London) 6(11): 117 1—1181.
Fahey, J. E., and N. Schecter. 1961. Diazotized Sulfanilic Acid Reagent
for Endrin Analysis. J. Agric. Food Chem. 9(3): 192—193.
-------
30
Food and Drug Administration. 1971 revised. Pesticide Analytical Manual.
Vol. 1 — Methods Which Detect Multiple Residues. U.S. Department of Health,
Education, and Welfare, Washington, D.C.
Goodwin, E. S., R. Goulden, and J. G. Reynolds. 1961. Rapid Identification
and Determination of Residues of Chlorinated Pesticides in Crops by
Gas—Liquid Chromatography. Analyst. 86(1028): 697—709.
Graham, R. E., and C. T. Kenner. 1969. Detection and Measurement of
Decomposition in Endrin Standards. J. Agric. Food Chem. 17(2): 259—263.
Gunther, F. A., and R. C. Blinn. 1955. Analysis of Insecticides and
Acaricides. Vol. 6 of Chemical Analysis. Interscience, New York.
Hastings, C. R., and W. A. Aue. 1974. Novel Polymer—deactivated
Adsorbents as Supports in Gas—Liquid Chromatography. J. Chromatogr.
89(2): 369—373.
Hathway, D. E. 1965. The Biochemistry of Dieldrin and Telodrin. Arch.
Environ. Health 11: 380—388.
lyle, G. W., and J. E. Casida. 1970. Enhancement of Photoalteratlon of
Cyclodiene Insecticide Chemical Residues by Rotenone. Science 167(3925):
1620—1622.
Kadoum, A. M. 1969. Partitioning Method for Sample Cleanup for Gas
Chromatographic Analysis of Common Organic Pesticide Residues in Biological
Materials. Bull. Environ. Contam. Toxicol. 4(3): 184—191.
Keith, L. H. 1971. Eu(DPM) 3 Transannularly Induced Paramagnetic Chemical
Shifts in the PMR Spectra of Endrin, Dieldrin, and Photodieldrin.
Tetrahedron Lett. (1): 3—6.
Keith, L. H., A. L. Alford, and J. D. McKinney. 1970. Long—Range Couplings
in the Chlorinated Polycyclodiene Pesticides. Tetrahedron Lett. (28)
(London): 2489—2492.
Klein, W., and F. Korte. 1967. Conversion of Pesticides Under Atmospheric
Conditions and in Soil. In: Proceedings of the First Annual Conference
on Trace Substances in Environmental Health. University of Missouri,
Columbia, Mo., pp. 71—80.
Lakshimarayana, V. 1974. Total Chlorine Determination in Organochlorine
Insecticides. J. Food Sd. Technol. 11(1): 15—17.
Lakshimarayana, V., and P. K. Menon. 1971. ThIn—Layer Chromatographic
Detection of Adulteration in Endrin Formulations. J. Food Sd. Technol.
8(4): 206—207.
Lidov, R. E., H. Bluestone, S. B. Soloway, and C. W. Kearns. 1950.
Alkali—Stable Polychloro Organic Insect Toxicants, Aidrin, and Dieldrin.
Adv. Chem. Ser. 1: 175—183.
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31
McDonald, S. 1962. Rapid Detection of Chlorinated Hydrocarbon Insecticides
in Aqueous Suspension with Gammarus Lacustris Lacustris (SARS.). Can. J.
Zool. 40: 719—723.
Melnikov, N. N. 1971. Chemistry of Pesticides. Vol. 36 of Residue
Reviews. Springer—Verlag, New York.
Metcalf, R. L. 1955. Organic Insecticides, Their Chemistry and Mode of
Action. Interscience, New York.
Mitchell, L. C. 1962. Identification and Differentiation of Dieldrin
and Endrin by Paper Chromatography. J. Assoc. Of f. Anal. Chem. 45(3):
682—688.
Munson, M. S. B., and F. H. Field. 1966. Chemical Ionization Mass
Spectrometry. I. General Introduction. J. Am. Chem. Soc. 88(12):
2621—2630.
Northrop, J. H. 1948. A Convenient Method for Potentiometric Titration
of Chloride Ions. J. Gen. Physiol. 31: 213—215.
Phillips, D. D., G. E. Pollard, and S. B. Soloway. 1962. Thermal
Isomerization of Endrin and Its Behavior in Gas Chromatography. J. Agric.
Food Chem. 10(3): 217—221.
Plinimer, J. R. 1971. Photochemistry of Organochlorine Insecticides.
In: Proceedings of the Second IUPAC Congress of Pesticides Chemistry:
Fate of Pesticides in Environment. Tel Aviv, Israel, pp. 413—432.
Porter, P. E. 1964. Endrin. Anal. Methods Pesticides, Plant Growth
Regulators, Food Additives. G. Zweig (ed.). Vol. 2. Academic Press.
pp. 1—24.
Reinke, J., J. F. Uthe, and H. O’Brodovich. 1973. Determination of
Polychlorinated Biphenyls in the Presence of Organochlorine Pesticide by
Thin—Layer Chromatography. Environ. Lett. 4(3): 201—210.
Robeck, G. G., K. A. Dostal, .1. N. Cohen, and J. F. Kreissl. 1965.
Effectiveness of Water Treatment Processes in Pesticide Removal. J. Am.
Water Works,. Assoc. 57(2): 181—189.
Roberts, R. L., and G. L. Blacknier. 1974. Carbon—13 Fourier Transform
Nuclear Magnetic Resonance with Eu (fod) for Configurational Confirmation
of Polychlorinated Pesticides, Endrin, and Dieldrin. J. Agric. Food Chem.
22(3): 542—545.
Roburn, J. 1963. Effect of Sunlight and Ultraviolet Radiation on
Chlorinated Pesticide Residues. Chem. Ind. 38(9/21): 1555—1556.
Roll, D. B., and F. J. Biros. 1969. Nuclear Quadropole Resonance
Spectrometry of Some Chlorinated Pesticides. Anal. Chem. 41(3): 407—411.
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32
Rondeau, R. E., and R. E. Sievers. 1971. New Superior Paramagnetic
Shift Reagents £ or Nuclear Magnetic Resonance Spectral Clarification.
J. Am. Chem. Soc. 93(6): 1522—1524.
Rosen, J. D., D. J. Sutherland, and G. R. Lipton. 1966. The Photochemical
Isomerization of Dieldrin and Endrin and Effects on Toxicity. Bull.
Environ. Contam. Toxicol. 1(4): 133—140.
Schutzmann, R. L., W. F. Barthel, and J. A. Warrington. 1966. Cleanup
and Confirmation of Identity of Pesticide Residues by Thin—Layer
Chromatography: Part I — Soil, Water, and Sediment. U.S. Department
of Agriculture, ARS 81—12, pp. 1—12.
Shell Chemical Corporation. 1959. Handbook of Aldrin, Dieldrin, and
Endrin Formulations, 2nd Edition. SC: 59—54, June. Agricultural
Chemicals Division, New York.
Sherma, J., and K. Bloomer. 1977. Separation, Detection, and Densitometric
Determination of Chlorinated Insecticides on Silica Gel and Aluminum
Hydroxide Papers. J. Chromatog. 135(1): 235—240.
Skerrett, E. J., and E. A. Baker. 1959. A New Color Reaction for Dieldrin
and Endrin. Chem. md. 17(4/25): 539.
Soloway, S. B. 1965. Correlation Between Biological Activity and
Molecular Structure of the Cyclodiene Insecticides. Adv. Pest. Control
Res. 6: 85—125.
Soloway, S. B., A. M. Damiana, J. W. Sims, H. Bluestone, and R. E. Lidov.
1960. Skeletal Rearrangements in Reactions of Isodrin and Endrin. J. Am.
Chem. Soc. 82(20): 5377—5385.
Stalling, D. L., R. C. Tindle, and J. L. Johnson. 1972. Cleanup of
Pesticide and Polychiorinated Biphenyl Residues in Fish Extracts by Gel
Permeation Chromatography. .J. Assoc. Of f. Anal. Chem. 55(1): 32—38.
Sun, Y. P., and J. Sanjean. 1961. Specificity of Bioassay of Insecticide
Residues with Special Reference to Phosdrin. J. Econ. Entomol. 54(5):
841—846.
Terriere, L. C. 1964. AnalytIcal Methods for Pesticide, Plant Growth,
Regulators, and Food Additives. Vol. II. Academic Press, New York,
Chapter 18.
Tew, R. P., and J. N. Sillibourne. 1961a. Pesticide Residues on Fruit.
I. Microbioassay of Pesticide Residues Using the Vinegar Fly, Drosophila
melanogaster. J. Sd. Food Agric. 12(9): 618—623.
Tew, R. P., and J. M. Sillibourne, 1961b. Pesticide Relsidues on Fruit.
II. Determination of Aidrin, Dleldrin, and Endrin Residues by the Organic
Chlorine and Phenyl Azide Methods and by Microbioassay. J. Sd. Food
Chem. 12(9): 623—628.
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33
Tewari, S. N., and I. C. Sharma. 1977. New Color Test for the Detection
of Endrin in Autopsy Tissues. Z. Anal. Chem. 283: 32.
Visweswariah, K., and N. Jayaram. 1971. Detection and Quantitative
Determination of Certain Chlorinated Pesticides by Micro—thin Layer
Chromatography. 3. Chromatogr. 62(3): 479—484.
Visweswariah, K., M. Jayaram, S. K. Majumder. 1971. Qualitative Tests
for the Detection of Certain Commonly Used Organochiorine Insecticides.
3. Food Sd. Technol. 8(2): 77—79.
Wiencke, W. W., and J. A. Burke. 1969. Derivatization of Dieldrin and
Endrin for Confirmation of Residue Identity. 3. Assoc. Of f. Anal. Chem.
52(6): 1277—1280.
Woodham, D. W., C. D. Loftis, and C. W. Collier. 1972. Identification
of the Gas Chromatographic Dieldrin and Endrin Peaks by Chemical Conversion.
J. Agric. Food Chem. 20(1): 163—165.
Young, S. 3. V., and 3. A. Burke. 1972. Microscale Alkali Treatment for
Use in Pesticide Residue Confirmation and Sample Cleanup. Bull. Environ.
Contam. Toxicol. 7(2/3): 160—167.
Zabik, N. 3., R. D. Schuetz, W. L. Burton, and B. E. Pape. 1971.
Photocheniistry of Bloactive Compounds: Studies of a Major Photolytic
Product of Endrin. 3. Agric. Food Chein. 19(2): 308—313.
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3. BIOLOGICAL ASPECTS IN MICROORGANISMS
31 SUMMARY
Endrin is degraded by only a few microorganisms, all of which also
degrade dieldrin. The metabolic pathways are speculative; however,
degradation appears to begin on the nonchlorinated epoxy ring, resulting
in the formation of ketones and aldehydes which may undergo dechlorination.
Ketoendrin Is the only metabolite which has been positively identified
to date. Degradation of endrin does not always result In detoxification.
Metabolites can be more toxic than the precursor and are often more stable.
Degradation products can also stimulate growth where endrin exhibited
an inhibitory effect.
Anaerobic conditions, such as those caused by flooding, and soils
of high organic content increase the transformation of endrin by soil
microorganisms (bacteria, fungi, and molds). In the marine environment,
only samples from those areas having large algal populations are active
in transformations.
3.2 BACTERIA
3.2.1 Metabolism
Relatively few bacteria are capable of degrading endrin. Only 2 to
17% of the microorganisms isolated from soil are active In endrin
degradation (Matsumura et al., 1971; Brooks, 1974b). Endrin persists
in soils for longer than nine months (Mulla, 1960, cited in Alexander,
1965b), implying that continued application will build up toxic levels
to nontarget organisms. Little is known of the chemical, biochemical,
and pedological bases for endrin resistance, but Alexander (1965b)
suggests several factors that may be involved:
• inaccessibility of the endrin substrate (adsorbed or embedded),
• absence of a growth factor (carbon, nitrogen, etc.),
• toxicity of the environment (temperature, salinity, etc.),
• inactivation of the requisite enzyme,
• structural characteristics that prevent enzyme activity (branching
molecule),
• physiological inadequacy (no enzyme to cope with the endrin substrate).
The generality that chiprine—containing rings are stable and that
the major microbial attack is on nonchlorinated rings appears to hold true
for endrin (Matsumura, 1973). Microorganisms rearrange the epoxy ring
34
-------
35
to form ketones, aldehydes, and alcohols (Fig. 3.1). While the ketone
(ketoendrin) appears to be the dominant product of biotransformation and
the only one identified to date, there are indications that reductive
dechlorination of both aldehydes and ketone occurs (Path et al., 1970;
Matsumura et al., 1971; Brooks, 1974b).
ENDRIN ALCOHOL
ORNL—DWG 79—8130
REDUCTIVE DECHLORINATION
OF ALDEHYDE
Fig. 3.1. Microbial degradation of endrin. Source: F. Matsumura,
Environmental Pollution by Pesticides, 1973. Copyright 1973 by Plenum
Publishing Corp.
All endrin—degrading bacteria were also found to degrade dieldrin
(but not the reverse) (Patil et al., 1970). Seven metabolities of
endrin (II I, lila, IV, V, VI, and two others) were separated from soil
cultures, of which only ketoendrin (IV) was identified (Table 3.1)
(Matsuniura et al., 1971). Ketoendrin ranged from undetectable to 46.3%,
and the unaltered endrin ranged from 5.8 to 97.1% in the cultures.
Biotransformation of endrin varied considerably, not only between
different bacterial cultures but also between cultures of the same genus
(e.g.,, Pseudcmonas spp.). Patil et al. (1970) found similar results with
soil isolates but separated only four endrin metabolites. The active
CI
C I
KETOENDRI N
C O
H
ENDRIN ALDEHYDE
H
CI OH
-------
36
17 91.9
18 6.7 81.3
19 91.3
20 41.0
26 44.9 44.9
44 32.2 19.6
48 93.1
49 90.8
52 81.9
53 37.8
83 18.5 80.3
93 36.5 9.5 38.0 9.5 5.8
95 Micro— 32.3 7.6 40.3 18.7
coccus
97 41.0
98 64.9
100 97.1
103 Pseudo— 9.0 15.0
monas
115 96.3
117 Pseudo— 82.5
monas
118 87.6
119 934
120 88.3
136 Pseudo— 10.1 78.2
monas
137 1.3 14.8 57.9
(173 Yeast 4.1 15.3)
Source: F. Matsumura et al., J. Agric. Food Chem. 19(1): 27—31
(1971). Copyright 1971 by the American Chemical Society.
Brooks (1974b) postulates that an endrin metabolite, if heated, would
lose CO to give a derivative of hexachlorobenzonorbornene. If both bridges
were removed by biological degradation, derivatives of tetrachloronaphtha—
lene would result. Microorganisms appear capable of genrating olef ins from
epoxides (i.e., dieldrin to aidrin), or molecules may be modified to
structures more vulnerable to conversion into water—soluble compounds
(conjugates), by reacting with endogenous chemicals through enzyme cataly—
zation (Brooks, l974b). For example, bacteria form glucosides by attaching
endogenous glucose with molecules such as alcohols in this way.
Table 3.1. Percent distribution of endrin and its
solvent—extractable metabolites due to
microorganisms (based on radioactivity)
Culture
number
Micro— Metabolite
organism (if
identified) 0 III lila IV V VI Endrin
Bacillus
2.7 3.4
4.2 3.2
2.1 4.6
10.4 27.9 19.3
1.9 3.4
20.6 5.9 19.5
2.5 3.3
2.7 3.3
16.0
13.3 19.0 29.4
12.5 10.8
6.8 9.4
2.3
13.0 Trace 46.3
2.0
4.6
2.0
1.4
4.9
2.2
1.1
3.2
2.1
0.5
1.2
0.7
1.1
0.6
3.6
0.6
0.5
0.6
1.4
1.4
0.8
2.1
1.9
35.1
15. 3
16.2
3.1
16.1
11.0
5.8
9.6
9.8
5.8 20.2
80.6
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37
bacteria included Pseudornonas spp., Bacillus app., Trichoderma spp.,
Micrococcus sp., Arthrobacter ep., as well as unidentified cultures.
Corynebacterium pyogenes appeared to decrease liquid endrin concentrations
in 7 to 16 days, but two species of Pseudomonas (P. fJ_uorescens and
P. aeruginosa) were without effect (Cope, 1963).
Endrin is very persistent under both aerobic and anaerobic conditions
(Pfister, 1972), but the creation of anaerobic conditions generally
stimulates microbial degradation of endrin. Support for this phenomenon
includes increasing transformation of endrin with increasing depth in field
soil (Nash et al., 1972) and decreasing endrin in flooded soil compared
with upland conditions (Castro and Yoshida, 1971; Guenzi et al., 1971).
Endrin degradation is not affected by temperature (Pfister, 1972) or soil
mixing, but it is improved by the amount of organic material in flooded
or naturally occurring soils (Table 3.2) (Guenzi at al., 1971; Castro
and Yoshida, 1971). Bacterial involvement was suggested by organic
enhancement (i.e., as an energy source) and by the apparent lag time in
endrin disappearance (i.e., adaptation time).
Table 3.2. Concentration of endrin under
different soil conditions (ppm)
Weeks
2.5
cm water/week
2.5
cm w
soil
ater/week,
mixed
Flooded
+
Alfalfa
+ Alfalfa
+
Alfalfa
0
25
25
25
25
25
25
2
20.4
21.9
20.0
20.5
19.4
21.7
6
19.5
20.5
20.9
19.3
18.6
19.5
10
19.8
19.5
20.3
20.2
17.1
15.2
14
20.1
19.9
20.7
19.4
15.5
12.7
18
20.5
21.0
18.9
20.7
14.1
10.8
22
19.2
19.9
19.1
19.9
14.6
11.0
Source: W. D. Guenzi et al., Soil Sci. Soc. Am. Proc. 35(6):
910—913 (1971). Copyright 1971 by the Soil Science Society of America.
Since the metabolic pathways of endrin in microorganisms are
speculative at this time, discussion of similar transformations may help
elucidate endrin reactions. All of the endrin metabolites classified so
far have the hexachiorinated norbornene moiety unchanged. However, under
anaerobic conditions, Clostridium butyricum reduced the dichioro—
methanobridge in hexachioronorbornene (compound 1, Fig. 3.2) to —CH 2
(compound 2, Fig. 3.2) and further hydroxylated it to —CH(OH)- (compound 3,
Fig. 3.2). A tetrachiorocyclodiene (compound 4, Fig. 3.2) was also found
in the bacterial culture, apparently formed only from the fully chlorinated
molecule by direct dechlorination without intermediate alcohol formation
(Schuphan and Ballschmiter, 1972).
-------
38
ORNL—DWG 79-8131
(2) (3)
CI CI
H
H
H
H
CI
H
ci
HEXACHLORONORBORNENE (4)
Fig. 3.2. Anaerobic transformations of hexachioronorbornene by
Clostridium butyricum. Source: I. Shupman and K. Ballschmiter, Nature
237: 100—101 (1972). Copyright 1972 by MacMillan Journals Ltd., London.
No dechlorinated products of hexachioronorbornene were found in yeast
(Saccharc. nyces) cultures or with soil microorganisms (Schuphan and
Ballschmiter, 1972). The extent to which these reactions can be generalized
for endrin is unknown; however, hypothetical transformations involving
oxidation (hydroxylation), oxidative dechlorination, reductive dechlorina-
tion, hydrochlorination, hydrolytic removal of chlorine, hydration of
epoxide rings, and skeletal rearrangements seem more probable in view of
similar reactions that are known.
The significance of the rearrangements is not known, but Matsumura
(1973) believes that it is unlikely that microbes derive any energy.
Usually biotransformation generates more polar and degradable products
than do the parent compounds, so rearrangements may provide further
opportunities to break down the molecules (Brooks, l974b; Matsuinura,
1973). It has also been suggested that anaerobic (reductive) dechlorina-
tion of endrin by microorganisms is precursory to aerobic (oxidative)
degradation, as indicated for DDT (Brooks, l974b). Thus, one way
organic matter may aid degradation of endrin is by decreasing the
oxidation—reduction potential of the soil, thereby creating conditions
favorable to reductive dechlorination (Castro and Yoshida, 1971).
The identification of “terminal residues” is important, because
biotransformation products may not follow the same pathways as do precursor
molecules. Metabolic products may be eliminated on the one hand or cause
CI
c i CI
Ci
(4)
-------
39
toxicity not demonstrated by parent compounds on the other hand. Thus,
different mechanisms of activation, transformation, and detoxification
are bases for variation on organism sensitivity to endrin.
3.2.2 Effects
Microorganisms that fix and release nitrogen are essential to the
biosphere, providing the major means of introducing elemental nitrogen
into organic compounds. The toxicity of endrin to these soil micro-
organisms is vitally important, but Pfister (1972) and Bollag and Henninger
(1976) reported that endrin was not excessively inhibitory to ammonifying
organisms or decomposers that liberated ammonia. In fact, Eno and Everett
(1958) conclude that pesticides appear to be toxic to higher plants
(12.5 ppm) before microbial responses are observed. The lack of effects
probably is explained by low solubility in water and low vapor pressure,
limiting the amount of chemical in soil solution and, therefore, the
quantity contacting microorganisms.
Many soil fungi (including Streptomyces, Penicillia, and molds)
and bacteria are not affected at concentrations below 1000 ppm (Pfister,
1972; Bollen and Tu, 1971). Endrin concentrations up to 50 mg/liter had
no toxic effect on sewage organisms for five days, based on BOD and COD
studies (Canter et al., 1969). Escherichia coli cultures grew for 24 hr
on agar and in suspension with 500 and 1500 mg/liter endrin added,
respectively, and complete growth inhibition occurred at 3000 mg/liter
(Canter et al., 1969). The decomposition rate of soil organic matter, as
measured by CO 2 evolution, was the same in treated and control samples,
as was sulfur oxidation and ammonification below 1000 ppm and nitrification
below 100 ppm (Bollen and Tu, 1971). Endrin was found to stimulate
degradation of organic matter in situ at levels below inhibition, but in
the laboratory, microbial plates were not affected (Bollen and Tu, 1971).
Bacterial sensitivity to endrin appears to be related to their gram
response (Trudgill et al., 1971). Gram—negative and —variable bacteria
were not affected by surface films of 0.5 mg/ml endrin, but 50% of the
gram—positive cultures were inhibited (Table 3.3). While some discrepancy
occurs in the effect of endrin on the growth of Bacillus species (Patil
et al., 1970; Trudgill et al., 1971), differences in methods of growth
determination and incubation periods may be responsible.
3.3 PROTOZOA AND PLANKTON
Conversions of chemical compounds in the natural environment may
result in more stable or sometimes more toxic products than the parent
compound. A degradation product of endrin, ketoendrin, produced by the
blue—green alga Anacystis nidulans, proved to inhibit growth as much as
the parent compound (Fig. 3.3) (Batterton et al., 1971). A9nlenellum
quacfruplicatwn, another blue—green alga, was slightly stimulated by
ketoendrin, while inhibited by endrin. Thus, not all degradation products
represent a detoxification step. A. nidulans had a lag period of up to
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40
Table 3.3. Effects of endrin on bacterial growth
Grain positive
Bacillus rnegateriwn
B. subtilis
Streptornyces antibioticus
Nocardia sp. B
Corynebacteriwn sp. T I
B. cereus —
Nocardia sp. 4 +
Microbacterium fiavwn +
Micrococcus lysodeilticus +
Staphylococcus aureus +
Sarcina lutea +
Gram variable
Arthrobacter sinrp Ze v +
Gram negative
Achromobacter butyri +
Achramobacter ep. PC 4 ÷
Eacherichia coli +
Klebsielia aerogenes +
P. aci-dovorans +
P. aureofaci ens (+)
P. dehalogens +
P. fluorescens +
P. fluorescens +
P. multivorans +
P. putida +
+, growth not inhibited; (+), growth slightly inhibited; —,
growth severely or completely inhibited.
Source: P. W. Trudgill et al., J. Gen. Microbiol. 69(1): 1—13.
Copyright 1971 by the Cambridge Univ. Press.
12 hr in the presence of 1 ppb endrin concentration during which apparently
adaptation or selection of resistant cells took place (Batterton et al.,
1971; Matsumura, 1972).
Mixed algal cultures isolated from fish—pond water and the fish—pond
water per se degraded radiocarbon—labeled endrin (Patil et al., 1972). Of
the introduced carbon label, 24.4% was recovered In ketoendrin from algal
cultures, and 35.5% from the pond water was in an unknown nietabolite.
Some blue-green algae have the capability of fixing elemental nitrogen
into organic compounds, thereby providing nitrogen in a usuable form to
other organisms. The effects of endrin on two cultures of these ecologi-
cally significant blue—greens were reported by Singh (1973). Both
-------
41
ORNL—OWG 79—8432
0
0 40 100 40000
ppb
40 400
ppb
4000
Fig. 3.3. Effect of endrin and one of its degradation products,
ketoendrin, on two species of blue—green algae, after 36 hr. Source:
J. C. Batterton, C. M. Boush, and F. Matsumura, Bull . Environ. Contain.
Toxicol. 6(6): 589—594 (1971). Copyright 1971 Springer—Verlag, N.Y.
Cylintfrospermujn sp. and Aulosira fertilissima showed increasing growth
inhibition with increasing endrin concentrations (Fig. 3.4). while an
aerobic, non—nitrogen—rixing blue—green alga (Plectonema bOryanuin) was
only slightly inhibited at 600 pg/mm endrin. No effect was observed on
morphology or sporulation of nitrogen—fixing algae by endrin. However,
heterocyst frequency was directly correlated with endrin concentration.
Cultures of four marine phytoplankton (Skeletonema costatwn,
Dunaliella tertiolecta, Coccolithus huxleyi, and Cyclotellcz nana) showed
varying responses to endrin (Menzel et al., 1970; Pfister, 1972). S.
costatwn and C. huxleyi had radiocarbon uptake and cell division reduced
at 10 and 100 ppb endrin respectively (Fig. 3.5). Cell division returned
to normal after five days in S. co8tatuin. C. nana proved most sensitive;
radiocarbon uptake and cell division were completely inhibited above
1 ppb, with the dose—response curve suggesting effective doses as low
as 0.01 ppb endrin (Menzel et al., 1970). There was no effect on D.
tertiolecta with endrin concentrations up to 1000 ppb.
Algae concentrated endrin manyfold, either through ad— or absorption
(Turnipseed, 1974; Vance and Drummond, 1969; Pfister, 1972). Concentration
factors ranged from 140 to 222 for seven days, with slightly higher bio—
accumulation in two blue—green algae, Microcystis aeruginosa and Anabaena
2
0
• 0
(I ,
C
0
0
w
I
I-
0
(9
KETOENDRIN
‘I
Is
\ I—
\ /
• AGMENELLUM QUADRUPLICATUM
o ANACYSTIS NIDULANS
-------
42
W ORNL—DWG 79— 8133
1:: I I
5 50 DAYS —
I i i
U 0
z
4
I— •
P
0 100 200 300 400 500
ENDRIN ( /mt)
Fig. 3.4. Effect of endrin on Cylindrospermun sp. Source:
P. K. Singh, Arch. Mikrobiol. 89(4): 317—320 (1973). Copyright 1973
Springer-Verlag, N.Y.
c:ilindrica, compared with two greens, Scenedesmus quadricauda and Qedogonium
spp. In contrast, lethal concentrations were higher for the greens
(>20 ppm) than for the blue—greens (<20 ppm) (Vance and Drununond, 1969).
Bioconcentration increased in algae with decreasing exposure levels,
although tissue accumulation per se was lower. For example, Oedogoniuin
spp. had bioconcentration factors of 140 and 4500 associated with tissue
levels of 140 and 11.6 ppm respectively (Metcalf et al., 1973; Vance
and Drummond, 1969). Chla .inydomonas reinhardtii had growth, respiration,
and photosynthesis inhibited to some degree by endrin, but concentration
levels were not given (Turnipseed, 1974).
Because of the low solubility of endrin, it was difficult to determine
incorporation into cell material (Pfister, 1972); however, the response
of some algae to concentrations above the solubility limits (about 0.2 ppm)
suggested that either saturation was maintained while endrin was accumu-
lated from solution or that there might be incorporation as small parti—
culates. This last pathway is supported by the association of endrin with
microscopic particles (0.15 pm or more) in Lake Erie water, including
organics, detritus, and microorganisms (Pfister et al., 1969).
-------
E
U,
C)
OTELLA
0.001 0.1 10 1000
ENDRIN IN WATER (ppb)
43
106
lo
4Q4
106
10
4Q4
106
10
ORNL—DWG 79—8129
I I I I
0 ENDRIN
- • CONTROL
I I
i Q
100
80
60
40
20
0
120
100
80
‘I ,
2 60
8 40
20
- 0
(ii ________
1 00
80
60
40
20
0
120
100
80
60
40
20
0
Fig. 3.5. Uptake of endrin by phytoplankton at various concentrations
over 24 hr (left side) and growth rates of same species in 100 ppb endrin
over seven days (right side). Source: D. W. Menzel, J. Anderson, and
A. Randike, Science 167(3926): 1724—1726 (1970). Copyright 1970
American Society for the Advancement of Science.
3.4 REFERENCES
Alexander, M. 1965b. Biodegradation: Problems of Molecular Recalcitrance
and Microbial Fallibility. Adv. Appi. Probab. 7: 35—80.
Batterton, J. C., G. M. Boush, and F. Natsumura. 1971. Growth Response
of Blue—Green Algae to Aidrin, Dieldrin, Endrin, and Their Metabolites.
Bull. Environ. Contam. Toxicol. 6(6): 589—594.
DAYS
106
1o
io 4
0 lo 7
P1
0 0
— 0
-
SKELE TONEMA 0
C’OSTATL/M
I I
I I I
T T T I
-------
44
Bollag, J. M., and N. N. Henninger. 1976. Influence of Pesticides on
Denitrification in Soil and with an Isolated Bacterium. J. Environ.
Qual. 5(1): 15—18.
Bollen, W. B., and C. N. Tu. 1971. Influence of Endrin on Soil Microbial
Populations and Their Activity. U.S.D.A. Forest Service Research
Paper—PNW 114: 1—4.
Brooks, G. T. 1974b. Chlorinated Insecticides. Vol. II: Biological
and Environmental Aspects. CRC Press, Cleveland, Ohio.
Canter, L. W., C. D. Nance, and D. R. Rowe. 1969. Effects of Pesticides
on Raw Wastewater. Water & Sewage Works 116(6): 230—234.
Castro, T. F., and T. Yoshida. 1971. Degradation of Organochlorine
Insecticides in Flooded Soils in the Philippines. J. Agric. Food Chem.
19(6): 1168—1170.
Cope, 0. B. 1963. Sport Fishery Investigations. In: Pesticide Wildlife
Studies: A Review of Fish and Wildlife Service Investigations During 1961
and 1962. Fish and Wildlife Service Cire. 167, Washington, D.C.,
pp. 26—42.
Eno, C. F., and P. H. Everett. 1958. Effects of Soil Applications of
10 Chlorinated Hydrocarbon Insecticides on Soil Microorganisms and the
Growth of Stringless Black Valentine Beans. Soil Sci. Soc. Am. Proc.
22: 235—238.
Guenzi, W. D., W. E. Beard, and F. G. Viets, Jr. 1971. Influence of
Soil Treatment on Persistence of Six Chlorinated Hydrocarbon Insecticides
in the Field. Soil Sd. Soc. Am. Proc. 35(6): 910—913.
Matsumura, F. 1972. Biological Effects of Toxic Pesticidal Contaminants
and Terminal Residues. Environ. Toxicol. Pestic. Proc. TJ.S.—Jap. 1971:
525—548.
Matsumura, F. 1973. Degradation of Pesticide Residues in the Environment.
In: Chapter 13, Environmental Pollution by Pesticides. C. A. Edwards
(ed.). Plenum Press, New York.
Matsumura, F., U. C. Khanvilkar, K. C. Patil, and G. N. Boush. 1971.
Metabolism of Endrin by Certain Soil Microorganisms. J. Agric. Food
Chem 19(1): 27—31.
Nenzel, D. W., J. Anderson, and A. Randike. 1970. Marine Phytoplankton
Vary in Their Response to Chlorinated Hydrocarbons. Science 176(3926):
1724—1726.
Metcalf, R. L., I. P. Kapoor, P. Y. Lu, C. K. Schuth, and P. Sherman.
1973. Model Ecosystem Studies of the Environmental Fate of Six Organo—
chlorine Pesticides. Environ. Health Perspec. 4: 35—43.
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45
Nash, R. G., M. L. Beau, Jr., and W. G. Harris. 1972. Endrin
Transformations in Soil. J. Environ. Sci. 1(4): 391—394.
Patil, K. C., F. Matsumura, and G. M. Boush. 1970. Degradation of
Endrin, Aldrin, and DDT by Soil Microorganisms. Appi. Microbiol. 19(5):
879—881.
Patil, K. C., F. Matsumura, and G. M. Boush. 1972. Metabolic
Transformation of DDT, Dieldrin, Aidrin, and Endrin by Marine
Microorganisms. Environ. Sci. Technol. 6(7): 629—632.
Pfister, R. M. 1972. Interactions of Halogenated Pesticides and
Microorganisms: A Review. CRC Critical Reviews in Microbiology 21(1):
1—33.
Pfister, R. M., P. R. Dugan, and J. I. Frea. 1969. Microparticulates:
Isolation from Water and Identification of Associated Chlorinated
Pesticides. Science 166(3907): 878—879.
Schuphan, I., and K. Eallschmiter. 1972. Metabolism of Polychiorinated
Norborrienes by Clostridiuin butyricurn. Nature (London) 237: 100—101.
Singh, P. K. 1973. Effect of Pesticides on Blue—Green Algae. Arch.
Mikrobiol. 89(4): 317—320.
Trudgill, P. W., R. Widdus, and J. S. Rees. 1971. Effects of
Organochiorine Insecticides on Bacterial Growth, Respiration, and Viability.
J. Gen. Microbiol. 69(1): 1—13.
Turnipseed, G. D. 1974. The Effects of Selected Chlorinated Hydrocarbon
Insecticides on Chiconydomonas reinhardtii. Diss. Abstr. 34(12):
5841B—5842B.
Vance, B. D., and W. Drummond. 1969. Biological Concentration of
Pesticides by Algae. J. Am. Water Works Assoc. 61(7): 360—362.
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4. BIOLOGICAL ASPECTS IN PLANTS
4.1 SUMMARY
The fungi Aspergillus niger, A. flavus, Penicilliwn notatu ’n, and
P. chrysogenwn metabilize endrin into ketoeridrin and a very hydrophilic
compound that are found in both mycelium and culture medium. The age
of the culture affects endrin metabolism. In growing cultures of
A. flavus, endrin was absorbed nearly quantitatively from the culture
medium and accumulated in the mycelium, while the endrin metabolites
(produced by a 2 to 3% metabolic rate) were excreted into the medium
quantitatively. In full—grown cultures of A. flavus, the metabolic rate
was 22%, and the endrin metabolites were found in both mycelium (20%)
and culture medium (74%).
An unidentified yeast metabolized endrin at the metabolic rate of
84.1%; ketoendrin was the only metabolite.
Endrin inhibits cell growth of the yeast Saceharomyces cerevisiae.
Inhibition was greater (17%) with the fermentable sugar glucose as
substrate than it was (6%) when the culture medium contained nonfermentable
lactate.
Uptake of endrin by vascular plants has been demonstrated. Plants
grown in soil that contains endrin absorb it by the roots. Endrin
applied to plant leaves is subsequently absorbed by the leaves. Leaves
also absorb endrin vapors (e.g., endrin that has volatilized from the
soil).
The amount of endrin taken up by vascular plants from soil depends
on the plant, on the type of soil, and on the endrin concentration in
the soil.
When they are grown under the same conditions, some plants develop
higher endrin residues (concentration based on fresh or dry weight)
than others. For example, carrot (Daucus carota) had higher concentra-
tions of endrin than did other root crops, including potato (Solanuin
tuberoswn), radish (Raphonus sativus), turnip (Brassica rapa), and
beet (Beta vulgaris). In another experiment, endrin concentrations in
aerial plant parts decreased in the order: bromegrass (Brornus inermis),
alfalfa (Medicago sativa), wheat (Triticum aestivum), corn (Zea maps),
and soybean (Glycine max).
Soil type also affects endrin uptake from soil. When plants were
grown in different soils, it was found that endrin residues in aerial
plant parts generally varied by a factor of 2, although the difference
was sometimes as great as fivefold. Residues were usually highest in
plants grown in sandy loam, and somewhat lower when the soil was clay
or loam. Silt in the soil retarded endrin uptake.
46
-------
47
Endrin uptake by plants appears to be proportional to the concen-
tration of endrin in soil, at least at low concentrations. Endrin
residues in plants grown in soil that contained 5.0 ppm endrin were
tenfold the residues in plants grown in soil with 0.5 ppm endrin.
The absorbed endrin is translocated throughout the plant. Endrin
concentrations in the various plant parts decrease with distance from
the site of uptake. When 1 C—endrin was applied to and absorbed by
leaves of cotton (Gossypium hirsutum) and cabbage (Brassica oleracea
capitata), most of the recovered radioactivity was associated with the
leaves. In cotton, radioactivity was also detected in stalks, pods,
fibers, and seeds, but not in roots. In cabbage, recovered radioactivity
was also associated with the stems and roots. Substantial amounts of
radioactivity (20% with cotton and 9.2% with cabbage) were recovered
in the soil in the translocated endrin and its metabolites that had
been excreted by the roots.
Absorbed endrin is metabolized by plants, and as many as five
metabolites have been detected. Three of the metabolites (including
ketoendrin) are slightly more hydrophilic than endrin, and two are
very hydrophilic. Delta—ketoendrin, the only identified metabolite,
was detected by most investigators, sometimes as the only metabolite
and sometimes as a minor constituent of the metabolite fraction, with
the major constituent(s) being very hydrophilic. Endrin alcohol and
traces of endrin aldehyde in plants have also been reported.
The rate of metabolism of endrin by vascular plants varies with
the plant species and probably also with the mode of endrin application.
The metabolic rate, as indicated by the proportion of metabolites in
the recovered endrin residues, was about 10% in cabbage four weeks after
foliar application of endrin at different rates. In tobacco (Nicotiana
tabacum), the metabolic rate was only 2.3% after four weeks. In carrot,
the metabolic rate three weeks after treatment with endrin was 32% with
foliar application, but 12% when endrin was injected into the roots and
5% when endrin was applied to the soil.
The amount of radioactivity recovered, when ‘ 1 C—endrin was used in
experiments, varied greatly. Recovery was always less than 50% four
weeks after endrin application. Because it is known that endrin and its
metabolites are excreted into soil by plant roots, most experiments of
this type did include soil analysis. The discrepancy between the amounts
of radioactivity applied and recovered has been attributed to vaporization
of the applied endrin and also to loss of absorbed endrin and/or its
metabolites by transpiration.
Endriri is somewhat phytotoxic to vascular plants. With the appli-
cation of a 0.03% endrin emulsion, scorching of the foliage of three
varieties of cucurbits was apparent to different degrees after seven days
of growth. A 0.04% emulsion effected high phytotoxicity within three
days of application. There are also reports that endrin is toxic to corn.
Some adverse effects attributed to endrin are actually caused by the
solvent used in the formulation.
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48
Endrin at 1 ppm did not affect the rates of germination and growth
of onion (Alliwn cepa). However, the gertninability of barley (Hordewn
vulgare) seeds soaked in endrin solutions at 500 and 1500 ppm for 24 hr
was reduced 50%.
Mitosis in seedling root cells was affected by endrin treatment. A
slight stickiness of anaphase chromosomes 48 hr after germination and an
increase in the number of anaphases with incompletely separated chromatids
ten days after germination were observed in onion. Endrin treatment
induced chromosome aberrations in mitotic root cells of seedlings at
mean frequencies of 7.59 and 18.55% in barley and broad bean (Vicia faba)
respectively.
Meiosis in barley was not affected when barley seeds were soaked
in a 1000—ppm solution of endrin for 12 hr prior to germination. However,
when endrin at 500 ppm was sprayed onto 16—day—old seedlings, the frequency
of chromosomal abnormalities in pollen mother cells increased about
3.5—fold.
The presence of endrin in the soil affects the uptake of various
macro— and microeleinents by vascular plants. The uptake of some elements
is increased, whereas the uptake of other elements is decreased. The
actual effect is a factor of the particular element, the plant species,
and the concentration of endrin.
The presence of endrin in soil alters the amino acid composition
of plants. There were significant increases and decreases in the contents
of various amino acids In corn grown in endrin—treated soil.
4.2 NONVASCTJLAR PLANTS
4.2.1 Metabolism of Endrin
Korte (1967) mentioned that the fungi Aspergilles niger, A. fiavus,
Penicilliwn notatwn, and P. chrysogenwn metabolize endrin. Metabolites
were isolated from both the mycelium and the culture medium; they were
more hydrophilic than endrin.
The experiments with Aspergillus flavus were later described in
more detail (Klein et al., 1968b). Carbon—l4—endrIn was applied at
concentrations of 0.044 to 0.132 ppm to cultures of A. fiavus. Three
weeks later, the mycellum and the culture medium were analyzed separately.
Twenty—five percent of the applied radioactivity was not recovered. The
3% of applied radioactivity found in the cotton plugs of the culture
flasks was associated only with endrin. It was concluded, therefore,
that volatilization of endrin accounted for the lost radioactivity and
that no metabolites were lost by volatilization. When the endrin was
applied to growing cultures of A. fiavus, it was absorbed nearly
quantitatively and was accumulated by the mycelium. The metabolic rate
-------
49
was 2 to 3%, and the metabolites were excreted quantitatively into the
culture medium. When the endrin was applied to full—grown (i.e., not
growing) cultures, 20% of the metabolites were found in ti’e inyceliuin
and 74% in the culture medium; the metabolic rate was 22%. Two metabo—
lites were produced by A. flavus — ketoendrin and a very hydrophilic
compound; these metabolites were identical with the endrin metabolites
of higher plants.
A yeast—mannitol medium was used to culture an unidentified yeast
that had been isolated from farm soil (Matsumura et al., 1971). Ten
microliters of 0.001 M 11 C—endrin solution was added to each culture
test tube. Of the total recovered radioactivity (21% of the applied
radioactivity), 80.6% was associated with ketoendrin and 15.3% with
endrin; ketoendrin was the only inetabolite.
4.2.2 Effects of Endrin
The effect of endrin on growth of the yeast Saccharonnjces cerevisiae
was examined by Nelson and Williams (1971). The liquid culture medium
contained either 1% glucose or 2% lactate as the energy source.
Immediately after the cultures were inoculated, 1 ml of 0.01 M endrin
solution in dimethylsulfoxide was added to the 100 ml of medium in each
flask. After a 20—hr incubation period, it was observed that cell growth
had been inhibited 17% in the glucose—containing culture medium, but only
6% in the lactate—containing medium. This finding was surprising because
the cyclodiene pesticides chiordane and heptachior completely inhibited
cell growth of S. cerevisiae when the substrate was nonfermentable
lactate, and other cyclodiene pesticides (heptachlor epoxide, aldrin,
and dieldrin) also strongly inhibited cell growth in lactate—containing
medium. When the energy source was the fermentable sugar glucose, cell
growth was inhibited 13 to 20% by the various cyclodiene pesticides
(37% by chlordane).
Chlorinated hydrocarbons, including endrin, inhibit fermentation
processes in Aspergillus niger and Saccharomyces oerevisiae (Singh et al.,
1977). Production of citric acid by A. niger was reduced 40 to 60%
compared with the control. A similar inhibition pattern was also
observed on fermentation of ethyl alcohol by S. cerevisiae. Initial
steps of fermentation do not seem to be affected by chlorinated
hydrocarbons, since sugar utilization is not inhibited by these compounds.
4.3 VASCULAR PLANTS
4.3.1 Metabolism of Endrin
Most of the earlier studies of endrin and plants were confined
primiarily to quantifying endrin residues (e.g., Brett and Bowery, 1958;
-------
50
Bowery et al., 1959; Gyrisco and Huddleston, 1961; Mattick et al., 1963;
Archer, 1968b; Bhalla et al., 1970; and Knutson et al., 1971). The
investigators did not, and often could not, distinguish between the
residues on the plant surfaces and those within the plant tissues.
More sophisticated experiments were designed to determine whether
endrin is absorbed into plants, translocated within the plants, and
metabolized by the plant. These experiments established that plants do
absorb, translocate, and metabolize endrin.
In order to demonstrate root uptake of endrin and its translocation,
plants were grown in soil which contained endrin that had been applied
to the surface of the soil or mixed in with the top soil layer. No
endrin was sprayed on the plants, and, therefore, the only source of
endrin was that present in the soil.
Although the quantity of endrin absorbed from the soil is affected
by several factors, root uptake of endrin does occur (Table 4.1). It
has been reported for many root crops (Foster et al., 1956; Harris and
Sans, 1967; Hermanson et al., 1970; Korte, 1967; Van Middelem, 1969b;
Wheeler et al., 1969; Winnett and Reed, 1968) as well as for diverse
plant types, including grasses (Beall and Nash, 1969; Saha and
co—workers, 1967, 1968), legumes (Barrentine and Cain, 1969; Beau and
Nash, 1969, 1971; Nash and co—workers, 1970, 1971, 1972, 1973, 1974b;
Saha et al., 1968; Van Middelem, l969b), cucurbits (Beall and Nash, 1969),
and pomes (Horsfall et al., 1970).
Working with turnips (Bra3sica rapa) and carrots (Daucus carota),
respectively, Wheeler et al. (1969) and Hermanson et al. (1970) proved
that endrin residues in root crops could not be attributed only to
surface contamination. The presence of endrin in peeled roots indicates
that the insecticide is absorbed from the soil.
Other investigators reported the presence of endrin residues in
aerial parts of plants, including the leaves of bromegrass (Bromus inerrnis)
and alfalfa (Medicago sativa) (Beall and Nash, 1969), sweet clover
(Melilotus sp.), oat (Avena sativa), barley (Hordewn vulgare) (Saha et al.,
1968), wheat (Triticwn aestivwn) (Beall and Nash, 1969; Saha and co—workers,
1967, 1968), turnIp (Van Middelem, 1969b; Wheeler et al., 1969), and
tobacco (Nicotictna tabacwn) (Van Middelem, 1969b). Endrin residues were
also detected in soybeans (Glycine nux) (Barrentine and Cain, 1969; Beall
and Nash, 1971; Nash and co—workers, 1970, 1973, 1974b) and in apples
(Malus dornestica) (Horsfall et al., 1970). These findings evidence trans—
location of endrin within the plant subsequent to its absorption by the
root.
The amount of endrin absorbed from the soil depends on various
factors, including plant species, insecticide concentration, and soil
type. Hermanson et al. (1970) noted that carrots usually take up more
endrin than do other root corps [ e.g., potato (Solanwn toberosum),
radish (Raphonus sativus), turnip, and beet (Beta vulgaris)]. Beau and
Nash (1969) grew soybean, wheat, corn (Zea Mays), alfalfa, bromegrass,
-------
Table 4.1.
Absorption of endrin from soil by plants
Treatment
Endrin In
(ppm)
soil°
Growth period Plant
Endrin residues
ConcentrationZ
(ppm) Reference
part
Compound
Plant (lb/acre) (ppm)
Soybean 2 0.59 5 months Beans Endrin 0.04 (F) Barrentine and Cain,
4 1.20 5 months Beans Endrin 0.08 (F) 1969
8 1.49 5 months Beans Endrin 0.12 (F)
Soybean 0.5 3 weeks Above cotyledon Endrin 0.024—0.045 (0) Beau and Nash, 1969
5.0 3 weeks Above cotyledon Endrin 0.303—0.410 (0)
Wheat 0.5 3 weeks Above coleoptile Endrin 0.176 (0)
sheath
5.0 3 weeks Above coleoptile Endrin 1.844 (0)
sheath
Corn 0.5 3 weeks Above coleoptile Endrin 0.068 (0)
sheath
5.0 3 weeks Above coleoptile Endrin 0.708 (0)
sheath
Alfalfa 0.5 3 weeks Above cotyledon Endrin 0.215 (0)
5.0 3 weeks Above cotyledon Endrin 2.464 (0)
Bromegrass 0.5 3 weeks Above coleoptile Endrin 0.304 (0)
sheath
6 weeks Above coleoptile Endrin 0.451 (D)
sheath
5.0 3 weeks Above coleoptile Endrin 3.127 (D)
sheath
6 weeks Above coleoptile Endrin 4.514 (0)
sheath
Cucumber 0.5 4 weeks Above cotyledon Endrin 0.028 (D)
5.0 4 weeks Above cotyledon Endrin 1.084 (D)
Soybean 20 20 53 days Above cotyledon Endrin + 2 metabolites 38.1 (D) Seall and Nash, 1971
Leaves 125.95 (0)
Stem 303.93 (0)
Pods 10.44 (D)
Seeds 3.30 (0)
Carrot 15 15.8 11.5 weeks Roots Total organic chlorine 4.0 (F) Foster et al., 1956
21.7 16.9 13 weeks Roots Total organic chlorine 3.0 (F)
Sweet potato 4.4 23 weeks Roots Total organic chlorine 7.3 (F)
Carrot 8.91 14 weeks Whole plant Endrin 0.06 (F) Harris and Sans, 1967
Raddish 8.91 5 wceks Whole plant Endrin 0.04 (F)
Sugar beet 5 Roots Endrin Significant Hermanson et al. , 1970
-------
Carrot 14 3.6—3.8 142 days
Table 4.1 (continued)
Treatment
Endrin j
(ppm)
5011 a
Endrin residues
Growth period Plant part Compound
concentratjonb
(ppm) Reference
Plant (lb/acre) (ppm)
163 days
P.aota
Peeled roots
Roots
Roots
Total organic chlorine
Total organic chlorine
Endrin
Endrin
1.2—1.6 (F)
0.5-0.7 (F)
1.2—4.0 (F)
1.0—3.2 (F)
Apple
2
2
4
4
11 months°
6 moqths°
a
6 months°
Fruit
Fruit
Fruit
Fruit
Endrin
Endrin
Endrin
Endrin
<0.0005—0.005 (F)
<0.002—0.028 (F)
<0.002—0.007 (F)
<0.002—0.023 (F)
Horsfall et al., 1970
Carrot
0.047
3 weeks
Roots
Endrin + metabolite
(Uptake, 26%)
Korte, 1967
Soybean
20
53 days
Leaves
Stems
Seeds
Endrin + setabolite(s)
Endrin + metabolite(s)
Endrin + metabolite(s)
(19.0% endrin)
(57.3% endrin)
(2.7% endrin)
Nash and Beall, 1970
Soybean
20
53 days
Stems and leaves
Endrin + 2 metabolites
Nash and BeaU., 1971
Soybean
20
75 days
Above cotyledon
Endrin + 3 metabolites
Nash et al., 1972
Soybean
7.52
21.44
99 days
118 days
99 days
118 days
Beans
Beans
Beans
Beans
Endrin + 3 metabolitea
Endrin + 2 metabolites
Endrin + 2 metabolltes
Endrin + 3 metsbolites
0.096 (F)
0.032 (F)
0.108 (F)
0.098 (F)
Nash and Harris, 1973
Soybean
20
43 days
99 days
160 days
160 days
Aerial
Aerial
Hay
Seed
Endrin + metabolites
Endrin + metabolites
Endrin + metabolites
Endrin atetabolites
0.266
0.202
0.195
0.026
Nash, 1974b
Wheat
2
8
1.00—1.12
3.66—3.76
45 days
60 days
112 days
45 days
60 days
112 days
Plants
Plants
Straw
Plants
Plants
Straw
Endrin
Endrin
Endrin
Endrin
Endrin
Endrln
0.009—0.021 (F)
0.014—0.020 (F)
0.022—0.028 (F)
0.040—0.050 (F)
0.068—0.082 (F)
0.046—0.054 (F)
Saha and McDonald, 1967
Sweet clover
8
1.20
Aerial
Endrin
0.14 (F)
Saha et al., 1968
Wheat
8
1.20
Aerial
Endrin
0.03—0.05 (F)
S ha et al., 1968
Oat
8
1.20
Aerial
Endrin
0.03—0.05 (F)
Barley
8
1.20
Aerial
Endrin
0.03—0.05 (F)
Soybean
8 4
Beans
Endrin
0.02—0.11
Van Middelem, 1969b
U’
I ’,
-------
Table 4.1
(continued)
Treatment
Endrin In
(ppm)
5011 a
Growth period
Endrin residues
Reference
Plant part
Compound
concentrationb
(ppm)
Plant
(lb/acre) (ppm)
TurnIp
4 2
Greens
Root peels
Endrin
Endrin
Insignificant
0.12
Tobacco
4 2
Green leaves
Endrin
0.04
Turnip
1
0.64
66 days
Greens
Peeled roots
Root peels
Endrin
Endrln
Endrin
0.01 (F)
0.02 (F)
0.03 (F)
Wheeler et al.,
1969
2
0.74
Greens
Peeled roots
Root peels
Endrin
Endrin
Endrin
0.01 (F)
0.02 (F)
0.07 (F)
4
1.98
Greens
Peeled roots
Root peels
Endrin
Endrin
Endrin
0.02 (F)
0.04 (F)
0.12 (F)
Potato
3
6
19 weeks
19 weeks
Tubers
Tubers
Endrin
Endrin
0.084—0.117 (F)
0.100—0.133 (F)
Winnett and Reed, 1968
-
aAf time of planting.
bBased on fresh (F) or dry (0) weight.
CTime from endrin application to harvest.
dEndrin applied twice at 2 lbs/acre: 11 months and 6 months before harvest.
-------
54
and cucumber (Cucumis sativus) in pots in a greenhouse. The soil contained
0.5 or 5.0 ppm endrin. The mean concentration of endrin in aerial parts
of three—week—old seedlings varied considerably with the species, ranging
from 0.045 ppm in soybean to 0.304 ppm in bromegrass for plants grown in
soil that contained 0.5 ppm endrin. For all the plants except cucumber,
however, endrin uptake by each species was proportional to the concentra-
tion of endrin in soil; that is, mean endrin residues in plants grown in
soil containing 5.0 ppm endrin were tenfold the residues found when soil
concentration was 0.5 ppm (Tables 4.1 and 4.2).
Harris and Sans (1967) noted that soil type as well as plant species
affects the amount of endrin absorption. When carrot, radish, turnip,
and onion (Alliwn cepa) were field grown in sandy loam soils containing
0.12 ppm endrin, no endrin residues were detected in the plants. With
muck soils that contained 8.91 ppm endrin, endrin residues were detected
in carrots (0.06 ppm) and in radishes (0.04 ppm), but not in turnips or
onions. The extensive experiments of Beau and Nash (1969) are probably
more indicative of the effect of soil type on root uptake of endrin
because the plants were grown in pots under controlled greenhouse conditions
(Table 4.2). Plants grown in sandy loam usually had the highest endrin
residues, whereas silt generally retarded endrin uptake.
It should be noted that the reported levels of endrin residues in
plants are probably of little value in a study of plant metabolism of
endrin. Hill (1971) emphasized that the dissipation of residues from
growing crops results from the combined effects of various factors,
including pesticide volatilization, photodegradation, mechanical removal
by wind and rain, metabolism, and dilution effected by plant growth. Hill
concluded that it cannot be generalized that a given pesticide will always
disappear from a given crop at the same rate.
Hill’s conclusions are supported by the experiments of Korte (1967)
and co—workers (Weisgerber et al., 1968). Although the same researchers
used the same plant species in experiments in which 1 C—endrin was applied
to the leaves of cabbage (Brassica oleracea capitata), the amount of
radioactivity recovered after four weeks was 6% in one experiment and
25% in the other. The amount of total recovered radioactivity is,
therefore, probably not significant.
The value of experiments of this type is, therefore, primarily in
the quantitative data, that is, the presence or absence of endrin and/or
its metabolites in the different plant parts, identification of the various
compounds, the relative amounts of the compounds at the different locations,
and the relative quantities of parent compounds and their metabolites and!
or degradation products.
Foliar absorption of endrin and its subsequent translocation within
the plant were demonstrated experimentally by a number of investigators.
In these experiments, endrin was applied directly to the leaves; the endrin
often contained ‘ C as a radioactive label. Radioactivity was subsequently
detected in unaltered endrin and in its metabolites as well. The data
are summarized in Table 4.3.
-------
Table 4.2. Plant uptake of endrin from soils
Soil Soil type
Endrin residue
(ppm)a
Soybean
Corn
Alfalfa
Bromegrass
Cucumber
Endrin concentration in soil, 0.5 ppm
Lakeland Sandy loam
0.066
0.084
0.424
0.249
0.206
Hagerstown Sandy clay loam
0.030
0.067
0.211
0.259
0.242
Chillum Silty loam
0.032
0.056
0.086
0.219
0.124
Sterling Loam
0.038
0.062
0.179
0.333
0.228
Sharkey Clay
0.060
0.069
0.174
0.462
0.238
Mean
0.045
0.068
0.215
0.304
0.208
Endrin concentration in soil, 5.0 ppm
Lakeland Sandy loam
0.594
1.132
5.989
3.912
1.734
Hagerstown Silty clay loam
0.260
0.461
1.037
1.659
1.118
Chillum Silty loam
0.256
0.497
1.330
2.031
0.670
Sterling Loam
0.365
0.575
1.407
3.020
0.812
Sharkey Clay
0.575
0.875
2.556
5.014
b
Mean
0.410
0.708
2.464
3.127
1.084
aBased on dry weight of three—week—old (soybean, corn, alfalfa, bromegrass) and four—week—old
(cucumber) seedlings.
bSeedlings killed by disease.
Source: N. L. Beau, Jr. and R. G. Nash, Argon. J. 61(4): 571—575 (1969.
Copyright 1970 American Society of Agronomy.
U i
Ui
-------
Table 4.3, Distribution of endrin and its metabolites in plants following foliar application of 11 ’C—endrin
Growth
period Recovered radioactivity
Plant Endrin applied (weeks)
(2) Location Compound Reference
Cabbage 1.3 mg/plant 4
(60 ppm)
l5ppm 4
On and in leaves, 80%;
in stalks, pods, fibers,
soil, 20%; in roots and
seeds, traces
In leaves
33 On and in leaves, 79.7%;
on stalks, pods, soil,
20.3%; in fibers and
seeds, traces
6 On and in leaves, 85.3%;
in soil, 9.2%; on and in
stems and roots, 5.5%
33.6 On plant surfaces, 1.2%;
inside plants, 95.2%; in
soil, 3.6%
30.1 On plant surfaces, 1.2%;
inside plants, 93.8%; in
soil, 5.0%
25.0 On plant surfaces, 1.0%;
inside plants, 92.5%; in
soil, 6.4%
6 On leaf surfaces, 13.6%;
inside leaves, 74.6%;
in stems and roots, 3.4%;
in soil, 8.5%
30
Endrin + 4 metabolites;
main metabolite: slightly
more hydrophilic than
endrin; 3 metabolites:
highly polar
Endrin + 5 metabolites;
3 metabolites: slightly
more hydrophilic than
endrin (1 ketoendrin);
2 metabolites: very hydro—
philic
Hill, 1970
Endrin + metabolites; Hill, 1971
some metabolites: slightly
more hydrophilic than endrin;
other metabolites: very
hydrophilic
Endrin + 2 metabolites; Korte, 1967;
main metabolite: very Weisgerber et
hydrophilic, 95%; ketoendrin, al., 1968
52
Korte, 1967;
Weisgerber et
al., 1968
Endrin, 90%; 2 metabolites, Korte et al., 1970
10%; main: very hydro—
philic; minor: ketoendrin
Endrin, 91%; 2 nietabolites,
9%; main: very hydrophilic;
minor: ketoendrin
Cotton 120 ppm 12 33
Ketoendrin; endrin
aldehyde, traces
Cotton 200 gIleaf
Cotton 12.6 mg/leaf 12
Cotton
Cabbage 60 ppm 4
Sppm 2
Cabbage 5 ppm 3
4
Soto and
Deichmann, 1967
Bayless et al.,
1970
0 ’
Cabbage 500 ig/p1ant
Leaves, stems, roots, Endrin, 90%; metabolites,
soil 10%
Brooks, 1969
-------
Table 4.3 (continued)
Cabbage 1.3 mg/plant 4 11
Growth
period Recovered radioactivity
Plant Endrin applied (weeks)
(%) Location Compound Reference
Brooks, 1974b
Tobacco
52 ppm
4
36
On
leaf surfaces, 80.6%;
in
plants,
19.4%
Tobacco
2.08 mg/plant
1
73—79
On
and in plants
(100 ppm)
2
4
6
61—66
42—47
32—47
1.04 mg/plant
1
75
On
and in plants
(50 ppm)
2
70
4
6
36
34
Carrot
14 ig/plant
3
Endrin, 90%; a very
polar metabolite,
10%;
A—ketoendrin, small
amt
Endrin, 97.7%;
2 metabolites, 2.3%;
main: very hydro—
philic; minor:
ketoendrin
Endrin, extremely
hydrophilic metabo—
lite(s)
Endrin, extremely
hydrophilic metabo—
lite(s)
Endrin, 68%;
2 metabolites, 32%;
main: very hydro—
philic; minor: keto—
endrin
Korte et al., 1970
Weisgerber et al.,
1969
Korte et al., 1970
‘JI
-4
-------
58
Hill (1970) reported that when about 120 ppm 1 C—endrin was applied
to leaves of cotton (Gossypium hirsutum) plants in three applications,
33% of the applied radioactivity was recovered after 12 weeks. Of the
recovered radioactivity, 80% was found on and in the leaves; 20% was
in the stalks, pods, and fibers and in the soil; only traces were detected
in the roots and seeds. The radioactivity compounds consisted of endrin
and four metabolites. The main metabolite was only slightly more hydro—
philic than endrin; the other three were highly polar. None of the
metabolites was identified.
The work of Burton and Potter demonstrated that endrin is rapidly
absorbed by leaves of cotton (Soto and Deichmann, 1967). Two hours after
200 g endrin was brushed onto each leaf of a cotton plant, ketoendrin
was detected in the leaves at a concentration of 0.35 ppm; after seven
days the concentration had decreased to less than 0.008 ppm. Traces of
endrin aldehyde were also detected in the leaves. Since the endrin used
in the experiment contained about 2% ketoendrin as well as traces of other
impurities, the investigators felt that the endrin aldehyde was not
necessarily a plant metabolite of endrin, that it may have been a
decomposition product or a metabolite of one of the impurities.
In their experiments, Bayless et al. (1970) applied 12.6 mg
1 C—endrin in three equal portions to the upper surfaces of cotton plant
leaves. Twelve weeks after the last application, 33% of the applied
radioactivity was recovered, primarily on and in the leaves and in the
soil (Table 4.4). Of the recovered radioactivity, 76% was associated
with endrin, 24% with endrin metabolites. The five metabolites were of
two types; those in group 1 were slightly more hydrophilic than endrin.
One of the three components was identified as ketoendrin; the two
components of group 2 were very hydrophilic.
Hill (1971) reported that when endrin was applied to the leaves
of cotton, endrin as well as degradation products was subsequently
detected in the plants. There were two groups of endrin metabolites — one
slightly more hydrophilic than endrin, the other very hydrophilic.
When deuterated endrin was applied to cotton, penetration of endrin
into the plants was not detected (Korte et al., 1970). Small amounts
of ketoendrin were found on leaf surfaces; this compound was attributed
to ultraviolet rearrangement of endrin.
Working with young cabbage plants which had not yet formed heads,
Korte (1967) and co—workers (Weisgerber et al., 1968) demonstrated that
endrin is absorbed by the leaves and then translocated throughout the
plant and even into the soil. When 60 ppm 1 C—endrin in acetone was
applied to the cabbage leaves, 6% of the applied radioactivity was
recovered four weeks later. Almost all of the recovered radioactivity
was found within the plant or in the soil, and there were only traces on
the plant surfaces. There was a gradient in the recovered radioactivity —
the concentration was greatest in the leaves; it diminished through the
stems and then the roots and was least in the soil (Table 4.5). There
-------
Table 4.4. Distribution and transformation of endrin 12 weeks after application
of 12.6 mg 11 C—endrin to leaves of cotton (Gossypium hirsutum)
CEndrin and group 1 inetabolites could not be distinguished.
Source: Reprinted with permission from Tetrahedron 26(3): 775—778 (1970). A Bayless,
I. Weisgerber, W. Klein, and F. Korte, “Contributions to Ecological Chemistry XXV. Conversion
and Residue Behavior of 14—C—Endrin in Cotton.” Copyright 1970, Pergamon Press, Ltd.
Location
Concentration
(ppm)
Radioactlvitya
(%)
Endrin
(%)
—
Metabolites
(%)
Group
1
Group
2
Total
Dead leaves
Surface
Interior
129.0
72.2
31.5
17.7
75
75
19
12
6
13
25
25
Living leaves
Surface
Interior
19.5
17.1
16.2
14.3
79
71
15
20
6
9
21
29
Stalks
Roots
0.33
NDb
0.27
ND
85
12
3
15
Pods
4.9
0.06
4 0c
10
>10
Fibers
0.36
0.003
12
>12
Seeds
0.033
0.0006
Soil
0.0053
20.0
81
16
3
19
aAS percentage of total recovered radioactivity.
not detected.
-------
60
Table 4.5. Concentration, distribution, and transformation of
endrin as measured four weeks after application of 60 ppm
14 C—endrin to leaves of cabbage
(Brassica oleracea capitata)
Location
Concentration
(ppm)
Radioactivitya
(%)
Metabolitesb
(%)
Withered leaves
Surface
Interior
2.55
5.10
3.9
8.1
\‘l
l
Living leaves
Surface
Interior
0.26
1.80
9.4
63.9
“il
7
Stem
Surface
Interior
0.13
0.26
1.5
2.8
l
26
Root
Surface
Interior
0.004
0.09
0.3
0.9
‘ 2
40
Soil
0.06
9.2
51
aM percentage of total recovered radioactivity.
percentage of radioactive compounds in each plant part.
Source: I. Weisgerber, W. Klein, A. Djirsarai, and F. Korte,
Justus Liebigs Ann. Chem. 713: 175—179 (1968). Copyright 1968 Verlag
Chemie GmbH.
was also a gradient in the ratio of metabolite concentration to endrin
concentration; this gradient, however, was in the reverse order. Whereas
only 7% of the recovered radioactivity in leaves was associated with
endrin metabolites, metabolites accounted for 26% of the radioactivity
in stems, 40% in roots, and 51% in the soil. Of the total recovered
radioactivity, 10.2% was attributable to the metabolites. Two metabolites
were distinguished; the main metabolite (95%) was very hydrophilic. The
other metabolite (5%) was slightly more hydrophilic than endrin; on the
basis of its chroinatographic behavior, it was identified as ketoendrin.
The investigators demonstrated that these radioactive compounds were
products of plant metabolism of endrin. In plants kept in the dark for
four weeks after the application of endrin, the concentrations of inetabo—
lites were about the same as in plants kept in the light. Consequently,
the compounds could not have been the products of photodecomposition of
endrin. Korte and co—workers also determined that decomposition on active
surfaces in the presence of light and air could not account for the
metabolities — less than 1% of the endrin applied to leaf surfaces, faded
leaves, glass plates, and Bilica gel plates degraded in four weeks under
the conditions of the experiment. Furthermore, the metabolites detected
in the soil had been excreted by the plants, since, under the experimental
conditions, less than 4% of endrin in soil degrades in four weeks.
-------
61
In another experiment with cabbage, Weisgerber et al. (1968) followed
the effect of time on the recovery of radioactivity. Carbon—14—endrin was
applied to the leaves at the rate of 5 ppm based on total plant weight.
Recovery of radioactivity decreased from 33.6% after two weeks to 25.0%
after four weeks (Table 4.6). During the same time interval, the amounts
of recovered radioactivity decreased on plant surfaces (from 0.40 to
0.26%) and inside the plants (from 32.0 to 23.1%), while it increased in
the soil (from 1.2 to 1.6%).
Table 4.6. Distribution of radioactivity after application
of 5 ppm 1 C—endrin to leaves of cabbage
(Brassica oleracea capitata)
Time after
application
(weeks)
Recovered
radioactivity (%)
On
plant surface
Inside plants
In
soil
Total
2
0.40
32.0
1.2
33.6
3
0.35
28.25
1.5
30.1
4
0.26
23.10
1.6
25.0
Source: I. Weisberger, W. Klein, A. Djirsarai, and F. Korte,
Justus Liebigs Ann. Chem. 713: 175—179 (1968). Copyright 1968
Verlag Cheinie GmbH.
Subsequent experiments with cabbage revealed that 1 hr after
application to upper leaf surfaces of 1.3 mg 1 C—endrin in acetone per
plant (which corresponds to 60 ppm based on plant weight at end of
experiment), 100% of the radioactivity was still present on the leaf
surfaces (Korte et al., 1970). After the plants had grown four weeks
in greenhouses, about 6% of the applied radioactivity was recovered:
0.8% on leaf surfaces, 4.4% inside the leaves, 0.2% in the stems and roots,
and 0.5% in the soil. On the basis of loss of radioactivity from surfaces
(glass, silica gel, paper), the disappearance of 60% of the applied
radioactivity was attributed to vaporization of endrin from the leaf
surfaces. The remainder of lost radioactivity was attributed to removal
from the plants by processes such as transpiration and excretion with
guttation water. The metabolic rate (i.e., the proportion of radioactivity
recovered in plants and soil that is attributable to metabolites) was
10%. When the cabbage plants were kept in the dark after application of
endrin, the metabolic rate was 14%. Conversion on active surfaces (dead
leaves, glass plates, silica gel, and plant homogenates) amounted to
less than 2%, so the conversion products detected in and on the plants
were endrin metabolites. Two metabolites were detected — the main one
was very hydrophilic, the other was ketoendrin.
When 75 ppm 14 C—endrin was applied to the upper surfaces of cabbage
leaves, 30% of the applied radioactivity was detected four weeks later
(Korte et al., 1970). Nine percent of the recovered radioactivity was
associated with hydrophilic metabolites of endrin.
-------
62
Brooks (1969) noted several of Korte’s experiments with cabbage.
In one experiment, when 50 pg 1 C—endrin was applied to leaves of growing
cabbage plants, 66% of the applied radioactivity was lost by evaporation
in two weeks. In another experiment, after 500 pg 1 C—endrin was applied
per plant, radioactivity was recovered, in decreasing order, from the
leaves, stems, roots and soil. The radioactive material recovered on
plant surfaces and in the leaves was mostly endrin. The proportion of
endrin metabolites, which constituted 10% of the recovered activity,
increased progressively in stems, roots, and soil. Brooks suggested
two explanations for this finding: (1) water—insoluble endrin is retained
in the leaves, while the hydrophilic conversion products are transported
to other parts of the plant; (2) metabolism of endrin occurs primarily
in the stems and roots.
Brooks (1974b) reported that when 1.3 mg 1 C—endrin per plant was
applied to the leaves of cabbage, 11% of the applied radioactivity was
recovered after four weeks. Of the recovered radioactivity, 90% was
associated with endrin, 10% with a very polar metabolite, and a small
amount with delta—ketoendrin.
Most of the experimental work on the tobacco was done by Korte and
co—workers. When 52 ppm 1 C—endrin was applied to tobacco leaves, 36% of
the applied radioactivity was recovered after four weeks: 29% on leaf
surfaces and 7% in the plants; the metabolic rate was 2.3%. The metabolite
fraction consisted of two compounds — a very hydrophilic main metabolite
and some ketoendrin (Korte et al., 1970). When 1 C—endrln was applied to
the upper surfaces of tobacco leaves at the rates of 2.08 and 1.04 mg per
plant (100 and 50 ppm respectively), 34 and 47% of the applied radio-
activity was recovered on and in the treated plants after six weeks
(Table 4.7). The investigators concluded that part of the applied endrin
was eliminated by the plants unaltered into the atmosphere, while the
roots excreted both unaltered endrin and endrin metabolite(s) into the
soil. The radioactive compounds consisted of endrin and at least one
extremely hydrophilic metabolite, which was chromatographically identical
to the main metabolite found in cabbage; it was neither ketoendrin nor
endrin aldehyde (Weisgerber et al., 1969).
In their work with carrot, Korte et al. (1970) found that the
metabolic rate depended on the mode of application. In these experiments,
14 pg ‘ C—endrin was applied per plant, and the material was analyzed
three weeks later. When the endrin was applied to the soil, the metabolic
rate was 5%. On the other hand, the metabolic rate was 12% when endrin
was injected into the roots and 32% when it was applied to the leaves near
the vegetation point. Two metabolites of endrin were distinguished — a
main metabolite that was very hydrophilic and also some ketoendrin.
Some experiments were designed specifically to demonstrate, and
also to compare, uptake of soil endrin by roots and of vaporized endrin
by leaves (Nash and Beall, 1970; Beall and Nash, 1971). Soybean plants
were grown in pots in a greenhouse for 53 days. Either the surface or the
subsurface soil layer was treated with endrin (concentration: 20 ppm),
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63
Table 4.7. Distribution and metabolism of 1 C—endrin after
application to upper surfaces of leaves of tobacco
(IVicotiana tabacuin)
Growth period
Recovered radioactivity (%)
Metabolic rate
(%)
Total Surfacea
Internala
Endrin application: 2.08
mg/plant
(100
ppm)
2 days
81.2 93.8
6.2
1 week
97.2 93.8
6.2
4.6
2 weeks
66.3 92.2
7.8
9.8
4 weeks
46.7 71.2
28.8
6.6
6 weeks
47.0 73.5
26.5
8.9
Endrin application: 1.04
mg/plant
(50
ppm)
2 days
87.9 96.3
3.7
1 week
75.2 95.2
4.8
8.9
2 weeks
69.6 90.1
9.9
5.8
4 weeks
36.4 80.7
19.3
20.8
6 weeks
34.3 42.4
57.6
7.2
aBased on radioactivity recovered on and in plants.
Source: I. Weisgerber, W. Klein, and F. Korte, Liebigs Ann. Chern.
729: 193—197 (1969). Copyright 1969 Verlag Chemie GmbH.
and the two were separated by a water— and vapor—impermeable barrier that
prevented movement of endrin through the soil from one layer to the other.
A glass tube that extended upward from the barrier isolated the stem of
each plant from the surrounding surface soil layer. Each pot was enclosed
in a polyethylene cage in order to localize the vapors around the plant.
These experiments demonstrated that soybean roots take up endrin from
soil and that leaves absorb endrin that has vaporized from treated soil
(Table 4.8). With root sorption, endrin concentrations were highest in
the stems and then, in decreasing order, in leaves, pods, and seeds. When
endrin vapor was sorbed, the concentrations were highest in the leaves,
then decreased through the pods, stems, and seeds. Endrin as well as
two metabolites was detected in the plants. The ratio of metabolites to
parent endrin was greater in leaves than in stems.
When seedlings of wheat were grown for 16 days in water that con-
tained 0.11 ppm 1 C—endrin, radioactivity was recovered in both water
and seedlings (Klein et al., 1968b). Endrin metabolites accounted
for 58% of the radioactivity in the water and 20% of that in the plants.
The endrin applied to crops and soils is seldom chemically pure, and
related compounds such as ketoendrin are frequently present as contaminants
and/or degradation products. Klein (1972) investigated the fate of
delta—ketoendrin applied to leaves of cabbage. Re found that ketoendrin
residues disappeared more slowly than did those of endrin. The metabolic
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64
Table 48. Sorption of endrin by soybean (Glycine max)
from soil and from air
Plant
part
Endrin concentration
(ppm)
Root sorptionCl
Leaf
sorptionb
Upper
leaves
87.71
15.95
Lower
leaves
160.55
33.78
Upper
stems
217.30
2.42
Lower
stems
359.62
1.66
Pods
10.44
2.84
Seeds
3.30
0.99
AverageC
38.1
6.7
asti of endrin from soil.
bSorption of endrin vaporized from soil.
0 Average concentration in aerial parts of plants.
Source: M. L. Beall and R. G. Nash, Agron. J. 63(3): 460—464
(1971). Copyright 1971 inerican Society of Agronomy.
rate in cabbage, four weeks after the application, was greater for keto—
endrin (15%) than for endrin (10%). The main metabolite of ketoendrin,
an unidentified polar compound, was present in highest concentrations
in leaves and stems.
In 1967, Nash and Harris (1973) examined the soil in some fields
that had been treated in 1951 with endrin at the rates of about 56 and
224 lb/acre (56 and 225 kg/ha; soil concentration, about 28 and 112 ppm).
Endrin, ketoendrin, two endrin aldehydes, and endrin alcohol were
identified in the soil. When soybean crops were grown in these fields,
endrin, ketoendrin, one endrin aldehyde, and endrin alcohol residues were
detected in the beans. Whereas the concentrations of endrin and keto—
endrin in soybeans were about 0.2 and 0.5% of the respective concentrations
in the soil, the endrin alcohol concentration in soybeans was about
10% of its concentration in soil. The reason f or the relatively greater
concentration of endrin alcohol in soybeans has not been ascertained.
Endrin alcohol may be more readily taken up from the soil and translocated
within the plant. Another possibility is that endrin, ketoendrin, and
possibly endrin aldehyde are metabolized by plants to endrin alcohol
(it is known that endrin and ketoendrin are converted to the alcohol
under severe conditions of acid and heat).
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65
It has been demonstrated that plants take up endrin from the soil
by root absorption and that leaves take up endrin applied directly to
leaf surfaces as well as vaporized endrin. Following uptake, endrin
is translocated to all parts of the plant. Endrin taken up by specific
root sections is subsequently translocated both acropetally and basipetally
(Beau and Nash, 1972). Plants metabolize endrin to delta—ketoendrin
and possibly to endrin aldehyde and as three additional inetabolites
(Brooks, l974b). The reported metabolites are of two types —one group,
including ketoendrin, is slightly more hydrophilic than endrin, whereas
the other is very hydrophilic.
4.3.2 Effects of Endrin
The major use of endrin is as a pesticide in agriculture (see
Sect. 2.5). The compound is usually applied to the fields by spraying
or dusting, and in this way it comes in direct contact with the plants.
It is essential that the plants suffer no adverse effects from this treat-
ment, and the paucity of information in the literature about the effects
of endrin on plants is therefore surprising.
Scholes (1955), in the 1951 progress reports by Julius Hyman and
Company on the development of endrin, noted that slight burning of corn
buds and cucumber foliage occured when plants were sprayed with endrin.
In his review of cholorinated insecticides, Brooks (1974a) reported
that “phytotoxicity appears to present few problems’ t if endrin is properly
applied. Adverse effects noted with some sensitive plants were traced to
the solvent used in the formulation. Endrin itself can be injurious to
corn (Zea maya).
Cucurbits (plants in the gourd family) are highly sensitive to
chemicals and were therefore selected by Sood et al. (1972) for use
in a study of the phytotoxicity of endrin. Bottlegourd (Lagenaria
sicararia), cucumber (Cuewnis sativus), and tinda (Citrullus vulgaris)
plants at the four—leaf stage were sprayed once with a 0.03 or a
0.04% endrin emulsion. Phytotoxicity was assessed by the number of spots
on the foliage that resulted from scorching. The 0.03% endrin emulsion was
slightly toxic to cucumber, but highly toxic to bottlegourd and tinda by
the seventh day. With the 0.04% endrin emulsion, high phytotoxicity to all
three varieties was apparent by the third day after spraying.
Abo El Liel et al. (1970) studied the effects of various insecticides
on Ashmouni cotton (Gossypiwn hirsutwn). They concluded that, when endrin
in a mixture with DDT—lindane is sprayed on cotton plants four to ten
times during the growing season, there are no undesirable effects which
could reduce the yield of cotton seed. The application consisted of
1.5 liters of endrin plus 1.5 liters of DDT—lindane per feddan (1 feddan
is about 1 acre or 0.4 ha); insecticide concentrations were not reported.
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66
Crouch and Radwan (1972) investigated the use of endrin in a coating
for Douglas fir (Pseudotsuga menziesii) seed as protection against seed—
eating deer mice. At 0.5%, endrin had little effect on seed germination.
Of the endrin—coated seeds, 82% germinated on perlite and 73% in soil;
for control (i.e., untreated) seeds, the germination rates were 83 and
80% respectively. Seedling growth was not affected by endrin.
Scholes (1955) investigated the effects of endrin on mitosis in
onion (Alliwn cepa) roots. When onion seeds were germinated in petri
dishes which contained endrin dust on gypsum at amounts equivalent to
0.4 and 2.0 lb/acre (about 0.4 and 2.0 kg/ha; soil concentration, about
0.2 and 1.0 ppm), there was very little effect on resting and on dividing
cells examined after a 48—hr growth period. A slight stickiness of the
chromosomes in anaphase delayed, but did not prevent, separation of the
chroinatids.
In another experiment. (Scholes, 1955), endrin was applied to and
mixed with the surface layer of soil at the heavy dose of 2.0 lb/acre
(about 2.0 kg/ha; soil concentration, about 1.0 ppm). The onion
(Alliwn cepa) seedlings were examined ten days after sowing. Rates
of germination and growth were within the normal variation for untreated
seed. Cytological examination of root cells did not provide any evidence
of toxic effects on the resting cell. In mitotic cells, there was an
increased number of anaphases with incomplete separation of chromatids,
but this was not sufficient to affect the growth rate.
Wuu and Grant (1966) investigated the phytotoxicity of endrin to
barley (Hordewn vulgare). Barley seeds were soaked in endrin solutions
at 500, 1000, or 1500 ppm for 6, 12, or 24 hr. They were then washed in
tap water, placed in petri dishes, and incubated. Germinability of the
seeds, as measured after 36 hr, decreased with increase in endrin con-
centration and lengthening of the soaking period. Duration of soaking
had the greater effect. The germination rate was severely reduced in
seeds soaked in endrin for 24 hr; at endrin concentrations of 500 and
1500 ppm, only 52 and 50% respectively, of treated seeds germinated
(see Table 4.9 for a tabulation of the data). Cytological studies of
root—tip cells confirmed the germination data. The mean frequency of cells
with chromosome aberrations was 6.01, 7.63, and 9.05% for the 6—hr, 12—hr,
and 24—hr treatment periods respectively. The overall mean was 7.59% for
endrin—treated barley seeds. The most common chromosome aberrations were
fragments in metaphase and in anaphase, and anaphase bridges. There were
no obvious morphological effects on root growth with any treatment.
In order to study the transmission of chromosomal abnormalities,
Wuu and Grant (1966) soaked barley (Hordewn vulgare) seeds in a 1000—ppm
solution of endrin for 12 hr; the seeds were then washed in tap water and
planted in soil. Seeds of the C—i generation were harvested and planted.
Among the 933 seedlings in the C—2 generation, there were three mutants
(one plant with a striped leaf and two dwarf plants). The mutation rate
-------
Table 4.9. Effect on barley seeds (Hordeum volgare)
of soaking in endrin solutions
Soaking period 6 hr 12 hr 24 hr
Concentration (ppm) 500 1000 1500 500 1000 1500 500 1000 1500
Germination (%) 92 88 90 84 84 80 52 80 50
Abnormal cells (%) 5.58 6.42 6.02 7.48 8.54 6.53 8.96 7.54 10.63
Chromosome aberrations
(No. of cells)
Metaphase fragments
Single 4 2 6 8 11 6 9 7 4
Double 0 1 1 3 3 0 1 0 1
Multiple 0 0 2 1 2 3 1 1 4
Anaphase bridges
Single 3 4 4 3 5 2 4 3 8
Anaphase fragments
Single 4 1 0 1 0 1 3 3 6
Double 0 1 0 1 1 1 0 3 1
Multiple 1 0 1 0 0 0 0 0 0
Othera 0 5 1 2 2 0 1 2 3
Total 12 14 15 19 24 13 19 19 27
alncludes telophase bridges, lagging chromosomes, bridges and fragments, and incomplete chromosome
breakages.
Source: K. D. Wuu and W. F. Grant, Can. J. Gent. Cytol. 8(3): 481-501 (1966).
Copyright 1966 Genetics Society of Canada.
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68
was therefore 0.32%, whereas it was 0.11% in the control group (1 yellow
plant out of 891). Only 1.55% of the root—tip cells examined had
chromosome aberrations, whereas the frequency in the C—i generation had
been 8.54%.
Wuu and Grant speculated that possible nonviability of cells with
chromosome aberrations resulted in the low transmission of chromosomal
abnormalities from the C—i to the C—2 generation. Cells with aberrations
of a lethal nature would have been eliminated in the course of the numerous
cell divisions which had occurred, and only chromosome aberrations with
less severe effects would have persisted.
Wuu and Grant (1967b) also investigated endrin induction of chromosome
aberrations in root—tip cells of broad bean (Vicia faba). Seedlings that
were 15 cm high (10 to 15 days old) were carefully removed from the soil
and immersed in aqueous endrin solutions for 3, 6, or 12 hr. After
washing and 24 hr in tap water, the roots were fixed and stained. Endrin
at concentrations of 200, 400, and 600 ppm was extremely toxic and strongly
inhibited root growth. Even at concentrations of 100, 200, and 300 ppm,
endrin greatly increased the frequency of chromosome aberrations. The
number of chromosomal abnormalities increased with increase in endrin
concentration and also with increase in duration of treatment. The mean
frequency of endrin—induced abnormal cells was 18.55%.
The effect of endrin on ineiotic cells of barley (Hordewn vulgare) was
also studied by Wuu and Grant (1967a). Barley seeds were soaked in a
1000—ppm solution of endrin for 12 hr; they were then washed in tap water
and sown in soil. Seeds of the C—i generation were harvested and sown.
Pollen mother cells of the C—i and C—2 generations were examined, and the
frequency of cells with chromosome aberrations was 0.26 and 0.37%
respectively. These frequencies were not significantly different from
those in control plants. In another experiment, barley seeds were soaked
12 hr in tap water and sown in soil; then on day 16 the seedlings were
sprayed with a 500—ppm solution of endrin at the rate of 2 ml per five
seedlings. Chromosome aberrations (anaphase bridges and fragments)
appeared in the pollen mother cells at a frequency of 0.98%. Spraying
barley plants with endrin at 500 ppm, therefore, induced a higher frequency
of chromosomal abnormalities in meiotic cells than did soaking the seeds
in endrin at 1000 ppm for 12 hr.
In addition to these studies of the phytotoxicity of endrin, there
have also been some studies of the effects of endrin—contaminated soil
on various constituents of plants growing in such soil.
Thakre and Saxena (1970) reported that the presence of endrin in the
soil at 10, 20, and 30 ppm affected calcium uptake by plants. Endrin at
these concentrations reduced calcium uptake by wheat but more than doubled
the calcium uptake by corn. In the same experiments, 10 ppm endrin did not
affect iron uptake, whereas 20 and 30 ppm did reduce iron uptake signif i—
cantly in wheat and slightly in corn. Wheat plants were harvested after
90 days of growth, corn after 50 days.
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69
Endrin in the soil at concentrations of 10, 20, and 30 ppm also
affected the amino acid composition of corn harvested after 50 days of
growth (Thakre and Saxena, 1972). The most significant changes were
increases in the contents of proline, lysine, arginine plus histidine,
and leucine, and decreases in the contents of tryptophan and valine.
Thakre and Saxena speculated that the presence of endrin in soil and
its absorption by plants could alter the nutritional value of these
plants as a consequence of changes in the amino acid composition.
Cole et al. (1968) investigated the effects of different concen—
trations of endrin in soil on the growth and on the macro— and microelement
contents of corn and green beans (Phaseolus vulgaris) (see Table 4.10).
The aboveground portions of the plants were analyzed after four and
eight weeks of growth. Endrin at all concentrations significantly
reduced the phosphorus contents of eight—week—old corn plants and of
four— and eight—week—old bean plants. The potassium content of all
four—week—old bean plants was decreased, but this change was noted in
eight—week—old bean plants only when the endrin concentration was 1 ppm.
Endrin increased the magnesium content of corn but decreased it in bean.
With the microelements, endrin effected significant decreases in the
contents of copper and zinc in both corn and bean and of boron in bean.
Significant increases in the levels of manganese and iron were detected.
The effect of endrin on the fresh weight was only slight in four—week—old
plants; however, the decreases were significant in eight—week—old corn
plants grown in soil that contained 100 ppm endrin and in eight—week—old
bean plants grown in soil with 10 and 100 ppm endrin.
-------
Table 4.10. Effect of soil endrin on aboveground portions of corn (Zea mays) and
bean (Vicia faba)
Macroelements
Microelements
Plant
Endrin
(ppm)
Fresh
weight (g)
(%
of
dry
weight)
(ppm of
dry
weight)
N
P
K
Ca
Mg
Mn
Fe
Cu
B
Al
Sr
Zn
Corn, 4 weeks
0
1
10
100
4.1
3.8
4.0
4.2
6.02
5.68
5.67
5.64
0.88
0 71 a
0.88
0.84
6.80
5.84
6.30a
6.08
0.80
0.87
0.89
0.94
0.29
0.31
033 a
0.32
434
454
533a
460
185
205
242 a
171
13.4
11 • 1 a
12.8
10 ga
19
25 a
21
18
121
166
137
117
11
11
11
12
117
83 a
91 a
96a
Corn, 8 weeks
0
1
10
100
27.1
27.8
24.8
23.la
3.45
3.43
3.20
3.15
0.54
0 • 44 a
0.48a
o 45a
4.71
5.00
5.53
4.87
0.73
0.75
0.68
0.84
0.27
0.25
0.26
O. 3 0a
362
331
350
318
119
117
120
124
8.5
8.5
7.9
7.6a
15
16
16
15
74
63
78
78
9
10
10
11 a
65
40
49
51
Bean, 4 weeks
0
1
10
100
7.0
6.0
6.4
6.0
6.25
6.25
6.45
6.09
0.65
0.45’ ’
0 50 a
0.60
5.40
495 a
4.89a
1.82
1.73
1.83
1.94
0.40
037 a
0.40
0.38
513
499
5 92a
574
257
224
275
259
10.6
9.la
10.0
11.2
41
33 a
35 a
39
205
171
210
186
23
22
22
22
96
75 a
94
79 a
Bean, 8 weeks
0
1
10
100
18.8
18.0
128 a
l2.4a
3.92
3.28a
3.83
4.24
0.54
036 a
038 a
0 • 47 a
3.82
295 a
3.90
3.93
1.74
1.98
1.52
1.88
0.36
0.36
0.32a
0.37
523
495
495
558
233
244
3Ø5a
234
10.5
7 7
8.2a
8 • 2 a
59
38a
38 a
43 a
132
177
198
119
22
21
20 a
22
76
51 a
62
69
asignificantly different from the control.
Source: modified from Cole et al., 1968.
0
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71
4.4 REFERENCES
Abo El Liel, G. A., F. A. Sorour, and H. Helmy. 1970. Effect of Some
Insecticides and Number of Sprays on Growth and Yield of Ashmouni Cotton.
Agric. Res. Rev. 48(6): 289—301.
Archer, T. E. 1968b. Location, Extraction, and Removal of Endrin
Residues on Alfalfa Hay. J. Dairy Sci. 51(10): 606—1611.
Barrentine, B. F., and J. D. Cain. 1969. Residues of Endrin and DDT
in Soybeans Grown on Soil Treated with These Compounds. Pesti. Monit.
J. 3(2): 77—79.
Bayless, A., I. Weisgerber, W. Klein, and F. Korte. 1970. Contributions
to Ecological Chemistry. XXV. Conversion and Residue Behavior of
14—C—Endrin in Cotton (in German with English abstract). Tetrahedron
26(3): 775—778.
Beall, N. L., Jr., and R. G. Nash. 1969. Crop Seedling Uptake of DDT,
Dieldrin, Endrin, and Heptachlor from Soils. Agron. J. 61(4): 571—575.
Beall, N. L., Jr., and R. G. Nash. 1971. Organochlorine Insecticide
Residues in Soybean Plant Tops: Root vs Vapor Sorption. Agron. J.
63(3): 460—464.
Beau, M. L., Jr., and R. C. Nash. 1972. Insecticide Depth in Soil —
Effect on Soybean Uptake in the Greenhouse. J. Environ. Qual. 1(3):
283—288.
Bhalla, J. S., H. R. Krueger, 0. S. Bindra, and S. N. Deshmukh. 1970.
Estimation of Endrin Residues in/on Bhindi Fruits by Gas—Chromatography.
Indian J. Entomol. 32(3): 189—193.
Bowery, T. G., W. R. Evans, F. E. Guthrie, and R. L. Rabb. 1959.
Insecticide Residues on Tobacco. J. Agric. Food Chem. 7(10): 693—702.
Brett, C. H., and T. G. Bowery. 1958. Insecticide Residues on Vegetables.
J. Econ. Entomol. 51(6): 818—821.
Brooks, G. T. 1969. The Metabolism of Diene—Organochiorine (Cyclodiene)
Insecticides. Residue Rev. 27: 81—138.
Brooks, G. T. 1974a. Chlorinated Insecticides. Vol. I: Technology and
Application. CRC Press, Cleveland, Ohio.
Brooks, G. T. 1974b. Chlorinated Insecticides. Vol. II: Biological
and Environmental Aspects. CRC Press, Cleveland, Ohio.
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72
Cole, H., D. MacKenzie, C. B. Smith, and E. L. Bergman. 1968. Influence
of Various Persistent Chlorinated Insecticides on the Macro and Micro
Element Constituents of Zea rnays and Phaseolus vulgari s Growing in Soil
Containing Various Amounts of These Materials. Bull. Environ. Contam. and
Toxicol. 3(3): 141—153.
Crouch, G. L., and N. A. Radwan. 1972. Arasan in Endrin Treatments to
Protect Douglas—Fir Seed from Deer Mice. U.S. Department of Agriculture,
Forest Service, Pacific Northwest Forest and Range Experiment Station,
Portland, Oregon.
Foster, A. C., V. R. Boswell, R. D. Chishoim, R. H. Carter, G. L. Gilpin,
B. B. Pepper, W. S. Anderson, and M. Gieger. 1956. Some Effects of
Insecticide Spray Accumulations in Soil on Crop Plants. U.S. Department
of Agriculture, Technical Bulletin 1149, 36 pp.
Gyrisco, G. G., and F. W. Huddleston. 1961. The Persistence of Aidrin,
Dieldrin, and Endrin Residues on Fresh Forage and on Hay Under Various
Conditions of Curing. J. Econ. Entomol. 54(4): 718—720.
Harris, C. R., and W. W. Sans. 1967. Absorption of Organochiorine
Insecticide Residues from Agricultural Soils by Root Crops. J. Agric.
Food Chem. 15(5): 861—863.
Hermanson, H. P., L. D. Anderson, and F. A Gunther. 1970. Effects of
Variety and Maturity of Carrots upon Uptake of Endrin Residues from
Soil. J. Econ. Entomol. 63(5): 1651—1654.
Hill, K. R. 1970. IUPAC Commission on Terminal Residues. J. Assoc. Of f.
Anal. Chem. 53(5): 987—1003.
Hill, K. R. 1971. IUPAC Commission on Terminal Residues. J. Assoc. Of f.
Anal. Chem. 54(6): 1316—1322.
Horsfall, F., R. E. Webb, N. 0. Price, and R. W. Young. 1970. Residues
in Apples Subsequent to Ground Sprays of Endrin. J. Agric. Food Chem.
18(2): 221—223.
Klein, W. 1972. Metabolism of Pesticides in Higher Plants. Envrion.
Qual. Saf. 1: 117—124.
Klein, W., F. Korte, I. Weisgerber, R. Kaul, W. Muller, and A. Djirsarai.
l968b. Uber Den Metabolismus Von Endrin, Heptachior Und Telodrin. Qual.
Plant Mater. 15: 225—238.
Knutson, H., A. M. Kadoum, T. L. Hopkins, G. F. Swoyer, and T. L.
Harvey. 1971. Insecticide Usage and Residues in a Newly Developed
Great Plains Irrigation District. Pestic. Monit. J. 5(1): 17—27.
Korte, F. 1967. Metabolism of Aldrin, Dieldrin, and Endrin. In:
Symposium on the Science and Technology of Residue Insecticides in
Food Production with Special Reference to Aldrin and Dieldrin, sponsored
by Shell Chemical Company, pp. 102—117.
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73
Korte, F., W. Klein, I. Weisgerber, R. Kaul, W. Mueller, and A. Djirsarai.
1970. Recent Results in Studies on the Fate of Chlorinated Insecticides.
Inter—American Conference on Toxicology and Occupational Medicine:
Pesticide Symposia Collection of Paper 6th, 7th, pp. 51—56.
Matsumura, F., U. G. Khanvilkar, K. C. Path, and G. M. Boush. 1971.
Metabolism of Endrin by Certain Soil Microorganism. J. Agric. Food Chem.
19(1): 27—31.
Mattick, L. R., D. L. Barry, F. M. Antenucci, and A. W. Avens. 1963.
The Disappearance of Endrin Residues in Cabbage. J. Agric. Food Chem.
11(1): 54—55.
Nash, R. C. l974b. Plant Uptake of Insecticides, Fungicides, and
Fumigants from Soils. In: Pesticides in Soil and Water, Soil Science
Society of America, Inc., Madison, Wisconsin, Chap. 11.
Nash, R. G., and M. L. Beau, Jr. 1970. Chlorinated Hydrocarbon
Insecticides: Root Uptake Versus Vapor Contamination of Soybean
Foliage. Science 168(3935): 1109—1111.
Nash, R. C., and M. L. Beau, Jr. 1971. Extraction and Identification of
Endrin and Heptachior Degradation Products. J. Assoc. Of f. Anal. Chem.
54(4): 959.
Nash, R. G., and W. G. Harris. 1973. Chlorinated Hydrocarbon Insecticide
Residues in Crops and Soil. J. Environ. Qual. 2(2): 269—273.
Nash, R. C., M. L. Beall, Jr., and W. G. Harris. 1972. Endrin Trans-
formation in Soil. J. Environ. Qual. 1(4): 391—394.
Nash, R. C., W. G. Harris, P. D. Ensor, and E. A. Woolson. 1973.
Comparative Extraction of Chlorinated Hydrocarbon Insecticides from
Soils 20 Years After Treatment. J. Assoc. Of f. Anal. Chem. 56(3):
728—732.
Nelson, D., and C. Williams. 1971. Action of Cyclodiene Pesticides
on Oxidative Metabolism in the Yeast Saccharomyces cerevisiae. J. Agric.
Food Chem. 19(2): 339—341.
Saha, J. G., and H. McDonald. 1967. Insecticide Residues in Wheat Grown
in Soil Treated with Aldrin and Endrin. J. Agric. Food Chem. 15(2):
205—207.
Saha, J. C., C. H. Craig, and W. K. Janzen. 1968. Organochiorine
Insecticide Residues in Agricultural Soil and Legume Crops in North-
eastern Saskatchewan. J. Agric. Food Chem. 16(4): 617—619.
Scholes, M. E. 1955. The Effects of Aldrin, Dieldrin, Isodrin, Endrin,
and DDT on Mitosis in Roots of the Onion (Alliwn cepa L.) J. Hortic.
Sci. 30: 181—187.
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74
Singh, R., L. Iyengar, and A. V. S. Prabhakara Rao. 1977. Effect of
Chlorinated Hydrocarbons (Insecticides) on Fermentation Processes.
J. Ferment. Technol. 55(3): 281—284.
Sood, N. K., U. K. Kaushik, and V. S. Rathore. 1972. Phytotoxicity
of Modern Insecticides to Cucurbits. Indian J. Hortic. 29(1): 111—113.
Soto, A. R., and W. B. Deichmann. 1967. Major Metabolism and Acute
Toxicity of Aidrin, Dieldrin, and Endrin. Environ. Res. 1: 307—322.
Thakre, S. K., and S. N. Saxena. 1970. Effect of Chlorinated
Insecticides on the Uptake of Calcium and Iron by Wheat (Triticum
vuigare viii.) and Maize. Andhra Agric. J. 17(6): 190—192.
Thakre, S. K., and S. N. Saxena. 1972. Effect of Soil Application of
Chlorinated Insecticides on Amino Acid Composition of Maize (Zea mays).
Plan. Soil. 37(2): 415—418.
Van Middelem, C. H. l969b. Cooperative Study on Uptake of DDT, Dieldrin,
and Endrin by Peanuts, Soybeans, Tobacco, Turnip Greens, and Turnips
Roots (Summary/Conclusions). Pestic. Monit. .1. 3(2): 100—101.
Wheeler, W. B., H. A. Moye, C. H. Van Middelem, N. P. Thompson, and
W. B. Tappan. 1969. Residues of Endrin and DDT in Turnips Grown in
Soil Containing These Compounds. Pesti. Monit. J. 3(2): 72—76.
Winnett, G., and J. P. Reed. 1968. Aldrin, Dieldrin, Endrin, and
Chiordane Persistence — A 3—Year Study. Pestic. Monit. J. 2(3): 133—136.
Weisgerber, I., W. Klein, A. Djirsarai, and F. Korte. 1968. Distribution
and Metabolism of Endrin—(14C) in White Cabbage (in German). Justus
Liebigs Ann. Chem. 713: 175—179.
Weisgerber, I., W. Klein, and F. Korte. 1969. Disappearance of Residues
and Metabolism of Endrin—(14C) in Tobacco (in German with English
abstract). Liebigs Ann. Chem. 729: 193—197.
Wuu, K. D., and W. F. Grant. 1966. Morphological and Somatic Chromosomal
Aberrations Induced by Pesticides in Barley (Hordewn vuigare). Can. J.
Genet. Cytol. 8(3): 481—501.
Wuu, K. D., and W. F. Grant. 1967a. Chromosomal Aberrations Induced
by Pesticides in Meiotic Cells of Barley. Cytologia 32: 31—41.
Wuu, K. D., and W. F. Grant. l967b. Chromosomal Aberrations Induced
in Somatic Cells of Vicia faba by Pesticides. Nucleus 10(1): 37—46.
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5. BIOLOGICAL ASPECTS IN ANIMALS
5.1 SUMMARY
Animals are exposed to endrin via all media (i.e., food, water, air,
soil). Endrin is absorbed through the digestive tract and through body
surfaces. Absorption of endrin is based on solubility differences between
water and liquid, with a continual residue exchange between tissues and
body fluids or, in the case of aquatic animals, the surrounding medium.
After an initial rapid uptake, endrin accumulation reaches a plateau that
appears to represent a balance between elimination and uptake. Both rate
of uptake and equilibrium concentrations are directly related to the
exposure level.
Endrin is not stored in tissues, but remains in a dynamic state,
equilibrating with ambient levels. After an equilibrium concentration
is reached, duration of exposure does not affect the amount of residue.
However, after chronic exposures, many insects, shrimp, and fish develop
a tolerance to increased endrin doses.
Evidence for transformation of endrin by aquatic animals and birds
is derived from “balance” studies that show incomplete recovery of the
introduced endrin and the presence of polar metabolites. Identification
of the metabolites in fish and aquatic invertebrates is speculative, but
a hydroxylated compound has been suggested by analogy with dieldrin
metabolism.
Endrin is eliminated from birds, mammals, and aquatic animals when
the exposure level is lowered. Passive equilibrium reactions that lower
residues in tissues appear to account for the major pathway of endrin
elimination; however, active excretion has been suggested to occur in
bluegill sunfish. The rate of endrin accumulation in bluegills drops
after initial uptake, possibly resulting from stimulation of an elimination
mechanism.
Aquatic invertebrates and fish are killed by endrin concentrations
of 1 ppb in water, while birds and mammals, acquiring endrin from food,
show mortality at doses from 2 to 20 ppm. Concentrations at a lower
magnitude caused pathologic and reproductive changes, suggesting that
chronic exposure to even lower concentrations may affect nerve function
and metabolism.
The central nervous system appears to be the primary site of endrin
toxicity in all animals. The symptoms of endrin poisoning reflect nerve
stimulation, and reactions to acute levels generally follow the order:
hypersensitivity, hyperactivity, tremors, loss of equilibrium, convulsions,
accelerated breathing, and paralysis. Ganglia in insects and the telen-
cephalic region of the brain in birds were identified as specific areas
of endrin action. Brain cell membranes from endrin—resistant fish were
75
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76
found to have structural differences associated with increased endrin
binding. Tissues of endrin—resistant insects also had higher endrin
binding. Binding may decrease toxicity by lowering the amount of endrin
entering the cells.
Other endrin effects include inhibition of certain enzymes and
impairment of liver function. Increased serum osmolality, due in large
part to high sodium and glucose levels, reflects the liver dysfunction.
Stress factors, such as starvation, nonoptimal temperature, and disease,
consistently tend to increase endrin toxicity. Low chronic exposure
levels occasionally have the reverse effect of acute doses; for example,
fecundity in red cotton bugs and growth of goldfish were increased at
endrin concentrations below those causing inhibitory effects. Chronic
endrin exposures reduced reproduction in fish and birds by decreasing
egg production. Decreased hatchability and viability of bird eggs were
also observed in some chronic feeding experiments (1 ppm endrin in the
diet).
No evidence of tumors or cancer was found in dogs after chronic
exposure to endrin (5 ppm in the daily diet). And no carcinogenicity
or teratogenicity was reported elsewhere, but the paucity of research
data is those areas makes any judgement inconclusive. Mutagenicity
Is suggested In fish by the inheritable tolerance to endrin, but mutations
were ruled out in endrin—resistant insects.
5.2 AQUATIC ANIMALS
5.2.1 Invertebrates
5.2.1.1 Metabolism
5.2.1.1.1 Uptake and absorption . Aquatic mollusks and arthropods are
exposured to endrin in the water, sediment, and food sources. Inverte-
brates act as extractors, continually exchanging residues between water
and body fluids until an equilibrium is eventually reached (Hamelink,
1971). The equilibrium concentration in an organism will depend on the
concentration of endrin in the water, species (physiology), bottom
composition, and exposure time (Table 5.1).
Endrin is rapidly accumulated initially by mollusks and arthropods,
achieving bioconcentration factors up to 49,000 and 2600 respectively
(Metcalf et al., 1973). However, endrin levels decreased progressively
after the initial uptake until equilibrium values were reached. This
supports Hamelink’s (1971) postulation that Invertebrates exchange
residues by physiological and chemical reactions until an equilibrium
is attained in about five days. Direct absorption has also been suggested
as contributing to body burdens of endrin (Metcalf et al., 1973).
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77
Table 5.1. Endrin accumulation factors in aquatic invertebrates
Species
Water
cone.
Exposure
time
(days)
Accumu—
.
lation
factor
Ref er—
ence
Clam (Mya arenaria)
0.5 ppg
5
1,240
1
Clam (Mercenaria mercenaria)
0.5 ppb
1.0 ppb
5
5
480
480
1
2
Mussel (Hyridella australis)
0.01 ppm
0.5 ppm
24
3
38
7
3
3
Oyster (species not given)
0.001 ppm
10
1,000
4
Eastern oyster (Crassostrea
virginica)
0.1 ppb
0.05 ppm
7
7
1,670
2,780
5
5
Snail (Physa sp.)
0.01 ppm (plus
contam. food)
33
49,218
6
Water flea (Daphnia magna)
1.0 ppb
1
3
2,600
330
6
Mosquito larva (Cuiex
pipiens quinquefasciatus)
1.0 ppb
1
3
2,100
310
6
1. Butler, 1971.
2. Duke and Dumas, 1974.
3. Ryan et al., 1972.
4. Pimentel, 1971.
5. Mason and Rowe, 1976.
6. Metcalf et al., 1973.
Whole—body accumulations depend on ambient concentrations and exposure
times. Endrin levels as much as 492, 3.44, and 2.6 ppm have been reported
in soft tissue of snails, mussels, and clams respectively (Metcalf et al.,
1973; Ryan et al., 1972; Butler, 1971).
5.2.1.1.2 Transformation and elimination . Biodegradability of
endrin was determined using radiocarbon—labeled endrin in a model ecosystem
(Metcalf et al., 1973). Approximately 17% of the labeled carbon was
recovered in metabolites from a snail, Physa sp. The metabolites could
not be identified, but one unknown was suggested to be 9—hydroxyendrin by
analogy with dieldrin degradation. Lower bioaccumulation factors for
the degradation product (1701) compared with endrin (49,000) also support
the formation of a hydroxylated compound that is more soluble than the
parent molecule (Metcalf et al., 1973). No metabolites were found after
the arthropod Daphnia sp. was exposed to endrin (Menzie, 1969).
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78
Endrin was eliminated by clams at a rate comparaoie to tnat or
uptake (Butler, 1971). Mya ccrenaria accumulated 2.6 times (620 ppb) as
much endrin as did Mercenaria mercenaria (240 ppb) in five days and re-
leased 3.1 times (610 ppb) more endrin in seven days of flushing.
The Australian freshwater mussel, HyrideiZa australis, also
demonstrated the capability for rapid uptake and elimination of endrin
(Ryan et al., 1972). The mussel released 88% of the tissue endrin within
24 h after transfer to fresh water (Fig. 5.1).
ORNL—DWG 79—8428
5
4
3
2
0
E
0 .
0.
z
0
H
z
U i
I.)
2
0
U
z
0
2
Ui
Ui
U)
U)
H
Fig. 5.1.
0.5 ppm endrin
S. Ryan, G. J.
Copyright 1972
0 4 8 12 46 20
DAYS
Endrin concentration in mussel tissues after exposure to
(stage 1) and transfer to fresh water (stage 2). Source:
Bacher, and A. A. Martin, Search 3(11/12): 446—447 (1972).
Australian and New Zealand Association for the Advancement
of Science.
5.2.1.2 Effects . Endrin is more toxic to the aquatic arthropods
than to mollusks. Lethal endrin concentrations are less than 10 ppb for
several species of marine shrimp, while clams (M. mercenaria) and mud
snails ( saa obsoleta) survive at levels a thousand times greater
(10 ppm) (Eisler, l970a).
Table 5.2 gives LC 50 endrin values for some aquatic invertebrates.
Effective endrin concentrations decrease with increasing exposure time
(Fig. 5.2). Small changes in endrin levels may make the difference between
STAGE I
STAGE 2
an ineffective concentration and lethality, as is demonstrated by death
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79
P1 anaria
Table 5.2.
Endrin LC 50 values for aquatic
5
invertebrates
1000 1
(Dugensia spp.)
Blue crab
(cal linectee spaidus)
Hermit crab
(Pagurus longicarpus)
Freshwater crayfish
(Cambarus spp.)
Red crawfish
(Procambaru.s sp.)
Grass shrimp
(Palaemonetes pugio)
(P. vulgaris)
Brown shrimp
(Penasus aztecus)
Sand shrimp
(Crangdon septum spinosa)
Waterf lea
(Daphnia magna)
(D. pulex)
(Simocepha lus serru latus)
(Moina macrocopa)
Stonefly naiads
(Acroneuria pacifica)
(Pteronarcys ca lifornica)
Mayfly nymph
(Bastis sp.)
Freshwater isopod
(Asillus app.)
Freshwater amphipod
(Gammarus sp.)
1. Georgacakis and Khan, 1971.
2. Butler, 1963.
3. Pimentel, 1971.
4. Eisler, l970a.
5. Hansen et al., 1973.
6. Sanders and Cope, 1966.
7. lyatomi et al., 1958.
8. Jensen and Gauf in, 1966.
Exposure
Species (hr)
LC 50 Reference
(ppb)
24
48
100
25
2
2
24
96
2.7
1.2
3
4
3.3
1800
1
48
300
3
24
1.5
5
24
96
10.3
10
3
4
24
48
0.6
0.3
2
2
24
96
2.8
1.7
3
4
24
50
0.1
48
24
48
900
352
1000
26
3200
56
6
6
1
3
7
7
96
0.32
8
24
48
96
4—24
0.9—6
2.4
3
3
8
48
5
3
1000
1
0.5
2.5
24
48
1000
8
5
1
3
3
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80
ORNL—DWG 79—8427
ACRONEURIA PA C/F/CA
100
80
60
40
20
0
400
80
60
40
20
0
0.0002
-J
4
>
>
U,
2
w
U i
a.
-J
>
U,
z
U i
0
Ui
a.
ENDRIN (ppm)
Fig. 5.2. Effects of endrin concentration and exposure time on two
stonefly naiad species. Source: L. D. Jensen and R. A. Gauf in, J. Water
PoiZu. Control Fed. 38(8): 1273—1286 (1966). Copyright 1966 Water
Pollution Control Federation.
ENDRIN (ppm)
0.0000 0.0004 0.0002 0.0005
PTERONARCVS CAL/FORN/CA
0.0005 QOOl 0.002 0.004
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81
of both water fleas (Dcphnia magna) and mosquito larvae (Culex pipiena
quinquefasciatus) when endrin is increased from 10 ppb to 60 ppb
(Metcalf et al., 1973).
Evidence of endrin toxicity in oysters (Crassostrea virginica) is
first manifested by decreasing shell growth, with the percent of inhibition
directly related to the concentration (Butler, 1966a, 1963). The percent
decrease in shell deposition over 96 hr was 70, 40, 20, and 0 for endrin
concentrations of 1.0, 0.1, 0.01, and 0.001 ppm respectively. The sequence
of poisoning symptoms in freshwater shrimp (Palaeomonetes kadiakensis)
and stone fly naiads (Pteronarcys app.) is similar (Sanders and Cope,
1968; Naqvi and Ferguson, 1970; Jensen and Gauf in, 1966). Initially there
is hyperactivity, increasing in intensity with exposure time. This is
followed by tremors, loss of equilibrium, convulsions (stone fly naiads),
paralysis (shrimp), and death. Once tremors and convulsions occurred in
two species of stone fly naiads (Pteronarcys californica and Acroneuria
pacifica), there was no recovery (Jensen and Gauf in, 1966). These obser-
vations suggest that endrin exerts its toxicity by affecting the nervous
system, possibly through action on critical enzyme systems (Jensen and
Gauf in, 1966).
Increasing temperature raises endrin lethality to oysters (Butler,
1966a, 1966b) but decreases effects in daphnids (Sanders and Cope, 1966).
The juvenile stages of aquatic invertebrates are generally more susceptible
to endrin than are adult forms, including oysters (Davis, 1961), daphnids
(Sanders and Cope, 1966), red crawfish (Proca’nbarus sp.), and stonef lies
(Jensen and Gauf in, 1966).
The lethal concentration of endrin may be dependent upon the morphology
of a species; for example, the 20—day LC 50 of the thin—shelled stone fly
(Acroneuria pacifica) was 0.25 ppb, approximately one—tenth of the level
for the hard—shelled stone fly (Pteronarcys californica sp.) (Jensen and
Gauf in, 1966). Stone fly data demonstrate an interspecific correlation
between size and mortality (Sanders and Cope, 1968). Stone fly naiads
of Pteronai’cys californica, Claasenia sabulosa, and P. badia (listed in
order of decreasing species size) had 24—hr LC 50 endrin of 4.0, 3.2, and
2.8 ppb respectively.
Sublethal endrin concentrations affect growth and reproduction of
many aquatic invertebrates. Survival and growth of oyster larvae (C.
virginica) exposed to endrin (0.5 to 10 ppm) were erratic, probably due
to solubility differences, but larvae were generally more sensitive than
eggs (Table 5.3) (Davis, 1961). Increased larval growth at 1.0 ppm may
be due to bacteriostatic action. Endrin concentrations (10 ppb) decreasing
oyster shell deposition 20% had no observable effect on mortality, spawning,
or median growth in mature oysters (Butler, 1971). Endrin reduced the
deposition of egg cases by mud snails (N. obsoleta) at 0.1 ppm but signi-
ficantly increased deposition after 33 days of exposure to 0.1 ppm
(Eisler, 1970a). Enhancement may not necessarily be beneficial,
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82
Table 5.3. Effects of endrin on survival and growth of oyster
(Crassostrea viginica) larvae and eggs
Endrin
(ppm)
Survival and growth (%)
Larvae
Eggs
0.50
36
72 a
1.00
92
18,
62 a
2.50
52
4,
60a
5.00
10
52’
10.00
0
0(2
Same stock suspension, two weeks later; probably flocculated.
Data from Davis, 1961.
since deposition over longer periods may be a means to avoid loss of an
entire reproductive effort. Experiments were not carried out long
enough to determine whether increased deposition continued or was the
result of a single effort. The molting rate of stone fly naiads was
significantly lowered by approximately 3 ppb endrin, decreasing the rate
of maturation (Jensen and Gauf in, 1966).
5.2.2 Fish
5.2.2.1 Metabolism
5.2.2.1.1 Uptake and accumulation . Direct sources of endrin to
fish include food, water, and sediment. Uptake in fish is based on
absorption and solubility differences between fat and water (Hamelink,
1971). Fish act as a multiphase exchange system with successive and
reversible partitionings between water, blood, and fat. Thus, endrin
is in a dynamic state and not stored in blood or tissue (Mount et al.,
1966).
Attainment of lethal endrin levels in the blood of channel catfish
is apparently Independent of both exposure time and water concentration.
In water containing concentrations of endrin that killed some fish but
not others, there was a distinct difference between the concentration
of endrin in the blood of fish that were killed and those that were
exposed but not killed. Figure 5.3 shows some blood levels for fish
that survived exposure for 4, 21, and 44 days in water containing endrin
concentrations that killed other fish. In 90% of the fish that were
analyzed, the endrin concentration in the blood of fish killed by endrin
was greater than the concentration of endrin in the blood of fish that
were exposed but not killed. No fish survived blood levels exceeding
0.28 ig/g, and no fish died with less than 0.23 pg/g.
-------
1.6 ORNL-0WG79-8126
— 1.2 • DEAD FISH
E I 0 LIVING 9 EXPOSED FISH
a
a
CD
0
S
0.8
0.4 —. ‘. __ .r__2_____
0 I I I
0 40 20 30 40 50
EXPOSURE TIME (doys)
Fig. 5.3. Blood levels of endrin in channel catfish exposed to
0.1 ppb endrin. Source: D. I. Mount et al., Science 152(3727): 1388—90
(1966). Copyright 1966 by the American Association for the Advancement of
Science.
A continuous mortality of channel catfish, Ictalurus punctatus., and
brown bullheads, I. nebulosis, in Alabama between September 1975 and
March 1976 was investigated by Plumb and Richburg (1977). Sera of mori-
bund catfish averaged 0.29 to 1.80 pg endrin/g. After cessation of
mortality in March 1976 the sera of apparently healthy catfish from the
affected ponds had <0.02 pg endrin/g. During the period of chronic
mortality, water samples from the affected ponds had very low concentra-
tions of endrin (0.06 to 0.Ol pg/liter). They postulated that survivors
of a 1975 pesticide kill absorbed insecticides and stored them in fat
tissue; the fat reserves were then utilized during a period of decreasing
food availability, releasing the endrin and producing toxicosis.
The rate of uptake from food by channel catfish is directly propor-
tional to the concentration (Argyle et al., 1973). After 20 days, whole—
body endrin concentrations were 310, 37, 6 ppm and undetectable from
exposure to 4, 0.4, 0.04, and 0.004 ppm respectively.
Endrin concentration in water also determines the initial uptake
rate and equilibrium levels (Argyl et al., 1973). However, uptake from
water far exceeds that from food, bioconcentration from water being 2000
times higher than that from food in channel catfish (Argyl et al., 1973).
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84
The lower bioconcentration from food could result from equilibration in
fish, since endrin absorbed from the gut is subsequently released to the
endrin—free water. Or uptake rates and/or routes may be less efficient
for endrin contained in food. The highest endrin residues in fish were
found in the gut, followed by liver, head, gills, heart and spleen,
bodies, and eggs (Ferguson et al., 1966).
Several factors suggest that one means of endrin uptake is through
the mouth; for example, young fish with nonfunctional mouths are more
resistant to endrin than adults (Ferguson and Goodyear, 1967). However,
the primary means of endrin entry into the fish body is absorption through
gill surfaces. The evidence of primary uptake by the gills includes:
• Similar mortality rates for starved and fed mosquito fish Ga’nbusia
affiniB) exposed to endrin (Ferguson and Goodyear, 1967).
• Mortality rates for black bullheads (Ictalurus melos) with ligated
esophagi, sham—operated, and controls were nearly identical
(Ferguson and Goodyear, 1967).
• Mosquito fish with only the head area exposed to endrin (1 ppm) had
higher mortality rates (100% within 31 tnin) than fish with only the
body exposed to 1 ppm endrin (15% mortality and 2.91 ppm average
residue) (Ferguson et al., 1966). (The fish were held in a taut
rubber membrane, sealed around the body posterior to the pectoral
fins. The membrane was stretched across the top of a jar, separating
the endrin solution in the jar from the tap water in which it was
immersed.)
• Endrin residues in dead mosquito fish exposed to endrin are about
equal to those in live fish without the head area exposed (6.25 and
6.34 ppm, respectively, after 11.25 hr in 1 ppm endrin) (Ferguson
et al., 1966).
Endrin absorption by bluegills (Leponris rnacrochirus) produced different
curves for lethal (2 ppb) and sublethal (0.2 ppb) exposures (Bennett and
Day, 1970). Lethal doses showed increasing body concentrations with
increasing time, while sublethal exposures gave an “N—shaped” curve. It
appears that, initially, endrin is rapidly absorbed, but after 7 or 8 hr,
a “coping” mechanism is developed that may allow metabolism or excretion
of endrin, resulting in a concentration drop. A gradual increase in
endrin follows, until the contending processes of uptake and excretion
reach their respective levels and an equilibrium is attained. Muscle
and liver tissue uptake curves are similar to those f or the whole body.
Gut uptake, on the other hand, showed no drop when bluegills were exposed
to either lethal or sublethal concentrations of endrin, probably as a
result of steady absorption from the swallowed water.
Endrin—resistant and —susceptible mosquito fish show significant
differences in endrin uptake in the brain and nervous tissue, suggesting
some sort of membrane barrier preventing or slowing endrin entry (Wells
-------
85
et al., 1972; Wells and Yarbrough, 1973; Fabacher and Chambers, 1976).
The ratio of endrin concentration in brain to that in liver was not only
higher in susceptible fish (1:30) than in resistant fish (1:8), but total
brain endrin was three to four times higher in susceptible fish (Wells
and Yarbrough, 1972; Yarbrough, 1974). Cell membrane fractions from
brains of endrin—resistant fish bind twice as much endrin as those from
susceptible fish, thus reducing the amount of endrin entering the cell
(Wells and Yarbrough, 1972). On the other hand, brain fractions other
than cell membranes (e.g., microsomal and myelin fractions) manifested
more endrin binding in susceptible fish than in resistant. Increased
binding of endrin to susceptible myelin fractions may lead to inter-
ference with nerve transmission (Wells and Yarbrough, 1972).
Fabacker and Chambers (1976) suggested that at higher concentrations
of endrin, mechanisms of resistance may be important in resistant mosquito
fish, Gambu.sia affinis, such as a more efficient blood—brain barrier. This
may prevent large amounts of endrin from accumulating in the brain, allowing
a more rapid accumulation in the lipid stores of the liver. To support
this they found that the brains and livers of susceptible fish killed with
20 ppb endrin contained 1.9 tImes more endrin than the same tissues from
resistant fish treated with the same amount of endrin. Fish mortality
in both the resistant and susceptible strains occurred with endrin con-
centrations of 1000 ppb. Brains of the susceptible fish had higher
endrin levels, and the livers of the resistant fish had 2.2 times more
endrin than those of the susceptible fish.
Endrin uptake was one—third as fast into muscle preparations of
resistant nervous tissue (identified as the primary site of endrin
action) as into susceptible nerve tissue at low exposure levels (10 ppb)
(Yarbrough, 1974). At acute concentrations, the difference in uptake
rates (resistant/susceptible) was only one—half, probably as a result
of comparing “tolerant” susceptible fish with resistant ones, since
only a few susceptible fish survived 1500 ppb endrin.
Whole—body uptake of endrin also decreased in fish previously exposed
to endrin (Ludke et al., 1968). Resistant golden shiners accumulate
approximately 60¼ of the endrin taken up by susceptible fish, 260 and
420 ppb, respectively, after 1 hr in 10 ppb endrin.
5.2.2.1.2 Transformation and elimination . The evidence for endrin
transformation by fish is based on one investigation by Metcalf et al.
(1973). Mosquito fish altered approximately 25% of introduced endrin
after 33 days of exposure. Identification of one of the metabolites as
a polar compound suggested a hydroxylated degradation product, 9—hydro—
xyendrin. Speculation of the product’s identity was made on the basis
of analogy with dieldrin metabolism in rats and a bioaccumulation factor
considerably lower (approximately one—fifth) than that for endrin. The
amount of endrin calculated to have been transformed into polar products
was small, 0.9% (Metcalf et al., 1973).
No evidence of metabolites was found in fathead minnows (Pimephales
promeZ as) (Menzie, 1969) or in dead and living mosquito fish by other
investigators (Ferguson et al., 1966).
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86
Endrin is released rapidly from fish withdrawn from endrin exposure.
Since the amount of endrin released from living mosquito fish Is not
significantly different from that released by dead ones, it appears that
active secretion is not involved (Johnson, 1968; Ferguson et al., 1966).
However, active endrin elimination at sublethal concentrations has been
demonstrated (Bennett and Day, 1970).
Endrin residues in spot (Leiostornus xanthurus) at levels of 78 ppm
whole—body weight disappeared within 13 days of endrin withdrawal
(Lowe, 1965). Channel catfish lost approximately two—thirds of a 310—ppb
residue after 28 days, with no detectable levels after 41 days of an
endrin—free diet (Argyl et al., 1973). The rapid decline in endrin
residues demonstrates that the compound can be eliminated in a relatively
short time.
5.2.2.2 Effects . Endrin is the most toxic to fish of the common
organochlorine insecticides (e.g., toxaphene, dieldrin, aidrin) (Eisler,
l970c). Table 5.4 lists some LC 50 values for a variety of fish, with
different exposure times. Because pollutants may drain into aquatic
environments for considerable periods of time and at low levels due to
the dilution factor, LC 50 values for 24 and 48 hr have questionable
value except to measure relative toxicity (Lowe, 1965; Butler, l966a).
For example, a 24—hr LC 50 of 1 ppm may not be considered dangerous,
because there is little chance of that concentration In the field.
However, the same fish may have a ten—day LC 50 of 0.03 ppb, a very possible
degree of pollution. Another factor to be considered in using LC 50 values
is that the margin of safety and lethality for fish exposed to endrin is
exceedingly narrow (Pimentel, 1971). Spot (Leiostomus santhurus) flourish
at 0.05 ppb, but an increase to 0.1 ppb causes 100% mortality in five
days (Butler, 1966a; Pimentel, 1971).
A correlation between concentration of endrin in the blood and
mortality in channel catfish (Mount et al., 1966) and gizzard shad
(Brungs and Mount, 1967) was found in both laboratory and field studies.
Critical blood concentrations were approximately 0.3 and 0.1 ppm endrin
for catfish and shad respectively. Some correlation between mortality
and whole—body residue is found in shiner perch (Cymatogaster aggregata)
and dwarf perch (Micrometrus minimus), but overlap occurs (Earnest and
Benville, 1972). The endrin residues found in dead and live shiner perch
averaged 0.13 (0.02 to 0.27) and 0.07 (0.03 to 0.09) ppm respectively.
Many factors influence the effective endrin concentration; among
these are: exposure time, temperature, salinity, body size, previous
exposure, flowing or static bioassay systems, species, synergism with
other compounds, route of endrin uptake, developmental stage, and the
season of the year.
The lethality of endrin to carp (Cyprinus carpio) and snakehead
fish (Channa argus) increased during the course of their development
(lyatomi et al., 1958). The fertilized eggs and 1—, 4—, 6—, and 12—day
-------
87
Table 5.4. Endrin toxicity to some fish as measured by LC 50 a
Exposure
Family and species (hr)
LC 50 Source
(ppb)
Anguillidae
American eel (Anguilla rostrata) 24 1.1 1
48 0.6 1
96 0.6 1, 2
Centratchidae
Bluegill sunfish (Lepomis 24 0.35—2.0 3, 4, 5
macrochirus) 36 1.5 6
72 0.95 7
96 0.25—0.6 7, 8
(LD 50 ) 6 200 9
24 10 9
Green sunfish (L. cyanellus) 36 3.4—5 6, 10
Clupeidae
Menhaden — juvenile (Brevoortia 24 0.8 11
sp.)
Cypr inidae
Bluntnose minnow (Pimephales 96 0.3 8
notatus)
Carp (Cyprinus carpio) 48 140 8
(LD 50 ) 24 5—9 12
48 5 12
Fathead minnow (P. prornelas) 1 700 9
48 0.57 13
96 0.39—1.8 8, 13, 14
Goldfish (Carassius auratus) 24 3 3
(LD 50 ) 48 2 3
96 2 8
Golden shiner (Notemigonus 36 3 6
cryso leucas)
Cyprinodontidae
Longnose killifish (Fundulus 24 0.3 3
s-irnilis) 96 0.3 3
(juvenile) 24 0.23 11
Mummichog (F. heteroclitus) 24 1.8 1
48 0.7 1
96 0.6 1, 2, 15
240 0.33 15
aNO resistant fish used knowingly.
-------
88
Table 5.4 (continued)
Family and species Exposure
(hr)
LC 50
Source
(ppb)
Sheepshead minnow — juvenile 24 0.32 11
(Cyprinodon variegatus)
Striped killifish (F. majalis) 24 1.8 1
48 0.7 1
96 0.3 1
Embiotocidae
Dwarf perch (Microme true minimus) 96 0.6 16
Shiner perch (Cymatogaster 96 0.8 16
aggregata)
Gasterosteidae
Three—spined stickleback 48 0.45—2 7, 14
(Casterosteua aculeatus) 72 0.45—1.7 7, 14
96 0.44—1.5 7, 14
Heteropneuatidae
Indian catfish (Heteropneuetes
fos8ilia) (LC 100 ) 5 120 17
24 6 17
Ictaluridae
Black bullhead (Icatalurus melas) 24 1.3 3
36 0.37 6
96 1.1 3
Channel catfish (I. punctatus) 24 0.45 3
96 0.29 3
Yellow bullhead (I. natalis) 36 1.25 18
Larbridae
Bluehead (ThaZassoim z bifasciatum) 24 0.6 1
48 0.5 1
96 0.1 1
Mugilidae
Striped mullet (M gil cephalus) 24 0.7 1
48 0.3 1
96 0.3 1, 19
(juvenile) 24 2.6 11
White mullet — juvenile 24 0.3—2.6 3, 20
(M. curema) 96 2.6 3
Ophicephalidae
Snakehead fish (Channa punctatu8) 24 8.5 21
48 4.1 21
72 2.7 21
96 1.9 21
-------
Table 5.4
89
(continued)
Family and species Exposure
(hr)
LC 50
Source
(ppb)
24
48
72
96
24
48
72
96
24
48
72
96
48
72
96
24
48
72
96
24
24
96
1.28
0.59
0.42
0.36
2
1.2—1.5
1.01—1. 2
0. 92—1. 2
1.3—12.
0.56—0.8
0.3—0.52
0.27—0.51
0.24
0.15
0.11
0.8—5.3
0.6—1.5
0.5—1.1
0.4—1.4
0.45
0. 5—4.4
0.6
25
25
25
25
14
7,
7,
7’
7, 14
7, 14
7, 14
7, 8, 14
25
25
25
7, 14
14
14, 25
7, 14,
96
0.09
22,
23
96
0.94
22,
23
24
0.5
1
48
0.08
1
96
0.05
1,
19
72
1.1
7
96
0.3—1.5
7,
8,
14
36
1
6
48
1—1.8
7,
24
72
1.05
7
96
0.75
7
Percichthyidae
Striped bass (Morons saxatil,is)
(juvenile)
Poeci lidae
Atlantic silversides (Menidia
menidia)
Guppy (Lebistes reticulatus)
Mosquito fish (Gainbusia affinis)
Salmonidae
Brook trout (Salve linus
fontinalis)
Chinook salmon (Oncorhyncus
tshawytscha)
Coho salmon (0. kisutch)
Cutthroat trout (Salmo clarki)
Rainbow trout (S. gairdneri)
Sciaenidae
Spot (Leiostomus santhurus)
(juvenile)
14
14
14
3,
7,
7,
3,
25
3
3, 11
3
-------
90
Table 54 (continued)
Family and
species
Exposure
(hr)
LC 50
(ppb)
Source
Tetraodontjdae
Northern puffer
maculatus)
(Sphaeriodes
(LC 50 )
24
48
96
24
3.1
3.1
3.1
10
1
1
1,
2
2
Sources: 1. Eisler, 1970c;
2. Eisler and Edmunds, 1966;
3. Holden, 1973;
4. Cope, 1963;
5. Bennett and Day, 1970;
6. Pimentel, 1971;
7. Katz and Chadwick, 1961;
8. Johnson, 1968;
9. Georgacakis and Khan, 1971;
10. Finley et al., 1970;
11. Lowe, 1965;
12. lyatomi et al., 1958;
13. Lincer et al., 1970;
14. Katz, 1961;
15. Eisler, 1970b;
16. Earnest and Benville, 1972;
17. Saxena and Aggarwall, 1970;
18. Ferguson and Bingham, 1966b;
19. Duke and Dumas, 1974;
20. Butler, 1963;
21. Javaid and Waiz, 1972;
22. Korn and Earnest, 1974;
23. Suffett et al., 1975;
24. Ferguson, 1967;
25. Post and Schroeder, 1971.
larvae of the snakehead fish had 24—hr median tolerance limits (LD 50 )
to endrin of 100, 62, 5, 6, 0.012, and 0.0065 ppm respectively.
After exposure to sublethal endrin concentrations (0.05 ppb) for
eight months, spots were more sensitive to lethal endrin concentrations
(0.56 ppb or more) than were unexposed control fish (Lowe, 1965). At
levels of 0.32 ppb endrin or less, both exposed and control fish showed
similar responses. Mummichogs were able to withstand short iminersions
In toxic concentrations of endrin (3 ppb, five times the 96—hr LC 50 )
(Elsier, 1970b). After 6 hr, survival rapidly decreased with extended
exposure (Fig. 5.4). Posttreatnient survival also was correlated to the
length of exposure.
-------
91
ORNL—DWG 79—8125
>-
I-
-J
0
I-
z
C)
LiJ
a-
w
>
-J
0
100 — ——— 3 ppb ENDRIN
24 days POST—
TREATMENT
80 —
60 —
40 —
20 —
0 —
I I I I
45 30 420 360 720
INITIAL EXPOSURE TIME (mm)
Fig. 5.4. Mortality of muinmichogs to various
treatment. Source: Eisler, 1970b.
1680 3000
durations of endrin
Endrin appears to primarily affect the nervous system of fish. The
typical symptoms of endrin poisoning bear out central nervous system
damage: hypersensitivity, hyperactivity, loss of sense of direction, loss
of equilibrium, increased ventilation, convulsions, and inert (except
for operculum moving) on the bottom (Johnson, 1968; Javaid and Waiz, 1972;
Saxena and Aggarwall, 1970; Argyl et al., 1973; Eisler and Edmunds, 1966).
El—Refai et al. (1976) also found that carp, Cypriznus carpio, and tilapia,
Tilapia milotica, slowly lost neural control of their swim bladders and
rose to the surface after exposure to endrin—contaminated water.
The increased activity resulting from endrin exposure may cause
the ineffective feeding behavior observed in goldfish (Grant and Mehrle,
1970) and disrupt normal swarming and displacement behavior in guppies
(Pimentel, 1971). Sheepshead minnows (Cyprinodon variegatus) showed
avoidance behavior to endrin concentrations only in the range 1.0 to
0.1 ppb (Hansen, 1969), but mosquito fish did not avoid 10 ppb endrin
or less (48—hr LC 50 = 1 ppb) (Hansen et al., 1972).
Chronic endrin exposures caused reduced reproduction in bluntnose
minnows and goldfish (143 pg/kg body weight per day), probably as a
result of decreased gonad development (Eisler and Edmunds, 1966; Grant
and Mehrle, 1970). Cutthroat trout fed 0.1 ppm endrin daily had
irregular oocytes (Eller, 1971), and exposure of guppies to 0.5 ppb
prevented reproduction (Eller, 1971). Adult carp at threshold toxicity
I I I
p
/
/
/
/
/
/
/
/
/
/
/
-------
92
(5 ppm) showed some degree of abortion, but egg embryo viability was
not affected below 1 ppm (Holden, 1973). Growth was halved in rainbow
trout fed 145 ppb endrin per body weight daily (Grant and Mehrle, 1973).
Endrin decreased growth in goldfish fed 430 ppb daily but increased
growth at 43 ppb or less (Grant and Mehrle, 1973).
Endrin impairs the function of liver tissue (Holden, 1973; Grant
and Mehrle, 1970, 1973; Eisler and Edmunds, 1966; Lowe, 1965; Eller,
1971). Eller (1971) reported a hepatitis—like response in cutthroat trout
liver, including increased blood coagulation time and degeneration of
the liver. The incidence and severity of liver degeneration increased
with exposure to increasing endrin concentrations (10 ppb or more). The
major liver effects encompassed energy transformations, such as reduc-
tion of liver glycogen (Eller, 1971; Lowe, 1965; Grant and Mehrle, 1973).
Eller (1971) suggests that endrin and nutritional stress interact to
impair the liver and fatty—acid metabolism.
The changes in blood and serum constituents reflect the liver
dysfunction. Serum glucose increased 50% over controls (145 ppb), and
there was a significant correlation between endrin dose (4.3 to 145 ppb)
and both serum sodium and increased osmolality in trout (Grant and
Nehrle, 1973). Other serum alterations included increased lactate,
decreased amino acids, and increased cortisol. Northern puffer (Sphaeroide8
maculatus) also exemplified cation transfer from liver to serum, 1.0 ppb
endrin causing increased sodium, potassium, and calcium in the serum and
decreased levels in the liver (Eisler and Edmunds, 1966). Fishes from
the Mississippi River fish kills in 1963—64 (generally attributed to
endrin) had lowered red and white blood cell counts (Johnson, 1968).
Pathologic conditions were generally found in the gills and pancreas
of fish as well as in liver. Gill tissue in trout was edematous as a
result of increased osmolality, undoubtedly interfering with gill function
and water circulation and contributing to the increased ventilation
observed in endrin—poisoned fish (Eller, 1971). Increased cell numbers
in the islets of Langerhans were observed in cutthroat and rainbow trout
(11 months in 0.01 ppm), but the implied alteration of carbohydrate
metabolism was not confirmed by biochemical analysis (Grant and Mehrle,
1973; Eller, 1971). LesIons were present in the brain, spinal cord,
liver, kidney, and stomach of spot chronically exposed to endrin (0.075 ppb)
(Holden, 1973).
Endrin has been identified as an inhibitor of several enzyme
systems, including ATPasea (Cutkomp et al., 1971; Davis etal., 1972),
oxidases (Staton and Khan, 1972), and s iccinic dehydrogenase (Yarbrough
and Wells, 1971). The inhibition of Na IC ATPase and Mg 2 +ATPase in
bluegill brain and muscle was almost the same, approximately 20% decrease
in activity with endrin concentrations of 16 ppm (Cutkomp et al., 1971).
Since endrin toxicity (24—hr LC 50 = 2 ppb) and ATPase inhibition (20% with
16 ppb) do not correlate, Davis et al. (1972) believe that endrin must act
on enzymes other than ATPase. Staton and Rhan (1972) reported that endrin
is a potent inhibitor of mixed—function oxidase from bluegill sunfish but
gave no further data.
-------
93
Evidence of membrane structural change in response to endrin may
be demonstrated by inhibition of succinic dehydrogenase, an inseparable
part of the inner mitochondrial membrane (Yarbrough and Wells, 1971).
Enzyme inhibition only occurred with intact mitochondria from fish sus-
ceptible to the toxic effects of endrin. Disruption of the organelle
permitted a similar degree of enzyme inhibition in preparations from both
resistant and susceptible organisms. Inhibition of succinic dehydrogenase
only after the outer membrane is removed demonstrates the existence of
an effective, but not absolute, membrane barrier.
Increased lipid content also appears to be an effect of endrin.
The whole—body lipid content was greater in fish exposed to endrin
(Fabacher and Chambers, 1971). Endrin—resistant, semiresistant (previously
removed to endrin—free water), and susceptible fish had lipid contents
of 17, 12, and 9% respectively. Resistant fish livers possess much more
fat than susceptible ones, but the amount of endrin solubilized in the fat
was comparable (approximately 90% of total endrin taken up) (Fabacher
and Chambers, 1971). That fish surviving endrin treatment (40 ppb) all
had approximately 50% more fat than did the mortalities (Fabacher and
Chambers, 1971) suggests that increased fat may provide a dilution factor.
5.3 BIRDS
5.3.1 Metabolism
A wide variety of possible methods for dispersion of endrin to the
natural environment have been noted (Sect. 7.2). Endrin in the avian
diet can come from fish, plankton, crustaceans, birds, eggs, or water.
Therefore, in considering wild birds, it can be assumed that exposure
to endrin is nearly inevitable.
The methods of endrin exposure to experimental avians have been
varied. The three primary types of exposure have been accomplished by
force—feeding contaminated natural foods (Gregory, 1970), dosing ad
libituni in a feed premixed with varying concentrations of endrin (Cummings
et al., 1967), or injection of endrin solutions into fertilized eggs
(Dunachie and Fletcher, 1969). Force—feeding and injection methods ensure
equal exposure of the experiinentals; however, ad libitum feeding is the
most natural procedure.
There appears to be general agreement that endrin is absorbed from
the avian gut and stored in various body tissues by both wild and
domestic species (Terriere et al., 1959; Reichel et al., 1969a). However,
experimental confirmation of this uptake and absorption was not found.
After absorption of endrin, residues have been reported to be
distributed in liver, brain, adipose, eggs, breast muscle, and gonadal
tissues. Adipose tissues generally contain the Lighest concentrations
(Gregory, 1970; Terriere et al., 1959), while brain tissues usually contain
the lowest residues (Reichel et al., 1969a).
-------
94
Endrin and four other organochlorine pesticides, lindane, dieldrin,
DDT, and heptachlor epoxide, were fed in combination to white leghorn
hens. Four groups were initiated on basal diets for two weeks, at which
time three of these groups were dosed with respective levels of 0.05,
0.15, and 0.45 ppm each of the five compounds in the feed, while the
control group continued the basal diet. The birds on contaminated feed
were returned to the basal diet after 14 weeks. The residual level of
endrin in fat and breast tissues was found to increase initially with a
subsequent plateau at concentrations proportional to dose levels (Fig. 5.5).
Since there were considerable differences recorded with respect to the
amount of abdominal fat found in the hens, it was concluded that the
accumulation of endrin in the abdominal fat did not appear to be dependent
upon the amount of adipose available as a repository but rather on the
level of pesticide in the feed. In this same experiment, it was also
determined that liver residues follow the same general pattern as observed
in adipose and breast tissues, that is, a sharp initial increase with
an approximate plateau thereafter and a decline during the withdrawal
period. Because of significant variations in liver pesticide content,
graphic representation was not attempted. The liver plateau levels
for the 0.45—, 0.15—, and 0.05—ppm dose levels were 0.35, 0.20, and 0.10
ppm, respectively, with no endrin detected in the controls (Cummings
et al., 1967).
ORNL-DWG 79-8124
FORTIFIED FEED (days)
0404731 4559 738796
‘IT
ENDRIN IN —
BREAST MUSCLE —
a
a
0.04 a I
-.
— 0 0 0
— 1 NO ENDRIN DETECTED —
IN CONTROLS
0.001
0—14 BASAL DIET (days) O—32
40
0.4
0.01
FORTIFIED FEED (days)
010 47 31 45 59 73 87 96
Fig. 5.5. Residual levels of endrin found in breast and fat tissues.
Source: 3. C. Cummings, M. Eidelman, V. Turner, D. Reed, and K. T. Zee,
J. Assoc. Off. Anal. Chem. 50(2): 418—425 (1967). Copyright 1967
Association of Official Analytical Chemists.
E
a.
a
a
z
U i
a
I -
U)
Ui
a.
0—44 BASAL DIET (days) 0—32
-------
95
In a related study conducted by Cummings et al. (1966), residue
levels were determined in eggs from hens maintained for 20 weeks on
the same low—pesticide--level diets (0.05, 0.15, and 0.45 ppm of each
of the five organochiorines). The background level of endrin detected
in the eggs before initiation of the pesticide feeding was less than
0.01 ppm. Within three days of exposure to the fortified feed, higher
levels were noted. Once again, a direct relationship between plateau
level and dosage was observed. The peak residues in the eggs after
the hens had been maintained on the diet of 96 days were approximately
0.03, 0.09, and 0.3 ppm for the respective feed levels of 0.05, 0.15,
and 0.45 ppm.
Terriere et al. (1959) examined the tissues and eggs of chickens
exposed to levels of 0.1, 0.25, and 0.75 ppm endrin in the feed. One—
month—old male Delaware X New Hampshire chicks were fed for six weeks
and then slaughtered, while six—month—old white leghorn pullets were
exposed to the endrin—fortified feed for eight weeks, with a return to
the basal diet for four additional weeks. A repeat of the male chick
experiment, using New Hampshire X Delaware chicks, was also reported
due to analytical discrepancies found in the original testing. In
all cases the deposits of adipose were found to be very meager; however,
weight gain and feed consumption appeared to be normal for the birds
utilized and the experimental conditions imposed. The data accumulated
during these experiments are compiled in Table 5.5. At a level of
0.25 ppm or higher, definite deposition of endrin in the egg tissue
occurred within two to four weeks after intake. This contamination
was still evident for at least one month after exposure had ceased.
Accumulation of endrin in adipose tissue was found in both experimental
groups, with even the lowest dietary level showing evidence of deposition.
Analysis of breast and tibia tissue revealed endrin contamination at
both the 0.25— and 0.75—ppm intake levels.
The fat tissue of the plain chachalacas, Ortalis vetula, was
analyzed by Marion (1976) for pesticide residues during 1971 and 1972.
Twenty—four birds, from four different study areas, had an average endrin
residue of 0.13 ± 0.52 ppm wet weight. There was no evidence that these
birds died of endrin exposure. Only 8 of the 24 birds sampled contained
detectable endrin residues.
The percentage of the dose retained by bobwhite quail appears to be
dependent upon administration time and dose according to Gregory et al.
(1972). Analyses of whole birds fed equal doses of endrin—contaminated
beans or beetles revealed retention of approximately 16% of the total
acute dose ingested, while 21% of the total chronic dose was retained.
The residues found in the body tissues during the acute and chronic
experiments differed, but not consistently. The average endrin content
of adipose in the acute dosage group was 0.014 ± 0.002 ppm, as compared
with 0.010 ± 0.001 ppm found in the chronic dosage group. Gonadal tis-
sues from both groups contained traces of endrin, while liver residues
in the chronic test were 0.007 ppm and in the acute test were 0.004 ppm.
-------
Table 5.5. Endrin content of eggs and adipose tissue from white leghorns
(ppm)
During endrin feeding After endrin feeding cessation
Dietary
level
1 week
2 weeks 4 weeks 8 weeks Eggs, 4 weeks
Adipose, 4 weeks
A B
A A B A B A B
A
B
0.00
0.1 0.02
0.1 0.1 0.1 0.1
0.1
0.04
0.10
0.1
0.1 0.1 0.1 0.1
0.1
0.21
0.25
0.1
0.1 0.1 0.05 0.2 0.31 0.1 0.13
0.3
0.59
0.75
0.1
0.1 0.1 0.3 0.36 0.2 0.17
1.1
1.07
Endrin content
of
broiler tissue from duplicate experiments after 6—week intake
(ppm)
Dietary
level
First experiment Second experiment
Adipose Breast Tibia, Adipose
A B A B A A B
0.00
0.1 0.02 0.1 0.1 0.1 0.1
0.10
0.5 0.66 0.1 0.04 0.1
0.25
0.7 1.46 0.1 0.1 0.6 1.0
0.75
1.6 3.10 0.2 0.24 0.3 3.6 4.3
2.25
17.0 18.0
0 ’
A — analyzed by spectrophotometric method with a detection limit of 0.1 ppm.
B — analyzed by bioassay method with a detection limit of 0.02.
Source: modified from Terriere et al., 1959.
-------
97
Ludke (1976) fed bobwhite quail (20) diets containing 10 ppm chiordane
for a ten—week period followed immediately by 10 ppm endrin for ten weeks.
Twenty other quail received 10 ppm endrin only in the diet for nine to ten
days. All birds lost weight; mortality from the endrin diet was associated
with as little as 0.34 ppm in the brain of the quail.
Evidence for the biotransformation of endrin by avians was not found.
Terriere et al. (1959) suggested that, based on estimates of the percent
retention of endrin by birds, either some of the endrin is metabolized
and stored in a chemical form not detected by the analytical methodology
used or that endrin or its metabolites are excreted. Supporting or
conflicting evidence for these theories was not found.
The distribution of endrin by egg—laying hens to their eggs, as
discussed previously, may be considered a method of elimination; however,
it has not been established that egg laying significantly reduces the
endrin body burden of the hen.
5.3.2 Effects of Endrin
In the literature, mortality appears as the most frequent effect of
endrin. The mean lethal concentrations (LD 50 ) for endrin and a group of
88 other chemicals were established by Heath et al. (1972). Using two—
to three—week—old bobwhites, pheasants, mallards, and Japanese quail at
the Patuxent Wildlife Research Center in Laurel, Maryland, the LC 50 and
RTD (relative toxicity to dieldrin) were derived by the method of probit
analysis. A dieldrin standard was consistently used to adjust for
possible experimental differences in animal sensitivity or physiological
and environmental variations. The selection of dieldrin was based on
its ability to provide an acceptable probit regression line to facilitate
comparison of experimental data. This investigation attempted to measure
the relative toxicities of each of the 89 chemicals on the basis of the
data compiled. Endrin ranked as one, or the most toxic chemical tested,
in all four of the experimental avian species (Table 5.6).
A 30—day empirical minimum lethal dosage (EMLD), the lowest daily
oral dose that produces one or two deaths by the end of the 30—day period,
of 0.125 mg endrin/kg/day was established for mallards. Since the LD 50
was 5.64 mg/kg in this experiment, it was calculated that the cumulative
toxicity index of endrin was 45 (5.64/0.125), indicating a moderately
high degree of cumulative action (Tucker and Crabtree, 1970).
A comprehensive study of the toxicity of endrin to quail and
pheasants, both adults and juveniles, was conducted by DeWitt (1955).
Severe tremors, muscular incoordination, and extreme nervousness ensued
in adult quail within 2 hr of administration of a diet containing 0.50%,
or 5000 ppm, endrin. All birds in this group died within 48 hr. It was
noted that lower dietary concentrations resulted in a lethargic condition
and bedraggled plumage prior to the onset of these symptoms of acute
toxicity. Endrin also proved highly toxic to adult pheasants. Diets
containing 0.025%, or 250 ppm, were refused by the birds, but satisfactory
-------
Table 5.6. Comparative dietary toxicity of endrin to birds
Species
No. of
concen—
trations
Birds per
concen—
tration
LC 50 : ppma
chemical
in feed
95% conf j
dence limits
Relative
toxicity of
dieldTin
(RTD)
95% conf 1—
dence limits
Bobwhite
6
10
14
11—24
0.370
c
Japanese
quail
6
13
18
15—20
0.304
0.257—0.359
Pheasant
4
8
14
11—17
0.335
0.236—0.527
Mallard
6
10
22
17—31
0.108
c
aLCSO:ppm endrin in ad libitum diet expected to produce 50% mortality in eight days, five days of
toxic diet followed by three days of untreated diet.
bRTD reads: “Dieldrin is x times as toxic as the given chemical as tested.”
CRelative toxicity of dieldrin applies only at LC 50 , since probit slope is significantly different
from that of dieldrin.
Source: Reprinted with permission from J. B. DeWitt, J. Agric. Food Chem. 3(8): 672—676
(1955). Copyright 1955 American Chemical Society.
-------
99
acceptance occurred at concentrations of 0.01%, or 100 ppm. All male
pheasants died within ten days of initiation of the toxic diet, while
females survived for longer periods (Table 5.7). Continuous feeding of
endrin—fortified diets at a level of 0.005%, or 5 ppm, to juvenile quail
and pheasants proved to be lethal, and short—time exposure to even lower
endrin levels produced a high mortality rate in juvenile quail (Tables
5.8 and 5.9).
Additional studies using quail and pheasant chicks reared on
endrin—fortified feed have been attempted; however, a maximum level
allowing growth and survival of the chicks was not established (DeWitt,
1956). Within 48 to 72 hr of initial feeding of 20 ppm endrin, symptoms
of acute poisoning appeared, and food consumption was significantly reduced
during the remainder of the test. Muscular incoordination, bedraggled
appearance, occasional tremors, and stiff—legged, hesitant movements were
followed by spasmodic leaping into the air and violent cartwheels which
could last for several minutes. Lower levels of endrin delayed the
onset of these symptoms; however, growth was depressed in the chicks,
and onset of acute poisoning symptoms was usually followed by death
within five days. Ataxia, drowsiness, and prostration have also been
reported in endrin—poisoned avians (Tucker and Crabtree, 1970).
Other symptoms noted in conjunction with endrin toxicity in chickens
include accelerated respiration followed by respiratory difficulty, loss
of equilibrium, and convulsive seizures before death. Postmortem inves-
tigation has revealed congestion of all internal organs; hemorrhagic
areas in serous membranes, epicardium, and endocardium; edematous lungs;
and dilated heart (Christopher, 1969).
Severely poisoned pigeons exhibited tonic—clonic convulsions beginning
20 to 30 mm after intravenous endrin injection. Within 1 hr of the
initial seizure, death usually occurred. However, surviving birds recovered
completely and exhibited no detectable symptomatology 4 hr after the
injection (Revzin, 1966).
An experimental determination of the toxicity of endrin to New
Hampshire chicks is represented in Table 5.10. The dosages listed were
administered in one capsule, and results were tabulated seven days later.
The deaths occurred between 6 hr and five days of treatment, and acute
toxicity symptoms were similar to those previously discussed. Although
the effect of treatment on weight gain was evaluated, no significant
difference could be determined (Sherman and Rosenberg, 1953).
General conclusions, derived from the experimental data, that may
or may not be applicable to all birds include:
1. There appears to be an age—mediated susceptibility difference, in
that juvenile avians more readily succumb to the toxicity of endrin
than do adults (Sherman and Rosenberg, 1953; DeWitt, 1955).
-------
Table 5.7. Toxicity of endrin to adult quail and pheasants
aEqual numbers of males and females were used.
Source: Reprinted with permission from J. B. DeWitt, J. Agric.
Copyright 1955 American Chemical Society.
0
0
Species
No. of
bird&
Concentration fed
Toxicant consumed
(mg/kg)
Mortality
(%)
Survival time
(days)
Daily
Total
%
ppm
Quail
10
10
10
10
10
10
10
10
10
0.50
0.25
0.125
0.0625
0.010
0.005
0.001
0.0005
0.0002
5000
2500
1250
625
100
50
10
5
2
62.9
7.2
2.6
1.8
0.9
0.6
0.7
0.5
0.2
92.5
13.9
9.2
4.5
4.4
2.8
16.7
11.3
6.4
100
100
100
100
100
100
100
100
100
2
2
4
3
5
5
26
22
36
Pheasants
Male
5
0.010
100
0.6
5.0
100
9
Female
5
0.010
100
1.1
25.3
100
23
Food Chem. 3(8): 672—676 (1955).
-------
Concen—
Toxicant consumed
Species
No. of
birds
Age at
start
(days)
Duration
of test
(days)
tration
in feed
(%)
(mg/kg)
Mortality
(%)
Daily
Total
Quail
10
10
10
20
20
32
22
1
1
1
16
1
1
1.
2
5
6
19
7
14
120
0.005
0.002
0.001
0.0005
0.0005
0.0001
0.00005
1.88
1.96
1.35
0.38
0.40
0.12
0.06
3.2
10.0
6.9
6.7
2.7
1.7
7.2
100
100
100
100
55.0
21.9
13.6
Pheasants
20
1
5
0.0005
0.36
2.0
100
Source: Reprinted with permission from J. B. DeWitt, J. Agric. Food Chem. 3(8): 672—676 (1955).
Copyright 1955 American Chemical Society.
Table 5.8. Toxicity of endrin to juvenile quail and pheasants
0
I- .
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102
Table 5.9. Toxicity of endrin to juvenile quail;
intermittent feeding, 28 days between tests
.
Concentration
in feed (%)
.
Duration
(days)
Toxicant consumed
(mg/kg)
.
Mortality (I .)
Daily
Total
Initial feeding
0.001
0.0005
0.00001
7
7
14
1.35
0.38
0.12
9.4
2.7
1.7
81.7
55.2
20.7
Second feeding
0.001
0.0005
0.00001
7
7
14
1.20
0.19
0.09
6.1
1.3
1.3
100
69.7
26.0
Source: Reprinted with permission from J. B. DeWitt, J. Agric.
Food Chem. 3(8): 672—676 (1955). Copyright 1955 American Chemical
Society.
Table 5.10. Toxicity of endrin to New Hampshire
chicks of various ages
Dosage
(mg/kg body weight)
Number
Mortality (%)
7 days old
4.3
3.8
3.6
3.3
2.5
1.9
1.4
Untreated
10
10
10
10
10
10
10
19
90
90
70
30
10
10
10
0
21 days old
4.3
3.4
10
10
50
0
4 .5 days old
4.3
3.4
10
20
40
0
64 days old
4.3
3.4
10
10
10
0
Source: C. H. Brett and T. C. Bowery, J. Econ. Entomol.
51(6): 818—821 (1958). Copyright 1958 Entomological Society
of America.
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103
2. A sex—mediated susceptibility variation occurs in adults birds,
since male pheasants died significantly earlier than females, although
no eggs were produced by the females (DeWitt, 1955).
3. Lowered feed consumption occurs in birds exposed to endrin—fortified
diets, which may result in prolonged survival times before death
(Sherman and Rosenberg, 1953; DeWitt, 1955).
Toxicity studies on wild birds are limited due to the difficulties
encountered in controlling the imposed conditions. Studies of fields
treated with 0.8 lb endrin per acre revealed five dead cackling geese,
one dead killdeer, a dead long—eared owl, a dead pheasant, and a dying
pheasant. In an attempt to study the effect of endrin on wildlife in a
more controlled situation, geese, pintails, widgeion, and pheasants were
placed in cages on a field that had been treated as previously described.
Within one week, four of eight geese, two of seven pintails, and one of
seven widgeon had died, while controls in untreated lots all survived.
The pheasants were not adversely affected for the first three days, after
which time the birds escaped. Endrin residues found in the tissues of
surviving birds were comparable to the levels detected in both the wild
and captive birds dying on the same field. Experimental data compiled
using widgeon revealed that a daily intake of 1.0 mg/kg would be hazardous
or fatal. A 500—g widgeon eating 25 g alfalfa contaminated with 20 ppm
endrin, a conservative part of the diet, will ingest 1.0 mg/kg daily
(Keith, 1963).
In determination of the hazards of endrin, the reproductive processes
are often studied. Egg production, fertility, hatchability, and viability
of chicks are the various stages of the avian reproductive process that
are often adversely affected by toxicants. Of these four phases, fertility
is the only one apparently not altered by endrin exposure.
DeWitt (1956) found that 10 ppm endrin administered in the diet during
the reproductive period significantly decreased egg production in pheasants.
The other concentrations tested, 2, 1, and 0.5 ppm, did not appreciably
alter egg production or any of the other previously mentioned parameters.
Fertility of the eggs laid was not decreased by the endrin—fortified diet
in either quail or pheasants, and the quail did not experience a decrease
in egg production at 1.0 ppm, the highest level administered (Table 5.11).
Hatchability was significantly lowered in pheasants receiving 10 ppm
endrin in their feed during the reproductive period. However, lower
concentrations did not substantially affect hatchability (DeWitt, 1956).
Quail receiving 1.0 ppm endrin in their diet during the winter months
and subsequently transferred to an endrin—free food source during the
reproductive period also suffered decreased egg hatchability. Reversal
of the time of endrin exposure, that is, during the reproductive period
rather than during winter, did not appear to reduce hatchability, egg
production, or fertility in the quail (Table 5.11) (DeWitt, 1956).
-------
Table 5.11. Effects of endrin upon reproduction
I - ’
0
ppm in diet
Number
of birds
Mortality
(%)
Eggs/hen,
average
Fertility
(%)
Hatcha—
bility
0
Hatch
0
(‘
survival
Winter
period
Repro—
ductlve
period
2
weeks
6
weeks
Quail
1.0
0
32
16
6.25
25.0
52
45
89.0
84.9
83.9
70.1
88.9
80.8
83.3
50.0
1.0
1.0
10
60.0
0
1.0
16
25.0
60
93.1
79.0
89.2
64.3
Pheasants
0
10
128
10
0
100
48
11
86.6
81.7
57.4
40.6
94.8
37.5
89.7
31.3
0
2
10
0
42
89.9
47.7
97.1
91.2
0
1
10
0
45
92.6
56.6
91.7
91.7
0
0.5
10
0
40
84.9
71.3
80.0
71.4
Source: modified from DeWitt, 1956.
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105
These same quail, maintained on an endrin—free during the winter and
transferred to endrin—fortified feed during the reproductive period, did
evidence a reduction in the viability of the hatched chicks, as did chicks
from quail fed endrin only during the winter. Pheasant chicks, from parents
receiving 10 ppm endrin during the breeding season, also had unusually
high mortality rates during the first two weeks. High mortality occurred
among quail receiving 1 ppm endrin during both winter and reproductive
periods, and, as a result, this group was eliminated from further experi-
mentation (Dewitt, 1956).
Previous experimental investigation using breeding quail fed an
0.001%, or 10 ppm, endrin—fortified diet revealed no visible signs of
toxicity as well as no affection of egg production, fertility, hatchability,
or viability until 23 days after the onset of the test. All of the
adults died within the next three days (DeWitt, 1955).
Other experimental investigations have been conducted on the
hatchability and viability of eggs, but they differ from the previous
studies in that they utilize egg injection techniques to expose the
embryo rather than transfer of endrin from the parents.
Injection of 5 mg endrin/egg, or 100 ppm, resulted in only 20%
hatchability compared with 100% hatchability of eggs injected with DDT
at the same concentration. A reduction in concentration to 0.5 mg/egg,
or 10 ppm, increased the hatchability to 40% (Dunachie and Fletcher, 1966).
Later investigation by Dunachie and Fletcher (1969) revealed that
the type of diluent used for endrin could alter the toxicity. Acetone—
dissolved endrin was found to be significantly more potent than corn
oil—dissolved endrin. Table 5.12 indicates this variation as well as
the inconsistency of endrin toxicity to hens’ eggs. These inconsistent
results were attributed to the possibility that the terminal stage is
the most susceptible and that a slight increase in the rigor of the con-
ditions of incubation could significantly reduce hatchability of the
treated eggs while not affecting the controls.
Table 5.12. Hatchability of hens’ eggs after endrin
injection (percentage of control)
ppm
Dissolved in acetone
Dissolved in corn oil
100
30
50
39
0
25
23
10
103
46
5
109
Source: modified from Dunachie and Fletcher, 1969.
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106
In a starvation experiment, the chicks hatched from eggs receiving
5 ppm endrin all died within five days, while the same chicks that
received feed after hatching from the eggs injected with endrin survived
(Dunachje and Fletcher, 1969). It was felt that this supported the
theory that rigorous conditions could adversely affect endrin—exposed
avians.
Dunachie and Fletcher (1969) also found that a delay in the time
of injection greatly reduced the toxicity of endrin to the embryo.
Injection on day 5 of 100 ppm endrin resulted in only 4% hatchability.
The same dose given on day 8 resulted in 25% hatchability, while
injection on the tenth day did not adversely affect the hatchability
of the eggs. These results may indicate that endrin toxicity is altered
by either the age of the exposed embryo or the duration of exposure.
Smith et al. (1970) found endrin to be highly toxic to the developing
embryo. Only 40% hatchability occurred In eggs injected with 0.2 mg/egg,
or 4 ppm, while the control eggs injected with diluent were hatched at
a rate of 86.2%. Although the hatchability was greatly affected, there
was no physiological effect on the day—old chicks.
Although these injection studies are pertinent, the effect of
injection of endrin into the egg may not be similar to the effect of
ingestion of endrin by the hen followed by deposition of endrin during
formation of the egg.
Endrin is thought to primarily induce central nervous system (CNS)
disorder, since behavioral observations indicate that death from
experimental endrin poisoning is preceded by convulsions and other CNS—
controlled responses. In order to obtain a more detailed knowledge of
the action of endrin on the CNS, the telencephalic function of the endrin—
exposed pigeon was investigated (Revzin, 1966).
Experiments conducted to determine whether endrin induces a selective
or a general pattern of CNS stimulation revealed evidence for both
possibilities. All telencephalic nuclei examined, after injection of
endrin doses in excess of 4 mg/kg, were induced to seizure with no clear
propagation from one center to another. Therefore, endrin at these doses
may be considered a nonspecific convulsant. In lower doses, however, the
seizures are not identical in all nuclei. The amplitude of the seizure
discharges is greater in the ectostriatum and adjacent neostriatum than
in the surface leads, paleostriatum or hyperstriatum. Buildup of the
high—frequency activity which precedes seizure as well as the initiation
of seizure discharge often occurred in the ectostriatum prior to their
appearance in other nuclei. Longer duration of the seizure discharges
appears to occur in the ectostriatum, and occasionally seizure activity
was only measurable in the ectostriatum. These findings, accompanied
by the absence of effect induced by endrin on the ascending reticular
activating system or on the nucleus rotundus, indicate that endrin also
acts as a selective toxicant in the avian CNS.
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107
Resulting from the facilitation of the rotundo—ectostriatal potential
after subconvulsive doses of endrin and the knowledge that the ecto—
striatuin is a visual projection area, it is probable that visual deficien-
cies will result from endrin exposure. These visual deficiencies could
reduce the avian ability to avoid predators and compete for food (Revzin,
1966).
Avoidance behavior in the gallinaceous chick occurs early and is of
obvious survival value in the wild. Measurement of this avoidance
response was tested in seven—day—old Coturnix quail treated with a 2—ppm
endrin—fortified diet for eight days and then with untreated feed for
six days. Group avoidance response of endrin—treated chicks was signifi-
cantly suppressed below the controls; however, after 48 hr on an endrin—
free diet the birds’ avoidance behavior returned to normal (Kreitzer and
Heinz, 1974). This alteration of avoidance response coupled with the
previously discussed visual deficiencies could greatly reduce the
possibility for survival.
A possible synergistic relationship between chlordane and endrin
given to Japanese quail was investigated by Kreitzer and Spann (1973).
Chlordane and endrin were given in respective mixtures of 80:20, 50:50,
and 20:80. None of these doses affected more than an additive mortality
in the birds. Therefore, the joint action of chiordane and endrin is
neither synergistic nor antagonistic.
5.4 INSECTS
5.4.1 Metabolism
Brooks (1960) treated different strains of houseflies (Misa dornestica)
with 1 C—labeled isodrin, aidrin, endrin, and dieldrin in order to determine
the metabolism as well as the mechanism of resistance of the adult flies
to these insecticides. The radioactive compounds were topically applied to
the dorsal thorax of pesticide—sensitive or dieldrin—resistant strains.
The results of this study indicated that insect resistance is not
related to the degree of penetration, and that there were no marked
differences in the way the radioactive insecticides were metabolized by
the different housefly strains. Thus, all strains enzymatically converted
isodrin and aidrin to the corresponding epoxides eridrin and dieldrin.
There was some evidence to show that this enzymatic oxidation took place
not only internally, but also occurred on or within the insect cuticle.
Acetone extracts of live susceptible and resistant insects treated
with isodrin or endrin contained similar small amounts of water—insoluble
products, one of which chromatographically behaved as the ketone, a known
rearrangement product of endrin (Bellin, 1956). Endrin and its precursor,
isodrin, were found together in all sampled tissues at the time of “knock—
down”; however, there was no evidence of endrin excretion by the house-
flies.
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108
A more systematic study concerned with the mode of entry, absorption,
metabolism, and excretion of endrin by susceptible (S) and resistant
(R) larvae was performed by Polles and Vinson, 1972.
In order to determine the mode of entry and the rate of cuticular
penetration of endrin, laboratory—reared third instar tobacco budworm
larvae (Heliothis virescens Fabrieius) and isolated tobacco budworm
cuticles were topically treated with 1 C—1abeled endrin on the dorsal
surface (between first and second abdominal segments). Samples analyzed
0, 1, 2, 4, 12, 24, and 48 hr after treatment revealed that penetration
of endrin into the endocuticle was slow, and that the rate of penetration
was higher in S larvae than in R larvae; however, no specific reason for
this difference was elucidated. According to Brooks (1960), the slower
penetration into the R strain may be due to the presence of inbred insec-
ticide in the tissues of these insects.
The metabolism of endrin and its distribution within insect tissues
was investigated by injecting large amounts [ 1.25 ig endrin per microliter
(0.5 lkC_labeled endrin per microliter)] of radioactive endrin in the
larvae. The concentration of endrin was then determined in the head,
digestive tract, hemolyinph, feces, ventral chord, and remaining tissues.
No differences were noted in the localization of endrin in the
tissues under study. In both strains the largest amount of endrin was
recovered from the fraction termed “remaining tissues” (largely composed
of body fat); however, storage of endrin in these tissues appeared to
be of no importance as a resistance mechanism, since both S and R strains
stored approximately the same amounts of endrin. There was also no dis—
cernable strain difference in the accumulation of endrin in nervous system
tissue. Differential extraction of nerve tissues with n—hexane and
chloroform—methanol solvent systems indicated some degree of affinity of
the insecticide for components of the nerve tissue as shown in Table 5.13.
Table 5.13. Quantity of lkC_endrln in S and R larvae of
Heliothi8 Vir98C9fl8 central nervous system extracted
with n—hexane and chloroform-methanol
Extraction
solvent
lkC_endrin
recovered at post injection” (%)
Susceptible
(S) ’
Resistant (R)b
1 6
24
1 6
24
n—Hexane 0
CucL 3 _CH 3 0ud
94.0 88.0
6.0 12.0
62.0
38.0
84.0 66.0
16.0 34.0
30.0
70.0
aPercentage represents total ameunt in nerve cord.
bReu
0 Lightly bound endrin.
4 rightly bound endrin.
Source: Reprinted with permission from S. G. Polles and
S. B. Vinson, J. Agric. Food Chem. 20(1): 38—41 (1972). Copyright
1972 American Chemical Society.
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109
From this data it was concluded that endrin forms complexes with
proteins in the nerves of R—strain larvae which are not involved in
toxicity. This indicated that the binding of endrin to proteins may
result in decreasing the concentration of insecticide available to exert
its toxic eff its toxic effect. Whether this phenomenon is of signif 1—
cance in the ability of the insect to withstand larger concentrations
of endrin is still uncertain.
The results of the metabolic study illustrated that both strains
(S and R larvae) produced two metabolites, each tentatively identified
as endrin aldehyde and endrin ketone. No evidence of endrin alcohol
formation by either strain was found. R—strain larvae produced two
additional unidentified metabolites having well—defined Rf values on
thin—layer chroinatographic plates. Finally, most of the radioactivity
excreted by both strains was unchanged endrin.
In an attempt to elucidate the role of insecticide penetration
into the insect body as one of the factors affecting the mechanism
of insect resistance to pesticides, Szeicz et al (1973) studied the
absorption rate of endrin and other 1 C—1abeled insecticides into two
strains of tobacco budworm, one a susceptible strain, MS, and one an
organophosphate resistant strain, CM. Each strain was topically treated
with 1 .il of an acetone solution of 1 C—labeled endrin. The dose was
applied on the dorsal surface of the first abdominal segment. The data
obtained in this experiment indicated a higher penetration rate for the
more polar materials into larvae of both strains. Thus, approximately 40
to 50Z of a 0.2— .ig dose of endrin was absorbed within 12 hr by both larval
strains. The initial buildup of 1 C—labeled insecticide in the cuticle
stopped 4 to 8 hr after application. The cuticular accumulation was
followed by a similar elevation of the concentration of endrin in the
internal fraction. In general the concentration of endrin in the internal
fraction exceeded the amount of endrin found in the cuticle after about 6
to 8 hr. The times for maximum internal absorption of endrin were approxi-
mately the same for both strains; however, the concentration of endrin at
those particular times was greater in the MS larvae. The reason for the
measured difference in the rate of penetration in the two strains of
larvae used was not discerned, but the results obtained seemed to correlate
with those of Polles and Vinson (1972).
5.4.2 Effects
The use of any pesticide for the control of any pest is based on
its chemical selectivity for that particular pest. Some insects, however,
develop resistance to pesticides; for example, the ability of the housefly
to develop resistant strains to DDT was shown by Perry and Hoskins (1951).
Perry suggested that insect resistance to DDT was due to the development
of detoxification mechanisms.
Mahar (1962) and Eldefrawi et al. (1964) reported the appearance of
highly cyclodiene—tolerant strains of the cotton leafworm (Spodop-tera
li-t-toralis boise). Later, Hassan et al. (1970) followed the development
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110
of endrin tolerance by different field strains of the cotton leafworm
in the laboratory. These investigations suggested that insecticide
tolerance was a function of the length of exposure of the worms to the
chemical. This was evidenced during 1961 by the inability of the endrin
concentrations used to effect an LD 50 . The cessation of the use of endrin
during the years 1963 through 1965 caused a decrease of endrin resistance
by the worms; however, in 1965, when endrin was once again liberally used,
most of the worm strains investigated regained their high tolerance to
endrin by the following year.
Attia (1976) found endrin resistance in three strains of the almond
moth, Cadra cczntelia (Walker), collected from stored foodstuffs and milk
products in New South Wales in 1975. Their endrin response was compared
with a human susceptible laboratory reference strain; the field moths
exhibited 35—, 57—, and 62—fold greater resistance to endrin.
The mutagenic potential of endrin was studied by Benes and Scram
(1969). These investigators used the fruit fly (Drosophila melc mogaster)
as the test organism. The Muller—5 genetic test, which detects recessive
lethality in the X—chromosome, as well as the eucentric—chromosome
aberration test, which ascertains the rearrangement of larger chromosome
groups, showed that endrin did not have any outstanding inutagenic activity
in Drosophila.
The effects of sublethal treatments of endrin on the biotic potential
(ability of a population to reproduce and survive, 1. e., natality vs
mortality) of lady beetles (Colcomegilla maculata De Geer) were investi-
gated by Atallah and Newsom (1966). The reproductive potential (natality
rate) was measured by recording the number of eggs produced by each female
until death, while the effect of the treatment on the survival potential
(ability of the organism to withstand environmental resistance) of the
progeny was determined by rearing the F 1 larvae and recording the number
reaching the adult stage. The results of these studies showed that
endria was toxic to both diapausing and active beetles. The LD 50 val es
found were 5.8 31g/active beetle (472 mg/kg) and 5.6 pg/diapausing beetle
(455 mg/kg). Although endrin decreased longevity, it had no effect on
oviposition or survival of the F 1 generation.
Somewhat similar results were reported by Singh and Lal (1966), who
studied the biology of red cotton bugs (D. koenigii) surviving DDT or
endrin treatments. Their findings showed that endrin at concentrations
higher than the LD 50 for the species not only reduced the life span of
adult bugs, but also reduced the fecundity of the females and the viability
of the eggs laid by the treated parents. On the other hand, lower dosages
of endrin (concentrations below the LD 50 ) had no effect on oviposition
and postoviposition periods. The number of egg batches per female was
not affected, and there was no deleterious effect on the first and second
generations as compared with controls. One of the most significant
findings by Siugh and his co—workers was that the female progeny of endrin—
treated adults were significantly more tolerant to endrin than the
controls and that lower endrin dosages may be responsible f or an increased
fecundity In the parents’ generation.
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111
The susceptibility variations of an insect to insecticides is largely
governed by the intrinsic changes in the environmental factors. Of these
factors, the quality and quantity of food significantly influence the
resistance of insects to insecticides (Gordon, 1961). Abhyankar and
Sanup (1970) studied endrin susceptibility of aphids (Lipaplus er Lsimi
Kalt) reared on different host plants (six host plants of the cruciferae
family). Abhyankar’s results showed statistically significant differences
in the susceptibility of certain groups of aphids to 11 insecticides:
phosphamidon, dimethoate ethyl parathion, methyl parathion, malathion,
endosuif an, lindane, nicotine sulfate, ppDDT, carbaryl, and nicotine.
However, the variations in the endrin susceptibility of aphids reared on
these host plants were not statistically significant, leading to the
conclusion that the same concentration of endrin can probably be used f or
the control of aphids irrespective of the host plant. Because there were
indications of endrin resistance developed by the aphids, the authors
suggested annual evaluations of LD 50 values.
The antagonistic effect of gossypol, a pigment present in the seeds
of glanded varieties of cotton, was studied by Abou—Donia et al. (1974).
Acetone solutions of gossypol or acetone alone were deposited on the
dorsal regions of army worms (Spodoptera littoralis) by means of micro—
pipettes, and the treated larvae were used for the determination of LD 50
values for endrin and other insecticides. Endrin LD 50 s increased 200%
in the gossypol—treated larvae as compared with the LD 50 obtained with
the non—gossypol—treated controls. Two mechanisms were suggested for the
mode of antagonistic action induced by gossypol: (1) gossypol may reduce
body penetration of the insecticide; (2) gossypol may enhance detoxifica-
tion of the absorbed insecticide. The second assumption is supported by
findings that liver microsomal oxidases increased in gossypol—fed rats
(Abou—Donia and Dieckert, 1971). However, Shaver arid Wolfenbarger (1976)
applied endrin (25 ug/larva) topically to tobacco budworm, Heliothis
viresoens (F.), larvae and placed them on diets containing 0.07 to
0.0082% (wt/vol basis) gossypol. They determined that the gossypol did
not affect endrin’s toxicity at this rate.
The mode of toxicity as well as the site of action of the cyclodiene
insecticides has not yet been defined. Based on some earlier investigations
reviewed by Winteringham and Lewis (1959), it was generally agreed that
cyclodienes affect the central nervous system. In an effort to elucidate
whether the site of action of endrin is in the ganglia or the axonal
membrane, Ryan and Shankland (1971) studied the synergistic action of
cyclodiene insecticides with DDT on the membrane and giant axons of the
American cockroach (PiripZaneta americana L.). From this study it was
concluded that the cyclodiene insecticides had no toxic action on the
axonal membrane of cockroach giant fibers located in the central nervous
system, but did affect the ganglia, suggesting that they are the primary
site of pesticide action. It was also found that DDT—cyclodiene mixtures
had a joint action on the axonal membrane of the giant fibers of the
American cockroach, but this effect did not represent enhancement of
the toxicity of either compound.
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112
Although it appears that endrin acts on the central nervous system,
the precise mechanism of action on other systems is not understood.
In many toxicological studies, insects are used as the test organisms;
therefore, d better understanding of the changes in metabolic processes
taking place within the test organisms should lead to the selection of
those materials ideally suited for their specific control. Following
this line of reasoning, Dikshith and Vasuki (1970) studied the changes
in phosphatase activity of mealybugs (Dacty Zopus confusus Cxii), a large
group of insect pests affecting potatoes.
The acid and alkaline phosphatases of the coccid CD. confusue)
homogenate showed a specificity toward glucose—i—phosphate as the substrate.
In vitro and in vivo tests with different doses of endrin revealed a
very significant pattern of enzyme inhibition. The inhibition of alkaline
phosphatase activity was gradual with the addition of endrin, whereas acid
phosphatase showed an initial increase in activity with a subsequent
decrease after the addition of higher doses of endrin.
5.5 MA}NALS
5.5.1 Domestic
5.5.1.1 Metabolism
5.5.1.1.1 Exposure, distribution, and accumulation . Domestic
herbivores are exposed to endrin primarily through ingestion of endrin—
treated foliage. Inhalation of vaporized endrin and absorption through
the skin following direct application of endrin to the animals represent
other known routes of exposure.
Little is known of the transport and distribution of endrin in mammals.
No evidence of storage in any particular tissue or organ, other than fat,
has been found. However, residues of endrin ranging from 0.001 to 23.7 ppm
have been detected in a variety of n tmn 1ian tissues.
Studies by Brooks (1969) demonstrated that steers, lambs, and hogs
receiving 0.1 ppm endrin in the diet for 12 weeks showed little tendency
to deposit endrin in body tissues. Continuous feeding of endrin at levels
up to 2 ppm resulted in a maximum body fat content of 1 ppm. Cattle with
only ambient environmental endrin exposure were analyzed for the presence
of endrin residues in their tissues by the U.S. Department of Agriculture
in 1967. Of the 2785 animals studied, 2783 contained no endrin residues;
one animal contained between 0.01 and 0.1 ppm endrin in fat and another
contained between 0.11 and 0.5 ppm, also in fat. By 1971, however,
similar testing revealed that endrin incidence in tissues was increasing.
Of 2403 cattle tested, 42 had levels of 0.01 to 0.1 ppm endrin in fat
(Spaulding, 1972).
Long et al. (1961) report high le els of storage in the adipose tissue
of lambs. Higher levels were detected in the internal fat surrounding the
stomach and thoracid cavity than in external fat deposits. Lambs were
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113
allowed to graze for 55 days on pastures treated with 2% endrin granules,
applied six times in May and June at a rate of 0.5 lb endrin per acre.
The lambs were then transferred to untreated pasture, and endrin in fat
was measured after 0, 14, and 42 days. After 0 days of grazing in un-
treated pastures, lambs had 18.3 to 23.4 ppm endrin in internal fat
and 11.5 to 14.0 ppm in external fat. After 14 days, endrin levels
were surprisingly higher, with 20.3 to 23.7 ppm detected in internal fat
and 146 to 20.1 ppm in external fat. Some loss did occur after 42 days.
Internal fat levels dropped to 8.9 to 13.8 ppm, and external fat contained
only 6.4 to 11.0 ppm. These findings seem to contradict later reports of
Brooks (1969 and 1974b) of no storage and no retention. However, the
Long et al. (1961) study did feed much higher levels of endrin to younger
animals, and younger animals have more fat than adults.
Sharma and Gautam (1971) detected endrin residues in the brain and
liver tissue of calves. In the domestic dog, endrin was reportedly
detected in the abdominal viscera (Reins et al., 1966) as well as in fat
(Richardson et al., 1967). The latter authors fed endrin to dogs at a
rate of 0.1 mg/kg per day for 128 days. Endrin did not accumulate in
the following tissues: blood, heart, liver, kidney, pancreas, spleen,
lung, or muscle. However, endrin had accumulated in fat to levels of
0.76 ppm.
5.5.1.1.2 Transformation and elimination . Biotransformation of
endrin in manunals is discussed in detail in Sect. 6.2.3.
With the exception of endosulf an, endrin is the least persistent in
mammals of all the commonly used pesticides. Endrin is rapidly metabolized
and eliminated from vertebrate tissues (Brooks, 1974b). Excretion occurs
through the milk as well as through the urine and feces. Residue levels
in excess of 0.25 ppm on a fat basis were detected in the milk of 40
Wisconsin dairy herds between 1964 and 1967 (Moubry et al., l968a).
Endrin was presumably retained in the milk fat for up to four weeks.
However, the quantities of endrin ingested during that period were not
controlled. Extracted milk fat from one of these herds average 6.76 ppm
endrin. One week following the removal of endrin sources, the average
endrin levels decreased to 0.81 ppm. After four weeks the endrin levels
in extracted milk fat had decreased to 0.13 ppm.
Williams and Mills (1964) studied the appearance of endrin in cow’s
milk under controlled feeding conditions. Cows were fed for 35 days
with a combination feed supplemented with 0.05, 0.15, or 0.30 ppm endrin.
Endrin concentratins in the milk increased progressively at all three
exposure levels during the first few days of feeding. When 0.15 or 0.3 ppm
endrin was ingested, the concentration in milk reached a maximum at approxi-
mately the 15th day. At an exposure level of 0.05 ppm, the plateau level
in milk was not attained until the 13th day. When ingestion of endrin
ceased, residues in milk declined sharply. Following 20 days on an
endrin—free diet, detectable (greater than 0.001 ppm) levels were present
only in milk samples from cows fed the highest levels of endrin (0.3 ppm).
It is possible that these data were not representative for endrin alone,
since several pesticides were fed together. The rate of transfer into
milk might have been affected by other pesticides in the mixture.
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114
Endrin is apparently excreted in milk in higher concentrations when
fed as a residue on hay than when fed dissolved in soybean oil (Ely et al.,
1957). When endrin—treated hay was fed to cows in doses of 0.05 mg
endrin/kg, no measurable amounts were detected in milk. Somewhat larger
doses (0.06 to 0.11 mg/kg) resulted in concentrations of 0.1 to 0.2 ppm.
ingestion of 0.11 to 0.24 mg/kg endrin in soybean oil, on the other hand,
was insufficient to produce detectable residues in milk. However, doses
ten times as large (1.11 to 2.33 mg/kg) did result in 0.15 to 0.27 ppm
endrin in milk on a fat basis. In general, a total daily endrin intake of
greater than 20 mg as a residue sprayed in forage is necessary for
excretion of measurable quantities of endrin in milk.
In another study (Saha, 1969) the average concentration of endrin
excreted in milk was found to be 0.05 to 0.08 ppm. The ratio of residue
in milk to feed was 0.07. This rate of excretion was higher than that
for DDT, heptochior, teraphene, chlordane, and methoxychior.
The levels of endrin in milk following ingestion of feed containing
various concentrations of endrin are presented in Table 5.14.
Table 5.14. Endrin residues in cow milk after feeding
Feed (ppm)
Milk (ppm)
Feeding (days)
Source
0.1
0.25
0.75
2.00
0.01
0.02
0.04
0.10
84
84
84
84
1
0.05
0.15
0.30
0.004
0.010
0.018
35
35
35
2
1.9
2.8
3.7
<0.05
0.14
0.15
48—63
48—63
48—63
3
Sources: 1 — Saha, 1969;
2 — Williams and Mills, 1964;
3 — Ely et al., 1957.
5.5.1.2 Effects
5.5.1.2.1 Acute exposure . Endrin is highly toxic to mammals in
large doses. Adverse effects have been reported following oral, respira-
tory, intravenous, and dermal exposure. Death from endrin has been
reported for the following domestic mammals: horse, rabbit, goat, dog,
cat, cow, and hamster. The dose lethal to 50% of the test animals is
presented in Table 5.15. Female mammals appear more susceptible than
males to endrin poisoning (Ely et al., 1957), possibly because females
store more fat. For this reason, horse LD 50 s are given as 10 mg/kg
for mares and 35 mg/kg for stallions and geldings (Catcott and Smithcors,
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115
1972). Other LD 50 s ranged from a low of 2.5 mg/kg for dogs to a high of
50 mg/kg for goats.
There are no known reports of dogs dying from environmental exposure
to endrin. However, the lethality of endrin to dogs has been demonstrated
through laboratory studies. Reins et al. (1966) injected up to 25 mg
endrin per ml intravenously into dogs. The increased blood pressure and
heart rate that resulted led to convulsions and finally death. At an
injection level of 2 mg/kg, 40% of the dogs died. At a rate of 3 mg/kg,
75% died. Between 5 and 10 mg/kg there was 100% mortality (Reins et al.,
1966). Brooks (l974b) reported mortality in dogs from 25 ppm endrin in
diets.
Table 5.15. Endrin lethal toxicity to mammals
Domestic animals
LD 50 (mg/kg)
Source
Horse
Hamster
Rabbit
Goat
Dog
10—35
10
5—10
25—50
2.5
1
8
2—7
2—4
3
Wild animals
Big brown
Pine mouse
bat
5—8
2.6
5
6
Sources: 1 — Catcott and Sinithcors, 1972;
2 — Pimentel, 1971;
3 — Reins et al., 1966;
4 — Tucker and Crabtree, 1970;
5 — Luckens and Davis, 1965;
6 — Petrella and Webb, 1973;
7 — Negherbon, 1959;
8 — Ottolenghi et al., 1974.
Sharma and Gautam (1971) report cows dying from both ingestion
and inhalation of endrin. Hematological changes and lesions were
reported.
Cattle mortality following dermal exposure has been reported by
Sharma and Gautam (1971), Moubry et al. (1968a), and Jerome (1958). The
last author reported the most extreme example of accidental poisoning.
After being sprayed for flies with a 0.34% endrin solution, 218 out
of 370 cattle were affected; the mortality rate was 71%. Acute
symptoms were: tetanic seizure, spasmodic actions, grinding teeth,
salivation, and falling. Peracute symptoms were: twitching, blinking,
and jumping, as well as respiratory and cardiac arrest. Postmortem
examinations revealed gross lesions, myocardial hemorrhages, tissue
anoxia, and cyanosis.
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116
Sharma and Gautam (1971) reported both derinal and oral poisoning in
calves. An endrin solution as small as 0.04% sprayed on calves caused
death within 6 hr. Oral doses of 4.5 to 5.5 mg per pound of body weight
were also lethal.
Goats appear to be more resistant to lethal doses of endrin than do
other domestic mammals. LD 50 varies from 25 to 50 mg/kg endrin. Acute
symtoms of poisoning were ataxia, slowness, tremors, tracheal congestion,
prostration, and convulsions. Goats died from one to five days after
oral treatment (Tucker and Crabtree, 1970).
5.5.1.2.2 Chronic exposure . Chronic exposure to endrin adversely
affects physiology, behavior, and reproduction; the last two are least
documented in domestic animals. Sublethal physiological effects observed
in some species are presented in Table 5.16. The symptoms of endrin
poisoning range from subacute nervous spasms and slight cyanosis (Jerome,
1958) to lesions, convulsions, and increased blood pressure and heart
rate.
Table 5.16. Endrin toxicity in domestic mammals — sublethal
MammRl
Storage in tissue
Effects (physiological)
Source
Cat
Unknown
Hematological changes
and lesions
1
Calf
Brain and liver
Hematological changes
and lesions
1
Cow
Fat and milk
Convulsions, high breathing
rate, lesions, tissue anoxia
2
Dog
Abdominal viscera
and fat
Changes in blood pressure
and heart rate, convulsions
3,
6
Rabbit
Unknown
Body and organ weight
increased
4
Goat
Unknown
Ataxia, tremors, convulsions
5
Sources: 1 — Sharma and Gautam, 1971;
2 — Jerome, 1958;
3 — Reins, et al., 1966;
4 — Takahama et al., 1972;
5 — Tucker and Crabtree, 1970;
6 — Richardson et al., 1967.
Siugh et al. (1977) treated buffalo calves with a 20% emulsible
concentrate formulation of endrin orally at a rate of 7.5 mg/kg body
weight. Within 2 to 3.5 hr after treatment the calves went into con-
vulsions lasting approximately 5 mm with a significant (P < 0.01) rise
in the level of blood glucose. Cholinesterase activity of the erythrocytes
was gradually restored as the signs subsided and returned to nearly normal
on the sixth day after treatment.
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117
The dose which can initiate the onset of symptoms of endrin poisoning
in calves is 2.0 mg/lb body weight (Sharma and Gautam, 1971). The
symptoms in calves and the results of postmortem analysis were as follows:
• nervous excitement,
• convulsions,
• accelerated respiratory rate,
• depressed erythrocyte count,
• increased total leukocyte count (lymphocytes),
• lesions of the gall bladder and kidney,
• albumin in the urine,
• congested kidney and lungs,
• endrin—positive brain and liver.
Long et al. (1961) reported that lambs grazing on endrin—treated
pastures stored up to 23. 7 ppm endrin in fat without exhibiting any
symptoms of endrin poisoning. In fact, there was not even a decrease
in weight gain.
Dogs fed 0,1 mg/kg per day had blood levels of endrin of less than
0.001 ppm and showed no toxicity symptoms (Richardson et al., 1967).
Brooks (1974b) reported no effect in dogs fed 1 ppm endrin. However, a
diet of 5 ppm/day increased liver and kidney weights. No evidence of
endrirt—related carcinogenesis has been reported (Brooks, 1974b).
Small doses of endrin may result in symptoms which might go unnoticed
outside of the laboratory or be improperly diagnosed. For example, cows
may show lack of appetite or decreased milk production (Ely et al., 1957).
In some animals, reproduction rates may be lowered (Pimentel, 1971;
Ottolenghi et al., 1974). Ingestion of small amounts of endrin (0.1 mg/kg)
by domestic rabbits resulted in increased weights of liver, kidney, heart,
lung, and whole body as compared with controls. Such effects would not
be obvious under natural conditions.
Not enough long—term or consistent data are available on the sublethal
effects of endrin, and endrin toxicology is not well known to veterinarians.
5.5.2 Wild Mammals
5.5.2.1 Exposure and metabolism . Wild mammals are exposed to endrin
following application of the pesticide to crops, orchards, and pastures.
Uptake may occur from dermal absorption, oral ingestion of contaminated
insects and vegetation, and by grooming the fur (Morris, 1970). Presumably,
wild lnRmmals inhale endrin, as do domestic mammals.
While extensive information is available on the effects of endrin
in several species of wild mice, very little has been published for other
species. Most of the literature deals with herbivores and insectivores,
with little available data concerning endrin in carnivores and omnivores.
Traces of endrin have been found in fat as well as other tissues of
wild mammals. Trace amounts of endrin (0.001 to 2.8 ppm) have been
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118
reported in the fat of white—tailed deer (Odocoileus virginianus) (Cotton
and Herring, 1971), pronghorn antelope (Antilocapra americana) (Moore et al.,
1968), and mule deer (0. hemionus) (Stickel, 1973; Jewel, 1966). Wilson
(1966) reported that the blubber of porpoises (Phocaenidae) contained 0.05
to 2.0 ppm endrin. Jewell (1966) reported that deer muscle tissue also
had traces of endrin (0.072 ppm). Ferrel (1963) reported that rabbits
(Lepus sp. and Sylvilagus sp.) had endrin residues of 1.6 ppm in kidney
and liver tissues. Hooven (1957) reported residues of endrin in the
following tissues: the stomach and intestine of the grey squirrel
(Sciurus carolinensis) (1.17 and 1.55 ppm respectively) and the intestine
of chickaree (Tamiasciurus doug7 asi) (0.56 ppm).
These data do not necessarily indicate endrin storage. However,
Morris (1968) hypothesized that endrin was stored in fat and translocated
to the nervous system during times of stress. Webb et al. (1972), on
the other hand, report that endrin was not stored in bodies of wild mice
(Pitymys pinetorwn) in detectable amounts.
Hepatic microsomes from mice converted endrin to the metabolite
12—OH—endrin (Petrella et al., 1974). Oral dosing of mice with endrin
resulted in the production of one fecal and three urinary metabolites.
The endrin metabolites were found to be excreted in the following propor-
tions: resistant mice, 18% in urine and 53% in feces; susceptible mice,
23% in urine and only 27% in feces. The greater amount of metabolites
released by resistant mice (71%) than by susceptible mice (50%) is well
documented (Webb et al., 1972, 1973; Petrella and Webb, 1973; Petrella
et al., 1974; Petrella et al., 1977). Thus, resistance may be due, in
part, to endrin degradation and the subsequent excretion of the metabolites.
5.5.2.2 Effects . VonRumker et al. (1974) defined wild—animal
toxicity in terms of population losses in habitats. “Highly toxic” means
severe losses occur if the pesticide is used over a given habitat.
“Moderately toxic” means moderate losses. “Slightly toxic” means slight
loss or injury to nontarget species. “Relatively nontoxic” was defined as
no loss or injury. Endrin seems to display all these levels of toxicity.
5.5.2.2.1 Acute toxicity . Endrin (2.0 lb/acre, or 2.2 kg/ha) has
been shown to be highly toxic to mouse populations for periods of up
to 70 days (Dana and Shav, 1958). Mortality in mouse populations of
33 to 100% was observed following field applications of endrin (0.5 to
2.5 lb/acre, or 0.55 to 2.75 kg/ha). Table 5 .17 lists mouse species
affected at varying rates of field spraying.
In addition to mice, the following species of mammalian wildlife
have been reported as receiving lethal doses of endrin: big brown bat
(Eptesicus fuscus), grey squirrel (Sciurus caroiinensis), chipmunk
(Tamais striatus), cottontail rabbit (Sylvilagus sp.), jackrabbit
(Lapus sp.), woodchuck (Marmota monax), and shrew (Sorex ep.). The only
species with established endrin LD 50 s are pine mouse, 2.6 mg/kg (Petrella
and Webb, 1973); brown bat, 5 to 8 mg/kg (Luckens and Davis, 1965); and
rabbit, 5 to 7 mg/kg (Negherbon, 1959).
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119
Wildlife symptoms of acute endrin toxicity are described for grey
squirrels and chipmunks by Hamrick (1969); they are tremors and reduced
vitality. Cotton rats exhibited severe tremors (Hamrick, 1969). Luckens
and Davis (1965) described tremors in bats before death by endrin poisoning.
Schindler (1956) described abnormal movements in wild mice for several
days preceding 100% mortality in a treated field.
Table 5.17. Applications of endrin in field to kill mice
Species
Rate of Application
Source
(lb/acre)
Pitymys pinetorum
Microtus sp.
2.5
2.0
1—1.5
1.6—2.4
0.5
1
2,
3
4
6
5
Perornyscus maniculatus
0.5
6
Sources: 1 Horsfall and Webb, 1966;
2 — Dana and Shaw, 1958;
3 — Schindler, 1956;
4 — Wolfe, 1957;
5 — Snyder, 1963;
6 — Morris, 1970.
5.5.2.2.2 Chronic toxicity . Endrin has been shown to have subacute
effects on wildlife populations by affecting reproduction, behavior,
ecology, and possibly evolution. The last can only be verified through
long—term observations of adaptation to endrin.
Sublethal effects of endrin are summarized in Table 5.18. Morris
(1972) describes sublethal effects of endrin due to direct toxicity
as either behavioral disorders or delayed reproduction. Indirect
toxicity may result when endrin is combined with environmental stress,
such as cold. Figure 5.6 shows various pathways of direct and indirect
biocide stress on small—mammal populations.
Reproductive disorders can occur in wild mammals due to endrin
exposure. Reproductive rates have both increased and decreased due
to endrin. Increases are due to larger amounts of territory (food,
water, and cover) available to survivors after population reduction due
to endrin. For example, continuing studies by Morris (1968, 1970, l97la,
b, 1972) have demonstrated that significant reductions occur in Microtus
populations after endrin spraying. However, populations recovered
quickly, and in two to three years demonstrated higher densities than
control groups. Morris (1972) attributes this phenomenon to repopulation
and higher survival rates of the young of surviving mice. The remaining
low—density Microtus population was able to expand territories and
avail itself of more food and cover. Reproductive potential was unharmed.
Driggers’ (1971) hypothetical conclusion was that endrin killed mouse
predators and parasites, allowing the population to prosper.
-------
Table 5.18. Endrin toxicity on wild niaininals — sublethal
1 — Morris, 1968;
2 — Morris, 1970;
3 — Morris, 1971b;
4 — Snyder, 1963;
5 — Luckens and Davis, 1965;
6 — Hamrick, 1969;
7 — Cotton and Herring, 1971;
8 — Jewell, 1966;
9 — Wilson, 1966.
Mammal
Classification
Storage in Tissue
Effects
1
Deer mouse
Perofl?y6CU8 8p.
Fat
Starvation stress,
unstable popula—
tion, and reproduc-
tion
Reproduction altered
2,
4
3
Meadow mouse
Microtus 8p.
Tremors
5
Big brown bat
E’pteBiCUB fuBcua
Tremors
6
Gray squirrel
Sciuru8 carolinensia
Tremors
6
Cotton rat
Sigmodon hi8pidu8
None known
7
White—tailed
deer
OdocoileUB Virgifl1 aflU8
Fat
muscle
None known
8
Mule deer
0. hemionua
Fat,
None known
9
Porpoises
Phocaenidae
Blubber
Sources:
0
-------
I IMPROPER
I MATERNAL CARE
I TEMPORARY
ACTIVITY LOSS
INCREASED
I VULNERABILITY
I TO PREDATORS
LAG IN POPULATION
GROWTH
+
EMBRYO
ABSORPTION
FOETAL DEATH
FEWER LITTERS
INDIRECT NONTOXIC
— DIRECT OR INDIRECT TOXIC
(LETHAUSUB LETHAL)
® THEORETICAL REPONSES
LONG TERM
UNREGULATED
FLUCTUATIONS
INDIRECT I
NONTOXIC
MORTALITY t- ———- -I SOCIAL
COMMUNITY F———
INDIRECT CHANGE IN
STRUCTURE
NONTOXIC _____________
121
ORNL-DWG 79-8123
AGGRESSION
COLD ENVIRONMENTAL
STRESS
FOOD
SHORTAGE
(UNCONTROLLED
DISPLACEMENT L TE
STRUCTURE I L DISRUPTION
(UNSTABLE POPULATIONS)
44
I
___________ I
— .1
Fig. 5.6. Generalized model of the ways in which a biocide may
affect a small—mrnnmal population. Source: R. D. Morris, Can. J. Zool.
50(6): 885—896 (1972). Copyright 1972, National Research Council of
Canada.
Peromycus populations, on the other hand, did not fare as well in
the same experiment. In 1970, Morris concluded that Peromycue populations
were severely reduced by endrin spraying and did not recover after a few
years. Peromycue showed long—term toxicological effects. No new
juveniles were found after spraying with endrin. However, in 1972,
Morris found that Peromycus were actually escaping from his enclosure.
His earlier findings could have been affected by this.
Other authors have found reduced reproductive potential due to
endrin. Good and Ware (1969) and Snyder (1963) showed reduction in
number of litters of Microtus after endrin application of 0.6 to 2.0
lb/acre. Snyder (1963) fed endrin to Microtus and found lower repro-
ductive rates due to reduced corpora lutea, implantation, and viable
embryos. Ottolenghi et al. (1974) fed endrin to mice during gestation
and found postnatal mortality of unweaned juveniles. This could have
been due to either endrin’s direct effects on fetuses or due to the
presence of endrin in milk.
Differential survival rates of wild mammals can have long—term
ecological or evolutionary effects which are still unknown. Morris’
studies demonstrated the potential for Peromyscus populations to be
replaced by Microtus in areas where endrin spraying is continuous year
after year.
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122
Pine mice (Pitynrys pinetorum), on the other hand, have been shown
to develop an inheritable resistance to endrin. Webb et al. (1973) report
that pine mice from areas sprayed regularly with endrin had an LD 50 as
high as 36.42 mg/kg. Pine mice from unsprayed areas had an LD 5 ç 1 as low
as 1.37 mg/kg. The endrin—resistant mice also exhibited a twofold cross—
resistance to dieldrin. Webb and Horsfall (1967) earlier found pine mice
with a 12—fold greater tolerance to endrin than susceptible mice from
unsprayed fields.
The resistance to endrin can be lost over time if endrin treatment
is stopped. Webb et al. (1973) report that three years after the last
endrin application the LD 50 in pine mice decreased from 36.42 mg/kg to
18.91 mg/kg. Webb et al. (1973) demonstrated that endrin resistance might
be hereditary as well as acquired. When susceptible males were crossed
with susceptible females, LD 50 values of progeny averaged 4.97 mg/kg.
When susceptible and resistance mice were crossed with resistant, LD 50 s
for progeny were 21.08 mg/kg. Therefore, in a field sprayed regularly
with endrin, resistant mammals would survive and produce resistant young.
At the same time, susceptible species would be killed or reproductive
rate affected. The long—term effect would be a different population
structure, loss of some species, and domination by other species.
Morris (1972) also discusses potential sublethal behavior changes in
wild mammals. These are related to maternal care, activity, and vulnera-
bility to predators. Endrin could also disrupt social patterns in popu-
lations, particularly when there is a sudden “vacuum” created by mortality.
Decreased competition leads to expansion of territories and changes in
rates of immigration and emigration, resulting in unstable and fluctuating
populations of small mammals. Predation rates may also increase (Ham—
rick, 1969), secondarily affecting larger predator populations as well.
Stickel (1973) reports that predatory mammals accumulate the highest
residues of chlorinated hydrocarbons. No data are given for endrin.
Schneeweis et al. (1974) report that endrin residues were below 1 ppm in
tongue and muscle tissue of timber wolves (Ccmis lupus) from Canada. These
data are inconclusive because wolves were not feeding in endrin—sprayed
areas; no fat was sampled, and minimum standards used were those established
for birds. No other mammalian predator data for endrin are known to date.
More research is necessary to determine whether endr n is accumulated
in carnivores, which feed on prey with high levels of pesticides. No
studies have been conducted on predators feeding on resistant populations
of mice.
5.6 REFERENCES
Abhyankar, K. M., and P. Sarup. 1970. Effect of Host Plants on the
Susceptibility of Lipaphis erysimi Kalt to Some Important Insecticides.
md. J. Entomol. 32(1): 74—85.
-------
123
Abou—Donia, M. B., and J. W. Dieckert. 1971. Gossypol: Subcellular
Localization and Stimulation of Rat Liver Microsomal Oxidases. Toxicol.
Appl. Pharmacol. 18: 507—516.
Abou—Donia, M. B., F. Taman, N. M. Bakery, and A. H. E1—Sebae. 1974.
Gossypol: Antagonistic Effect on Toxicity of Insecticides to Spadop-
tera Z.ittoralis. Experienta 30(10): 1151—1152.
Argyl, R. L., G. C. Williams, and I-I. K. Dupree. 1973. Endrin Uptake
and Release by Fingerling Channel Catfish (Ictalurus punctatus). J. Fish
Res. Board Can. 30(11): 1743—1744.
Atallah, Y. H., and L. D. Newsom. 1966. Ecological and Nutritional
Studies on Coleomegilla maculatcz De Greer (Coleoptera: Coccinellidae)
III — The Effect of DDT, Toxaphene, and Endrin on the Reproductive and
Survival Potentials. J. Econ. Entomol. 59(5): 1181—1187.
Attia, F. I. 1976. Insecticide Resistance in Cadra cautella in New
South Wales, Australia. J. Econ. Entomol. 69(6): 773—774.
Beck, J. R. 1957. Investigations on Use of Endrin—Ohio. Correspondence
to Patuxent Res. Reguge, Laurel, Maryland, November 29, 1957.
Bellin, R. H. 1956. Endrin Stabilization Using Inorganic and Organic
Nitrite Salts. U.S. Patent No. 2,768,178. Washington, D.C.
Benes, V., and R. Scram. 1969. Mutagenic Activity of Some Pesticides
in Drosophila melanogaster. md. Med. 38(12): 50—52.
Bennett, H. J., and J. W. Day, Jr. 1970. Absorption of Endrin by the
Bluegill Sunfish, Lepomis macrochirus. Pesti. Monit. J. 3(4): 201—203.
Brooks, G. T. 1960. Mechanisms of Resistance of the Adult Housefly
(l sco domestica) to Cyclodiene Insecticides. Nature 186(4718): 96—98.
Brooks, G. T. 1969. The Metabolism of Diene—Organochiorine (Cyclodiene)
Insecticides. Residue Rev. 27: 81—138.
Brooks, G. T. 1974a. Chlorinated Insecticides. Vol. 1: Technology
and Application. CRC Press, Cleveland, Ohio.
Brooks, G. T. 1974b. Chlorinated Insecticides. Vol. II: Biological
and Environmental Aspects. CRC Press, Cleveland, Ohio.
Brungs, W. A., and D. I. Mount. 1967. Lethal Endrin Concentration in
the Blood of Gizzard Shad. J. Fish. Res. Board Can. 24(2): 429—431.
Butler, P. A. 1963. Commercial Fisheries Investigations. In: U.S.
Department of the Interior, Fish Wildi. Serv. Circ. 167: 11—25.
-------
124
Butler, P. A. 1966a. The Problem of Pesticides in Estuaries. Reprint
from Am. Fish. Soc., Special Publication No. 3, pp. 110—115.
Butler, P. A. 1966b. Pesticides in the Marine Environment. J. Appi.
Ecol. 3(Suppl.): 253—259.
Butler, P. A. 1971. Influence of Pesticides on Marine Ecosystems. Proc.
R. Soc. London 177(1048): 321—329.
Catcott, E. J., and J. F. Smithcors (eds.). 1972. Equine Medicine
and Surgery. 2nd ed. Ainerican Vetenarian Publishers, Wheaton, Illinois.
Christopher, J. 1969. Endrin Poisoning in Chicken. Indian Poultr. Gaz.
53(3): 5—7.
Cope, 0. B. 1963. Sport Fishery Investigations. In: Pesticide Wild-
life Studies: A Review of Fish and Wildlife Service Investigations During
1961 and 1962. Fish and Wildl. Serv. Circ. 167: 26—42, Washington, D.C.
Cotton, D., and J. Herring. 1971. A Preliminary Survey of Pesticide
Residues in Whitetail Deer (Odoooileue virginianua). 24th Annual Con-
ference of Southeastern Association of Game and Fish Commissioners:
23—25, 28—29.
Cummings, J. G., K. T. Zee, V. Turner, F. Quinn, and R. E. Cook. 1966.
Residues in Eggs from Low—Level Feeding of Five Chlorinated Hydrocarbon
Insecticides to Hens. J. Assoc. Of f. Anal. Chew 49(2): 354—364.
Cummings, J. G., M. Eidelman, V. Turner, D. Reed, and K. T. Zee. 1967.
Residues in Poultry Tissues from Low—Level Feeding of Five Chlorinated
Hydrocarbon Insecticides to Hens. J. Assoc. Of f. Anal. Chew. 50(2):
418—425.
Cutkomp, L. K., H. H. Yap, E. Y. Cheng, and R. B. Koch. 1971. ATPase
Activity in Fish Tissue Homogenates and Inhibitory Effects of DDT and
Related Compounds. Chew. Bi.ol. mt. 3(6): 439—447.
Dana, R. H., and D. H. Shaw. 1958. Meadow Mouse Control In Holly. Calif.
Dep. Agric. Bull. 47(3): 224—226.
Davis, H. C. 1961. Effects of Some Pesticides on Eggs and Larvae of
Oysters (Craasoatrea virginic a) and Clams (Venus rnercenaria). Conuner.
Fish. Rev. 23(12): 8—23.
Davis, P. W., J. M. Friedhoff, and G. A. Wedemeyer. 1972. Organochlorine
Insecticide, Herbicide, and Polychiorinated Biphenyl (PCB) Inhibition of
NaK—ATPase in Rainbow Trout. Bull. Environ. Contain. Toxicol. 8(2): 69—72.
DeWitt, 3. B. 1955. Effects of Chlorinated Hydrocarbon Insecticides
upon Quail and Pheasants. 3. Agric. Food Chew. 3(8): 672—676.
-------
125
DeWitt, J. B. 1956. Chronic Toxicity to Quail and Pheasants of Some
Chlorinated Insecticides. J. Agric. Food Chem. 4(10): 863—866.
Dikshith, T. S. S., and K. Vasuki. 1970. Alkaline and Acid Phosphatases
and the Effect of Endrin on Dactylopius canfusus. Enzymol. 39(2): 77-83.
Driggers, B. F. 1971. Ground Spraying with Endrin to Control Orchard
Mice May Result in Severe Tree Damage by the Meadow Mouse, Microtus.
Hortic. News 52(4): 18—20.
Duke, T. W., and D. P. Dumas. 1974. Implications of Pesticide Residues
in the Coastal Environment. In: Pollut. Physiol. Mar. Organ. F. J.
Vernberg and W. B. Vernberg, eds. Academic Press, New York.
Dunachie, J. F., and W. W. Fletcher. 1966. Effect of Some Insecticides
on the Hatching Rate of Hens’ Eggs. Nature (London) 212(5066): 1062—1063.
Dunachie, J. F., and W. W. Fletcher. 1969. An Investigation of the
Toxicity of Insecticides to Birds Eggs Using the Egg—Injection Technique.
Ann. Appi. Biol. 64(3): 409—423.
Earnest, R. D., and P. E. Benville, Jr. 1972. Acute Toxicity of Four
Organichiorine Insecticides to Two Species of Surf Perch. Calif. Fish
Game 58(2): 127—132.
Eisler, R. 1970a. Latent Effects of Insecticide Intoxication to Marine
Mollusks. Hydrobiologia 36(3—4): 345—352.
Eisler, R. 1970b. Factors Affecting Pesticide—Induced Toxicity in an
Estuarine Fish. Tech. Pap. Bur. Sport. Fish. Wildi. 45: 1—20.
Eisler, R. l970c. Acute Toxicities of Organochiorine and Organo—
phosphorus Insecticides to Estuarine Fishes. Tech. Pap. Bur. Sport Fish.
Wildl. 46: 1—12.
Eisler, R., and P. H. Edmunds. 1966. Effects of Endrin on Blood and
Tissue Chemistry of a Marine Fish. Trans. Am. Fish. Soc. 95(2): 153—159.
Eldefrawi, M. E., A. Toppozada, A. Salama, and S. A. Eskishen. 1964.
Toxicological Studies on the Egyptian Cotton Leafworm, Prodenia litura.
II. Reversion of Toxaphene Resistance in the Egyptian Cotton Leafworm.
J. Econ. Entomol. 57(4): 593—595.
Eller, L. L. 1971. Histopathologic Lesions in Cutthroat Trout (Salmo
clarkii) Exposed Chronically to the Insecticide Endrin. Am. 3. Pathol.
64(2): 321—336.
El—Refal, A., F. A. Fahemy, N. F. A. Abdel—Lateef, and A. K. E. Imam.
1976. Toxicity of Three Insecticides to Two Species of Fish. Intern.
Pest Cont. 18(6): 4—8.
-------
126
Ely, R. E., L. A. Moore, R. H. Carter, and B. A. App. 1957. Excretion
of Endrin in the Milk of Cows Fed Endrin—Sprayed Alfalfa and Technical
Endrin. J. Econ. Entomol. 50: 348—349.
Fabacher, D. L., and H. Chambers. 1971. Possible Mechanism of Insecti-
cide Resistance in Mosquito Fish. Bull Environ. Contam. Toxicol. 6(4):
372—376.
Fabacher, D. L., and H. Chambers. 1976. Uptake and Storage of 1 C—
labeled Endrin by the Livers and Brains of Pesticide—Susceptible and
Resistant Mosquito Fish. Bull. Environ. Contain. Toxicol. 16(2): 203—207.
Ferguson, D. E. 1967. The Ecological Consequences of Pesticide Resistance
in Fishes. North American Wildlife and Natural Resources Conference
(32nd): 103—107.
Ferguson, D. E., and C. R. Bingham. 1966b. Endrin Resistance in the
Yellow Bullhead Ictalurua natalis. Trans. Am. Fish. Soc. 95(3): 325—326.
Ferguson, D. E., and C. P. Goodyear. 1967. The Pathway of Endrin Entry
in Black Bullheads, Icta7urua melas. Copeia 2: 467—468.
Ferguson, D. E., J. L. Ludke, and C. G. Murphy. 1966. Dynamics of Endrin
Uptake and Release by Resistant and Susceptible Strains of Mosquito Fish.
Trans. Am. Fish. Soc. 95(4): 335—344.
Ferrel, C. M. 1963. Detection of Wildlife Losses Caused by Pesticides.
Calif. Dept. of Fish and Game. 4 pp.
Finley, M. T., D. E. Ferguson, and J. L. Ludke. 1970. Possible Selective
Mechanisms in the Development of Insecticide—Resistant Fish. Pestic.
Monit. J. 3(4): 212—218.
Georgacakis, E., and M. A. Q. Khan. 1971. Toxicity of the Photoisomers
of Cyclodiene Insecticides to Freshwater Aniamals. Nature (London)
233 (5315).
Good, E. E., and G. W. Ware. 1969. Effects of Insecticides on Reproduc-
tion in the Laboratory Mouse. IV. Endrin and Dieldrin. Toxicol. Appl.
Pharinacol. 14(1): 201—203.
Gordon, H. T. 1961. Nutritional Factors in Insect Resistance to Chemicals.
Annu. Rev. Entomol. 6: 27—54.
Grant, B. F., and P. M. Nehrle. 1970. Chronic Eridrin Poisoning in
Goldfish Carassius auratus. 3. Fish. Res. Board Can. 27(12): 2225—2232.
Grant, B. F., and P. M. Mehrle. 1973. Endrin Toxicosis in Rainbow
Trout (SaZrno gairdneri). 3. Fish. Res. Board Can. 30(1): 31—40.
-------
127
Gregory, W. W. 1970. Bioaccumulation of Endrin from Natural Food
Sources in the Eastern Bobwhite Quail, Colinus v-i rginianus Virginanus
L. Diss, Abstr. mt. 31(2): 736B—737B.
Gregory, W. W., J. K. Reed, and L. G. Webb. 1972. Bioaccumulation of
Endrin from Natural Food Sources in the Eastern Bobwhite Quail, Colinus
virginanus virginianus L. In: Proceeding of the Annual Conference of
the Southeast Association for Gasm Fish 25: 156—164.
Hamelink, J. 1971. The Fate and Effects of Pesticides in Aquatic Environ-
ments. Proc. 2nd Symp. Haz. Chem. Handi. and Dis. Indianapolis, Indiana.
19—24.
Hamrick, W. J. 1969. The Effects of Arasan—Endrin Treated Pine Seed
on Bobwhite Quail, Gray Squirrel, and Turkey. 22nd Annual Conference
Southeastern Game & Fish Commissioners, pp. 106—113.
Hansen, D. 1969. Avoidance of Pesticides by Untrained Sheepshead
Minnows. Trans. Am. Fish. Soc. 98(3): 426—429.
Hansen, D. J., E. Matthews, S. L. Nall, and D. P. Dumas. 1972. Avoidance
of Pesticides by Untrained Mosquito Fish Gambusia affinis. Bull. Environ.
Contam. Toxicol. 8(1): 46—51.
Hansen, D. J., S. C. Schimmel, and J. M. Keltner, Jr. 1973. Avoidance
of Pesticides by Grass Shrimp (Palasnionetes pugio). Bull. Environ.
Contam. Toxicol. 9(3): 129—133.
Hassan, M. H., A. M. Ali, and M. S. E. El—Sawy. 1970. Development of
Tolerance of the Cotton Leafworm, Spodoptera littoralis boisd, to
Currently Applied Insecticides. Agric. Res. Rev. 48(1): 1—11.
Health, R. G., J. W. Spann, E. F. Hill, and J. F. Kreitzer. 1972. Com-
parative Dietary Toxicities of Pesticides to Birds. U.S. Dept. of mt.
Bur. Sport Fish. and Wildl. Wildlife No. 152, GPO. Washington, D.C.
Holden, A. V. 1973. Effects of Pesticides on Fish. Environ. Pollu.
by Pestic. Chap. 6. C. A. Edwards, ed. Plenum Press, New York.
Hooven, E. F. 1957. Field Test of Endrin—Treated Douglas Fir Seed.
Research Note No. 28, Oregon Forest Lands Research Center, Corvallis,
Oregon.
Horsf all, F., Jr., and R. E. Webb. 1966. Endrin Resistance in Pine
Mice. Va. Fruit 54(11): 18—20.
Iyatomi, K., T. Tamura, Y. Itazawa, I. Hanyu, and S. Sugiura. 1958.
Toxicity of Endrin to Fish. Prog. Fish Cult. 20(4): 155—162.
-------
128
Javaid, M. Y., and A. Waiz. 1972. Acute Toxicity of Five Chlorinated
Hydrocarbon Insecticides to the Fish, Channa punclzztuts. Pak. J. Sci.
md. Res. 15(4—5): 291—293.
Jensen, L. D., and R. A. Gauf in. 1966. Acute and Long—Term Effects
of Organic Insecticides on Two Species of Stonefly Naiads. J. Water
Pollu. Control Fed. 38(8): 1273—1286.
Jerome, Q. R. 1958. Endrin Poisoning: A Case Report. Vet. Med. 53(8):
409—412.
Jewell, S. R. 1966. Pesticide Residue Concentrations in Mule Deer.
Cob. Coop. Wildi. Res. Unit. Fort Collins, Colorado, Tech. Paper
No. 8: 11.
Johnson, B. W. 1968. Pesticides and Fishes — A Review of Selected
Literature. Trans. Am. Fish. Soc. 97(4): 398—424.
Katz, N. 1961. Acute Toxicity of Some Organic Insecticides to Three
Species of Salmonids and to the Threespine Stickleback. Trans. Am. Fish.
Soc. 90(3): 264—268.
Katz, N., and G. Chadwick. 1961. Toxicity of Endrin to Some Pacific
Northwest Fishes. Trans. Am. Fish. Soc. 90: 394—397.
Keith, J. 0. 1963. Wildlife Hazards of Endrin Used as a Rodenticide
in Alfalfa. In: Pesticide—Wildlife Studies: A Review of Fish and Wild-
life Service Investigations During 1961 and 1962: 51—52. Fish and Wild-
life Service Circ. 167, Washington, D.C.
Korn, S., and R. Earnest. 1974. Acute Toxicity of Twenty Insecticides
to Striped Bass, Morone sa catilis. Calf. Fish. and Game 60(3): 128—131.
Kreitzer, J. F., and G. H. Heinz. 1974. The Effect of Sublethal Dosages
of Five Pesticides and a Polychborinated Biphenyl on the Avoidance
Response of Coturnix Quail Chicks. Environ. Polbu. 6(1): 21—29.
Kreitzer, J. F., and J. W. Spann. 1973. Test of Pestidal Synergism with
Young Pheasants and Japanese Quail. Bull. Environ. Contam. Toxicob.
9(4): 250—256.
Lincer, J. L., J. M. Solon, and J. H. Nair III. 1970. DDT and Endrin
Fish Toxicity under Static Versus Dynamic Bioassay Conditions. Trans.
Am. Fish. Soc. 99(1): 13—19.
Long, W. H., L. B. Newsom, and A. M. Mullins. 1961. Endrin Residues
in the Fat of Lambs Grazed on Endrin—Treated Pasture. J. Econ. Entomol.
54(3): 605—606.
-------
129
Lowe, 3. L. 1965. Some Effects of Endrin on Estuarine Fishes (pre-
sented at the 19th Annual Conference of the Southeastern Association of
Game and Fish Commissioners, Tulsa, Oklahoma, October 10—13, 1965,
pp. 271—276.
Luckens, M. M., and W. H. Davis. 1965. Toxicity of Dieldrin and Endrin
to Bats. Nature (London) 207(4999): 879—880.
Ludke, J. L. 1976. Organochlorine Pesticide Residues Associated with
Mortality: Additivity of Chiordane and Endrin. Bull. Environ. Contain.
Toxicol. 16(3): 253—260.
Ludke, J. L., D. E. Ferguson, and W. D. Burke. 1968. Some Endrin
Relationships in Resistant and Susceptible Populations of Golden Shiners
Noternigonus crysoleucas. Trans. Am. Fish. Soc. 97(3): 260—263.
Naher, A. A. 1962. On the Resistance of the Cotton Leafworm (Prodenia
litura) to Insecticides. Agric. Res. Rev. (Cairo) 40: 51—70.
Marion, W. R. 1976. Organochlorine Pesticide Residues in Plain
Chachalacas from South Texas, 1971—72. Pesticide Monit. J. 10(3): 84—86.
Mason, J. W., and 0. R. Rowe. 1976. The Accumulation and Loss of Dieldrin
and Endrin in the Eastern Oyster. Arch. Environ. Contam. Toxicol.
4(3): 349—360.
Menzie, C. N. 1969. Metabolism of Pesticides. Spec. Sci. Rep. Wild-
life No. 127: 30—31. Bureau of Sport Fisheries and Wildlife.
Metcalf, R. L., I. P. Kapoor, P. Y. Lu, C. K. Schuth, and P. Sherman.
1973. Model Ecosystem Studies of the Environmental Fate of Six Organo—
chlorine Pesticides. Environ. Health Perspec. 4: 35—43.
Moore, G. L., Y. A. Creichus, and E. J. Hugghins. 1968. Insecticide
Residues in Pronghorn Antelope of South Dakota. Bull. Environ. Contam.
Toxicol. 3(5): 269—273.
Morris, R. D. 1968. Effects of Endrin Feeding on Survival and Repro-
duction in the Deer Mouse, Peromyscus maniculatus. Can. J. Zool. 46(5):
951—958.
Morris, R. D. 1970. The Effect of Endrin on Microtus and Perornyacus.
I. Unenclosed Field Populations. Can. J. Zool. 48(4): 695—708.
Morris, R. D. l97la. Biocides and Mammals. Blue Jay 29(3): 136—140.
Morris, R. D. l971b. Effects of Endrin on Small Mammal Populations.
Diss. Abstr. Int. 31(8): 5079B—5080B.
Norris, R. D. 1972. The Effects of Endrin on Microtus and Peromyscus.
II. Enclosed Field Populations. Can. 3. Zool. 50(6): 885—896.
-------
130
Moubry, R. J., G. R. Myrdal, and A. Sturges. 1968a. Residues in Food
and Feed. Rate of Decline of Chlorinated Hydrocarbon Pesticides in
Dairy Milk. Pestic. Monit. J. 2(2): 72—79.
Mount, D. I., L. W. Vogir, and N. L. Schafer. 1966. Endrin: Use of
Concentration in Blood to Diagnose Acute Toxicity to Fish. Science
152(3727): 1388—1390.
Naqvi, S. M., and D. E. Ferguson. 1970. Levels of Insecticide Resis—
tance in Freshwater Shrimp, Palaernonete8 kadiaken8is. Trans. Am. Fish.
Soc. 99(4): 696—699.
Negher.bon, W. 0. 1959. Handbook of Toxicology. Vol. III: Insecticides.
Div. of Biol. and Agric. NAS Nat’l Res. Council, W. B. Saunders Co.,
Philadelphia, Pa., pp. 310—316.
Ottolenghi, A. D, J. K. Haseman, and F. Suggs. 1974. Teratogenic Effects
of Aldrin, Dieldrin, and Endrin in Hamsters and Mice. Teratology 9(1):
11—16.
Perry, A. S., and W. N. Hoskins. 1951. Detoxification of DDT as a Factor
in the Resistance of House Flies. J. Econ. Entomol. 44: 850—857.
Petrella, V. J., and R. E. Webb. 1973. Excretion of Carbon—14 Endrin
and its Metabolities in Endrin Susceptible and Resistant Pine Mice
(Microtus pinetorwn). Fed. Proc., Fed. Am. Soc. Exp. Biol. 32 (3—Part 1).
Petrella, V. J., R. S. Hartfrove, J. P. Fox, and R. E. Webb. 1974. Iden-
tification of the Metabolites of Endrin in Endrin—Resistant and Susceptible
Pine Mice. Fed. Proc., Fed. Am. Soc. Exp. Biol. 33(3): 219.
Petrella, V. J., J. D. McKinney, J. P. Fox, and R. E. Webb. 1977.
Identification of Metabolities of Endrin. Metabolism in Endrin Sus-
ceptible and Resistant Strains of Pine Mice. J. Agric. Food Chem. 25(2):
393—398.
Pimentel, D. 1971. Ecological Effects of Pesticides on Non—Target Species.
Cornell Univ., Ithaca, New York for Office of Science and Technology, GPO,
Washington, D.C.
Plumb, J. A., and R. W. Richburg. 1977. Pesticide Levels in Sera of
Moribund Channel Catfish from a Continuous Winter Mortality. Trans. Am.
Fish Soc. 106(2): 185—188.
Polles, S. G., and S. B. Vinson. 1972. Penetration, Distribution, and
Metabolism of 14—C Endrin in Resistant and Susceptible Tobacco Budworm
Larvae. J. Agric. Food Chem. 20(1): 38—41.
Post, G., and T. R. Schroeder. 1971. The Toxicity of Four Insecticides
to Four Salmonid Species. Bull. Environ. Contam. Toxicol. 6(2): 144—155.
-------
131
Reichel, W. L., E. Cromartie, T. G. Lamont, B. N. Nulhern, and R. N.
Prouty. l969a. Pesticide Residues in Eagles, Pestic. Monit. J. 3(3):
142—144.
Reins, D. A., J. A. Rieger, Jr., W. B. Stavinoha, and L. B. Hinshaw.
1966. Effect of Endrin on Venous Return and Catecholamine Release in
the Dog. Can. J. Physiol. Pharmacol. 44(1): 59—67.
Revzin, A. N. 1966. Effects of Endrin on Telencephalic Function in the
Pigeon. Toxicol. Appi. Pharmacol. 9: 75—83.
Richardson, L. A., J. R. Lane, W. S. Gardner, J. T. Peeler, and J. E.
Campbell. 1967. Relationship of Dietary Intake to Concentration of
Dieldrin and Endrin in Dogs. Bull. Environ. Contam. Toxicol. 2(4):
207—219.
Ryan, W. H., and D. L. Shankland. 1971. Synergistic Action of Cyclo—
diene Insecticides with DDT on the Membrane of Giant Axons of the
American Cockroach Periplaneta amer-ican. Life Sci. 10(1): 193—200.
Ryan, S., G. J. Bacher, and A. A. Martin. 1972. The Mussel Hyridella
austra7 is as a Biological Monitor of the Pesticide Endrin in Fresh
Water. Search 3(11—12): 446—447.
Saha, J. G. 1969. Significance of Organochlorine Insecticide Residues
in Fresh Plants as Possible Contaminants of Milk and Beef Products.
Residue Rev. 26: 89—126.
Sanders, H. 0., and 0. B. Cope. 1966. Toxicities of Several Pesticides
to Two Species of Cladocerans. Trans. Am. Fish. Soc. 95: 165—169.
Sanders, H. 0., and 0. B. Cope. 1968. The Relative Toxicities of Several
Pesticides to Naiads of Three Species of Stoneflies. Limnol. Oceanogr.
13: 112—117.
Saxena, P. K., and S. Aggarwall. 1970. Toxicity of Some Insecticides
to the Indian Catfish, Heter’opneustes fossilia. Anat. Anz. 127: 502—503.
Schindler, U. 1956. Rodent Control with Toxaphene and Endrin in Forest
in Western Germany. FAO Plant Prot. Bull. 4(5): 67—68.
Schneeweis, J. C., Y. A. Creichus, and R. L. Linder. 1974. Organochiorine
Pesticide Residue Levels in North American Timber Wolves — 1969—71.
Pestic. Monit. J. 8(2): 142—144.
Sharma, R. D., and 0. P. Gautam. 1971. Experimental Endrin Poisoning in
Calves. J. Res. (Punjab) 8(3): 394—403.
Shaver, T. N., and D. A. Wolfenbarger. 1976. Gossypol: Influence on
Toxicity of Three Insecticides to Tobacco Budworm. J. Environ. Entomol.
5(1): 192—194.
-------
132
Sherman, M., and N. N. Rosenberg. 1953. Acute Toxicity of Four
Chlorinated Domethanonaphthalene Insecticides to Chicks. J. Econ. Entomol.
46(6); 1067—1070.
Singh, H., and R. Lal. 1966. Effects of DDT and Endrin Treatments on
the Biology of Surviving Red Cotton Bugs. Indian J. Agric. Sci. 36(2):
85—94.
Singh, S. P., G. A. Shivnani, and H. S. Bahga. 1977. A note on the
Effect of Insecticides on Blood Glucose Values and Erythrocyte Cholines—
terase Activity of Buffalo Calves. Indian J. Anim. Sci. 47(6): 365—366.
Smith, S. I., C. W. Weber, and B. L. Reid. 1970. The Effect of Injection
of Chlorinated Hydrocarbon Pesticides on Hatchability of Eggs. Toxicol.
Appi. Pharmacol. 16(1): 179—185.
Snyder, D. B. 1963. Effects of Endrin on Vole Microtus penn8y1. vanicue
Reproduction in Bluegrass Meadows. Ph.D. Thesis. Ohio State University,
118 pp.
Spaulding, J. E. 1972. Pesticide and Heavy Metal Residues. Proceedings
of the Meat Industry Research Converence: 11—23. March 1972. American
Meat Institute Foundation, Chicago, Ill.
Staton, B.. H., and N. A. Q. Khan. 1972. Oxidation of Cyclodiene Insecti-
cides by Sunfhish, Mouse, and Rat Liver Mixed—Function Oxidase. Am. Soc.
Zool. 12(3): 38.
Stickel, L. F. 1973. Pesticide Residues in Birds and M inm ls. Environ-
mental Pollution by Pesticides. Chap. 7, C. A. Edwards, ed. Plenum
Press, New York.
Suffett, I. H., S. Friant, C. Marcindiewicz, M. J. McGuire, and D. T.
L. Wong. 1975. Organics. Literature Review. 3. Water Pollu. Contro.
Fed. 47(6): 1169—1241.
Szeicz, F. M., F. W. Plapp, Jr., and S. Bradleigh Vinson. 1973. Tobacco
Budworm: Penetration of Several Insecticides into the Larva. 3. Econ.
Entomol. 66(1): 9—15.
Takahama, K., Y. Ishil, and M. Kanda. 1972. Toxicological Studies on
Organochlorine Pesticides. 1. Effects of Long Term Administration of
Organochlorine Pesticides on Rabbitt Body Weight and Organ Weight. Jpn.
3. Legal Med. 26(1): 5—10.
Terriere, L. C., G. H. Arscott, and U. Kiigemagi. 1959. The Endrin Con-
tent of Eggs and Body Tissue of Poultry Receiving Endrin in Their Daily
Diet. J. Agric. Food Chem. 7(7): 502—5—4.
Tucker, R. K., and D. G. Crabtree. 1970. Handbook of Toxicity of Pesti-
cides to Wildlife. U.S. Dep. of mt. Bur. of Sport Fish. and Wildi.
Resource Publication No. 84, NTIS, PB—198—8l5, Springfield, Virginia.
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VonRuinker, R., E. W. Lawless, and A. F. Meiners. 1974. Production,
Distribution, Use, and Environmental Impact Potential of Selected Pesti-
cides. U.S. Environmental Protection Agency—EPA 540/1—74—001.
Webb, R. E., and F. W. Horsf all. 1967. Endrin Resistance in the Pine
Mouse. Science 156(3783): 1762.
Webb, R. E., W. C. Randolph, and F. Horsfall, Jr. 1972. Hepatic
Benzpyrene Hydroxylase Activity in Endrin—Susceptible and Resistant Pine
Mice. Life Sd. 11(9 Pt 2): 477—483.
Webb, R. E., R. W. Hartgrove, W. C. Randolph, V. J. Petrella, and F.
Horsfall, Jr. 1973. Toxicity Studies in Endrin—Susceptible and
Resistant Strains of Pine Mice. Toxicol. Appl. Pharmacol. 25(1): 42—47.
Wells, M. R., and J. D. Yarbrough. 1972. Vertebrate Insecticide
Resistance: in vivo and in vitro Endrin Binding to Cellular Fractions
from Brain and Liver Tissues of Gainbusia. J. Agric. Food Chem. 20(1):
14—16.
Wells, M. R., and J. D. Yarbrough. 1973. The in vivo and in vitro
Binding of Endrin, Aidrin, and DDT to Liver and Brain Particulate Frac-
tions of Insecticide—Resistant and Susceptible Mosquito Fish (Gambusia
affinis). Physol. 16(3): 485.
Wells, M. R., J. D. Yarbrough, and B. Glick. 1972. The in vivo and
in vitro Retention of Organochiorine Compounds by Tissues of Insecti-
cide Resistant and Susceptible Mosquito Fish. Fed. Proc. 31(2): Abstract
3375: 3370.
Williams, S., and P. A. Mills. 1964. Residues in Milk of Cows Fed
Rations Containing Low Concentrations of Five Chlorinated Hydrocarbon
Pesticides. J. Assoc. Off. Anal. Chem. 47(6): 1124—1128.
Wilson, A. J., Jr. 1966. Report of the Bureau of Commercial Fisheries
Biological Laboratory. Circ. 260: 5. Gulf Breeze, Florida.
Winteringham, F. P. W., and S. E. Lewis. 1959. On the Mode of Action
of Insecticides. Annu. Rev. Entomol. 4: 303—318.
Wolfe, H. R. 1957. Endrin Spray for Orchard—Mouse Control. Proc. 53rd
Wash. State Hortic. Assoc. 230.
Yarbrough, J. D. 1974. Insecticide Resistance tn Vertebrates. In:
Survival in Toxic Environments. M. A. W. Khan, ed. Academic Press, New
York. pp. 373—397.
Yarbrough, J. D., and M. R. Wells. 1971. Vertebrate Insecticide Resis-
tance: The in vitro Endrin Effect on Succinic Dehydrogenase Activity
on Endrin—Resistant and Susceptible Mosquito Fish. Bull. Environ. Contam.
Toxicol. 6(2): 171—176.
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6. BIOLOGICAL ASPECTS IN HUMANS
6.1 SUMMARY
Endrin, the most acutely toxic of all the cyclodiene insecticides,
is highly hazardous to all mammals regardless of route of exposure. Endrin
is less persistent, however, than most other organochlorine compounds. It
is quickly metabolized in mammals and excreted as hydrophilic metabolites.
Endrin is eliminated much more rapidly than DDT or dieldrin from mammalian
tissues.
Human exposure to endrin occurs through the diet, through inhalation,
and through derinal contact. The average dietary intake in the United
States from 1965 to 1970 was 0.005 tg/kg body weight per day. This level
is far below the maximum acceptable daily intake of 0.002 mg/kg body weight
established by the World Health Organization. Respiratory or dermal ex-
posure to endrin is possible during manufacture and distribution but is
more likely to result, directly or indirectly, from agricultural uses.
Outbreaks of human poisoning have resulted from accidental contamina-
tion of foods and have been traced to doses as low as 0.2 mg/kg. The
symptoms usually observed in victims of endrin poisoning were convulsions,
vomiting, abdominal pain, nausea, dizziness, and headache. In severe
cases, convulsive seizures of several minutes duration may be followed by
semiconsciousness. Convulsions can result in death through respiratory
failure. The toxicity of endrin appears to result primarily from the
effect of endrin on the central nervous system. Endrin loads in the
general population, however, are probably not sufficient to induce changes
in brain function.
Endrin poisoning can be fatal. The mean lethal dose (LD 50 ) values
for acute oral exposures of laboratory animals range from 3 to 43 mg/kg
body weight.
Chronic exposures to low levels of endrin can be toxic to mammalian
species. Significant mortality has been observed in mice exposed to 2 ppm
endrin in the diet for seven months. Fatalities were observed following
inhalation exposure of animals to 0.36 ppm endrin vapor for 7 hr on each
of 130 days.
There is no evidence indicating carcinogenicity of endrin. Endrin
can, however, cause mutations in mammalian cells. Endrin is teratogenic
in mice and hamsters. Exposure to endrin causes an increase in fetal and
postnatal mortality, but fertility of parents is generally not affected.
134
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6.2 METABOLISM
6.2.1 E posure
The general population is exposed to very little endrin in the
diet. In the United States, Duggan and Lipscomb (1969) and Duggan and
Corneliussen (1972) found that the total average intake from food ranged
from about 0.01 pg/kg body weight per day in 1965 and in 1968, to
0.0005 pg/kg body weight per day in 1970. The six—year average intake
was 0.005 pg/kg body weight per day. These levels are far below the
maximum acceptable daily intake of 0.002 mg/kg body weight which has
been established by the Joint FAO/WHO Meeting on Pesticide Residues in
Food (World Health Organization, 1973).
Agricultural workers, anyone using endrin in a home garden, and those
involved in manufacture or distribution of endrin might be exposed to
endrin through inhalation or dermal contact. Probably the greatest hazard
associated with the use of endrin occurs when measuring and pouring the
emulsifiable concentrate material (Wolfe et al., 1963).
The most significant occupational exposure to endrin comes during
spraying of fields. Kale and Dangwal (1970) measured endrin concentra-
tions during cropland spraying ranging from trace amounts to 7.0 pg/m 3 .
In dust or spray machine operations, dermal exposure is almost always
greater than respiratory exposure (Wolfe et al., 1963). Dermal exposure
during orchard spraying is likely to range up to 3 mg/br, while respiratory
exposure would be likely to reach 0.01 mg/hr (Wolfe et al., 1963; Wolfe
et al., 1967).
A threshold limit value of 0.1 pg/rn 3 for an 8—hr time weighted average
occupational exposure has been established by OSHA (U.S. Code of Federal
Regulations, 1972).
6.2.2 Distribution and Accumulation
Humans do not tend to store endrin in significant quantities. No
residues were detected in plasma, adipose tissue, or urine of workers
occupationally exposed to endrin (Hayes and Curley, 1968). Measurable
levels of endrin have not been found in human subcutaneous fat or blood,
even in areas where it is extensively used, as in India or the lower
Mississippi area (Brooks, l974b). Despite its high acute toxicity
(Sect. 6.3.2), endrin is a relatively nonpersistent pesticide in man.
Endrin residues are only detected in body tissues of humans immediately
after an acute exposure.
As a result of acute endrin poisoning, high endrin content has been
observed in blood and urine, but no endrin has been detected in cerebral
spinal fluid (Cobel et al., 1967). Poisoned humans have been reported
to have an endrin content as high as 400 ppm in fat and 10 ppm in other
tissues (Cobel et al., 1967). The 400—ppm value was obtained by a bioassay
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technique no longer regarded as dependable. The 10—ppm value was determined
in a patient who died after repeated exposures to endrin. Much lower
levels of endrin were found at autopsy in body tissues of endrin poisoning
victims during an outbreak in Saudi Arabia (Table 6.1). Samples of blood
and urine taken from patients 29 to 31 days after the outbreak (Sect.
6.3.1.1) were uniformly negative for endrin (Curley et al., 1970). Low
blood levels were found in three humans who recovered after accidental
ingestion of endrin. In one case the concentration of endrin in the
blood 30 mm after convulsions occurred was 0.053 ppm, and 20 hr later
it was 0.038 ppm. The same patient excreted 0.02 ppm endrin in his urine
during the next 24 hr (Cobel et al., 1967). Endrin is not found in blood,
urine, or tissue samples from the general population or even from workers
who manufacture and formulate endrin (Hayes and Curley, 1968).
Table 6.1. Endrin concentrations found In victims
of endrin poisoning in Saudi Arabia
Sample
Endrin concentration (ppm)
Blood
0.007—0.032
Urine
0.004—0.007
Vomitas
5.24
Tissues (autopsy)
Stomach wall
Liver
Kidney
from:
0.16
0.685
0.116
Source: A. Curley, R. W. Jennings, H. T. Mann, and
V. Sedlak, Bull. Environ. Contain. To r icol. 5(1): 24—29
(1970). Copyright 1970 Springer-Verlag.
Oral administration of 11 C—labeled endrin to rats in daily doses
of 8 g in peanut oil for 12 days resulted in equilibrium after six
days. After 12 days the spleen had the highest concentration, 3 ppm;
the blood, 1.1 ppm; the skin and subcutaneous adipose tissue, 0.74 ppm;
the peritoneal adipose tissue, 0.38 ppm; and the brain, 0.25 ppm. Four
days after cessation of feeding, male rats were found to have retained
only 5.3% of the total radioactive material given, and the females,
15% (Klein et al., 1968a).
Richardson et al. (1967) fed endrin to nine—month—old dogs for
128 days at a level of 0.1 mg/kg body weight per day. Blood concentra-
tions during the experiment ranged from 0.002 to 0.008 ppm. At the end
of the experiment, concentrations In adipose tissue ranged from 0.3 to
0.8 ppm; heart, pancreas, and muscle were at the lower end of this range,
while the concentration in liver was 0.077 to 0.084 ppm; kidneys and
lungs had similar concentrations.
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The amounts of endrin found in the tissues of dogs that survived
after being fed for almost six months on diets containing endrin in
concentrations of 4 to 8 ppm were: 1 ppm in fat; 1 ppm in liver; and
0.5 ppm in kidneys (Treon et al., 1955).
6.2.3 Biotransformation and Elimination
Endrin is metabolized and excreted more rapidly than other chlorinated
hydrocarbon insecticides (Jager, 1970). There is good evidence that endrin
is quickly metabolized in mammals and excreted as hydrophilic metabolites.
Experiments of Korte (1967) demonstrate that conversion of endrin to
metabolites takes place in the mammalian organism itself and is not caused
by microorganisms in the intestinal tract. The liver appears to be the
site of biotransformation (Korte et al., 1970; Jager, 1970).
In vitro studies appear to support the hepatic metabolism of endrin.
A metabolite behaving as a monohydroxy derivative was produced when endrin
was incubated at 30°C for several hours with both rat liver and pig liver
microsomes and NADPH (Brooks, 1969). Formation of the derivative was
suppressed by sesamex, an inhibitor of microsoinal oxidations.
Endrin is apparently degraded to derivatives which are less toxic to
mammalian organisms. When endrin was given orally and intra-
venously to rats, the ketoanalogue of endrin and other hydrophilic meta—
bolites were present in trace amounts in the urine (Klein et al., l968a).
Since the acute oral LD 50 of ketoendrin to rats (62 mg/kg) is higher
than that of endrin (25 mg/kg), the rearrangement would be detoxification
reaction (Brooks, 1969).
Endrin is metabolized in the rat to at least three metabolites
(Baldwin et al., 1970). One is 9—ketoendrin, which is found in the urine.
The other two metabolites are excreted in the feces and have not been
found in body tissues (Baldwin et al., 1970). In all experiments utilizing
rats, an isomer of 9—hydroxyendrin accounts for 95% of the radioactivity
excreted (Korte et al., 1970). This isomer has the hydroxyl group endo
with respect to the epoxy group (Fig. 6.1). The third metabolite is a
monohydroxylated endrin, but the hydroxyl group is not on carbon 9
(Baldwin et al., 1970). Nethanobridge hydroxylation occurs in the rat,
and the corresponding ketone is found in adipose tissue, liver, and
brain.
Rabbits excreted radioactivity after intravenous administration of
1 C—labeled erzdrln mainly in the urine and only as metabolites (Korte
at al., 1970). Hydroxylation seems to occur in the rabbit without major
skeletal rearrangement (Brooks, l974b). Four metabolites were found in
order of decreasing polarity in the ratio of 1:1:3:1. The second most
polar one is identical with the isomer of 9—hydroxyendrin, which was the
main metabolite fouLtd in rats. When NADU was added to 100 g of rabbit
liver homogenate, 38 iig of endrin was metabolized within 72 hr to an
extent of 39.6% (Korte et al., 1970).
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ORNL-DWG 79-8950
8 1
8a 2
40
5 4
NUMBERING SYSTEM
C I
CI
CI
CI
CI
H H CI
DIEL DR IN
Fig. 6.1. Structures of the metabolities I and II, endrin, keto—
endrin, and dieldrin. Source: Reprinted with permission from M. K.
Baldwin, J. Robinson, and D. V. Parke, J. Agric. Food Chern. 18(6):
1117—1123 (1970). Copyright 1970 American Chemical Society.
Oxidations without skeletal rearrangement predominate in mammals.
There is, as yet, no evidence for epoxide ring hydration, and trans—diol
formation may be sterically difficult (Brooks, l974b).
Studies indicate attainment of plateau storage levels for endrin.
For a given level of endrin intake, a steady state should be achieved in
which the rate of intake is balanced by the rate of elimination (Brooks,
1969). Rats given a daily oral dose of 8 pg 1 C—labeled endrin for
12 days reached a plateau level of endrin storage in nine to ten days
(Brooks, 1969). When endrin is given orally to rats at a daily dose
corresponding to 0.4 ppm in the diet, a steady state of storage is
reached after about six days for male and female rats (Korte, 1967;
Korte et al., 1970). The storage level for females (27%) is about twice
as high as that for males (14%). Four days after administration was
METABOLITE I! (9- HYDROXYENDRIN) METABOLITE I (9- KETOENDRIN)
ENDRIN A-KETOENDR IN
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139
stopped, males retained only 5.3% and females 15% of the administered
radioactive substance.
At high dosage levels, excretion of endrin appears to be slower.
Korte et al. (1970) determined the biological half—life of endrin to
be one to two days after an oral dose of 16 or 64 pg/kg body weight.
However, after an oral dose of 128 pg/kg body weight, the half—life
increased to approximately six days.
Females metabolize endrin more slowly than males (Brooks, 1969).
The biological half—life of endrin in male rats receiving 0.4 ppm in
the diet is two to three days; in females approximately four days (Korte
et al., 1970). Following intravenous injection of 200 pg of 1 C —1abeled
endrin per kilogram body weight in two doses, male rats retained 5.2%
and females 12.1% of the administered dose after 24 hr. The radioactivity
was totally excreted as metabolites (Korte et al., 1970). Similar
results were obtained by Jager (1970) in feeding experiments. When
1 C—labeled endrin was fed to male and female rats, the males excreted
60% of it in the feces within the first 24 hr, and the females only
39%; less than 1% was excreted in the urine. Of the total radioactivity
excreted in the feces, 70 to 75% occurred in the form of hydrophilic
metabolites; the remainder was in unchanged endrin. Twenty—four hours
after the last dose, only hydrophilic metabolites were excreted (Jager, 1970).
The difference in rates of metabolic conversion between endrin and
dieldrin is likely to be related to the stereochemistry of the endrin
molecule, which predisposes it to skeletal rearrangements. When dogs,
fed a daily diet containing 0.1 mg/kg dieldrin, were compared with others
similarly fed with endrin, the blood dieldrin level approached a maximum
after 114 to 121 days, but there was no accumulation of endrin in the blood
(Richardson et al., 1967).
Body content of endrin declines fairly rapidly after a single dose
or when a continuous feeding experiment is terminated. When exposure
ceases, endrin concentration in tissues declines, and the rate of decline
is proportional to tissue concentration at that time (Brooks, 1969).
Most endrin is excreted in the feces, much of it through the bile.
The liver has been identified as the major excretory organ for endrin
in the rat. The amount of radioactivity in the feces of rats, administered
1 C—1abeled endrin intravenously, reflects the amount of radioactivity
entering the gastrointestinal tract via the bile (Cole et al., 1970).
Cole et al. (1970) studied rates of excretion of radiocarbon—labeled
endrin in whole rats, bile—f istula rats, and isolated perfused rat livers.
Over 90% of the excreted radioactivity was found in the feces of the
intact animals and in the bile of fistula animals. Fifty percent of the
radioactive endrin was excreted within the first day. In fistula animals,
50% of the endrin radioactivity was excreted in the bile in approximately
1 hr in the perfusion experiments (Cole et al., 1970). A similar set of
experiments using radiolabeled dieldrin indicated that excretion of
radioactivity from endrin was greater than that from dieldrin in the feces
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140
of intact animals, bile of bile—fistula animals, and bile of isolated,
perfused rat liver preparations.
The liver appears to be the major controlling factor in the different
rates of excretion of radioactivity from 11 C—labe1ed endrin and 1 C—labeled
dieldrin. The more rapid fecal elimination of endrin can be explained by
its more rapid biliary excretion (Cole et al., 1970). Since endrin is
excreted more rapidly than dieldrin, it is less available for storage.
6.3 EFFECTS
6.3.1 Human Exposure
6.3.1.1 Accidental poisonings . Several incidents of human endrin
poisoning have been reported in the literature.
The first report of acute endrin poisoning was from Wales in 1956.
Sacks of flour were contaminated during shipment in a railway car in which
3 gal of endrin had leaked several months earlier. Bread made in a bakery
from this flour resulted in almost 60 cases of acute endrin poisoning;
no deaths occurred. The bread was contaminated with 150 ppm endrin (Davies
and Lewis, 1956). Between 1958 and 1963, endrin poisoning in the state
of Andra Pradesh, India, increased from two a year to 140 a year, paralleling
increased use of the insecticide (Reddy et al., 1966). Two three—week—old
babies died from endrin poisoning in Israel in 1970. The stomach contents
of one baby contained 103 ppm endrin and a trace of dieldrin. The cause
was presumably a contaminated recycled glass milk bottle (Tadjer and Dore,
1971).
Between June 3 and July 15, 1967, four explosive outbreaks of acute
poisoning with endrin occurred in Doha in Qatar and Hofuf in Saudi Arabia
(Weeks, 1967; Curley et al., 1970). The outbreaks resulted in hospitali—
zation of 874 persons and death of 26 persons. It was estimated that
another 500 to 750 persons were poisoned but not hospitalized. Flour in
a lower deck of each of two ships had been contaminated by an emulsifiable
concentrate of endrin carried on an upper deck of the same hold. Poisoning
resulted when the flour was made into bread and eaten (Curley et al., 1970).
Three cases of accidental poisoning of infants have been reported in the
United States (Cobel et al., 1967).
The most common symptoms observed in these outbreaks were vomiting,
convulsions, abdominal pain, nausea, dizziness, and headache. The first
indication of acute poisoning was often a sudden epileptical convulsion
lasting several minutes and accompanied by frothing of the mouth.
Contractions were violent and, in severe cases, followed by a sudden loss
of consciousness (Cobel et al., 1967; Weeks, 1967).
An endrin intake of 0.2 to 0.25 mg/kg produced convulsions in humans
during the Wales outbreak in 1956 (Davies and Lewis, 1956). Doses estimated
at 5 to 50 mg/kg were responsible f or the endrin poisoning in Andhra Pradesh,
India. Of the 290 cases from 1958 to 1963, 60 were fatal (Reddy et al.,
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141
1966). In the majority of fatal cases, individuals died within an hour or
two after ingestion of endrin. Respiratory failure was the most common
mode of death (Reddy et al., 1966).
In many nonfatal endrin poisonings, a rapid recovery to a normal
sense of well—being usually ensued within 24 hr, particularly in patients
who vomited. In a few cases, headache, lethargy, weakness, and anorexia
persisted for a few weeks (Cobel et al., 1967). With more severe poisoning,
convulsions were multiple or continuous and resulted in residual damage
to the central nervous system from anoxia (Cobel et al., 1967).
6.3.1.2 Occupational exposure . Versteeg and Jager (1973) report,
in a study done by Shell Internationale Research, that occupational
exposure to endrin in a manufacturing plant (Shell Netherlands Chemical
Industries at Pernis near Rotterdam) for periods up to 17 years did not
result in any persistent adverse effect as far as could be demonstrated
by the following parameters: miniature chest radiograph, electroencephalo—
grain, routine urinalysis, blood analysis, general physical examination,
and a blood chemistry profile which included 12 biochemical tests. Versteeg
and Jager (1973) claimed that all symptoms of endrin intoxication were
fully reversible within a few days.
A study of the pattern and rate of sickness absenteeism at the Shell
Netherlands Chemical Industries Plant at Pernis among endrin—exposed
workers and their nonexposed colleagues from other plants revealed no
significant differences between the two groups (Hoogendam et al., 1965).
Analytical tests were performed on men employed in a factory where
endrin, aidrin, dieldrin, a nematocide, and certain organic phosphorus
compounds were manufactured. Eleven isomers or inetabolites representing
six insecticides were detected in plasma samples; seven isomers or metabo—
lites representing five insecticides were found in fat samples in the
urine; and nine isomers or metabolites representing four insecticides were
found in the urine. No endrin was found in any sample, even though the
men had been exposed to it for an average of 2106 hr (Hayes and Curley,
1968).
Men engaged in the manufacture of endrin have significantly increased
activity of hepatic microsomal enzymes. Hunter et al. (1972) assessed
hepatic microsomal enzyme activity of workers engaged in the manufacture
of pesticides by measuring changes in the urinary excretion of D—glucaric
acid. Men employed in the manufacture of endrin alone had greater D—glucaric
acid excretions than workers exposed to aldrin or dieldrin.
Low DDE [ l,l—dichloro—2, 2—bis(p—chloropheny1)ethylene 1 levels found
in endrin workers also suggest enzyme induction, since DDE is metabolized
by microsomal enzymes (Hunter et al., 1972). A significant inverse
relationship between the blood DDE level and urinary D—glucaric acid
excretion is further evidence that this is the effect of enyzme induction.
Increased urinary concentrations of 6—beta—hydroxycortisol have
also been reported in endrin workers (Hunter et al., 1972). This
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probably results from induction of the hepatic enzyme cortisol 6—beta—
hydroxylase.
6.3.2 Acute Toxicity
Acute exposure can be defined as exposure to a test agent for 24 hr
or less (National Academy of Sciences, 1975). Dosages in acute toxicity
tests are usually selected to provide data for estimating the lethal dose
for 50% of a group of animals and the slope of the dosage mortality curve.
The LD 50 is expressed as milligrams of endrin per kilogram of the weight
of the test animal. Less toxic chemicals have larger LD 50 values, since
it takes a larger quantity to be fatal.
Endrin is classified as “very highly hazardous,” meaning that any
contact with very small amounts of the substance may result in severe
injury or death (Thompson, 1971). Endrin is the most acutely toxic of
the cyclodiene insecticides in use and yet, except for endosulfan, is
least persistent in mammals (Brooks, 1974b). Endrin is toxic to all
mammals regardless of route of exposure. When ingested in one dose by
rats, endrin is about three times as toxic as aldrin and about 15 times
as toxic as DDT (Treon et al., 1955). Upon intravenous administration
in mice, endrin is five times as toxic as dieldrin (Walsh and Fink, 1972).
The onset of endrin toxicity symptoms is rapid. The return to normal
among those who survive is also rapid. The recovery from endrin intoxica-
tion is quicker than from other cyclodiene insecticides (Weeks, 1967).
The symptoms of acute endrin poisoning in manmials clearly indicate
that endrin is a neurotoxicant. The first indication of acute endrin
poisoning is often central nervous system excitation evidenced by hyper-
sensitivity to external stimuli associated with generalized tremors and
followed by severe tonic—clonic convulsions (Brooks, l974b). Convulsions
may occur as soon as 30 mm after acute endrin exposure (Weeks, 1967).
Convulsions can culminate in death through respiratory failure (Brooks,
1974b). In the range of the acute oral LD 50 (17 to 43 mg/kg), death of
rats may result in about 48 hr (Boyd and Stefec, 1969).
Other symptoms of acute endrin poisoning include bradycardia (slowed
heartbeat), increase in blood pressure, salivation, increased body
temperature, leukocytosis (increased number of white blood cells), increased
hemoconcentration, decreased blood pH, increased cerebrospinal fluid
pressure and cerebral venous pressure, increased renal vascular resistance
with decreased renal blood flow and glomerular filtration rate, decrease
in catecholamine concentration of the adrenals, and increased levels of
circulating epinephrine and norepinephrine (Emerson et al., 1964; Reins
et al., 1966). Pulmonary edema was observed by Sen et al. (1969) in rats
and mice. Pathological observations of rats at autopsy reveal signs
of a stress reaction, degenerative changes in kidneys, liver and brain
capillary and venous congestion, loss of weight, and dehydration of many
organs (Boyd and Stefec, 1969).
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The symptoms in man include headache, dizziness, abdominal disturbances,
nausea, vomiting, mental confusion, muscle twitching, and epileptiform
convulsions which may occur suddenly and without prior warning (Brooks,
1974b).
6.3.2.1 Oral toxicity . Mammalian susceptibility to endrin toxicity
varies greatly with age, sex, and species, as shown in Table 6.2. The
LD 50 values range from 3 to 43 mg/kg.
Table 6.2. Acute oral toxity of endrin to mammals
Animal
LD 50 (mg/kg)
References
Bats
5—8
Luckens and Davis,
1965
Rats (M)
17.8
Speck and Maaske,
1958
Rats (6 months,
M)
43
Treon et al., 1955
Rats (6 months,
F)
7
Treon et al., 1955
Rats (30 days,
M)
30
Treon et al., 1955
Rats (30 days,
F)
17
Treon et al., 1955
Rabbits (F)
7—10
Treon et al., 1955
Guinea pigs (F)
16
Treon et al., 1955
Guinea pigs (M)
36
Treon et al., 1955
Monkey
3
Treon et al., 1955
Sources: Luckens and Davis, 1965;
Speck and Maaske, 1958;
Treon et al., 1955.
It appears that monkeys are more susceptible than rats, and guinea
pigs are more resistant. Rabbits appear to be somewhat more resistant
than monkeys to a single dose of endrin. The acute toxicity of endrin
is, however, high for all these species.
In rats and guinea pigs, females are more susceptible than males.
The greater susceptibility of female rats six months of age than of younger
female rats is the reverse of the more normal relationship between age
and susceptibility in the case of males.
6.3.2.2 Dermal toxicity . When endrin, as a dry 100—mesh powder, was
maintained in contact with either the intact or abraded skin of female
rabbits for 24 hr, the minimum lethal dosage was found to be greater than
60 and less than 94 mg/kg. Poisoned animals had convulsions, but neither
gross nor microscopic evidence of damage to the skin was found. Degenera—
tion of the cells in the central zones of the lobules of the livers of
rabbits was observed (Treon et al., 1955).
6.3.2.3 Other routes of administration . Graves and Bradley (1965)
determined an LD 50 of 5.6 mg/kg for endrin injected into the peritoneal
cavity of Swiss albino mice. An intravenous LD 50 value of 2.3 mg/kg was
determined by Walsh and Fink (1972) for adult male mice. Endrin injected
into dogs intravenously at a dosage of 3 mg/kg caused death in approximately
75% of the animals (Hinshaw et al., 1966).
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6.3.3 Chronic and Subchronic Toxicity
Subchronic toxicity studies are designed to determine the adverse
effects that may occur during repeated exposure over a period of a few
days to about three months (National Academy of Sciences, 1975). Exposure
levels in these studies are usually lower than in acute toxicity experi-
ments. Studies involving repeated or continuous exposures to low dose
levels for longer intervals could be considered chronic toxicity studies.
Target organs found in acute experiments are not always the same as
those following repeated exposure over long periods of time. The central
nervous system is the target of acute endrin poisoning. When an animal
is exposed repeatedly to low doses (0.8 to 3.5 mg/kg/day) of endrin, it
can often make compensatory adjustments to cope with the initial nervous
system injury until damage to liver or other organ intervenes (Speck
and Maaske, 1958).
After exposure of rats, rabbits, guinea pigs, cats, dogs, and monkeys
to varying doses of endrin via several routes and frequencies of administra-
tion, diffuse degenerative changes were observed in the livers, kidneys,
and brains of all fatally poisoned animals. Alternations were also ob-
served in tissues of some of the surviving animals (Treon et al., 1955).
Rabbits subjected to multiple dermal applications (20 to 44 mg/kg) exhibited
severe fatty degeneration of the liver (Treon et al., 1955). A series of
50 oral doses of 1 to 5 mg/kg per day in a rabbit caused diffuse degeneration
and fatty vacuolizatlon of the hepatic and renal cells and degeneration
of the heart. Rabbits that survived 118 periods of inhalation of 0.36 ppm
endrin developed a granulomatous type of pneumonitis (Treon et al., 1955).
Chronic administration of endrin can lead to convulsions. Revzin
(1970) administered endrin to squirrel monkeys at a minimum rate of
0.2 mg/kg per day, inducing characteristic change in the electroencephalogram
(EEG) after relatively small total doses (0.5 to 1.0 mg/kg). At total
doses of 5 to 10 mg/kg, electrographic seizures developed. Endrin admini-
stration was discontinued after seizures, but three weeks later, EEGs and
behavior were still abnormal (Revzin, 1970). Recurrence of seizures,
under stress conditions, months after termination of endrin administration
demonstrates that even the small amounts of endrin stored in the body after
exposure cannot be regarded as toxicologically inert (Revzin, 1970). Endrin
mobilized by stress may cause toxic responses in the brain. If
concentrations in fat in these monkeys (about 25 ppm after four months)
were sufficient to cause seizures, the same stress to an animal storing
2.5 ppm may induce EEG and presumably behavioral changes (Revzin, 1970).
The chronic toxicity of endrin is greater than that of other organo—
chlorine pesticides. In prolonged feeding experiments, rats can consume
diets containing approximately three times as much aldrin and 12 times
as much DDT as endrin without increase in the relative weight of specific
organs. Dogs are at least ten times as susceptible to the toxic effects
of endrin as to those of DDT (Treon et al., 1955). Species and sex
differences exist in susceptibility to chronic endrin toxicity. Females
are generally more susceptible than males. Rabbits and dogs are more
susceptible than rats (Treon et al., 1955).
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Exceptions to the usual higher susceptibility of females have been
observed at low doses. Mortality rates observed by Nelson et al. (1956)
indicate that male rats were significantly more susceptible to the toxic
effects of endrin at the lower levels (1 and 5 ppm) than were females.
Deichmann et al. (1970) found that mean survival rates for female rats
fed 12 ppm endrin in laboratory chow was 18.2 months, while the mean
survival of control rats were 19.5 months for females and 19.7 months
for males.
Female rats appeared to be less susceptible than female rabbits
but more susceptible than male rats to the cumulative action of endrin
administered orally in multiple doses. Given an oral dosage of 1 mg
endrin per kilogram of body weight on each of five days per weeks, four
of five female rabbits died. This level of dosage (1 mg/kg) was tolerated
by five female rats, but 2 mg/kg was fatal to two out of five female
rats. Male rats survived when the level of dosage was 2 mg of endrin
per kilogram, but died in the early period of the experiment when the
level was 5 mg/kg (Treon et al., 1955).
6.3.3.1 Oral exposure . Mammalian species are sensitive to the
toxic effects of endrin at low levels in the diet. Significant mortality
over a seven—month period appeared in deer mice at 2 ppm in the diet
(Morris, 1968). The deer mice showed symptoms of hypertension, incoordina—
tion, muscle tremors, and convulsions which increased in intensity until
death occurred.
Endrin fed for a lifetime to Osborne—Mendel rats at 12 ppm in the
diet decreased viability. Mean survival time fell from 19.7 months to
17.6 months for males and from 19.5 months to 18.2 months for females
(Deichmann et al., 1970). Rats on the endrin diet experienced moderate
increases in incidence of congestion and focal hemorrhages of the lung;
slight enlargement, congestion, and mottling of the liver; and some
enlargement, discoloration, or congestion of the kidneys (Deichmann et al.,
1970).
Nelson et al. (1956) observed hypersensitivity to sound, touch, and
pressure stimuli in all rats ingesting 1 to 100 ppm endrin for periods
up to 16 weeks. In rats ingesting 25 ppm or more, the extreme
sensitivity was followed by convulsions. Once convulsive patterns were
established, rats rarely lived more than a week. Rats on a diet containing
25 ppm endrin also suffered from intermittent blindness, dysenteric
symptoms, and slight bleeding through the nostrils. All rats receiving
100 ppm endrin died within two weeks. Of the ten rats that received
50 ppm, only two females survived the 16—week experiment (Nelson et al.,
1956).
Groups of Carworth rats were given diets containing endrin in
concentrations of 1, 5, 25, 50, and 100 ppm. The rats that died by the
80th and 106th weeks of feeding are shown in Table 6.3. Endrin in diets
of female rats at levels of 25 ppm or higher caused significant mortality.
Dietary levels of 50 ppm resulted in the early deaths of all but a few
resistant rats. Male rats were less susceptible than female rats to the
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Table 6.3. Mortality among groups of control rats and rats fed
two years on diets containing endrin
Concentration
(ppm)
No.
that died/No.
fed on diet
Males
Females
80 weeks
106 weeks
80 weeks
106 weeks
100
50
25
5
1
0
18/20
13/20
5/20
5/20
5/20
7/20
18/20
16/20
9/20
13/20
9/19
12/20
18/20
19/20
12/20
7/20
4/20
5/20
19/20
20/20
15/20
12/20
9/20
13/20
Source: Reprinted with permission from J. F. Treon, F. D. Cleveland,
and J. Cappel, J. Agric. Food Chem. 3(10): 842—848 (1955). Copyright
1955 American Chemical Society.
Among rats fed on diets containing 50 to 100 ppm endrin, hyper-
sensitivity to external stimuli and occasional convulsions were observed.
These symptoms were not seen in those fed at 25 ppm (Treon et al., 1955).
After rats had been fed diets containing endrin at levels of either 25 or
5 ppm for two years, the average ratios of the weights of their livers to
their body weights were significantly greater than that of controls
(Treon et al., 1955).
effects of endrin in the diet. A dietary level of 50 ppm caused a mortality
increase over controls barely significant at the 5% level. At the dietary
level of 100 ppm, however, only 5% of the males survived beyond two weeks.
Rats that died exhibited diffuse degeneration of the brain, liver, kidneys,
and adrenal glands. The incidence of neoplasia was no greater among the
experimental animals than among the controls (Treon et al., 1955).
Dogs can consume safely about half the concentration of endrin in
the diet that rats can tolerate. Dogs died when fed diets containing
endrin in concentrations of 10 to 50 ppm (18 to 44 days). More than
half of the dogs fed S to 8 ppm died. Dogs fed 10 ppm or more suffered
extensive losses in weight. Dogs that died when fed on diets containing
toxic concentrations (5 ppm or more) of endrin regurgitated their food,
became lethargic, salivated, and later refused to eat. They became
emaciated and developed respiratory distress and signs of irritation of
the central nervous system (Treon Ct al., 1955).
Dogs fed 8 ppm endrin in the diet for almost six months exhibited
enlargement of the liver, kidneys, and brain and reduction in the deposition
of free peritoneal and omental fat. After dogs had been fed for almost
19 months on diets containing endrin at the level of 3 ppm, their kidneys
and hearts were significantly enlarged (Treon et al., 1955).
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Fatally poisoned dogs had diffuse degenerative lesions in the brain,
heart, liver, and kidneys, together with pulmonary hyperemia and edema.
Renal damage was severe and was characterized by the diffuse degeneration
and neurosis of the convoluted tubules. The liver exhibited diffuse
degeneration and fatty vacuolization and, in some instances, necrosis of
the liver cells (Treon et al., 1955).
Speck and Maaske (1958) evaluated effects of chronic exposure by
administering repeated oral doses (0.8, 1.7, and 3.5 mg/kg) of endrin
daily, five days a week, to rats. Rats given these doses for one week had
similar symptoms (red liver and contracted spleen) to rats receiving
single high doses (20 to 80 mg/kg), but effects in animals receiving
chronic doses were less severe. From three months up to the maximum
tolerated exposure at seven months, there was a progressive decrease in
color and an increase of spottiness of the liver, while spleens, blood,
and lungs appeared normal. At the seventh month of repeated exposures to
3.5 mg/kg, there was a dramatic upsurge in the death rate (Speck and
Maaske, 1958). Rats removed from a chronic exposure to endrin before
irreversible liver damage occurred returned to normal. Rats removed
from endrin exposure after three months showed no withdrawal symptoms
(Speck and Maaske, 1958).
6.3.3.2 Inhalation . Following 7 hr of exposure on each of 130 days
to air containing the sublimed vapor of endrin in the concentration
of 0.36 ppm, two rabbits and a mouse died out of a group consisting of
a cat, guinea pigs, hamsters, mice, rats, and rabbits. No convulsions
were observed (Treon et al., 1955).
6.3.3.3 Dermal exposure . The intact skin of each of three female
rabbits was maintained in contact with 150 mg dry endrin for 2 hr on
each of five days per week. The rabbits died after 19, 19, and 25 such
applications respectively (Treon et al., 1955).
6.3.4 Carcinogenesis and Mutagenesis
No malignancies attributed to endrin exposure have been found in the
literature. Endrin fed to weanling Osborne—Mendel rats for a lifetime at
levels of 2, 6, or 12 ppm in laboratory chow was neither tumorigenic
nor carcinogenic (Deichmann et al., 1970; Deichmann and MacDonald, 1971;
Deichmann, l972a).
Endrin as well as aidrin and dieldrin can cause chromosome damage
(Grant, 1973). Symptoms of cellular degeneration have been observed in
germinal tissue of male albino rats treated with 0.25 mg of endrin
administered intratesticularly (Dikshith and Datta, 1972). The most
conspicuous effects were chromosomal aberrations, including stickiness,
bizarre configurations, formation of chromosome fragments, and abnormal
restitution of chromosomes. Formation of single and double bridges with
acentric fragments was very common, disturbing the normal disjunction of
chromosomes and eventually affecting the chromosome complements of the
division products (Dikshith and Datta, 1973). Unequal distribution of
chromosomes at anaphase was also observed. Severe cell damage resulted
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in liquefaction and transformation of the chromatin mass into an amorphous
lump (Dikshith and Datta, 1972).
6.3.5 Reproduction and Teratogenesis
Endrin exposure appears to cause an increase in fetal and postnatal
mortality, but fertility of the parents is generally not affected.
Endrin (5 ppm) in the diet of Sprague—Dawley rats for 60 days prior
to conception and during pregnancy caused an increased number of resorptions
and a decreased number of viable embryos (Green, 1967).
Good and Ware (1969) studied reproductive effects of endrin in Swiss
mice. Virgin males and females were randomly paired. During four months
of feeding 5 ppm endrin in the diet, adult mortality occurred in one—third
of the pairs. Litters were significantly smaller than those produced by
controls. The influence of endrin on reproduction is probably a direct
effect on fetal mortality.
Postnatal mortality of young may be the main effect of endrin on
reproductive performance in deer mice. Data of Horns (1968) suggest
that average litter productivity of the deer mouse (Perymys cus rnan culatus)
is not adversely affected by endrin at doses up to 2 ppm in diet. Survival
of parents was, however, significantly decreased at levels of 2 ppm or
more.
Litter survival was adversely affected by feeding endrin to the
parents. A severe postnatal effect on young was observed in deer mice
whose parents ingested 4 or 7 ppm endrin in the diet.
If quantities of endrin sufficient to affect viability of young were
to move across the placenta, the insecticide would first have to be moved
from storage in the fat tissue into the blood stream. This movement might
occur under conditions of parental stress or if stored levels reached a
saturation point so that additional quantities would be circulated. Under
these conditions, It is likely that parental death would precede parturition
(Norris, 1968).
Endrin exerted embryocidal and teratogenic effects on pregnant hamsters
(Ottolenghi et al., 1974). Both soft and skeletal tissue malformations
were produced. Single oral doses of endrin (5 mg/kg) administered to
pregnant Syrian golden hamsters on day 7, 8, or 9 of gestation caused a
high Incidence of fetal death, congenital abnormalities, and growth
retardation. Thirty—two percent of the implantations resulted in fetal
mortalities. Teratogenic effects were observed in 28% of the fetuses
from hamsters treated on day 8. Open eye occurred In 22%, webbed foot in
16%, cleft palate in 5%, cleft lip in 1%, and fushed ribs in 8%.
Endrin is teratogenic in mice, but frequency and gravity of the defects
produced were less pronounced than in the hamsters when a single oral dose
(2.5 mg/kg In mice and 5 mg/kg in hamsters) of half the LD 50 was administered.
Abnormalities in mice Included open eye and cleft palate (Ottolenghi et al.,
1974).
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The only reported effect on fertility was caused by a single admini-
stration of endrin into the rat testes, which produced hypertrophic changes
in the testis and induced total arrest of spermatogenesis. Endrin action
was not specific to any group of spermatogenic cells; rather, the entire
tubular and intertubular areas suffered total and irreversible damage.
All the spermatogenic cells of the tubules revealed massive necrosis.
Seminiferous epithelium and cellular architecture of the tubules were
totally altered, and the necrotic cells coalesced to form a mass (Dikshith
and Datta, 1972).
6.3.6 Physiological Effects
6.3.6.1 Nervous system . The toxicity of endrin to humans appears to
result primarily from the effect of endrin on the central nervous system.
The major clinical manifestation of endrin intoxication in humans is
convulsive seizures of several minutes duration followed by semiconsciousness
(Weeks, 1967; Cobel et al., 1967; Jacobziner and Raybin, 1959). Convulsions
and hypersensitivity are probably caused by endrin acting directing on the
motor cortex and/or spinal cord (Emerson et al., 1964).
Convulsions usually occur in humans within 2 to 4 hr following
ingestion of endrin—contaminated food. Children are less likely to have
convulsions from acute poisoning than are adults, but there is a wide range
of sensitivity in both adults and children.
In rats, a latent period of 45 to 60 mm elapsed before the appearance
of convulsions regardless of size of an effective single dose (20 to 80 mg/kg)
(Speck and Maaske, 1958). The data suggest that the concentration of
endrin had to reach a critical level in the brain and/or other tissues for
convulsions to occur. Severe clonic convulsions were apt to be set off by
touch or auditory stimuli. Some rats survived repeated severe attacks
and showed catatonic behavior for 30 mm afterward (Speck and Maaske, 1958).
Severe tonic—clonic convulsions in dogs commenced within five to ten mm
after beginning intravenous infusion with 10 mg/kg endrin (Emerson et al.,
1964). Convulsions, as well as hyperexcitability to stimulation, and
copious, mucoid salivation lasted until death. Symptoms manifested were
similar to those observed in humans. Death occurred from respiratory
failure.
Electroencephalogram changes frequently precede convulsions, and
withdrawal from exposure usually results in a normal EEC within one to
six months (Cobel et al., 1967). During endrin exposure, the EEC may show
bilateral synchronous spikes, spike—and—wave complexes, and slow theta
waves.
Seven daily injections (0.2 mg/kg) of endrin in the squirrel monkey
caused increases in EEC amplitude and a tendency toward increased spiking.
These changes became more marked as a function of total dosage until
seizure activity developed. The EEG remained abnormal for more than one
month after administrations were terminated (Revzin, 1968).
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Joy (1976) injected cats with 1 to 2 mg/kg endrin and found that
spontaneous seizures occurred within 5 to 15 mm. Higher doses produced
seizures in 0.5 to 2 mm. Some test animals developed transient hypotension
followed by hypertension and arrytbniias. EEG changes were clearly defired
and consistently present. Following the administration of endrin, hyper—
synchrony, rhythmic bursts of high—voltage spikes, and isolate spikes
invariably developed immediately prior to the seizure. Seizures were
bilateral and symmetrical and of a tonic—clonic type. Evolution of the
entire EEG sequence leading to a seizure was found to occur within 2 mm
after injection of endrin.
EEG recordings made on rats after an 80 mg/kg dose of endrin showed
irregular slowing, some irregular spikes, and frequent convulsive discharges
(Speck and Haaske, 1958). EEG changes were minimal, however, in rats
receiving chronic doses of 3.5 mg/kg or less. After one week of exposure
to endrin, some rats had bursts of multiple spikes accompanied by clonic
convulsions, and additional runs of spikes without full—fledged convul-
sions. Convulsions were usually preceded by a period of hyperventilation.
After two weeks of exposure, the rats had normal EEGs until liver damage
began to appear after three months of repeated doses. At three months the
animals again became susceptible to audiogenic convulsions. At seven
months, convulsions were easily started (Speck and Maaske, 1958). Rats
withdrawn from chronic exposure were no longer susceptible to convulsion
after seven weeks of withdrawal (Speck and Maaske, 1958).
Endrin can affect central nervous system processing at doses substan-
tially below lethal or convulsive levels. Consequently, behavior can be
affected in the absence of the tremors and seizures generally considered
signs of endrin poisoning. Revzin (1970) observed EEG changes in a
squirrel monkey receiving a total endrin dose of 1 mg/kg. Seizures were
not observed until the total dose reached 10 mg/kg. Endrin levels in the
general human population, however, are probably not sufficient to induce
changes in brain functions (Revzin, 1970).
Other symptoms of endrin toxicity may result indirectly from the
effect of endrin on the central nervous system. Convulsions may interfere
with normal respiratory exchanges of blood gases, resulting in the acidosis
and hyposia found consistently in endrin poisoning (Hinshaw et al., 1966).
Action of endrin on the central nervous system seems to indirectly affect
both sympathetic and parasympathetic nervous systems and the adrenals
(Hinshaw et al., 1966). Stimulation of parasympathetic nerves may cause
bradycardla and excessive salivation, while the sympathetic nerves may
be responsible for other cardiovascular symptoms in endrin intoxication
(Fig. 6.2).
6.3.6.2 Cardiovascular effects . Endrin poisoning in mammals is
accompanied by marked cardiovascular effects, including bradycardia,
hypertension, increased venous return and corresponding elevation in
cardiac output, and decreased renal blood flow. Most of these cardio-
vascular effects appear to be caused indirectly by endrin acting on the
central nervous system (Fig. 6.2). The symptoms suggest that both sym-
pathetic and parasympathetic nervous systems are hyperactive after endrin
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ORNL—DWG 79-8951
ENDRIN
INTRAVENOUS
INJECTION
CNS LEFT VENTRICLE
HEART FAILURE
SYMPATHETIC ADRENALS PARASYMPATHETIC
NERVES NERVES
I DECREASED
CARDIAC OUTPUT
MARKED EXCESSIVE
INCREASED INCREASE SALIVATION
VENOUS IN PLASMA
RETURN CATECHOLAMINES
L BRADYCARDIA
CONVULSIONS
(SKELETAL
MUSCLES)
INCREASED
CARDIAC
OUTPUT DECREASE IN
I EFFECTIVE GASEOUS
I DECREASE IN TRANSPORT IN LUNGS
VASCULAR
RESISTANCE
HYPOXIA
Fig. 6.2. Suggested schema for physiological changes produced by
endrin. Source: Hinshaw et al., 1966.
administration. Stimulation of the parasympathetic nerves would cause
bradycardia. When the sympathetic nervous system throughout the body is
stimulated to cause direct effects on the blood vessels, it also causes
the adrenal medul].ae to secrete catecholamines (epinephrine and nor—
epinephrine). These hormones then circulate everywhere in the body
fluids and act on all vasculature (Guyton, 1971). Dogs given endrin
exhibited large mean increases in catecholamine concentration from less
than 4 ig per liter of plasma to over 55 mg/liter (Hinshaw et al., 1966).
Adrenalectomy significantly decreased catecholamine concentrations, which,
however, were significantly elevated above pre—endrin values (Hinshaw
et al., 1966). The slight, though significant, elevation in total plasma
catecholamines after endrin exposure in adrenalectomized dogs suggests
the active particpation of the sympathetic nervous system. Many sympathetic
postganglionic axons are adrenergic fibers, capable of releasing norepi—
nephrine and smaller amounts of epinephrine (Hinshaw et al., 1966).
Increases in levels of epinephrine and norepinephrine in the blood with
probable parasympathetic activation make it difficult to evaluate the
exact role of catecholamines in the cardiovascular effects of these compounds
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(Reins et al., 1966). These high levels of epinephrine and norepinephrine
are probably enough to increase systemic arterial pressure through increased
cardiac output following elevation of venous return. High levels of
epinephrine apparently do not increase heart rate because of an overriding
reflex vagal effect (Reins at al., 1966).
Increased systemic arterial pressure has been observed as an early
effect of a lethal dose of endrin administered to dogs immobilized with
succinylcholine (Reins et al., 1964). This rise in systemic arterial
pressure depends primarily on increased cardiac output. Endrin does not
have a direct excitant action on the heart to cause an increase in cardiac
output, thus elevating venous return. The increased volume of blood re-
turning to the right atrium of the heart after endrin exposure appears
to originate primarily in the abdominal viscera (Reins et al., 1966).
Release of stored blood results in a continued maintenance of a high
cardiac output. Since the released blood remains in the active circula-
tion, venous return is continually maintained at a higher level. The
increase in venous return is not induced by circulating catecholamines,
since adrenalectomy does not modify the response (Hinshaw at al., 1966).
Systemic peripheral resistance markedly falls with endrin administration,
which could be due to the marked rise in blood flow. Total peripheral
resistance is ordinarily related inversely to blood flow (Hinshaw et al.,
1966). Total vascular resistance represents net changes In resistance.
Some vascular beds may be dilating and some constricting. Dogs administered
10 mg/kg endrin showed marked renal vasoconstriction and, therefore,
elevated resistance in the renal bed (Reins et al., 1964).
Emerson and Hinshaw (1965) investigated the effects of endrin
on vascular resistances in forelimbs of anesthetized dogs. Endrin admini-
stration resulted in large increases in total limb vascular resistance,
most of which were due to small—vessel (small artery to small vein) re-
sistance. The arterioles constitute a major resistance to blood flow.
Arterial and venous segmental resistances also increased. Sympathetic
innervation of limb vessels is not necessary for the large resistance
increases which follow .. ndrin administration. The resistance patterns of
the innervated and denervated groups are similar for the first 10 to 15
mm after endrin exposure (Emerson and Hinshaw, 1965). Resistance then
increases considerably more in denervated limbs than in innervated.
Increased vascular resistance in the kidney following endrin infusion
(10 mg/kg body weight) has been shown to be due primarily to circulating
catecholamine—like agents, but renal nerves also play a role (Reins at al.,
1964).
In addition to cardiovascular effects exerted through the central
nervous system, endrin appears to exert a toxic action directly on the
left ventricle (Fig. 6.2). Left ventricle failure demonstrated by elevated
left atrial pressure occurred regularly in endrin—treated dogs (Hinshaw
et al., 1966). Cardiac standstill occurred in more than 20% of the dogs.
It is not understood why endrin has a damaging action on the left ventricle,
while the right ventricle appears to be unaffected.
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6.3.6.3 Enzyme systems . Some symptoms of endrin intoxication may
arise through effects of endrin on mammalian enzyme systems.
Metabolic effects of endrin are particularly likely to be influenced
by change in enzyme levels. Metabolic changes after endrin exposure have
been indicated by weight loss and by changes in both oxygen uptake and
carbon dioxide production.
Nelson et al. (1956) observed a significant relation between endrin
consumed and weight change at various time intervals. Rats on 100 ppm
lost the greatest weight followed by those on 50 and 25 ppm. A greater
weight loss was found in male rats than in females. Although the total
average feed consumption of rats receiving endrin was less than controls,
a reduced food intake was not entirely responsible for the weight loss.
Even where control and experimental animals consumed the same amount of
food, the endrin—fed animal lost considerably more weight than its control.
Marked increases in both oxygen uptake and carbon dioxide production
resulted from intravenous injection of 3 mg/kg endrin into dogs. Mean
respiratory quotient values, however, remain relatively unchanged. Arterial
and venous concentrations of oxygen are very low within 30 mm after
administration of endrin (Hinshaw et al., 1966).
The ability of a single dose of endrin to significantly enhance the
potential of kidney cortex and liver to synthesize glucose from non—
carbohydrate sources in animals has been demonstrated (Singhal and Kacew,
1973). Alterations in carbohydrate metabolism produced by endrin may be
related to an enhanced capacity of liver and kidney cortex to synthesize
cyclic AMP (adenosine monophosphate). The cyclic AMP—adenyl cyclase system
is believed to play an important role in the action of several chemicals
on carbohydrate metabolism. A single oral dose of endrin (50 mg/kg body
weight) to rats stimulated the activities of the following key rate—limiting
enzymes involved in the pathway of gluconeogenesis: renal and hepatic
pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose,1,6—
diphosphatase, and glucose 6—phosphatase. In addtion, endrin depressed
liver glycogen and elevated the concentration of serum glucose and urea
(Kacew and Singhal, 1973a; Kacew et al., 1973; Singhal and Kacew, 1976).
When kidney cortex homogenates, kidney slices, or liver slices were
incubated with endrin in vitro, a significant stimulation of cyclic AMP
formation from radioactive adenosine was noted (Kacew and Singhal, l973b;
Singhal and Kacew, 1973). Administration of exogenous cyclic AMP was
found to mimic the action of endrin on gluconeogenous and glycogenolysis
as well as the hyperglycemic and hyperuremic responses (Singhal and Kacew,
1973). Since endrin—induced changes in carbohydrate metabolism are similar
to those produced by exogenous cyclic AMP, endrin—induced changes in
carbohydrate metabolism of kidney and liver might involve alterations on
the cyclic AMP system.
Endrin may affect major components of the terminal oxidation system.
The possibility that endrin exerts an effect on electron transport enzymes
by Its ability to associate with lipoprotein components of the mitochondrion
raises the question of whether the phosphorylative capacity of endrin—treated
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154
mitochondria is altered. Preliminary experiments on phosphorylation in
rat liver mitochondria treated with endrin revealed that ATP formation,
measured as radioactive—labeled P0 incorporation into glucose—6—phosphate
in the presence of excess hexokinase, was inhibited up to 10% (Colvin and
Phillips, 1968).
Colvin and Phillips (1968) suggest that any inhibition by endrin of
the transmission of nerve impulses would be due to binding of endrin to
lipoprotein components essential for mitochondrial oxidation and not
directly due either to inhibition or stimulation of acetyicholinesterase.
They propose that endrin and its analogues bind to lipid—rich structural
components of mitochondrial and certain other organelles. This binding
may subsequently affect the activity of enzymes associated directly with
the lipid—rich fractions.
A single intraperitoneal injection of endrin (10 mg/kg) significantly
inhibited the total lipid content of the liver form 12 to 48 hr after
treatment. An increase in total liver weight, however, indicated increased
protein synthesis. Kidney protein levels were not affected, but glycogen
levels were increased. Therefore, when rats are exposed to single doses
of endrin, the total lipid and phospholipid levels are decreased, but there
is no significant change in cholesterol levels (Gupta and Kaushal, 1977;
Kaushal and Gupta, 1977).
Pardino et al. (1971) investigated the effect of endrin on in vitro,
mitochondrial electron transport. Endrin was found to be a marginal
inhibitor of the beef heart mitochondrial succinoxidase system and the
beef heart mitochondrial—reduced nicotinamide adenine dinucleotide—oxidase
system. Endrin depressed the activity of both enzyme systems to approxi-
mately 80% of controls. Other evidence indicates that endrin induces
hepatic microsomal enzymes. Measurements of urinary 6—beta—hydroxycortisol
in workers exposed to endrin indicate that endrin can induce hydroxylating
enzymes of hepatic microsomes (Chamberlain, 1971). Levels of 6—hydroxylating
enzyme activity in the group exposed to endrin were significantly higher
than in control groups or a group exposed to aidrin and dieldrin.
Endrin causes an increased serum alkaline phosphatase level. When
various levels of endrin (0, 1, 5, 25, 50, and 100 ppm) were added to a
basal diet, the serum alkaline phosphatase levels were higher among rats
consuming endrin than in the control group, and this increase was related
to the quantity of endrin consumed during a period of time (Nelson et al.,
1956). The liver plays an important role as a source of alkaline phos—
phatase. Elevated serum alkaline phosphatase levels have been associated
with functional impairment of the liver and also with abnormalities in
dephosphorylation mechanisms (Nelson et al., 1956).
The administration of a single oral convulsive dose (20 mg/kg) of
endrin to albino mice significantly increased serum enzyme levels of
glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and
lactic dehydrogenase (Luckens and Phelps, 1969). Serum enzyme activity
levels appear to be directly related to cellular damage. Damaged organs
and tissues have been found to show a decrease in enzyme activity. The
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155
proportions of enzymes from such organs agree with those concomitantly
found in the serum (Luckens and Phelps, 1969). This may account for the
fact that although Luckens and Phelps (1969) observed an increase in
serum lactic dehydrogenase upon endrin exposure, Hendrickson and Bowden
(1973, 1976) found endrin inhibiting to rabbit muscle lactic dehydrogenase.
6.3.6.4 Hematology . Various changes in blood composition have been
observed following endrin exposure. Endrin appears to cause hemocentration
as evidenced by increases in hematocrit (the percentage of total blood
volume consisting of erythrocytes) and in leukocyte concentration.
Dogs given lethal doses of endrin (30 mg/kg) exhibited large increases
in the concentration of leukocytes (Emerson et al., 1964). Both mobiliza-
tion of stored leukocytes and increased bone marrow production appear to
have contributed to the increased plasma leukocyte concentration. Hemo—
concentration was observed in most animals. The trend toward acidosis during
endrin intoxication did not appear to be of respiratory origin, since
increasing ventilatory rate did not prevent the decreased pH (Emerson et al.,
1964).
Hematocrit increases in dogs were observed during acute endrin
poisoning (Emerson, 1965). A hematocrit increase can be due to increase
in size or number of erythrocytes. Emerson (1965) showed that approximately
half the postendrin rise in hematocrit is prevented by removal of the
spleen. This indicates the expulsion of cell—rich blood from spleen
storage is responsible for an appreciable portion of hematocrit elevation.
Other mechanisms must also be involved, however, to account for the
hematocrit elevation. Other mechanisms must also be involved, however, to
account for the hematocrit increase in splenectomized dogs. Loss of
filtration is possible. Severe acidemia could lead to an increased
hematocrit subsequent to an increased erythrocyte size (Emerson, 1965).
Coleman (1968) analyzed blood serums of rats given daily intraperitoneal
endrin doses (1 mg/kg). No changes were found in general serum protein,
serum lipoproteins, albumin, and in alpha, beta, or gamma globulins.
Protein—bound sialic acid, methyl pentose, and bound hexose rose to above
normal levels. Bound hexosamine was decreased. Alterations in bound
carbohydrates would indicate metabolic alterations in serum glycoproteins.
6.3.6.5 Trace—metal mobilization . Endrin intoxication produces, in
the initial stages, significant changes in concentration of metals in
various organs (Coleman et al., 1968). Shifts in certain trace metals at
the molecular level may be related to observed symptoms of endrin intoxica-
tion (Lawrence et al., 1968). Such trace—metal shifts resulting from
endrin exposure might precede and contribute to gross physiological
manifestations of endrin intoxication. Metal concentrations in organs,
tissues, and body fluids of rats were studied under conditions of actue
endrin intoxication by Lawrence et al. (1968) and under conditions of
subacute endrin intoxication by Coleman et al. (1968).
Lawrence et al. (1968) exposed rats to a single oral dose of 25 mg
of endrin per kilogram body weight. The rats experienced increases in
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156
size of all organs except the spleen within 2 hr of administration.
Increases were greatest for the liver and heart. The heart and spleen
demonstrated the greatest mobilization of metals. In both organs the
total amounts of iron, magnesium, and zinc increased, while the total
amount of copper decreased. Changes in unit concentrations paralleled
those of the total organ contents, indicating trace—metal shifts over
and above that attributable to change in the organ size parameters.
The kidney was intermediate in metal translocation, demonstrating
significant increases in concentration of iron, magnesium, and zinc.
The principal trace—metal shifts experienced by the brain and liver
included decreases in both total and unit concentrations of magnesium and
copper in the brain, and of copper in the liver. These decreases occurred
in opposition to increases in sizes of both of these organs. Total amounts
of zinc in brain and liver and iron in liver increased, while unit con-
centrations did not change significantly.
Zinc exhibited increases in the total organ content of heart, liver,
brain, spleen, and kidney. An observed decrease in zinc in red blood cells
provides one possible source of the mobilized zinc.
Copper concentrations and total amount of copper present decreased
in all organs studied except the kidney. The appearance of increased
plasma levels of this metal indicates that copper was mobilized toward
the circulatory system.
Magnesium increased in kidney, spleen, and heart. The increases
in unit concentrations, accompanied by increases in size of kidney and
heart, indicate extreme migration of magnesium into these organs. Decreased
magnesium levels observed in the brain, red blood cells, and plasma suggest
that magnesium was mobilized at the expense of the circulatory and central
nervous systems.
Total iron content, as well as unit concentration, increased in kidney,
spleen, and heart. Total iron content of liver increased without significant
change in unit concentrations.
Coleman et al. (1968) investigated the possibility that mobilization
of some of the most biologically significant metals (iron, magnesium, zinc,
and copper) occurs in those organs, tissues, and body fluids most responsive
to endrin exposure.
After eight daily sublethal exposures (1 mg/kg body weight per day),
the number of trace—metal translocations was small compared with those
occurring during the initial intoxication, indicating a tendency of most
organs to recover. Two exceptions to this trend were concentrations of
magnesium in the liver and copper in the kidney, both of which remained
essentially unaltered during the initial stages of intoxication but later
increased.
Under acute exposure (single oral dose of 25 mg/kg body weight) the
spleen demonstrated significant changes in all metals studied, but no
changes In organ size (Lawrence et al., 1968). After eight daily exposures,
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157
the spleen decreased drastically in size, but the number of metal shifts
was comparatively small. Subacute oral exposure of rats to multiple doses
of endrin (1 mg/kg body weight per day) produced, over an eight—day period,
effects on organs differing from effects observed in an earlier acute
study (Lawrence et al., 1968) in the same laboratory. In the subacute,
a decrease in size of spleen was the only significant change (Coleman et al.,
1968). In the acute study the spleen was the only organ that did not
experience a significant change in size.
Significant increases in excretion of magnesium and decreases in
excretion of zinc in the urine and feces accompanied endrin intoxication
(Coleman et al., 1968).
6.3.6.6 Liver . Endrin produces liver damage similar to that seen
after poisoning by other chlorinated hydrocarbons.
After an acute lethal dose of endrin (10 mg/kg body weight), dogs
exhibited mild to moderate congestion and irregularly distributed cloudy
swellings in the liver (Reins et al., 1964). Elevated serum alkaline
phosphatase levels associated with addition of various levels of endrin
to the diet of rats may indicate functional impairment of the liver
(Nelson et al., 1956).
A major difference between acute and chronic endrin exposure manifests
itself in effects on the liver. Rats receiving chronic low doses developed
zones of basophilic cells around the central and portal veins. These
abnormal cells were seen as early as seven days and increased in severity
and incidence as exposure was increased. The livers of acute animals showed
no discernible microscopic changes (Speck and Maaske, 1958).
6.3.6.7 Kidney . Studies by Reins et al. (1964) offer no evidence
that endrin has a direct toxic effect on the kidney. Renal alterations
appear to result secondarily from hemodynamic effects of circulating humoral
agents, systemic hypertension in acute poisoning, and terminal systemic
hypotension in animals with chronic exposure.
Dogs given acute doses of endrin (10 mg/kg) by intravenous infusion
developed increased renal vascular resistance largely attributable to
sympathoadrenal action. Only a small increase in renal resistance was
seen in adrenalectomized animals. Acute effects of endrin were predominantly
afferent arteriolar vasoconstriction as evidenced by decreases in renal
blood flow, glomerular filtration rate, and urine flow. Although renal
vascular resistance appears to be due primarily to circulating catecho—
lamines, renal sympathetic nerves have a minor but variable role in
control of resistance of the renal vasculature (Reins et al., 1964).
Changes in renal function of dogs in chronic studies were minimal
and appeared to be due to secondary alterations in systematic hemodynamics.
Dogs received 1—mg/kg doses of endrin five days a week until death (Reins
et al., 1964). No definite tubular changes were detected in the kidneys.
6.3.6.8 Spleen . After an acute lethal dose of endrin (10 mg/kg body
weight), dogs exhibited moderate to severe congestion of the spleen,
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158
with early degenerative changes and a mild degree of necrosis in the
reticular cells associated with the germinal centers. Degenerative changes
were more prominent in the large active germinal centers (Reins et al.,
1964).
6.4 REFERENCES
Baldwin, M. K., J. Robinson, and D. V. Parke. 1970. Metabolism of
Endrin in the Rat. J. Agric. Food Chem. 18(6): 1117—1123.
Boyd, E. N., and I. Stefec. 1969. Dietary Protein and Pesticide
Toxicity with Particular Reference to Endrin. Can. Med. Assoc. J.
101(20): 335—339.
Brooks, G. T. 1969. The Metabolism of Diene—Organochlorine (Cyclodiene)
Insecticides. Residue Rev. 27: 81—138.
Brooks, C. T. l974b. Chlorinated Insecticides. Vol. II: Biological
and Environmental Aspects. CRC Press, Cleveland, Ohio.
Chamberlain, J. 1971. The Determination of Urinary 6—Oxygenated Cortisol
in Evaluating Liver Function. Clin. Chim. Acta. 34: 269—271.
Cobel, Y., P. Hildebrandt, J. Davis, F. Raasch, and A. Curley. 1967.
Acute Endrin Poisoning. JAMA 202(6): 153—157.
Cole, J. F., L. N. Klevay, and N. R. Zavon. 1968. Endrin and Dieldrin:
A Comparison of Hepatic Excretion Rates in the Rat. (Abstract) Toxicol.
Appi. Pharmacol. 12(2): 298.
Cole, J. F., L. M. Klevay, and N. R. Zavon. 1970. Endrin and Dieldrin:
A Comparison of Hepatic Excretion in the Rat. Toxico. Appi. Pharmacol.
12(2): 547—555.
Coleman, R. L. 1968. Endrin—Induced Alterations in Bound Carbohydrates
in Rat Serum. Bull. Environ. Contam. Toxicol. 3(6): 348—353.
Coleman, R. L., C. H. Lawrence, and W. L. Sowell. 1968. Trace—Metal
Alterations Following Sub—Acute Exposure to Endrin. Bull. Environ. Contam.
Toxicol. 3(5): 284—295.
Colvin, H. J., and A. T. Phillips. 1968. Inhibition of Electro Transport
Enzymes and Cholinesterases by Endrin. Bull. Environ. Contam. Toxicol.
3(2): 106—115.
Curley, A., R. W. Jennings, H. T. Mann, and V. Sedlak. 1970. Measurement
of Endrin Following Epidemics of Poisoning. Bull. Environ. Contam.
Toxicol. 5(1): 25—29.
Davies, G. M., and I. Lewis. 1956. Outbreak of Food Poisoning from Bread
Made of Chemically Contaminated Flour. Brit. Med. J. II: 393—398.
-------
159
Deichmann, W. B. 1972a. Toxicology of DDT and Related Chlorinated
Hydrocarbon Pesticides. J. Occup. Med. 14(4): 285—292.
Deichinann, W. B., and W. E. MacDonald. 1971. Organochiorine Pesticides
and Human Health. Food Cosmet. Toxicol. 9(1): 91—103.
Deichmann, W. B., W. E. MacDonald, E. Blum, M. Bevilacqua, J. Radomski,
M. Keplinger, and M. Balkus. 1970. Tumorigenicity of Aidrin, Dieldrin,
and Endrjn in the Albino Rat. md. Med. Surg. 39(10): 37—45.
Dikshith, T. S. S., and K. K. Datta. 1972. Effect of Intratesticular
Injection of Lindane and Endrin on the Testes of Rats. Acta Pharmacol.
Toxicol. 31(1): 1—10.
Dikshith, T. S. S., and K. K. Datta. 1973. Endrin—Induced Cytological
Changes in Albino Rats. Bull. Environ. Contam. Toxicol. 9(2): 65—69.
Duggan, R. E., and P. E. Corneliussen. 1972. Dietary Intake of Pesticide
Chemicals in the United States (III), June 1968—April 1970. Pesti. Monit.
J. 5(4): 331—341.
Duggan, R. E., and C. Q. Lipscomb. 1969. Dietary Intake of Pesticide
Chemicals in the United States (II), June 1966—April 1968. Pesti. Monit.
J. 2(4): 153—162.
Emerson, T. E. 1965. Mechanisms of Hemoconcentration in the Dog During
Acute Endrin Insecticide Poisoning. Can. J. Physiol. Pharmacol. 43: 793—800.
Emerson, T. E., and L. B. Hinshaw. 1965. Perpheral Vascular Effects of
the Insecticide Endrin. Can. J. Physiol. Pharmacol. 43: 532—539.
Emerson, T. E., C. M. Brake, and L. B. Hinshaw. 1964. Cardiovascular
Effects of the Insecticide Endrin. Can. J. Physiol. Pharmacol. 42(1):
41—51.
Good, E. E., and G. W. Ware. 1969. Effects of Insecticides on Reproduction
in the Laboratory Mouse. IV. Endrin and Dieldrin. Toxicol. Appl. Pharmacol.
14(1): 201—203.
Grant, W. F. 1973. Cytological Effects of Environmental Mutagens —
Pesticides. Mutat. Res. 21(4): 221—222.
Graves, J. B., and J. R. Bradley. 1965. Response of Swiss Albino Mice
to Intraperitoneal Injection of Endrin. J. Econ. Entomol. 58(1): 178—179.
Green, V. A. 1967. Effects of Pesticides on Rat and Chick Embryo.
In: Proceedings of the First Annual Conference on Trace Substances in
Environmental Health. University of Missouri, Kansas City, No., pp. 183
209.
Gupta, P. K., and M. Kaushal. 1977. Endrin Intoxification in Normal and
Irradiated Rats. I. Protein and Glycogen Pattern. Chemosphere 6(1):
41—49.
-------
160
Guyton, A. C. 1971. Textbook of Medical Physiology. 4th Ed. Saunders,
Philadelphia.
Hayes, W. J., and A. Curley. 1968. Storage and Excretion of Dieldrin
and Related Compounds. Arch. Environ. Health 16: 155—162.
Hendrickson, C. H., and J. A. Bowden. 1973. The In Vitro Inhibition
of Lactic Dehydrogenase by Selected Polychiorinated Pesticides. (Abstract)
Fed. Proc. 32(3): 132—235.
Hendrickson, C. M., and J. A. Bowden. 1976. In Vitro Inhibition of
Lactic Acid Dehydrogenase by Insecticidal Polychiorinated Hydrocarbons.
2. Inhibition by Dieldrin and Related Compounds. J. Agric. Food Chem.
24(4): 756—759.
Hinshaw, L. B., L. A. Solomon, D. A. Reins, V. Fiorical, and T. E. Emerson.
1966. Effects of the Insecticide Endrin on the Cardiovascular System
of the Dog. J. Pharmacol. Exp. Ther. 153(2): 225—236.
Hoogendam, I., J. P. J. Versteeg, and H. DeVlieger. 1965. Nine Years’
Toxicity Control in Insecticide Plants. Arch. Environ. Health 10(3):
441—448.
Hunter, J., J. D. Maxwell, D. A. Stewart, R. Williams, J. Robinson, and
A. Richardson. 1972. Increased Hepatic Microsomal Enzyme Activity from
Occupational Exposure to Certain Organochiorine Pesticides. Nature
(London) 237(5355): 399—401.
Jacobziner, H., and H. Raybin. 1959. Briefs on Accidental Chemical
Poisonings in New York City. N.Y. State J. Med. 59: 2017—2022.
Jager, K. W. 1970. Aldrin, Dieldrin, Endrin and Telodrin. Elsevier,
New York.
Joy, R. N. 1976. Convulsive Properties of Chlorinated Hydrocarbon
Insecticides in the Cat Central Nervous System. Toxic. Appi. Pharmacol.
35(1): 95—106.
Kacew, S., and R. L. Singhal. 1973a. The Influence of P,P’—DDT,
Alpha—Chlordane, Heptachior, and Endrin on Hepatic and Renal Carbohydrate
Metabolism and Cyclic Amp—Adenyl Cyclase System. Life Sd. 13(10): 1363—
1371.
Kacew, S., and R. L. Singhal. l973b. Stimulation of Kidney Cortex
Cyclic 3’,5’—Adenosine Monophosphate—H 3 Formation by DDT and Related
Insecticides. (Abstract) Fed. Proc. 32(2): 3297:802.
Kacew, S., D. J. B. Sutherland, and R. L. Singhal. 1973. Biochemical
Changes Following Chronic .idministration of Heptachlor, Heptachlor Epoxide,
and Endrin to Male Rats. Environ. Physiol. Biochem. 3(5): 221—229.
-------
161
Kale, S. C., and S. K. Dangwal. 1970. Hazards During the Use of
Pesticides/Insecticides in Agricultural Farms. Seminar on Pollution
and Human Environment, Bombay Proceedings: 192—204.
Kaushal, M., and P. K. Gupta. 1977. Endrin Intoxification in Normal
and Irradiated Rats. II. Lipid, Phospholipid, and Cholesterol Content.
Bull. Environ. Contam. Toxicol. 18(3): 355—360.
Klein, W., W. Mueller, and F. Korte. 1968a. Excretion, Distribution,
and Metabolism of Endrin —(l4C) in Rats. Justus Liebigs Ann. Chem.
713: 180—185.
Korte, F. 1967. Metabolism of Aidrin, Dieldrin, and Endrin. In:
Symposium on the Science and Technology of Residual Insecticides in Food
Production with Special Reference to Aldrin and Dieldrin. pp. 102—117.
Korte, F., W. Klein, I. Weisgerber, R. Kaul, W. Mueller, and A. Djirsarai.
1970. Recent Results in Studies on the Fate of Chlorinated Insecticides.
In: Inter—American Conference on Toxicology and Occupational Medicine:
Pesticide Symposia Collection of Paper Sixth and Seventh, pp. 51—56.
Lawrence, C. H., R. L. Coleman, and W. L. Sowell. 1968. Endrin—Induced
Trace—Metal Alterations Following Acute Exposure. Bull. Environ. Contam.
Toxicol. 3(4): 229—239.
Luckens, M. M., and W. H. Davis. 1965. Toxicity of Dieldrin and Endrin
to Bats. Nature (London) 207(4999): 879—880.
Luckens, M. M., and K. I. Phelps. 1969. Serum Enzyme Patterns in Acute
Poisoning with Organochlorine Insecticides. J. Pharm. Sd. 58(5): 569—572.
Morris, R. D. 1968. Effects of Endrin Feeding on Survival and Reproduction
in the Deer Mouse, Peromyscus maniculatus. Can. J. Zoo. 46(5): 951—958.
National Academy of Sciences. 1975. Principles for Evaluating Chemicals
in the Environment. Washington, D.C. 454 pp.
Nelson, S. C., T. L. Bhaler, W. V. Hartwell, D. A. Greenwood, and L. E.
Harris. 1956. Serum Alkaline Phosphatase Levels. Weight Changes and
Mortality Rates of Rats Fed Endrin. J. Agric. Food Chem. 4(8): 696—700.
Ottolenghi, A. D., J. K. Haseman, and F. Suggs. 1974. Teratogenic Effects
of Aldrin, Dieldrin, and Endrin in Hamsters and Mice. Teratology 9(1):
11—16.
Pardino, R. S., J. C. Heidker, and B. Payne. 1971. The Effects of Some
Cyclodiene Pesticides, Benzenhexachloride and Toxaphene, on Mitochondrial
Electron Transport. Bull. Environ. Contam. Toxicol. 6(5): 436—444.
Reddy, D. B., V. D. Edward, G. J. S. Abraham, and K. V. Rao. 1966. Fatal
Endrin Poisoning. A Detailed Autopsy, Histopathological, and Experimental
Study. J. Indian Med. Assoc. 46(3): 121—124.
-------
162
Reins, D. A., D. D. Holmes, and L. B. Hinshaw. 1964. Acute and Chronic
Effects of the Insecticide Endrin on Renal Function and Renal Hemodynamics.
Can. J. Physiol. Pharmacol. 42(5): 599—608.
Reins, D. A., J. A. Rieger, Jr., W. B. Stavinoha, and L. B. Hinshaw. 1966.
Effect of Endrin on Venous Return and Catecholamine Release in the Dog.
Can. J. Physiol. Pharinacol. 44(1): 59—67.
Revzin, A. N. 1968. Effects of Chronic Endrin Administration on Brain
Electrical Activity in the Squirrel Monkey. Fed. Proc. 27(2): 597.
Revzin, A. N. 1970. Some Acute and Chronic Effects of Endrin on the
Brains of Pigeons and Monkeys.
Richardson, L. A., J. R. Lane, W. S. Gardner, J. T. Peeler, and J. E.
Campbell. 1967. Relationship of Dietary Intake to Concentration of
Dieldrin and Endrin in Dogs. Bull. Environ. Contam. Toxicol. 2(4): 207—219.
Sen, P., S. Arora, and P. K. Lahiri. 1969. An Experimental Study of
Endrin — An Insecticide. Indian J. Chest. Dis. 11: 26—30.
Singhal, R. L., and S. Kacew. 1973. Evidence for the Role of Cyclic
AMP in Mechanism of Action of Organochlorine Pesticides. (Abstract 642)
J. Cell Biol. 59(2, Pt 2): 321a.
Singhal, R. L., and S. Kacew. 1976. The Role of Cyclic AMP in Chlorinated
Hydrocarbon—Induced Toxicity. Fed. Am. Soc. Exp. Biol. 35(14): 2618—2623.
Speck, L. B., and C. A. Naaske. 1958. The Effects of Chronic and Acute
Exposure of Rats to Endrin. AMA Arch. Ind. Health 18(3): 268—272.
Tadjer, C. S., and I. Dore. 1971. Possibility of Contamination of Bottles
Used by Food Industries by Insecticides (in Hebrew). Harefuah 81(8): 385.
Thompson, F. B. 1971. Insecticides. II. Toxicity Hazards. N. Z. J.
Agric. 4(123): 84—87.
Treon, J. F., F. D. Cleveland, and J. Cappel. 1955. Toxicity of Endrin
for Laboratory Animals. Agric. Food Chein. 3(10): 842—848.
Versteeg, J. P. J., and K. W. Jager. 1973. Long—Term Occupational Ex-
posure to the Insecticides Aldrin, Dieldrin, Endrin, and Teoldrin.
British J. Ind. Med. 30(2): 201—202.
Walsh, G. M., and G. B. Fink. 1972. Comparative Toxicity and Distribution
of Endrin and Dieldrin After Intravenous Administration in Nice. Toxicol.
Appl. Pharmacol. 23(3): 408—416.
Weeks, D. E. 1967. Edrin Food Poisoning. A Report on Four Outbreaks
Caused by Two Separate Shipments of Endrin—Contaminated Flour. Bull.
WHO. 37: 499—512.
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Wolfe, H. R., W. F. Durham, and J. F. Armstrong. ‘1963. Health Hazards
of the Pesticides Endrin and Dieldrin. Arch. Environ. Health 6: 458—464.
Wolfe, H. R., W. F. Durham, and J. F. Armstrong. 1967. Exposure of
Workers to Pesticides. Arch. Environ. Health 14(4): 622—633.
World Health Organization. 1973. Pesticide Residues in Food. Report
of the 1972 Joint Meeting of the FAO and WHO in Rome. WHO Technical
Report Series No. 525, Geneva.
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7. MEDIA DISTRIBUTION, TR.ANSFORNATION, AND TRANSPORT
7.1 SUMMARY
Endrin was introduced in the United States in 1951 and is manufactured
both domestically and abroad. Its primary use is as an insecticide, and
its major application is to cotton. A wide variety of other crops may
also be protected from insect pests by endrin. The most recent year for
which consumption data are available is 1971. In that year a total of
643,772 kg (1,418,000 ib) of endrin was used. This value represents a
significant decrease from the 1964 figure of 984,726 kg (2,169,000 ib).
Endrin enters the environment as a result of direct application to
soil and crops. The persistence of endrin in the soil is, however,
dependent upon so wide a variety of factors that half—lives ranging from
24 hr to 11.8 years have been reported. Included among these factors are
properties of the soil, agricultural processes, topography, and numerous
meteorological determinants. Soils contaminated by endrin are located
predominantly in the cotton belt or delta states (such as Arkansas,
Louisiana, and Mississippi), where endrin is used extensively. Concen-
trations as high as 0.64 ppm were observed in Mississippi soils during
1972, while maximum concentrations in Arkansas and Louisiana soils during
1973 where 0.24 and 0.48 ppm respectively.
Many pathways have been established for the removal of endrin from
the soil. Mechanisms such as volatilization, leaching into groundwater,
wind erosion, and surface runoff result in the translocation of endrin to
other compartments of the environment, namely, the atmosphere and hydro-
sphere. Other pathways, including photodecomposition, thermal decomposi-
tion, and microbial degradation actually result in the dissipation of
endrin from the environment as well as from the soil.
The major source of endrin in rivers and other freshwater bodies
is surface runoff from fields and crops following application. Factors
similar to those affecting the persistence of endrin in the lithosphere
also influence the extent to which surface runoff will occur. Where
intense precipitation falls on sites of low permeability and low organic
content, runoff usually occurs. Steep topography accentuates runoff losses.
Additional sources of endrin in the hydrosphere are runoff from
endrin—coated seeds, contaminated industrial effluents, contaminated
fallout and precipitation, and carelessness in application and handling.
Pesticide surveillance of the surface waters of United States river basins
has been in effect since 1957. From 1961 through 1964 the number of
samples containing endrin progressively increased until, in 1964, 50% of
all samples tested were contaminated. Consistent contamination over the
years of a large percent of the samples occurred only in the lower
Mississippi basin. In addition, the highest concentrations recorded during
the six consecutive years from 1960 to 1965 were all from this area. Endrin
contamination of the lower Mississippi is apparently declining. While the
164
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residue levels reported between 1970 and 1975 were significant (20 ppt),
they did not approach the maximum of 214 ppt present in 1963 when numerous
endrin—related fish kills occurred.
Removal of endrin from the hydrosphere occurs by several routes.
Volatilization and codistillation, although extremely significant, merely
involve a reallocation of the endrin to the atmosphere. True dissipation
occurs as a result of biochemical and photochemical degradation. While
degradation of endrin by aquatic microorganisms has been reported, no
studies in support of photochemical decomposition in the hydrosphere are
available. It is believed, however, that such decomposition does take
place to some extent.
Endrin adsorbs to suspended particulates in the hydrosphere and is
transported to the sediment. The large—scale use of endrin in the agri-
cultural lands surrounding the Mississippi River basin prior to 1964 was
reflected in the levels of the pesticide detected in bottom deposits
(10,000 ppt) in that year. The highest concentration of endrin in the
sediment of any river basin between 1970 and 1975 was also found in the
lower Mississippi. This value, 6700 ppt, was somewhat less than that
reported in 1964. Decreased input, resuspension of sediment following
turbulent periods (such as storms), and some transport of contaminated
sediment to the sea are probably all responsible.
Vaporization of endrin from treated soils and crops is believed to
represent the major source of atmospheric contamination. In one experiment,
only 6% of the endrin sprayed on cabbage plants was detected in soil or
leaves four weeks following application. Codistillation from water, wind
transport of pesticide—laden dust, aerial drift from spraying operations,
and vapor emissions from industrial sources also contribute to the presence
of endrin in the atmosphere. Endrin is present in the atmosphere both in
the vapor phase and adsorbed to wind—borne particulates.
Extensive monitoring for organochlorine pesticides in the atmosphere
has not been conducted, and data for endrin are limited. From what little
data are available, it is apparent that concentrations are highest in the
agricultural centers of the delta states, where use of endrin predominates.
The highest concentration reported to date was 58.5 ng/m 3 in Stoneville,
Mississippi, in 1971. Urban communities far removed from agricultural
areas are unlikely to experience significant contamination. The majority
of organochlorine insecticides released to the atmosphere are eventually
returned to the earth’s surface. While some dissipation in the atmosphere
via photodecomposition is possible, no real evidence that such transforma-
tion actually takes place is available. Therefore the major hazard involved
in release of endrin to the atmosphere is the subsequent contamination of
the hydrosphere and lithosphere. The atmosphere transports far larger
quantities of organochlorine insecticides than does any other mechanism,
and atmospheric transport is considered to be primarily responsible for the
worldwide dissemination of these poisons. Although endrin per se has not
been detected in remote areas, the structural, chemical, and toxicological
similarities between endrin and related compounds detected at great distances
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166
from their point of application suggest that similar patterns of transport
may be operative.
Transport of endrin to the open ocean is expected to occur primarily
via the atmosphere. While river transport of contaminated, suspended
particulate matter may also contribute, codistillation and sedimentation
would probably remove most of the endrin from the flowing water long before
it reached the sea.
Atmospheric endrin Is conveyed to the ocean by particle fallout or
precipitation washout. Upon arriving at the surface of the sea, the
endrin may adsorb to the organic materials present in the surface micro—
layer and be subject to revolatilization, or it may adhere to large
suspended particulates and be carried to the sediment. Due to the depth
of the ocean, the chances for resuspension of contaminated sediment are,
at best, limited. The sediment of the oceanic abyss therefore represents
the ultimate sink for endrin and related compounds. The fate of endrin
in the ocean sediment remains unknown.
7.2 PRODUCTION AND USE
Endrin was introduced in the United States in 1951 by the Hyman
Company and is manufactured domestically by the Velsicol Chemical Corpora-
tion and in the Netherlands by Shell Nederland Chemie. The only known uses
of endrin are as an avicide, a rodenticide, and an insecticide, the last
of these being the most important. The endrin sold in the United States
is a technical—grade product containing not less than 95% active ingredient.
It Is available in a variety of diluted formulations including wettable
powders, dusts, emulsifiable concentrates, granules, oil solutions, and
baits (Shell Chemical Corporation, 1959; International Agency f or Research
on Cancer, 1974).
Endrin is approved for use in the protection of forest seeds against
birds, mice, and chipmunks, and for the control of birds on buildings and
mice in orchards (International Agency for Research on Cancer, 1974).
As an insecticide, its major application is to cotton crops, which it
protects from sucking, leaf—eating, and boll—damaging varieties of insects
throughout the growing season (Brooks, l974a). Insects that attack a wide
variety of vegetables, field crops, fruits, nuts, and pasture are also
controlled by endrin (Eichers et al., 1968; Eichers et al.,, 1970;
Adrilenas, 1974).
The use of endrin Is apparently declining. In 1964, endrin was
included among the 12 leading insecticides with a total consumption of
2,169,000 lb. By 1971, consumption had decreased to approximately 65% of
the 1964 value, or to 1,427,000 lb (Eichers et al., 1968; U.S. Department
of Agriculture, 1968; Andrilenas, 1974). The current consumption figures
are not available. Endrin usage has been banned in Switzerland, Italy,
and Germany (International Agency for Research on Cancer, 1974).
-------
167
7.3 ENDRIN IN TIlE ATMOSPHERE
7.3.1 Introduction
Evidence suggests that more than half of the organochiorine
insecticides sold annually eventually enter the atmosphere (Frost, 1969).
Although photochemical decomposition of many of these insecticides does
take place, even generous allowances for this factor result in the
conservative estimate that thousands of tons are transported to the oceans
via the atmosphere each year (Frost, 1969). The atmosphere transports far
larger quantities than any other mechanism, and atmospheric transport is
considered to be primarily responsible for the worldwide dissemination of
these poisons. In order to control the escape of organochiorine insecti-
cides into the atmosphere, it is first necessary to understand the
mechanisms by which such escape takes place. Losses are known to occur
by several routes, including: volatilization from soil and crops,
evaporation and codistillation from contaminated bodies of water, wind
transport of pesticide—laden soil and dust, aerial drift from spraying
and dusting applications, venting of vapors from pesticide manufacturing
and formulating plants, and open burning of discarded pesticide containers
at inadequate temperatures.
All of the above routes have not been investigated for every
organochlorine insecticide. However, the structural, chemical, and
toxicological similarities among these compounds (especially the
chlorinated cyclodienes) suggest that similar patterns of loss may be
expected. The number of experimental studies dealing specifically with
loss of endrin to the atmosphere are adequate in some areas but nonexistent
in others. Where experimental data are lacking for endrin, but are suff i—
cient to implicate a given route to the atmosphere as significant for a
related compound, this route must be considered as a potential source of
endrin as well. Only after studies have definitely ruled out a mechanism
is it safe to assume that the mechanism does not apply.
In interpreting what little experimental evidence is available, care
must be taken to assure that release to the atmosphere has actually been
observed. Studies dealing with “disappearance” of endrin from soil and
crops are particularly suspect. Endrin may “disappear” for other reasons
as well. Photodecomposition, bacterial degradation, absorption by plants,
etc., must also be taken into account. If an analytical procedure does
not extend to the decomposition products as well as to endrin itself, then
one cannot be certain that vaporization is wholly responsible for loss.
Monitoring data for ambient atmospheric endrin concentrations have
also been reported. Data, however, are scarce and generally not totally
reliable. Analytical difficulties, problems associated with monitoring
sufficiently large volumes of air, failure to trap vapors as well as parti-
culate matter, interfering compounds, and equipment failure are all
responsible. However, some feeling for the extent and degree of atmospheric
contamination by endrin is provided by these data, and despite their
inaccuracies they seem worthy of presentation.
-------
168
7.3.2 Sources of Endrin in the Atmosphere
7.3.2.1 Vaporization from soil and crops . Vaporization of endrin
from treated soils and crops is believed to represent the major source of
atmospheric contamination (Abbott et al., 1966; Frost, 1969; Chesters
and Konrad, 1971; U.S. EPA, 1972). Some idea of the evaporative potential
of endrin under controlled laboratory conditions is provided by the work
of Bowman et al. (1965). Samples of endrin (375 mg in 4 ml of hexane)
were placed in glass beakers with a bottom surface area of 8 cm 2 and
incubated in a gravity convection—type oven at 45°C. This temperature
was arbitrarily chosen as the highest temperature to which soils in a
southern state (Georgia) are likely to be exposed under field conditions.
Samples were analyzed for endrin and possible degradation products by
electron—capture gas chromatography following four and eight days of
Incubation. After four days, 38% of the endrin had volatilized; eight
days of incubation resulted in the loss of 82% of the initial quantity.
No degradation products were observed under the conditions of this
experiment.
Studies conducted in the field appear to confirm the expected rapid
loss of endrin to the atmosphere following application to soil and/or
crops. Volatilization from sugarcane was investigated by Willis et al.
(1969). Granular endrin (2% active ingredient) was applied by hand to a
sugarcane plot located within a larger field of sugarcane at a rate of
2 lb/acre. Half of the endrin was applied to the soil surface and half
to the sugarcane Itself. A special apparatus, designed for continuous
collection of volatilized endrin, was set up in the field. Air was
drawn through the apparatus at a rate of 1 liter/mm. This relatively
low flow rate reduced the possibility of creating a “sink” which may have
led to erroneous conclusions concerning the rate and extent of volatiliza-
tion. The vapors were collected in an ethylene glycol trap, and the air
was recycled back into the atmosphere. The collection apparatus, located
4 ft above the soil surface, was allowed to run continuously for 11 weeks
following application of the pesticide. Ethylene glycol was replaced in
the trap at three—day intervals thereafter. Thus each sample represented
an average value for a given collection period. Analyses were performed
by electron—capture gas chromatography, and the results are presented in
Fig. 7.1. The cumulative recovery (in thousands of nanograms) is also
given. The initial data point (540 ng/m 3 ) is an average concentration for
the first three days following application and does not represent the
highest level occurring during that time period. Shorter sampling periods
would have been necessary In order to determine the actual peak concentra-
tion. The average atmospheric concentration decreased rapidly to 123 ng/m 3
at 21 days following treatment and continued to decrease less rapidly to
a value of 30 ng/m 3 after 77 days. The asymptotic nature of the curve
possibly indicates a dependence of volatilization upon concentration. The
cumulative recovery approached 12,000 ng, and the shape of the recovery
curve was also indicative of a decrease in rate of volatilization with time.
It was estimated that about 5% of the total endrin applied was lost to the
atmosphere; but this estimate was based upon assumptions as to the rate of
air turnover above the plot and should not be taken as absolute.
-------
169
ORNL—DWG 79—8952
14
12
0
10 <
8
uJ
>
0
U
Gw
z
4
w
2
0
60 70 80 90
Fig. 7.1. Atmospheric concentration of endrin 4 ft above ground
level In a sugarcane field and cumulative recovery. Source: modified
from Willis et al., 1969.
A similar curve for disappearance of endrin from rice seedlings was
obtained using an entirely different method (All and Nair, 1973). Rice
seedlings were sprayed with an endrin emulsion, and plants were collected
at given intervals following treatment. The concentration of endrin
remaining in the plants was determined by exposing Corcyra cephalonica
larvae to acetone extracts of the plants (which contain the residual endrin)
and comparing the observed percent mortality to a standard dose—mortality
curve. The results are presented in Fig. 7.2. While the primary factor In
the loss of endrin activity was most likely volatilization, other possi-
bilities, such as decomposition to compounds nontoxic to the test organisms,
are not to be ruled out by this type of study.
The disappearance of endrin from treated cabbage was studied by
Mattick et al. (1963). An emulsified formulation of endrin was sprayed
on maturing cabbage at rates of 0.8, 0.5, and 0.25 lb of actual pesticide
per acre. The cabbage was harvested on successive days following treatment
and analyzed for endrin and its degradation products by electron—capture
gas chromotography. The results are presented in Table 7.1. In each case,
more than 95% of the endrin present in the cabbage at the time of treatment
was lost within 21 days. Presumably, a fair percentage of this loss can be
attributed to vaporization.
In another study (Klein and Korte, 1967), 1 to 2 mg 1 C—labeled
endrin per plant was applied to white cabbage. Four weeks following
application, only 6% of the radioactivity could be found in plants and
560
480
400
N,
E
320
z
0
2 240
w
160
80
0
0 10 20 30 40 50
TIME (days)
-------
170
200
460
E
- 120
Li
C
U)
Li
z
C
z
Li
80
40
0
ORNL-DWG 79-8953
Fig. 7.2. Endrin residues remaining in rice plants as determined
from mortality of Corcyra cepholonica larvae. Source: K. A. All
and M. R. G. K. Nair, MadraB Agric. J. 60(7): 439—440 (1973). Copyright
1973 Tam.il Nadu Agricultural University.
Table 7.1.
Disappearance of endrin residues from cabbage
D
ays after
spraying
Endrin (ppm)
remaining at each
treatment level
0.8
lb/acre
0.5 lb/acre
0.25 lb/acre
0
1
2
5
7
10
14
21
4.17
4.79
2.36
2.08
0.81
0.95
0.30
0.13
2.26
2.45
1.06
0.48
0.32
0.18
0.17
0.10
Sample lost
0.72
0.50
0.34
0.21
0.10
0.09
0.004
%
remaining
(day
21)
3.1
4.4
0 , 56 a
%
lost
(day
21) 9
6.9
95.6
99.44
aBased on day 1 value.
Source: Reprinted with
J. Agric. Food Chem. 11(10):
Chemical Society.
permission from L. R. Mattick et al.,
54—55 (1963). Copyright 1963 American
0 4 8 12 46
INTERVALS AFTER SPRAYING (doys)
-------
171
soil; the remaining 94% had disappeared into the atmosphere. The authors
attributed 60% of the loss to evaporation of 34% to transpiration by the
plants. This interpretation may also apply to the previous study as well.
The extent of pesticide vaporization from plants and soil under field
conditions is determined by a complex, interacting collection of parameters
and is not easily predicted. Some of these parameters, such as the vapor
pressure of the pesticide, the temperature of the soil, and the wind
velocity at the time of measurement, are obvious. Others are revealed
only through extensive experimentation. While each observed parameter
influences the volatilization of every organochiorine insecticide, the
direction and extent of that influence may differ drastically among the
various compounds. One particularly important variable appears to be
the organic content of the soil in question (Bowman et al., 1965; Adams,
1967; Frost, 1969; Chesters and Konrad, 1971). Due to their lipophilic,
hydrophobic nature, the chlorinated hydrocarbon insecticides (including
endrin) strongly absorb to the organic material present in soil.
Vaporization is therefore retarded from soils rich in organic matter.
This phenomenon may also explain why the rates of vaporization are highest
immediately following pesticide application, before the pesticide has
become completely adsorbed.
The effect of soil organic matter on the vaporization of a series of
chlorinated insecticides was studied by Bowman et al. (1965). Eight
types of soil representing a wide range of organic content were equili-
brated at 45°C to ensure roughly comparable moisture retention at the start
of the experiment. Solutions of each pesticide in minimal amounts of
hexane were added to samples of each of the soils, and the samples were
incubated in a gravity convection—type oven at 45°C. Analyses for residual
insecticide and degradation products were conducted after 4 and 8 days of
incubation, using electron—capture gas chromatography. The results for
dieldrin and endrin in three types of soil are presented in Table 7.2.
Loss of dieldrin from Lynchburg loamy sand, poor in organic matter, was
rapid and extensive. Following eight days of exposure, 88% had evaporated.
Only 16% of the dieldrin was lost from Rutledge sand, rich in organic matter,
after a similar incubation period. Endrin, however, did not behave at
all like its isomer. Complete degradation to three products occurred in
each soil type, and little loss was observed. Furthermore, the greatest
relative loss (11%) took place from that soil containing the highest
organic content. No explanation was presented for these unexpected results.
The moisture content of the soil also plays a role in determining the
extent of volatilization of organochiorine insecticides (Bowman et al.,
1965; Frost, 1969; Beau and Nash, 1971; Chesters and Konrad, 1971). In
general, more volatilization is expected from wet soils than from dry soils.
Bowman et al. (1965) studied the effects of moisture on the volatilization
of a series of insecticides from four soils. Acetone solutions of each
insecticide were applied to dry soil, to soil which was subsequently
saturated with distilled water, and to soil previously saturated with
distilled water. The treated samples were incubated at 45°C in a gravity
convection—type oven f or four days and analyzed for residues and degrada-
tion products by electron—capture gas chromatography. The results for
dieldrin and endrin are presented in Table 7.3.
-------
172
Table 7.2. Persistence and behavior of dieldrin and
endrin in various types of soil at 45°C
Insecticide
Added
insecticide
periods
recovered from soils
of exposure (%)
after
Days of
exposure
Lynchburg
loamy sand
(0.17%)
Lakeland sand
deep phase
(O 42 %)
Rutledge
sand I
( 6 . 56 %)a
Dieldrin
4
8
24
22
50
46
93
84
Endrinlb
4
0
0
0
11°
1 1 1 d
4
4
25
17
48
0
2
33
1V 5
4
56
45
54
Total endrin
4
98
93
89
Endrjn lb
8
0
0
0
11 C
1 11 d
8
8
39
5
50
0
1
33
lye
8
55
46
55
Total endrin
8
99
96
89
a ganic content in the soil (2).
bCalcalated by comparison with endrin standard.
Cjmo degradation product of endrin.
dEfldrin aldehyde.
eEdrin ketone.
Source: Reprinted with permission from N. C. Bowman, N. S.
Schecter, and R. L. Carter, J. Agric. Food Chain. 13(4): 360—365 (1965).
Copyright 1965 American Chemical Society.
In three of the four soil types, more dieldrin was lost from
water—saturated soils than from dry soils. The exception was Rutledge
sand. In all four soils, addition of dieldrin, prior to saturation with
water, suppressed volatilization relative to the situation where
saturation with water occurred first.
Loss of total endrin from water—saturated soils was greater than from
dry soils in two of the four soil types. In this case the exceptions were
Rutledge sand and Greenville clay. In three soil types, loss of total
endrin from water—saturated soils was greatest when saturation occurred
prior to addition of the insecticide. Here the exception was Lakeland
sand. Once again, the complicated nature of the interactions involved
renders predictions difficult.
A parameter closely associated with soil moisture content is humidity.
Kalkat et al. (1961) studied the effects of relative humidity on the
-------
Table 7.3. Effects of moisture on persistence and behavior of dieldrin and endrin
in four types of soils exposed at 45°C for 4 days
Soil
Condition
Added
insecticide recovered
(%)
Dieldrin
Endrin
Total
endrin
i
j b
1 1 1 b
ivb
Lakeland sand
deep phase
(0.42%)
Dry soil
H 2 0 + insecticide
Insecticide + 1120
59
43
48
0
15
21
18
8
8
7
4
4
44
31
33
69
58
56
Greenville
sandy clay
( 057 %)a
Dry soil
H 2 0 + insecticide
Insecticide + 1120
84
61
67
46
40
67
10
2
2
0
0
0
8
8
8
64
50
77
Magnolia
sandy loam
(l.33%)a
Dry soil
H 2 0 + insecticide
Insecticide + 1120
83
50
69
6
32
30
40
9
30
0
0
0
33
15
16
79
56
76
Rutledge sand
(l 943 %)a
II
Dry soil
H 2 0 + insecticide
Insecticide + H 2 0
70
75
84
64
72
92
3
1
3
0
0
0
13
11
2
80
84
97
H
(-k)
aorganic content in soil (%).
bDegradation product of endrin.
Source: Reprinted with permission from
J. Agric. Food C1-iem. 13(4): 360—365 (1965).
M. C. Bowman, N. S. Schecter, and R. L. Carter,
Copyright 1965 American Chemical Society.
-------
174
volatility of several insecticides and found that their fumigant action
increased significantly when the relative humidity was raised from 55 ± 5%
to 90 ± 5% under similar temperature conditions (43.3°C in all cases).
Loss of heptachior epoxide through volatilization more than doubled when
the relative humidity was raised from 7 ± 5% to 70 ± 5% at 34.4°C. The
effect of increased humidity on the vaporization of several organochiorine
insecticides, including endrin, was also studied (though unintentionally)
by Bowman et al. (1965). In one case the insecticide solutions were added
to soil previously dried at 45°C and returned immediately to a low—humidity
environment. In the second case the insecticide solutions were added in
an indentical manner, but the soil samples were returned to an oven also
containing water—saturated soils and, therefore, to a highly humid
atmosphere. The results f or dieldrin and endrin in four soil samples
after four days of incubation at 45°C are presented in Table 7.4. In
three of the four soil types tested, the amount of dieldrin lost to the
atmosphere was greater under humid conditions. Loss of total endrin was
greater in all four soil types under humid conditions. Results in conflict
with these have, however, also been reported. Lyon and Davidson (1965)
studied the effects of humidity on the volatilization of certain insecti-
cides. Insecticide residues were weighed before and after exposure in
petri dish halves at 43.3 ± 1.1°C to a relative humidity of either
8 ± 5% or 80 ± 5%. The total weight loss for each group of replicate
samples was determined. Of nine compounds tested, seven showed the
expected greater weight loss at higher humidity. Two compounds, coumaphos
and endrin, exhibited a greater weight loss at lower humidity. The total
loss for endrin at 8 ± 5% relative humidity was 2.0 mg; at 80 ± 5% humidity,
the loss was 1.1 mg. The exact cause of this devious behavior remains
unknown.
Any treatment that increases the exchange of air over the soil surface
will increase the rate of pesticide volatilization (Frost, 1969). The
cultivation practice of disking or mixing the soil is an example of such
treatment. Harvesting the crops also bares the soil to the air. Conversely,
any treatment which reduces the air flow will retard volatilization. For
example, pesticides persist much longer where a cover crop such as alfalfa
is planted, or in forests where trees provide a canopy over the soil
surface. In both of these instances, shade is also provided which helps
keep the soil cool and retards vaporization (Frost, 1969).
A parameter which may possibly affect evaporation from crops is the
surface area of the plant. Brett and Bowery (1958) studied the disappear-
ance of endrin as a function of plant surface area. Three types of plants
were used in these experiments: tomatoes (great volume with little surface
area), collards (small volume with large surface area), and snap beans
(intermediate in both surface area and volume). Crops were dusted in the
field with 2% endrin and sampled at given intervals for analysis of
residual pesticide levels; the results are presented in Table 7.5.
Collards, with the largest ratio of surface area to volume, contained
the highest levels of endrin and retained residues for a longer period of
time than did the other two types of vegetables. Endrin could not be
detected in tomatoes one day following treatment.
-------
Table 7.4. Effects of humidity on the persistence and behavior of dieldrin and
endrin in four types of soils exposed at 45°C for 4 days
aorganjc content in soil (%).
bDegradation product of endrin.
Source: Reprinted with permission from N. C. Bowman, M. S. Schecter, and R. L. Carter,
J. Agric. Food Chem. 13(4): 360—365 (1965). Copyright 1965 American Chemical Society.
Soil
.
Condition
Added insecticide
recovered
(%)
Dieldrin
Endrin
I
1I
1 1 1 b
ivb
endrin
Lakeland sand
deep phase
(O• 42 %)a
Dry
Humid
50
59
0
0
48
18
0
7
45
44
93
69
Greenville
sandy clay
(0.57%)a
Dry
Humid
94
84
0
46
49
10
0
0
34
8
83
64
Magnolia
sandy loam
(l . 33 %)a
Dry
Humid
90
83
0
6
48
40
0
0
44
33
92
79
Rutledge sand
(lg.4 3 %)a
II
Dry
Humid
97
70
47
64
5
3
5
0
41
13
98
80
H
Ln
-------
Table 7.5. Endrin residues on tomatoes, snap beans, and collards
Days after
application
Tomatoes
Snap beans
Collards
(°F
Temp
max/mm)
ppm
(°F
Temp
max/mm)
ppm
(°F
Temp
max/mm)
ppm
0
82/62
0.31
80/54
0.48
64/37
17.3
1
91/65
oa
81/58
0.25
64/36
15.2
2
96/71
0 a
78/59
0.25
63/42
3.4
3
98/73
0 a
81/62
0 a
69/40
2.7
4
95/70
0 a
85/59
0 a
80/60
a low the minimum detection level (<0.10 ppm).
Source: C. 11. Brett and T. G. Bowery, J. Econ. Entoinol. 51(6): 818—821 (1958). Copyright
1958 Entomological Society of merica.
0 ’
-------
177
While loss of residues may be attributed at least partially to
volatilization, the role of surface area per se in determining the extent
to which volatilization occurs might be questioned. The organic content
of the plant surface would also be an important factor. Endrin may be
more strongly adsorbed to the waxy cuticle of a collard leaf than to the
surface of a tomato. This selective adsorption, in conjunction with a
larger surface area, appears to provide a more complete explanation for
the observed results.
Vaporization of endrin from soil surfaces may contribute to
contamination of nearby plants. The extent to which vaporized endrin is
taken up by the aerial portions of soybean plants was investigated by
Beall and Nash (1971). Soybean seedlings were planted in specially de-
signed pots which enabled the surface soil to contain 1.5 pCi of 1 C—labeled
endrin at a concentration of 20 ppm, while the subsurface soil (to which
the roots were exposed) remained pesticide free. Surface and subsurface
soil layers were separated by a water— and vapor—tight disk as well as
by an airspace. To confine vapors around the plant, a polyethylene cage,
open at the top, was provided. The soil was kept moist for the duration
of the 53—day experiment. At that time the plants were harvested and
separated Into lower stem, lower leaves, upper stem, upper leaves, pods,
and seeds. Uptake of endrin was determined through complete combustion
of the dried plant parts followed by quantification of the released
1 C—labe1ed CO 2 . The results are presented in Table 7.6. Residue concen-
trations resulting from vapor sorption were highest in the leaves. The
lower leaves contained more residues than the upper leaves, most likely
Table 7.6. Concentration of residuesa found in soybean
plants exposed to topsoil treated with ‘ 1 C—endrin
Plant part Residues (ppm)
Upper leaves 15.95
Lover leaves 33.78
Total leaves 23.81
Upper stem 2.42
Lower stem 1.66
Total stem 1.89
Pods 2.84
Seeds b 0.99
Average concentration 6.7
aBased on - C content of combusted dried plant
parts.
bAverage concentration in total aerial parts.
Source: M. L. Beau, Jr. and R. G. Nash, J.
Environ. Qual. 1(3): 283—288 (1972). Copyright 1972
American Chemical Society.
-------
178
due to their closer proximity to the treated soil and their distribution
over the soil. Pods contained higher concentrations than stems. The
large hairy surfaces of the pods along with their semipendulous growth
habits provided a greater surface area for vapor sorption than did the
single upright stem. Although 43% of the applied endrin had vaporized by
the end of the experiment, residue concentrations resulting from vapor
sorption averaged only 6.7 ppm. One explanation is that most of the
endrin may have volatilized during the early growth stages, at a time when
the plants provided little canopy over the soil. Additionally, some of
the residues originally adsorbed to the plant surfaces may have revolatilized
and escaped to the environment. The authors suggest that the low organic
content of the soil, the shallow (1—cm) depth of the treated soil layer,
and the observance of moist conditions throughout the experiment may have
resulted in a greater degree of volatilization than would occur in the
field. These factors may, however, have been counterbalanced by the fact
that the endrin was uniformly distributed throughout the soil as opposed
to being applied merely to the surface.
7.3.2.2 Vaporization and codistillation from water . Vaporization
and codistillation of organochiorine insecticides from fresh and marine
waters is another well—established route of atmospheric contamination
(Risebrough et al., 1968; Frost, 1969; Koeman et al., 1972). As a
result of their tendency to accumulate at the surface of the water,
these compounds are carried off into the atmosphere as the surface water
evaporates. Most of the pesticides in laboratory suspensions are lost
in this way within a few days (Frost, 1969), and the pesticide content
of rivers and lakes subjected to surface runoff from agricultural lands
is seen to decrease rapidly. No studies dealing with the extent to which
endrin is lost from bodies of water have been reported. However, circum-
stantial evidence implies that such loss may be significant. Birds and
fish were collected from Lake Nakuru in Kenya, and their tissues were
analyzed for residues of organochiorine insecticides including endrin
(Koeman et al., 1972). Residues in general were found to be extremely
low, indicating that chlorinated hydrocarbon pesticides were not major
pollutants at the time of sampling. Lake Nakuru, which has no outlet, is
surrounded by agricultural land where insecticides (including endrin) are
frequently used. Under the circumstances, it was expected that the
residues in birds and fish would be equal to those found in similar
ecosystems in other parts of the world. The results may indicate that the
rate of disappearance of chlorinated hydrocarbon pesticides in tropical
areas is relatively high as compared with more temperate areas and that
vaporization and codistillation from water is a major route of disappearance.
It is possible that tropical regions where pesticides are used extensively
may be significant sources of the observed global atmospheric pollution
by these compounds.
7.3.2.3 Other sources . Other potential sources of organochiorine
insecticides in the atmosphere have not been studied specifically as
they relate to endrin. These sources are, however, well established for
similar compounds and therefore must be considered as probably routes of
contamination for endrin as well. One major source of atmospheric con—
tainination is pesticide—laden dust picked up directly from soils by winds
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179
(Risebrough et al., 1968; Frost, 1969; Yobs et al., 1972). These airborne
dusts are of more than local significance, since they may be transported
thousands of miles by the prevailing winds, especially during storms.
Pesticides adsorbed to large particulates (size range > 1 i) will be
deposited fairly close to their point of origin. Pesticides adsorbed to
finer particles (size range < 1 p) will travel greater distances.
Risebrough et al. (1968) collected gram quantities of airborne particulate
matter over Barbados. From the mineralogical and biological composition
of these samples, it was apparent that they had originated from Europe
and Africa and had traveled, carried by trade winds, over 6000 km across the
Atlantic Ocean. Using the pesticide concentration on the dust (41 ppb)
and estimates of the rate of dust sedimentation throughout the areas
affected by the trade winds, Risebrough concluded that approximately
600 kg organochlorine insecticides was deposited over this portion of the
Atlantic every year. This estimate represents a minimum figure, since
the method of collection did not trap particles of less than 1 i in diameter.
The percentage of aerial dust—borne pesticides that actually arrive there
as such is difficult to determine, since vaporization from, and/or adsorp’-
tion to, particulates undoubtedly takes place in the atmosphere. It is
possible that the dust itself did not represent the original source of the
pesticides, but rather that free pesticide vapors, also carried by the
winds, were picked up by dusts from totally different origins.
Another source of atmospheric contamination closely related to the
one just discussed is aerial drift from spraying or dusting applications
(Tabor, 1965; Abbott et al., 1966; Frost, 1969; Chesters and Konrad, 1971;
U.S. EPA, 1972; Yobs et al., 1972). Such contamination is mainly local,
with concentrations likely to vary inversely as the distance from the point
of application. However, appreciable distances may be effected if the
wind conditions are appropriate, and a potentially serious situation exists
if a water body is located within drift distance. Ground spraying is
four to five times less likely to result in drift than is aerial spraying,
but aerial spraying is generally more popular. The best weather conditions
for aerial spraying are on days when there is little or no wind and when
a temperature inversion exists between 3 and 10 m above the ground (Chesters
and Konrad, 1971). The temperature inversion prevents the upward movement
of the pesticides and subsequent transportation by the wind. These ideal
conditions seldom prevail, and significant amounts of pesticides are
transported great distances following application. Due to their smaller
particle size, dusting applications are more likely to result in widespread
dissemination than are aerosolic applications. Some evidence for widespread
drift of applied pesticides is the observation that the mineral talc used
as a carrier and diluent for pesticides occurs in the solid—mineral phases
of rain, glaciers, and rivers and in dusts recovered from the atmosphere
in concentrations much higher than can be expected from natural occurrences
(Risebrough et al. 1968). Unfortunately, this talc cannot be used as a
quantitative tracer because it is gradually being displaced by water and
light petroleum bases.
Vapors from industrial sources such as pesticide manufacturing or
formulating plants are yet another source of atmospheric contamination
(Tabor, 1965; Abbott et al., 1966). Once again, the greatest effects are
local, but transport over great distances is possible.
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180
One final route by which pesticides may be released to the atmosphere
is during disposal of unused product or empty containers. The most popular
method used by farmers to dispose of empty containers is burning in an
open fire along with other trash. While burning containers is recommended
by most manufacturers, reliable estimates suggest that temperatures
obtained in open burning are not sufficient to destroy these compounds
(U.S. EPA, 1972). As a result, vaporization occurs.
7.3.3 Monitoring for Endrin in the Atmosphere
Extensive monitoring for organochiorine pesticides in the atmosphere
has not been conducted, and data for endrin are limited. One reason for
the paucity of studies in this area is the difficulty of accurate analysis
at low ambient levels. The most sensitive quantitative analytical tech-
nique available at this time is electron—capture gas chroniotography. This
technique, however, cannot distinguish among certain similar compounds, and
the sought—after peaks are sometimes hidden by those of contaminants
present in higher concentrations (such as the ubiquitous polychlorinated
biphenyls). Mass spectrometry is an accurate qualitative tool. However,
it is not very sensitive and cannot detect “trace” amounts of pesticide.
Mass spectrometers are also very expensive and require highly trained
technicians for their operation. As a result they are generally not
available for confirmatory studies during ambient air sampling programs
(Lewis, 1976).
Despite these problems, some studies have been reported. Tabor (1965)
conducted a study in which the concentrations of particulate pesticide
pollutants in the atmosphere of urban areas were measured. The communities
chosen were surrounded by agricultural areas where large amounts of
pesticides are applied annually during the growing season. If substantial
amounts of pesticides were not found under these conditions, the probability
of significant contamination in cities far removed from agricultural
activity would be rather slight.
Sampling stations were set up in the center of town, and sampling was
conducted during the periods of greatest application of pesticides to
crops. Particulate matter was collected on glass—fiber filters and analyzed
by electron—capture gas chromotography. The limits of detection were less
than 1 ng (lO g).
Of the agricultural communities sampled, two had histories of endrin
usage. Leland, Mississippi, and Newellton, Louisiana, are both surrounded
by cotton fields where numerous pesticides, including endrin, are applied
during the growing season. DDT and chlordane were detected at both sampling
sites at maximum concentrations of 20 and 2 ng/m 3 respectively. Toxaphene
and malathion were detected in Newellton. No trace of endrin was found
in any samples from either community. These studies, however, were
limited to particulate pesticide sampling. Accurate measurement of
atmospheric pesticides requires a simultaneous quantitative collection
of vapors as well as particulates. The concentrations reported here must
be interpreted as minimum estimates, and it is quite possible that vaporized
endrin is present in the atmospheres of both of these communities.
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181
In 1970 and 1971, the Division of Pesticide Community Studies of the
United States Environmental Protection Agency (no longer in operation)
conducted a survey of pesticide levels in ambient air in the United States
(U.S. EPA, 1970b; U.S. EPA 1971a; U.S. EPA l971b; Yobs et al., 1972).
During 1970, 30 sites in 19 states were sampled; during 1971, 45 sites
in 27 states and the island of Bimini in the Bahamas were sampled. The
sampling system consisted of a fiberglass cloth filter and an ethylene
glycol trap through which air was drawn at a constant rate by a vacuum
pump. Thus, both particulate matter and vapors were collected. Analysis
was by electron—capture gas chromatography. Several problems inherent
in this study became apparent at its conclusion (Lewis, 1976). Samples
from stations located 5 miles apart had been pooled, even though one was
representative of an urban community and the other of an agricultural area.
Due to apparatus malfunction, airflow measurements were discovered to be
inaccurate. Interfering compounds were present in the gas chromatograms,
and confirmation of pesticide identity by mass spectrometry was not
obtained. Therefore, both qualitative and quantitative estimates of
ambient atmospheric concentrations, as determined by these studies, are
generally unreliable. Nevertheless, these studies represent the only
broad survey of ambient endrin concentrations, and the results are worthy
of discussion. We can assume a 50% probability that the compound observed
was, in fact, endrin. The chances are even less that the concentrations
are correct (Lewis, 1976). The levels of endrin detected at those sites
where it was observed are presented in Table 7.7.
Table 7.7. Endrin residues in ambient air 1970 and 1971
Site (by state)
Max endrin (ng/m 3 )
Mm endrin (ng/m 3 )
1.970
Alabama
0.9
0.6
Arkansas
8.8
0.3
Kentucky
3.1
1.5
South Dakota
1.8
0.5
Tennessee a
2.2
0.6
Tennessee b
2.2
0.4
1971
Arkansas
7.7
1.6
Colorado
25.6
0.2
Mississippi
0.9
a
Montana
2.9
a
Ohio
1.7
0.2
Oklahoma
4.6
0.3
Tennessee
12.4
0.2
aN O minimum value reported.
Source: modified from U.S. EPA, 1970b, l97la.
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182
Endrin was detected in 6 out of 30 and 7 out of 45 sampling sites
in 1970 and 1971 respectively. The maximum concentration reported in
1970 was 8.8 nglm 3 in Little Rock, Arkansas; the maximum in 1971 was
25.6 ng/m 3 in Greeley, Colorado. Maximum levels for each year were reported
during the pesticide use season as expected.
In another study (Stanley et al., 1971), air was sampled at nine
locations in the United States and analyzed in a similar fashion for
19 pesticides and their metabolites. Sites were representative of both
urban and agricultural areas, and levels were found to be much lower in
the urban samples. Endrin was found at only one site, Stoneville,
Mississippi, in 25 out of 98 samples collected. Stoneville is representa-
tive of large, southern agricultural areas. The highest concentration
reported was 58.5 ng/m 3 . Arthur et al. (1976) collected weekly air
samples at Stoneville, using a similar technique, and found average yearly
atmospheric levels of endrin (ng/m 3 ) as follows: for 1972, 3.2; for
1973, 2.3; and for 1974, 5.3.
In 1972 an eight—station experimental airborne pesticide monitoring
network was established by the Syracuse University Research Corporation.
Sampling was conducted over a 12—month period at each of the eight sites,
using an experimental air sampling device. The device collected particu—
lates on a fiberglass filter and adsorbed vapors onto cottonseed—oil—coated
glass beads. Samples were analyzed for the presence of 14 pesticides by
electron—capture gas chromatography. The limit of detection for endrin
was 0.29 ng/m 3 . No endrin was detected in any sample from any sampling
site. Sites included six locations in upstate New York; Winter Haven,
Florida; and Lubbock, Texas (Compton et al., 1972).
During this past year a small pilot program for monitoring pesticides
in air was established by the National Human Monitoring Program for Pesti-
cides of the United States Environmental Protection Agency. From April
through July 1975, 15 air samples were collected and analyzed from suburban
sites in Miami, Florida; Jackson, Mississippi; and Fort Collins, Colorado.
Analysis was by electron—capture gas chromatography. Only one sample
contained endrin at a concentration of 0.5 ng/m 3 ; this sample was collected
at the Jackson, Mississippi, site (Kutz et al., 1976).
The final study to be reported was designed to measure the extent of
air contamination in the homes of occupationally exposed men (Tessori and
Spencer, 1971). Inside and outside air was monitored monthly for one year
at the homes of 12 families in which the head of the household worked
directly with pesticides. The collection device, installed for five days
each month, consisted of a nylon chiffon screen saturated with ethylene
glycol and suspended in a wooden frame. The screen trapped both particu—
lates and vapors but was not designed to measure concentrations in any
given volume of air. After each five—day sampling period, the screen was
removed, extracted, and analyzed for pesticides by electron—capture gas
chromatography. The results for two groups of exposed workers (five
farmers and seven formulators) are presented in Table 7.8.
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183
Table 7.8. Concentrations (pg/rn 2 ) of endrin collected
on ethylene—glycol—saturated screens
Statistic
Farmers
(5)
Formulators (7)
Indoor
air
Outdoor
air
Indoor air
Outdoor
air
N
38
37
52
54
F_
15
24
30
36
NX
0.17
0.13
0.50
0.13
FX
0.43
0.19
0.86
0.20
Range
0.07—1.
88
0.04—0.53
0.24—2.69
0.04—1.70
Note: N = number of samples taken,
F = frequency of endrin found out of N,
NX = numerical mean,
FX = frequency mean.
Source: J. D. Tessari and D. L. Spencer, J. Assoc. Off. Anal.
Chern. 54(6): 1376—1382 (1971). Copyright 1971 Association of Official
Analytical Chemists.
Outdoor air samples exhibited similar degrees of contamination for
both groups, although the highest collected level outside of a formulator’s
home (1.70 pg/rn 2 ) was over three times as high as the outside of a farmer’s
home (0.53 pg/m 2 ). Since the sample locations were widely distributed
throughout the study area (Greeley, Colorado), it appears likely that
these levels prevail throughout the entire area and are indicative of the
ambient levels to which the general population is exposed. Analyses of
indoor samples revealed that formulators bring home two to three times as
much endrin on their person as do farmers. Consequently, the families of
pesticide formulators are exposed to somewhat higher ambient concentrations
than are either the families of farmers or the general population.
Although available data are far too limited to yield definite
conclusions concerning the ambient levels of endrin in the atmosphere,
certain trends do appear probable.
1. Endrin concentrations are highest in the atmosphere over
agricultural areas and probably reach their peak levels during the
pesticide use season.
2. Of all urban communities, those surrounded by farmlands run the
highest risk of atmospheric contamination. Endrin adsorbed to particulates
could not be detected in the air over representative communities, but may
perhaps be present at very low concentrations in the vapor phase. Urban
communities far removed from agricultural areas are unlikely to experience
significant contamination.
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184
3. The homes of occupationally exposed workers have higher levels
of atmospheric contamination than do those of the general population.
Formulators appear to bring home more endrin than do farmers.
4. In the few studies reported to date, no levels approaching the
threshold limit value of 100 iig/m 3 adopted by the American Conference of
Governmental Industrial Hygienists for 1971 have been detected (Yobs et al.,
1972).
More extensive monitoring data, using confirmatory techniques such as
mass spectrometry, are needed before further conclusions may be drawn
concerning the concentration, distribution, and residence time of endrin
in the atmosphere.
73.4 Mechanisms for Removal of Endrin from the Atmosphere
The majority of organochiorine insecticides released to the atmosphere
are eventually returned to the earth’s surface. Pesticides adsorbed to
large, heavy particulates usually fall out close to their point of origin,
while those associated with the smaller, lighter dusts or present as vapors
may travel long distances before redoposition takes place. Cleansing of
the atmosphere may occur as a result of particle fallout or washout of both
particles and vapors during precipitation. Rainwater samples were collected
continuously at seven widely distributed sites in the British Isles from
August 1966 through July 1967 and analyzed for the presence of organo—
chlorine insecticides (Tarrant and Tatton, 1968). Even though the sites
were chosen so as to represent a variety of locations from urban to remote,
the average total pesticide concentrations in annual rainfall were sur-
prisingly similar (range, 104 to 229 ppt). Assuming an average pesticide
concentration of 170 ppt in rainfall throughout the entire British Isles,
it may be calculated that, in this area, 1 in. of rainfall would deposit
1 ton of pesticide. Since the average annual rainfall in the British
Isles exceeds 40 in., approximately 40 tons of pesticide is deposited
annually by this route. This value is four times greater than the quantity
of pesticide annually dumped into the Gulf of Mexico by the Mississippi
River (Frost, 1969). Endrin was not detected in any of the samples;
however, endrin is not commonly applied in Britain, and there is every
reason to expect that endrin would be detected in the rainfall of countries
(such as the United States) which use this compound extensively.
The photochemical isomerization of endrin is a well—established
phenomenon, and a variety of products, all considerably less toxic to
mammals than is the parent compound, are formed (Klein and Korte, 1967;
Soto and Deichmann, 1967; Pliinmer, 1971).
Due to the difficulty of simulating atmospheric conditions in the
laboratory, all studies have been conducted with endrin either in the
solid state or dissolved in organic solvents. It is believed, however,
that similar reactions occur in the vapor phase and when endrin is adsorbed
to airborne particulates. A great deal of work is needed in the area of
atmospheric photodecomposition in order to assess the extent to which
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185
this process contributes to the removal of endrin from the atmosphere.
For a more in—depth discussion of endrin photodecomposition, refer to
Sect. 2.3 and 7.5.
Other pathways for removal of endrin from the atmosphere include
inhalation by animals and birds and absorption and metabolism by airborne
microbes. Aside from the obvious undesirability of these mechanisms, their
contribution to cleansing the air is, at best, minimal.
From the information available, it may be concluded that contamination
of the atmosphere by endrin per se at any given moment is a transient
occurrence, and that the major hazard involved in release of endrin to
the atmosphere is the subsequent contamination of the hydrosphere and
lithosphere. This situation results from the fact that the established
mechanisms for removal of endrin from the atmosphere do not remove endrin
from the environment, but rather relocate endrin to other environmental
compartments. Some dissipation via photodecomposition is possible;
however, no real evidence that such transformations actually take place
is available.
7.4 ENDRIN IN THE HYDROSPHERE
7.4.1 Introduction
The pathways for the entrance of endrin into the hydrosphere are
numerous. They include: surface runoff following application of endrin
to soil and crops, runoff from endrin—coated seeds, contaminated effluents
from pesticide manufacturing and formulating plants, careless aerial
application, dumping of unused pesticide into waterways, cleaning spray
equipment in rivers and lakes, and contaminated rainout and fallout. Some
of these routes may be controlled by voluntary action or legislation.
Others are inevitable consequences of application of the pesticide.
Considerable progress has been made in recent years in the development
of suitable technology for assessing the extent of hydrospheric contamina-
tion by organochlorine insecticide. The older carbon adsorption sampling
systems were not very accurate, since quantitative retention of pesticide
was not guaranteed (Lauer et al., 1966). In addition, due to the limited
sensitivity of the analytical methods available prior to the later 1960s,
large sample volumes were required. With the development of
electron—capture gas chrotnatographic techniques for organochiorine
compounds, ppt quantities in water could be detected, and much smaller
sampling volumes were required. At present, 1—gal or l—qt grab samples
are sufficient for accurate analyses, and extensive monitoring is easily
achieved. When levels of contamination are expected to approach the limits
of sensitivity, larger grab samples may be collected and concentrated to
an appropriate volume. The state of the art is therefore far more advanced
in the case of hydrospheric monitoring than in the atmospheric counterpart,
where complicated sampling equipment must be installed individually at
each site. The large collection of monitoring data available for
pesticides in water testifies to this fact.
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186
Several points must be considered when interpreting the monitoring
data for endrin, for it is virtually insoluble in water (Pfister et al.,
1969). The failure to detect endrin in filtered water samples is therefore
not indicative of the absence of hydrospheric contamination. Endrin is
carried in water as a suspension, as an emulsion, or, most commonly,
adsorbed onto soil and sediment particles. Thus, suspended particulates
as well as water must be analyzed. The old carbon adsorption methods
filtered out particulates and therefore led to minimum estimates of con-
tamination. With the new grab—sample techniques, both water and particulate
matter are analyzed.
If both water and suspended particulate are endrin free, it is still
not safe to conclude that the hydrosphere is free of the pesticide. Recent
contamination may be ruled out; however, previous episodes of contamination
will have left their more persistant mark on the bottom sediment. It is
therefore important that bottom deposits also be monitored. While less of
a threat to life, contamination of bottom deposits with endrin implies a
chronic source of contamination throughout the hydrosphere.
In general, the worst effects of contamination in a given body of
water are observed immediately following the episode of pollution. Due
to such processes as codistillation and sedimentation, a large proportion
of the endrin is either transferred somewhere else or rendered relatively
harmless. However, entire populations of birds and fish may be destroyed
during the short period of acute contamination, and years may be required
for the ecosystem to return to normal (Breldenbach et al., 1967; Rowe et al.,
1971; Anonymous, l975c).
7.4.2 Sources of Endrin in the Hydrosphere and Sediment
7.4.2.1 Surface runoff following application . The major source of
endrin in rivers and other freshwater bodies is surface runoff from fields
and crops following application (U.S. EPA, 1972; Chesters and Konrad,
1971). The factors which affect the extent of surface runoff contamination
are numerous and complex. Included among these are: the rate of applica-
tion of the pesticide, the runoff volume, the amount of intensity of pre-
cipitation, irrigation practices, topographic relief, soil permeability,
soil organic content, and the degree of vegetative cover. Where intense
precipitation falls on soil of low permeability and low organic content
(e.g., soils with high clay content), runoff usually occurs. Steep
topography accentuates runoff losses, since soil erosion Is more severe,
water infiltration is reduced, and, as a result, movement of soil particles
is increased (Working Group on Pesticides, 1970). Conditions opposite to
these would be unfavorable for excess surface runoff, and loss of pesticide
by this route would be comparatively small.
Studies were conducted in 1961 and 1964 to determine the modes,
extent, and duration of surface water contamination by endrin from sugarcane
fields near Franklin, Louisiana (Lauer et al., 1966). From the end of
June through August 1961, the Bayou Yokely basin, containing 3300 acres
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187
of sugarcane, was treated with almost 2000 lb of endrin. A carbon adsorp-
tion unit was operated continuously at the downstream end of Bayou Yokely
from late April through November 1961. Of 18 samples collected by this
unit, six contained endrin at concentrations ranging from 1 to 360 ppt,
with a median concentration of 100 ppt. The occurrence of these residues
in relation to endrin usage, rainfall, and runoff is shown in Fig. 7.3.
Detectable (>1 ppt) quantities of endrin were recovered from Bayou Yokely
water during the 90—day period July 8 to October 5, 1961, commencing
shortly after the first of three sets of endrin applications in the basin
and extending until shortly after the final set. The first and third sets,
which totaled 500 and 800 lb of technical endrin, respectively, were
followed by high levels of endrin recovery from the stream. Frequent
intense rains and runoff occurred throughout both of these sampling periods.
ORNL-DWG 79-8954
.
L
L 1
II
JUN JUL AUG
(+ (+) (—) (—) C .— .) —
I I
SEPT OCT NOV
Fig. 7.3. Results from endrin pollution study of the Bayou Yokely
watershed in Louisiana during 1961. Lower panel: pesticide recoveries
from Bayou Yokely water, (+) sampled; endrin recovery at level of 1 ppt,
(—) sampled; endrin, if present, was recovered at less than 1 ppt.
Source: G. J. Lauer et al., Trans. Am. Fish. Soc. 95(3): 310—316
(1966). Copyright 1966 American Fisheries Society.
-J
-J
2
4
4
2
0
400
— 300
w -
400
0
600
400
2 .D
LU 200
0
1200
800
-uJ .
>0.
00.
400
0
APR MAY
II 11111 ii
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188
Six hundred pounds of endrin was applied during the second set of treat—
ments. In this case, however, recoveries decreased during two subsequent
sampling periods. Few intense rains and little runoff occurred during
these sampling periods.
In 1964, both carbon adsorption samples and 1—gal grab samples were
collected from each of three stations along Bayou Yokely at given intervals
following the endrin application season. The maximum recoveries from grab
samples and carbon adsorption samples taken from the second to the fourth
of September were 820 and 700 ppt respectively. The mean recoveries from
the three stations on those dates were 440 ppt for grab samples and 530 ppt
for carbon adsorption samples. Recoveries of endrin still averaged 30
and 40 ppt for the two methods three months following the final application
to the fields. Although less endrin (1200 lb) was used in the basin in 1964
than in 1961, larger recoveries over a longer period of time were observed.
These results probably reflect both the improved sampling methods available
at the time of the later study and the occurrence of more rain during
October and November 1964 as compared with 1961. However, the pattern of
surface water contamination remained the same in both studies. Maximum
recoveries of endrin were observed immediately after the initial rains and
runoff following application; but recoveries rapidly decreased thereafter.
Sediment and soil samples were also collected during the 1964 study.
Endrin recovery from sediment was 165 ppb immediately following the applica-
tion season in early September. Although concentrations decreased
significantly during the subsequent three—month period, samples still
contained an average of 70 ppb in late November, when the study was
discontinued. Difficulties in obtaining representative samples of soil
resulted in highly variable values for endrin contamination. However,
concentrations averaging 1450 ppb were detected in soil at the conclusion
of the study. The persistence of endrin in soil over a period of months
implies that contamination of surface waters as a result of runoff
probably takes place long after the application season is over.
Several studies have been conducted which deal specifically with the
relationship between rainfall and runoff contamination. In July 1967 and
1968, endrin was surface—applied to sugarcane plots in Louisiana at the
rate of 0.337 kg/ha, and surface runoff was sampled following each
subsequent precipitation event (Willis and Hamilton, 1973). Rainfall,
runoff volume, runoff contamination, and endrin loss data are presented
in Table 7.9; concentrations remaining in soil are presented in Table 7.10.
In 1967 the amount of rainfall varied considerably, ranging from 0.53 to
11.43 cm. Runoff volumes varied with the amount of rainfall but were also
influenced by other factors such as rainfall intensity and soil surface
conditions. The highest endrin concentration (1.23 ppb) occurred with the
first runoff event three days following application. Since the weather
conditions remained uncooperative during the immediate posttreatment
period, a sprinkler system was employed to simulate rainfall on the first
two sampling dates. It is believed that had the runoff occurring on day 3
resulted from 2.54 cm of natural rainfall, the intensity and impact energy
would have been greater, and endrin loss in runoff would have been higher.
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189
Date of runoff
August 2, 1967
August 14, 1967
August 27, 1967
September 11, 1967
September 12, 1967
September 27, 1967
December 10, 1967
December 27, 1967
January 2, 1968
January 9, 1968
February 19, 1968
March 4, 1968
March 22, 1968
May 17, 1968
July 19, 1968
July 22, 1968
Rainfall
(cm)
Endrin applied
2.
•
11.43
1.27
2.21
0.53
7.09
2.01
4.19
0.81
2.39
1.50
4.52
3.63
Endrin applied on
5.08
3.51
Lost
(mg / ha)
66.05
57.0
94.49
15.28
18.25
3.11
43.68
10.09
30.02
2.34
3.65
5.97
5.94
346.8
65.5
Table 7.9. Rainfall, runoff,
sugarcane plots following
and endrin loss in runoff from
a single endrin application
Runoff Conc. in
volume runoffC
(m 3 /plot) (ppb)
on July 31, 1967
0.24 0.37—2.73
1.23
0.48 0.20—1.34
0.53
1.40 0.13—0.53
0.30
0.17 0.10—1.03
0.40
0.27 0.13—0.51
0.30
0.03 0.09—1.12
0.53
1.39 0.07—0.18
0.14
0.24 0.10—0.44
0.19
0.64 0.06—0.42
0.21
0.09 0.04—0.19
0.11
0.08 0.12—0.25
0.20
0.16 0.08—0.27
0.17
0.44 0.01—0.12
0.06
0.31 0.00
July 13, 1968
0.54 0.94—5.02
2.85
0.15 0.63—3.00
1.95
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190
Table 7.9 (continued)
Date
of runoff
Rainfall
(cm)
Runoff
volume
(m 3 /plot)
Conc. in
runoffa
(ppb)
Lost
(mg/ha)
August
5,
1968
3.15
0.06
0.15—2.88
17.0
1.19
August
13,
1968
9.32
0.57
0.75—4.09
1.56
199.5
aData from six plots. The first two numbers refer to the minimum
and maximum concentration; the lower number is the mean concentration.
bSprinkler irrigation used to simulate rainfall.
Source: G. H. Willis and R. A. Hamilton, J. Environ. Qual.
2(4): 463—466 (1973). Copyright 1973 American Society of
Agronomy.
Table 7.10. Concentration of endrin in soil
Date
Concentration
at depth
(ppb)
of
Application
Sample
0—15 cm
15—30 cm
July 31, 1967
January 10, 1968
7.5—9.0
8.1
0.0
July 9, 1968
1.2—6.5
3.3
0.6—1.2
0.8
July 13, 1968
July 29, 1968
34.2—124.9
76.3
2.1—13.0
5.2
August 22, 1968
17.4—51.8
42.9
2.2—5.0
3.4
aD from six plots. The first two numbers refer to the minimum
and maximum concentration; the lower number is the mean concentration.
Source: G. H. Willis and R. A. Hamilton, J. Environ. Qual.
2(4): 463—466 (1973). Copyright 1973 American Society of
Agronomy.
-------
191
Endrin concentrations decreased to 0.53 ppb or less during subsequent
runoff events, and no endrin (<0.01 ppb) was detectable ten months after
application.
Endrin losses were greatest in the first month following application,
although a significant loss occurred in mid—December during a storm that
resulted in a large volume of runoff. Accumulated losses in runoff during
the ten months following a single application amounted to only 0.1% of
that applied.
Only four runoff events occurred between the endrin application in
July 1968 and harvest in November. Endrin concentrations ranged from
1.19 to 2.85 ppb, with an accumulated loss of 0.2% of that applied. As
in 1967, runoff contamination was highest immediately after application
and decreased with time. However, a large runoff event occurring one
month after treatment resulted in considerable loss.
In 1969, as part of the same study, Willis and Hamilton investigated
the effect of the time interval between application and runoff on the
amount of endrin found in the initial runoff and soil. A sprinkler
irrigation system was used once again to simulate rainfall and initiate
runoff 24 or 72 hr after application. The results are presented in
Table 7.11. Mean concentrations of endrin in runoff water when rainfall
occurred 24 hr after application were more than twice those observed when
rainfall was postponed for 72 hr. The lower concentrations after 72 hr
may have been due to the smaller amounts of endrin remaining at the soil
surface as a result of volatilization. The lower endrin concentrations
associated with the 72—hr time interval between application and rainfall
were also reflected in soil concentrations 5.5 months following application.
Approximately 43 and 17% of the applied endrin were present in soil
receiving rainfall after 24 and 72 hr respectively.
Table 7.11. Effect of time interval between endrin applica ion
and rainfalla on endrin concentration in runoff and soil
Time between application
and rainfall (hr)
Concentration
(ppb)
RunoffC
Soil
24
0.00—2.12
1.06
39.0—83.4
64.9
72
0.07—0.84
0.46
11.3—55.9
24.8
asprinkler irrigation used to simulate rainfall.
samples (0 to 15 cm) collected 5.5 months after application.
CData from six plots. The first two numbers refer to the minimum
and maximum concentration; the lower number is the mean concentration.
Source: C. H. Willis and R. A. Hamilton, J. Environ. Qual.
2(4): 463—466 (1973). Copyright 1973 American Society of Agronomy.
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192
The effect of rainfall upon endrin contamination of the surface waters
of Greenville, Mississippi, was studied by Iverson (1967). The study area
consisted of 300 acres of cultivated land and contained a slough in which
the surface runoff from the fields was collected. During 1965, when the
study was conducted, a cotten field within the 300—acre tract received
weekly applications of endrin from July 14 through September 3. Water
from the slough was sampled on 19 different occasions between April 1965
and February 1966, and samples of runoff water were obtained whenever
precipitation caused water to move rapidly and in quantity from the treated
areas. The dates on which endrin was detected in the slough or runoff
and the concentrations present on those dates are summarized in Table 7.12.
Table 7.12. Concentration of endrin in a drainage slough in
Greenville, Mississippi, and in surface runoff
Slough
Runoff
Date
ppb
Date
ppb
Apr. 20
0.18
May 22
0.96
May 17
0.72
May 27
1.37
Aug. 9
0.09
Sept.
9
0.12
Aug. 23
0.72
Sept.
21
0.21
Sept. 8
Feb. 21
0.07
1.49
Jan.la
Feb.J
0.72
1.74
3.34
(ZN 0 exact dates given.
Source: L. C. K. Iverson, Agriculture and the Quality of Our
Environment (1967). Copyright 1967 American Association for the
Advancement of Science.
Measurable residues of endrin were detected on only six of the sampling
dates. The highest level (1.49 ppb) occurred In late February, during
which time, heavy rains caused flooding in the study area, and at the peak
residue period, 6 in. fell within 11 hr. Samples of runoff contained up
to 3.34 ppb endrin.
The surface water contamination resulting from irrigation and rainfall
following foliar application of endrin to cotton was studied by Sparr
et al. (1966). A 5—acre cotton field in Kelso, Arkansas, was sprayed
with 2 lb of endrin on three successive occasions. Irrigation water flowed
through a furrow within the plot to a drainage ditch, which was sampled as
it left the field. The ditch ended in a check dam, where the water was
held for reuse. It was estimated that the water was diluted 20—fold at
the dam site. During irrigation, water samples were collected before
and after spraying from the irrigation furrow and the drainage ditch at
the check dam. Rain runoff samples were taken from the end of a furrow
during a rain storm. The results of analysis for endrin are presented
in Table 7.13.
-------
Table 7.13. Residues in water from spraying a cotton field
with 0.4 lb/acre endrin
No. of
sprays
Interval
last spray
from
(days)
Endrin conc
(ppb)
Input irrigation H 2 0
Used irrigation H 2 0 from furrowsa
Input irrigation H 2 0
Used irrigation H 2 0 from furrowsa
Rain runoff, 1.15 in.
H 2 0 held by check dam 5/8 mile from
plot
1
1
2
2
3
1
1
1
1
1
3
3
40
7
2
3
0.08
0.36
0.12
0.11
0.05
0.66
0.006
0.008
a
1/4 mile long.
Source: B. I. Sparr et al., Agriculture and the Quality of Our Environment (1967).
Copyright 1967 American Association for the Advancement of Science.
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194
A 4.5—fold increase in endrin concentration (0.08 ppb to 0.36 ppb)
was observed in the irrigation water when sampled one day following the
initial application. About five—sixths of the endrin in this sample
(0.30 ppb) remained on a glass filter, indicating that it was adsorbed to
soil particles. Three days after the second application, the input
irrigation water contained 0.12 ppb endrin. No increase in concentration
was observed following irrigation on the same day. In this case, however,
only one—tenth of the endrin was retained on a filter. It may be concluded
that more soil was dislodged during the first irrigation than during
the second, and that contamination of surface runoff is dependent to a
large extent upon the degree of soil errosion. Forty days after the final
spraying, the endrin concentration in the used irrigation water was only
0.05 ppb. The concentration of endrin in water held by the check dam
was less than 10 ppt, significantly less than could be accounted for by
the 20—fold dilution. No endrin was detected in the mud from the check
dam, although the analytical sensitivity was only 0.01 ppm. Whether the
observed 45—fold dilution was due to adsorption onto sediment or to loss
by evaporation is not certain. However, these concentrations are believed
to be representative of those which may enter streams from Cotton fields
contiguous to them.
A 1.15—in, rainfall which occurred seven days after the first
application gave rise to the highest water concentration observed In these
studies (0.66 ppb). This high concentration may have resulted from the
washing of endrin off the foliage, which probably held most of the
applied pesticide. This conclusion was supported by soil residue data,
which indicated that only 10% or less of the applied endrin (0.04 to
0.02 ppb) was lost from the foliar canopy at the time of application. If
all of the endrin had reached the ground, the concentration in soil would
have been 0.4 ppb.
In June 1963, the Cedar Bluff Irrigation District was created along
the Smokey Hill River from Cedar Bluff Dam eastward in central Kansas.
This area was transformed from one of dry—land farming practices with
little insecticide usage to land with intensified crop production requiring
the use of significant quantities of pesticides. The extent of surface—
water and groundwater contamination by endrin as a result of this trans-
formation was investigated in a four—year study conducted from 1965 through
1969 (Knutson et al., 1971). A cornfield of approximately 3.25 acres was
sprayed with 0.3 to 0.4 lb/acre endrin annually for the duration of the
study. Foliage samples were collected soon after application and at harvest
time along with grain samples. Water and silt samples were taken on the
Smokey Hill River just above and below where drainage from the experi-
mental field occurred, in the Cedar Bluff Reservoir near the dam, and
where water entered the test field from the irrigation canal. Groundwater
samples and samples of surface runoff were also collected. Foliage samples
collected soon after spraying showed endrin residues of from 0.9 to
6 ppm over the four—year period. Endrin residues persisted in the foliage
at harvest time (range, 0.06 to 2.43 ppm); however, none were detected
in the corn grain. No residues were detected in surface runoff or ground-
water at any time, or in reservoir and river silt or water in 1969. From
1966 through 1968, endrin was detected once in reservoir water at 13 ppt
-------
195
and twice in river water at 3 and 10 ppt. The absence of rainfall probably
accounted for the persistance of large quantities of endrin on the foliage
with little transference to the soil. Thus, the surface waters remained
relatively free of pesticide.
Examples of extensive contamination of surface waters from
pesticide—laden irrigation runoff are also available. One such example
is the situation existing at the Tule Lake and Lower Klamath Lake National
Wildlife Refuge in northern California during the early l960s. The deaths
of unusually large numbers of fish—eating birds were attributed to the
use of pesticides on agricultural lands within the surrounding refuge.
Drainage from these lands carried the pesticides through the extensive
irrigation system serving the refuge. This situation prompted an investi-
gation of the occurrence of chlorinated hydrocarbon insecticides at various
locations within the Lost River system draining into and out of the refuge
(Godsil and Johnson, 1968). Monitoring of water, suspended material, and
various organisms (both free and caged) was conducted from April 1965
through January 1967. Endrin predominated in all analytical results due
to its abundant usage (14,000 lb in 1966) and persistence in drainage
water following application. Data for endrin contamination were reported
for a representative location known as drainage pump B, which discharged
into the Tule Lake sump. Water used throughout the entire irrigation
system eventually passed through pump B, and model studies indicated
that this water could be recycled in irrigated lands up to 5.2 times.
Consequently, the highest levels of endrin relative to those found at
other stations were observed there. The occurrence of endrin in the
water and biota of the Tule Lake sump at pump B is shown in Fig. 7.4, and
the data for water and organism analyses are presented in Table 7.14. Most
striking is the increase and subsequent decrease of endrin in the water and
all levels of biota during the main growing season from May through September.
During the two years shown (1965 and 1966), concentrations in water
increased from below the levels of detection in April to peaks of 0.1
and 0.069 ppb, respectively, at the height of the growing season. The
patterns of endrin contamination in captive fish paralleled those in
water, with maximum accumulations of 97 ppb in 1965 and 107 ppb in 1966.
Concentrations decreased once again to below the levels of detection in
late fall and remained so throughout the winter. The most important
conclusion is that short—term contamination of an aquatic environment
with endrin does not result in permanent residual concentrations in water
or biota. However, sediment samples were not analyzed in this study, and
accumulation of pesticides in sediment, and their consequent low—level
but continuous release, is certainly possible.
7.4.2.2 Runoff from endrin—coated seeds . Endrin is often applied
to seeds prior to seeding operations in order to protect them from
decimation by rodents. Loss of endrin from these seeds during runoff
following precipitation or irrigation may result in contamination of
neighboring streams. Samples of Douglas fir seed, coated with 1 lb of
active endrin per 100 lb of seed and soaked in distilled water for varying
lengths of time, rapidly lost endrin during the first hour (Marston
et al., 1969). For the remainder of the 32—day experiment, endrin con-
tinued to be removed at a fairly constant but greatly reduced rate. The
-------
.L O
ORNL—DWG 79—8955
O VASCULAR PLANTS
• FILAMENTOUS ALGAE
O SUSPENDED MATERIAL
• WATER
• CAGED LARGE MOUTH BASS
WILD CHUBS
O CAGED CLAMS
6 WILD CLAMS
0.100
0.50
.0
a
a
0.20
4
O.f 0
0.5
Fig. 7.4. Occurrence of endrin in water and biota at pump B.
Source: Godsil and Johnson, 1968.
actual losses for a typical sample are presented in Table 7.15 and in
Fig. 7.5, where a linear regression curve is also shown. The deviations
from linearity observed in Fig. 7.5 were probably due to irregularities
in seed shape and surface area and to differences in the thickness of
the endrin coating. The total amount of endrin recovered, 28.2 ppb,
amounted to approximately l1.3Z of the amount contained in the sample.
In a field experiment using the sane seed, losses were less pronounced.
Grab samples of water from Needle Branch were collected and analyzed for
endrin before, during, and after the aerial application of endrin—coated
200
1o0
50H j
£
20
.0
a
a
4
I-
0
10 —
5—
2
WATER
SENSITIVITY
1963 1966 1967
-------
197
Table 7.14. Pumb B water and biota analyses (residues)
(ppb)
Date Date
Water
collected collected
Suspended
material
4/01/65 4/20/66 1.5
5/14/65 6/22/66 6.0
6/22/65 7/22/66 1.3
7/22/65 8/22/66 57.7
8/11/65 0.100 9/13/66 13.0
8/27/65 0.015 10/26/66 5.3
9/10/65 0.017 11/16/66
10/01/65 0.007 1/06/67 1.5
10/11/65
10/20/ 65 Vascular
11/09/65 plants
1/18/66
2/17/66 6/22/66
3/22/66 7/22/66 1.6
4/26/66 8/22/66 12.2
6/07/66 9/13/66 12.5
6/22/66 9/29/66 4.8
7/06/66 10/20/66 8.0
7/20/66 11/16/66 1.8
7/28/66
8/04/ 66 Algae
8/05/ 66
8/09/66 0.008 4/20/66 2.0
8/11/66 6/22/66
8/18/66 0.023 7/22/66
8/20/66 0.011 8/22/66 22.3
8/22/66 0.021 9/13/66 10.8
8/24/66 0.069
8/26/66 0.057 Chubs
8/29/66 0.056
9/02/66 0.030 8/27/65 198.0
9/07/66 0.007 4/20/66 10.0
9/13/66 0.010 6/22/66 6.0
9/22/66 0.007 7/22/66 4,0
9/29/66 0.010 8/22/66 30.5
10/04/66
10/19/66 0.009 Clams
11/04/66
11/18/66 8/10/65 34.0
11/25/66 0.007 12/28/65 4.0
11/30/66 7/22/66 2.0
12/14/66
1/11/67
2/06/ 67
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198
Table 7.15. Concentrations of endrin in water from samples of
Douglas fir seed soaked for different lengths of time
Solvent
Length of soaking
period (days)
Concentration
(ppb)
Distilled water
1/24
1/8
1/4
1
1
2
3
7
7
14
21
30
32
1.34
2.36
3.65
5.02
2.98
5.22
10.2
4.57
7.26
18.4
20.0
23.2
28.2
pH 4.5—5.0
7
10.1
pH 4.5—5.1
7
10.5
pH 9.5—7.0
7
9.47
pH 9.5—7.0
7
11.2
Source: modified from Marston et al., 1969.
seeds to the Needle Branch watershed. Sampling started 0.5 hr prior to
seeding on January 23, 1967, and continued at increasingly longer intervals
through January 28. Three samples were also taken during a winter frost
freshet that occurred on January 29; the results are presented in
Table 7.16. The total amount of endrin detected in runoff amounted to
1.05 x l0 kg/km 2 or only 0.l25 of that theoretically applied
(0.84 kg/kin 2 ). Ninety—six percent of this amount was lost during the
winter freshet. The remaining 4 was lost during the 2—hr period after
seeding started and probably came from loose powder that rubbed off the
seeds.
In another study (Mann et al., 1971), two lots each of loblolly and
slash pine seeds were coated with an endrin formulation and surface—sown.
One lot of each type of seed had been presoaked for 24 hr prior to treat-
ment in order to approximate the moisture content obtained by cold
stratification, a procedure frequently employed to condition the seed.
Samples were taken from each sublot and analyzed for endrin content
after 0, 15, 30, and 45 days of exposure to natural conditions; the results
are presented in Table 7.17. After the first 15 days, more than 80%
remained on three of the four lots. The soaked slash pine had apparently
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199
ORNL-DWG 79-8956
I I S
• SUBSAMPLE SOAKED IN DISTILLED WATER
£ WATER FOR SOAKING ADJUSTED TO pH 4.5
• WATER FOR SOAKING ADJUSTED TO pH 9.5
.
-o
0.
0.20—
.
a:
I —
z
w
Y=3.9 1+O.74X
o rO.96
1O— •
zz•
OO . 10 20 30
LENGTH OF SOAKING PERIOD (days)
Fig. 7.5. Concentrations of endrin in water from subsamples of
Douglas fir seed soaked for different lengths of time. Source: modified
from Marston et al., 1969.
been coated too heavily (23.6 mg as opposed to an average of 12.6 for the
other three lots) and, due to excess flaking, contained only 58% on the
same sampling date. The small initial losses were attributed to low
rainfall (only 0.16 in. total during that period). After 30 days the
three lots treated correctly contained 60 to 70% of their endrin and had
lost slightly more during this period than during the first 15 days.
Rainfall had been near normal, totaling 2.33 in. Between 30 and 45 days,
above average rainfall occurred (3.36 in.) and resulted in heavy losses
from all four lots. Only 22 to 23% of the endrin remained regardless
of how much had originally been applied. Both studies make obvious the
importance of rainfall in determining the extent of endrin loss from
treated seeds.
7.4.2.3 Contaminated industrial effluents . Another route of endrin
into fresh waters, of significance in certain localities, is the release
of contaminated effluents from pesticide manufacturing or formulating
plants (Tabor, 1965; Abbott et al., 1966; Barthel et al., 1969; Eichelberger
and Lichtenberg, 1971). Studies of pesticide residues in sediments of the
lower Mississippi and its tributaries conducted in 1964 and again in 1966
revealed one major area of endrin contamination — that associated with a
-------
Table 7.16. Endrin analysis of water samples, Needle Branch Watershed, January 23—29, 1967
aThat no results are given for the samples taken between the one at 5 PM on January 23,
the one at 12:15 AN on January 29, .1967, indIcates that no endrin was detected in any of the
taken between these two 0 entries.
Sampling
time
Instantaneous
concentration
(pg/liter)
Average
concentration
(pg/liter)
Streamf low
(liters per
square mile)
Weight of endrin
pg per
square mile
lb per
square mile
1/23/67
2:30PM
0
0
3:00
0
0
3:15
0.04
0.02
340,882
6,818
0.00002
3:30
3:45
4:00
4:15
0.10
0.04
0.04
0.04
0.07
0.07
0.04
0.04
340,882
340,882
340,882
340,882
23,862
23,862
13,635
13,635
0.00005
0.00005
0.00003
0.00003
4:30
4:45
5:00
0.04
0.04
0 2
0.04
0.04
0.02
334,812
328,741
328,741
13,392
13,150
6,575
0.00003
0.00003
0.00001
1/29/67
12:15
AN
0 a
0
10:30
AN
0.04
0.02
51,271,481
1,025,430
0.00226
11:15
PM
0
0.02
76,446,331
1,528,927
0.00337
Total
0.00588
t’ .)
0
0
1967, and
samples
Source: Marston et al., 1969.
-------
201
Table 7.17. Endrin remaining on 200 repellent—coated
seeds after different periods of exposure
Days of
exposure
Loblolly
Slash
Dry
Soaked
Dry
Soaked
(mg)
(%)
(mg) (%)
(mg) (%)
(mg)
(%)
0
10.5
10.3
17.1
23.6
15
8.8
83.8
9.3 90.3
13.8
80.7
13.7 58.1
30
7.0
67.7
7.2 69.9
10.2
59.7
9.6 40.7
45
3.0
28.6
4.0 38.8
3.8
22.2
6.1 25.8
Source: Mann et al., 1971.
pesticide manufacturing operation in the Memphis Wolf River—Cypress Creek
complex (Barthel et al., 1969). No endrin was found in bottom sediments
from any of the other Mississippi River tributaries or from any of the
11 Mississippi River sampling sites investigated. In 1964, endrin was
found in Cypress Creek at concentrations of 824, 12,800, and 172 ppm in
sediment samples taken upstream, midstream, and downstream, respectively,
from a primary manufacturer of endrin and heptachlor; in 1966, 10,200 ppm
endrin was detected on a spoil bank 20 to 60 ft southwest of that stream.
Old Wolf River was not sampled in 1964, but concentrations of 0.57, 0.26,
and 0.31 ppm endrin in sediment samples taken upstream, midstream, and
downstream, respectively, from the confluence with Cypress Creek were
detected in 1966. A further study of endrin contamination of the Wolf
River—Cypress Creek complex was conducted in April 1967. In this study,
water as well as sediment samples was collected both upstream and down-
stream from (1) the pesticide manufacturing plant and (2) the confluence
of Cypress Creek and Wolf River. Endrin was not detected in water from
Wolf Creek but was present at a concentration of 1.01 ppm in a bank
deposit sample from that stream. Water from Cypress Creek contained from
0.27 to 2.03 ppb endrin and 5.04 to 6.50 ppb endrin ketone. Concentra-
tions of endrin in Cypress Creek sediment ranged from 0.24 to 23.6 ppm,
and endrin ketone was detected at concentrations of 2.08 to 2.80 ppm.
Samples of Cypress Creek dredge spoils contained from 47.4 to 10,676 ppm
endrin and from 24.8 to 3509 ppm endrin ketone, while sediment from a
stream deposition area contained 1.93 to 294 ppm endrin and 4.78 to
96.10 ppm endrin ketone.
Pesticide residues in Wolf River sediment samples upstream from the
confluence with Cypress Creek probably originated from three sources:
(1) Cypress Creek water from the vicinity of the manufacturing plant,
transported upstream by backwater from the Mississippi River; (2) direct
discharge of manufacturing wastes into the Wolf River or into the
Mississippi River with subsequent transport upstream during high stages
-------
202
of the Mississippi River; and (3) seepage from wastes buried in recent
years at a nearby dump.
7.4.2.4 Careless practices . Carelessness in the application and
handling of pesticides represents yet another route of hydrospheric
contamination, and specific cases of undesirable practices resulting in
contamination by endrin have been reported (Lauer et al., 1966; Iverson,
1967; Saunders, 1969). In one study (Lauer et al., 1966) in which pilots
were cautioned to avoid direct contamination of nearby streams during
aerial spraying (a common source of pesticides in streams bounded by
agricultural lands), a pilot was observed applying endrin immediately
after a heavy rain, when water was running Out of the fields. This
incident undoubtedly contributed to the high concentrations observed in
the drainage basin following application.
Practices such as filling pesticide sprayers at streams, washing
spray equipment in streams, or draining excess spray materials into
drainage facilities have been routinely observed. Saunders (1969)
reported a case in which extensive mortalities occurred among brook
trout and juvenile Atlantic salmon following the cleansing of an endrin—
containing potato sprayer into Mill River, Prince Edward Island. Concen-
trations in the water at the time of the fish kill were not determined.
The burning of insecticide containers, such as paper cartons or sacks,
where ashes can blow or be washed into a stream must also be included among
practices which lead to contamination, although no instance involving endrin
per se has been reported.
7.4.2.5 Contaminated fallout and precipitation . A detailed
discussion of the pathways by which endrin enters the atmosphere was
presented in Sect. 7.2.2. Loss to the atmosphere does not, however,
represent a mechanism for the dissipation of endrin from the environment,
since the bulk of what is released is eventually returned to the earth’s
surface. As was stated previously, pesticides borne by the wind may
travel long distances, either as vapors or adsorbed to small particulates,
before being redeposited to the hydrosphere and lithosphere as a result
of fallout or rainout. Therefore, areas far removed from agricultural
lands as well as those nearby are subject to contamination.
The difficulties involved in determining to what extent the
contamination of a steam, river, or lake, located in an agricultural
area, is due to airborne pesticides are obvious; other forms of con-
tamination (such as surface runoff), operating simultaneously, interfere
with analyses. However, one can be reasonably certain that aerial drift
following spraying operations, wind—borne transport of pesticide—laden
dusts, and rainout of pesticides vaporized from crops and soils have
contributed significantly to the contamination of freshwater bodies.
While no evidence testifying to the existence of endrin in distant ocean
waters has been reported, the presence of related compounds suggests
that endrin may be transported similar distances by similar mechanisms
(Risebrough et al., 1968; Frost, 1969).
-------
203
River transport represents one possible mechanism. Pesticides
entering rivers from agricultural runoff are subject to codistillation,
biodegradation, and sedimentation prior to reaching the sea. Even so,
an estimated 1.9 x l0 kg of pesticide reaches San Francisco Bay via the
San Joaquin River each year, and l0 kg/year is transported to the Gulf
of Mexico by the Mississippi River (Risebrough et al., 1968). Surface
currents in the ocean, traveling at speeds of up to 100 miles/day, carry
these pesticides to areas far removed from their point of origin. The
Gulf Stream, for instance, is quite capable of moving pesticides from
the coastal areas of the United States to Iceland and the Arctic areas
beyond. However, none of these currents is capable of carrying pesticides
to Antarctica, and the only route of dispersal able to account for the
presence of pesticide residues in the fish and aquatic mammals of
Antarctica is atmospheric transport (Frost, 1969). As discussed in
Sect. 7.2.2, Risebrough et al. (1968) estimated that approximately 600 kg
of dust—borne pesticides was deposited over one particular section of
the Atlantic Ocean in a given year. This value clearly underestimated
the actual amounts of pesticide delivered to the ocean via the atmosphere,
because the method of dust collection used in the study discriminated
against materials carried on particles of less than several microns in
diameter or present as vapors and subject to rainout. Thus the atmosphere
is able to transport significant quantities of pesticides to the open
ocean, where river drainage and ocean currents cannot be invoked to
explain their presence.
7.4.3 Monitoring for Endrin in the Hydrosphere and Sediment
7.4.3.1 Monitoring for endrin in fresh water and sediment . Pollution
surveillance of the surface waters of United States river basins has been
in effect since 1957. From 1957 through 1965, monitoring was conducted
under the auspices of the Federal Water Pollution Control Administration
within the Department of Health, Education, and Welfare. During this
period, approximately 6000 samples were collected at more than 100 stations,
using a carbon adsorption method (CAN). This method permitted large
volumes of water (up to 5000 gal) to be sampled and quantities of con-
taminant, sufficient for detection by the analytical procedures available
at that time, to be recovered. These samples were stored for future
reference following analysis.
The advent of highly sensitive analytical technology for chlorinated
hydrocarbon insecticides (e.g., electron—capture gas chromotography)
rendered possible the analysis of smaller volumes of water. In 1964
and 1965, surveys were performed f or selected pesticides at approximately
100 sites, using bottled l—qt grab samples (Breidenbach et al., 1967).
CAM samples were collected at all sites in 1964 but only at sites in the
upper and lower Mississippi River basins in 1965. The stations selected
for sampling in 1964 and 1965 were predominantly located in areas with
known pesticide usage. On the basis of the 1964 survey, old CAN samples
were chosen for reanalysis so as to obtain a historic review of pesticide
pollution in the surface waters of the United States. The chosen samples
also included those representative of areas experiencing pesticide—related
fish kills. Analysis of CAN sample extracts and grab—sample extracts was
-------
204
by electron—capture gas chromotography; the lowest detectable concentration
was 0.001 pg/liter. Since quantitative adsorption on and desorption from
carbon does not always take place with all organic compounds, and since
the old CAM method filtered out suspended particulates to which the
pesticides may have adsorbed, values from CAM samples must be considered
as minimum.
The results of analyses for endrin in CAM samples (1958 to 1965) and
in grab samples (1964 and 1965) are presented in Table 7.18, and the ten
locations at which the highest levels were observed in grab samples (1964
and 1965) are listed In the first two columns of Table 7.19. The frequency
of occurrence in each year by river basin is sttmm rized in Fig. 7.6.
Examination of the data for combined CAM samples in Table 7.18 and Fig. 7.6
reveals that fluctuations in both concentration and frequency of occurrence
took place during the early years. From 1961 through 1964, the fraction
of samples containing endrin progressively increased until, in 1964, 50%
of all samples tested were contaminated with this pesticide (Fig. 7.6).
Although some degree of contamination was observed at every river
basin studied in at least one year, consistent contamination of a large
percent of the samples occurred only in the lower Mississippi basin. In
addition, the highest concentrations recorded f or CAM samples during the
five consecutive years from 1960 to 1964 were all from this area
(Table 7.18). A comparative of the frequency of occurrence in grab samples
taken in 1964 and 1965 (Fig. 7.6) indicates that the incidence of endrin
contamination decreased in all but one river basin in 1965. The exception
was the Southeast basin, which remained the same (14% contamination in
each year). However, endrin was still present in 60% of the samples
from the lower Mississippi basin, which, for the sixth consecutive year,
had the highest concentration measured (Table 7.18). In a separate study
conducted from July 1964 to July 1965, endrin was detected on three
occasions at a concentration of 10 ppb (10,000 ng/kg) in mud from the
lower Mississippi River (Novak and R.ao, 1965).
During the fall and winter months of 1963, recurrent fish kills took
place in the lower Mississippi, and endrin was identified as the
causative agent (Anonymous, 1964; Breidenbach et al., 1967; Rowe et al.,
1971). The history of endrin contamination in the Mississippi River
main stem from St. Paul, Minnesota, to New Orleans, Louisiana, is
presented in Fig. 7.7. The occurrence of high concentrations at and
below West Memphis from October 1962 through July 1964 is striking.
However, a general decrease in concentration took place beginning in the
sumer of 1964, and no major fish kills were reported on the lower
Mississippi River between 1964 and 1966 (Breidenbach et al., 1967).
From 1966 through 1968, monitoring of surface waters for pesticide
contamination was conducted by the Federal Water Quality Administration
within the U.S. Department of the Interior. ApproxImately 100 stations
were surveyed each year by electron—capture gas chromotographic analysis
of grab—sample extracts (Lichtenberg et al., 1970). Endrin was found
in approximately 23 and 2% of all samples tested in 1966 and 1967
respectively. No endrln was detected in any sample in 1968. The percent
-------
Water year
(Oct. 1—Sept. 30)
Northeast basin
CAM samples
1958
1959
1960
1961
1962
1963
1964
Grab samples
1964
1965
North Atlantic basin
CAM samples
1958
1959
1960
1961
1962
2 0.025
0
Water year
(Oct. 1—Sept. 30)
Southeast basin
CAN samples
1958
1959
1960
1961
1962
1963
1964
Grab samples
1964
1965
Ohio, Tennessee, and
Lake Erie basins
CAM samples
1958
1959
1960
1961
1962
2 :i
1 0
6 1
3 0
3 1
14 0
10 1
7 1
7 1
4 0
4 0
3 0
6 0
5 2
0.001
P
0.001
P
0.015
Table 7.18. Occurrence of positive and presumptive endrin determinations
in carbon adsorption method (1958—1965)
and in grab samples (1964 and 1965)
‘-I
a)
a)
C a ) r4
a))
H
H
8 U)
0 C. )’— ’
C l ) 0..
1 -4
a) a)
I ______
C 1 -4
z _______
1-4
a)
a)) 14J
U)
a)) H
H 4.J
0-. H
8 U) O
C )j 0 C.)’—’
U) 0..
1-1
(1) a)
-
8 8
Z Z
1
0
0
1
1
0
0
0.001
P
0.001
6
5
4
6
7
9
7
7
7
<0.001
2
1 P
1
0
7
1
5
0
10
1
P
P
P
-------
Table 7.18 (continued)
‘
,.
Water year
(Oct. 1—Sept.
30)
U)
C)
,...4
E
C
U)
. ‘
C)
z
ai
4.J
• - i
U)
0
0..
1
C)
.0
E
11
w
ii.j
r-
v- i
.j . ._
o
o
C.)’-’
O
E.r4
4
Water year
(Oct. 1—Sep •
t
30)
U)
I - i
E
C
C / )
-1
C l )
z
C.)
>
.t i
••i
r4
CC
0
0..
I -i
C)
0
z
Q)
IU
c:•.-i
v- i
u—
00
O
Q’ —’
0
Er4
U
1963 9 1 P 1963 11 4 0.012
1964 5 2 P 1964 18 7 P
Grab samples Grab samples
1964 8 3 >0.094 1964 12 4 0.015
1965 8 1 0.018 1965 12 4 0.014
0
Upper Mississippi Missouri River basin
River basin
CAN samples c samples
1958 4 0 1958 4 1 P
1959 2 1 0.013 1959 6 0
1960 4 1 P 1960 6 2 0.004
1961 7 1 0.001 1961 7 2 P
1962 2 0 1962 8 4 0.003
1963 15 11 0.007 1963 8 1 P
1964 12 9 0.004 1964 14 4 0.001
1965 8 0
Grab samples Grab samples
1964 8 5 0.023 1964 11 6 0.026
1965 8 1 0.009 1965 11 3 P
-------
Table 7.18 (continued)
Water year
(Oct. 1—Sept.
30)
U)
a)
E
(
U)
,-l
a)
.
E
Z
a)
>
o
,
)-l
a)
E
Z
‘-S
a)
I 1
a) 4
(
‘_ ‘
E
O
r-4
• H4J
4c j
C .4
Water year
(Oct. 1—Sept.
30)
(
G)
‘—1
E
ai
U)
_1
a)
‘
—
Z
a)
.
H
4 -
•r-1
U)
0
4
‘
—
Z
‘-S
-1
a)
, j
OJr—
( )—. .
o
0 ’ —’
O
. i
CU
CU
>
Western Great Lakes basin Southwest basin
cAN samples CAM samples
1958 1 0 1958 1 0
1959 3 0 1959 0
1960 3 0 1960 0
1961 4 0 1961 0
1962 3 0 1962 1 0
1963 2 0 1963 6 6 0.007
1964 7 2 <0.001 1964 10 6 0.002
Grab samples Grab samples
1964 4 1 0.006 1964 6 5 0.014
1965 4 0 1965 6 0
Lower Mississippi Western Gulf basin
River basin
CAN samples CAM samples
1958 3 3 0.004 1958 4 1 0.008
1959 4 3 0.002 1959 3 1 0.001
1960 3 3 0.064 1960 5 1 0.002
1961 6 2 0.029 1961 4 3 0.008
1962 3 3 0.160 1962 4 4 0.009
1963 12 12 0.214 1963 10 3 0.011
1964 25 74 0.150 1964 7 5 0.004
1965 34 22 0.015
-------
Table 7.18 (continued)
1.1 )-i
4 ) 4)
4) a ii.i
U)
Wateryear w .r1 vI )
Water year
r-1 .1.1
C) —
r4
(Oct. 1—Sept. 30) (Oct. 1—Sept. 30)
E U) o
(4 0 U—’ (4 0 U ’-’
U) U)
I-i O
4) 4) .t-4 4 ) 4)
4cvj
z z z z
Grab samples Grab samples
1964 6 6 0.025 1964 5 2 0.007
1965 5 3 0.110 1965 6 1 0.014
Colorado River basin Pacific Northwest
basin
0
CAN samples CAN samples
1958 0 1958 3 0
1959 0 1959 4 0
1960 1 0 1960 1
1961 0 1961 7 1 P
1962 1 0 1962 5 0
1963 0 H 1963 12 0
1964 2 0 1964 13 1 P
Grab samples Grab samples
1964 7 3 0.012 1964 10 4 0.019
1965 7 1 P 1965 11 0
California, Hawaii, and Combined
Great Basin
CAN samples CAN samples
1958 0 1958 34 8 0.008
1959 0 I 1959 33 5 0.013
•1
-------
Table 7.18 (continued)
‘-1
Q)
14-i
U)
U) U)
(1) O)r-I
Water year — c i — . -.. Water year . -
(Oct. 1—Sept 30)
U)
U)
(Oct. 1—Sept. 30)
U) U)
1 -4 O I 1-1 1-4
C l) C l) 8r4 I C l) U)
1 - .r. _J I -
I E
z Z Z Z
1960 0 1 1960 43 9 0.064
1961 1 0 1961 56 10 0.029
1962 5 0 1962 57 16 0.160
1963 9 1 0.001 1963 117 39 0.214
1964 8 1 P 1964 118 108 0.150
Grab samples Grab samples
0
1964 5 2 0.009 1964 96 44 >0.094
1965 7 1 0.005 1965 99 16 0.116
-I—
P = presumptive. Data are reported as presumptive in instances where the results of chromatography
were highly indicative but did not meet all requirements for positive identification and quantification.
Source: modified from Breidenbach et al., 1967.
-------
Table 7.19. Top ten locations at which highest levels of endrin were observed
Potomac River,
Great Falls, Md.
Rio Grande River,
El Paso, Tex.
Big Horn River,
Hardin, Mont.
Mississippi River,
Vicksburg, Miss.
Connecticut River,
Northfield, Mass.
Red River (North),
Grand Forks, N.D.
Mississippi River,
New Roads, La.
Yellowstone River,
Sidney, Mont.
Columbia River,
Clatskanie, Oreg.
Atchafalaya River,
Morgan City, La.
Location
Hudson River,
Narrows, N.Y.
South Platte River,
Julesburg, Cob.
Savannah River,
Port Wentworth,
Ga.
St. Joseph River,
Denton Harbor,
Mich.
Lake Superior,
Duluth, Minn.
Savannah River,
N. Augusta, S.C.
Bear River,
Preston, Idaho
Clearwater River,
Lewiston, Idaho
Connecticut River,
Northfield, Mass.
Mississippi River,
Delta, La.
____________ 1967
Location
Kansas River,
Lawrence Kan.
Maumee River,
Toledo, Ohio
1964 1965 1966
Location pg/liter pg/liter pg/liter
pg/liter
0.094
Mississippi River,
West Memphis, Ark.
0.116
0.067
Atchafalaya River,
Morgan City, La.
0.019
0.026
Delaware River,
Trenton, N.J.
0.018
0.025
Tombigbee River,
Columbus, Miss.
0.015
0.025
Clinch River,
Kingston, Tenn.
0.015
0.023
Rio Grande River,
Alamosa, Cob.
0.014
0.023
Monongahela River,
Pittsburgh, Pa.
0.014
0.021
Tennessee River,
Lenoir City, Tenn.
0.009
0.019
Red River (North),
Grand Forks, M.D.
0.009
0.018
Mississippi River,
Delta, La.
0.008
0.133
0.086
0.069
0.063
0,031
0.029
0.022
0.022
0.019
0.015
0.014
0.014
0
Source: modified from Lichtenberg et al., 1970.
-------
ORNL—DWG 79-8957
CAM SAMPLES
BASINS
GRAB SAMPLES
100
QL I
100
0
LAKES
MISSOURI RIVER
SOUTHW EST
100
0
NORTHEAST
100
Q
100
0
—
NORTH ATLANTIC
100
0
100
SOUTHEAST
100
Q
100
0
F
OHIO RIVER,
TENNESSEE RIVER,
AND LAKE ERIE
WESTERN GREAT
UPPER MISSISSIPPI
RIVER
LOWER MISSISSIPPI
RIVER
WESTERN GULF
COLORADO RIVER,
CALIFORNIAAND
GREAT BASIN
PACIFIC NORTHWEST
COMBINED
100
. R
0
100
0
100
I
100
I
100
1
I
100
0
100
R
100
i I
0
i .11 100
0
100
0
100
0
100
0
100
0
100
0 — —
1OO —
0 (%J-
IL) (0 (0(0
0 ’ O ) 0)0)
. IL)
tD (0
o_) 0)
100
w
>
I-
a-
U)
w
a:
a-
a:
0
LU
>
I—
U)
0
a-
I-
z
LU
( )
a:
LU
a-
Fig. 7.6. Percent occurrence of endrin in CAM samples, 1958—65,
and in grab samples, 1964—65. Source: modified from Breidenbach et
al., 1967; Lichtenberg et al., 1970.
211
LU
>
a-
U)
LU
a:
a-
a:
0
LU
>
I —
U)
0
a-
I-
z
LU
C.)
a:
LU
a-
-------
212
ORP4L-D*G 79—8958
0.05 L . _hhhhhhhhh1h1Uhhh1
0 L
SAINT PAUL
ii iii iii
111111111111111111111111
i
o 05
F
0
.________________
DUBUQUE
•• —o c
O 05 F
0
BURLINGTON
. o—a
IJ
E—
0
EAST SAINT LOUIS
0.05
0.2
0.4
0
4.0
0_
0.2
0.1 —
CAM SAMPLE
o ABSENT
• PRESUMPTIVE
I PRESENT
GRAB SAMPLE
A ABSENT
A PRESENT OR PRESuMPTIvE
1
NEW ORLEANS
I
ii
ILLL
11111111111 IlIllIllIll IIIIIIIJIiIllI IJIIIIIrrIIIIrrII II
4958 4959 I 1960 4964 1962 1963 4964 I 4965
WATER YEAR
Fig. 7.7. Historical occurrence of endrin in the Mississippi River
main stem, CAM samples from water years 1958—65. Source: modified from
Breidenbach et al., 1967.
occurrence of endrin in grab samples throughout the United States from
1964 through 1968 is suiiimarized in Fig. 7.8. The locations at which the
highest levels were observed in 1966 and 1967 are presented (along with
similar data for 1964 and 1965 grab samples) in Table 7.19. The lower
Mississippi River still exhibited significant concentrations of endrin In
1966, although it now ranked tenth in contamination as compared with first
in 1965. Neither of the two sampling sites at which endrin was observed
in 1967 was located in the Mississippi River.
I
CAPE GIRARDEAL)
.0
WEST MEMPHIS
I
I
VICKSBURG
ii A —
IIL.ai...i...
II
1
-------
213
50
40
U
C-)
z
U
0
0
0
I.-
U 20
0
U
30
10
0
ORNL-DWG 79-8959
Fig. 7.8. Occurrence of endrin in river basins throughout the United
States (grab samples, 1964—68). Source: data as given by Breidenbach
et al., 1967; Lichtenberg et al., 1970.
Monitoring of the surface water and sediment of major drainage basins
was conducted from 1970 through 1975 by the U.S. Geological Survey within
the Department of the Interior, and the results of these surveys were
analyzed by the National Water Monitoring Program of the U.S. Environmental
Protection Agency (U.S. EPA, 1975b).
The data for 1970 through 1975 (or the last year monitored) were pooled
for each drainage basin and are presented in Table 7.20. Unfortunately,
the results, as tabulated, cannot be directly compared with those available
for previous years, since the number of samples positive for endrin in a
given year and the year in which the maximum concentration was observed are
not reported. However, some conclusions may be drawn from the data.
Endrin was observed in 10 out of 17 drainage basins at some time
between 1970 and 1975. The failure to detect endrin at any site in 1968
was, therefore, only a temporary phenomenon and not indicative of a
permanent trend. While the levels of contamination in the lower Mississippi
were significant (20 ng/liter), they did not approach the maximum of
214 ng/liter present in 1963 at the time of the fish kills.
Fish kills have, however, been known to occur at similarly low
concentrations. In 1961, fish kills attributed to endrin took place
1964 4965 1966 4967 1968
YEAR
-------
Table 7.20. Endrin residues in whole —water samples (us/liter) and bottom deposits (ug/kg)
in drainage baain of the United States and Puerto Rico
Whole—water samples Bottom deposits
No. of Arithmetic Standard
Minimum Maximum
observations mean deviation
379 0.0004 0.0053 0.0000 0.1000
Time
period
6/22/70—
1/6/75
705 0.0013 0.0058 0.0000 0.1000 3/1/70—
No. of
observations
Arithmetic
mean
Standard
deviation
Minimum
Maximum
226
0.0442
0.2334
0.0000
2.4000
Drainage
basins
1. North
Atlantic
slope
2. South
Atlantic
slope and
eastern Gulf
of Mexico
3. Ohio River
4. St. Lawrence
River
5. Hudson Bay
and upper
Mississippi
River
6. Missouri
River
7. Lower
Mississippi
8. Western gulf
of Mexico
9. Colorado
River
10. The Great
Basin
11. Pacific
slope basins
in Califor-
nia
12. Pacific
slope basins
in Washing-
ton
0. 0000
0.00 15
0. 0000
Time
period
6/22/70—
3/20/75
1/12/70—
4/3/75
1/15/JO-
4/2/7 5
4/17/70—
3/26/75
3/5/ 70—
3/19/75
1/6/70—
3/13/75
1/6/70—
3/13/74
1 / 2/70—
11/15/74
1/6/70—
3/11/75
1/2/70-..
8/15/74
1/29/ 70—
5/31/74
2/16/ 70—
5/24/74
0. 0000
0. 0000
0. 0000
0.1575 0.0000 2.1000
571 0.0280
20 0.1000 0.1026
97 0.0144 0.0520
53 0.0189 0.05745
235 0.0000
263 0.0002
133 Q.000u
596 0.0001
920 0.0003
1723 0.0001
251 0.0001
117 0.0015
289 0.0001
0. 0000
0.0000
0. 2000
0.2000
0. 0000
0. 0200
0. 0000
0. 0100
0.0200
0.0200
0. 0100
0. 0400
0.0100
9/21/70—
11/14/74
9/9/ 70.-
2/4/75
10/29/70—
3/19/75
8/24/70—
3/11/7 5
4/ 28170—
3/11/7 5
7 / 20/ 70—
10/9/74
10/8/ 70—
8/28/74
9/2/70—
4/18/74
6/14/71—
1/9/74
0.0004 0.0000
0.0018 0.0000
0.0005 0.0000
0.0006 0.0000
0.0058 0.0000
0.0006 0.0000
I ’ . )
I - ’
0.0000 0.2000
0.0000 0.2000
0.0000 6.7000
0.0000 1.9000
58 0.1069
260 0.1285
656 0.0889
20 0.1000
20 0.1100
53 0.1245
0. 1006
0.5005
0.1217
0.1026
0. 1021
0. 0979
63 0.0000 0.0000 0.0000 0.0000 9/2/70—
5/23/ 74
0. 0000
0. 0000
0. 0000
0. 2000
0.2000
0.2000
20 0.1000 0.1026 0.0000 0.2000
-------
Table 7.20 (continued)
Whole—water samples
Bottom deposits
Orainage
basin8
Time No. of
period observations
Arithmetic
mean
Standard
deviation
Minimum
Maximum
Time
period
No. of
observations
Arithmetic
mean
Standard
deviation
Minimum
Maximum
13. Snake River
1/13/70— 33
5/6/76
0.0000
0.0000
0.0000
0.0000
9/1/70—
5/6/74
8
0.1500
0.0926
0.0000
0.2000
14. Pacific
slope basins
in Oregon
and lower
Columbia
River
1/14/70— 31
4/17/74
0.0000
0.0000
0.0000
0.0000
3/22/72—
3/22/72
1
0.2000
0.0000
0.2000
0.2000
15. Alaska
9/29/71— 1
9/29/71
0.0000
0.0000
0.0000
0.0000
9/29/71—
9/29/71
3
0.0667
0.1155
0.0000
0.2000
16. Hawaii
10/13/70— 4
9/28/73
0.0000
0.0000
0.0000
0.0000
10/13/70—
9/28/73
4
0.1500
0.1000
0.0000
0.2000
17. Puerto Rico
1/13/70— 216
3/20/74
0.0175
0.0066
0.0000
0.0200
2/28/73—
4/4/74
8
0.0000
0.0000
0.0000
0.0000
Source: U.S.
EPA, 1975b.
I -I
tJl
-------
216
in three Louisiana streams: a borrow pit canal near Centerville, Bayou
L’Onion near Chegley, and the Franklin Canal in Franklin. During these
episodes the streams contained 29, 9, and 40 ppt (ng/liter) endrin
respectively (Lauer et al., 1966).
The levels present in fish from the lower Mississippi during the
summer of 1975 were apparently high enough to result in the death of
80% of Louisiana’s brown pelican population. All of the birds examined
contained lethal doses of endrin in their tissues (Anonymous, l975c;
King and Fllckinger, 1977).
Although endrin contamination of the surface waters of the lower
Mississippi has decreased since 1964, the large—scale use of endrin in
the agricultural lands surrounding this basin prior to that period is
reflected in the levels of the pesticide detected in bottom deposits.
The highest concentration of endrin in the sediment of any river basin
(6700 ng/kg) between 1970 and 1975 was found in the lower Mississippi.
This value has, however, decreased since 1964—65, when a concentration
of 10,000 ng/kg was reported.
The basins experiencing the highest levels of contamination in
surface water from 1970 to 1975 (100 ng/liter) were the North Atlantic
slope and the South Atlantic slope—eastern Gulf of Mexico. The North
Atlantic basin had demonstrated similar levels of contamination
(>94 ng/liter) in 1964 (Table 7.18). Levels of endrin in the bottom
deposits of the North Atlantic slope and South Atlantic slope—eastern
Gulf of Mexico basins were 2400 and 2100 ng/kg respectively. Except for
the western Gulf of Mexico (1900 ng/kg) and the lower Mississippi basin
(previously discussed), these levels were ten times greater than those
observed in the bottom deposits of all other basins.
Monitoring for pesticides in the surface water and sediment of
Louisiana waterways has recently been conducted by the U.S. Army, New
Orleans District Corps of Engineers, as part of a program to assess the
impact of proposed maintenance dredging on the water quality in the
area of the work (U.S. Army, 1975). Endrin was nor detected in any of
the surface water samples but was found at concentrations ranging from
0.00 to 2.00 jig/kg in the bottom sediments of various waterways. The
exact locations at which endrin was found and the concentration range
for each location are presented in Table 7.21.
From fall 1965 through fall 1971 the U.S. Geological Survey
monitored selected streams west of the Mississippi for pesticide
contamination. In the 1965—66 survey, 11 streams, located within
agricultural areas, were chosen for investigation. From 1967 through
1971, the number of streams monitored was increased to 20, including
the original 11. Grab samples consisting of water and suspended sediment
were analyzed by electron—capture gas chromatography with a limit of
detection of 5 ppt. The streams which were positive for endrin are
presented in Table 7.22. In 1965—66, endrin was detected once at each
of four sites and three times at one site. The location of the last
site was the Rio Grande River below Anzulduos Dam, Texas. Concentrations
-------
Z.LI
Table 7.21. Endrin in bottom sediments of Louisiana waterways—1975
Concentration range
Location
(pg/kg)
Atchafalaya Bay 0.00—0.40
Atchafalaya basin,
east access channel 0.00—
-------
218
at all sites ranged from 5 to 35 ppt (Brown and Nishioko, 1967). From
1966 through 1968, endrin was detected once at each of four sites with
concentrations ranging from 10 to 70 ppt (Nanigold and Schuize, 1969).
From 1968 through 1971, endrin was detected three times at one location,
the Gila River at Gillespie Dam, Arizona. Concentration ranged from 10
to 30 ppt (Schuize et al., 1973).
Other freshwater bodies monitored for endrin in the United States
include Lake Head, Arizona (Lyons and Salman, 1972); Lake Poinsett, South
Dakota (Harmon et al., 1970); and Everglades National Park, Florida
(Kolipinski et al., 1971). Endrin was not detected at any of these sites.
Samples of bottom sediment from three locations in the Bid Muddy Creek
watershed, Kentucky, showed endrin to be present in quantities less than
0.01 ppm (Golden and Twilley, 1976).
Municipal water supplies fed by contaminated streams are themselves
subject to contamination, and endrin has been detected in the raw and
finished water of several treatment plants. All studies were conducted
in areas with a history of high endrin usage and where mass fish kills,
due to endrin, had occurred. One such treatment plant was located on
Bayou Teche in the city of Franklin, Louisiana (Lauer et al., 1966).
Synchronous carbon adsorption samples were collected from the raw—water
pump on Bayou Teche, from a pump located between the open—air holding
reservoir and the treatment plant, and from a finished waterline at the
treatment plant, continuously from Nay 1961 through January 1962 and
intermittedly from that time through Nay 1962. Water treatment consisted
in prechiorination, alum—lime coagulation, use of activated charcoal at
the rate of 1 to 2 ppm, sedimentation, rapid sand filtration, chlorine
disinfection, and softening. The results are presented in Table 7.23.
Table 7.23. Concentration of endrin recovered by the carbon
adsorption method from the Franklin Municipal Treatment Plant
on Bayou Tech, Louisiana, 1961—62
Number of
samples
analyzed
Number of
containing
samples
endrin
Concentration (ppt)
Range of
positive
samples
Median of
positive
samples
Raw water
(pumphouse)
22
7
1—35
7
Raw water
(holding reservoir)
21
5
1—12
3
Finished water
(treatment plant)
18
2
223
11
Source: G. J. Lauer, H. P. Nicolson, W. S. Cox, and J. I. Teasley,
Trans. Am. Fish. Soc. 95(3): 310—316 (1966). Copyright 1966 American
Fisheries Society.
-------
219
Despite the rigorous treatments, endrin was recovered from the finished
water going to the consumer as well as from the raw river water and the
raw water after storage. In fact, the concentration in one contaminated
sample of finished water (23 ppt) exceeded that of the most contaminated
sample of stored raw water (12 ppt). Whether this phenomenon was due to
an error in sampling or analysis or whether further contamination occurred
during the treatment process itself remains unknown. All samples con-
taining detectable quantities of endrin were collected from early June
through late November 1961. The highest value (35 ppt) occurred in raw
water from a late July sample. Dead fish floated past the Franklin water
intake for several days during that period.
In a study conducted between March 1964 and June 1967, over 500 grab
samples of finished drinking water and corresponding raw water were
collected from ten selected municipal water treatment plants whose source
was either the Mississippi or the Missouri River (Schafer et al., 1969b).
Grab samples consisting of 100 ml in 1964, 100 ml and 1 gal (3.785 liters)
in 1965, and 3.785 liters in 1966—67 were collected and analyzed by
electron—capture gas chromotography. The decision to use a larger
sampling volume resulted from the poor precision obtained with the 100—nil
aliquots. The results are presented in Table 7.24.
Of the 458 finished water samples assayed between 1964 and 1967 by
both methods, 156 (34%) contained detectable concentrations of endrin.
However, the number of finished water samples containing concentrations
of endrin in excess of 0.1 ppb, which is a suggested maximum reasonable
stream allowance (Schafer et al., 1969b), decreased from 23 (10%) in the
period 1964—65 to zero in the period 1966—67.
The most recent study of endrin contamination of drinking water was
conducted by the U.S. Environmental Protection Agency (1974a). Endrin
was detected in the finished water from the Carroilton Water Plant in
New Orleans, Louisiana. The highest concentration measured was 4 ppt.
The results of similar investigations at the Jefferson Parish No. 1
water plant (Metairie, Louisiana) and the Jefferson Parish No. 2 water
plant (Marerro, Louisiana) were not reported.
Approximately five months following a single application of endrin
to Louisiana sugarcane fields on July 6, 1967, endrin was detected in
the groundwater (Willis and Hamilton, 1973). Concentrations decreased
from 0.17 ppb to 0.04 ppb over the ensuing three—month period. Endrin was
also detected in the groundwater following a similar application in July
1968. In this case the endrin appeared at a concentration of 0.78 ppb
immediately following treatment and decreased to a concentration of
0.25 ppb after one month. In both years the occurrence of endrin in
groundwater could be correlated with rainfall and runoff following periods
of drought which had caused numerous deep cracks in the soil. It is likely
that the pesticide, adsorbed to either carrier granules or soil particles,
was washed downward into these cracks and was subsequently transported to
the groundwater supply. When rainfall occurred 72 hr following application,
contamination of the groundwater amounted to 0.07 ppb; if precipitation
followed 24 hr after application, the groundwater contained 0.45 ppb. Thus,
heavy rains occurring immediately after endrin application and following
-------
Table
1—gal samples of water
7.24. Endrin in drinking water and associated river water
lOOinl samples of water
Number of samples
Location Date Ratid 2 with concentrations Location
>0.1 ppb
Number of samples
Date p atioa with concentrations
>0.1 ppb
Piniehed d.rinking b)ater
Algiers
03/31/65
08/25/65
4/12
0
0
Algiers
03/03/64
12/11/74
Carrolton
03/31/65
08/25/65
3/12
0
Carrolton
03/03/64
12/17/64
Carville
03/29/65
12/14/67
1/19
0
Carville
04/16/64
06/08/66
Vicksburg
03/29/65
05/25/67
7/45
0
vick sburg
03/31/64
06/30/66
Cape Cirardeau
04/19/65
06/07/67
3/39
0
Cape Cirardeau
06/02/64
03/14/66
naha
05/04165
05(23/67
1/19
0
Burlington
06/30/64
03/22/66
St. Louis
12/11/66
05/25/67
1/7
0
St. 1 ouis
06/11/64
06/16/66
Burlington
03/24/65
06/06/67
0/11
0
Jefferson City
06/04/64
07/16/64
Jefferson City
05/30/66
05/26/67
0/15
0
Kansas City
06/11/64
05/23/66
Kansas City
03/19/65
05/23/67
4/54
0
06aha
06/01/64
03/07/66
Total
24/233
0
Total
Rcn water
Carville
12/14/66
01/05/67
0/2
0
Carville
06/17164
03/10/66
Vicksburg
02/27/67
05/25/67
1/4
0
Cape Girardeau
06/02/64
03/14/66
Cape Cirardeau
03/29/65
06/07/67
2/8
0
Kansas City
04/27/66
05/23/66
Jefferson City
05/30/66
05/26/6 7
0/15
0
Kansas City
05/04/66
05/23/67
1/22
0
Omaha
04/20/66
05/23/67
1/16
0
Total
5/67
0
Total
aRatio of
number of samples
with detectable concentrations <0.1 ppb to total number of samples.
Source:
modified from Schafer et al., l969b.
14/19
14/20
2 4/39
34/41
11/25
4/10
10/32
6/7
5/12
10/20
132/225
3(10
4/12
0/2
7/24
1
2
3
6
3
1
1
0
3
3
23
1
3
4
I . . ,
0
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221
a prolonged drought will favor contamination of the groundwater supply
and potentially the drinking water supply.
Endrin contamination of freshwater bodies in Ontario, Canada, has
also been reported (Miles and Harris, 1973). In 1971, in order to compare
residue contributions from areas with differing degrees of pesticide
usage, a study was conducted in which three streams draining an agricul-
tural, an urban—agricultural, and a resort area, respectively, were
monitored. Both water (including suspended particulates) and bottom
sediment were sampled from mid—April to mid—October 1971 and analyzed
by electron—capture gas chromotography. The results are presented in
Table 7.25.
Table 7.25. Endrin concentration in water and bottom mud from
three streams in Ontario, Canada — 1971
Date
Concentration in wa
(ppt)
ter
Date
Concentration in bottom mud
(ppb)°
Big Creek
(agrioultural)
Apr. 13
<1
Apr.
<0.2
26
<1
May
0.2
May 4
<1
June
<0.2
11
<1
July
<0.2
25
1
Aug.
<0.2
June 8
3
Sept.
0.2
22
July 26 to Oct.
12Z
7
Oct.
0.3
Average
1
Range
<1—3
Thojne8 River
(urbø-agricultural)
Apr. 15
—
May
-
26
—
June
-
May5
—
July
12
—
Aug.
-
26
June 9 to Sept.
b
—
Sept.
Oct.
—
-
Average
—
Range
-
Sept. 29
—
Oct. 13
—
28
—
Mtskoka
River (resort)
May 5
2
May
0.3
26
<1
June
<0.3
June 10
June 23 to Nov.
4 b
<1
July
Aug.
<0.3
<0.3
Average
<1
Sept.
<0.3
Range
<1-1
a cause concentrations were very uniform, results for each month have been averaged for
presentation in this table.
of the leveling off of insecticide residues at lover concentrationa for these uniform
periods, data have been condensed by reporting average concentrations and ranges.
— not detected.
qualitative identification of the compound was made but the amount was less than the lowest
level of reporting.
Source: modified from Miles and Harris, 1973.
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222
Endrin was present in both the water and bottom mud of Big Creek,
which drains 280 square miles of primarily tobacco farms. Concentrations
in water ranged from <1 to 7 ppt, while concentrations in sediment ranged
from <0.2 to 0.3 ppb. An earlier survey of this region reported endrin
absent in both water and sediment; but in this case the limits of detection
were 3 ppb (Miles and Harris, 1973).
The Thames River, which drains the urban—agricultural city of London,
showed no evidence of endrin contamination in either water or bottom mud
(Miles and Harris, 1973). However, endrin was detected at concentrations
of less than 0.01 ppm in fish from this river and must therefore have been
present at low concentrations in the water and/or sediment.
Surprisingly, the resort area of Muskoka Lakes exhibited endrin
concentrations equal to or in excess of those detected in the agricultural
area. Concentrations in water ranged from less than 1 to 2 ppt;
concentrations in sediment ranged from less than 0.3 to 0.3 ppb. No
explanation was proposed for these unexpected results (Miles and Harris,
1973).
Another study (Stewart et al., 1977) of two New Brunswick streams
draining agricultural land and analyzed for organochiorine and organo—
phosphorus insecticide residues indicated as much as 0.45 ppm endrin in
bottom sediments.
Although concentrations of endrin in fish are not directly proportional
to those in water, the presence of endrin in fish is indicative of
hydrospheric contamination. Additional information concerning the
locations of problem areas may be obtained by consulting Sect. 5.2.2.
7.4.3.2 Monitoring for endrin in estuarine water and sediment .
Estuaries receiving water from rivers draining agricultural lands are
susceptible to contamination by insecticides. Due to the westerly tide,
which may carry Mississippi River water into Barataria Bay, the possibility
of contamination of the surrounding estuarine area by endrin was considered
likely. A study was conducted from October 1968 through May 1969 in which
water, sediment, and oysters from Grand Bayou, Hackberry Bay, and Creole
Bay (all adjacent to Barataria Bay) were sampled and analyzed for the
presence of endrin by electron—capture gas chromatography (Rowe et al.,
1971). This study area, located some 40 miles south of New Orleans,
eventually drains the entire agricultural watershed to the north.
Water samples from all stations on every sampling date contained less
than 1 ppb endrin, and the maximum concentration of endrin detected in
bottom sediment was less than 5 ppb. Sixty—nine percent of the oyster
samples analyzed were positive for endrin. The highest concentration
observed was less than 6 ppb. Comparison of endrin levels in oysters with
those from a similar study conducted in 1965—66 reveals that influx of
endrin into the study area decreased between 1966 and 1968 (Rowe et al.,
1971). The 1968—69 maximum endrin concentration was 29 times lower than
that observed in 1965—66. These results are reasonable in light of the
failure to detect any endrin in the lower Mississippi basin during the
1968 survey (see Sect. 7.4.3.2).
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223
Monitoring of estuarine waters for endrin by analysis of shellfish
was conducted along the coast of California in 1967 (Modin, 1969). Nine
estuaries from Humboldt Bay to Hedionda Lagoon were sampled. Endrin was
found in the Asiatic clam (Corbicula fluininea) at only one site, West
Island in San Francisco Bay. The highest concentration detected was
10 ppb.
A study was conducted from September 1969 to June 1970 to determine
the levels of endrin in Arkansas Bay, Texas, and its adjacent contributing
bays (Fay and Newland, l972a). The land surrounding these bays Is
primarily ranchiand with secondary agricultural usage. Samples of water,
sediment, and eight types of organisms were analyzed by electron—capture
gas chromotography. Endrin was detected in only 1 out of 80 water samples
from Arkansas Bay at a concentration of 4.4 ppb. No endrin was found in
either sediment or organisms.
Monitoring of estuarine waters by analysis of mollusks was conducted
in 15 coastal states from 1965 through 1972 (Butler, 1973). Endrin was
found at concentrations above 5 ppb only in organisms from California
and Texas. Endrin appeared in 14 out of 772 samples collected from
California waters. The maximum concentration observed was 19 ppb and was
found in Crossostrea gigas from Elkhorn Slough in 1968. In Texas, Out
of 728 samples, endrin appeared in 22. The highest value was 32 ppb
and was found in Crossostrea virginica from the Arroyo Colorado in 1965.
7.4.4 Mechanisms for Removal of Endrin from the Hydrosphere and Sediment
In June 1959 a fish kill occurred in a pond located in Weld County,
Colorado. Dead and dying fish were observed several days following the
aerial application of endrin to a nearby beetfield. Samples of water,
mud, and vegetation were taken from the pond and analyzed for the presence
of endrin (Bridges, 1961). The concentration of endrin in water four
days after spraying was 40 ppb. After 23 days the concentration had
decreased to 4 ppt. By the 31st day, endrin could no longer be detected
in water samples. The endrin concentrations in vegetation and mud 16 days
after spraying were 250 and 170 ppb respectively. Endrin was no longer
detected in vegetation 51 days after spraying or in mud 70 days after
spraying. Even though the analytical technique employed in this study
(paper chromatography) is not as sensitive as others and might not have
detected very low levels of residual contamination, rapid reduction in
concentration appears to have occurred.
Several mechanisms for the removal of pesticides from the hydrosphere
are known (Chesters and Konrad, 1971). Volatilization and codistillation
most likely accounted for a large proportion of the losses occurring in
the situation described above. The pond in question consisted of four
well—exposed acres with an average depth of 3 ft. Significant wind action
was observed during the summer sampling period (no wind velocities were
given), and water temperatures averaged 24°C (75°F). The combination of
large surface area, shallow depth, warm temperatures, winds, and lack of
vegetative cover provided the ideal setting for maximum evaporative loss.
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224
Dissipation of pesticides from the environment occurs as a result
of biochemical, photochemical, and thermal degradation. However, the
degradation products themselves may be of equal or greater toxicity and
just as persistent as the parent compounds; under such circumstances,
degradation would result in little benefit to the environment.
Endrin Is known to undergo rearrangement reactions under the influence
of both sunlight and heat when treated either in the solid state or as a
solution in an organic solvent such as hexane (Sect. 2.3). All of the
rearrangement products studies have proved to be less toxic to test animals
than eridrin itself (Soto and Deichmann, 1967). From an environmental
point of view, such rearrangements are therefore desirable. Similar
reactions are believed likely when endrin is adsorbed to particulates
(as when present in the hydrosphere) (Klein and Korte, 1967); however,
studies in support of this prediction have not been reported. No
photolytic reaction was observed when endrin, at a concentration of
10 pg per liter of distilled water, was exposed to both sunlight and
artificial fluorescent light for a period of three weeks (Eichelberger and
Lichtenstein, 1971).
Degradation of endrin by aquatic microorganisms has been reported
and probably contributes at least to some extent to the dissipation of
that pesticide from the aquatic environment (Sect. 3.2). Microbial
degradation appears to be most important In freshwater systems.
Due to their hydrophobic, lipophilic nature, organochiorine
Insecticides adsorb onto particulate matter suspended In water and are
transported to the sediment. The association of pesticides with suspended
particulates is borne out by comparative studies of ponds during periods
of murky water and clear water following a settling period. Measurable
pesticide residues in the water often drop to nondetectable levels within
a week (Iverson, 1967). Evidence that endrin behaves in this predicted
fashion was provided by the work of Pfister et al. (1969). Particulate
matter from a sample of water collected from the western basin of Lake
Erie was layered onto a sucrose gradient and centrifuged. The gradient
was subsequently divided into portions and analyzed for the presence of
organochiorine insecticides. Endrin was found attached to the less dense
upper fractions, which consisted of organics, detritus, and microorganisms.
All positive samples appeared to be associated with particles equal to or
greater than 0.15 pm in diameter. The highest concentration observed was
9.6 ng per liter of water. No endrin was detected in the raw lake water
following the centrifugation procedures used to separate the particulates.
In an environment such as Lake Erie, where the shallow waters are
easily disturbed by wind action, the turnover and accumulation of
pesticides in bottom sediments may be quite significant.
Adsorption is an indirect form of dissipation from the hydrosphere,
since the availability of the pesticides for uptake by plants and aquatic
organisms is markedly reduced by the process. However, biochemical
degradation and rates of volatilization are also reduced, leading to the
conclusion that adsorption and sedimentation result in a safer but more
persistent form of contamination.
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225
When natural processes are insufficient, it is possible to remove
trace amounts of endrin from water by the use of large quantities of
activated carbon (Chesters and Konrad, 1971). An example of such a
situation was reported by Stoltenberg (1972). In June 1971 a man
deliberately dumped 0.5 gal of a mixture of endrin and strychnine Into
Shawnee Lake, a three—acre reservoir in the Shawnee State Forest near
Portsmouth. Within one day, 4000 fish along with other aquatic organisms
in the lake had died. Concentrations of endrin ranged as high as 15 ppb,
25 times greater than the concentration needed to kill minnows in 43 hr.
With the aid of a controlled activated—carbon filtration system, 98 to
99% of the endrin was removed from the lake. Removal of pesticides from
large bodies of water is not feasible.
7.5 ENDRIN IN THE LITHOSPHERE
7.5.1 Introduction
Since a large proportion of the endrin entering the environment
is initially released to the soil, the fate of endrin in the soil
determines, to a great extent, the degree to which the rest of the
environment will become contaminated. Depending upon conditions, the soil
may act as either a barrier or a link in the physical transfer of endrin
from one point In the environment to another (Adams, 1967). Some types
of soil adsorb endrin and prevent it from escaping to the atmosphere, while
others show litt Le affinity for the pesticide and permit extensive
volatilization. The situation is even more complicated when the variety
of climates and topographies which may enhance or reverse the restraining
effects of soil retention is considered. For example, rainfall on sloping
lands may result in surface erosion leading to transport of endrin to the
hydrosphere despite its being tightly adsorbed by the soil.
Many mechanisms by which endrin can be dispelled from the environment
also transpire in the lithosphere. It is in the field that granular
endrin may undergo photodecomposition through exposure to natural sunlight
(Sect. 2) or where anaerobic conditions favorable for microbial degradation
(Sect. 3) may develop.
Whether endrin undergoes transportation from the soil, degradation
in the soil, or retention by the soil depends upon so large a number of
factors that the formulation of hard—and—fast generalizations becomes
exceedingly difficult. The availability of extensive soil monitoring
data has aided in identification of seriously contaminated areas and has
revealed the levels of residues in the vicinity of sites where endrin—
related environmental disasters have occurred. Residue levels in root
crops and soil invertebrates may also be an effective indicator of soil
contamination (Sect. 8).
7.5.2 Sources of Endrin in the Lithosphere
The major source of endrin in the lithosphere is direct application.
Endrin may be applied to the soil per se or may reach the soil indirectly
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226
following treatment of crops. The quantities of endrin used and the number
of acres treated during 1964, 1966, and 1971 are summarized by crop in
Table 7.26 and by region in Table 7.27. The regions are presented
pictorially in Fig. 7.9 (Eichers et al., 1968; Eichers et al., 1970;
Andrilenas, 1974). Although endrin usage was apparently widespread,
especially in 1964, the largest single use of endrin in the United States
during each of these years was for the control of lepidopterous larvae
attacking cotton crops in the southeastern and delta states. In 1971,
75% of all enclrin used was applied to cotton, while 99% of the total
usage was confined to the southeastern and delta states. When the quantity
of endrin applied to cotton in 1971 (4.849 x i0 5 kg) is compared with
that applied in 1964 (8.467 x l0 kg), it appears as though a 43% reduction
in endrin usage had occurred. These figures are, from one standpoint,
quite misleading in that the number of acres treated in 1971 (2.62 x i0 )
was only 22% of the number treated in 1964 (1.194 x 106), so that the
number of pounds applied per acre increased by a factor of 2.6. Thus,
while contamination of the lithosphere was less diffuse in 1971 than in
1964, pockets of more extensive contamination were created. The marked
Table 7.26. Quantities of endrin used on specified crops and
number of acres treated (by crop)
Crop
1964
1966
1971
1000
acres
1000
pounds
1000
acres
1000
pounds
1000
acres
1000
pounds
Corn
9 a
75
30
Cotton
1194
1865
403
510
262
1068
Soybeans
48
9
58
23
Tobacco
149
150
24
20
Other field
crops
49
12
55
17
193
256
Irish potatoes
141
61
3
5
Other vegetables
10
20
1
1
Apples
Other fruits and
nuts
30
b
30
b
22
18
13
175
9
47
2
33
Total
1630
2125
522
735
648
1418
aLess than 10,000 acres treated; 9000 assumed.
b
Not reported.
Source: modified from Eichers et al., 1968; Eichers et al., 1970;
Andrilenas, 1974.
-------
ZLI
7.27. Quantities of endrin used on all crops and
number of acres treated (by region)
Region
1964
1966
1971
1000
1000
1000
1000
1000
1000
acres
pounds
acres
pounds
acres
pounds
Northeast
40
13
12
5
7
5
Lake states
60
12
b
Corn belt
4 5
1.5
127
37
Northern Plains
1.5
6
4
Appalachian
168
155
47
194
Southeast
218
484
31
67
156
339
Delta states
628
893
358
435
273
990
Southern Plains
291
231
71
34
Mountain
80
42
3
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228
decrease in the use of endrin during 1966 may have resulted from variations
in the weather, pest infestations, and crop production during that year.
The massive fish kills attributed to endrin in the early sixties may also
have contributed to a temporary decline in use of the pesticide during
that year.
The amount of endrin reaching the soil during treatment depends upon
the method of application, the type of crop, and the type of soil. Four
examples are presented in Table 7.28 (Harris et al., 1966). When endrin
was applied to tall dense crops (such as tobacco at site 1), residues
did not appear in the soil. Application of endrin directly to the soil
(as in sites 2 and 3) only resulted in trace amounts actually contaminating
the soil, since both of these soils have limited retentive ability for
endrin, and dissipation of the pesticide by wind or runoff readily occurs.
Table 7.28. Endrin in soil as a function of soil type,
crop, and mode of application
Site
Soil
type
Crop
Mode of
application
Year
applied
Detected
(late 1964)
(ppm)
1
Sandy
loam
Tobacco, rye
Foliar
1963
None
2
Clay
loam
Sugar beets
Surface
1963
<0.1
3
Clay
Sugar beets
Surface
1964
<0.1
4
Muck
Radishes
Surface
1960—1964
3.8
Source: Reprinted with permission from N. L. Schafer et al., J.
Agric. Food Chem. 14(4): 398—403 (1966). Copyright 1966 American
Chemical Society.
The most serious problem arises when endrin is applied directly to a
soil with high organic content such as muck (site 4). In this case the
pesticide Is adsorbed relatively quickly, clings tenaciously, and is only
removed with difficulty.
Fallout and rainout of airborne particulate matter to which endrin
has adsorbed are Important mechanisms for contamination of nonagricultural
soil or soil on which endrin, specifically, has never been used. These
mechanisms have been discussed in detail in the sections dealing with
removal of endrin from the atmosphere (Sect. 7.3.4) and sources of endrin
In the hydrosphere (Sect. 7.4.2).
In one study (Abbott et al., 1965), rainwater was examined for traces
of pesticides. Endrin was not detected; but the quantities of those
pesticides which were detected were insufficient to account for more than
a very small percentage of their representation in untreated soils.
Although the concentrations of these compounds in air were lower by a
factor of 10 to 100 than that In rainwater (Abbott et al., 1965), the vastly
greater volume of air which passes over the soil may have rendered its
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229
contribution of greater significance. Along with the constantly changing
contact between air and soil, the mass of air within the surface soil may
alter by up to 5% due to variations in temperature throughout the day.
Thus the soil may act as a gas—solid chromatographic “column,” and,
assuming a tendency toward equilibrium, treated soils will lose pesticides,
while untreated soils will gain them.
Wind drift and irrigation with contaminated water are other possible
routes of endrin to the soil. They are also discussed in Sect. 7.4.2,
which deals with sources of contamination of the hydrosphere. Small amounts
of endrin may also be transported to untreated soils by migration of
contaminated soil invertebrates, primarily earthworms. The extent to
which these organisms bioaccumulate endrin is discussed in Sect. 8.2.
7.5.3 Monitoring for Endrin in the Lithosphere
A comprehensive program for monitoring levels of pesticide residues
in soils of the United States (the National Soils Monitoring Program,
NSMP) was initiated in 1969 as part of the National Pesticide Monitoring
Program. Approximately 257. of some 13,300 officially designated sites
are surveyed each year (Carey et al., 1973). The results for the first
two years (1969 and 1970) have been reported and comprise a baseline
against which future trends may be evaluated (Crockett et al., 1971;
Wiersma et al., 1972a). In 1969, both cropland and noncropland soil
was sampled from 43 and 11 states respectively. The 1970 study was
limited to cropland soil, and only 35 states were included. Soil samples
were extracted with hexane—isopropanol and analyzed for organochiorine
insecticides by electron—capture gas chromatography. The limit of detec-
tion for endrin was 0.01 ppm in dry soil sample. The data for the cropland
soil surveys are presented in Tables 7.29 (by state) and 7.30 (by cropping
region). No endrin was detected in the noncropland sites investigated
in the earlier study.
Of the 1729 sites sampled in 1969, 39 (2.3%) contained endirn residues.
The mean residue level was less than 0.01 ppm, with a range of 0.00 to
0.56 ppm.
In 1970, 27 (1.79%) of the 1506 sites sampled were positive for endrin.
The mean residue level was once again less than 0.01 ppm, with values
ranging from 0.00 to 0.90 ppm. Although endrin was not detected in soils
from Indiana, Iowa, or South Dakota in either year, an Independent survey
of 400 NSMP sites in the corn—belt region, conducted in 1970, detected
endrin in one site in each of these states. The concentrations reported
were 0.02, 0.02, and 0.04 ppm for Indiana, Iowa, and South Dakota
respectively (Carey et al., 1973).
Ketoandrin was detected at nine (0.5%) of the sites sampled in 1969
at a mean concentration of less than 0.01 ppm (range of 0 to 0.13 ppm),
while endrin aldehyde was detected in only one sample in the same year
at a concentration of 0.03 ppm.
-------
Table 7.29. National Soils Monitoring Program for endrin residues:
cropland soil FY 1969 and FY 1970
Number of
State Year sites
analyzed
Number
sites
positive
Sites
positive (%)
Mean
residue
level (ppm)
Maximum
level de—
tected (ppm)
Alabama 1969 22 2 9.1 <0.01 0.05
1970 21 2 9.52 0.01 0.16
Arizona 1969 8 3 37.5 0.07 0.22
(endrin ketone) (8) (2) (25) (0.01) (0.07)
1970 NS
Arkansas 1969 47 5 10.6 0.01 0.29
(endrin ketone) (47) (2) (4.3) (<0.01) (0.13)
1970 47 3 6.38 <0.01 0.03
California 1969 65 9 13.9 0.01 0.16 0
1970 65 5 7.69 <0.01 0.10
Colorado 1969 60 3 5.0 <0.01 0.02
(endrin ketone) (60) 1 1.7 <0.01 0.05
1975 NS
Connecticut 1969 2 ND
1970 20a ND
Delaware 1969 3 ND
1970 NS
Florida 1969 18 2 11.1 0.03 0.38
(endrin aldehyde) (18) (1) (5.6) (<0.01) (0.03)
(endrin ketone) (18) (1) (5.6) (<0.01) (0.03)
1970 17 1 5.88 0.05 0.90
-------
Table 7.29 (continued)
Number of
State Year sites
analyzed
Number
sites
positive
Sites
positive (%)
Mean
residue
level (ppm)
Maximum
level de—
tected (ppm)
Georgia 1969 22 1 4.6 0.02 0.42
1970 28 ND
Idaho 1969 33 ND
1970 NS
Illinois 1969 142 ND
1970 140 ND
Indiana 1969 78 ND
1970 78 ND
Iowa 1969 151 ND
1970 150 ND
Kentucky 1969 31 ND
1970 30 ND
Louisiana 1969 27 1 3.7 <0.01 0.06
(endrin ketone) 27 1 3.7 <0.01 0.02
1970 26 2 7.69 <0.01 0.03
Maine 1969 8 1 12.5 0.02 0.15
1970 20a ND
Maryland 1969 12 ND
1970 19b ND
Massachusetts 1969 2 ND
1970 20a ND
-------
Table 7.29 (continued)
Number of
State Year sites
analyzed
Number
sites
positive
Sites
positive
Mean
residue
level (ppm)
Maximum
level de—
tected (ppm)
Michigan 1969 51 1 2.0 <0.01 0.01
1970 54 ND
Minnesota 1969 NS
1970 120 2 1.67 <0.01 0.02
Mississippi 1960 29 1 3.5 0.01 0.19
(endrin ketone) 29 1 3.5 <0.01 0.11
1970 29 3 10.34 0.01 0.11
Missouri 1969 82 1 1.2 <0.01 0.01
1970 81 1 1.23 <0.01 0.02
Nebraska 1969 106 1 0 ,9 <0.01 0.02
1970 106 4 3.77 <0.01 0.03
Nevada 1969 2 ND
1970 NS
New Hampshire 1969 2 ND
1970 20a ND
New Jersey 1969 5 ND
1970 19b ND
New Mexico 1969 10 ND
1970 NS
New York 1969 38 1 2.6 0.01 0.56
(endrin ketone) 38 1 2.6 <0.01 0.05
1970 38 ND
-------
Table 7.29 (continued)
Number of
State Year sites
analyzed
Number
sites
positive
Sites
positive (%)
Mean
residue
level (ppm)
Maximum
level de—
tected (ppm)
North Carolina 1969 31 2 6.5 <0.01 0.08
1970 30 2 6.67 <0.01 0.03
North Dakota 1969 157 1 0.6 <0.01 0.01
1970 NS
Ohio 1969 68 ND
1970 69 1 1.45 <0.01 0.02
Oklahoma 1969 64 ND
1970 65 1 1.54 <0.01 0.06
Pennsylvania 1969 29 ND
1970 32 ND
Rhode Island 1969 1 NI)
1970 20a ND
South Carolina 1969 17 3 17.7 <0.01 0.05
1970 17 ND
South Dakota 1969 106 ND
1970 106 ND
Tennessee 1969 27 1 3.7 <0.01 0.02
1970 25 ND
Utah 1969 12 ND
1970 NS
Vermont 1969 5 ND
1970 20a ND
-------
Table 7.29 (continued)
State
Year
Number o
sites
analyzed
f Number
sites
positive
Sites
positive
Mean
residue
level (ppm)
Maximum
level de—
tected (ppm)
VIrginia
1969
1970
21
26c
N I)
ND
Washington
1969
1970
45
NS
West Virginia
1969
1970
6
26c
ND
ND
Wisconsin
1969
1970
67
67
ND
NI)
Wyoming
1969
1970
17
NS
ND
ND = not detected; NS = not sampled in that year; a = 20 sites sampled in Maine, New Hampshire,
Vermont, Massachusetts, Rhode Island, and Connecticut; b = 19 sites sampled in New Jersey, Maryland, and
Delaware; c = 26 sites sampled in Virginia and West Virginia.
(-‘)
Source: modified from Crockett et al., 1971; Wiersma et al., 1972a.
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235
Table 7.30. Summary of endrin residues in cropland soil
by cropping region, FY 1969 and FY 1970
Crop
Sites
detectable
showing
residues (%)
Mean
concentration
(ppm)
1969
1970
1969
1970
Corn
0.3
0.42
<0.01
<0.01
Cotton
7.3
5.94
0.01
<0.01
Cotton and
general farming
2.6
4.27
<0.01
<0.01
General farming
3.6
1.36
<0.01
<0.01
Hay and
general farming
ND
1.36
ND
ND
Irrigated land
11.1
2.56
0.01
0.01
Small grains
0.9
0.95
<0.01
<0.01
Vegetable
3.2
1.39
0.01
<0.01
Vegetable and
fruit
6.1
4.76
0.01
0.01
ND = not detected.
Source: modified from Crockett et al., 1971; Wiersma et al., 1972a.
When soil samples were collected, an attempt was made to determine
whether eudrin had been used on the sites for the year of sampling. The
locations at which endrin was admittedly applied are listed in Table 7.31.
Endrin was applied to far fewer sites than the number at which it was
detected. In 1969, 1684 sites were surveyed, but only 0.48% of these
reported the use of endrin. In 1970, 0.45% of the 1346 sites surveyed
had been treated with the pesticide. One explanation for the presence
of endrin in nontreated soils is the persistence of residues from previous
years of treatment. Under such circumstances, both the percentage of
sites exhibiting contamination and the maximum residue level observed
should decrease from year to year. One example is the state of Arkansas
(Table 7.31), where endrin was applied in 1969 but not in 1970. Whereas
10.6% of the sites analyzed were positive for endrin in 1969, only 6.38%
contained residues in 1970. The maximum levels detected for the two years
were 0.29 and 0.03 ppm respectively.
The situation in Louisiana cannot, however, be explained in the same
manner. In this case (Table 7.31), endrin was not applied in either year.
Although the maximum detectable level decreased from 0.06 ppm in 1969 to
0.03 ppm in 1970, the percentage of samples exhibiting contamination more
than doubled (3.7% in 1969 to 7.69% in 1970). Since the number of positive
samples was small, this observation may not be statistically important.
However, the possibility of other sources of contamination, such as soil
drift, aerial fallout, and precipitation, must not be overlooked.
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236
Table 7.31. States where endrin was used in FY 1969 and/or FY 1970
State
Year
Number
of sites
investigated
Number of
sites treated
with endrin
Sites
treated
endrin
with
(%)
Alabama
1969
1970
23
22
2
1
8.70
4.55
Arkansas
1969
1970
45
47
1
NU
2.22
Calif ornia
1969
1970
66
43
NU
1
2.33
Colorado
.
1969
1970
60
NS
3
5.00
Georgia
1969
1970
28
30
NU
1
3.33
Mississippi
1969
1970
29
31
1
1
3.45
3.23
Nebraska
1969
1970
103
106
NU
2
1.89
North Dakota
1969
1970
159
NS
1
0.63
NU = no endrin used; NS = state not studied.
Source: modified from Crockett et al., 1971; Wiersma et al., 1972a.
The presence of endrin in cropland soil by crop in 1970 is presented
in Table 7.32. During this year, endrin was applied only to cotton, and
the highest percentage of contaminated sites as well as the highest levels
of contamination were found in cotton fields. Once again, the occurrence
of residues in fields where no endrin was applied suggests other means of
contamination.
Monitoring for endrin in soils from the cotton—belt states was
continued through 1973, and the data are presented in Table 7.33. Data
for 1969 and 1970 are also included in this table so that trends may be
easily observed (U.S. EPA, 1975c). Levels of endrin contamination reached
their minimum values in Arkansas, Louisiana, and Mississippi in 1971. The
trend, however, did not continue. Concentrations as high as 0.64 ppm were
observed in Mississippi soils during 1972, while maximum concentrations in
Arkansas and Louisiana soils during 1973 were 0.24 and 0.48 ppm respec-
tively. No data are available as to the use of endrin in these states
during 1972 and 1973.
Monitoring for endrin in soils planted to specific types of crops
other than cotton has also been reported. Fields in the eastern states
planted to root crops were surveyed in the fall of 1965 (Seal et al., 1967).
-------
ND = not detected.
Table 7.32. Endrin in cropland soil by crop — FY 1970
-J
Source: modified from Crockett et al., 1971.
Crop
Number
of sites
sampled
Number
of times
detected
Occurrence
(%)
Mean
concentration
(ppm)
Maximum
concentration
(ppm)
Alfalfa and
bur cloves
114
3
2.63
<0.01
0.07
Field corn
363
4
1.10
<0.01
0.03
Cotton
49
7
14.29
0.01
0.16
Grass and hay
29
ND
Mixed hay
118
ND
Soybeans
254
2
0.79
<0.01
0.03
-------
Table 7.33. Endrin in cotton—belt soils: 1969—1973
Number
Number
Sites
Mean
resi—
Maximum level
State Year of sites
of sites
positive
due
level
detected
analyzed
positive
(70
(ppm)
(ppm)
Alabama 1969 22 2 9.1 <0.01 0.05
1970 12 2 95 0.01 0.16
1971 0 NA NA NA NA
1972 23 1 4.3 0.02 0.42
1973 22 1 4•5 <0.01 0.10
Arkansas 1969 47 10.6 0.01 0.29
1970 3 6.4 <0.01 0.03
1971 22 NA NA NA NA
1972 46 1 2.2 <0.01 0.10
1973 43 2 4.7 0.01 0.24
Louisiana 1969 27 1 3.7 <0.01 0.06
1970 26 2 7.7 <0.01 0.03
1971 22 ND NA NA NA
1972 26 ND NA NA NA
1973 27 1 3.7 0.02 0.48
Mississippi 1969 29 1 3.4 0.01 0.19
1970 29 3 10.3 0.01 0.11
1971 38 1 2.6 <0.01 0.01
1972 31 2 6.5 0.02 0.64
1973 30 ND NA NA NA
Texas 1971 113 1 0.8 <0.01 0.05
Source: modified from U.S. EPA, 1975c.
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239
Endrin was detected in 10 Out of 49 fields sampled. Eight of the fields
were planted with potatoes, and the concentration of endrin ranged from
0.08 to 0.50 ppm (average was 0.27 ppm). The remaining two fields were
planted with carrots. The range of endrin concentrations was 0.05 to
0.10 ppm (average was 0.08 ppm). Endrin residues were not detected in
either crop.
Commercially grown onions and the soils on which they were grown
were sampled in the ten major onion—producing states in 1969 and analyzed
for the presence of endrin (Wiersma et al., 1972c). Endrin was detected
in 15.5% of the 76 sites sampled at an average concentration of 0.06 ppm
(range was 0.01 to 2.05 ppm). Residues were absent from onions per se.
Soil from commercial wheat fields was sampled in the 16 major wheat—
producing states during the summer of 1969 (Wiersma et al., l971a).
Endrin had been applied at the rate of 0.33 lb/acre to four of the 100
wheat fields sampled. Endrin was detected at each of these four sites at
an average concentration of 0.03 ppm (range was 0.02 to 0.08 ppm), but
was not detected at any other site. No endrin was detected in the harvested
wheat crops.
The NSMP sampled several urban areas annually for pesticide residues.
The results of the 1969 to 1973 surveys on endrin are present in Table 7.34
(U.S. EPA, l975c; Wiersma et al., l972a). From the limited data available,
accumulation of endin residues does not appear to present a major problem
to urban environments.
Monitoring for pesticide residues in soils from agricultural regions
in Canada has also been conducted. Southwestern Ontario is an area of
intensive farming with a wide variety of soil types and crops. The cyclo—
diene insecticides were utilized to a considerable extent between 1954
and 1960 and to a lesser extent in subsequent years. In 1964, soil samples
were collected from 31 farms throughout the region and analyzed for the
presence of organochlorine insecticides (Harris et al., 1966). Fifty
percent (16) of the samples contained significant amounts of cyclodiene
insecticides (greater than or equal to 0.1 ppm). However, only eight of
the samples were active enough to cause mortality in appropriate test
organisms. Endrin was found at a concentration of 3.8 ppm at one site
where the pesticide had been applied annually since 1960. Trace amounts
(less than 0.1 ppm) were detected at two other sites where endrin had been
surface applied either in 1963 or in 1964. Endrin was neither used nor
detected at any other site surveyed that year. The study was continued
through 1969 on 16 of the original 31 farms (Table 7.35) (Harris and Sans,
1971). In the 1964 survey, endrin had been found on only two of these
farms; by 1966, residues were present on seven farms, and by 1969, detect-
able levels were reported on nine farms. Concentration ranges were 0.11
to 3.76 ppm in 1964, 0.01 to 6.55 ppm in 1966, and 0.01 to 3.54 ppm in
1969. Although endrin was reportedly applied to only 3 of the 16 farms
sampled, more extensive use during this period was probable. Endrin was
a likely substitute for certain other pesticides phased out between 1958
and 1969 due to development of resistant strains or to bans. Endrin usage
was apparently most extensive in tobacco fields, but the highest residue
levels were present in soils where vegetables had been grown. These soils
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240
Table 7.34. Endrin residues in urban soils 1969—1973
No. of
Urban area
sites
No. of
positive
detections
Positive
detections
(%)
Mean
(ppm)
Highest
level de—
tected (ppm)
1969
Bakersfield, CA 50 3 6.0 0.01 0.03
Camden, NJ 50 ND
Houston, TX 50 1 2.0 0.01 0.01
Manhattan, KS 50 ND
Miami, FL 50 ND
Milwaukee, WI 50 ND
Salt Lake City, UT 50 1 2.0 0.01 0.06
Waterbury, CT 50 ND
1970
Augusta, ME 27 ND
Charleston, SC 27 ND
Cheyenne, WY 19 ND
Grand Rapids, MI 23 ND
Greenville, MS 28 ND
Honolulu, HI 21 ND
Memphis, TN 28 1 3.6 0.01 0.07
Mobile, AL 29 ND
Portland, OR 25 ND
Philadelphia, PA 26 ND
Richmond, VA 27 ND
Sikeston, MO 27 ND
Sioux City, LA 22 ND
Wilmington, DE 27 ND
1971
Baltimore, MD 156 ND
Gadsen, AL 55 ND
Hartford, CT 48 ND
Macon, GA 43 1 2.3 0.01 0.17
Newport News, VA 78 ND
1972
Des Moines, IA 82 ND
Fitchburg, MA 35 ND
Lake Charles, LA 70 ND
Pittsburgh, PA 189 ND
Reading, PA t9 ND
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241
Table 7.34 (continued)
Urban area
No. of
sites
No. of
positive
detections
Positive
detections
(%)
Mean
(ppm)
Highe
level
tected
st
de—
(ppm)
:1973
Evansville,
IN
82
ND
Greenville,
SC
86
ND
Pittsvield,
MA
45
ND
Tacoma, WA
95
ND
Washington,
DC
116
ND
ND = not detected.
Source: modified from U.S. EPA, l975c.
Table 7.35. Residues of endrin found in agricultural soils on
16 farms in southwestern Ontario in 1964, 1966, and 1969
Endrin
residues in soil
V
Site
number
(ppm)
Endrin
applied
(year)
General •
classification
1964
1966
1969
1
Field
ND
0.01
0.01
2
Field
ND
ND
0.10
3
Field
ND
ND
ND
4
Field
ND
ND
ND
5
Tobacco
0.11
0.10
0.06
1966, 1969
6
Tobacco
ND
0.10
0.07
7
Tobacco
ND
0.03
0.03
8
Tobacco
ND
0.05
0.04
1964
9
Vegetable
ND
ND
NS
10
Vegetable
ND
0.38
0.08
11
Vegetable
3.76
6.55
3.54
1960—1964
12
Vegetable
ND
ND
ND
13
Vegetable
ND
ND
ND
14
Vegetable
ND
ND
1.06
15
Fruit
ND
ND
ND
16
Fruit
ND
ND
ND
ND = not detected (<0.01 ppm in 1964; <0.001 ppm in 1966 and 1969);
NS = not sampled in that year.
Source: modified from Harris and Sans, 1971.
were classified primarily as “muck” and, as such, contained a large quantity
of organic matter to which the insecticides readily adsorbed. Since only
0.13% of the total area of the Province of Ontario is devoted to nonfield
crop farming (vegetable, tobacco, and orchard), where insecticides are
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242
used extensively, contaminated soils are expected to be concentrated in
relatively small pockets and are not representative of the entire province.
The levels of organochlorine insecticide residues in soil and legume
crops in the northeastern agricultural area of Saskatchewan, Canada, were
studied in September 1966 (Saha et al., 1968). Soil and foliage samples
were taken from 16 sweet clover and 4 alfalfa fields. Fifteen percent of
the soil samples contained endrin residues at concentrations ranging
from 0.01 to 0.02 ppm. Residues of endrin in the crops were either
undetectable or present in only trace amounts (less than 0.01 ppm).
Saha and Sumner (1970) analyzed 41 agricultural soil samples from
21 vegetable farms in Saskatchewan for the presence of organochiorine
insecticide residues. Aldrin and/or dieldrin were present in 61%
of the samples; endrin was detected only once at a cOncentration of
0.48 ppm.
Agricultural soil from Japan was analyzed for organochiorine
insecticide residues in a study by Suzuki et al. (l973a). Endrin was
detected in 29 out of 99 samples tested. The concentration range was
0.016 to 0.629 ppm with a mean of 0.183 ppm.
7.5.4 Persistence of Endrin in the Lithosphere
Many pathways have been established for the removal of endrin from
the soil. Mechanisms such as volatilization, leaching into groundwater,
wind erosion, and surface runoff result in the translocation of endrin
to the atmosphere or hydrosphere and were discussed in detail in the
sections dealing with sources of endrin in those compartments (Sect. 7.3.2
and 7.4.2). Other pathways, such as direct root uptake by plants and
ingestion by soil invertebrates, lead to contamination of living things
and are also dealt with in the appropriate sections (4. and 5.6). The
only remaining pathways for the removal of endrin from the soil are
photodecomposition, thermal decomposition, and bacterial degradation.
Although the first two were discussed in Sect. 2.3 and the third in
Sect. 3.2.1, the fact that these pathways comprise the only mechanism
for actual dissipation of endrin from the environment (as opposed to
mere translocation) deems it appropriate that they be briefly discussed
in this section as well.
7.5.4.1 Mechanisms for Removal of Endrin from the Lithosphere
7.5.4.1.1 Photodecomposition and thermal decomposition . It has
been known for some years that endrin undergoes chemical isomerization
under the influence of sunlight and heat (Klein and Korte, 1967). Most
of the laboratory studies dealing with the photo— and thermochemistry
of endrin have been conducted either in the solid state or in solution
in an organic solvent. The results of these studies appear most relevant
to endrin in the lithosphere, since the pesticide may reside there either
as a solid or adsorbed to the organic matter in the soil.
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243
The extent to which endrin may be expected to disappear as a result
of the light and heat received from sunlight was studied by Baker and
Applegate (1974). Samples of solid endrin were placed in a petri dish
and exposed to ultraviolet radiation in the biologically active range
(300 to 400 nm) for from 4 to 24 hr. Half of the samples were covered
with aluminum foil in order to separate the effects of the uv rays from
those of heat (35°C). Samples were analyzed for endrin at four intervals
by electron—capture gas chromatography; the results are presented in
Table 7.36.
After 24 hr of uv exposure, 52.4% of the primary gas—chromatographic
endrin peak had been lost. In the presence of heat alone, the losses
amounted to only 20.1%. The net effect of uv radiation on the primary
peak was, therefore, 32.3% over the 24—hr period. The effects of uv
radiation on the secondary peak were similar to those for the primary
peak. Ultraviolet exposure resulted in the loss of 59.4% of the secondary
peak after 24 hr, while heat alone diminished the peak by only 29.9%.
The net uv decomposition as indicated by the secondary peak was 29.5%.
Since decomposition products were neither identified nor quantitated, it
is not known whether exposure to heat resulted in thermal isomerization,
vaporization, or both. The experiment only indicates that under these
conditions of simulated sunlight, uv decomposition does, in fact, occur.
The major products resulting from the photochemical and thermochemical
isomerization of endrin have been identified, and their structures, along
with that of the parent compound, are presented in Sect. 2.
7.5.4.1.2 Degradation by soil microorganisms . The removal of
persistent pesticides from soil may be accomplished by microbfal degrada-
tion, providing that an appropriate microbial species is present and that
the soil conditions are suitable.
Natsumura et al. (1971) screened about 150 microbial isolates from
various soil samples for their ability to degrade 1 C—labeled endrin.
Twenty—five of these organisms were active in degrading endrin, but the
degree to which degradation occurred and the number of products varied
considerably (Sect. 3.).
In a similar study (Patil et al., 1970), 20 microorganisms, which
had previously been shown to degrade dieldrin, were tested for their
ability to degrade endrin. All were positive; however, no degradation
products were described (Sect. 3.).
The importance of such factors as soil pH, moisture content, the
presence or absence of crops, and soil depth in determining whether or
not microbial degradation of endrin is probable was studied by Nash et
al. (1972). In one experiment, Lakeland sandy loam, pH 6.4, was treated
with 20 ppm 1 C—labeled endrin at one of three soil depths (1 to 2 cm,
16 to 17 cm, or 31 to 32 cm). A soybean plant was grown in the soil for
75 days, after which time the 1—cm treated sections were extracted and
analyzed for endrin and its degradation products by both gas and thin—layer
-------
Table 7.36. Effect of ultraviolet radiation on the loss of endrin from petri dishes
treated with 100 pg of sample
Quantity remaining after the given number of hours
(ug)
0 4 8 16 20 24
Primary peak 100 87.2 ± 1.2 77.9 ± 5.1 65.4 ± 2.4 51.1 ± 1.3 47.6 ± 1.3
(+uv)
Primary peak 100 96.2 ± 1.4 89.8 ± 2.1 86.8 ± 1.5 82.1 ± 2.3 79.9 ± 3.9
(-uv)
Secondary peak 100 78.3 ± 3.8 71.8 ± 1.2 60.8 ± 1.6 44.4 ± 2.8 40.6 ± 1.1
(+uv)
Secondary peak 100 88.0 ± 1.3 84.5 ± 1.6 82.1 ± 1.1 75.9 ± 1.9 70.1 ± 2.2
(-uv)
Source: R. D. Baker and H. G. Applegate, Tex. J. Sci. 25(1—5): 53—59 (1974). Copyright 1974
Texas Academy of Science.
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245
chromatography. At least three and possibly five different soil transf or-
mation products were detected. Endrin ketone and endrin alcohol were
positively confirmed by both analytical techniques; endrin aldehyde was
tentatively confirmed. Two other polar degradation products remained
unidentified. The amount of endrin and its three major transformation
products found in the treated soil layers are given in Table 7.37. Con-
siderable transformation occurred at all depths, with endrin ketone being
the primary product. Ratios of the three products to recovered endrin
indicate that transformation increased with depth, suggesting that the
responsible organisms require anaerobic conditions.
In another experiment by the same group, two uncultivated samples of
(1) the pH 6.4 Lakeland sandy loam and (2) a more acid variety of the
same soil (pH 4.2 Lakeland sandy loam) were sprayed with endrin. One
sample of each had been kept in an air—dried state, while the other had
been moistened with a water spray. Following a 75—day incubation, all
four samples were extracted and analyzed for endrin and its transformation
products; the results are presented in Table 7.38.
In the absence of the soybean plant, no transformation was
detected in the pH 6.4 soil in either the dry or moist state. With the
more acidic soil, some transformation occurred following treatment of the
dry soil only. The major product was endrin ketone, but a second product,
tentatively identified as endrin aldehyde, was also detected.
Erroneous conclusions as to the probable persistence of endrin in the
soil may result if the fate of the pesticide is studied in only one type
of soil under a single set of conditions. Bartha et al. (1967) studied
the stability of endrin and its effect upon CO 2 production and nitrifica—
don in Nixon sandy—loam soil, pH 6.0. Soil samples supplemented with
}I H 2 PO and containing either 250 to 2500 ppm endrin were brought
to 70% of moisture holding capacity and incubated at 28°C for 30 days.
Carbon dioxide production was measured at intervals throughout the
duration of the experiment. Microbial degradation of the endrin would
have resulted in an increased CO 2 production relative to that of an
identical soil sample in the absence of endrin. No such increase occurred.
On the contrary, a 20% decrease in CO 2 production was observed at both
endrin concentrations, indicating that the pesticide was toxic to some
of the soil microorganisms. Addition of glucose reversed this inhibition
of respiration and brought CO 2 production back to 100% of the control
levels. Endrin, at a concentration of 250 ppm, had no effect on nitrate
production in this soil under similar conditions. The higher concentration
(2500 ppm) was not studied for effects upon nitrification. From these
experiments it might be concluded that endrin is not degraded by the
microbial population of Nixon sandy—loam soil. However, as was observed
in the study by Nash et al. (1972), actual field conditions and the
presence of crops may alter the circumstances sufficiently to allow
degradation to take place.
7.5.4.2 Factors affecting the persistence of endrin in the
lithosphere . The extent to which any of the pathways succeed for removal
of endrin from the soil depends, in turn, upon the interplay of a large
-------
Table 7.37. Influence of treatment depth and
endrin residues in Lakeland sandy loam
one soy
(pH =
bean crop on
6.4)
Compound
Total products
(ratio 1 ’)
Total
residues
g/g %
Soil depth
(cm)
Endrin
alcohol
Endrin aldehydea
Endrin
ketone
%
Ratiob
Ratio 1’
%
Ratio ’
7.8
0.13
9.4 0.16
27.7
0.48
0.78
1.856 79.4
8.4
0.20
14.1 0.33
35.5
0.84
1.38
1.018
8.2
0.23
16.0 0.45
40.5
1.15
1.83
1.849
Endrin _________________ ______________
(%)
1—2 57.3
16—17 42.1
31—32 35.3
aT ll identif led.
b i of transformation product to endrin.
Source: R. G. Nash, M. L. Beau, Jr., and W. G. Harris, J. Environ. Quczl. 1(4): 391—394 (1974).
Copyright 1974 American Society of Agronomy.
C’
-------
Table 7.38. Influence of soil moisture on endrin treatment of Lakeland sandy loam
Soil pH
Compounds found
Soil
moisture
Endrin
Endrin
alcohol
Endrin
ketone
Endrin
aldehydea
4.2
Dry
b
C
+
+
4.2
Moist
+
—
—
—
6.4
Dry
+
-
-
6.4
Moist
+
—
—
—
a
Tentatively identified.
bp 0 5 j j
C
Not detected.
Source: R. G. Nash, N. L. Beall, Jr., and W. G. Harris, J. Environ. Qual. 1(4): 391—394
(1974). Copyright 1974 American Society of Agronomy.
-------
248
number of influential parameters. Included among these are the physical
and chemical properties of the pesticide, physical and chemical properties
of the soil, microbial population of the soil, type of crops planted,
agricultural practices employed, topography, temperature, humidity, amount
of rainfall, irrigation and dew, average wind velocity, and intensity of
sunlight. Since many of these parameters affect more than one pathway, it
is only possible to evaluate the effect of each parameter upon persistence
per Se. To estimate the net result of the combined effects of all param—
eters upon all pathways under natural conditions is, however, exceedingly
difficult. An understanding of the direction and extent of a given
parameter upon persistence can, therefore, only serve as a guideline for
assessing the probability that the pesticide in question will persist
under a given set of conditions.
7.5.4.2.1 Soil organic content . Due to their hydrophobic, lipophilic
nature, organochiorine insecticides are expected to adsorb to the organic
matter present in soil. It follows that a correlation should exist between
persistence of these insecticides in various soils and the percent organic
matter in those soils. The difficulties of establishing such correlations
are revealed in the laboratory studies of Bowman et al., 1965. The
adherence of endrin to various soils was examined by determining the
extent to which the pesticide could be removed from soil columns by
percolation with either hexane or distilled water. Endrin was applied
to the top 2 cm of the columns, and the soils were eluted at atmospheric
pressure. Fractions were extracted, pooled, and analyzed by electron—
capture gas chromatography; the results are summarized in Table 7.39.
Endrin remained totally adsorbed to three of the eight soils tested and
moderately adsorbed to two others following elution with hexane. No
relationship existed between the percent organic matter in these soils
and the amount of endrin eluted. However, the range of soil organic
content among these soils was narrow (0.17 to 1.33%) and might not have
been sufficient for a statistically significant comparison.
The Rutledge sands I and II containing 6.56 and 19.43% organic matter,
respectively, exhibited the least retention of endrin, releasing virtually
all of the bound pesticide to hexane with the first 100 ml of eluate.
The unexpected behavior of these soils, which responded in a similar
fashion toward a variety of other organochlorine insecticide as well, was
most probably related to some property other than percent organic content.
One other soil, Greenville sandy clay, also released 98% of the bound
endrin to hexane. In this case, however, the behavior was not inconsistent
with soil organic content (0.57%).
The Rutledge sands behaved as expected when an attempt was made to
elute the adsorbed endrin with distilled water. No trace of endrin was
detected following elution with 1600 ml of water. Difficulties in relating
this behavior to organic content arise, however, when it is considered
that Magnolia sandy—clay loam (organic content 0.72%) and Magnolia sandy
loam (organic content 1.33%) also retained the major portion of the applied
endrin under the same elution conditions. Trace amounts of endrin
degradation products were detected in the aqueous eluates from Magnolia
-------
Eluate
fraction
(ml)
Aa
CC
A
B
C
A
B
C
A
B
C
A
B
C
A
B
C
A
B
C
A
B
C
Eluate
fraction
(ml)
D
E
0
E
U
S
U
B
U
S
U
S
U
B
Organic
Soil matter
(2)
Lynchburg loamy 0.17
sand
Lakeland sand 0.42
deep phase
Greenville sandy 0.57
clay
Magnolia sandy— 0.72
clay loam
Susquehanna sandy 0.77
clay
Magnolia sandy 1.33
loam
Rutledge sand I 6.56
Rutledge sand II 19.43
aA 0 to 100 ml.
bB 100 to 300 ml.
CC = 300 to 500 ml.
dD = 0 to 800 ml.
= 800 to 1600 ml.
= Trace (<0.5%).
Source: modified from Bowman et al., 1965.
Table 7.39.
as
Elution characteristics
determined by percolation
of endrim
with hexane
on various types of soil
and distilled water
Hexane
1120
Endrin
aldehyde
in eluate
(2)
Endrin
ketone in
eluate
(%)
Unidentified
degradation
product
(2)
Added
endrin in
eluste
(2)
Added
endrin in
eluate
(2)
g} 0
g}o
}5
5 }56
}l
l O}
Q}72
}T
}o
}i
981
0 98
oJ
15151
36J
010
oJ
Ti
TJT
0
0
2l}26
g}o
g}o
}T
g}o
g} 0
}95
g}o
}T
g}o
g}
g}o
g}o
}T
g}o
9 r}98
}o
g}o
}o
‘° .r}lo4
g}o
}o
o
}o
-------
250
sandy loam, Magnolia sandy—clay loam, Greenville sandy clay, and Susque—
hanna sandy clay. Seven percent of the endrin residues eluted from
Lakeland sand (deep phase) and 62% of those eluted from Lynchburg loamy
sand consisted of degradation products. The major degradation product
observed in all cases was endrin ketone. However, endrin aldehyde and
another unidentified product were also detected. No degradation occurred
in the Rutledge sands, but whether the lack of degradation is related to
the high organic content of these soils is uncertain.
In a study by Gish (1970), agricultural soils were collected from
67 fields in 8 states of the southern and midwestern United States and
analyzed for the presence of endrin. Since the soil types and organic
contents were also reported, it was possible to examine the data for
correlation between endrin persistence and soil organic content. Sixteen
of the 67 sites surveyed contained endrin residues. The range was from
less than 0.005 to 3.47 ppm, with a median of 0.051 ppm and an arithmetic
mean of 0.49 ppm. Once again, no relationship was noted between the
percent organic content of the soil and the degree to which endrin persisted
The highest endrin concentration (3.47 ppm) was, in fact, detected in
the soil having the lowest organic content (2.98%). However, as in the
case of the Bowman study, the range of organic content was also rather
small (2.98 to 6.70%) and, under the complex conditions which exist
naturally in the field, may not allow for realistic correlation.
Evidence that organic content of soil may indeed influence persistence
can be found in the data of Harris and Sans (1969). Three experimental
plots, set up in 1967 at different locations throughout southwestern
Ontario, were sampled for organochlorine insecticide. Although the
pesticide use records for these plots were not revealed, it was believed
that all had received reasonably similar treatments in previous years.
The soils were sandy loam, clay, and muck and contained 1.4, 3.6, and
66.5% organic matter respectively. The concentrations of total cyclodiene
residues for these soils were 0.76 ppm for the sandy loam, 1.34 ppm for
the clay, and 10.44 ppm for the muck. Although endrin concentrations were
higher in the sandy loam (0.14 ppm) than in the clay, the highest residues
observed were in the highly organic muck soil (5.94 ppm). It therefore
seems probable that the quantity of organic matter present in soil does
influence persistence but that a significant effect is observed only when
the percentage of organic matter is large.
7.5.4.2.2 Moisture and mixing . Since microbial degradation of
organochiorine insecticide occurs predominantly under anaerobic conditions,
little loss of surface—applied pesticide can be expected to occur by this
route. In an attempt to accelerate the disappearance of six chlorinated
insecticides from the top 10 cm of soil, the effects of alternately wetting
and drying the soil and of mixing the soil were examined (Guenzi et al.,
1971). It was believed that the former practice would accelerate volati—
lization, codistillation, and leaching, while the latter would continuously
expose new residues to the surface layer for volatilization and possible
thermal degradation. Experimental plots of Nunn silty—clay loam were set
up at the Colorado State University farm. Each of the pesticides to be
-------
251
studied was added to the top 10 cm of soil to a final concentration of
25 ppm. After application, soils were treated in one of two ways:
(1) 2.5 cm of water was added every week, or (2) 2.5 cm of water was added
every week and the surface 8 cm of soil was mixed every two weeks. For
each of these sets of treatments, one plot received no added energy source,
while a second received 0.25% alfalfa mixed in the top 10 cm of soil.
Soils were sampled and analyzed for the presence of the added pesticide
immediately after pesticide applications and at given intervals thereafter
for a period of 22 weeks, after which all mixing and water treatments were
discontinued, and the plots received only natural precipitation. The soils
were sampled once more for distribution and recovery of pesticides one year
following the initiation of the experiment. All analyses were by electron—
capture gas chromatography; the results for endrin are presented in
Table 7.40.
Table 7.40. Recovery of endrin from soil at various depths after
one year; initial concentration was 25 ppm
Depth
(cm)
WandDa
WandD+Nb
OA
A
OA°
Ad
ppm
%
ppm
%
ppm
%
ppm
%
0—16
12.05
85.5
12.73
89.0
11.63
82.0
12.68
88.0
16—32
0.60
3.2
1.30
7.1
1.70
3.7
0.72
3.7
32—48
0.13
0.7
0.18
0.8
0.10
0.4
0.10
0.4
Total
89.4
96.9
86.1
92.1
a 2 • 5 cm of water added every week and no soil mixing for 22 weeks —
then discontinued.
b 2 5 cm of water added every week and the surface 7.6 cm of soil
mixed every 2 weeks for 22 weeks — then discontinued.
added energy source.
d 0257 alfalfa mixed in the top 10 cm of soil.
Source: W. D. Guenzi, W. E. Beard, and F. G. Viets, Jr., Soil
Sci. Soc. Am. Proc. 35(6): 910—913 (1971).
No differences in endrin concentration in the 0 to 8 cm of soil layer
were observed among the variously treated experimental plots over the
22—week period. The mean concentration during the 22—week period remained
at 20 ppm or 80% of the initial amount. The low recovery (expected
95 to 100%) was attributed to a small vertical distribution of the endrin
as a result of the mechanics of adding and packing and amended soil. In
addition, some of the pesticide may have remained in the emulsion form
-------
252
in which it was applied and been leached to a small extent during the
first water addition.
The total recovery of endrin one year following the initiation of
the study (Table 7.40) was also approximately the same for each of the
experimental plots (91%). The endrin was, however, found to be distributed
throughout the 48 cm of soil depth. Most of the pesticide was found in
the 0— to 16—cm layer, and about 4% and less than 1% were detected in the
16— to 32—cm layer and the 32— to 48—cm layer respectively.
It is interesting to note that concentrations of some other pesticides,
namely, lindane and heptachlor, were greatly affected by similar treat-
ments. After 22 weeks, only 54% of the lindane was recovered from the
top 8—cm layer following alternate wetting and drying, while only 44%
remained when mixing was also performed. Forty—three percent of the added
heptachior remained after 22 weeks of alternate wetting and drying, while
mixing reduced this value to 27%. Alfalfa amendment had no influence upon
the persistence of either pesticide. One year later, 82% of the lindane
was recovered from the combined 48—cm soil plot which had been subjected
to wetting and drying only, while 70% was recovered from the mixed soil.
The disappearance of lindane observed during the initial 22 weeks was
therefore due primarily to leaching into the lower soil strata, although
some volatilization did occur. Loss of heptachior, on the other hand,
was predominantly through volatilization, since only 57% was recovered
from the undisturbed soil and 42% from the mixed soil after one year.
From these studies it would be predicted that decontamination of soil
containing lindane and heptachior could be accelerated by tilling the
soil. This process would, however, have little effect on reducing residues
of endrin under similar conditions.
7.5.4.2.3 Flooding . Microbial degradation of persistent pesticides
may be accelerated by practices leading to anaerobic soil conditions.
Flooding the soil is one method by which anaerobiosis may be stimulated.
In addition, amendment of the soil with a supplementary microbial energy
source such as alfalfa assists the process. The readily available energy
source allows the aerobic soil microorganisms to rapidly deplete the
available oxygen, thereby creating a suitable environment for the anaerobic
degradation of the pesticides (Guenzi et al., 1971) (Sect. 3.).
Castro and Yoshida (1971) studied the degradation of endrin in soils
from the Philippines under both flooded and upland conditions. Four
types of soil were tested, and their characteristics are presented in
Table 7.41.
Endrin proved unstable only in the flooded Casiguron soil. After
two months, only 8.4% of the pesticide was recovered from the flooded soil
as compared with 88.24% from the upland soil. Endrin persisted in all
of the other soils regardless of flooding. Casiguron soil contained a
higher percentage of organic matter (4.4%) than any of the other three
soils studied.
-------
253
Table 7.41. Soils tested for their ability to degrade endrin
.
Soil type
Total
Organic matter
nitrogen
7
p
Maahas clay
2.0
0.14
6.6
Luisiana clay
3.2
0.21
4.7
Pila clay loam
1.5
0.09
7.6
Casiguran sandy loam
4.4
0.2
4.8
Source: modified from Castro and Yoshida, 1971.
Studies to determine the persistence of endrin in flooded vs
nonflooded soils indicated endrin to be degraded more rapidly under
anaerobic (flooded) conditions. Aerobic soil conditions increased per-
sistence of endrin in soil. The addition of rice straw to the water
enhanced endrin’s degradation. Data also indicated microbial participation
in the decomposition process (Gowda and Sethunathan, 1976; Gowda and
Sethunathan, 1977).
7.5.4.2.4 Crop rotation . Some evidence exists that crop rotation may
aid in the dissipation of endrin from the soil. Endrin at the rate of
1.6 lb of active ingredient per acre was applied to two sets of dry—land
plots (Pullman clay loam soil) in June 1959 (Daniels, 1966). One set was
continuously cropped for 11 years with grain sorghum, while the other set
was a rotation of grain sorghum, fallow, and wheat. The plots were
cultivated normally. Soils were analyzed 5 and 11 years after pesticide
application for the presence of endrin; the results are presented in
Table 7.42. Less endrin residues were found in the rotation plots than
in the continuously cultivated plots, and concentrations were generally
Table 7.42. Endrin residues found in Pullman clay loam
soil 5 and 11 years after application
Crop
Residues at indicated soil
(ppm)
depth
.
Upper 6 in.
Lower
.
6 in.
5 years
11 years
5 years
11 years
Continuous
sorghum
Sorghum—fallow—
wheat rotation
0.069
0.029
0.02
<0.0009
0.009
<0.003
<0.0009
0
Source: modified from Daniels, 1966.
-------
254
greater in the first 6 in. than in the lower 6 in., indicating that
movement into lower soil strata is minimal. Even though the endrin
concentration was considerably diminished, the remaining residues continued
to provide satisfactory control of wireworms and grubs for 11 years after
treatment.
The type of crop used for rotation and the subsequent treatment of
the crop undoubtedly affect persistence under field conditions. Rye,
for instance, is usually ploughed down in order to build up the soil and
will not help remove endrin when rotated with an endrin—treated crop such
as tobacco. Rotation of tobacco with winter wheat to corn will help in
removal of endrin from the soil, since these crops will absorb the
pesticide prior to harvest (Harris et al., 1966).
7.5.4.2.5 Type of endrin formulation . Endrin formulations are
prepared as dusts, wettable powders, emulsions, and sprays. The type of
formulation may affect the persistence of the pesticide in the soil.
Sprays tend to disappear sooner than dusts due to a faster initial
volatilization. However, loss from drift is more significant in the
case of dusts (Carey et al., 1973).
The mineral clays used as diluents for the dust and wettable powder
formulations have been shown to catalyze the decomposition of endrin
(Fowkes et al., 1960). Investigations showed that the decomposition was
promoted by the acid sites on the clay and that appropriate neutralization
could reduce decomposition to negligible rates. Since the introduction
and widespread use of clay deactivators, the probability of decomposition
by this mechanism is virtually zero.
7.5.4.3 Studies on the persistence of endrin in the lithosphere .
Several studies have been performed to determine the long—term persistence
and rates of disappearance of endrin in the soil. In 1951, duplicate soil
plots of Congaree sandy—loam soil were established at the Plant Industry
Station, Beltsville, Maryland (Nash and Woolson, 1967). Endrin was applied
to the soil at rates of 56 and 224 kg/ha (25 and 100 ppm), and the soils
were thoroughly mixed prior to placement in the 38—cm plots. The soils
were cropped at various times through 1962, after which time cultivation
was discontinued and weeds were cut when necessary. Soil samples were
taken at intervals through 1966 and analyzed for the persistence of endrin
residues either by estimation of total chlorine content (through 1962)
or by electron—capture gas chromatography. The decline of endrin in
Congaree sandy—loam soil is presented in Fig. 7.10. The quantity of endrin
remaining in the soil 14 years after application was 41% of the applied
amount, and the calculated half—life under the experimental conditions was
approximately 11.8 years. No difference in persistence was noted between
the higher and lower rates of application.
In 1967, the plots were sampled again and degradation products
were identified (Nash and Harris, 1973). The total remaining residues
were 39.2% of the originally applied amount. Of the remaining residues,
54.8% was endrin itself, 38.4% was endrin ketone, 5.7% was tentatively
Identified as endrin aldehyde, and 1.1% was endrin alcohol.
-------
100
75
50
25 —
0—
0 5
255
10
ORNL—DWG 79-8961
15
YEARS
Fig. 7.10. Persistence of endrin in Congaree sandy—loam soil.
Source: R. G. Nash and E. A. Woolson, Science 157: 924—927 (1967).
Copyright 1967 by the American Association for the Advancement of Science.
Due to the manner in which these experimental plots were established
and maintained, an upper limit of soil persistence would be expected
(Nash and Woolson, 1967). Photodecomposition, which occurs only near the
surface of the soil, was probably minimal due to the initial thorough
mixing of endrin throughout the soil and absence of tillage. Volatilization,
which occurs most rapidly at the soil surface, would also have been
depressed by the same procedures, although some losses may have occurred
following upward diffusion of the pesticide or possibly through codistilla—
tion with water. The extremely high rates of endrin application may have
eliminated much of the soil’s zoological and microbial populations, thereby
reducing both microtillage and microbial degradation. Leaching was
minimized by the placement of a gravel layer beneath the soil column.
Mechanical removal via absorption by crops and subsequent harvest was also
negligible, since these plots were not cultivated as extensively as normal
agricultural soils. Thus, endrin is expected to be somewhat less persistent
in the same soil under natural field conditions.
The degree to which endrin accumulates in the soil following repeated
foliar applications over the course of two to three years was studied by
Foster et al. (1956). Experimental plots of Congaree sandy loam, Kouf man
sandy loam, and Sassofras sandy loam were set up at Beltsville, Maryland;
State College, Mississippi; and New Brunswick, New Jersey respectively.
Due to differences in climate and soil among the three locations, the
test crops grown differed widely. Successions of crops were planted,
sprayed with endrin (in the form of a 50% wettable powder), and harvested
over a two— to three—year period from 1951 to 1954. The cumulative amount
of endrin applied at each location and the percent remaining in the soil
at the end of the experiment are presented in Table 7.43. Since all
.
.
0
.
z
z
w
z
w
0
w
0
CONCENTRATION
• 100 ppm
0 25 ppm
0
•
0
-------
256
Table 7.43. Accumulation of endrin in soil
following repeated foliar application
Location
Soil
type
Years
of study
Total amount
applied
(ib)
Amount
remaininga
(%)
Beltsville, MD
Congaree
sandy loam
1951—1954
65
78
State College,
MS
Kaufman
sandy loam
1951—1953
35
25
New Brunswick,
NJ
Sassafras
sandy loam
1952—1954
30
32
apercentage of amount applied.
Source: modified from Foster et al., 1956.
analyses were for total organic chlorine in the soil, they include degrada-
tion products as well as endrin Itself. The percent accumulation of endrin
in the State College and New Brunswick soils was strikingly less than that
observed at Beltsville. It is not known to what extent these differences
were caused by differences in the soils, the crops, the climate, or the
cultivation practices. But these results do indicate the inadvisability
of predicting how much endrin will accumulate in an area of a given soil
on the basis of studies conducted at a different location with other types
of soil.
The distribution of endrin throughout the Congaree sandy—loam plots
at Beltsville 13 years following the last foliar application was studied
by Nash and Woolson (1968). Soil cores from each plot were taken and
sectioned into 7.6—cm lengths. The soils were extracted and the extracts
analyzed for endrin by gas chromatography; the results are presented in
Fig. 7.11. Approximately 80Z of the residual endrin was found in the
upper 23 cm of soil, which probably corresponds to the cultivated layer.
Due to the gravel layer and tile drainage underlying these soil plots,
leaching was minimal. Under normal field conditions in which leaching
would be a more important factor, the downward movement of endrin might
be greater. Another, less obvious fact is that the quantity of endrin
in the surface 7.6 cm was less than the mean quantity between the 7.6—
and 23—cm depths. This indicates that volatility and photodecomposition
may have played a significant role in the dissipation of the endrin from
the surface layers. The total amount of endrin remaining in the soil
in 1966 was 28% of that remaining in 1954 following the last foliar
application. When endrin was incorporated into and thoroughly mixed with
the soil (Nash and Woolson, 1967), the total amount remaining in the
soil in 1966 was 44% of that remaining 1954, three years following
treatment. Thus, endrin persistence is greater when incorporated into
the soil than when surface—applied to the crops. These figures also
suggest that photodecomposition and volatilization are quite significant.
-------
257
0 ORNL-Dw( ( b
7.6
.
15.3
I
I-
0
U i
22.9
30.5
EN DR IN
38.0 I I I I
0 10 20 30 40
PERCENT
Fig. 7.11. Distribution of endrin in a 38—cm Congaree sandy—loam
soil profile 13 years after the last foliar application. Source:
R. G. Nash and E. A. Woolson, Soil Sci. Soc. Am Proc. 32: 525—527 (1968).
Copyright 1968 by the Soil Science Society of America.
The disappearance of endrin from a soil surface in the field, as
indicated by loss of biological activity, was investigated by Mulla (1960).
Samples of Coachella fine sand were placed in wooden boxes and treated
(to a depth of 6 in.) with endrin emulsion at a rate equivalent to 4.8 lb
(2.2 kg) of toxicant per acre. After treatment, the boxes were placed
in the ground, their tops flush with the surface, in an open vineyard in
Southern California which was exposed to sunlight throughout the day.
Soil temperatures ranged from lows of 38°F (3.3°C) at 6 AN and 10 PM to
highs of greater than 120°F (49°C) at noon. The disappearance of endrin
from the soil was determined by the mortality of Hippelates colluson
(eye gnat) and Culex quinquefasciatus larvae (mosquito larvae) following
exposure to the treated soil at intervals following endrin application.
The data are presented in Table 7.44 and summarized in Fig. 7.12. The loss
of endrin appears to follow the same trend in the tests conducted using
both insects. After 48 hr the percentages remaining as indicated by eye
gnat and mosquito larvae were 30 and 35 respectively. After 144 hr (six
days) the figures were 25 and 22%. Half of the applied dosage was lost
24 hr after application. Since the toxicity of endrin degradation products
for these species was not indicated and since degradation products were
not measured, the possibility exists that some undetected degradation
products also remained in the soil. Nevertheless, endrin did disappear
-------
258
Table 7.44. Loss of endrin activity from the surface of soil in the
field as tested against Hippelates colluson and
Culex quinquefasciatus larvae
Treatment
Hippelates colluson
Hours
after
treatment
Average Reduc— Toxicant
No. gnats! tion recovered!
jara (%) acre (lb)
Loss
Endriè
1
7 93 4.8
0
24
53 49 2.1
56
48
84 20 1.4
70
96
84 20 1.4
70
144
90 14 1.2
75
Control
1
104
Treatment
Cu lex quinquefasciatus
Hours
after
treatment
Average
Insecticide
mortality presentC
of larvae
(ppm)
(%)
Average
lossC
(%)
Endrin’
1
100 0.0490
0
24
81 0.0260
47
48
50 0.0170
65
96
16 0.0102
79
144
19 0.0108
78
aFive replicates.
quantity detectable is 0.7 lb/acre.
°Average of 3 tests each with 3 replicates per test. The percent
loss was calculated from standard dosage mortality line for each
material.
dMinimum quantity detected was 0.007 ppm.
Source: C. U. Brett and T. C. Bowery, J. Econ. Entomol.
51(6): 818—821 (1958). Copyright 1958 Entomological Society of
America.
quite rapidly, probably as a result of volatilization from the sandy soil
(low organic content) in the hot sun.
In conclusion, it appears that knowledge of the persistence of endrin
in a particular soil at a given location may only be obtained with
-------
ORNL—DWG 79—8963
80
70
60
— 50
U)
U) 40
0
-J
30
20
10
0
120 144
Fig. 7.12. Loss of endrin from surface of the soil as determined
by bioassay procedure against eye gnats and mosquito larvae. Source:
M. S. Mulla, J. Econ. Entomol. 53(4): 650—653 (1960). Copyright 1960
Soil Science Society of America.
certainty through investigations conducted with that soil at that location.
Auxiliary studies may, however, provide guidelines as to what might be
expected. Included among these guidelines are the following:
1. Endrin appears to be less persistent if applied to crops or to soil
surface than if mixed throughout the soil.
2. Volatilization and photodecomposition are primarily responsible for
the disappearance of endrin from soil surfaces.
3. Microbial degradation of endrin occurs anaerobically, and conditions
which lead to a decrease in the soil oxidation—reduction potentional
(such as flooding) accelerate endrin decomposition by this route.
Microbial degradation is more significant at lower soil depths.
4. Cultivating the soil aids in the dissipation of endrin. Crop rotation
is more effective than continuous cropping.
5. Soil organic content encourages persistence only when the percentage
of organic matter is very large, as in the case of the muck soils
used fot growing vegetables. Volatilization is most substantial from
sandy soils.
6. Unless conditions are specified, it is not correct to label endrin
as persistent in the lithosphere. Half—lives ranging from 24 hr
to 11.8 years have been observed.
0 24 48 72 96
EXPOSURE TIME (hr)
-------
260
7.6 REFERENCES
Abbott, D. C., R. B. Harrison, J. O’G. Tatton, and J. Thompson. 1965.
Organochlorine Pesticides in the Atmospheric Environment. Nature (London)
208(5017): 1317—1318.
Abbott, D. C., R. B. Harrison, J. O’G. Tatton, and J. Thompson. 1966.
Organochiorine Pesticides in the Atmosphere. Nature (London) 211(5046):
259—261.
Adams, R. S. 1967. Effect of Soil Organic Matter on the Movement and
Activity of Pesticides in the Environment. In: Proceedings of the First
Annual Conference on Trace Substances in Environmental Health. University
of Missouri, Columbia, Mo., pp. 81—93.
All, K. A., and M. R. G. K. Nair. 1973. Microbioassay of Endrin Residues
on Rice 2. Determination of Residues on Rice Plants. Madras Agric. J.
60(7): 439—440.
Andrilenas, P. A. 1974. Farmers’ Use of Pesticides in l971...Quantities.
Economic Research Service, U.S. Department of Agriculture, Washington,
D.C. Agric. Econ. Rep. 252, 56 pp.
Anonymous. 1964. Catfish vs. Insecticides. Agric. Chem. 19(5): 20.
Anonymous. 1975c. Pesticide Blamed as Pelican Killer. The Washington
Star, July 2, UPI story, p. A—9.
Arthur, R. D., J. D. Cain, and B. F. Barrentine. 1976. Atmospheric Levels
of Pesticides In the Mississippi Delta. Bull. Environ. Contain. Toxicol.
15(2): 129—134.
Baker, R. D., and H. G. Applegate. 1974. Effect of Ultraviolet Radiation
on the Persistence of Pesticides. Tex. J. Sd. 25(1—4): 53—59.
Bartha, R., R. P. Lanzilotta, and D. Pramer. 1967. Stability and Effects
of Some Pesticides In Soil. Appi. Microbiol. 15(1): 67—75.
Barthel, W. F., J. C. Hawthorne, J. H. Ford, G. C. Bolton, L. L. McDowell,
B. H. Grissinger, and D. A. Parsons. 1969. Pesticide Residues in Sediments
of the Lower Mississippi River and Its Tributaries. Pestic. Monit. J.
3(1): 8—68.
Baall, N. L., Jr., and R. G. Nash. 1971. Organochlorine Insecticide
Residues in Soybean Plant Tops: Root vs. Vapor Sorption. Agron. J.
63(3): 460—464.
Beau, N. L., Jr., and R. G. Nash. 1972. Insecticide Depth in Soil — Effect
on Soybean Uptake In the Greenhouse. J. Environ. Qual. 1(3): 283—288.
-------
261
Bowman, M. C., M. S. Schechter, and R. L. Carter. 1965. Behavior of
Chlorinated Insecticides in a Broad Spectrum of Soil Types. J. Agric.
Food Chein. 14(4): 360—365.
Breidenbach, A. W., C. G. Gunnerson, A. B. Kawahara, J. J. Lichtenberg,
and R. S. Green. 1967. Chlorinated Hydrocarbon Pesticides in Major
River Basins, 1957—65. Pubi. Health Rep. 82(2): 139—156.
Brett, C. H., and T. G. Bowery. 1958. Insecticide Residues on Vegetables.
J. Econ. Entomol. 51(6): 818—821.
Bridges, W. R. 1961. Disappearance of Endrin from Fish and Other Materials
of a Pond Environment. Trans. Am. Fish. Soc. 90: 332—334.
Brooks, G. T. 1974a. Chlorinated Insecticides. Vol. 1: Technology and
Application. CRC Press, Cleveland, Ohio.
Brown, E., and Y. A. Nishioka. 1967. Pesticides in Selected Western
Streams — A Contribution to the National Program. Pestic. Monit. J.
1(2): 38—45.
Burton, W. B., and G. E. Pollard. 1974. Rate of Photochemical Isomerization
of Endrin in Sunlight. Bull. Environ. Contain. Toxicol. 12(1): 113—116.
Butler, P. A. 1973. Organochlorine Residues in Estuarine Mollusks,
1965—72 — National Pesticide Monitoring Program. Pestic. Monit. J. 6(4):
238—362.
Carey, A. E., G. B. Wiersina, H. Tai, and W. G. Mitchell. 1973.
Organochlorine Pesticide Residues in Soils and Crops of the Corn Belt
Region, United States — 1970. Pestic. Monit. J. 6(4): 369—376.
Castro, T. F., and T. Yoshida. 1971. Degradation of Organochlorine
Insecticides in Flooded Soils in the Philippines. J. Agric. Food Chem.
19(6): 1168—1170.
Castro, T. F., and T. Yoshida. 1974. Effect of Organic Matter on the
Biodegradation of Some Organochiorine Insecticides in Submerged Soils.
Soil. Sd. Plant Nutr. 20(4): 363—370.
Chesters, G., and J. G. Konrad. 1971. Effects of Pesticide Usage on
Water Quality. BioScience 21(12): 565—569.
Compton, B., P. P. Bazydlo, and G. Zweig. 1972. Field Evaluation of
Methods of Collection and Analysis of Airborne Pesticides. Vol. 1 —
EPA—R4—72—004a, Research Triangle Park, N.C., 149 pp.
Crockett, A. B., G. B. Wiersina, H. Tai, W. G. Mitchell, and P. .1. Sand.
1971. National Soils Monitoring Program for Pesticide Residues — FY 1970.
Monitoring Panel of the Federal Working Group on Pest Management, .J.S.
Environmental Protection Agency and U.S. Department of Agriculture, 85 pp.
-------
262
Daniels, N. E. 1966. Soil Insect Control and Insecticide Residue
Detection. J. Econ. Entomol. 59(2): 410—413.
Daryodel, F., M. Behboody, and S. Teimury. 1971. Searching for Endrin
Residue on Cotton Seed, by Gas Chromatography Method. Iran Institu
des Recherches Entomologigues et Phytopathologigues Entomologie et
Phytoputhologie Appliques 31: 15—16.
Eichelherger, 3. W., and J. J. Lichtenberg. 1971. Persistence of
Pesticides in River Water. Environ. Sci. Technol. 5(6): 541—544.
Eichers, T., P. Andrilenas, R. Jenkins, and A. Fox. 1968. Quantities of
Pesticides Used by Farmers in 1964. U.S. Government Printing Office,
Washington, D.C., 37 pp.
Eichers, T., P. Andrilenas, H. Blake, R. Jenkins, and A. Fox. 1970.
Quantities of Pesticides Used by Farmers in 1966. U.S. Department of
Agriculture, Economic Research Service, Washington, D.C. Agricultural
Economic Report No. 179, 61 pp.
Pay, R. R., and L. W. Newland. 1972a. Organochiorine Insecticide Residues
in Water, Sediment, and Organisms, Arkansas Bay, Texas — September 1969—
June 1970. Pestic. Monit. 3. 6(2): 97—102.
Foster, A. C., V. R. Boswell, R. D. Chishoim, R. H. Carter, G. L. Gilpin,
B. B. Pepper, W. S. Anderson, and N. Geiger. 1956. Some Effects of
Insecticide Spray Accumulations in Soil on Crop Plants. U.S. Department
of Agriculture, Technical Bulletin 1149, 36 pp.
Fowkes, F. N,, H. A. Benesi, L. B. Ryland, W. M. Sawyer, K. D. Detling,
E. S. Loeffler, F. B. Folckemer, N. R. Johnson, and Y. P. Sun. 1960.
Clay—Catalyzed Decomposition of Insecticides. J. Agric. Food Chem.
83(3): 203—210.
Frost, 3. 1969. Earth, Air, and Water. Environment 11(6): 14—29 and
31—33.
Gish, C. D. 1970. Organochiorine Insecticide Residues in Soils and Soil
Invertebrates from Agricultural Lands. Pestic. Monit. 3. 3(4): 241—252.
Codsil, P. 3., and W. C. Johnson. 1968. Pesticide Monitoring of the
Aquatic Biota at the Tule Lake National Wildlife Refuge. Pestic. Nonit.
3. 1(4): 21—26.
Golden, M. F., and C. E. Twilley. 1976. Fisheries Investigation of a
Channelized Stream, Big Muddy Creek Watershed, Kentucky. Trans. Ky. Acad.
Sci. 37(3—A): 85—90.
Gowda, T. K. S., and N. Sethunathan. 1976. Persistence of Endrin in
Indian Rice Soils Under Flooded Conditions. 3. Agric. Food Chem. 24(4):
750—753.
-------
263
Gowda, T. K. S., and N. Sethunathan. 1977. Endrin Decomposition in Soils
as Influenced by Aerobic and Anaerobic Conditions. Soil Sci. 124(1):
5—9.
Guenzi, W. D., W. E. Beard, and F. G. Viets, Jr. 1971. Influence of Soil
Treatment on Persistence of Six Chlorinated Hydrocarbon Insecticides in
the Field. Soil Sci. Soc. Am. Proc. 35(6): 910—913.
Hannon, M. R., Y. A. Greichus, R. L. Applegate, and A. C. Fox. 1970.
Ecological Distribution of Pesticides in Lake Poinsett, South Dakota.
Trans. Am. Fish. Soc. 99(3): 496—500.
Harris, C. R., and W. W. Sans. 1969. Absorption of Organochlorine
Insecticide Residues from Agricultural Soil by Crops Used for Animal
Feed. Pestic. Monit. J. 3(3): 182—185.
Harris, C. R., and W. W. Sans. 1971. Insecticide Residues in Soils on
16 Farms in Southwestern Ontario — 1964, 1966, and 1969. Pestic. Monit.
J. 5(3): 259—267.
Harris, C. R., W. W. Sans, and J. R. W. Miles. 1966. Exploratory Studies
on the Occurrence of Organochiorine Insecticide Residues in Agricultural
Soils in Southwestern Ontario. J. Agric. Food Chem. 14(4): 398—403.
International Agency for Research on Cancer. 1974. Evaluation of
Carcinogenic Risk of Chemicals to Man. Vol. 5, Some Organochiorine
Pesticides, pp. 157—172.
Iverson, L. G. K. 1967. Monitoring of Pesticide Content in Water in
Selected Areas of the United States. In: Agricultural and the Quality
of Our Environment. N. C. Brady (ed.). AAAS Publication 85, Washington,
D.C., pp. 157—162.
Kalkat, G. S., R. U. Davidson, and C. L. Brass. 1961. The Effect of
Controlled Temperature and Humidity on the Residual Life of Certain
Insecticides. J. Econ. Entomol. 54(6): 1186—1190.
Kennedy, M. V., B. J. Stojanovic, and F. L. Shuman, Jr. 1969. Chemical
and Thermal Methods for Disposal of Pesticides. Residue Rev. 29: 89—104.
King, K. A., and E. L. Flickinger. 1977. The Decline of Brown Pelicans
on the Louisiana and Texas Gulf Coast. Southwest Nat. 21(4): 417—431.
Klein, W., and F. Korte. 1967. Conversion of Pesticides Under Atmospheric
Conditions and in Soil. In: Proceedings of the First Annual Conference
on Trace Substances in Environmental Health. University of Missouri,
Columbia, No., pp. 71—80.
Knutson, H., A. M. Kadoum, T. L. Hopkins, G. F. Swoyer, and T. L. Harvey.
1971. Insecticide Usage and Residues in a Newly Developed Great Plains
Irrigation District. Pestic. Monit. J. 5(1): 17—27.
-------
264
Koeman, J. H., J. H. Pennings, 3. 3. M. DeGoeij, P. S. Tjioe, P. M. Olindo,
and 3. Hopcraft. 1972. A Preliminary Survey of the Possible Contamination
of Lake Nakuru in Kenya with Some Metals and Chlorinated Hydrocarbon
Pesticides. 3. Appi. Ecol. 9(2): 411—416.
Kolipinski, N. C., A. L. Higer, and M. L. Yates. 1971. Organochlorine
Insecticide Residues in Everglades National Park and Loxahatchee National
Wildlife Refuge, Florida. Pestic. Monit. 3. 4(3): 281—288.
Kutz, F., A. Yobs, and H. Yang. 1976. In: Air Pollution from Pesticides
and Agricultural Processes, R. Lee, Jr. (ed.). CRC Press, Cleveland, Ohio,
pp. 95—136.
Lauer, G. J., H. P. Nicholson, W. S. Cox, and J. I. Teasley. 1966.
Pesticide Contamination of Surface Waters by Sugarcane Farming in Louisiana.
Trans. Am. Fish. Soc. 95(3): 310—316.
Lichtenberg, J. 3., 3. W. Eichelberger, R. C. Dressman, and J. E. Longbottom.
1970. Pesticides in Surface Waters of the United States — A 5—Year
Summary — 1964—68. Pestic. Monit. 3. 4(2): 71—86.
Lyon, W. F., and R. H. Davidson. 1965. The Effect of Humidity on the
Volatilization of Certain Insecticides. 3. Econ. Entomol. 58(5): 1037.
Lyons, E. T., and H. A. Salman. 1972. Development of Analytical Procedures
for Determining Chlorinated Hydrocarbon Residues in Waters and Sediments
from Storage Reservoirs. U.S. Department of the Interior, Bureau of
Reclamation, NTIS, Springfield, Va. REC—ERC—72—l5.
Manigold, D. B., and 3. A. Schuize. 1969. Pesticides in Water—Pesticides
In Selected Western Streams — A Progress Report. Pestic. Monit. 3. 3(2):
124—135.
Mann, W. F., Jr., T. E. Campbell, and 3. P. Barnett. 1971. Loss of Endrin
from Repellent—Coated Pine Seed. U.S. Department of Agriculture, Forest
Service, Southern Forest Experiment Station, New Orleans, La. U.S. Forest
Service Research Note 50—135.
Marston, R. B., R. M. Tyo, and S. C. Middendorff. 1969. Endrin in Water
from Treated Douglas Fir Seed. Pestic. Nonit. 3. 2(4): 167—171.
Matsumura, F., U. C. Khanvilkar, K. C. Patil, and C. N. Boush. 1971.
Metabolism of Endrin by Certain Soil Microorganism. J. Agric. Food Chem.
19(1): 27—31.
Lewis, R. 1976. In: Air Pollution from Pesticides and Agricultural
Processes. R. Lee (ed.). CRC Press, Cleveland, Ohio. pp. 51—94.
Mattick, L. R., D. L. Barry, F. N. Antenucci, and A. W. Avens. 1963.
The Disappearance of Endrin Residues in Cabbage. 3. Agric. Food Chem.
11(1): 54—55.
-------
265
Miles, J. R. W., and C. R. Harris. 1973. Organochlorine Insecticide
Residues in Streams Draining Agricultural, Urban—Agricultural, and Resort
Areas of Ontario, Canada 1971. Pestic. Monit. J. 6(4): 363—368.
Modin, J. C. 1969. Chlorinated Hydrocarbon Pesticides in California
Bays and Estuaries. Pestic. Nonit. J. 3(1): 1—7.
Mulla, M. S. 1960. Loss of Chlorinated Hydrocarbon Insecticides from
Soil Surface in the Field. J. Econ. Entomol. 53(4): 650—653.
Nash, R. G., and W. G. Harris. 1973. Chlorinated Hydrocarbon Insecticide
Residues in Crops and Soil. J. Environ. Qual. 2(2): 269—273.
Nash, R. G., and E. A. Woolson. 1967. Persistence of Chlorinated
Hydrocarbon Insecticides in Soils. Science 157(3791): 924—927.
Nash, R. C., and E. A. Woolson. 1968. Distribution of Chlorinated
Insecticides in Cultivated Soil. Soil Sd. Soc. Am. Proc. 32: 525—527.
Nash, R. C., H. L. Beall, Jr., and W. G. Harris. 1972. Endrin
Transformations in Soil. J. Environ. Qual. 1(4): 391—394.
Novak, A. F., and M. R. Rao. 1965. Food Safety Program: Endrin
Monitoring in the Mississippi River. Science 150(3704): 1732.
PaUl, K. C., F. Matsumura, and G. M. Boush. 1970. Degradation of
Endrin, Aidrin, and DDT by Soil Microorganisms. Appi. Microbiol. 19(5):
879—881.
Personal communication with F. W. Kutz. U.S. Environmental Protection
Agency, Washington, D.C. October 1975.
Personal communication with R. Lewis. National Environmental Research
Center, Rasearch Triangle Park, N.C. September 1975.
Pfister, R. M., P. R. Dugan, and J. I. Frea. 1969. Nicroparticulates:
Isolation from Water and Identification of Associated Chlorinated Pesticides.
Science 166(3907): 878—879.
Plimmer, J. R. 1971. Photochemistry of Organochlorine Insecticides.
In: Proceedings of the Second UIPAC Congress of Pesticides Chemistry:
Fate of Pesticides in Environment, Tel Aviv, Israel, pp. 413—432.
Risebrough, R. W., R. J. Huggetc, J. J. Griffin, and E. D. Goldverg.
1968. Pesticides: Transatlantic Movements in the Northeast Trades.
Science 159(3/15): 1233—1236.
Rowe, D. R., L. W. Canter, P. J. Snyder, and J. W. Mason. 1971. Dieldrin
and Endrin Concentrations in a Louisiana Estuary. Pestic. Monit. J. 4(4):
177—183.
-------
266
Saha, J. C., and A. K. Sumner. 1971. Organochiorine Insecticide
Residues in Soil from Vegetable Farms in Saskatchewan. Pestic. Nonit. J.
5(1): 28—31.
Saha, J. G., C. H. Craig, and W. K. Janzen. 1968. Organochiorine
Insecticide Residues in Agricultural Soil and Legume Crops in Northeastern
Saskatchewan. J. Agric. Food Chem. 16(4): 617—619.
Saunders, J. W. 1969. Mass Mortalities and Behavior of Brook Trout and
Juvenile Salmon in a Stream Polluted by Agricultural Pesticides. Can.
Fish. Res. Board J. 26(3): 695—699.
Schafer, H. L., J. T. Peeler, W. S. Gardner, and J. E. Campbell. 1969b.
Pesticides in Drinking Water — Waters from the Mississippi and Missouri
Rivers. Environ. Sci. Technol. 3(12): 1261—1269.
Schuize, J. A., D. B. Manigold, and F. L. Andrews. 1973. Pesticides in
Selected Western Streams — 1968—71. Pestic. Monit. 3. 7(1): 73—84.
Seal, W. L., L. H. Dawsey, and G. E. Cavin. 1967. Monitoring for
Chlorinated Hydrocarbon Pes.ticides in Soil and Root Crops in the Eastern
States in 1965. Pestic. Monit. J. 1(3): 22—25.
Shell Chemical Corporation. 1959. Handbook of Aldrin, Dieldrin and
Endrin Formulations, 2nd ed. SC:59—54—June. Agricultural Chemicals
Division, New York.
Soto, A. R., and W. B. Deichmann. 1967. Major Metabolism and Acute
Toxicity of Aidrin, Dieldrin, and Endrin. Environ. Res. 1: 307—322.
Sparr, B. I., W. G. Appleby, D. N. DeVries, 3. V. Osmun, J. N. McBride,
and G. L. Foster. 1966. Advances in Chemistry Series No. 60, A. A.
Rosen and H. F. ICraybill, Eds. Insecticide Residues in Waterways from
Agricultural Use. In: Organic Pesticides in the Environment. ACS,
Washington, D.C., pp. 146—162.
Stanley, C. W., J. E. Barney II, M. H. Helton, and A. R. Yobs. 1971.
Measurement of Atmospheric Levels of Pesticides. Environ. Sd. Technol.
5(5): 430—435.
Stewart, 0. K. R., A. A. MacLean, and E. R. Kimball. 1977. Insecticide
Residues in Bottom Sediments of Two New Brunswick Streams Draining
Agricultural Land. Can. J. Soil Sd. 57: 15—20.
Stoltenberg, 0. H. 1972. How to Reclaim a Poisoned Lake. Public Works
103(3): 59—61.
Suzuki, N., Y. Yamato, and T. Watanabe. 1973a. Multiple Organochlorine
Pesticide Residues in Japan. Bull. Environ. Contain. Toxicol. 10(3):
145—150.
-------
267
Tabor, E. C. 1965. Pesticides in Urban Atmospheres. J. Air Pollu.
Control Assoc. 15(9): 415—418.
Tarrant, K. R., and J. Tatton. 1968. Organochiorine Pesticides in
Rainwater in the British Isles. Nature (London) 219(5155): 725—727.
Tessari, J. D., and D. L. Spencer. 1971. Air Sampling for Pesticides
in the Human Environment. J. Assoc. Of f. Anal. Chem. 54(6): 1376—1382.
U.S. Army, Corps of Engineers. 1975. Maintenance Dredging—Sediment
and Water Quality Assessment. New Orleans District, New Orleans, La.
U.S. Department of Agriculture. 1968. The Regulation of Pesticides
in the United States. U.S. Department of Health, Education, and Welfare,
and Food and Drug Administration.
U.S. Environmental Protection Agency. 1970b. Pesticide Residues in
Ambient Air, 1970, Maximum—Minimum Levels (Nanograms/Cubic Meter).
Division of Pesticide Community Studies, Chamblee, Ga.
U.S. Environmental Protection Agency. l97la. Pesticide Residues in
Ambient Air, 1971. Division of Pesticide Community Studies, Chamblee,
Ga.
U.S. Environmental Protection Agency. 197lb. Incidence of Pesticide
Residues in Ambient Air. Division of Pesticide Community Studies,
Chamblee, Ga.
U.S. Environmental Protection Agency. 1972. Development of a Case Study
of the Total Effect of Pesticides in the Environment, Non—Irrigated
Croplands of the Mid—West. Pesticide Study Report 4 in compliance of
PL91—224.
U.S. Environmental Protection Agency. 1974a. Draft Analytical
Report — New Orleans Area Water Supply Study. Lower Mississippi River
Facility, Surveillance and Analysis Division, Region VI, Dallas, Tex.
U.S. Environmental Protection Agency. 1975b. Endrin Residues in Whole
Water Samples (pg/l) and Bottom Deposits (ag/kg) in Drainage Basins of
the United States and Puerto Rico.
U.S. Environmental Protection Agency. 1975c. National Urban Monitoring
Program, Endrin Data — ppm. Data charts from the Office of Pesticide
Programs. 5 pp.
Wiersma, G. B., P. F. Sand, and R. L. Schutzmann. l971a. Chlorinated
Hydrocarbon and Organophosphate Residues in Wheat and Soil. Agricultural
Research Service, United States Department of Agriculture, ARS 81—44, 5 pp.
Wiersnia, G. B., H. Tai, and P. F. Sand. l972a. Pesticide Residues in
Soil from Eight Cities — 1969. Pestic. Monit. J. 6(2): 126—131.
-------
268
Wiersma, G. B., W. G. Mitchell, and C. L. Stanford. 1972c. Pesticide
Residues in Onions and Soil — 1969. Pestic. Monit. J. 5(4): 345—347.
Willis, C. H., and R. A. Hamilton. 1973. Agricultural Chemicals in
Surface Runoff Ground Water and Soil: I. Endrin. J. Environ. Qual.
2(4): 463—466.
Willis, G. H., J. F. Parr, R. I. Papendick, and S. Smith. 1969. A
System f or Monitoring Atmospheric Concentrations of Field—Applied
Pesticides. Pestic. Monit. J. 3(3): 172—176.
Winnett, G., and J. P. Reed. 1968. Aidrin, Dieldrin, Endrin, and
Chiordane Persistence — A 3—Year Study. Pestic. Monit. J. 2(3): 133—136.
Working Group on Pesticides. 1970. Ground Disposal of Pesticides: The
Problem and Criteria for Guidelines. NTIS, Springfield, Va. PB 197 144,
pp. 1—61.
Yobs, A. R., J. A. Hanan, B. L. Stevenson, J. J. Boland, and H. F. Enos.
1972. Levels of Selected Pesticides in Ambient Air of the United States
(presented at National American Chemical Society — Symposium on Pesticides
in Air, Boston, Mass., April 11, 1972).
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8. ENVIRONMENTAL INTERACTIONS AND THEIR CONSEQUENCES
8.1 SUNMARY
Endrin enters the terrestrial environment primarily by deliberate
application to crops. Associated routes of entry such as disposal and
cleaning of equipment, vaporization, and surface runoff serve to transfer
endrin to the aquatic and atmospheric compartments.
In the latest available figures (for the fiscal year 1973), the
average daily intake of endrin by a man was 0.033 pg. This is at least
two orders of magnitude below the WHO/FAO acceptable daily intake of
138.2 pg. Daily intakes of 1 pg or less have been reported since 1965,
while the frequency of endrin occurrence in food composites has decreased
from 2.8% in 1965 to 0.3% in 1973.
The concentrations of endrin found in water and air are also far
below accepted limits, except for occasional high levels in the immediate
vicinity of endrin usage. The maximum air concentration of endrin in 1975
was found in Jackson, Mississippi, 0.5 ng/m 3 . The threshold limit value
is 100 pg/m 3 . And drinking water from a high endrin usage area in
Louisiana contained a maximum endrin concentration of 23 ppt, less than
one—fourth the suggested reasonable level of 100 ppt for potable water.
Processing of foods by storage, heating, freezing, and peeling root
vegetables serves to lower endrin residues by as much as 80%. However,
endrin residues in or on tobacco are not lost after curing (when approxi-
mately 40% of the residual endrin disappears); an average of 0.2 pg of
endrin is present in a commercial cigarette.
Endrin has been shown to alter the nutritional value of some crops.
Calcium, iron, and amino acid composition in wheat were reported to be
significantly changed by soil concentrations of endrin as low as 10 ppm.
Biomagnification of endrin does not occur in succeedingly higher
trophic levels of food chains. Bioconcentration does take place up to
thousands of times the ambient concentrations. However, residue con-
centrations are based on partition between tissues, body fluids, and
ambient concentration and are correlated to exposure levels and duration,
solubilization in fat, and physiological changes.
Endrin resistance develops in a number of animals in response to
chronic endrin exposure. The resistance apparently is controlled
genetically and affords the resistant animal not only cross—resistance
to many other organochlorine pesticides but also tolerance to higher
endrin residues. It is these high residues (as much as 200 times the
levels tolerated by susceptible animals) that pose a potential hazard
to the environment. Both ingestion of prey with high endrin residues
and release of the residues to ambient water cause mortality to other
269
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270
components of the ecosystem. Sublethal endrin effects such as reproductive,
growth, and behavioral changes also disrupt the structure of a community.
Plants do not bioconcentrate endrin much above soil concentrations,
but they translocate endrin from aerial parts to roots and soil as well
as from soil to leaves and air. Thus, plants act to distribute endrin in
the environment and expose more members of the ecosystem. The large
biomass of plants makes them important in endrin cycling.
Worldwide monitoring data show that endrin occurs at very low
levels, if at all. Since the massive fish kills in the Mississippi
River and delta in 1963—64, the occurrence of endrin in the United States
has steadily decreased. However, endrin has the highest acute toxicity
of the common organochlorine insecticides, making even low levels of
endrin a potential threat to the environment.
8 • 2 ENVIRONNENTAL CYCLING OF ENDRIN
Pesticides do not remain localized at the point of application but
undergo cycling, by numerous pathways, throughout the envrionment. The
function of a transport model is to define these pathways and estimate
their relative importance in terms of frequency and quantity. Although
the processes resulting in release of endrin to the environment and the
mechanisms by which it is transported are known, the data necessary for
a quantitative model are not available. Qualitative judgments as to
which transport mechanisms predominate are, however, possible from
analysis of both experimental and circumstantial evidence.
The routes by which endrin enters the environment are presented in
Fig. 8.1. Although any one of these pathways might predominate under
specialized conditions, vaporization from treated crops and soil, surface
runoff, and direct application represent the major routes to the atmosphere,
freshwater hydrosphere, and lithosphere respectively (Sects. 7.2 through
7.5).
An often overlooked, but unquestionably significant, route of endrin
dispersion is the disposal and cleaning of contaminated containers and
applicators. In one report, disposal of empty containers was listed as
the third major source of endrin into the environment (U.S. EPA, 1972).
The results of a survey to determine the disposal methods most frequently
used by farmers are presented in Table 8.1. The most common procedure,
open burning, undoubtedly results in volatilization of significant quan-
tities of endrin, while the second most common procedure, rinsing and
saving, is often carried out in streams, resulting in contamination of
the hydrosphere (Saunders, 1969). Rinsing of spray equipment is usually
performed at the same time. The third ranking practice, intermixing with
other solid waste for dumping or incineration, leads to possible
contamination of the lithosphere and the atmosphere respectively.
-------
ORNL-DWG 79-8644
AND WIND
KEY
- .4
I—I
RESERVOIR
FLOW PATH
> ROUTE INTO THE AIR IA ),
WATER (WI. OR TERRESTRIAL
IT) ENVIRONMENT
Fig. 8.1. Possible routes of endrin into the environment.
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272
Table 8.1. Disposal methods used by farmers
Rank
Disposal
method
Comment
1
Burn
Containers burned with other
trash in open fire
2
Wash and
save
Containers rinsed out and stored
or reused
3
Throw in
trash
Containers thrown for pickup with
other solid waste
4
Bury
Farmer buries containers on his
property
5
Discard
Farmers throw containers in ditch
or field edge
Source: U.S. EPA, 1972.
A schematic representation of the movement of endrin through the
environment following its release to the atmosphere, hydrosphere, or
lithosphere is presented in Fig. 8.2.
While pathways such as surface runoff, irrigation, and dredging
may be of significant consequence in terms of transport from one
compartment of the environment to another, the effects, although often
quite serious, are for the most part local. The only mechanisms able
to account for the worldwide distribution of appreciable quantities of any
pesticide are those which occur via the atmosphere. A typical cycle of
atmospheric transport is presented in Fig. 8.3.
On one day in January 1965, 5 to 6 tons of dust per square mile was
deposited in Cincinnati, Ohio, during a light rain. The dust originated
in western Texas, where it had been picked up in a large wind stream
on the previous day. At the time the dust fall occurred in Cincinnati,
the dust cloud resulting from the storm stretched for 1500 miles in a
200—mile—wide band extending from the Gulf of Mexico to Lake Erie. The
dust contained a total of 1.3 ppm chlorinated hydrocarbon insecticides
(Frost, 1969).
The majority of endrin released or transported to the hydrosphere
becomes adsorbed to suspended particulate matter and is eventually carried
to the sediment. High levels of endrin residues in fresh water are almost
always temporary, being associated with eroded soil particles which
subsequently settle out (Frost, 1969). Although some redissolution may
occur under normal circumstances, it is usually during periods of turbulence
(such as heavy storms or dredging operations) that the sediment is suf-
ficiently disturbed to effect resuspension of particulate matters with
maximum release of pesticide back to the water. During such periods it
would appear that significant river transport of endrin to the sea might
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273
OR N L—DWG 79 .8652
Fig. 8.2. Movement of endrin through the environm nt.
occur. However, resuspension and dissolution also carry the endrin up
to the surface, where codistillatlon takes place. Furthermore, when the
storm subsides, redeposition to the sediment follows. Thus, in actuality,
only a small percent of the endrin released to freshwater bodies reaches
the sea by this route.
Atmospheric transport provides the major route to the sea. While
adsorption to the organic matter in the surface microlayer does occur
with the reemission to the atmosphere (via codistillation and other
processes) a distinct possibility, sedimentation once again predominates.
FALLOUT AND
PRECIPITATION
PARTICLE SCAVENGING
AND
SEDIMENTATION
DREDGING AND
DUMPING
REDISSOLUTION
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274
ORNL- DWG 79—865
U N
CROP DUSTING PORIZATION AM)
ADSORPT TO AIRBORPE BY TI€ WINO
PARTICUL ATES
Fig. 8.3. Transport of vaporized endrin. Source: J. Frost,
Environment 11(6): 14—29; 31—33 (1969). Copyright 1969 Wadham
Publishers Ltd., Toronto, Ontario.
Due to the depth of the ocean, the chances for resuspension of contami-
nated sediment are, at best, limited. The sediment of the oceanic abyss,
therefore, represents the ultimate sink for endrin and similar compounds.
Whether these compounds remain dormant and relatively harmless, are degraded
by microorganisms, or are ingested by bottom feeders is uncertain. The
only real certainties are that the quantity of organochiorine insecticides
and other toxic pollutants which are ultimately carried to the sea is
enormous, and that the sea, while vast indeed, is not infinite.
8.2.1 Endrin in Food
Endrin residues may be ingested by man directly from plant material
or from primary and secondary consumers of the contaminated plants. Man
is also exposed to low levels of endrin in water and air. Potentially
hazardous levels apparently occur only as a result of accidental mishaps
such as spray drift or in the immediate vicinity of endrin use where high
residues on plants or in water occasionally are detected.
The latest available figure for the average daily intake of endrin
from food by a 69.1—kg man (June 1972 to July 1973) was 0.033 pg (0.5 x
10.6 mg/kg) (Bureau of Foods, 1975). Thls is well below the WHO/FAO
acceptable daily intake of 138.2 iig (0.2 x lQ mg/kg) for a 69.1—kg man
(WHO, 1973; U.S. EPA, 1974b).
While no standards have been set f or water concentrations of endrin,
0.1 ppb is suggested as a reasonable limit for potable water (Schafer
et al., 1969b). Occasionally, groundwater may contain more than 0.1 ppb,
but high levels were correlated with precipitation and runoff following
endrin application. Drinking water from Franklin, Louisiana, a region of
high endrin usage, was found to contain a maximum of 23 ppt, well below
0.1 ppb (Lauer et al., 1966).
RAtNOuT AND
FALLOUT
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275
Exposure to endrin in the air has decreased from a maximum finding
in 1971 in Greely, Colorado, of 25.6 ng/m 3 (U.S. EPA, 197la) to a maximum
in 1975 in Jackson, Mississippi, of 0.5 ng/m 3 (Kutz at al., 1976). No
monitoring data contained endrin levels even approaching the threshold
limit value of 100 pg/rn 3 set by the American Conference of Governmental
Industrial Hygienists for 1971 (Yobs et al., 1972).
In a series of analyses of total diets, the average daily intake of
endrin in FY 1973 remained at the trace levels found in FY 1965 to 1970,
but the frequency of occurrence decreased in FY 1973 compared with the
six—year average of FY 1965 to 1970, 0.3 and 2.05% respectively (Table 8.2)
(Bureau of Foods, 1975). The total diets were determined from market
basket samples in four regions of the U.S. northeast, southeast, central,
and west. A “market basket’ t consisted of approximately 117 individual
Table 8.2. Average incidence and daily intake of endrin
FY
Positive composites (%)
Daily intake (mg)
1965
2.8
Ta
1966
2.0
T
1967
1.7
T
1968
1.1
0.001
1969
3.3
T
1970
1.4
T
1971
0.6
T
1972
1.6
T
1973
0.3
T
a
T = trace, <0.001 mg.
Source: Bureau of Foods, 1975.
food items grouped into 12 composites (Table 8.3) required for the total
14—day diet of a 15— to 20—year—old American male (69.1 kg) in the region
of collection. All foods were normally treated before analysis, that is,
meats were cooked, etc. The calculated daily intake of endrin by food
class from F? 1964 to FY 1973 is given in Table 8.4. Only potatoes
contained detectable endrin residues in FY 1973. Recommendations for
acceptable daily intake, tolerances, and practical residue limits in
food by WHO are given in Table 8.5.
Commercial catfish from Arkansas and Mississippi were reported to
contain average residues ranging from 0.01 to 0.41 ppm. Four percent
of the samples exceeded the FDA action level for maximum permissible
endrin concentration in the edible portion of fish, which is 0.3 ppm
(Hawthorne et al., 1974; Corckett et al., 1975). Humans may also be
exposed to endrin in cow’s milk and in steer, lamb, and hog meat
(Sect. 6.5.1).
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276
Table 8.3. Relative composition of diet by food class
Food group
Ày/day
% of total diet
Dairy
769
22.6
Meats
273
8.0
Grain and cereal
417
12.3
Potatoes
200
5.9
Leafy vegetables
63
1.9
Legume vegetables
72
2.1
Root vegetables
34
1.0
Garden fruits
89
2.6
Fruits
222
6.5
Oil and fats
51
1.5
Sugars and adjuncts
82
2.4
Beverages
1130
33.2
Total
3402
100.0
Source: Bureau of Foods, 1975.
Endrin disappearance from growing and harvested crops is so variable
that “half—life” data for endrin persistance on food plants should be
viewed with skepticism (Hill, 1971). The largest factor in concentration
decrease in plants is probably the dilution effected by plant growth
(Hill, 1971). The loss of endrin residue depends on the sum of many
factors, including temperature, volatization, metabolism, and dislodgement
by wind and rain (Sect. 5.3.1). Since generalizations cannot be made
that endrin on a given crop will always “disappear” at the same rate
(Hill, 1971), only residue analyses on harvested crops can ascertain the
potential hazard to humans.
Processing of some foods before human consumption significantly
changed endrin residues. Endrin increased in soybean oils (0.28 ppm)
relative to whole—crop levels (0.07 ppm) by the extraction process (Hill,
1970; U.S.D.A., Plant Pest Control Division, 1968). Storage above 12 weeks
decreased endrin residues in Irish and sweet potatoes by 20% (Solar et
al., 1971; Solar, 1971). Heat processing and freezing further lowered
potato residues 65 and 52% respectively. Studies on turnips (Wheeler
et al., 1969) and carrots (Hermanson et al., 1970) identified 50 to 80%
of the endrin in the peels (Table 4.1).
The nutritional value of food may be affected by endrin. Thakre
and Saxena (1970) reported that 10 to 30 ppm endrin in the soil decreased
calcium uptake in wheat by 30 to 40% and increased calcium uptake in maize
by 2.5 to 3 times. Iron uptake was not affected in maize but was decreased
40% in wheat by 20 to 30 ppm endrin. The amino acid composition was signif i—
cantly changed in maize by 10 ppm endrin (Thakre and Saxena, 1972). The
amino acids arginine, histine, leucine, proline, and lysine were increased
two— to fivefold by 20 ppm or more, while a slight increase was noted in
glutamine, asparagine, phenylalanine, glycine, serine, and tyrosine.
Trytophan and valine were decreased by 33 and 10% respectively.
-------
Table 8.4. Calculated daily intake of endrin by food class
(mg/day)
Fiscal
year
Neat, fish,
and poultry
Potatoes
Leafy
vegetables
Root
vegetables
Garden
fruit
0
and
us, fats,
shortening
1965
Ta
T
1966
T
T
T
T
1967
T
T
T
1968
1969
T
T
T
T
T
0.001
1970
T
T
T
1971
T
1972
T
1973
T
aT = trace, <0.001.
Sources: Corneliussen, 1969, 1970, 1972.
Duggan and Lipscomb, 1969.
Duggan et al., 1967, 1971.
Manske and Corneliussen, 1974.
Bureau of Foods, 1975.
Duggan and Weatherwax, 1967.
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278
Table 8.5. Recommendations for endrin concerning acceptable daily
intakes, tolerances, and practical residue
limits as of November 1972
Maximum acceptable
daily intake
(mg/kg body weight)
Commodity
Residue limits
(ppm)
Tolerances
Practical
limits
0.002
Cottonseed, cottonseed
311 (crude)
0.1
Corn (sweet)
0.02
Apples, barley, rice
(husked and/or polished),
sorghum, wheat
0.02
Edible cottonseed oil
002
Milk and milk products
(fat basis)
0.02
Fat of poultry
1.0
Eggs (shell free)
0.2
Source: World Health Organization, WHO Technical Report Series No.
525,, Geneva, 1973. Copyright 1973 World Health Organization.
Tobacco retains an average of 0.2 ig of endrin per commercial cigarette
(Bowery et al., 1959). Forty percent of the residual endrin disappears
during curing, but the remainder persists during cigarette manufacture.
Endrin residues in chewing tobacco and pipe tobacco increased approximately
threefold from 1969 (0.05 ppm) to 1971 (0.114 ppm) (Domanski et al., 1973).
Cigar and snuff residues remained at approximately 0.06 and 0.16 ppm,
respectively, from 1969 to 1972 (Domanski et al., 1973; Domanski and
Guthrie, 1974). Cigarette residues decreased from 0.18 to 0.09 ppm from
1969 to 1971 (Domanski et al., 1973).
Respiratory and dermal exposure of a dust or spray machine operator,
estimated by Wolfe et al. (1963), is shown in Table 8.6. In all operations
studied, calculations indicated that the dermal exposure was greater than
the respiratory exposure. Potential dermal exposure during orchard
spraying with 0.05% spray (1.2 lb active ingredient/acre) ranges from
2.5 to 3 mg/hr and for respiratory exposure reaches 0.01 mg/hr (Wolfe
et al., 1963; Wolfe et al., 1967). Higher levels of exposure occurred
during dusting of potatoes with 1% endrin dust, where levels of 18.5 mg/hr
for dermal exposure and 0.41 mg/hr for respiratory exposure were found
(Wolfe et al., 1963). During the spraying of row crops, a dermal exposure
of 0.15 mg/hr was found, but the respiratory exposure was below the limits
of detection of the analytical method employed (Jegier, 1964). The EPA
worker protection standards for agricultural use of endrin are given in
Table 8.7.
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279
Table 8.6. Exposure of workers to endrin
•
Activity
Dermal
(mg/hr)
Respiratory
(mg/hr)
Total
.
I. toxic dose
(hr)
Spraying orchard cover crops
for mouse control
2.6
0.01
0.21
High—pressure power handgun
3
0.01
0.25
Operating power air blast or
boom sprayers
2.5
0.01
0.21
Dusting potatoes
18.7
0.41
1.5
Spraying row crops
0.15
Piloting airplane during
air application
1.18
0.08
0.29
Source: H. R. Wolfe, W. F. Durham, and J. F. Armstrong, Arch.
Environ. Health 14(4): 622—633 (1967). Copyright American Medical
Association.
Table 8.7. U.S. Environmental Protection Agency worker
protection standards for agricultural use of endrin
General standard:
No endrin should reenter a field treated with endrin for
at least 48 hr
Tolerances for endrin residues:
A tolerance of zero for residues in or on the following
raw agricultural commodities:
broccoli
brussels sprouts
cabbage
caulif lower
cottonseed
cucumber
eggplant
peppers
potatoes
sugar beets, sugar—beet tops
summer squash
tomatoes
Source: U.S. EPA, 197lc.
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280
8.2.2 Terrestrial Ecosystems
8.2.2.1 Introduction . In tracing the movement of endrin in terrestrial
food chains, both direct and indirect reactions between trophic levels must
be anticipated. A well—planned food web may easily fall apart under the
biocidal and physiological effects exerted by endrin (Fig. 8.2). Sources,
transport in and out, and persistence of endrin in a terrestrial ecosystem
have been discussed in Sect. 7.5.
Factors influencing the Introduction of endrin Into the environment
may be artifical or natural. Certainly, economics is the chief artificial
factor. The return on a one—dollar expenditure for agricultural pesticides
was approximately four dollars according to J. C. Headly (Decker, 1974).
But not only profit is involved. Crop demands continually increase, and
more produce must come from the same or shrinking land area. Thus,
pesticide residues of some type are likely to remain, and it becomes a
matter of wisely choosing the most beneficial and least hazardous compound.
Other artificial factors Include the type of endrin formulation (granules,
dust, and emulsion) with its associated persistence and toxicity. As
would be expected, formulations with a longer active life (granules) exert
less toxicity than formulations with shorter effective duration (emulsions),
even though the endrin concentration is equal (lyatomi et al., 1958).
Natural factors influence endrin residues in a subtle way. They
include soil type, absorption by plants or animals, weather, and food—chain
transfers, among others. The longer a compound remains in the environment,
the greater is the likelihood of movement out of the target area in soil,
air, water, and migrating carriers (Fig. 8.4). Prolonged exposure also
allows development of resistence and natural selection processes in the
biota.
Currently, scientists are more competent to confirm the presence of
endrin than to assess Its ecological impact. The consensus appears to be
that man and most other mammals are able to cope effectively with ingested
endrin, but that many birds and cold—blooded animals are less able to
do so (Decker, 1974). Food—chain studies tend to show that predators
at the highest trophic levels are in the most danger. However, the
knowledge of endrin’s actions in terrestrial food uains is scant and in-
complete, lacking the data to elucidate potentially hazardous trends.
While there Is no doubt of endrin’s toxicity to most fauna, it usually
Is true that species extinction is only likely to occur if the population
at risk is already in a perilous situation for other reasons (Edwards, 1973).
Pesticides often set off an unpredicted sequence of events due to
toxic effects on nontarget organisms. The response of nontarget species
usually has not been evaluated and poses the greatest hazard in pesticide
use. Thus, information in addition to lethal doses is needed to determine
populational, trophodynamic consequences (Finlayson and MacCarthy, 1973).
Endrin influences the food—chain transfers by both immediate,
differential mortality and by long—term accumulation of residues (Khan
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281
TRANSPORT
FLUX
ORNL—DWG 79-8650
MIGRATION PREDATION
KEY
E:.:.:. INTRAWEB FLUX BY PREDATION AND
:: ::: FEEDING
E: OTHER TRANSPORT AND TRANSFER WITHIN
THE FOOD WEB OR BETWEEN FOOD WEBS OF
DIFFERENT REGIONS OR ZONES.
Fig. 8.4. Food web module. Source: Gillett et al., 1974.
et al., 1971). Some of the impacts of endrin on the terrestrial ecosystem
include (Pimental and Goodman, 1974):
• influence on structure and function of a community by
differential toxicity,
• reduction of population numbers,
• alteration of natural habitats by effects on flora and fauna,
LIFE
I I CYCLE
CHANGES
-------
282
• changes in normal behavior patterns,
• stimulation or suppression of growth,
• increase or decrease in reproduction,
• alteration in nutritional content and preference of food,
• increase or decrease in susceptibility to disease and predation,
• change in the natural evolution of a species population.
In the terrestrial ecosystem, the major pathway of endrin uptake is
feeding on treated vegetation or contaminated prey. The apparent lack
of endrin storage in plants and animals makes biomagnification of endrin
by food—chain transfers less aggravated. But short—term endrin buildups
present a source of food with high endrin residues that can cause predator
mortality. This is particularly true of endrin in small animals (Craig
and Rudd, 1974). Small predators take in higher endrin residues per
body weight than do large predators because small prey have increased
surface area for absorption of endrin. In addition, the higher metabolic
rates in small animals require greater food intake (and endrin residues)
per gram of body weight than do larger animals, creating a hazard both
to self and predator (Craig and Rudd, 1974).
8.2.2.2 Plants . Transport of endrin in the terrestrial food chain,
using plants as an intermediary vehicle, is important because of the large
biomass of plants. Endrin residues in or on plants may originate from
accidental or intentional contamination. Accidental sources include
volatilization from soil and drift from aerial application. However, most
plant residues result from deliberate treatments used to control insects.
Plants accumulate endrin from leaf and soil applications, but not to
concentrations much in excess of ambient levels (Sect. 4.3). Uptake
depends upon plant species, soil type, and soil concentrations of endrin
(Table 4.2). Endrin applied to plant leaves or soil was translocated
throughout the plant, occurring in ever decreasing concentrations at
distances increasingly further from the source. Endrin was found in the
soil after application to aerial parts of plants, demonstrating release
as well as uptake of endrin by plants. Thus, plants make endrin available
to both herbivores and soil organisms.
Endrin treatment (4 and 2 oz/acre, 0.28 and 0.14 kg/ha) of an
alfalfa—bromegrass field produced the highest residues (0.87 and 0.55 ppm
respectively) when applied 14 days before harvest (Gyrisco and Huddleston,
1961). Treatments at 21 and 10 days before harvest reduced residues
approxImately 40 and 50 respectively. Alfalfa treated immediately before
harvest had endrin residues reduced 30—fold by air—drying three days, plus
one day of oven—drying. Thus, timing of endrin application and processing
before use as fodder can substantially reduce the amount of endrin ingested
by livestock. However, Archer (1968b) determined that endrin residues were
located in the cuticle of alfalfa. Heat removed 35% of the residue, and
adding water doubled the loss.
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283
8.2.2.3 Invertebrates . Endrin was used as an effective poison for
snails (Achatine fulica) that attacked crops in India (Manna and Ghose,
1972). Baits were prepared by combining different amounts of endrin with
wheat bran and molasses. Snail mortality was directly related to the
percent of endrin in the bait; seven—day periods of feeding 2.0, 1.0, 0.5,
and 0.25% endrin produced 100, 90, 40, and 10% mortality respectively.
Endrin damaged the snail gut, inhibited mucus secretion, and interfered
with peristalsis. No residue determinations were made by Manna and Ghose
(1972), buth Thompson (1973) reported endrin residues of 0.90 ppm (dry
weight) in snails from soils containing 1.74 ppm. Gish (1970) determined
endrin residues of 2.72 ppm in snails from locations of 3.47 ppm in the
soil. The data available suggest that snails do not bioaccumulate large
amounts of endrin relative to the soil concentration.
Bloaccumulation factors for endrin in slugs were considerably higher
than those for snails (Gish, 1970; Thompson, 1973). Slugs collected in
endrin—treated orchards contained residues as high as 134 ppm when soil
residues were 3.47 ppm (Gish, 1970). Generally, lower soil residues
(0.013 ppm) produced lower residues in slugs (1.14 ppm), but bioconcentra—
tion factors increased (88—fold in 0.013—ppm soil compared with 39—fold in
3.47—ppm soil).
There was no significant relationship between endrin residues in
soil and earthworms (Gish, 1970). As an illustration, earthworms collected
from cotton fields contained endrin residues of 0.20, 0.23, 5.40, 9.40,
and 11.04 ppm in soils of 0.024, 1.29, 0.11, 0.09, and 3.47 ppm respectively.
Bioconcentration factors ranged from 14.0 to 103.3 (Gish, 1970). Soil
invertebrates, and especially slugs and earthworms, provide a first step
in endrin transfer to birds, moles, shrews, and snakes. Additionally,
fecal matter and decomposition spread endrin in the soil.
Information on endrin residues in insects was not available, but
endrin is absorbed through body surfaces and by ingestion (Sect. 5.5).
Undoubtedly, surface residues account for the major source of endrin
transfer to other trophic levels in the food chain by insects. Cotton
leafworms exposed to endrin concentrations of 19.5% developed a degree of
tolerance correlated to the duration of exposure (Hassan et al., 1970).
The economic benefits of endrin in pest control are particularly
important. Some of the crops treated with endrin are: cabbage (Harris
and Svec, 1970; Gupta and Sharma, 1971), soybeans (Lee, 1962), eggplant
(Pal, 1971), cotton (Khan et al., 1971; Misra, 1970; Loutfy et al., 1970),
rice (Israel et al., 1969), wheat (Bindra and Singh, 1973; Khan et al.,
1972), sugarcane (Sithanantham and Daniel, 1972; Kavadia et al, 1970),
and corn (Bindra and Singh, 1973). Residue levels in food plants are
discussed in Sect. 8.2.1.
8.2.2.4 Vertebrates . Almost all mammals appear to have the ability
to accumulate endrin. Data on endrin residues in wild animals are
essentially from isolated samples, except for birds. This probably re-
flects the low endrin levels encountered away from immediate application
areas, as well as the obvious problems involved in collecting large
sample numbers.
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284
Continuous feeding of 2.0 ppm endrin to steers, lambs, and hogs
produced accumulations of 1.0 ppm in fat tissue (Brooks, 1969). Forty
Wisconsin dairy herds had endrin residues in milk of 0.25 ppm (fat basis)
in 1964 to 1967 (Moubry et al., 1968a). Endrin residues in cow milk were
directly related to the duration and level of exposure to endrin—treated
hay, with a minimum daily endrin intake of 20 mg as forage residue before
endrin detection in milk (Ely et al., 1957). Lambs grazing on pasture
treated with endrin granules accumulated up to 23.7 ppm in external fat
deposits without showing adverse effects (Long et al., 1961). In all
cases, withdrawal of endrin was followed by a decrease in endrin
accumulations.
Residues detected in wild birds cannot be related to specific intake
concentrations, but they are indicative of the distribution of a compound.
A report of pesticide residues in eagles (Reichel et al., 1969a) revealed
a total of 6 of the 29 bald eagles analyzed had endrin residues in liver
tissue with a median value of 0.09 ppm. Brain tissue contained a trace
of endrin, while a level of 0.09 ppm was determined for the carcass.
Endriti was detected in a composite sample of brain, heart, kidney, liver,
and muscle tissue at a medial level of less than 0.1 ppm in four golden
eagles (Reidinger and Crabtree, 1974). No endrin was detected in brain
tissue alone, and of ten adipose samples containing endrin, the highest
residue detected was 0.3 ppm with a median of less than 0.1 ppm for the
other nine samples.
An analysis of brain tissue from common egrets found dead or moribound
at the Audubon Canyon Ranch in California during 1970 revealed endrin
residues In all five of the birds tested. A mean level of less than
0.18 ppm was reported with a range of less than 0.10 to 0.28 ppm detected.
It was revealed that endrin was still being used at the time to treat
conifer seeds as a protection against seed—eating mice in the forest
regions, but whether this was the principal dietary source of the endrin
detected was not clear (Faber et al., 1972).
Ring—necked pheasants from southwestern Idaho collected during 1969
were analyzed for endrin content of adipose tissue and eggs. Only trace
amounts were detected in the samples (Messick, 1972). Juvenile pheasants
from southeastern South Dakota were collected and tested during July 1967.
The brain tissues of the birds as well as the plant and animal material
from the crop contents revealed no endrin residues at a detection limit
of 0.03 ppm (Linder and Dahigren, 1970). No endrin was detected at a
minimum limit of 0.05 ppm In adipose tissue from pheasants or sharp—tailed
grouse from South Dakota (Greichus et al., 1968).
Songbirds from regions in California where endrin was used contained
residues in muscle (1.23 ppm average) and gizzard (1.45 ppm average)
(Keith and Hunt, 1966). Waterfowl from the same regions had only a trace
(0.03 to 0.07 ppm) of endrin in fat and egg yolk. Sixty—eight percent of
avian samples from the Gulf coast of Texas had endrin residues (Flickinger
and King, 1972). The birds included waterfowl, shorebirds, and passerines.
The highest (0.7 ppm) and most frequent (100%) residues were found in
geese, and the least amount of endrin (0.1 ppm or less in 15%) was found in
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285
shorebirds (stilt, rail, and sandpiper, for example). Of the aquatic
food sources tested, only one sample of crayfish contained traces of
endrin. This suggests that local food sources were not responsible for
the endrin accumulations, since endrin was not being used in field
applications.
These experimental data indicate that the residues of endrin in wild
birds appear to be quite low if detectable at all. However, Health et al.
(1972) found endrin to be the most toxic of the 89 chemicals tested in
bobwhites, Japanese quail, ring—necked pheasants, and mallards. If this
toxic ranking of endrin is applicable to all avians, levels similar to
those reported in food sources may be sufficient to induce injury or
death.
8.2.3 Aquatic Ecosystems
8.2.3.1 Introduction . The introduction of end in into aquatic
ecosystems presents a hazard to the environment, ranging from the micro-
organisms, which are necessary for decompositon and cycling of nutrients,
to man, who may eventually consume harmful amounts of endrin residues in
fish and shellfish. The Environmental Defense Fund has indicated that
concentrations in water in excess of 2 ppt (2 i.ig/liter) would result in
consumption of quantities of endrin, by human populations relying heavily
upon fish, in excess of the WHO/FAO acceptable daily intake of 2 x lO
mg/kg per day (U.S. EPA, l974b).
Bioconcentration (the ability of an organism to concentrate a sub-
stance against a gradient) by aquatic organisms is the immediate cause
of the adverse effects observed in aquatic food—chain relationships,
while biomagnification (the increasing concentrations of a substance with
increasingly higher trophic levels) per se is relatively unimportant.
As presented in Sect. 5.2., the data support equilibrium reactions
between ambient and organismal endrin levels as the basis for ultimate
endrin concentrations. Endrin has the highest acute toxicity to aquatic
organisms of the common organochlorine insecticides, causing mortality at
concentrations less than 1 ppb. Bioconcentration factors of 1000 or more
are commonly found in fish and aquatic invertebrates, resulting in the
ingestion of high, and often fatal, endrin concentrations by predator
species. Louisiana’s brown pelican population disappeared entirely in the
early 1960s, and three—fourths of a restocking effort was eliminated in
1975 as a result of lethal endrin doses presumably acquired from fish
(Anonymous, 1975c).
In the process of controlling insect populations by endrin, natural
insect predators are also eliminated. Field applications of endrin at
0.5 lb/acre (0.55 kg/ha) completely killed all bullfrog tadpoles (Rana
catesbeiana) (Sanders, 1970). Frog (Pseudacris triseriata) and toad (Bufo
woodhousii) tadpoles were more sensitive to endrin than to other common
insecticides such as lindane, DDE, and dieldrin (Sanders, 1970).
A series of processes influence the bioconcentration of endrin in
aquatic organisms. The concentration of endrin in the water is directly
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286
related to the bottom concentration, with sediment effectively removing
endrin from the water and the adsorption capacity increased by the amount
of organics present. Sediment has been described as “a way station,
not a graveyard” by Hamelink (1971), because decreasing water concentration
will release endrin from the sediment until an exchange equilibrium is
again reached.
Algae also act as adsorbants of endrin, with their endrin concentra-
tions dependent not only on water concentration but the amount of adsorbants
present. For example, more endrin is adsorbed per algal unit weight
when the standing crop is low than when It is high, assuming the endrin
concentration remains constant (Hamelink, 1971).
Both invertebrates and fish act as multiphase exchange systems.
Because invertebrates, such as oysters, accumulate endrin an order of
magnitude higher than do algae, it is often assumed that the source is
from the algal food. However, it appears that the endrin concentration
in algae and invertebrates is unrelated, except for a mutual correlation
with the water concentration (Hamelink, 1971). Fish bioaccumulate endrin
from food and by absorption form water (Sect. 5.2.2). The food probably
contains the major amount under natural conditions, since it may be
bioconcentrated in invertebrates to levels far above that it water.
However, the residue concentration in fish tissue eventually depends
on the water concentration, since equilibrium is reached in the different
exchange phases of tissue—blood-water. Residue equilibria, in turn, are
affected by the amount of fat present for solubilization of the highly
lipid—soluble endrin and the length of time available for exchange to
take place. Thus, Hamelink (1971) and Johnson (1968) suggest that endrin
accumulation is ultimately controlled by partitioning (i.e., solubility
differences between water and lipid) in fish and invertebrates.
As endrin solubility is increased in waters, residue levels in
organisms should decrease if, indeed, endrin bloaccumulation is controlled
by solubility differences. Hamelink (1971) states that low concentration
factors between water and fish are found in turbid, highly eutrophic
water (water with high organic content), supporting the partition role in
endrin biomagnification. Sediments in eutrophic waters are in a reductive
state, due to the oxygen depletion. Thus, microorganisms probably con-
tribute to the lowering of endrin levels in water and, therefore, tissues
by reductive degradation of the compound.
Aquatic ecosystems present a number of conditions that tend to
intensify the effects of endrin pollution. Among these are the following:
• maximized exposure because the medium containing endrin surrounds
the organisms at all times,
• adsorption of endrin onto algal cells, resulting in concentration
factors at least an order of magnitude higher than ambient levels,
• long food chains creating more steps in the short—term biomagnification
residues,
• oceans and lakes acting as endrin sinks.
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287
The total impact of endrin on aquatic ecosyste.ns depends on its
effect on each member of the food chain, whether directly, through
predation, or by differential toxicity. The readily apparent effects
of endrin may overshadow less obvious ones. For example, alterations
in normal behavior (such as hyperactivity) may lead to exposure of the
organism to predation; and changes in developmental timing may prevent
emergence during favorable times, leading to eventual extinction
(Jensen and Gauf in, 1966).
In general, endrin pollution patterns parallel drainage basins of
intensive agricultural areas, and the seasonal distribution of endrin
in aquatic environments supports an agricultural origin. Levels begin
to rise in the late spring and peak during the summer (Butler, 1971).
This appears to reflect endrin application and maximum runoff during
the first precipitations following use. The seasonal maximum of endrin
in aquatic ecosystems unhappily coincides with the time of maximal
numbers of larval fish and shellfish (Butler, 1971). Thus the danger of
a single large pollution incident wiping out an entire season of larvae
is present. Of secondary importance in endrin pollution of aquatic
environments is drainage from large urban areas and from industrial
plants formulating endrin.
8.2.3.2 Plankton . Endrin may significantly influence succession and
dominance of species within a phytoplankton community by not being equally
toxic to all organisms. Marine phytoplankton isolated from markedly
different oceanic environments showed varying responses to endrin (Menzel
et al., 1970; Pfister, 1972). The isolates were S7
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288
C 3 —1.5
P—20. 810
ENERGY FLOW: kcal/m 2 /year
ORNL—DWG 79-8649
P — PRODUCERS
C 1 — PRIMARY CONSUMERS
C 2 — SECONDARY CONSUMERS
C 3 — TERTIARY CONSUMERS (TOP CARNIVORES)
S — SAPROTROPHS (BACTERIA AND FUNGI)
Fig. 8.5. Generalized standing—crop and energy—flow (trophic
level) pyramids. Source: E. P. Odum, Fundcrinentala of Ecology, 3rd ed.
(1971). Copyright W. B. Saunders Company.
equilibrium between invertebrates and the ambient concentration (Table 8.8)
(Moubry et al., 1968b). Further, wild clams (Gonidea sp.) responded to
endrin applications (June and August) on the surrounding cropland by
rapid uptake with fluctuations paralleling ambient changes (Fig. 8.6)
(Godsil and Johnson, 1968).
Response to ambient endrin concentration was also demonstrated by
rainfall and tissue residue correlation in freshwater mussels kept in
an endrin—polluted pond (Ryan et al., 1972). The lowered endrin resi-
dues in the pond (after a heavy rainfall caused water to overflow the
dam) were reflected in the decreased endrin concentration in mussel
tissues (Fig. 8.7).
C 2 — 11
C 1 —37
STANDING CROP: kcal/m 2
C 3 —21
C 2 —383
C 1 —3368
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Table 8.8.
289
Endrin residues from two anastomosing
creeks in Wisconsin
Location/organism
Endrin residues
(ppm dry weight)
Silt
Debris
North Branch
0.003
0.025
Alderfly larvae
0.009
Caddisfly larvae
0.003
Freshwater shrimp
0.025
South Branch 0.002
Composite of bottom organisms 0.004
0.011
Confluence
0.013
0.014
Freshwater shrimp
0.013
Source: data from Moubry et al., 1968b.
ORNL-DWG 79-8648
100
50
20
10
5
2
-a
0
a.
2
2
w
Fig. 8.6.
Johnson, 1968.
YEAR AND MONTH
Endrin accumulation in clams. Source: Godsil and
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E
U
-J
-J
Li
z
E
a
a
z—
c Z
zo
c i
p —u
z
0
U
290
ORNL—DWG 79—8647
0
6
4
2
0
0.4
0.3
0.2
0.4
0
I I 1 I
,
1111 -
I 1 i I I1
1 I //4 /•\SSSSs\i\\\I I I —
ENDRIN •
ADDED / DAM BEGAN —
OVERFLOWING
.1
I
._•1• I I I I I —
10 0 10 20 30 40 50 60 70
DAYS
Fig. 8.7. Endrin concentration in mussel tissues and rainfall
during ten—day periods of study. Source: S. Ryan, G. J. Bacher, and
A. A. Maryin, Search 3(11/12): 446—447 (1972). Copyright 1972
Australian and New Zealand Association for the Advancement of Science.
Another factor involved in bioaccumulatiOfl of endrin by invertebrates
appears to be the surface—area-to—Volume ratio, suggesting that direct
absorption contributes to body burdens. Under identical experimental
conditions, higher endrin concentrations occurred in water fleas (with
the larger area/volume ratio) than in mosquito larvae (Metcalf et al.,
1973). However, species differences may complicate the relationship.
The rapid adjustment to ambient endrin concentrations makes
mollusks a good monitoring organism for endrin pollution (Modin, 1969;
Butler, 1971), but several factors must be considered before interpreting
the results. The need to use consistent sample species is illustrated
by the varying rates of uptake and elimination in different species.
For example, substituting the hardshell clam (M. mercenaria) for the
softshell clam (M. arenaria) results in approximately a one—third
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291
decrease in bioaccumulation and elimination rates (Duke and Dumas, 1974;
Butler, 1971). Sequential data are necessary to draw valid conclusions
from bioaccumulation levels. Heavy rainfall may flush out an estuarine
system almost overnight and, concurrently, tissue residues. A series of
samples would be needed to correlate tissue cleansing with rainfall and
not assume a drop in pollution input. Other anomalous cases of bio—
accumulation as a mirror of endrin pollution may result from cycling of
the pesticide. For example, the rapid elimination of endrin by one
organism and accumulation by another may cause erroneous indications of
continuing pollution in a closed system (Fig. 5.1).
Resistance to endrin was found in freshwater shrimp (Palaemonetes
kadiakensis) (Naqvi and Ferguson, 1970). Shrimp populations gathered
from different areas had endrin tolerances that correlated with the
amount of endrin in the source water. The 24—hr LD 50 values for shrimp
from a nonpolluted lake, a lake containing cotton—field runoff, a pond
draining a cotton field, and a drainage ditch located in cotton fields
were 0.9, 2.8, 4.7, and 13.7 ppb endrin, respectively (Naqvi and Ferguson,
1970).
Another source of variation in endrin toxicity is the use of static
(with continuously renewed concentration) or continuous—flow bioassay
tanks. Endrin levels causing death to the stone—fly naid P. californica
in static bioassays produced only tremors and convulsions in continuous—
f low aquaria (Jensen and Gauf in, 1966). Static conditions may cause
oxygen depletion, a buildup of metabolic products, or other conditions
detrimental to stone flies.
Following the major fish kill in the lower Mississippi River in
1963, endrin application was reduced, in turn decreasing endrin concen-
trations in the water (Fig. 7.8) and the wildlife (Rowe et al., 1971).
For example, oysters (Crassostrea virginica) from estuaries below
New Orleans in 1965—66 had endrin concentrations up to 70 ppb, but
the levels were below 2.5 ppb (median 1 ppb) by 1968—69 (Rowe et al.,
1971). Adsorption of endrin by sediment would allow endrin to be
released back to solution as water concentrations fell, thereby
extending the contact time with oysters and resulting in the cycling of
the low concentrations of endrin.
The highest endrin concentrations reported were below 100 ppb in
1969, occurring in Pacific oysters (Crassostrea gigas) and Atlantic
clams (Corbicula fluminea) from San Francisco Bay (Modin, 1969). Major
rivers draining the agricultural basins of California terminate in the
bay, so it appears that endrin runoff was diluted by tidal flow.
Samples of oysters along the Gulf and southeast Atlantic coast
in 1966 contained endrin levels up to 70 ppb (Bugg et al., 1967).
Negative results were obtained from pelecypods in Long Island (New York)
estuaries (Foehrenback et al., 1971) and near Baton Rouge, Louisiana
(Novak and Rao, 1965). Data are absent on endrin levels in aquatic
invertebrates outside the United States and in more recent (1973 to
1975) years.
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ORNL-DWG 79-8643
292
8.2.3.4 Fish . The level of endrin accumulated by fish depends upon
the concentration and exposure time (Sect. 5.2.2). Largemouth bass and
tui chubs rapidly adjust their endrin residues to environmental
concentrations (Codsil and Johnson, 1968). Maximum concentration in
tui chubs was 198 ppb (1980 times maximum water concentration) during
the agricultural growing season when endrin application rose. At the end
of the season, as the concentration in water fell to 0.007 ppb, the
biota had levels of 4.0 ppb. The largemouth bass showed similar fluctua-
tions (Fig. 8.8).
Fig. 8.8. Endrin accumulation in largemouth bass. Source: Godsil
and Johnson, 1968.
In general, increasing exposure time and temperature increases
endrin toxicity (Lowe, 1965; Pimental, 1971; lyatomi et al. 1958). A
good example of the exposure time and toxicity relationship is demonstrated
by the Indian catfish (Heteropneu8tea fossiliB) (Saxena and Aggarwall,
0.
2
z
w
100
50
20
10
5
2
I
YEAR AND MONTH
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293
1970). Endrin levels of 120, 14, and 5.98 ppb caused 100% mortality
in 5, 12 to 16, and 24 hr, respectively, while a level of 5.78 ppb could
be tolerated indefinitely. The salmonids appear to experience maximum
toxicity at 72 hr, after which increasing exposure times do not cause
increasing lethality (Katz, 1961).
Rainbow trout (Salmo gairdneri) and bluegills (Lepomis macrochirus)
show increased susceptibility to endrin with increased temperature
(Table 8.9) (Holden, 1973; Katz and Chadwick, 1961; Macek et al., 1969;
Pimentel, 1971). Marine three—spined sticklebacks (Gasterosteus aculeatus)
also have a direct correlation between temperature and endrin toxicity
(Katz and Chadwick, 1961). Minor (no values given) temperature fluctuations
do not affect endrin toxicity to the Indian catfish (Saxena and Aggarwall,
1970). Mummichogs (Fundulus heteroclitus) are most sensitive to endrin
in the 20 to 25°C range and do not appear to be affected outside that
temperature spread (Eisler, l970b) (Fig. 8.9). The temperature—toxicity
relationships may reflect enzymatic activity (Macek et al., 1969), which
generally increases with temperature to an optimum within the tolerance
range of the organism. At 30°C the optimal enzyme temperature for the
muimnichog would appear to be exceeded and toxicity drops.
Table 8.9. Temperature—toxicity relationships
for endrin in rainbow trout and bluegills
Species, TL 50
(ppb)
Rel
in
ative increase
susceptibility
1.6°C
7.2°C
12.7°C
Rainbow trout
24 hr TL 50
96 hr TL 50
15
2.5
5.3
1.4
2.8
1.1
5.35
2.27
12.7°C
18.3°C
23.8°C
Bluegill
24 hr TL 50
96 hr TL 50
2.8
0.61
1.5
0.41
0.8
0.37
3.5
1.64
Note: TL is median tolerated limit of toxin in aquatic media.
Source: K. J. Macek, C. Hutchinson, and 0. B. Cope, Bull. Environ.
Conta’n. Toxicol. 4(3): 174—183 (1969). Copyright 1969 Springer-Verlag.
Salinity does not exert much effect on endrin toxicity (Eisler, l970b;
Katz, 1961; Katz and Chadwick, 1961; Lowe, 1965). Interestingly, only
estuarine fish ( ujmmichogs) responded consistently to increasing salinity,
showing a 20% increase in mortality for a doubling of salinity [ from 18
to 36 parts per thousand (Eisler, l970b)].
Direct application of laboratory LC 50 to field exposures may not
be possible. It appears that acute toxicity generally occurs at higher
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294
100 ORNL-DWG79-8645
>-75
I—
-J
o 50
I-
z
25
0
20
TEMPERATURE (°C)
Fig. 8.9. Effect of temperature on toxicity of endrin (0.6 ppb)
to mummichogs. Source: modified from Elsier, 1970b.
concentrations in the field than in the laboratory (Johnson, 1968). For
example, 40 ppb did not result in a total fish kill in a pond but was
well above the laboratory LC 50 (Johnson, 1968). On the other hand,
sublethal field concentrations of as little as 0.009 ppb have produced
fish kills.
Static and continuous—flux conditions in the laboratory produced
conflicting evidence as to the effect on endrin toxicity (Earnest and
Benville, 1972; Holden, 1973; Lincer et al., 1970). However, flux tests
are probably more meaningful, since stress may be caused in static water
by oxygen depletion and waste buildup (Korn and Earnest, 1974).
Seasonal variation in susceptibility to endrin has been reported by
Fabacher and Chambers (1971). Mosquito fish are more susceptible to endrin
in the winter and early spring, apparently correlated with low body lipid
at those times.
Symptoms of endrin poisoning in the field were similar to those
observed in the laboratory (Sect. 5.2.2). In addition, channel catfish
from the Mississippi River also had distended abdomens at death (Holden,
1973). Survivors of an accidental endrin poisoning that killed several
thousand brook trout and juvenile Atlantic salmon on Prince Edward Island,
Nova Scotia, demonstrated unusual downstream movements (Nielsen, 1971).
Fish are among the many organisms that demonstrate resistance to
endrin. Maintenance of resistance over several generations in an endrin—
free environment suggests a genetic base for the tolerance (Ferguson, 1967).
I I
10 15
I I
25
30
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295
Endrin—resistant populations may develop by natural selection favoring
the rare individual(s) in a wild population that exhibits resistance, and
then passing on the genetic capability for tolerance to succeeding
generations. Artificial selection in the laboratory when mosquito fish
were exposed to endrin for consecutive generations resulted in strains
with increased tolerances (Ferguson, 1967). A comparison of fish gathered
from uncontaminated areas with populations exposed to heavy concentrations
from adjoining cotton fields disclosed as much as a 200—fold resistance
in the exposed fish (Pimentel, 1971); the data are presented in Table 8.10.
Table 8.10. 36—hr LC 50 values for field fish from endrin—polluted
and nonpolluted areas in Mississippi
Species
36—hr LC 50 (ppb)
Nonpolluted
Endrinpolluted
Golden shiners
3.0
310.0
Bluegills
1.5
300.0
Green sunfish
3.4
160.0
Mosquito fish
1.0
120.0
Black bullhead
0.37
2.5
Source: data from Pimentel, 1971.
Endrin resistance in fish has the advantage not only of affording
protection against endrin but also of providing cross—resistance to other
organochiorine insecticides such as dieldrin and toxaphene (Ferguson, 1967).
However, resistant fish can tolerate higher body burdens of endrin than
do susceptible fish, and it is these residues that present a source of
environmental concern. Field—collected resistant mosquito fish contained
residues up to 11.95 ppm (Ferguson et al., 1966), while susceptible fish
contained up to 0.88 ppm. Resistant fish exposed to 500 ppb for two
weeks in the laboratory accumulated endrin in amounts ranging from
201.6 to 214.3 ppm. These high body burdens may adversely affect aquatic
communities in two ways: through ingestion by predators and by release
to the ambient water.
Endrin—resistant mosquito fish (average residues of 180 ppm) were
fed to endrin—resistant and susceptible green sunfish (Finley et al.,
1970). The resistant sunfish survived 96 hr, while the susceptible fish
died within an average of 11 hr. Ninety percent of the susceptible sun-
fish regurgitated the mosquito fish but died nevertheless, suggesting
absorption of endrin from water. It was found that endrin—treated
resistant mosquito fish (exposed to 2 ppm for seven days) contained
sufficient endrin to kill predators several hundred times their own
weight (Table 8.11). While endrin levels of 2 ppm are not normally
encountered under natural conditions, the possibility exists of isolated
areas where run—off, equipment washing, or direct spraying may drastically
raise endrin concentrations.
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296
Table 8.11. Effect of force—feeding on endrin—resistant
mosquito fish (average 890 ppm endrin) to a predator
Mortality
Predator (%)
Time
(hr)
Ratio of
predator:prey
(mean weight)
Red—eared turtle 72 112.8 757:1
(Pseudemys scripta
elegans)
Yellow—bellied water 100 65.4 402:1
snake (Natrix erthrogaster
fiavigaster)
Diamond—backed water snake 100 54.0 714:1
(Natrix rhornbifera)
Cottonmouth 91 27.1 311:1
(Ancistrodon piscivorus)
Bullfrog 100 15.6 418:1
(Rana catesbe uzna)
Redf in pickerel 100 7.1 35:1
(Esox ajneri canus
vermiculatus)
Largeinouth bass 100 12.6 168:1
(Micropterus sa imoides)
Bluegill sunfish 100 9.4 113:1
(Lepomis macrochirus)
Purple grackle 100 8.2 77:1
(Quiscalus quiscula)
Starling 100 1.0 93:1
(Sturnus Vulgaris)
Coturnix quail 100 1.3 134:1
(Corturnix corturnix
japonicwn)
Source: P. Rosato and D. E. Ferguson, Bioscience 18(8): 783—784
(1968). Copyright 1968 An rican Institute of Biological Sciences.
An experiment involving resistant fish in a field environment
was conducted by Ferguson (1967). Thirty—nine mosquito fish (each
containing approximately 400 ppm endrin) were added to a woodland pool
previously stocked with 41 susceptible sunfish. In 16.5 hr, 11 of the
sunfish were dead, and only 8 sunfish and no mosquito fish were recovered
after eight days. The results indicate that one possible consequence
of bioconcentration is the extinction of top piscivores, an occurrence
illustrated by the absence of largemouth bass in waters heavily containina—
ted with endrin (Ferguson, 1967).
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297
Laboratory experiments demonstrate the hazard that resistant fish
pose to other fish by means of endrin release to the water. Ferguson
et al. (1966) exposed a single resistant mosquito fish to 1000 ppb endrin
for 36 hr and then transferred it to 10 liters of tap water. Sufficient
endrin was released to kill five susceptible mosquito fish in 38.5 hr,
implying water concentrations of 2 to 3 ppb according to bioassay fish
tolerances.
Higher trophic levels are not necessarily more resistant than lower
ones. And not all fish have the same potential for developing resistance.
For example, black bullheads are able to resist only a sevenfold increase
in endrin (2.5 vs 0.37 ppb), while yellow bullheads can develop tolerance
for a 60—fold increase (75 vs 1.25 ppb) (Ferguson and Bingham, 1966b).
While the benefits of endrin are evidence in the control of insects,
the positive use of endrin in fisheries is often overlooked. Sreenivasan
and Natarajan (1962) reported on the successful use of endrin in fishery
management in India. Carp failed to reproduce in Ooty Lake because
mosquito fish, inadvertently introduced, interfered with carp breeding.
Prior to treating the lake, test ponds (l.m deep) were sprayed with 15 ppb
endrin (no quantity given) twice in one month. All of the mosquito fish
were killed. A month later, adult mirror and scale carp successfully
spawned in the ponds, and fry and fingerlings were recovered. The shallow
margins of Ooty Lake were then sprayed with 20% endrin (4.5 liters, but
no area was given). Approximately 90% of the mosquito fish and some adult
carp died. However, ten weeks after treatment, carp spawned successfully.
The breeding produced many fingerlings, allowing over 53,000 to be taken
for stocking other lakes.
In 1967 and 1968, fish from approximately one—half of the sampling
stations in the United States had endrin residues ranging from 0.01 to
1.5 ppm, but consistent residues were found at only three stations in
cotton areas: the White River, Mississippi River, and Arkansas River
(Henderson et al., 1969). While variations occurred, bottom fish and fish
from agricultural drainage areas generally had the highest residues. By
1969 no endrin residues were detected in fish from 50 nationwide nonitoring
stations operated by the Bureau of Sport Fisheries and Wildlife (Henderson
et al., 1971).
Endrin residues in catfish from commercial catfish farms were
directly correlated to the surrounding number of acres planted in cotton
(Crockett et al., 1975; Hawthorne at al., 1974). In 1970, catfish
accumulations averaged 0.06 ppm (0 to 0.41 ppm) and were detected in
76% of the catfish (Hawthorne et al., 1974; Crockett et al., 1975). It
appears that aerial transport of endrin was the primary source, since
sediment, feed, and water were not contaminated (Crockett et al., 1975).
No significant amount of endrin (no level given) was found in
commercially caught fish in Canada in 1970 (Relnke et al., 1972). However,
endrin concentrations in the waters around Ontario, Canada, increased from
less than 3 ppb in 1970 to 1 ppm in 1971 (Miles and Harris, 1971, 1973).
Fish, however, remained at low residue levels. Rock bass and bluegills
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298
had less than 10 ppb, except in agricultural regions in 1971 (30 ppb), and
suckers and chubs ranged from 10 to 18 ppb in 1970, although endrin was
not detected in the mud or water.
Worldwide reports indicate that endrin is not a significant pollutant.
No residues were found in threadtail, black—tip shark, or catfish from
undeveloped or developed areas of northern Australia (Best, 1973). Fish
(Talapia graha’ni) from Lake Nakuru in Kenya, an area of intensive agricul-
ture and pesticide use, had low endrin levels of 2 ppb (Koeman et al.,
1972). No endrin was detected in a nonmigrating marine bathydemersal
(deep—bottom) fish (Antirnora rostrata) by Meith—Avcin et al. (1973).
8.2.3.5 Effects on community structure . Some examples of the more
drastic environmental impacts caused by endrin are worth discussing.
Probably the most far—reaching and extensive occurrences were the fish
kills in the drainage basins of the Mississippi River.
Beginning in November 1960 and continuing for four years, large
numbers of dying fish and shrimp were observed in the lower Mississippi
River and adjacent Gulf of Mexico (Anonymous, 1964; Mount and Putnicki,
1966). Endrin was Identified as the toxicant by laboratory investigations
using extracts from the dead fish. Other pesticides were also found, but
feeding different fractions to fish showed the endrin fraction to be the
active one. As further support for endrin causation of the fish kills,
lethal threshold concentrations of endrin in catfish blood (0.3 ppm)
determined in the laboratory corresponded to those found in dying specimens
(0.40 ppm or more) from the kills. Catfish and bream from the fish—kill
areas consistently had endrin residues of 10 ppb from July 1964 to
June 1965 (Novak and Rao, 1965). At the time of the 1963 Mississippi River
fish kills, Johnson (1968) reports fish (species not given) residues of
7 ppm in surface waters of 0.1 ppb, and mosquito fish had levels of 6.8
to 11.95 ppm.
Endrin concentrations found in the Mississippi River during fish kills
ranged from 0.1 to 0.2 ppb, levels acutely toxic to channel catfish,
largemouth buffalo, and gizzard shad (Mount and Putnickj, 1966). Lauer
et al. (1966) measured endrin levels of 0.009 to 0.040 ppb in Louisiana
streams at fish—kill sites, but later apparently concurred with the data
of Mount and Putnickl (1966). In 1964, there were no large fish kills,
but all water samples from the lower Mississippi River region were positive
and ranged as high as 0.145 ppb (Breidenbach et al., 1967). While fish
kills were associated with the first precipitation and runoff following
endrin application, endrin residuals persist in soil from one agricultural
season to the next and in river sediment. This persistence along with
continued endrin usage probably accounts for the continuing presence of
endrin.
In another example of an environmental calamity, over 2000 lb of
carp and buffalo fish was killed by endrin runoff (U.S. HEW, 1969). Endrin
was sprayed on tobacco plants (no concentration or location was given) on
a hill above some lakes. A 4—in, rainfall occurred within a few hours of
application, flushing endrin into the lakes and causing the fish kill.
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299
A deliberate disaster was created by dumping 0.5 gal of endrin and
strychnine into 3—acre Shawnee Lake, Portsmouth, Ohio (Stoltenberg, 1972).
Within 24 hr, 4000 fish and other aquatic life were dead. Endrin was
found to be stratified in the upper 5 ft of the lake, reaching concentra-
tions of 15 ppb. The toxic effects lasted for at least eight weeks.
To interpret the effects of endrin on an entire aquatic ecosystem it
is necessary to understand not only changes in a species but how the
changes intermesh and affect the whole ecosystem (Fig. 8.10). In some
instances, low concentrations of endrin may produce more severe results
than higher concentrations. For example, low endrin exposures may cause
resistance in fish, with the corresponding increase in endrin body burdens.
Predators on the resistant fish may be killed by ingesting the high endrin
level, or they may further transfer endrin across trophic levels as they,
in turn, become prey. At high endrin concentrations, all of the exposed
fish may be killed immediately, limiting the effects of endrin to
mortality in the initial area of contamination.
Endrin may alter the population of an area by differential impact on
the various species and their developmental steps. For example, eggs
are generally resistant to endrin, so that levels killing adult predators
ORNL—DWG 79-8646
Fig. 8.10. Compartment model of an aquatic ecosystem. Source:
R. B. Craig and F. L. Rudd, Survival in Toxic Environments (1974).
Copyright 1974 Academic Press.
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300
may not affect later hatched populations of prey. Food chains may also
be disrupted by the higher toxicity of endrin to crustaceans, insects, and
fish than to flatworms, snails, and annelids (Johnson, 1968). Bottom and
plankton populations may be depleted without an immediate effect on fish
populations, but in time the situation may change.
As Sect. 5 illustrates, a quantitative report on the processes and
parameters involved in endrin cycling is impossible, not only because of
biological and chemical inconsistencies but also because a completely
definitive description of an aquatic ecosystem defies compilation. As
a result, partial system studies have been undertaken. A short food chain
is studied in order to gain information for comparison with other laboratory
or field studies. While model ecosystems have limited applicability to
natural conditions, they do provide a basis for comprehensive and prediction
of eudrin behavior in the aquatic environment.
Metcalf et al. (1973) set up a model ecosystem in an aquarium that
consisted of a sloping terrestrial portion interfacing with sand at the
water portion. Radiocarbon—labeled endrin (5 mg, equivalent to 1.1 kg/ha)
was applied to sorghum seedlings on the terrestrial portion. Fourth instar
salt—marsh caterpillars (Estiginene ac t ’ea) fed until all the leaves were
eaten and the fecal products and larvae themselves contaminated the aquatic
portion of the ecosystem. The distribution of the radiolabeled products
was determined in the ecosystem after 33 days. Several members of the food
chain were analyzed: alga (Oedogoniwn cardiacwn), snail (Physa sp.),
water flea (Daphnia rnagna), mosquito larvae (Culex pipiens quinquefasciatus),
and fish (Gambusia affinis); the data are given in Table 8.12. Endrin
was highly toxic to the salt—marsh caterpillar, which had difficulty
ingesting it. When the water concentration of endrin was 0.06 ppm, both
water fleas and mosquito larvae were killed and had to be reintroduced
repeatedly. The water was also extremely toxic to the fish, which died
after violent convulsions or within a few minutes of being added. The
water toxicity persisted for more than 60 days from the initial addition
of endrin to the seedlings and apparently occurred at concentrations from
1 to 2 ppb.
The model ecosystem data disclose several important features of endrin
transfer in the food chain. The relative stability of endrin is demon-
strated by the movement of toxic amounts of unchanged endrin from seedling
to caterpillar to aqueous solution. Disruption of trophic levels was
shown by the greater sensitivity of primary consumers (water fleas and
mosquito larvae) than by primary producers (algae). The secondary
consumers (fish) were also sensitive to endrin in solution, dying even
before consuming endrin—contaminated food. Further adverse effects from
the introduction of endrin were apparent in the high bioconcentration of
endrin by snails, resulting in an almost certain lethal dose of endrin to
predators.
Analysis of endrin contamination of a natural ecosystem provided
results consistent with those obtained in the laboratory. Bingharn (1970)
compared an endrin—polluted lake (Wolf Lake) with a comparatively clean
lake (Mossy Lake) in the Mississippi delta region in 1967 and 1968.
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301
Table 8.12. Distribution of endrin in
some components of a model ecosystem
Comrrnnent
Total 1L+Ca
(ppm)
Endrin
B.I.b
E.M.C
% total
ppm
Water
0.0134
0.00254
19.0
Alga
13.62
11.56
84.9
Not given
4,551
Snail
150.58
125.00
82.8
0.0127
49,213
Fish
4.48
3.40
75.8
0.009
1,335
aI dd as 14 C—endrin.
bBiodegradability index = _ polar products
nonpolar products
CEcological magnification endrinin organism
endrin in water
Source: R. L. Metcalf et al., Environ. Health Perspec. 4: 35—43
(1973). Copyright 1973 National Institute of Health Sciences.
However, insecticides such as DDT and toxaphene were found along with
endrin in Wolf Lake, so the results probably represent the composite
influence. Wolf Lake was chosen for study as being representative of
declining productivity as manifested by poor fishing, while Mossy Lake
displayed excellent fishing.
Determinations of total insecticide concentration in the two lakes
showed that Wolf Lake samples were higher than those of Mossy Lake on
every occasion except two, in both of which abnormally high insecticide
levels were obtained at the mouth of a cotton—field drainage ditch
entering Mossy Lake. Bioassays using bluegills from Wolf and Mossy lakes
showed endrjn LD 50 values of 300 and 15 ppb, respectively, a reflection of
previous endrin exposure levels. No largemouth bass were found in Wolf
Lake, and none survived a stock attempt. Benthic sampling of Wolf and
Mossy lakes showed the average number of organisms per square foot to be
37.2 and 54.6 respectively. The composition of the bottom communities also
disclosed different characteristics, with small mussels and oligochaetes
comprising 8.9 and 54.5%, respectively, of the benthic fauna in Wolf Lake
and 56.6 and 0.06%, respectively, of Mossy Lake fauna. Plankton ratios
in Mossy Lake compared with Wolf Lake were: zooplankton, 0.84 in 1967 and
2.34 in 1968; and phytoplankton, 1.47 in 1967 and 2.27 in 1968. There was
a decrease in both plankton in Wolf Lake relative to Mossy Lake, but no
data were given as to whether decreases occurred in Wolf Lake or increases
occurred in Mossy Lake. However, taking pollution into consideration, it
seems reasonable to assume a decrease in populations in Wolf Lake. If
1967 is taken as a base year, zooplankton have decreased approximately
twice as much as the phytoplankton. Since successively fewer numbers of
organisms make up increasingly higher food—chain levels (Fig. 8.3), a
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302
decreased producer population would be expected to alter the consumer level
by at least double. Further support for a threefold decrease in Wolf Lake,
rather than the corresponding increase in Mossy Lake, comes from finding
that primary consumers in the model ecosystem are much more sensitive to
endrin than are primary producers.
8.3 REFERENCES
Anonymous. 1964. Catfish vs. Insecticides. Agric. Chem. 19(5): 20.
Anonymous. 1975c. Pesticide Blamed as Pelican Killer. Wash. Star
July 2 — UPI Story, A—9.
Archer, T. E. 1968b. Location, Extraction, and Removal of Endrin
Residues on Alfalfa Hay. J. Dairy Sci. 51(10): 1606—1611.
Best, S. M. 1973. Some Organochiorine Pesticide Residues in Wildlife of
the Northern Territory, Australia, 1970—71. Aust. J. Biol. Sd. 26(5):
1161—1970.
Bindra, 0. S., and J. Singh. 1973. Bionomics of the Arm—worm, Mythimna
separata (Walker) (Lepidoptera: Noctuidae), at Ludhiana, Punjab. Indian
J. Agric. Sci. 43(3): 299—303.
Bingham, C. R. 1970. Comparison of Insecticide Residues from Two
Mississippi Oxbow Lakes. Proc. Ann. Southeast. Assoc. Gaines Fish
Comm.: 275-280.
Bowery, T. G., W. R. Evans, F. E. Guthrie, and R. L. Rabb. 1959.
Insecticide Residues on Tobacco. J. Agric. Food Chem. 7(10): 693—702.
Brooks, G. T. 1969. The Metabolism of Diene—Organochiorine (Cyclodiene)
Insecticides. Residue Rev. 27: 81—138.
Breidenbach, A. W., C. G. Gunnerson, A. B. Kawahara, J. J. Lichtenberg,
and R. S. Green. 1967. Chlorinated Hydrocarbon Pesticides in Major
River Basins, 1957—65. Pubi. Health Rep. 82(2): 139—156.
Bugg, J. C., J. E. Higgins, and E. A. Robertson. 1967. Chlorinated
Pesticide Levels in the Eastern Oyster (Crassostrea virginica) from
selected areas of the South Atlantic and Gulf of Mexico. Pesti. Monit.
J. 1(3): 9—12.
Bureau of Foods. 1975. Compliance Program Evaluation — Total Diet Studies:
FY 1973. Prepublication material.
Butler, P. A. 1963. Commercial Fisheries Investigations. In: U.S.
Department of the Interior, Fish and Wildlife Circular 167, Washington,
D.C., pp. 11—25.
Butler, P. A. 1971. Influence of Pesticides on Marine Ecosystems. Proc.
R. Soc. London 177(1048): 321—329.
-------
303
Corneliussen, P. E. 1969. Pesticide Residues in Total Diet Samples (IV).
Pesti. Monit. J. 2(4): 140—152.
Corneliussen, P. E. 1970. Pesticide Residues in Total Diet Samples (V).
Pesti. Monit. J. 4(3): 89—105.
Corneliussen, P. E. 1972. Pesticide Residues in Total Diet Samples (VI).
Pesti. Monit. J. 5(4): 313—330.
Craig, R. B., and R. L. Rudd. 1974. The Ecosystem Approach to Toxic
Chemicals in the Biosphere. In: Survival in Toxic Environments, M. A. Q.
Khan and J. P. Bederka, eds., Academic Press, New York, pp. 1—24.
Crockett, A. B., G. B. Wiersma, H. Tai, and W. Mitchell. 1975. Pesticide
and Mercury Residues in Commercially Growth Catfish. Pesti. Monit. J.
8(4): 235—240.
Decker, G. C. 1974. Costs and Benefits of Pesticides: An Overview. In:
Survival in Toxic Environments, M. A. Q. Khan and J. P. Bederka, eds.,
Academic Press, New York, pp. 447—471.
Doinanski, J. J., and F. E. Guthrie. 1974. Pesticide Residues in 1972
Cigars. Bull. Environ. Contam. Toxicol. 11(4): 312—314.
Domanski, J. J., J. M. Laws, P. L. Haire, and T. J. Sheets. 1973.
Insecticide Residues on 1971 U.S. Tobacco Products. Tob. Sci. 17: 80—81.
Duggan, R. E., and G. 0. Lipscomb. 1969. Dietary Intake of Pesticide
Chemicals in the United States (II), June 1966 — April 1968. Pesti. Monit.
J. 2(4): 153—162.
Duggan, R. E., and J. R. Weatherwax. 1967. Dietary Intake of Pesticide
Chemicals. Science 157(3792): 1006—1010.
Duggan, R. E., H. C. Barry, and L. Y. Johnson. 1967. Pesticide
Residues (II). Pesti. Monit. J. 1(2): 2—12.
Duggan, R. E., G. 0. Lipscomb, E. L. Cox, R. E. Heatwole, and R. C. Kling.
1971. Pesticide Residue Levels in Foods in the United States from July 1,
1963, to June 30, 1969. Pesti. Monit. J. 5(2): 73—212.
Duke, T. W., and D. P. Dumas. 1974. Implications of Pesticide Residues
in the Coastal Environment. In: Pollution and Physiology of Marine
Organisms, F. J. Vernberg and W. B. Vernberg, eds., Academic Press, New
York.
Earnest, R. D., and P. E. Benville, Jr. 1972. Acute Toxicity of Four
Organochiorine Insecticides to Two Species of Surf Perch. Calif. Fish
Game 58(2): 127—132.
Edwards, C. A. 1973. Pesticide Residues in Soil and Water. In:
Environmental Pollution by Pesticides, C. A. Edwards, ed., Plenum Press,
New York, Chap. 11.
-------
304
Elsier, R. 1970b. Factors Affecting Pesticide—Induced Toxicity in an
Estuarine Fish. Tech. Pap. Bur. Sport Fish Wildi. 45: 1—20.
Ely, R. E., L. A. Moore, R. H. Carter, and B. A. App. 1957. Excretion
of Endrin in the Milk of Cows Fed Endrin—Sprayed Alfalfa and Technical
Endrin. J. Econ. Entomol. 50: 348—349.
Fabacher, D. L., and H. Chambers. 1971. Possible Mechanism of Insecticide
Resistance in Mosquito Fish. Bull. Environ. Contam. Toxicol. 6(4): 372—376.
Faber, R. A., R. W. Risebrough, and H. N. Pratt. 1972. Organochiorines
and Mercury in Common Egrets and Great Blue Herons. Environ. Pollu.
3(2): 111—122.
Ferguson, D. E. 1967. The Ecological Consequences of Pesticide Resistance
in Fishes. North American Wildlife and Natural Resources Conference
(32nd): 103—107.
Ferguson, D. E., and C. R. Bingham. l966b. Endrin Resistance in the
Yellow Bullhead Ictalurus natalis. Trans. Am. Fish. Soc. 95(3): 325—326.
Ferguson, D. E., J. L. Ludke, and G. G. Murphy. 1966. Dynamics of Endrin
Uptake and Release by Resistant and Susceptible Strains of Mosquito Fish.
Trans. Am. Fish. Soc. 95(4): 335—344.
Finlayson, D. G., and H. R. MacCarthy. 1973. Pesticide Residues in Plants.
In: Environmental Pollution by Pesticides, C. A. Edwards, ed., Plenum
Press, New York, Chap. 2.
Finley, M. T., D. E. Ferguson, and J. L. Ludke. 1970. Possible Selective
Mechanisms in the Development of Insecticide—Resistant Fish. Pesti.
Monit. J. 3(4): 212—218.
Flickinger, E. L., and K. A. King. 1972. Some Effects of Aldrin—Treated
Rice on Gulf Coast Wildlife. J. Wildi. Manage. 36(3): 706—727.
Foehrenback, J., C. Mabmood, and D. Sullivan. 1971. Chlorinated
Hydrocarbon Residues it t Shellfish (Pelecypoda) from Estuaries of Long
Island, New York. Pesti. Nonit. J. 5(3): 242—247.
Frost, J. 1969. Earth, Air, and Water. Environment 11(6): 14—29; 31—33.
Gi].lett, J. W.., J. Hill IV, A. W. Jarvinen, and W. P. Schoor. 1974.
A Conceptual Model for the Movement of Pesticides through the Environment:
A Contribution of the EPA Alternative Chemicals Program. U.S. Environmental
Protection Agency, National Ecological Research Laboratory, Corvalis,
Oregon, NTIS: PB—238—653.
Gish, C. D. 1970. Organochlorine Insecticide Residues in Soils and Soil
Invertebrates from Agricultural Lands. Pestic. Monit. J. 3(4): 241—252.
Codsil, P. S., and W. C. Johnson. 1968. Pesticide Monitoring of the
Aquatic Biota at the Tule Lake National Wildlife Refuge. Pestic. Monit.
5. 1(4): 21—26.
-------
305
Greichus, Y. A., A. Greichus, and E. G. Reider. 1968. Residues in Fish,
Wildlife, and Estuaries. Insecticide Residues in Grouse and Pheasant
of South Dakota. Pesti. Monit. J. 2(2): 90—92.
Gupta, B. N., and J. C. Sharma. 1971. Efficacy of Certain Insecticidal
Control Schedules Against Insect Pests of Cabbage. Madras Agric. J.
58(12): 889—891.
Gyrisco, G. G., and F. W. Huddleston. 1961. The Persistance of Aidrin,
Dieldrin, and Endrin Residues on Fresh Forage and on Hay Under Various
Conditions of Curing. J. Econ. Entomol. 54(4): 718—720.
Hamelink, J. 1971. The Fate and Effects of Pesticides in Aquatic
Environments. Proc. 2nd Symp. Haz. Chem. Handl. Dis., Indianapolis,
Indiana: 19—24.
Harris, C. R., and H. J. Svec. 1970. Laboratory Studies of the Toxicity
of Technical Formulations of Some Insecticides to Cabbage Loopers. J.
Econ. Entomol. 63(2): 666—667.
Hassan, M. H., A. M. Au, and M. S. E. El—Sawy. 1970. Development of
Tolerance of the Cotton Leafworm, Spodoptera littoralis Boisd, to Currently
Applied Insecticides. Agric. Res. Rev. 48(1): 1—11.
Hawthorne, J. C., J. H. Ford, and C. P. Markin. 1974. Residues of Mirex
and Other Chlorinated Pesticides in Commercially Raised Catfish. Bull.
Environ. Contam. Toxicol. 11(3): 258—264.
Heath, R. G., J. W. Spann, E. F. Hill, and J. F. Kreitzer. 1972.
Comparative Dietary Toxicities of Pesticides to Birds. U.S. Department of
Interior, Bureau of Sport Fisheries and Wildlife, Wildlife No. 152, GPO,
Washington, D.C.
Henderson, C., W. L. Johnson, and A. Inglis. 1969. Organochiorine
Insecticide Residues in Fish (National Pesticide Monitoring Program).
Pesti. Nonit. J. 3(3): 145—171.
Henderson, C., A. Inglis, and W. L. Johnson. 1971. Organochiorine
Insecticide Residues in Fish — Fall 1969 National Pesticide Monitoring
Program. Pesti. Nonit. J. 5(1): 1—11.
Hermanson, H. P., L. D. Anderson, and F. A. Gunther. 1970. Effects of
Variety and Maturity of Carrots upon Uptake of Endrin Residues from
Soil. J. Econ. Entomol. 63(5): 1651—1654.
Hill, K. R. 1970. IUPAC Commission on Terminal Residues. J. Assoc.
Off. Anal. Chem. 53(5): 987—1003.
Hill, K. R. 1971. IUPAC Commission on Terminal Residues. J. Assoc.
Off. Anal. Chem. 54(6): 1316—1322.
Holden, A. V. 1973. Effects of Pesticides on Fish. In: Environmental
Pollution by Pesticides, C. A. Edwards, ed., Plenum Press, New York,
Chap. 6.
-------
306
Israel, P., M. B. Kalade, P. S. Prakasa Rao, and C. P. Yadava. 1969.
Persistence of Some Insecticides and Their Compatibility with Urea
Against Newly Hatched Larvae of Tryporyza incertuals Walker in Rice.
Indian J. Entomol. 31(4): 346—349.
lyatomi, K., T. Tamura, Y. Itazawa, I. Hanyu, and S. Sugiura. 1958.
Toxicity of Endrin to Fish. Prog. Fish Cult. 20(4): 155—162.
Jegier, Z. 1964. Health Hazards in Insecticide Spraying of Crops.
Arch. Environ, Health 8: 670—674.
Jensen, L. D., and R. A. Gauf in. 1966. Acute and Long—Term Effects
of Organic Insecticides on Two Species of Stonefly Naiads. J. Water
Pollu. Control Fed. 38(8): 1273—1286.
Johnson, D. W. 1968. Pesticides and Fishes — A Review of Selected
Literature. Trans. in. Fish. Soc. 97(4): 398—424.
Katz, N. 1961. Acute Toxicity of Some Organic Insecticides to Three
Species of Salmonids and to the Threespine Stickleback. Trans. Am. Fish.
Soc. 90(3): 264—268.
Katz, M., and G. G. Chadwick. 1961. Toxicity of Endrin to Some Pacific
Northwest Fishes. Trans. Am. Fish Soc. 90(4): 394—397.
Kavadia, V. S., R. C. Srivastava, and H. C. L. Gupta. 1970. Laboratory
Evaluation of Insecticides Against Psalis pennatula (Lymantriidae:
Lepidoptera). Indian J. Entomol. 32(3): 255—288.
Keith, J. 0., and E. G. Hunt. 1966. Levels of Insecticide Residues in
Fish and Wildlife in California. In: Transactions of the 31st North
American Wildlife Conference, Wildlife Management Institute, Washington,
D.C., pp. 150—177.
Khan, I. A., R. I. Zuberi, Z. I. Khan, A. All, and S. N. H. Naqvi. 1971.
Effectiveness of Petkolin, Endrin and Their Combination Against Jassids
and Thrips on Cotton Crop at Multan. Sci. md. (Karachi) 8(2): 147—151.
Khan, R. N., S. K. Sharina, and B. M. Gupta. 1972. Appearance of Armyworms
on Wheat Crop in Outbreak Form and Their Control. Madras Agric. J.
59(11—12): 663—665.
Koeman, H. H., J. H. Pennings, J. J. M. DeGoeij, P. S. Tjioe, P. N. Olindo,
and J. Hopcraft. 1972. A Preliminary Survey of the Possible Contamination
of Lake Nakuru in Kenya with Some Metals and Chlorinated Hydrocarbon
Pesticides. J. Appl. Ecol. 9(2): 411—416.
Korn, S., and R. Earnest. 1974. Acute Toxicity of Twenty Insecticides to
Striped Bass, Morone saxatilis. Calif. Fish Game 60(3): 128—131.
Kutz, F., A. Yobs, and H. Yang. 1976. In: Air Pollution from Pesticides
and Agricultural Processes, R. Lee, Jr. (ed.), CRC Press, Cleveland, Ohio,
pp. 95—136.
-------
307
Lauer, G. J., H. P. Nicholson, W. S. Cox, and J. I. Teasley. 1966.
Pesticide Contamination of Surface Waters by Sugar Cane Farming in
Louisiana. Trans. Am. Fish. Soc. 95(3): 310—316.
Lee, S. Y. 1962. The Node of Action of Endrin on the Bean Stem Miner,
Melanogromyza sojae, with Special Reference to Its Translocation in Soybean
Plants. J. Econ. Entomol. 55(6): 956—964.
Lincer, J. L., J. M. Solon, and J. H. Nair III. 1970. DDT and Endrin
Fish Toxicity Under Statis Versus Dynamic Bioassay Conditions. Trans. Ma.
Fish. Soc. 99(1): 13—19.
Linder, R. L., and R. B. Dahigren. 1970. Occurrence of Organochiorine
Insecticides in Pheasants of South Dakota. Pesti. Monit. J. 3(4):
227—232.
Long, W. H., L. D. Newsom, and A. M. Mullins. 1961. Endrin Residues
in the Fat of Lambs Grazed on Endrin—Treated Pasture. J. Econ. Entomol.
54(3): 605—606.
Loutfy, M. S., F. A. Khalil, and A. H. E1—Hemaesy. 1970. Effect of
Certain Soil Insecticides on the Cutworm Agrotis ipsilon in Cotton.
Agric. Res. Rev. 48(1): 12—21.
Lowe, J. L. 1965. Some Effects of Endrin on Estuarine Fishes.
Presented at the 19th Annual Conference of the Southeastern Association
of Game and Fish Commissioners, Tulsa, Oklahoma, October 10—13, 1965,
pp. 271—276.
Macek, K. J., C. Hutchinson, and 0. B. Cope. 1969. Effects of Temperature
on the Susceptibility of Blue Gills and Rainbow Trout to Selected
Pesticides. Bull. Environ. Contam. Toxicol. 4(3): 174—183.
Manske, D. D., and P. E. Corneliussen. 1974. Pesticide Residues in
Total Diet Samples (VII). Pesti. Monit. J. 8(2): 110—124.
Manske, D. D., and R. D. Johnson. 1975. Pesticide Residues in Total
Diet Samples (VIII). Pesti. Monit. J. 9(2): 94—105.
Manna, B., and K. C. Ghose. 1972. Histopathological Changes in the Gut
of Achatincz fulica Bowdich Caused by Endrin — A Molluscicide. Indian J.
Exp. Biol. 10(6): 461—463.
Meith—Avcin. N., S. M. Warlen, and R. T. Barber. 1973. Organochiorine
Insecticide Residues in a Bathyl—Demersal Fish from 2,500 Meters. Environ.
L.ett. 5(4): 215—221.
Menzel, D. W., J. Anderson, and A. Randtke. 1970. Marine Phytoplankton
Vary in Their Response to Chlorinated Hydrocarbons. Science 176(3926):
1724—1726.
Messick, J. P. 1972. organochlorine Residues in Wild Ringnecked Pheasants
from Southwestern Idaho. Bull. Environ. Contam. Toxicol. 8(6): 356—360.
-------
308
Metcalf, R. L., I. P. Dapoor, P. Y. Lu, C. K. Schuth, and P. Sherman.
1973. Model Ecosystem Studies of the Environmental Fate of Six
Organochiorine Pesticides. Environ. Health Perspec. 4: 35—43.
Miles, J. R., and C. R. Harris. 1971. Insecticide Residues in a Stream
and a Controlled Drainage System in Agricultural Areas of Southwestern
Ontario, 1970. Pesti. Monit. J. 5(3): 289—294.
Miles, J. R. W., and C. R. Harris. 1973. Organochlorine Insecticide
Residues in Streams Draining Agricultural, Urban—Agricultural, and
Resort Areas of Ontario, Canada — 1971. Pesti. Monit. J. 6(4): 363—368.
Misra, S. S. 1970. Residual Toxicity of Insecticides on Cotton in the
Field to Adults of Cotton Grey Weevil, Myllocerus undecinipustulatus
maculoaus. Sci. Cult. 36(10): 563—565.
Modin, 3. C. 1969. Chlorinated Hydrocarbon Pesticides in California
Bays and Estuaries. Pestic. Monit. 3. 3(1): 1—7.
Moubry, R. J., G. R. Myrdal, and A. Sturges. 1968a. Residues in Food
and Feed. Rate of Decline of Chlorinated Ilydrocarbon Pesticides in Dairy
Milk. Pestic. Nonit. 3. 2(2): 72—79.
Moubry, R. 3., 3. M. Helm, and G. R. Nyrdal. 1968b. Chlorinated Pesticide
Residues in an Aquatic Environment Located Adjacent to a Commercial
Orchard. Pesti. Nonit. J. 1(4): 27—29.
Mount. D. I., and G. 3. Putnlcki. 1966. Summary Report of the 1963
Mississippi Fish Kill. In: Transactions of the 31st North American
Wildlife Conference, Wildlife Management Institute, Washington, D.C.,
pp. 177—184.
Naqvi, S. N., and D. E. Ferguson. 1970. Levels of Insecticide Resistance
in Fresh—Water Shrimp, Palaemonetes kadiakensis. Trans. Am. Fish. Soc.
99(4): 696—699.
Nielson, S. W. 1971. Environmental Pollutants Pathogenic to Animals.
3. Am. Vet. Ned. Assoc. 159(9): 1103—1107.
Novak, A. F., and N. R. Rao. 1965. Food Safety Program: Endrin
Monitoring in the Mississippi River. Science 150(3704): 1732.
Odum, E. P. 1971. Fundamentals of Ecology, 3rd ed., W. B. Saunders,
Phildelphia, Pennsylvania.
Pal, S. K. 1971. Relative Efficacy of Different Insecticides on Urentius
echinus Dist. and Enrpoasca app. Infesting Brinjal Crop in Methania Area
of Western Rajasthan. Madras Agric. 3. 58(4): 323—325.
Personal communication with R. W. Kutz. U.S. Environmental Protection
Agency, Washington, D.C. October 1975.
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Pfister, R. M. 1972. Interactions of Halogenated Pesticides and
Microorganisms: A Review. CRC Critical Reviews in Microbiology 21(1):
1—33.
Pimentel, D. 1971. Ecological Effects of Pesticides on Non—Target Species.
Cornell University, Ithaca, New York, for Office of Science and Technology,
GPO, Washington, D.C.
Pimentel, D., and N. Goodman. 1974. Environmental Impact of Pesticides.
In: Survival in Toxic Environments, N. A. Q. Khan and J. P. Bederka, Jr.,
eds., Academic Press, New York, pp. 25—52.
Reichel, W. L., E. Cromartie, T. C. Lamont, B. M. Mulhern, and R. M.
Prouty. 1969a. Pesticide Residues in Eagles. Pesti. Nonit. J. 3(3):
142—144.
Reidinger, R. F., Jr., and D. G. Crabtree. 1974. Organochiorine Residues
in Golden Eagles, United States — March 1964—July 1971. Pesti. Monit. J.
8(1): 37—43.
Reinke, J., J. F. Uthe, and D. Jamieson. 1972. Organochiorine Pesticide
Residues in Commercially Caught Fish in Canada — 1970. Pesti. Monit. J.
6(1): 43—49.
Rosato, P., and D. E. Ferguson. 1968. The Toxicity of Endrin—Resistant
Mosquito Fish to Eleven Species of Vertebrates. Bioscience 18(8): 783—784.
Rowe, D. R., L. W. Canter, P. J. Snyder, and J. W. Mason. 1971. Dieldrin
and Endrin Concentrations itt a Louisiana Estuary. Pesti. Nonit. J. 4(4):
177—183.
Ryan, S., C. 3. Bacher, and A. A. Martin. 1972. The Mussel Byridella
australia as a Biological Monitor of the Pesticide Endrin in Fresh Water.
Search 3(11—12): 446—447.
Sanders, H. 0. 1970. Pesticide Toxicities to Tadpoles of the Western
Chorus Frog Pseudacris triseriata and Fowler’s Toad Bufo woodhousii fowleri.
Copeia (2): 246—251.
Saunders, 3. W. 1969. Mass Mortalities and Behavior of Brook Trout and
Juvenile Atlantic Salmon in a Stream Pollution by Agricultural Pesticides.
Can. Fish. Res. Baord J. 26(3): 695—699.
Saxena, P. K., and S. Aggarwall. 1970. Toxicity of Some Insecticides
to the Indian Catfish, Heteropneustes fossilis. Anat. Anz. 127: 502—503.
Schafer, M. L., 3. T. Peeler, W. S. Gardner, and 3. E. Campbell. 1969b.
Pesticides in Drinking Water — Waters from the Mississippi and Missouri
Rivers. Environ. Sci. Technol. 3(12): 1261—1269.
Sithanantham, S., and S. C. Daniel. 1972. Potash with Endrin Spray for
Control of Sugarcane Shoot Borer. Fert. News 17(8): 36.
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Sithananthain, S., and S. C. Daniel. 1972. Potash with Endrin Spray for
Control of Sugarcane Shoot Borer. Fert. News 17(8): 36.
Solar, J. M. 1971. Pesticidal Residue Alterations in Potatoes During
Processing (abstract). Diss. Abstr. Tnt. 31(8): 4766B.
Solar, J. M., J. A. Luizzo, and A. F. Novak. 1971. Removal of Aldrin,
Heptachior Epoxide, and Endrin from Potatoes During Processing. J. Agric.
Food Chem. 19(5): 1008—1010.
Sreenivasan, C. W.., and M. V. Natarajan. 1962. Use of Endrin in Fishery
Management. Prog. Fish Cult. 24(4): 181.
Stoltenberg, 0. H. 1972. How to Reclaim a Poisoned Lake. Public Works
103(3): 59—61.
Thakre, S. K., and S. N. Saxena. 1970. Effect of Chlorinated Insecticides
on the Uptake of Calcium and Iron by Wheat (Triticum vulgare Vill.) and
Maize. Andhra Agric. 3. 17(6): 190—192.
Thompson, A. R. 1973. Pesticide Residues in Soil Invertebrates. In:
Environmental Pollution by Pesticides, C. A. Edwards, ed., Plenum Press,
New York, Chap. 3.
U.S. Department of Agriculture, Plant Pest Control Division. 1968.
Monitoring for Chlorinated Hydrocarbon Insecticide Residues in Soybeans —
1966. Pesti. Monit. 3. 2(1): 58—67.
U.S. Department of Health, Education and Welfare. 1969. Report of the
Secretary’s Commission on Pesticides and Their Relationship to Environmental
Health, Parts I and II. GPO, Washington, D.C.
U.S. Environmental Protection Agency. l971a. Pesticide Residues in Ambient
Air, 1971. Division of Pesticide Community Studies, Chaniblee, Georgia.
U.S. Environmental Protection Agency. 1971c. Part 180 — Tolerances and
Exemptions from Tolerances for Pesticide Chemicals in or on Raw Agricultural
Commodities (Subpart C — Specific Tolerances): 180.131, Endrin.
U.S. Environmental Protection Agency. 1972. Development of a Case Study
of the Total Effect of Pesticides in the Environment, Non—Irrigated
Croplands of the Mid—West. Pestic. Study Report 4 in compliance of
PL91—224.
U.S. Environmental Protection Agency. 1974b. Comments of Environmental
Defense Fund in Opposition to the Proposed Effluent Standards. Re:
proposed toxic pollutant effluent standards for Aldrin/Dieldrin et al.,
FWPCA (307) Docket No. 1.
Wheeler, W. B., H. A. Moye, C. H. Van Middelem, N. P. Thompson, and
W. B. Tappan. 1969. Residues of Endrin and DDT in Turnips Grown in
Soil Containing These Compounds. Pesti. Monit. 3. 3(2): 72—76.
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Wolfe, H. R., W. F. Durham, and J. F. Armstrong. 1953. Health Hazards
of the Pesticides Endrin and Dieldrin. Arch. Environ. Health 6: 458—464.
Wolfe, H. R., W. F. Durham, and J. F. Armstrong. 1967. Exposure of
Workers to Pesticides. Arch. Environ. Health 14(4): 622—633.
World Health Organization. 1973. Pesticide Residues in Food. Report of
the 1972 Joint Meeting of the FAO and WHO in Rome. WHO Technical Report
Series No. 525, Geneva.
Yobs, A. R., J. A. Hanan, B. L. Stevenson, J. J. Boland, and H. F. Enos.
1972. Levels of Selected Pesticides in Ambient Air of the United States.
Presented at National American Chemical Society Symposium on Pesticides
in Air, Boston, MA, April 11.
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9. ENVIRONMENTAL ASSES SMENT
9.1 PRODUCTION, CONSUMPTION, AND USES
9.1.1 Production and Consumption
Endrin was introduced into the United States in 1951 by the Hyinan
Company. It is being produced in the United States by Velsicol Chemical
Corporation, while Shell Nederland Chemie manufactures endrin in the
Netherlands. Endrin is snythesized by the oxidation of isodrin at tem-
peratures below 100° C.
Consumption of endrin Is apparently declining. Current consumption
figures are not available; however, the figures for 1971, the most recent
year for which data are available, indicated that usage had decreased by
35% from the 1964 figure of 984,726 kg (Eichers et al., 1968: U.S.
Department of Agriculture, 1968; Andrilenas, 1974).
9.1.2 Uses
Endrin is used as an avicide, rodenticide, and insecticide, the last
being the most important. As an insecticide its major application is to
cotton. A wide variety of other crops may also be protected from insect
pests by endrin. Endrin is also approved for use in the protection of
forest seeds against birds, mice, and chipmunks, and for the control of
birds on buildings and mice in orchards.
9.2 BIOLOGICAL EFFECTS IN THE ENVIRONMENT
9.2.1 Microorganisms
Only a few microorganisms are able to degrade endrin; but these are
also able to degrade dieldrin. Metabolic pathways for microbial degradation
are still speculative, but degradation appears to begin on the nonchiori—
nated epoxy ring, thus forming ketones and aldehydes which may undergo
dechlorination. Ketoendrin is the only metabolite positively identified
to date. Detoxification does not always result from the degradation of
endrin. Metabolites formed may be more toxic and often are more stable.
Transformation of endrin by soil microorganisms is increased by anaerobic
conditions and highly organic soils. In the ocean, algae are active in
endrin transformations.
Endrin does not appear to be excessively inhibitory to ammonifying
organisms or decomposers that liberate ammonia. Eno and Everett (1958)
concluded that higher plants exhibited signs of phytotoxicity before
microbial responses were observed. Many of the soil fungi (including
Streptomyces and Penicillia) and bacteria are not affected by concen-
trations below 1000 ppm. Some algae concentrate endrin manyfold, and
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growth, respiration (Pfister, 1972; Bollen and Tu, 1971), and photosynthesis
may be inhibited to some degree.
Only 2 to 17% of isolated soil microorganisms are active In endrin
degradation (Matsumura et al., 1971; Brooks, 1974). Its persistence in
the soil for longer than nine months implies continued use will build
up toxic levels to nontarget organisms.
Endrin is very persistent under both aerobic and anaerobic conditions,
but the creation of anaerobic conditions generally stimulates microbial
degradation. Temperature does not seem to affect the degradation of
endrin (Pfister, 1972), nor does soil mixing, but degradation is enhanced
by the amount of organic material in flooded or naturally occurring soils
(Guenzi et al., 1971; Castro and Yoshida, 1971).
9.2.2 Vascular Plants
Endrin uptake by vascular plants has been demonstrated. Plants grown
in soil that contains endrin absorb it through their root systems. Endrin
is taken up by plant leaves both upon topical application and by absorption
of endrin vapors which volatilize from the soil. Endrin uptake by plants
from soil depends on the plant, the type of soil, and the endrin concen-
tration in the soil. Residues are usually highest in plants grown in sandy
loam and somewhat lower in clay or loam soils. Endrin uptake by the plant
is retarded by the presence of silt in the soil.
The absorbed endrin is translocated through the plant. Concentrations
vary in the different parts of the plant, decreasing with distance from
the site of uptake. As many as five metabolites have been detected in
plants after absorption. The rate of metabolism by plants varies with
the plant species and probably with mode of endrin application. Endrin
and its metabolites are excreted into soil by plant roots.
Endrin is somewhat phytotoxic to vascular plants; however, some
adverse effects attributed to endrin are actually caused by the solvent
used in the formulation. A 0.03% endrin emulsion produced scorching of
the foliage of three varieties of cucurbits after seven days. A 0.04%
emulsion produced high phytotoxicity after three days. Endrin can affect
the rate of seed germination as well as mitotic and maiotic processes.
The presence of endrin in the soil affects the uptake of various
macro— and microelements, either increasing or decreasing uptake, depending
upon the particular element, plant species, and the endrin concentration.
9.2.3 Aquatic and Higher Animals
Animals are exposed to endrin through their contact with several
components of their environment, including food, water, air, and soil.
Endrin may be absorbed through the digestive tract and/or body surfaces.
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After an initial rapid uptake, endrin accumulation reaches an equilibrium
between elimination and uptake. Both rate of uptake and equilibrium
concentration are directly related to the exposure level.
Endrin is not stored in tissues, but remains in a dynamic state,
equilibrating with ambient levels. After reaching the equilibrium
concentration, the duration of exposure does not affect the amount of
residue. However, after chronic exposures, many insects, shrimp, and
fish develop a tolerance to increased endrin doses. If the exposure level
is lowered, endrin is eliminated from birds, mammals, and aquatic animals.
Aquatic mollusks and arthropods are exposed to endrin in the water,
sediment, and food sources. These aquatic invertebrates act as extractors,
continually exchanging residues between body fluids and water until reaching
an equilibrium. This equilibrium will depend on the concentration of
endrin in the water, species, bottom concentration, and exposure time.
Endrin is rapidly accumulated initially by mollusks and arthropods,
achieving bioconcentration factors up to 49,000 and 2600 respectively
(Metcalf et al., 1973).
Endrin is more toxic to aquatic arthropods than to mollusks. Lethal
concentrations are less than 10 ppb for several species of marine shrimp,
while clams and mud snails survive at levels a thousand times greater,
that is, 10 ppm. Sublethal endrin concentrations also affect growth and
reproduction of many aquatic invertebrates. Oyster larvae exposed to
sublethal endrin concentrations were generally more sensitive than eggs
(Davis, 1961).
Direct sources of endrin to fish include food, water, and sediment.
Uptake in fish is based on absorption and solubility differences between
fat and water, with fish acting as a multiphase exchange system with
successive and reversible partitionings between water, blood, and fat.
Endrin concentration in water determines the initial uptake rate and
equilibrium levels in fish. The uptake from water far exceeds that
from food, bioconcentration from water being 2000 times higher than
that from food in channel catfish (Argyl et al., 1973). The primary
means of endrin entry into the fish body is absorption through gill
surfaces.
Endrin is most toxic of the organochlorine insecticides to fish
(Eisler, 1970a, b, c). Many factors influence the toxicity of endrin
to fish; among these are exposure time, temperature, salinity, body size,
previous exposure, flowing or static bioassay systems, species, synergism
with other compounds, route of entry, developmental stage, and season.
Mortality occurs in aquatic invertebrates and fish at endrin con-
centrations as low as 1 ppb in water, while birds and mammals, acquiring
endrin from feed sources, exhibit mortality at doses of 2 to 20 ppm.
Lower concentrations may cause pathological and reproductive changes,
suggesting that chronic exposure to lower concentrations may affect nerve
function and metabolism.
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The central nervous system apparently is the primary site of endrin
toxicity in all animals. The signs of endrin poisoning reflect nerve
stimulation, with reactions to acute levels generally following the pattern
of hypersensitivity, hyperactivity, tremors, equilibrium loss, convulsions,
hyperventilation, and paralysis. Endrin may also inhibit certain enzymes
and impair liver function. Chronic endrin exposures of 1 ppm in the
diet reduced reproduction of fish and birds by decreasing egg production,
and in some cases decreased hatchability and viability of bird eggs were
observed.
9.3 EFFECTS ON HUMAN HEALTh
9.3.1 Toxicity
Endrin poisoning in humans has resulted from accidental contamination
of foods and has been traced to endrin doses as low as 0.02 mg/kg. Human
symptoms of endrin poisoning are convulsions, vomiting, abdominal pain,
nausea, dizziness, and headache. In severe cases, convulsive seizures of
several minutes duration may be followed by semiconsciousness and can
lead to death through respiratory failure. Endrin toxicity appears to be
primarily due to its effect on the central nervous system.
Chronic exposure studies in laboratory animals indicate that exposures
to low levels of endrin can be toxic. Significant mortality has been
observed in mice exposed to 2 ppm endrin in the diet for seven months.
Fatalities have been observed following inhalation exposure of animals
to 0.36 ppm endrin vapor for 7 hr on each of 130 days.
Humans do not tend to store endrin in significant quantities:
residues have not been detected in plasma, adipose tissue, or urine of
workers occupationally exposed. Thus despite its high acute toxicity,
endrin is relatively nonpersistent in man. Residues are only detected
in body tissues of humans immediately after an acute exposure.
9.3.2 Carcinogenesis, Mutagenesis, and Teratogenesis
No malignancies in humans attributed to endrin exposure have been
reported in the literature. Endrin can, however, cause mutations in mam-
malian cells and appears to be teratogenic in mice and hamsters. Endrin
exposure may cause an increase in fetal and postnatal mortality, but
parental fertility is not affected.
9.3.3 Potential Health Hazards
Human exposure to endrin occurs through the diet via inhalation and
by dermal contact. The average dietary intake in the United States
from 1965 to 1970 of 0.005 pg of endrin per kg was well below the maximum
acceptable daily intake of 0.002 mg of endrin per kg of body weight
established by the World Health Organization.
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Agricultural workers, home gardeners, and those involved in endrin
manufacture and distribution might be exposed through inhalation or
dermal exposure. The most significant occupational exposure to endrin
comes during spraying of fields, and dermal exposure is almost always
greater than respiratory exposure. A threshold limit of 0.1 g/m 3 for
an 8—hr time—weighted average occupational exposure has been established
by OSHA (U.S. Code of Federal Regulations, 1972).
9.4 SOURCES OF PERSISTENCE IN THE ENVIRONMENT
9.4.1 Lithosphere
Direct application is the greatest source of endrin in the lithosphere.
Endrin may be applied to the soil directly or indirectly following the
treatment of crops. The largest single use of endrin in the United States
is for the control of lepidopterous larvae attacking cotton crops in the
southeastern and delta states. Endrin—contaminated soils in the United
States are located predominantly in the cotton belt or delta states, where
endrin is extensively used. Fallout and rainout of airborne particulate
matter to which endrin has adsorbed are important mechanisms for contami-
nation of nonagricultural soil or soil on which endrin has never been
used. Wind drift and irrigation with contaminated water are also possible
routes of endrin to the soil.
Since a large proportion of the endrin entering the environment is
initially released to the soil, the fate of endrin in the soil largely
determines to what extent the rest of the environment will become con-
taminated. The persistence of endrin in the soil is dependent upon a
wide variety of factors, including soil properties, agricultural processes,
topography, and weather conditions.
Endrin is removed from the soil in several ways. Volatilization,
leaching into groundwater, wind erosion, and surface runoff translocate
endrin to other parts of the environment. Other pathways, such as uptake
by plants and ingestion by soil invertebrates, contribute to removal of
endrin from the lithosphere. Degradation of endrin through photodecomposi—
tion, thermal decomposition, and microbial degradation also occurs,
resulting in the dissipation of endrin from the environment. Endrin
removal by microbial degradation, however, is contingent upon the presence
of an appropriate microbial species and favorable soil conditions. Half—
lives ranging from 24 hr to 11.8 years have been observed, depending upon
all of the previously mentioned conditions.
Since most of the endrin entering the environment is initially
released to the soil, the soil type largely determines to what extent
the rest of the environment will become contaminated. Some soil types
adsorb endrin, preventing it from escaping to the atmosphere, while others
permit extensive volatilization. Climate and topography affect the fate
of endrin in the environment also. Rainfall on sloping ground may result
in surface erosion, which causes endrin to be transported to the hydro-
sphere regardless of the soil’s adsorption ability.
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9.4.2 Hydrosphere
The major source of endrin in rivers and other freshwater bodies is
surface runoff from fields and crops following application. Other sources
of endrin in the hydrosphere include runoff from endrin—coated seeds, con-
taminated effluents from pesticide manufacturing and formulating factories,
careless aerial application, dumping of unused pesticide into waterways,
cleaning spray equipment in rivers and lakes, and contaminated rainout
and fallout.
The worst effects of contamination in a given body of water, generally,
are recorded immediately following the episode of pollution. Codistillation
and sedimentation transfer a large proportion of the endrin elsewhere or
render it relatively harmless. However, entire populations of birds or
fish may be destroyed during the short period of acute contamination.
Pesticide surveillance of surface waters of the United States river
basins has been in effect since 1957. From 1961 through 1964 the number
of samples containing endrin progressively increased until, in 1964, 50%
of all samples tested were contaminated. However, over this time period,
consistent contamination of a large percentage of the samples occurred
only in the lower Mississippi basin. Highest concentrations recorded
during this six—year period were also from this area. Endrin usage in
this area is apparently declining, since the residue levels reported in
1970 and 1975 were only 20 ppt as compared with a maximum of 214 ppt
reported in 1963.
The highest concentration of endrin in the sediment of any river
basin monitored between 1970 and 1975 was found in the lower Mississippi.
This value, 6700 ppt, was significantly less than the amount found in
1964, that is, 10,000 ppt.
Removal of endrin from the hydrosphere occurs by several routes.
Volatilization and codistillation reallocate endrin to the atmosphere.
Dissipation of endrin from the hydrosphere occurs as a result of bio-
chemical and photochemical degradation. Degradation by aquatic micro-
organisms has been reported and probably contributes to some extent to
the dissipation of endrin from the aquatic environment.
9.4.3 Atmosphere
Vaporization of endrin from treated soils and crops is believed to
represent the major source of atmospheric contamination. In one experi—
ntent, only 6% of the endrin applied on cabbage plants could be detected
on the soil or leaves four weeks after treatment. Codistillation from
water, wind transport of pesticide—laden dust, aerial drift from spraying
operations, and vapor emissions from industrial sources also contribute
to the presence of endrin in the atmosphere.
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Since atmospheric monitoring equipment and technology are extremely
complex and expensive, they are not in common use. However, the highest
endrin concentration in air reported to date was 58.5 mg/rn 3 at Stoneville,
Mississippi, in 1971. Atmospheric endrin is present both in the vapor
phase and adsorbed to wind—borne particulates.
Some dissipation of endrin in the atmosphere via photodecomposition is
possible; however, no real evidence that this transformation actually
occurs is available. Thus the major hazard involved in the release of
endrin to the atmosphere is the subsequent contamination of the hydrosphere
and the lithosphere.
Atmospheric transport of endrin far exceeds any other mechanism and
is considered to be primarily responsible for the worldwide dissemina-
tion of the pesticide. Transport of endrin to the open ocean is thought
to occur largely via the atmosphere, from which it is removed by parti-
cle fallout or precipitation washout. After deposition in the ocean,
endrin may adsorb to the organic materials present and later be revolati—
lized, or it may adhere to large particulates and be deposited in the
sediment. Ocean sediment therefore represents the ultimate sink f or endrin
and related compounds. The fate of endrin in the ocean sediment remains
unknown.
9.4.4 Detection and Analysis
Many techniques for endrin determination have been reported. These
include bloassays, total chlorine content, silylation, acetylation, spectro—
photometry, and colorimetry. The most sensitive methods available, however,
both qualitatively and quantitatively, involve variations in gas chroma-
tography. Gas—liquid chromatography methods are rapid and highly sensitive,
permitting detection of a very small quantities of endrin residues.
Although analytical methods are adequate in determining the presence
of endrin residues, detection of endrin in the environment is rather
difficult at times because of the inadequacy of sampling methods.
9.5 STANDARDS AND REGULATIONS
Several concentrations have been recommended and/or established as
acceptable environmental levels for endrin residues. A threshold limit
value of 100 g/m 3 was adopted by the American Conference of Governmental
Industrial Hygienists for atmospheric concentrations. While no standards
have been set for water concentrations of endrin, 0.1 ppb has been sug-
gested as a maximum reasonable allowance for potable water. Maximum
acceptable daily intake for humans was established at 138.2 pg/day by
the World Health Organization (1973).
Concentrations of endrin found in air and water are well below accepted
limits, except for sporadic high levels in the immediate vicinity of
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endrin usage. The maximum air concentration of endrjn in 1975 was found
at Jackson, Mississippi (0.5 mg/rn 3 ). The maximum concentration of endrin
in drinking water (23 ppt) was found in Louisiana, from a high endrin
usage area, and was less than one—fourth the suggested allowance for
potable water. The average daily intake of endrin by man according to
the latest available figures was 0.033 pg; this is far below the acceptable
daily intake established by the WHO/FAO (1973).
9.6 ENVIRONMENTAL IMPACT
Worldwide monitoring data show that endrin occurs at very low levels.
However, endrin has the highest acute toxicity of the common organochlorine
insecticides, making even low levels a potential threat to the environment.
Major uses of endrin occurred in the l960s in the southeastern cotton—
producing areas for control of lepidopterous larvae. However, since the
large—scale fish kills in the Mississippi River and delta region in the
mid—1960s, the levels of endrin in the United States have progressively
declined. Environmental contamination is mainly restricted to those areas
where intensive use has occurred. Concentrations of endrin, away from
areas of heavy use, are generally below the levels of detection.
Bioaccumulation of endrin has been reported in blue—green algae, and
growth inhibition occurs in several species of algae and phytoplankton,
after endrin exposure. Vascular plants absorb, translocate, and metabolize
endrin, but it is generally nontoxic to them. Aquatic invertebrates and
fish can bioconcentrate endrin from the water. It is the most toxic to
fish of all the commonly used organochiorine insecticides. Birds are
extremely susceptible to endrin, with mortality commonly occurring.
Mammals rapidly degrade and eliminate endrin even though it can be extremely
toxic at times. Endrin in not stored in mammalian tissues, and residues
can only be detected immediately after an acute exposure.
The threat to nontarget organisms, mainly birds and fish, does exist
becuase of their high degree of susceptibility. However, since endrin
usage is declining, the threat for environmental contamination is reduced.
The possibility of human food, water, or air supplies being highly
contaminated with endrin apparently exists only in those areas immediately
adjacent to high endrin use areas.
However, since endrin is such a highly toxic pesticide to fish, birds,
and mammals, any increased usage would pose a serious threat to the
environment in localized areas.
9.7 REFERENCES
Andrilenas, P. A. 1974. Farmers’ Use of Pesticides in 1971 ... Quantities.
Economic Research Service, U.S. Department of Agriculture, Washington, D.C.,
Agric. Econ. Rep. 252, 56 pp.
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Argyl, R. L., C. C. Williams, and H. K. Dupree. 1973. Endrin Uptake and
Release by Fingerling Channel Catfish (Ictaburus punctatus). J. Fish Res.
Board Can. 30(11): 1743—1744.
Bollen, W. B., and C. M. Tu. 1971. Influence of Endrin on Soil Microbial
Populations and Their Activity. USDA Forest Service Research Paper — PNW
114: 104.
Brooks, G. T. 1974. Chlorinated Insecticides. Vol. II: Biological and
Environmental Aspects. CRC Press, Cleveland, Ohio.
Castro, T. F., and T. Yoshida. 1971. Degradation of Organochlorine
Insecticides in Flooded Soils in the Phillippines. J. Agric. Food Chem.
19(6): 1168—1170.
Davis, H. C. 1961. Effects of Some Pesticides on Eggs and Larvae of
Oysters (Crassostrea virginica) and Clams (Venus merc,encwia). Coinmer.
Fish Rev. 23(12): 8—23.
Eichers, T., P. Andrilenas, R. Jenkins, and A. Fox. 1968. Quantities of
Pesticides Used by Partners in 1964. U.S. Government Printing Office,
Washington, D.C., 37 pp.
Eisler, R. 1970a. Latent Effects of Insecticide Intoxication to Marine
Mollusks. Hydrobiologia 36(3—4): 345—352.
Eisler, R. 197Db. Factors Affecting Pesticide—Induced Toxicity in a
Estuarine Fish. Tech. Pap. Bur. Sport Fish. Wildi. 45:1—20.
Eisler, R. l970c. Acute Toxicities of Organochlorine and Organophosphorus
Insecticides to Estuarine Fishes. Tech. Pap. Bur. Sport Fish. Wildi.
46: 1—12.
Eno, C. F., and P. H. Everett. 1958. Effects of Soil Applications of
10 ChlorInated Hydrocarbon Insecticides on Soil Microorganisms and the
Growth of Stringless Black Valentine Beans. Soil Sd. Soc. Am. Proc.
22: 235—238.
Guenzi, W. D., W. E. Beard, and F. G. Viets, Jr. 1971. Influence of
Soil Treatment on Persistence of Six Chlorinated Hydrocarbon Insecticides
in the Field. Soil Sci. Soc. Am. Proc. 35(6): 910—913.
Matsumura, F., U. G. Khanvilkar, K. C. Path, and G. M. Boush. 1971.
Metabolism of Endrin by Certain Soil Microorganisms. J. Agric. Food Chem.
19(1): 27—31.
Metcalf, R. L., I. P. Kapoor, P. Y. Lu, C. K. Schuth, and P. Sherman.
1973. Model Ecosystem Studies of the Environmental Fate of Six Organo—
chlorine Pesticides. Environ. Health Perspec. 4: 35—43.
-------
321
Pfister, R. M. 1972. Interactions of Halogenated Pesticides and
Microorganisms: A Review. CRC Critical Reviews in Microbiology 21(1):
1—33.
U.S. Code of Federal Regulations. 1972. Washington, D.C.
U.S. Department of Agriculture. 1968. The Regulation of Pesticides in
the United States. U.S. Department of Health, Education, and Welfare;
and Food and Drug Administration.
World Health Organization. 1973. Pesticide Residues in Food. Report of
the 1972 Joint Meeting of the FAO and WHO in Rome. WHO Technical Report
Series No. 525, Geneva.
-------
BIBLIOGRAPHY
323
-------
325
A
Adler, C. 1969. Ocean Pollution Problems. Sci. Technol. 93: 18—25.
Agricultural Pesticide Chemicals Handbook. 1967a. Fruits, Bush and
Vine Fruits and Deciduous Fruits and Nuts. Insecticides.
Agricultural Pesticide Chemicals Handbook. 1967b. Hay and Grass
Crops. Insecticides. H—7 and H—7—l.
Agricultural Pesticide Chemicals Handbook. 1967c. Cotton. Insecticides.
E— 8.
Agricultural Pesticide Chemicals Handbook. l967d. Corn. Insecticides.
D—6.
Agricultural Pesticide Chemicals Handbook. l967e. Small Grains and
Miscellaneous Crops. Insecticides. L—l2 and L—13.
Agricultural Pesticide Chemicals Handbook. 1967f. Vegetables and
Truck Crops. Insecticides. P—45 and P—46.
Ahiawat, Y. S., and K. K. Sardar. 1976. Efficiency of Certain Insecti-
cides in Controlling Leaf Curl Disease in Chillies. Sci. Cult.
42(5): 273—275.
Ahmed, M., and A. Abdullah. 1971. Determination of Residues of Dimecron,
Endrin, and Malathion on Tobacco Plants Using Bioassay Technique. Pak.
J. Sci. Res. 23(1—2): 34—41.
Ahmed, S., S. Amin, and M. A. Uddin. 1971. Viscosities of Dilute
Polymer Solutions: Significance of the Mark—Houwink Constants. Pak.
J. Sd. Indian Res. 23(1—2): 34—36.
Alexander, M. 1965a. Persistence and Biological Reactions of Pesticides
in Soils. Soil Sci. Soc. Am. Proc. 29(1): 1—7.
Altmeier, G., W. Klein, and F. Korte. 1969. Ecological Chemistry XXIV.
Metabolism of Endrin—l4C in Perfused Rat Liver (in German). Tetrahedron
Lett. (49): 4269—4271.
Anderson, D. W., and J. J. Hickey. 1970. Oological Data on Egg and
Breeding Characteristics of Brown Pelicans. Wilson Bull. 82(1): 14—28.
Anderson, D. W., J. J. Hickey, R. W. Risebrough, D. F. Hughes, and
R. E. Christensen. 1969. Significance of Chlorinated Hydrocarbon
Residues to Breeding Pelicans and Cormorants. Can. Field Nat.
83(2): 91—112.
Anonymous. 1969a. Curbs on Panic and Pesticides. Nature 224(5226): 1249.
-------
326
Anonymous. 1969b. Mrak Committee Molds Pesticides’ Future. Farm
Chem. 132(12): 24—25.
Anonymous. 1970a. Finland — Ban on Organochiorine Insecticides.
Food Cosmet. Toxicol. 8(2): 200.
Anonymous. 1970b. USDA to Review Uses of Seven Insecticides. Am. Vet.
Med. Assoc. J. 157(7): 914.
Anonymous. 1970c. Pesticide Industry’s Long, Hot Summer. Chein. Week
107(6): 21—22.
Anonymous. 1970d. Severe Restrictions on Use of Persistent Pesticides.
Chem. Week. 106(1): 22.
Anonymous. 1972a. CSMA Chemical Analysis Test Methods. Soap Cosmet.
Chem. Spec. 48(4): 155—163.
Anonymous. 1972b. Pressure on Pesticides. Chem. Week 110(16): 22.
Anonymous. 1973. British Columbia — Control of Poisonous Substances:
Agricultural Pesticides. mt. Dig. Health Leg. 24(1): 28—29.
Anonymous. 1974a. Events Force Toxic Substances Issue. Environ.
Sci. Tech. 8(5): 408—409.
Anonymous. 1974b. EPA Administrator Suspends Pesticides Aidrin,
Dieldrin for Cancer Risk. Toxic Mater. News. 10/1/74: 103.
Anonymous. l974c. EPA Moves Against Two More Pesticides as Potential
Cancer Risk to Man. Toxic Mater. News. 11/1/74.
Anonymous. 1975a. EPA Begins Second Try at Setting Water Discharge
Standards for Nine Toxic Pollutants. Toxic Mater. News. Jan. 15: 13—15.
Anonymous. 1975d. EPA, Caught in the Middle, Is Upheld on Aidrin—
Dieldrin. Chem. Mark. Rep. 207(15): 5, 23.
Archer, T. E. 1968a. Quantitative Measurement of Combinations of
Aramite, DDT, Toxaphene, and Endrin in Crop Residues. Bull. Environ.
Contain. Toxicol. 3(2): 71—79.
Archer, T. E., and D. C. Crosby. 1969. The Decontamination of Animal
Feeds. Residue Rev. 29: 13—37.
Arias, A. C., J. S. Lozano, and J. N. Creus Vidal. 1966. Lethal
Intoxication by Endrin (Spanish). An. R. Acade Farm (Santiago)
32(2): 131—146.
Arsenault, C. P., J. J. Doihun, and K. Biemann. 1971. Alternate or
Simultaneous Electron Impact — Chemical Ionization Mass Spectrometry of
Gas Chromatographic Effluent. Anal. Chem. 43(12): 1720—1722.
-------
327
Asai, R. I., W. E. Sestlake, and F. A. Gunther. 1969. Endrin
Decomposition on Air—Dried Soils. Bull. Environ. Contain. Toxicol.
4(5): 278—284.
Ashe, H. B., E. J. Baier, A. L. Coleman, H. B. Elkins, B. Grabois,
W. J. Hayes, Jr., K. Jacobson, H. N. MacFarland, E. Mastromatteo,
W. F. Reindollar, R. G. Scovill, R. C. Smith, M. R. Zavon, and
H. E. Stokinger. 1964. Threshold Limit Values for 1964. AMA Arch.
Environ. Health 9: 545—554.
Bagon, D. A., N. T. Crosby, H. L. Hardy, and J. H. Simmons. 1973.
A Personal Sampling Technique for Simultaneous Determination of Hydro-
gen Sulphide and Carbon Disulphide in Air. Ann. Occup. Hyg. 16(2):
133—139.
Baluja, G., and J. N. Franco. 1971. Thermal Decomposition of Labile
Chlorinated Pesticides and Efficiency of Mixed Stationary Phases in
Gas—Liquid Chromatography Analysis. Fate of Pesticides. In: Pro-
ceedings of the 2nd International IUPAC Congress of Pesticides Chemistry,
Tel—Aviv, 6: 263—271.
Barker, R. J. 1958. Notes on Some Ecological Effects of DDT Sprayed
on Elms. J. Wildl. Manage. 22(3): 269—274.
Barroga, S. F. 1969. Control of Lepidopterous Pests Attacking Bush
Bean (Phaseolus vulgaris L.) Blossoms and Pods. Philipp. J. Plant
md. 34(3—4): 159—162.
Bartlett, B. R. 1963. The Contact Toxicity of Some Pesticide Residues
to Hymenopterous Parasites and Coccinellid Predators. J. Econ. Entomol.
56(5): 694—698.
Bartlett, B. R. 1966. Toxicity and Acceptance of Some Pesticides Fed
to Parasitic Hymenoptera and Predatory Coccinellids. J. Econ. Entomol.
59(5): 1142—1149.
Bates, A. 1960. Analysis of Endrin Residues in Flour by Infra—Red
Spectroscopy. J. Sci. Food Agric. 11(12): 750—754.
Bedford, C. T., D. H. Hutson, and I. L. Natoff. 1975. The Acute
Toxicity of Endrin and Its Netabolites to Rats. Toxicol. Appl. Pharmacol.
33: 115—121.
Begliomini, A., and A. Fravilini. 1971. Residui Di Insetticidi Nei
Mangimi. Nota II. Identificazione E Dosaggio Gas Chroinatografico
Di Insetticidi Clorurati Ed Esteri Fosforici in Mangimi Composti (in
Italian). Arch. Vet. Ital. 22(2—3): 109—118.
-------
328
Benson, W. R. 1969b. The Chemistry of Pesticides. Ann. New York
Acad. Sci. 160: 7—29.
Best, S. M. 1973. Some Organochlorine Pesticide Residues in Wildlife
of the Northern Territory, Australia, 1970—71. Aust. J. Biol. Sci.
26(5): 1161—1970.
Bhatia, S. K., and S. Pradhan. 1970. Studies on Resistance to Insecti-
cides in Triboliwn castcznewn (Herbst). II. Cross—Resistance Char-
acteristics of the p,p’—DDT—Resistant Strain. Indian J. Entomol.
32(1): 32—38.
Bidlenian, T. F., and C. E. Olney. 1974. High—Volume Collection of
Atmospheric Polychiorinated Biphenyls. Bull. Environ. Contain. Toxicol.
11(5): 442—447.
Bindra, 0. S., and J. Singh. 1973. Bionomics of the Arm—Worm, Mythimna
separata (Walker) (Lepidoptera: Nocutidae), at Ludhiana, Punjab.
Indian. J. Agric. Sci. 43(3): 299—303.
Bingham, C. R. 1970. Comparison of Insecticide Residues from Two
Mississippi Oxbow Lakes. Proc. Ann. Southeast. Assoc. Games Fish
Comm. 275—280.
Bird, C. W., R. C. Cookson, and E. Crundwell. 1961. Cyclisations and
Rearrangements in the Isodrin—Aidrin. J. Chem. Soc. (London): 4809—4816.
Bird, C. W., and R. Khan. 1976. The Addition of p—Chlorobenzenethiol
to Isodrin. Tetrahed. Lett. 32: 2813—2814.
Blevins, R. D., and W. C. Dunn, Jr. 1975. Effects of Carbaryl and
Dieldrin on the Growth, Protein Content, and Phospholipid Content of
Hela Cells. J. Agric. Food Chem. 23(3): 377—382.
Bluestone, H. 1954. 1,2,3,4,1O,10—Hexachloro—6,7—epoxy,l,4,4a,5,6,7,8,Ba--
octahydro—1’ ,4,5,8, dimethanonathalene and Insecticidal Composition
Thereof. U.S. Patent No. 2,676,132. Washington, D.C.
Bluestone, H., R. E. Lidov, J. H. Kuaus, and P. W. Howerton. 1951.
Process for Producing Heptachlor. US. Patent No. 2,576,666. Washington,
D.C.
Bogusz, M., and T. Borkowski. 1973. The Application of the Thin—Layer
Chromatographic—Enzyme Inhibition Technique to Organochiorine Insecti-
cides. Anal. (London) 98(1164): 190—193.
Borror, D. J., and D. M. DeLong. 1954. An Introduction to the Study
of Insects. Rinehard, New York.
-------
329
Bourquin, A. W., S. K. Alexander, H. K. Speidel, J. E. Mann, and
J. F. Fair. 1972. Microbial Interactions with Cyclodiene Pesticides.
In: Developments in Industrial Microbiology 13: 264—276. American
Institute of Biological Sciences, Washington, D.C.
Bowery, T. G., and F. E. Guthrie. 1961. Determination of Insecticide
Residues on Green and Flue—Cured Tobacco and in Main—Stream Cigarette
Smoke. Agric. Food Chem. 9(3): 193—197.
Boyd, E. M. 1969. Dietary Protein and Pesticide Toxicity in Male
Weanling Rats. Bull. W.H.O. 40(5): 801—805.
Boyd, C. E., and D. E. Ferguson. 1964. Susceptibility and Resistance
of Mosquito Fish to Several Insecticides. J. Econ. Entomol.
57(4): 430—431.
Brady, N. C. (ed.). 1967. Agriculture and the Quality of Our Environ-
ment. American Association for the Advancement of Science, Publication
85. Washington, D.C.
Bresch, H., and U. Arendt. 1977. Influence of Different Organochiorine
Pesticides on the Development of the Sea Urchin Embryo. Environ. Res.
13(1): 121—128.
Brodtmann, N. V. 1976. Continuous Analysis of Chlorinated Hydrocarbon
Pesticides in the Lower Mississippi River. Bull. Environ. Contam.
Toxicol. 15(1): 33—39.
Bugg, J. C., J. E. Higgins, and E. A. Robertson. 1967. Chlorinated
Pesticide Levels in the Eastern Oyster (Crassostrea virginica) from
Selected Areas of the South Atlantic and Gulf of Mexico. Pesti. Monit.
J. 1(3): 9—12.
Bureau of Foods. 1975. Compliance Program Evaluation — Total Diet
Studies: FY 1973. Prepublication material.
Burke, J. A. 1973. Report on Chlorinated Pesticides. J. Assoc. Of f.
Anal. Chem. 56(2): 296—299.
Burke, J. A. 1974. Report on Chlorinated Pesticides. J. Assoc. Of f.
Anal. Chem. 57(2): 296—298.
Burke, W. D., and D. E. Ferguson. 1969. Toxiclties of Four Insecti-
cides to Resistant and Susceptible Mosquito Fish in Static and Flowing
Solutions. Mosq. News 29(1): 96—101.
Butler, P. A. 1972. DDT in Estuarine Molluscs. Bioscience
22(12): 690—691.
Butler, P. A. 1974. Trends in Pesticide Residues in Shellfish. Proc.
Nat. Shellfish. Assoc. 64: 77—81.
-------
330
Butler, P. A., and P. F. Springer. 1963. Pesticides — A New Factor in
Coastal Environments. Reprinted from Transactions of the 28th North
American Wildlife and Natural Resources Conference, March 4—6, Wildlife
Management Institute, Washington, D.C.
C
California Department of Agriculture. 1972. State Pesticide Use Report,
January—December 1971. Pesti. Use Rep.: 78.
California Department of Agriculture. 1973. State Pesticide Use Report,
January—December 1972. Pesti. Use Rep.: 85—86.
Casper, V. L., R. J. Hammerstroin, E. A. Robertson, Jr., J. C. Bugg, Jr.,
and J. L. Gaines. 1969. Study of Chlorinated Pesticides in Oysters and
Estuarine Environment of the Mobile Bay Area. U.S. Department of
Health, Education, and Welfare, Bureau of Water Hygiene, Cincinnati,
Ohio, 47 pp.
Chand, N., and S. N. Deshmukh. 1973. Some Observations on the Behavior
of the Dispersing Larvae of Bissetia steniella (Hampson) and Their
Susceptibility to Some Common Insecticides. Indian Sugar 23(7): 603—605.
Cahu, A. S. Y. 1974. Confirmation of Pesticide Residue Identity. VII.
Solid Matrix Derivation Procedure for the Simultaneous Confirmation of
Heptachlor and Endrin Residues in the Presence of Large Quantities of
Polychiorinated Biphenyls. J. Assoc. Of f. Anal. Chem. 57(3): 585—591.
Christudas, S., P. S. Mathai, and M. R. G. K. Nair. 1971. Field
Evaluation of Insecticides. Agric. Res. J. Kerala 9(1): 29—30.
Claeys, R. R., and R. D. Inman. 1974. Adsorption Chromatographic
Separation of Chlorinated Hydrocarbons from Liquids. J. Assoc. Of f.
Anal. Chem. 57(2): 399—404.
Cochrane, W. P., and A. S. Y. Chau. 1971. Chemical Derivatization
Techniques for Confirmation of Organochiorine Residue Identity. Adv.
Chem. Series 104: 11—26.
Coleman, G. R., and J. H. Baker. 1974. Resistance to Dieldrin and
Gamma—BIIC in the Wood—Boring Insect (Coleoptera lyctidae). mt.
Biodeterior. Bull. 10(4): 115—116.
Cookson, R. C., and E. Crundwell. 1959. Transannular Reactions in the
Isodrin Series. Chem. md.: 703—704, June 6.
Corneliussen, P. B. 1969. Pesticide Residues in Total Diet Samples
(IV). Pesti. Monit. J. 21(4): 140—152.
Corneliussen, P. E. 1970. Pesticide Residues in Total Diet Samples
(V). Pesti. Monit. J. 4(3): 89—105.
-------
331
Corneliussen, P. E. 1972. Pesticide Residues in Total Diet Samples
(VI). Pesti. Monit. J. 5(4): 313—330.
Cotton, D., and J. Herring. 1971. A Preliminary Survey of Pesticide
Residues in Whitetail Deer. Proceedings of the 24th Annual Conference
Southeastern Assoc. of Game and Fish Commissioners: 23—30.
Craig, R. B., and R. L. Rudd. 1974. The Ecosystem Approach to Toxic
Chemicals in the Biosphere. In: Survival in Toxic Environments,
M. A. Q. Khan and J. P. Bederka (eds.), Academic Press, New York,
pp. 1—24.
Crockett, A. B., G. B. Wiersina, H. Tai, and W. Mitchell. 1975.
Pesticide and Mercury Residues in Commercially Grown Catfish. Pesti.
Monit. J. 8(4): 235—240.
D
Dale, W. E., M. F. Copeland, and W. J. Hayes, Jr. 1965. Chlorinated
Insecticides in the Body Fat of People in India. Bull. W.H.0.
33: 471—477.
Daniels, N. E. 1971. Detection of Insecticidal Residue and Control
of Soil Insects. J. Econ. Entomol. 64(1): 175—177.
Davies, J. E. 1972. Recognition and Management of Pesticide Toxicity.
Adv. mt. Medi. 18: 23—38.
Davies, J. E. 1973. Pesticide Residues in Man. In: Environmental
Pollution by Pesticides, C. A. Edwards (ed.), Plenum Press, New York,
Chap. 8.
Decker, C. C. 1967. Significance of Pesticide Residues in the
Environment. Span 10(1): 5—7.
Decker, G. C. 1974. Costs and Benefits of Pesticides: An Overview.
In: Survival in Toxic Environments, M. A. Q. Rhan and J. P. Bederka, Jr.
(eds.), Academic Press, New York, pp. 447—471.
Deelstra, H., J. L. Power, and C. T. Kenner. 1976. Chlorinated Hydro-
carbon Residues in the Fish of Lake Tanganyika. Bull. Environ. Contam.
Toxicol. 15(6): 689—698.
Deichmann, W. B. l972b. The Debate on DDT. Arch. Toxikol. 29(1): 1—27.
DePew, L. J. 1971. Evaluation of Foliar and Soil Treatments for
Greenbug Control on Sorghum. J. Econ. Entomol. 64(1): 169—172.
Deshmukh, S. N., and S. C. Dutta. 1973. Study of the Residues of DDT
and Endrin in or on Maize by Gas—Liquid Chromatography. Indian J.
Agric. Sd. 43(1): 94—96.
-------
332
deVos, R. H., J. Bouwman, and A. B. Engel. 1972. Residues of Organo—
chlorine Pesticides in Broilers from Feed Fortified with Known Levels
of These Compounds. Pesti. Sci. 3(4): 421—432.
DeWitt, J. B., C. M. l4enzie, V. A. Adomaitis, and W. L. Reichel. 1960.
Pesticidal Residues in Animal Tissues. Reprint from Transactions of
the 25th North American Wildlife Conference, Wildlife Management
Institute, Washington, D.C.
DeWitt, J. B., W. H. Stickel, and P. F. Springer. 1963. Wildlife
Studies, Patuxent Wildlife Research Center. U.S. Department of the
Interior, Fish and Wildlife Service. No. 67: 74—96.
Dhindsa, K. S., S. H. Singhvi, S. K. Gupta, and N. D. Verma. 1974.
Effect of Soil Application of Aidrin and Dleldrin on Yield and Chemical
Composition of Groundnut (Arachis hypogasa L.). Ann. Arid Zone
13(1): 59—61.
Dodson, P. 1975. Functional and Ecological Significance of Relative
Growth in Alligator. J. Zool. (London) 175(3): 315—355.
Dolan, J. W., and J. N. Seiber. 1977. Chlorine—Selective Detection
for Liquid Chromatography with a Coulson Electrolytic Conductivity
Detector. Anal. Chem. 49(2): 326—331.
Domauski, J. J., J. N. Laws, P. L. Haire, and T. J. Sheets. 1973.
Insecticide Residues on 1971 U.S. Tobacco Products. Tob. Sci. 17: 80—81.
Domanskl, J. J., and F. E. Guthrie. 1974. Pesticide Residues in 1972
Cigars. Bull. Environ. Contain. Toxicol. 11(4): 312—314.
Dorough, H. W., and J. R. Gibson. 1972. Chlorinated Insecticide
Residues in Cigarettes Purchased 1970—72. Environ. Entomol. 1(6): 739—743.
Dorough, H. W., and N. N. Randolph. 1969. Residues of DDT and Endrin
in Peanuts and Soybeans Grown in Soil Containing These Pesticides.
Pesti. Nonit. J. 3(2): 90—93.
Drake, J. L., G. W. Ware, and F. G. Werner. 1971. Insecticidal Effects
on Soil Arthropods. J. Econ. Entomol. 64(4): 842—845.
Dugan, P. B.. 1972. Biochemical Ecology of Water Pollution. Plenum
Press, New York. p. 106.
Duggan, R. E., and M. B. Duggan. 1973. Pesticide Residues in Food.
In: Environmental Pollution by Pesticides, C. A. Edwards (ed.),
Plenum Press, New York, Chap. 9.
Duggan, R. E., II. C. Barry, and L. Y. Johnson. 1966. Pesticide
Residues in Total—Diet Samples. Science 151(1/7): 101—104.
-------
333
Duggan, R. E., H. C. Barry, and L. Y. Johnson. 1967. Pesticide
Residues in Total—Diet Samples (II). Pesti. Monit. J. 1(2): 2—12.
Duggan, R. E., G. Q. Lipscomb, E. L. Cox, R. E. Heatwolfe, and
R. C. Kling. 1971. Pesticide Residue Levels in Foods in the United
States from July 1, 1963, to June 30, 1969. Pesti. Monit. J.
5(2): 73—212.
Duke, T. W., and A. J. Wilson. 1971. Chlorinated Hydrocarbons in
Livers of Fishes from the Northeastern Pacific Ocean. Pesti. Monit.
J. 5(2): 228—232.
Dustman, E. H., and L. F. Stickel. 1969. The Occurrence and Signifi-
cance of Pesticide Residues in Wild Animals. N.Y. Acad. Sd. Ann.
160(1): 162—172.
Dyte, C. E., and P. S. Tyler. 1960. The Contamination of Flour by
Insecticidal Lacquers Containing Endrin and Dieldrin. J. Sci. Food
Agric. 11: 745—750.
Dziuk, L. J., and F. W. Plapp. 1973. Insecticide Resistance in
Mosquito Fish from Texas. Bull. Environ. Contam. Toxicol. 9(1): 15—19.
E
Edwards, C. A. 1970. Persistent Pesticides in the Environment. CRC
Press, Cleveland, Ohio.
Edwards, C. A. 1973. Pesticide Residues in Soil and Water. In:
Environmental Pollution by Pesticides, C. A. Edwards (ed.), Plenum
Press, New York, Chap. 11.
Edwards, C. A. (ed.). 1973. Environmental Pollution by Pesticides.
Plenum Press, New York.
Egan, H. 1969a. IUPAC Commission on Terminal Residues. J. Assoc.
Off. Anal. Chem. 52(2): 299—305.
Egan, H. l969b. IUPAC Commission on the Development, Improvement,
and Standardization of Methods of Pesticide Residue Analysis. J. Assoc.
Off. Anal. Chem. 52(2): 306—309.
Eisler, R. 1966. Acute Toxicities of Insecticides to Marine Decapod
Crustaceans. Crustaceana 16(3): 302—310.
El—Kifl, A. H., A. E. A. Wahab, M. A. Assem, and A. A. Metwally. 1973.
Note on the Insecticidal Control of Bean-Fly, Melanagromyza phaseoli
(Tryon) (Diptera: Agromyzidae). Indian J. Agric. Sci. 43(5): 518—519.
-------
334
El Sayed, E. I., J. B. Graves, and F. L. Bonner. 1967. Chlorinated
Hydrocarbon Insecticide Residues in Selected Insects and Birds Found
In Association with Cotton Fields. J. Agric. Food Chem. 15(6): 1014—1017.
Environmental Defense Fund, Inc., and National Audubon Society vs Envi-
ronmental Protection Agency and Russell Train. 1975. FIFRA—Aidrin and
Dieldrin — Suspension. Environ. Rep. No. 19(51): 1689—1697.
Epstein, S. S., E. Arnold, J. Andrea, W. Bass, and Y. Bishop. 1972.
Detection of Chemical Mutagens by the Dominant Lethal Assay in the
Mouse. Toxicol. Appl. Pharmacol. 23: 288—325.
Erney, D. R. 1974. Rapid Screening Method for Analysis of Chlorinated
Pesticide and Polychlorinated Biphenyl Residues in Fish. J. Assoc.
Of f. Anal. Chem. 57(3): 576—579.
Fabacher, D. L. 1976. Toxicity of Endrin and an Endrin—methyl Parathion
Formulation to Largemouth Bass Fingerlings. Bull. Environ. Contam.
Toxicol. 16(3): 376—378.
Faber, R. A., R. W. Risebrough, and H. M. Pratt. 1972. Organochiorines
and Mercury in Common Egrets and Great Blue Herons. Environ. Pollu.
3(2): 111—122.
Farb, R., and B. G. Moore. 1971. A Preliminary Investigation of
Pollution and Its Distribution in Mobile Bay. Ala. Acad. Sci. J.
42(3): 138.
Fay, R. R., and L. W. Newland. l972b. Elution of Some Organochiorine
Insecticide Mixtures by Florisil Column Chromatography. Tex. 3. Sd.
24(2): 191—196.
Ferguson, D. E., and C. R. Bingham. 1966a. Effects of Combinations of
Insecticides on Susceptible and Resistant Mosquito Fish. Bull. Environ.
Contam. Toxicol. 1(3): 97—103.
Ferguson, D. E., and C. C. Gilbert. 1967. Tolerances of Three Species
of Anuran Amphibians to Five Chlorinated Hydrocarbon Insecticides.
J. Miss. Acad. Sd. 13: 135—138.
Ferguson, D. E., W. D. Cotton, D. T. Gardner, and D. D. Culley. 1965a.
Tolerances to Five Chlorinated Hydrocarbon Insecticides in Two Species
of Fish from a Transect of the Lower Mississippi River. 3. Miss. Acad.
Sci. 11: 239—245.
Ferguson, D. E., 3. L. Ludke, 3. P. Wood, and J. W. Prather. l965b.
The Effects of Mud on the Bloactivity of Pesticides on Fishes. J. Miss.
Acad. Sci. 11: 219—228.
Ferguson, D. E., 3. L. Ludke, M. T. Finley, and G. G. Murphy. 1967.
Insecticide—Resistant Fishes: A Potential Hazard to Consumers. 3. Miss.
Acad. Sd. 13: 138—140.
-------
335
Field, F. H. 1966. Chemical Ionization Mass Spectrometry. IX.
Temperature and Pressure Studies with Benzyl Acetate and t—Amyl Acetate.
J. Am. Chem. Soc. 91(11): 2621—2838.
Field, F. H. 1968. Chemical Ionization Mass Spectrometry. VIII.
Alkenes and Alkynes. J. Am. Chem. Soc. 90(21): 5649—5656.
Field, F. H. 1970. Chemical Ionization Mass Spectrometry. XII.
Alcohols. J. Am. them. Soc. 92(9): 2672—2676.
Finlayson, D. G., and H. R. MacCarthy. 1973. Pesticide Residues in
Plants. In: Environmental Pollution by Pesticides, C. A. Edwards
(ed.), Plenum Press, New York, Chap. 2.
Flickman, E. L., and K. A. King. 1972. Some Effects of Aidrin—Treated
Rice on Gulf Coast Wildlife. J. Wildl. Manage. 36(3): 706—727.
Fletcher, W. W. 1971. Pests, Pesticides and the Environment. Sci.
Hortic. 23: 139—142.
Foehrenbach, J., G. Mahmood, and D. Sullivan. 1971. Chlorinated
Hydrocarbon Residues in Shell Fish (Pelecypoda) from Estuaries of Long
Island, New York. Pesti. Monit. J. 5(3): 242—247.
Food and Agriculture Organization of the United Nations. 1975a.
Production Yearbook — 1974 (Rome) 28(1).
Food and Agriculture Organization of the United Nations. 1975b.
Production Yearbook — 1974 (Rome) 28(2).
Forbes, .J. E. 1968. Controlling Pine Mouse Damage in Orchards. N.Y.
State Horti. Soc. Proc. Ann. Meeting 113: 265—267.
Frank, R., H. E. Braun, K. Ishida, and P. Suda. 1976. Persistent
Organic and Inorganic Pesticide Residues in Orchard Soils and Vineyards
of Southern Ontario. Can. J. Soil Sd. 56: 463—484.
Frear, D. E., and N. S. Kawar. 1967. Use of Dczphnia magna for the
Microbioassay of Pesticides. II. Comparison of Microbioassay with Gas
Chromatography for Analysis of Pesticide Residues in Plant Extracts.
J. Econ. Entomol. 60(5): 1236—1239.
G
Gabliks, J. 1965. Responses of Cell Cultures to Insecticides. II.
Chronic Toxicity and Induced Resistance. Reprint from Proc. Soc. Exp.
Biol. Med. 120: 168—171.
Gabliks, J., and L. Friedman. 1965. Responses of Cell Cultures to
Insecticides. I. Acute Toxicity to Human Cells. Reprint from Proc.
Soc. Exp. Biol. Med. 120: 163—168.
-------
336
Ganguly, S. K., and 3. Bhattacharyya. 1973. Detection of Small Amounts
of Pesticides in Human Biological Material by Thin—Layer Chromatography.
Forensic Sci. 2(3): 333—338.
Gast, R. T. 1961. Factors Involved in Differential Susceptibility of
Corn Earworm Larvae to DDT. 3. Econ. Entomol. 54(6): 1203—1206.
Gawaad, A., A. Hamad, and F. H. El—Gayar. 1971. Effect of the Canal
Irrigation System Used in the UAR on the Persistence of Soil Insecti-
cide. mt. Pest. Control (London) 13(4): 8—10, 28.
Gershman, L. L. 1961. Infrared Determination of Endrin Residues.
J. Assoc. Off. Anal. Chem. 44(2): 212-214.
Gibson, J. R., G. A. Jones, H. Dorough, C. I. Lusk, and R. Thurston.
1974. Chlorinated Insecticide Residues in Kentucky Burley Tobacco:
Crop Years 1963—72. Pesti. Monit. J. 7(3/4): 205—213.
Gillett, 3. W., 3. Hill IV, A. W. Jarvinen, and W. P. Schoor. 1974.
A Conceptual Model for the Movement of Pesticides Through the Environ-
ment: A Contribution of the EPA Alternative Chemicals Program. U.S.
Environmental Protection Agency, National Ecological Research Laboratory,
Corvalis, Oregon, NTIS: PB—238—653.
Goerlitz, D. F., and M. L. Law. 1974. Determination of Chlorinated
Insecticides in Suspended Sediment and Bottom Material. 3. Assoc.
Off. Anal. Chem. 57(1): 176—181.
Gomez—Taylor, M. M., D. Kuehl, and P. R. Griffiths. 1976. Vibrational
Spectroinetry of Pesticides and Related Materials on Thin Layer Chroma-
tography Absorbents. Appi. Spectroscopy 30(4): 447—452.
Goodwin, E. S., R. Goulden, A. Richardson, and J. G. Reynolds. 1960.
The Analysis of Crop Extracts for Traces of Chlorinated Pesticides by
Gas—Liquid Partition Chromatography. Chem. End. (London) (9/24): 1220—1221.
Gordon, S. C., and C. E. Taylor. 1977. Chemical Control of the Raspberry
Leaf and Bud Mite, PhylZ.ocaptea gracl-l1..8 (Nal.) (Eriophyidae). 3. Hort.
Sd. 52: 517—523.
Cough, R. H. 1971. Reduction of Chlorinated Hydrocarbon Insecticide
Residues in Milk and Milk Products. Diss. Abstr. mt. 31(9): 5093B.
Gould, R. F. (ed.). 1966. Organic Pesticides in the Environment.
Advances in Chemistry Series 60, American Chemical Society, Washington,
D.C.
Grant, B. F. 1976. Endrin Toxicity and Distribution in Fresh Water: A
Review. Bull. Environ. Toxicol. 15(3): 283—290.
-------
337
Greichus, Y. A., A. Greichus, and E. G. Reider. 1968. Residues in
Fish, Wildlife, and Estuaries. Insecticide Residues in Grouse and
Pheasant of South Dakota. Pesti. Monit. J. 2(2): 90—92.
Greve, P. A. 1972. Potentially Hazardous Substances in Surface Waters.
Part 1. Pesticides in the River Rhine. Sci. Total Environ. 1(2): 173—180.
Guenzi, W. D. (ed.). 1974. Pesticides in Soil and Water. Proceedings
of Soil Science Soc. of Am. Symposium held in 1965, Madison, Wisconsin.
Gupta, B. M., and J. C. Sharma. 1971. Efficacy of Certain Insecticidal
Control Schedules Against Insect Pests of Cabbage. Madras Agric. J.
58(12): 889—891.
Guthrie, F. E., P. V. Shah, and D. E. Moreland. 1974. Effects of
Pesticides on Active Transport of Glucose Through the Isolated Intestine
of the Mouse. J. Agric. Food Chem. 22(4): 713—715.
H
Handy, E. I. 1970. Laboratory Trials on the Effect of Some Insecticides
on Ascaris lwnbricoides Eggs. J. Egypt. Med. Assoc. 53(7—8): 603—607.
Hamelink, J. L., R. C. Waybrant, and R. C. Ball. 1971. A Proposal:
Exchange Equilibria Control the Degree Chlorinated Hydrocarbons Are
Biologically Magnified in Benthic Environment. Trans. Am. Fish. Soc.
100(2): 207—214.
Hainrick, W. J. 1968. The Effects of Arasan—Endrin Treated Pine Seed on
Bobwhite Quail, Gray Squirrel and Turkey. Proceedings of the 22nd Annual
Conference, Southeastern Association of Game and Fish Commissioners.
Hansen, D. J. 1969. Avoidance of Pesticides by Untrained Sheepshead
Minnows. Trans. Am. Fish. Soc. 98: 426—429.
Hansen, D. J., and A. J. Wilson, Jr. 1970. Significance of DDT Residues
from the Estuary Near Pensacola, Fla. Pesti. Monit. J. 4(2): 51—56.
Haque, R., and D. Hansen. 1975. New Colored Chlorinated Hydrocarbon—
Clay Complexes. Bull. Environ. Contam. Toxicol. 13(4): 497—500.
Harris, C. I. 1969. Movement of Pesticides in Soil. J. Agric. Food
Chem. 17(1): 80—82.
Harris, C. R., R. A. Chapman, and J. R. W. Miles. 1977. Insecticide
Residues in Soils of Fifteen Farms in Southwestern Ontario, 1964—1974.
J. Environ. Sci. Health, Part B. 12(3): 163—177.
Harris, C. R., and H. J. Svec. 1970. Laboratory Studies of the Toxicity
of Technical Formulations of Some Insecticides to Cabbage Loopers. J.
Econ. Entomol. 63(2): 666—667.
-------
338
Harris, C. R., and H. J. Svec. 1973. Toxicological Studies on Cutworms.
XI. Laboratory and Field Microplot Studies on the Effectiveness of
Some Experimental Insecticides in controlling the Redbacked Cutworm in
Organic Soil. J. Econ. Entomol. 66(2): 444—446.
Harris, C. R., and H. .1. Svec. 1976. Susceptibility of the Colorado
Potato Beetle in Ontario to Insecticides. J. Econ. Entoinol. 69(5):
625—629.
Harrison, R. B. 1966. The Detection and Determination of Organo—
chlorine Pesticide Residues in Wildlife with Special Reference to Endrin.
J. Sci. Food Agric. 17(1): 10—13.
Hattula, M. L. 1974. Some Aspects of the Recovery of Chlorinated
Residues (DDT—type Compounds and PcB) from Fish Tissue by Using Different
Extraction Methods. Bull. Environ. Contam. Toxicol. 12(3): 301—307.
Hawthorne, i. C., J. H. Ford, and G. P. Markin. 1974. Residues of
Mirex and Other Chlorinated Pesticides iii Commercially Raised Catfish.
Bull. Environ. Contain. Toxjcol. 11(3): 258—264.
Hayama, K., and S. Kuwabara. 1962. Studies on Enzymes in Fish Blood —
II. Effect of Organophosphorus Insecticides on Cholinesterase Activity.
(English summary). Bull. Jpn. Soc. Sci. Fish. 28(2): 179—183.
Heath, R. G. 1969. Nationwide Residues of Organochlorine Pesticides
in Wings of Mallards and Black Ducks. Pestj. Monit. J. 3(2): 115—123.
Hekinati, M., and R. L. Bradley, Jr. 1971. Degradation of Organochlo jne
Pesticides and Hydrogen Peroxide. Milchwissenschaft 26(4): 224—226.
Henderson, c., W. L. Johnson, and A. Inglis. 1969. Organochiorine
Insecticide Residues in Fish (National Pesticide Monitoring Program).
Pesti. Monit. J. 3(3): 145—171.
Henderson, c., A. Inglis, and W. L. Johnson. 1971. Organochloririe
Insecticide Residues in Fish — Fall 1969 National Pesticide Monitoring
Program. Pesti. Monit. J. 5(1): 1—11.
Hermanson, H. P., F. A. Gunther, L. D. Anderson, and M. J. Garber. 1971.
Installment Application Effects upon Insecticide Residue Content of a
California Soil. J. Agric. Food Chew. 19(4): 722—726.
Hill, IL w., and P. L. McCarty. 1967. Anaerobic Degradation of Selected
Chlorinated Hydrocarbon Pesticides. J. Water Pollu. Control Fed.
39(8): 1259—1277.
Hoffman, w. S., W. I. Fishbein, and N. B. Andelman. 1964. The Pesticide
Content of Hufllafl Fat Tissue. Archi. Environ. H. 9: 387-394.
-------
339
Holland, H. T., and D. L. Coppage. 1970. Sensitivity to Pesticides in
Three Generations of Sheepshead Minnows. Bull. Environ. Contam. Toxicol.
5(4): 362—367.
Hopkins, A. R. 1957. Effect of Several Insecticides on the English
Red Worm. J. Econ. Entomol. 50(5): 699—700.
Horsfall, F., Jr. 1956. Rodenticidal Effect on Pine Mice of Endrin
Used as a Ground Spray. Science 123(3185): 61.
Howard, W. E., R. E. Marsh, and R. E. Cole. 1970. A Diphacinone Bait
for Deer Mouse Control. J. For. 68(4): 220—222.
Hunt, E. G. 1970. The Effects of Pesticides on Pelicans, Owls,
Pheasants, Falcons, Egrets, Herons Aren’t Fully Known. But Could We
Do Without Birds? Calif. Health 27(8): 7—9.
Hurley, J. T. 1974. Pesticide Analysis in Water. J. Am. Water
Work Assoc. 66(1): 27—31.
Hurter, J., H. Zurrer, and E. Reuthinger. 1966. RUckstandsbestimmunger
von Endrin im Boden, auf Gras und in der Much (in German). Z. Lebensm.
Unters. Forsch. 130: 20—25.
I
Ifeadi, C. N. 1975. Screening Study to Develop Background Information
and Determine the Significance of Air Contaminant Emissions from
Pesticide Plants. Final report to EPA. Battelle Columbus Labs.
Irving, G. W., Jr. 1970. Agricultural Pest Control and the Environ-
ment. Science 168(3938): 1419—1424.
Ismail, R. J., and F. L. Bonner. 1974. New, Improved Thin Layer
Chromatography for Polychlorinated Biphenyls, Toxaphene, and Chiordane
Components. J. Assoc. Off. Anal. Chem. 57(5): 1026—1032.
Israel, P., M. B. Kalode, P. S. Prakasa Rao, and C. P. Yadava. 1969.
Persistence of Some Insecticides and Their Compatibility with Urea
Against Newly Hatched Larvae of Tryporyza incertulas Walker in Rice.
Indian J. Entomol. 31(4): 346—349.
Iyengar, L., M. P. Pandey, C. Venkobachar, and A. V. S. Prabhakara Rao.
1972. Biochemical Evaluation of Pesticides. Biochem. J. 128(1): 39—40.
J
Jackson, G. A. 1976. Biological Half—Life of Endrin in Channel Catfish
Tissues. Bull. Environ. Contam. Toxicol. 16(5): 505—507.
-------
340
K
Kaira, A. N. 1970. Efficiency of Endrin and Endosuif an Granules in
Controlling Top Borer of Sugarcane. Indian Sugar 20(2): 185—186.
Kandra, M., K. Takahama, Y. Waseda, Y. Ishli, and Y. Miyazaki. 1968.
Studies on the Influences of Organochioric Pesticides, PCP and Endrin
to Nitochondrial Respiration and Oxydative Phosphorylation of Rat
Brain. (English summary). Jpn. 3. Legal Med. 22(3): 223—228.
Kaplan, H. N., and J. G. Overpeck. 1964. Toxicity of Halogenated
Hydrocarbon Insecticides for the Frog, Rana pipiens. Herpetrologica
20(3): 163—169.
Katz, N, and C. G. Chadwick. 1961. Toxicity of Endrin to Some Pacific
Northwest Fishes. Trans. Am. Fish. Soc. 90(4): 394—397.
Katz, N., G. L. Pdereson, M. Yoshinika, and D. Sjolseth. 1969. Effects
of Pollution of Fish Life. J. Water Pollu. Control Fed. 41(6): 994—1016.
Kavadia, U. S., R. C. Srivastava, and H. C. L. Gupta. 1970. Laboratory
Evaluation of Insecticides Against Psalis pennatula (Lymantriidae:
Lepidoptera). Indian J. Entomol. 32(pt. 3): 255—288.
Kawar, N. S., G. C. deBatista, and F. A. Gunther. 1973. Pesticide
Stability in Cold—Stored Plant Parts, Soils, and Diary Products, and
In Cold—Stored Extractives Solutions. Residue Rev. 48(0): 45—77.
Keith, L. H., and A. L. Alford. 1970. Review of the Application of
Nuclear Magnetic Resonance Spectroscopy in Pesticide Analysis. J. Assoc.
Anal. Chem. 53(5): 1018—1035.
Keith, J. 0., and E. C. Hunt. 1966. Levels of Insecticide Residues in
Fish and Wildlife in California. In: Transactions of the 31st North
American Wildlife Conference, pp. 150—177. Wildlife Management
Institute, Washington, D.C.
Keith, L. H., A. L. Alford, J. D. McKinney. 1972. N.M.R. Studies of
Chlorinated Polycyclodiene Pesticides. Anal. Chim. Acta. (The
Netherlands) 60(1): 1—11.
Kerr, S. R., and W. P. Vass. 1973. Pesticide Residues in Aquatic
Invertebrates. In: Environmental Pollution by Pesticides, C. A. Edwards
(ed.), Plenum Press, New York, Chap. 4.
Kahn, I. A., R. I. Zuberi, Z. I. Khan, A. Au, and S. N. H. Naqvi. 1971.
Effectiveness of Petkolin, Endrin and Their Combination Against Jassids
and Thrips on Cotton Crop at I4ultan. Sci. md. (Karachi) 8(2): 147—151.
Khan, R. 14., S. K. Sharma, and B. N. Gupta. 1972. Appearance of
Armyworms on Wheat Crop in Outbreak Form and Their Control. Madras
Agric. J. 59(11—12): 663—665.
-------
341
Kirkpatrick, H. E., G. S. Linton, B. M. Mountjoy, and L. C. Aibright.
1955. Flavor of Sebago Potatoes Grown in Soil Treated with Chiodan,
Heptachlor, Dieldrin, Aldrin, or Endrin. J. Agric. Food Chem.
3(5): 409—412.
Klaassen, H. E., and A. H. Kadoum. 1973. Pesticide Residues in Natural
Fish Populations of the Smoky Hill River of Western Kansas — 1967—69.
Pesti. Monit. J. 7(1): 53—61.
Klevay, L. M. 1971. Endrin Excretion by the Isolated Perfused Liver:
A Sexual Difference. Proc. Soc. Exp. Biol. Med. 136(3): 878—879.
Knoevenagel, K., and R. Himmelreich. 1976. Degradation of Compounds
Containing Carbon Atoms by Photooxidation in the Presence of Water.
Arch. Env. Contam. Tox. 4(3): 324—333.
Koeman, H. H., and J. H. Penning. 1970. An Orientational Survey on the
Side—Effects and Environmental Distribution of Insecticides Used in
Tsetse—Control in Africa. Bull. Environ. Contam. Toxicol. 5(2): 164—170.
Konar, S. K. 1972. Toxicity of Nicotine to Aquatic Life. Indian Sci.
Congr., Part III (Abstracts) 59(3): 458.
Konrad, J. B., H. B. Pionke, and G. Chesters. 1969. An Improved Method
for Extraction of Organochiorine and Organophosphate Insecticides from
Lake Siaters. Analyst 94: 490—492.
Kornberg, W. 1964. So What Did Kill the Fish? Chem. Week 95(4): 19—26.
Koshy, G., N. M. Das, and R. G. K. Nair. 1972. Deterioration of Insec-
ticides on Glass and on Leaf Surface. Agric. Res. J. Kerala 10(2):
128—132.
Koudela, K., A. Soya, V. Pujman, J. Janda, A. Vrbenska, J. Houska,
I. Mostkova, D. Trefny, A. Hrdinova, and Z. Nemec. 1972. Activity
of Some Plasma and Liver Enzymes in Pheasants Following Administration
of Low Doses of Endrin During Recovery. (Abstract) Cesk. Fysiol.
21(4): 376—377.
L
Ladish, H., and H. W. Zeschma. 1971. Insecticides as the Causes of Fish
Poisonings (in German). Aquarien Terrarien 18(2): 52—53.
Lakshminarayana, V., and P. K. Menon. 1972. Exposure of the General
Population in Hyderabad to DDT. J. Food Sci. Technol. 9(2): 82—85.
Langlois, B. E., B. J. Laska, and D. L. Hill. 1965. The Effects of
Processing and Storage of Dairy Products on Chlorinated Insecticide
Residues: II. Endrin, Dieldrin, and Heptachior. J. Milk Food Technol.
28(1): 9—il.
-------
342
Larose, R. H. 1974. High—Speed Liquid Chromatographic Cleanup of
Environmental Samples Prior to the Gas Chromatographic Determination of
Lindane. J. Assoc. Of f. Anal. Chem. 57(5): 1046—1049.
Lee, S. Y. 1962. The Mode of Action of Endrin on the Bean Stem Miner,
Melanogromzya sojae, with Special Reference to Its Translocation in
Soybean Plants. J. Econ. Entomol. 55(6): 956—964.
Lichtenstein, E. P., G. R. Myrdal, and K. R. Schulz. 1965. Absorption
of Insecticidal Residues from Contaminated Soils into Five Carrot
Varieties. J. Agric. Food Chem. 13(2): 126—131.
Linder, R. L., and R. B. Dahlgren. 1970. Occurrence of Organochiorine
Insecticides in Pheasants of South Dakota. Pesti. Monit. J. 3(4): 227—232.
Lindstrotn, F. T., J. W. Gillett, and S. E. Rodecap. 1975. Distribution
of Heod (Dieldrin) in Mammals: II. Some Applications of the Preliminary
Model. Archi. Environ. Contain. Toxicol. 3(2): 166—182.
Lofgren, J. A., and L. K. Cutkomp. 1963. Insecticides and Their Uses
in Minnesota. Extension Bulletin 263. University of Minnesota.
Loutfy, N. S., F. A. Khalil, and A. H. El—Hemaesy. 1970. Effect of
Certain Soil Insecticides on the Cutworm Agrotis ipsi ion in Cotton.
Agric. Res. Tev. 48(1): 12—21.
Loutfy, N. S., A. H. E1—Hemaesy, S. A. El—Monsef, H. I. Youssef, and
S. M. Tantawy. 1972. Studies on the Effect of Certain Insecticides
on the Greasy Cutworm Agrotis ipsilon. Agric. Res. Rev. 50(1): 25—30.
Luard, E. .J. 1973. Sensitivity of Dunalielia and Scenedesmus (Chloro—
phyceae) to Chlorinated Hydrocarbons. Phycologia 12(1/2): 29—33.
Luckens, M. M. 1970. A Rapid Procedure for the Laboratory Diagnosis of
Poisoning by Organochiorine Insecticides. Inter—American Conference
on Toxicology and Occupational Medicine: Pesticides Symposia Collection
of Papers 6th, 7th. pp. 177—182.
Lykken, L. 1961. Total Chlorine and Infrared Methods for the Determina-
tion of Aidrin, Dieldrin, and Endrin Formulations. J. Assoc. Of f. Anal.
Chein. 44(3): 595—605.
N
Nclngvale, C. R., L. Ludke, and D. E. Ferguson. 1968. Oxygen Consump-
tion of Endrin—Susceptible and Endrin—Resistant Ganibusia During Sublethal
and Acute Endrin Exposure. J. Miss. Acad. Science 14: 116—121.
Macke, K. J., C. Hutchinson, and 0. B. Cope. 1969. Effects of Tempera-
ture on the Susceptibility of Blue Gills and Rainbow Trout to Selected
Pesticides. Bull. Environ. Contain. Toxicol. 4(3): 174—183.
-------
343
Mackenzie, K., and W. P. Lay. 1970. Fragmentation of Tetrahydro—
methanonaphthalenes and Their Diaza— and Benzo—Analogues. Tetrahedron
Lett. (37): 3241—3244.
MacNay, C. G. 1965. Control of Mice, Rabbits, and Deer in Orchards.
Can. Dep. Agric. Publ. 1115: 4—10.
Malone, C. R., and B. G. Blaylock. 1970. Toxicity of Insecticide
Formulations to Carp Embryos Reared In Vitro. J. Wildi. Manage.
34(2): 460—463.
Manna, B., and K. C. Ghose. 1972. Histopathological Changes in the Gut
of Achatina fulica Bowdich Caused by Endrin — A Molluscicide. Indian
J. Exp. Biol. 10(6): 461—463.
Manske, D. D., and R. D. Johnson. 1975. Pesticide Residues in Total
Diet Samples (VIII). Pesti. Monit. J. 9(2): 94—105.
Marishima, I., A. Mizuno, and T. Yonezawa. 1971. Anomalous Features
of Nuclear Magnetic Resonance Spectra of Methyl and Methylene Halides
Oriented in a Nematic Solvent. Unusual Ordering Due to Specific Solute—
Solvent Interaction. J. Am. Chem. Soc. 93(6): 1520—1522.
Narkin, G. P., 3. H. Ford, and J. C. Hawthorne. 1972. Mirex Residues
in Wild Populations of the Edible Red Crawfish (Procainbarus clarki).
Bull. Environ. Contam. Toxicol. 8(6): 369—374.
Marliac, 3. P., M. 3. Verrett, 3. McLaughlin, Jr., and 0. G. Fitzhugh.
1965. A Comparison of Toxicity Data Obtained for Twenty—One Pesticides
by the Chicken Embryo Technique with Acute, Oral LD—50’s in Rats.
(Abstract #40). Toxicol. Appl. Pharmacol. 7(3): 490.
Martin, R. J., and R. E. Duggan. 1968. Pesticide Residues in Total
Diet Samples (III). Pesti. Monit. 3. 1(4): 11—14.
Mason, 3. W., and R. D. Rowe. 1969. How Pesticides are Threatening
Our Oysters. Ocean md. 4(7): 60—61.
Matthews, G. A. l966a. Investigations of the Chemical Control of Insect
Pests of Cotton in Central Africa. I — Laboratory Rearing Methods and
Tests of Insecticides by Application to Bollworm Eggs. Bull. Entomol.
Res. 57(1): 69—76.
Matthews, G. A. l966b. Investigations of the Chemical Control of Insect
Pests of Cotton in Central Africa. II — Tests of Insecticides with
Larvae and Adults. Bull. Entomol. Res. 57(1): 77—91.
Mayer, F. L., D. L. Stalling, and J. L. Johnson. 1972. Phthalate Esters
as Environmental Contaminants. Nature 238(364): 411—413.
-------
344
McPherson, R. N., S. D. Hensley, J. B. Graves, and E. G. King. 1976.
Dosage—Mortality Responses of the Parasite Lixophaga diatraeae to
Selected Insecticides in the Laboratory. 3. Econ. Entomol. 69(1): 105—108.
Meith—Avcin, N., S. N. Warlen, and R. T. Barber. 1973. Organochiorine
Insecticide Residues in a Bathyl—Deniersal Fish from 2,500 Meters. Environ.
Lett. 5(4): 215—221.
Menzer, R. E. 1973. Biological Oxidation and Conjugation of Pesticidal
Chemicals. Residue Rev. 48: 79—116.
Menzie, C. N. 1972. Fate of Pesticides in the Environment. Ann. Rev.
Entomol. 17: 199—222.
Menzie, C. N. 1974. Metabolism of Pesticides, an Update. U.S. Depart-
ment of the Interior, Fish and Wildlife Service: Special Scientific
Report — Wildlife No. 184, Washington, D.C.
Messick, J. P. 1972. Organochiorine Residues in Wild Ring—Necked
Pheasants from Southwestern Idaho. Bull. Environ. Contam. Toxicol.
8(6): 356—360.
Miles, J. R., and C. R. Harris. 1971. Insecticide Residues in a Stream
and a Controlled Drainage System in Agricultural Areas of Southwestern
Ontario, 1970. Pesti. Monit. J. 5(3): 289—294.
Misra, S. S. 1970. Residual Toxicity of Insecticides on Cotton in the
Field to Adults of Cotton Grey Weevil, Myllocerus undecimpustulatus
maculosus. Sd. Cult. 36(10): 363—365.
Mistric, W. J., and 3. C. Gaines. 1953. Effect of Wind and Other
Factors on the Toxicity of Certain Insecticides. J. Econ. Entomol.
46(2): 341—349.
Mitchell, L. C. 1953. Separation and Identification of Chlorinated
Organic Pesticides by Paper Chromotography. III. Aidrin, Isodrin,
Dieldrin, and Endrin. J. Assoc. Of f. Anal. Chem. 36(4): 1183—1186.
Maria, E. W., A. Robertson, and M. Beauregard. 1970. Endrin Poisoning
in Chickens. Can. Vet. J. 11(4): 74—77.
Moubry, R. 3., 3. N. Helm, and G. R. Nyrdal. 1968b. Chlorinated
Pesticide Residues in an Aquatic Environment Located Adjacent to a
Commercial Orchard. Pesti. Nonit. J. 1(4): 27—29.
Mount, D. I., and C. 3. Putnicki. 1966. Summary Report of the 1963
Mississippi Fish Kill. In: Transactions of the 31st North American
Wildlife Conference: 177—184. Wildlife Management Institute,
Washington, D.C.
-------
345
Mozai, T., T. Muro, Y. Yoshino, and Y. Shimada. 1971. Poisoning by
Agricultural Chemicals (Japanese). Naika 27(5): 870—871.
Mukherjee, A. B., and V. S. Srivastava. 1970. Bioassay of the Relative
Toxicity of Some Pesticides to the Larvae of Spodoptera jitura. Indian
J. Entomol. 32(pt. 3): 251—255.
Mukherjee, G., T. V. Mathew, A. K. Mukherjee, and S. N. Mitra. 1971.
Identification and Separation of Chlorinated Pesticides by TLC on
Magnesium Hydroxide. J. Food Sci. Technol. 8: 152-153.
Mulla, M. S. 1962. Frog and Toad Control with Insecticides. Pest
Control 30: 20, 64.
Mulla, M. S. 1963. Toxicity of Organochiorine Insecticides to the
Mosquito Fish Gambusia affinis and the Bullfrog Rana catesbeiana.
Mosquito News 23(4): 299—303.
Mullins, D. E., R. E. Johnson, and R. I. Starr. 1971. Persistence
of Organochiorine Insecticide Residues in Agricultural Soils of
Colorado. Pesti. Monit. J. 5(3): 268—275.
Mumma, R. 0., W. B. Wheeler, D. E. H. Frear, and R. H. Hamilton. 1966.
Dieldrin: Extraction of Accumulations by Root Uptake. Science
152(4/22): 530—531.
Muncy, R. J., and A. D. Oliver, Jr. 1963. Toxicity of Ten Insecticides
to the Red Crawfish, Pr ocambarus clarki (Girard). Trans. Am. Fish.
Soc. 92: 428—431.
Musial, C. J., M. E. Peach, and D. A. Stiles. 1976. A Simple Procedure
for the Confirmation of Residues of ct— and —Endosu1f an, Dieldrin,
Endrin, and Heptachlor Epoxide. Bull. Environ. Contam. Toxicol.
16(1): 98—100.
Musty, P. R., and C. Nickless. 1974. Use of Amberlite XAD—4 for
Extraction and Recovery of Chlorinated Insecticides and Polychiorinated
Biphenyls from Water. J. Chroznatogr. 89: 185—190.
N
Naqvi, S. M., and D. E. Ferguson. 1968. Pesticide Tolerances of
Selected Freshwater Invertebrates. J. Miss. Acad. Sci. 14: 121—127.
Nash, R. G. 1974. Improved Gas—Liquid Chromatographic Method for
Determining Ethylenethiourea in Plants. J. Assoc. Of f. Anal. Chem.
57(5): 1015—1021.
National Academy of Sciences. 1971. Chlorinated Hydrocarbons in the
Marine Environment. National Research Council, Washington, D.C.,
PB—204—738, NTIS, Springfield, Virginia.
-------
346
National Academy of Sciences. 1972. Degradation of Synthetic Organic
Molecules in the Biosphere. Proceedings of a Conference, San Francisco,
California, June 1971.
Nebeker, A. V., and A. R. Gaufin. 1964. Bioassays to Determine
Pesticide Toxicity to the Mnphipod Crustacean, Gcvnmarus lacustris.
Utah Acad. Proc. 41(1): 64—67.
Nelson, N. J., and P. R. Datta. i 68. Microdetermination of Endrin
in Presence of Aldrin and Dieldrin by Infrared Spectroscopy. Nicrochem.
J. 13(1): 91—97.
Neuhaus, V. K. 1956. Eine Polarographische Bestiimnungsmethode fur
das Kontakinsektizid Endrin (in German). Chem. Ztg. 80(24): 851—854.
Nielsen, S. W. 1971. Environmental Pollutants Pathogenic to Animals.
J. Mn. Vet. Med. Assoc. 159(9): 1103—1107.
Nimbalkar, S. A., and N. N. Bone. 1970. Efficacy of Different Insec-
ticides Against Pupae of Cabbage Leaf Miner, Liriomyza brassicae Riley.
Indian J. Entomol. 32(pt. 3): 290—292.
P
Pal, S. K. 1971. Relative Efficacy of Different Insecticides on
Urentius echinus dist. and Empoasca spp. Infesting Brinjal Crop in
Mathania Area of Western Rajasthan. Madras Agric. J. 58(4): 323—325.
Panel on Pesticide Monitoring. 1971. Criteria for Defining Pesticide
Levels to Be Considered an Alert to Potential Problems. Pesti. Monit.
J. 5(1): 36.
Pank, L. F., and G. H. Marschke. 1972. Decline and Reinvasion of Deer
Mouse Populations After Baiting Douglas—Fir Clearcuts with 6-Amino—
nicotinamide. J. For. 70(11): 678—680.
Parsons, A. N. 1970. Pesticide Residues in Fats and Other Lipids.
Prog. Chem. Fats Other Lipids l1(pt. 2): 243—293.
Parsons, A. N., and D. J. Moore. 1966. Some Reactions of Dieldnin and
the Proton Magnetic Resonance Spectra of the Products. J. Chem. Soc.
(London): 2026—2031.
Patel, H. K. 1960. Earthworms in Tobacco Nursery and Their Control.
Indian Tob. 10(1): 56.
Payne, W. R., and W. S. Cox. 1960. Micro—Infrared Analysis of Dieldrin,
Endrin, and Other Chlorinated Pesticide Residues in Complex Substrates.
J. Assoc. Off. Anal. Chem. 49(5): 989—996.
-------
347
Penfound, W. J., and E. S. Hathaway. 1938. Plant Communities in the
Marshlands of Southeastern Louisiana. Ecol. Monogr. 8(1): 1—56.
Peterson, J. E., K. N. Stahl, and D. L. Mecker. 1976. Simplified
Extraction and Cleanup for Determining Organochiorine Pesticides in
Small Biological Samples. Bull. Environ. Contam. Toxicol. 15(2): 135—139.
Phillips, J. N. 1973. Endrin Poisoning in Poultry: A Case History.
Vet. Rec. 92(8): 211—212.
Pimentel, D., and N. Goodman. 1974. Environmental Impact of Pesticides.
In: Survival in Toxic Environments, N. A. Q. Khan and J. P. Bederaka, Jr.
(eds.), Academic Press, New York, pp. 25—52.
Pionke, H. B., J. G. Konrad, G. Chesters, and D. E. Armstrong. 1968.
Extraction of Organochiorine and Organophosphate Insecticides from
Lake Waters. Analyst. 93(1107): 363—367.
Pionke, H. B., C. Chesters, and D. E. Armstrong. 1969. Dual Column and
Derivative Techniques for Improved Specificity of Gas—Liquid Chromato—
graphic Identification of Organochlorine Insecticide Residues in Soils.
Analyst 94(1123): 900—903.
Pollero, R., R. Goyema, N. Siquiroff, and R. Tumino. 1976. Removal of
Pesticides in Water of Rio de la Plata (In Vitro Assay). Bull. Environ.
Contam. Toxicol. 15(5): 617—622.
Porter, N. L., S. J. V. Young, and J. A. Burke. 1970. A Method for
the Analysis of Fish, Animal, and Poultry Tissue for Chlorinated
Pesticide Residues. J. Assoc. Off. Anal. Chem. 53(6): 1300—1303.
Powell, D. M. 1966. Endosulfan Oxydemetonmethyl, and Endrin in Control
of the Green Peach Aphid and Suppression of Leaf Roll in Potatoes in
Eastern Washington. J. Econ. Entomol. 59(6): 1354—1357.
Princi, F. 1957. Toxicology, Diagnosis and Treatment of Chlorinated
Hydrocarbon Insecticide Intoxications. Archi. md. Health 16: 333—336.
R
Rao, N. S., and G. R. K. Murty. 1977. Chemical Control of Sugarcane
White Grubs, Holotrichia serrata F. (Melolonthidae: Coleoptera). Sci.
Cult. 43(5): 228—229.
Reichel, W. L., T. G. Lamont, E. Cromartie, and L. N. Locke. 1969b.
Residues in Two Bald Eagles Suspected of Pesticide Poisoning. Bull.
Environ. Contam. Toxicol. 4(1): 24—30.
Reidinger, R. F., Jr., and D. G. Crabtree. 1974. Organochiorine
Residues in Golden Eagles, United States — March 1964—July 1971. Pesti.
Monit. J. 8(1): 37—43.
-------
348
Reinke, J., J. F. Uthe, and D. Jamieson. 1972. Organochiorine Pesticide
Residues in Conunercially Caught Fish in Canada 1970. Pesti. Monit. J.
6(1): 43—49.
Reith, J. F., T. H. Drost, C. A. Schrijver, and R. J. Albers. 1969.
Demonstration of Poisoning Substances Through Trails on the Fish
Species (in German). Lebistes Retriculatus Pharmaceutisch Weekblad
104(14): 273—287.
Rettich, F. 1977. The Susceptibility of Mosquito Larvae to Eighteen
Insecticides in Czechoslovakia. Mosq. News 37(2): 252.
Ritchey, S. J., R. W. Young, and E. 0. Essary. 1972. Effects of
Heating and Cooking Method on Chlorinated Hydrocarbon Residues in
Chicken Tissues. J. Agric. Food Chein. 20(2): 291—293.
Robel, R. J., C. D. Stalling, M. E. Westfahl, and A. M. Kadoum. 1972.
Effects of Insecticides on Populations of Rodents in Kansas — 1965—69.
Pesti. Monit. J. 6(2): 115—121.
Robertson, G. W. 1968. A Biometeorology Time Scale for a Cereal Crop
Involving Day and Night Temperatures and Photoperiod. mt. J. Biom.
12(3): 191—223.
Robinson, J. 1971. Organochiorine Compounds in Man and His Environment.
Chem. Bri. 7: 472—475.
Robinson, J. l973 . Dynamics of Pesticide Residues in the Environment.
In: Environmental Pollution by Pesticides, C. A. Edwards, ed., Plenum
Press, New York, Chap. 12.
Robinson, J., and A. E. J. McGill. 1966. Organochiorine Insecticide
Residues In Complete Prepared Meals in Great Britain During 1965.
Nature 212(5066): 1037—1038.
Rosato, P., and D. E. Ferguson. 1968. The Toxicity of Endrin—Resistant
Mosquito Fish to Eleven Species of Vertebrates. Bioscience 18(8): 783—784.
Rosen, 3. D., and D. 3. Sutherland. 1967. The Nature and Toxicity of
the Photoconversion Products of Aidrin. Bull. Environ. Contain. Toxicol.
2(1): 1—9.
Rowe, D. R., L. W. Canter, and J. W. Mason. 1970. Contamination of
Oysters by Pesticides. 3. Sanit. Eng. Div. Proc. Am. Soc. Civ. Eng.
96(SA5): 1221—1234.
Rudd, R. L., and R. E. Genelly. 1956. Pesticides: Their Use and
Toxicity in Relation to Wildlife. Game Bulletin No. 7, State of
California Department of Fish and Game, Davis, California, pp. 92—93.
-------
349
Ruzicka, H. H. 1973. Methods and Problems in Analyzing for Pesticide
Residues in the Environment. In: Environmental Pollution by Pesticides,
C. A. Edwards, ed., Plenum Press, New York, Chap. 1.
S
Sachan, 3. N. 1972. Studies on the Control of Lily Moth Polytela
glorioaae Fabr. (Lepidoptera, Noctuidae). Indian 3. Hortic. 29(1): 94—96.
Sanders, H. 0. 1969. Toxicity of Pesticides to the Crustacean Gcvninarus
lacustris. Technical Paper 25 of the Bureau of Sport Fisheries and
Wildlife, Washington, D.C., 18 pp.
Sanders, H. 0. 1970. Pesticide Toxicities to Tadpoles of the Western
Chorus Frog Pseudacris triseriata and Fowler’s Toad Bufo woodhousii
fowleri. Copeia (2): 246—251.
Sandhu, J. S.,, and Y. P. Madan. 1971. Evaluation of New Chemicals for
the Control of Sugarcane Pyrilla (Pyriila perpusilla WIK). Indian
Sugar 21(8): 561—563.
Sandhu, 3. S., and Y. P. Madan. 1972. Studies of the Chemical Control
of the Sugarcane Lygaeid Bug (Macropes excavatus). 3. Res. Punjab
Agric. Univ. 9(1): 64—67.
Sarup, P. 1970. Effect of Formulation on the Toxicity of Insecticidal
Dusts to the Larvae of Prodenia litura. I. Choice of Diluents. Indian
3. Entomol. 32(4): 365—375.
Schafer, E. W. 1972. The Acute Oral Toxicity of 369 Pesticidal,
Pharmaceutical and Other Chemicals to Wild Birds. Toxicol. Appi.
Pharmacol. 21: 315—330.
Schafer, E. W., R. R. West, and D. 3. Cunningham. 1969a. New Starling
Toxicant: DRC—1347. Pest Control 37(9): 22—30.
Schwabe, Von U., and I. Wendling. 1967. Beschleunigung des Arzneimittel—
Abbaus durch Kleine Dosen von DDT und anderen Chlorkohlenwasserstaf f—
Insekticiden. Arzneimittel—Forschungen 17(5): 614—618.
Sen, R., H. B. Kaur, and N. L. Dave. 1970. Studies of Mechanism of
Action of Endrin. Indian 3. Physiol. Pharmacol. 14(2): 59.
Shah, A. H., V. 3. Vora, and K. P. Godhania. 1973. Aerial Application
of Insecticides to Control the Sugarcane Pyrilla in South Gujarat.
Indian Sugar 23(3): 205—206.
Shell Chemical Company. 1967. Symposium on the Science and Technology
of Residual Insectides in Food Production with Special Reference to
Aldrin and Dieldrin. Presented at Gaithersburg, Maryland, October 26—27
and St. Charles, Illinois, November 2—3.
-------
350
Sherman, M., and M. N. Rosenberg. 1954. Subchronic Toxicity of Four
Chlorinated Dimethanonaphthalene Insecticides to Chicks. J. Econ.
Entoniol. 47(6): 1082—1083.
Shorey, H. H., W. C. Evans, R. H. Burrage, and C. G. Gyrisco. 1958.
The Residual Effect of Insecticides Applied to Meadow and Pasture
Sod for Control of the European Chafer. J. Econ. Entomol. 51(6): 765-767.
Sithanantham. S., and S. C. Daniel. 1972. Potash with Endrin Spray
for Control of Sugarcane Shoot Borer. Fert. News 17(8): 36.
Skerrett, E. J., and E. A. Baker. 1960. The Micro—Determination of
Endrin. Analyst 85(1013): 606—607.
Smart, N. A., A. R. C. Hill, and P. A. Roughan. 1974. Chlorinated
Hydrocarbon Pesticide Residues in Foodstuffs: Comparison of Methods.
J. Assoc. Off. Anal. Chem. 57(1): 153—164.
Smith, D. C., R. Leduc, and L. Tremblay. 1975. Pesticide Residues
in the Total Diet in Canada. IV. 1972 and 1973. Pesti. Sd. 6: 75—82.
Smith, K. J., P. B. Polen, 1). N. DeVries, and F. B. Coon. 1968. Removal
of Chlorinated Pesticides from Crude Vegetable Oils by Simulated Com-
mercial Processing Procedures. J. Am. Oil Chem. Soc. 45(12): 866—869.
Sneeringer, P. V., F. Belkin, N. Straff on, and S. A. Costick. 1977.
The Army’s Drinking Water Surveillance Program. Environ. Sci. Technol.
11(8): 767—771.
Solar, J. N. 1971. Pesticidal Residue Alterations in Potatoes During
Processing (Abstract). Diss. Abstr. mt. 31(8): 4766B.
Solar, J. M., J. A. Liuzzo, and A. F. Novak. 1971. Removal of Aldrin,
Heptachlor Epoxide, and Endrin from Potatoes During Processing. J.
Agric. Food Chem. 19(5): 1008—1010.
Solon, J. N., J. L. Lincer, and J. H. Nair III. 1969. The Effect of
Sublethal Concentration of Las on the Acute Toxicity of Various Insec-
ticides to the Fathead Minnow (Pimephales promelas rafinesque). Water
Res. (London) 3: 767—775.
Sommers, C. E., Jr. 1971. New Problems: Pesticide Regulations.
Successful Farm. 69(6): 23.
Sreenivasan, C. W., and M. V. Natarajan. 1962. Use of Endrin in
Fishery Management. Prog. Fish Cult. 24(4): 181.
Stadelman, W. J. 1973. Record of Some Chemical Residues in Poultry
Products. Bioscience 23(7): 424—428.
-------
351
Starr, H. G., F. D. Aldrich, W. D. McDougall III, and L. M. Mounce.
1974. Contribution of Household Dust to the Human Exposure to
Pesticides. Pesti. Monit. J. 8(3): 209—212.
Stemp, A. R., B. J. •Liska, B. E. Langlois, and W. J. Stadelman. 1964.
Analysis of Egg Yolk and Poultry Tissues for Chlorinated Insecticide
Residues. Poult. Sci. 43(1): 273—275.
Stemp, A. R., B. J. Liska, R. L. Wesley, and W. J. Stadelman. 1965.
Effect of High Temperature Cooking on Chlorinated Insecticide Residues
in Chicken Tissues (Abstract). Poult. Sd. 44(5): 1417.
Stevenson, 3. 1968. Laboratory Studies on the Acute Contact and Oral
Toxicities of Insecticides to Honeybees. Ann. Appi. Biol. 61(3): 467—472.
Stickel, L. F. 1968. Organochiorine Pesticides in the Environment.
U.S. Department of the Interior, Fish and Wildlife Service, Special
Scientific Report — Wildlife No. 119, Washington, D.C., 32 pp.
Stijve, T., and E. Cardinale. 1972. Confirmation of Identity of
Heptachlor Residues by Hydroxy Derivatization on Thin Layers of Aluminum
Oxide. Mitt. Geb. Lebensmitteiunters. Hyg. 63(2): 308—310.
Stojanovic, B. 1968. Pesticide Disposal. Nat. Agric. Chem. Assoc.
News Pesti. Rev. 27(1): 13.
Stokinger, H. E. 1968. Spectre of Today’s Environmental Pollution — USA
Brand: New Perspectives from an Old Scout. Am. md. Hyg. Assoc. 3.
29: 195—217.
Storherr, R. W. 1973. Report on Carbamate Pesticides, Fumigants, and
Miscellaneous. 3. Assoc. Of f. Anal. Chem. 56(2): 296—299.
Stout, V. F. 1968. Pesticide Levels in Fish of the Northeast
Pacific. Bull. Environ. Contam. Toxicol. 3(4): 240—246.
Stretz, P. E., and H. M. Stahr. 1973. Determination of Chlorinated
Pesticides in Whole Blood. J. Assoc. Of f. Anal. Chem. 56(5): 1173—1177.
Su, G. C. C., and H. A. Price. 1973. Element Specific Gas Chromato—
graphic Analyses of Organochlorine Pesticides in the Presence of PCBs by
Selective Cancellation of Interfering Peaks. 3. Agric. Food Chem.
21(6): 1099—1102.
Suzuki, K., K. Miyashita, H. Nagayoshi, and T. Kashiwa. 1973b. Separa-
tion and Identification of 20 Pesticides in Their Mixture. Agric. Biol.
Chem. 37(8): 1959—1962.
Suzuki, K, H. Nagayoshi, and T. Kashiwa. 1974. The Systemic Separation
and Identification of Pesticides in the First Division. Agric. Biol.
Chem. 3. 38(2): 279—285.
-------
352
Suzuki, M., Y. Yainato, and T. Watanabe. 1976. Organochiorine Insecticide
Residues in Vegetables of the Kitakyushu District, Japan, 1971—74.
Pestic. Monit. J. 10(2): 35—40.
T
Tabb, D. C., and A. C. Jones. 1962. Effect of Hurricane Donna on the
Aquatic Fauna of North Florida Bay. Trans. Am. Fish Soc. 91: 375—378.
Tabet, J. C. K., and E. P. Lichtenstein. 1976. Degradation of { 1 C]
Photodieldrin by Trichoderma viride as Affected by Other Insecticides.
Can. J. Nicrobiol 22(9): 1345—1356.
Tarzwell, C. M. 1964. The Toxicity of Synthetic Pesticides to Aquatic
Organisms and Suggestions for Meeting the Problem. Ecol. md. Soc.
Symp., Swansea, Engi. 1964: 197—218.
Terriere, L. C. 1964. Analytical Methods for Pesticide, Plant Growth,
Regulators, and Food Additives. Vol. II, Academic Press, New York,
Chap. 18.
Tewari, S. N., and I. C. Sharma. 1976. TLC Determination of Endrin
In Biological Tissues. Z. Anal. Chem. 278: 127.
Tewari, S. N., and S. P. Harpalanl. 1977. Detection and Determination
of Dichiorvos (DDVP) in Toxicological Analysis. Z. Anal. Chem. 285: 48.
Thomas, P. C., and T. L. Murthy. 1976. Studies on the Impact of a Few
Organic Pesticides on Certain Fish Enzymes. Indian J. Anita. Sd.
46(11): 619—624.
Thompson, A. R., Jr. 1970. Effects of Nine Insecticides on the Numbers
and Biomass of Earth Worms In Pasture. Bull. Environ. Contain. Toxicol.
5(6): 577—586.
Thompson, A. R. 1973. Pesticide Residues in Soil Invertebrates. In:
Environmental Pollution by Pesticides, C. A. Edwards (ed.), Plenum
Press, New York, Chap. 3.
Thompson, W. T. 1973. Agricultural Chemicals. Book 1 — Insecticides,
Acaricides, and Ovicides. 1973 Revision. Thompson, Indianapolis, md.
300 pp.
Thomson, 3. M., and G. A. Cash. 1976. Pesticides in Commercial Fish
Foods. Search 7(3): 101—102.
Tietjen, H. P. 1969. Orchard Mouse Control — A Progress Report. Mass.
Fruit Grow. Assoc. Rep. Annu. Rep.: 60—66.
-------
353
Toor, H. S., K. Mehta, and S. Chhina. 1973. Toxicity of Insecticides
(Commercial Formulations) to the Exotic Fish, Common Carp Cyprinus carpio
cornmunis Linnaeus. J. Res. Punjab Agric. Univ. 10(3): 341—345.
Trautmann, W. L., G. Chesters, and H. B. Pionke. 1968. Pesticides in
Soil. Organochiorine Insecticide Composition of Randoml 1 Selected Soils
from Nine States — 1967. Pesti. Monit. .3. 2(2): 93—96.
Tuinstra, L. G. N., and 3. B. H. deGraaff. 1971. Data Processing of GLC
Pesticide Analyses by Means of a Time—Shared Computer System. Chromato—
graphia 4: 468—471.
Turner, J. W., and L. W. RIgby. 1976. Use of DDT in Combination with
Endrin and Parathion for Controlling Cotton Pests in Queensland.
Queensland 3. Agric. Anim. Sci. 33(1): 77—82.
U
U.S. Department of Agriculture. 1956. Some Effects of Insecticide
Spray Accumulations in Soil on Crop Plants. Technical Bulletin No.
1149: 34—36.
U.S. Department of Agriculture. 1968b. The Pesticide Review 1968.
Agricultural Stabilization and Conservation Service, Washington, D.C.,
54 pp.
U.S. Department of Agriculture, Plant Pest Control Division. 1968.
Monitoring for Chlorinated Hydrocarbon Insecticide Residues in Soybeans —
1966. Pesti. Monit. 3. 2(1): 58—67.
U.S. Department of Agriculture. 1974. Farmers’ Use of Pesticides in
1971 Quantities. Agriculture Economic Report.
U.S. Department of Commerce. 1974. Re: proposed regulations of
effluent standards for toxic pollutants. Letter of March 28 to. C. H.
Thompson, Chairman — Hazardous and Toxic Substances Regulation Task
Force, Environmental Protection Agency; from General Counsel of the
Department of Commerce, Washington, D.C.
U.S. Department of Health, Education, and Welfare. 1969. Report of
the Secretary’s Commission on Pesticides and Their Relationship to Envi-
ronmental Health, Parts I and II, Washington, DC.
U.S. Department of the Interior. 1969. FWPCA Method for Chlorinated
Hydrocarbon Pesticides in Water arid Wastewater. Federal Water Pollution
Control Administration, CincInnati, Ohio.
U.S. Environmental Protection Agency. 1970a. Investigation of Means
for Controlled Self—Destruction of Pesticides. Water Pollution Control
Research Series No. 16040 ELO 06/70.
-------
354
U.S. Environmental Protection Agency. 1970c. Maximum Pesticide Residue
Levels by Site, Nanograins/Cubic Meter. Division of Pesticide Community
Studies, Chamblee, Georgia.
U.S. Environmental Protection Agency. 1971c. Part 180 — Tolerances and
Exemptions from Tolerances for Pesticide Chemicals in or on raw Agricultural
Commodities (Subpart C — Specific Tolerances): l80.l3l.Endrin.
U.S. Environmental Protection Agency. l973a. Water Pollution Preven—
tion and Control — Proposed List of Toxic Pollutants. Fed. Regi.
38(129): 18044—18045.
U.S. Environmental Protection Agency. 1973b. Toxic Pollutant Effluent
Standards — List of Toxic Pollutants. Fed. Regi. 38(173): 24342—24344.
U.S. Environmental Protection Agency. 1974b. Comments of Environmental
Defense Fund in Opposition to the Proposed Effluent Standards. Re:
proposed toxic pollutant effluent standards for aldrin/dieldrin et al.,
FWPCA (307), Docket No. 1.
U.S. Environmental Protection Agency. 1975a. Papers of a Seminar on
Early Warning Systems for Toxic Substances. EPA-560/l—75—003, pp. 77, 78.
U.S. International Trade Commission. 1975. Synthetic Organic Chemicals,
United States Production and Sales, 1973. Government Printing Office,
Washington, D.C., ITC Publication 728.
V
Van Middelem, C. H. 1969a. Cooperative Study on Uptake of DDT, Dieldrin,
and Endrin by Peanuts, Soybeans, Tobacco, Turnip Greens, and Turnip Roots.
Pesti. Monit. J. 3(2): 70—71.
Varadharajan, G., and P. R. Nagaraja Rao. 1966. Control of Rice Stem—
Borer (Tryoryza incertujas WLK.) by the Application of Parathion and
Endrin. Indian J. Agric. Sd. 36(6): 334—339.
Vasuki, K., and T. S. S. Kikshith. 1968. Alkaline and Acid Phosphatases
in the Grasshopper Poecilocerus pictus FAB (Orthoptera: Acrididae) and
the Effect of Endrin. Enzymol. 39(2): 1968.
Velsicol Chemical Corporation. 1964. Statement of Velsicol Chemical
Corporation Relating to Recent Reports of Fish Kills on the Mississippi
River Submitted Pursuant to Notice of Public Hearing. 21 pp.
Verma, A. N., and B. S. Sohi. 1971. Susceptibility of Different Instars
of Bihar Hairy Caterpillar, Diacrisia obliqua Walker, to Some Contact
Insecticides. J. Res. Punjab Agric. Univ. 8(1): 61—66.
-------
355
Verma, M. P., H. S. Mahga, B. K. Soni, and S. P. Singh. 1970. Effect
of Insecticides on Lactic Acid Concentration in the Blood of Buffalo
Calves. Indian Vet. J. 47: 1056—1059.
Vermeer, K., and L. M. Reynolds. 1974. Organochiorine Residues in
Aquatic Birds in the Canadian Prairie Provinces. Can. Field Nat.
84: 117—129.
Vinson, S. B., and P. K. Law. 1971. Cuticular Composition and DDT
Resistance in the Tobacco Budworm. J. Econ. Entomol. 64(6): 1387—1390.
Vinson, S. B., C. E. Boyd, and D. E. Ferguson. 1963. Resistance to DDT
in the Mosquito Fish, Gainbusia affinis. Science 139: 217—218.
Vogt, H. H. 1970. Chlorinated Hydrocarbons Influence Marine Phyto—
plankton (in German). Naturwiss. Rudsch. 23(7): 296.
W
Walker, C. H., G. A. Hamilton, and R. B. Harrison. 1967. Organochiorine
Insecticide Residues in Wild Birds in Britain. J. Sci. Food Agric.
18: 123—129.
Walker, P. T. 1972. Effect of the Physical Properties of Granules on
Their Insecticidal Performance. Pesti. Sd. 3(6): 805—809.
Walsh, G. M. 1971. A Pharmacologic and Toxicologic Comparison of Two
Isomeric Chlorinated Hydrocarbon Insecticides: Endrin and Dieldrin.
Diss. Abstr. mt. B. 32(4): 2316.
Walsh, G. M., and G. B. Fink. 1971. Tissue Distribution and Comparative
Toxicity of Endrin and Dieldrin in Mice. Fed. Proc. 30(2): Abstract
2052: 562.
Waseda, Y. 1971. Studies on the Mechanism of Toxic Actions of Organo—
chloric Pesticides, Drin Compounds. Jpn. J. Leg. Med. 25(1): 64—80.
Water Resources Scientific Information Center. 1972. Aidrin and Endrin
in Water — A Bibliography. Office of Water Resources Research,
Washington, D.C., PB—210—922.
Weil, E. D., H. G. Colson, P. E. Hoch, and R. H. Gruber. 1969. Toxic
Chlorinated Methanoisobenzofuran Derivatives. J. Heterocycl. Chem.
6: 643—649.
Welborn, M. E., R. B. Borchard, L. C. Hansen, and R. L. Metcalf. 1974.
Extraction and Analysis of Aroclor 1254 Components in Blood. J. Assoc.
Off. Anal. Chem. 57(6): 1248—1252.
-------
3.6
Wessel, J. R. 1969. Comparison of Four Extraction and Cleanup
Procedures for Chlorinated Pesticide Residues in Eggs. J. Assoc.
Of f. Anal. Chem. 52(1): 172—175.
Wheatley, G. A. 1973. Pesticides in the Atmosphere. In: Environmental
Pollution by Pesticides. C. A. Edwards (ed.), Plenum Press, New York,
Chap. 10.
Wheatley, C. A., and J. A. Hardman. 1965. Indications of the Presence
of Organochiorine Insecticides in Rainwater in Central England. Nature
207 (4966): 486—487.
Whetstone, R. R. 1964. Chlorinated Derivatives of Cyclopentadiene.
Encyci. Che. Technol. 5(2nd Ed.): 240—252.
White, T. T, and G. G. McKinley. 1961. Determination of Aldrin,
Dieldrin, or Endrin in Formulations. J. Assoc. Of f. Anal. Chein.
44(3): 591—605.
Wiersma, C. B., P. F. Sand, and R. L. Schutzmann. 197lb. National
Soils Monitoring Program — Six States, 1967. Pesti. Monit. J. 5(2):
223—227.
Wiersma, G. B., H. Tai, and P. 1. Sand. 1972b. Pesticide Residue
Levels in Soils, FY 1969 — National Soils Monitoring Program. Pesti.
Moult. J. 6(3): 194—201.
Williams, D. T., and B. J. Blanchfield. 1972. Screening Method for
the Detection of Chlorodibenzo—p—dioxins Presence of Chiorobiphenyls,
Chloronaphthalenes, and Chlorodibenzofurans. J. Assoc. Of f. Anal. Chem.
55(1): 93—95.
Wood, B. J. 1966. Elution of Dieldrin and Endrin from Florisil.
J. Assoc. Off. Anal. Chem. 49(2): 472—474.
Woodham, D. W. 1967. IdentifIcation of the Gas Chromatographic Endrin
Peak by Its Conversion to Delta—Keto Endrin. U.S. Department of
Agriculture, ARS 81—16, Gulfport, Mississippi.
Woolson, E. A. 1974. Extraction of Chlorinated Hydrocarbon Insecticides
from Soil: Collaborative Study. J. Assoc. Off. Anal. Chem. 57(3): 604—609.
z
Zitko, V. 1972. Absence of Chlorinated Dibenzodioxins and Dibenzofurans
from Aquatic Animals. Fisheries Research Board of Canada, Biological
Station, St. Andrews, New Brunswick, Canada.
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357
TECHNICAL REPORT DATA
(Please read Instructions on i -. ;everse before completing)
1. REPORT NO. 2. 3. RECIPIENTS ACCESSION NO.
EPA—600/l—79—005 -____________
4. TITLE AND SUBTITLE
Reviews of the Environmental Effects of Pollutants:
XIII. Endrin
5. REPORT DATE
6.PERFORMINGORGANIZATIONCODE
7. AUTHOR(S)
J. Donoso, J. Dorigan, B. Fuller, J. Gordon,
N. Kornreich, S. Saari, L. Thomas, and P. Walker
8. PERFORMING ORGANIZATION REPORT NO.
ORNL EIs—131
9. PERFORMING ORGANIZATION NAME AND ADDRESS
Information Center Complex/Information Division
Oak Ridge National Laboratory
Oak Ridge, Tennessee 37830
10. PROGRAM ELEMENT NO.
lHA6l6
11.CONTRACT/GRANTNO.
lAG D5—0403
12. SPONSORING AGENCY NAME AND ADDRESS
Health Effects Research Laboratory, Cm—OH
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati, Ohio 45268
13. TYPE OF REPORT AND PERIOD COVERED
14. SPONSORING AGENCY CODE
EPA/6 0 0/lo
15. SUPPLEMENTARY NOTES
16. ABSTRACT
This document is a multidisciplinary review of the health and environmental
effects of endrin. Included in the review are a general summary and a compre-
hensive discussion of the following topics: physical and chemical properties;
synthesis and use; analytical methodology; biological aspects in microorganisms,
plants, wild and domestic animals, and humans; distribution, mobility, and
persistence in the environment; assessment of the present and potential health
and environmental hazards; and review of standards and governmental regulations.
More than 600 references are cited.
7. KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS J DENTIFIERS/OPEN ENDED TERMS
*pollutaflts
Endrin Health Effects
Toxicology
C. COSATI Field/Group
0€ ’
06T
8. DISTRIBUTION STATEMENT
.
Release to public
19. SECURITY CLASS (This Report)
Unclassified
21. NO. OF PAGES
20. SECURITY CLASS (This page)
Unclassified
22. PRICE
EPA Form 2220—1 (Rev. 4._ l i) PREVIOUS EDITION IS OBSOLETE *U.S. GOVERNMENT PRINTING OFFICE: 1979-640-079- 149
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