Aldrin and Dieldrin (EHC 91, 1989)

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

ENVIRONMENTAL HEALTH CRITERIA 91

ALDRIN AND DIELDRIN

This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.

Published under the joint sponsorship of
the United Nations Environment Programme,
the International Labour Organisation,
and the World Health Organization

World Health Orgnization
Geneva, 1989

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WHO Library Cataloguing in Publication Data

Aldrin and Dieldrin.

(Environmental health criteria ; 91)

1.Aldrin 2.Dieldrin I.Series

ISBN 92 4 154291 8 (NLM Classification: WA 240)
ISSN 0250-863X

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CONTENTS

ENVIRONMENTAL HEALTH CRITERIA FOR ALDRIN AND DIELDRIN

1. SUMMARY

1.1. General
1.2. Environmental transport, distribution, and transformation
1.3. Environmental levels and human exposure
1.4. Kinetics and metabolism
1.5. Effects on organisms in the environment
1.5.1. Accumulation
1.5.2. Toxicity for microorganisms
1.5.3. Toxicity for aquatic organisms
1.5.4. Toxicity for terrestrial organisms
1.5.5. Population and ecosystem effects
1.6. Effects on experimental animals and in vitro test systems
1.7. Effects on man

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS

2.1. Identity
2.1.1. Primary constituent: aldrin
2.1.2. Primary constituent: dieldrin
2.2. Physical and chemical properties
2.2.1. Aldrin
2.2.2. Dieldrin
2.3. Analytical methods
2.3.1. Sampling methods
2.3.2. Analytical methods

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1. Natural occurrence
3.2. Man-made sources
3.2.1. Production levels and processes; uses
3.2.1.1 World production figures
3.2.1.2 Manufacturing processes
3.2.1.3 Release into the environment during
normal production
3.2.2. Uses
3.2.2.1 Aldrin
3.2.2.2 Dieldrin

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION

4.1. Transport and distribution between media
4.1.1. Leaching of aldrin and dieldrin
4.1.2. Surface run-off

4.1.3. Loss of aldrin and dieldrin from soils -
volatilization
4.1.3.1 Movement within the soil profile - mass
flow
4.1.3.2 Movement within the soil profile -
diffusion
4.1.3.3 Actual volatilization losses - laboratory
studies
4.1.3.4 Actual volatilization losses - field
studies
4.1.4. Losses of residues following treatment of soil
with aldrin
4.1.5. Losses of residues from water
4.1.6. Aldrin and dieldrin in the atmosphere
4.1.7. Aldrin and dieldrin in water
4.2. Translocation from soil into plants
4.3. Models of the behaviour of water and chemicals in soil
4.4. Biodegradation of aldrin and dieldrin
4.4.1. Epoxidation of aldrin
4.4.2. Other metabolic pathways of aldrin
4.4.3. Biotransformation of dieldrin
4.4.4. Conclusions
4.5. Abiotic degradation
4.5.1. Photochemistry
4.5.1.1 Photochemistry of aldrin and dieldrin in
water
4.5.1.2 Photochemistry of aldrin and dieldrin in
air
4.5.1.3 Photochemistry of aldrin and dieldrin on
plant surfaces
4.5.1.4 Photochemistry of aldrin and dieldrin in
soils
4.5.1.5 Conclusions
4.5.2. Other abiotic processes
4.5.2.1 Reaction with ozone
4.5.2.2 Clay-catalysed decomposition
4.6. Bioaccumulation
4.7. The fate of aldrin and dieldrin in the environment
4.7.1. Aldrin and dieldrin in soils
4.7.2. Aldrin and dieldrin in the atmosphere
4.7.3. Conclusion

5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

5.1. Environmental levels
5.1.1. Air and rainwater
5.1.1.1 Aldrin
5.1.1.2 Dieldrin
5.1.2. Concentrations in houses
5.1.2.1 Aldrin used for subterranean termite
control
5.1.2.2 Aldrin and dieldrin used for remedial
treatment of wood
5.1.3. Aquatic environment
5.1.4. Soil

5.1.5. Drinking-water
5.1.6. Food and feed
5.1.6.1 Joint FAO/WHO food contamination
monitoring programme
5.1.6.2 Information summarized by GIFAP (1984)
5.1.6.3 United Kingdom (UK MAFF, 1983-1985)
5.1.6.4 USA
5.1.6.5 Appraisal of intake studies
5.1.7. Concentrations of dieldrin in non-target species
5.1.7.1 Occurrence of dieldrin in birds of prey
and fish-eating birds
5.2. General population exposure
5.2.1. Adults
5.2.1.1 Aldrin
5.2.1.2 Concentrations of dieldrin in adipose
tissue
5.2.1.3 Concentrations of dieldrin in blood
5.2.1.4 Concentrations of dieldrin in other
tissues
5.2.2. Babies, infants, and mother's milk

6. KINETICS AND METABOLISM

6.1. Absorption
6.1.1. Aldrin
6.1.1.1 Ingestion
6.1.1.2 Inhalation
6.1.2. Dieldrin
6.1.3. Photodieldrin (and other metabolites of dieldrin)
6.2. Distribution
6.2.1. Aldrin
6.2.1.1 Mouse
6.2.1.2 Rat
6.2.1.3 Dog
6.2.1.4 Human studies
6.2.2. Dieldrin
6.2.2.1 Laboratory animals
6.2.2.2 Transplacental transport
6.2.2.3 Domestic animals
6.2.2.4 Human volunteers
6.2.2.5 General population
6.2.3. Photodieldrin (and major metabolites of dieldrin)
6.2.3.1 Laboratory animals
6.2.3.2 Human beings
6.3. Metabolic transformation
6.3.1. Aldrin and dieldrin
6.3.1.1 Laboratory animals
6.3.1.2 Human studies
6.3.1.3 Non-domestic organisms
6.3.2. Photodieldrin (and major metabolites of dieldrin)
6.3.2.1 Rat
6.3.2.2 Monkey
6.4. Elimination and excretion
6.4.1. Aldrin
6.4.1.1 Rat

6.4.2. Dieldrin
6.4.2.1 Laboratory animals
6.4.2.2 Human studies
6.4.3. Photodieldrin (and major metabolites of dieldrin)
6.4.3.1 Rat
6.4.3.2 Monkey
6.5. Retention and turnover
6.5.1. Non-domestic organisms
6.5.2. Biological half-life in human beings
6.5.3. Body burden and (critical) organ burden; indicator
media
6.6. Appraisal

7. EFFECTS ON ORGANISMS IN THE ENVIRONMENT

7.1. Microorganisms
7.2. Aquatic organisms
7.2.1. Aquatic invertebrates
7.2.1.1 Acute toxicity
7.2.1.2 Short-term toxicity, reproduction, and
behaviour
7.2.2. Fish
7.2.2.1 Acute toxicity
7.2.2.2 Long-term toxicity
7.2.2.3 Reproduction
7.2.3. Amphibia and reptiles
7.3. Terrestrial organisms
7.3.1. Higher plants
7.3.2. Earthworms
7.3.3. Bees and other beneficial insects
7.3.4. Birds
7.3.4.1 Acute toxicity
7.3.4.2 Short- and long-term toxicity
7.3.4.3 Reproductive studies
7.3.4.4 Eggshell thinning
7.3.4.5 Concentrations of dieldrin in tissues of
experimentally poisoned birds
7.3.5. Mammals
7.4. Effect on populations and ecosystems
7.4.1. Exposure to dieldrin
7.4.2. Effects on populations of birds
7.4.3. Effects on populations of mammals

8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS

8.1. Single exposures
8.1.1. Aldrin and dieldrin
8.1.1.1 Oral
8.1.1.2 Dermal
8.1.1.3 Inhalation
8.1.1.4 Parenteral
8.1.2. Formulated materials
8.1.2.1 Oral and dermal
8.1.2.2 Inhalation

8.2. Short-term exposures
8.2.1. Oral
8.2.1.1 Rat
8.2.1.2 Dog
8.2.1.3 Domestic animals
8.2.2. Dermal
8.2.3. Inhalation
8.3. Skin and eye irritation; sensitization
8.3.1. Skin and eye irritation
8.3.2. Sensitization
8.4. Long-term toxicity and carcinogenicity
8.4.1. Mouse
8.4.1.1 Appraisal
8.4.2. Rat
8.4.2.1 Appraisal
8.4.3. Hamster
8.4.4. Monkey
8.4.5. Mode of action
8.5. Reproduction, embryotoxicity, and teratogenicity
8.5.1. Reproduction
8.5.1.1 Mouse
8.5.1.2 Rat
8.5.1.3 Dog
8.5.1.4 Appraisal
8.5.2. Embryotoxicity and teratogenicity
8.5.2.1 Mouse
8.5.2.2 Rat
8.5.2.3 Hamster
8.5.2.4 Rabbit
8.5.2.5 Appraisal
8.6. Mutagenicity and related end-points
8.6.1. Microorganisms
8.6.2. Mammalian cell point mutations
8.6.3. Dominant lethal assays and heritable translocation
assays in mice
8.6.4. Micronucleus test
8.6.5. Chromosome and cytogenicity studies
8.6.6. Host-mediated assays
8.6.7. Cell transformation in mammalian cell systems
8.6.8. Drosophila melanogaster and other insect systems
8.6.9. Effects on DNA
8.6.10. Cell to cell communication
8.6.11. Appraisal
8.7. Special studies
8.7.1. Liver enzyme induction
8.7.2. Nervous system
8.7.2.1 Rat
8.7.2.2 Dog
8.7.2.3 Monkey
8.7.3. Weight loss and stress
8.7.3.1 Rat
8.7.4. Immunosuppressive action
8.8. Toxicity of photodieldrin and major metabolites

8.8.1. Photodieldrin
8.8.1.1 Acute toxicity
8.8.1.2 Short-term toxicity
8.8.1.3 Long-term toxicity
8.8.1.4 Reproduction, embryotoxicity, and
teratogenicity
8.8.1.5 Appraisal
8.8.2. Major metabolites of dieldrin
8.8.2.1 Acute toxicity
8.8.2.2 Short-term toxicity
8.9. Mechanisms of toxicity; mode of action
8.9.1. Central nervous system
8.9.2. Liver

9. EFFECTS ON HUMAN BEINGS

9.1. General population exposure
9.1.1. Acute toxicity - poisoning incidents
9.1.2. Effects of short- and long-term exposure -
controlled human studies
9.1.2.1 Accidental poisoning
9.1.2.2 Controlled human studies
9.1.3. Tissue concentrations of dieldrin in hospitalized
people
9.1.3.1 Pathological findings
9.1.3.2 Influence of weight loss and stress on
dieldrin concentrations in tissues
9.1.4. Exposure in treated homes
9.2. Occupational exposure
9.2.1. Acute toxicity - poisoning incidents
9.2.1.1 Blood levels diagnostic of
aldrin/dieldrin poisoning
9.2.1.2 Electroencephalography
9.2.2. Effects of short- and long-term exposure
9.2.3. Epidemiological studies

10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE
ENVIRONMENT

10.1. Evaluation of human health risks
10.2. Evaluation of effects on the environment
10.3. Conclusions

11. RECOMMENDATIONS

12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES

REFERENCES

APPENDIX I. NOMENCLATURE

FRENCH TRANSLATION OF SUMMARY, EVALUATION, AND RECOMMENDATIONS

WHO TASK GROUP ON ALDRIN AND DIELDRIN

Members

Dr G. Burin, Office of Pesticide Programs, US Environmental
Protection Agency, Washington DC, USA

Dr I. Desi, Department of Hygiene and Epidemiology, University
Medical School, Szeged, Hungary (Vice-Chairman)

Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
Experimental Station, Abbots Ripton, Huntingdon, United Kingdom

Dr R. Goulding, Guy's Hospital, London, United Kingdom (Chairman)

Dr A. Furtado Rahde, Ministry of Public Health, Porto Alegre,
Brazil

Dr S.K. Kashyap, National Institute of Occupational Health,
Ahmedabad, India

Dr M. Takeda, Division of Environmental Chemistry, National
Institute of Hygienic Sciences, Tokyo, Japan

Dr H.G.S. Van Raalte, The Hague, Netherlands

Observers

Dr R. Rimpau, European Chemical Industry, Ecology and Toxicology
Centre, Brussels, Belgium

Dr R.C. Tincknell, International Group of National Associations of
Agrochemical Manufacturers, Brussels, Belgium

Dr H.G.S. Van Raalte, International Commission on Occupational
Health, Geneva

Secretariat

Dr J.R.P. Cabral, International Agency for Research on Cancer,
Lyons, France

Dr J. Copplestone, Pesticide Development and Safe Use Unit, World
Health Organization, Geneva, Switzerland

Dr M. Gilbert, International Programme on Chemical Safety, World
Health Organization, Geneva, Switzerland

Ms B. Goelzer, Office of Occupational Health, World Health
Organization, Geneva, Switzerland

Dr H. Galal Gorchev, Food Safety Unit, World Health Organization,
Geneva, Switzerland

Secretariat (contd.)

Dr K.W. Jager, International Programme on Chemical Safety, World
Health Organization, Geneva, Switzerland (Secretary)

Dr G.J. van Esch, Bilthoven, Netherlands (Rapporteur)

Dr N. Watfa, Safety and Health Branch, International Labour Office,
Geneva, Switzerland

NOTE TO READERS OF THE CRITERIA DOCUMENTS

Every effort has been made to present information in the
criteria documents as accurately as possible without unduly
delaying their publication. In the interest of all users of the
environmental health criteria documents, readers are kindly
requested to communicate any errors that may have occurred to the
Manager of the International Programme on Chemical Safety, World
Health Organization, Geneva, Switzerland, in order that they may be
included in corrigenda, which will appear in subsequent volumes.

* * *

A detailed data profile and a legal file can be obtained from
the International Register of Potentially Toxic Chemicals, Palais
des Nations, 1211 Geneva 10, Switzerland (Telephone no. 7988400 -
7985850).

* * *

The proprietary information contained in this document cannot
replace documentation for registration purposes because the latter
has to be closely linked to the source, the manufacturing route,
and the purity/impurities of the substance to be registered. The
data should be used in accordance with paragraphs 82 - 84 and
recommendations paragraph 90 of the Second FAO Government
Consultation (FAO, 1982).

ENVIRONMENTAL HEALTH CRITERIA FOR ALDRIN AND DIELDRIN

A WHO Task Group on Environmental Health Criteria for Aldrin
and Dieldrin met in Geneva from 13 to 17 July 1987. Dr K.W. Jager,
IPCS, opened the meeting and welcomed the participants on behalf
of the heads of the three IPCS cooperating organizations
(UNEP/ILO/WHO). The group reviewed and revised the draft criteria
document and made an evaluation of the risks for human health and
the environment from exposure to aldrin and dieldrin.

The first draft of this document was prepared by Dr G.J. VAN
ESCH of the Netherlands on the basis of a review of all studies on
aldrin and dieldrin including the proprietary information, made
available to the IPCS by Shell International Chemical Company
Limited, London, United Kingdom.

The second draft was also prepared by Dr van Esch,
incorporating comments received following the circulation of the
first draft to the IPCS contact points for Environmental Health
Criteria documents.

Dr K.W. Jager and Dr P.G. Jenkins, both members of the IPCS
Central Unit, were responsible for the technical development and
editing, respectively, of this monograph.

The assistance of Shell in making available to the IPCS and the
Task Group its toxicological proprietary information on aldrin and
dieldrin is gratefully acknowledged. This allowed the Task Group
to make its evaluation on a more complete data base.

The efforts of all who helped in the preparation and
finalization of the document are gratefully acknowledged.

* * *

Partial financial support for the publication of this criteria
document was kindly provided by the United States Department of
Health and Human Services, through a contract from the National
Institute of Environmental Health Sciences, Research Triangle Park,
North Carolina, USA - a WHO Collaborating Centre for Environmental
Health Effects. The United Kingdom Department of Health and Social
Security generously supported the cost of printing.

INTRODUCTION

Aldrin and dieldrin are the common names of insecticides
containing 95% HHDN and 85% HEOD, respectively.

Throughout this monograph the names aldrin and dieldrin are
used, although concentrations determined in the different matrices
are actually those of the active molecules HHDN and HEOD.

Aldrin is readily metabolized to dieldrin (HEOD) in plants and
animals. Only rarely are aldrin residues present in food or in the
great majority of animals, and then only in very small amounts.
Therefore, national and international regulatory bodies have
considered these two closely related insecticides together. The
practicality of considering them jointly is further emphasized by
the lack of significant difference in their acute and chronic
toxicity and by their common mode of action.

1. SUMMARY

1.1. General

Aldrin and dieldrin, both organochlorine pesticides and
manufactured commercially since 1950, were used throughout the
world up to the early 1970s. Both compounds were used as
insecticides in agriculture for the control of many soil pests and
in the treatment of seed. Insects controlled by these compounds
include termites, grasshoppers, wood borers, beetles, and textile
pests. Dieldrin has also been used in public health for the
control of tsetse flies and other vectors of debilitating tropical
diseases. Both aldrin and dieldrin act as a contact and stomach
poison for insects.

Since the early 1970s, both compounds have been severely
restricted or banned, in a number of countries, from use,
especially in agriculture. Nevertheless, the use for termite
control continues in other countries. Global production, which was
estimated to be 13 000 tonnes/year in 1972, decreased to less than
2500 tonnes/year in 1984.

The purity of technical grade aldrin and dieldrin is 90%
and > 95%, respectively. Impurities for aldrin include
octachlorocyclopentene, hexachlorobutadiene, and polymerization
products, and for dieldrin polychloroepoxyoctahydrodimethano-
naphthalenes.

Both compounds are practically insoluble in water and
moderately to highly soluble in most paraffinic, aromatic, and
halogenated hydrocarbons, and in esters, ketones, and alcohols.
The vapour pressure of aldrin is 6.5 x 10^-5mmHg at 25 °C and that
of dieldrin is 3.2 x 10^-6 mmHg at 25 °C.

Analytical methods for the determination of aldrin and dieldrin
in food, feed, and the environment are described in section 2.

1.2. Environmental Transport, Distribution, and Transformation

A major use of aldrin is as a soil insecticide. Hence, aldrin-
treated soil is an important source of aldrin and its reaction
product dieldrin in the environment.

Aldrin has a low propensity for movement away from treated
areas, either through volatilization or by leaching. It is mainly
and rapidly adsorbed on soils with a high organic matter content,
but only moderately adsorbed by clay soils. Aldrin and dieldrin
rarely penetrate more than 20 cm beneath the top treated layer of
soil. Aldrin adheres to soil particles to such an extent that only
traces can be removed by water. For this reason, contamination of
ground water does not generally occur.

The disappearance of aldrin from soil resembles a first-order
reaction. Immediately after application, there is a short period
of rapid loss due to volatilization and thereafter a second longer

exponential period of decline, mainly due to conversion to
dieldrin, which is slower to dissipate. However, there is the
possibility of migration by way of soil erosion, as wind drift,
sediment transport, and surface run-off. From data on residues of
aldrin in the environment, it appears that it is mainly retained in
the soil and that 97% of the primary residue is not the parent
compound but its epoxide, dieldrin.

Photodieldrin is a photodegradation product of dieldrin and
does not occur widely in the environment.

Aldrin applied to soils is lost slowly in temperate areas,
three-quarters of the applied aldrin being lost during the first
year in a typical case. The rate of loss slows later as aldrin is
converted to dieldrin. There is some evidence that the rate of loss
is greater under the anaerobic conditions of rice paddies than under
aerobic conditions. Dieldrin is lost from the soil very rapidly in
tropical areas, up to 90% disappearing within 1 month, whereas the
half-life of dieldrin in temperate soils is approximately 5 years.
Volatilization appears to be the principal route of loss from the
soil, though atmospheric levels of dieldrin and aldrin are generally
low. Some dieldrin is washed from the atmosphere by rain, but
levels in ground water are very low because of strong adsorption to
soil particles. Dieldrin has been detected, in small amounts, in
surface water contaminated by run-off from agricultural land.

1.3. Environmental Levels and Human Exposure

Aldrin and dieldrin have been found in the atmosphere, in the
vapour phase, adsorbed on dust particles, or in rainwater at
variable levels according to the situation. They have been
detected mainly in agricultural areas, where the mean level in the
air has been of the order of 1 - 2 ng/m³, with maximum levels of
about 40 ng/m³. In rainwater, concentrations of the order of
10 - 20 ng/litre, or occasionally higher, have been found.

Concentrations found in the air in houses treated for the
control of termites were much higher, ranging from 0.04 to 7 µg/m³,
depending on the time of sampling (i.e., the number of days of
after application) and the type of house. Within 8 weeks, the
concentrations decreased rapidly. Treatment of internal wood in
houses resulted in dieldrin concentrations in the air ranging from
0.01 to 0.5 µg/m³. Aldrin and dieldrin migrated into food from
treated laminated timber and plywood, and by direct contact and/or
sorption from the atmosphere.

The occurrence of dieldrin in the aquatic environment has been
reported. However, the concentrations were very low, mainly less
than 5 ng/litre. Higher levels have been generally attributed to
industrial effluents or soil erosion during agricultural usage.
River sediments may contain much higher concentrations (up to 1 mg/kg).

Aldrin is found only rarely in food, but dieldrin is more
common, especially in dairy products, meat products, fish, oils and
fats, potatoes, and certain other vegetables (especially the root
vegetables). Maximum residue limits (MRLs) in the range of 0.02 to
0.2 mg/kg product have been recommended over the years by the
FAO/WHO Joint Meetings on Pesticide Residues. Recent studies in
different countries have shown that the actual concentrations of
dieldrin in these food commodities are generally lower. Studies
from the United Kingdom indicate this decrease clearly. In
1966 - 67, the mean level of dieldrin residues in a total diet
study was 0.004 mg/kg food, whereas in the period 1975 - 77 it was
0.0015 mg/kg, and in 1981, 0.0005 mg/kg. This downward trend has
been confirmed in other countries, for instance in the USA. This
may be due to the restriction or banning of the use of these
compounds.

A large number of investigations has been reported in which the
adipose tissue, organs, blood, or other tissues of the general
population have been examined for the presence of dieldrin. Over
the last 25 years, surveys have been carried out in many countries
all over the world. Most of the mean values for adipose tissue
have been in the range of 0.1 - 0.4 mg/kg. Surveys in the
Netherlands, the United Kingdom, and the USA have indicated a
decline in concentrations in adipose tissue, since the mid-1970s.
Blood concentrations range from 1 to 2 µg/litre. Levels in the
liver are below 0.4 mg/kg, while those in other tissues, including
the kidneys, brain, and gonads, are below 0.1 mg/kg tissue.

As a result of transplacental exposure, dieldrin is present in
the blood, adipose tissue, and other tissues of the fetus and
newborn infants. The concentrations are one tenth to one half of
those of their mothers. There is no difference between infants and
adults in the brain/liver/fat ratio of dieldrin concentrations.
Dieldrin is also excreted in mother's milk. Over the last 15
years, samples of mother's milk have been analysed for the presence
of organochlorine pesticides, including dieldrin, in various
countries. In most countries, the dieldrin concentration in milk
amounts to 6 µg/litre, though higher levels have occasionally been
found.

1.4. Kinetics and Metabolism

In both animals and human beings, aldrin and dieldrin are
readily absorbed into the circulating blood from the
gastrointestinal tract, through the skin, or through the lungs
following inhalation of the vapour. A study on human volunteers
showed that absorption through the intact skin amounts to 7 - 8% of
the applied dose. Inhalation studies with human volunteers
suggested that up to 50% of inhaled aldrin vapour is absorbed and
retained in the human body. After absorption, it is rapidly
distributed throughout the organs and tissues of the body and a
continuous exchange between the blood and other tissues takes
place. In the meantime, aldrin is readily converted to dieldrin,
mainly in the liver but also to a much lesser extent in some other
tissues, such as the lungs. This conversion proceeds very rapidly.

When 1-day-old rats were given oral doses of 10 mg aldrin/kg
body weight, their livers contained dieldrin 2 h after treatment.
Over the course of the next few hours, dieldrin concentrated to a
greater extent in the lipid tissues.

Numerous studies carried out with ¹⁴C-labelled aldrin and
dieldrin have shown that part of the ingested material is passed
unabsorbed through the intestinal tract and eliminated from the
body, part is excreted unchanged from the liver into the bile, part
is stored in the various organs and tissues particularly in the
adipose tissue, and part is metabolized in the liver to more polar
and hydrophilic metabolites. In human beings and most animals, the
metabolites are excreted primarily via the bile in the faeces. It
has also been shown that both aldrin and dieldrin are biodegraded
into the same metabolites.

Most of the currently available information on the
biodegradation metabolism in mammals is based on studies on
dieldrin in the mouse, rat, rabbit, sheep, dog, monkey, chimpanzee,
and in human beings. The overall picture shows only quantitative
variations between species, and the mechanisms in rats seem to be
similar to those in primates.

The major metabolite, except in the case of the rabbit, is the
9-hydroxy derivative. This metabolite is found in the faeces and
in a free or conjugated form in the urine. Small amounts of three
other metabolites have been found and identified in experimental
animals. These are the trans-6,7-dihydroxy derivative,
dicarboxylic acid derived from the dihydroxy compound, and the
bridged pentachloroketone.

Only the 9-hydroxy compound has been demonstrated in the faeces
of human beings and neither this nor the other metabolites have
been found in human blood or other tissues. Dieldrin was found to
be present in the faeces of occupationally exposed workers, whereas
the concentrations in the samples from the general population were
below the limits of detection. Examination of the urine of five
workers indicated that urinary excretion of dieldrin and its four
metabolites was minor compared to the elimination of the 9-hydroxy
metabolite via the faeces.

The conversion of aldrin to dieldrin by mixed-function
monooxygenases (aldrin-epoxidase) in the liver and the distribution
and the subsequent deposition of dieldrin (mainly in lipid-
containing tissues, such as adipose tissue, liver, kidneys, heart,
and brain) proceed much more rapidly than the biodegradation and
ultimate elimination of unchanged dieldrin and its metabolites from
the body. Thus, at a given average daily intake of aldrin and/or
dieldrin, dieldrin slowly accumulates in the body. However, this
accumulation does not continue indefinitely. As dosing continues,
a "steady state" is eventually reached at which the rates of
excretion and intake are equal. The upper limit of storage is
related to the daily intake. This has been demonstrated in rats,
dogs, and human beings.

When the intake of aldrin/dieldrin ceases or decreases, the
body burden decreases. The biological half-life in man is
approximately 9 - 12 months. Significant relationships have been
found between the concentrations of dieldrin in the blood and those
in other tissues in rats, dogs, and human beings.

Numerous investigations of the concentrations of dieldrin in
the blood, adipose tissue, and other tissues of members of the
general population and from special groups, carried out in several
different countries, have shown that at equilibrium the ratio of
dieldrin concentrations in the adipose tissue, liver, brain, and
blood is about 150:15:3:1.

Dieldrin is transported via the placenta and reaches the fetus.
Accumulation takes place in the same organs and tissues as in the
adult, but to a much lower level. There seems to be an equilibrium
between the levels in the mother and the fetus.

Photodieldrin is also metabolized into bridged pentachloroketone
in the rat and dog. Both compounds were found in the adipose
tissue, liver, and kidneys when animals were administered high
levels of photodieldrin. No residues of these compounds could be
detected in human adipose tissue, kidneys, or breast milk. The
accumulation of photodieldrin in the adipose tissue of experimental
animals was much less than that of dieldrin.

1.5. Effects on Organisms in the Environment

1.5.1. Accumulation

Most residues in organisms are of dieldrin, since aldrin is
readily converted to dieldrin in all organisms.

The uptake of dieldrin from medium into fungi, streptomycetes,
and bacteria over 4 h has yielded concentration factors ranging
from 0.3 to >100. Protozoa take up more dieldrin than algae.
Algae take up dieldrin from the culture medium very rapidly, maxima
often being reached within a few hours.

Many species of aquatic invertebrates concentrate dieldrin from
very low water concentrations, yielding high concentration factors.
A steady state is reached within a few days. On transfer to clean
water, the loss of dieldrin is rapid, the half-life being 60 - 120 h.

Bioconcentration factors for whole fish are greater than
10 000. The half-life for loss of accumulated dieldrin was found
to be 16 days for one species of fish.

The bioconcentration of dieldrin in aquatic organisms is
principally from the water rather than by ingestion of food.

Earthworms take up dieldrin from the soil and concentrate it to
a maximum of about 170 times. There is little correlation between
levels in earthworms and levels in most types of soil.

Many investigations have been carried out to estimate the
occurrence of dieldrin in the tissues or eggs of non-target
species. The concentrations found cover a wide range from 0.001
mg/kg up to 100 mg/kg tissue, but most are below 1 mg/kg tissue.

Both the body tissues and eggs of birds accumulate dieldrin
readily. Similarly, various mammal species have been shown to
accumulate dieldrin, particularly in the fatty tissues.

1.5.2. Toxicity for microorganisms

The effects of dieldrin on unicellular algae are very variable,
some species being markedly affected by 10 µg/litre and others
unaffected even by 1000 µg/litre. Aldrin and dieldrin have only
minor effects on soil bacteria, even at levels far exceeding those
normally encountered. Most studies have shown no effects at
exposure levels of 2000 mg/kg soil. Effects on photosynthesis have
been reported in several different species of algae, with aldrin
showing a more marked effect than dieldrin at the same
concentration. However, these slight effects on the biochemical
processes of soil algae were only transitory.

1.5.3. Toxicity for aquatic organisms

Aldrin and dieldrin are highly toxic for aquatic crustaceans,
most 96-h LC₅₀values being below 50 µg/litre. However, a few
reported results of up to 4300 µg/litre illustrate species
variability. Daphnids are less sensitive to dieldrin than aldrin,
with 48-h tests yielding LC₅₀values of 23 - 32 µg/litre for aldrin
and 190 - 330 µg/litre for dieldrin. Molluscs are significantly
more resistant, with 48 h values ranging up to >10 000 µg/litre.
The results of studies over several weeks have confirmed the
relative resistance of daphnids and molluscs. The most susceptible
aquatic invertebrates are the larval stages of insects with 96-h
values of 0.5 - 39 µg/litre for dieldrin and 1.3 - 180 µg/litre for
aldrin.

Both aldrin and dieldrin were highly toxic in acute tests on
fish. Values for 96-h LC₅₀s in various fish species varied from
2.2 to 53 µg/litre for aldrin, and from 1.1 to 41 µg/litre for
dieldrin. Several studies have revealed that toxicity increases
with increasing temperature. In a long-term study on Poecilia
latipinna, there was 100% mortality at dieldrin concentrations of
3 µg/litre or more. Dieldrin administered in the food of rainbow
trout at up to 430 µg/kg body weight per day did not have any
effects on mortality, but enzymic changes were reported.
Morphological changes in liver mitochondria were seen using the
electron microscope. The ammonia-detoxifying mechanism of fish is
sensitive to dieldrin, the no-observed-adverse-effect level being
less than 14 µg/kg body weight per day. Different life stages of
fish have been found to have different susceptibilities to
dieldrin. Eggs were resistant and juvenile stages were less
susceptible than adults.

The acute toxicity of both aldrin and dieldrin is high for
larval amphibia with 96-h LC₅₀s of the order of 100 µg/litre.

1.5.4. Toxicity for terrestrial organisms

The toxicity of dieldrin for higher plants is low, crops only
being affected at application rates greater than 22 kg/ha. Aldrin
is more phytotoxic, to tomatoes and cucumbers particularly, but
only at application rates many times greater than those
recommended. Cabbage is the most sensitive crop to aldrin.

Oral LD₅₀s for honey bees ranging from 0.24 to 0.45 µg/bee for
aldrin and from 0.15 to 0.32 µg/bee for dieldrin have been reported.
Contact toxicity ranged from 0.15 to 0.80 µg/bee for aldrin and from
0.15 to 0.41 µg/bee for dieldrin. Two studies have indicated that
dieldrin is relatively non-toxic for predatory insects eating pest
species.

In laboratory studies, earthworms tolerated aldrin at a level
of 13 mg/kg of artificial soil with <1% mortality. The 6-week
LC₅₀was 60 mg aldrin/kg soil.

The acute toxicities of aldrin and dieldrin have been found to
vary by more than an order of magnitude for 13 species of birds,
ranging from 6.6 to 520 mg/kg body weight for aldrin and from 6.9
and 381 mg/kg body weight for dieldrin. In four bird species,
subacute oral toxicity varied between 34 and 155 mg/kg for aldrin
and 37 and 169 mg/kg for dieldrin. Repeated testing over a period
of time did not indicate the development of resistance in these
species. Reproductive studies on several species of domestic birds
have indicated that levels of dieldrin in the diet of more than
10 mg/kg cause some adult mortality. There are no reproductive
effects on egg production, fertility, hatchability, or chick
survival at levels of dietary dieldrin not causing maternal
toxicity. Eggshell thickness is not directly affected by dieldrin.
However, reduced food consumption is a symptom of dieldrin
poisoning, and eggshell thickness can be reduced by decreased food
intake.

Among non-laboratory mammals, the response to dieldrin varies
from species to species. Four vole species showed acute LD₅₀s
ranging from 100 to 210 mg/kg body weight, making them less
susceptible to dieldrin than laboratory species. Shrews survived a
diet containing 50 mg dieldrin/kg but died with a dietary level of
200 mg/kg. Blesbuck (antelope) survived for 90 days at 5 and 15
mg/kg diet but all died within 24 days at levels of 25 mg/kg or
more. All blesbuck in an area sprayed with dieldrin at 0.16 kg/ha
died, the calculated dietary intake being 1.82 mg/kg per day. Thirty
percent of springbok survived the spray with no after-effects.
Toxicological signs of dieldrin poisoning were similar to those of
laboratory mammals.

1.5.5. Population and ecosystem effects

It has been suggested that some mammal populations have been
affected by dieldrin. Small mammals were probably killed by eating
dieldrin-dressed seed, but populations were replenished by
immigration. Bats have been killed by dieldrin in wood preservatives.

Residues of dieldrin have been reported in many species of
birds. Throughout the world, the highest residues have been found
in birds of prey at the top of foodchains. The dieldrin content of
bird tissues and eggs has paralleled usage patterns and decreased
with restrictions in the use of aldrin and dieldrin. It is not
easy to identify the effects of dieldrin, because residues occur
together with residues of other organochlorines. Dieldrin is more
toxic to birds than DDT and probably has been responsible for more
adult deaths that DDT. However, the reproductive effects of
dieldrin in the field are more difficult to prove. There are
seasonal changes in the contents of dieldrin in bird tissues.
Furthermore, effects can occur long after exposure to the source of
the pollutant.

1.6. Effects on Experimental Animals and In Vitro Test Systems

Aldrin and dieldrin are of a high order of toxicity; the oral
LD₅₀s for both compounds in the mouse and rat range from 40 to 70
mg/kg body weight. The dermal toxicity is in the range of 40 - 150
mg/kg body weight, depending on the animal species and the solvent
used. Technical aldrin and dieldrin were found to produce slight
to severe irritation in the rabbit skin, but this effect was mainly
caused by the solvent. In the Magnusson & Kligman guinea-pig
maximization test, aldrin produced a sensitization effect.
However, during 20 years of manufacture and formulation, no cases
of skin sensitization occurred in a group of over 1000 workers.

The vapour pressures of both aldrin and dieldrin are low and
acute inhalation effects do not normally arise. The effects
observed in acute toxicity studies by all routes involve the
central nervous system and include hyperexcitability, tremors, and
convulsions.

Short- and long-term oral studies have been carried out with
aldrin and dieldrin on the mouse, rat, dog, hamster, and monkey.
The liver is the major target organ in the rat and mouse, with an
increased liver/body weight ratio and hypertrophy of the
centrilobular hepatocytes occurring, which in the early stages may
be reversible. Microscopically these changes include increased
cytoplasmatic oxyphilia and peripheral migration of basophilic
granules. These changes were not found in the liver of the hamster
and the monkey. In the dog, mild liver changes (fatty changes and
slight hepatic cell atrophy) were accompanied by kidney changes
consisting of vacuolization in the epithelia of distal renal
tubules and tubular degeneration. In the rat, the overall no-
observed-adverse-effect level from the available short-term and
long-term studies is 0.5 mg/kg diet, equivalent to 0.025 mg/kg body

weight. With feeding levels equivalent to 0.05 mg/kg body weight
or more, an increasing dose-related hepatomegaly and histological
changes occurred. In the dog, no-effect levels of 0.04 - 0.2 mg/kg
body weight were found.

A number of long-term carcinogenicity studies on mice of
different strains were carried out with aldrin or dieldrin. In all
studies, benign and/or malignant liver cell tumours were found.
Females seemed to be less sensitive than males. No other types of
tumours were induced.

Long-term studies on the other animal species (rat, hamster)
did not show any increase in tumour incidence. Photodieldrin, fed
at concentrations up to 7.5 mg/kg diet, did not induce tumours.

In addition, a number of special studies have been published
that have so far failed to elucidate the mechanism of the induction
of the liver tumours in mice.

In most of the reproduction studies (over 1 - 6 generations)
carried out with aldrin or dieldrin on mice and rats, the major
effect was an increased mortality rate in pre-weaning pups.
Reproductive performance was only affected at doses causing
maternal intoxication. Studies on dogs were too limited to draw
firm conclusions, apart from a consistent increase in pre-weaning
pup mortality.

It can be concluded from the results of these reproduction
studies that 2 mg dieldrin/kg in the rat diet and 3 mg dieldrin/kg
in the mouse diet, equivalent to 0.1 and 0.4 mg/kg body weight per
day, respectively, are no-observed-adverse-effect levels for
reproduction.

No evidence of teratogenic potential was found in studies on
the mouse, rat, or rabbit using oral doses of aldrin and dieldrin
of up to 6 mg/kg body weight. Single doses of aldrin and dieldrin,
equal to about half the LD₅₀, caused severe fetotoxicity and an
increased incidence of teratogenic abnormalities in the mouse and
hamster. The significance of these findings in the presence of
likely maternal toxicity is doubtful.

Many in vivo and in vitro mutagenicity studies have been
carried out, but the results of nearly all these studies were
negative.

The acute oral toxicity of photodieldrin is higher than that of
dieldrin in the mouse, rat, and guinea-pig. In acute and short-
term toxicity studies, the symptoms of intoxication and the effects
on target organs are quantitatively and qualitatively similar to
those of dieldrin. Photodieldrin did not induce tumours in mice
and rats.

Like most other chemical substances, aldrin and dieldrin do not
have a single mechanism of toxicity. The target organs are the
central nervous system and the liver. In human beings and other

vertebrates, intoxication following acute or long-term overexposure
is characterized by involuntary muscle movements and epileptiform
convulsions. Survivors recover completely after a short period of
time of residual signs and symptoms. In the liver there is an
increased activity of microsomal biotransformation enzymes,
particularly of the monooxygenase system with cytochrome P-450.
This induction of the microsomal enzymes is reversible and, if it
exceeds a certain level, it appears to be linked to cytoplasmic
changes and hepatomegaly in the liver of rodents.

All the available information on aldrin and dieldrin taken
together, including studies on human beings, supports the view that
for practical purposes these chemicals make very little
contribution, if any, to the incidence of cancer in man.

1.7. Effects on Man

Aldrin and dieldrin are highly toxic for human beings. Severe
cases of both accidental and occupational poisoning have occurred
but only rarely have fatalities been reported. The lowest dose
with a fatal outcome has been estimated to be 10 mg/kg body weight.
Survivors of acute or subacute intoxications recovered completely.
Irreversible effects or residual pathology have not been reported.

Adverse effects from aldrin and dieldrin are related to the
level of dieldrin in the blood. Determination of the level of
dieldrin in the blood provides a specific diagnostic test of
aldrin/dieldrin exposure. The level of dieldrin in the blood of
male workers below which adverse effects do not occur, (the
threshold no-observed-adverse-effect level) is 105 µg/litre blood.
This corresponds to a daily intake of 0.02 mg dieldrin/kg body
weight per day.

Environmental exposure (mainly dietary though also, to a small
extent, respiratory) leads to the presence of dieldrin at very low
levels in organs, adipose tissue, blood, and mother's milk. As far
as can be judged from the extensive clinical and epidemiological
studies, there is no reason to believe that these prevailing body
burdens constitute a health hazard for the general population. In
a continuing study lasting more than 20 years, involving more than
1000 industrial workers in an aldrin/dieldrin insecticide-
manufacturing plant, no increase in cancer incidence occurred among
workers who had been exposed to high levels of aldrin and dieldrin.
More significantly, there were no signs of any premonitory change
in liver function in these workers.

An epidemiological mortality study was carried out at a
manufacturing plant in the USA on a cohort of 870 workers exposed
to aldrin, dieldrin, and endrin. With almost 25 000 man-years of
observation, no specific cancer risk associated with employment at
this plant could be identified.

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS

2.1. Identity

2.1.1. Primary constituent: aldrin^a

Chemical formula: C₁₂H₈Cl₆

Relative molecular mass: 364.9

IUPAC chemical name^b: (1 R,4 S,4a S,5 S,8 R,8 R,a R)-1,2,3,4,10,
10-hexachloro-1,4,4a,5,8,8a-hexahydro-1,
4:5,8-dimethanonaphthalene or 1,2,3,4,10,
10-hexachloro-1,4,4a,5,8,8a-hexahydro-
exo-1,4- endo-5,8-dimethanonaphthalene

Common synonyms
and trade names: ENT 15 949 (compound 118), HHDN,
Octalene, OMS 194

CAS registry number: 309-00-2

RTECS registry number: I02100000

Technical product

Common trade name: Aldrin. This is the common name of an
insecticide containing 95% of HHDN.

Purity: The minimum content of aldrin (as defined
above) in technical aldrin is 90%.

Impurities: octachlorocyclopentene (0.4%),
hexachlorobutadiene (0.5%), toluene (0.6%),
a complex mixture of compounds formed by
polymerization during the aldrin reaction
(3.7%) and carbonyl compounds (2%)
(FAO/WHO, 1968b)

-------------------------------------------------------------------
^aFrom: Worthing & Walker (1983).
^bOther chemical names are given in Appendix I.

2.1.2. Primary constituent: dieldrin^a

Chemical formula: C₁₂H₈OCl₆

Relative molecular mass: 380.9

IUPAC chemical name^b: (1 R,4 S,4a S,5 R,6 R,7 S,8 S,8a R)-1,2,3,
4,10,10-hexachloro-1,4,4a,5,6,7,8,8a-
octahydro-6,7-epoxy-1,4:5,8-
dimethanonaphthalene or 1,2,3,4,10,10-
hexachloro-6,7-epoxy-1,4,4a,5,6,7,8,8a-
octahydro- endo-1,4- exo-5,8,-
dimethanonaphthalene

Common synonyms ENT 16 225 (compound 497), HEOD, Alvit,
and trade names: Octalox, OMS 18, Quintox

CAS registry number: 60-57-1

RTECS registry number: I01750000

Technical product

Common trade name Dieldrin. This is the common name of an
insecticide containing 85% of HEOD.

Purity: Technical dieldrin contains not less than
95% of dieldrin, as defined above.

Impurities: other polychloroepoxyoctahydrodimethano-
naphthalenes, endrin 3.5% (FAO/WHO,
1968b)

-------------------------------------------------------------------
^aFrom: Worthing & Walker (1983).
^bOther chemical names are given in Annex I.

2.2. Physical and Chemical Properties

2.2.1. Aldrin

Pure aldrin is a colourless crystalline solid. It has a
melting point of 104 - 104.5 °C.

Technical aldrin (90%) is a tan to dark brown solid with a
melting point of 49 - 60 °C. Its vapour pressure is 8.6 mPa at
20 °C (6.5 x 10^-5mmHg at 25 °C). Its density is 1.54 g/ml at
20 °C. Its solubility in water is 27 µg/litre at 27 °C
(practically insoluble), and in acetone, benzene, and xylene
is > 600 g/litre. Aldrin is stable at < 200 °C and at pH 4 - 8,
but oxidizing agents and concentrated acids attack the
unchlorinated ring. Aldrin is non-corrosive or slightly corrosive
to metals because of the slow formation of hydrogen chloride on
storage (Shell, 1976, 1984; Worthing & Walker, 1983).

2.2.2. Dieldrin

Technical dieldrin (95%) consists of buff to light tan flakes
(setting point > 95 °C) with a mild odour. Its melting point is
175 - 176 °C. Its vapour pressure is 0.4 mPa at 20 °C (3.2 x 10^-6
mmHg at 25 °C). Its density is 1.62 g/ml at 20 °C. Its solubility
in water is 186 µg/litre at 20 °C (practically insoluble), but it
is moderately soluble in most paraffinic and aromatic hydrocarbons,
halogenated hydrocarbons, ethers, esters, ketones, and alcohols.
Dieldrin is stable to alkali, mild acids, and to light. It reacts
with concentrated mineral acids, acid catalysts, acid oxidizing
agents, and active metals (iron, copper). It is non-corrosive or
slightly corrosive to metals in the same way as aldrin (Shell,
1976; Worthing & Walker, 1983).

2.3. Analytical Methods

2.3.1. Sampling methods

Methods of sampling and storage have been reviewed by Beynon &
Elgar (1966). Sample collection is broadly divisible into two types:
adventitious sampling (particularly of wildlife) and systematic
sampling (soil, total diet surveys) in which samples are collected
in accordance with the principles of statistical design. Surveys
of dieldrin in human blood and adipose tissue are a partial
combination of these two classes of sample collection. The
sampling methods for total diet surveys were reviewed by Cummings
(1966), and the sampling of air for pesticide residues has been
discussed in detail by Lewis (1976).

2.3.2. Analytical methods

Since the introduction of the method of gas-liquid
chromatography with electron capture detection (GLC/EC) (Goodwin et
al., 1961), old methods, based on, for instance, total organic
chlorine or the colorimetric phenyl azide procedure, have been
abandoned. The great majority of analytical data relating to the

occurrence of residues of aldrin or dieldrin since that time have
been based on GLC/EC procedures. There has been considerable
evolution of various aspects (especially extraction and clean up
procedures) of the methodology. The many publications on specific
procedures are reviewed in the Codex Publication "Recommendations
for methods of analysis of pesticide residues", CAC/PR 8-1986,
(FAO/WHO, 1986b). This review lists 22 individual publications,
four of which refer to simplified methods. It also lists the
following compendia of methods which may also be consulted.

- Official methods of analysis of the Association of Official
Analytical Chemists, 14th Edition 1984.

- Pesticide analytical manual, Food & Drug Administration,
Washington DC, USA.

- Manual on Analytical methods for pesticide residues in foods,
Health Protection Branch, Health and Welfare, Ottawa, Canada,
1985.

- Methodensammlung zur Rueckstandsanalytik von
Pflanzenschutzmitteln (Methods for analysing residues of plant
protective agents) 1984 Verlag Chemie GmbH, Weinheim, Federal
Republic of Germany.

- Chemistry Laboratory Guidebook, USDA.

Whatever procedure is adopted should be carried out within the
requirements of the CAC publication "Codex Guidelines on Good
Laboratory Practice in Pesticide Residue Analysis", CAC/PR 7-1984,
(FAO/WHO, 1984).

It is important to recognize that the electron capture detector
is not specific for aldrin and dieldrin and in the analysis of
samples without a precise history of treatment, confirmation of the
identity of the residue is an essential part of the analysis.
Reports of the occurrence of aldrin in environmental samples in the
past, are now thought, in many cases, to have been instances of
misidentification. The occurrence of PCBs in the same sample has
been a particularly troublesome source of interference. Many
procedures for the confirmation of identity are available and
include comparison of the position of the peak on different
chromatographic columns, thin-layer chromatography, and
derivatization. The most definitive method, however, involves the
uses of mass spectrography as the detector. With this procedure,
much of the uncertainty with regard to the identification of the
residue has been eliminated. The mass spectrography procedure
described by Hargesheimer (1984) is effective for the determination
of chlorinated hydrocarbon residues in the presence of PCBs. The
limit of determination of individual methods depends to a
considerable extent on the amount of effort the analyst devotes to
extraction and clean-up procedures. With samples of food and
feeds, for example, a limit of determination of 0.01 mg/kg is
normally regarded as acceptable, but in water and air far lower
levels are achievable, depending on the care and effort taken.

It should be recognized that there is considerable variation in
the results that can be obtained on the same sample by different
analysts and in different laboratories and variations of 100% are
by no means uncommon at the lower end of the scale. A valuable
account of the variation found among 120 laboratories for a sample
of butterfat containing known amounts of 11 different chlorinated
hydrocarbon insecticides was given by Elgar (1979).

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1. Natural Occurrence

Aldrin and dieldrin are not known to occur as natural products.

3.2. Man-Made Sources

3.2.1. Production levels and processes; uses

3.2.1.1 World production figures

The first laboratory synthesis of aldrin and dieldrin was in
1948 by J. Hyman & Co. (Thompson, 1976). The method was licensed
to Shell and manufacture began in 1950, first in the USA and later
on in the Netherlands (IARC, 1974).

Production has decreased since the early 1960s. The production
capacity was 20 000 tonnes in 1971, and the estimated 1972
production was 13 000 tonnes. In 1984, less than 2500 tonnes of
aldrin and dieldrin were manufactured, approximately one third of
which was used in Australia, the United Kingdom, and the USA (Van
Duursen, 1985).

Up to the late 1960s and early 1970s, aldrin and dieldrin were
used throughout the world. Since then, many countries have
severely restricted or banned their use, especially in agriculture,
because of their persistent character in the environment (IARC,
1974). The main remaining uses are in the control of disease
vectors and termites and industrial applications.

3.2.1.2 Manufacturing processes

Aldrin is synthesized by the Diels-Alder reaction of
hexachlorocyclopentadiene with an excess of bicycloheptadiene at
100 °C. The yield is more than 80%, calculated on the
hexachlorocyclopentadiene (Melnikov, 1971).

Commercial production of dieldrin is believed to be through
epoxidation of aldrin with a peracid (e.g., peracetic or perbenzoic
acid), but an alternate synthetic route involves the condensation
of hexachlorocyclopentadiene with the epoxide of bicycloheptadiene
(Galley, 1970).

3.2.1.3 Release into the environment during normal production

Loss of aldrin and dieldrin, together with isobenzan, in waste
water from a manufacturing plant in the Botlek area of the
Netherlands caused deaths among sandwich terns (Sterna
sandvicentis), eider ducks (Somateria mollissima), and, to a lesser
extent, some other bird species, feeding on marine organisms
containing high levels of these insecticides in the Wadden Sea
during 1962 - 65. Following improvement of the waste-water
purification of the plant, the residue levels in the marine
organisms decreased during subsequent years (Koeman, 1971).

3.2.2. Uses

3.2.2.1 Aldrin

Aldrin is a highly effective broad-spectrum soil insecticide.
It kills insects by contact and ingestion, and possesses slight
fumigant action within the soil, which ensures distribution in the
top soil where the pests are found.

It is used to control soil insects, including termites, corn
rootworms, seed corn beetle, seed corn maggot, wireworms, rice
water weevil, grasshoppers, and Japanese beetles, etc. Crops
protected by aldrin soil treatment include corn and potatoes; it is
used as a seed dressing on rice. Aldrin is also used for the
protection of wooden structures against termite attack. It is
supplied mainly as an emulsifiable concentrate or wettable powder.

3.2.2.2 Dieldrin

Dieldrin is used mainly for the protection of wood and
structures against attack by insects and termites and in industry
against termites, wood borers, and textile pests (moth-proofing).
It acts as a contact and stomach poison.

Dieldrin is no longer used in agriculture. It has been used as
a residual spray and as a larvacide for the control of several
insect vectors of disease. Such uses are no longer permitted in a
number of countries.

It is available as an emulsifiable concentrate or wettable
powder.

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION

4.1. Transport and Distribution Between Media

4.1.1. Leaching of aldrin and dieldrin

As would be expected from their very low water solubility,
hydrophobic character, and strong adsorption by soil, aldrin and
dieldrin are very resistant to downward leaching through the soil
profile.

Since one of the major uses of aldrin is as a soil insecticide,
aldrin-treated soil is an important source of aldrin in the
environment.

Bowman et al. (1965) studied the leaching of aldrin through six
different types of soil, by passing water through them. In five
out of six soil types, only traces were recovered in the leachates.
However, 16% of applied aldrin was found in the leachate from a
sandy soil type. Other studies indicate that leaching of aldrin
through soil is minimal (Harris, 1969; Herzel, 1971; El Beit et
al., 1981a,b).

A study was carried out to determine the possible involvement
of aldrin applied for the control of termites around house
foundations. Seven types of soil collected from different
geographical areas in the USA were investigated by placing the
soils (adjusted to 0, 5, 10, or 15% water content) in glass
columns. The soil columns were separated into five layers of 5 cm
by filter paper support cloth. An emulsion of aldrin was placed on
the top of the column, equivalent to 0.365 kg aldrin/m². The
layers of soil were removed approximately 24 h after application of
the emulsion and the concentration of aldrin determined.
Penetration below 20 cm did not occur in any soil at any of the
water contents. In certain soils, penetration only took place in
the first 5 cm and, in others, in the third layer (10 - 15 cm).
Water content also plays a role in the penetration. In another
study, layers of 4 cm were used, with comparable results (Carter &
Stringer, 1970).

Several field studies on the leaching of aldrin through
different types of soil have been carried out. In these studies,
aldrin was applied to the surface or tilled to a depth of about 15
cm at dose levels of 1.8 - 20.7 kg/ha. From the results, it is
clear that, even up to 5 years after application, aldrin and
dieldrin were still present in the treated layer, with little
penetration to layers immediately below the treated layer. From
these studies, it appears that there is little movement
(Lichtenstein et al., 1962; Daniels, 1966; Park & McKone, 1966).
However, Wiese & Basson (1966) found some movement, even in clay
soil.

In studies by Powell et al. (1979), sandy soil in which tomato
plants were growing was sprayed with an aldrin emulsion (2.2 kg/ha)
on six occasions at intervals of 1 - 2 weeks. Approximately one

year after the final treatment, soil core samples were taken and
the concentrations of aldrin and dieldrin in the 0 - 5, 5 - 10,
10 - 15, 15 - 22.5 cm layers were determined. About 73% of the
total residue in the 0 - 22.5 cm layer was in the 0 - 15 cm layer.
The ratio of aldrin to dieldrin in the four strata was similar.
The remark should be made that in this study there were a number of
confounding factors (e.g., the field was ploughed).

Stewart & Fox (1971) applied aldrin as a spray to four turf
plots at doses of 3.3, 4.4, or 6.6 kg/ha. Loam and silt soil core
samples were taken to a depth of 30 cm 9 - 13 years after
treatment. Aldrin was not detected; 93 - 100% of the total
dieldrin in the 30 cm core was in the top 15 cm layer of soil.

In studies by Lichtenstein et al. (1971), aldrin was applied to
a silt loam at a rate of 4.4 kg/ha and rototilled to a depth of
10 - 12.5 cm. After 10 years, the percentage of the applied aldrin
in the 0 - 22.5 cm layer was 0.18% as aldrin and 5.2% as dieldrin.
The ratios of concentrations in the 0 - 15 cm layer relative to the
15 - 22.5 cm layer were: aldrin, 2.5; dieldrin, 4.9.

¹⁴C-Aldrin was incorporated to a depth of 15 cm in experimental
plots in which potatoes were grown in the Federal Republic of
Germany (sandy loam; equivalent to 2.9 kg/ha) and England (sandy
clay loam; equivalent to 3.2 kg/ha). After 6 months, the
concentrations of aldrin in both cases were as follows: at 0 - 10
cm, 0.58 and 0.59 mg/kg; at 10 - 20 cm, 0.23 mg/kg and < 0.01
mg/kg; at 20 - 40 cm 0.02 and < 0.01 mg/kg and at 40 - 60 cm, < 0.01
mg/kg (in both locations) (Klein et al., 1973). In a parallel
study, the ¹⁴C activity in leach water collected at a depth of 60
cm was determined over a 3-year period; the cumulative rainfall
during this period was 160 cm. About 10% of the ¹⁴C activity,
applied initially to a depth of 15 cm, was found in the leachate
over a period of 3 years. Almost all the ¹⁴C activity was present
as dihydrochlordene dicarboxylic acid (Moza et al., 1972).

In studies by Stewart & Gaul (1977), aldrin (5.6 and 11.2
kg/ha) was incorporated to a depth of 15 cm into a sandy loam soil
for three successive years. Various crops were grown and soil
samples were collected for 14 years. Residues of aldrin and
dieldrin below 15 cm were negligible in the tenth year after the
initial application, whereas the residues of aldrin plus dieldrin
in the 0 - 15 cm layer were 0.2 and 1.7 mg/kg, respectively, at the
two different treatments levels.

The results of these leaching studies indicate the almost
quantitative adsorption of aldrin by organic matter and clay
minerals. Water molecules compete with aldrin for the adsorption
sites in clay minerals, and it has been found that aldrin is bound
to a greater extent in dry soil (Baluja et al., 1975; Kushwaha et
al., 1978b). The adsorption and desorption of aldrin has been
studied by Tejedor et al. (1974) in whole soil and in the clay and
organic (humic) fractions. It was concluded that the organic
fraction was mainly involved in the adsorptive uptake of aldrin and
that the clay fraction was the major factor affecting the retention

of aldrin. There does not appear to be a simple relationship
between water solubility and leaching, presumably because of the
variations in the adsorptive capacity of clay minerals in various
types of soil (Yaron et al., 1967). A chromatographic model of the
movement of pesticides through soils has been proposed (King &
McCarty, 1968; Oddson et al., 1970).

In the laboratory, the investigations by Eye (1968) and Harris
(1969) of the transport of dieldrin by water through soil are
particularly relevant and are consistent with the chromatographic
model for chemicals in soil of King & McCarty (1968). The elution
of dieldrin from soil by 1600 ml water was investigated in a study
of six types of soil placed in chromatographic columns. The
dieldrin content of the total eluate, as a proportion of the
applied dieldrin, varied from 1% (loam soil) to 65% (soil
containing 93% sand) (Bowman et al., 1965).

The leaching of dieldrin through soil columns (30 cm diameter)
was studied by Thompson et al. (1970). A dieldrin emulsion was
applied to the surface (equivalent to 31 kg dieldrin/ha) of soil
columns 35 cm deep, and water was added to the surface until about
30 litres (equivalent to about 6 months rainfall) had passed down
the columns in 120 h. It was concluded that dieldrin did not
readily leach from the three types of soil investigated into
drainage water, and that cracks and crevices caused by drying or by
earthworms and other animals favour the leaching of dieldrin. The
results of an investigation using sloping troughs gave results
consistent with the soil column study.

4.1.2. Surface run-off

Run-off from treated land caused by soil erosion is a potential
source of dieldrin residues in surface waters in areas where
erosion is not controlled by good farming practice. Sediments
bearing aldrin and dieldrin can result in low concentrations in
aqueous solution, although these are limited due to adsorption onto
the sediments. Thus, rain-water run-off (without sediment) does
not appear to be a major contributor.

Richard et al. (1975) and Sparr et al. (1966) sampled various
surface waters in the USA and reported levels of dieldrin ranging
from < 1 to 42 ng/litre and of aldrin in the region of 0.05
µg/litre.

To gain data on the erosion of treated land, Caro & Taylor
(1971) and Caro et al. (1976) incorporated dieldrin into the soils
of two small watersheds in Ohio, USA, and studied run-off losses
over a three-year period. In the first case, there was practically
no surface soil erosion and the total loss of dieldrin was confined
to run-off water. The area was 1.07 ha and the loss over the
period was less than 0.5 g dieldrin, the highest level in the water
being 4 µg/litre. In the second study, there was a substantial
loss of soil by erosion and the amount of dieldrin lost in the
solid sediment was 77 g in only 8 months. The loss in the water
itself was just under 2.5 g and the highest water concentration was

20 µg/litre. It should, however, be borne in mind that in this
case the soil had been mechanically compacted to aggravate the
effects of erosion, so that it is questionable whether the results
bear much relation to normal agricultural practice. The authors
commented that there was only a poor correlation between rainfall
events and the amounts of dieldrin lost.

Sediment-bearing residues of aldrin or dieldrin will yield some
of their burden to true solution in the water which they enters.
Sharom et al. (1980) showed that the ratio of dieldrin
concentration in soil to that in water (in equilibrium with the
soil) was between 100 and 500 for mineral soils, whilst that same
ratio for aldrin was likely to be around 5 - 6 times higher. Thus,
with 1 mg dieldrin/kg sediment, one could expect a water
concentration of about 10 µg/litre.

The movement of aldrin and dieldrin by run-off and soil erosion
was studied by Haan (1971). Each pesticide was applied at 1.65
kg/ha to the surface of small plots, mainly consisting of silt loam
(slope, 1 - 2%), in a greenhouse. Water was applied and the run-
off water, sediment, and surface soil (0.6 cm deep) were analysed.
It was estimated that 94.8% and 95.4%, respectively, of the applied
aldrin and dieldrin remained in the surface soil (0.6 cm depth).
It was concluded that there was no difference in the potential for
loss from soil by rainfall, whether the rainfall occurred shortly
after aldrin application or several days later.

4.1.3. Loss of aldrin and dieldrin from soils - volatilization

Most authors consider that the principal loss of aldrin and
dieldrin from soils is by volatilization. There is widespread
evidence for this, although other mechanisms (sections 4.4.1 and
4.4.2) may also play an important role.

Volatilization from soils was first demonstrated when it was
shown that mosquitoes were killed by vapour emanating from treated
soil blocks (Barlow & Hadaway, 1955, 1956; Gerolt, 1961).

When aldrin is incorporated into the soil, it is most readily
lost from the surface layer. Subsequently, material from deeper
layers has to rise to the surface to replenish what was lost. The
position is somewhat complicated by its gradual conversion to the
less volatile dieldrin, although this, too, behaves in a
qualitatively similar manner.

There are two routes to the surface: transport in ascending
capillary water - analogous to the process of salinization - and
vapour diffusion through the soil pores. Both of these processes
are strongly affected by hydrophobic adsorption, a phenomenon
common to many hydrophobic pesticides of low water solubility.
Adsorption by the soil has the effect, at practical rates of
application, of reducing the vapour pressure and hence the
saturation vapour density in the soil atmosphere. It also reduces
the maximum concentration in the soil solution.

There is a very extensive literature on soil adsorption,
especially of dieldrin and the following general situation is now
well established.

Adsorption, as measured by reduced vapour density, takes place
in all soils but is greatest at low moisture levels; that is to say
soils in equilibrium with air of relative humidity below around
95%. (Barlow & Hadaway, 1955, 1956; Gerolt, 1961; Harris, 1964,
1972; Igue et al., 1972).

In dry soils, mineral components play the most important part,
whereas in moist soils it is organic matter that dominates (Harris
& Lichtenstein, 1961; Harris et al., 1966; Harris & Sans, 1967;
Harris, 1972). In fact, Harris demonstrated a linear relation
between organic matter and adsorption in moist soils. On the other
hand, in a dry mineral soil with predominantly montmorillonitic
clay and very low organic matter, practically no dieldrin
volatilized until the relative humidity of the air in equilibrium
with soil reached saturation. At this point volatilization readily
resumed.

In moist soils, Spencer et al. (1969) found that adsorption,
expressed as a reduction in vapour density, became less marked as
the dieldrin level increased. At 20 °C, 10% moisture in the soil,
and 1 mg dieldrin/kg soil, the dieldrin vapour density was only 2
ng/litre, compared with 52 ng/litre when the dieldrin level in the
soil was increased to 25 mg/kg. This level is close to the figure
for free dieldrin. Similar results were reported at 30 °C and
40 °C by Spencer & Cliath (1973).

In dry soils, however, adsorption is far stronger. At 100 mg
dieldrin/kg moist soil (Spencer et al., 1969), the depression in
vapour pressure was negligible. However, as the moisture content
of the soil fell to a critical level of 2.1%, there was a dramatic
decrease in vapour density, so that below 2% moisture the vapour
density was practically zero. The same authors showed that the
level of water in their soil needed to provide a monomolecular
layer was 2.8%. They concluded that the critical point at which
adsorption increased was when the monomolecular layer started to be
lost, leaving adsorption sites available for occupation by
dieldrin. Restoration of the moisture status of the soil, however,
restored the vapour density to its original level.

Whilst most of these studies were carried out on one soil, Gila
silt loam, and whilst the figures would be different for other
soils, the qualitative conclusions are largely valid for all soils.
Adsorption is expected to be least on sandy soils of low organic
matter content.

Adsorption by soils can also be determined by measuring the
reduction in the saturation concentration of the soil solution
(Eye, 1968; Tejedor et al., 1974; Baluja et al., 1975). As in the
case of reduced vapour pressure caused by adsorption by moist
soils, the organic matter content of the soil was the principal
soil characteristic affecting adsorption from solution. Eye (1968)

also demonstrated the dominating influence of organic matter,
whereas clay content, surface area, and cationic exchange capacity
showed very little correlation. These findings are compatible with
those of Yaron et al. (1967).

In studies involving the percolation of dieldrin, dissolved in
water, through columns of soils with differing contents of organic
matter, Sharom et al. (1980) also showed that the soil capacity for
adsorption was largely determined by its content of organic matter.
Moreover, adsorption followed the Freundlich adsorption equation.
They reported Freundlich adsorption constants for a range of soils
and pesticides, including dieldrin, and showed that, for a given
pesticide, adsorption was strongly dependent on the organic matter
content of the soil. Moreover, the strength of adsorption by a
given soil depended mainly on the water solubility of the
pesticide, so that dieldrin, with its low water solubility, was
more strongly adsorbed than, for instance, the much more water-
soluble lindane. Although aldrin was not studied, it may be
inferred from these data that aldrin would be adsorbed
correspondingly more strongly, owing to a much lower water
solubility than that of dieldrin.

4.1.3.1 Movement within the soil profile - mass flow

Spencer & Cliath (1973) concluded from laboratory studies that
dieldrin could ascend the soil profile by mass flow in capillary
water moving up to the surface through a moisture gradient, and
that this mechanism could account for 3 - 30% of the total upward
movement. However, with low solubility products such as dieldrin,
Jury et al. (1983) pointed out that volatilization decreases with
time, because ascent to the surface is rate limiting. With high
solubility compounds, however, the reverse is true as more material
reaches the surface, dissolved in capillary water, to become
available for evaporation. However, it is not only water
solubility that determines the behaviour, but the value of Henry's
constant for the partition of the compound between air and water.
These authors considered the critical value to be 2.7 x 10^-5; above
this value mass flow is progressively less important. The value of
Henry's constant for dieldrin (6.7 x 10^-4) is substantially higher
(Jury et al., 1983) and that for aldrin higher still, so that on
this basis it is doubtful whether mass flow ever does play a
significant role in the transport of aldrin or dieldrin up the soil
profile.

In support of the view that transport by mass flow is not
appreciable, the mathematical models that have been proposed to
describe the loss of aldrin and dieldrin from soils (Farmer &
Letey, 1974; Mayer et al., 1974; Jury et al., 1983) tend to
demonstrate, in comparisons with laboratory data, that ascent to
the surface is predominantly by vapour diffusion rather than mass
flow.

4.1.3.2 Movement within the soil profile - diffusion

Diffusion is regarded as the main route by which aldrin and
dieldrin ascend the soil profile to reach the surface. Diffusion
increases with soil temperature, concentration, decreasing
adsorption capacity (usually the same as decreasing organic
matter), maintenance of moisture content above the wilting point,
and the "tortuosity" of the soil pore system (a measure of the
openness of the soil). With regard to moisture content, Farmer &
Jensen (1970) found that diffusion coefficients of dieldrin in
three soils in equilibrium with air of 94% relative humidity were
9.7, 4.4, and 3.8, but at 75% relative humidity the values were
0.6, 0.4, and 0.4, respectively. According to Farmer & Letey
(1974), the critical moisture level is probably the "fifteen
atmosphere percentage", usually considered to be a reasonable
measure of the water content at the wilting point.

Tortuosity increases as soils are compacted. Working with
moist soils of differing bulk densities, Farmer et al. (1973),
showed that diffusion of dieldrin was about twice as fast in a soil
with a density of 0.75 g/cm³as when it was compressed to a bulk
density of 1.5 g/cm³.

4.1.3.3 Actual volatilization losses - laboratory studies

Lichtenstein & Schulz (1970) reported that aldrin was lost by
volatilization from a silt loam soil about 20 times faster than
dieldrin. Helene et al. (1981) reported a 31% loss of aldrin from
a highly humic soil after 120 days but 62% from a soil of low
organic matter content.

In studies of moist soils in volatilization chambers, Farmer et
al. (1972) and Igue et al. (1972) found that the rate of loss by
volatilization gradually decreased with time. However, if
translated into terms of the open field, this could still represent
a loss of between 0.2 and 1.4 kg/ha per year, depending on the
depth of incorporation.

With a surface application of dieldrin in a microagroecosystem
chamber, Nash (1983) reported loss of dieldrin at the rate of 1 - 4
g/day, but this rate fell to about a half of its initial value
within 6 - 7 h. Incorporation of the dieldrin had the effect of
greatly slowing this loss rate (Nash, 1983).

4.1.3.4 Actual volatilization losses - field studies

The data on volatilization losses in the field are limited and
refer only to dieldrin. Caro & Taylor (1971) reported loss by
volatilization from an incorporated dieldrin application (5.6
kg/ha) of 2.8% of that applied (after 18 weeks). Spencer et al.
(1973) cited unpublished studies by Caro & Taylor (1971) where a
surface application was lost at the rate of 3% per hour. In a
later study, Caro & Taylor (1976) found that 4.5% of a dieldrin
application was lost by volatilization in the first year after
treatment. By the autumn, the loss rate was only 0.2 g/ha per day,

although this increased to 0.9 g/ha per day immediately after the
land was cultivated, due, presumably, to the exposure of fresh
soil.

Taylor et al. (1972, 1976) estimated a loss of dieldrin of 0.2
kg/ha from an incorporated application of dieldrin. However, only
6% remained from a surface application after 16 weeks, although in
this case a small amount was recovered as photodieldrin (Turner et
al., 1977).

Willis et al. (1972) demonstrated an 18% loss from a very high
application (22 kg/ha) of dieldrin after 5 months where the soil
was kept moist by irrigation. However, losses were substantially
less when the soil was not irrigated or when maintained under flood
conditions. The maximum rate of loss by volatilization was 0.2
kg/ha per day.

4.1.4 Losses of residues following treatment of soil with aldrin

One of the earliest systematic studies of the decline of aldrin
and dieldrin residues in soils, arising from the application of
aldrin to the soil, was by Decker et al. (1965), who sampled a wide
range of soils of known treatment history from Illinois, USA. They
demonstrated the transformation of aldrin to dieldrin and
considered that the loss of residues was a two-stage process.
There was a comparatively rapid loss in the first year after
treatment, a typical loss being 75% of the applied dose.
Thereafter, residues declined with a half-life of 2 - 4 years, the
reduced rate being apparently due to the greater proportion of
dieldrin in the residues. Elgar (1966) incorporated 2.2 kg
aldrin/ha into soils in the United Kingdom and reported somewhat
similar results for the decline of residues, although there were
indications that the rate of decline slowed in later years as the
level in the soil fell to around 0.3 mg/kg. Further studies of
this kind have been reported by Lichtenstein et al. (1970), Onsager
et al. (1970), and Korschgen (1971). Although the rates of decline
were very variable, they were not inconsistent with the data of
Decker et al. (1965), bearing in mind the inherent variability of
soil data.

There are indications that loss rates are higher in tropical
soils than in temperate climates. Whilst Agnihotri et al. (1977)
found that epoxidation was faster in tropical than temperate soils,
leading to the possibility of slower decline because of higher
dieldrin levels, Gupta & Kavadia (1979) found in India that
declines were often much faster. In one case, half of the aldrin
applied had been lost in only 38 days. Wiese & Basson (1966) also
reported comparatively high loss rates in South Africa. Using
three rates of treatment and three soils, they found that half of
the original application was lost between 1 and 2 months.

Elgar (1975) conducted a series of studies in temperate, warm
temperate, and tropical soils and reported rates of decline that
were compatible with those of Decker et al. (1965). Again, losses
from the tropical sites occurred more rapidly than from the

temperate sites. He deduced the following empirical expression to
describe loss rates, expressed as the sum of aldrin and dieldrin
residues surviving n years after a single application.

C(n) = fC(o)(1-p)^n-1

In this expression, C(o) is the initial residue level, C(n) is the
level after n years, f is the proportion remaining after the first
year, and p is the proportion lost in each of the succeeding years.
In Elgar's studies, the mean estimate of these latter two
parameters was f = 0.25 and p = 0.44, but in the Decker work, the
value of p was somewhat less. It is also possible to derive an
equation that describes the accumulation of residues in a soil
subject to a regular routine of annual applications. The
implications of this equation are that residue levels do not
continue to increase indefinitely, but reach a plateau. In the
case of Elgar's data, the plateau level, one year after the last of
n applications, would be around 60% of the level observed
immediately after the first application. This prediction is well
borne out by the soil monitoring data presented in Table 1.

Studies of the decline of residues arising from aldrin applied
for the control of termites (Bess & Hylin 1970; Carter & Stringer,
1970) reveal slower rates of decline than would be expected,
considering the deep application.

Separate studies have been carried out on dieldrin residue
losses. These show considerably slower rates of decline than in
the case of aldrin, but there is a very wide range in the data
reported. Thus, Edwards (1966) reported that the average time for
the disappearance of 95% of the residues was 8 years, but Wiese &
Basson (1966) found much faster rates. Intermediate rates were
reported by Stewart & Fox (1971) and Beyer & Gish (1980). It seems
probable that the rate of decline of dieldrin in the soil is
reasonably well reflected by Elgar's equation for the years that
succeed the first year of aldrin application.

4.1.5. Losses of residues from water

The partition of dieldrin between the vapour phase and water
was determined by a dynamic gas-flow method using ¹⁴C-dieldrin
(Atkins & Eggleton, 1970). The partition coefficient at 20 °C
(expressed on a weight/volume basis for air and water) was constant
at 540, up to a concentration of 0.033 mg dieldrin/litre water. At
higher concentrations, there was a rapid increase in the partition
coefficient, which was attributed to the aqueous solution becoming
saturated at 0.033 mg/litre. Using the values for vapour pressure
(3.47 x 10^-4Pa) and water solubility found in this study, the
wash-out ratio for the removal of dieldrin vapour from atmospheric
air by rain was 0.65. It was suggested that the concentration of
dieldrin in the rainfall in London (Abbott et al., 1965) (Table 6)
may indicate the presence of dieldrin in particulate matter in the
atmosphere rather than in the vapour phase.

Table 1. Concentrations of aldrin and dieldrin in soil^a
------------------------------------------------------------------------------------------------------------------------------
Location Year Use Number Mean concentration Comments Reference
of in mg/kg (maximum
sites value in brackets)
aldrin dieldrin
------------------------------------------------------------------------------------------------------------------------------
United aldrin: potatoes 21 0.02 0.09 LD < 0.03 mg/kg Wheatley et
Kingdom (0.12) (0.41) al. (1962)

1965 aldrin: potatoes; 10 0.15 0.48 LD not reported; apparently Davis (1968)
dieldrin: seed-dressing, (0.7) (0.7) < 0.02 mg/kg; various soil
carrots, and wheat; types; residues in soil
cumulative applications microfauna also determined
during 5 years prior to
sampling (0.14-3.4
kg/ha)

Canada

S.W. Ontario 1964-65 aldrin: various crops; 13 0.19 0.57 LD < 0.1 mg/kg; soil of Harris et al.
known usage (0.8) (1.3) various types (sandmuck); (1966)
aldrin used to a
considerable extent
(1954-60) on 27 sites

no reported use 1961-64 14 0.18 0.25
(2.1) (1.6)

none used 1954-64 5 LD LD

Atlantic 1965 aldrin: 1-5 applications LD 0.01 mg/kg; no detectable Duffy & Wong
provinces during 15 years prior to residues of aldrin or (1967)
sampling; cumulative dieldrin in orchard soils to
application 0.5-45 kg/ha; which aldrin/dieldrin had
not been applied

root crops 18 0.46 0.41
(1.5) (1.45)

vegetables 17 0.66 0.36
(2.5) (1.35)
------------------------------------------------------------------------------------------------------------------------------

Table 1. (contd.)
------------------------------------------------------------------------------------------------------------------------------
Location Year Use Number Mean concentration Comments Reference
of in mg/kg (maximum
sites value in brackets)
aldrin dieldrin
------------------------------------------------------------------------------------------------------------------------------
Southern 1971 aldrin: tobacco 4 (50 ND 0.16 LD 0.001 mg/kg; woodlots Frank et al.
Ontario samples) (0.19) were adjacent to treated (1974)
areas, but not directly
sprayed

cereals 4 (60 ND 0.16
samples) (0.19)

woodlots 12 ND trace
samples

Saskatchewan 1970 soil from 21 vegetable 41 0.03 0.06 LD 0.005 mg/kg; aldrin found Saha & Sumner
farms samples (0.28) (0.77) in 25% of samples; dieldrin (1971)
found in 55% of samples

Southern 1972-75 soil samples from LD < 0.0004 mg/kg; dieldrin Frank et al.
Ontario orchards had been used (1955-65) (1976)
at recommended rates of
0.8-1.3 kg/ha

apple: 0-15 cm 31 ND 0.03
(0.38)
15-30 cm ND 0.001
(0.03)

Southern 1972-75 sweet cherry: 16 Frank et al.
Ontario 0-15 cm ND 0.001 (1976)
(0.01)
15-30 cm ND LD

sour cherry: 12
0-15 cm ND 0.005
(0.04)
15-30 cm ND 0.003
(0.02)
------------------------------------------------------------------------------------------------------------------------------

Table 1. (contd.)
------------------------------------------------------------------------------------------------------------------------------
Location Year Use Number Mean concentration Comments Reference
of in mg/kg (maximum
sites value in brackets)
aldrin dieldrin
------------------------------------------------------------------------------------------------------------------------------
Southern peach: 11
Ontario 0-15 cm ND 0.04
(contd.) (0.11)
15-30 cm ND 0.02
(0.07)
vineyards: 16
0-15 cm ND 0.009
(0.035)
15-30 cm ND 0.004
(0.023)

USA

Seven eastern 1965 aldrin and dieldrin in 3 LD 0.05 mg/kg; proportions Seal et al.
states crops: of soil samples with (1967)
measurable residues:

peanuts: 5 ND 0.15 potatoes, 76%; carrots,
(0.20) 21%; peanuts, 100%
carrots: 19 ND 0.19
(0.26)
potatoes: 25 ND 0.10
(0.20)

1965-67 aldrin and dieldrin used 17 (278 0.02 0.21 LD 0.01 mg/kg; aldrin Stevens et al.
regularly samples) (0.47) (2.84) detected in 15% of samples (1970)
and dieldrin in 67% of
samples from areas of
regular use

limited use 16 LD 0.001
(0.001)

no known use 18 LD LD
------------------------------------------------------------------------------------------------------------------------------

Colorado 1967 aldrin: various soil 11 0.16 0.19 LD < 0.02 mg/kg; some Mullins et al.
types (1-4.3% organic (0.61) (0.44) fields had been treated (1971)
matter); nominal annually for 9 years; time
concentrations in soil at of last treatment prior to
time of application: sampling varied from 0-9
0.06-6.75 mg/kg years

dieldrin: nominal 9 ND 0.05
concentrations in soil at (0.30)
time of application:
0.13-0.63 mg/kg

Arizona 1968 3 types of soil (organic 13 LD 0.0003 LD not defined; appears to Laubscher et
matter 0.5-6.6%) from (0.0013) be about 0.0001 mg/kg; no al. (1971)
area downwind of relationship between
an area of insecticide concentration of dieldrin
use and distance from area of
application

10 major 1969 samples of soil 71 0.02 0.79 LD 0.01 mg/kg; aldrin in Wiersma et al.
areas of (0.96) (16.72) 4.2% of samples and (1972)
onion growing dieldrin in 73% of samples

9 areas 1969 samples of soil 92 0.01 0.17 LD 0.01 mg/kg; aldrin in Sand et al.
growing sweet (0.11) (2.18) 3.3% and dieldrin in 60.9% (1972)
potatoes of samples

Rice-growing 1972 samples of soil 99 0.01 0.04 LD 0.01 mg/kg; aldrin in Carey et al.
areas (0.25) (0.27) 39% and dieldrin in 85% of (1980)
samples

USA National 1970 samples of soil 1506 0.02 0.04 LD 0.01 mg/kg; aldrin in Crockett et al.
Monitoring (4.25) (1.85) 13% and dieldrin in 31% of (1974)
Program samples
(35 states)
------------------------------------------------------------------------------------------------------------------------------

12 states in 1970 average application of 12 (389 0.05 0.07 LD <0.01 mg/kg; dieldrin Carey et al.
the cornbelt dieldrin was 1.3 kg/ha samples) (2.98) (2.04) residues attributed (1973)
region primarily to the use of
aldrin; aldrin had been
used in one or more years
from 1954

14 cities 1970 soil from urban areas 356 LD 0.1 LD < 0.03 mg/kg; aldrin Carey et al.
sampled to a depth of (12.8) not detected in any (1976)
7.6 cm samples; dieldrin in
samples from 22 sites
(6.5%) in 6 cities

Japan, S.W.

Kyushu 99 0.07 0.29 LD 0.001 mg/kg Suzuki et al.
district samples (1.01) (1.73) (1973)
------------------------------------------------------------------------------------------------------------------------------
^aLD = limit of detection; ND = not determined.
The rate of dry deposition of dieldrin (vapour phase) on grass,
calculated from the results of wind tunnel studies, was 4 x 10^-2
cm/second. The average lifetime of dieldrin in the atmosphere,
assuming loss by wash-out and dry deposition only, was estimated to
be 28 weeks (Atkins & Eggleton, 1970).

The rate of transfer of dieldrin from water to air and vice
versa has been determined (Slater & Spedding, 1981). The transfer
velocity from water, measured in a wind tunnel, increased as the
air speed (measured at 6 cm above the water surface) increased.
When there was no air movement, the transfer velocity was 2.6 x
10^-5cm/second compared to 15 x 10^-5cm/second at an air velocity
of 31.1 km/h. The transfer velocity from air to water was measured
by passing air through a column of downward-flowing water, and was
found to increase as the interfacial velocity increased from 0.9 x
10^-2cm/second (at 10 km/h) to 5.2 x 10^-2cm/second (at 34.2 km/h).
It was suggested that the exchange of dieldrin between water and
air was controlled by diffusive processes either in the air
boundary or water boundary layers. The Henry's law constant (ratio
of the concentrations in air and aqueous phases at equilibrium) for
dieldrin was 1.3 x 10^-3at 20 °C. It was concluded that the
resistances to transfer of dieldrin from water to air and vice
versa were similar.

The physical and thermodynamic principles of exchanges of
chemicals between water and air have been discussed (Mackay &
Wolkoff, 1973; Liss & Slater, 1974; Mackay & Leinonen, 1975; Mackay
et al., 1979; Smith et al., 1981). An estimate of the half-life of
the evaporation of dieldrin at 25 °C from a column of water of 1 m
depth was derived by Mackay & Leinonen (1975). Although this
estimate (539 days) is not based on the most recent and reliable
values for the vapour pressure and water solubility of dieldrin, it
is probably of the right order.

4.1.6. Aldrin and dieldrin in the atmosphere

Small amounts of dieldrin have been detected in the atmosphere
(Table 6). Baldwin et al. (1977) conducted a study at Bantry Bay
on the west coast of Ireland, well away from point sources of
emission. They found concentrations of dieldrin between 0.06 and
1.6 ng/kg, with an average of 0.36 ng/kg, but no aldrin,
photodieldrin, or photoaldrin. No dieldrin was detected on solid
matter trapped on filter pads; the limit of determination ranged
from 1.1 to 7.2 pg/kg (parts per thousand trillion of air).

The reason for the very low level of occurrence of dieldrin in
the global atmosphere, if, as seems probable, a major part of the
aldrin used in agriculture escapes from the soil by evaporation,
has been the subject of considerable speculation. It appears
unlikely that direct photochemical reactions are involved, since
there have been no reports of photodieldrin being detected.
Washout by rain may be an important factor. Indeed, Baldwin et al.
(1977) cited literature figures for Hawaii of 1 - 97 ng/litre, and
Abbott et al. (1965) reported 1 - 95 ng/litre in rainfall in London
and other locations in the United Kingdom. MacCuaig (1975), on the

other hand, working in the vicinity of a dieldrin application in
Ethiopia, reported 100 µg/litre in rainwater. These results
support the suggestion of Atkins & Eggleton (1970) that, though
washout of the atmosphere by rain would be inefficient in the case
of dieldrin, it could lead to substantial losses. If this were so,
dieldrin deposits would be expected on soil adjacent to treated
areas, but the fact that large areas of soil in the cornbelt of the
USA (Carey et al., 1973) have no detectable levels of aldrin or
dieldrin seems to cast doubt on the extent to which rain acts to
disperse aldrin and dieldrin onto untreated land near to treated
areas.

It would appear possible, therefore, that there are losses of
aldrin and dieldrin in the atmosphere. Glotfelty (1978) mentioned
the high reactivity of free radical species in the atmosphere, in
particular hydroxyl radicals. These could presumably play an
important role in the degradation of molecules occurring as vapour.

4.1.7. Aldrin and dieldrin in water

The data regarding the occurrence of aldrin and dieldrin in
both ground and surface waters are summarized in Table 7 (section
5.1.3). As would be expected from the extreme resistance of
dieldrin and, especially, aldrin to leaching from soil, the
occurrence of either compound in groundwater is rare. Spalding et
al. (1980) took a series of groundwater samples in Nebraska, USA,
where aldrin had been used extensively for the control of corn
rootworm and could not detect it in any of the samples. Their
limit of determination was between 5 and 10 ng/litre. Junk et al.
(1980) reported somewhat similar results from Nebraska. Richard et
al. (1975), in a wide-ranging study, examined the water supplied to
a series of cities in Iowa, USA, from boreholes. Again, no aldrin
or dieldrin was reported; their limit of determination appears to
have been 0.5 ng/litre.

Surface waters, by contrast, have often been reported to
contain small amounts of dieldrin. In a programme of sampling
various surface waters in Iowa, Richard et al. (1975) reported
levels of dieldrin ranging from 3 to 75 ng/litre in rivers and
streams and levels in reservoirs from 3 to 18 ng/litre. In rivers
in Iowa and Louisiana, levels ranged from < 1 to 42 ng/litre.
During the period 1976 - 80, dieldrin was found in 2.4% of samples
from national surface waters in the USA, (maximum concentration of
0.61 µg/litre) and in 21.7% of national surface water sediments
(maximum concentration of 5300 µg/kg) (Carey & Kutz, 1985).

The dieldrin in surface water probably comes from run-off from
treated land. Sparr et al. (1966) sampled drainage ditches and a
river in a maize growing area in northwest Indiana, USA. Levels
reached 0.6 µg/litre in the river but, in the ditches from fields
treated with aldrin at up to 5.6 kg/ha, levels seldom exceeded the
limit of determination (0.05 µg/litre). Water draining from rice
paddies that had been planted with aldrin-treated seed also
contained small amounts of dieldrin (1 µg/litre after seeding and

falling by the 14th week to 0.07 µg/litre). The authors calculated
that about 1 g of aldrin had been lost from the rice paddy surface
water during the whole 14-week period.

Hindin et al. (1964) reported aldrin in irrigation water up to
2.3 µg/litre, but no dieldrin. However, in view of the readiness
with which aldrin is epoxidized to dieldrin in surface waters,
there must be some doubt as to the identity of the residue they
actually measured.

It does appear that dieldrin can occur in surface waters
draining from agricultural areas, but the amounts are usually so
small that they could not be expected to represent a major
proportion of the product applied to the soil. The ultimate fate
of these small levels of dieldrin in water is not known. It is
probably that adsorption onto particulate matter, volatilization,
and various degradation mechanisms all play a role.

4.2 Translocation From Soil Into Plants

The uptake of aldrin and dieldrin by plants is much higher in
root crops than in grain crops. It is influenced by the levels in
soils, the strength of adsorption, and the depth of application.

In grain crops, it is rare for residues to reach detectable
levels in the grain (FAO/WHO, 1970a; Gupta & Kavadia, 1979). Root
crops are much more prone to take up residues from treated soils,
as observed by Harris & Sans (1967) who found that carrots,
radishes, and turnips had the highest residues. Onions, lettuce,
and celery were intermediate and cole crops showed no detectable
uptake at all (Lichtenstein, 1959).

The level of aldrin and dieldrin in the soil influences the
degree of uptake as shown by Lichtenstein et al. (1970) and Edwards
(1973a,b), who both reported on ratios of the concentrations in
plants to those in the soil. Further work by Onsager et al.
(1970), Voerman & Besemer (1975), Bruce & Decker (1966), and Saha
et al. (1971) provided compatible results.

The availability of aldrin and dieldrin for uptake by plants
depends on the strength of adsorption by the soil and especially
the organic matter fraction. Harris & Sans (1967), Beall & Nash
(1969), Beestman et al. (1969), and Nash et al. (1970) demonstrated
that crops tend to take up more residues from soil of low than of
high organic matter. Adding activated charcoal to soil reduced
dieldrin uptake by 70% or more in carrots and potatoes
(Lichtenstein et al., 1971).

Deep application of dieldrin greatly reduces the uptake (Beall
& Nash, 1972). Residues in the plants from a deep (31 - 32 cm)
application were only 1% of those from superficial application.
The authors commented that a possible treatment for reducing the
uptake of old soil residues by crops would be simply to plough them
under.

The mechanism of uptake by crops is not entirely clear and
appears to vary considerably from species to species. Beall & Nash
(1971), in work with soyabeans grown on soil treated with ¹⁴C-
labelled dieldrin, found that residues were taken up both by
absorption through the roots and by absorption of vapour through
the leaves. In the case of cereals, it seems unlikely that root
uptake occurs to any great extent (Powell et al., 1970; Gutenmann
et al., 1972; Gupta et al., 1979). This probably accounts for the
very low levels found in cereal grains from treated crops. On the
other hand, it would seem almost certain that it is root uptake
which accounts for the residues found in root crops.

4.3. Models of the Behaviour of Water and Chemicals in Soil

Various models for the movement of water and chemicals in
porous media have been developed, based on physical variables such
as vapour pressure, diffusibility, and adsorption, etc. (Keller &
Alfaro, 1966; Bresler & Hanks, 1969; Lindstrom et al., 1971;
Davidson & McDougal, 1973; Pionke & Chester, 1973; Van Genuchten et
al., 1974). Models for run-off from soil have also been proposed
(Crawford & Donigian, 1973; Bailey et al., 1974; Bruce et al.,
1975). These models may be useful as a means of defining more
precisely the behaviour of aldrin and dieldrin in soil.

4.4. Biodegradation of Aldrin and Dieldrin

When used to protect crops from soil insects, aldrin is usually
incorporated into the soil in which the plants are grown. For this
reason, most of the work on the biodegradation of aldrin in
agriculture has been concerned with the soil system.

4.4.1. Epoxidation of aldrin

The most important transformation of aldrin in the soil is its
conversion by epoxidation to dieldrin (Fig. 2, section 6.3.1.1).
Epoxidation, essentially biological in nature (Lichtenstein &
Schulz, 1960), occurs in all aerobic and biologically active soils,
and about 50 - 70% of the residues remaining in a soil at the end
of the season in which the application was made consist of
dieldrin. Lichtenstein & Schulz (1959) reported that epoxidation
was slower on peat than on mineral soils and was inhibited at low
soil temperatures; very little conversion occurred at 7 °C.
Subsequently, many authors have demonstrated that a large number of
microorganisms are capable of promoting epoxidation, and these were
reviewed by Tu & Miles (1976).

Aldrin is also epoxidized by plants, as demonstrated by Gannon
& Decker (1958), while Yu et al. (1971) have showed that root
homogenates are very effective promoters of aldrin-to-dieldrin
epoxidation.

Aldrin is not epoxidized under anaerobic conditions. In their
studies on the degradation of aldrin in anaerobic cultures of
sewage sludge, Hill & McCarty (1967) found no dieldrin, although
aldrin was completely decomposed within 60 days. Sethunathan (1973)
reported that epoxidation of aldrin was arrested in flooded soils.

4.4.2. Other metabolic pathways of aldrin

The transformation of aldrin in the soil to aldrin dicarboxylic
acid (V, Fig. 2) appears to be well established (Klein et al.,
1973; Kohli et al., 1973b; Weisgerber et al., 1974). The
occurrence of photodieldrin (III, Fig. 2) as a metabolite derived
from aldrin soil treatment is less well established either in soil
(Lichtenstein et al., 1970) or in the leaves of wheat grown in
aldrin-treated soils (Weisgerber et al., 1974).

4.4.3. Biotransformation of dieldrin

Dieldrin is much more resistant to biodegradation than aldrin,
and microbial degradation is probably a minor route of loss from
soils, even under anaerobic conditions (Sethunathan, 1973; El Beit,
1981). Kohli et al. (1973b) added ¹⁴C-labelled dieldrin to a soil
and detected very little degradation, though he did report trace
quantities of photodieldrin. Similarly, small amounts of
photodieldrin were detected after dieldrin had been applied to
onion seed (Kohli et al., 1972).

In the search for organisms that would degrade dieldrin,
Matsumura & Boush (1967) found that only a few soil samples
produced detectable transformation of dieldrin, although, in some,
up to 6% of the dieldrin added was transformed to water-soluble
metabolites. Separation of the organisms responsible revealed that
Pseudomonas, Bacillus, and Trichoderma species were able to attack
the dieldrin molecule. Tu & Miles (1976) list organisms that have
been reported to attack dieldrin; these include bacteria, fungi,
and one actinomycete.

In spite of the large number of studies on this topic, it is
difficult to estimate the extent to which photodieldrin is evolved
in soils treated with aldrin. It is perhaps significant that the
microorganisms capable of producing photodieldrin in the laboratory
have been isolated mainly from anaerobic environments, so that
their activity would be very limited in a well-managed agricultural
soil. This is borne out by the study of Suzuki et al. (1974) who
sampled 52 soils with a history of aldrin treatment in Japan.
Photodieldrin levels were very low compared with dieldrin levels
and ranged from < 0.001 to 0.035 mg/kg soil (section 4.4.2.1).

The further fate of photodieldrin in soils has received little
attention, but Weisgerber et al. (1975) considered it to be less
persistent in the soil than dieldrin itself. They also identified
two breakdown products, the bridged equivalent of aldrin
dihydrochlordene dicarboxylic acid (XII, Fig. 2) and the bridged
equivalent of the transdiol (XI, Fig. 2), though these were only
present in very small amounts.

4.4.4. Conclusions

Although many studies have been carried out on the
biodegradation of aldrin and dieldrin, it seems improbable that
this is a major source of loss from soil. On the other hand, it

does seem as if transformation of aldrin to aldrin acid in aldrin-
treated soils can be a significant pathway, although there is
little evidence in the literature that aldrin acid occurs widely as
an environmental residue.

4.5. Abiotic Degradation

Abiotic processes play a limited role in the degradation of
aldrin and dieldrin in the environment. Of these abiotic processes,
the greatest amount of research has been carried out on photochemically
induced changes.

4.5.1. Photochemistry

Aldrin and dieldrin are susceptible to chemical change as a
result of irradiation. Robinson et al. (1966b) assigned structure
III (Fig. 2) to the transformation product generally referred to as
"photodieldrin".

Rosen & Carey (1968) demonstrated the formation of the
unepoxidized analogue from aldrin (photoaldrin) (XIII, Fig. 2) when
aldrin was irradiated by sunlight or UV light in abiotic conditions,
but the major reaction product under these conditions was an
unbridged product where a single chlorine atom had been lost at the
3 position. The addition of benzophenone greatly enhanced yields of
photoaldrin from aldrin and also photodieldrin from dieldrin.
Fischler & Korte (1969) showed that other ketones also increased the
formation of photodieldrin.

4.5.1.1 Photochemistry of aldrin and dieldrin in water

Henderson & Crosby (1968) demonstrated that saturated aqueous
solutions of dieldrin exposed outdoors to sunlight produced
photodieldrin. However, Ross & Crosby (1974, 1975) found that when
oxygenated aqueous solutions of aldrin were irradiated with UV
light there was little effect in the absence of sensitizers. The
addition of acetone or acetaldehyde led to epoxidation; no caged
products were formed. Aldrin in rice paddy water was epoxidized
but not in the absence of irradiation. Ross & Crosby (1985) showed
that a series of amino acids present in natural waters and even
humic acids were capable of initiating photooxidation of aldrin to
dieldrin in natural sunlight.

Further evidence for the role of oxidants in the photo-
transformation of aldrin was reported by Draper & Crosby (1984).

4.5.1.2 Photochemistry of aldrin and dieldrin in air

As noted by Miller & Zepp (1983), data on the atmospheric
photodegradation of aldrin and dieldrin are sparse. Turner et al.
(1977) reported small levels of photodieldrin above a field of
grass that had been treated with dieldrin, but considered that it
had arisen from volatilization of the photodieldrin from the
foliage rather than from formation in the air itself.

In their studies on the occurrence of dieldrin and its
photoisomer in the atmosphere on a global scale, Baldwin et al.
(1977) reported detectable levels of dieldrin (0.35 ng/m³) but were
unable to detect any photodieldrin (limit of determination of
approximately 0.1 ng/m³) and considered, therefore, that
photodieldrin does not accumulate in the atmosphere.

4.5.1.3 Photochemistry of aldrin and dieldrin on plant surfaces

MacCuaig (1975) reported substantial conversion of dieldrin to
photodieldrin on the leaves of plants growing in areas of Africa
sprayed for locust control. In a more detailed study, Turner et
al. (1977) reported the formation of photodieldrin on grass that
had been sprayed with dieldrin. They also found that it was lost
fairly readily from the foliage but were uncertain whether
evaporation was the sole cause.

Harrison et al. (1967) demonstrated the rapid epoxidation of
aldrin to dieldrin on apple leaves. Ivie & Casida (1970) showed
that rotenone had a very marked effect on the rate of
transformation of leaf deposits to photodieldrin and found its
activity as a sensitizer to be some 100 times that of benzophenone.

4.5.1.4 Photochemistry of aldrin and dieldrin in soils

Lotz et al. (1983) studied the irradiation of aldrin on a
series of mineral substrates. The substrate had a marked influence
on the rate of aldrin loss, river sand showing the greatest effect.
El Beit et al. (1983) irradiated dieldrin in contact with various
substrates and found that degradation was less in the case of a
clay soil than a glass surface. However, the relevance of some of
the laboratory studies to the practical situation is questionable
because of the frequent use of very hard UV as the radiation
source.

It appears that photodieldrin does not occur in large amounts
in aldrin-treated soil. Lichtenstein et al. (1970) treated a field
soil with very high levels of aldrin and found that 98 - 99% of the
surviving residues 6 or 10 years after the last treatment were in
the form of dieldrin. Photodieldrin formed 1.6% of the dieldrin
residue. Suzuki et al. (1974) sampled 52 soils with a history of
aldrin treatment in Japan and measured dieldrin levels ranging from
0.002 to 1.73 mg/kg and photodieldrin levels ranging from < 0.001
to 0.035 mg/kg.

4.5.1.5 Conclusions

The photochemistry of aldrin and dieldrin has been intensively
studied and it seems that the use of dieldrin for certain disease
vector control operations could lead to photodieldrin formation,
although its persistence seems uncertain. Current uses would seem
unlikely to represent a significant source, and it is doubtful
whether photodieldrin occurs widely in the environment.

4.5.2. Other abiotic processes

4.5.2.1 Reaction with ozone

Ross et al. (1976) reported that ozonization of water
contaminated with dieldrin led to substantial reductions in
dieldrin levels and suggested that this process could be used
commercially to help clean-up contaminated water.

4.5.2.2 Clay-catalysed decomposition

Fowkes et al. (1960) showed that clay diluents in the dust
formulations of many pesticides caused decomposition. In the case
of aldrin and dieldrin, the most pronounced reactions occurred with
kaolinite and attapulgite, especially when they were acidic. In
the case of kaolinite at 65 °C, the half-life of dieldrin was 400
min, which was reduced to only 30 min when the kaolinite had been
acidified. Although, these effects were observed at relatively
high temperatures, it is possible that this type of decomposition
could be significant in the soil environment, though evidence for
this has not been reported.

4.6. Bioaccumulation

The relationship between the bioaccumulation factor and the
partition coefficient (K_ow) of a chemical between octanol and water
has been investigated intensively for a number of compounds. The
partition coefficient has been shown to be a useful preliminary
indicator of the tendency for a chemical to accumulate in
organisms, particularly aquatic ones. The partition coefficient of
hydrophobic compounds is usually given as its logarithm (log₁₀
K_ow). The values reported for aldrin and dieldrin (Briggs, 1981)
are 7.4 and 6.2, respectively.

Estimates of the bioaccumulation factors for aquatic organisms,
determined under controlled laboratory conditions, are given in
Table 2.

Aldrin bioaccumulates and biomagnifies mainly in the form of
its conversion products. In one model ecosystem study (Metcalf et
al., 1973), conversion to dieldrin occurred rapidly and nearly
quantitatively. Only 0.5% of the original radioactive aldrin was
stored as aldrin in the mosquitofish (Gambusia affinis), which was
the organism at the top of this model food chain.

The uptake of dieldrin from water (0.1 - 1 mg/litre), after
4 h, by three species each of fungi, streptomycetes, and bacteria
gave ratios for the concentration of dieldrin in cells or mycelia
to that in the supernatant ranging from 0.3 to more than 100. The
rate of uptake of dieldrin by mycelia of Streptomyces venezuelae
and Trichoderma viride was very rapid, reaching equilibrium after
about 15 min (Chacko & Lockwood, 1967).

Table 2. Bioaccumulation of dieldrin
-----------------------------------------------------------------------------------------
Species Concentration in Duration Bioaccumulation Reference
water (µg/litre) of factor
or food (mg/kg) exposure
-----------------------------------------------------------------------------------------
Guppy 0.8, 2.3, or 4.2 32 days whole fish: 12 500 Reinert (1972)
(Poecilia reticulata)

Sailfin molly 0.075 34 weeks muscle: 3900 Lane &
(Poecilia latipinna) gill: 50 100 Livingston
(1970)

1.5 34 weeks muscle: 4900 Lane &
gill: 36 400 Livingston
(1970)

Channel catfish 0.013 70 days dorsal muscle: 2400 Shannon
(Ictalurus punctatus) 0.027 70 days 1800 (1977a)
0.049 70 days 3300

small 0.075 28 days dorsal muscle: 2300 Shannon
large 0.075 28 days 3600 (1977b)
small 2 mg/kg food 28 days 0.27
large 2 mg/kg food 28 days 0.62

Sculpins 0.017, 0.17, or 32 days whole fish: 13 300 Chadwick &
(Cottus perplexus) 0.86 Brocksen
(1969)

Alga 1, 5, or 20 14 days 1300 (based on dry Reinert (1972)
(Scenedesmus obliquus) weight of alga)

Waterflea 2.1, 4.5, or 6 days 14 000 (dry weight) Reinert (1972)
(Daphnia magna) 12.8

Common frog
(Rana temporaria) 0.8 2 days whole body 387.5 Cooke (1972)

Common toad 20 2 days whole body 280 Cooke (1972)
(Bufo bufo)

Barn owl 0.5 mg/kg food 2 years carcass: 18.8 Mendenhall et
(Tyto alba) al. (1983)

Short-tailed shrew 50 mg/kg food 17 days carcass: 1.6 Blus (1978)
(Blerina brevicauda)

Mink 2.5 mg/kg food 4-10 weeks fat: 8.4 Aulerich et
(Mustela vision) al. (1972)
-----------------------------------------------------------------------------------------
The uptake of ¹⁴C-dieldrin by Chlorella pyrenoidosa or by six
species of marine algae (Skeletonema costatum, Tetraselmis chuii,
Isochrysis galbana, Olisthodiscus luteus, cyclotella nana,
Amphidinium carteri) has been studied. In Chlorella pyrenoidosa,
rapid penetration of algal cells occurred and a maximum
radioactivity was reached after 6 - 24 h, whereas in the six marine
algae, it was reached within 1 h. From the study on Chlorella, it
was concluded that the movement of dieldrin into subcellular
organelles occurs within 72 h, and that algae are scavengers of
dieldrin. The study on the six marine algae showed that there was
no correlation between the dieldrin accumulation in the different
algae and the number of cells per ml culture. However, the amount
accumulated was related to the concentration of dieldrin in the
culture (range, 1 - 1000 µg/litre), and, for each algal species, to
the number of cells per culture. No metabolites were detected
(Wheeler, 1970; Rice & Sikka, 1973).

In studies by Jefferies & Davis (1968), medium size worms
(Lumbricus terrestris) were placed in containers, and water and
dieldrin-treated compost were added to give a final concentration
of 25 mg dieldrin (nominal)/kg moist compost. The containers were
kept at 10 °C for 20 days, and the worms were then collected. The
average concentration of dieldrin in six batches of worms ranged
from 18.4 - 24.9 mg/kg live weight of worms.

When two species of earthworms (Lumbricus terrestris and
Allolobophora caliginosa) were placed in containers with compost
containing 17 mg dieldrin/kg for 4 weeks at 10 °C, the mean
concentration of dieldrin in Lumbricus terrestris (two studies) was
13.3 mg/kg live weight. The gut content of L. terrestris was
determined using worms kept in compost (32 mg dieldrin/kg) for 20
days. The mean concentration of dieldrin in whole worms was 13.8
mg/kg live weight, the air-dried gut contents constituted 11.3% of
the total live weight, and the mean dieldrin concentration in the
tissues of the dissected worms was 10.8 mg/kg tissue. The uptake
of dieldrin by L. terrestris was compared with that by A.
caliginosa; after 4 weeks, the concentration of dieldrin in A.
caliginosa (27.3 mg/kg) was more than twice that in L. terrestris.
The concentrations of dieldrin in A. caliginosa placed in five
different soils for 4 weeks are given in Table 3 (Davis, 1971).
Table 3. The concentration of dieldrin in A. caliginosa placed in five different
soils for 4 weeks^a
-------------------------------------------------------------------------------------
Soil type Estimated concentration Organic matter Mean concentration of dieldrin
of dieldrin (mg/kg air- (% w/v) in A. caliginosa (mg/kg)
dried soil)
-------------------------------------------------------------------------------------
Peaty loam 3.1 30.1 0.23
Organic loam 2.7 6.6 0.78
Loamy sand 1.7 1.3 2.99
Silty loam 2.2 2.8 3.56
Clay loam 2.0 1.7 4.55
-------------------------------------------------------------------------------------
^aFrom: Davis (1971).
A number of field studies have been carried out in which the
concentrations of aldrin and dieldrin in earthworms from fields
treated with aldrin were determined. Six species of earthworms
were collected from a field to which excessive applications of
aldrin had been made for 8 years, and two species from experimental
plots to which dieldrin had been applied (single treatment).
Samples of soil and earthworms from the aldrin-treated fields were
analysed for aldrin and dieldrin, and the mean concentrations in
the worms are given in Table 4. The overall mean geometric
concentrations in soil (dry weight) were 0.72 mg/kg (aldrin) and
0.64 mg/kg (dieldrin). It was suggested that residual soil in the
gut may have contributed appreciably to the residues of aldrin in
the earthworms. The low residues in L. terrestris, relative to the
other species, were attributed to the deeper burrowing behaviour of
this species, which enable it to live in non-treated layers of soil
for part of its life. The concentrations of dieldrin in the soil
and earthworms from the experimental plots 6 months after treatment
with dieldrin are given in Table 5. The relationship between the
concentration of dieldrin in the two species of earthworms and the
concentration in the soil was thought to be given by the function,
W = aS^b, where W is the concentration of dieldrin in the earthworm
and S the concentration in the soil. The fact that the estimated
value of b (0.794) was significantly less than unity indicates that
residues tend to be relatively greater in worms when the
concentrations in the soil are low than when higher concentrations
are present (Wheatley & Hardman, 1968).

Table 4. Mean concentrations of aldrin and
dieldrin in six species of earthworms from
aldrin-treated fields
--------------------------------------------
Species Geometric mean concentration
(mg/kg wet weight)
Aldrin Dieldrin
--------------------------------------------
L. terrestris 0.053 1.6
A. longa 0.28 2.2
A. caliginosa 0.52 3.8
A. chlorotica 0.98 4.6
A. rosea 0.64 3.9
O. cyaneum^a 0.84 2.4
--------------------------------------------
^aOne sample only.

Beyer & Gish (1980) measured the concentrations of dieldrin in
four species of earthworms collected from a depth of 0 - 50 cm in
plots that had received a single surface application of a dieldrin
wettable powder (0.6, 2.2, or 9 kg dieldrin/ha). Samples of
earthworms were collected over a period of 11 years, and the
following relationship was derived between the concentration of
dieldrin in the worms and the time interval between dieldrin
application and worm collection:

C(n) = aE^bn

where C(n) is the concentration in the earthworms n years after
soil treatment, and a and b are constants calculated from the data.
The mean values of a and b were as follows:

Application rate a b
(kg dieldrin/ha)

0.6 7.8 -0.41
2.2 21 -0.32
9.0 53.5 -0.16

The average time required for the initial residues of dieldrin in
soil to be reduced by 50% was 5.1 years, and the corresponding time
for dieldrin in earthworms was 2.6 years (Beyer & Gish, 1980).

Table 5. Concentrations of dieldrin in the soil and earthworms
from experimental plots 6 months after treatment with aldrin
---------------------------------------------------------------
Applied dieldrin Concentrations of dieldrin^a (mg/kg)
(kg/ha) (nominal) Soil^b A. longa^c A. chlorotica^c
(dry weight)
---------------------------------------------------------------
0 0.003 0.033 0.028
0.50 0.50 0.70 1.8
0.75 0.85 1.0 2.0
1.0 1.1 1.3 2.9
1.25 1.2 1.3 2.1
---------------------------------------------------------------
^aGeometric means.
^bSoil samples taken 6 weeks before earthworm samples.
^cWet weight.

In studies by Gish & Hughes (1982), small experimental pasture
plots were sprayed with a suspension of a dieldrin wettable powder
at application rates of 0.56, 2.24, or 8.97 kg dieldrin/ha.
Samples of soil and earthworms were collected on 12 occasions over
a period of 2 years, the soil being sampled to a depth of 2.5 cm.
The concentration of dieldrin in the soil did not decline during
the 2-year period, but that in the earthworms from the two plots
treated at the two lower rates declined significantly. The maximum
concentration of dieldrin in the earthworms occurred 4 months after
treatment. The ratios of dieldrin concentration in earthworms to
that in the soil were examined. Residues in earthworms averaged
166 times those in soil in the sampling period 4 months after
application when earthworm residues reached a maximum. The effects
of several variables on the concentration of dieldrin in earthworms
was investigated, and a multiple regression relationship,
incorporating five variables, accounted for about 77.2% of the
variability of the residues in earthworms.

The accumulation of dieldrin in live fish-food organisms,
tubificid worms, and midge larvae (Chironomidae) was investigated
by Chadwick & Brocksen (1969), in Daphnia magna by Johnston et al.
(1971) and Reinert (1972), in crab (Leptodius floridanus) and
Artemia salina nauplii by Epifanio (1973), in mollusc (Rangia

cuneata) and blue crab (Callinectes sapidus) by Petrocelli et al.
(1973, 1975), in oyster (Crassostrea virginica) by Mason & Rowe
(1976) and Emanuelsen et al. (1978), and in an ostracod
(Chlamydotheca arcuata) by Kawatski & Schmulbach (1972). These
studies were carried out at concentrations (in fresh water or sea
water) of 0.5 - 100 µg/litre or by feeding feed or organism
containing aldrin or dieldrin. The duration of the studies was a
few days up to 43 days. In all organisms, there was a rapid
increase of dieldrin concentration in organs and tissues. A steady
state was reached after 3 - 4 and 2 days, respectively, in Daphnia
magna and Cassostrea virginica. In all organisms tested, the
elimination was slow and the half-life of dieldrin for tubificed
worms and Crassostrea virginica was approximately 16 days and 75 h,
respectively.

The rate of insecticide accumulation is partly dependent on the
concentration in the water, the duration of exposure, and the
activity of the animals. The concurrent feeding of aldrin- or
dieldrin-containing feed did not have a significant effect on
dieldrin accumulation. It can be concluded that water is the
principle source of dieldrin accumulation (Kawatski & Schmulbach
1972; Reinert, 1972; Epifanio, 1973).

A number of studies on different species have been carried out
by Gakstatter (1968) (Carassius auratus), Chadwick & Brocksen
(1969) (Cottus perplexus), Lane & Livingston (1970) (Poecilia
latipinna), Hogan & Roelofs (1971) (Lepomis cyanellus), Ludke et
al. (1972) (Notemigonus chrysoleucas, Gambusia affinis, Lepomis
cyanellus, L. macrochirus, Ictalurus natalis), Reinert (1972)
(Poecilia reticulata), Wells et al. (1973) (Gambusia affinis),
Wells & Yarbrough (1973) (Gambusia affinis), Addision et al.
(1976), (Salmo salar), and Shannon (1977a,b) (Ictalurus
punctatus). In these studies, dieldrin was added to the water at
different concentrations, and in a few of the studies the dieldrin
was radiolabelled. Distribution and accumulation were examined in
various organs and tissues (section 6.3.1.3).

Chadwick & Brocksen (1969) found that the accumulation of
dieldrin in whole fish (sculpins) was related to the concentration
in the water (0.017 - 8.6 µg/litre) and appeared to reach a steady
state by day 32. Reinert (1972) found such a state after only 17
days in Poecilia reticulata. Shannon (1977a) studied this aspect
in channel catfish (Ictalurus punctatus) (length 15 cm) exposed
continuously to 0.013, 0.027, or 0.049 µg dieldrin/litre. The
concentration of dieldrin in dorsal muscle increased in a
curvilinear fashion. Little change occurred within 56 days in the
two lower exposure groups, but a significant increase occurred in
the 0.049 µg/litre group. Steady-state concentrations appear to
have been established in the dorsal muscle of the fish exposed to
the two lower concentrations (but not in those exposed to 0.049
µg/litre) after 56 - 70 days.

Feeding studies using dieldrin-contaminated tubificid worms
(25 - 350 mg/kg) as food source showed that the retention of
dieldrin by sculpins was inversely related to the amount of
dieldrin they consumed. However, sculpins fed worms containing
0.4 - 26 mg dieldrin/kg did not show this relationship. It was
suggested that the metabolism and excretion of dieldrin was
stimulated at the higher concentrations. The findings showed that
a maximum of 16% of the dieldrin accumulated would have come from
the contaminated food. Thus dieldrin is accumulated in fish far
more readily from water than from food (Chadwick & Brocksen, 1969;
Reinert, 1972).

In studies on sailfin molly (Poecilia latipinna), exposed to
concentrations of 0.75 and 1.5 µg/litre for 34 weeks (flow-through
system), Lane & Livingston (1970) found that the ratio of the
concentration of dieldrin in the tissues to that in water in the
steady state was about 10 000.

From a study on green sunfish (Lepomis cyanelles) that were
exposed to dieldrin at 6 µg/litre for 124 - 139 h, it was concluded
that the lethal concentrations of dieldrin in blood and brain were
approximately 6 and 9 mg/kg tissue, respectively (Hogan & Roelofs,
1971).

Shannon (1977b) exposed channel catfish to 0.075 µg
dieldrin/litre water and/or 2 mg dieldrin/kg food for 28 days.
Small (15 - 22.5 cm) and larger fish (3 - 40 cm) were used and
dorsal muscle of the fish was analysed. After 28 days, fish
exposed to 0.075 µg/litre had a mean concentration of dieldrin in
muscle of 0.175 (small fish) and 0.274 (large fish) mg/kg tissue,
fish fed 2 mg dieldrin/kg contained 0.544 (small fish) and 1.243
(large fish) mg/kg tissue, and those given the combined treatment
contained 0.898 (small fish) and 2.418 (large fish) mg/kg tissue.
The elimination of dieldrin from the dorsal muscle in clean water
showed that when fish were exposed to dieldrin in water only, a 50%
decrease took place in 8 days. For fish exposed to dietary or
combined exposure, it required 20 days.

In a study with different early-life stages of rainbow trout,
the bioconcentration factor in the different stages was determined
using ¹⁴C-dieldrin. It increased during embryonic development from
120, reached a maximum at the sac fry stage of 12 000 and fell
again at the early fry stage to 1500. The clearance rate constant
sharply increased at the early fry stage. Almost all the dieldrin
was recovered from the yolk (Van Leeuwen, 1986).

The yolks of eggs from chickens fed aldrin or dieldrin
(1 mg/kg) or 10 mg dieldrin/kg for 2 years contained dieldrin
concentrations of 6 - 25 mg/kg (Brown et al., 1965). Several other
studies on the accumulation of dieldrin into avian eggs have been
made, details of these being given in Tables 17 and 18 (section
5.1.6).

Clark (1975) fed red-winged blackbirds (Agelaius phoeniceus) a
diet containing 10 mg aldrin/kg, some of the birds being
artificially stressed. The mean number of days that the birds
survived was 29.9 for unstressed and 22 for stressed birds. The
mean values of brain residue levels at death were 19.8 mg
dieldrin/kg for unstressed birds and 22.2 mg dieldrin/kg for
stressed birds. Three unstressed birds, sacrificed after 76 days,
had dieldrin levels of 6.7, 7.28, and 7.4 mg/kg. The carcass
levels of dieldrin increased linearly with time and showed no
tendency to level off, as occurred in the brains of unstressed
birds. The three unstressed birds sacrificed had the highest
carcass dieldrin levels (70.3, 82.8, and 147 mg/kg).

Stickel et al. (1969) fed Japanese quail (Coturnix coturnix
japonica) diets containing 2, 10, 50, or 250 mg/kg dieldrin for up
to 158 days. The mean dieldrin levels in the brain of dead and
sacrificed birds were 18.25 mg/kg and 3.35 mg/kg (wet weight),
respectively, while the mean liver residues were 19.7 mg/kg (wet
weight) and 28.8 mg/kg (wet weight), respectively.

Mendenhall et al. (1983) fed captive barn owls (Tyto alba)
with diets containing 0.5 mg/kg dieldrin for 2 years. The mean
carcass residues were 9.4 mg/kg (wet weight) after 2 years, and the
mean dieldrin levels in eggs were 3.6 mg/kg in the first year and
8.1 mg/kg in the second.

Enderson & Berger (1970) fed each of three captive female
prairie falcons (Falco mexicanus) with 11 starlings, one per day.
The starlings had been treated for 14 days with 10 mg/kg dieldrin
in their diet. One bird died and showed levels of dieldrin in
brain, liver, and muscle of 11, 29, and 4.6 mg/kg (wet weight),
respectively. The other two were sampled and found to have mean
adipose tissue and brain levels of 532 and 5.84 mg/kg,
respectively. The authors also fed wild falcons for 6 weeks prior
to egg laying. The analysis of one egg from each clutch showed a
mean egg dieldrin content of 41.5 mg/kg, and the mean adipose
tissue level of dieldrin in dosed adult falcon, was 83 mg/kg
dieldrin.

Turtles (Pseudemys scripta elegans) were given intraperitoneal
injections of dieldrin (20 mg/kg body weight) and the accumulation
in organs and tissues was determined over a period of 70 days. The
turtles were fasted during the study. The rate of absorption of
dieldrin into the tissues was slow, and there were no clear
indications of an approach to steady-state concentrations by day
70. The highest levels of dieldrin were found in body fat and
liver, and the levels in plasma and brain were also high (Pearson
et al., 1973).

Cooke (1972) studied the effect of dieldrin at nominal
concentrations of 0.0008, 0.02, or 0.5 mg/litre on groups of 40
common frog (Rana temporaria) tadpoles with hindlimb paddles or
hind legs. The exposure lasted 24 or 48 h in amphibian saline. At
the highest dose level the mean dieldrin content after 48 h
exposure was 42.9 mg/kg tissue. At the dose levels of 0.0008 and

0.02 mg/litre, there were 0.31 and 6.1 mg/kg dieldrin in tissues,
respectively. Toad (Bufo bufo) tadpoles exposed to 0.02 or 0.5
mg/litre contained 138 mg dieldrin/kg tissue at the higher dose
level, after 48 h, and 5.6 mg/kg at the lower.

A laboratory study was undertaken concerning the lethal brain
levels for dieldrin in adult and juvenile brown bats (Myotis
lucifugus), using 47 female bats collected from a church attic in
Maryland, USA. Meal worms containing an average of 0.38 mg
dieldrin/kg (wet weight) were fed to the bats for 52 days, and then
untreated worms were administered for another 22 days. The amount
of dieldrin in bats increased during dosing and decreased
afterwards. These changes did not appear as changes in average
dieldrin concentrations in the fat because the amounts were highly
variable. During the exposure period a continuous build up of the
concentration in fat was seen, but an equilibrium was not reached.
The initial half-life for dieldrin loss was estimated to be 24
days. Measurable dieldrin was found in the brains of only 6 out of
47 bats. The levels measured (0.5 to 0.9 mg/kg tissue) were all
far below lethal levels. The highest dieldrin level determined in
the carcass of 37 bats was 110 mg/kg tissue (lipid weight) (Clark &
Prouty, 1984).

Short-tailed shrews (Blerina brevicauda) were fed diets
containing dieldrin (nominal concentrations of 50, 100, or 200
mg/kg diet) for up to 14 days. All of the animals fed 50 mg/kg
survived, but all those fed 200 mg/kg died. The mean dieldrin
concentration in the brains of 14 shrews that died was 6.8 mg/kg
(range, 3.7 - 12.6). Some animals sacrificed after 17 days of
feeding the 50 mg/kg diet contained mean residues in the brain of
1.8 mg/kg and in the carcass of 58 mg/kg. After 14 days on an
untreated diet, the concentrations in the carcass declined by 76%
in both sexes, and in the brain by 59% and 84% in males and
females, respectively. The half-life of dieldrin was estimated to
be less than 14 days (Blus, 1978).

Male mink (3 months old) were fed a diet containing dieldrin
(nominal concentrations of 0 and 2.5 mg/kg diet) for 10 weeks, and
samples of abdominal fat were taken by biopsy at two-weekly
intervals. The mean concentration of dieldrin after 2 weeks was
12.5 mg/kg body fat. For weeks 4 - 10, an average concentration of
21 mg was found, a steady state being reached after approximately 4
weeks (Aulerich et al., 1972).

4.7. The Fate of Aldrin and Dieldrin in the Environment

On the basis of the current uses of aldrin in agriculture, the
first point at which aldrin and dieldrin enter the environment is
the soil, dieldrin being derived from aldrin by biological
epoxidation. Understanding the fate of aldrin and dieldrin in the
environment, therefore, depends firstly on an understanding of its
behaviour in the soil.

4.7.1. Aldrin and dieldrin in soils

It was concluded in section 4.1.4 that the regular application
of aldrin to soils for the control of soil pests does not lead to
an indefinite accumulation in the soil. The results of a
considerable number of soil monitoring studies, summarized in
Table 1, support this conclusion. Some of the individual
monitoring studies are discussed at greater length in this section.

Carey et al. (1973) monitored residues of aldrin and dieldrin
over a very wide area of the corn belt in the USA in 1970, when the
use of aldrin on maize was probably close to its maximum and the
levels were representative of residues in a situation of continuing
use. Average values for aldrin plus dieldrin, recalculated for
samples that contained positive residues, ranged from 0.05 to 0.87
mg/kg for each of the twelve states. The maximum levels for the
whole study were 2.98 mg aldrin/kg and 2.04 mg dieldrin/kg (these
values were not both derived from the same sample). In many cases
the residues had come from relatively recent applications, as may
be judged from the comparatively high proportion of aldrin still
remaining. The average was greater than 50% of the combined
residues in four of the twelve states, so that many of the samples
were probably taken from soils in the same year in which they were
treated.

Carey et al. (1980) carried out a further study on rice soils
in the USA during the year 1972. At that time, aldrin was used
extensively as a rice seed dressing and, according to the data
presented by Sparr et al. (1966), overall application rates of
aldrin would have been between 0.2 and 0.4 kg/ha. Between 50% and
100% (depending on the state) of the land sampled had received
aldrin-dressed seed. As in the case of the maize data, figures for
aldrin and dieldrin were presented separately and not paired, so
that total residue levels are difficult to deduce. The average
level for aldrin was only about 0.02 mg/kg soil and for dieldrin
was 0.05 mg/kg, although there were occasional samples that reached
0.25 mg/kg for either aldrin or dieldrin. According to the
information presented earlier, degradation of aldrin occurs more
readily in the anaerobic conditions of a rice paddy than in fully
aerobic soils, and this may have contributed to the much lower
level of residues surviving in rice compared with maize. However,
it should also be remembered that the initial rates of application
were substantially lower in rice than in maize.

In Canada, Harris et al. (1966) reported a series of data for
soils in S.W. Ontario and there was limited information on the
treatment history of the soils sampled. About a half of the soils
showed residues, and these ranged from < 0.01 to 1.5 mg/kg for
aldrin plus dieldrin residues. One high figure of 3.5 mg/kg seems
anomalous in that it was reported from land that had no treatment
history with aldrin or dieldrin. With the exception of this
anomalous sample, there was no evidence for accumulation. Fairly
similar results were reported by Duffy & Wong (1967), who sampled a
series of vegetable-growing areas in Canada in 1965. In cases

where it was reported that aldrin or dieldrin had been used
(sometimes over a period of several years) residues were mostly
below 2 mg/kg.

None of these studies mentioned the occurrence of any dieldrin
degradation products, in particular photodieldrin, and yet this
would presumably have been detected had it been present. This,
taken in conjunction with the work of Suzuki et al. (1974) (section
4.4.2) would seem to be useful evidence that photodieldrin does
not, to any appreciable extent, represent a terminal metabolite of
aldrin in the soil.

4.7.2. Aldrin and dieldrin in the atmosphere

The relative contributions of the various mechanisms for the
loss of aldrin and dieldrin from the soil have not been estimated
(as far as can be judged from the literature) but, as mentioned in
section 4.1.3, volatilization is usually considered to be the major
loss route. Consequently, the occurrence of aldrin or dieldrin
vapour in the atmosphere has been the subject of considerable
study.

Spencer & Cliath (1975) considered that many pesticides enter
the atmosphere after application. This occurs by volatilization
during spraying, from treated crops or soils, or from dust from
treated soil surfaces blown up by the wind. These routes are
difficult to quantify, and only sparse data are available, though a
few relating to dieldrin have been cited in section 4.1.3.

Small amounts of dieldrin have been detected in the atmosphere,
particularly in agricultural areas and, in one case, close to a
formulating plant (section 5.1.1.2). Aldrin has also been
detected, though relatively less often (section 5.1.1.1). There is
further information on the levels in the atmosphere of aldrin and
dieldrin in section 4.1.6.

4.7.3. Conclusion

In spite of the slow rate at which aldrin and dieldrin are lost
from soils when applied to them for insect control, there is no
evidence for their indefinite accumulation in the environment,
either in the soil itself, in water, or in the atmosphere. The
evidence suggests that photodegradation products do not accumulate
either.

Although there is evidence that a considerable proportion of
the aldrin and dieldrin used in agriculture reaches the atmosphere,
it seems probable that the degradation processes in the atmosphere
described by Glotfelty (1978) for pesticides in general operate to
prevent accumulation of aldrin and dieldrin.

5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

5.1. Environmental Levels

5.1.1 Air and rainwater

5.1.1.1 Aldrin

Residues of aldrin in the general atmosphere, either in the
vapour phase, adsorbed by dust particles, or in rainwater, have
been reported less frequently than for other organochlorine
insecticides. Concentrations in the range 0.1 - 4 ng/m³have been
found in the air of agricultural communities (Tabor, 1966). In a
pilot survey in 1967 - 1968, out of nine localities in the USA,
only one sample from a total of 880 contained aldrin (8 ng/m³)
(Stanley et al., 1971). Aldrin was detected in 13.5% of 2479 air
samples collected from 16 states in the USA in the 3-year period
1970 - 1972. The mean value in these positive samples was 1.6
ng/m³and the maximum was 24.6 ng/m³(Kutz et al., 1976).

Aldrin was found at a level of 0.9 ng/m³in 16 out of 66 air
samples taken within 800 m of two formulation plants in 1970 (Lewis
& Lee, 1976). One year later, 6 out of 60 samples were found to
contain a level of 1.5 ng/m³, and in 1972 no aldrin could be
detected.

5.1.1.2 Dieldrin

In a pilot survey in 1967 - 1968 in the USA, dieldrin was found
in 6% of the 880 samples analysed. The maximum level was 29.7
ng/m³(Stanley et al., 1971).

In a survey mentioned above (Kutz et al., 1976), dieldrin was
detected in 94% of the 2479 samples. The mean value in these
positive samples was 1.7 ng/m³and the maximum was 23.9 ng/m³.

A summary of the concentrations of dieldrin in air and
rainwater (washout from the air) is given in Table 6.

5.1.2. Concentrations in houses

5.1.2.1 Aldrin used for subterranean termite control

Aldrin EC (480 g/litre) was applied in a 0.5% solution as a
termiticide to typical slab and crawl-space type houses in
California, 1982. Samples of air were taken in the kitchen,
bedroom, and crawl-space at intervals up to 1 year after
application. Kitchen wipe samples were taken at the same time.
Air concentrations of aldrin in kitchen and bedrooms of the treated
houses showed transient peaks 24 h after treatment. In the slab-
type houses, concentrations were 0.04 - 0.27 µg/m³and in the
crawl-space houses 0.09 - 7 µg/m³. These concentrations fell
rapidly. The air concentrations in slab houses were < 0.04 - 0.09
µg/m³at day 28 and were < 0.05 µg/m³at day 56, whereas those in
crawl-space houses were 0.06 - 1.5 µg/m³at day 7, 0.04 - 0.36

µg/m³at day 28, and 0.06 - 0.55 µg/m³at day 56. One year after
application the air concentration of aldrin was 0.08 µg/m³or less,
whereas dieldrin was not detected in any of the samples of air.
The concentrations of aldrin in surface wipes from kitchens showed
transient peaks 7 days after treatment, the concentrations being
higher in wipes from crawl-space houses (0.09 µg/m²) than from slab
houses (0.012 µg/m2). Between day 28 and day 56 the concentrations
remained at about 0.04 µg/m2 in crawl-space houses and 0.002 µg/m²
in slab houses. One year after application, aldrin and dieldrin
were not detectable in the kitchen wipe samples from the slab
houses, while in the samples from the crawl-space houses the
concentration of aldrin amounted to 0.04 µg/m²and that of dieldrin
to 0.018 µg/m2 (Marlow et al., 1982; Marlow & Wallace, 1983).

5.1.2.2 Aldrin and dieldrin used for remedial treatment of wood

One to ten years after the remedial treatment of inside wood in
houses with dieldrin, its concentration in the air was measured.
Forty samples from 16 houses in the United Kingdom, covering a wide
range of construction type, size, and occupational pattern, were
analysed. The concentrations of dieldrin in the air in all
interior areas other than roof-voids were between 0.01 and 0.51
µg/m³, and in roof-voids, they were between 0.03 and 2.7 µg/m³
(Dobbs & Williams, 1983).

Paton et al. (1984) observed that aldrin and dieldrin migrated
from treated laminated timber and plywood, used as structural
components of commercial containers, into flour in polyethylene
bags or metal tubes that were stored in the containers for up to 40
days. The migration was thought to occur through contact with the
floor or sorption from the atmosphere. The residues in the flour
varied widely depending on temperature, type of packaging material,
and location of the flour in the container.

5.1.3. Aquatic environment

Dieldrin occurs more commonly in the aquatic environment than
does aldrin, albeit at very low concentrations. The major sources
of contamination of rivers, etc., by aldrin and dieldrin are
industrial effluents (manufacturing, formulation, and moth-proofing
in the textile industry) and soil erosion during agricultural usage
(Lichtenstein et al., 1962; Park & McKone, 1966; Epstein & Grant,
1968; Eye, 1968; Croll, 1969; Lowden et al., 1969; Rowe et al.,
1971; Burns et al., 1975; Brown et al., 1979). Local use appears
to contribute to the presence of dieldrin in sediments in urban
areas (Mattraw, 1975). In the USA, the Environmental Protection
Agency found that between 118 kg and 14.2 tonnes of dieldrin was
carried in the Mississippi River past St. Louis each year.
Although this is certainly not the case today, it does illustrate
the contribution of run-off to the pesticide load in river systems.
This is of special concern with dieldrin because of its stability
in water (Eichelberger & Lichtenberg, 1971).

Table 6. Concentration of dieldrin in air, rainwater, and dust
----------------------------------------------------------------------------------------------------------------
Location Year Number Medium Analytical^a Mean Comments Reference
of procedure concentration
samples (range)
----------------------------------------------------------------------------------------------------------------
Netherlands

Delft 1979-81 55 air glass fibre 0.073 ng/m³ 24-h samples Guicherit
filter; GC/EC (maximum, 370 & Schulting
ng/m³) aldrin: (1985)
0.039 ng/m³
(maximum, 640
ng/m³)

United Kingdom

Wellesbourne 1964-65 11 rain- TLC followed by 24 ng/litre samples of monthly Wheatley
water GLC/EC (10-36) rainfall & Hardman
(1965)

1965 5 9 ng/litre samples collected
(3-16) during periods of
prolonged rainfall

London 1965 11 rain- GLC/EC 42 ng/litre samples of monthly Abbott et
water (10-95) rainfall; 2 sampling al. (1965)
sites; limit of
determination: 10
ng/litre

London 1965 1 air TLC followed by 20 ng/kg Abbott et
GLC/EC al. (1966)

United 1966-67 28 rain- alumina column 8 ng/litre samples from 7 Tarrant
Kingdom water chromatography (1-35) locations during 12 & Tatton
and TLC followed months; limit of (1968)
by GLC/EC determination:
1 ng/litre
----------------------------------------------------------------------------------------------------------------

Table 6. (contd.)
----------------------------------------------------------------------------------------------------------------
Location Year Number Medium Analytical^a Mean Comments Reference
of procedure concentration
samples (range)
----------------------------------------------------------------------------------------------------------------
USA

Cincinnati 1965 1 dust florisil column 3 ng/g dust source of the dust was Cohen &
washed chromatography the Southern High Pinkerton
out by followed by Plains, approximately (1966)
gentle GLC/EC 1500 km southwest of
rain Cincinnati

16 states 1970-72 2479 air florisil column 1.7 ng/m³ limit of determination: Kutz et al.
chromatography (1-23.9) 1-10 ng/m³ (1976)
followed by
GLC/EC

Hawaii 1970-71 5 rain- GLC/EC 5 ng/litre Bevenue et
water (1-27) al. (1972a)

1971-72 14 12 ng/litre Bevenue et
(1-97) al. (1972b)

West Indies

Barbados 1965-66 15 dust TLC followed by 2.2 ng/g dust samples of dust Risebrough
GLC/EC (1-8.1) collected in nylon et al. (1968)
screens; limit of
determination:
1 ng/g (?)

Barbados July 12 air- silicic acid 49 ng/m³air source of dust in air Prospero &
1970 borne column (1-190) probably North Africa Seba (1972)
dust chromatography
followed by
GLC/EC
----------------------------------------------------------------------------------------------------------------

Bantry Bay 1973 17 air florisil column 0.36 ng/m³ aldrin and photo- Baldwin et
chromatography (0.06-1.6) dieldrin less than al. (1977)
followed by limits of detection
GLC/EC (0.1 ng/kg); origin
of air samples either
westerly from Atlantic
Ocean (13 occasions)
or easterly from
continental Europe
(4 occasions)
----------------------------------------------------------------------------------------------------------------
^aTLC = thin-layer chromatography; GC/EC = gas chromatography/electron capture detection; GLC/EC = gas-liquid
chromatography/electron capture detection.
Dieldrin has been detected in the northern Atlantic Ocean at a
mean concentration of 5.8 ng/litre (Jonas & Pfaender, 1976), and it
is of interest that the dieldrin concentration was apparently
unrelated to depth or distance from shore. It was suggested that
this may be the result of adsorption to particulate matter. The
identification of the component measured as dieldrin was based on
gas-liquid chromatographic behaviour (three different stationary
phases), but was not rigorously confirmed. Other investigators
(Harvey et al., 1973, 1974; Bidleman & Olney, 1974) did not report
the presence of dieldrin in the northern Atlantic Ocean, although
the analytical methods were appropriate for the detection of aldrin
and dieldrin.

Dieldrin residues (0.01 - 0.3 ng/litre) have also been reported
off the coast of Ireland, in the English Channel, and in the North
Sea (Dawson & Riley, 1977).

Low levels of dieldrin have been reported in surface waters
from several countries. The results of several surveys are
summarized in Table 7.

5.1.4. Soil

Aldrin is applied more frequently to the soil (directly or
indirectly) than dieldrin. However, as a result of the relatively
rapid conversion of aldrin to dieldrin, residues of dieldrin are
usually found more frequently in soil and at higher concentrations,
except shortly after the application of aldrin to soil. Sediment
residue levels tend to lie between those of soil and water, with
values up to 140 µg/kg) (Dawson & Riley, 1977). Dieldrin has been
reported in the sediments of Lake Ontario and Lake Superior (Frank
et al., 1974; Frank et al., 1981), rivers of the USA (Ryckman et
al., 1972), bays (Sheets et al., 1970), and off the coasts of
Ireland (Dawson & Riley, 1977). A summary of some of the results
of monitoring surveys was given in Table 1 (section 4.1.4). This
is not a comprehensive review of residues, but it indicates the
variations of the concentrations that occur in practice. These
results also illustrate the potential for absorption into root
crops, and for uptake by soil organisms.

5.1.5. Drinking-water

Studies on drinking-water in the USA have indicated dieldrin
residue values up to 8 µg/litre (Kraybill, 1977; Sandhu et al.,
1978). In a comprehensive study in the USA, dieldrin residues were
found in less than 17% of the samples with 78% of these positive
results lying within the range 4 - 10 ng/litre. The highest
residue level found in this study was 110 ng/litre. Dieldrin has
also been found in drinking-water in Canada (0.1 - 4 ng/litre)
(Williams et al., 1978) and in the Virgin Islands (average
concentration 0.19 µg/litre (Lenon et al., 1972).

Table 7. Concentrations of aldrin and dieldrin in the aquatic environment
--------------------------------------------------------------------------------------------------------------------------
Location Year Type Number Mean concentration Comments Reference
of of (ng/litre) (maximum)^a
water sites aldrin dieldrin
--------------------------------------------------------------------------------------------------------------------------
Argentina

Santa Fe 1981 surface water 4 4 (29) LD LD not defined; samples Lenardon et
and Parana (20 cm depth) collected twice monthly al. (1984)
(March-December)

suspended 4 150 ng/g LD occasional high residues of
solids (1625) aldrin attributable to local
source of application
(1966-68)

Canada

Ontario 1971 agricultural 2 1 (7) 11 (41) LD less than 1 ng/litre Miles & Harris
and urban (1973)
rivers

resort rivers 1 1 4 (11)

bottom mud 2 LD 0.9 LD less than 1 ng/g mud
(dry weight)
(4.5)
1 LD 0.9
(dry weight)
(1.4)

Nova Scotia 1972-73 river 7 (23 77 (670) 979 LD not defined; water, Burns et al.
samples) (11 800) probably less than 10 (1975)
ng/litre; sediment, probably
less than 1 ng/g

artesian wells 4 LD 10 (10)

holding pond 3 37 (40) 100 (200)
and reservoirs

natural 2 (4 90 (330) 17.5 (50) national drainage ditch in a
drainage samples) tobacco-growing area
--------------------------------------------------------------------------------------------------------------------------

Table 7. (contd.)
--------------------------------------------------------------------------------------------------------------------------
Location Year Type Number Mean concentration Comments Reference
of of (ng/litre) (maximum)^a
water sites aldrin dieldrin
--------------------------------------------------------------------------------------------------------------------------
Canada (contd.)

Nova Scotia 1972-73 sediment from 25 31 (368) 4.9 (86) high residues in water and
stream bed sediments attributable to
soil erosion, particularly
during and after prolonged
heavy showers

sediment from 4 1088 670
natural (2220) (13 750)
drainage ditch

Lake 1974 filtered lake 34 LD 0.5 (0.5) LD: filtered water, less than Glooschenko
Superior water 0.5 ng/litre; sediment, less et al. (1976)
and Lake than 1 ng/g; dieldrin detected
Huron sediment 34 LD 0.1 mg/kg (0.5 ng/litre) in one sample
dry weight of filtered water and in 5
(0.1) samples of sediment (0.1 ng/g)

Greece

Northern 1981-82 coastal water 10 ND 0.55 (1.1) Fytianos et
Greece al. (1985)

United Kingdom

Kent and 1965-66 rivers 9 (224 LD (4) LD (59) LD less than 3 ng/litre; Croll (1969)
Essex samples aldrin found in one sample
collected only
at 2-weekly
intervals)

Great 1965-66 rivers 11 (75 LD 24.3 (423) high residues of dieldrin Croll (1969)
Britain samples attributable to effluent from
collected moth-proofing plants using
at 2-monthly dieldrin
intervals)
--------------------------------------------------------------------------------------------------------------------------

Kent 1965-66 underground 11 LD LD Croll (1969)
water

Hereford- 1966 River Lee 6 LD LD LD less than 2 ng/litre Lowden et al.
shire (1969)

Yorkshire 1966-68 rivers 14 (30 LD 114 (650)
samples)

Birmingham 1966 sewage 24 LD 132 (1900) high concentrations of Lowden et al.
and effluent dieldrin attributable to (1969)
Hertford- industrial effluent from
shire moth-proofing plants

Yorkshire 1976-77 rivers 7 (18 LD 902 (4900) LD less than 1 ng/litre; high Brown et al.
samples) concentrations of dieldrin in (1979)
individual rivers (and sewage
sewage 1 sample LD 6240 effluent) attributable to the
effluent use of dieldrin for moth-
river 10 LD 124 ng/g proofing of wool
sediments (dry weight)
(432)

Netherlands 1969-75 raw water 11 (120 LD LD (50) unfiltered water to be used Greve (1972);
samples) for drinking-water preparation Wegman & Greve
(1978)

surface water 26 (1246 LD 10 (140) aldrin was detected Wegman & Greve
(depth about samples) occasionally at low (1978)
1 m) concentrations; limit of Greve (1972)
detection about 10 ng/litre
--------------------------------------------------------------------------------------------------------------------------

suspended 26 LD LD LD not given (appears to be
solids approximately 10 ng/litre)

USA

Major river 1965 surface water 99 LD 1 (100) LD 1 ng/litre; aldrin not Breidenbach et
basins detected in any sample; al. (1967)
dieldrin detected in 42% of
samples

Western USA 1965, rivers 11 0.2 (5) 2.3 (15) lower LD 5 ng/litre Brown &
1966 Nishioka
(1967)

1966-68 rivers 20 LD (40) LD (70) LD not defined; presumed to be Manigold &
about 10 ng/litre Schulze (1969)

Major river 1964-68 surface water about 100 LD range: 4-407 LD 2 ng/litre; in 37% of the Lichtenberg et
basins stations samples dieldrin was present al. (1970)

Iowa 1968 rivers 6 LD 2 (10) LD about 1 ng/litre; dieldrin Johnson &
1969 10 LD 8.5 (63) found in 40% of samples (179) Morris (1971)
1970 10 LD 9 (65) analysed

Western USA 1968-71 rivers 20 LD (10) LD (30) LD 5 ng/litre; aldrin detected Schulze et al.
in only 1 sample (total 716); (1973)
dieldrin detected in 5% of
samples

Hawaii 1970-71 non-potable 10 LD 4.8 (18.6) LD about 0.2 ng/litre Bevenue et al.
(1972a)

canals 3 LD 11.9 (18.6)
--------------------------------------------------------------------------------------------------------------------------

Gulf coast 1971 canal water 1 90 (440) drainage water from a rice Ginn & Fisher
of Texas field-marshland ecosystem; (1974)
samples (7) collected for 15
weeks after aldrin-dressed
rice seed had been planted;
one sample out of 7 contained
aldrin (270 ng/litre)

Lower surface water 1 LD 5 (10) LD not defined Brodtmann
Mississippi (samples (1976)
River taken
monthly)

Iowa 1974 surface water, 18 (104 not 12 (76) LD less than 0.5 ng/litre Richard et al.
rivers, and samples) reported (1975)
reservoirs

Western 1972 ocean surface 10 0.2 6.4 (19.4) lower LD: aldrin, less than Jonas &
North (0.2) 0.2 ng/litre; dieldrin, less Pfaender
Atlantic than 0.4 ng/litre; (1976)
50 m depth 7 LD 6.2 (9.8) concentrations of aldrin
below LD in 29 samples;
500 m depth 7 LD 3.7 (11.9) one surface sample contained
a component with the same
1000 m depth 6 LD 7 (18.3) retention time of aldrin,
corresponding to 0.2 ng/litre

USA 1976-80 rivers LD 610 occurrence of dieldrin in 2.4% Carey & Kutz
of samples (1985)
--------------------------------------------------------------------------------------------------------------------------
^aConcentrations in bottom mud, sediments, and suspended solids (ng/g); LD = limit of detection; ND = not determined.
Maximum concentration indicated in parentheses.
5.1.6. Food and feed

Aldrin is rarely found in plants and animals, since it is
readily converted to dieldrin (IARC, 1974). A total-diet study of
Balby pensioners in Sweden did not detect any aldrin (Abdulla et
al., 1979). Similarly, a market-basket study in the USA in
1974 - 1975 (Johnson & Manske, 1977) found aldrin in only one
composite out of 240, with a value of 7 µg/kg. Traces or low
levels of aldrin have been found in vegetable products and meat
products (Balayannis, 1974; Saschenbrecker, 1976; Chaudry et al.,
1978; Wessels, 1978). In all cases, dieldrin residues were greater
than those of aldrin, even when aldrin was the only compound
applied. Aldrin is rarely found in milk or milk fat or in the body
fat of cows fed aldrin (Frank et al., 1985; Vreman & Poortvliet,
1982). In one study where aldrin was found in dairy products, milk
samples contained 0.04 mg/litre, butter samples 0.02 mg/kg, and
cheese samples 0.02 mg/kg (Heeschen, 1972). For the occurrence of
residues in breastmilk, see section 5.2.2.

The analytical procedures used in well conducted dietary
surveys are capable of detecting all of the commonly used
organochlorine pesticides, so that if aldrin did occur in a dietary
sample it would be detected. The lack of mention of aldrin,
therefore, can usually be taken as an indication that it was not
detected.

Dieldrin residues in food and feed, resulting from the
application of aldrin and dieldrin in normal use as well as from
field studies, have been reviewed by the FAO/WHO Joint Meeting on
Pesticide Residues (JMPR) at its meetings in 1963, 1965, 1966,
1967, 1968, 1969, 1970, 1974, 1975, and 1977 (FAO/WHO, 1964,
1965a,b, 1967a,b, 1968a,b, 1969a,b, 1970a,b, 1971a,b, 1975a,b,
1976a,b, 1978a,b).

Australia, Canada, Japan, the Netherlands, the United Kingdom,
and the USA have all reported daily intakes below the ADI (Duggan &
Lipscomb, 1969; Uyeta et al., 1971; Duggan & Corneliussen, 1972;
IARC, 1974; Smith, 1978; de Vos et al., 1984).

In Australia, Canada, Italy, Japan, the United Kingdom, and the
USA, analyses of total diets revealed dieldrin residues (Cummings,
1966; Duggan et al., 1967; Abbott et al., 1969; Corneliussen, 1972;
Duggan & Corneliussen, 1972; Johnson & Manske, 1977; Dick et al.,
1978; Smith, 1978) ranging from 0.06 mg/kg (Cummings, 1966;
Corneliussen, 1972) to 0.2 mg/kg (Duggan et al., 1967;
Corneliussen, 1970). In 1982 - 1983, dieldrin was determined in 73
typically composed, prepared daily meals in Switzerland, and was
detected in 46 of the meals. It was calculated from these results
that the average daily intake of the Swiss consumer was 0.9 ng/day.
The levels in 1971 - 1972 were 3.4 ng/day (Wüthrich et al., 1985).
Residue levels of up to 0.125 mg/kg in Canadian pork
(Saschenbrecker, 1976) and of 0.03 - 0.1 mg/kg in herring oil
(Addison et al., 1972) have been reported.

In a market-basket survey in 1974 - 1975, dieldrin was present
in only three food groups, with maximum residues of 5 µg/kg in
dairy products, 15 µg/kg in meat, fish, and poultry, and 8 µg/kg in
potatoes (Johnson & Manske, 1977).

The JMPR meeting in 1970 summarized data concerning dieldrin
residues from the feeding of dieldrin to cattle and poultry. The
average ratio of dieldrin levels in fat to levels in feed was
2.43:1 in milking cows and 3.95:1 in steers (Gannon et al., 1959a).
At intake rates of less than 1 mg/kg, the average ratio of dieldrin
levels in milk to levels in feed was about 0.1:1 after 12 weeks
(Gannon et al., 1959b; Williams et al., 1964). In Denmark, the
average concentration of dieldrin in butter fat declined from 0.05
mg/kg in 1964 to 0.03 mg/kg in 1966 and to 0.02 mg/kg in 1968
(Bro-Rasmussen et al., 1968). Similar residue levels and decreases
were found in Australia, Ireland, New Zealand, Norway, and the
United Kingdom. In Canada and the USA, residues in milk fat of
0.011 - 0.09 mg dieldrin/kg have been measured (Duggan et al.,
1967; Wedberg et al., 1978; Frank et al., 1985).

Dieldrin losses resulting from cooking or processing food can
be quite substantial, as demonstrated with trout and soybean
(Chaudry et al., 1978; Zabik et al., 1979).

More recent information on the occurrence of dieldrin residues
in foods is relatively scarce. However, a number of reviews exist.

5.1.6.1 Joint FAO/WHO Food Contamination Monitoring Programme

Information on dietary intakes of aldrin and dieldrin were
collected from seven collaborating centres participating in the
Joint FAO/WHO Food Contamination Monitoring Programme. The data
cover the period from 1971 - 1983, and the countries involved were
Australia, Canada, Guatemala, Japan, New Zealand, the United
Kingdom, and the USA. The mean daily intake during this period
varied from 0.007 to 0.056 µg/kg body weight (the 90th percentile
varied from 0.016 to 0.105 µg/kg body weight). During the later
years of this period, the mean values ranged from 7% to 56% of the
acceptable daily intake (ADI). A decrease in the dietary intake of
aldrin and dieldrin residues was noted during this period in some
of the countries. Possibly this decrease was the result of
restricting or banning the use of aldrin and dieldrin (Gorchev &
Jelinek, 1985).

5.1.6.2 Information summarized by GIFAP (1984)

Australia, 1980: Twenty-four samples of each of 50 different
foods were analysed for a range of organochlorine pesticides.
In the case of dieldrin, the limit of determination was 0.01
mg/kg. Dieldrin occurred above this level in only 0.04% of the
samples, and the maximum level was 0.05 mg/kg.

Canada, 1976 - 1978: The results of analyses of food
commodities were expressed in terms of estimated intakes for
the population. The average daily dietary intake of dieldrin
for this period was 0.002 µg/kg body weight.

Italy, 1982: Apples were sampled from a variety of locations
representing 70% of the country's apple production. There were
300 samples and 80% or 90% were below the limit of determination
for aldrin and dieldrin, respectively.

Netherlands, 1977 - 1978: During the period 1977 - 1978,
residues of organochlorine pesticides were determined in a wide
range of market baskets composed of items considered to be
representative of the diet of 16 - 18-year-old boys. Although
dieldrin was not specifically mentioned, the studies revealed
that none of the organochlorine pesticides contributed
residues in excess of the Maximum Residue Limit (MRLs).

5.1.6.3 United Kingdom (UK MAFF, 1982-1985)

Residues of dieldrin found in a range of dietary components in
1981 are listed in Table 8.

Table 8. Dieldrin residues in individual food groups of
the total-diet study (24 sets of total diet samples,
January - December 1981)^a
----------------------------------------------------------
Food group Range of residues Average residues
(µg/kg) (µg/kg)
----------------------------------------------------------
Bread ND ND
Other cereal products ND ND
Carcass meat ND - 40 3.5
Offals ND - 5 0.5
Meat products ND ND
Poultry ND - 4 1
Fish ND - 8 2
Oils and fats ND - 15 1
Eggs ND - 4 0.5
Green vegetables ND ND
Potatoes ND - 1 < 0.5
Other vegetables ND - 10 1
Fresh fruit ND ND
Milk ND - 2 0.5
Dairy products ND - 150 4
----------------------------------------------------------
^aThe limit of detection in these studies varied with the
food group but was sometimes as low as 1 µg/kg.
ND = not detectable.

On the basis of these data, it was estimated that the mean
level of dieldrin residues in the total diet in 1981 in the United
Kingdom was 0.5 µg/kg. This figure compares with 1.5 µg/kg for the
period 1975 - 1977 and 4 µg/kg for the period 1966 - 1967. The
computed daily intake derived from the 1981 figure was < 0.8
µg/person or < 0.01 µg/kg body weight.

Further data on certain individual products were also reported.

Maize: Two samples of imported maize, representing 3% of the
total number of samples taken in a survey conducted in 1981,
contained detectable levels of dieldrin, the highest
concentration being 0.04 mg/kg. The rest of the samples did
not contain dieldrin residues above the limit of determination
of 0.01 mg/kg.

Pulses: Separate surveys of residues in pulses obtained from
retail outlets were carried out in 1982 and 1983. In 1982, 42
samples involving 12 different kinds of pulses were analysed.
In this case, aldrin was found in one sample of haricot beans
(0.04 mg/kg) but was below the limit of determination (< 0.01
mg/kg) in all the others. Dieldrin was found in a limited
number of mung beans (0.05 mg/kg) but was below the limit of
determination (< 0.01 mg/kg) in all of the others. Thus,
neither aldrin nor dieldrin were detected in the majority of
pulses sampled in 1982.

In 1983, 40 samples were analysed and there were no residues
reported for aldrin or dieldrin above the level of
determination, with the exception of limited samples of mung
beans containing dieldrin (maximum, 0.04 mg/kg; mean, < 0.01
mg/kg).

Fruit and vegetables, 1981 - 1984: A large-scale monitoring
project of fruit and vegetables was undertaken in the United
Kingdom during the period 1981 - 1984. Some 40 commodities
were sampled during that period, 1649 samples being obtained
from retail outlets and analysed. The data were not
individually reported but, although most of the commodities
were analysed for organochlorine pesticide residues, there were
no reports of any sample containing residues of dieldrin
exceeding either Codex or EEC maximum residue limits.
Information on the incidence of detectable residues of dieldrin
was not presented in this case. It is of interest to note that
648 of the samples were grown in the United Kingdom and 1001
were imported.

Lamb meat: Sampling of kidney fat from home-grown lamb
destined for export began in October 1984 and data for 988
samples were reported. None contained dieldrin residues above
the limit of determination of 0.02 mg/kg.

Fish: The information in Table 9 was obtained from fish caught
in areas around the English and Welsh coast where the levels of
chemical contamination were known to be high.

Residues of dieldrin in processed fish imported into the United
Kingdom were determined in 155 samples of different products
obtained from retail outlets in 1983. The data are summarized
in Table 10. In a further study, dieldrin residues were
determined in a limited number of fish oil products obtained
through retail outlets (Table 11).

Table 9. Mean residue levels of dieldrin (mg/kg)
in the liver and muscle of marine fish from
England and Wales, 1982
------------------------------------------------
Fish Muscle Number Liver Number
of samples of samples
------------------------------------------------
Cod 0.003 43 0.26 73
Dab 0.003 50 0.13 50
Flounder 0.003 49 0.027 49
Mackerel 0.007 29 0.053 23
Plaice 0.004 43 0.040 68
Sole 0.003 50 0.031 50
Whiting 0.009 62 0.26 62
------------------------------------------------

Table 10. Residues of dieldrin (mg/kg) in
processed imported fish and shellfish in 1983
---------------------------------------------
Fish Range^a Average Number of
samples
---------------------------------------------
Pilchards < 0.009 0.001 21
Plaice < 0.006 0.001 19
Salmon < 0.02 0.002 36
Sardines < 0.004 0.001 11
Tuna ND ND 15
Cockles and < 0.01 0.004 5
mussels
Crab ND ND 15
Prawns < 0.001 < 0.001 17
Shrimps < 0.004 0.001 16
---------------------------------------------
^aND = not detectable.

Table 11. Residues of dieldrin (mg/kg) in fish
oil products, 1984
-----------------------------------------------
Product Range Mean Number of
samples
-----------------------------------------------
Cod liver oil
Mixtures 0.01-0.21 0.08 8
Capsules 0.06-0.20 0.12 3

Halibut liver oil
Capsules 0.01-0.1 0.04 5

"Fish lipid" oil
Capsules 0.01 0.01 1
-----------------------------------------------

5.1.6.4 USA

Surveys were carried out in the USA, during the period
1980 - 1982, covering the diets of infants (aged 6 months),
toddlers (aged 2 years) (Gartrell et al., 1986a), and adults
(youths aged 16 - 19 years) (Gartrell et al., 1986b). In each
case, the samples were taken from a number of locations (13 in the
case of infants and toddlers and 27 in the case of youths). They
were selected as being representative of the composition of diets
for the three population groups studied. Individual foods were
bulked together in food groups and the bulked samples analysed.
The lower level of determination was not precisely stated, since it
varied according to the food group concerned, but from the data
presented it would appear to have been either 1 or 2 µg/kg food
item. Results that were below these limits (and hence
unquantifiable), but where the identity of the residue could be
confirmed, were reported as "T". The analysts' estimate of the
value of "T" was used to estimate the average level of residues in
the whole food group. Data for dieldrin residues are given in
Tables 12, 13, and 14.

Table 12. Dieldrin residues (lg/kg) in infant dietary
components^a
---------------------------------------------------------
Food group Range of residues Average level
---------------------------------------------------------
Drinking-water 0 0
Whole milk T 0.1
Other dairy products T - 1 0.3
Meat, fish, poultry T - 2 0.5
Grain and cereals 0 0
Potatoes T - 2 0.2
Vegetables T - 1 0.1
Fruit and fruit juices 0 0
Oils and fats 0 0
Sugar and adjuncts 0 0
Beverages 0 0
---------------------------------------------------------
^aFor breast milk, see section 5.2.2.

5.1.6.5 Appraisal of intake studies

The above data demonstrate that in the United Kingdom and the
USA the intake of dieldrin residues in food is well below the ADI
of 0.1 µg/kg body weight. Moreover, taking into account the rather
high dietary intake estimated for adults in the USA, the agreement
between estimates for the United Kingdom and the USA is striking,
notwithstanding the widely differing origins of the basic food
commodities, especially the relatively high proportion of imports
in the case of the United Kingdom. The estimated levels of intake
in Canada were even lower. The residues in Australia, though very
low, were not expressed in terms of intakes.

Table 13. Dieldrin residues (µg/kg) in toddler dietary
components
--------------------------------------------------------
Food group Range of residues Average level
--------------------------------------------------------
Drinking-water 0 0
Whole milk T 0.1
Other dairy products T - 3 1.2
Meat, fish, poultry T - 3 0.8
Grain and cereals 0 0
Potatoes T - 3 0.3
Vegetables T - 2 0.5
Fruit and fruit juices 0 0
Oils and fats 2 0.3
Sugar and adjuncts 0 0
Beverages 0 0
--------------------------------------------------------

Table 14. Dieldrin residues (µg/kg) in adult dietary
components
------------------------------------------------------
Food group Range of residues Average level
------------------------------------------------------
Dairy products T - 3 0.6
Meat, fish, poultry T - 4 1.2
Grain and cereals 4 0.1
Potatoes T - 2 0.4
Leafy vegetables T - 2 0.2
Legume vegetables 0 0
Root vegetables T - 5 0.4
Garden fruits T - 11 2.1
Fruits 1 0.1
Oils and fats T - 2 0.3
Sugar and adjuncts 0 0
Beverages 0 0
------------------------------------------------------

Dietary levels of dieldrin residues in both the United Kingdom
and the USA appear still to be decreasing, though less so than in
previous years.

In 1966, the JMPR established an acceptable daily intake (ADI)
of 0 - 0.1 µg/kg body weight (combined total for aldrin + dieldrin).

5.1.7. Concentrations of dieldrin in non-target species

There have been many investigations of the occurrence of
dieldrin in the body tissues or eggs of non-target species. The
residues range from less than 0.001 mg/kg to about 100 mg/kg, but
most reported residues are less than 1 mg/kg. The wide range of
concentrations is partly a reflection of the extreme sensitivity of
modern analytical techniques, but there are a number of other
factors involved, e.g., the source and magnitude of the exposure;

the component analysed (brain, adipose tissue, eggs, etc.), and
whether the samples are representative of living, apparently
healthy populations (specimens collected by capture, shooting,
etc., during systemic monitoring surveys) or consist of animals
found dead or dying. Interspecies differences in rates of
metabolism also contribute to the variability of residues. The
highest residues are found in two main groups of organisms. The
first group consists of organisms living near the source of release
into the environment; thus, high residues may be found in aquatic
organisms near the point of release of an industrial effluent, or
in seed-eating birds in areas where seed dressed with aldrin or
dieldrin is used in agriculture. The second group of organisms
consists of predators, particularly those feeding on aquatic
organisms or seed-eating birds or mammals.

The results of some analyses of various species from different
geographical areas are summarized in Tables 15 and 16.

There have been very extensive surveys of dieldrin residues in
biota that are not directly associated with a particular use of
aldrin/dieldrin or their waste disposal.

Soil and earthworms (four genera) were collected from 67 fields
from eight states in the USA. The geometric mean concentrations of
aldrin and dieldrin in soil were 0.014 and 0.023 and, in
earthworms, 0.088 and 0.19 mg/kg dry weight, respectively.
Correlation coefficients between the concentrations of dieldrin in
earthworms and soil were derived for six types of crops, but none
were significant. They were also derived from four different soil
types; only the concentrations in the earthworms from silt loam
soils were significantly related to the concentration in the soil
(Gish, 1970).

Henderson et al. (1969, 1971) studied the occurrence during the
period 1967 - 1969, of dieldrin in various species of fish from 50
monitoring stations located in the Great Lakes and in major river
basins in the USA. The mean concentrations of dieldrin in whole
fish lay in the range 0.01 - 0.28 mg/kg, and the maximum value
found was 1.94 mg/kg. The concentrations above 1 mg/kg were found
in fish from the Atlantic coast streams, Gulf coast streams, and
Great Lake drainage.

Koeman et al. (1967, 1971) and Koeman (1971) studied the
presence of dieldrin in fish, mussels, zooplankton, and birds in
the Wadden area of the Netherlands during the period 1965 - 1971.
The mean concentrations in mussels, marine fish, freshwater fish,
and zooplankton were below 0.1 mg/kg (maximum concentration, 0.23
mg/kg), except in three species of marine fish. In these, the mean
concentration was 0.27 mg/kg (maximum concentration, 0.42 mg/kg).
The levels in the liver and/or eggs of the sandwich tern (Sterna
sandwincensis) and grey heron (Ardea cinerea) were up to 5.1 mg/kg
(maximum concentration, 12 mg/kg). Mortality among sandwich terns
(Sterna sandvicensis), eider duck (Somateria mollissima), and a few
other bird species was reported.

Table 15. Residues of dieldrin in non-target species and their environment
----------------------------------------------------------------------------------------------------------------------------------------
Geographical Species Type of Number of Mean Range^c Comments^c Reference
area/Year sample samples (mg/kg) (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
Antarctica

Signy Island 1966 Chinstrap penguin liver 11 0.002 0.001-0.006 LD not defined; Tatton &
(Pygoscelis antarctica) presumably < 0.001 Ruzicka (1967)
mg/kg

Fish liver 4 0.003 0.001-0.009
(Notothenia neglecta)

Skuas and shags liver 4 0.001 LD - 0.002

Sheathbills 3 0.009 LD - 0.015 sudden deaths of
(Chionis alba) sheathbills of
unknown causes had
occurred

Canada

Southwestern Fish (two species) river water 52 0.000005 LD - 0.00011 LD: water, Miles & Harris
Ontario 1970 bottom mud 14 0.002 LD - 0.01 < 0.000001 mg/litre; (1971)
30/4^a 0.071 0.023-0.189 bottom mud, < 0.001
mg/kg

Province of Fish (various species) composites of 62 0.10 LD - 0.56 LD < 0.005 mg/kg Reinke et al.
Ontario headless dressed (1972)
specimens

Four other Fish (various species) composites of 119 0.01 LD - 0.08 76 composites from Reinke et al.
provinces headless dressed these four provinces (1972)
specimen contained residues;
LD < 0.005 mg/kg

Eastern Canada Leach's storm egg 18 0.05 0.03-0.13 Pearce et al.
1970-1976 petrel (Oceanodroma (1979)
leucorhoa)

Double-crested cormorant egg 90 0.13 0.01-0.68
(Phalacrocorax auritus)
----------------------------------------------------------------------------------------------------------------------------------------

Table 15. (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical Species Type of Number of Mean Range^c Comments^c Reference
area/Year sample samples (mg/kg) (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
Eastern Canada Common eider egg 25 0.02 0.01-0.04
1970-1976 (contd.) (Somerteria mollissima)

Common tern egg 50 0.04 0.01-0.13
(Sterna hirundo)

Razorbill egg 13 0.12 0.01-0.52
(Alca torda)

Common guillemot egg 4 0.02 0.02-0.03
(Uria aalge)

Black guillemot egg 3 0.02 0.01-0.05
(Cepphus grylle)

Atlantic puffin egg 48 0.06 0.03-0.13
(Fratercula arctica)

Falkland Islands Marine, coastal, and egg 46 0.002 LD - 0.011 LD not defined, but Hoerschelmann
1977 freshwater birds < 0.002 mg/kg et al. (1979)

Greece

Saronikos Gulf Striped mullet muscle 74 0.004 0.0001-0.050 residues attributed Voutsinou-
1975 (Mullus barbatus) to the discharge of Taliadouri &
domestic waste and Satsmadjis
industrial effluents (1982)

Iraq

Shatt al-Arab Cyprinid muscle 2 0.003 ND - 0.008 Douabul et al.
river (Barbus xanthopetrus) (1987)

Indian shad muscle 2 0.028 0.016-0.041 Douabul et al.
(Tenualosa ilistra) (1987)
----------------------------------------------------------------------------------------------------------------------------------------

Lake Nakuru 1975 water 10 < 0.0001 - Greichus et
al. (1978b)

bottom sediment 10 < 0.001^b -

Plankton composite 1 0.03^b - Greichus et
al. (1978b)
Chironomids composite 1 < 0.01^b -

Water boatmen composite 1 < 0.01^b -
(Coroxidae)

Fish composite 100/10^a 0.02^b -
(Tilapia grahami)

Netherlands 1965 Mussel 22 0.033 0.014-0.084 Koeman (1971)
(Mytilus edulis)

1965 marine fish (3 species) whole body 103 0.27 0.16-0.42 Koeman et al.
(1967)

1966 marine fish (2 species) whole body 37 0.07 0.01-0.23 fish species on Koeman et al.
which sandwich terns (1967)
feed

1965 Sandwich tern liver 19 5.1 1.9-12 found dead or dying Koeman et al.
(Sterna sandvincensis) (1967)

1965-1966 Sandwich tern liver 14 0.6 0.2-2 killed, shot, or Koeman et al.
found dead after a (1967)
storm

1967 freshwater fish 28 0.02 LD - 0.05 LD < 0.01 mg/kg Koeman (1971)
(3 species)

1969 Mussel 10/2^a 0.012 0.007-0.016 Koeman et al.
(Mytilus edulis) 199/8^a 0.013 0.007-0.023 (1971)
----------------------------------------------------------------------------------------------------------------------------------------

Table 15. (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical Species Type of Number of Mean Range^c Comments^c Reference
area/Year sample samples (mg/kg) (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
Netherlands (contd.)
1970 Pike whole body 10 0.01 LD - 0.022 LD < 0.003 mg/kg Koeman et al.
(Esox lucius) (1971)

1971 Roach whole body 81/6^a 0.004 LD - 0.013 LD < 0.005 mg/kg Koeman et al.
(Rutilus rutilus) (1971)

1971 zooplankton composite - 0.005 - Koeman et al.
(1971)

1970 Shrimp 50/1^a 0.009 - Koeman et al.
(Crangon vulgaris) (1971)

1969-1970 marine fish (5 species) 37/5^a 0.022 0.008-0.043 Koeman et al.
(1971)

1970 Sandwich tern egg 10 0.082 0.054-0.099 Koeman et al.
(1971)

1971 Grey heron egg 27/4^a 1.25 0.5-1.9 Koeman et al.
(Ardea cinerea) (1971)

New Zealand and Marine birds egg, 7 0.01 LD - 0.05 LD not defined, but Bennington et
sub-Antarctic (various spp.) breast muscle 7 0.1 0.03-0.28 < 0.02 mg/kg al. (1975)
islands 1970-1971

Norway

Four regions 1983 Shags (Phalacrocorax egg approx- 0.126-0.286 Barrett et al.
aristotelis) imately in 7.1% of (1985)
Herring gull (Larus 10 samples
argentatus)
Kittwakes (Rissa
tridactyla)
Common guillemots
(Uria aalge)
Razorbills (Alca torda)
Puffins (Fratercula
arctica)
----------------------------------------------------------------------------------------------------------------------------------------

England, Brown shrimp homogenates of 12 0.0055 0.0012-0.020 Van Den Broek
Medway estuary (Crangon vulgaris) 50 specimens (1979)
1974-1975
Sand goby homogenates of 9 0.047 0.024-0.077 Van Den Broek
(Pomatoschistus minutus) 50 specimens (1979)

Sprat homogenates of 13 0.084 0.030-0.142 Van Den Broek
(Sprattus sprattus) 50 specimens (1979)

Eel liver 16 0.051 0.0085-0.090 Van Den Broek
(Anguilla anguilla) (1979)

Whiting liver 9 0.57 0.25-1.10 Van Den Broek
(Merlangius merlangus) (1979)

Flounder liver 16 0.21 0.043-0.39 Van Den Broek
(Platichthys flesus) (1979)

Plaice liver 12 0.12 0.015-0.23 Van Den Broek
(Pleuronectes platessa) (1979)

Scotland, Plankton 12 0.072 0.019-0.230 Williams &
Firth of Clyde (various estuarine Holden (1973)
1971-1972 and marine species)

North Atlantic, Plankton 14 0.003 LD - 0.015 LD < 0.001 mg/kg Williams &
northeast transect (various estuarine Holden (1973)
from Mull of and marine species)
Kintyre 1971-1972

Firth of Clyde Mussel 25 0.178 0.012-2.43 Cowan (1981)
(coastal waters) (Mytilus edulis) homogenates of 80 0.022 0.006-0.216
1977 50-100 specimens
----------------------------------------------------------------------------------------------------------------------------------------

Table 15. (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical Species Type of Number of Mean Range^c Comments^c Reference
area/Year sample samples (mg/kg) (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
Shetland Isles Mussel 12 0.013 0.006-0.029 Cowan (1981)
(8 other coastal (Mytilus edulis)
sites) 1977

Irish Sea and Seabirds liver 21 1.23 0.07-5 heavy mortality of Lloyd et al.
Firth of Clyde (various species) seabirds in Irish (1974)
1974 Sea; continuous
winter storms may
have been cause of
mortality

Irish Sea 1969 Guillemot liver high mortality of Parslow &
(Uria aalge) guillemots in 1969; Jefferies
shot birds 9 0.09 0.01-0.41 primary cause of (1973)
dead birds 8 0.48 0.10-0.80 death was probably
malnutrition: mean
body weights for
shot and dead birds,
963 g and 580 g,
respectively; mean
liver weights,
43.8 g and 12.5 g,
respectively; PCBs
may also have been
responsible for the
death of guillemots

Great Britain Grey heron egg
1964-1977 (Ardea cinerea)
March 135 0.75 0.65-0.86^b concentration Cooke et al.
April 103 1.19 1.05-1.35^b increased (1982)
May 45 3.20 2.64-3.88^b significantly
between March and
May

Shetland Isles, Great skua egg 12 0.091 0.022-0.15 Furness &
Foula 1976 (Catharacta skua) Hutton (1979)
----------------------------------------------------------------------------------------------------------------------------------------

Table 15. (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical Species Type of Number of Mean Range^c Comments^c Reference
area/Year sample samples (mg/kg) (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
USA 15 states:
1965-1972 Estuarine molluscs composites of LD 0.005 mg/kg Butler (1973)
(10 species) meat from 15
or more mature
molliscs

North Carolina, 71 0.01 LD - 0.019 concentrations in 69
Point of Marsh samples below 0.005
mg/kg
Mississippi, 78 0.01 LD - 0.019 concentrations
Biloxi Bay in 70 samples below
0.005 mg/kg
Texas, 48 0.021 LD - 0.046
Arroyo Colorado
New York, 74 0.024 LD - 0.132
Hempstead Harbor
Georgia, 64 0.028 LD - 0.230
Lazaretta Creek

Major river fish composites of LD < 0.001 mg/kg Henderson et
basins in the (various species) whole fish al. (1969,
USA: 1971)

Atlantic coast 741/141^a,d 0.14 LD - 1.94
streams 157/36^a,e 0.13 LD - 0.55
Gulf coast 204/48^a,d 0.12 LD - 1.26
streams 59/12^a,e 0.28 LD - 1.59
Great Lakes 378/63^a,d 0.05 LD - 0.50
drainage 81/18^a,e 0.06 LD - 0.37
Mississippi River 657/139^a,d 0.06 LD - 0.52
system 153/34^a,e 0.06 0.01-0.49
Hudson Bay 51/13^a,d 0.12 0.03-0.37
drainage 5/2^a,e 0.01 0.01
Colorado River 112/24^a,d 0.02 LD - 0.10
system 24/6^a,e 0.01 0.01
Interior basins 120/25^a,d 0.01 LD - 0.06
30/6^a,e 0.02 LD - 0.03
----------------------------------------------------------------------------------------------------------------------------------------

California 90/24^a,d 0.06 LD - 0.31
streams 28/6^a,e 0.10 0.01-0.36
Columbia River 246/64^a,d 0.02 LD - 0.10
system 70/16^a,e 0.03 LD - 0.09
Pacific Coast 83/20^a,d 0.06 LD - 0.52
streams 29/6^a,e 0.01 LD - 0.02
Alaskan streams 105/24^a,d 0.003 LD - 0.01
30/6^a,e 0.006 LD - 0.01

Upper continental Bathyl-demersal liver 4 0.017 0.011-0.026 fish caught by trawl Meith-Avcin et
rise (southeast fish (Antimora at a depth of 2500 m al. (1973)
of (Cape rostrata)
Hatteras)

California 1970 Common egret brain 5 4.36 0.60-6.76 birds found dead or Faber et al.
(Casmerodius albus) moribund; dieldrin (1972)
considered to be a
contributory cause
of death of 4 birds

South Dakota Pheasant adipose tissue 48 0.08 LD - 1.07 LD < 0.01 mg/kg; 13 Greichus et
1965-1967 (Phasianus colchicus) samples of fat al. (1968)
contained < 0.01
mg/kg

Sharp-tailed grouse living birds 46 0.17 LD - 1.71 13 samples of fat
(Pedioecetes phasianellus contained < 0.01
campestris) mg/kg

South Dakota 1967 Pheasant egg 67 0.02 LD - 0.12 LD < 0.01 mg/kg; 13 Linder &
eggs contained 0.01 Dahlgren
mg/kg (1970)

Maine and Common eider and herring egg 88 LD LD LD < 0.1 mg/kg Szaro et al.
Virginia 1977 gull (1979)
----------------------------------------------------------------------------------------------------------------------------------------

Maine and Great black-backed egg 28 0.12 LD - 0.55 24 of the eggs
Virginia (contd.) gull contained < 0.1 mg/kg

Texas, Corpus Wintering shorebirds carcass 56 0.11 LD - 1 LD < 0.1 mg/kg; 2 White et al.
Christi Bay (7 species) (shot birds) carcasses contained (1980)
1976-1977 < 0.1 mg/kg

Lake Michigan Red-breasted merganser egg 206 0.77 0.2-2.3 LD < 0.1 mg/kg Haseltine et
1977-1978 (Mergus serrator) al. (1981)

Mallard egg 27 0.07 LD - 0.53 22 of the eggs
(Anas platyrhynchos) contained < 0.1
mg/kg

Gadwall egg 9 0.1 LD - 0.56 5 of the eggs
(Anas strepera) contained < 0.1
mg/kg

Florida Brown pelican LD < 0.05 mg/kg Blus et al.
(Pelecanus occidentalis) egg (1974b)

Atlantic coast egg 22 0.36 LD - 1.52
Gulf coast egg 27 0.10 trace - 0.40
Florida carcass 16 0.65 LD - 1.60 Blus et al.
1969 (shot birds) (1974b)
South Carolina carcass 5 0.51 LD - 1.50
(shot birds)
1969 Brown pelican egg 11 0.94 0.60-1.62 Blus et al.
1970 egg 10 0.62 0.20-1.30 (1974b, 1977,
1971 egg 65 0.46 0.20-1.02 1979b)
1972 egg 72 0.45 LD - 1.76
1973 egg 104 0.45 0.16-1.65
1974 egg 116 0.54 0.17-2.89
1975 egg 102 0.36 LD - 1.04
----------------------------------------------------------------------------------------------------------------------------------------

Table 15. (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical Species Type of Number of Mean Range^c Comments^c Reference
area/Year sample samples (mg/kg) (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
Louisiana
1971 Brown pelican egg 3 0.33 0.24-0.54 Blus et al.
1972 egg 12 0.45 0.30-0.79 (1979a)
1973 egg 21 0.64 0.30-1.12
1974 egg 25 0.84 0.49-1.61
1975 egg 30 1.08 0.64-2.25
1976 egg 25 0.94 0.44-3.03

Zimbabwe

Lake McIlwaine water 10 < 0.0001 Greichus et
1974 al. (1978a)
bottom sediment 10 0.004

Plankton composite 1 < 0.01^b

Oligochaete composite 1 0.08^b
(Branchiura sowerbyi)

Fish (3 spp.) composite 200/15^a 0.04b 0.03-0.07

Cormorant (2 spp.) brain 10 1.4^b
----------------------------------------------------------------------------------------------------------------------------------------
^aN₁/N₂: N₁is the number of individuals incorporated into N₂composites; the range corresponds to the composites.
^bConcentration expressed on dry weight basis.
^cLD = limit of detection, ND = not detectable.
^dSamples taken in 1967-1968.
^eSamples taken in 1969.
Table 16. Concentrations of dieldrin in non-target organisms
------------------------------------------------------------------------------------------
Species Geographical Year Concentration of dieldrin Reference
(component area (mg/kg wet weight)
analysed) Geometric Arithmetic Range
mean mean (N)^c
------------------------------------------------------------------------------------------
Fish (3 spp.) Great Britain 1977-79 - 0.00042^a <0.00035- Rickard &
(muscle) R. Thames 0.0020 (83) Dulley (1983)
(tidal)

Oysters USA: 1968-69 - 0.0014^a <0.001- Rowe et al.
(flesh) Louisiana 0.0034 (113) (1971)

Penguin Antarctic 1966-67 - 0.008^a <0.006-0.010 Tatton &
(abdominal (5) Ruzicka
fat) (1967)

Fish, USA: Virgin 1972-74 - 0.005^a <0.005-0.021 Reimold
invertebrates Islands, (141) (1975)
(various spp.) Puerto Rico
(whole body)

Fish (various USA: Western 1967-69 - 0.01^a <0.01-0.08 Klaassen &
spp.) (whole Kansas (393) Kadoum (1973)
body/tissues)

Northern fur USA: Alaska 1968-69 - 0.05^a <0.01-0.091 Anas & Wilson
seals (liver) (23) (1970a,b)

Birds (various Zimbabwe 1973-76 - 0.004^b <0.01-0.67 Tannock et
spp. including (34) dry al. (1983)
birds of prey) weight
(eggs)

Woodcock USA: eastern, 1970-71 - 0.018^a <0.01-0.55 Clark & McLane
(breast mid-western (129) (1974)
muscle)

Starlings USA 1967-68 - 0.139^a <0.005-1.18 White (1976)
(carcass) (360)

1970 - 0.117^a <0.005-3.59 White (1976)
(125)

Starlings USA 1972 - 0.098^a <0.005-1.56 White (1976)
(carcass) (130)

1974 - 0.057^a <0.005-1.01 White (1976)
(126)

Migratory USA: Florida 1964-73 - 0.2^a <0.01-1.10 Johnston
birds (various (829) (1975)
spp.) (breast
muscle)
------------------------------------------------------------------------------------------

Table 16. (contd.)
------------------------------------------------------------------------------------------
Species Geographical Year Concentration of dieldrin Reference
(component area (mg/kg wet weight)
analysed) Geometric Arithmetic Range
mean mean (N)^c
------------------------------------------------------------------------------------------
Bats (3 spp.) USA: 1973 0.2^a - <0.1-3.2 Clark &
(carcass) Maryland, (110) Prouty (1976)
West Virginia

Golden eagle USA: western, 1964-70 - 0.1 <0.1-12 Reidinger &
(fat) mid-western (69) Crabtree
states (1974)

Golden eagle Scotland 1964-74 0.12 - <0.05-6.9 Cooke et al.
(eggs) (100) (1982)

Tawny owl Great Britain 1963-65 0.15 - <0.05-12.7 Cooke et al.
(liver) (55) (1982)

Peregrine Great Britain 1964-77 0.20 - <0.05-7.6 Cooke et al.
falcon (eggs) (145) (1982)

Bald eagle USA 1971-72 0.6^b - <0.05-7.8 Cromartie et
(brain) (37) al. (1975)

Barn owl Great Britain 1963-75 1.21^b - <0.05-70.2 Cooke et al.
(liver) (251) (1982)

Hawks, Netherlands 1968-69 - 10.8 0.45-31 Koeman et al.
falcons, owls (19) (1969)
(liver)
------------------------------------------------------------------------------------------
^aIndicates living organisms collected by capture, shooting, etc.
^bIndicates organisms found dead or dying.
^cNumber in parentheses is the number of specimens.

Butler (1973) found mean dieldrin concentrations of 0.01 -
0.028 mg/kg (maximum concentration, 0.23 mg/kg) in estuarine
molluscs collected from 15 coastal states in the USA during the
period 1965 - 1972.

Fish sampled in Canada, in 1970, were found to have a mean
concentration of 0.071 mg dieldrin/kg (maximum concentration, 0.189
mg/kg). The concentrations in the water and bottom mud were of the
order of 0.005 µg/litre and 0.002 mg/kg, respectively (Miles &
Harris, 1971). In another study, fish from five provinces (78
locations) in Canada showed mean concentrations of 0.1 - 1 mg/kg
(maximum concentration, 0.56 mg/kg) (Reinke et al., 1972).

In coastal waters around England, Scotland, and Ireland, a
number of studies were carried out to determine dieldrin levels in
plankton, mussels, shrimp, and various other marine species
(1971 - 1975). The mean concentrations ranged from 0.003 to 0.178
mg/kg (maximum level, 2.43 mg/kg). Mussels showed the highest
levels (Williams & Holden, 1973; Lloyd et al., 1974; Van Den Broek,
1979; Cowan, 1981).

The presence of dieldrin in water, bottom sediment, and living
organisms has been studied in Africa (Kenya, Zimbabwe), Signy
Island (Antartica), New Zealand, and sub-antartic islands. The
concentrations of dieldrin in water were very low (< 0.01
µg/litre), those in bottom sediment were up to 0.004 mg/kg, and
those in water organisms (mainly plankton and invertebrates) were
0.01 - 0.03 mg/kg (dry weight basis). Penguin abdominal fat
contained 0.008 mg/kg and liver 0.002 mg/kg. The levels in fish
were < 0.1 mg/kg (dry weight) (Tatton & Ruzicka, 1967; Bennington
et al., 1975; Greichus et al., 1978a,b).

In the different areas where water, invertebrates, and fish
were analysed, birds and eggs were also studied for the presence of
dieldrin. In the eggs of a number of bird species from the
Falkland Islands, Hoerschelmann et al. (1979) found an average of
about 0.005 mg/kg dieldrin in 17 of the 46 eggs. In eggs of
coastal birds in the Federal Republic of Germany, the average
concentration (in 27 eggs) was higher (average, 0.031 mg/kg; range,
0.004 - 0.187 mg/kg).

Parslow & Jefferies (1973) found mean concentrations of up to
0.48 mg/kg in the liver of guillemots (Uria aalge) in the Irish
Sea. In eggs of the great skua (Catharacta skua), collected on the
Shetland Islands, Furness & Hutton (1979) measured a concentration
of 0.091 mg/kg (maximum concentration, 0.15 mg/kg). In South
Dakota, USA (1965 - 1967), Greichus et al. (1968) and Linder &
Dahlgren (1970) determined concentrations of up to 0.08 mg/kg in
the adipose tissue of pheasants and 0.02 mg/kg in eggs. In adipose
tissue of grouse, a mean concentration of 0.17 mg/kg was found.

When a number of eggs of several bird species was analysed in
eastern Canada (1970 - 1976), the mean concentrations were 0.06
mg/kg (maximum level, 0.68 mg/kg) (Szaro et al., 1979). In
different species of birds (and eggs) in the north and south of the
USA, White et al. (1980) found average concentrations in the
carcass of 0.13 - 0.47 mg/kg and Haseltine et al. (1981) found in
eggs of mergansers (Mergus serrator) a geometric mean concentration
of 0.78 mg/kg.

It is of interest that very low residues are found in the great
majority of eggs from areas remote from the regions of major
aldrin/dieldrin use. This is true of samples from the Falkland
Islands and Antartica and it is also true of a survey of 440 eggs
from 19 species of seabirds collected in 1973 - 1976 in Alaska
showing that residues in 410 eggs were less than 0.05 mg/kg (wet
weight). The highest residue found was 0.6 mg/kg (Ohlendorf et
al., 1982).

In Florida, Louisiana, and South Carolina, Blus et al. (1974b,
1977, 1979a,b) studied the dieldrin concentrations in the carcass
and eggs of the brown pelican (Pelecanus occidentalis) during the
period 1969 - 1976. The mean concentration in the carcass was
about 0.6 mg/kg (maximum concentration, 1.6 mg/kg) and, in the
eggs, about 0.6 mg/kg (maximum concentration, 2.89 mg/kg).

Jefferies (1972) carried out a survey of the residue levels in
bats from the East Anglian area, United Kingdom, to provide more
information on the situation concerning the British bat population.
Four species of bats were studied, Pipistrellus pipistrellus,
Plecotus auritus, Myotis nattereri, and Myotis daubentoni.
Thirty specimens were collected during the period 1963 - 1970.
Dieldrin was found in eight liver specimens (range 0.04 to 3.3 mg/kg
tissue), in two adipose tissue samples (4.0 and 7.9 mg/kg), and in
six total body samples (0.07 to 0.50 mg/kg tissue).

Clark et al (1978) estimated the dieldrin levels in 28 juvenile
grey bats (Myotis grisesceus) taken from three caves in Missouri,
USA. The concentrations varied between the individual animals and
between the caves. Dieldrin was detected in the brain of 18/28
bats, the range being 0.4 - 10 mg/kg tissue (wet weight basis), and
in the carcass of 22/28 bats (range 1.7 - 1379 mg/kg carcass; lipid
weight). The authors believed that there was a direct link between
the field mortality of bats and dieldrin residues acquired through
the food chain.

Clark et al. (1980, 1983b) detected dieldrin in the brain and
carcass of grey bats found dead in a Missouri cave in 1976 and
1977. In 1976, the geometric mean was 7.5 and 650 mg/kg tissue
(respectively for brain on wet weight basis and for carcass on
lipid weight basis) and in 1977, 8.6 and 867 mg/kg tissue,
respectively. Other chlorinated hydrocarbons were also present
such as heptachlor epoxide, DDE, and PCBs.

Clark (1981) studied the brain to carcass lipid relationship
for dieldrin and estimated a minimum lethal level for brain tissue
of 4.6 mg dieldrin/kg (wet weight) and for carcass of 390 (210 -
800) mg dieldrin/kg tissue (lipid weight).

In two other caves in Missouri, dead grey bats were found in
1980, and dieldrin and other halogenated insecticides were found in
the brain and carcass. Seven animals were studied and dieldrin
concentrations ranging from not detectable to 21 mg/kg tissue (wet
weight) were found in the brain and 4.1 - 970 mg/kg in the carcass
(lipid weight). The concentrations in brain were of the same order
as those found in the other caves in Missouri. Bat mortality in
July 1981 occurred simultaneously, in one case, with the death of
macroinvertebrates in the outlet stream of the cave (Clarke et al.,
1983a).

Dieldrin residues ranging from trace to 3.3 mg/kg have been
detected in marine mammals, including whales and seals (Holden,
1975; Rosewell et al., 1979). Other mammals in which dieldrin has
been found include the fisher, fox, marten, mink, raccoon, and

skunk (Frank et al., 1979), the highest concentrations being found
in the predators at the top of the food chain, i.e., mink and
marten (9.7 µg/kg wet tissue).

Other studies on the presence of dieldrin in non-target species
and their environment are summarized in Tables 15 and 16 (Bugg et
al., 1967; Koeman et al., 1967; Rowe et al., 1971; Faber et al.,
1972; Meith-Avcin et al., 1973; Voutsinou-Talia-Douri & Satsmadjis,
1982). Most of these results are an indication of adventitious
contamination, i.e., there is no close relationship to a particular
use of aldrin or dieldrin.

The use of aldrin and dieldrin as seed-dressing agents has
undoubtedly resulted in high concentrations of dieldrin in the body
tissues of animals found dead. An association between the use of
aldrin and dieldrin seed dressings and the deaths of wood-pigeons
(Columba palumbus) was first noted by Carnaghan & Blaxland (1957)
and Turtle et al. (1963, 1965). In wood-pigeon, pheasant,
partridge, and corvids found dead, Turtle et al. (1965) found mean
concentrations of 10, 2.3, 7.3, and 2 mg/kg liver, respectively,
(maximum concentrations of 59.2, 28.8, 46.3, and 14 mg/kg liver).
The concentrations in birds that had been shot were much lower.

Table 17 summarizes the residue levels found following the use
of dieldrin for the control of the tsetse fly and arising from
other uses of aldrin and dieldrin, e.g., as seed-dressing agents.
Several other reports on seed-dressing incidents in the United
Kingdom have been published, e.g., Murton & Vizoso (1963) and
Jefferies et al. (1973).

5.1.7.1 Occurrence of dieldrin in birds of prey and fish-eating
birds

Changes in the populations of hawks, falcons, and other raptors
have prompted extensive studies of the concentrations of dieldrin
in the tissues of birds and eggs. These data are summarized in
Table 18.

The concentrations of dieldrin in the tissues of bald eagles
(Haliacetus leucocephalus) that were found dead during the period
1967 - 1977 were estimated by Mulhern et al. (1970), Belisle et al.
(1972), Cromartie et al. (1975), Prouty et al. (1977), and Kaiser
et al. (1980). The concentrations (geometric mean) in the brain
were 0.1 - 2.0 mg/kg tissue, with a maximum of 11 mg/kg. Because
the population declines of some birds of prey and some fish-eating
birds have been associated with the use of aldrin and dieldrin, the
residues in some of these species will be discussed in more detail.

Table 17. Residues in non-target species - concentrations related to particular uses or discharges of
aldrin/dieldrin
---------------------------------------------------------------------------------------------------------
Species Component Geographical Year No. of Concentration of Comments Reference
analysed area speci- dieldrin (mg/kg)
mens^a Mean^b Range
---------------------------------------------------------------------------------------------------------
Woodpigeon liver Netherlands 1966 20 2.8^b 0.05-27.1 seed dressing Fuchs
(Columba 4 79^c 44.2-136 (1967)
palumbus)

Pink-footed liver United 1972 6 31^c 15-48 seed dressing Stanley &
goose (Anser Kingdom -73 Bunyan
branchyrhynchus) (1979)

Pheasant egg USA: 1966 120 0.3 0.02-2.82 soil Greenberg &
(Phasianus Illinois insecticide Edwards
colchicus) (1970)

Birds (various liver Kenya 1968 12 28.2^c 18-57 tsetse fly Koeman &
spp.) 21 1.7^b 0.16-6 control (dead Pennings
brain 10 14.3^c 6-22 birds found (1970)
11 0.2^b 0.06-0.68 during 10 days
after spray
application;
live birds
collected 2
months later)

Insects (various whole Cameroon 1979 227 0.2^c ND^e- 13.2 tsetse fly Mueller et.
spp.) body control al. (1981)

Fish whole 124 0.09 ND - 214.3
(Aphyosemion body
bualanum)

Birds (various liver 40 1.51^b ND - 7.24
spp.)

Fruit bat liver 20 79.2^b ND - 174.81
(2 spp.)
---------------------------------------------------------------------------------------------------------

Table 17. (contd.)
---------------------------------------------------------------------------------------------------------
Species Component Geographical Year No. of Concentration of Comments Reference
analysed area speci- dieldrin (mg/kg)
mens^a Mean^b Range
---------------------------------------------------------------------------------------------------------
Rat (Praomys liver 13 0.37 ND - 1.20 Mueller et
tullbergi) al. (1981)

Common gallinule egg USA: 1965 4/23^d 9.6 2.23-13.17 rice fields Causey et
(Gallinula Louisiana sown with al. (1968)
chloropus) 1966 14 9.4 1.13-22.12 aldrin-treated
seed

Purple gallinule egg 1965 2/16^d 9.7 6.47-12.94
(Porphyrula 1966 56 6.5 0.49-15.35
martinica)

Common gallinule egg USA: 1968 6 17.5 4.69-28.07 rice fields Fowler et
Louisiana sown with al.(1971)
1969 12 4.8 1.16-10.7 aldrin-treated
seed

Purple gallinule egg 1968 26 9.4 3.23-16.43
1969 33 3.8 1.56-13.62

Invertebrates composites USA: Texas 1967 1208/ 1.1^b LD^f- 3.2 aldrin-treated Flickinger
of whole Gulf coast -71 16 (3.1) (LD - 16.3) seed & King
body (1972)

Crayfish whole 105/8 6.3^c LD - 17
(2 spp.) body (2.1) (LD - 9)

Cricket frog whole 18/3 0.1^b LD - 0.1
(Acris crepitans body
blanchardi)

Fish (4 spp.) whole 592/4 1.2^b 0.4-2.8
body

Turtles (2 spp.) whole 5/2 0.9^b 0.6-1.2
body (2.4) (LD - 4.8)

---------------------------------------------------------------------------------------------------------

Table 17. (contd.)
---------------------------------------------------------------------------------------------------------
Species Component Geographical Year No. of Concentration of Comments Reference
analysed area speci- dieldrin (mg/kg)
mens^a Mean^b Range
---------------------------------------------------------------------------------------------------------
Snakes (3 spp.) whole USA: Texas 1967 3/3 2.4^b 0.1-5.7 Flickinger
body Gulf coast -71 & King
(1972)

Great horned owl brain 1 6.3^c -

Birds (various brain 27 8.5^c LD - 22 192 dead birds
spp.) (0.1) (LD - 0.2) collected from
1967-71

Fulvous tree egg 69/14 2.5 <0.1-9.5
duck
(Dendrocygna
bicolor)

Owls (various liver United 1974 22 24^c 1.7-46 death of many Jones et
spp.) Kingdom -76 owls due to al. (1978)
(London Zoo) dieldrin
poisoning;
sawdust from
dieldrin-
treated wood
the probable
source of
contamination
---------------------------------------------------------------------------------------------------------
^aN₁/N₂: N₁is the number of incorporated into N₂composites; the range corresponds to the composites.
^bIndicates living organisms collected by capture, shooting, etc. Values in parentheses are the
concentrations of aldrin.
^cIndicates organisms found dead or dying. Values in parentheses are the concentrations of aldrin.
^dClutches/eggs.
^eND = not determined.
^fLD = limit of detection.

Table 18. Concentrations of dieldrin in tissues and eggs of birds of prey and fish-eating
birds found dead
-------------------------------------------------------------------------------------------
Species Type of Geographical Year No. of Concentration of Reference
sample area speci- dieldrin (mg/kg)
mens Mean^a Range^b
-------------------------------------------------------------------------------------------
Kestrel (Falco liver Netherlands 1968-69 7 - 1.1-24 Koeman et
tinnunculus) al. (1969)

Kestrel (Falco liver United 1963-65 74 1.09 0.94-1.27 Cooke et
tinnunculus) Kindgom 1966-71 144 1.06 0.91-1.24 al. (1982)
1972-75 125 1.43 1.19-1.72
1977 31 0.31 0.21-0.45

Sparrow-hawk liver Netherlands 1969 3 - 0.9-19 Koeman et
(Accipiter nisus) al. (1969)

Sparrow-hawk liver United 1963-65 30 1.20 0.97-1.49 Cooke et
(Accipiter nisus) Kingdom 1966-71 82 0.29 0.22-0.38 al. (1982)
1972-75 83 0.61 0.48-0.78
1977 26 0.22 0.15-0.32

Sparrow-hawk egg United 1963-65 24 2.09 1.63-2.67 Cooke et
(Accipiter nisus) Kingdom 1966-71 154 0.69 0.60-0.79 al. (1982)

Buzzard liver Netherlands 1968-69 5 - 0.45-31 Koeman et
(Buteo buteo) al. (1969)

Grey heron liver United 1963-65 26 1.13 0.66-1.94 Cooke et
(Ardea cinerea) Kingdom 1966-67 69 0.92 0.67-1.26 al. (1982)
1972-75 57 0.74 0.57-0.96
1977 12 0.17 0.08-0.37

Kingfisher liver United 1964-65 4 6.83 3.95-11.8 Cooke et
(Alcedo atthis) Kingdom 1966-71 37 1.56 1.23-1.98 al. (1982)
1972-75 22 1.16 0.89-1.53

Peregrine falcon liver United 1963-77 15 1.91 1.35-2.71 Cooke et
(Falco peregrinus) Kingdom al. (1982)

Barn owl liver United 1963-65 48 1.31 1.08-1.60 Cooke et
(Tyto alba) Kingdom 1966-71 94 1.42 1.19-1.69 al. (1982)
1972-75 114 1.07 0.90-1.28
1977 29 0.26 0.18-0.37

Long-eared owl liver United 1963-77 30 1.75 1.14-2.70 Cooke et
(Asio otus) Kingdom al. (1982)

Bald eagle liver USA 1964-65 44 0.28 LD - 11.9 Reichel et
(Haliacetus (LD <0.05 al. (1969)
leucocephalus) mg/kg)
-------------------------------------------------------------------------------------------

Table 18. (contd.)
-------------------------------------------------------------------------------------------
Species Type of Geographical Year No. of Concentration of Reference
sample area speci- dieldrin (mg/kg)
mens Mean^a Range^b
-------------------------------------------------------------------------------------------
Peregrine falcon egg United 1963-65 23 0.59 0.49-0.71 Cooke et
(Falco peregrinus) Kingdom 1966-71 76 0.14 0.11-0.17 al. (1982)
1972-75 34 0.18 0.11-0.28
1977 12 0.34 0.25-0.46

Bald eagle egg USA 1969-70 12 0.08^c LD - 0.3 Wiemeyer et
(Haliacetus (LD <0.05 al. (1972)
leucocephalus) mg/kg)

USA: 11 0.83^c 0.15-2.3
Alaska, 4
other states
-------------------------------------------------------------------------------------------
^aGeometric mean, except for footnote ^cwhich is arithmetic mean.
^bRange of value within 1 standard error.
^cArithmetic mean.

(a) Grey heron (Ardea cinerea)

This is one of the highly contaminated species in the United
Kingdom. Relatively high levels of dieldrin have been measured in
the livers of herons found dead, together with high levels of DDT-
type compounds and polychlorinated biphenyls (Cooke et al., 1982).
The geometric mean concentrations of dieldrin for various periods
within the range 1963 - 1977 are given in Table 18. The geometric
mean concentration of dieldrin in the livers of 143 samples over
the period 1963 - 1975 was 0.9 mg/kg. Of the herons found dead,
50% contained less than 1 mg dieldrin/kg liver, whereas 14%
contained 10 mg/kg or more.

(b) Kestrel (Falco tinnunculus)

The geometric mean concentration of dieldrin in the livers of
374 kestrels found dead in the United Kingdom during the period
1963 - 1977 was 1.2 mg/kg (Cooke et al., 1982). Some 50% of the
kestrels found dead contained less than 1 mg dieldrin/kg liver, 18%
contained more than 10 mg/kg, and 8% more than 20 mg/kg. Higher
levels were found in the Netherlands (Fuchs, 1967; Koeman et al.,
1969).

Sierra et al. (1987) studied the presence of residues of aldrin
and dieldrin in the liver, muscle, fat, kidneys, and brain of four
kestrels from the province of Leon, Spain. The concentrations of
aldrin ranged from 0.003 to 0.65 mg/kg tissue (highest in fat and
kidneys), whereas those of dieldrin ranged from 0.005 to 0.151
mg/kg tissue (highest in liver; fat not estimated). All values
were based on wet weight.

The geometric mean concentration of dieldrin in the liver of
195 sparrow-hawks found dead in the United Kingdom over the period
1963 - 1977 was 0.5 mg/kg (Cooke et al., 1982). About 62% of the
dead sparrow-hawks contained less than 1 mg dieldrin/kg liver, and
about 7% contained more than 10 mg dieldrin/kg liver.

Three sparrow-hawks found dead or dying in the Netherlands in
1969 contained 0.89, 1.1, and 19 mg dieldrin/kg liver, respectively
(Koeman et al., 1969). One dead sparrow-hawk (1966) contained 18.4
mg dieldrin/kg liver (Fuchs, 1967).

Sierra et al. (1987) studied the presence of residues of aldrin
and dieldrin in three sparrow-hawks in Leon, Spain. The average
concentrations of dieldrin ranged from 0.1 to 0.45 mg dieldrin/kg
tissue (liver, kidneys, brain) but in fat an average level of 17.3
mg/kg was found (all values were based on wet weight). Only low
levels (< 0.01 mg/kg tissue) of aldrin were found in fat.

(d) Barn owl (Tyto alba)

The geometric mean concentration of dieldrin in the liver of
251 barn owls found dead in the United Kingdom (1963 - 1977) was
1.2 mg/kg (Cooke et al., 1982). About 49% of the barn owls
contained less than 1 mg dieldrin/kg liver, while about 15%
contained at least 10 mg dieldrin/kg liver.

The concentration of aldrin and dieldrin in the muscle, liver,
fat, brain, and kidneys of 23 barn owls, collected in the province
of Leon, Spain, was determined (91 samples in total). The
incidence of aldrin in the tissues ranged from 76 to 83%, and of
dieldrin from 4 to 27%. The average concentration in these organs
and tissues was 0.03 - 0.11 mg aldrin/kg and 0.009 - 0.2 mg
dieldrin/kg tissue (wet weight). The highest concentration was in
the kidneys for aldrin and in the brain for dieldrin (Sierra &
Santiago, 1987).

The concentrations in all four of the above species in the
United Kingdom showed seasonal, annual, and regional trends.
Residue levels in herons decreased progressively after 1963 - 1965
until 1977, whereas the main decrease in levels in sparrow-hawks
occurred between 1963 - 1965 and 1966 - 1971, there being little
subsequent change. In kestrels and barn owls, there was no overall
trend between 1963 and 1974 - 1975, but significant declines in
levels had occurred by 1977. The residues in the livers of herons,
kestrels, and barn owls were significantly higher in areas of
eastern England (the main wheat bulb fly infestation areas) than in
other regions of the United Kingdom. These differences are
probably indicative of the use of aldrin- or dieldrin-dressed grain
in eastern England. Few samples of sparrow-hawk's livers were
available from eastern England, but the residues showed a similar
regional difference.

(e) Bald eagle (Haliacetus leucocephalus)

A survey of the residues of dieldrin in the carcass, liver, and
brain of bald eagles was initiated in 1960 by the Patuxent Wildlife
Research Centre, USA. The median concentration (1964 - 1965) was
0.1 mg dieldrin/kg brain and about 0.3 mg dieldrin/kg liver
(Reichel et al., 1969). During the period 1966 - 1977, mean
concentrations ranged from 0.1 to 2 mg dieldrin/kg brain (Mulhern
et al., 1970; Belisle et al., 1972; Cromartie et al., 1975; Prouty
et al., 1977; Kaiser et al., 1980).

(f) Other birds of prey and fish-eating birds

The surveys of the residues of dieldrin in other raptors have
been less extensive than those for the five species discussed
above. The geometric mean concentrations in the livers of 12 other
species (283 birds) in the United Kingdom (Cooke et al., 1982) in
the period 1963 - 1977 were between 0.02 and 2.35 mg/kg. Those for
the golden eagle (14 birds) in the USA during the period 1964 -
1965 were between trace levels and 0.4 mg/kg (Reichel et al.,
1969).

5.2. General Population Exposure

5.2.1. Adults

5.2.1.1 Aldrin

In the great majority of investigations into the presence of
organochlorine compounds in human blood and other tissues, the
level of aldrin was below the limits of detection. However, there
are a few reports of aldrin being present in human blood, placenta,
adipose tissue, and other tissues (Radomski & Fiserova-Bergerova,
1965; Kanitz & Castello, 1966; Selby et al., 1969a,b; Herrera
Marteache et al., 1978; Fernicola & Azevedo, 1982; Mossing et al.,
1985). These findings are unusual. The report that aldrin was
present in eight samples of blood, when none was found in the
matched adipose tissue samples, also seems anomalous (Selby et al.,
1969b). Fernicola & Azevedo (1982) suggested that some other
compounds with the same retention time as aldrin had perhaps led to
false results. None of these investigators established the
identity of the component, reported as "aldrin".

5.2.1.2 Concentrations of dieldrin in adipose tissue

Following the introduction of gas-liquid chromatography, there
have been numerous investigations of the concentration of dieldrin
in the adipose tissue of members of the general population who have
had no know occupational exposure to aldrin or dieldrin. Surveys
have been made in more than 20 countries, but in some surveys the
number of samples of fat analysed was small. In the USA and the
United Kingdom, there have been several surveys during the period
1961 - 1977. The results are summarized in Table 19, using two
statistics to define the samples: arithmetic mean (or geometric
mean in some American surveys) and maximum value as an indication
of the upper limit of variability (upper confidence limit in a few
surveys). The distribution tends to be skewed to the right, i.e.,

there is a greater number of high values than would be expected if
the samples had a normal distribution (Hunter et al., 1963; Morgan
& Roan, 1970). The maximum values in some surveys are so large
that they may correspond to individuals with an occupational
exposure. The results for stillborns and young babies and children
are discussed in section 5.2.2.

Most of the mean values are in the range 0.1 - 0.3 mg dieldrin
kg body fat and are usually smaller than those of total DDT by at
least a factor of 10. Surveys in the USA, United Kingdom, and
Netherlands indicate that there has been a decline of about 50% in
the concentration of dieldrin in the body fat since the mid 1970s
(Abbott et al., 1981; Ministry of Welfare, Health and Culture, The
Netherlands, 1983).
Table 19. Concentrations of dieldrin in the body fat of the general population
------------------------------------------------------------------------------------------
Country Year No. of Method of Dieldrin Reference
samples^a clean-up^b Mean Maximum
(mg/kg fat)
------------------------------------------------------------------------------------------
North America

Canada 1966 47 (N) I 0.22 0.53 Brown (1967)
1967-68 51 (N) II 0.12 0.83 Kadis et al. (1970)
1969 221 (N) II 0.12 0.46 Ritcey et al. (1973)
1969 5 (-) - 0.08 - Mastromatteo (1971)
1970 3 (-) - 0.22 - Mastromatteo (1971)
1972 168 (N) II 0.069 0.35 Mes et al. (1977)
1969-74 448 (N) - 0.12 0.88 Holdrinet et al.
(1977)
1976 99 (N) 0.049 0.211 Mes et al. (1982)
1979-81 175 (N) II 0.04 0.13 Williams et al.
(1984)
1980 29 (N) 0.046 Mes et al. (1985)

USA 1961-62 28 (B) II 0.15 0.36 Dale & Quinby (1963)
1962-66 221 (N) II 0.14 1.39 Hoffman et al. (1967)
1964 25 (N) II 0.29 1.15 Hayes et al. (1965)
1964 64 (N) - 0.31 2.82 Zavon et al. (1965)
1964-67 42 (N) none 0.21 0.70 Radomski et al.
(1968)
1965-67 146 (N) none 0.22 0.77 Edmundson et al.
(1968)
1966-68 70 (N) II 0.14 - Morgan & Roan (1970)
1967 30 (N) II 0.03^f - Casarett et al.
(1968)
1968 48 (N) II 0.20 - Warnick (1972)
1969 15 (N) II 0.15 - Warnick (1972)
1969 26 (B) II 0.33^f 0.80^c Burns (1974)
1970 40 (N) II 0.15 - Warnick (1972)
1970 68 (B) II 0.29^f 0.73^c Burns (1974)
1970 202 (B) II 0.2 1.0 Wyllie et al. (1972)
1970 1412 (N/B) II 0.18^f 15.20 Kutz et al. (1979)
1971 88 (B) II 0.36^f 0.78^c Burns (1974)
1971 1615 (N/B) II 0.22^f 2.91 Kutz et al. (1979)
1972 39 (B) II 0.43^f 1.00^c Burns (1974)
------------------------------------------------------------------------------------------

1972 1913 (N/B) II 0.18^f 2.91 Kutz et al. (1979)
1973 1094 (N/B) II 0.18^f 5.64 Kutz et al. (1979)
1974 898 (N/B) II 0.15^f 2.21 Kutz et al. (1979)
Louisiana 1980 8 (B) II 0.15^f 0.34 Holt et al. (1986)
1984 10 (B) II 0.10^f 0.19 Holt et al. (1986)

Central and South America

Mexico 1975 19 (N) II 0.06^f 0.24 Albert et al. (1980)
1975 9 (B) II 0.18^f 0.49 Albert et al. (1980)
1975 9 (N) II 0.05^f 0.12 Albert et al. (1980)

Argentina - 47 (N) IV 0.38 0.66^c Wassermann et al.
(1969)

Brazil 1969-70 17 (N/B) III 0.02^e 0.12 Wassermann et al.
(1972a)
1969-70 69 (N/B) III 0.12^e 1.62 Wassermann et al.
(1972a)

Europe

Belgium 1968-69 37 (N) II 0.13 0.50 Wit (1971)
1975 60 (N) II 0.26 1.16 Dejonckheere et al.
(1977)
1977 58 (N) II 0.12 0.69 Van Haver et al.
(1978)

Denmark 1965 18 (N) - 0.20 0.34 Weihe (1966)
1972-73 70 (N) II 0.16^f 0.53 Kraul & Karlog (1976)

France 1971 100 (N) II 0.45 1.45 Fournier et al.
(1972)

Germany, 1967 15 (B) I 0.18^f 0.36 Wuenscher & Acker
Federal (1969)
Republic of 1973 50 (N) - 0.14 0.23 Acker & Schulte
(1974)

Greece - 50 (N/B) II 0.23 0.87 Panetsos et al.
(1975)

Italy 1965 9 (N) II 0.59 2.77 Kanitz & Castello
(1966)
1966 22 (N/B) II 0.68^f 1.55 Del Vecchio & Leoni
(1967)
------------------------------------------------------------------------------------------

Table 19. (contd.)
------------------------------------------------------------------------------------------
Country Year No. of Method of Dieldrin Reference
samples^a clean-up^b Mean Maximum
(mg/kg fat)
------------------------------------------------------------------------------------------
Italy 1965-68 33 (B) - 0.32 3.15 Paccagnella et al.
(contd.) (1971)
1965-68 11 (B) - 1.95 5.70 Paccagnella et al.
(1971)
1965-68 52 (N) - 0.91 3.55 Paccagnella et al.
(1971)

Netherlands 1964 34 (N) II 0.31^f - Wit (1971)
1966 11 (N) II 0.20 0.50 De Vlieger et al.
(1968)
1968-69 34 (N) II 0.27^f 1.5 Wit (1971)
1973-74 102 (N) - 0.2 - Greve & Wegman (1985)
1975 25 (N) - 0.11 - Greve & Wegman (1985)
1976 74 (N) - 0.09 - Greve & Wegman (1985)
1977-78 78 (N) - 0.11 - Greve & Wegman (1985)
1979 25 (B) - 0.09 - Greve & Wegman (1985)
1980 24 (N) - 0.10 - Greve & Wegman (1985)
1981 53 (N) - 0.07 - Greve & Wegman (1985)
1982 54 (N) - 0.07 - Greve & Wegman (1985)
1983 78 (N) - 0.06 - Greve & Wegman (1985)

Spain - 40 (B) III 0.15 0.49 Herrera Marteache et
al. (1978)

Switzerland 1972 13 (B) II 0.29 0.57 Zimmerli & Marek
(1973)

United 1961 131 (N) II 0.21 1.29 Hunter et al. (1963)
Kingdom 1963-64 66 (N) II 0.26 0.9 Egan et al. (1965)
1964 50 (N) II 0.27 0.85 Robinson et al.
(1965)
1964 50 (B) II 0.25 0.65 Robinson et al.
(1965)
1965 101 (N) II 0.34 1.80 Cassidy et al. (1967)
1966 53 (B) II 0.21 0.60 Hunter et al. (1967)
1965-67 248 (N) II 0.21 1.0 Abbott et al. (1968)
1967 18 (B) II 0.27 0.68 Hunter et al. (1967)
1969-71 201 (N) II 0.16 0.68 Abbott et al. (1972)
1976-77 236 (N) II 0.11 0.49 Abbott et al. (1981)
1982-83 187 (N) - 0.074 0.27 UK-HMSO (1986)

Africa

Kenya 1969-70 32 (N) III 0.030^d 0.18 Wassermann et al.
(1972b)
1969-70 51 (N) III 0.064^e 0.28 Wassermann et al.
(1972b)
------------------------------------------------------------------------------------------

Nigeria 1969 46 (N) III 0.059^d 0.73 Wassermann et al.
(1972c)
1969 90 (N) III 0.13^e 0.98 Wassermann et al.
(1972c)

South Africa 1969 114 (N/B) IV 0.039 - Wassermann et al.
(1970)

Uganda 1969-70 16 (N) III 0.023^d 0.058 Wassermann et al.
(1974a)
1969-70 39 (N) III 0.031^e 0.59 Wassermann et al.
(1974a)

Asia

India 1964 35 (N) II 0.04 0.36 Dale et al. (1965)

Iran 1974-76 170 II 0.049 0.75 Hashemy-Tonkabony &
Soleimani-Amiri
(1978)

Israel 1967-69 61 (N) III 0.10^d 0.315 Wassermann et al.
(1974b)
1967-69 162 (N) III 0.14^e 3.96 Wassermann et al.
(1974b)

Japan Prior to 1973 241 (N) II 0.13 0.98 Curley et al. (1973)
1974-75 59 (N) II 0.09^f 0.51 Yoshimura et al.
(1979)

Thailand 1969-70 8 (N) III 0.077^d 0.459 Wassermann et al.
(1972d)
1969-70 27 (N) III 0.10^e 1.20 Wassermann et al.
(1972d)
1975-76 9 II 0.322 - Department of
Agriculture Thailand
(1976)^g

Oceania

Australia 1965 53 (N) II 0.046 0.43 Bick (1967)
1965-66 12 (N) IV 0.67 0.99 Wassermann et al.
(1968)
1969-70 75 (N) II 0.21 2.60 Brady & Siyali (1972)
------------------------------------------------------------------------------------------

New Zealand Prior to 1967 45 (N) II 0.28 0.77 Brewerton & McGrath
(1967)
1965 43 (B) II 0.41 - Copplestone et al.
(1973)
1966 54 (B) II 0.30 - Copplestone et al.
(1973)
1967 68 (B) II 0.43 - Copplestone et al.
(1973)
1968 64 (B) II 0.33 - Copplestone et al.
(1973)
1969 25 (B) II 0.27 - Copplestone et al.
(1973)

Papua New 1969-70 38 (N) II 0.17 0.72 Brady & Siyali (1972)
Guinea
------------------------------------------------------------------------------------------
^aSamples taken at necropsy (N) or during elective surgery (B).
^bMethod of clean-up:

I Removal of neutral lipids at -70 °C.
II Separation into two or more fractions by eluting from a Florisil column (with prior
liquid/liquid partition to reduce neutral lipid content, in most investigations using
this clean-up procedure).
III Florisil column clean-up without separation into two or more fractions.
IV Kontes co-distillation.
- Method not reported.

^cUpper confidence limit ( P = 0.025) for the set of samples.
^dAge group 5-24 years.
^eAge group 25 years and older.
^fResults expressed in terms of extractable lipid content.
^gPersonal communication to IPCS in 1987.
5.2.1.3 Concentrations of dieldrin in blood

The concentrations of dieldrin in whole blood or serum of
members of the general population have been determined in a few
countries and are summarized in Table 20. The concentrations are
very low (µg/litre) and it is essential that the sensitivity of the
analytical method is at least 0.1 µg/litre. Two analytical
procedures have been used (Dale et al., 1966; Richardson et al.,
1967a), which give significant different results: the acetone
extraction procedure (method II in Table 20) gives results that are
about 50% higher than the hexane extraction procedure (method I in
Table 20) and showed a better reproducibility (Robinson et al.,
1967a). An interlaboratory comparison of the hexane extraction
method showed that large variations in results may occur (Thompson,
1976).

Table 20. Concentration of dieldrin in the blood of the general population
------------------------------------------------------------------------------------------
Country Year Number of Analytical Dieldrin Reference
samples^a method^b Mean Maximum
(µg/litre)
------------------------------------------------------------------------------------------
USA 1965 10 (B) I 1.4 2.8 Dale et al. (1966)
1967-68 1000 (S) I 0.5 25 Watson et al. (1970)
1967-71 970 (S) I 0.9 - Warnick (1972)
1967-68 37 (H) III 4 - Morgan & Roan (1970)
1970 202 (S) I 0.9 10 Wyllie et al. (1972)
Prior to 1981 59 (S) I 0.6 10.1 Barquet et al.
(1981)
1976-80 6078 (S) ? ~1.4^c 16 Murphy & Harvey
(1985)

Hawaii 1968-70 1107 (S) I 1.46 11 Klemmer et al.
(1973)
Lanai Island 1968-70 484 (S) I 1.3 26 Klemmer et al.
(1973)

Europe

Netherlands 1978 70 (B) - < 0.5 - Greve & Wegman
(1985)
1980 48 (B) - < 0.4 - Greve & Wegman
(1985)
1981 127 (B) - < 0.4 - Greve & Wegman
(1985)
1982 54 (B) - < 0.5 - Greve & Wegman
(1985)

Switzerland 1972 ~100 (S) I 1.1 - Zimmerli & Marek
(1973)

United Kingdom 1962 20 (B) II 1.6 10.0 Hunter et al. (1967)
1964 61 (B) II 1.4 5.0 Hunter et al. (1967)
1965 25 (B) II 1.7 8.7 Hunter et al. (1967)
1966 55 (B) II 1.8 4.3 Hunter et al. (1967)
1968 18 (B) II 0.9 1.1 Robinson & Roberts
(1969)

Oceania

Australia - 52 (B) I^ust 2.3 13 Siyali (1972)
- 47 (B) I^ust none - Siyali (1973)
------------------------------------------------------------------------------------------
^aSamples of whole blood (B), serum (S), whole blood from heart chamber (during autopsy)
(H).
^bAnalytical methods (all use gas-liquid chromatography with an electron-capture detector):
I Hexane extraction.
I^ustHexane extraction combined with ultrasonic treatment.
II Acetone extract on silica gel column.
III Solvent extraction and Florisil column clean-up.
^cIn 260 positive samples.
5.2.1.4 Concentration of dieldrin in other tissues

A few investigations of the concentrations of dieldrin in other
body tissues have been made and some of the results are summarized
in Table 21.
Table 21. Concentration of dieldrin in various tissues from members of the general
population
------------------------------------------------------------------------------------------
Tissue Country Year No. of Dieldrin Reference
samples Mean Maximum
(mg/kg)
------------------------------------------------------------------------------------------
Liver Canada 1967-68 50 0.25^a 3.0^a Kadis et al. (1970)

USA 1967 42 0.009 - Casarett et al. (1968)

USA 1966 42 0.035 0.22 Fiserova-Bergerova et al. (1967)

USA 1966-68 35 0.047 - Morgan & Roan (1970)

Denmark 1972-73 18 0.29^a - Kraul & Karlog (1976)

Netherlands 1966 11 0.034 0.081 De Vlieger et al. (1968)

Japan 1974-75 30 0.39^a 1.73^a Yoshimura et al. (1979)

Thailand 1975-76 16 0.010 - Dept. of Agriculture, Thailand
(1976)^b

Kidneys Canada 1967-68 47 0.10^a 1.35^a Kadis et al. (1970)

USA 1967 38 0.021 - Casarett et al. (1968)

USA 1966 42 0.013 0.04 Fiserova-Bergerova et al. (1967)

USA 1966-68 35 0.014 - Morgan & Roan (1970)

USA 1973 12 0.006 0.009 Anon (1974c)

Thailand 1975-76 16 0.010 - Dept. of Agriculture, Thailand
(1976)^b

Brain Canada 1967-68 30 0.002^a - Kadis et al. (1970)

USA 1967 32 0.003 - Casarett et al. (1968)

USA 1966 42 0.035 0.10 Fiserova-Bergerova et al. (1967)

USA 1966-68 35 0.007 - Morgan & Roan (1970)

Denmark 1972-73 21 0.057^a - Kraul & Karlog (1976)

Netherlands 1966 28 0.0075 0.021 De Vlieger et al. (1968)
------------------------------------------------------------------------------------------

Table 21. (contd.)
------------------------------------------------------------------------------------------
Tissue Country Year No. of Dieldrin Reference
samples Mean Maximum
(mg/kg)
------------------------------------------------------------------------------------------
Brain Thailand 1975-76 16 0.010 - Dept. of Agriculture, Thailand
(contd.) (1976)^b

Gonads Canada 1967-68 39 0.06^a 0.86^a Kadis et al. (1970)

USA 1967 36 0.008 - Casarett et al. (1968)

USA 1966 42 0.035 0.20 Fiserova-Bergerova et al. (1967)
------------------------------------------------------------------------------------------
^aResults expressed in terms of extractable lipid content.
^bPersonal communication to IPCS in 1987.
5.2.2. Babies, infants, and mother's milk

Dieldrin penetrates the placenta and, as a result of
transplacental exposure, may occur in the blood, adipose tissue,
and other tissues of the fetus and newborn baby (Table 22). The
concentrations are lower by a factor of 2 - 10 than those of their
mothers or other adults (Table 19). There is no difference between
infants and adults in the brain/liver/fat ratio of dieldrin
concentrations (Fiserova-Bergerova et al., 1967; Casarett et al.,
1968). A similar situation exists in animals, e.g., pigs (Uzoukwu
& Sleight, 1972).

Dieldrin is also excreted in the milk of human beings and
various animal species. Table 23 summarizes the concentrations of
dieldrin found in human milk over the last 15 years in various
countries, mean concentrations up to 6 µg/litre having been
reported. Higher values, occurring occasionally in a few regions,
have been associated with house and garden use of aldrin/dieldrin.
Thus, in the first several months, a breast-fed infant drinking
approximately 150 ml milk/kg body weight per day has a daily intake
of 0.15 - 0.9 µg dieldrin/kg body weight.

Acker et al. (1984) studied the problem of residues in human
milk and the importance of breast-feeding for the newborn baby.
They concluded that, at least in the early months, the value of
breast-feeding outweighed the possible risks from residues of
dieldrin, in this case, in human milk. They calculated that the
average daily intake of dieldrin by newborn babies was
approximately 0.7, 0.75, 0.65, and 0.65 µg/day, respectively, for
the 1st, 2nd, 3rd, and 4th months of breast-feeding.

Aldrin has rarely been detected in human milk. It was not
detectable in 202 samples of Dutch human milk (Wegman & Greve,
1974; Greve & Wegman, 1985), and in only one (21.8 µg/litre) of 50
Norwegian samples (Bakken & Seip, 1976).

Table 22. Concentration of dieldrin in blood and fat of fetus, newborns, infants, and adults
---------------------------------------------------------------------------------------------------------
Country Year Age Number Dieldrin in Number Dieldrin in Reference
of blood of fat
samples Mean Maximum samples Mean Maximum
(µg/litre) (mg/kg fat)
---------------------------------------------------------------------------------------------------------
North America

Canada 1982 mothers during 16 0.1 - Mes et al.
lactation (1984)

USA 1966 fetus, stillborn 6 0.17 0.38 Fiserova-
0-5 years 12 0.14 0.34 Bergerova et
6-10 years 6 0.07 0.26 al. (1967)
31-83 years 12 0.34 0.7

USA 1968 newborn 26 0.7 1.5 3^a 0.24 0.35 Curley et al.
stillborn 4 ND^b 7 ND (1969)

South America

Argentina 1969 mothers 13 1.63 Radomski et al.
-70 newborn 13 0.59 (1971)
1-5 years 19 0.54
5-10 years 18 0.94
adults 20 1.43

1970 newborn 3 0.12 0.13 Astolfi et al.
0-4 months 6 0.02 0.07 (1973)
4-12 months 4 0.05 0.07
1-4 years 14 0.06 0.13
over 4 years 20 0.07 0.25

Brazil 1969 stillborn 28 0.011 0.174 Wassermann et
-70 5-24 years 17 0.023 0.122 al. (1972a)

Europe

Netherlands 1979 newborn 87 0.3 4.6 Eckenhausen et
2 weeks 22 0.5 - al. (1981)
2 months 17 0.4 -
3 months 8 0.5 -
---------------------------------------------------------------------------------------------------------

Table 22. (contd.)
---------------------------------------------------------------------------------------------------------
Country Year Age Number Dieldrin in Number Dieldrin in Reference
of blood of fat
samples Mean Maximum samples Mean Maximum
(µg/litre) (mg/kg fat)
---------------------------------------------------------------------------------------------------------
Netherlands mothers, pre-natal 48 0.8 3.5
(contd.) mothers, post-natal 73 0.4 4.1

Spain 1982 mothers 10 6 23 Gonzalez-
(Cordoba) babies 10 8 50 Rodriquez
Cordoba et al.
(1983)

United 1969 1 newborn, stillborn 3 0.01 0.02 Abbott et al.
Kingdom -71 1 day-3 months 8 0.03 0.07 (1972)
3 months-4 years 9 0.05 0.10
over 4 years 201 0.16 0.68

1976 newborn 1 0.03 - Abbott et al.
-77 2 months 1 0.02 - (1981)
3 months 1 0.09 -
over 4 years 236 0.11 0.49

Africa

Nigeria 1969 stillborn 31 0.002 0.014 Wassermann et
0-11 months 47 0.019 0.087 al. (1972c)
1-4 years 54 0.023 0.083
adults 90 0.13 0.98

Asia

Israel 1968 fetus 23 1.3 - - - - Polishuk et al.
-69 pregnant woman 24 1.6 - 16 0.084 - (1970)
non-pregnant woman - - - 33 0.172 -

Israel 1967 stillborn 44 0.019 0.118 Wassermann et
-69 0-11 months 40 0.021 0.125 al. (1974b)
5-24 years 61 0.101 0.315
adults 162 0.136 3.96
---------------------------------------------------------------------------------------------------------
^aStillborn.
^bND = not determined.
Table 23. Concentration of dieldrin in mother's whole milk
-------------------------------------------------------------------
Country Year No. of Dieldrin Reference
samples Mean Maximum
(µg/litre)
-------------------------------------------------------------------
North America

Canada 1969-70 48 0.09^g 0.25^g Holdrinet et al.
(Ontario) 1971-72 34 0.04^g 0.17^g (1977)
1973-74 24 0.04^g 0.08^g
1978-79 154 1^a 26^b Dillon et al.
(1981)
1982 ~128^c ~1.3 1.8 Mes et al. (1984)

USA 1972-73 57 < 10 50 Kutz et al. (1979)
1973-74 57 4 50 Strassman & Kutz
(1977)
1973-75 40 6 42^b Barnett et al.
(1979)
1972-75 1436 ~5 15 Savage et al.
(1981)

Hawaii 1979-80 54 0.04^g 0.09^g Takei et al.
(1983)

Central America

El Salvador 1973-74 40 5 15 De Campos &
Olszyna-Marzys
(1979)

Guatemala 1971 46 2 10 De Campos &
Olszyna-Marzys
(1979)

Europe

Belgium 1968 20 3.4 8 Heyndrickx & Maes
(1969)

Denmark 1982 57 0.04^g 0.47^g Anderson & Orbaek
(1984)

Germany, 1981 91 0.05^g 0.44^g Rohwer (1983b)
Federal
Republic of 1982 132 0.01^g 0.3^g Cetinkaya et al.
(1984)

Netherlands 1969 48 3 11 Tuinstra (1971)
1972 202 5 - Wegman & Greve
(1974)
1983 278 0.03^g 0.22^g Greve & Wegman
(1985)
-------------------------------------------------------------------

Netherlands 1979 69 2.3 - Eckenhausen et al.
(1981)

Norway 1975 50 2.75 3.6 Bakken & Seip
(1976)

Portugal 1972 164 11 21 Graca et al.
(1974)

Spain 1981 20 3 14 Baluja et al.
(1982)

Sweden 1978 51^d 22^g 54^g Noren (1983a,b)
(Stockholm) 1979 54^d 20^g 31^g
1980 36^d 18^g 23^g

Switzerland 1983 6 0.5 1 Disler et al.
(1984)

United 1963-64 19 6 13 Egan et al. (1965)
Kingdom 1979-80 102 2 12 Collins et al.
(1982)
1983-84 40 5 32 UK-HMSO (1986)

Africa

Kenya 1983-85 292 range: 2.3-98 Kanja et al.
(1986)

Asia

Israel 1975 29 7 - Polishuk et al.
(1977)

Japan 1973-77 116 2.3 - Yakushiji et al.
(1979)

Oceania

Australia 1970-71 23 5 11 Stacey & Thomas
(1975)
1971-72 40 25 68 Miller & Fox
(1973)
-------------------------------------------------------------------

Table 23. (contd.)
-------------------------------------------------------------------
Country Year No. of Dieldrin Reference
samples Mean Maximum
(µg/litre)
-------------------------------------------------------------------
Oceania (contd.)
Australia 1973 45 5 13 Siyali (1973)
1979-80 267^c ~8.5 31 Stacey et al.
(1985)
1981 74^e 13 35 Stacey & Tatum
(1985)

New Guinea 1972 74 0.7 13.2 Hornabrook et al.
(1972)
-------------------------------------------------------------------
^aThe authors stated that they found aldrin. However, they
probably meant dieldrin, since, in mother's milk, the presence of
aldrin without dieldrin is highly unlikely, whereas the reverse
is the rule.
^bIn an area of high pesticide use.
^c128 samples from 16 women.
^dNumber of samples included 745, 805, and 973, respectively.
^e74 samples from 14 women.
^fMany of the houses had been treated against termites, but the
pesticides used were unknown.
^gOn lipid basis in mg/kg.

During the first trimester, and usually during the first year,
of a baby's life, the concentration of dieldrin in the blood and
adipose tissue does not increase and, in most cases, decreases
(Astolfi et al., 1974) (Table 22).

The concentration of dieldrin in the blood of breast-fed babies
is not higher that that in bottle-fed babies (Eckenhausen et al.,
1981), and it is lower than it is in adults.

A study on organochlorine insecticides in the blood of mothers
and newborn babies was carried out in an agricultural rural area in
the Mississippi Delta (USA). In total, 209 black and 130 white
mother-newborn pairs participated. Dieldrin was detected in the
blood of 43.5% of black and 51.5% of white mothers and in the blood
of 19.1% of black babies and 10% of white babies. The blood
concentrations of both mothers and babies were less than 1
µg/litre. Maternal age and birth weight of the baby did not
correlate significantly with the prevalence, or with the mean
level, of maternal and infant insecticide residues in the blood
(d'Ercole et al., 1976).

Data on the occurrence of aldrin and dieldrin in human milk
have been submitted by Australia, Guatemala, Japan, and
Switzerland, Japan reporting a decline of the concentrations in
human milk during the period 1971 - 1979. Data on dieldrin in
human milk have been reported by Canada, the Federal Republic of
Germany, Mexico, the Netherlands, Sweden, Switzerland, and the USA,

none of the median levels exceeding 3 µg/kg milk. Levels in the
USA were below 10 µg/kg milk (limit of detection) (National Food
Administration, Uppsala, 1982).

6. KINETICS AND METABOLISM

6.1. Absorption

6.1.1. Aldrin

6.1.1.1 Ingestion

Aldrin is readily absorbed from the gastrointestinal tract and
through the skin; it is stored as dieldrin, mainly in adipose
tissue (section 6.2.1). Aldrin is readily metabolized to dieldrin
in plants and animals and is rarely found as such in food or in the
great majority of animals.

6.1.1.2 Inhalation

Inhalation studies by Beyermann & Eckrich (1973) on human
volunteers suggested that about 50% of inhaled aldrin vapour was
absorbed and retained in the human body. However, a study on 10
male volunteers exposed to actual aldrin vapour concentrations of
1.31 µg/m³and some weeks later to 15.5 µg/m³air for a period of
60 min suggested an actual retention in man of 20%.

Physical exertion did not have any significant effect on the
retention. Dieldrin could not be detected in the exhaled air. The
concentration of dieldrin in the blood of the volunteers was lower
than 1 µg/litre before and after exposure (Bragt et al., 1984).

6.1.2. Dieldrin

Studies on rabbits, dogs, monkeys, and human beings have shown
that dieldrin is absorbed through the intact skin (Shah & Guthrie,
1976; Sundaram et al., 1978; Fisher et al., 1985). There have been
many studies demonstrating the absorption of dieldrin through the
gastrointestinal tract (section 6.2).

6.1.3. Photodieldrin (and other metabolites of dieldrin)

Studies demonstrating the absorption of photodieldrin through
the gastrointestinal tract are summarized in section 6.2.3.

6.2. Distribution

6.2.1. Aldrin

6.2.1.1 Mouse

In studies by Deichmann et al. (1975), Swiss-Webster mice were
fed diets containing 0, 5, or 10 mg aldrin/kg, over seven
generations. The retention of dieldrin following the feeding of
aldrin over four generations significantly increased the
concentration of dieldrin in abdominal fat and in the lipids of the
total carcass. There was also a significantly increased retention
of dieldrin in the carcass in the F₁generation, with some further
(but not statistically significant) increase in concentration and

total retention of dieldrin in the F₂and F₃generation. The
dieldrin concentration in the total lipids of mouse carcasses were:
for the F₀generation, 60 mg/kg; for the males in the F₁, F₂, and
F₃generations, a mean of 100 mg/kg; and for the females in the F₁,
F₂, and F₃generations, a mean of 132 mg/kg. The dieldrin
concentration was below 1 mg/kg in pups from the F₄generation,
born of parents that carried a considerable load of aldrin or
dieldrin (thus exposed in utero and via lactation) and fed the
control diet from weaning to the age of 260 days. The
concentrations of dieldrin in the F₅and F₆generations were
similar to those in the 2nd - 4th generations.

6.2.1.2 Rat

When single oral doses of 10 mg aldrin/kg body weight were
given to neonate Sprague Dawley rats, aldrin was detectable up to 6
days after dosing in the stomach and small intestine, but only for
72 h in the kidneys. In the liver, the aldrin concentration
increased during the first 6 h, and then declined during the
following days. Dieldrin was detected as early as 2 h after dosing
and had reached a maximum after 24 h. It then declined. The only
metabolic conversion product detected in the liver was dieldrin.
The concentration of aldrin was very low relative to that of
dieldrin, except in the case of studies in which tissues were
analysed within a few hours of dosing with aldrin (Farb et al.,
1973).

In studies by Ludwig et al. (1964), two male Wistar rats were
given daily oral doses of 4.3 µg ¹⁴C-aldrin by stomach tube for 3
months and were killed 24 h after the final dose. The total
radioactivity in the body as a proportion of the total cumulative
dose was 3.6%, but, after 82 days, the value had fallen to 0.21%.
The ratio of dieldrin to aldrin in the carcass was approximately
15:1; in abdominal fat, it was about 18:1.

6.2.1.3 Dog

Deichmann et al. (1969, 1971), gave beagle dogs oral doses of
aldrin in capsules. Three males were given 0.3 mg aldrin/kg body
weight and 4 females were given 0.15 or 0.3 mg aldrin/kg body
weight, 5 days per week, for 14 months. During the last 10 months
of the dosing period, the concentration of dieldrin in the blood of
dogs given 0.3 mg aldrin/kg body weight was in the range 42 - 183
µg/litre, while the concentration in the subcutaneous fat was
37 - 208 mg/kg. The levels in the animals receiving 0.15 mg
aldrin/kg body weight were 40 - 130 µg/litre and 12 - 67 mg/kg in
blood and subcutaneous fat, respectively. The apparent partition
ratio, subcutaneous fat/blood, was about 1000.

6.2.1.4 Human studies

Little is known about the distribution of aldrin in the human
body after transfer from the gastrointestinal tract or skin into
the circulating blood. As a result of its relatively rapid
conversion to dieldrin, aldrin is rarely detected in human tissues.

6.2.2. Dieldrin

6.2.2.1 Laboratory animals

(a) Mouse

Following a preliminary comparison of the distribution of
dieldrin and three known animal metabolites in CFE rats and CFI
mice (Baldwin et al., 1972), a more detailed comparison was made of
male CFE rats and two strains of male mice (CFI and LACG) (Hutson,
1976). The latter study also included a comparison of the effects
of a pretreatment with diets containing dieldrin at 20 mg/kg diet
(rats) or 10 mg/kg diet (mice) for 4 weeks. ¹⁴C-Dieldrin was
administered orally as a single dose of about 3 mg/kg body weight
to both the pretreated and non-pretreated groups, and the animals
were killed 8 days after dosing. The concentrations of the
6,7-dihydroxy metabolite were below the limits of detection (less
than 0.02 mg/kg) in the fat, liver, and kidneys of all the animals.
The concentrations of the 9-hydroxy metabolite were very small or
below the limits of detection (less than 0.03 mg/kg) in the fat and
kidneys; small concentrations (about 0.4 mg/kg) were found in the
livers of the two strains of mice. The bridged pentachloroketone
(PCK) was present in the liver of CFE rats in small amounts (about
0.04 mg/kg), but quite large concentrations were found in the
kidneys: 2.48 (no pretreatment) and 6.11 mg/kg (4-week
pretreatment). The concentrations in the fat in both groups were
small (mean, 0.17 mg/kg). In the two strains of mice, the
concentrations of PCK in the liver were very small (about 0.5
mg/kg) except in the pretreated animals. Concentrations in the
kidneys of the two strains of mice were below the limits of
detection (less than 0.02 mg/kg) in the absence of pretreatment or
small (about 0.15 mg/kg) in pretreated mice. In the fat of the
mice (no pretreatment), the PCK concentrations were below the
limits of detection (less than 0.04 mg/kg), but, in the pretreated
mice, the concentrations were about 1.3 mg/kg. The concentrations
of dieldrin in the fat were much higher than in the other tissues,
and those in the mice were about twice those in the rat.

(b) Rat

Heath & Vandekar (1964) studied the transport of ³⁶Cl-dieldrin
from the gastrointestinal tract by cannulation of the thoracic
lymph duct in rats. They found that only one-seventh of the
absorbed dieldrin was recovered from the lymph and most of the
dieldrin was absorbed via the portal vein.

Iatropoulos et al. (1975) indicated that the transport of
dieldrin from the gastrointestinal tract to the liver of Sprague-
Dawley rats is mainly through the portal venous system. However,
during the subsequent redistribution of dieldrin, the lymphatic
system seemed to be a major route.

When female Osborne-Mendel rats were fed a diet containing 50
mg technical dieldrin (87%)/kg for 6 months, the concentrations of
dieldrin in the blood, liver, and fat increased rapidly during the

first 2 weeks. During the next 26 weeks, the concentrations
fluctuated but did not appear to increase significantly. The mean
concentrations for the final 4 months were (groups of four to six
animals): in blood, 240 µg/litre; in liver, 6.8 mg/kg; and in fat,
159.5 mg/kg tissue. The distribution ratios (blood = 1) for this
period were: liver, 28 and fat, 666 (Deichmann et al., 1968).

In the studies by Walker et al. (1969b), groups of 25 male and
25 female Carworth Farm E rats were fed diets containing 0.1, 1, or
10 mg dieldrin (99%)/kg diet. The control group consisted of 45
animals of each sex. Small groups of rats were killed after 26,
52, and 78 weeks and the remaining animals after 104 weeks. The
concentration of dieldrin in blood, brain, liver, and fat was
estimated. An approximate plateau level was reached during the
first 26 weeks. The tissue uptake ratios (concentration of
dieldrin in tissues/concentration in diet) for female rats in the
three test groups were: in blood, 0.056; in brain, 0.19; in liver,
0.35; and in fat, 8.8. The uptake ratios for male rats were
significantly lower than those for females. The partition ratios
(concentration in tissues relative to that in blood) for
males/females, respectively, were: in brain, 3.3/2.6; in liver,
7.8/5.9; and in fat, 104/137. It was considered that the results
were consistent with the use of a compartmental model.

Osborne-Mendel rats (6 male and 6 female) were orally
administered approximately 50 µg ¹⁴C-dieldrin/kg body weight,
dissolved in corn oil, 5 days/week, for 9 weeks. The animals were
killed 24 h after the last dose, and the radioactivity in nine
tissues was measured. More radioactivity was retained in the
tissues by females than by males, except in the case of kidneys
(where the female:male ratio was about 0.3:1). Adipose tissue was
the main storage site for dieldrin. The lowest levels were present
in spleen, brain, and heart, while higher levels were found in
liver, lung, adrenals, and especially in the kidneys (Dailey et
al., 1970).

In a study on Charles River rats, administered ¹⁴C-dieldrin in
the diet for 8 h, Matthews et al. (1971) found a high level of
radioactivity in the kidneys. The same was found in the kidneys of
male rats in the study by Iatropoulos et al. (1975).

In studies by Baron & Walton (1971), male Osborne-Mendel rats
were fed diets containing 25 mg dieldrin/kg diet for 8 weeks. On
the first 4 days of the 9th week, oral doses of ¹⁴C-dieldrin were
administered, together with sufficient non-radioactive dieldrin to
maintain a 24-h intake equivalent to 25 mg/kg diet. Groups of five
rats were killed on days 1 - 4 of the 9th week. The remaining rats
were divided into two groups, one group being fed the diet
containing 25 mg dieldrin/kg and the other being given the control
diet. An equilibrium level of 50 mg dieldrin/kg adipose tissue was
reached by the 8th week. The concentration of dieldrin in the
adipose tissue of the animals given the control diet in the 9th
week declined rapidly during the subsequent 18 days. The rate of
decline corresponded to a half-life of about 4 - 5 days. It was

postulated that an active transport of dieldrin into and out of
fat, differing from the mechanism for lipids, may have occurred
(Baron & Walton, 1971).

Groups of two male and two female Sprague-Dawley rats were
administered dietary concentrations of 0.04 mg ¹⁴C-dieldrin/kg,
0.04 mg ¹⁴C-dieldrin/kg plus 0.16 mg dieldrin/kg, or 0.04 mg
¹⁴C-dieldrin/kg plus 1.96 mg dieldrin (99%)/kg, for 39 weeks, and
the animals were then killed. The daily intake of food was
restricted to 12 and 15 g for female and male animals,
respectively. In all three groups, the recovery of ¹⁴C activity in
whole carcasses, as a proportion of the total administered dose,
was significantly higher in female rats (mean 6.9%) than in male
rats (mean 2.1%) (Davison, 1973).

When single doses of 10 mg dieldrin/kg body weight (in corn
oil) were administered orally to male Sprague-Dawley rats, the
concentration of dieldrin in the plasma attained a maximum value
(500 µg/litre) after about 2 h. Up to 48 h after dosing, it
fluctuated between 200 and 500 µg/litre, but then declined quite
rapidly to about 10 µg/litre during the next 8 days. In the brain,
the highest concentration (about 1 mg/kg) was attained after about
4 h; it remained essentially steady for a further 44 h, and then
declined in a similar manner to that in the plasma. The
concentration/time relationships for muscle, kidneys, and liver
were similar to those for the brain. A slower approach to a
maximum value was observed in retroperitoneal fat, the 4 h and 24 h
concentrations being about 10 and 40 mg dieldrin/kg fat,
respectively. After 48 h, the concentration in fat declined in a
similar manner as did those in the plasma and brain (Hayes, 1974).

Moss & Hathway (1964) administered ¹⁴C-dieldrin
intraperitoneally to rats, and determined the partition of
radioactivity between plasma and erythrocytes. The ratio
(plasma:erythrocytes) 2 h after dosing was 2.1:1; 4 days after
dosing, it was 1.6:1, though the activities had declined by 49% and
32%, respectively, in plasma and erythrocytes.

The partition of ¹⁴C-dieldrin-related activity between the
soluble proteins of blood and the cellular components has been
studied in vitro. The radioactivity was located mainly in the
erythrocytes and plasma of rats and rabbits, whereas that in
leukocytes, platelets, and erythrocyte membranes was much lower.
The activity in the erythrocytes was associated with haemoglobin
and an unknown constituent. The radioactivity in the serum of rats
(electrophoresis at pH 8.6) was associated with pre- and post-
albumin, whereas that in rabbit serum was associated with albumin
and alpha-globulin. Electrophoresis at pH 4.5 gave a pattern which
was similar in rats and rabbits but the patterns at pH 4.5 were
different from those at pH 8.6; there were four incompletely
separated peaks of radioactivity (Moss & Hathway, 1964).

It has been demonstrated in vitro that the transport of
dieldrin between rat hepatocytes and the extracellular medium is a
much faster process than the metabolic transformation reaction in
hepatocytes (Ichinose & Kurihara, 1985).

(d) Dog

In studies by Richardson et al. (1967b), three beagle dogs were
fed a diet containing dieldrin (equivalent to 0.1 mg/kg body
weight) for 128 days, and two animals were used as controls. The
concentration of dieldrin in the blood increased in an
approximately curvilinear manner up to day 93. There were
fluctuations during the next 5 weeks, but any increase was small
relative to that during the first 5 weeks of the study (a mean
plateau concentration of about 130 µg/litre blood appears to be
consistent with the data). One week after the dieldrin diet was
discontinued, the dogs were killed and samples of blood, fat,
heart, liver, kidneys, pancreas, spleen, lung, and muscle were
taken for analysis. The mean concentrations of dieldrin in the
organs and tissues were 150 µg/litre in blood, 1090 µg/kg in the
heart, 4420 µg/kg in liver, 2330 µg/kg in kidneys, 14 030 µg/kg in
pancreas, 710 µg/kg in spleen, 1227 µg/kg in lungs, 25 333 µg/kg in
fat, and 566 µg/kg in muscle. The mean partition ratio fat/blood
was 161. There was a highly significant linear relationship
between the logarithm (log₁₀) of the concentration of dieldrin in
the blood and the logarithm (log₁₀) of the length of the dosing
period.

Six mongrel dogs (four males, two females) were orally dosed
daily with dieldrin dissolved in corn oil for 5 days (1 mg
dieldrin/kg body weight) and thereafter at doses of 0.2 mg/kg body
weight for a further 54 days. Six control animals were used.
Samples of blood were taken twice weekly from day 7 onwards and
analysed for dieldrin content. The concentration of dieldrin in
the blood of all the animals showed a small but significant
increase from day 7 to day 59. Biopsy samples of subcutaneous fat
were obtained on days 16 and 50. The fat/blood partition ratio on
day 16 was 216 and that on day 50 was 117 (Keane & Zavon, 1969b).

In studies by Walker et al. (1969b), groups of five male and
five female beagle dogs were given daily oral doses (by capsule in
olive oil) of dieldrin (99%) at 0, 0.005, or 0.05 mg/kg body
weight, for 2 years. The concentration of dieldrin in the blood
increased in all animals during the first 12 weeks of the study and
reached an approximately steady state value from week 18 to about
week 76. During the last 6 months, there were significant
deviations from the apparent asymptotic value for weeks 18 - 76.
The reasons for this are not understood, but there was also an
upward tendency in the concentration of dieldrin in the control
animals. There were statistically significant relationships
between the concentrations of dieldrin in the diet (calculated
from the daily oral dose) and those in the blood, brain, liver, and
adipose tissue. The tissue uptake ratios were similar in both
males and females, those for males being (concentration of dieldrin
in diet = 1): blood, 0.06; brain, 0.22; liver, 4.4; and adipose

tissue, 10.0. There were also statistically significant
relationships between the concentrations of dieldrin in the blood
and those in the other three tissues. The partition ratios
(concentration of dieldrin in blood = 1) for the male dogs were:
brain, 3.7; liver, 10; and adipose tissue, 169.

(e) Monkey

Two female rhesus monkeys were given an intravenous injection
of ¹⁴C-dieldrin (2.5 mg/kg body weight) in 1,2-propylene glycol and
two male rhesus monkeys received, respectively, a single oral dose
of ¹⁴C-dieldrin at 0.5 or 0.36 mg/kg body weight. The females were
killed 75 days after dosing and the males 10 days after dosing.
With both routes of administration, the highest radioactivity was
found in the adipose tissue, bone marrow, and liver. The activity
in the brain was relatively low (about 2% of that in the adipose
tissue). Metabolites were not found in the organs, but they were
present in the bile (Mueller et al., 1975b).

In studies by Mueller et al. (1979), groups of 1 - 5 male
rhesus monkeys were fed diets containing 0, 0.01, 0.1, 0.5, or 1 mg
dieldrin/kg diet for 70 - 74 months. Two other rhesus monkeys were
fed 5 mg dieldrin/kg diet for 4 months, 2.5 mg/kg for the next 5
months, and 1.75 mg/kg for a further 64 months. One rhesus monkey
was fed 5 mg/kg for 4 months, 2.5 mg/kg for the next 5 months, and
then 1.75 mg/kg diet, this dietary concentration gradually
increasing until after 23 months from the onset of the trial it had
reached 5 mg/kg (this feeding level being continued for a further
46 months). The mean concentrations of dieldrin in the livers of
these monkeys were: in the 0.01 mg/kg group, 1.2 mg/kg; in the 0.1
mg/kg group, 1.3 mg/kg; in the 0.5 mg/kg group, 4.1 mg/kg; in the 1
mg/kg group, 5.5 mg/kg; in the 5.0/2.5/1.75 mg/kg group, 13.6
mg/kg; and in the one animal fed 5, 2.5, 1.75, and 5 mg/kg diet,
23.3 mg/kg. The distribution of dieldrin in liver subcellular
fractions was determined by isotope dilution. The highest
proportion of dieldrin was present in the microsomal fraction, with
about 60% of the total in the subcellular fractions, and about
12.5% of the total in the soluble fraction. The remaining 3
fractions (nuclear, mitochondrial, and lysosomal) contained similar
proportions, about 9% in each fraction (Wright et al., 1978). The
modes of distribution of dieldrin (and metabolites) in rhesus
monkeys were similar to those in rats.

6.2.2.2 Transplacental transport

(a) Mice

Pregnant mice were each given 0.4 mg ¹⁴C-dieldrin
intramuscularly and its distribution was studied by means of whole-
body autoradiography. The highest values for ¹⁴C activity were
found in the fat, liver, intestines, and mammary glands, while
moderate activity was found in the ovaries and brain. Moderate
levels were also found in fetal liver, fat, and intestines,
indicating transfer across the placenta (Baeckstroem et al., 1965).

(b) Rat

Transplacental transfer of ¹⁴C-dieldrin was found in Sprague
Dawley rats that were administered the compound intravenously (tail
vein) on days 13, 16, or 21 of gestation. Relatively high levels
were present in the fetus 5 min after injection, and they continued
to increase for 40 - 60 min after which they declined by about 60%
in 2 - 3 days. The transfer of ¹⁴C activity was greater during
late gestation. Phenobarbital pretreatment decreased the amount of
radioactivity in the fetus (Eliason & Posner, 1971).

The transport of ¹⁴C activity from mother to blastocyst and
from mother to fetus was demonstrated in pregnant New Zealand white
rabbits following intravenous injection of ¹⁴C-dieldrin into the
ear vein (0.14 mg dieldrin/kg body weight). The ¹⁴C activity in
blastocysts of rabbits injected on the 6th day of pregnancy was
generally low compared with the activity in maternal blood.
However, 40 - 60 min after dosing, the activities were very
similar. After 60 min, the ¹⁴C activity in blastocysts declined
rapidly, relative to that in maternal blood. In rabbits dosed
intravenously on the 16th day of pregnancy, the transfer of ¹⁴C
activity was transplacental, no activity being detected in
allantoic or amnionic fluids. The ratio of ¹⁴C activity in the
whole fetus to that in the maternal blood remained fairly constant
up to 100 min after dosing, suggesting an equilibrium between the
mother and the fetus. The results for rabbits injected on the 24th
day of pregnancy indicated that two-way placental transport of ¹⁴C
activity was occurring (Hathway et al., 1967).

6.2.2.3 Domestic animals

Studies on domestic animals, in which body tissues, milk, or
eggs were analysed, indicate that the pharmacokinetics of aldrin
and dieldrin in these species are broadly similar to those in
laboratory animals (Gannon et al., 1959a,b; Ivey et al., 1961;
Williams et al., 1964; Cummings et al., 1966; Davison, 1970, 1973;
Brown et al., 1974). None of the known metabolites of dieldrin
were detected in the body tissues or milk of cows fed ¹⁴C-dieldrin
in their diet for 41 days (Baldwin, 1972; Potter et al., 1972).

Dieldrin accumulation ratios (concentration in tissues, milk,
or eggs relative to the concentration in the diet) are given in
Table 24.

Table 24. Accumulation ratios for dieldrin in domestic animals
-----------------------------------------------------------------------------
Animal Sample Feeding period Accumulation Reference
analysed (months) ratio
-----------------------------------------------------------------------------
Cow renal body fat 3 2.43 Gannon et al. (1959a)

whole milk 3 0.18 Gannon et al. (1959b)

milk fat 12 6 Vreman et al. (1980)

Hen renal body fat 3 43.1 Gannon et al. (1959a)

body fat 13 10-24 Brown et al. (1974)

egg 7 1.5 Cummings et al. (1966)

Hog renal body fat 3 2.9 Gannon et al. (1959a)

Hog body fat 2 1.14 Dobson & Baugh (1976)
(young) (body weight
increase, 290%)

Lamb renal body fat 3 1.05 Gannon et al. (1959a)

Steer renal body fat 3 3.95 Gannon et al. (1959a)
-----------------------------------------------------------------------------
6.2.2.4 Human volunteers

A study on volunteers was carried out in which daily oral doses
of 0, 10, 50, or 211 µg dieldrin/man (three men per dose group)
were given in gelatine capsules for 18 months (Hunter & Robinson,
1967; Hunter et al., 1969). The control group comprised four men.
From the 18th month to the 24th month, the volunteers given 50 µg
continued to receive dieldrin at this level, whereas all other
volunteers, including those in the control group, received 211
µg/day. The concentrations of dieldrin in the blood of the
volunteers given 211 µg dieldrin daily throughout the study had
increased 10-fold by the end of 18 months to 15 µg/litre, while
that of the group given 50 µg/day had increased 4-fold to 5
µg/litre. The increase in the case of the group given 10 µg/day
was slight; after 5 months, a 2-fold increase had occurred to 3
µg/litre, and there was little change during the subsequent 13
months. From 21 - 24 months, the concentrations of dieldrin in the
blood of the groups given 50 or 211 µg/day fluctuated, but there
was no indication of a significant continuing increase in either
set of samples. The concentrations of dieldrin in adipose tissue
after 15 months had increased approximately 3-fold in the group
given 10 µg/day (mean: 0.4 mg/kg tissue), approximately 4-fold in
the group given 50 µg/day (mean, 0.7 mg/kg tissue), and
approximately 11-fold in the group given 211 µg/day (mean, 2 mg/kg
tissue). The concentrations of dieldrin in the adipose tissue
showed an apparent increase at 24 months relative to those at 18
months, but this may be partly related to the fact that the samples
were taken by needle biopsy at 24 months. Overall, it was

concluded that the results for the groups given 50 or 211 µg/day
indicated an approach to an upper limit (asymptote), the
relationship being of the form:

concentration of dieldrin in tissues = A - Be^-kt

where A is the asymptotic value attained as time (t) approaches
infinity, and B and k are empirical constants (k corresponds to the
first-order rate constant for the elimination of dieldrin). The
mean values of the asymptote (A) for blood were 5.9 µg/litre in the
group given 50 µg/day and 20.2 µg/litre in the group given 211
µg/day. Relationships were also derived between the daily intake
of dieldrin and the steady-state (asymptotic) values for blood and
adipose tissue, respectively:

concentration of dieldrin in
blood (µg/litre)
amount of dieldrin ingested = -------------------------------------
(µg/day) 0.086

concentration of dieldrin in
adipose tissue (mg/kg)
= -------------------------------------
0.0185

It is emphasized that these relationships correspond to the
condition of a steady state between intake, storage, and
elimination of this compound. The distribution ratio
(concentration of dieldrin in adipose tissue/concentration in
blood) was 136 (Hunter & Robinson, 1967; Hunter et al., 1969).

6.2.2.5 General population

De Vlieger et al. (1968) collected samples of brain tissue,
liver, and adipose tissue from 11 routine autopsies in the
Netherlands, and found a significant relationship between the
dieldrin concentrations in the various tissues. They suggested a
tentative scheme for the distribution of dieldrin between the
various tissues. This scheme is reproduced in Fig. 1, but the
figures have been updated by recalculation conforming to the latest
empirical formula of Hunter et al. (1969) (Jager, 1970).

6.2.3. Photodieldrin (and major metabolites of dieldrin)

6.2.3.1 Laboratory animals

(a) Rat

Brown et al. (1967) fed rats diets containing 3 or 10 mg
photodieldrin/kg diet for 26 days, the 10 mg/kg-group then being
fed a control diet for a further 2 or 8 days. The half-life of
photodieldrin in adipose tissue was calculated to be 1.7 days in
male rats and 2.6 days in female rats. The storage ratio in
adipose tissue was considerably higher in females (1.3) than in
males (0.5).

In studies by Dailey et al. (1970), young rats were given daily
oral doses of 5 µg ¹⁴C-photodieldrin per rat, orally or
intraperitoneally, for 12 weeks. Although there was considerable
variation, the radioactivity in the tissues of female rats was
3 - 10 times greater than in male rats, except in the kidneys,
where the ¹⁴C activity in males was about 13 times that in females,
regardless of the route of administration.

When rats were fed diets containing 0, 0.1, 1, 10, or 30 mg
photodieldrin/kg diet for 13 weeks, the concentrations of
photodieldrin in the body tissues of female rats receiving up to 10
mg/kg diet were 2 - 15 times greater than those in males. High
concentrations of pentachloroketone (PCK) were found in the kidneys
of male rats receiving 30 mg/kg (276 mg PCK/kg kidney weight
compared with 29 mg photodieldrin/kg). The corresponding
concentrations for females were lower: 13.55 mg PCK and 1.85 mg
photodieldrin per kg kidneys (Walker et al., 1971).

In studies by Walton et al. (1971), groups of weanling rats
(Charles River strain) were fed photodieldrin at concentrations of
0, 1, 5, or 25 (decreased to 12.5 mg) mg/kg diet for 90 days, while
other groups of rats were fed dieldrin at the same concentrations.
The concentrations of both photodieldrin and dieldrin in the
adipose tissue of female rats were higher than in male rats.

(b) Dog

Following the administration of a single oral dose of
photodieldrin to one male and one female dog (160 and 120 mg/kg
body weight, respectively), the concentrations of photodieldrin in
the female dog's tissues, with the exception of the liver, were
much higher than those in the male (Brown et al., 1967).

The concentrations of photodieldrin in the liver and adipose
tissue of dogs fed photodieldrin at 0, 0.005, 0.05, or 0.2 mg/kg
body weight for 3 months were related to the dose rate and similar
in males and females. In the kidneys, the concentrations of
photodieldrin and its metabolite (PCK) were similar in male and
female dogs and much lower (of the order of 0.1 - 0.2 mg/kg
kidneys) than in rats (Walker et al., 1971).

6.2.3.2 Human beings

In samples of human adipose tissue, kidneys, and breast milk,
no residues of photodieldrin or the pentachloroketone metabolite
were detected (Robinson et al., 1966b; Anon., 1973, 1974a,c).

6.3. Metabolic Transformation

6.3.1. Aldrin and dieldrin

The initial and major step in the biotransformation of aldrin
is the formation of the corresponding epoxide dieldrin. There is
considerable evidence that this transformation is mediated by
mixed-function monooxygenases, sometimes called aldrin-epoxidase,
which have been found in a wide variety of organisms, e.g., plant
roots (Mehendale et al., 1972), insects (Krieger & Wilkinson, 1969;
Terriere & Yu, 1976), fish (Burns, 1976), and various mammals,
including man. The endoplasmic reticulum of the liver of
vertebrates is an important site of these enzymes.

6.3.1.1 Laboratory animals

(a) In vitro

The in vitro metabolism of ¹⁴C-dieldrin by unwashed microsomes
from a male rat pretreated with phenobarbital has been investigated
by Hutson (1976). The addition of uridine 5'-diphosphoglucuronic
acid (UDPGA) increased the yield of a polar metabolite. The
9-hydroxy derivative was not detected either in the presence or
absence of UDPGA, and investigation of the polar metabolite
indicated that it was the glucuronide of the 9-hydroxy derivate.
The rate of conversion of dieldrin to the glucuronide of 9-hydroxy
dieldrin, measured after 30 min incubation, was 0.0028 nmols/min
per mg protein. In the absence of UDPGA, the conversion of
dieldrin to 9-hydroxy dieldrin could not be detected, and the rate
was estimated to be less than 0.0002 nmols/min per mg protein.

A rat hepatocyte culture suspension effectively epoxidized
aldrin to dieldrin (Kurihara et al., 1984).

(b) In vivo

From the results of a comparative metabolic study on rat and
mouse (section 6.2.2.1), it appears that the main differences
between the species are a more rapid metabolism of dieldrin in
rats, a much greater production of the pentachloroketone by rats,
and the production of small amounts of polar urinary metabolites by
mice. The two strains of mice (CF1 and LACG) were similar to one
another in most, but not all, parameters measured. Thus, the
distinguishing features of the metabolism of dieldrin in CF1 mice,
unique to this strain and which could account for tumour initiation
in mice, have not been found. The hydroxylation of dieldrin in
mice is less efficient than in rats, and the formation of the
glucuronide of 9-hydroxy dieldrin is the result of the consecutive
action of hepatic microsomal monooxygenase and uridine

diphosphoglucuronyl transferase. The 9-hydroxy dieldrin formed
initially is probably bound to the microsomal membrane, and the
availability of UDPGA may be rate-limiting in the overall formation
of the glucuronide. The binding of 9-hydroxy dieldrin to the
microsomal membrane may inhibit the first oxidative step, unless
the concentration of bound metabolite is reduced by conversion to
the water-soluble glucuronide (Hutson, 1976).

Of the species studied, rats, mice, rabbits, sheep, rhesus
monkey, and chimpanzee (Feil et al., 1970; Mueller et al., 1975a),
the major metabolite, except in the case of the rabbit, is the
9-hydroxy derivative (Fig. 2, compound VI). This derivative is
found in the faeces and free or conjugated in the urine. Excretion
of the glucuronide occurs via the bile duct into the lower
intestines, where it is converted to the free 9-hydroxy compound.
The initial chemical identification of this metabolite was based on
a combination of physical and chemical methods (Richardson et al.,
1968; Baldwin et al., 1970; Feil et al., 1970), but it was
subsequently synthesized and the structure confirmed (Bedford &
Harrod, 1972a). The stereochemical configuration of the 9-hydroxy
group has been shown to be syn oriented with respect to the
6,7-epoxy group (Baldwin et al., 1973).

The other metabolites, the chemical identities of which have
been rigorously established, are detailed below.

(a) The trans-6,7-dihydroxy compound (Fig. 2, compound IV) is
formed by the hydration (formal) of the epoxide ring of dieldrin
(Korte & Arent, 1965). This compound is a major metabolite in
rabbit urine, but of relatively minor importance in other species.
The formation of the cis-diol by rat microsomes has been
demonstrated, together with its epimerization to the trans-diol
(McKinney et al., 1973). Both the cis- and trans-diols have been
synthesized (Korte & Arent, 1965; Chau & Cochrane, 1970b; Bedford &
Harrod, 1972b).

(b) The dicarboxylic acid (Fig. 2, compound V) is derived from
the dihydroxy metabolite (Baldwin et al., 1972; Oda & Mueller,
1972). This compound has also been synthesized (Buechel et al.,
1966), and has been shown to undergo further degradation (formation
of two isomers of a monodechlorinated derivative) after intravenous
injection into male and female rats (Lay et al., 1975).

(c) The bridged pentachloroketone (PCK) (Fig. 2, compound VII)
is mainly found in the urine and kidneys of male rats, but, even in
rats, it is a minor metabolite (Damico et al., 1968; Klein et al.,
1968; Richardson et al., 1968). In other species, it is a very
minor metabolite of dieldrin. It is also a metabolite of
photodieldrin (Klein et al., 1970), and has been synthesized
(Bedford & Smith, 1978).

The Chemical Abstract or Von Baeyer AG/IUPAC names of aldrin,
dieldrin, photodieldrin, and metabolites are given in Appendix I.

Methods for the quantitative determination of the four
metabolites are available. They depend on the availability of
authenticated analytical standards (Ludwig & Korte, 1965;
Richardson, 1971; Baldwin et al., 1972).

6.3.1.2 Human studies

A metabolite of dieldrin detected in human faeces has been
shown to be the 9-hydroxy derivative (Richardson & Robinson, 1971).

6.3.1.3 Non-domestic organisms

The conversion of aldrin to dieldrin was studied in algae
( Chlorella and diatoms) and protozoa (Dinoflagellates and mixed
protozoa) after exposure for 24 h to 0.1 mg aldrin/litre. The
amount of dieldrin present in the cultures was of the order of
0.06 - 0.2 µg/litre). The amounts of dieldrin were greater in the
protozoa than in the algae; it was concluded that these planktonic
species have enzyme systems that epoxidize aldrin (Khan et al.,
1972b).

The conversion of aldrin to dieldrin in 12 species of fresh-
water invertebrates has been compared. Ten species were exposed
for 2 h to concentrations of 0.1 or 0.25 mg aldrin/litre, and two

species of molluscs were exposed to 0.25 mg aldrin/litre for 4 h.
The concentrations of dieldrin relative to aldrin in the whole
bodies of eight species from four phyla (Coelenterata,
Platyhelminthes, Annelida, and Arthropoda) were in the range
1.03 - 8.48%. In two species of Insecta (dragon fly nymphs and
Aedes larvae), the values were 24.9% and 42.4%, respectively. The
two species of molluscs had dieldrin concentrations (relative to
aldrin) of 17 - 19% (Khan et al., 1972b).

In a study on an ostracod (Chlamydotheca arcuata) exposed to
¹⁴C-labelled aldrin (5.5 - 11.2 µg/litre), aldrin was readily
converted to dieldrin, 83% conversion occurring within 24 h. The
elimination of aldrin and dieldrin appeared to involve both passive
and active processes, and it was concluded that dieldrin was
eliminated more rapidly after dieldrin exposure than after aldrin
exposure (Kawatski & Schmulbach, 1972).

A number of in vitro studies have been carried out concerning
the influence of these insecticides on mixed-function oxidase
activity. The epoxidation of aldrin to dieldrin by this enzyme
system has been demonstrated in crayfish (Cambarus) (Khan et al.,
1972a,b), in snail (Lymnea palustris) and clam (Khan et al.,
1972b), and in midge larvae (Chironomus riparius) (Estenik &
Collins, 1979).

The conversion of aldrin to dieldrin by lobsters (Homarus
americanus) was reported by Carlson (1974).

The mixed-function oxidase activities in five species of fresh
water fish, as measured by the conversion of aldrin to dieldrin,
were investigated by Ludke et al. (1972). The fish were exposed to
aldrin (50 µg/litre) for 4 h, and the concentrations of aldrin and
dieldrin in the liver were determined. Contrary to earlier
reports, the conversion by epoxidation of aldrin to dieldrin in
fish may be the rule rather than an exception.

The epoxidation of ¹⁴C-aldrin to dieldrin in susceptible and
resistant mosquitofish (Gambusia affinis) has been investigated.
The fish were exposed to 5 µg ¹⁴C-aldrin/litre for 4 or 8 h and the
concentration of aldrin and dieldrin in liver and brain were
determined. The concentration of dieldrin (expressed in terms of
protein content) was significantly higher in the livers of
resistant fish than in susceptible fish). It was concluded that
resistant mosquitofish convert aldrin to dieldrin and/or water-
soluble compounds at a greater rate than susceptible mosquitofish
(Wells et al., 1973).

In studies by Addison et al. (1976), Atlantic salmon fry (Salmo
salar) were injected intramuscularly with ¹⁴C-aldrin, to initial
whole-body concentration of 5 mg/kg. The fish were maintained in
flowing fresh water, and were removed at five intervals up to 56
days for the measurement of whole-body residues. The time required
for 50% epoxidation of aldrin was between 1 and 2 days. Less than
10% of the radioactivity remained in the fish at the end of the
exposure. It was concluded that there was rapid elimination either
of unchanged aldrin or its epoxide, dieldrin, from the fish.

6.3.2. Photodieldrin (and major metabolites of dieldrin)

6.3.2.1 Rat

Besides unchanged photodieldrin, bridged pentachloroketone
(PCK) (Fig. 2, compound VII), a metabolite of photodieldrin, was
isolated from the brain, liver, adipose tissue, and blood of rats
(Carworth Farm, type E) fed diets containing 10 or 30 mg
photodieldrin/kg for 13 weeks (Baldwin & Robinson, 1969).

In studies by Klein et al. (1970), Osborne-Mendel rats were
given ¹⁴C-photodieldrin, orally or intraperitoneally, 5 days/week,
for 12 weeks, and urine was collected quantitatively every day. A
metabolite was found in the urine of male rats and shown to be PCK.
Small amounts of other (unidentified) more polar urinary
metabolites were also present.

6.3.2.2 Monkey

Metabolites were detected in the urine and faeces of a female
rhesus monkey given daily oral doses of 0.8 mg ¹⁴C-photodieldrin/kg
body weight for 175 days. Two metabolites were identified in the
urine: the trans-diol (Fig. 2, compound XI) and its glucuronide
conjugate. A faecal metabolite was tentatively identified as the
diol. A third metabolite was present in both urine and faeces, and
it was suggested that this might be a monohydroxy derivative of
photodieldrin (Nohynek et al., 1979).

6.4. Elimination and Excretion

6.4.1. Aldrin

6.4.1.1 Rat

When male rats were given daily oral doses of 4.3 µg ¹⁴C-aldrin
(equivalent to about 0.2 mg aldrin/kg diet) for 3 months, the
radioactivity in the urine increased from about 2% of the dose of
aldrin during the first week to about 10% during the 12th week. In
the faeces, the excreted radioactivity increased from about 48%
during the first week to about 93% during the 12th week. After
about 8 weeks, a saturation level was reached (i.e., there was a
balance between the rates of intake of aldrin and excretion of
aldrin plus aldrin-related materials). Extracts of urine and
faeces were examined by paper chromatography. Because the urine
was probably contaminated by faeces in the metabolism cages, only
the trend is given. In both faeces and urine, the aldrin content
decreased during the 12 weeks. The hydrophilic metabolites
increased, reaching 75% (faeces) and 95% (urine) of total
radioactivity after 12 weeks. The level of dieldrin was more or
less constant (Ludwig et al., 1964).

6.4.2. Dieldrin

6.4.2.1 Laboratory animals

As described in section 6.2.2.1, Hutson (1976) studied the
comparative metabolism of dieldrin in CFE rats and two strains of
mice after a single oral dose of 3 mg/kg body weight ¹⁴C-dieldrin.
The excretion of ¹⁴C activity in the faeces of the rats was 62.4%
of the administered dose in the non-pretreated group and 69% in the
dieldrin-pretreated group. In the case of the CF1 mice, the
pretreatment period did not have any effect on the faecal excretion
(51.5%), whereas, in the LACG mice, the faecal excretion of ¹⁴C
activity increased from 27.2% for the non-pretreated group to 48.8%
for the 4-week pretreated group. The total ¹⁴C activity excreted in
the urine of the two strains of mice was low (0.42 - 2.6% of dose)
compared with that in the urine of male rats (5.5 - 6.6%). In both
species of rodents, the faeces was the major route of excretion of
¹⁴C activity. In the urine of both the male CFE rat and the male
CF1 mice, the amount of the dicarboxylic acid metabolite in the
urine was small compared with that of pentachloroketone plus
dieldrin, while in the male LACG mice, the amount of the acidic
metabolite was twice that of pentachloroketone plus dieldrin. Both
strains of mice excreted, proportionally, much larger amounts of a
polar (unidentified metabolite) in the urine than did the CFE rats.
In the faeces of the male CFE rats (no pretreatment), the major
component was the 9-hydroxy derivative. This was also found by
Matthews et al. (1971). However, in both mouse strains (no
pretreatment), this compound was a minor metabolite, but it became
the major product in the dieldrin-pretreated group. In isolated
liver microsomes, most of the ¹⁴C activity appeared to be present
as dieldrin, and the 9-hydroxy metabolite was not detected.

A number of other studies on the excretion of dieldrin via
urine and/or faeces have been carried out. Dailey et al. (1970)
found that male rats excreted higher levels of ¹⁴C radioactivity
via urine and faeces than females. Davison (1973) confirmed this
in a study lasting 39 weeks. Maximal excretion of ¹⁴C activity
occurred in the 6th week in both sexes, regardless of the amount of
dieldrin given. A steady state was reached and maintained from the
6th to the 39th week.

In studies by Robinson et al. (1969), rats were fed a diet
containing 10 mg dieldrin/kg diet for 8 weeks. The decline in the
concentration of dieldrin in blood, brain, liver, and adipose
tissue was studied during the subsequent 12 weeks when a control
diet was fed. There was an initial rapid decline in the dieldrin
concentration during the first 10 days of the post-exposure period
in the blood, liver, and brain, followed by a slower decline. The
changes in the concentration of dieldrin in the brain, adipose
tissue, blood, and liver corresponded to biological half-lives of 3
to about 10 days.

When male and female rats were administered 3 g of diet
containing 10 mg ¹⁴C-dieldrin/kg diet, followed by a control diet
ad libitum, ¹⁴C activity in the kidneys of male rats was 10-fold
higher than in the female rats (the animals were killed 9 days
after administration of ¹⁴C-dieldrin). Most of the activity in the
male kidneys was due to pentachloroketone, whereas, in the female
kidneys, only dieldrin was detected (Matthews et al., 1971).

The excretion of ³⁶Cl activity by female rats dosed
intravenously (680 µg/h for 2.5-5 h; total doses of 8 - 16 mg/kg
body weight) with ³⁶Cl-dieldrin has been studied. The ³⁶Cl
activity detected in the faeces was about 7 times that found in the
urine, indicating excretion via the bile (Heath & Vandekar, 1964).

Comparable results were found by Cole et al. (1970), who gave
male rats a single intravenous dose of 0.25 mg ¹⁴C dieldrin/kg body
weight. Similar doses of ¹⁴C-dieldrin were administered
intravenously to male rats with bile fistulas. About 30% of the
administered ¹⁴C activity was excreted via the bile during the
first 24 h after dosing, and after 4 days a total excretion of
about 60% had occurred. Isolated perfused rat liver preparations
were also investigated; some 20% of the original perfusate dose was
collected in the bile over a period of 8 h.

Rapid excretion of ¹⁴C-dieldrin (or its metabolites) from
isolated perfused rat livers via the bile of rats has also been
reported by Klevay (1970), the rate of excretion by male rats being
about 3 times as rapid as that by female rats.

In studies by Mueller et al. (1975a), mice, rats, rabbits,
rhesus monkeys, and one chimpanzee were given a single oral dose of
0.5 mg/kg body weight ¹⁴C-dieldrin, and urine and faeces were
collected for 10 days. For all species except the rabbit, the main
route of excretion was the faeces. The faecal excretion of
unchanged dieldrin was high in the first 48 h and then declined
rapidly. The urine samples contained only metabolites of dieldrin.
The mean total amount of radioactive material excreted (males
and/or females) in faeces and urine within 10 days after dosing
(expressed as percentage of administered dose) was 37% in mice, 11%
in rats, 2% in rabbits, 20% in rhesus monkeys, and 6% in the
chimpanzee. In all five species, 9-hydroxy-dieldrin and
4,5-aldrin- trans-dihydrodiol were the major metabolites. The
metabolism in the rat seems to be comparable to that of primates;
however, mice and rabbits showed the opening of the epoxide to diol
as the predominant reaction.

6.4.2.2 Human studies

The occurrence of a neutral metabolite of dieldrin in human
urine in amounts indicative of exposure to aldrin/dieldrin was
reported by Cueto & Hayes (1962) and Cueto & Biros (1967).

Quantitative estimates of the amounts of a metabolite of
dieldrin, 9-hydroxy-dieldrin, in the faeces of seven workmen
occupationally exposed to aldrin/dieldrin and five male members of
the general population have been made. The average concentration
of the 9-hydroxy derivative in 24-h collections of faeces of the
seven workmen was 1.74 mg/kg (range, 0.95 - 2.80 mg/kg), whereas

the average concentration in faeces of the five members of the
general population was 0.058 mg/kg (range, 0.033 - 0.12 mg/kg).
Dieldrin was present in the faeces of the workmen (average
concentration, 0.18 mg/kg), but, in samples from the general
population, it was below the limit of detection. Examination of
the urine of five of the workmen indicated that this route of
elimination of dieldrin and four known metabolites was minor. It
was concluded that the 9-hydroxy-dieldrin in the faeces represented
the major excretory pathway of dieldrin from male human beings. It
should be noted, however, that the urine was not examined for
glucuronide or other conjugates of the hydroxy metabolites). There
was good correlation between the estimated daily intake of dieldrin
(calculated from the concentrations of dieldrin in the blood) and
excretion in faeces of total equivalent dieldrin (Richardson,
1971). This relationship is based on a number of assumptions, and
it is probably more relevant that the concentration of the
9-hydroxy-dieldrin in the faeces (produced by the metabolism of
absorbed dieldrin) is significantly related to the concentration of
dieldrin in the blood, which is a measure of the body burden
arising from absorption of aldrin plus dieldrin.

When ¹⁴C-Dieldrin was applied in acetone (4 µg/cm²) once to the
forearm of volunteers, 7.7% of the applied ¹⁴C activity was
excreted in the urine over a 5-day period. A single intravenous
injection of ¹⁴C-dieldrin resulted in 3.3% being excreted in the
urine over a 5-day period (Feldman & Maibach, 1974).

6.4.3. Photodieldrin (and major metabolites of dieldrin)

6.4.3.1 Rat

In studies by Dailey et al. (1970), young rats were given daily
doses of 5 µg ¹⁴C-photodieldrin, orally or intraperitoneally, for
12 weeks. Urine and faeces were collected daily and pooled in
weekly groups. The excretion of ¹⁴C activity via the urine of
females was considerably less than that by males, by either method
of dosing. The ¹⁴C activity in urine after oral and ip
administration increased slowly during the 12 weeks (males about
10% and females 5%), the highest levels in urine (up to 33%) being
found in males dosed intraperitoneally. Faecal excretion of ¹⁴C
activity was initially lower in females, but greater during the
latter half of the study (of the order of 20 - 40%). In males,
during the whole study, it was about 30%.

6.4.3.2 Monkey

A juvenile female rhesus monkey was given daily oral doses of
2 mg ¹⁴C-photodieldrin (equivalent to 0.8 mg/kg body weight), and
the treatment was continued until, between days 70 and 76, the
daily excretion of ¹⁴C activity was in balance with the daily
intake. When dosing ceased, the animals had retained about 50% of
the cumulative dose of photodieldrin. Collection of excreta was
continued for a further 100 days, during which a further 30.1% of
the dose, administered during the 76-day period, was excreted.
During the period of dosing, a major part of the faecal ¹⁴C

excretion consisted of photodieldrin (probably indicating
incomplete absorption in the gastrointestinal tract), while
20 - 50% of the excreted activity was in the urine. After dosing
ceased, 60% of the excreted ¹⁴C activity appeared in the urine
(Nohynek et al., 1979).

In studies by Nohynek et al. (1979), one male and one female
juvenile rhesus monkey were given single intravenous doses of
4.5 mg ¹⁴C-photodieldrin (2 mg/kg body weight). Urine and faeces
were collected separately every 24 h, and the animals were killed
after 21 days. Excretion of ¹⁴C activity was high during the first
7 days (male, 39%; female, 27.3%, of the given dose). It then
decreased rapidly and reached a nearly constant value of 0.2% of
the administered dose. Approximately 45% (male) and 34% (female)
of the dose had been excreted by day 21.

6.5. Retention and Turnover

6.5.1. Non-domestic organisms

A few studies have been carried out on the uptake and
elimination of aldrin and/or dieldrin in invertebrates: marine
clams (Mya arenaria and Mercenaria mercenaria) (Butler, 1971);
naiad mollusc (Amblema plicata) (Fikes & Tubb, 1972); mussel
(Lampsilis siliquiodea) (Bedford & Zabik, 1973); crab (Leptodius
floridanus) (Epifanio, 1973); and ostracod (Chlamydotheca arcuata)
(Kawatski & Schmulbach, 1972). The concentration of aldrin or
dieldrin in organs and tissues increased rapidly during the first
1 - 2 weeks of exposure, but remained virtually constant
thereafter. When the organisms were placed in clean water, the
concentration declined in a (semi)-logarithmic manner in relation
to time. The estimated half-life for the tested organisms varied,
e.g., for Lampsilis siliquiodea, it was 4.7 days, whereas for
Amblema plicata, it was about 3 - 4 weeks.

The elimination of ¹⁴C-dieldrin from bluegills (Lepomis
macrochirus) and goldfish (Carassius auratus) was studied by
Gakstatter & Weiss (1967). The fish were exposed to 30 µg
¹⁴C-dieldrin/litre (initial concentration) until toxic symptoms
appeared (5 - 8 h), and were then placed in recovery aquaria
together with unexposed fish. The water in the recovery aquaria
was continuously renewed. Samples of five fish were taken on 10
different occasions during the recovery period. The ¹⁴C activity
in whole fish of both species, expressed as equivalent dieldrin,
declined by about 90% within 16 days, the half-time for elimination
being about 4 days. The control bluegills and goldfish accumulated
a maximum equivalent dieldrin concentration of 0.29 and 0.22 mg/kg,
respectively, on day 4 of the period in the recovery aquaria,
indicating transfer of dieldrin or derived material from
contaminated to uncontaminated fish.

In another study, the distribution of aldrin and dieldrin in
the tissues of Carassius auratus was determined following an 8-h
exposure to ¹⁴C-aldrin (50 µg/litre) in a static study. After the
exposure, fish were placed in a continuously flushed aquarium for

32 days. Dieldrin was found in all tissues examined immediately
after the exposure. The percentage of dieldrin in the total
residues in the tissue increased with time, reaching about 95% on
day 32 (except in visceral fat). During the recovery period, the
total concentration of aldrin plus dieldrin in the blood declined
from 2.1 mg/litre (as aldrin) to 0.4 mg/litre. The corresponding
changes in the brain concentrations were 5.45 mg/kg to 2.3 mg/kg.
Total residues in the nerve cord did not show a consistent decline
and varied from 4.56 to 21.6 mg/kg throughout the 32-day period;
however, these residues were determined by thin-layer
chromatography, not by gas-liquid chromatography (Gakstatter,
1968).

The partitioning of ¹⁴C activity into particulate fractions of
the brain and liver of resistant and susceptible mosquitofish has
been studied after exposure of the fish to ¹⁴C-aldrin or ¹⁴C-
dieldrin. The ¹⁴C activities in total brain, cell membrane, and
five cellular fractions were significantly higher in susceptible
fish than in resistant fish for both aldrin and dieldrin. However,
this difference was much less marked in the case of the liver. It
was suggested that a basic structural change in polarity exists in
the myelin of resistant fish, which could provide a membrane
barrier (Wells & Yarbrough, 1973).

The fate of dieldrin in the digestive tract of juvenile lake
trout (Salvelinus namaycush) has been studied. Macerated trout
flesh containing an average of 1.05 mg/kg was injected in the
stomach. The decline in the dieldrin content of the stomach was
parallel to that of the food from the stomach. Little or no
dieldrin was found in the intestines (Stewart & Stein, 1974).

In studies by Chadwick & Brocksen (1969), groups of sculpins
(Cottus perplexus) were exposed to 1.3 µg dieldrin/litre for 12
days, followed by removal to uncontaminated continuously renewed
water. The concentration in whole fish declined in a curvilinear
fashion from about 2.5 mg/kg fish to about 1 mg/kg fish in 60 days
and to about 0.5 mg/kg fish in 90 days.

Sailfin molly (Poecilia latipinna) were exposed to 12 µg
dieldrin/litre for up to 6 h by Lane et al. (1970). Two products,
thought to be metabolites of dieldrin, were detected in the liver
and other organs, and it was suggested that they were partially
dechlorinated derivatives of dieldrin.

6.5.2. Biological half-life in human beings

The concentration of dieldrin in the blood of volunteers given
oral daily doses for 2 years (section 6.2.2.4) was determined over
a period of 8 months after termination of the deliberate exposure
(Hunter et al., 1969). A small, but statistically significant,
decline occurred, corresponding to a mean value of 369 days for the
half-life of dieldrin in blood. However, there were significant
differences between the rates of decline of the individual
volunteers.

The concentration of dieldrin in the blood of 15 workmen was
determined for a period of 3 years following termination of
occupational exposure to aldrin/dieldrin (Jager, 1970). The mean
half-life was 266 days.

When a state of equilibrium has not yet been reached, the
apparent half-life will be much shorter, due mainly to a
redistribution of dieldrin between compartments in the body.

6.5.3. Body burden and (critical) organ burden; indicator media

Whatever the route of exposure, the effect, if any, will be
determined by the concentration of the chemical in the target organ
or tissue. It has been shown that the distribution between the
various tissues of mammals is fairly constant within and between
species (Robinson & Hunter, 1966; Hunter & Robinson, 1967; Hunter
et al., 1967; Robinson & Roberts, 1969; Walker et al., 1969b).
Thus, at a state of equilibrium, the dieldrin level in the blood
reflects the concentration of the active compound in the target
tissues and therefore represents the best practical parameter for
the internal exposure that is associated with a biochemical,
clinical, or pathological effect. Since the biological half-life
of dieldrin in human blood is known (266 days) (Jager, 1970),
a reliable estimation of the blood level at the time of
discontinuance of the exposure can be made. This, in turn enables,
better than anything else, the evaluation of the likelihood of an
observed symptom of disease or indisposition being associated with
exposure to dieldrin. Also, the established mathematical
relationship between the dieldrin level in the blood and the total
daily equivalent oral intake thus enables, on the basis of the
concentration of dieldrin in the blood, the evaluation of a current
exposure or an exposure of a short time ago vis-à-vis the
acceptable daily intake established by the FAO/WHO Joint Meeting on
Pesticide Residues.

Determination of the dieldrin concentration in blood is the
method of choice in monitoring exposed workers or the general
population (section 9.2.1.1).

6.6. Appraisal

Aldrin is readily absorbed through the skin, by inhalation of
the vapour, or into the circulating blood from the gastrointestinal
tract. It has not been possible to determine the percentage of an
ingested dose of aldrin or dieldrin that is actually absorbed into
the body because of the intestinal hepatic biliary cycle. Work
with human volunteers (Feldmann & Maibach, 1974) showed that
absorption through the skin amounted to 7 - 8% of the applied dose.
Inhalation studies with human volunteers (Beyermann & Eckrich,
1973; Bragt et al., 1984) suggested that about 50% of inhaled
aldrin vapour is absorbed and retained in the human body. After
absorption, it is rapidly distributed to the organs and tissues of
the body, and a continuous exchange between the blood and other
tissues takes place. In the meantime, aldrin is readily converted

to dieldrin, mainly in the liver but, to a much lesser extent, in
some other tissues, e.g., the lungs (Mehendale & El-Bassiouni,
1975).

This conversion proceeds very rapidly. The livers of even
24-h-old rats, given oral doses of 10 mg aldrin/kg body weight,
contained dieldrin 2 h after treatment (Farb et al., 1973). In the
course of the next few hours, dieldrin and what little is left of
the aldrin in blood and other tissues, concentrates more in the
lipid tissues (Heath & Vandekar, 1964; Hayes, 1974). In human
beings, aldrin is found rarely, if at all, in human blood or other
tissues, except in cases with acute poisoning by accidental or
intentional ingestion of massive doses.

Studies carried out with ¹⁴C-labelled aldrin and dieldrin have
shown that part of the ingested material is passed unabsorbed
through the intestinal tract and eliminated from the body, part is
excreted unchanged from the liver into the bile, part is stored
unchanged in the various organs and tissues (particularly the
adipose tissue), and part is metabolized in the liver to more polar
and hydrophilic metabolites. These metabolites, in human beings
and most animals, are excreted primarily via the bile in the
faeces. It had also been shown that aldrin and dieldrin are both
biodegraded into the same metabolites (Damico et al., 1968; Klein
et al., 1968). The biodegradation products have been identified in
the rat within 15 min after an intravenous injection (Moersdorf et
al., 1963). Most of the currently available information on the
biodegradation metabolism in mammals is based on studies with
dieldrin on the mouse, rat, rabbit, sheep, dog, monkey, chimpanzee,
and human beings (Ludwig et al., 1964; Datta et al., 1965; Korte,
1965; Korte & Arent, 1965; Richardson et al., 1967b, 1968; Klein et
al., 1968; Matthews & Matsumura, 1969; Baldwin et al., 1970, 1972;
Feil et al., 1970; Richardson & Robinson, 1971; Mueller et al.,
1975a,b). Although there appear to be differences between species
and, in the rat, differences between the sexes, the overall picture
shows only quantitative variations between species.

In the species studied (with the exception of the rabbit) the
major metabolite is the 9-hydroxy derivative. This is found in the
faeces and free or conjugated in the urine. Three other
metabolites have been found and identified in experimental animals:

(a) trans-6,7-dihydroxy derivative;
(b) dicarboxylic acid derived from the dihydroxy compound; and
(c) the bridged pentachloroketone (PCK).

The latter is also a metabolite of photodieldrin (Klein et al.,
1970).

Only the 9-hydroxy compound was found in the faeces of seven
occupationally exposed industrial workers (1.74 mg/kg) and five
male members of the general population (0.058 mg/kg). Neither the
9-hydroxy compound nor the other metabolites have been found in
human blood or other tissues. Dieldrin was present in the faeces
of the workmen (average 0.18 mg/kg), whereas the concentrations in

the samples from the general population were below the limits of
detection. Examination of the urine of five workmen indicated that
urinary excretion of dieldrin and its four metabolites is minor
relative to elimination of the 9-hydroxy metabolite via the faeces
(Richardson, 1971).

The conversion of aldrin to dieldrin and the distribution and
the subsequent deposition of dieldrin (mainly in lipid tissues)
proceed much faster than the biodegradation and ultimate
elimination of unchanged dieldrin and its metabolites from the
body. At a given average intake of aldrin and/or dieldrin,
dieldrin slowly accumulates in the body. This accumulation or
"storage", however, does not increase indefinitely. As the
concentration of dieldrin in the liver cells increases, the
metabolizing enzyme activity in the microsomes increases, and so
the rate of biodegradation of dieldrin, and hence the elimination
from the body, is enhanced. Thus, the accumulation proceeds at an
ever slower rate until the concentrations of dieldrin in blood and
tissues approach upper limits of storage and an amount of dieldrin
equal to the average daily intake is eliminated each day. These
upper limits of storage are related to the daily intake. This has
been demonstrated in rats and dogs (Walker et al., 1969b) and in
human beings (Hunter & Robinson, 1967; Hunter et al., 1969). When
the intake of aldrin/dieldrin ceases or decreases, the body burden
decreases. The biological half-life in human beings is 9 - 12
months (Hunter & Robinson, 1967; Hunter et al., 1969; Jager, 1970).
Significant relationships exist between the concentrations of
dieldrin in the blood and those in other tissues of rats, dogs, and
human beings (Hunter & Robinson, 1967; Deichmann et al., 1968;
Keane & Zavon, 1969b; Hunter et al., 1969; Walker et al., 1969b).

Numerous investigations of the concentrations of dieldrin in
body fat, blood, and other tissues from members of the general
population and from special groups have been carried out in several
countries. The results are summarized and discussed in section
5.2. The ratio of dieldrin concentrations in fat, liver, brain,
blood is about 150:15:3:1.

Dieldrin penetrates the placenta and is present in the blood,
fat, or other organs of the fetus, newborn babies, and infants
(Table 22). The concentrations are much lower (by 50% or more)
than those in adults. The ratio of dieldrin concentrations in
blood, brain, liver, and fat in infants is not different from that
ratio in adults (Fiserova-Bergerova et al., 1967; Casarett et al.,
1968). Dieldrin is excreted in mother's milk, average values being
about 3 - 5 µg/litre mother's milk (Table 23). The ratio of the
dieldrin concentration in mother's blood to that in mother's milk
is about 1:2 - 3.

7. EFFECTS ON ORGANISMS IN THE ENVIRONMENT

7.1. Microorganisms

Neither aldrin nor dieldrin have significant effects on
populations of microorganisms in soil or fresh water at realistic
concentrations. Some physiological processes of microorganisms are
affected by low concentrations of both aldrin and dieldrin, but
these would appear to have little or no environmental significance.
Aldrin and dieldrin have only minor deleterious effects on soil
bacterial populations, even at concentrations that are much higher
than those used in agricultural practice.

The effects of insecticides on soil microbes have been reviewed
by Tu & Miles (1976). Of 15 strains tested, aldrin did not have
any effect on the growth of 11 bacterial species (single cultures)
but caused some growth inhibition in four species. Dieldrin did
not have any effect on 13 bacterial species but had some inhibitory
effect in two species. Neither aldrin nor dieldrin at 2000 mg/kg
soil had effects on bacteria in laboratory studies; soil fungi were
also little affected. In pot studies, using aldrin at 4 and 120
mg/kg soil, there were no quantitative changes in bacteria during
any part of the vegetative period. Aldrin inhibited the growth of
Rhizoctonia solani in plate cultures by 20% or more at 6.2 mg/litre
and higher concentrations. Dieldrin was less toxic, producing an
average inhibition of about 15%, which was not dose related over
the range of 1 - 100 mg/litre. The evolution of carbon dioxide
(CO₂) (a measure of soil organisms respiration) was significantly
reduced by dieldrin at 1000 mg/kg soil (but not at 100 mg/kg),
whereas aldrin produced a significant reduction at concentrations
as low as 25 mg/kg soil. Slight effects on nitrification were
initially found when aldrin and dieldrin were incorporated at 2000
mg/kg in a sandy loam soil, but nitrification was normal after
about 10 weeks. Short-term inhibition of nitrification was also
produced by aldrin and dieldrin at 25 mg/kg in a sandy loam soil
(aldrin for 1 week, dieldrin for 2 weeks). Decreased sulfur
oxidation was observed in soil containing aldrin or dieldrin (2000
mg/kg), the inhibition decreasing considerably after 3 months.
Five annual applications of aldrin or dieldrin (5.5 - 22 kg/ha) to
a Ramona sandy loam had no measurable effect on the numbers of soil
bacteria or fungi, did not influence the ability of the soil
population to decompose plant residue, and did not alter soil
aggregation.

The effect of dieldrin on the activities of three soil enzymes
was determined at concentrations of 5 or 10 mg dieldrin/kg soil by
Tu (1981). The dehydrogenase activity of the dieldrin-treated soil
(10 mg/kg) did not differ from controls, whereas at 5 mg
dieldrin/kg, the activity was significantly greater than controls
after 2 weeks (50% increase). Urease activity at both treatment
levels was significantly reduced after a 1-week incubation but
significantly increased after 2 weeks. Phosphatase activity was
significantly reduced at 5 mg dieldrin/kg, but not at 10 mg/kg.

The 96-h EC₅₀(growth) for algae (Chlamydomonas sp.,
Phaeodactylum tricornutum, Dunaliella sp., Chlorella ovalis, and
Chlorella pyrenoidosa) was > 100 µg dieldrin/litre (Adema & Vink,
1981).

The photosynthetic activity of four species of marine
phytoplankton in the presence of dieldrin was investigated using
¹⁴C-labelled Na₂CO₃. A range of nominal concentrations
(0.01 - 1000 µg/litre) was used, and the plant cultures were
exposed for 24 h. The ¹⁴C uptake of Dunaliella tertiolecta during
7 days post-treatment was unaffected by up to 1000 µg
dieldrin/litre. Two other species (Skeletonema costatum and
Coccolithus huxleyi) showed significant reductions in ¹⁴C uptake at
levels of dieldrin above 10 µg/litre, and the photosynthetic
activity of Cyclotella nana was reduced at concentrations above 1
µg dieldrin/litre (Menzel et al., 1970).

In studies by Schauberger & Wildman (1977), three species of
fresh-water algae (Anabaena cylindrica, Anacystis nidulans, Nostoc
muscorum) were exposed to aldrin or dieldrin at concentrations of
0 - 1000 µg/litre. After exposure for 7 days, there was no
significant effect on the photosynthetic pigment absorption of the
three species at concentrations up to 10 µg (nominal)/litre.
However, at 1 mg/litre, aldrin almost completely suppressed the
absorption by photosynthetic pigments (chlorophyll and
phycocyanin), these being indicators of physiological health and
growth. Dieldrin (1 mg/litre) produced a reduction of about 40%.

The growth response of two cyanobacteria (blue-green algae) in
the presence of aldrin, dieldrin, or two metabolites of dieldrin,
photoaldrin, or photodieldrin was determined at nominal
concentrations of 0.2 - 950 µg/litre (Batterton et al., 1971).
None of these compounds had significant effects on the growth rate
constants at concentrations of 95 µg/litre or at lower
concentrations over periods of 26 - 30 h. The investigators
considered that dieldrin and its derivatives reduced the growth
rate constant at 475 and 950 µg/litre, Agmenellum quadriplicatum
being more sensitive than Anacystis nidulans. Aldrin did not have
a significant effect on either species, but photoaldrin affected
Agmenellum quadriplicatum at 950 µg/litre.

In studies by Powers et al. (1977), a marine dinoflagellate
(Exuviella baltica) was incubated with dieldrin (0.1, 1, or 10 µg
(nominal)/litre), and the numbers of cells were counted during a
period of 6 days. No adverse effects on optical counts were
observed at the two lower concentrations, but there was a marked
reduction in the size and number of cells at 10 µg dieldrin/litre.

7.2. Aquatic Organisms

The toxicity of aldrin and dieldrin to aquatic invertebrates is
very variable. For some species both compounds are highly toxic,
whereas for others there is no effect until the compounds are
dissolved to artificially high concentrations, many times their
solubility in water. Both aldrin and dieldrin are highly toxic to

most species of fish in laboratory tests, with acute LC₅₀values
well within the solubility of the compounds. It should be borne in
mind that aldrin and dieldrin are strongly bound to particulate
matter in water, which reduces their availability to aquatic
organisms and, in consequence, their potential toxicity.

7.2.1. Aquatic invertebrates

7.2.1.1 Acute toxicity

A convenient overview, in graphical format, of the toxicity of
aldrin and dieldrin to many aquatic organisms was produced by Craig
(1977). The 96-h LC₅₀values of aldrin and dieldrin for
crustaceans and molluscs were in the range 0.2 - 10 000 µg/litre.

Dieldrin is moderately toxic to fresh-water annelids
(4000 - 7000 µg/litre) and molluscs (> 100 - 640 µg/litre).
Insects are the most sensitive group (aldrin, 1 - 200 µg/litre;
dieldrin, 0.2 - 40 µg/litre). The values for a number of species
are given in Table 25.

7.2.1.2 Short-term toxicity, reproduction, and behaviour

(a) Short-term toxicity

When naiads of two species of stonefly were exposed for 30 days
in a continuous-flow system, the 30-day LC₅₀s for aldrin and
dieldrin were, respectively, 2.5 and 2 µg/litre for Pteronarcys
californica, and 22 and 0.2 µg/litre for Acroneuria pacifica
(Jensen & Gaufin, 1966).

The LC₅₀for adult molluscs (Mytilus edulis and Dreissena
polymorpha) exposed for 3 - 4 weeks was 180 - 200 µg dieldrin/litre
(Adema & Vink, 1981).

McLeese et al. (1982) exposed polychaete worms (Nereis vireus)
to dieldrin in sea water or sediment for 12 days. The LC₅₀in sea
water was > 170 µg/litre (in surficial water > 20 µg/litre; in
sediment > 13 mg/kg).

Table 26 gives the LC₅₀values for a number of invertebrate
species.

(b) Reproduction

The effects of dieldrin on the embryonic development of the
American oyster (Crassostrea virginica) and of aldrin on that of
the hard clam (Mercenaria mercenaria) were studied by Davis & Hidu
(1969). Table 27 gives the concentrations producing approximately
50% reduction in the development of fertilized eggs during 48 h,
those producing about 50% reduction in larval survival during 12
days (clams) or 14 days (oysters), and the effects on larval growth
during 10 or 12 days of exposure (expressed as a percentage of
growth of control larvae).

Table 25. Acute toxicity of aldrin and dieldrin for aquatic invertebrates
---------------------------------------------------------------------------------------------------------
Species Developmental Vehicle Temperature 96-h LC₅₀(static test) Reference
stage, body (°C) -----------------------
weight, or Aldrin Dieldrin
length (µg/litre)
---------------------------------------------------------------------------------------------------------
Daphnids

Daphnia magna (29)^a 330^a Anderson (1959)

Simocephalus first instar dispersed via 15 (23)^a (240)^a Johnson & Finley
serrulatus acetone 21 (32)^a (1980)

Daphnia pulex first instar dispersed 15 (28)^a (190)^a Johnson & Finley
(1980)

Crustacea

Seed shrimp mature dispersed via 21 (18)^a - Johnson & Finley
(Cypridopsis acetone (1980)
vidua)

Sowbug (Asellus mature dispersed via 21 - 5 Johnson & Finley
brevicaudus) acetone (1980)

Scud (Gammarus mature dispersed via 21 4300 640 Johnson & Finley
fasciatus) acetone (1980)

Sand shrimp 0.25 g, dispersed via 20 8 7 Eisler (1969)
(Crangon 2.6 cm acetone
septemspinosa)
2 g dispersed via 20 - 0.4 McLeese & Metcalfe
hexane (1980)

2 g dispersed in 10 - 4.1 McLeese & Metcalfe
sediment (1980)

Grass shrimp 0.47 g, dispersed via 20 9 50 Eisler (1969)
(Palaemonetes 3.1 cm acetone
vulgaris)
---------------------------------------------------------------------------------------------------------

Table 25. (contd.)
---------------------------------------------------------------------------------------------------------
Species Developmental Vehicle Temperature 96-h LC₅₀(static test) Reference
stage, body (°C) -----------------------
weight, or Aldrin Dieldrin
length (µg/litre)
---------------------------------------------------------------------------------------------------------
Crustacea (contd.)

Grass shrimp mature dispersed via 21 50 - Johnson & Finley
(Palaemonetes acetone (1980)
kadiakensis)

Crayfish mature dispersed via 21 - 740 Johnson & Finley
(Orconectes acetone (1980)
nais)

Hermit crab 0.28 g, dispersed via 20 33 18 Eisler (1969)
(Pagurus 0.35 cm acetone
longicarpus)

Molluscs

Mercenaria egg dispersed via 24 (> 10 000)^a - Davis & Hidu (1969)
mercenaria acetone

Crassostrea egg dispersed via 24 - (640)^a Davis & Hidu (1969)
virginica acetone

Slipper limpet veliger - - - > 100 Adema & Vink (1981)
(Crepidula
fornicata)

Pond snail egg - - - > 200 Adema & Vink (1981)
(Lymnaea juvenile
stagnalis)

Insects

Pteronarcys naiad, dispersed via 15.5 1.3 0.5 Sanders & Cope
californica 3-3.5 cm ethanol (1968); Johnson &
Finley (1980)
---------------------------------------------------------------------------------------------------------

Pteronarcella naiad, dispersed via 15.5 - 0.5 Sanders & Cope
badia 1.5-2 cm ethanol (1968); Johnson &
Finley (1980)

Claassenia naiad, dispersed 15.5 - 0.6 Sanders & Cope
sabulosa 2-2.5 cm (1968); Johnson &
Finley (1980)

Pteronarcys naiad, 2-5 cm dispersed via 12.8 180 39 Jensen & Gaufin
californica acetone (1966)

Acroneuria naiad, dispersed via 12.8 143 24 Jensen & Gaufin
pacifica 2-2.5 cm acetone (1966)

Damselfly juvenile dispersed via 24 - 12 Johnson & Finley
(Ischnura acetone (1980)
venticalis)

Other invertebrates

Bristle worm 2-3-day-old dispersed via 21 - > 100 Hooftman & Vink
(Ophryotrocha larva acetone (1980)
diadema)
4-week-old dispersed via 21 - > 100 Hooftman & Vink
adult worm acetone (1980)
---------------------------------------------------------------------------------------------------------
^aValues in parentheses are the 48-h LC₅₀.
Table 26. Short-term LC₅₀s of dieldrin in invertebrates
-------------------------------------------------------------------
Species Stage LC₅₀at end of Reference
study (µg/litre)
(time of exposure)
-------------------------------------------------------------------
Ophryotrocha larva >10 Hooftman & Vink
diadema (2-3 days) (5-6 weeks) (1980)

adult 60 Hooftman & Vink
(4 weeks) (5-6 weeks) (1980)

Daphnia magna larva 100 Adema & Vink
(3 weeks) (1981)

adult 200 Adema & Vink
(0.3 cm) (7 days) (1981)

Artemia salina larva 40 Adema & Vink
(4 weeks) (1981)

adult 50 (male) Adema & Vink
(1 cm) (7 days) (1981)
110 (female)
(7 days)

Chaetogammarus larva 1.8 Adema & Vink
marinus (4 weeks) (1981)

adult 3.6 Adema & Vink
(1 cm) (14 days) (1981)

Palaemonetes adult 0.3 Adema & Vink
varians (4 cm) (7 days) (1981)

Crangon crangon adult 4 Adema & Vink
(4 cm) (14 days) (1981)
-------------------------------------------------------------------

When adult mud snails (Nassa obsoleta) were exposed to up to
10 000 µg dieldrin/litre for 96 h, and then transferred to
dieldrin-free sea water for 33 days, no mortality occurred
throughout the study and the length of the animals was normal after
33 days. There was a significant increase in total egg deposition
during the 33-day post-treatment period in the case of snails
exposed to 10 µg dieldrin/litre, but there was a significant
reduction at 100, 1000, and 10 000 µg dieldrin/litre (Eisler,
1970).

In studies by Klein & Lincer (1974), fiddler crabs, (Uca
pugilator) were fed diets containing 0, 0.1, 1, 10, and 50 mg
dieldrin/kg diet for 14 days and observed for another 25 days.
Behaviour, measured as righting response, was modified at dose

levels of 1 mg/kg or more, and even in the group given 0.1 mg/kg,
difficulty in righting was seen after 11 days. With 10 and 50
mg/kg diet, an increase in mortality was observed, but not with 1
mg/kg diet.

Table 27. Concentrations producing about 50%
reduction in the development of fertilized eggs
during 48 h, in larval survival during 12 days
(clams) or 14 days (oysters), and effects on
larval growth during 10 or 12 days exposure^a
(Davis & Hidu, 1969)
--------------------------------------------------
Organism Effect Aldrin Dieldrin
(µg/litre) (µg/litre)
--------------------------------------------------
Clam development of > 10 000 -
Oyster fertilized eggs - 640

Clam larval survival 410 -
Oyster - > 10 000

Clam larval growth 250^b -
Oyster - 500^c
--------------------------------------------------
^aExpressed as a percentage of growth of control
larvae.
^b80% reduction.
^c50% reduction.

7.2.2. Fish

7.2.2.1 Acute toxicity

Both aldrin and dieldrin are highly toxic to fish under
laboratory conditions. A summary of reported 96-h LC₅₀values for
fresh water and marine species is given in Table 28. In parallel
studies, dieldrin was consistently more toxic than aldrin. The
96-h LC₅₀s range from 2.2 to 53 µg aldrin/litre and from 1.1 to 41
µg dieldrin/litre in various fish species. It should be noted that
the range for aldrin exceeds the water solubility of the compound.

The results of studies by Macek et al. (1969) indicate that a
rise in temperature increases the toxicity of aldrin and dieldrin
for bluegills and rainbow trout. However, Johnson & Finley (1980)
stated that toxicity was not appreciably (only a factor of 2)
changed by variations in temperature or water hardness.

Macek (1975) investigated the effects of simultaneous exposure
of bluegills to DDT and dieldrin and concluded that the acute
toxicity of dieldrin in the concentration range 5.9 - 6.6 µg/litre
was not increased by the presence of DDT (concentration range,
4.5 - 5 µg/litre).

Anderson & Weber (1975) found that new-born and juvenile
guppies (Lebistes reticulatus) were more resistant to dieldrin
than adults. A relationship between the LC₅₀and body weight was
derived for mature, juvenile, and new-born guppies:

LC₅₀= aW^b

where W is the body weight. The best fit value for the exponent b
was 0.81.
Table 28. Acute toxicity of aldrin and dieldrin for fish
------------------------------------------------------------------------------------------
Species Weight Vehicle Temperature 96-h LC₅₀ Reference
(g) (°C) (static test)
----------------
Aldrin Dieldrin
(µg/litre)
------------------------------------------------------------------------------------------
Fresh-water

Rainbow trout 0.6 dispersed 13 2.6 - Johnson &
(Salmo via acetone Finley (1980)
gairdneri)
1.4 dispersed 13 - 1.2 Johnson &
via acetone Finley (1980)

3.2 dispersed 20 17.7 9.9 Katz (1961)
via acetone

0.6-1.5 dispersed 1.6 3.2 2.4 Macek et al.
via acetone 7.2 3.3 1.1 (1969)
12.7 2.2 1.4

Cutthroat trout 1.1 dispersed 9 - 6^a Johnson &
(Salmo clarki) via acetone Finley (1980)

Chinook salmon 1.45-5 dispersed 20 7.5 6.1 Katz (1961)
(Oncorhynchus via acetone
tshawytscha)

0.8 dispersed 15 14.3 - Johnson &
via acetone Finley (1980)

Coho salmon 2.7-4.1 dispersed 20 45.9 10.8 Katz (1961)
(Oncorhynchus via acetone
kisutch)

Goldfish 1-2 dispersed 25 32 41 Henderson et al.
(Carrassius via acetone (1959)
auratus)

Goldfish 1 dispersed 18 - 1.8 Johnson &
(Carassius via acetone Finley (1980)
auratus)
------------------------------------------------------------------------------------------

Table 28. (contd.)
------------------------------------------------------------------------------------------
Species Weight Vehicle Temperature 96-h LC₅₀ Reference
(g) (°C) (static test)
----------------
Aldrin Dieldrin
(µg/litre)
------------------------------------------------------------------------------------------
Fresh-water (contd.)

Carp (Cyprinus NA NA 20 4^b - Rehwoldt et al.
carpio) (1977)

Fathead minnow 0.6 dispersed 18 8.2 3.8 Johnson &
(Pimephales via acetone Finley (1980)
promelas)
1-2 dispersed 25 32 18 Henderson et al.
via acetone (1959)

Guppy (Lebistes 0.1-0.2 dispersed 25 37 25 Henderson et al.
reticulatus) via acetone (1959)

NA^d NA 20 20^b - Rehwoldt et al.
(1977)

NA NA 24 - 3.2-7 Adema & Vink
(young) (1981)

NA NA 24 - 35^c Adema & Vink
(adult) (1981)

juvenile NA 25 10.9 Anderson & Weber
(1975)

newborns NA 36.7 Anderson & Weber
(1975)

Black bullhead 1.5 dispersed 24 19 - Johnson & Finley
(Ictalurus via acetone (1980)
melas)

Channel catfish 5.2 dispersed 18 53 - Johnson & Finley
(Ictalurus via acetone (1980)
punctatus)
1.4 dispersed 18 - 4.5 Johnson & Finley
via acetone (1980)

Bluegill 0.7 dispersed 18 6.2 - Johnson & Finley
(Lepomis via acetone (1980)
macrochirus)
1.3 dispersed 18 - 3.1 Johnson & Finley
via acetone (1980)

1-2 dispersed 25 15 8.8 Henderson et al.
via acetone (1959)
------------------------------------------------------------------------------------------

Pumpkinseed NA NA 20 20^b - Rehwoldt et al.
sunfish (1977)
(Lepomis
gibbosus)

Largemouth bass 2.5 dispersed 18 5 3.5 Johnson & Finley
(Micropterus via acetone (1980)
salmoides)

Striped bass NA NA 20 10^b - Rehwoldt et al.
(Marone (1977)
saxatilis)

Banded killyfish NA NA 20 21^b - Rehwoldt et al.
(Fundulus (1977)
diaphanus)

White perch NA NA 20 42^b - Rehwoldt et al.
(Roccus (1977)
americanus)

American eel NA NA 20 16^b - Rehwoldt et al.
(Anguilla (1977)
rostrata)

Marine species

Common goby NA NA 15 - 3.5 Adema & Vink
(Gobius microps) (adult) (1981)

Plaice length: NA 15 - 1.7 Adema & Vink
(Pleuronectes 2-3 cm (1981)
platessa)
length: NA 15 - 4 Adema & Vink
10 cm (1981)

yolk-sac NA 5-10 - 30 Adema & Vink
larva (1981)

egg-metam NA 5-10 - > 32 Adema & Vink
larva (1981)
------------------------------------------------------------------------------------------

Threespine 0.4-0.8 dispersed 20 27.4 13.1 Katz (1961)
stickleback via acetone
(Gasterosteus
aculeatus)
------------------------------------------------------------------------------------------
^aHardness = 162 mg CaCO₃/litre.
^bHardness = 50 mg CaCO₃/litre.
^c48-h LC₅₀.
^dNA = not available.
7.2.2.2 Long-term toxicity

Sailfin mollies (Lebistes latipinna) were exposed in groups of
20 to 0, 0.75, 1.5, 3, 6, or 12 µg dieldrin/litre using a flow-
through system for 34 weeks. The mortality of the 0.75 µg/litre
group was similar to that of the control group. At 1.5 µg/litre,
there was an increase in mortality, and, at 3 µg/litre or more,
100% mortality occurred. The growth rates and reproduction
performances were adversely affected in the surviving fish (Lane &
Livingstone, 1970).

Rainbow trout (Salmo gairdneri) were fed food containing
dieldrin for 240 days, the nominal dietary concentrations
corresponding to 14, 43, 143, or 430 µg dieldrin/kg body weight per
day. The growth rate was not affected at any of the concentrations
throughout the 240 days, and there was no mortality or visible
adverse effects. The activities of liver glutamate-pyruvate
transaminase (GPT) and glutamate-oxaloacetate transaminase (GOT)
were not affected, except, in the case of the latter, at the
highest dose level. Liver glutamate dehydrogenase (GDH) activity
was increased at all dose levels. Electron micrographs of liver
cells demonstrated changes in mitochondrial morphology, the highest
dose causing swelling and membrane disruption. Since GDH is an
intramitochondrial enzyme, examination by electron microscopy gave
further evidence that dieldrin altered mitochondrial metabolism.
In the brain, GOT activity was significantly decreased at 43 µg/kg
and GTP was decreased at 14 µg/kg or more. At all dose levels,
brain GDH was decreased and brain glutamine transferase (GT) was
increased. Electron microscopy of the medulla and cerebral
hemispheres did not show any effects of dieldrin. The
concentrations of 16 free amino acids in the brain were determined.
The concentrations of four were not significantly changed, whereas
eight were significantly altered at 143 µg dieldrin/kg and 12 at
430 µg/kg. Serum ammonia concentrations were significantly
increased at 143 and 430 µg dieldrin/kg, but the concentration of

ammonia in the brain was not affected. The increase in brain GT
was considered to be a possible reason for this lack of effect on
brain ammonia, since it compensated for the decrease in GDH
activity. Alternatively, brain ammonia may have been transported
via the blood to the liver with consequent effects on the liver.
The ammonia-detoxifying mechanism of fish seemed to be very
sensitive to dieldrin, the no-effect dose being below 14 µg/kg body
weight per day (equivalent to 0.36 mg/kg food) (Mehrle &
Bloomfield, 1974).

Several studies have described the influence of aldrin and/or
dieldrin on enzymes such as mitochondrial succinic hydrogenase, the
epoxidative activities of liver microsomes and the ATPase activity
of microsomes of the gills or brain (Chan et al., 1967; Davis et
al., 1972; Moffet & Yarbrough, 1972; Yap et al., 1975).
Furthermore, the influence of dieldrin during thermal stress has
been studied in darters (Etheostoma nigrum) (Silbergeld, 1973).

In studies by Verma & Tonk (1984), Heteropneustes
(Saccobranchus) fossilis was exposed to aldrin for 30 days at a
concentration of 0.03 mg/litre. Respiration, haematological
parameters, and the activity of two enzymes in liver, kidneys, and
gills were determined. The respiration rate decreased and the
blood concentrations of glucose, sodium, and chloride ions showed
significant increases. The cholesterol content and clotting time
were decreased, and the ATPase activity in the three tissues was
significantly reduced.

7.2.2.3 Reproduction

Van Leeuwen (1986) carried out studies with dieldrin to study
the susceptibility of early-life stages of rainbow trout. The test
was performed with fertilized eggs before and after water
hardening, and with early eye point eggs, late eye point eggs, sac
fry, and early fry. No mortality was found in the different early-
life stages using concentrations greater than aqueous solubility
(> 10 mg/litre), except for the early fry where a very low 96-h
LC₅₀of 0.003 mg/litre was found.

In studies by Cairns et al. (1967), nine populations of guppies
(Lebistes reticulatus) were exposed in a semi-static system to
nominal concentrations of 0 (three populations), 1.8, 5.6, and 10
µg dieldrin/litre (two populations of each) for 14 months. During
the first 2 - 3 months, the exposed populations in five tanks
developed greater numbers of individuals (mature, immature, and
fry) than did the controls (except one population at 5.6 µg/litre,
which was similar to the controls). The difference between the
controls and five treatment groups was attributed to the higher
predation and harassment observed in the control groups. The total
numbers of individuals in control and treatment groups became
similar during the final 6 - 8 months of the study. The average
total monthly body weights of the groups treated with 1.8 µg/litre
and 5.6 µg/litre began to increase steadily after about 8 months,
whereas the total monthly body weights of the group exposed to 10
µg/litre were similar to the controls throughout the 14 months of

the study. The production of fry by one of the groups treated with
10 µg/litre declined markedly after the thirty-second week of the
study, no new broods of fry being born after the forty-second week.
No such marked decline occurred in the other five treatment groups
(including one population exposed to 10 µg/litre).

Chadwick & Shumway (1970), conducted studies lasting 130 days
on rainbow trout (Salmo gairdneri) to determine survival from time
of fertilization through to hatching in continuously cycled water.
Embryos, alevins, and fry were exposed to dieldrin concentrations
ranging from 0.012 to 52 µg/litre. Eggs (embryos) exposed to up to
52 µg dieldrin/litre from the time of fertilization survived until
hatching as well as controls, but the mean weight of newly-hatched
alevins (minus yolk material) was reduced by higher concentrations
(not specified). Alevins were more susceptible than embryos.
Their survival was reduced at all concentrations above 0.39
µg/litre. Trout fry, whose survival was unaffected at dieldrin
levels of 0.12 µg or less, quickly succumbed at concentrations of
0.39 µg/litre or more.

Smith & Cole (1973), exposed adult winter flounder (Pseudo-
pleuronectes americanus) to 2 µg/litre in aquaria continuously
supplied with filtered sea water. When fish became ripe, they were
artificially spawned, and approximately 30 000 eggs were collected
from each of the 24 spawning pairs and cultured. The remaining
eggs were analysed. The percentage fertilization of eggs
containing 0.61 mg dieldrin/kg or less was 99% (controls, 97.8%).
The percentage fertilization of eggs containing 1.21 mg dieldrin/kg
was 12%, and all the eggs containing 1.74 mg/kg were infertile.
There was no effect on egg development except in the case of the
two groups of eggs containing the higher concentrations of
dieldrin. The effects on egg mortality were not due to dieldrin in
the gametes, and the milt of exposed male flounders contained no
detectable residue of dieldrin.

7.2.3. Amphibia and reptiles

The LC₅₀values for tadpoles of two species of frogs (1 week
old) and toads (4 - 5 weeks old) were determined by Sanders (1970).
The 96-h LC₅₀(at 15.5 °C) of dieldrin for Western chorus frog
tadpoles (Pseudacris triseriata) was 100 µg/litre, whereas that of
both aldrin and dieldrin for Fowler's toad tadpoles (Bufo
woodhousii fowleri) was 150 µg/litre.

Cooke (1972) studied the effect of dieldrin at nominal
concentrations of 0.008, 0.02, or 0.5 mg/litre on groups of 40
common frog (Rana temporaria) or toad (Bufo bufo) tadpoles with
hindlimb paddles or hind legs. The exposure was for 24 or 48 h in
amphibian saline, and the observation period 5 or 15 days. At the
highest dose level, the frogs showed an increased mortality, the
mean dieldrin content being 42.9 mg/kg tissue. At the two lower
dose levels (0.008 and 0.02), there were 0.31 and 6.1 mg/kg
dieldrin in tissues, respectively. When toad tadpoles were exposed
to 0.02 or 0.5 mg/litre, the animals with the higher dose level
showed clear behavioural and structural abnormalities and a reduced

rate of development, but these changes returned to normal a few
days after exposure. The mean dieldrin content was 138 mg/kg
tissue at a dose level of 0.5 mg/litre.

The in vitro exposure of toad embryo tissue (Bufo arenarum) to
dieldrin (4 x 10^-5mol/litre) produced an inhibition of acetyl and
butyryl cholinesterase activity. In in vivo studies with open-
mouth stage embryos, dieldrin produced acetyl cholinesterase
inhibition at 0.5 x 10^-6mol/litre. Furthermore, hyperactivity in
swimming larvae was observed (de Llamas et al., 1985).

The in vitro activity of ATPase in a number of tissues of the
male turtle (Graptemys geographica) was determined by Wells et al.
(1974). There was no consistent dose relationship for either aldrin
or dieldrin, except perhaps in the case of the cloacal bladder in
the aldrin treatments. The inhibition of Na/K/Mg ATPase by aldrin
and dieldrin was in the range of 4 - 13%. It was suggested that
aldrin and dieldrin may affect the transport of metabolites across
the cellular membranes as a result of decreased energy for active
transport.

7.3. Terrestrial Organisms

7.3.1. Higher plants

Dieldrin has low phytotoxicity, tomatoes and cucumber, for
example, being affected only at application rates greater than 22
kg/ha. Aldrin affects some crops at rates greater than 22 kg/ha,
beans and cereals being most sensitive. Tomatoes and cucumbers are
sensitive to aldrin but only at unrealistically high application
rates (Edwards, 1965).

Studies in greenhouses showed that aldrin, administered weekly
as an emulsifiable concentrate at a rate of 16 kg active
ingredient/ha to 2 - 3-week-old seedlings of tomato, cauliflower,
and Chinese cabbage, inhibited root development and reduced growth
rate of cauliflower and Chinese cabbage seedlings. A ten-fold
reduction in the aldrin level failed to produce these effects
(Hagley, 1965).

Aldrin and dieldrin at 11 kg active ingredient/ha had no effect
on the emergence, growth, yield, or chemical composition of
soybeans (Probst & Everly, 1957).

7.3.2. Earthworms

In studies by Cathey (1982), earthworms (Lumbricus terrestris)
were maintained in an artificial nutritionally complete soil, based
on shredded paper containing aldrin. The LC₅₀value (6-week
exposure) was 60 mg aldrin/kg bedding, and the tolerance level,
producing less than 1% mortality, was 13 mg aldrin/kg bedding.

When aldrin (2.5 - 4.6 kg/ha) was applied as a spray or dust,
respectively, to the surface of soil plots and incorporated into
the soil, the numbers of earthworms in treated plots were either
similar to or greater than those in control plots (Edwards et al.,
1967; Griffiths et al., 1967; Edwards & Lofty, 1977).

7.3.3. Bees and other beneficial insects

In a review of five investigations on the toxicity of aldrin
and dieldrin to honey bees (Sanger, 1959), the oral LD₅₀values for
aldrin ranged from 0.24 to 0.45 µg/bee, while the values for
dieldrin were in the range 0.15 - 0.32 µg/bee. Contact LC₅₀values
were 0.15 - 0.8 µg/bee for aldrin and 0.15 - 0.41 µg/bee for
dieldrin.

Cowie (1967) reported an oral LD₅₀of 0.3 µg dieldrin/bee
(range, 0.13 - 0.54) and a contact LD₅₀of 0.21 µg/bee.

The toxicity of dieldrin to two important predators of cotton
pests was investigated by Burke (1959). The contact LD₅₀value for
Hippodamia convergens was 1.6 mg/g body weight.

In a review of the effects of pesticides on soil fauna, it was
concluded that aldrin (and, by implication, dieldrin) is relatively
non-toxic for predatory mites ( Acarina spp.), and that this may
contribute to its success as a soil insecticide (Edwards &
Thompson, 1973).

7.3.4. Birds

7.3.4.1 Acute toxicity

Estimates of the LD₅₀values for several species of birds are
given in Table 29. The variation in acute oral toxicity of
dieldrin among six species of birds tested by Tucker & Haegele
(1971) was more than ten fold.

Table 29. Acute oral toxicity of aldrin and dieldrin for avian
species^a
-------------------------------------------------------------------
Species LD₅₀ Reference
-------------------
Aldrin Dieldrin
(mg/kg body weight)
-------------------------------------------------------------------
Fulvous whistling duck male: female: Tucker & Crabtree
(Dendocygna bicolor) 29.2 100-200 (1970)

Mallard duck female: female: Tucker & Crabtree
(Anas platyrhynchos) 520 381 (1970)

Canada goose 50-150 Tucker & Crabtree
(Branta canadensis) (1970)
-------------------------------------------------------------------

Table 29. (contd.)
-------------------------------------------------------------------
Species LD₅₀ Reference
-------------------
Aldrin Dieldrin
(mg/kg body weight)
-------------------------------------------------------------------
Domestic fowl 25.5 43 Sherman &
(Gallus domesticus) Rosenberg (1953)

Japanese quail male: Tucker & Crabtree
(Coturnix coturnix 69.7 (1970)
japonica)

Bobwhite quail female: Tucker & Crabtree
(Colinus virginianus) 6.6 (1970)

California quail 8.7 Hudson et al.
(Callipepla californica) (1984)

Gray partridge female: Tucker & Crabtree
(Perdix perdix) 8.8 (1970)

Chukar partridge 23.4 Tucker & Crabtree
(Alectoris graeca) (1970)

Sharp-tailed grouse male: McEwen & Brown
(Pedioecetes phasianellus) 6.9 (1966)

Ring-necked pheasant female: female: Tucker & Crabtree
(Phasianus colchicus) 16.8 79 (1970)

Pigeon 55 67 Turtle et al.
(Columba livia) (1963)
26.6 Tucker & Crabtree
(1970)

House sparrow female: Tucker & Crabtree
(Passer domesticus) 47.6 (1970)
-------------------------------------------------------------------
^aDetails concerning age and weight of birds are not summarized
here but can found in the original publications.

7.3.4.2 Short- and long-term toxicity

Values for the subacute LC₅₀s of aldrin and dieldrin,
determined using the procedure developed at the Patuxent Wildlife
Centre (Hill et al., 1975), are given in Table 30. The LC₅₀values
of aldrin and dieldrin for each of the four species tested were of
the same order. The annual variations in the LC₅₀of dieldrin over
a period of up to 8 years for these four species have been
investigated by Hill et al. (1977) (18 times per species). No
time-related changes in LC₅₀values were found for any of the
species. However, differences were found between birds of
different ages in some species, e.g., Japanese quail and mallards

(Hudson et al., 1984). There were also differences between the
slopes of the average regression lines for the four species. These
authors emphasized the need to evaluate both the LC₅₀and the slope
of the regression line. Food consumption was reduced by aldrin or
dieldrin in the diet.

Table 30. Subacute dietary toxicity of aldrin and dieldrin
for avian species^a
-----------------------------------------------------------
Species Age LC₅₀(95% confidence limits)
(days) ----------------------------
Aldrin Dieldrin
(mg/kg diet)
-----------------------------------------------------------
Mallard duck 5 155 153
(Anas platyrhynchos) (129-186) (123-196)
10 - 169

Japanese quail 14 34 62
(Coturnix coturnix (28-41) (53-71)
japonica)

Bobwhite quail 14 37 37
(Colinus virginianus) (33-41) (30-46)

Ring-necked pheasant 10 57 58
(Phasianus colchicus) (50-64) (51-67)
-----------------------------------------------------------
^aAldrin or dieldrin fed for 5 days followed by 3 days of
untreated diet.

Wiese et al. (1969) fed diets containing up to 500 mg technical
dieldrin (85%)/kg diet to male and female 6-month-old crowned
guinea-fowl (Numida meleagris). None of the birds fed 1.5 mg/kg
for 21 months died. The median survival time for birds fed 5 mg/kg
was 524 days; for birds fed 150 and 500 mg/kg, it was 3 and 1 days,
respectively. No differences in susceptibility between males and
females were found.

The subacute toxicities of technical dieldrin (85%) to three
species of birds are given in Table 31 (Basson, 1971).

7.3.4.3 Reproductive studies

The first experimental studies of the effects of aldrin or
dieldrin on avian reproduction showed that these compounds were
toxic for quail and pheasants. Quail fed a diet containing aldrin
or dieldrin at a toxic dose of 0.5 or 1 mg/kg diet did not show any
clear effects on egg production, percentage fertility, or
percentage hatchability (the birds had not been exposed earlier to
the compounds) (DeWitt, 1955, 1956). No significant effect was
found on the fertility or hatchability of eggs of pheasants fed
25 mg dieldrin/kg diet, but at 50 mg/kg there was a clear effect
(Genelly & Rudd, 1956).

Table 31. Subacute toxicity of technical dieldrin for three species
of birds
-------------------------------------------------------------------
Species Concentration Median time Median lethal
(mg/kg diet) till death dose (mg
(days) dieldrin/kg
body weight)
-------------------------------------------------------------------
Guinea fowl 20 72 72.4
(Numida meleagris) 150 12 11.2

Laughing dove 5 49 15.8
(Stigmatopelia 90 4.7 17.3
senegalensis)

Sparrow (Passer 5 85.1 > 41
melanurus melanurus) 45 7 43.8
-------------------------------------------------------------------

Eggs from chickens fed 1 mg aldrin or dieldrin/kg diet for
2 years showed normal fertility and hatchability, although the
concentrations of dieldrin in the yolks of the eggs were in the
range of 6 to 25 mg/kg. The fertility and hatchability slightly
decreased at 10 mg dieldrin/kg diet (Brown et al., 1965).

Other studies on avian reproduction are summarized in Table 32.
This table gives the available information on five criteria
relevant to reproduction (parental survival, production, fertility
and hatchability of eggs, and chick survival) in relation to oral
intake of dieldrin and (where reported), the residues of dieldrin
in eggs. These studies show that, depending on the duration of
exposure, dose levels of 5 - 10 mg dieldrin/kg diet reduce the
survival of the parent birds. Egg production was reported to be
significantly increased in some studies but reduced in others. In
general, egg fertility was not influenced, except in one study.
Hatchability was not affected, neither in most cases, was the
survival of chicks. There seems to be a trend that overall
reduction in reproductive success occurs only if the parent birds
are showing signs of being affected by dieldrin, e.g., reduced food
intake with consequent loss of weight and poor condition. It
should be noted that in these studies (with one exception) the eggs
were placed in incubators for hatching. Consequently, one aspect
of the reproductive process was not studied, namely, parental
behaviour. However, in the study on homing pigeons (Robinson &
Crabtree, 1969), the parents (and subsequently, their offspring)
were free-flying, they brooded their eggs, and fed their young
until they fledged.

A 3-generation study of the effects of dieldrin on pheasants
(Phasianus colchicus), has not been included in Table 32 because
of the complexity of the experimental design. The doses of
dieldrin (hens, 6 or 10 mg dieldrin/bird per week; cocks, 4 or 6 mg
dieldrin/bird per week) were sufficient to cause mortality of
breeding birds, but the production, fertility, and hatchability of
eggs and the viability of chicks at the time of hatching were not

affected in a consistent manner in relation to dose or generation.
The survival of chicks from hens given 6 or 10 mg dieldrin/week was
reduced. Residues of dieldrin in eggs or tissues were not
determined in this study (Dahlgren & Linder, 1974).

When seven-week-old Japanese quail were given diets containing
3.1 or 50 mg dieldrin/kg diet for 21 days, a significant reduction
in egg production occurred in both groups (Call & Harrell, 1974).

With the exception of the study with the barn owl (Mendenhall
et al., 1983) and the homing pigeon (Robinson & Crabtree, 1969),
the birds that were tested are precocial species which show no
parental feeding of the young. Most birds are not precocial and
reproduction involves a period of full dependency of the offspring
on parental care. Results should, therefore, be interpreted with
care; extrapolation directly from the laboratory to the field is
difficult.

7.3.4.4 Eggshell thinning

Ratcliffe (1967a) reported that the ratio of eggshell weight to
size in three species of birds of prey in the United Kingdom had
declined during the period after 1947 relative to pre-1947. This
report has stimulated considerable interest in the relationship
between egg-shell thickness (or the related eggshell index based on
the weight/size ratio) and the breeding success of birds,
particularly as eggshell thinning seems to be quite a widespread
phenomenon, particularly among birds of prey (Hickey & Anderson,
1968; Ratcliffe, 1970; Anderson & Hickey, 1972). There has been
considerable speculation on the causes and mechanism of these
changes (Cooke, 1973; Mueller & Leach, 1974). Experimental studies
on the effects of dieldrin on eggshell thickness have given
conflicting results. The results are summarized in Table 33.

Eggshell weights of crowned guinea-fowl (Numida meleagris) fed
diets containing up to 15 mg dieldrin/kg diet for 21 months were
not affected by the treatments (Wiese et al., 1969).

American sparrow hawks (Falco sparverius) were given diets
containing dieldrin and North American prairie falcons (Falco
mexicanus) were fed starlings contaminated with an average of 29 mg
dieldrin/kg body weight, along with DDT and DDE at different
levels. The purpose of these studies was to show the influence of
these pesticides on shell thickness. The results of the two
studies, in relation to the effects of dieldrin, cannot be
interpreted, in view of the possible effects of DDE on eggshell
thinning (Porter & Wiemeyer, 1969; Enderson & Berger, 1970). It
has slowly become accepted that metabolites of DDT, particularly
DDE, are the most likely cause of eggshell thinning (Cooke, 1973;
Newton, 1979; Bunyan & Stanley, 1982). It is also pertinent that
the onset of eggshell thinning in wild birds preceded the use of
aldrin/dieldrin. There is evidence that eggshell thinning after
exposure to dieldrin is related to reduced food consumption.
Untreated Coturnix and Mallard, when fasted for 36 h, laid thin-
shelled eggs for a few days during and after fasting (Haegele &
Tucker, 1974).

Table 32. Reproductive success of birds in relation to oral intake of dieldrin and the concentration of HEOD in eggs
--------------------------------------------------------------------------------------------------------------------
Species Intake of Duration Mean concen- Survival Reproductive success relative to Reference
dieldrin tration of of controls
(mg/kg diet) dieldrin in parents Eggs Fer- Hatcha- Chick
eggs (mg/kg) /hen tility bility- survival
(range) of eggs of eggs
--------------------------------------------------------------------------------------------------------------------
Mallard duck 4 90 days - - NC^g NC Red.^c - Muller &
(Anas platy- Lockman (1972)
rhinchos)

Japanese quail 1 16 weeks - - NC NC NC - Shellenberger
(Coturnix 10 16 weeks - - NC NC NC - & Newell
coturnix (1965)
japonica)
10 18 weeks 19 NC NC NC NC NC Walker et al.
(6.9-26.9) (1969a)
20 9 weeks 39 Red. Red. DC NC Red.
(19.8-54.1)
30 7 weeks 48 Red. Red. DC Red. Red.
(34.7-63.2)
40 6 weeks 84 Red. Red. - - -
(76.9-92.5)

0.1 multi- - NC NC NC NC NC Shellenberger
generation (1978)
P; F₁,
1 F₂, F₃ - NC NC NC NC NC

Bobwhite quail 10 34 weeks - Red. NC - - - Fergin &
(Colinus 20 34 weeks - Red. Red. - - - Schafer (1977)
virginianus) 40 34 weeks - Red. Red. - - -

Pheasant 2 mg/hen/ 13 weeks (0.6-26.5) NC NC NC^a Inc.^c NC Atkins &
(Phasianus week^b (yolks) Linder (1967)
colchicus) 2 mg/hen/ 13 weeks - NC NC NC NC NC
week
4 mg/hen/ 13 weeks (5.3-40.1) DR NC NC NC NC
week (yolks)
4 mg/hen/ 13 weeks (7.5-20.6) NC NC NC NC NC
week (yolks)
--------------------------------------------------------------------------------------------------------------------

Table 32. (contd.)
--------------------------------------------------------------------------------------------------------------------
Species Intake of Duration Mean concen- Survival Reproductive success relative to Reference
dieldrin tration of of controls
(mg/kg diet) dieldrin in parents Eggs Fer- Hatcha- Chick
eggs (mg/kg) /hen tility bility- survival
(range) of eggs of eggs
--------------------------------------------------------------------------------------------------------------------
Pheasant 6 mg/hen/ 13 weeks (13.3-52.4) NC Red.^a NC NC NC
(Phasianus week (yolks)
colchicus)
(contd.) (0) 6 mg/hen/ 14 weeks - Red. Inc.^c Red.^c NC NC Baxter et al.
week^d (1969)
(0) 8 mg/hen/ 14 weeks - Red. Inc.^c NC NC NC
week
(0) 12 mg/ 14 weeks - Red. Red.^c NC - -
hen/week
(4) 0 mg/hen/ 14 weeks - NC Inc.^c Red.^c Red. NC
week
(4) 6 mg/hen/ 14 weeks - Red. NC Red.^c NC NC
week
(6) 0 mg/hen/ 14 weeks - NC Red.^c NC - -
week
(6) 6 mg/hen/ 14 weeks - Red. Red.^c Red.^c - -
week

Gray partridge 3 1.5 - DR NC NC NC Neill et al.
(Perdix perdix) (1-2) (1971)

Domestic fowl 2 16 weeks (0.34-1.45) NC NC - NC NC Graves et al.
(Gallus 5 16 weeks (1.2-4.8) NC NC - NC NC (1969)
domesticus)
10 13 months (7.6-16) NC NC NC NC NC Brown et al.
(1974)
20 13 months (19.6-35.7) Red. Inc.^a NC NC Red.

Crowned guinea- 0.5 21 months 1.11/1.17^e NC Inc.^a NC NC NC Wiese et al.
fowl (Numida (1969)
meleagris) 1.5 21 months 2.38/3.35^e NC Inc.^a NC NC NC
5 21 months 7.18/13.56^e PR Inc.^a NC NC NC
15 21 months 15.79^e Red. Inc.^a NC NC Red.
--------------------------------------------------------------------------------------------------------------------

--------------------------------------------------------------------------------------------------------------------
Homing pigeon _~2 mg/kg 2 years (0.03-13.4)^f NC NC NC NC NC Robinson &
(free-flying) body weight/ (4.5-16.7)^f NC NC NC NC NC Crabtree
(Columba livia) week (1969)

Barn owl 0.5 2 years 3.6 (first NC NC NC NC NC Mendenhall et
(Tyto alba) year) al. (1983)
8.1 (second
year)
--------------------------------------------------------------------------------------------------------------------
^aSignificant at a probability of < 0.01.
^bDoses of 2, 4, or 6 mg dieldrin/hen were administered once per week in capsules.
^cSignificant at a probability of < 0.05.
^dSecond-generation hens; offspring of birds used in study by Atkins & Linder (1967). The doses in parentheses
refer to the doses administered to the first-generation hens.
^eResidues in eggs of successive years.
^fFirst and second laying periods, respectively.
^gThe term "no change" (NC) indicates that any differences between controls and treatment groups were within the
limits of experimental variation. If any of the results for treatment groups are reported to be increased (Inc.)
or reduced (Red.), the statistical significance, if reported, is given. Equivocal results have been described
"doubtful reduction" (DR), "probably reduced" (PR), and "doubtful change" (DC).

Table 33. Effects of dieldrin on eggshell thickness
--------------------------------------------------------------------------------------------------------------
Species Dose of dieldrin Duration Difference between egg- Reference
(mg/kg diet) shell thickness of treated
and control birds (%)
--------------------------------------------------------------------------------------------------------------
Mallard duck 1.6 16 months -3.4^a Lehner & Egbert (1969)
(Anas platyrhynchos)
4 16 months -2^a Lehner & Egbert (1969)

10 16 months -4.3^a Lehner & Egbert (1969)

4 90 days -4.2 Muller & Lockman (1972)

Japanese quail 3.1 21 days with -8^a Call & Harrell (1974)
(Coturnix coturnix changes in
japonica) 50 photoperiod -8^a Call & Harrell (1974)

Domestic fowl 10 12 weeks 0 Davison & Sell (1972)
(Gallus domesticus) 20 12 weeks +0.3 Davison & Sell (1972)

10 13 months 0 Brown et al. (1974)
20 13 months +9.7 Brown et al. (1974)

Pheasant 6 mg/hen/week^b - 0 Dahlgren & Linder (1970)
(Phasianus colchicus)
10 mg/hen/week^b - 0 Dahlgren & Linder (1970)
(6) 0 mg/hen/week^c - +4.1 Dahlgren & Linder (1970)
(6) 6 mg/hen/week^c - +4.1 Dahlgren & Linder (1970)
(10) 0 mg/hen/week^c - +4.1 Dahlgren & Linder (1970)
--------------------------------------------------------------------------------------------------------------
^aSignificant at or below 0.05.
^bAdministered in capsules once per week (see footnote^b Table 32).
^cSee footnote^d Table 32.
7.3.4.5 Concentrations of dieldrin in tissues of experimentally
poisoned birds

Many studies have been carried out to estimate the
concentrations of dieldrin in the liver, brain, or other tissues of
birds that died following oral intake of aldrin or dieldrin. The
intakes were either single acute doses or long-term dietary
exposure. In some investigations, the concentrations of dieldrin
in the tissues of birds that survived after treatment were also
reported. The results of these studies are not comparable, because
the dose levels and duration of the studies are different. The
concentrations that were found in the different studies ranged from
a few mg/kg up to about 100 mg/kg tissue (wet weight) (Turtle et
al., 1963; Koeman et al., 1967; Robinson et al., 1967b; Robinson,
1969; Robinson & Crabtree, 1969; Stickel et al., 1969; Enderson &
Berger, 1970; Linder et al., 1970; Brown et al., 1974; Clark, 1975;
Heinz & Johnson, 1981; Mendenhall et al., 1983) (Table 34).

Attempts to define tissue concentrations that can be used as
indicators of death by dieldrin poisoning of wild birds lack
precision as a result of the overlap between the lowest
concentrations in the tissues of birds dying under experimental
conditions and the highest concentrations in survivors. Thus, it
has been proposed that concentrations of 5 or 10 mg dieldrin/kg
brain (Robinson, 1969; Stickel et al., 1969) are indicative of
death from aldrin/dieldrin poisoning. Liver concentrations of 10
or 20 mg/kg (Robinson, 1969; Cooke et al., 1982) have been proposed
as levels diagnostic of dieldrin poisoning of birds.

As a general point, interpretation of residue data must be done
with extreme caution. Brain residues of dieldrin are probably a
good indicator of lethality. However, most bird carcasses
collected in the field cannot be analysed for brain residues,
because the brain deteriorates rapidly after death. For this
reason, most residue data from the field are for levels in the
liver, which remains discrete and usable for much longer. A liver
residue level symptomatic of death from dieldrin poisoning is more
difficult to define. A large, acutely toxic, dose of dieldrin may
leave a low residual level of dieldrin in liver because the bird
dies rapidly. A smaller, less acutely toxic, dose of dieldrin
usually leads to loss of body weight before death because of a lack
of ability or desire to feed. This period of starvation prior to
death boosts liver residues considerably as dieldrin is released
from mobilized fat and concentrated in the liver as detoxification
is attempted.

7.3.5. Mammals

The acute and long-term toxicity of aldrin and dieldrin for
laboratory mammals is summarized in section 8.

Values for the acute oral LD₅₀and subacute oral LC₅₀in the
diet (30 days) of dieldrin for four species of voles ( Microtus sp.)
are given in Table 35.

Table 34. Concentrations of dieldrin in the tissues of experimentally poisoned birds and
in survivors
------------------------------------------------------------------------------------------
Species Tissue Concentration of dieldrin (mg/kg wet weight) Reference
analysed geometric mean, (range of values)
No. of Survivors No. of Dead birds
samples samples
------------------------------------------------------------------------------------------
Domestic pigeon liver 11 8 20 45.6 Robinson et
(Columba sp.) (3.1-51.2) (23-81) al. (1967b)
brain 11 3.6 19 20
(1.6-8.5) (13.5-32.5)

House sparrow liver - - 19 44.7 Robinson
(Passer domesticus) (38.4-52.3) (1969)
brain - - 19 20
(17.6-22.7)

Japanese quail liver - 36 40 Robinson et
(Coturnix coturnix (17.7-90.4) al. (1967b)
japonica) brain 12 6.9 65 17.4
(3.1-15) (8.7-34.6)

Japanese quail liver 8 28.8 9 19.7 Stickel et
(Coturnix coturnix (2.7-140.8) (5.7-51.7) al. (1969)
japonica) brain 20 3.4 17 17.3
(0.25-11.9) (6.2-32.9)

Redwinged blackbird brain 3 7.1 27 19.8 Clark
(Agelaius phoeniceus) (6.7-7.4) (1-34.5) (1975)
27 22.2
(13.5-29.5)

Prairie falcon brain 2 2.9 1 11 Enderson &
(Falco mexicanus) (2.8-3) Berger
(1970)

Barn owl brain 2 10 Mendenhall
(Tyto alba) (5-15) et al.
carcass 19 9.4 - - (1983)
------------------------------------------------------------------------------------------
The toxicological signs in these studies were similar to those
in laboratory animals, and these four microtine rodents appear to
be less susceptible than laboratory rodents to dieldrin
intoxication (Cholakis et al., 1981). When short-tailed shrews
(Blerina brevicauda) were fed diets containing 50, 100, or 200 mg
dieldrin (nominal)/kg diet for up to 14 days, all the animals fed
50 mg/kg dieldrin survived, whereas all those fed 200 mg/kg diet
died (Blus, 1978).

Luckens & Davis (1965) studied the acute oral toxicity in big
brown bats (Eptericus fuscus) caught in Kentucky, USA. Death
occurred at all dose levels above 20 mg/kg body weight. The
approximate LD₅₀seemed to be within the range 20 - 40 mg/kg body
weight.

Table 35. Acute and subacute toxicity of dieldrin for voles^a
------------------------------------------------------------------------
Species Acute LD₅₀ Subacute LC₅₀(30 days)
(mg/kg body weight) (mg/kg body weight)
Average males/females Average males/females
------------------------------------------------------------------------
Microtus orchrogaster 210 105

Microtus canicaudus 100 40

Microtus montanus 205

Microtus pennsylvanicus 175
------------------------------------------------------------------------
^aFrom: Cholakis et al. (1981).
White-tailed deer (Odocoileus virginianus) were fed 0, 5, or
25 mg dieldrin/kg diet for up to 3 years as were their progeny. No
signs of intoxication were observed, and the survival of adults was
not affected. The growth rate of treated females was decreased.
Relative liver weights increased at 25 mg/kg. Fertility and in
utero mortality were comparable for the three groups. Fawns from
treated does were smaller at birth, and greater postpartum
mortality occurred. The weight gain of fawns was reduced during 2
of the 3 years. Whole milk from doses fed 25 mg/kg contained
residues of 17 mg/litre. Residues in the liver of surviving
animals were about 4 mg/kg in the low-dose group and 16 mg/kg (wet
weight) in the high-dose group. Highest brain residues (12 mg/kg
wet weight) occurred in fawns only a few days before death (Murphy
& Korschgen, 1970).

When blesbuck (Damaliscus dorcas phillipsi) were fed diets
containing 5, 15, 25, 35, or 50 mg dieldrin (nominal)/kg diet, none
of the animals fed 5 or 15 mg/kg diet died during the 90 days of
the study. However, all the animals given higher dose levels died
within 24 days. The concentration of dieldrin in the liver was 3.3
and 8.2 mg/kg for the two lowest dose levels, after 90 days. The
concentrations of dieldrin in the livers of the dead animals were
9.4, 15.1, and 18.4, respectively, for the three highest treatment
groups (Wiese et al., 1973).

In studies by Wiese et al. (1973), an experimental grazing site
(250 ha) with a resident population of 35 blesbuck and 20 springbok
(Antidorcas marsupialis) was aerially sprayed with dieldrin at a
rate corresponding to 0.16 kg/ha. The concentration of dieldrin on
the veld declined rapidly from 27.6 mg/kg immediately after
treatment to 5.04 mg/kg after 14 days. The decline during the
following 106 days was much slower (it was 0.75 mg/kg on the 85th
day and 0.23 on the 120th day). Behavioural changes were observed
in both antelope species after 3 days. From the 4th day, there
were further nervous symptoms, including clonic convulsive attacks,
and partial or even complete blindness was also noted. Blesbuck
died from the 4th day onwards, and the entire population of 35
animals had died by the 19th day. The median time to death was
7.08 days, and there was no significant difference between adults

(male or female) and juveniles. The calculated mean intake of
dieldrin was 1.82 mg/kg herbage per day. This estimate was much
lower than that derived from the feeding trial (the total intake of
animals that died was 9.08 mg/kg). The mean concentration in the
livers of six blesbuck that died was 8.3 mg/kg. It was inferred
that dieldrin was unlikely to be the cause of death of the blesbuck
(further investigations implicated photodieldrin). Springbok were
less adversely affected: deaths occurred from the 6th day, and 70%
had died by the 13th day. Surviving animals recovered with no
after-effects, and two ewes lambed normally in the spring following
the winter treatment. The average dieldrin concentration in the
livers of three springbok that died was 9.2 mg/kg. The
pathological findings were similar to those in the common
laboratory species.

Few other mammalian species have been investigated. Reduced
reproductive success and some mortality has been reported in
raccoons fed 2 mg dieldrin/kg diet (Stickel, 1975).

7.4. Effect on Populations and Ecosystems

In order to show that a chemical has had an effect on
populations of organisms in the environment it is necessary to
satisfy a combination of several criteria. Ideally the exposure to
the chemical in the field should be established to compare exposure
with effects produced. Population declines should correlate with
usage of the chemical and should be reversed by controls on the use
of the chemical. Although it is generally recognized that dieldrin
affected populations of some animals when its use was widespread,
there are some difficulties in establishing its precise effects on
the environment. These difficulties arise because the use of
dieldrin coincided with the use of other persistent
organochlorines, which themselves affect populations of organisms,
and also because poisoning by dieldrin was often secondary
(poisoned organisms did not take in dieldrin directly but from prey
that had concentrated the chemical from the environment).

7.4.1. Exposure to dieldrin

It is difficult to establish the exposure of wildlife to
dieldrin unless animals are directly feeding on dressed grain or
directly exposed to preserved wood. Even where this occurs, the
animal will frequently die some distance from the source of
exposure. This is particularly true for birds but less so for
small mammals. Since exposure cannot be readily monitored
directly, most investigators have estimated exposure from the
residue remaining in dead or dying animals. Monitoring programmes
in several countries sampled both dead and dying animals and
compared them with healthy animals taken from the wild. Eggs of
birds were also monitored as a measure of dieldrin contamination
of populations. These monitoring programmes had to establish
criteria by which it could be definitively stated that particular
individuals had died from dieldrin poisoning. The criteria were
based on residue levels in experimentally poisoned animals and were
set at 5 - 10 mg/kg brain tissue and 10 - 20 mg/kg liver tissue for

birds (Robinson, 1969; Stickel et al., 1969; Cooke et al., 1982).
These criteria are probably conservative; 20 - 30% of dead wood
pigeons examined in the UK during the period 1961 - 1964 were
judged, by these criteria, to have died from dieldrin poisoning.
During this period many seed-eating birds were killed directly by
eating dieldren-dressed grain (Robinson, 1969); the actual
percentage of death attributable to dieldrin should probably be
higher. A high proportion of dead birds from areas of tsetse fly
control contained residues which would be judged lethal by these
criteria. The great majority of birds sampled contained non-lethal
residues of dieldrin (Tables 15, 16, 17, 18, and 34). It should be
remembered that all of these sampled birds contained residues of
other organochlorines, in addition to dieldrin. Although there
have been reports of populations with no dieldrin contamination,
but contamination with other organochlorines, there have been no
reports of populations contaminated by dieldrin alone. Furthermore,
residues of dieldrin always correlate well with residues of other
organochlorines; birds retaining large quantities of dieldrin also
retain large quantities of DDE and often polychlorinated biphenyls
(PCB) (Newton, 1979).

The literature reporting the presence of dieldrin in birds and
mammals from the wild is very extensive and has been selectively
reviewed elsewhere (section 5.1.6). Analysis of a few dead animals
serves to indicate the presence of dieldrin in wildlife but is of
little use in establishing effects at the population level. Only
long-term monitoring programmes, measuring changes in dieldrin
residues in the population with time and correlating this to
ecological monitoring of the size and reproductive success of the
population, can approach an objective assessment of the effects of
dieldrin. Such programmes have been reviewed by Newton (1979).

7.4.2. Effects on populations of birds

Populations of birds of prey declined during the period of
large scale use of organochlorine insecticides. Major studies of
changes in bird populations concentrated on a few species mainly in
the United Kingdom and North America, though also to some extent in
areas of mainland Europe. The following references are
illustrative on this subject of the literature: general
references, Anon (1964), Prestt (1965), Prestt & Bell (1966),
Parslow (1973), Bijleveld (1974), Cooke et al., (1976, 1982),
Havera & Duzan (1986); peregrine falcon (Falco peregrinu),
Ratcliffe (1963, 1965, 1967b, 1970, 1972, 1980, 1984), Lockie &
Ratcliffe (1964), Cade et al. (1968), Enderson & Berger (1968),
Hickey (1969); heron (Ardea cinerea), Reynolds (1974); golden eagle
(Aquila chrysaetos), Brown (1969), Lockie et al. (1969); sparrow-
hawk (Accipiter nisus), Koeman et al. (1972), Newton (1973a,b,
1974, 1976, 1979), Newton & Bogan (1974, 1978); Newton et al.
(1979), Marchant (1980); kestrel (Falco finnunculus), O'Connor
(1982).

In most of these studies, population decline correlated with
organochlorines residues in adult birds and their eggs. Reduced
breeding success was associated with thinning of eggshells,

behavioural changes resulting in egg breakage, and aggressive
interaction between adults resulting in a reduction of the number
of young fledged successfully from the clutches. The death of
adult birds was reported at the same time as seed-eating species
were dying from dieldrin poisoning.

As reported earlier in this section, dieldrin cannot be held
responsible for the eggshell-thinning effect, which has been shown
to be attributable to DDE (Cooke, 1973). Embryo deaths in shell
correlate best with PCB residues in eggs (Newton, 1979). The
contribution of dieldrin to these declines is difficult to
determine because the birds were subjected to residues of all
organochlorines. It is probable that dieldrin contributed to
population declines in some areas but not others (Newton, 1979;
Newton & Haas, 1984).

The studies of Blus et al. (1974a,b, 1975, 1979a,b) and Blus
(1982) on the brown pelican (Pelicanus occidentalis) conclude that
the decline in numbers could be ascribed entirely to DDE. The
population size of birds of prey in some of the Eastern states of
the USA declined when no dieldrin residues were present, DDE alone
being a contaminant in these populations. Newton (1979) pointed
out that the decline in populations of birds of prey contaminated
by DDE is gradual, a result of progressive effects of failure in
breeding. The decline of populations of peregrine falcon and
sparrow-hawk in the United Kingdom was more sudden and was
associated with the death of breeding adults. This was attributed
to dieldrin usage, which correlated well with the decline (Newton,
1979; Newton & Haas, 1984).

7.4.3. Effects on populations of mammals

Some mammal species in addition to birds, have been affected by
the use of organochlorine pesticides. There are reports of
decreases in the number of badgers (Meles meles) in some areas of
the United Kingdom (Jefferies, 1969, 1975). Declines in the number
of bats have been reported in the United Kingdom and the
Netherlands (Jefferies, 1972); furthermore, the grey bat (Myotis
grisesceus) in the USA (Clark et al., 1978) and the otter (Lutra
lutra) have also been affected (Jefferies et al., 1974; Chanin &
Jefferies, 1978).

Declines in bat numbers have been associated with the use of
dieldrin and lindane in wood preservatives in the United Kingdom
(Jefferies, 1972). In the United States, they appear to be related
to a combination of organochlorines. Many species migrate long
distances, using fat reserves on the journey, and are susceptible
to DDE poisoning en route (Clark & Kroll, 1977). No contribution
of dieldrin to declines in bat numbers in the USA has been proven.
Other declines have been attributed to dieldrin (Chanin &
Jefferies, 1978). Jefferies & Pendlebury (1968) studied the effect
of aldrin/dieldrin seed dressings on the populations of stoats,
weasels, and hedgehogs in the United Kingdom. None of these
species showed a decline during the period 1959 to 1962, and there
was no evidence that aldrin/dieldrin had any detrimental effects.

Jefferies et al. (1973) studied the behaviour of small mammals
in and adjacent to a field sown with dieldrin-dressed wheat. The
field mouse Apodemus, which lives on the field margin and the open
field, immediately fed on dosed grain. Residues of dieldrin in
sampled mice was very high. The bank vole Clethrionomys, which
lives in field margins, did not take the dosed grain. Residues of
dieldrin in these small mammals were monitored regularly after
sowing. These very quickly dropped to very low levels. The
authors propose that those individuals eating dressed grain died
quickly or were taken by predators. Populations were quickly
replenished by immigration from surrounding areas.

8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS

8.1. Single Exposures

8.1.1. Aldrin and dieldrin

8.1.1.1 Oral

The acute oral LD₅₀values for technical aldrin and dieldrin in
various animal species are shown in Table 36. Intoxication with
cyclodiene insecticides consists of increased irritability and
tremor, followed later by tonic-clonic convulsions. In rats,
convulsions appear within 1 h following oral dosing at high
concentrations; death follows within 6 h, or from 2 - 7 days later.
This depends on factors such as the contents of the rat's
gastrointestinal tract, the concentration of aldrin/dieldrin in the
solvent, and the type of solvent used (Borgmann et al., 1952b;
Heath & Vandekar, 1964). Fox & Virgo (1986) reported that dieldrin
induced hyperglycemia.
Table 36. Acute oral LD₅₀values for technical aldrin and dieldrin
------------------------------------------------------------------------------------------
Species Vehicle LD₅₀ Reference
Aldrin Dieldrin
(mg/kg body weight)
------------------------------------------------------------------------------------------
Mouse corn oil 44 38 Borgmann et al. (1952a,b)

Mouse olive oil _~75 Jolly (1954)

Rat (newborn) arachis oil 168^a Lu et al. (1965)

Rat (pre-weaning) arachis oil 25 Lu et al. (1965)

Rat (adult) arachis oil 37 Lu et al. (1965)

Rat arachis oil 51-64 Heath & Vandekar (1964)

Rat various 38-67 Lehman (1951); Borgmann et al.
(1952a); Treon & Cleveland (1955);
Gaines (1960); Worthing & Walker
(1983)

Rat various 37-87 Lehman (1951); Borgmann et al.
(1952b); Treon & Cleveland (1955);
Gaines (1960); Lu et al. (1965);
Worthing & Walker (1983)

Hamster olive oil 320 330 Gak et al. (1976)

Hamster corn oil 100 Cabral et al. (1979a,b)

Guinea-pig corn oil 33 49 Borgmann et al. (1952a,b)
------------------------------------------------------------------------------------------

Table 36. (contd.)
------------------------------------------------------------------------------------------
Species Vehicle LD₅₀ Reference
Aldrin Dieldrin
(mg/kg body weight)
------------------------------------------------------------------------------------------
Guinea-pig olive oil between 10 Jolly (1954)
and 25

Rabbit corn oil 50-80 45-50 Borgmann et al. (1952a,b)

Dog corn oil 65