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

         The International Programme on Chemical Safety (IPCS) is a
    joint venture of the United Nations Environment Programme, the
    International Labour Organisation, and the World Health
    Organization. The main objective of the IPCS is to carry out and
    disseminate evaluations of the effects of chemicals on human health
    and the quality of the environment. Supporting activities include
    the development of epidemiological, experimental laboratory, and
    risk-assessment methods that could produce internationally
    comparable results, and the development of manpower in the field of
    toxicology. Other activities carried out by the IPCS include the
    development of know-how for coping with chemical accidents,
    coordination of laboratory testing and epidemiological studies, and
    promotion of research on the mechanisms of the biological action of
    chemicals.

    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 10-5 mmHg 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 LC50 values 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 LC50 values 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 
LC50 was 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: aldrina

Chemical formula:         C12H8Cl6

Relative molecular mass:  364.9

IUPAC chemical nameb:     (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)

-------------------------------------------------------------------
a From:  Worthing & Walker (1983).
b Other chemical names are given in Appendix I.

2.1.2.  Primary constituent: dieldrina

Chemical formula:         C12H8OCl6

Relative molecular mass:  380.9

IUPAC chemical nameb:     (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)

-------------------------------------------------------------------
a From:  Worthing & Walker (1983).
b Other 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 10-5 mmHg 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/cm3 as 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 10-4 Pa) 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 soila
------------------------------------------------------------------------------------------------------------------------------
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
------------------------------------------------------------------------------------------------------------------------------

Table 1.  (contd.)
------------------------------------------------------------------------------------------------------------------------------
Location       Year     Use                        Number    Mean concentration  Comments                      Reference
                                                   of        in mg/kg (maximum
                                                   sites     value in brackets)
                                                             aldrin    dieldrin
------------------------------------------------------------------------------------------------------------------------------
USA (contd.)

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)
------------------------------------------------------------------------------------------------------------------------------

Table 1.  (contd.)
------------------------------------------------------------------------------------------------------------------------------
Location       Year     Use                        Number    Mean concentration  Comments                      Reference
                                                   of        in mg/kg (maximum
                                                   sites     value in brackets)
                                                             aldrin    dieldrin
------------------------------------------------------------------------------------------------------------------------------
USA (contd.)

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)
------------------------------------------------------------------------------------------------------------------------------
a LD = 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 
10-5 cm/second compared to 15 x 10-5 cm/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 
10-2 cm/second (at 10 km/h) to 5.2 x 10-2 cm/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 10-3 at 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 (Kow) 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 
Kow).  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 weeksa
-------------------------------------------------------------------------------------
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
-------------------------------------------------------------------------------------
a From:  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 = aSb, 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. cyaneuma    0.84                2.4
--------------------------------------------
a One 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) = aEbn

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 dieldrina (mg/kg)     
(kg/ha) (nominal)   Soilb          A. longac    A. chloroticac
                   (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
---------------------------------------------------------------
a Geometric means.
b Soil samples taken 6 weeks before earthworm samples.
c Wet 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/m3 have 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/m3 and the maximum was 24.6 ng/m3 (Kutz et al., 1976). 

    Aldrin was found at a level of 0.9 ng/m3 in 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/m3 and 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/m3 and 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/m3 at day 28 and were < 0.05 µg/m3 at day 56, whereas those in 
crawl-space houses were 0.06 - 1.5 µg/m3 at day 7, 0.04 - 0.36 

µg/m3 at day 28, and 0.06 - 0.55 µg/m3 at day 56.  One year after 
application the air concentration of aldrin was 0.08 µg/m3 or 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/m2 and 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  Analyticala       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  Analyticala       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/m3 air    source of dust in air    Prospero &
              1970              borne   column            (1-190)         probably North Africa    Seba (1972)
                                dust    chromatography                                             
                                        followed by       
                                        GLC/EC
----------------------------------------------------------------------------------------------------------------

Table 6.  (contd.)
----------------------------------------------------------------------------------------------------------------
Location      Year     Number   Medium  Analyticala       Mean            Comments                 Reference
                       of               procedure         concentration
                       samples                            (range)
----------------------------------------------------------------------------------------------------------------
 Ireland

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)
----------------------------------------------------------------------------------------------------------------
a TLC = 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)
--------------------------------------------------------------------------------------------------------------------------

Table 7.  (contd.)
--------------------------------------------------------------------------------------------------------------------------
Location     Year     Type            Number       Mean concentration       Comments                        Reference
                      of              of           (ng/litre) (maximum)a
                      water           sites        aldrin     dieldrin
--------------------------------------------------------------------------------------------------------------------------
Great        1965-67  rivers          15           LD         292 (2840)    high residues of dieldrin       Croll (1969)
Britain                                                                     attributable to effluent from    
                                                                            moth-proofing plants using
                                                                            dieldrin

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

Table 7.  (contd.)
--------------------------------------------------------------------------------------------------------------------------
Location     Year     Type            Number       Mean concentration       Comments                        Reference
                      of              of           (ng/litre) (maximum)a
                      water           sites        aldrin     dieldrin
--------------------------------------------------------------------------------------------------------------------------
 Federal      1970-71  unfiltered      28 (119      LD         LD (45)       dieldrin reported in only one   Herzel (1972)
 Republic of           surface water   samples)                              sample of water                 
 Germany                                                          
                                                                 
                      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)
--------------------------------------------------------------------------------------------------------------------------

Table 7.  (contd.)
--------------------------------------------------------------------------------------------------------------------------
Location     Year     Type            Number       Mean concentration       Comments                        Reference
                      of              of           (ng/litre) (maximum)a
                      water           sites        aldrin     dieldrin
--------------------------------------------------------------------------------------------------------------------------
Hawaii                sewage          1            LD         198
(contd.)              discharge                                    
                                                                   
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)
--------------------------------------------------------------------------------------------------------------------------
a Concentrations 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
----------------------------------------------------------
a The 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         Rangea   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
---------------------------------------------
a ND = 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 
componentsa
---------------------------------------------------------
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
---------------------------------------------------------
a For 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      Rangec        Commentsc             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)
                                                                30/4a       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      Rangec        Commentsc             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)         
----------------------------------------------------------------------------------------------------------------------------------------

Table 15.  (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical        Species                   Type of           Number of   Mean      Rangec        Commentsc             Reference
area/Year                                     sample            samples     (mg/kg)   (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
 Kenya

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

                                              bottom sediment   10          < 0.001b  -
                                                    
                    Plankton                  composite         1           0.03b     -                                   Greichus et
                                                                                                                          al. (1978b)
                    Chironomids               composite         1           < 0.01b   -

                    Water boatmen             composite         1           < 0.01b   -
                     (Coroxidae)

                    Fish                      composite         100/10a     0.02b     -
                     (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                                      10/2a       0.012     0.007-0.016                         Koeman et al.
                     (Mytilus edulis)                            199/8a      0.013     0.007-0.023                         (1971)
----------------------------------------------------------------------------------------------------------------------------------------

Table 15.  (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical        Species                   Type of           Number of   Mean      Rangec        Commentsc             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        81/6a       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                                      50/1a       0.009     -                                   Koeman et al.
                     (Crangon vulgaris)                                                                                    (1971)

1969-1970           marine fish (5 species)                     37/5a       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               27/4a       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)
----------------------------------------------------------------------------------------------------------------------------------------

Table 15.  (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical        Species                   Type of           Number of   Mean      Rangec        Commentsc             Reference
area/Year                                     sample            samples     (mg/kg)   (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
 United Kingdom
              
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      Rangec        Commentsc             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      0.65-0.86b    concentration         Cooke et al.
                                              April             103         1.19      1.05-1.35b    increased             (1982)
                                              May               45          3.20      2.64-3.88b    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      Rangec        Commentsc             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                                                  741/141a,d  0.14      LD - 1.94
 streams                                                        157/36a,e   0.13      LD - 0.55
Gulf coast                                                      204/48a,d   0.12      LD - 1.26
 streams                                                        59/12a,e    0.28      LD - 1.59
Great Lakes                                                     378/63a,d   0.05      LD - 0.50
 drainage                                                       81/18a,e    0.06      LD - 0.37
Mississippi River                                               657/139a,d  0.06      LD - 0.52
 system                                                         153/34a,e   0.06      0.01-0.49
Hudson Bay                                                      51/13a,d    0.12      0.03-0.37
 drainage                                                       5/2a,e      0.01      0.01
Colorado River                                                  112/24a,d   0.02      LD - 0.10
 system                                                         24/6a,e     0.01      0.01
Interior basins                                                 120/25a,d   0.01      LD - 0.06
                                                                30/6a,e     0.02      LD - 0.03
----------------------------------------------------------------------------------------------------------------------------------------

Table 15.  (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical        Species                   Type of           Number of   Mean      Rangec        Commentsc             Reference
area/Year                                     sample            samples     (mg/kg)   (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
 USA (contd.)

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

Table 15.  (contd.)
----------------------------------------------------------------------------------------------------------------------------------------
Geographical        Species                   Type of           Number of   Mean      Rangec        Commentsc             Reference
area/Year                                     sample            samples     (mg/kg)   (mg/kg)
----------------------------------------------------------------------------------------------------------------------------------------
 USA (contd.)

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      Rangec        Commentsc             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           < 0.01b

                   Oligochaete                composite         1           0.08b
                    (Branchiura sowerbyi)
                            
                   Fish (3 spp.)              composite         200/15a     0.04b    0.03-0.07
                   
                   Cormorant (2 spp.)         brain             10          1.4b
----------------------------------------------------------------------------------------------------------------------------------------
a N1/N2: N1 is the number of individuals incorporated into N2 composites; the range corresponds to the composites.
b Concentration expressed on dry weight basis.
c LD = limit of detection, ND = not detectable.
d Samples taken in 1967-1968.
e Samples 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  -          0.00042a    <0.00035-     Rickard &
(muscle)        R. Thames                                      0.0020 (83)   Dulley (1983)
                (tidal)                                                     

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

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

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

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

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

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

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

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

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

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

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

Migratory       USA: Florida   1964-73  -          0.2a        <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     0.2a       -           <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  0.6b       -           <0.05-7.8     Cromartie et 
(brain)                                                        (37)          al. (1975)

Barn owl        Great Britain  1963-75  1.21b      -           <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)
------------------------------------------------------------------------------------------
a Indicates living organisms collected by capture, shooting, etc.
b Indicates organisms found dead or dying.
c Number 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)
                                                  mensa   Meanb  Range
---------------------------------------------------------------------------------------------------------
Woodpigeon        liver       Netherlands   1966  20      2.8b   0.05-27.1    seed dressing   Fuchs 
 (Columba                                          4       79c    44.2-136                     (1967)
 palumbus)                                     

Pink-footed       liver       United        1972  6       31c    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      28.2c  18-57        tsetse fly      Koeman &
spp.)                                             21      1.7b   0.16-6       control (dead   Pennings
                  brain                           10      14.3c  6-22         birds found     (1970)
                                                  11      0.2b   0.06-0.68    during 10 days 
                                                                              after spray 
                                                                              application; 
                                                                              live birds 
                                                                              collected 2 
                                                                              months later)

Insects (various  whole       Cameroon      1979  227     0.2c   NDe - 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      1.51b  ND - 7.24
spp.)         

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

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

Common gallinule  egg         USA:          1965  4/23d   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  2/16d   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/   1.1b   LDf - 3.2    aldrin-treated  Flickinger 
                  of whole    Gulf coast    -71   16      (3.1)  (LD - 16.3)  seed            & King 
                  body                                                                        (1972)

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

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

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

Turtles (2 spp.)  whole                           5/2     0.9b   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)
                                                  mensa   Meanb  Range
---------------------------------------------------------------------------------------------------------
Snakes (3 spp.)   whole       USA: Texas    1967  3/3     2.4b   0.1-5.7                      Flickinger 
                  body        Gulf coast    -71                                               & King 
                                                                                              (1972)

Great horned owl  brain                           1       6.3c   -

Birds (various    brain                           27      8.5c   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      24c    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
---------------------------------------------------------------------------------------------------------
a N1/N2: N1 is the number of incorporated into N2 composites; the range corresponds to the composites.
b Indicates living organisms collected by capture, shooting, etc.  Values in parentheses are the 
  concentrations of aldrin.
c Indicates organisms found dead or dying.  Values in parentheses are the concentrations of aldrin.
d Clutches/eggs.
e ND = not determined.
f LD = 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    Meana  Rangeb
-------------------------------------------------------------------------------------------
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    Meana  Rangeb
-------------------------------------------------------------------------------------------
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      0.08c  LD - 0.3    Wiemeyer et
 (Haliacetus                                                         (LD <0.05   al. (1972)       
 leucocephalus)                                                      mg/kg)

                             USA:                    11      0.83c  0.15-2.3
                             Alaska, 4      
                             other states
-------------------------------------------------------------------------------------------
a Geometric mean, except for footnote c which is arithmetic mean.
b Range of value within 1 standard error.
c Arithmetic 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. 

(c)   Sparrow-hawk (Accipiter nisus)

    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
                             samplesa    clean-upb  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         0.03f   -        Casarett et al. 
                                                                     (1968)
              1968           48 (N)      II         0.20    -        Warnick (1972)
              1969           15 (N)      II         0.15    -        Warnick (1972)
              1969           26 (B)      II         0.33f   0.80c    Burns (1974)
              1970           40 (N)      II         0.15    -        Warnick (1972)
              1970           68 (B)      II         0.29f   0.73c    Burns (1974)
              1970           202 (B)     II         0.2     1.0      Wyllie et al. (1972)
              1970           1412 (N/B)  II         0.18f   15.20    Kutz et al. (1979)
              1971           88 (B)      II         0.36f   0.78c    Burns (1974)
              1971           1615 (N/B)  II         0.22f   2.91     Kutz et al. (1979)
              1972           39 (B)      II         0.43f   1.00c    Burns (1974)
------------------------------------------------------------------------------------------

Table 19.  (contd.)
------------------------------------------------------------------------------------------
Country       Year           No. of      Method of     Dieldrin      Reference
                             samplesa    clean-upb  Mean    Maximum
                                                      (mg/kg fat)
------------------------------------------------------------------------------------------
 USA (contd.)              
        
              1972           1913 (N/B)  II         0.18f   2.91     Kutz et al. (1979)
              1973           1094 (N/B)  II         0.18f   5.64     Kutz et al. (1979)
              1974           898 (N/B)   II         0.15f   2.21     Kutz et al. (1979)
Louisiana     1980           8 (B)       II         0.15f   0.34     Holt et al. (1986)
              1984           10 (B)      II         0.10f   0.19     Holt et al. (1986)

 Central and South America

Mexico        1975           19 (N)      II         0.06f   0.24     Albert et al. (1980)
              1975           9 (B)       II         0.18f   0.49     Albert et al. (1980)
              1975           9 (N)       II         0.05f   0.12     Albert et al. (1980)
                                         
Argentina     -              47 (N)      IV         0.38    0.66c    Wassermann et al. 
                                                                     (1969)

Brazil        1969-70        17 (N/B)    III        0.02e   0.12     Wassermann et al. 
                                                                     (1972a)
              1969-70        69 (N/B)    III        0.12e   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         0.16f   0.53     Kraul & Karlog (1976)

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

Germany,      1967           15 (B)      I          0.18f   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         0.68f   1.55     Del Vecchio & Leoni
                                                                     (1967)
------------------------------------------------------------------------------------------

Table 19.  (contd.)
------------------------------------------------------------------------------------------
Country       Year           No. of      Method of     Dieldrin      Reference
                             samplesa    clean-upb  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         0.31f   -        Wit (1971)
              1966           11 (N)      II         0.20    0.50     De Vlieger et al. 
                                                                     (1968)
              1968-69        34 (N)      II         0.27f   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        0.030d  0.18     Wassermann et al. 
                                                                     (1972b)
              1969-70        51 (N)      III        0.064e  0.28     Wassermann et al. 
                                                                     (1972b)
------------------------------------------------------------------------------------------

Table 19.  (contd.)
------------------------------------------------------------------------------------------
Country       Year           No. of      Method of     Dieldrin      Reference
                             samplesa    clean-upb  Mean    Maximum
                                                      (mg/kg fat)
------------------------------------------------------------------------------------------
 Africa (contd.)

Nigeria       1969           46 (N)      III        0.059d  0.73     Wassermann et al. 
                                                                     (1972c)
              1969           90 (N)      III        0.13e   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        0.023d  0.058    Wassermann et al. 
                                                                     (1974a)
              1969-70        39 (N)      III        0.031e  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        0.10d   0.315    Wassermann et al. 
                                                                     (1974b)
              1967-69        162 (N)     III        0.14e   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         0.09f   0.51     Yoshimura et al. 
                                                                     (1979)

Thailand      1969-70        8 (N)       III        0.077d  0.459    Wassermann et al. 
                                                                     (1972d)
              1969-70        27 (N)      III        0.10e   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)
------------------------------------------------------------------------------------------

Table 19.  (contd.)
------------------------------------------------------------------------------------------
Country       Year           No. of      Method of     Dieldrin      Reference
                             samplesa    clean-upb  Mean    Maximum
                                                      (mg/kg fat)
------------------------------------------------------------------------------------------
 Oceania (contd.)
                                                                                          
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
------------------------------------------------------------------------------------------
a Samples taken at necropsy (N) or during elective surgery (B).
b Method 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.

c Upper confidence limit ( P = 0.025) for the set of samples.
d Age group 5-24 years.
e Age group 25 years and older.
f Results expressed in terms of extractable lipid content.
g Personal 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
                               samplesa   methodb     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)   ?           ~1.4c  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)     Iust        2.3    13       Siyali (1972)
                -              47 (B)     Iust        none   -        Siyali (1973)
------------------------------------------------------------------------------------------
a Samples of whole blood (B), serum (S), whole blood from heart chamber (during autopsy) 
  (H).
b Analytical methods (all use gas-liquid chromatography with an electron-capture detector):
   I Hexane extraction.
   Iust Hexane extraction combined with ultrasonic treatment.
   II  Acetone extract on silica gel column.
   III Solvent extraction and Florisil column clean-up.
c In 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       0.25a   3.0a     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       0.29a   -        Kraul & Karlog  (1976)

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

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

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

Kidneys  Canada       1967-68  47       0.10a   1.35a    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       0.002a  -        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       0.057a  -        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       0.06a   0.86a    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)
------------------------------------------------------------------------------------------
a Results expressed in terms of extractable lipid content.
b Personal 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      3a       0.24   0.35     Curley et al.
                   stillborn             4        NDb            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
---------------------------------------------------------------------------------------------------------
a Stillborn.
b ND = 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       0.09g   0.25g     Holdrinet et al.
(Ontario)    1971-72  34       0.04g   0.17g     (1977)
             1973-74  24       0.04g   0.08g
             1978-79  154      1a      26b       Dillon et al.
                                                 (1981)
             1982     ~128c    ~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       42b       Barnett et al.
                                                 (1979)
             1972-75  1436     ~5      15        Savage et al. 
                                                 (1981) 

Hawaii       1979-80  54       0.04g   0.09g     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       0.04g   0.47g     Anderson & Orbaek
                                                 (1984)

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

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

Table 23.  (contd.)
-------------------------------------------------------------------
Country      Year     No. of      Dieldrin       Reference
                      samples  Mean    Maximum
                                 (µg/litre)
-------------------------------------------------------------------
 Europe (contd.)

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

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  267c     ~8.5    31        Stacey et al.
                                                 (1985)
             1981     74e      13      35        Stacey & Tatum
                                                 (1985)

New Guinea   1972     74       0.7     13.2      Hornabrook et al.
                                                 (1972)
-------------------------------------------------------------------
a The 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.
b In an area of high pesticide use.
c 128 samples from 16 women.
d Number of samples included 745, 805, and 973, respectively.
e 74 samples from 14 women.
f Many of the houses had been treated against termites, but the 
  pesticides used were unknown.
g On 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/m3 and some weeks later to 15.5 µg/m3 air 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 F1 generation, with some further 
(but not statistically significant) increase in concentration and 

total retention of dieldrin in the F2 and F3 generation.  The 
dieldrin concentration in the total lipids of mouse carcasses were: 
for the F0 generation, 60 mg/kg; for the males in the F1, F2, and 
F3 generations, a mean of 100 mg/kg; and for the females in the F1, 
F2, and F3 generations, a mean of 132 mg/kg.  The dieldrin 
concentration was below 1 mg/kg in pups from the F4 generation, 
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 F5 and F6 generations 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. 

    (c)   Rat and rabbit in vitro

    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). 

    (c)   Rabbit

    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 LC50 values 
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 LC50 values 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 LC50 for 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 LC50 in sea
water was > 170 µg/litre (in surficial water > 20 µg/litre; in 
sediment > 13 mg/kg). 

    Table 26 gives the LC50 values 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        330a         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)
---------------------------------------------------------------------------------------------------------

Table 25.  (contd.)
---------------------------------------------------------------------------------------------------------
Species          Developmental  Vehicle        Temperature  96-h LC50 (static test)   Reference
                 stage, body                   (°C)         -----------------------
                 weight, or                                 Aldrin       Dieldrin
                 length                                          (µg/litre)
---------------------------------------------------------------------------------------------------------
Insects (contd.)

 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)
---------------------------------------------------------------------------------------------------------
a Values in parentheses are the 48-h LC50.
Table 26. Short-term LC50s of dieldrin in invertebrates
-------------------------------------------------------------------
Species          Stage       LC50 at 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). 

    (c)   Behaviour

    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 exposurea 
(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    250b        -
Oyster                     -           500c
--------------------------------------------------
a Expressed as a percentage of growth of control 
  larvae.
b 80% reduction.
c 50% 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 LC50 values 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 LC50 and body weight was 
derived for mature, juvenile, and new-born guppies: 

    LC50 = aWb

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            -       6a         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           4b      -          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)

                  NAd        NA           20           20b     -          Rehwoldt et al. 
                                                                          (1977)

                  NA         NA           24           -       3.2-7      Adema & Vink 
                  (young)                                                 (1981)

                  NA         NA           24           -       35c        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)
------------------------------------------------------------------------------------------

Table 28.  (contd.)
------------------------------------------------------------------------------------------
Species           Weight     Vehicle      Temperature  96-h LC50          Reference
                  (g)                     (°C)         (static test)                       
                                                       ----------------
                                                       Aldrin  Dieldrin       
                                                       (µg/litre)           
------------------------------------------------------------------------------------------
Bluegill          0.6-1.5    dispersed    12.7         7.7     17         Macek et al. 
(contd.)                     via acetone  18.3         5.8     14         (1969)
                                          23.8         4.6     8.8

Pumpkinseed       NA         NA           20           20b     -          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           10b     -          Rehwoldt et al. 
 (Marone                                                                   (1977)
 saxatilis) 

Banded killyfish  NA         NA           20           21b     -          Rehwoldt et al. 
 (Fundulus                                                                 (1977)
 diaphanus) 

White perch       NA         NA           20           42b     -          Rehwoldt et al. 
 (Roccus                                                                   (1977)
 americanus) 

American eel      NA         NA           20           16b     -          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)
------------------------------------------------------------------------------------------

Table 28.  (contd.)
------------------------------------------------------------------------------------------
Species           Weight     Vehicle      Temperature  96-h LC50          Reference
                  (g)                     (°C)         (static test)                       
                                                       ----------------
                                                       Aldrin  Dieldrin       
                                                       (µg/litre)           
------------------------------------------------------------------------------------------
Marine species (contd.)               

Threespine        0.4-0.8    dispersed    20           27.4    13.1       Katz (1961)
stickleback                  via acetone
 (Gasterosteus  
 aculeatus)     
------------------------------------------------------------------------------------------
a Hardness = 162 mg CaCO3/litre.
b Hardness = 50 mg CaCO3/litre.
c 48-h LC50.
d NA = 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 
LC50 of 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 LC50 values 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 10-5 mol/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 10-6 mol/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 LC50 value (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 LD50 values 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 LC50 values 
were 0.15 - 0.8 µg/bee for aldrin and 0.15 - 0.41 µg/bee for 
dieldrin. 

    Cowie (1967) reported an oral LD50 of 0.3 µg dieldrin/bee 
(range, 0.13 - 0.54) and a contact LD50 of 0.21 µg/bee. 

    The toxicity of dieldrin to two important predators of cotton 
pests was investigated by Burke (1959).  The contact LD50 value 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 LD50 values 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 
speciesa
-------------------------------------------------------------------
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)
-------------------------------------------------------------------
a Details 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 LC50 values 
of aldrin and dieldrin for each of the four species tested were of 
the same order.  The annual variations in the LC50 of 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 LC50 values 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 LC50 and 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 speciesa                                
-----------------------------------------------------------
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)
-----------------------------------------------------------
a Aldrin 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     -              -         NCg    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     NCa    Inc.c    NC         Atkins &
 (Phasianus       weekb                     (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.
                 weekd                                                                               (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   1.11/1.17e     NC        Inc.a  NC     NC       NC         Wiese et al.
fowl  (Numida                                                                                          (1969)
 meleagris)       1.5           21 months   2.38/3.35e     NC        Inc.a  NC     NC       NC
                 5             21 months   7.18/13.56e    PR        Inc.a  NC     NC       NC
                 15            21 months   15.79e         Red.      Inc.a  NC     NC       Red.
--------------------------------------------------------------------------------------------------------------------

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          
                                                                                                                   
--------------------------------------------------------------------------------------------------------------------
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)
--------------------------------------------------------------------------------------------------------------------
a Significant at a probability of < 0.01.
b Doses of 2, 4, or 6 mg dieldrin/hen were administered once per week in capsules.
c Significant at a probability of < 0.05.
d Second-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.
e Residues in eggs of successive years.
f First and second laying periods, respectively.
g The 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     -3.4a                       Lehner & Egbert (1969)
 (Anas platyrhynchos)   
                       4                    16 months     -2a                         Lehner & Egbert (1969)

                       10                   16 months     -4.3a                       Lehner & Egbert (1969)

                       4                    90 days       -4.2                        Muller & Lockman (1972)

Japanese quail         3.1                  21 days with  -8a                         Call & Harrell (1974)
 (Coturnix coturnix                          changes in
 japonica)              50                   photoperiod   -8a                         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/weekb       -             0                           Dahlgren & Linder (1970)
 (Phasianus colchicus)
                       10 mg/hen/weekb      -             0                           Dahlgren & Linder (1970)
                       (6) 0 mg/hen/weekc   -             +4.1                        Dahlgren & Linder (1970)
                       (6) 6 mg/hen/weekc   -             +4.1                        Dahlgren & Linder (1970)
                       (10) 0 mg/hen/weekc  -             +4.1                        Dahlgren & Linder (1970)
--------------------------------------------------------------------------------------------------------------
a Significant at or below 0.05.
b Administered in capsules once per week (see footnoteb Table 32).
c See footnoted 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 LD50 and subacute oral LC50 in 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 LD50 seemed to be within the range 20 - 40 mg/kg body 
weight. 

Table 35.  Acute and subacute toxicity of dieldrin for volesa
------------------------------------------------------------------------
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
------------------------------------------------------------------------
a From: 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 LD50 values 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 LD50 values 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            168a         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       65-95   65-80        Borgmann et al. (1952a,b)
------------------------------------------------------------------------------------------
a Transcutaneous intragastric injection.
    The minimum toxic and the maximum non-toxic doses of aldrin and 
dieldrin, administered orally to livestock, are indicated in Table 
37. 
Table 37.  Acute oral toxicity of aldrin and dieldrin for livestock
-------------------------------------------------------------------
Compound  Species  Age          Maximum    Minimum    Reference
                                non-toxic  toxic
                                dose       dose
                                tested     found
                                -------------------
                                (mg/kg body weight)
-------------------------------------------------------------------
Aldrin    calf     1-2 weeks    2.5        5          Radeleff et 
                                                      al. (1955)

          cattle   1 year       10         25         Radeleff et 
                                                      al. (1955)

          sheep    1-2 years    10         15         Radeleff et  
                                                      al. (1955)

Dieldrin  calf     1-2 weeks    5          10         Radeleff et 
                                                      al. (1960)

          cattle   1 year       10         25         Radeleff et 
                                                      al. (1955)

          horse    -            -          25         Radeleff et 
                                                      al. (1960)

          pig      3 weeks      25         50         Radeleff et 
                                                      al. (1960)

          sheep    1 year       15         25         Radeleff et 
                                                      al. (1960)

          sheep    9-12 months  -          LD50       Jolly (1954)
                                           50-75
-------------------------------------------------------------------
8.1.1.2  Dermal

    The minimum lethal dose of aldrin or dieldrin when applied as a 
dry powder on the intact skin of female rabbits for 24 h was 
between 600 and 1250 mg aldrin/kg body weight and between 250 and 
360 mg dieldrin/kg body weight.  In olive oil, the range for aldrin 
was the same as for dry powder, and the range for dieldrin was 
between 360 and 600 mg/kg body weight (Treon et al., 1953). 

    The acute dermal LD50 values for technical aldrin and dieldrin 
in various animal species are shown in Table 38.  The signs of 
intoxication are similar to those that follow oral administration. 

Table 38.  Dermal LD50 values for technical aldrin and dieldrin
---------------------------------------------------------------
Species     Vehicle    LD50                 Reference
                       Aldrin  Dieldrin
                       (mg/kg body weight)
---------------------------------------------------------------
Mouse       solvent    -       40-80a       Jolly (1954)
            naphtha

Rat         xylene     ~100    60-90        Gaines (1960)

Guinea-pig  solvent    -       120a         Jolly (1954)
            naphtha

Rabbit      dimethyl-  150     150          Lehman (1952)
            phthalate
---------------------------------------------------------------
a With complete immersion of body.

8.1.1.3  Inhalation

    The vapour pressures of technical aldrin and dieldrin are 
sufficiently low that an acute inhalation hazard from aldrin or 
dieldrin vapour does not normally arise. 

8.1.1.4  Parenteral

    The acute LD50 values for technical dieldrin (in glycerol 
formal) in the rat via intraperitoneal and intravenous routes are 
56 and 8 - 9 mg/kg body weight, respectively (Heath & Vandekar, 
1964). 

8.1.2.  Formulated materials

8.1.2.1  Oral and dermal

    The acute toxicity of formulated products, particularly the 
dermal toxicity, is a more realistic guide than that of the 
technical product to the acute hazard to the user.  The percentage 
of aldrin or dieldrin in the formulation, the solvent used, and the 
type of formulation (such as an emulsion, wettable powder, dust, 
etc.) will determine the acute toxicity of the formulated product. 

Depending on these factors, the oral and dermal LD50s vary from 100 
to 4500 and 500 to 16 000 mg total aldrin formulation/kg body 
weight, respectively.  For dieldrin formulations, these figures are 
100 - 400 mg/kg and 200 - 2700 mg formulation/kg body weight, 
respectively (Muir, 1970; Rose, 1982, 1984a,b). 

    For a dieldrin formulation for termite control (680 g/litre 
suspension concentrate), the dermal LD50 in the male rat was 645 mg 
formulation/kg body weight and in the female rat 284 mg 
formulation/kg body weight (Rose, 1984c). 

8.1.2.2  Inhalation

    The acute inhalation LC50 (4-h exposure) in rats for aqueous 
dilutions of a 48% (w/v) emulsifiable concentrate of aldrin (high 
aromatic solvent) in the form of a spray was estimated to be 
equivalent to 3% (w/v) aldrin.  The median droplet size was 52 µm, 
and the animals were exposed "nose only".  Deaths occurred up to 6 
days after exposure, but most of the animals died on the 2nd day 
after exposure.  Signs of intoxication consisted of a subdued 
and hunched appearance with piloerection, progressing to 
hypersensitivity and convulsions in the more seriously affected 
animals.  Surviving animals recovered within 2 - 3 days after 
exposure.  Oral intake (due to grooming) contributed significantly 
to the results (MacDonald, 1982). 

8.2.  Short-Term Exposures

    Short-term studies on rodents have shown that aldrin and 
dieldrin affect the liver.  The liver/body weight ratio is 
increased, and histopathological changes that have become known as 
"Chlorinated Hydrocarbon Insecticide Rodent Liver" (CHIRL) are 
observed.  Microscopically, these CHIRLs consist of enlarged 
centrilobular hepatocytes with somewhat increased cytoplasmic 
oxyphilia and peripheral migration of the basophilic granules 
(Treon & Cleveland, 1955; Ortega et al., 1957). 

    The cellular and subcellular changes in the liver of different 
mammalian species have been studied by Wright et al. (1972, 1977, 
1978).  These studies have shown that dieldrin produces a 
generalized enlargement of the liver, which, in rats and dogs, is 
associated with increased size of liver parenchymal cells but, in 
mice, is associated with an increase in both cell size and cell 
number.  The earliest ultrastructural change in the livers of mice, 
rats, and dogs treated with dieldrin was the proliferation of the 
smooth endoplasmic reticulum (SER).  During the initial phase of 
the exposure to dieldrin, and also to phenobarbital, the increases 
in the SER in the liver cells of mice, rats, and dogs were of the 
vesicular type.  These changes were associated with an enhanced 
microsomal mixed-function oxidase, and intracellular whorls of 
smooth membranes appeared in the liver cells of rats and dogs but 
not in those of the mouse.  The changes in liver subcellular 
structure and function were reversible in mouse, rat, and dog.  In 
contrast, no liver enlargement or other ultrastructural changes 
were observed in the livers of rhesus monkeys.   In vitro 

determinations showed that the activity of the liver microsomal 
monooxygenase system was increased after treatment, and this was 
the most sensitive effect observed.  In all species examined, the 
biochemical and subcellular structural response of the liver to 
dieldrin was shown to be similar to that found with a number of 
other chemicals, such as DDT, heptachlor, and phenobarbital 
(Jansen, 1979).  These chemicals also induce in the mouse a type of 
liver tumour identical to that found with dieldrin (Stevenson & 
Walker, 1969; Thorpe & Walker, 1973). 

8.2.1.  Oral

8.2.1.1  Rat

    A number of short-term feeding studies (3 - 9 months duration) 
were carried out on rats with aldrin.  Dose levels of 0.5 - 300 mg 
aldrin/kg diet were tested.  The results of these old studies 
showed that dose levels up to 5 mg/kg diet produced no effects, but 
that levels of 25 mg/kg or more gave an increased liver/body weight 
ratio and reversible hypertrophy of centrilobular hepatocytes with 
cytoplastic changes (CHIRL) (section 8.4.2).  Dose levels of 150 
mg/kg or more resulted in increased mortality (Treon et al., 1951; 
Borgmann et al., 1952a). 

    Five further studies were carried out with dieldrin (3 - 10 
months duration), using dose levels of 1 - 300 mg/kg diet.  No 
effects were seen up to 5 mg/kg, except that Walton et al. (1971) 
found an increased liver/body weight ratio in females at 5 mg/kg 
and Ortega et al. (1957) found occasional liver changes at 2.5 
mg/kg diet.  These changes, e.g., liver enlargement and induction 
of CHIRL, were found in the other studies at 10 mg/kg diet or more. 
At 150 mg/kg or more, there was increased mortality (Treon et al., 
1951; Borgmann et al., 1952b; Ortega et al., 1957; Walton et al., 
1971). 

    When groups of male albino rats were fed diets equivalent to 
2 mg/kg body weight for 6 months, the alkaline phosphatase, SGPT, 
SGOT, and LD-hydrogenase activities in the serum were increased 
after 6 months.  The urea content decreased after 3 months, and 
some other parameters were also changed.  The growth of the animals 
was considerably inhibited (Shakoori et al., 1986). 

8.2.1.2  Dog

    Dogs appear to be more susceptible to aldrin and dieldrin than 
rats.  Dogs administered aldrin in the diet for 5 or 6 days at dose 
levels equivalent to 0.9 - 9.1 mg/kg body weight died within 7 
months.  However, beagle dogs (two males and two females) survived 
15.6 months when given 0.043 - 0.25 mg aldrin/kg body weight.  With 
dieldrin, dogs survived dose levels up to 0.23 mg/kg body weight 
for 15.7 months.  In aldrin- and dieldrin-treated animals, no 
effects on growth and no changes in haematology were seen.  The 
dogs with 0.25 mg aldrin/kg showed hepatomegaly, and the females 
had local hyaline (droplet) degeneration of hepatocytes and 
vacuolization in the epithelia of distal renal tubules.  One of the 

males of this group showed hepatocyte degeneration, while the other 
exhibited the renal tubular changes seen in the females.  In the 
group fed 0.09 mg/kg, no effects were seen in the males, while the 
females (and also one female in the group fed 0.23 mg/kg) showed 
vacuolization in the epithelia of the distal renal tubules.  The 
liver weights of the dieldrin-treated animals were increased.  No 
other dogs showed gross or microscopic abnormalities in the viscera 
(Treon & Cleveland, 1955). 

    Four beagle dogs fed dieldrin at daily oral doses of 0.4 - 0.8 
mg/kg body weight showed blood concentrations of 0.27 - 1.27 
mg/litre blood after eight episodes of convulsions (Brown et al., 
1964).  When two dogs were given 0.2 mg dieldrin/kg body weight, in 
gelatin capsules daily for 8 months, no signs of intoxication were 
observed.  The concentration in the blood was 0.11 - 0.22 mg/litre. 

    In studies by Fitzhugh et al. (1964), twelve mongrel dogs of 
various ages received aldrin, 6 days/week for periods up to 25 
months, at doses of 0.2, 0.5, 1, 2, or 5 mg/kg body weight. 
Dieldrin was tested in 14 mongrel dogs at doses of 0.2, 0.5, 1, 2, 
5, or 10 mg/kg body weight.  In both cases, there were two animals 
per dose level (one male, one female), with the exception of four 
animals in the groups given 0.5 mg/kg.  In the animals tested with 
aldrin, the 5 mg/kg dogs and one 2 mg/kg dog died in 3 - 4 weeks; 
the remaining male dog in the 2 mg/kg group was killed at 25 weeks 
because of poor condition.  All four dogs showed weight loss and 
fatty changes in the liver and renal tubules.  The bone marrow 
showed a reduced number of mature granulocytes and erythroid cells. 
At 1 mg/kg, the two dogs survived for 15 and 49 weeks and, at 
autopsy, showed the same lesions.  In the 0.5 mg/kg group, one dog 
died after 4 days.  The remaining three dogs survived for 2 years, 
one male among these having convulsions during the last 2 months. 
At 0.2 mg/kg body weight, there were no effects.  In the animals 
tested with dieldrin, all six dogs on 2, 5, and 10 mg/kg died 
during weeks 2 - 5.  These dogs showed weight loss, fatty changes 
and slight hepatic cell atrophy in the liver, and a small amount of 
atypically distributed fat in the kidneys.  The bone marrow showed 
a reduced number of mature granulocytes and erythroid cells.  The 
reported bone marrow findings, which were not replicated in other 
studies, cannot be interpreted, because of the inadequacy of 
clinical details, and no control dogs were used in this study.  The 
two dogs given 1 mg/kg survived for 12 and 43 weeks and, at 
autopsy, showed the same lesions.  One dog given 0.5 mg/kg was 
sacrificed after 2 weeks because of anorexia and marked emaciation. 
Detailed histological examination, including that of the brain, did 
not show any distinct organ damage.  The remaining three dogs in 
the 0.5 mg/kg group died with terminal convulsions or were 
sacrificed in poor condition at weeks 29, 43, and 81.  Two of the 
dogs showed weight loss.  No effects were observed in the 0.2 mg/kg 
group. 

    Repeated daily oral administration of 0.2, 1, or 2 mg 
dieldrin/kg body weight to groups of six mongrel dogs was carried 
out until intoxication occurred between the 18th and 85th day.  A 
direct relationship was established between the dieldrin 

concentration in the blood and the severity of clinical signs of 
intoxication.  On the first day of muscle spasms, the average 
concentration of dieldrin in the blood was about 0.50 mg/litre and, 
at the time of the first full-blown convulsion, about 0.90 mg/litre 
(Keane & Zavon, 1969a). 

    In studies by Walker et al. (1969b), groups of five beagle dogs 
of each sex received, by capsule, daily doses of 0.005 or 0.05 mg 
dieldrin (in olive oil)/kg body weight, for 2 years.  Control dogs 
were given capsules containing olive oil.  The health, behaviour, 
and body weight were unaffected, and EEG recordings did not differ 
between the dogs fed 0.05 mg/kg and the controls.  In females given 
0.05 mg/kg, liver/body weight ratio was increased.  In both sexes, 
serum alkaline phosphatase activity was increased.  However, urine, 
haematology, clinical chemistry, bromosulfthalein clearance, and 
relative organ weight data were not affected.  No gross or 
histopathological anomalies were observed. 

    Deichmann et al. (1969) gave groups of six beagle dogs (aged 
1.5 - 3.5 years) 0 or 0.6 mg aldrin/kg body weight, 5 days/week for 
10 months, and then observed them for an additional 12 months.  The 
treated dogs showed hyperexcitability, tremors, and weight loss. 
One dog died.  After 14 - 18 months, the dogs with aldrin showed 
cloudy swelling and fatty degeneration in the liver and hypertrophy 
of hepatocytes.  Renal vascular congestion and tubular degeneration 
were seen in some of the animals. 

8.2.1.3  Domestic animals

    A dairy cow given aldrin in soybean oil daily by capsule (2.2 
mg/kg body weight) exhibited hyperirritability after 27 days.  The 
animal was in heat and was bred the next day.  She died on day 29 
with convulsions.  Autopsy showed a slightly discoloured, pulpy, 
congestive liver and one slightly enlarged congested kidney.  No 
mortality occurred among cows given 0.8, 1, or 1.5 mg/kg body 
weight for 48 days (Ely et al., 1954). 

    In studies by Gannon et al. (1959b), groups of four dairy cows 
were fed rations containing 0, 0.1, 0.25, 0.75, or 2.25 mg 
dieldrin/kg for 12 weeks (average total intake, 0, 0.293, 0.75, 
2.17, or 6.55 mg dieldrin/kg body weight).  No signs of illness and 
no abnormalities were found when the cows were slaughtered at the 
end of the test feeding period or after an additional 6-week period 
on dieldrin-free rations. 

    Ivey et al. (1961) fed groups of 2 - 3 steers, sheep, and hogs 
rations containing 0, 0.25, 0.75, or 10 mg aldrin/kg diet for 12 
weeks.  Two steers received rations with 2 mg/kg diet for the same 
period.  The control groups consisted of two animals each.  No 
evidence of illness and no postmortem pathology were found. 

    Goats administered 50 mg aldrin/kg body weight showed mild 
degenerative changes, congestion and petechial haemorrhages, in 
various organs.  In the kidneys degenerative changes of the 
proximal convoluted tubules were found.  Clinical changes were also 
found, e.g., salivation and convulsions (Singh et al., 1985). 

8.2.2.  Dermal

    In studies by Treon et al. (1953), aldrin and dieldrin, as dry 
powders or in solutions, were applied daily to the skin of groups 
of three female rabbits for 2 h on each of 5 days per week over a 
period of 10 weeks.  A series of graded doses was used to determine 
the doses resulting in no mortality.  It was clear that aldrin 
or dieldrin dissolved in kerosene was very toxic (LD50 of 
approximately 5 mg/kg body weight).  Dissolved in vegetable oil 
they were about 6 times less toxic and as dry powder about 20 times 
less toxic than when dissolved in kerosene. 

8.2.3.  Inhalation

    Mice, hamsters, and guinea-pigs did not show any adverse 
effects when exposed to vapourized aldrin at a concentration of 18 
mg/m3 for 178 days (Baker et al., 1959). 

8.3.  Skin and Eye Irritation; Sensitization

8.3.1.  Skin and eye irritation

    Treon et al. (1953) reported that technical aldrin or dieldrin 
applied on the intact rabbit skin for 24 h occasionally caused 
slight erythema.  Repeated application of aldrin or dieldrin for 10 
weeks (2 h per day, 5 days per week) as a dry powder did not alter 
the gross condition of the rabbit skin.  Slight irritation and 
scaliness were observed when the compounds were applied in 
vegetable oil, but their application in kerosene resulted in 
damage, attributable to the solvent. 

    An undiluted aldrin emulsifiable concentrate formulation (48% 
aldrin in high aromatic hydrocarbon solvent), applied at a dose of 
0.5 ml at each test site for 24 h on the intact skin and abraded 
skin of rabbits under an occlusive patch, caused severe irritation 
and necrosis of the skin.  One male died on day 13. When applied to 
the rabbit eye, this undiluted 48% emulsifiable concentrate caused 
severe initial pain and mild irritation (Rose, 1982). 

8.3.2.  Sensitization

    In the Magnusson and Kligman guinea-pig maximization test, 48% 
aldrin emulsifiable concentrate caused positive responses (at 24 h 
and 48 h after removal of the challenge patches) in 3 out of the 20 
test animals.  Rechallenge of these animals, one week later, 
confirmed that they had been sensitized to the test material (Rose, 
1982). 

    Aldrin emulsifiable concentrate (48%) is not a skin sensitizer 
under the EEC Dangerous Substances Directives (EEC, 1983). 

    No cases of skin sensitization occurred over a period of 20 
years among a group of over 1000 workers involved in the 
manufacture and formulation of aldrin and dieldrin (Jager, 1970). 

8.4.  Long-Term Toxicity and Carcinogenicity

8.4.1.  Mouse

    Davis & Fitzhugh (1962) fed groups of 100 male and 100 female 
C3HeB/Fe mice a diet containing aldrin or dieldrin at 0 or 10 mg/kg 
diet for 2 years.  The average lifespan of the treated mice was 
shortened by 2 months.  A significant increase in the incidence of 
benign liver tumours was observed. 

    In a further study, 100 male and 100 female C3HeB/Fe/J mice 
received aldrin or dieldrin at 0 or 10 mg/kg diet for 2 years.  An 
increase in the number of animals with hepatic hyperplasia and 
benign liver tumours was seen in the treated groups, but no 
increase in malignant liver tumours was found.  The survival in the 
treated groups was lower than that of controls (Davis et al., 1965). 

    Groups of 300, 125, 125, and 200 CF1 mice of each sex were fed 
diets containing dieldrin (> 99%) at 0, 0.1, 1, or 10 mg/kg, 
respectively, for 2 years.  A positive control group fed 600 mg 
4-amino-2,3-dimethylazobenzene for 6 months, followed by a control 
diet, was used.  After 9 months, the morbidity of the mice fed 10 
mg/kg started to increase, but the lifespan of the mice fed 0.1 or 
1 mg/kg was unaffected.  The animals with 4-amino-2,3-
dimethylazobenzene died within 14 months.  The frequency of liver 
tumours was increased in all groups fed dieldrin.  Two types of 
tumours were observed, one of which was considered benign 
(hyperplastic nodules) and the other malignant.  The malignant 
tumours were clearly hepatocarcinomas, though no fibrosis or bile 
duct proliferation, as seen in the positive control group, occurred 
in the dieldrin-treated groups.  A reversibility study in a 
separate group fed 10 mg dieldrin/kg in the diet for up to 15 
months, followed by a control diet for the rest of the 2-year 
study, showed that the tumours did not regress or disappear upon 
discontinuation of the treatment.  However, the dieldrin induced 
hepatomegaly, and cytoplasmic changes were found to be reversible 
(Walker et al., 1972; Hunt et al., 1975). 

    In a study by Thorpe & Walker (1973), a group of 30 CF1 mice of 
each sex were fed a diet containing 10 mg dieldrin/kg for 2 years. 
The control group consisted of 45 mice of each sex.  Liver 
enlargement was detected after 50 weeks in both sexes, and liver 
lesions were observed, classified as hyperplastic nodules (Type a) 
and hepatocellular carcinoma (Type b) (sometimes associated with 
lung metastases).  In a separate study, it was shown that dieldrin 
Type b liver cell tumours were capable of growing as subcutaneous 
transplants in mice of the same strain and sex (Thorpe, 1973). 

    To compare the pathological responses to dieldrin in different 
mouse strains, groups of 30 mice of each sex of the CF1, LACG, and 
hybrid CF1-LACG strains were fed diets containing 10 mg dieldrin/kg 
for 2 years.  There was also a control group of 45 animals of each 
sex for each strain.  The incidence of liver tumours, particularly 
Type b tumours, in male CF1 and hybrid mice and in females of all 

three strains was higher than in controls.  In male LACG mice, the 
incidence of liver tumours was low.  Qualitatively, there was no 
difference in tumours between strains, and there was no increased 
incidence of neoplasms in other tissues, nor were unusual tumours 
found.  Metastases of liver carcinoma were found in the lungs in 
some of the mice (Thorpe & Hunt, 1975). 

    In studies by Benitz et al. (1977), nine groups of 100 Charles 
River CD1 mice of each sex were given dieldrin in the diet at 
concentrations ranging from 0.15 to 15 mg/kg.  Six hundred mice of 
each sex were used as controls.  Groups of animals were sacrificed 
at time intervals ranging from 2 to 25 months.  Initial changes in 
the liver consisted of various degrees of centrilobular and 
pericentral hypertrophy.  These changes were later associated with 
the appearance of hepatic nodules, the occurrence of which was time 
and dose related.  These nodules consisted of hypertrophic 
hepatocytes, which, in a few instances, were mixed with 
hyperplastic cells.  Various degrees of loss and distortion of 
lobular architecture were seen within these nodules.  Metastases in 
the lung were observed in three nodule-bearing animals given 15 mg 
dieldrin/kg for 25 months.  These metastases contained similar 
hypertrophic hepatocytes as did the primary liver tumours. 

    Groups of 50 B6C3F1 mice of each sex were fed diets containing 
aldrin (4 or 8 mg/kg diet for males and 3 or 6 mg/kg diet for 
females) or dieldrin (2.5 or 5 mg/kg for both sexes) for 80 weeks, 
followed by an observation period of 10 - 13 weeks.  Concurrent 
controls consisted of groups of 20 male and 10 female mice.  The 
pooled controls, used for statistical evaluation, consisted of the 
concurrent control groups combined with 92 male and 79 female mice 
from similar bioassays of other chemicals.  All surviving mice were 
killed at 90 - 93 weeks.  Body weight was not affected in the 
treated animals, but there was a dose-related increase in 
mortality, especially in the high-dose groups in the second half of 
the study.  In the dieldrin-treated mice, clinical symptoms, such 
as irritability, tremors, and alopecia occurred.  Hepatocellular 
carcinomas were found, as indicated in Table 39.  The incidence of 
hepatocellular carcinomas was clearly higher in male than female 
mice.  There was no difference in tumour frequencies in other 
tissues (NCI, 1978a). 

    Groups of weanling male C3H/HE mice were fed a diet containing 
10 mg dieldrin/kg diet until an age of 57 weeks and then were 
either administered a control diet (12 mice) or continued on the 
dieldrin diet (11 mice) for another 10 weeks.  A third group served 
as an untreated control group (21 mice).  Laparatomies were 
performed and biopsy specimens taken when about 30% of the mice in 
each dieldrin-treated group had tumours.  Further biopsy samples 
were taken approximately 10 weeks later.  Tumours were observed at 
the first laparotomy in 6/21 controls and 14/23 dieldrin-treated 
animals.  At the second laparotomy, adenomas were seen in some 
animals in which there had been no tumour at the first laparotomy. 
In one animal in the continuous dieldrin-treatment group, there was 
histological progression from adenoma to hepatocellular carcinoma. 
Additional hepatocellular carcinomas were observed in some animals 

autopsied at 2 years of age.  A strong tendency to tumour 
progression was found in both treated and control mice (Ruebner et 
al., 1984a,b). 

Table 39.  Incidence of hepatocellular tumours 
in mice (NCI, 1978a)
----------------------------------------------
Groups               Males        Females
----------------------------------------------
Concurrent controls  3/20 (15%)a  0/10 (0%)a
                     3/18 (17%)b  0/20 (0%)b

Pooled controls      17/92 (18%)  3/78 (4%)

Aldrin (4 mg)        16/49 (33%)
       (8 mg)        25/45 (56%)

Aldrin (3 mg)                     5/48 (10%)
       (6 mg)                     2/43 (5%)

Dieldrin (2.5 mg)    12/50 (24%)  6/50 (12%)
         (5 mg)      16/45 (36%)  2/49 (4%)
----------------------------------------------
a Concurrent controls of aldrin study.
b Concurrent controls of dieldrin study.
                                                     
    In a study by Meierhenry et al. (1983), groups of 50 - 70 male 
mice of three strains (C57Bl6J, C3H/He, and C57Bl6J x C3H/He B6C3F1 
hybrid) were administered a diet containing 10 mg dieldrin/kg diet 
for 85 weeks.  The control groups consisted of approximately 60 
mice of the same strains.  After 4 months, the livers in a small 
number of animals showed swellings of hepatocytes in the central 
zone with nuclear atypia, small nodules containing basophilic or 
eosinophilic foci, and multiple tumours.  The percentage of benign 
hepatic tumours was 28, 20, and 29, respectively, and in the 
control groups, 19, 18, and 4.  The percentage of hepatocellular 
carcinomas was 30, 38, and 42, respectively, and, in the controls, 
0, 12, and 4%.  Mallory bodies were seen in all the dieldrin-
treated mice that had either benign or malignant tumours, but only 
rarely in mice without tumours. 

    It seems from the available studies that dieldrin facilitates 
and exacerbates the expression of an endogenous oncogenic factor in 
CF1 mice (Tennekes et al., 1981).  The dose-response characteristics 
of dieldrin-mediated enhancement of liver tumour formation in CF1 
mice were analysed using existing tumour data from long-term 
feeding studies at six levels of continuous exposure, involving a 
total of more than 1500 animals.  Using the Druckrey equation, the 
actual contribution of dieldrin to tumour formation was considered 
to be negligible (Tennekes et al., 1985). 

8.4.1.1  Appraisal

    A number of long-term carcinogenicity studies have been carried 
out in which mice of different strains were fed aldrin and/or 
dieldrin at one or more dose levels.  In all these studies, there 
was an increased incidence of liver changes, some of which were of 
the nature of hepatocellular carcinomas while others were regarded 
as non-malignant.  Females seem to be less sensitive than males.  
No other tumours were induced. 

8.4.2.  Rat

    Borgmann et al. (1952a) fed six groups of 10 male and 10 female 
weanling Sprague-Dawley rats a diet containing 0, 5, 10, 50, 100, 
or 150 mg aldrin/kg diet over a period of 2 years.  At the two 
highest dose levels, an increased mortality was found at 16 months, 
which was not seen in the other groups.  Liver enlargement was 
observed in the groups with high dose levels, but not in the groups 
with 10 mg/kg diet or less. 

    When groups of 40 Carworth rats of each sex were given diets 
containing aldrin or dieldrin at 0, 2.5, 12.5, or 25 mg/kg diet for 
2 years, there was no increase in mortality and the growth rate was 
comparable with that of controls.  At all dose levels, the 
liver/body weight ratio was increased in males and there were 
histological liver cell changes characteristic of CHIRL.  No 
tumours were reported (Treon & Cleveland, 1955).  In a review of 
all the aldrin and dieldrin studies, it was reported that there was 
no excess of tumours in these rats (Cleveland, 1966). 

    When groups of 12 Osborne-Mendel rats of each sex were given 
diets containing aldrin or dieldrin (0, 0.5, 2, 10, 50, 100, or 
150 mg/kg diet) for 2 years, growth was not affected.  However, 
survival was markedly decreased at dose levels of 50 mg or more in 
a dose-related manner.  The liver/body weight ratio was increased 
in males fed 10 mg/kg or more, while, in females, an increase at 
all dose levels was found (no dose-response relationship at the 
lower doses).  CHIRL was observed in all treated groups, although 
at 0.5 mg/kg only a few animals showed a trace of CHIRL.  Rats at 
dose levels of 50 mg/kg or more showed haemorrhagic urinary 
bladders and nephritis.  An overall increase in tumour incidence 
was noted, but this was not dose related.  On the contrary, the 
lowest dose levels showed the highest tumour incidence.  Only one 
liver tumour was found (Fitzhugh et al., 1964). 

    In a study at the National Institute of Public Health of the 
Netherlands, no increased incidence of tumours was found in rats 
fed diets containing 75 mg dieldrin/kg for 2 years (Van Genderen, 
1965, 1979). 

    When groups of 30 Osborne-Mendel rats of each sex were fed 
5 mg/kg aldrin (95%) or a control diet for 2 years, there was no 
increase in mortality, liver/body weight ratios, or tumour 
incidence in the aldrin-fed group (Deichmann et al., 1967). 

    In studies by Walker et al. (1969b), groups of 25 Carworth Farm 
E rats of each sex were given dieldrin at 0.1, 1, or 10 mg/kg diet 
for 2 years.  A control group consisted of 45 males and 45 females. 
There was no effect on body weight.  After 2 - 3 months, the 
animals fed 10 mg/kg exhibited irritability and, as the study 
progressed, tremors and occasional convulsions, usually during 
handling.  Mortality, haematology, serum enzyme levels, and 
urinalysis were not affected.  The females fed 1 mg/kg and 10 mg/kg 
had increased liver/body weight ratios.  At 10 mg/kg, one male and 
six females exhibited CHIRL.  In two females of the group fed 10 
mg/kg and in one female control rat, microscopic nodules in the 
liver parenchyma were seen.  There was no increase in tumour 
incidence.  Subsequent re-evaluation of these data (Stevenson et 
al., 1976) confirmed that there was no treatment-related increase 
in tumour incidence. 

    Nine groups of 50 Osborne-Mendel rats of each sex were fed 
diets containing aldrin or dieldrin at 0, 20, 30, or 50 mg/kg for 
up to 31 months.  A control group consisted of 100 male and 100 
female rats.  Dose-related tremors and convulsions, always 
associated with weight loss, occurred at all dose levels, 
particularly in females.  Female rats fed 50 mg aldrin/kg or 30 or 
50 mg dieldrin/kg had a shortened lifespan.  The liver/body weight 
ratio was increased in all dieldrin-treated groups and in males fed 
30 or 50 mg aldrin/kg, but was decreased in females fed 20 mg/kg. 
A moderate increase (not dose related) in the incidence of hepatic 
centrilobular cloudy swelling, necrosis, or, rarely, foci of acute 
or chronic inflammatory cellular infiltration was observed in all 
treated groups.  Hyperplasia in the liver was found in two male 
rats fed 30 mg aldrin/kg.  There was no increase in tumour 
incidence (Deichmann et al., 1970; Deichmann, 1974). 

    Groups of 50 Osborne-Mendel rats of each sex were given diets 
containing aldrin at levels of 30 or 60 mg/kg.  Treatment of male 
rats lasted 74 weeks followed by 37 - 38 weeks of observation, 
while that of female rats lasted 80 weeks followed by 32 - 33 weeks 
of observation.  In a similar study, dieldrin was fed at a level of 
29 mg/kg diet (time-weighted average dose) for 80 weeks followed by 
observation for 30 - 31 weeks or 65 mg/kg diet (time-weighted 
average dose) for 59 weeks followed by observation for 51 - 52 
weeks.  Concurrent control groups consisted of 10 rats of each 
sex.  Pooled controls, used for statistical evaluation, consisted 
of concurrent control groups combined with 58 males and 60 females 
from similar bioassays with other chemicals.  All surviving rats 
were killed at 110 - 111 weeks.  Typical signs of organochlorine 
intoxication (such as hyperexcitability) were observed with 
increasing frequency and severity, especially in the second year, 
but mortality was not affected.  No significant increase in tumour 
incidence was found (NCI, 1978a) (Table 40). 

    Groups of 24 Fischer 344 rats of each sex were given dieldrin 
at 0, 2, 10, or 50 mg/kg diet for 2 years.  Typical signs of 
organochlorine intoxication were observed during the second year in 
the 50 mg/kg group.  Body weight and survival were not adversely 

affected in any of the dieldrin groups.  Liver tumours were not 
observed.  No significant increase in tumours was found (NCI, 
1978b) (Table 40). 

Table 40.  Incidence of hepatocellular tumours in rats 
(NCI, 1978a,b)
-------------------------------------------------------
Groups                        Males        Females
-------------------------------------------------------
 Osborne-Mendel rats

Concurrent controls           1/10 (10%)a  1/10 (10%)a
                              1/10 (10%)b  0/9  (0%)b

Pooled controls               ?            5/59 (8.5%)a

Aldrin (30 mg/kg diet)        1/47 (2%)    0/48 (0%)
       (60 mg/kg diet)        1/47 (2%)    3/49 (6%)

Dieldrin (40-20 mg/kg diet)d  0/44 (0%)    1/47 (2%)
         (80-40 mg/kg diet)e  1/47 (2%)    1/44 (2.3%)

 Fischer F 344 rats

Concurrent controls           2/24 (8.3%)  0/24 (0%)

Pooled controls               ?            ?

Dieldrin ( 2 mg/kg diet)      0/23 (0%)    0/24 (0%)
         (10 mg/kg diet)      0/23 (0%)    0/24 (0%)
         (50 mg/kg diet)      4/23 (17%)c  0/23 (0%)
-------------------------------------------------------
a Concurrent controls of aldrin study.
b Concurrent controls of dieldrin study.
c Nodular hyperplasia.
d Time-weighted average dose = 29 mg/kg.
e Time-weighted average dose = 65 mg/kg.

    When groups of 50 female rats of two different strains 
(Osborne-Mendel and Sprague-Dawley) were fed 0, 20, or 50 mg 
aldrin/kg diet, the survival rate was reduced at 50 mg/kg but not 
at 20 mg/kg.  There was no increase in the incidence of mammary or 
liver tumours (Deichmann, 1974; Deichmann et al., 1979). 

    Photodieldrin, which has metabolites identical to those of 
dieldrin, was fed to groups of rats for 80 weeks at concentrations 
of up to 7.5 mg/kg diet NCI (1977).  No increase in tumour 
incidence was found (see section 8.8.1.3). 

    Ito et al. (1983) studied the promoting activity of dieldrin on 
the induction of hyperplastic (neoplastic) liver nodules using a 
short-term test system.  F344 rats received a single dose (200 
mg/kg body weight) of  N-nitrosodiethylamine, and 2 weeks later, 
were treated for 6 weeks with dieldrin in the diet at a 
concentration of 100 mg/kg.  Dieldrin had a weak promoting 
potential in this test system. 

8.4.2.1  Appraisal

    A number of long-term/carcinogenicity studies have been carried 
out in which rats of different strains were fed one or more dose 
levels of aldrin and/or dieldrin.  The overall no-effect level in 
these long-term studies, both for aldrin or dieldrin, was 0.5 mg/kg 
diet.  At feeding levels of 1 mg/kg or more, an increasing, dose-
related hepatomegaly and histological changes in the liver 
characterized as CHIRL occurred.  At levels of 10 mg/kg diet or 
more, typical signs of organochlorine toxicity occurred such as 
irritability, tremors, and convulsions.  In all these studies, no 
increase in tumour incidence in liver or other organ/tissue systems 
was found. 

8.4.3.  Hamster

    When groups of 34 - 40 Syrian golden hamsters of each sex were 
fed diets containing dieldrin (99%) at 0, 20, 60, or 180 mg/kg for 
120 weeks, there was no significant increase in tumour incidence 
(Cabral et al., 1979b). 

8.4.4.  Monkey

    In studies on rhesus monkeys, groups of five males were given 
diets containing dieldrin (88.4%) at 0, 0.01, 0.1, 0.5, 1, or 5 
mg/kg (0.0002 - 0.07 mg/kg body weight) for approximately 6 years. 
After two monkeys in the group fed 5 mg/kg died, the level of 
exposure to the remaining three animals was reduced to 2.5 mg/kg 
and, later, to 1.75 mg/kg.  Subsequently, one of these animals had 
his dieldrin intake progressively increased until at the end of the 
second year, he was receiving dieldrin at the initial dietary 
concentration of 5 mg/kg.  Clinical and haematological examinations,
liver and kidney function studies, urinalysis, and pathology did not
reveal any abnormalities.  The liver/body weight ratios and liver
DNA and RNA of the test animals were not different from those of
control animals.  No subcellular changes were seen in the
hepatocytes.  Dose-related increases in microsomal cytochrome P-450
and in the activity of the liver mono-oxygenase enzyme system were
observed at the two highest dose levels.  These alterations in 
cytochrome P-450 in the liver microsomes were significant in the 
monkeys fed 0.1 mg/kg or more.  No effect was observed at 0.01 
mg/kg.  The concentrations of dieldrin in the subcutaneous fat of 
the monkeys fed 0.1 mg/kg were similar to those measured in human 
beings receiving a daily oral intake of similar concentration.  The 
dieldrin concentrations in the monkey livers were approximately 200 
times higher than those in male rats receiving a daily intake of 
dieldrin 3 times higher than the monkeys, and they were similar to 
the concentration in the livers of male mice daily ingesting 
dieldrin at a level approximately 50 times higher (Zavon & Stemmer, 
1975; Wright et al., 1977, 1978). 

8.4.5.  Mode of Action

    From long-term feeding experiments, it seems that aldrin and 
dieldrin may be carcinogenic to mice, but not to rats or hamsters. 
Mutagenicity findings have been consistently negative (see section 
8.6).  There is insufficient knowledge of the mechanism by which 
these chemicals might behave epigenetically. 

    The latest evaluation of IARC (1987) is that there is 
inadequate evidence of carcinogenicity in humans and limited 
evidence for carcinogenicity in experimental animals. 

8.5.  Reproduction, Embryotoxicity, and Teratogenicity

8.5.1.  Reproduction

8.5.1.1  Mouse

    Groups of 100 pairs of male and female virgin CFW Swiss mice 
were fed diets containing 5 mg dieldrin/kg for 30 days before 
mating, after which time they were randomly paired and fed the same 
diet for a further 90 days.  Mortality in the dieldrin-treated 
group was similar to that of a control group (size not specified). 
No major biological effects on fertility, fecundity, gestation 
period, size of the first litters, or numbers of young produced per 
day were noted as a result of feeding dieldrin.  A statistically 
significant (6%) decrease in mean size of all litters combined was 
the only difference observed between the dieldrin-treated and 
control groups (Good & Ware, 1969). 

    In a reproductive study, groups of 4 male and 14 female Swiss 
white mice (120 days old) were fed diets containing 3, 5, 10, or 
25 mg aldrin/kg or 3, 10, or 25 mg dieldrin/kg.  Six groups served 
as controls.  The study covered six generations, and two litters 
per generation.  For both aldrin and dieldrin, the 25 mg/kg dose 
was too toxic and resulted in high litter mortality in the few dams 
reaching gestation.  This dose level was therefore discontinued. 
Pup survival was low in mice fed 10 mg dieldrin/kg, and so 
treatment was terminated after the first generation.  The most 
pronounced effect observed in the group fed 10 mg aldrin/kg and, to 
a lesser extent, 5 mg aldrin/kg was a low pre-weaning pup survival. 
No effects on fertility, viability, or gestation were observed in 
six generations of mice fed 3 mg dieldrin/kg.  A decrease in pre-
weaning survival was observed in the F2b litters, but a similar 
decrease was also found in one of the six control groups (Keplinger 
et al., 1970). 

    In studies by Virgo & Bellward (1975), groups of 18 - 19 
uniparous female Swiss-Vancouver mice were given diets containing 
0, 2.5, 5, 10, 15, 20, or 25 mg dieldrin/kg, 4 weeks prior to their 
second mating, continuing until day 28 postpartum.  Significant 
mortality of the females occurred at 20 and 25 mg/kg, all deaths 
occurring before parturition (89 and 56%, respectively).  Fertility 
in the groups fed 10 and 15 mg/kg was decreased, though survivors 
at higher doses were fertile.  Oestrus and gestation period were 

not affected.  Litter size was decreased only in the group 
receiving 25 mg/kg.  The major effect was an increase in pre-
weaning pup mortality; 47% at 2.5 mg/kg, 80% at 5 mg/kg, and 100% 
at 10 mg/kg or more (31% mortality in control animals).  Dams 
receiving 10 mg/kg or more exhibited hyperactivity, which was a 
contributory factor to the high pup mortality.  No gross 
abnormalities were detected in the pups, none of whom showed 
tremors or convulsions.  Within the litters raised at 2.5 and 5 
mg/kg, pup survival was not different from controls.  The only 
effect on reproductive capacity or pup survival observed in female 
mice fed 2.5 mg/kg was an increase in pre-weaning pup mortality. 

    A study was carried out on primiparous female Swiss-Vancouver 
mice to investigate whether diets containing up to 15 mg 
dieldrin/kg affect maternal behaviour and pup viability.  Viability 
was investigated in dams fed diets containing 0, 5, 10, or 15 mg 
dieldrin/kg for 4 weeks prior to mating.  Pups fed 10 mg/kg were 
nursed by foster dams not fed dieldrin, and all died by day 4; the 
foster dams' own pups showed a very low mortality and survived 
until weaning.  Similar results were obtained at 5 mg/kg.  Dieldrin 
did not have any influence on serum progesterone levels, milk 
production, or the dam's tendency to retrieve pups or build nests. 
However, at 5 mg/kg or more, nursing was reduced.  It was concluded 
that dieldrin causes irreversible congenital inviability (not 
through any effect on progesterone levels) and it was suggested 
that the inviability and the reduced tendency to nurse increased 
the pup mortality (Virgo & Bellward, 1977). 

8.5.1.2  Rat

    In studies by Treon & Cleveland (1955), rats (Carworth strain) 
were fed aldrin or dieldrin at dietary concentrations of 2.5, 12.5, 
or 25 mg/kg for three consecutive generations, two litters being 
produced for each generation.  (There was no mention of a control 
group, and tabulation and description of results was limited in 
this report).  A reduction in the number of pregnancies, which 
gradually disappeared over successive generations, was initially 
observed at 12.5 and 25 mg aldrin/kg and at all three doses of 
dieldrin.  No effects on litter size or pup weights were observed 
at any dietary concentration.  A marked increase in mortality in 
pre-weaning pups was found at dietary concentrations of 12.5 and 
25 mg/kg for both compounds.  This was thought by the authors to 
be due to the high concentration of dieldrin in the milk of the 
mothers.  Neither aldrin nor dieldrin had any effect on 
reproductive capacity.  No effects, except a "slight to moderate" 
increased pre-weaning pup mortality, were observed in the rats fed 
for three generations with aldrin or dieldrin at 2.5 mg/kg. 

    When groups of 10 male and 20 female Long Evans rats were fed 
dietary concentrations of 0, 0.1, 1, or 2 mg dieldrin/kg over three 
generations (each generation producing two litters), no effects 
were observed on the general health (including weight gain), 
behaviour, fertility, gestation, viability, lactation, or organ 
weight ratios.  No pathological changes were found in parents or 
pups.  Increased pre-weaning mortality (compared to that in 

controls) in the F1a litter was observed in the animals fed 2 
mg/kg.  This effect was not found in the five subsequent litters 
from this group and was not considered to be a major toxic effect. 
No changes in reproductive capacity were observed over three 
generations at dietary concentrations up to and including 2 mg/kg 
dieldrin (Eisenlord et al., 1967). 

    In studies by Harr et al. (1970), groups of 20 male and 20 
female 28-day-old OSU-Wistar rats were fed 0, 0.08, 0.16, 0.31, 
0.63, 1.25, 2.5, 5, 10, 20, or 40 mg dieldrin/kg diet throughout 
their lifespan.  Ten females from each group were mated at 146 days 
of age.  Mortality occurred in dams at 20 and 40 mg/kg.  Fertility 
and litter size were decreased in several dose groups without a 
clear dose relationship.  The number of pups at weaning was 
markedly reduced at 2.5 mg/kg or more; none survived at 20 and 40 
mg/kg.  The nursing pups died in convulsions or starved.  No 
effects were noted at 1.25 mg/kg or less.  Neural lesions, such as 
cerebral oedema and hydrocephalus, occurred in pups of nursing dams 
at dieldrin concentration of 0.08 mg/kg.  Hepatic lesions were 
found in rats fed concentrations of 0.31 mg/kg or more. 

    When groups of 18 - 20 Long Evans pregnant rats were given 4 mg 
dieldrin/kg body weight daily by gavage from day 15 of gestation to 
21 days post partum, fecundity, number of stillbirths, perinatal 
mortality, and total litter weights did not differ from the control 
group.  No malformations in pups were observed (Coulston et al., 
1980). 

8.5.1.3  Dog

    In study by Kitselman (1953), seven groups of three dogs, each 
group having at least one member of each sex, were fed either 
aldrin or dieldrin for one year at dietary concentrations 
equivalent to 0, 0.2, 0.6, or 2 mg/kg body weight (in corn oil). 
Out of a total of 11 bitches fed either aldrin or dieldrin, 9 
conceived.  All pregnant bitches produced litters of at least four 
pups/litter.  The survival of pups was generally lower in the 
groups fed aldrin or dieldrin.  Histopathological examinations of 
dead pups revealed degenerative changes in the liver and mild 
degenerative changes in renal tubules.  Liver changes were also 
observed in treated bitches.  The design and size of this study was 
too limited to deduce a dose-response relationship for pup 
survival, but no effects were observed in dogs receiving 0.2 mg 
dieldrin/kg body weight. 

8.5.1.4  Appraisal

    In the reproductive studies (over one to six generations) 
carried out with aldrin or dieldrin on mice and rats, the major 
effect observed in most of the studies was an increased mortality 
rate in pre-weaning pups.  Reproductive performance,  per se, was 
only affected at doses causing maternal intoxication.  The studies 
on dogs are of a too limited nature to draw firm conclusions, apart 
from the consistent increase in pre-weaning pup mortality. 

    The results of these reproductive studies indicate that 
dieldrin at levels of 2 mg/kg in the rat diet and 3 mg/kg in the 
mouse diet (equivalent to 0.1 and 0.4 mg/kg body weight per day, 
respectively) are no-effect levels for reproduction.  It is not 
possible to establish a no-effect level for aldrin for 
reproduction, because no adequate data are available. 

8.5.2.  Embryotoxicity and teratogenicity

8.5.2.1  Mouse

    Ottolenghi et al. (1974) gave groups of 10 pregnant CD-1 mice 
single oral doses of 25 mg aldrin/kg body weight or 15 mg 
dieldrin/kg body weight (in corn oil; equivalent to half the LD50 
values) on day 9 of gestation.  Control groups consisted of 
untreated and corn-oil-dosed mice.  No effects on fetal survival or 
weight were observed.  Abnormalities, such as webbed feet, cleft 
palate, and open eyes, were increased in both treated groups, but 
they may have been related to maternal toxicity.  The percentage of 
the total live fetuses that were malformed was 33% for aldrin-
treated mice and 17% for dieldrin-treated ones. 

    In two comparable studies, pregnant CD-1 mice (6 - 16 per 
group) were given daily oral doses of dieldrin in peanut oil at 0, 
1.5, 3, or 6 mg/kg body weight from day 7 to day 16 of gestation. 
At 6 mg/kg, reduced body weight gain and increased liver/body 
weight ratio were observed.  There was an increase in supernumerary 
ribs and a decreased number of caudal ossification centres in the 
fetuses of mice given 6 mg/kg.  In one study, the number of 
supernumerary ribs was increased at all three dose levels, 
(significant at the two highest dose levels) (Chernoff et al., 
1975).  In the other study, the increase in supernumerary ribs at 
6 mg/kg was not significant.  The increase in the number of 
supernumerary ribs may be an expression of developmental toxicity. 

    Doses of dieldrin (99%) were given either in corn oil (0, 1.5, 
or 4 mg/kg body weight) or in dimethylsulfoxide (DMSO) (0, 0.25, 
0.5, or 1 mg/kg) daily by gavage to pregnant CF-1 mice (7 - 14 
mice/group) on days 6 - 14 of gestation.  No maternal or fetal 
toxicity was seen in groups treated with dieldrin in corn oil or in 
the corn oil control groups, but some was seen in the dieldrin/DMSO 
and DMSO-control groups.  No compound-related teratogenic effects 
were observed (Dix et al., 1978). 

8.5.2.2  Rat

    In a study by Chernoff et al. (1975), pregnant CD rats (9 - 25 
per group) were given daily oral doses of dieldrin in peanut oil 
(0, 1.5, 3, or 6 mg/kg body weight) from days 7 to 16 of gestation. 
At 6 mg/kg, increased mortality and reduced body weight gain were 
observed in the dams, but no changes in the liver/body weight 
ratios were found.  Fetuses did not show any differences from the 
controls in mortality, body weight, or occurrence of anomalies. 
There were no differences in the average number of sternal or 

caudal ossification centres (as were seen in mice).  No evidence of 
teratogenicity was observed at a dose level of 6 mg aldrin/kg body 
weight per day. 

    No malformations were observed in fetuses or pups from 18 - 20 
Long Evans rats given 0 or 4 mg dieldrin/kg, by gavage, daily from 
day 15 of gestation to day 21 of lactation (Coulston et al., 1980). 

8.5.2.3  Hamster

    Pregnant Syrian golden hamsters (41 - 43 per group) were given 
single oral doses in corn oil of either 50 mg aldrin/kg body weight 
or 30 mg dieldrin/kg body weight on either day 7, 8, or 9 of 
gestation.  Untreated and vehicle-control groups (respectively, 57 
and 41 animals) were used.  The high dose levels of both aldrin and 
dieldrin caused reductions in the number of live fetuses and fetal 
weight and an increased incidence of abnormalities (cleft palate, 
open eyes, and webbed feet).  The effects were more pronounced 
after treatment on days 7 and 8 of gestation than on day 9.  It was 
suggested that, since webbed foot and open eye were frequently 
associated with low fetal weight, these effects might be simply the 
expression of growth retardation (Ottolenghi et al., 1974). 

8.5.2.4  Rabbit

    No teratogenic effects were observed in the offspring of groups 
of pregnant Banded Dutch rabbits dosed with dieldrin in 
carboxymethylcellulose (2 or 6 mg/kg body weight per day) from 
days 6 to 18 of gestation.  The animals were killed on day 28 of 
gestation and the fetuses were examined for visceral and skeletal 
abnormalities (Dix & Wilson, 1971). 

8.5.2.5  Appraisal

    No evidence of a teratogenic potential has been found from 
studies on rats, mice, or rabbits using oral doses up to 6 mg/kg 
body weight.  Single high oral doses, equivalent to half the LD50, 
have been found to cause fetotoxicity and abnormal development of 
the fetuses in hamsters and, to a lesser extent, in mice.  The 
significance of these abnormalities in the presence of severe 
maternal toxicity is doubtful but a specific teratogenic potential 
cannot be ruled out completely.  No gross malformations have been 
reported in reproductive studies. 

8.6.  Mutagenicity and Related End-Points

8.6.1.  Microorganisms

    Most research workers have reported that aldrin and dieldrin, 
with or without microsomal activation, are not mutagenic in 
bacterial or yeast test systems.  In one study, it was reported 
that dieldrin, without activation, was mutagenic in two out of 
three strains of  Salmonella typhimurium, but there was no dose-
response relationship (Majumdar et al., 1977).  The results of the 
other mutagenicity studies with aldrin and dieldrin in bacterial 

test systems have been negative (Table 41).  A critical survey of 
the published reports indicates clearly that neither aldrin nor 
dieldrin is mutagenic in microbial systems (Ashwood-Smith, 1981). 

8.6.2.  Mammalian cell point mutations

    Only one study on the  in vitro mutagenicity of dieldrin to 
mammalian cells has been reported.  Dieldrin was weakly mutagenic 
when tested at a single concentration (0.01 mmol/litre) in ouabain-
resistant Chinese hamster V-79 cells.  The significance of this 
result is difficult to assess because of the lack of a dose-
response relationship, and a positive control group was not used 
(Ahmed et al., 1977a). 

8.6.3.  Dominant lethal assays and heritable translocation assays 
in mice

    Aldrin did not show any detectable dominant lethality when 
given as a single intraperitoneal dose (8 or 40 mg/kg) or in daily 
oral doses (0.5 or 1 mg/kg body weight) for 5 days to male ICR/Ha 
Swiss mice (Epstein et al., 1972). 

    Dieldrin, also, revealed no detectable dominant lethality in 
four assays in male mice following a single intraperitoneal 
injection (5.2 or 26 mg/kg) or daily oral doses of 2 or 3 mg/kg 
body weight for 5 days (Epstein et al., 1972).  Likewise, a single 
oral dose of 12.5, 25, or 50 mg/kg body weight did not produce 
dominant lethality in CF-1 mice (Dean et al., 1975).  Bidwell et 
al. (1975) carried out a dominant lethal test on B6D2F1/J mice 
orally administered 0.08, 0.8, and 8 mg/kg body weight dieldrin for 
5 days, but no effects were seen. 

    In further studies by Bidwell et al. (1975), a heritable 
translocation test was performed on male mice after oral intake of 
0.008, 0.08, or 0.2 mg dieldrin/kg body weight per day for a period 
of 6 weeks.  The cytogenetic determination of somatic cells using 
the micronucleus test and the usual analysis of spermatocytes did 
not reveal an increase in the rate of translocations. 

8.6.4.  Micronucleus test

    Aldrin did not induce a significant increase in the frequency 
of micronuclei in the bone marrow of mice treated orally with 13 
mg/kg body weight (Usha Rani et al., 1980). 

    No cytogenetic abnormalities were seen in a standard metaphase 
analysis and micronucleus test after oral gavage of mice with 0.8 
or 8 mg dieldrin/kg body weight per day for 5 days (Bidwell et al., 
1975). 

8.6.5.  Chromosome and cytogenicity studies

    Chinese hamsters (three groups of four males and four females) 
were orally dosed with 30 and 60 mg dieldrin/kg body weight.  No 
chromosome abnormalities were found in femoral bone marrow cells 
(Dean et al., 1975). 

Table 41.  Aldrin and dieldrin:  mutagenicity tests in microorganisms
---------------------------------------------------------------------------------------------------------
Organism                  Strain             Activation  Compound/dose         Result    Reference
                                             system
---------------------------------------------------------------------------------------------------------
 E. coli                   WP2 Try-           none        aldrin and dieldrin;  negative  Ashwood-Smith et
                                                         1000 µg/plate                   al. (1972)

 E. coli                   WP2 hcr            rat S9      up to 5000 µg/plate   negative  Moriya et al.
                                                                                         (1983)

 E. coli                   Ga1 Rs             none        aldrin and dieldrin;  negative  Fahrig (1974)
 Serratia marcescens       alpha 21 and 742               dose not stated
 Saccharomyces cerevisiae

 Aspergillus nidulans      diploid P1 and     none        dieldrin; 13 or 26    negative  Crebelli et al.
                          haploid strain 35              mmol                            (1986)

 Saccharomyces cerevisiae  632/4              none        aldrin; 5 µg/ml on    positive  Guerzoni et al.
                                                         disc                            (1976)
 Bacillus subtilis         (Rec-assay)        none        aldrin and dieldrin;  negative  Shirasu (1975)
 Salmonella typhimurium    TA 1535, 1536,
                          1537, 1538
 E. coli                   WP2 hcr+, hcr-

 Salmonella typhimurium    TA 98, 100, 1535,  rat S9      dieldrin; 10, 50,     negative  Bidwell et al.
                          1536, 1537, 1538,              100, or 500 µg/plate            (1975)
                          G46          

 Salmonella typhimurium    TA 98, 100, 1535,  rat S9      dieldrin; dose not    negative  McCann et al.
                          1537                           stated                          (1975)

 Salmonella typhimurium    TA 1535, 1536,     rat S9      dieldrin; 1000        negative  Marshall et al.
                          1537, 1538                     µg/plate                        (1976)

 Salmonella typhimurium    TA 98, 100         none        dieldrin; 10, 30,     negative  Glatt et al.
                                                         100, 300, 1000, 3000            (1983)
                                                         µg/plate

 Salmonella typhimurium    TA 90, 100, 1535,  rat S9      up to 5000 µg/plate   negative  Moriya et al.
                          1537, 1538                                                     (1983)
---------------------------------------------------------------------------------------------------------

Table 41.  (contd.)
---------------------------------------------------------------------------------------------------------
Organism                  Strain             Activation  Compound/dose         Result    Reference
                                             system
---------------------------------------------------------------------------------------------------------
 Salmonella typhimurium    TA 98, 100, 1535,  mouse S9    dieldrin; 1000        negative  Van Dijck & Van
                          1537, 1538, 1950,              µg/plate                        de Voorde (1976)
                          1978         

 Salmonella typhimurium    not specified      S9          dieldrin; dose not    "weak"    Ercegovich &
                                                         stated                response  Rashid (1977)

 Salmonella typhimurium    TA 98, 100, 1535   mouse S9    dieldrin; 1, 25, or   positive  Majumdar et al.
                                                         50 µg/ml                        (1977)

 Salmonella typhimurium    TA 98, 100, 1535,  rat S9      dieldrin; up to 2500  negative  Purchase et al.
                          1538                           µg/plate                        (1978)

 Salmonella typhimurium    TA 98, 100         rat S9      dieldrin; 50 or 1000  negative  Wade et al.
                                                         µg/plate                        (1979)

 Salmonella typhimurium    TA 98, 100, 1535,  rat,        aldrin; dose not      negative  Simmon et al.
                          1537, 1538         mouse, and  stated                          (1977)
                                             human S9
                                             
 Salmonella typhimurium    TA 98, 100         rat S9      aldrin and dieldrin;  negative  Nishimura et al.
                                                         364 and 380 µg/plate            (1982)

 Salmonella typhimurium    TA 98, 100 1535,   rat S9      dieldrin 2.6 x 104    negative  DeFlora (1981)
                          1537, 1538                     nmoles/plate
---------------------------------------------------------------------------------------------------------

    The effect on the bone marrow cells of STS mice was examined 
after applying a single dose of dieldrin intraperitoneally at 0, 1, 
30, or 50 mg/kg body weight.  A decrease in the mitotic index was 
noted, as dieldrin concentration increased, and differences in 
chromosome aberrations (a slight increase in breaks, fragments, 
and interchanges) were found (Majumdar et al., 1976). 

    Seventy-one juvenile mallard ducks, the parents of which had 
been exposed to various dietary levels of dieldrin for 6 months or 
longer, were grouped and fed dieldrin at a level that corresponded 
to the diet fed to the parents (0, 4, 10, or 30 mg dieldrin/kg 
diet) for approximately 60 days.  At the end of this period, no 
chromosomal aberrations were found in femoral bone marrow cultures. 
However, the mitotic index of ducks exposed to 30 mg/kg was 
significantly reduced (Bunch & Low, 1973). 

    When lymphocytic cultures from adult mallard ducks (which had 
not been exposed to dieldrin) were treated with 0, 0.1, 1, 10, 30, 
or 100 mg dieldrin/kg, there was a significant increase in the 
incidence of chromosome structural alterations, but only at the 
highest dose level.  The mitotic index was significantly reduced at 
all dose levels, the greatest decreases occurring at the two 
highest dose levels (Bunch & Low, 1973). 

    Chromosome studies in cultured lymphocytes from current 
dieldrin plant workers (12) former plant workers (9), and control 
(17) did not show any differences in the frequency of chromosome 
aberrations (Dean et al., 1975).  In one study, it was reported 
that aldrin produced chromosomal aberrations in cultured human 
lymphocytes at concentrations of 19 and 38 µg/ml.  In mice and 
rats, an intraperitoneal injection of a dose of 19 mg/kg body 
weight was reported to induce chromosomal gaps, breaks, deletions, 
and fragments in bone marrow cells (Georgian, 1975). 

    Cultured human peripheral lymphocytes from agricultural and 
public health (anti-Chagas' disease) workers with at least 10 years 
exposure to dieldrin were examined for structural chromosome 
aberrations and sister chromatid exchange.  No differences were 
seen when they were compared with lymphocytes derived from a 
control group (Bordon, 1980). 

8.6.6.  Host-mediated assays

    Bidwell et al. (1975) carried out a host-mediated assay, 
incorporating blood- and urine-recovery studies, for mutagenic 
substances on B6D2F1/J mice.  Five daily oral doses of 20 mg 
dieldrin/kg body weight were given, and the mice were then injected 
intraperitoneally with  Salmonella tester strains.  The results were 
negative.  In a further host-mediated assay using  Saccharomyces 
 cerevisiae (strain D4, heteroallelic at the ade-2 and trp-5 loci) 
as tester microorganism, CF-1 mice were treated with a single oral 
dose of 25 or 50 mg dieldrin/kg body weight or with five daily 
doses of 5 or 10 mg/kg body weight.  No mutagenic activity was 
found (Dean et al., 1975). 

8.6.7.  Cell transformation in mammalian cell systems

    Dieldrin (0.08 - 250 mg/litre) proved negative in mammalian 
cell transformation tests using cell lines derived from baby Syrian 
hamster kidney (BHK-21 C13) and from human lung (Wl-38), either 
with or without metabolic activation by rat liver S9 microsomal 
fraction (Purchase et al., 1978). 

    In a 6-thioguanine resistance mutation assay using FM 3A mouse 
cell cultures, aldrin was weakly mutagenic (Morita & Umeda, 1984). 

8.6.8.   Drosophila melanogaster and other insect systems

    There is no evidence of a mutagenic activity of aldrin or 
dieldrin in  Drosophila melanogaster (Benes & Sram, 1969; Bidwell et 
al., 1975).  No increase in recessive or dominant lethal mutations 
was found following exposure of the wasp  Bracon hebetor to 
sublethal doses of dieldrin (95%) (Grosch & Valcovic, 1967). 

8.6.9.  Effects on DNA

    DNA strand breakage was not detected in Chinese hamster V-79 
cells exposed to dieldrin (0.1 - 1 mmol/litre) in the presence of 
rat liver S9 microsomal fraction using the alkaline elution assay 
(Swenberg et al., 1976). 

    Aldrin (1 - 1000 µmol/litre) and dieldrin (1-100 µmol/litre) 
induced unscheduled DNA synthesis in SV-40 transformed human 
fibroblast cells (VA-4) both in the presence and absence of rat 
liver microsomes (Ahmed et al., 1977b).  This study was repeated by 
Zelle & Lohman (1977).  After exposure to dieldrin, the rate of DNA 
synthesis in normal primary human fibroblasts (AH) decreased, but 
returned to the control level in a few hours.  This suggests that 
dieldrin interferes with semiconservative DNA replication without 
damaging DNA.  The effect of dieldrin on the induction of repair 
replication was studied with both AH cells and SV-40 transformed 
human cells (MM-SV-40).  No evidence that dieldrin could induce DNA 
repair was found (Zelle & Lohman, 1977). 

    The DNA breakage rates in an  Escherichia coli plasmid after 
treatment with aldrin or dieldrin did not differ from those in 
untreated plasmid DNA, suggesting that, at least in these studies, 
the compounds did not interact directly with DNA (Griffin & Hill, 
1978). 

    The effects of aldrin and dieldrin (both at 100 µg/ml) on the 
uptake of tritiated thymidine by cultured rat thymocytes and human 
lymphocytes were tested under different experimental conditions. 
Both compounds appeared to have marginal effects on thymidine 
uptake, suggesting inhibition of DNA synthesis (Rocchi et al., 
1980). 

    Aldrin (100 mmol/litre) and dieldrin (500 mmol/litre) did not 
induce unscheduled DNA synthesis in primary cultures of Fischer 344 
rat hepatocytes (Probst et al., 1981).  Williams (1982) reported 

the results of the hepatocyte primary culture/DNA repair test, 
using freshly isolated hepatocytes of high metabolic capability to 
monitor the production of DNA damage by measuring DNA repair 
synthesis.  Aldrin and dieldrin gave equivocal results concerning 
DNA repair, but there was no damage to DNA.  Aldrin (0.3 - 3 
mmol/litre) induced DNA strand breaks in an alkaline elution/rat 
hepatocyte assay (Sina et al., 1983). 

    Cultured hepatocytes from male Balb/c mice treated with 
dieldrin at a concentration of 4 x 10-4 mol/litre showed no 
unscheduled DNA synthesis.  The results were no different with 
cells from mice treated  in vivo with phenobarbital (Klaunig et al., 
1984). 

    A DNA synthesis inhibition/damage test on HeLa cells with S9 
showed inhibition to 60% of the control value within 90 min of 
treatment with 4 x 10-4 mol dieldrin/litre (Painter, 1981). 

8.6.10.  Cell to cell communication

    Both aldrin and dieldrin inhibited gap junctional intercellular 
communication between 6-thioguanine-sensitive and 6-thioguanine-
resistant human teratocarcinoma cells in culture (Zhong-Xiang et 
al., 1986). 

    The inhibition of cell to cell communication was observed in 
human teratocarcinoma cells in culture in the presence of dieldrin, 
using dye transport methods (Wade et al., 1986). 

    Metabolic cooperation between 6TG-resistant and HGPRT-deficient 
Chinese hamster V79 cells was inhibited when aldrin (2.5 - 10 
µg/ml) or dieldrin (2.5 - 5 µg/ml) was added to the medium (Kurata 
et al., 1982). 

    Trosko et al. (in press) studied the inhibition of gap 
junctional-mediated intercellular communication using co-cultures 
of Chinese hamster cells.  To do this, an  in vitro assay (in which 
the metabolic cooperation between V79-6-thioguanine-sensitive (6 
TGs) and resistant (6 TGr) cells is studied) has been developed to 
detect the ability of non-cytotoxic and non-mutagenic chemicals to 
inhibit gap junctional communication.  Aldrin and dieldrin 
inhibited metabolic cooperation at concentration of about 4 µg/ml 
or more. 

8.6.11.  Appraisal

    Aldrin and dieldrin are not mutagenic to mammals in a variety 
of mutagenicity test systems with unrelated different end-points. 

8.7.  Special Studies

8.7.1.  Liver enzyme induction

    Aldrin and dieldrin have been shown to increase the activity of 
liver microsomal enzymes, generally associated with enlargement of 
the liver.  They have also been found to induce microsomal 

dimethylaminoantipyrine-N-demethylase and aldrin-epoxidase, and 
increase the cytochrome P-450 level (Campbell et al., 1983).  This 
enzyme induction is the earliest and most sensitive indicator of an 
effect of exposure in mouse, rat, beagle dog, and rhesus monkey 
(Wright et al., 1972). 

    Studies on rats indicated a no-effect level for enzyme 
induction, by either aldrin or dieldrin, at 1 mg/kg diet (Gillett & 
Chan, 1968; Kinoshita & Kempf, 1970; Den Tonkelaar & Van Esch, 
1974). 

    In the rhesus monkey, the activity of the liver microsomal 
monooxygenase system was increased by dieldrin (at daily feeding 
levels of 1.75 and 5 mg/kg diet for approximately 6 years), but no 
associated liver enlargement was observed.  The dietary intake of 
dieldrin required for the induction of this enzyme system in 
monkeys was approximately 1 mg/kg diet, corresponding to an intake 
of 25 - 30 µg/kg body weight per day (section 8.4.4) (Wright et 
al., 1978). 

    In human beings, oral dosing with 211 µg dieldrin/day 
(approximately 3 µg/kg body weight per day) for two years, in 
addition to the daily intake of 19 µg dieldrin from the diet, did 
not increase the activity of microsomal liver enzymes as measured 
by the concentration of  p,p'-DDE in adipose tissue and blood.  No 
evidence of enzyme stimulation was observed in a group of 10 
workers (at the time, they were the most highly exposed workers) in 
a manufacturing plant with a mean exposure equivalent to a daily 
oral intake of 17 µg/kg body weight (maximum 24 µg/kg body weight) 
(Hunter & Robinson, 1967; Hunter et al., 1969; Jager, 1970). 

8.7.2.  Nervous system

8.7.2.1  Rat

    When three groups of eight male albino rats were fed diets 
containing 0, 25, or 50 mg dieldrin/kg for 60 days, there was no 
effect on body weight or learning, but muscular efficiency, 
measured by pulling weights of increasing magnitude in a 250-cm 
runway, was decreased (Khaïry, 1960).  This finding is in agreement 
with the results of a study on nerve muscle (gastrocnemius) 
preparations of pre-treated rats (Ibrahim, 1964). 

8.7.2.2  Dog

    Groups of five dogs of each sex, given daily oral doses of 
dieldrin (0.05 mg/kg body weight) by capsule for 2 years, did not 
show any changes in behaviour or EEG recordings compared with 
controls (Walker et al., 1969b). 

8.7.2.3  Monkey

    When groups of three or four adult male squirrel monkeys were 
given daily oral doses of 0, 0.01, or 0.1 mg dieldrin/kg body 
weight for 54 days, learning ability was impaired and changes (high 
amplitude slow waves) in the EEG occurred in both test groups (Van 
Gelder & Cunningham, 1975). 

8.7.3.  Weight loss and stress

    It is known that in birds, and perhaps in some small mammals, 
dieldrin intoxication may be induced by starvation, weight loss, 
and stress in animals having a previously harmless body burden of 
dieldrin.  Concern is sometimes expressed that, by analogy to these 
observations, a similar course of events might occur in human 
beings.  Therefore, this phenomenon was studied in rats as well as 
in human beings (for human beings see section 9.1.3.2). 

8.7.3.1  Rat

    In studies by Treon & Cleveland (1955), rats previously fed 
diets containing aldrin or dieldrin at levels of 5, 10, or 15 mg/kg 
diet for 7 - 18 months were starved.  The complete withdrawal of 
food did not result in the release of aldrin or dieldrin from the 
adipose tissue stores to an extent sufficient to induce symptoms of 
intoxication of any type. 

    When Osborne-Mendel rats fed 7.5 mg aldrin/kg diet for 4 weeks 
were subsequently starved for 6 days with free access to water, 
there was a marked loss of body weight and fat and a decrease in 
the liver/body weight ratio.  The total body burden of dieldrin 
decreased during starvation regardless of age, sex, or the previous 
level of exposure.  The total quantity of dieldrin in the liver 
decreased in all rats.  In females, particularly older females, the 
concentration of dieldrin in abdominal fat increased, whereas in 
all males, the level in fat decreased.  The concentration of 
dieldrin in the blood was not increased.  Young weanling rats 
reacted similarly (Deichmann et al., 1972). 

8.7.4.  Immunosuppressive action

    Loose et al. (1981) found that macrophages from mice fed 50 mg 
dieldrin/kg diet had a marked impairment in antigen processing.  
The effect was statistically significant in Kupffer cells at 50 
mg/kg diet, in alveolar and splenic macrophages at 0.5, 5 and 50 
mg/kg diet, and in peritoneal macrophages at 5 and 50 mg/kg diet. 
There was an impairment of  in vivo phagocytic clearance in mice 
receiving 5 or 50 mg/kg diet for 8 weeks but not at 0.5 mg/kg diet. 
This was related to a decrease in serum fibronectin.  Tumour cell 
killing after challenge with EL-4, P388, or mKSA tumour cells was 
significantly impaired in mice fed either 1 or 5 mg dieldrin/kg 
diet.  The mean survival time after challenge with EL-4 was reduced 
by 3 weeks, and with the P388 or mKSA tumour cells impairment was 
observed after 3 or 18 weeks, respectively.  There was no 

alteration in the oxygen uptake by isolated macrophages either at 
rest or during phagocytosis, and no effect on phagocytic activity 
or capacity or on chemotaxis  in vitro was observed. 

    Loose (1982) found that dieldrin caused immunosuppression in 
mice.  Levels of 1 or 5 mg dieldrin/kg diet were fed to BALB/c mice 
for 3.5 or 10 weeks, and the mice were challenged intradermally 
with  Leischmania tropica.  Dieldrin acted synergistically on 
lethality in a dose- and time-related manner, indicating an effect 
on host mechanisms.  It also resulted in decreased antibody 
formation to PVP, a T-independent antigen (direct splenic plague 
assay).  The mitogenic response of cultured T-cells to 
phytohaemagglutinin (PHA) in dosed mice was depressed.  Mitomycin C 
and anti-Thy-1 abolished the mitogenic response.  When splenic 
T-cells from treated mice were mixed with T-cells from control 
mice, there was inhibition of PHA mitogenesis.  The data indicated 
an active cell-mediated suppressor.  A soluble macrophage factor 
from the hepatic Kupffer cells (but not from alveolar or peritoneal 
macrophages) suppressed the T-cell response to PHA.  It was 
concluded that administration of 5 mg dieldrin/kg diet to mice for 
10 weeks caused a profound impairment of macrophage antigen 
processing. 

8.8.  Toxicity of Photodieldrin and Major Metabolites

    The relevance of photodieldrin lies in the fact that it has 
metabolites identical to those of dieldrin and is quantitatively 
and qualitatively similar in toxicity. 

8.8.1.  Photodieldrin

    The photodecomposition of deposits of dieldrin on leaves and 
grass has been reported (Roburn, 1963), and the physical and 
chemical properties and structure of this decomposition product 
have been determined (Robinson et al., 1966b; Rosen et al., 1966). 
It appears to be the pentacyclo isomer of dieldrin (hexacyclo 
isomer by the alternative nomenclature used by Rosen et al. 
(1966)).  Photodieldrin residues were less than the limits of 
detection in most of the food samples analysed (Robinson et al., 
1966a). 

8.8.1.1  Acute toxicity

    Photodieldrin is more acutely toxic than dieldrin for mice, 
rats, and guinea-pigs (Table 42).  The toxicity for dogs is about 
equal to that of dieldrin.  Dieldrin-like convulsions have been 
observed in all species given photodieldrin. 

8.8.1.2  Short-term toxicity

    (a)   Mouse

    When groups of five male and five female Carworth Farm No. 1 
mice were fed 1, 3, or 10 mg photodieldrin/kg diet for 1 month, all 
animals fed 10 mg/kg and two animals fed 3 mg/kg died.  No changes 
were observed at necropsy (Brown et al., 1967). 

Table 42.  Oral LD50 values for photodieldrin
-------------------------------------------------------------------
Species       Vehicle    LD50                     Reference
                         Photodieldrin  Dieldrin
                         (mg/kg body weight)
-------------------------------------------------------------------
Mouse         dimethyl-  6.8            77.3      Brown et al.
              sulfoxide                           (1967)

Rat           dimethyl-  9.6            46.8      Brown et al.
              sulfoxide                           (1967)

Guinea-pig    dimethyl-  2.3-3.9        18-30     Brown et al.
              sulfoxide                           (1967)

Dog (male)    gelatin    120-160        120       Brown et al.
              capsule                             (1967)

Dog (female)  gelatin    80-120         80-100    Brown et al.
              capsule                             (1967)
-------------------------------------------------------------------
                            
    (b)   Rat

    Groups of five male and five female Carworth Farm E rats were 
fed 3 or 10 mg photodieldrin/kg diet for one month without apparent 
ill effects (Brown et al., 1967). 

    In studies by Walton et al. (1971), groups of 28 male and 
28 female Charles River rats were fed 0, 1, 5, or 25 mg 
photodieldrin/kg diet for 3 months.  A similar study was carried 
out concurrently with dieldrin.  The concentrations of 
photodieldrin given in the diet were lowered from 25 to 12.5 mg/kg 
diet within the first week of the study because of high mortality. 
At the end of 3 months, no significant differences were found in 
growth or food intake, and no gross evidence of toxicity was 
observed.  Liver/body weight ratios were increased at 12.5 mg/kg 
diet.  Increases in the activity or concentration of liver mixed-
function oxidase and microsomal cytochrome P-450 at 5 and 12.5 
mg/kg diet indicated the occurrence of a dose-dependent enzyme 
induction.  The total protein content of the liver was not 
affected.  The short-term toxicities of photodieldrin and dieldrin 
appeared to be similar. 

    Walker et al. (1971) fed groups of 12 Carworth Farm E rats of 
each sex diets containing 0.1, 1, 10, or 30 mg photodieldrin/kg 
diet for 3 months.  The control group consisted of 24 male and 24 
female rats.  Six females given 30 mg/kg and two females given 10 
mg/kg died.  The animals in these groups that survived were 
irritable and showed tremors when handled.  Growth was reduced, 
increases in serum urea and glutamic pyruvic transaminase (SGPT) 
activity were seen in females fed 30 mg/kg, and the liver/body 
weight ratio was increased in this group.  In the groups fed 10 or 
30 mg/kg, kidney/body weight ratio was increased in males.  At 
autopsy, no gross lesions were seen.  Some of the animals fed 10 or 

30 mg/kg showed CHIRL and centrilobular fatty changes in the liver. 
Eosinophilic droplets were seen in the cytoplasm of the proximal 
convoluted tubules and in the lumen of affected tubules in the 
kidneys of males fed 10 or 30 mg/kg.  No evidence of nephron damage 
was found.  No effects were observed in the animals dosed with 1 
mg/kg. 

    (c)   Dog

    In a study by Walker et al. (1971), groups of four male and 
four female beagle dogs received photodieldrin in olive oil by 
capsule (daily oral doses of 0.005, 0.05, or 0.2 mg/kg body weight) 
for 3 months.  A control group of six males and six females 
received olive oil in gelatine capsules.  The health, behaviour, 
body weight, and haematology were unaffected.  In the 0.2 mg/kg 
males, increases occurred in the plasma alkaline phosphatase and 
SGPT activities, and, after 13 weeks, their serum protein levels 
were slightly reduced.  Increases in the liver/body weight ratios 
occurred in the 0.2 mg/kg animals and the 0.05 mg/kg females.  At 
autopsy, no pathological changes associated with photodieldrin were 
observed.  No effects were observed at 0.005 mg/kg body weight. 

8.8.1.3  Long-term toxicity

    (a)   Mouse

    In a study on the long-term toxicity of photodieldrin, groups 
of 50 B6C3F1 mice of each sex were fed diets containing 0.32 or 
0.64 mg/kg for 80 weeks.  After 80 weeks, the animals were fed a 
control diet for 12 or 13 weeks.  Concurrent control groups 
consisted of 10 untreated mice of each sex.  Pooled controls, used 
for statistical evaluation, consisted of the concurrent controls 
plus 60 male and female mice from similarly performed bioassays 
with six other test chemicals.  All surviving mice were killed at 
93 weeks.  Mean body weights and mortality were not affected by 
treatment, but convulsions and hyperactivity were noted in treated 
male mice.  No statistically significant increase in tumour 
incidence was found (NCI, 1977). 

    (b)   Rat

    In similar studies to those on mice, groups of 50 Osborne-
Mendel rats of each sex were given 5 or 10 mg photodieldrin/kg diet 
for 80 weeks.  After 80 weeks, the animals were fed a control diet 
until sacrifice at 111 - 112 weeks.  Because of neurotoxicity, the 
doses in the females were reduced after 30 weeks, so that the time-
weighted average doses were 3.4 or 7.5 mg/kg diet for the females. 
Concurrent control groups consisted of 10 rats of each sex.  Pooled 
controls, used for statistical evaluation, consisted of the 
concurrent controls combined with 65 rats of each sex from similarly
performed bioassays with six other chemicals.  All surviving animals
were killed at 111 - 112 weeks.  Mean body weights and mortality
were not affected by treatment, but convulsions and hyperactivity
occurred in treated male and female rats.  Photodieldrin was not
carcinogenic in this study (NCI, 1977). 

8.8.1.4  Reproduction, embryotoxicity, and teratogenicity 

    (a)   Mouse

    Chernoff et al. (1975) fed groups of pregnant CD-1 mice (16 - 
20 per group) photodieldrin in peanut oil (daily oral doses of 0, 
0.15, 0.3, or 0.6 mg/kg body weight) from day 7 to day 16 of 
gestation.  At a dose of 0.6 mg/kg, one animal died.  Liver/body 
weight ratios were increased in a dose-related manner, but no 
significant differences in fetal mortality, litter weight, 
percentage of supernumerary ribs, or sternal or caudal ossification 
centres were observed at any of the doses used.  Photodieldrin was 
not teratogenic or fetotoxic in CD-1 mice at doses up to and 
including 0.6 mg/kg body weight. 

    (b)   Rat

    In a study by Chernoff et al. (1975), groups of 24 - 27 
pregnant CD rats were given daily oral doses of photodieldrin in 
peanut oil (0, 015, 0.3 or 0.6 mg/kg) on days 7 - 16 of gestation.
Some maternal mortality (5 out of 24 animals) occurred in the 
0.6-mg/kg group.  No significant differences in liver/body weight 
ratios, fetal mortality, weight of the pups, or occurrence of 
anomalies in litters of treated animals, compared with the 
controls, were noted.  No evidence of teratogenicity in CD rats was 
observed at doses of photodieldrin up to and including 0.6 mg/kg 
per day. 

8.8.1.5  Appraisal

    The acute oral toxicity of photodieldrin to rodents is greater 
than that of dieldrin.  In short-term toxicity and teratogenicity 
studies, no major differences between the two compounds were found. 
Photodieldrin did not induce tumours in mice and rats.  The 
accumulation of photodieldrin in the adipose tissue of experimental 
animals was less than that of dieldrin (section 6.2.3). 

8.8.2.  Major metabolites of dieldrin

8.8.2.1  Acute toxicity

    The acute oral toxicity of the major metabolites of dieldrin is 
far less than that of dieldrin itself (Table 43). 

8.8.2.2  Short-term toxicity

    In a study by Granville et al. (1973), groups of 12 male and 12 
female rats (control group of 24 males and 24 females) were fed 
diets containing aldrin dicarboxylic acid (0, 0.1, 1, 10, 100, or 
1000 mg/kg diet) for 13 weeks.  No adverse effects attributable to 
the dosing were observed in general health, behaviour, body weight, 
clinical chemical and haematological values, organ weights, or on 
pathological examination of the viscera. 

Table 43.  Oral LD50 values for metabolites of aldrin and dieldrin 
in mice
-------------------------------------------------------------------
Compound                      LD50                  Reference
                              (mg/kg body weight)
-------------------------------------------------------------------
 trans-6,7-dihydroxy-dihydro-  1250                  Korte & Arent
aldrin                                              (1965)

9-hydroxy-dieldrin            > 400                 Baldwin et al.
                                                    (1970)

hexachlorohexahydromethano-   > 850                 Baldwin et al.
indenedicarboxylic acid                             (1972)
(aldrin dicarboxylic acid)
-------------------------------------------------------------------

8.9.  Mechanisms of Toxicity; Mode of Action

    Like most chemicals, aldrin and dieldrin do not have a single 
mechanism of toxicity.  The main target organs of these chemicals 
are the central nervous system and the liver. 

8.9.1.  Central nervous system

    Intoxication following acute or long-term overexposure is 
characterized by involuntary muscle movements and epileptiform 
convulsions.  Survivors, after a short period of residual signs and 
symptoms, recover completely (Hoogendam et al., 1962; Avar & 
Czegledi-Janko, 1970; Jager, 1970).  In rare cases, a residual 
brain injury has been reported, but this has been found to be due 
to the convulsive state or prolonged cerebral anaemia rather than 
to the dieldrin  per se.  Apparently, a still unidentified receptor 
site in the central nervous system is reversibly occupied, and when 
this occupation exceeds a certain degree, myoclonics and 
convulsions occur (Van Genderen, 1979).   In vitro, the dieldrin 
metabolite aldrin transdiol appears to be more potent in this 
respect that is dieldrin itself (Van den Bercken, 1972; Van den 
Bercken & Narahashi, 1974).  However, in cats, the aldrin transdiol 
appeared to be inactive (Joy, 1977).  The mechanism of action seems 
to be a presynaptic inhibition as well as an increased release of 
an unidentified transmitter (Akkermans, 1974; Akkermans et al., 
1975; Joy, 1976). 

    Joy (1982) suggested that dieldrin acts by intensifying 
synaptic activity through a presynaptic locus of action and 
possibly a post-synaptic action as well.  Neurons having a large 
number of synapses will be affected most.  There does not appear 
to be any selective action on a particular neurotransmitter or 
neurotransmitter system.  The modification of behaviour is dose 
dependent and performance in complex behavioural tasks is readily 
disrupted. 

    Aldrin and dieldrin and other cyclodiens inhibit the gamma 
amino butyric acid (GABA)-induced chloride ion uptake into skeletal 
muscles and the binding of tritiated dihydropicrotoxinin (anion 
channel probe) to the membrane.  This results in central nervous 
system excitation and convulsions due to the blocking of GABA 
transmitters (Lawrence & Casida, 1984; Abalis et al., 1985). 

8.9.2.  Liver

    The mode of action of aldrin and dieldrin on the liver involves 
an increase in the activity of microsomal biotransformation 
enzymes, particularly of the monooxygenase system with cytochrome 
P-450.  This induction of liver microsomal enzymes is reversible 
and, if exceeding a certain degree, appears to be associated with 
the occurrence of CHIRL and hepatomegaly in the liver of rodents 
(sections 6.3 and 8.2) (Jager, 1970; Wright et al., 1972, 1977, 
1978). 

9.  EFFECTS ON HUMAN BEINGS

9.1.  General Population Exposure

9.1.1.  Acute toxicity - poisoning incidents

    When a toxic dose of aldrin or dieldrin has been ingested or 
has contaminated the skin, effects appear from 20 min to 24 h 
afterwards.  Signs and symptoms may include headache, dizziness, 
nausea, general malaise, and vomiting, followed by muscle 
twitchings, myoclonic jerks, and convulsions.  Death may result 
from cerebral anoxaemia (Nelson, 1953; Princi, 1954; Hayes, 1957, 
1963; Hoogendam et al., 1962, 1965; Kazantzis et al., 1964; 
Schafer, 1968; Jager, 1970). 

    The duration of the interval between oral intake or skin 
contact and onset of symptoms (as well as the clinical picture) 
depends on the dose absorbed.  With massive overexposure, 
convulsions may occur even in the absence of any premonitory 
symptoms. 

    Initially, there is no fever or change in blood count or in 
blood chemistry.  However, later the temperature may be elevated 
and leukocytosis may occur.  Terminal hyperthermia has been 
reported.  Abnormal EEG patterns showing spike and dome complexes 
and multiple spike and wave discharges, or in less serious 
intoxications, bilateral synchronous theta discharges may be seen. 
The diagnosis needs to be confirmed by determining the insecticide 
concentration in the blood. 

    The onset of clinical intoxication is practically always acute 
also in those cases where the accumulation of dieldrin in the 
target tissues has taken place during a much longer period.  The 
latter cases are, therefore, usually indistinguishable from acute 
intoxication.  Survivors almost always recover completely (Jager, 
1970; Hayes, 1982). 

    Estimates of dosages in anecdotal cases suggest that fatalities 
have occurred with ingestion of approximately 10 mg dieldrin/kg 
body weight, (Hayes, 1982) but Hodge et al. (1967) estimate the 
lethal dose of aldrin and/or dieldrin for the adult man to be about 
5 g. 

    Cases of poisoning have occurred by ingestion of formulated 
material, mostly in children by mistake (for instance when aldrin 
is used in granules as bait to control ants) or by adults with 
suicidal intent.  Several cases of poisoning have been the result 
of ingesting food contaminated with aldrin or dieldrin during 
storage or transport. 

    Van Raalte (1965) surveyed the world literature for all cases 
of fatal poisoning by aldrin and dieldrin, and found 13 cases:  
four suicides, three due to accidental ingestion, five due to 
accidental contamination, and only one (a spray operative) due to 

occupational exposure.  No cases of fatal poisoning have been 
reported during the course of aldrin and dieldrin manufacture and 
formulation. 

    A non-exhaustive overview of published poisoning cases is given 
in Table 44.  A more complete review is provided by Hayes (1982). 
Table 44.  Case reports on accidental and suicidal acute aldrin and dieldrin poisoning
------------------------------------------------------------------------------------------
Number  Fatal  Causative agent       Circumstances                   Reference
of      cases
cases
------------------------------------------------------------------------------------------
1       -      aldrin emulsifiable   attempted suicide               Spiotta (1951)
               concentrate

53      -      aldrin and other      consumption of seed grain       WHO (1958)
               pesticides

        13     aldrin and dieldrin   review of all fatal cases from  Van Raalte (1965)
                                     literature:
                                     - 4 suicides, 3 accidental
                                       ingestion, 5 accidental 
                                       contaminations, 1 sprayer

2       1      5% dieldrin           accidental ingestion            Garrettson & Curley 
                                                                     (1969)

79                                   consumption of dieldrin-        WHO (1977)
                                     contaminated rice in Mali

1       -      dieldrin (120 mg/kg)  attempted suicide               Black (1974)

2       -      dieldrin                                              Fry (1964)

12      -      aldrin + BHC          consumption of seed grain       Gupta (1975)
------------------------------------------------------------------------------------------
9.1.2.  Effects of short- and long-term exposure - controlled human
studies

9.1.2.1  Accidental poisoning

    Twelve cases of neurotoxicity, resulting from the repeated 
consumption of wheat into which aldrin dust and gammexane (BHC) 
powder had been mixed accidentally, have occurred in India (Gupta, 
1975).  The patients consumed this wheat for 6 - 12 months before 
showing typical clinical symptoms, including convulsions. 
Electroencephalographic tracings were consistent with a diagnosis 
of organochlorine insecticide poisoning.  The patients were treated 
with phenobarbital and diazepam.  The latter was more effective in 
controlling seizures.  All patients recovered. 

    The threshold dieldrin concentration in the blood below which 
no adverse effects have been observed (and none are to be expected) 
is 105 µg/litre (see also section 9.2.1.1).  The dieldrin 
concentration in the blood of the general population, in the 
countries where this has been investigated, is well below this 
threshold level.  However, there are rare cases in which it seems 
that low concentrations of dieldrin have induced effects. 

    A rare, well investigated and well reported case of dieldrin-
induced immunohaemolytic anaemia was observed in Iowa, USA.  The 
patient had a haemolytic anaemia with a positive direct 
antiglobulin (Coombs) test and a positive Ham test in the serum. 
The serum contained anti-bodies selectively active against 
erythrocytes coated with dieldrin.  The patient improved following 
splenectomy.  Dieldrin concentrations in blood and fat were similar 
to those of the general Iowa population (Hamilton et al., 1978).  A 
similar case was reported by Muirhead et al. (1959). 

9.1.2.2  Controlled human studies

    In section 6.2.2.4, reference was made to a pharmacodynamic 
study in human volunteers.  This study had three objectives: 

    (a)  to establish the relationship between the daily intake of 
         dieldrin and its concentration in human blood and adipose
         tissue;

    (b)  to establish the blood/fat ratio in human beings; and

    (c)  to establish the relationship between the concentrations 
         of dieldrin in blood and fat and the length of exposure 
         (Hunter & Robinson, 1967, 1968; Hunter et al., 1969).

In addition, the opportunity was taken to monitor the health of the 
human subjects during and after the exposure by full clinical, 
physiological, and laboratory examinations as well as full 
electroencephalographic (EEG) studies, polygraphic recording of 
cardio-respiratory function, measurement of basal metabolic rate, 
and electroneuromyographic studies at frequent intervals to detect 
the possible occurrence of changes in physiological function.  The 
study involved 13 adult male college graduates without a history of 
recent occupational exposure to pesticides.  The subjects received 
0, 10, 50, or 211 µg dieldrin per day for 2 years.  All the men 
continued in excellent health.  Clinical, physiological, and 
laboratory findings remained essentially unchanged throughout the 
whole experimental period of 24 months and the 8 months after 
exposure.  No departures from what is regarded as normal for the 
general population were observed.  The concentration of  p,p'-DDE in 
adipose tissue and blood did not show any significant change during 
or after the study, indicating that the liver microsomal enzyme 
activity had not been induced.  Thus, the total daily intake of 
230 µg (211 µg plus intake from food) of dieldrin per person for 2 
years had no effect on health.  The concentrations of dieldrin in 
both adipose tissue and blood were shown to be proportional to the 
daily intake (section 6.2.2.4). 

9.1.3.  Tissue concentrations of dieldrin in hospitalized people

9.1.3.1  Pathological findings

    Specimens of human abdominal subcutaneous fat, obtained from 
four hospitals in Chicago were analysed for residues of dieldrin. 
Dieldrin was not present in 103 out of 221 samples analysed for 
this pesticide.  Positive samples contained 0.01 - 1.39 mg 
dieldrin/kg fat (mean value 0.14 mg/kg).  There was no correlation 
between the dieldrin concentration in adipose tissue and 
pathological findings (Hoffman et al., 1967). 

    When organochlorine pesticide concentrations were determined in 
the adipose tissue and liver of 271 hospital patients in Miami, 
USA, patients with typical alcoholic (Laennec's) cirrhosis of the 
liver had about twice the dieldrin concentration in the liver of 
that found in the normal population.  In patients with post-
necrotic cirrhosis, fatty metamorphosis of the liver, metastatic 
malignancy of the liver, or primary hepatocellular carcinoma, 
dieldrin concentrations were "normal".  Terminal cases with 
carcinomas of different organs had elevated concentrations of 
organochlorine pesticides in the fat, but no association with any 
particular neoplastic disease was found (Radomski et al., 1968). 

    In Hawaii, emaciated patients who had carcinoma and/or focal or 
generalized liver pathology were found to have "normal" (for the 
USA) concentrations of dieldrin in the liver and body fat (Casarett 
et al., 1968). 

    When concentrations of organochlorine pesticides were 
determined in specimens of liver, brain, and adipose tissue from 
autopsies of patients with cirrhotic liver disease in Vancouver 
(Canada) hospitals, the concentrations of dieldrin appeared to be 
no higher than in tissues from controls (Oloffs et al., 1974). 

    In a case-control study on 122 matched cancer patients in south 
Florida, USA, a comparison was made of dieldrin residues in the 
adipose tissue of cancer patients and controls.  The mean dieldrin 
concentration in the adipose tissue was 0.3 mg/kg fat in both 
cancer patients and controls (Davies et al., 1975). 

9.1.3.2  Influence of weight loss and stress on dieldrin 
concentrations in tissues

    It is well known that, in birds, and perhaps in some small 
mammals, dieldrin intoxication may be induced by starvation, weight 
loss, or stress in animals having a previously harmless body burden 
of dieldrin.  Concern is sometimes expressed that, by analogy to 
these observations, a similar course of events might occur in human 
beings. 

    Twenty-nine patients (14 males, 15 females) undergoing surgery 
were investigated.  The concentrations of dieldrin in the blood 
were unaffected by the catabolic responses to surgery.  In another 
study, these authors determined the concentrations of dieldrin in 

the blood of 4 women undergoing voluntary near-starvation for 
slimming purposes, which resulted in weight losses of up to 7.5 
kg/week.  There was no increase in the concentration of dieldrin in 
the blood (Hunter & Robinson, 1968). 

    No significant difference was found between the dieldrin blood 
concentrations of slimming or non-slimming mothers before and after 
delivery (Eckenhausen et al., 1981). 

    On the basis of these results and calculations, it is suggested 
that significant weight loss does not result in increased 
concentrations of dieldrin in human tissues (Van Raalte, 1965; 
Hunter & Robinson, 1968). 

9.1.4.  Exposure in treated homes

    From the data on aldrin concentrations in the air of houses 
treated for termite control (section 5.1.2), an estimate of the 
dieldrin concentration in the blood of occupants of these houses 
can be made using the mathematical formulas given by Hunter et al. 
(1969) for deriving blood concentrations from the average daily 
intake.  The average daily intake is based on an estimated average 
in-house volume of air inhaled per day (15 m3).  The dieldrin blood 
levels of home dwellers, calculated in this way, remain far below 
the blood concentration no-effect level for the general population 
(secton 9.2.1.1). 

    The blood dieldrin concentrations of 59 female residents of 
Dade County (Florida, USA), where many houses had been treated for 
termite control, were of the order of 1 µg/litre (Barquet et al., 
1981). 

    Also relevant to the health of home dwellers is the experience 
obtained in the 1950s and 1960s when tens of thousands of houses in 
more than 30 countries were sprayed with dieldrin for malaria and 
yellow fever eradication.  Although exposures were presumed to have 
been high, as a result of surface spraying inside and outside 
houses, no adverse health effects were reported in home dwellers. 
Neither were adverse effects observed in well-trained and 
medically-supervised spray operators (Soper, 1955 (Personal 
communication at the 2nd Meeting of the Industrial Council on 
Tropical Health, Boston); Fletcher et al., 1959). 

9.2.  Occupational Exposure

9.2.1.  Acute toxicity - poisoning incidents

    With the exception of poisoning cases resulting from massive 
acute overexposure, most reported cases of poisoning with aldrin 
and dieldrin in occupationally-exposed men have been the result of 
a slow build-up of the insecticide in the body, the daily intake 
exceeding the daily excretion (Jager, 1970; Hayes, 1982). 

    Based on the experience of Jager (1970), it was suggested that 
the classification of types of intoxication by Hayes (1963) be 
modified as follows: 

    Type 1:  an acute convulsive intoxication with no (or only 
minor) prodomi, resulting from one or several gross overexposures. 

    Type 2:  a greater number of smaller doses may cause an 
accumulative intoxication.  Clinically, this results in a syndrome 
of headache, dizziness, drowsiness, hyperirritability, general 
malaise, nausea, anorexia, occasional vomiting.  At times muscle 
twitchings, myoclonic jerks and convulsions may occur.  In these 
circumstances minor increases in the insecticide level in the 
blood, perhaps caused by minor fluctuations in exposure, may bring 
about a convulsive intoxication. 

    Type 3:  this is actually a combination of Types 1 and 2.  In 
this type an overexposure, in itself not significant, causes an 
acute convulsive intoxication superimposed upon a subclinical 
accumulative intoxication of Type 2. 

    These three types of intoxication are schematically illustrated 
in Fig. 3. 

    Table 45 gives a non-exhaustive overview of occupational aldrin 
and dieldrin poisonings.  Hayes (1982) contains further information 
on this subject. 

Table 45.  Published case reports on occupational aldrin and dieldrin poisoning
------------------------------------------------------------------------------------------
Number     Fatal  Acute  Causative agent   Circumstances                   Reference
of         cases  cases
cases
------------------------------------------------------------------------------------------
3          -      ?      25% aldrin dust   formulation with inadequate     Nelson (1953)
                                           safety precautions

~100       -      ?      various           spraying in malaria-            Hayes (1957, 
                                           eradication programmes          1959)

1          -      1      aldrin            gross overexposure in aldrin    Bell (1960)
                                           packer

1          1      ?      dieldrin          sprayer                         Van Raalte 
                                                                           (1965)

4          -      ?      aldrin            formulation of aldrin           Kazantzis et 
                                                                           al. (1964)

17         -      some   aldrin and        manufacturing and formulation   Hoogendam et 
                         dieldrin                                          al. (1962, 
                                                                           1965)

32 (15 in  -      some   aldrin,           manufacturing and formulation   Jager (1970)
addition                 dieldrin,  
to                       endrin, 
previous                 isobenzan
reference)
------------------------------------------------------------------------------------------
    No cases of fatal poisoning have been reported during the 
manufacture and formulation of aldrin and dieldrin (Jager, 1970). 
However, there has been one case of a spray operator being fatally 
poisoned (Van Raalte, 1965). 

    In developing countries it is, however, difficult to establish 
the actual number of poisoning cases.  Experience shows that even 
when pesticides are banned, cases may occur in areas where control 
is poor and where large quantities of pesticide are stocked.  In 
May 1987, four cases of occupational poisoning with aldrin were 
reported from an area of cocoa plantations in Bahia (Brazil).  One 
of them was fatal, while three recovered.  The fatal case had a 
dieldrin level in whole blood exceeding 600 µg/litre two days after 
poisoning (Rahde, personal communication). 

9.2.1.1  Blood levels diagnostic of aldrin/dieldrin poisoning

    Because the symptoms of aldrin/dieldrin intoxication are non-
specific, a differential diagnostic test is required to confirm 
that the symptoms, signs, and clinical course of a particular case 
are the result of aldrin or dieldrin intoxication. 

    The results of animal studies, together with those obtained 
subsequently during medical surveillance of workmen employed in the 
manufacture (or formulation) of aldrin/dieldrin, have shown that 
adverse effects induced by aldrin/dieldrin are related to the 
dieldrin blood concentration (Brown et al., 1964; Jager, 1970). 
Therefore, the determination of this concentration provides a 
specific differential diagnostic test. 

    Concentrations of dieldrin ranging from 40 to 530 µg/litre have 
been reported in the blood of people who had been poisoned 
relatively recently and who had recovered (Kazantzis et al., 1964; 
Jager, 1970; Avar & Czegledi-Janko, 1970; Siyali & Simson, 1973). 

    From the limited information available, Brown et al. (1964) 
concluded that the threshold concentration of dieldrin in the blood 
of human beings, critical for intoxication, is approximately 
150 - 200 µg/litre. 

    Dieldrin is present in the blood at very low concentrations in 
the general population of many countries throughout the world.  It 
is also found at considerably higher concentrations in the blood of 
healthy workers.  These "healthy workmen" were men between 18 and 
60 years of age who had no complaints or clinical or laboratory 
signs attributable to occupational exposure, but they were, of 
course, subject to the same ailments and diseases as are members of 
the general population (Hayes & Curley, 1968; Jager, 1970).  No 
complaints of ill health and no positive results in objective 
clinical or laboratory tests of ill health have ever been noted in 
workers whose blood contained less than 200 µg/litre.  This 
concentration may, therefore, be considered to be a no-observed-
adverse-effect level in human beings.  Higher concentrations may 
have effects.  The maximum concentration reported to be without 
complaints or clinical signs or symptoms was 430 µg/litre (Jager, 
1970). 

    Studies on animals have shown that the earliest physiological 
sign of exposure to dieldrin is an increase in the activity of 
certain liver microsomal enzymes.  No enzyme induction has ever 
been found in workers with dieldrin blood concentrations at or 
below 105 µg/litre (Jager, 1970).  (When liver enzyme induction 
test methods became available, workers with dieldrin levels in the 
blood exceeding 105 µg/litre were no longer encountered.) 

    Sometimes, dieldrin concentrations in plasma or serum, rather 
than in whole blood, have been reported.  The ratio of the dieldrin 
concentration in plasma to that in erythrocytes is approximately 
4:1 (Dale et al., 1965; Mick et al., 1972) (the conversion factor 
to calculate the concentration of dieldrin in whole blood from the 
concentration in plasma or serum is 0.66). 

    Great differences exist between the average concentrations of 
dieldrin in the blood of the general population and of 
occupationally exposed workers with or without complaints (Table 
46). 
Table 46.  Concentrations of dieldrin in whole blood of human beings (µg/litre)
-------------------------------------------------------------------------------
                    No. of
Subjects            persons   Geometric  Range      Reference
                    involved  mean
-------------------------------------------------------------------------------
General population  4592      <1        <1-16.1a   US EPA (1983)

Unexposed persons   25        0.5        0-3.3      Sandifer et al. (1981)

                    20        2.5        0.5-10     Brown et al. (1964)

Healthy workers     35        29         <10-90     Jager (1970)

                    21        120e                  Mick et al. (1972)

                    37        55         -f         Morgan & Roan (1974)

                    27        20         4.5-54     Sandifer et al. (1981)

                    89        38g        2-220      Brown et al. (1964)

Patients with       18        160g       8-280      Avar & Czegledi-Janko 
clinical symptoms                                   (1970) 
                                                    
                    4                    40-530b    Kazantzis et  al. (1964)

                    5                    130-370c   Brown et al. (1964)

                    5                    160-430d   Brown et al. (1964)

Deceased (suicide)  1                    850        Hayes (1982)
-------------------------------------------------------------------------------
a In serum.
b The low level of 40 µg/litre was found in a man with chronic nephritis, 
  complaining of headache and nausea; the occupational cause of the symptoms 
  is, therefore, doubtful.  In one other worker, a blood level of 530 µg/litre 
  was found 1 month after a mild acute episode when he was exposed to aldrin 
  again.
c Determined some time after the acute episode.
d Estimated to be the concentration at the time of the acute episode.
e Converted from plasma figures using a factor of 0.66 (see 9.2.1.1).
f Highest value 231 kg/litre.
g Average.
    Among 13 adolescent patients with colon-rectal adenocarcinomas, 
who had lived in rural areas of Mississippi, USA, where pesticides 
are widely sprayed, dieldrin blood levels were no higher than those 
in controls (Caldwell et al., 1981). 

9.2.1.2  Electroencephalography

    Changes in the electroencephalogram (EEG) are sometimes of 
practical importance for confirming a diagnosis of aldrin/dieldrin 
intoxication (Spiotta, 1951; Winthrop & Felice, 1957; Hoogendam et 
al., 1962, 1965; Kazantzis, 1964; Avar & Czegledi-Janko, 1970; 
Jager, 1970).  These EEG changes were first used as a practical 
tool for monitoring workers and determining when they should 
discontinue exposure and when they could be allowed to resume work 
with aldrin/dieldrin.  Characteristic changes - which, however, are 
not pathognomonic for aldrin/dieldrin poisoning - include bilateral 
synchronous spikes, spike and wave complexes, and slow theta waves, 
thought to be possibly associated with brain stem stimulation 
(Hoogendam et al., 1962, 1965).  The interesting parallelism 
between the rate of diminution of the EEG changes and the rate of 
decrease in the dieldrin blood concentration was also reported in 
the case of an accidentally poisoned child (Garrettson & Curley, 
1969). 

    Nowadays, analysis for dieldrin in the blood has replaced EEG 
examination as the method of choice for monitoring exposed workers 
(Jager, 1970). 

9.2.2.  Effects of short- and long-term exposure

    Occupational exposure occurred in the 1950s and early 1960s 
among sprayers in malaria and yellow fever control programmes. 
These men sprayed dieldrin inside houses day after day in prolonged 
cycles without appreciable intervals of non-exposure.  Quite often, 
precautions and supervision were less than would be required today. 
At the time, methods for the determination of blood concentrations 
had not been developed.  A significant percentage of these sprayers 
became sick after having worked for as little as 2 days or as much 
as 2 years (Hayes, 1957, 1959; Patel & Rao, 1958; Zavon & Hamman, 
1961).  According to communications by the Pan-American Sanitary 
Bureau (Soper, 1955a), it appeared that no clinical symptoms were 
observed in well-executed, well-supervised malaria and yellow fever 
control programmes. 
                                                          
    In a study carried out in East Africa, where workers were 
spraying dieldrin 6 h/day for 180 days per year (with an interim of 
2 months between spraying cycles) no clinical symptoms were seen. 
The potential average dermal exposure of spray operators who 
observed the protective measures laid down was 1.8 mg/kg body 
weight per day (Fletcher et al., 1959). 

    Long et al. (1969) studied 159 farmers in Iowa, USA.  Extensive 
clinical and laboratory examinations of 33 pesticide users among 
these farmers did not reveal evidence of any disease that could be 
attributed to the use of pesticides, neither was the dieldrin blood 
concentration correlatable with any parameter examined. 

-------------------------------------------------------------------
a Personal communication at the 2nd Meeting of the Industrial 
  Council on Tropical Health, Boston.

    The dieldrin blood concentrations in 8 locust-control workers 
in Ethiopia were measured on two occasions and were found to range 
between 0 and 9 µg/litre (MacCuaig, 1976). 

    Wolfe et al. (1963) studied the hazards from spraying orchards 
with dieldrin in the US Pacific Northwest.  Potential contamination 
of the skin and respiratory exposure were measured.  From the 
results, potential skin and respiratory exposures were calculated 
to amount to 14.2 and 0.25 mg/h, respectively. 

    Princi & Spurbeck (1951) studied a group of workers exposed 
to chlordane, aldrin, and dieldrin for several years in a 
manufacturing and formulating plant.  The atmospheric 
concentrations of aldrin were reported to be as high as 2.6 mg/m3. 
Physical examinations and chest-röntgenograms did not reveal 
respiratory anomalies. 

    A study was carried out on 71 men employed in the manufacture 
and formulation of aldrin, dieldrin, endrin, and some other non-
related pesticides.  Twenty-eight of these workers each contributed 
a sample of blood and a sample of fat on the same day.  The average 
concentration of dieldrin in fat (6.12 ± 1.24 mg/kg) was 247 times 
greater than the mean plasma concentration (0.025 ± 0.006 
mg/litre).  There was no relation between the amount of dieldrin in 
the samples and the use of sick leave (Hayes & Curley, 1968). 
                                            
    In another study, 68 pesticide workers (including pest control 
operators) and 29 unexposed controls were examined quarterly over a 
period of four years.  Determinations of serum pesticide 
concentrations and enzyme activity, blood chemistry, haematology, 
and urinalysis were carried out.  The mean serum dieldrin 
concentration was 3.6 ± 6.3 µg/litre (1.1 ± 1.6 µg/litre in the 
controls).  There was no difference between the exposed workers and 
the controls in the incidence of disease or disability (Warnick & 
Carter, 1972). 

    In a pesticide formulation plant, the blood of 21 employees was 
examined at the conclusion of a 5-week period during which 900 kg 
of technical aldrin was formulated.  The mean dieldrin 
concentration in plasma was 11 and 182.5 µg/litre for herbicide 
formulators and aldrin formulators, with a maximum of 317 µg/litre 
in the latter case.  No mention was made of any intoxications (Mick 
et al., 1972). 

    In a group of 42 occupationally exposed pesticide workers with 
a dieldrin serum concentration 5 times as high as that in a group 
of 23 controls, no indication of disturbed renal- or adrenocortical 
function was found (Morgan & Roan, 1969, 1973). 

    A study was carried out in California, USA, where aldrin (EC as 
a 0.5% solution) at 480 g/litre was applied as a termiticide to 
typical slab and crawl space type houses.  Personal air samples, 
samples of blood, and samples of pads on clothes and gloves were 
taken to monitor the exposure of the pest-control operators.  The 
personal air samples during application contained less than 0.3 

µg/m3 aldrin for the slab houses and 30 - 75 µg/m3 for the crawl 
space houses.  The total work day (9 - 18 h) time-weighted average 
concentration of aldrin in air was 6 - 17 µg/m3.  This is far below 
the threshold limit value (TLV) for aldrin established by the 
American Conference of Governmental Industrial Hygienists (ACGIH, 
1986) of 250 µg/m3.  Data from dermal exposure samples showed large 
variation.  However, the maximum calculated percentage of the toxic 
dose per h, based on the acute percutaneous toxicity (rat LD50) of 
the formulation, was less than 0.01%.  The concentration of aldrin 
and dieldrin in the blood of the operators was below the limit of 
detection (less than 1 µg/litre) (Marlow et al., 1982). 

    A case-control study, carried out on 27 pesticide workers 
(4 formulators and 23 pest-control operators) with elevated blood 
concentrations of dieldrin, revealed a mean blood concentration of 
19.59 µg/litre (range:  4.45 - 54 µg/litre).  In an extensive 
clinical examination, including physical examination, comprehensive 
neurological examinations, laboratory tests, and physiological and 
psychomotor testing, no important differences were found compared 
with results in a control group of 25 people with a mean dieldrin 
blood concentration of 0.48 µg/litre (range of 0 - 3.34 µg/litre) 
(Sandifer et al., 1981). 

9.2.3.  Epidemiological studies

    An extensive study on workers in an aldrin/dieldrin 
manufacturing plant has been in progress since the plant began 
operations in the 1950s.  The results from the first 15 years of 
this epidemiological study were reported in 1970 (Jager, 1970). 
From a total of more than 800 exposed workers, all those exposed 
for more than 4 years (233 men) or those who had experienced an 
intoxication (20 men) underwent extensive physical, neurological, 
haematological, and other laboratory examinations.  Clinical 
chemical determinations, including SGOT, SGPT, LDH, alkaline 
phosphatase, total serum protein, and serum protein spectrum, were 
made every 3 months and remained within normal limits.  A no-effect 
level in this group of workers, including those who had previously 
suffered intoxications, was established at a dieldrin blood 
concentration of 200 µg/litre.  This level corresponds to a total 
equivalent daily oral intake of 33 µg/kg body weight or a total 
daily intake of 2300 µg/person per day (Hunter & Robinson, 1967). 

    In experimental animals, the earliest, reversible effect of 
dieldrin is the induction of liver microsomal enzyme systems 
(Wright et al., 1977, 1978).  This finding led to an investigation 
of a group of 10 workers.  At the time, due to further improvements 
in the industrial hygiene of the above-mentioned plant, the 
geometric mean concentration of dieldrin found in the blood of 
workers was 105 µg/litre.  As criteria of enzyme induction 
measurements were made of the blood levels of  p,p'-DDE, the urinary 
ratio of 6-beta-hydroxycortisole and 17-hydroxycorticosteroids, and 
the urinary excretion of D-glucaric acid.  No difference in these 
values was found between the 10 exposed workers and a control 
group.  On the basis of these data, the no-effect level was 105 µg 
dieldrin/litre blood, equivalent to an oral daily intake of 17.4 

µg/kg body weight per day (or 1220 µg/person per day) (Jager, 1970; 
Hunter et al., 1969; Hunter & Robinson, 1967; Versteeg & Jager, 
1973). 

    Further results from this long-term survey of an industrial 
population were subsequently published, based on a study of 1000 
workers.  Because not all of the workers had severe and/or 
prolonged exposure, smaller groups with an exposure meaningful 
enough for carcinogenicity evaluation were included.  One group 
consisted of 166 men (including workers who were still exposed and 
workers who had left the company), with a mean exposure time of 
16.9 years (range 4 - 19 years), who had been under observation for 
more than 15 years (mean observation period 17 years; range, 
15 - 20 years).  A sub-group comprised 69 men with a mean exposure 
time of 14.9 years (range 10 - 19 years) and a mean observation 
period of 17.2 years.  Among the group of 166 workers, 51 were more 
than 50 years old.  One man with only 5 years of comparatively mild 
exposure died because of a gastric carcinoma.  A lymphosarcoma 
occurred in a man with 7 years of very mild exposure.  Both 
incidences occurred before 1964.  No new cases were noted in the 
final 11 years of study, and no undue mortality from other causes 
that could have masked a higher cancer incidence was observed 
(Versteeg & Jager, 1973; Van Raalte, 1977). 

    In a follow-up study on the original group of 233 men with more 
than 4 years of exposure and an observation period ranging from 4 
to 29 years (mean, 24 years), there were no indications of a 
specific carcinogenic activity.  Total observed mortality was 25 
deaths versus 38 expected.  Of nine cancer deaths, three were 
caused by lung cancer, while the remaining six were each of a 
different nature.  No primary liver tumours were observed (Ribbens, 
1985). 

    In a study by Morgan & Roan (1974), 28 pesticide formulators 
and applicators, plus a separate group of 43 termite-control 
workers, with occupational exposures of 5 - 22 years were examined, 
together with 56 controls.  The highest levels of dieldrin among 
these 71 workers were found in a group of 37 men who had a mean 
serum dieldrin concentration of 84 µg/litre (equivalent to about 
55 µg/litre whole blood).  There were no signs of liver cell injury 
and the serum enzyme activities SGOT, SGPT, LDH, alkaline 
phosphatase and creatine phosphokinase (CPK) were within normal 
limits.  There was no indication of drug-metabolizing enzyme 
induction and urinary excretion of D-glucaric acid was not 
different from that in a control group. 

    A study comparing liver cancer deaths in the USA and the 
"domestic disappearance" of organochlorine pesticides, revealed 
that, in 1962, 18 and 10 years after the introduction of DDT and 
aldrin/dieldrin, respectively (when an increase in primary liver 
cancer due to the organochlorines would be manifest), the cases of 
primary liver cancer as a percentage of the total number of liver 
cancer deaths began a gradual and steady decline (from 61.3% in 
1962 to 56.9% in 1972).  The death rate (per 100 000 per year) of 
primary liver cancer for this period declined from 3.46 to 3.18 
(Deichmann & MacDonald, 1977). 

    An epidemiological mortality study in a plant manufacturing 
aldrin, dieldrin, and endrin was carried out on a cohort of 1155 
workers who had been employed for at least 6 months between 1946 
and 1976 (almost 25 000 man-years of observation).  The mortality 
due to all malignant neoplasms was 31, lower than expected 
(standardized mortality ratio (SMR) 82).  The total mortality from 
all causes was 173 (SMR 84).  The only disease with an SMR above 
100 (SMR 212) was "non-malignant respiratory system disease", 
specifically pneumonia.  There was a slight excess of oesophagus 
and rectum cancer (two and three cases observed with an SMR of 235 
and 242, respectively), liver cancer (two cases observed versus 
0.57 expected), and cancer of the lymphatic and haematopoietic 
system (six cases observed versus 4.07 expected).  However, there 
was a deficit of cancer of other sites.  The authors concluded that 
"the study has not identified a specific cancer risk associated 
with employment at this manufacturing plant, but several causes 
should be examined further" (Ditraglia et al., 1981). 

    In a 1981 health survey, a total of 567 serum samples from 1811 
Florida citrus workers were collected during the spraying and the 
harvest season and were compared with the national ("Hanes") 
sample.  There were no differences in serum dieldrin levels; the 
mean in both groups being 1.8 - 1.9 µg/litre serum (Griffith & 
Duncan, 1985). 

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

10.1.  Evaluation of Human Health Risks

    Aldrin and dieldrin, organochlorine pesticides, were used 
throughout the world from 1950 until the early 1970s as 
insecticides in agriculture and as a seed treatment, for the 
control of soil pests and other types of insects (e.g., termites, 
grasshoppers, and textile pests), and for the control of tsetse 
flies and other disease vectors.  The compounds act as contact and 
stomach poisons in the insects.  Since the early 1970s, both 
compounds have been restricted or banned from use in several 
countries, especially in agriculture.  Nevertheless, use continues 
in other countries for termite control. 

    Both compounds are practically insoluble in water and 
moderately to highly soluble in many organic solvents.  The vapour 
pressure is low. 

    Dairy and meat products, fish, oils and fats, and certain 
vegetables such as root vegetables often contain dieldrin.  Maximum 
residue limits recommended by the FAO/WHO Joint Meeting on 
Pesticide Residues range from 0.02 to 0.2 mg/kg product.  Recent 
measurements have shown that actual levels are lower, and this has 
been confirmed by total diet studies.  Since the use of these two 
compounds has been restricted, a steady but slow decrease in 
residue levels in the different food commodities has taken place. 

    The intake by human beings of low concentrations in the daily 
diet has resulted in dieldrin being present in adipose tissue and 
in some other tissues and organs.  Global surveys have shown that 
mean values range from 0.1 to 0.4 mg/kg adipose tissue.  Since the 
early 1970s, this concentration has slowly decreased. 

    Transplacental exposure of the fetus occurs, with the result 
that the fatty tissues of the fetus also contain dieldrin, but at 
concentrations 10 - 50% of those of the mother.  There seems to be 
an equilibrium between levels in the fetus and those in the mother. 
Dieldrin is also excreted with the milk.  Inhabitants of houses 
that have been treated for termite control may be exposed by 
inhalation.  Concentrations in the air found after indoor treatment 
may range from 0.01 to 7 µg/m3, depending on the type of 
applications, concentration used, type of ventilation, and time of 
sampling.  Under these conditions food may also be contaminated by 
direct contact or by sorption from the atmosphere. 

    Metabolism takes place mainly in the liver where aldrin is 
readily transformed to dieldrin.  Dieldrin is degraded at a slower 
rate to hydrophilic metabolites, which are then excreted via the 
bile and urine.  The structures of these metabolites have been 
established.  In all species examined, including human beings, it 
has been shown that there is a steady state of aldrin/dieldrin 
storage corresponding to the level of intake and a linear 
relationship between the log of intake and storage has been 

demonstrated.  The concentration of dieldrin in body tissues 
decreases exponentially on termination of exposure to the 
compounds. 

    The acute oral toxicity of aldrin and dieldrin for mammals is 
high, while the dermal toxicity is moderate.  Dermal sensitization 
has not been found.  Effects observed in acute, short-term and 
long-term studies involve the central nervous system.  The liver is 
also a target organ.  In the liver of mice and rats, changes known 
as "chlorinated hydrocarbon insecticide rodent liver" are found. 

    Aldrin and dieldrin do not appear to cause teratogenic effects 
at doses below those causing maternal toxicity and fetotoxicity. 
Male or female reproductive toxicity has not been reported. 

    Numerous  in vitro and  in vivo mutagenicity studies have 
demonstrated that neither aldrin nor dieldrin have mutagenic 
potential. 

    In long-term studies, aldrin and dieldrin induced benign and 
malignant liver tumours in the mouse.  However, no increased 
incidence of liver tumours or other tumours were found in rats and 
hamsters. 

    IARC (1987) has stated that there is inadequate evidence of 
carcinogenicity in human beings and limited evidence of 
carcinogenicity in experimental animals.  Both aldrin and dieldrin 
have been classified in Group 3:  the chemicals cannot be 
classified as to their carcinogenicity in human beings. 

    On the basis of available short-term and long-term toxicity 
data, the overall no-observed-adverse-effect level in the rat is 
0.5 mg dieldrin/kg diet, equivalent to 0.025 mg/kg body weight.  In 
the dog, the lowest no-observed-adverse-effect level found was 0.04 
mg/kg body weight.  The Joint Meeting on Pesticide Residues (JMPR) 
established an Acceptable Daily Intake (ADI) of 0.1 µg/kg body 
weight in 1966 and 1977 based on the conclusion that aldrin and 
dieldrin were not human carcinogens. 

    Aldrin and dieldrin are highly toxic to human beings.  Both 
accidental and occupational cases of poisoning have occurred but 
reported fatalities have been rare.  Survivors of acute or subacute 
intoxications recovered completely.  Adverse effects are related to 
the dieldrin blood concentration, the determination of which 
provides a specific diagnostic test for aldrin/dieldrin exposure. 
At a dieldrin blood concentration below 105 µg/litre, no adverse 
effects can be expected.  This level is considered a threshold no-
observed-adverse-effect level and corresponds to a daily intake of 
0.02 mg dieldrin/kg body weight per day. 

    Environmental, mainly dietary, exposure leads to the presence 
of dieldrin in low concentrations in the human body.  The results 
of extensive clinical and epidemiological studies indicate that 
these body burdens do not present a health hazard to human beings. 

    No signs of any premonitory change in liver function were found 
in a 20-years study, involving more than 1000 industrial workers 
exposed to aldrin and dieldrin.  In this study and another study in 
the USA, no specific cancer risk could be identified associated 
with occupational exposure to (sometimes high levels of) aldrin and 
dieldrin. 

    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 human beings. 

    Photodieldrin, the photo-decomposition product of dieldrin, is 
similar to dieldrin in its short-term toxicity.  It is not 
teratogenic or carcinogenic in mice and rats.  The accumulation of 
photodieldrin in the adipose tissue of experimental animals was 
less than that of dieldrin. 

10.2.  Evaluation of Effects on the Environment

    Aldrin, used as a soil insecticide, is the major source of 
dieldrin (up to 97%) in the environment.  Aldrin and its reaction 
product dieldrin are rapidly adsorbed on soils, especially soils 
containing a high level of organic matter.  Consequently there is 
little penetration into the soil, and contamination of groundwater 
does not generally occur.  Transport of both compounds takes place 
mainly through soil erosion (as wind drift) and sediment transport 
(surface run-off), but not through leaching. 

    The use of aldrin and dieldrin in agriculture leads to residues 
(mainly of dieldrin) in the soil that can persist for years; the 
estimated half-life of dieldrin is between 4 and 7 years.  Under 
tropical conditions, the compounds are less persistent than under 
temperate conditions. 

    Aldrin and dieldrin enter the atmosphere through volatilization 
from treated crops and soil or, directly, during the application of 
the pesticide.  Dieldrin returns to soil and water surfaces by 
washout and dry deposition.  Thus, the compounds are found either 
in the vapour phase (very low levels, in general 1 - 2 ng/m3), 
adsorbed by dust particles, or in rainwater (of the order of 
10 - 20 ng/litre). 

     The occurrence of dieldrin in the aquatic environment has been 
reported by several authors.  The concentrations in surface water 
are mainly very low, less than 5 ng/litre.  However, concentrations 
in areas of soil erosion or agricultural use may be higher. 
Sediment in rivers in these areas may contain up to 1 mg 
dieldrin/kg.  The high capacity for aquatic organisms to 
concentrate dieldrin from very low levels in water could lead to 
toxic levels in aquatic organisms.  Concentration through aquatic 
foodchains is of less importance than direct uptake from water. 

     Because of the widespread occurrence of dieldrin in the 
environment and its persistence, there is a wide range of 
concentrations in non-target organisms.  Whereas the concentrations 
previously ranged from 0.001 mg to 100 mg/kg tissue, they are now 
mostly below 1 mg/kg tissue. 

     In terrestrial ecosystems, aldrin and dieldrin are accumulated 
by a wide variety of organisms, principally as dieldrin.  Dieldrin 
is probably responsible for the deaths of mammals in the field and 
for the decline in population size in some species, such as the 
otter.  Small mammals would be killed by eating dieldrin-dressed 
grain, but populations of these animals are likely to have been 
replenished by immigration from surrounding areas.  Birds of prey 
eating small mammals and small birds contaminated by dieldrin take 
up and accumulate dieldrin in their own tissues and eggs. 
Granivorous birds have been killed by eating dressed grain.  It is 
probable that the population decline in birds of prey was caused by 
dieldrin residues (among other organochlorine residues) in their 
tissues.  The effects of dieldrin are seen some time after the 
exposure, because residues are stored in fat over winter, to be 
released in the spring.  When dieldrin was used only at certain 
times of the year, this did not prevent bird mortalities. 

     The widespread use of aldrin and dieldrin, in conjunction with 
other organochlorine pesticides, has led to severe detrimental 
effects on the environment, though with drastic curtailment of use, 
particularly in seed dressings, there has been some recovery in 
bird populations. 

10.3.  Conclusions 

(a)  Both aldrin and dieldrin have been subjected to intensive and 
     wide-ranging study, toxicologically, clinically, and 
     epidemiologically.  The body burden is mainly the result of 
     the oral ingestion of residues in the diet (which seem 
     generally to fall within the promulgated ADIs) and, to a 
     lesser extent, of inhalation.  Evaluation of the data suggests 
     strongly that the body burden resulting from the present level 
     of exposure constitutes no health risk to the general 
     population. 

(b)  Dieldrin occurs almost ubiquitously in human breast milk. 
     However, its concentration in the blood and adipose tissue of 
     suckling infants does not increase with age during the first 
     six months, nor is their blood dieldrin level higher than that 
     of bottle-fed babies.  Under these circumstances, the benefits 
     of natural breast feeding still make it the preferred method 
     of infant feeding, in spite of the dieldrin residues. 

(c)  In the treatment of premises, notably for termite control, the 
     exposure of occupants does not appear to be increased to a 
     level that endangers their health, as long as the directions 
     for safe practice are conscientiously respected. 

(d)  Despite the highly toxic nature of aldrin and dieldrin, both 
     of these chemicals can be handled safely as long as the 
     recommended precautions to minimize worker exposure are always 
     observed.  Neglect of these rules may lead to the poisoning of 
     operators. 

(e)  During the period of high aldrin and dieldrin use between 1950 
     and 1970, detrimental effects were undoubtedly inflicted upon 
     species in the environment.  These effects were due partly to 
     dieldrin and partly to other organochlorines.  Since the 
     drastic curtailment of the use of these materials, the 
     affected species have recovered in numbers. 

11.  RECOMMENDATIONS

1.   A further, properly designed, teratogenic investigation is 
     required in the hamster, with dieldrin at realistic dose 
     levels. 

2.   Research into the mechanism of carcinogenesis should be 
     directed to explaining why the hepatic reaction in the mouse 
     is different from that of other species. 

3.   Dieldrin should be selected as an agent for further study of 
     neurotoxic mechanisms, both experimentally and clinically. 

4.   To protect the environment, large-scale use of aldrin and 
     dieldrin must not be resumed, and applications should be 
     confined to those situations in which no safer, equally 
     effective alternatives can be recommended. 

5.   For the health and welfare of workers and the general 
     population, the handling and application of aldrin and 
     dieldrin should only be entrusted to well trained competent 
     operators, who will follow adequate safety measures. 

6.   To avoid accidental poisoning from aldrin, especially among 
     children, the use of aldrin granules as an ant bait should be 
     forbidden. 

12.  PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES

     Aldrin and dieldrin were evaluated by the FAO/WHO Joint 
Meeting on Pesticide Residues (JMPR) 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, 1978a,b). 
From 1966 onwards, the JMPR established an acceptable daily intake 
(ADI) of 0 - 0.0001 mg/kg body weight (combined total for aldrin 
plus dieldrin).  This was based on a level causing no toxicological 
effect of: 

     0.5 mg/kg diet, equivalent to 0.025 mg/kg body weight, in the 
     rat; and

     1 mg/kg diet, equivalent to 0.025 mg/kg body weight, in the 
     dog. 

     The maximum residue limits (MRLs) listed in Table 47 were 
recommended by the FAO/WHO Joint Meeting on Pesticide Residues in 
1970 and 1975 and are quoted as the sum of aldrin plus dieldrin. 

Table 47.  Maximum residue limits (MRL's) recommended by the Codex
Alimentarius Commission (FAO/WHO, 1986)
-------------------------------------------------------------------
Commodity                                   Aldrin and dieldrin
                                            (mg/kg)
-------------------------------------------------------------------
Potatoes                                    0.1

Fat of meat                                 0.2a

Carrots, lettuce, fat of meat               0.1a

Asparagus, aubergines, broccoli, Brussels   0.1
 sprouts, cabbage, cauliflower, cucumbers,
 horse radish, onions, parsnips, peppers,
 pimentos, radishes, radish tops

Eggs (shell-free)                           0.1a

Milk and milk products (fat basis)          -

Milk                                        0.006a

Fruit                                       0.05

Rice (in husks)                             0.02

Raw cereals (other than rice)               0.02a
-------------------------------------------------------------------
a Extraneous residue limit.

     WHO (1984) recommended that the level of aldrin and dieldrin 
in drinking-water should not exceed 0.03 µg/litre. 

     IARC evaluated aldrin and dieldrin on several occasions. 
Aldrin and dieldrin were found to be carcinogenic in the liver in 
mice, but there was no evidence for carcinogenicity in other 
organs.  The data available did not provide evidence of 
carcinogenicity in rats.  Data on dogs, monkeys, and human beings 
were too limited to allow any conclusions (IARC, 1974).  IARC 
considered that there was inadequate evidence of carcinogenicity 
in humans and limited evidence of carcinogenicity in experimental 
animals.  Accordingly, both chemicals were classified in Group 3 
(IARC, 1987). 

     The Pesticide Development and Safe Use Unit, Division of 
Vector Biology and Control, WHO, classified the acute hazard to 
health for technical dieldrin as "highly hazardous" (WHO, 1988). 
The same division published a data sheet on aldrin (79.41) and 
dieldrin (75.17) (WHO/FAO, 1975-85). 

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APPENDIX I.  NOMENCLATURE

     Two major systems are currently used for the nomenclature of 
these compounds:  "polyhydroaromatic" names used by Chemical 
Abstracts (American Chemical Society) and IUPAC and the von 
Baeyer/IUPAC system for polycylic aliphatic compounds.  That the 
latter system should be used for the cyclodiene insecticides was 
proposed by Benson (1969) and Bedford (1974).  The "polyaromatic" 
system has, unfortunately, been subject to historical variation, 
and there are differences between the IUPAC, British and American 
conventions for defining the 3-dimensional stereochemistry in this 
system. As a consequence of the differences in the numbering of the 
carbon atoms in the two major systems, and the modification of the 
Chemical Abstracts "polyaromatic" name for dieldrin since 1971, 
considerable confusion can occur regarding the nomenclature of 
metabolites. 

     The various alternative names for aldrin, dieldrin, and photo-
dieldrin are summarized in Table 48.  A useful discussion of 
nomenclature is given by Brooks (1974). 

     For convenience, in view of the much more extensive usage in 
the literature of the former Chemical Abstracts names for aldrin 
and dieldrin, the names of their metabolites in this review are 
based (if appropriate) on the former Chemical Abstracts names of 
the parent compounds given in Table 48.  The names of the 
metabolites are given in Table 49, together with some alternative 
names based on either the current Chemical Abstracts name for 
dieldrin or the von Baeyer/IUPAC system. 

     The possible misunderstandings that may occur, particularly 
for those not familiar with the various conventions of chemical 
nomenclature, are illustrated by the different names that may be 
given to the major faecal metabolite of dieldrin.  This one 
compound may be designated: 

     (a)  9-hydroxy dieldrin (former CA system);
     (b)  8-hydroxy dieldrin (current CA system); or
     (c)  12-hydroxy dieldrin (von Baeyer/IUPAC system).

Table 48.  Alternative chemical names for aldrin, dieldrin, and photodieldrin
---------------------------------------------------------------------------------------------------------------
Compounda              Polyhydroaromatic name                             Polycyclic aliphatic name
           Chemical Abstracts              IUPAC                          (von Baeyer/IUPAC)
---------------------------------------------------------------------------------------------------------------
Aldrin      Formerly:                       Formerly:                      1,8,9,10,11,11-hexachloro-2,3-7,6-
(HHDN)     1,2,3,4,10,10-hexachloro-       1,2,3,4,10,10-hexachloro-      endo-2,1-7,8-exo-tetracyclo[6.2.13,6
(I)        1,4,4a,5,8,8a-hexahydro-        1,4,4a,5,8,8a-hexahydro-       02,7] dodeca-4,9-diene
           endo-1,4-exo-5,8-               exo-1,4-endo-5,8-
           dimethanonaphthalene            dimethanonaphthalene

            Currently:                      Currently:
           1,2,3,4,10,10-hexachloro-       (IR,4S,5S,8R)-1,2,3,4,10,10-
           1 alpha,4 alpha,4a-beta,        hexachloro-1,4,4a,5,8,8a-
           5 alpha,8a,8a beta-hexahydro-   hexahydro-1,4:5,8-
           1,4:5,8-dimethanonaphthalene    dimethanonaphthalene

Dieldrin    Formerly:                       Formerly:                      1,8,9,10.11,11-hexachloro-4,5-exo-
(HEOD)     1,2,3,4,10,10-hexachloro-       1,2,3,4,10,10-hexachloro-      epoxy-2,3-7,6-endo-2,1-7,8-exo-
(II)       6,7-epoxy-1,4,4a,5,6,7,8,8a-    6,7-epoxy-1,4,4a,5,6,7,8,8a-   tetracyclo[6.2.1.13,6.02,7] dodec-
           octahydro-endo-1,4-exo-         octahydro-exo-1,4-endo-5,8-    9-ene
           5,8-dimethanohaphthalene        dimethanonaphthalene

            Currently:                      Currently:
           3,4,5,6,9,9-hexachloro-         (IR,4S,5S,8R)-1,2,3,4,10,10-
           1a alpha,2 beta,2a alpha,       hexachloro-1,4,4a,5,6,7,8,8a-
           3 beta,6 beta,6a alpha,7 beta,  octahydro-6,7 epoxy-1,4:5,8-
           7a alpha-octahydro-2,7:3,6-     dimethanonaphthalene
           dimethanonaphth[2,3-b]oxirene

Photo-     1,1,2,3,3a,7a-hexachloro-                                      3,exo-4,5,6,6,7-hexachloro-11,12-
dieldrin   6,7-epoxy-2,4,7-metheno-                                       exo-epoxy-pentacyclo[6.4.0.02,10.
(III)      decahydro-3H-cyclopenta[a]-                                    03,7.05,9]-dodecane
           pentalene
---------------------------------------------------------------------------------------------------------------
a Roman numerals in parentheses refer to the structures in Fig. 2 of the main document.
Table 49.  Chemical nomenclature of metabolites of aldrin and dieldrin
---------------------------------------------------------------------------------------------------------
Trivial name(s)a        Chemical name used in this review    Alternative chemical names
---------------------------------------------------------------------------------------------------------
9-Hydroxy dieldrin      9-hydroxy-1,2,3,4,10,10-hexa-        9-(syn-epoxy)hydroxy-1,2,3,4,10,10-hexa-
(VI) (9-Hydroxy HEOD)   chloro-6,7-epoxy-1,4,4a,5,6,7,       chloro-6,7,-epoxy-1,4,4a,5,6,7,8,8a-octa-
                        8,8a-octahydro-1,4-endo-5,8-exo-     hydro-1,4-endo,exo-5,8-dimethanonaphthalene
                        dimethanonaphthalene
                                                             8-hydroxy-3,4,5,6,9,9-hexachloro-1a alpha,
                                                             2 beta, 2a alpha, 3 beta, 6 beta, 6a alpha,
                                                             7 beta, 7a alpha-octahydro-2,7:3,6-
                                                             dimethanonapth[2,3-b]oxirene

                                                             1,8,9,10,11,11-hexachloro-4,5-exo-epoxy-12-
                                                             (synepoxy)hydroxy-2,3-7,6-endo-2,1-7,8-exo-
                                                             tetracyclo[6.2.1.13,602,7]dodec-9-ene

Aldrin trans-diol (IV)  trans-6,7-dihydroxy-1,2,3,4,10,10-   1,8,9,10,11,11-hexachloro-4,5-trans-
                        hexachloro-1,4,4a,6,7,5,8,8a-hexa-   dihydroxy-2,3-7,6-endo-2,1-7,8-exo-
                        hydro-1,4-endo-5,8-exo-dimethano-    tetracyclo[6.2.1.13,6.02,7]dodec-9-ene
                        naphthalene

Aldrin dicarboxylic     4,5,6,7,8,8-hexachloro-4,7-methano-  1,7,8,9,10,10-hexachloro-2,3-6,5-endo-
acid (V)                3a,4,7,7a-tetrahydro-indane-1,3-     tricyclo[5.2.1.02,6]dec-8-ene-3,5-exo-
                        dicarboxylic acid                    dicarboxylic acid

Bridged pentachloro-    3,5,6,6,7-pentachloro-11,12-exo-
ketone (VII) (PCK,      epoxy-pentacyclo[6.4.0.02,10.03,7
Klein's metabolite)     .05,9]dodecan-4-one

Dechloro-aldrin         4,5,6,7,8-pentachloro-4,7-methano-
dicarboxylic            3a,4,7,7a-tetrahydro-indane-1,3-
acid (VIII)             dicarboxylic acid

Dieldrin ketone (IX)    1,2,3,4,10,10-hexachloro-1,4,4a,5,   1,8,9,10,11,11-hexachloro-2,3-7,6-endo-
                        6,7,8,8a-octahydro-6-keto-endo-      2,1-7,8-exo-tetracyclo[6.2.1.13,6.02,7]-
                        1,4-exo-5,8-dimethanonaphthalene     dodec-9-en-4-one

Photodieldrin           3-exo-4,5,6,6,7-hexachloro-
ketone (X)              pentacyclo[6.4.0.02,10.03,7.05,9]
                        dodecan-11-one
---------------------------------------------------------------------------------------------------------

Table 49.  (contd.)
---------------------------------------------------------------------------------------------------------
Trivial name(s)a        Chemical name used in this review    Alternative chemical names
---------------------------------------------------------------------------------------------------------
Photodieldrin trans-    3,exo-4,5,6.6,7-hexachloro-11,12
diol (XI) (caged        dihydroxy-pentacyclo[6.4.0.02,10.
aldrin trans-diol)      03,7.05,9]dodecane

Photoaldrin dicarbo-    1,7,8,exo-9,10,10-hexachlorotetra-
xylic acid (XII)        cyclo[5.2.1.02,6.04,8]decane-3,5-
(caged aldrin acid)     exo,exo-dicarboxylic acid

Photoaldrin (XIII)      3,exo-4,5,6,6,7-hexachloropenta-
                        cyclo[6.4.0.02,10.03,7.05,9]dodec-
                        11-ene
---------------------------------------------------------------------------------------------------------
a Roman numerals in parentheses refer to the structures in Fig. 2 of the main document.
RESUME

1.  Généralités

     L'aldrine et la dieldrine qui sont l'une et l'autre des 
pesticides organochlorés fabriqués industriellement depuis 1950, 
ont été utilisés dans le monde entier jusqu'au début des années 70 
comme insecticides en agriculture, contre de nombreux ravageurs 
présents dans le sol, et pour le traitement des semences.  Ces 
insecticides étaient actifs contre les termites, les sauterelles, 
les xylophages, les coléoptères et les ravageurs des textiles.  La 
dieldrine a également été employée en santé publique, pour la lutte 
contre la mouche tsé-tsé et d'autres vecteurs de maladies 
tropicales invalidantes.  L'aldrine comme la dieldrine agissent par 
contact et par ingestion. 

     Depuis le début des années 70, ces deux composés sont 
interdits ou font l'objet de limitations rigoureuses dans un 
certain nombre de pays, spécialement en agriculture.  Néanmoins, 
ils continuent d'être employés pour la destruction des termites 
dans d'autres pays.  La production annuelle mondiale, estimée à 
13 000 tonnes en 1972, est tombée à moins de 2500 tonnes en 1984. 

     L'aldrine et la dieldrine de qualité technique ont une pureté 
respective de 90% et plus de 95%.  Les principales impuretés sont, 
pour l'aldrine, l'octachlorocyclopentène, l'hexachlorobutadiène et 
des produits de polymérisation et, pour la dieldrine, des 
polychloroépoxy-octahydrodiméthanonaphtalènes. 

     Les deux composés sont pratiquement insolubles dans l'eau et 
modérément à très solubles dans la plupart des alcanes, des 
hydrocarbures aromatiques et des hydrocarbures halogénés, ainsi que 
dans les esters, les cétones et les alcools. 

     La tension de vapeur de l'aldrine est de 6,5 x 10-5 mmHg à 
25°C et celle de la dieldrine de 3,2 x 10-6 mmHg à 25°C. 

     Les méthodes utilisables pour le dosage de l'aldrine et de la 
dieldrine dans les aliments, les aliments pour animaux et le milieu 
sont décrites à la section 2. 

2.  Transport, distribution et transformation dans l'environnement

     L'aldrine est principalement utilisée comme insecticide épandu 
au niveau du sol.  Les sols ainsi traités constituent donc dans 
l'environnement une source importante d'aldrine et de son produit 
de réaction, la dieldrine. 

     L'aldrine n'a qu'une faible capacité de migration à partir des 
zones traitées, par volatilisation ou lessivage.  Elle s'adsorbe 
préférentiellement, et rapidement, sur les sols riches en matières 
organiques, mais faiblement sur les sols argileux.  Il est rare que 
l'aldrine et la dielrine pénètrent au-delà des 20 premiers 
centimètres de la couche de sol traité.  L'aldrine adhère si 

solidement aux particules du sol que seules des traces peuvent être 
retirées par l'eau.  C'est pourquoi il n'y a généralement pas 
contamination des eaux souterraines. 

     L'aldrine s'élimine du sol selon une cinétique qui évoque une 
réaction du premier ordre.  Immédiatement après épandage, on 
observe une courte période d'élimination rapide par volatilisation, 
suivie d'une seconde période, plus longue, de décroissance 
exponentielle, principalement du fait de la transformation en 
dieldrine, plus lente à se dissiper.  Néanmoins, il peut y avoir 
une certaine migration du fait de l'érosion du sol, sous l'action 
du vent, des eaux de ruissellement de du déplacement des sédiments. 
Les observations faites sur les résidus d'aldrine dans la nature 
montrent que, apparemment, ce composé est essentiellement retenu 
dans le sol et que pour 97%, le résidu essentiel n'est pas le 
composé d'origine mais l'époxyde correspondant, la dieldrine. 

     La photodieldrine est un produit de photodégradation de la 
dieldrine, peu répandu dans l'environnement. 

     Après épandage sur le sol, l'aldrine disparaît lentement dans 
les régions tempérées puisque, dans le cas type, il faut un an pour 
qu'elle s'élimine aux trois quarts.  La vitesse d'élimination 
diminue ensuite à mesure que l'aldrine se transforme en dieldrine. 
Il semblerait que la vitesse d'élimination soit plus élevée en 
anaérobiose, comme c'est le cas dans les rizières, qu'en aérobiose. 
Dans les régions tropicales, la dieldrine s'élimine du sol très 
rapidement, jusqu'à hauteur de 90% au cours du premier mois, alors 
que, dans le sol des régions tempérées, la dieldrine a une demi-vie 
d'environ 5 ans.  La volatilisation semble être le principal 
mécanisme d'élimination à partir du sol, bien que la teneur 
atmosphérique de la dieldrine et de l'aldrine soit généralement 
faible.  Une partie de la dieldrine est éliminée de l'atmosphère 
par les précipitations, mais la concentration de ce produit est 
très faible dans les eaux souterraines par suite de son adsorption 
énergique sur les particules telluriques.  On trouve de la 
dieldrine en petites quantités dans les eaux de surface qui sont 
contaminées par les eaux de ruissellement provenant de terres 
agricoles. 

3.  Concentrations environnementales et exposition humaine

     On trouve de l'aldrine et de la dieldrine dans l'atmosphère en 
phase vapeur, adsorbées sur des poussières ou dans les eaux de 
pluie, à des teneurs variables selon la situation.  Ces produits 
s'observent principalement dans les régions agricoles où leur 
concentration atmosphérique moyenne est de l'ordre de 1 - 2 ng/m3 
avec des maximums d'environ 40 ng/m3.  Dans l'eau de pluie, on 
relève des concentrations de l'ordre de 10 - 20 ng/litre ou parfois 
plus. 

     Dans les habitations traitées avec ces produits contre les 
termites, on observe une concentration dans l'air allant de 0,04 à 
7 µg/m3, selon le moment de l'échantillonnage (c'est-à-dire le 
nombre de jours après l'épandage) et le type d'habitation.  Au bout 

de 8 semaines, la concentration a très nettement diminué. Lorsqu'on 
traite le bois en profondeur dans ces maisons, la concentration de 
la dieldrine dans l'air va de 0,01 à 0,5 µg/m3.  On a constaté que 
l'aldrine et la dieldrine migraient dans les produits alimentaires 
à partir de panneaux lamellés et de contreplaqués traités, ainsi 
que par contact direct ou sorption à partir de l'atmosphère. 

     On a signalé la présence de dieldrine en milieu aquatique. 
Mais les concentrations étaient très faibles, le plus souvent 
inférieures à 5 ng/litre.  Les concentrations plus élevées ont 
généralement étéattribuées au rejet d'effluents industriels ou à 
l'érosion du sol à la suite de l'utilisation de ces produits en 
agriculture.  Dans les cours d'eau, les sédiments peuvent présenter 
des teneurs beaucoup plus élevées (allant jusqu'à 1 mg/kg). 

     On trouve rarement de l'aldrine dans les aliments, alors que 
la dieldrine est plus courante, spécialement dans les produits 
laitiers, les produits carnés, le poisson, les huiles et les 
graisses, les pommes de terre et certains autres légumes 
(principalement des légumes-racines).  Des limites maximales de 
résidus (LMR) de l'ordre de 0,02 - 0,2 mg/kg de produit ont été 
recommandées lors des réunions conjointes successives FAO/OMS sur 
les résidus de pesticides.  Les études récentes réalisées dans 
différents pays montrent que la concentration effective de la 
dieldrine dans les denrées alimentaires est généralement plus 
faible. Le recul est net au Royaume-Uni.  En 1966 - 67, la 
concentration moyenne des résidus de dieldrine observée lors d'une 
étude sur la ration totale était de 0,004 mg/kg d'aliments tandis 
que, pendant la période 1975 - 77, elle n'était plus que de 0,0015 
mg/kg pour tomber à 0,0005 mg/kg en 1981.  Cette évolution en 
baisse est confirmée dans d'autres pays, par exemple aux Etats-Unis 
d'Amérique.  Cela tient peut-être à l'interdiction ou à la 
limitation d'emploi de ces composés. 

     Dans un grand nombre de travaux publiés, on a recherché la 
présence de dieldrine dans le tissu adipeux, les organes, le sang 
et d'autres tissus, chez des sujets de la population générale.  Au 
cours des 25 dernières années, des enquêtes ont été réalisées dans 
de nombreux pays, partout dans le monde.  La plupart des 
concentrations moyennes observées dans le tissu adipeux se situent 
entre 0,1 et 0,4 mg/kg.  Aux Etats-Unis d'Amérique, aux Pays-Bas et 
au Royaume-Uni, on note une diminution de la concentration dans les 
tissus adipeux depuis le milieu de la décennie 70.  La 
concentration sanguine varie de 1 à 2 µg/litre.  Dans le foie, elle 
est inférieure à 0,4 mg/kg tandis que, dans les autres tissus, à 
savoir les reins, l'encéphale et les gonades, elle est inférieure à 
0,1 mg/kg. 

     A la suite d'une exposition par voie transplacentaire, on 
trouve de la dieldrine dans le sang, les tissus adipeux et d'autres 
tissus du foetus et du nouveau-né.  Les concentrations sont 2 à 10 
fois plus faibles que chez la mère.  Il n'existe aucune différence 
entre le nourrisson et l'adulte pour ce qui est des concentrations 
relatives de la dieldrine dans le cerveau, le foie et les tissus 
adipeux.  La dieldrine est également excrétée dans le lait 

maternel.  Depuis une quinzaine d'années, on recherche dans divers 
pays la présence de pesticides organochlorés dans le lait de femme. 
Dans la plupart des pays, la concentration plafonne à 6 µg/litre, 
sauf cas exceptionnels. 

4.  Cinétique et métabolisme

     Chez les animaux comme chez l'homme, l'aldrine et la dieldrine 
passent rapidement des voies digestives dans le courant sanguin. 
L'absorption a également lieu au niveau de la peau ou des poumons 
après inhalation de la vapeur.  Une étude sur des volontaires a 
montré que la quantité résorbée par la peau intacte représente 
7 - 8% de la dose appliquée.  Selon des études d'inhalation 
conduites sur des volontaires, le taux d'absorption et de rétention 
de l'aldrine dans l'organisme peut atteindre 50% de la vapeur 
inhalée.  Après absorption, le composé se répartit rapidement dans 
tous les organes et tissus, et il existe un échange permanent entre 
le sang et les autres tissus.  Entre-temps,l'aldrine se transforme 
en dieldrine, principalement au niveau du foie mais aussi, dans une 
moindre proportion, dans d'autres tissus comme les poumons.  Cette 
conversion est très rapide. 

     Après administration par voie orale d'une dose de 10 mg 
d'aldrine par kg de poids corporel à des rats de 1 jour, on a 
retrouvé ce composé dans le foie des animaux d'expérience 2 heures 
après l'administration.  Au cours des quelques heures suivantes, la 
dieldrine s'est concentrée dans une beaucoup plus large mesure dans 
les tissus lipidiques. 

     Comme l'ont montré de nombreuses études effectuées avec de 
l'aldrine ou de la dieldrine marquées au 14C, une partie du produit 
ingéré passe telle quelle dans l'intestin d'où elle est éliminée de 
l'organisme, une partie est excrétée telle quelle à partir du foie 
dans la bile, une autre fraction est stockée dans les divers 
organes et tissus, en particulier le tissu adipeux, et une dernière 
fraction est métabolisée dans le foie en produits à caractère 
hydrophile et polaire plus prononcé.  Chez l'homme et la plupart des 
animaux, les métabolites sont principalement éliminés dans les 
excreta, par l'intermédiaire de la bile.  On a établi par ailleurs 
que la biodégradation de l'aldrine et de la dieldrine aboutit aux 
mêmes métabolites. 

     La plupart des connaissances actuelles sur le catabolisme de 
la dieldrine chez les mammifères proviennent d'études chez la 
souris, le rat, le lapin, le mouton, le chien, les petits singes, 
le chimpanzé et l'homme.  Dans l'ensemble, on n'observe que des 
différences quantitatives entre les diverses espèces et les 
mécanismes sont apparemment semblable chez le rat et les primates. 

     Le principal métabolite, sauf chez le rat, est le dérivé 
hydroxylé en 9.  On le trouve dans les déjections ainsi que dans 
l'urine, sous forme libre ou conjuguée.  On a découvert et 
identifié chez les animaux d'expérience trois autres métabolites, 
présents en petites quantités. Il s'agit d'un dérivé 6,7-
dihydroxylé en position  trans, d'un acide dicarboxylique dérivé du 
composé dihydroxylé et d'une pentachlorocétone pontée. 

     Seul le composé hydroxylé en 9 a été mis en évidence chez 
l'homme, dans les matières fécales, tandis que ni ce composé ni les 
autres métabolites n'apparaissaient dans le sang ou les autres 
tissus.  On a observé la présence de dieldrine dans les selles 
d'ouvriers professionnellement exposés, tandis que, dans la 
population générale, les quantités étaient inférieures au seuil de 
détection.  L'examen des urines de cinq ouvriers a montré que 
l'excrétion de la dieldrine et de ses quatre métabolites par voie 
urinaire était minime par rapport à l'élimination du métabolite 
hydroxylé en 9 par voie fécale. 

     La transformation de l'aldrine en dieldrine dans le foie, sous 
l'action de mono-oxygénases à fonction mixte (aldrine-époxydase) et 
la distribution, puis le dépôt ultérieur, de la dieldrine 
(principalement dans les tissus à contenu lipidique, tels que le 
tissu adipeux, le foie, les reins, le coeur et le cerveau) sont 
beaucoup plus rapides que le catabolisme et l'élimination finale de 
la dieldrine intacte et de ses métabolites.  Dans ces conditions, 
pour un apport quotidien moyen déterminé d'aldrine ou de dieldrine, 
il y a accumulation lente de dieldrine dans l'organisme.  Mais 
cette accumulation n'est pas indéfinie.  Quand l'administration se 
poursuit, on finit par aboutir à un état d'équilibre dynamique, la 
quantité excrétée compensantexactement l'apport.  La quantité 
stockée maximale dépend de l'apport quotidien, tout comme on l'a 
montré chez le rat, le chien et l'homme. 

     Quand l'apport d'aldrine/dieldrine est réduit ou interrompu, 
la charge de l'organisme diminue.  Chez l'homme, la demi-vie 
biologique est de l'ordre de 9 à 12 mois.  Chez le rat, le chien et 
l'homme, on a démontré l'existence de relations significatives 
entre la concentration de la dieldrine dans le sang et sa 
concentration dans d'autres tissus. 

     De nombreuses études sur la concentration de la dieldrine dans 
divers tissus, dont le sang et les tissus adipeux, aussi bien dans 
la population générale que dans des catégories particulières, ont 
été réalisées dans plusieurs pays et ont montré que, à l'équilibre, 
les concentrations respectives dans les tissus adipeux, le foie, le 
cerveau et le sang sont sensiblement proportionnelles à 150, 15, 3 
et 1. 

     La dieldrine est transportée par le placenta jusqu'au foetus. 
Il y a accumulation dans les mêmes organes et tissus que chez 
l'adulte, mais en quantités moindres.  Il existe apparemment un 
équilibre entre les concentrations chez la mère et chez le foetus. 

     Chez le rat et le chien, la photodieldrine est également 
métabolisée sous forme de pentachlorocétone pontée.  On a retrouvé 
les deux composés dans les tissus adipeux, le foie et les reins des 
animaux à qui l'on avait administré de la photodieldrine à forte 
dose.  Chez l'homme, aucun résidu de ces composés n'a été mis en 
évidence dans le tissu adipeux, les reins ni le lait maternel. 
L'accumulation de photodieldrine dans les tissus adipeux des 
animaux d'expérience était beaucoup moins importante que celle de 
la dieldrine. 

5.  Effets sur les êtres vivants dans leur milieu natural

5.1  Accumulation

     La plupart des résidus présents chez les êtres vivants sont 
des résidus de dieldrine, car l'aldrine se transforme facilement 
chez eux en dieldrine. 

     Les champignons, les streptomycètes et les bactéries 
concentrent la dieldrine du milieu ambiant dans une proportion qui 
peut aller en 4 h de 0,3 à plus de 100.  Les protozoaires absorbent 
la dieldrine davantage que les algues.  Celles-ci absorbent très 
rapidement la dieldrine présente dans le milieu de culture, les 
concentrations maximales étant souvent atteintes en quelques 
heures. 

     De nombreuses espèces d'invertébrés aquatiques concentrent 
fortement la dieldrine à partir d'une eau à très faible teneur. 
L'équilibre est atteint en quelques jours.  Lorsqu'on les remet en 
eau pure, la dieldrine s'élimine rapidement, avec une demi-vie de 
60 - 120 h. 

     Pour les poissons entiers, le facteur de bioconcentration 
dépasse 10 000.  Chez une espèce de poissons, la demi-vie 
d'élimination de la dieldrine accumulée s'est établie à 16 jours. 

     La bioconcentration de dieldrine chez les organismes 
aquatiques se fait principalement à partir de l'eau et non par 
ingestion d'aliments. 

     Les lombrics absorbent la dieldrine présente dans le sol et 
laconcentrent jusqu'à un facteur maximal d'environ 170.  Pour la 
plupart des types de sol, il n'existe guère de corrélation entre la 
concentra-tion atteinte chez le lombric et la concentration dans le 
sol. 

     De nombreux travaux ont été consacrés à la présence de la 
dieldrine dans les tissus ou dans les oeufs d'espèces non visées. 
Les concentrations observées sont extrêmement variables, allant de 
0,001 mg/kg à 100 mg/kg de tissu, mais elles restent le plus 
souvent inférieures à 1 mg/kg de tissu. 

     Chez les oiseaux, il y a accumulation rapide de dieldrine 
aussi bien dans les tissus que dans les oeufs.  De même, on a 
montré que diverses espèces de mammifères accumulent la dieldrine, 
en particulier dans les graisses. 

5.2  Toxicité pour les micro-organismes

     La dieldrine a des effets très variables sur les algues uni-
cellulaires, avec une action sensible sur certaines espèces dès la 
concentration de 10 µg/litre tandis que d'autres espèces ne sont 
pas touchées même à la concentration de 1000 µg/litre.  L'aldrine 
et la dieldrine n'ont que peu d'effets sur les bactéries 
terricoles, même à des concentrations très supérieures aux valeurs 

habituelles.  Dans la plupart des études, aucun effet n'a été 
constaté après exposition à une concentration de 2000 mg/kg de 
terre.  Des effets ont été signalés sur la photosynthèse chez 
différentes espèces d'algues, avec une action plus marquée de 
l'aldrine que de la dieldrine à concentrations égales.  Mais ces 
effets minimes sur la biochimie des algues n'étaient que 
transitoires. 

5.3  Toxicité pour les organismes aquatiques

     L'aldrine et la dieldrine sont extrêmement toxiques pour les 
crustacés aquatiques, avec des valeurs de la DL50 à 96 h 
inférieures à 50 µg/litre.  Cependant, les quelques résultats plus 
élevés signalés (jusqu'à 4300 µg/litre) illustrent les différences 
de sensibilité selon les espèces.  Les daphnies sont moins 
sensibles à la dieldrine qu'à l'aldrine, avec des DL50 à 48 h de 
23 - 32 µg/litre dans le premier cas et de 190 - 330 µg/litre dans 
le second.  Les mollusques sont nettement plus résistants, les CL50 
à 48 h pouvant atteindre plus de 10 000 µg/litre.  Des études de 
plusieurs semaines ont confirmé la résistance relative des daphnies 
et des mollusques.  Les invertébrés aquatiques les plus sensibles 
sont les stades larvaires des insectes, avec des CL50 à 96 h de 
0,5 - 39 µg/litre pour la dieldrine et de 1,3 - 180 µg/litre pour 
l'aldrine. 

     Lors d'épreuves de toxicité aiguë, l'aldrine comme la 
dieldrine se sont montrées très toxiques vis-à-vis des poissons. 
Chez diverses espèces de poisson, on a relevé des valeurs de la 
CL50 à 96 h allant de 2,2 à 53 µg/litre pour l'aldrine et de 1,1 à 
41 µg/litre pour la dieldrine.  De nombreuses études ont montré que 
la toxicité augmente avec la température.  Dans une étude prolongée 
sur  Poecilia latipinna, on a obtenu un taux de mortalité de 100% en 
présence d'une concentration de dieldrine égale ou supérieure à 3 
µg/litre.  L'addition de dieldrine à la nourriture de truites arc-
en-ciel jusqu'à des concentrations de 430 µg/kg de poids corporel 
par jour, n'a exercé aucune influence sur la mortalité mais a 
entraîné des modifications enzymatiques.  Des altérations 
morphologiques ont été observées aumicroscope électronique dans les 
mitochondries hépatiques.  Le mécanisme de détoxification de 
l'ammoniaque chez les poissons est sensible à la dieldrine, la dose 
sans effet nocif apparent étant inférieure à 14 µg/kg de poids 
corporel par jour.  La sensibilité à la dieldrine s'est révélée 
variable selon le stade de développement des poissons.  Les oeufs 
étaient résistants et les formes juvéniles moins sensibles que les 
adultes. 

     La toxicité aiguë de l'aldrine comme de la dieldrine est 
élevée pour les larves d'amphibiens, avec des CL50 à 85 h de 
l'ordre de 100 µg/litre. 

5.4  Toxicité pour les organismes terrestres

     La dieldrine est peu toxique pour les végétaux supérieurs 
puisque les cultures ne sont affectées que par des doses 
supérieures à 22 kg/ha.  La phytotoxicité de l'aldrine est plus 

importante, notamment pour les tomates et les concombres, mais 
uniquement à des doses plusieurs fois supérieures aux valeurs 
recommandées.  Le chou est la plante cultivée la plus sensible à 
l'aldrine. 

     Vis-à-vis des abeilles, la DL50 par voie orale varie, selon 
les observations publiées, de 0,24 à 0,45 µg/abeille pour l'aldrine 
et de 0,15 à 0,32 µg/abeille pour la dieldrine.  Les quantités 
toxiques par contact vont de 0,15 à 0,80 µg/abeille pour l'aldrine 
et de 0,15 à 0,41 µg/abeille pour la dieldrine.  D'après deux 
études, la dieldrine est relativement plus toxique vis-à-vis des 
insectes prédateurs qui se nourrissent de ravageurs. 

     Selon des études effectuées en laboratoire, le lombric 
supporte des doses d'aldrine de 13 mg/kg en sol artificiel, le taux 
de mortalité étant inférieur à 1%.  La CL50 à six semaines était de 
60 mg d'aldrine par kg de sol. 

     Pour 13 espèces d'oiseaux, la toxicité aiguë de l'aldrine et 
de la dieldrine variait de plus du simple au décuple, avec des 
valeurs de 6,6 - 520 mg/kg de poids corporel pour l'aldrine et de 
6,9 - 381 mg/kg de poids corporel pour la dieldrine.  Chez quatre 
espèces d'oiseaux, la toxicité subaiguë par voie orale 
correspondait à des doses comprises entre 34 et 155 mg/kg pour 
l'aldrine et 37 et 169 mg/kg pour la dieldrine.  Des épreuves 
répétées au cours d'une certaine période n'ont révélé aucun signe 
de résistance acquise chez ces espèces.  D'après des études sur la 
reproduction de plusieurs espèces de volaille, une concentration de 
la dieldrine dépassant 10 mg/kg dans les aliments provoque une 
certaine mortalité chez les adultes.  Aucun effet ne s'est fait 
sentir sur la production des oeufs, la fécondité, le taux 
d'éclosion ni la survie des poussins en présence de dieldrine dans 
les aliments à des concentrations qui ne sont pas toxiques pour la 
mère.  La dieldrine n'a aucune influence directe sur l'épaisseur de 
la coquille des oeufs.  Cependant, la diminution de la consommation 
de nourriture, qui constitue un symptôme de l'intoxication par la 
dieldrine, peut entraîner une diminution de l'épaisseur de la 
coquille. 

     Chez le mammifères non élevés au laboratoire, la réponse à la 
dieldrine varie selon les espèces.  Chez quatre espèces de 
campagnols, on a observé des valeurs de la DL50 aiguë, allant de 
100 à 210 mg/kg de poids corporel, ce qui montre que ces animaux 
sont moins sensibles àla dieldrine que les animaux de laboratoire. 
Des musaraignes ont survécu à la consommation d'une nourriture 
contenant 50 mg de dieldrine par kg mais sont mortes quand la 
concentration est passée à 200 mg/kg.  Des damalisques (une espèce 
d'antilope) ont survécu 90 jours à une nourriture contenant de la 
dieldrine à raison de 5 ou 15 mg/kg mais sont toutes mortes dans 
les 24 jours pour une concentration égale ou supérieure à 25 mg/kg. 
Tous les damalisques d'une région où l'on avait pulvérisé de la 
dieldrine à raison de 0,16 kg/ha sont mortes et le calcul a montré 
que l'apport alimentaire était de 1,82 mg/kg par jour.  Trente pour 
cent des springboks ont survécu aux épandages, sans manifester 

d'effets tardifs.  Les signes toxicologiques de l'intoxication par 
la dieldrine étaient sensiblement les mêmes que chez les mammifères 
de laboratoire. 

5.5  Effets sur les populations et les écosystèmes

     Certaines études donnent à penser que des populations de 
mammifères ont été intoxiquées par de la dieldrine.  Il est 
probable que de petits mammifères sont morts après avoir mangé des 
semences enrobées de dieldrine mais les populations se sont 
reconstituées par immigration.  Des chauves-souris ont été tuées 
par la dieldrine contenue dans les agents de protection du bois. 

     Des résidus de dieldrine ont été signalés chez de nombreuses 
espèces d'oiseaux.  Partout dans le monde, c'est chez les oiseaux 
de proie que les résidus sont les plus abondants car les animaux se 
situent en fin de chaîne alimentaire.  La teneur en dieldrine des 
tissus et des oeufs d'oiseau suit l'évolution de l'emploi de 
l'aldrine et de la dieldrine, et elle a diminué à la suite des 
restrictions imposées à leur usage.  Il n'est pas facile de repérer 
les effets de la dieldrine car les résidus de cet insecticide 
s'accompagnent de résidus d'autres organochlorés.  La dieldrine est 
plus toxique que le DDT pour les oiseaux et il est probable qu'elle 
a provoqué chez les adultes une plus forte mortalité que le DDT.  
Il est encore plus difficile de démontrer l'existence d'effets de 
la dieldrine sur la reproduction à l'état naturel.  En outre, il se 
peut que les effets interviennent longtemps après l'exposition. 

6.  Effets sur les animaux d'expérience et les systèmes d'épreuve 
 in vitro

     L'aldrine et la dieldrine sont extrêmement toxiques : pour ces 
deux composés, la DL50 varie, chez la souris et chez le rat, de 40 
à 70 mg/kg de poids corporel.  Par voie percutanée, la dose toxique 
se situe entre 40 et 150 mg/kg de poids corporel selon l'espèce en 
cause et le solvant utilisé.  On a constaté que l'aldrine et la 
dieldrine de qualité technique déterminent chez le lapin une 
irritation cutanée légère à intense, mais la cause en est le 
solvant.  Dans l'épreuve de maximalisation de Magnusson & Kligman 
chez le cobaye, l'aldrine a provoqué un effet de sensibilisation. 
Pourtant, au cours de 20 années de fabrication et de préparation 
des formules, aucun cas de sensibilisation cutanée n'a été observé 
dans un groupe comptant plus de 1000 travailleurs. 

     L'aldrine, comme la dieldrine, a une faible tension de vapeur 
de sorte que, en principe, il n'y a aucun effet aigu par 
inhalation.  Les effets observés lors des études de toxicité aiguë 
après exposition par toutes les voies possibles concernent le 
système nerveux central etconsistent en hyperexcitabilité, 
tremblements et convulsions. 

     Des études d'exposition par voie orale, de courte ou longue 
durée, ont été réalisées avec l'aldrine et la dieldrine, chez la 
souris, le rat, le chien, le hamster et les petits singes.  Chez le 
rat et la souris, le foie est le principal organecible : on observe 

une augmentation de son poids par rapport au poids du corps et une 
hypertrophie des hépatocytes centrilobulaires, la réversibilité 
étant possible à un stade précoce.  Au microscope, ces altérations 
se traduisent par une augmentation de l'oxyphilie cytoplasmique et 
une migration périphérique des granules basophiles.  Ces 
altérations ne se rencontrent pas au niveau du foie chez le hamster 
et le singe.  Chez le chien, l'atteinte hépatique est peu prononcée 
(dégénérescence graisseuse et légère atrophie des hépatocytes); 
elle s'accompagne d'une atteinte rénale consistant dans une 
vacuolisation de l'épithélium des tubules distaux et une 
dégénérescence tubulaire.  Chez le rat, la dose sans effet nocif 
observable se situe dans l'ensemble, d'après les résultats dont on 
dispose sur le court et le long terme, aux alentours de 0,5 mg/kg 
de nourriture, soit l'équivalent de 0,025 mg/kg de poids corporel. 
En augmentant les quantités incorporées à la nourriture, jusqu'à 
obtenir l'équivalent de 0,05 mg/kg de poids corporel ou davantage, 
on observe une hépatomégalie et des altérations histologiques 
d'importance proportionnée à la dose.  Chez le chien une dose de 
0,04 - 0,2 mg/kg de poids corporel s'est révélée sans effet. 

     Plusieurs études de cancérogénicité à long terme ont été 
effectuées sur différentes souches de souris, avec de l'aldrine ou 
de la dieldrine.  Chaque fois, on a observé des tumeurs 
hépatocellulaires bénignes ou malignes.  Apparemment, les femelles 
étaient plus sensibles que les mâles.  Aucun autre type de tumeur 
ne s'est manifesté dans ces études. 

     Des études à long terme sur d'autres espèces (rat, hamster) 
n'ont révélé aucune augmentation de l'incidence tumorale. 
L'administration de photodieldrine incorporée à la nourriture, 
jusqu'à une concentration de 7,5 mg/kg d'aliments, ne s'est pas 
révélé tumorigène. 

     En outre, on a publié un certain nombre d'études spéciales qui 
n'ont, jusqu'ici, pas permis d'élucider le mécanisme de la 
production des tumeurs hépatiques chez la souris. 

     Dans la plupart des études de reproduction (sur 1 à 6 
générations), réalisées avec l'aldrine ou la dieldrine sur des 
souris et des rats, le principal effet constaté a été 
l'augmentation du taux de mortalité dans la descendance, avant 
sevrage.  La capacité génésique n'a été atteinte qu'à des doses 
toxiques pour la mère.  Les études sur le chien étaient trop 
limitées pour permettre les conclusions catégoriques, si ce n'est 
qu'on a noté une augmentation systématique de la mortalité des 
chiots à la mamelle. 

     D'après les résultats de ces études sur la reproduction, on 
peut conclure que, de ce point de vue, les doses sans effet nocif 
décelable sont de 2 mg de dieldrine par kg de nourriture chez le 
rat et de 3 mg de dieldrine par kg de nourriture chez la souris, 
soit l'équivalent quotidien de 0,1 et 0,4 mg/kg de poids corporel 
respectivement. 

     Aucun signe de tératogénicité n'a été observé chez la souris, 
le rat ou le lapin, après administration par voie orale de doses 
d'aldrineet de dieldrine atteignant 6 mg/kg de poids corporel. 
L'administration d'une dose unique d'aldrine et de dieldrine, 
représentant environ la moitié de la DL50, a provoqué des effets 
toxiques intenses chez le foetus de souris et de hamster, ainsi 
qu'une incidence accrue d'anomalies tératogènes. La signification 
de ces observations est douteuse en présence d'effets toxiques 
probables chez les femelles gravides. 

     Les études de mutagénicité  in vivo ou  in vitro ont été 
nombreuses, mais elles ont presque toujours donné des résultats 
négatifs. 

     La toxicité aiguë de la photodieldrine par voie orale est plus 
élevée que celle de la dieldrine chez la souris, le rat et le 
cobaye.  Lors d'études de toxicité aiguë ou à long terme, on a 
observé des symptômes d'intoxication et des effets sur les organes 
cibles analogues à ceux de la dieldrine, tant sur le plan 
quantitatif que sur le plan qualitatif.  La photodieldrine ne s'est 
pas montrée tumorigène chez la souris ni chez le rat. 

     Comme la plupart des autres substances chimiques, l'aldrine et 
la dieldrine exercent leurs effets toxiques selon plusieurs 
mécanismes.  Les organes cibles sont le système nerveux central et 
le foie.  Chez l'homme et les autres vertébrés, l'intoxication 
secondaire à une exposition aiguë ou chronique, se caractérise par 
des mouvements musculaires involontaires et des convulsions 
épileptiformes.  En cas de survie, la récupération est totale après 
une courte durée marquée par des symptômes résiduels.  Au niveau du 
foie, on observe une activité accrue des enzymes microsomales de 
biotransformation, en particulier du système enzymatique cytochrome 
P-450/monooxygénase.  Cette induction des enzymes mircosomales est 
réversible et, au-delà d'un certain niveau, elle semble liée aux 
altérations cytoplasmiques au niveau du foie et à l'hépatomégalie 
chez les rongeurs. 

     Dans l'ensemble, d'après les observations faites sur l'aldrine 
et la dieldrine, notamment dans le cadre des études sur l'homme, on 
peut penser que, en pratique, ces produits ne contribuent guère à 
l'incidence des cancers humains. 

7.  Effets chez l'homme

     L'aldrine et la dieldrine sont très toxiques pour l'homme.  Il 
y a eu de graves cas d'intoxication accidentelle ou professionnelle 
mais il est rare qu'ils aient fait des victimes.  La plus faible 
dose ayant provoqué une issue fatale a été estimée à 10 mg/kg de 
poids corporel.  Les personnes ayant survécu à une intoxication 
aiguë ou subaiguë se sont complètement rétablies.  Aucun effet 
irréversible ni atteinte anatomopathologique résiduelle n'a été 
signalée. 

     Les effets nocifs de l'aldrine et de la dieldrine sont 
fonction de la concentration de la dieldrine dans le sang.  Le 
dosage de la dieldrine dans le sang permet de diagnostiquer avec 
précision une exposition à l'aldrine/dieldrine.  Chez les 
travailleurs, le taux sanguin au-dessous duquel on n'observe aucun 
effet nocif (dose limite sans effet nocif décelable) est de 105 
µg/litre de sang.  Cela correspond à un apport quotidien de 
dieldrine de 0,02 mg/kg de poids corporel. 

     L'exposition environnementale (principalement par 
l'intermédiairedes aliments mais aussi, dans une faible mesure, par 
voie respiratoire) entraîne l'apparition de dieldrine à une très 
faible concentration dans les organes, le sang et le lait maternel. 
Autant qu'on puisse en juger d'après des études épidémiologiques et 
cliniques poussées, il n'existe aucun raison de penser que les taux 
couramment observés dans l'organisme constituent une menace pour la 
santé de la population en général.  Lors d'une étude poursuivie 
pendant plus de 20 ans auprès de 1000 travailleurs de l'industrie, 
employés dans une fabrique d'insecticides à base d'aldrine/dieldrine, 
aucune augmentation de l'incidence des cancers n'a été observée chez 
les sujets fortement exposés à ces deux produits.  Phénomène encore 
plus significatif, aucun signe avant-coureur, sous forme d'une 
altération de la fonction hépatique, n'a été observé. 

     Une étude épidémiologique sur la mortalité a été réalisée dans 
une unité de production aux Etats-Unis, sur une cohorte de 870 
travailleurs exposés à l'aldrine, à la dieldrine et à l'endrine. 
Malgré près de 25 000 années-homme d'observation, il n'a pas été 
possible de repérer un risque particulier de cancer attributable au 
travail dans cette usine. 

EVALUATION DES DANGERS POUR LA SANTE DE L'HOMME ET DES EFFETS SUR 
L'ENVIRONNEMENT

1.  Evaluation des dangers pour la santé de l'homme

     L'aldrine et la dieldrine sont des pesticides organochlorés 
qui ont été utilisés partout dans le monde entre 1950 et le début 
des années 70 comme insecticides en agriculture et pour le 
traitement des semences, pour la destruction des ravageurs 
terricoles et d'autres types d'insectes (par exemple les termites, 
les sauterelles et les ravageurs des textiles) ainsi que pour la 
lutte contre les glossines et autres vecteurs de maladies.  Chez 
les insectes, ces composés exercent leur effet toxique par contact 
et par voie digestive.  A partir des années 70, on en a limité ou 
interdit l'emploi dans plusieurs pays, spécialement en agriculture. 
Pourtant, ils continuent d'être utilisés dans d'autres pays pour la 
destruction des termites. 

     Les deux composés sont pratiquement insolubles dans l'eau et 
modérément à très solubles dans de nombreux solvants organiques. 
Leur tension de vapeur est faible. 

     On trouve souvent de la dieldrine dans des produits laitiers 
ou carnés, le poisson, les huiles et les graisses et certains 
légumes, notamment des légumes-racines.  La limite maximale de 
résidus recommandée par les instances compétentes de la FAO/OMS 
lors des réunions conjointes sur les résidus de pesticides varie de 
0,02 à 0,2 mg/kg de produit.  Des mesures récentes ont montré que 
les teneurs effectives sont plus faibles, comme l'ont d'ailleurs 
confirmé les études sur la ration globale.  Comme l'utilisation de 
ces deux composés fait maintenant l'objet de restrictions, on 
observe une diminution lente mais régulière de la teneur en résidus 
des différentes denrées alimentaires. 

     Les quantités ingérées par l'homme avec sa ration quotidienne 
se traduisent, malgré la faible concentration de ces produits dans 
les aliments, par la présence de dieldrine dans le tissu adipeux et 
dans certains autres tissus et organes.  Des enquêtes à l'échelle 
mondiale montrent que les teneurs moyennes varient de 0,1 à 0,4 
mg/kg de tissu adipeux.  Depuis le début des années 70, cette 
concentration diminue lentement. 

     Comme le foetus est exposé par voie transplacentaire, ses 
tissus adipeux contiennent également de la dieldrine, mais à une 
concentration qui n'est que de 10 à 50% de la concentration chez la 
mère.  Il semble exister un équilibre entre les concentrations 
foetales et les concentrations maternelles.  La dieldrine est 
également excrétée dans le lait.  Une exposition est possible par 
inhalation dans les habitations où l'on utilise ce produit pour la 
destruction des termites.  Après traitement, on observe des 
concentrations atmosphériques allant de 0,01 à 7 µg/m3, selon le 
mode d'épandage, la concentration utilisée, les modalités de 
l'aération et le moment où les échantillons sont prélevés.  En 
pareilles circonstances, les aliments peuvent aussi être 
contaminés, par contact direct, ou par sorption à partir de l'air 
ambiant. 

     Le métabolisme s'effectue principalement dans le foie où 
l'aldrine se transforme rapidement en dieldrine.  Le catabolisme de 
la dieldrineest plus lent que celui de ses métabolites hydrophiles 
qui sont excrétés dans la bile et dans les urines.  La structure de 
ces métabolites a été établie.  Chez toutes les espèces étudiées, 
notamment l'homme, on a montré que les quantités 
d'aldrine/dieldrine accumulées se stabilisent à un niveau qui est 
fonction de l'apport puisqu'il existe une relation linéaire entre 
les quantités accumulées et le logarithme de l'apport.  Quand 
l'exposition prend fin, la concentration de la dieldrine dans les 
tissus de l'organisme diminue selon une loi exponentielle.  La 
toxicité aiguë de l'aldrine et de la dieldrine est importante chez 
les mammifères par voie orale, tandis que la toxicité par voie 
cutanée est modérée.  Aucune sensibilisation cutanée n'a été 
observée.  Les effets constatés à la suite d'une exposition 
expérimentale aiguë ou de courte ou longue durée intéressent le 
système nerveux central.  Le foie est également un organe cible. 
Chez les souris et les rats, on observe à ce niveau des altérations 
désignées sous le nom de "foie de rongeur sous insecticide 
organochloré". 

     Apparemment, l'aldrine et la dieldrine ne sont pas tératogènes 
à des doses inférieures à celles qui sont toxiques chez la femelle 
gravide et chez le foetus.  On n'a pas fait état de toxicité pour 
la fonction de reproduction chez le mâle ou la femelle. 

     De nombreuses études de mutagénicité  in vitro et  in vivo ont 
montré que ni l'aldrine ni la dieldrine ne sont mutagènes. 

     Lors d'études à long terme, ces deux produits ont déterminé 
chez la souris des tumeurs hépatiques, bénignes ou malignes.  En 
revanche, aucune augmentation de l'incidence des tumeurs hépatiques 
ou autres n'a été observée chez le rat ni le hamster. 

     Selon le CIRC (1987), il n'existe pas de preuves suffisantes 
d'un pouvoir cancérogène chez l'homme et les preuves de 
cancérogénicité chez l'animal d'expérience sont limitées.  
L'aldrine comme la dieldrine ont été classées dans le groupe 3, à 
savoir celui des produits chimiques dont il est impossible de 
préciser le pouvoir cancérogène chez l'homme. 

     Compte tenu des résultats obtenus lors des études de toxicité 
de courte ou de longue durée, la dose globale sans effet nocif 
décelable se situe chez le rat à 0,5 mg de dieldrine par kg de 
nourriture, soit l'équivalent de 0,025 mg/kg de poids corporel. 
Chez le chien, la dose sans effet nocif décelable est de 0,04 mg/kg 
de poids corporel.  Lors des réunions conjointes FAO/OMS de 1966 et 
1977 sur les résidus de pesticides, on a fixé la dose journalière 
admissible (DJA) à 0,1 µg/kg de poids corporel, en tenant compte de 
la non-cancérogénicité de ces deux substances pour l'homme. 

     L'aldrine et la dieldrine sont très toxiques pour l'homme.  On 
connaît des cas d'intoxication accidentelle ou professionnelle, 
mais qui ont rarement fait des victimes.  Les survivants à une 
intoxication aiguë ou subaiguë se sont entièrement rétablis.  Les 

effets nocifs sont fonction de la concentration sanguine de la 
dieldrine, dont le dosage permet de diagnostiquer avec précision 
une exposition à l'aldrine/dieldrine.  Pour taux sanguins inférieur 
à 105 µg/litre, aucun effet indésirable n'est à craindre.  Cette 
concentration constitue la dose limite sans effet nocif décelable 
et correspond à un apport quotidien de 0,02 mg de dieldrine par kg 
de poids corporel.  

    L'exposition liée à l'environnement, principalement par la voie
alimentaire, entraîne la présence de faibles concentrations de
dieldrine dans l'organisme.  D'après des études épidémiologiques et
cliniques poussées, ces teneurs ne constituent pas une menace pour
la santé humaine. 

     Aucun signe avant-coureur d'une altération de la fonction 
hépatique n'a été observé lors d'une enquête de 20 ans portant sur 
plus de 1000 ouvriers de l'industrie exposés à l'aldrine et à la 
dieldrine.  Dans cette étude ainsi que dans une autre effectuée aux 
Etats-Unis d'Amérique, aucun risque particulier de cancer n'a été 
repéré chez les personnes profesionnellement exposées à l'aldrine 
et à la dieldrine (parfois à de fortes concentrations). 

     Dans l'ensemble, d'après les observations faites sur l'aldrine 
et la dieldrine, notamment dans le cadre des études sur l'homme, on 
peut estimer que, en pratique, ces produits chimiques ne 
contribuent que très peu, sinon pas du tout, à l'incidence des 
cancers humains. 

     La photodieldrine, produit qui résulte de la dégradation de la 
dieldrine sous l'action de la lumière, est analogue à la dieldrine 
pour ce qui est de sa toxicité sur une courte durée.  Elle n'est ni 
tératogène ni cancérogène chez la souris et le rat.  L'accumulation 
de photodieldrine dans les tissus adipeux d'animaux d'expérience 
s'est révélée inférieure à celle de la dieldrine. 

2.  Evaluation des effets sur l'environnement

     La principale source de dieldrine (jusqu'à 97%) dans 
l'environnement est l'aldrine, un insecticide épandu au niveau du 
sol. L'aldrine et son produit de réaction, la dieldrine sont 
rapidement absorbé par les sols, spécialement ceux qui sont riches 
en matières organiques.  De ce fait, la pénétration est limitée et 
il n'y a généralement aucune contamination des eaux souterraines. 
Les deux composés sont entraînés principalement du fait de 
l'érosion (sous l'action du vent) et du transport des sédiments 
(eaux superficielles de ruissellement), mais non par lessivage. 

     L'emploi d'aldrine et de dieldrine en agriculture donne lieu à 
la présence de résidus (principalement de dieldrine) dans le sol où 
ils peuvent persister plusieurs années; la demi-vie de la dieldrine 
est estimée à 4 - 7 ans.  La persistance de ces composés est 
moindre dans les régions tropicales que dans les régions tempérées. 

     L'aldrine et la dieldrine passent, par volatilisation, des 
récoltes et du sol traités à l'atmosphère; elles peuvent aussi y 
pénétrer directement lors de l'épandage.  La dieldrine retourne au 
sol ou dans les étendues d'eau par les précipitations ou par dépôt 

de particules sèches.  Les composés se rencontrent donc soit en 
phase vapeur (à des concentrations très faibles, en général de 
l'ordre de 1 - 2 ng/m3), soit adsorbés sur des particules de 
poussière, soit encore dans les eaux de pluie (à des concentrations 
de l'ordre de 10 - 20 ng/litre). 

     Plusieurs auteurs ont signalé la présence de dieldrine en 
milieu aquatique.  Dans les eaux de surface, les concentrations 
sont le plus souvent très faibles, inférieures à 5 ng/litre.  Mais 
des valeurs plus élevées s'observent dans les régions soumises à 
l'érosion ou danscelles où l'on utilise ce produit en agriculture. 
Dans ces régions, les sédiments des cours d'eau peuvent renfermer 
jusqu'à 1 mg de dieldrine par kilogramme.  La forte capacité qu'ont 
les organismes aquatiques à concentrer la dieldrine à partir de 
teneurs très faibles peut aboutir à l'accumulation de doses 
toxiques.  La concentration de ce produit tout au long de la chaîne 
alimentaire aquatique est moins importante qu'une absorption 
directe à partir de l'eau. 

     Comme la dieldrine est très répandue dans l'environnement et 
qu'elle y persiste, on observe des concentrations très variées chez 
les organismes non visés.  Alors qu'auparavant les valeurs 
observées allaient de 0,001 mg à 100 mg/kg de tissu, elles sont 
aujourd'hui le plus souvent inférieures à 1 mg/kg de tissu. 

     Dans les écosystèmes terrestres, l'aldrine et la dieldrine 
s'accumulent chez divers organismes, principalement sous forme de 
dieldrine.  Cette dernière est probablement responsable de la mort 
de mammifères dans la nature et de la raréfaction de certaines 
espèces, comme la loutre.  Certains petits mammifères périssent 
sans doute après avoir mangé des céréales traitées mais il est 
probable que leurs populations se reconstituent par immigration à 
partir des zones voisines.  Les oiseaux de proie qui mangent de 
petits mammifères et de petits oiseaux contaminés par la dieldrine 
absorbent et concentrent cet insecticide dans leurs tissus et leurs 
oeufs.  Des oiseaux granivores ont été tués par la consommation de 
céréales traitées.  Il est probable que la raréfaction des oiseaux 
de proie s'explique par la présence dans leurs tissus de résidus de 
dieldrine (entre autres organochlorés).  Les effets de la dieldrine 
se manifestent avec un certain retard car les résidus s'accumulent 
dans les graisses pendant l'hiver d'où ils ne se libèrent qu'au 
printemps.  Le fait de n'utiliser la dieldrine qu'à certaines 
époques de l'année n'a pas réduit la mortalité des oiseaux. 

     La large utilisation d'aldrine et de dieldrine, parallèlement 
à celle d'autres organochlorés, a exercé des effets très nocifs sur 
l'environnement mais grâce à des restrictions draconiennes, 
particulièrement en ce qui concerne les semences traitées, les 
populations d'oiseaux commencent à se reconstituer. 

3.  Conclusions

     a) L'aldrine et la dieldrine ont donné lieu à des études 
poussées et variées sur le plan toxicologique, clinique et 
épidémiologique.  La charge de l'organisme résulte principalement 

de l'ingestion de résidus présents dans la nourriture (les 
quantités ingérées semblant diminuer de façon générale et tomber 
en-dessous des DJA fixées) et, dans une moindre mesure, de 
l'inhalation de ces produits.  D'après l'étude des données, on a 
tout lieu de penser que la charge de l'organisme résultant du 
niveau actuel d'exposition ne menace en aucun cas la santé de la 
population dans son ensemble. 

     b) La dieldrine se rencontre presque partout dans le lait 
maternel.  Mais, sa concentration dans le sang et dans le tissu 
adipeux des nourrissons n'augmente pas avec l'âge au cours des six 
premiers mois de leur vie et le taux sanguin n'est pas plus élevé 
que chez un enfant nourri au biberon.  Dans ces conditions, 
l'allaitement au sein reste la méthode de choix pour nourir les 
nourissons malgré la présence de résidus de dieldrine. 

     c) Lors du traitement de locaux, notamment pour la destruction 
des termites, l'exposition des occupants ne semble pas présenter 
des risques pour leur santé, pour autant que le traitement 
s'effectue correctement. 

     d) Malgré leur toxicité élevée, l'aldrine et la dieldrine 
peuvent être manipulées sans danger dans la mesure où l'on observe 
toujours les précautions recommandées en vue de réduire au minimum 
l'exposition des opérateurs.  Dans le cas contraire, il y a risque 
d'intoxication. 

     e) Pendant la période où l'on a massivement utilisé l'aldrine 
et la dieldrine, c'est-à-dire de 1950 au début des années 70, il 
est certain que cette pratique a eu des effets dommageables sur 
diverses espèces.  Ces effets sont imputables en partie à la 
dieldrine à côté d'autres organochlorés.  Depuis qu'on a limité de 
façon draconienne l'utilisation de ces produits, les espèces 
touchées se sont reconstituées. 

RECOMMENDATIONS

     1. Il faut effectuer des études de tératogénicité 
complémentaires sur le hamster, bien conçues, avec des doses 
réalistes de dieldrine. 

     2. Dans l'étude du mécanisme de la cancérogenèse, on 
s'efforcera d'expliquer pourquoi les réactions hépatiques sont si 
différentes chez la souris et chez les autres espèces. 

     3. On continuera d'utiliser la dieldrine pour l'étude des 
mécanismes neurotoxiques, à la fois sur le plan expérimental et sur 
le plan clinique. 

     4. Pour des raisons écologiques, toute reprise d'une 
utilisation massive d'aldrine et de dieldrine est exclue, et on 
n'utilisera ces produits que s'il n'existe pas de produit moins 
nocif d'efficacité équivalente. 

     5. Afin de préserver la santé et le bien-être des travailleurs 
et de la population en général, il convient de ne confier la 
manipulation et l'épandage de l'aldrine et de la dieldrine qu'à des 
opérateurs compétents et dûment formés, qui devront appliquer les 
mesures de sécurité qui s'imposent. 

     6. En raison du risque d'intoxication accidentelle par 
l'aldrine, spécialement chez les enfants, il faut en interdire 
l'utilisation sous forme de granulés contre les fourmis. 

    See Also:
       Toxicological Abbreviations
       Aldrin and dieldrin (HSG 21, 1989)