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    INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY



    ENVIRONMENTAL HEALTH CRITERIA 83






    DDT AND ITS DERIVATIVES - ENVIRONMENTAL ASPECTS


                          








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

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

    World Health Orgnization
    Geneva, 1989


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CONTENTS

ENVIRONMENTAL HEALTH CRITERIA FOR DDT AND ITS DERIVATIVES - ENVIRONMENTAL 
ASPECTS 

1. SUMMARY AND CONCLUSIONS

    1.1. Physical and chemical properties
    1.2. Uptake, accumulation, and degradation
    1.3. Toxicity to microorganisms
    1.4. Toxicity to aquatic invertebrates
    1.5. Toxicity to fish
    1.6. Toxicity to amphibians
    1.7. Toxicity to terrestrial invertebrates
    1.8. Toxicity to birds
    1.9. Toxicity to non-laboratory mammals

2. PHYSICAL AND CHEMICAL PROPERTIES OF DDT AND RELATED COMPOUNDS

3. KINETICS, METABOLISM, BIOTRANSFORMATION, AND BIOACCUMULATION

    3.1. Retention in soils and sediments and plant uptake 
    3.2. Uptake and accumulation by organisms
         3.2.1. Plants
         3.2.2. Microorganisms
         3.2.3. Aquatic invertebrates
         3.2.4. Fish                                            
         3.2.5. Terrestrial invertebrates                       
         3.2.6. Birds                                           
         3.2.7. Mammals                                         

4. TOXICITY TO MICROORGANISMS                                      
  
    4.1. Bacteria and cyanobacteria (blue-green algae)           
    4.2. Freshwater microorganisms                               
    4.3. Marine microorganisms                                   
    4.4. Soil microorganisms                                     
    4.5. Fungi                                                   

5. TOXICITY TO AQUATIC ORGANISMS                                   

    5.1. Aquatic invertebrates                                   
         5.1.1. Short-term and long-term toxicity               
         5.1.2. Physiological effects on aquatic invertebrates
    5.2. Fish                                                    
         5.2.1. Short-term and long-term direct toxicity to fish 
         5.2.2. Sublethal behavioural effects on fish
         5.2.3. Physiological effects on fish
         5.2.4. Development of tolerance
    5.3. Toxicity to amphibians

6. TOXICITY TO TERRESTRIAL ORGANISMS                               
   
    6.1. Terrestrial invertebrates
    6.2. Birds                                                   
         6.2.1. Short-term and long-term toxicity to birds      

         6.2.2. Toxicity to birds' eggs                         
         6.2.3. Reproductive effects on birds                   
         6.2.4. Reproductive hormones and behaviour             
         6.2.5. Reproductive effects on the male                
         6.2.6. Effects on the thyroid and adrenal glands in birds
         6.2.7. Special studies in birds                        
         6.2.8. Synergism with other compounds in birds         
    6.3. Non-laboratory mammals                                  

7. ECOLOGICAL EFFECTS FROM FIELD APPLICATION                       

8. EVALUATION                                                      

    8.1. Aquatic organisms                                       
    8.2. Terrestrial organisms                                   
                                                                        
REFERENCES
                                                             
WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR
DDT AND ITS DERIVATIVES - ENVIRONMENTAL ASPECTS

 Members 

Dr L.A.  Albert, Environmental Pollution Programme, National Institute
   for Research on Biotic Resources, Xalapa, Mexico
Mr H.   Craven,  Ecological  Effects  Branch,   Office  of  Pesticides
   Programs, US Environmental Protection Agency, Washington DC, USA
Dr A.H.  El-Sebae,  Division  of  Pesticide  Toxicology,  Faculty   of
   Agriculture, Alexandria University, Alexandria, Egypt
Dr J.W.  Everts,  Department  of Toxicology,  Agricultural University,
   Wageningen, Netherlands
Dr W.  Fabig,  Fraunhofer  Institute for  Environmental  Chemistry and
   Ecotoxicology,   Schmallenberg-Grafschaft,   Federal  Republic   of
   Germany
Dr R. Koch, Division of Toxicology, Research Institute for Hygiene and
   Microbiology, Bad Elster, German Democratic Republic (Chairman)
Dr Y.  Kurokawa,  Division  of Toxicology,  Biological Safety Research
   Centre, National Institute of Hygienic Sciences, Tokyo, Japan
Dr E.D.  Magallona,  Pesticide  Toxicology and  Chemistry  Laboratory,
   University of the Philippines at Los Baos, College of Agriculture,
   Laguna, Philippines
Professor   P.N.   Viswanathan,   Ecotoxicology   Section,   Industrial
   Toxicology Research Centre, Lucknow, India

 Observers 
---------

Dr M.A.S.  Burton, Monitoring and Assessment  Research Centre, London,
   United Kingdom
Dr I.   Newton,   Institute   of  Terrestrial   Ecology,   Monks  Wood
   Experimental Station, Huntingdon, United Kingdom

 Secretariat 
-----------

Dr S.   Dobson,   Institute   of  Terrestrial   Ecology,   Monks  Wood
   Experimental Station, Huntingdon, United Kingdom ( Rapporteur )
Dr M.  Gilbert,  International  Programme on  Chemical  Safety,  World
   Health Organization, Geneva, Switzerland ( Secretary )
Mr P.D.   Howe,   Institute   of  Terrestrial   Ecology,   Monks  Wood
   Experimental Station, Huntingdon, United Kingdom

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.  988400 - 985850).

ENVIRONMENTAL HEALTH CRITERIA FOR DDT AND ITS DERIVATIVES -ENVIRONMENTAL 
ASPECTS 

    A WHO Task Group on Environmental Health Criteria for DDT and its
Derivatives - Environmental Aspects met at the Institute of Terrestrial
Ecology, Monks Wood, United Kingdon, from 14 to 18 December 1987.  Dr. I.
Newton welcomed the participants on behalf of the three co-sponsoring 
organizations of the IPCS (ILO/UNEP/WHO).  The Task Group reviewed and
revised the draft criteria document and made an evaluation of the risks
for the environment from exposure to DDT and its derivatives.

     The first draft of this document was prepared by Dr. S. Dobson and
Mr. P.D. Howe, Institute of Terrestrial Ecology.  Dr. M. Gilbert and Dr.
P.G. Jenkins, both members of the IPCS Central Unit, were responsible for
the overall scientific content and editing, respectively.


                                *    *    *


     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.



INTRODUCTION

    There  is  a  fundamental  difference  in  approach   between   the
toxicologist  and the ecotoxicologist  concerning the appraisal  of the
potential  threat posed by  chemicals.  The toxicologist,  because  his
concern  is with  human health  and welfare,  is preoccupied  with  any
adverse  effects on  individuals, whether  or not  they  have  ultimate
effects  on performance or survival.  The ecotoxicologist, in contrast,
is  concerned primarily with  the maintenance of  population levels  of
organisms in the environment.  In toxicity tests, he is  interested  in
effects on the performance of individuals - in their  reproduction  and
survival - only insofar as these might ultimately affect the population
size.  To him, minor biochemical and physiological effects of toxicants
are irrelevant if they do not, in turn, affect reproduction, growth, or
survival.

    It  is the aim of this document to take the ecotoxicologist's point
of  view  and  consider effects  on  populations  of organisms  in  the
environment.   The risk to human health of the use of DDT was evaluated
in  Environmental Health  Criteria 9:  DDT and  its  Derivatives  (WHO,
1979).   This  document did  not consider effects  on organisms in  the
environment,  but did consider  environmental levels of  DDT likely  to
arise from recommended uses.  No attempt has been made here to reassess
the  human  health  risk; the  interested  reader  should refer  to the
original  document,  which contains  the  relevant literature  in  this
area.

    This  document,  although  based  on  a  thorough  survey  of   the
literature,  is not intended to be exhaustive in the material included.
In  order to  keep the  document concise,  only those  data which  were
considered to be essential in the evaluation of the risk posed  by  DDT
to the environment have been included.

    The term bioaccumulation indicates that organisms take up chemicals
to  a  greater concentration  than that found  in their environment  or
their  food.   'Bioconcentration  factor'  is  a  quantitative  way  of
expressing  bioaccumulation:   the ratio  of  the concentration  of the
chemical  in the organism to  the concentration of the  chemical in the
environment or food.  Biomagnification refers, in this document, to the
progressive accumulation of chemicals along a food chain.

1.  SUMMARY AND CONCLUSIONS

1.1 Physical and Chemical Properties

    DDT is an organochlorine insecticide which is a  white  crystalline
solid,  tasteless  and  almost  odourless.   Technical  DDT,  which  is
principally  the  p,p'  isomer, has  been  formulated in  almost every
conceivable form.

1.2  Uptake, Accumulation, and Degradation

    The  physicochemical properties of  DDT and its  metabolites enable
these  compounds  to  be taken  up  readily  by organisms.   High lipid
solubility  and low water solubility  lead to the retention  of DDT and
its stable metabolites in fatty tissue.  The rates of accumulation into
organisms vary with the species, with the duration and concentration of
exposure, and with environmental conditions.  The high retention of DDT
metabolites means that toxic effects can occur in organisms  remote  in
time and geographical area from the point of exposure.
   
    These compounds are resistant to breakdown and are readily adsorbed
to  sediments  and soils  that can act  both as sinks  and as long-term
sources of exposure (e.g., for soil organisms).
   
    Organisms  can  accumulate  these chemicals  from  the  surrounding
medium and from food.  In aquatic organisms, uptake from the  water  is
generally  more important, whereas, in terrestrial fauna, food provides
the major source.
   
    In general, organisms at higher trophic levels tend to contain more
DDT-type compounds than those at lower trophic levels.
   
    Such compounds can be transported around the world in the bodies of
migrant animals and in ocean and air currents.

1.3 Toxicity to Microorganisms

    Aquatic  microorganisms are more sensitive than terrestrial ones to
DDT.
    
    An  environmental exposure concentration of 0.1 g/litre  can cause
inhibition of growth and photosynthesis in green algae.
    
    Repeated  applications  of  DDT can  lead  to  the  development  of
tolerance in some microorganisms.
    
    There  is  no  information  concerning  the  effects   on   species
composition  of microorganism communities.  Therefore,  it is difficult
to  extrapolate the relevance of  single-culture studies to aquatic  or
terrestrial  ecosystems.   However,  since microorganisms  are basic in
food  chains,  adverse effects  on  their populations  would  influence
ecosystems.   Thus,  DDT and  its metabolites should  be regarded as  a
major environmental hazard.


1.4 Toxicity to Aquatic Invertebrates

    Both the acute and long-term toxicities of DDT vary between species
of   aquatic  invertebrates.   Early  developmental   stages  are  more
sensitive than adults to DDT.  Long-term effects occur  after  exposure
to  concentrations ten  to a  hundred times  lower than  those  causing
short-term effects.
    
    DDT is highly toxic, in acute exposure, to aquatic invertebrates at
concentrations  as low as 0.3 g/litre.   Toxic effects include impair-
ment of reproduction and development, cardiovascular modifications, and
neurological  changes.  Daphnia reproduction  is adversely affected  by
DDT at 0.5 g/litre.
    
    The  influence  of  environmental variables  (such  as temperature,
water  hardness,  etc.) is  documented but the  mechanism is not  fully
understood.    In  contrast  to  the  data  on  DDT,  there  is  little
information on the metabolites DDE or TDE.  The reversibility  of  some
effects, once exposure ceases, and the development of  resistance  have
been reported.

1.5 Toxicity to Fish

    DDT  is  highly toxic  to fish; the  96-h LC50s   reported  (static
tests) range from 1.5 to 56 g/litre  (for largemouth bass  and  guppy,
respectively).  Smaller fish are more susceptible than larger  ones  of
the same species.  An increase in temperature decreases the toxicity of
DDT to fish.
   
    The  behaviour of  fish is  influenced by DDT.  Goldfish exposed to
1  g/litre   exhibit hyperactivity.  Changes  in the feeding of  young
fish  are caused by DDT levels commonly found in nature, and effects on
temperature preference have been reported.
   
    Residue levels of > 2.4 mg/kg in eggs of the winter flounder result
in  abnormal embryos in the  laboratory, and comparable residue  levels
have been found to relate to the death of lake trout fry in the wild.
   
    Cellular  respiration  may be  the main toxic  target of DDT  since
there are reports of effects on ATPase.
   
    The toxicity of TDE and DDE has been less studied than that of DDT.
However,  the data available on rainbow trout and bluegill sunfish show
that TDE and DDE are both less toxic than DDT.

1.6 Toxicity to Amphibians

    The toxicity of DDT and its metabolites to amphibians  varies  from
species to species; although only a few data are  available,  amphibian
larvae seem to be more sensitive than adults to DDT.  TDE seems  to  be
more  toxic than DDT to amphibians, but there are no data available for
DDE.  All the studies reported have been static tests  and,  therefore,
results should be treated with caution.

1.7 Toxicity to Terrestrial Invertebrates

    There  have  been  few reports  on  the  effects  of  DDT  and  its
metabolites on non-target terrestrial invertebrates.
 
    Earthworms  are insensitive to the  acutely toxic effects of  these
compounds  at  levels  higher than  those  likely  to be  found  in the
environment.   The  uptake  of DDT  by  earthworms  is related  to  the
concentrations  in soil and  to the activity  of the worms;  seasonally
greater  activity  increases  uptake.  Thus,  although  earthworms  are
unlikely to be seriously affected by DDT, they pose a major  hazard  to
predators because of the residues they can tolerate.
 
    Both  DDT and DDE are  classified as being relatively  non-toxic to
honey bees, with a topical LD50 of 27 g/bee.
 
    There  are no reports  on laboratory studies  using DDE or  TDE, in
spite of the fact that these are major contaminants of soil.

1.8 Toxicity to Birds

    DDT and its metabolites can lower the reproductive rate of birds by
causing eggshell thinning (which leads to  egg breakage) and by causing
embryo  deaths.  However,  different groups  of birds  vary greatly  in
their  sensitivity to these  chemicals; predatory birds  are  extremely
sensitive  and, in the wild,  often show marked shell  thinning, whilst
gallinaceous   birds  are  relatively  insensitive.    Because  of  the
difficulties  of  breeding  birds of  prey  in  captivity, most  of the
experimental  work has been done  with insensitive species, which  have
often  shown little  or no  shell thinning.   The few  studies on  more
sensitive  species have shown shell thinning at levels similar to those
found in the wild.  The lowest dietary concentration of DDT reported to
cause shell thinning experimentally was 0.6 mg/kg for the  black  duck.
The mechanism of shell thinning is not fully understood.

1.9 Toxicity to non-laboratory Mammals

    Experimental  work suggests that  some species, notably  bats,  may
have  been  affected by  DDT and its  metabolites.  Species which  show
marked  seasonal  cycles in  fat content are  most vulnerable, but  few
experimental  studies on such species  have been made.  In  contrast to
the   situation   in  birds,  where  the  main  effect  of  DDT  is  on
reproduction,  the main  known effect  in mammals  is to  increase  the
mortality  of migrating  adults.  The  lowest acute  dose  which  kills
American big brown bats is 20 mg/kg.  Bats collected from the wild (and
containing residues of DDE in fat) die after  experimental  starvation,
which simulates loss of fat during migration.

2.  PHYSICAL AND CHEMICAL PROPERTIES OF DDT AND RELATED COMPOUNDS
    
    The  term DDT  is  generally  understood  throughout  the world and
refers   to  p,p' -DDT   (1,1 -[2,2,2-trichloroethylidine]-bis [4-chloro-
benzene]).  The compound's structure permits several different isomeric
forms,  such  as   o,p' -DDT   (1-chloro-2-[2,2,2-trichloro-1-(4-chloro-
phenyl)  ethyl] benzene).  The term  DDT is also applied  to commercial
products  consisting predominantly of  p,p' -DDT  with smaller amounts of
other  compounds.  A typical example of technical DDT had the following
constituents:  p,p' -DDT,    77.1%;  o,p' -DDT,    14.9%;  p,p' -TDE,  0.3%;
 o,p' -TDE,    0.1%;  p,p' -DDE,   4%;  o,p' -DDE,   0.1%;  and  unidentified
products, 3.5%.
    
    All   isomers   of  the  compound  DDT  are   white,   crystalline,
tasteless,   almost  odourless  solids,  with   the  empirical  formula
C14H9Cl5  and a relative  molecular mass of  354.5.  The  melting
range  of  p,p' -DDT  is 108.5   to  109 C and  its  vapour pressure  is
2.53  x 10-5   Pa  (1.9 x 10-7  mmHg) at 20 C.   DDT is  soluble  in
organic  solvents as follows (g/100  ml):  benzene, 106; cyclohexanone,
100;  chloroform, 96; petroleum  solvents, 4-10; ethanol,  1.5.  It  is
highly  insoluble in water  (solubility approximately 1 g/litre)   but
very soluble in animal fats.  The octanol-water  partition  coefficient
(log kow) is 7.48
    
    The  chemical structure of some of the analogues of DDT is shown in
Table  1.   The  structure  of  the  o,p' - and  m,p' -compounds can be
inferred  from those of the  p,p' -isomers  presented in the table.  The
table   is   confined  to  compounds  that  occur  in  commercial  DDT,
metabolites formed from them, and analogues that have had some  use  as
insecticides.   It  must  be  emphasized  that  even  the commercially-
available  insecticidal analogues have strikingly different properties.
Especially  remarkable is the slow metabolism and marked storage of DDT
and  its metabolite DDE and the rapid metabolism and negligible storage
of methoxychlor.
    
    Technical  DDT has been formulated in almost every conceivable form
including  solutions in xylene  or petroleum distillates,  emulsifiable
concentrates,   water-wettable   powders,  granules,   aerosols,  smoke
candles,  charges  for  vaporizers  and  lotions.   Aerosols  and other
household formulations are often combined with synergized pyrethroids.
    
    This   is  a  summary  of   part  of  the  relevant   section  from
Environmental Health Criteria 9: DDT and its Derivatives  (WHO,  1979).
Further   details,  including  information  on   analysis,  sources  of
pollution,   and  environmental  distribution  can  be  found  in  this
document.

Table 1.  Structure of  p,p' -DDT and its analogues of the form:

TABLE 1
------------------------------------------------------------------------------------
Name                 Chemical name                       R       R'    R"
DDT and its major
metabolites
------------------------------------------------------------------------------------
DDT                  1,1'-(2,2,2-trichloroethylidene)-   -Cl     -H    -CCl3
                     bis[4-chlorobenzene]
DDEa                 1,1'-(2,2-dichloroethenylidene)-    -Cl     None  =CCl2
                     bis[4-chlorobenzene]
TDE(DD)a,b           1,1'-(2,2-dichloroethylidene)-      -Cl     -H    -CHCl2
                     bis[4-chlorobenzene]
DDMUa                1,1'-(2-chloroethenyldene)-         -Cl     None  =CHCl
                     bis[4-chlorobenzene]-
DDMSa                1,1'-(2-chloroethylidene)-          -Cl     -H    -CH2Cl
                     bis[4-chlorobenzene]
DDNUa                1,1'-bis(4-chlorophenyl)ethlyene    -Cl     None  =CH2
DDOHa                2,2-bis(4-chlorophenyl)ethanol      -Cl     -H    -CH2OH
DDAa                 2,2-bis(4-chlorophenyl)-            -Cl     -H    -C(O)OH
                     acetic acid

Some related insecticides
                                                                       NO2
Bulan(r)             2-nitro-1,1-bis-                    -Cl     -H    |
                     (4-chlorophenyl)butane                           -CHC2H5

                                                                       NO2
Prolan(r)            2-nitro-1,1-bis-                    -Cl     -H    |
                     (4-chlorophenylpropane                           -CHCH2

DMC                  4-chloro-a-(4-chlorophenyl)-        -Cl     -OH   -CH3
                     a-(methyl)benzenemethanol
dicocol              4-chloro-a-(4-chlorophenyl)-a-      -Cl     -OH   -CCl3
(Kelthane(r))        (trichloromethyl)benzenemethanol
chlorobenzilatec     ethyl 4-chloro-a-(4-chlorophenyl)-  -Cl     -OH   -C(O)OC2H5
                     a-hydroxybenzeneacetate
chloropropopylatec   1-methylethyl 4-chloro-a-           -Cl     -OH   -C(O)OCH(CH3)2
                     (4-chlorophenyl)-a-hydroxy-
                     benzeneacetate

   Table 1.  Structure of  p,p' -DDT and its analogues of the form (continued)
------------------------------------------------------------------------------------
Name                 Chemical name                       R       R'    R"
DDT and its major
metabolites
------------------------------------------------------------------------------------

methoxychlorc        1,1'-(2,2,2-trichloroethylidene)-   -OCH3   -H    -CCl3
                     bis[4-methoxybenzene]
Perthane(r)          1,1'-(2,2-dichloroethylidene)-      -C2H5   -H    -CHCl2
                     bis[4-ethylbenzene]
DFDT                 1,1'-(2,2,2-trichloroethylidene)-   -F      -H    -CCl3
                     bis[4-fluorobenzene]
------------------------------------------------------------------------------------
a Recognized metabolite of DDT in the rat.
b As an insecticide, this compound has the ISO approved name of TDE, and it has been 
  sold under the name Rothane(r); in metabloic studies the same compound has been 
  referred as DDD; as a drug, it is called mitotane.
c Common name approved by the International Organization for Standardization (ISO).
(r) Registered.

3.  KINETICS, METABOLISM, BIOTRANSFORMATION, AND BIOACCUMULATION

Appraisal

     The  physicochemical properties of  DDT and its  metabolites enable
 these  compounds  to be  taken up readily  by organisms.  The  rates of
 accumulation vary with the species, with the duration and concentration
 of exposure, and with environmental conditions.

     These compounds are resistant to breakdown and are readily adsorbed
 to  sediments  and  soils, which can act both as sinks and as long-term
 sources of exposure (e.g., for soil organisms).

     Organisms  can  accumulate  these chemicals  from  the  surrounding
 medium and from food.  In aquatic organisms, uptake from the  water  is
 generally  more important, whereas, in terrestrial fauna, food provides
 the major source.

     In general, organisms at higher trophic levels tend to contain more
 DDT-type compounds than those at lower trophic levels.

     Such compounds can be transported around the world in the bodies of
 migrant animals and in ocean and air currents.

    Different  organisms metabolise DDT via different pathways.  Of the
two  initial metabolites, DDE  is the more  persistent, though not  all
organisms produce DDE from DDT.  The alternative route  of  metabolism,
via  TDE leads  to more  rapid elimination  (WHO, 1979).   Much of  the
retained  DDT and  its metabolites  are stored  in lipid-rich  tissues.
Because  there is an annual  cycle in lipid storage  and utilization in
many  organisms, there is also a related annual cyclic pattern  in  the
handling of DDT.

3.1 Retention in Soils and Sediments and Plant Uptake

    Shin et al. (1970) investigated the adsorption of DDT by  soils  of
various  different types and by isolated soil fractions.  A sandy loam,
a clay soil, and a highly organic muck were either used intact  or  had
various   components  extracted  before  estimating   their  adsorptive
capacity for the insecticide.  Adsorption was least in the  sandy  loam
and  greatest in the muck  (distribution coefficients [Kd] were  in the
ratio   1:10:80   for  sandy   loam,  clay  soil,   and  organic  muck,
respectively).   All soils showed a strong adsorptive capacity for DDT.
The adsorption of DDT was closely related to the organic matter content
of the soils; progressive removal of lipids,  resins,  polysaccharides,
polyuronides, and humic matter identified the organic  fractions  which
bound  the DDT.  Humic material represents a major source of adsorptive
capacity  for  DDT;  the  degree  of  sorption,  however,  is  strongly
connected  with  the degree  of  humification.  Soil  containing  large
amounts  of humic material may not adsorb DDT as greatly as other soils
where humification is more advanced.  Wheatley (1965)  estimated  half-
times for the loss of DDT applied to soils.  After surface application,
50% of DDT was lost within 16-20 days.  The estimated time for the loss
of 90% of surface-applied DDT was 1.5 to 2 years.  With  DDT mixed into
the  soil, 50% loss occurred in 5 to 8 years, and it was estimated that
90% of applied insecticide would be lost in 25-40 years.

    Albone   et   al.  (1972)  investigated  the  capacity   of   river
sediments,  from the Severn  Estuary, United Kingdom,  to degrade  DDT.
 p,p' -DDT   (14C-labelled)   was applied to sediments either  in situ  on
the  mud flats or in the laboratory.   Sediment movement in the area of
the  in situ  study was sufficiently  small to neither bury  nor expose
the  incubation  tubes set  into the mud.   Incubation  in situ  over  46
days  led  to very  little  metabolism of  DDT in the  sediments.  Some
 p,p' -TDE    was produced, but the  ratio of DDT to  TDE was 13 : 1  and
48 : 1  in  two  replicate experiments.   There  was  no production  of
extractable  polar  products; metabolism  beyond  TDE did  not   occur.
Incubation of the same sediments in the laboratory, over 21  days,  led
to  much greater metabolism (ratios of 1 : 1.1 and 1 : 3.3, DDT to TDE,
in  replicate  incubations) and  the  production of  some unidentified,
further  breakdown products.  Investigation of the microbial population
of  the sediment  showed that  some of  the organisms  were capable  of
degrading DDT; little metabolism appeared to take place  in situ .

3.2 Uptake and Accumulation by Organisms

    The  uptake  and  accumulation of  DDT  and  its  metabolites  into
organisms,  as  determined  in controlled  laboratory  experiments,  is
summarized  in  Table 2.   Results  are expressed  as  bioconcentration
factors (the ratio of the concentration of the compound in the organism
to the concentration in the medium).
   
    Concentration  factors can be misleading with compounds such as DDT
when exposure is high.  The compound is readily taken up  and  retained
at very low concentrations.  At high concentrations, no  more  material
can  be  taken  up because  a  plateau  has  been  reached.   The  only
meaningful  way   to assess  the capacity of  organisms to take  up and
retain  DDT is by looking  over a wide range  of exposure levels.   The
low concentration factor quoted in Table 2 for earthworms, for example,
reflects  the high exposure rather  than a low capacity  for uptake and
retention  of  DDT, because  concentration  factors are  simple  ratios
between "exposure" and final concentration in the organism.
    
    Concentration  factors for fish are generally higher than for their
invertebrate prey (Table 2).  It is now generally agreed that  most  of
the DDT taken into aquatic organisms comes from the water  rather  than
from their food (Moriarty, 1975).  Again, the concentration factors can
be  misleading.   Aquatic  organisms take  in  a  small  proportion  of
ingested DDT.  However, they retain a large proportion of the DDT which
has  been absorbed into the  body from the food.   There has been  some
controversy in the past over explanations for higher  accumulations  of
DDT  at higher trophic levels  in aquatic systems.  It  now seems clear
that this is not due primarily to biomagnification up food  chains  but
rather  to  a  tendency  for  organisms  at  higher trophic  levels  to
accumulate more DDT directly from the water.

    Terrestrial organisms do not live in a uniform medium surrounded by
a relatively constant concentration of a chemical.  Even soil organisms
live  in  a  medium with  very  variable  concentrations of  DDT or its
metabolites at different levels of the soil profile or  patchy  distri-
bution of the chemical.  Some terrestrial organisms could  be  directly
exposed  to DDT during application of the insecticide, but most will be

exposed  to what  remains of  the DDT  after  application.   Therefore,
higher  terrestrial  organisms will  accumulate  DDT mostly  from their
food.   The  data  in Table  2  are  taken from  controlled  laboratory
investigations.  There is ample evidence from the field that  DDT  does
accumulate  in many organisms in  different media.  There is  similarly
evidence  that  the  residues of  DDT  or  its metabolites  persist  in
organisms  for long periods after  exposure has ceased.  The  following
should not be regarded as a comprehensive review of the  literature  on
this  subject, which is  too large to  be included.  Rather,  these are
examples from different groups of organisms.


Table 2.  Bioaccumulation of DDTa 
---------------------------------------------------------------------------------------------------------
Organism                Biomass  Flow   Organ  Tem-     Duration   Exposure    Bioconcen-  Reference 
                        (g/ml)  statb         perature            (g/litre)  tration
                                               ( C)                           factorc
---------------------------------------------------------------------------------------------------------
Bacteria

 Aerobacter aerogenes    100                    22       24 h       1.2         3736        Johnson & 
 Bacillus subtilis       130                    22       24 h       0.676       4303        & Kennedy 
 Aerobacter aerogenes    25                     22       4 h        0.64        10 639      (1973)
                        200                    22       4 h        0.64        1784        Johnson & 
 Bacillus subtilis       43                     22       4 h        0.64        13 880      Kennedy 
                        348                    22       4 h        0.64        1805        (1973)

Marine algae

 Cyclotella nana         17                     23       2 h        0.7         37 600      Rice & Sikka 
                        8                      23       2 h        0.7         58 100      (1973)
 Isochrysis galbane      39                     23       2 h        0.7         11 300      Rice & Sikka
                        19                     23       2 h        0.7         28 800      (1973)
 Olisthodiscus luteus    108                    23       2 h        0.7         4600        Rice & Sikka
                        54                     23       2 h        0.7         7000        (1973)

 Amphidinium carteri     66                     23       2 h        0.7         4300        Rice & Sikka
                        33                     23       2 h        0.7         9600        (1973)
 Tetraselmis chuii       106                    23       2 h        0.7         5200        Rice & Sikka
                        53                     23       2 h        0.7         6300        (1973)
 Skeletonema costatum    29                     23       2 h        0.7         31 900      Rice & Sikka
                        15                     23       2 h        0.7         38 400      (1973)

Diatom

 Cylindrotheca                                           21 days    100         300         Keil & Priester 
 closterium                                                                                 (1969)

Pond snail                       stat                   6 days     3.0         6000        Reinbold et al. 
 (Physa 5 sp.)                                                                              (1971)

Freshwater mussel                flow          20       3 weeks    0.62        3990d       Bedford & Zabik 
 (Anodonta grandis)                                                                         (1973)

Table 2.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism                Biomass  Flow   Organ  Tem-     Duration   Exposure    Bioconcen-  Reference
                        (g/ml)  statb         perature            (g/litre)  tration
                                               ( C)                           factorc
---------------------------------------------------------------------------------------------------------

Earthworm                                      10       4 weeks    17 000      0.47d       Davis (1971)
 (Lumbricus terrestris) 

Water flea                       stat          30       3 days     2.0         1330        Metcalf et al.  
                                                                                           (1973)
 (Daphnia magna)                  flow          21       3 days     0.08        114 100     Johnson et al.  
                                                                                           (1971)
Scud                             flow          21       3 days     0.081       20 600      Johnson et al.  
 (Gammarus fasciatus)                                                                       (1971)

Glass shrimp                     flow          21       3 days     0.1         5000        Johnson et al.  
 (Palaemonetes kadiakensis)                                                                 (1974)

Pink shrimp                      flow          8-15     13 days    0.14        1500        Nimmo et al.  
 (Penaeus duorarum)                                                                         (1970)

Crayfish                         flow          21       3 days     0.08        2900        Johnson et al.  
 (Orconectes nais)                                                                          (1971)

Mayfly larva                     flow          21       3 days     0.052       32 600      Johnson et al.  
 (Hexagenia bilineata)                                                                      (1971)

Mayfly larva                     flow          21       3 days     0.047       22 900      Johnson et al.  
 (Siphlonurus sp.)                                                                          (1971)

Dragonfly nymph                  flow          21       2 days     0.101       3500        Johnson et al.  
 (Ischnura verticalis)                                                                      (1971)

Dragonfly nymph                  flow          21       2 days     0.079       910         Johnson et al.  
 (Libellula sp.)                                                                            (1971)

Midge larva                      flow          21       3 days     0.046       47 800      Johnson et al.  
 (Chironomus sp.)                                                                           (1971)

Mosquito larva                   flow          21       2 days     0.105       133 600     Johnson et al.  
 (Culex pipiens)                                                                            (1971)

Table 2.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism                Biomass  Flow   Organ  Tem-     Duration   Exposure    Bioconcen-  Reference
                        (g/ml)  statb         perature            (g/litre)  tration
                                               ( C)                           factorc
---------------------------------------------------------------------------------------------------------

Mosquito larva                   stat          30       3 days     2.0         110d        Metcalf et al.
 (Culex quinquifasciatus)         stat          30       3 days     0.9         74d         (1973)
                                        
Mosquito fish                    stat          30       3 days     2.0         344d        Metcalf et al.
 (Gambusia affinis)               stat          30       3 days     0.9         217d        (1973)

Rainbow trout                    flow          5        12 weeks   0.176       21 363d     Reinert et al.  
 (Salmo gairdneri)                flow          10       12 weeks   0.137       43 158d     (1974)
                                 flow          15       12 weeks   0.133       51 355d     Reinert et al.  
                                                                                           (1974)
Brook trout                      flow          14       120 days   3 mg        0.64d       Macek & Korn 
 (Salvelinus fontinalis)                                            /kg diet                (1970)
                                 flow          14       120 days   0.003       8533d       Macek & Korn 
                                                                                           (1970)
Pinfish                          flow                   14 days    0.1         40 000d     Hansen & Wilson
 (Lagodon rhomboides)             flow                   14 days    1.0         11 020d     (1970)

Atlantic croaker                 flow                   14 days    0.1         12 500d     Hansen & Wilson
 (Micropogon undulatus)           flow                   14 days    1.0         12 170d     (1970)

Fathead minnow                   flow          24-25.5  14 days   45.6 mg/kg   1.17d       Jarvinen et al.
 (Pimephales promelas)            flow          24-25.5  14 days    0.5         85 400d     (1977)
                                 flow          24-25.5  14 days    2.0         69 100d     Jarvinen et al.
                                 flow          24-25.5  112 days   45.6 mg/kg  1.33d       (1977)
                                 flow          24-25.5  112 days   0.5         93 200d     Jarvinen et al.
                                 flow          24-25.5  112 days   2.0         154 100d    (1977)

Tilapia                          stat                   31 days    1.0         6800        Reinbold et al.
 (Tilapia mossambica)                                    31 days    10          10 600      (1971)

Green sunfish                    stat                   31 days    1.0         3900        Reinbold et al.
 (Lepomis cyanellus)                                     31 days    10          4020        (1971)
                                 stat          22       15 days    0.1-0.3     17 500d     Sanborn et al.  
                                                                                           (1975)

Table 2.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism                Biomass  Flow   Organ  Tem-     Duration   Exposure    Bioconcen-  Reference
                        (g/ml)  statb         perature            (g/litre)  tration
                                               ( C)                           factorc
---------------------------------------------------------------------------------------------------------
Chicken                                 eggs            8 weeks    0.1         1.87d       Foster et al.
                                        fat             8 weeks    0.1         5.8d        (1972)
                                        
Broiler hen                             fat             6 weeks    1.0         10.3d       Kan et al. 
                                                                                           (1978)

White pelican                           WB              10 weeks   72          11.9d       Greichus et al.  
 (Pelecanus erythrorhynchos)                                                                (1975)

Double-crested cormorant                WB              9 weeks    0.95        236.3d      Greichus & 
 (Phalacrocorax a. auritus)                                                                 Hannon (1973)

American kestrel                        WB              11-16      2.8         103.9       Porter & 
 (Falco sparverius)                                      months                             Wiemeyer (1972)

Mule deere                              muscle          30 days    5 mg/day    122.8 ug    Watson et al.  
 (Odocoileus heminonus)                                  oral                   /kgd        (1975)

---------------------------------------------------------------------------------------------------------
 a  Unless specified otherwise, bioconcentration factors are based on whole body (WB) measurements.
 b  Stat = static conditions (water unchanged for duration of experiment); 
    Flow = flow-through conditions (DDT concentration in water continuously maintained).
 c  Bioconcentration factor = concentration of DDT in organism/concentration of DDT in medium or food.
    Concentrations of DDT in organisms represents total DDT, i.e., DDT plus its stable metabolites, 
    principally DDE.  Bioconcentration factors calculated on a dry weight basis unless otherwise stated.
 d  Calculated on a wet weight basis.
 e  Oral dose (by capsule) given daily.
3.2.1 Plants

    Fuhremann & Lichtenstein (1980) applied 14C-labelled  p,p' -DDT to
loam or sandy soil (at 4 and 2 mg/kg, respectively) and grew oat plants
on the treated soils for 13 days. At harvest, residues of DDT  and  its
metabolites  were analysed in soil and plant by scintillation counting,
thin  layer chromatography, and GLC.   Of the total applied  DDT, 95.7%
was  recovered from loam soil and 88.6% from sandy soil.  Almost all of
the  DDT  present was  extractable in organic  solvent (only 2.8%,  for
loam,  and  0.7%,  for  sand,  was  present  in  a  water-bound  form),
indicating little or no metabolism of the compound except to persistent
organically   extractable residues.  DDE  was detected in  both  soils,
accounting  for 3.4% of the  total extracted in loam  soil and 2.2%  in
sand.   Other metabolites, including  o,p' -DDT, TDE, and dicofol  were
recovered in very small quantities.  Very little DDT (and none  of  its
metabolites) was detected in oat roots grown on loam, amounting to 0.2%
of  the  total  DDT applied.  The uptake was greater (4.6%) in roots of
oats  grown on sand, but the uptake of labelled carbon into plant tops,
from both soils, was so low that it could not be analysed.

    DDT was not translocated into the foliage of alfalfa  when  applied
to  the  soil  (Ware, 1968; Ware et al., 1970) or into soybeans (Eden &
Arthur, 1965).  Harris & Sans (1967)  found only trace amounts  of  DDT
or  its metabolites  in the  storage roots  of carrots,  radishes,  and
turnips  after  growing  the plants  in  soils  containing up  to 14 mg
DDT/kg.

3.2.2 Microorganisms

    The  uptake and  accumulation of  DDT from  the culture  medium  by
microorganisms  has been reviewed by  Lal & Saxena (1982).   All of the
microorganisms studied showed some capacity to take up DDT  from  their
growth  medium, but the  relative amount taken  up varied greatly  from
species to species.  Many species took up more than 90% of the DDT when
exposed to concentrations ranging from 1 to 1000 g/litre,   whereas  a
few  species took in only 0.5% of the available DDT.  The concentration
factors  (i.e., the concentration  within the organism  expressed as  a
ratio  against the concentration in  the medium) for DDT  were variable
but always high (Table 2).

3.2.3 Aquatic invertebrates

    Concentration  factors are also variable  in aquatic invertebrates.
In  all cases there  is considerable uptake  and retention of  the DDT,
though  often  as DDE  or other metabolites  rather than as  the parent
compound.   The  main  point of  interest  is  the ability  of  aquatic
organisms  to take up  large amounts of  the compound, over  time, from
water  where DDT is present  at very low concentrations,  and to retain
it.

    Risebrough et al. (1976) measured DDT in sea water and  in  mussels
( Mytilus  sp.) from  San Fransisco  Bay  and the  French Mediterranean
coast.  Concentration factors varied between 40 000 and 690 000 for DDT
and between 45 000 and 310 000 for DDE.

    Eberhardt  et al. (1971) applied  radioactively labelled DDT, at  a
rate of 220 g/ha, to a freshwater marsh and followed  the  distribution
of  the compound  and its  metabolites.  Concentration  factors in  ten
species  of  plants varied  between 5500 and  84 000.  Various  invert-
ebrates    showed   high   concentration   factors:    ramshorn   snail
( Planorbidae ), 4700; backswimmer ( Notonectidae ),   10  000; crayfish
( Orconectes  immunis ),  22 000; bloodworm ( Tendipes ), 25 000; and red
leech ( Erpobdella  punctata ),  47 000.  Reporting earlier on  the  same
study,  over  15 months,  Meeks (1968) showed  that plants and  invert-
ebrates accumulated DDT to a maximum mainly within the first week after
treatment,  whereas  vertebrates  required  longer  to  attain  maximum
residues.  Residues of DDT in the surface water and suspended particles
had  fallen  below  detectable levels  within  1  month.   Residues  in
sediments stabilized at about 0.3 mg/kg after 9 months.

3.2.4 Fish

    The uptake of DDT from water is affected by the size of  the  fish;
smaller  fish  take  up relatively  more  DDT  from water  than  larger
specimens  of the  same species.   A range  in weight  of  mosquitofish
between  70  and  1000 mg  led  to  a four-fold  difference between the
smallest and largest fish in DDT uptake from water over 48  h  (Murphy,
1971).

    A  rise in temperature results  in increased uptake of  DDT by fish
(Reinert et al., 1974).  Rainbow trout were exposed to a  single  water
concentration of DDT (nominally 330 ng/litre) at temperatures of 5, 10,
or  15 C;  the  actual concentrations  of  DDT  in water  varied  with
temperature   and   were  measured  at  176,  137,  and  133  ng/litre,
respectively, for 5, 10, and 15 C.  Whole body residues of DDT (total)
after  12 weeks exposure were   3.8, 5.9, and 6.8  mg/kg for the  three
temperatures, respectively.  Expressing the results as bioconcentration
factors to allow for the differences in dissolved DDT showed a similar,
clear  increase  in the  relative amount of  DDT taken up  and retained
(Reinert et al., 1974).

    Increasing   salinity decreases  DDT uptake  significantly, but has
no  effect  on  the uptake  of  DDE  or TDE  by  fish  (Murphy,  1970).
Increasing  the  salinity from  0.15o/oo    to 10o/oo    decreased  DDT
uptake  over 24 h from 22% of the dose to 18%  (body residues decreased
from  658 to  329 ng).   There was  a further  significant decrease  in
uptake when the salinity was increased to 15o/oo (Murphy, 1970)

    Fish  accumulate DDT from  food in a  dose-dependent manner.   When
Macek et al. (1970) fed rainbow trout on diets containing 0.2 or 1.0 mg
DDT/kg,  the  fish  retained more than 90% of the dietary intake of DDT
(measured as total DDT) over the 90-day exposure period.   The  authors
estimated the time required for the elimination of 50%  of  accumulated
DDT  to be 160  ( 18) days.   When Warlen et  al. (1977) fed  Atlantic
menhaden on a diet containing 14C-labelled  DDT at three  dose  levels,
the fish assimilated and retained between 17% and 27% of the cumulative
dose  from  food  containing 0.58,  9.0,  or  93 g/kg.   There  was  a
straight-line  relationship between exposure  time and body  burden  of
total  DDT, with no tendency for residues to reach a plateau within the
45  days of feeding with  DDT.  At the end  of the feeding period,  the

fish had accumulated DDT or its metabolites, to levels of approximately
1.1,  11,  and  110 g/kg   for  the  three  doses  respectively.   The
biological  half-time  of  DDT in the fish was estimated to be 428, 64,
and  137 days,  for groups  exposed to  0.58, 9.0,  or 93 g/kg   diet,
respectively.

3.2.5 Terrestrial invertebrates

    Relatively  low  concentration  factors  have  been  reported   for
terrestrial molluscs by Dindal & Wurtzinger (1971), who  also  reviewed
the  earlier literature.  However,  low concentration factors,  derived
from  short-term studies, can be misleading for these organisms because
of the high persistence of DDT in soil.  Residues of DDT were  as  high
as  40 mg/kg and, therefore,  molluscs represent a source  of DDT which
will  be concentrated by  organisms which eat  them.  The same  is true
for earthworms, which also show low concentration factors (Davis, 1971;
Edwards  & Jeffs, 1974).  Gish & Hughes (1982) investigated residues of
DDT  and other pesticides  in earthworms for  2 years following  appli-
cation.   They showed that body residue levels were cyclic, with higher
levels  of  DDT and  its metabolites occuring  between late spring  and
early  autumn and lower levels from late autumn to early spring.   Peak
high  levels occurred in May and low levels in January, coinciding with
the  seasonal  high  and low  activity  periods  of earthworms.   These
changing  residue levels presumably  indicate that DDT  is retained  in
soil  and that earthworms contain more of the residual metabolites when
they are processing more soil through the gut.

3.2.6 Birds

    Laboratory studies on birds have shown them capable of accumulating
DDT from food, yielding high concentration factors (Table 2).

    The accumulation of DDT and its metabolites in birds in  the  field
has  been regularly and  extensively reviewed (Moore,  1965;  Moriarty,
1975;  Newton,  1979).   The results  of  an  analysis of  a  long-term
sampling  programme of birds in the United Kingdom (Cooke et al., 1982)
confirm many of the early theories.  Birds with the highest residues of
DDT  or its metabolites  were either terrestrial  predators feeding  on
other  birds or aquatic predators  feeding on fish.  Thus,  residues of
DDE in the liver of the peregrine falcon, with birds as  its  principal
dietary  component, averaged 7.56  mg/kg, whereas for  the rough-legged
buzzard,  with mammals  as the  principal dietary  component, mean  DDE
levels  were 0.05 mg/kg over a period extending from the early 1960s to
the late 1970s.

    There  are  marked  geographical differences  throughout the United
Kingdom,  related to usage  patterns of DDT  (Cooke et al.,  1982), and
also  marked  seasonal changes  in  residues.  These  seasonal  changes
appear  to relate more  to physiological changes  in body  composition,
which  occur with climatic and  breeding seasons, than to  the environ-
mental  availability of pollutants.   Some species, e.g.,  heron,  barn
owl,  and kingfisher, showed a  decline in DDE residues  with time, but
others, e.g., sparrowhawk, kestrel, and great-crested grebe,  did  not,
levels  in 1977 being similar to those in 1963.  Eventually residues of
DDT in  wildlife decline with time after a ban is imposed on the use of

the pesticide.  However, the highly persistent nature of DDE means that
significant  residues will  continue to  be found  for  a  considerable
period.   The situation in the United Kingdom and the USA appears to be
broadly similar (O'Shea & Ludke, 1979).

3.2.7 Mammals

    DDT  is taken up by, and retained in, wild mammals.   The degree of
uptake and retention varies with the species.  In a study  following  a
single  application  of  DDT to a forest to control spruce budworm at a
rate of 0.89 kg/ha, Dimond &  Sherburne (1969) and Sherburne  &  Dimond
(1969) reported residues of DDT and its metabolites in mammals  over  9
years.    Herbivorous mice, voles,  and hares contained  less DDT  than
carnivorous  mink  and  insectivorous shrews.   In herbivores, residues
approached  pre-treatment levels after 6-7 years, whereas residues were
still  significantly higher in shrews and mink than in the same species
taken from untreated areas 9 years after the single treatment with DDT.
In  these species, the authors calculate that it would take at least 15
years  for residues to reach  background levels.  They regard  the high
residue  levels  in  mammals  at  higher  trophic  levels  as  deriving
principally  from DDT retained in the soil, since there is little long-
term retention on vegetation.

    In  a 3-year study,  after treating a  field ecosystem  with  36Cl-
ring-labelled  DDT at  a dose  rate of  0.92 kg/ha,  Forsyth &  Peterle
(1973)  measured DDT  residues in  various tissues  of two  species  of
shrew.   The highest residue (135 mg/kg) occurred in fat, compared with
10,  10, and 4 mg/kg in liver, muscle, and brain, respectively.  Shrews
of the species  Blarina brevicauda  released into treated areas accumu-
lated  DDT  to  the same degree as resident shrews within 15-20 days of
exposure.   Equilibrium between intake  and excretion of  DDT  occurred
within  approximately  30 days in muscle, liver, and brain  and  within
40  days  in  fat.   The  second  species  of  shrew ( Sorex cinereus )
accumulated  residue levels of DDT during the following 2  years  which
were  successively  greater  than levels  present  in  the first  year,
indicating  that DDT was   increasing in availability  to this  species
with  the passage  of time.   The levels  of DDT  in  muscle  were  not
influenced  by sex  but were  influenced by  breeding condition.   Male
shrews  with   scrotal testes  and  lactating females  developed  lower
levels  of DDT  in muscle  and viscera  than did  males with  abdominal
testes or non-lactating females.

    Benson & Smith (1972) measured levels of DDT and its metabolites in
deer exposed to DDT used for spruce budworm control, and found that, in
the  year of spraying,  there was up  to 20 mg/kg  in fat.   Males  had
considerably  higher levels of DDT than females.  Fawns also had higher
levels  than their mothers, though  this was from a  small sample.  The
majority of the residues consisted of  p,p' -DDT,  with almost insignifi-
cant levels of DDE.  Five years later, the residue levels in males were
still higher than those in females, though these had  fallen  to  about
1%  of original levels.  Most of the deer population was 3 years old or
less,  and so  the figures  for 5  years after  spraying represent  DDT
ingested from the environment and not from direct exposure.

    Some,  though very  little, DDT  was detected   in black  bears  by
Benson  et al. (1974).  There  was no evidence that  the area had  been
directly  sprayed  with DDT.   This study illustrates  that there is  a
general  environmental contamination with DDT, which can be accumulated
by mammals, though to a small degree, without direct application of the
material to their habitat.

4.  TOXICITY TO MICROORGANISMS

Appraisal 

     Aquatic  microorganisms are more sensitive than terrestrial ones to
 DDT.

     An  environmental exposure concentration of 0.1 g/litre  can cause
 inhibition of growth and photosynthesis in green algae.

     Repeated applications of DDT can lead to tolerance in  some  micro-
 organisms.

     There  is no information on  effects concerning the species  compo-
 sition  of microorganism communities.   Therefore, it is  difficult  to
 extrapolate  the  relevance of  single-culture  studies to  aquatic  or
 terrestrial  ecosystems.   However,  since microorganisms  are basic in
 food  chains,  adverse effects  on  their populations  would  influence
 ecosystems.   Thus,  DDT and  its metabolites should  be regarded as  a
 major environmental hazard.

    Studies cited in this section will be restricted to  those  effects
produced by low concentrations of DDT.  Some studies still use  DDT  at
concentrations above its water solubility.  Reviews of other effects of
DDT and its analogues, at higher concentrations, on cell  division  and
several biochemical parameters have been produced by Luard  (1973)  and
Lal & Saxena (1979).

4.1 Bacteria and Cyanobacteria (Blue-green Algae)

    Ledford  &  Chen (1969)  cultured  bacteria isolated  from surface-
ripened  cheese with 0.5 mg DDT/litre or 0.5 mg DDE/litre, but found no
effect on growth.

    At  a concentration  of 10 g/litre   in the  culture  medium,  DDT
stimulated the growth of the bacterium  Escherichia coli  (Keil  et  al.,
1972).  Yields of cultures exposed to 100 g/litre  did not differ from
controls.  There was no effect of DDT on denitrification (conversion of
nitrate  to  nitrite)  at a  concentration  of  100 mg/kg  in soil and,
similarly,  no effect on this  process when carried out  by a bacterial
culture  (Bollag  & Henninger,  1976).  DDT at  up to 22  kg/ha did not
affect the numbers of soil bacteria in outdoor-treated plots (Bollen et
al.,  1954),  and  five annual applications of DDT to a sandy loam soil
did  not significantly  affect the  numbers of  soil bacteria  (Martin,
1966).

    Concerning  cyanobacteria  (blue-green  algae),  Goulding  &  Ellis
(1981)  found no effect on  the growth of  Anabaena variabilis  at a DDT
concentration of 1 g/litre.   Batterton et al. (1972)  suggested  that
DDT  reduced  the  tolerance of  Anocystis nidulans  to sodium chloride.
The organism is resistant to salt and to DDT, at concentrations  up  to
8000 mg/litre, but not to combinations of the two stressors.


4.2 Freshwater Microorganisms

    Lee et al. (1976) showed that DDT inhibited photosynthesis  in  the
green  alga  Selenastrum capricornutum  at concentrations between 3.6 and
36 g/litre, inhibition increasing with time of exposure.
   
    Two different  species of  green algae were shown to  be  resistant
to   DDT and its   metabolites, DDE and  TDE, at  concentrations  up to
1000 mg/litre in culture.  Scenedesmus  and  Dunaliella  revealed rates of
photosynthetic  uptake  of  14C-labelled CO2 similar   to  those  of
controls  (Luard, 1973).  Considerable variation exists between species
of  microorganisms concerning  the effect  of DDT  and  its  analogues;
resistance  to  DDT is  not restricted to  one taxonomic group,  either
freshwater  or marine (Luard, 1973).   The source of the  resistance is
unclear.   The two species studied show very different characteristics;
 Dunaliella  has no cell wall, whereas  Scenedesmus  has a complex  cell
wall.   Since both  show resistance  to DDT,  it is  unlikely that  the
chemical  is excluded from the  cell by the cell  wall.  Cell membranes
and  chloroplast membranes are an alternative barrier to DDT uptake and
effect.   It is not known how these structures might be involved in DDT
resistance; studies with isolated chloroplasts suggest that there is no
barrier to DDT uptake there.

    Cole & Plapp (1974) found inhibition of growth  and  photosynthesis
of  the green alga  Chlorella pyrenoidosa  with DDT at 1 g/litre  in the
medium.   However, inhibition was  inversely related to  the number  of
cells   in   the  culture.   With  high  cell  counts,  there  was   no
inhibition of either growth or photosynthesis with DDT present at up to
1 mg/litre.  Inhibition only occurred at low cell densities in culture.

    Goulding & Ellis (1981) found that the green alga  Chlorella fusca 
was   affected by DDT  at 0.1 g/litre.   The  amount of inhibition  of
growth  varied with time and  with the method of  assessing the result.
Cell numbers were maximally affected (75% inhibition) after  72  hours,
and  after  200 hours  cell numbers had  reached control levels.   When
growth  was assessed by chlorophyll  content or biovolume, the  initial
inhibition  was  more  marked and  cultures  were  only  equivalent  to
controls  after  480  hours.  The  apparent  anomaly  is  explained  by
reductions in cell size in response to DDT.

    Christie  (1969)  reported  no  effect  of  DDT  on the  growth  of
 Chlorella  and attributed  this  to the  ability  of  the organism  to
metabolize the compound.

    Lal & Saxena (1980) reported that DDT did not affect growth and DNA
synthesis  in  the ciliate Stylonychia  notophora at  concentrations of
1 mg/litre or less.

4.3 Marine Microorganisms

    MacFarlane  et  al.  (1972)  showed  that  DDT,  at  concentrations
between   9.4  and   1000 g/litre,   reduced    photosynthetic  carbon
fixation and the cell content of  chlorophyll a relative  to   controls
in  a marine diatom   Nitzschia delicatissima ,  over a   24-h  period.

The  diatom  was cultured  with DDT under  four different light  inten-
sities.  The insecticide had the greatest effect at the  highest  light
intensity, where carbon fixation was reduced by 94% in water containing
100 g   DDT/litre.  At higher DDT concentrations, there was no further
reduction in either carbon fixation or chlorophyll content.

    The photosynthesis of several species of marine  phytoplankton  has
been found to be inhibited by DDT at concentrations of 100 g/litre  or
less  (Wurster,  1968).   Four  different  species  showed   increasing
inhibition  up to DDT concentrations  of 100 g/litre,  but no  greater
effect  at  higher  concentrations.  A  green  alga,  Pyramimonas , was
affected by DDT only at concentrations higher than  10 g/litre.    The
other  three species, a diatom, a coccolithophore, and a dinoflagellate
were   affected at  DDT concentrations  between 1 and 10 g/litre.   In
a  similar  study  (Menzel et  al., 1970)   four different  species  of
marine   phytoplankton  were  studied.  Inhibition  of  photosynthesis,
where  it  occurred,  followed a   similar dose-response  relationship.
For  three  species  ( Skeletonema costatum , a   diatom;  Coccolithus 
 huxleyi , a  coccolithophorid;  and  Cyclotella nana , a  second  diatom)
inhibition began between 1 and 10 g  DDT/litre and reached  a  maximum
at 100 g/litre.   The other organism, a green  flagellate  Dunaliella 
 tertiolecta , was  unaffected by DDT at concentrations up to 1 mg/litre,
the highest exposure tested.

    The   marine  dinoflagellate  Exuviella baltica  showed  significant
inhibition  of growth after exposure to DDT at concentrations as low as
0.1 g/litre (Powers et al., 1979).

4.4  Soil Microorganisms

    TDE had no significant effects on growth and reproduction  of  soil
amoebae  except at concentrations  higher than 1  mg/litre (Prescott  &
Olson, 1972).  Populations of protozoa in garden soil were  reduced  by
DDT  at a concentration  of 5 mg/kg  (MacRae & Vinckx,  1973).  Numbers
were still significantly reduced after 3 months.

4.5  Fungi

    Two  aquatic  and  one terrestrial fungi showed  stimulated  growth
in  response  to  DDT  present  at  concentrations  of  between  2  and
60 g/litre of growth medium (Hodkinson & Dalton, 1973)

5.  TOXICITY TO AQUATIC ORGANISMS

    DDT  and its  derivatives are  highly toxic  to aquatic  organisms;
water  concentrations of a few  micrograms per litre are  sufficient to
kill a large proportion of populations of aquatic organisms in acute or
short-term  exposure.  In addition to its high short-term toxicity, DDT
also  has  long-term  sublethal  effects  on  aquatic  organisms.  Many
physiological  and  behavioural parameters  have  been reported  to  be
affected  by the  insecticide.  This  toxicity, coupled  with its  high
capacity  for  bioconcentration  and biomagnification,  means  that DDT
presents a major hazard to aquatic organisms.

5.1 Aquatic Invertebrates

Appraisal 

     Both the acute and long-term toxicities of DDT vary between species
 of   aquatic  invertebrates.   Early  developmental   stages  are  more
 sensitive than adults to DDT.  Long-term effects occur  after  exposure
 to  concentrations ten  to a  hundred times  lower than  those  causing
 short-term effects.

     DDT is highly toxic, in acute exposure, to aquatic invertebrate, at
 concentrations   as  low  as  0.3 g/litre.     Toxic  effects  include
 impairment    of    reproduction   and    development,   cardiovascular
 modifications,  and  neurological  changes.   Daphnia  reproduction  is
 adversely affected by DDT at 0.5 g DDT/litre.

     The  influence  of  environmental variables  (such  as temperature,
 water  hardness,  etc.) is  documented but the  mechanism is not  fully
 understood.   In contrast to the data on DDT, there is less information
 on  the metabolites DDE or TDE.  The reversibility of some effects once
 exposure  ceases  has  been reported,  as  well  as the  development of
 resistance.

5.1.1  Short-term and long-term toxicity

    The short-term toxicity to aquatic invertebrates is  summarized  in
Table 3.

    Most aquatic invertebrates are killed by low  water  concentrations
of DDT and its metabolites, though the majority of the  published  data
is  on DDT itself.  Six invertebrate species studied by Macek & Sanders
(1970) showed 96-h LC50   values ranging from 1.8 to  54.0 g/   litre.
Adult  molluscs are  relatively resistant  to DDT and the  compound has
been used to control crustacean pests on oyster beds (Loosanoff, 1959).
However, the larval stages of molluscs are affected by DDT; clam larvae
showed 90% mortality after exposure to DDT at 0.05 mg/litre (Calabrese,
1972).   Molluscs exhibit effects  on shell growth  at low DDT  concen-
trations.   Tubifex worms are resistant to DDT; 3 mg/litre did not kill
any  Tubifex tubifex  (Naqvi & Ferguson, 1968).  Many aquatic crustaceans
yield  LC50 values   less  than 1 g/litre.    Muirhead-Thomson  (1973)
showed  that  predator invertebrates,  such  as dragonfly  nymphs, were
more tolerant of DDT than  prey organisms.  Since the  prey   organisms
are  also  food for  fish, the balance  of aquatic ecosystems  could be

changed by very low levels of DDT.  Lowe (1965)  reported that juvenile
blue  crabs ( Callinectes sapidus ), exposed to 0.25 g   DDT/litre for 9
months,  grew and moulted  normally; there were  no apparent  sublethal
effects.   However, exposure to 5 g DDT/litre killed all crabs.

    The  metabolite  TDE has  been studied in  parallel tests with  the
parent compound in some organisms.  There is no consistent relationship
between  the toxicity of the  two compounds.  TDE is  considerably less
toxic  to stonefly larvae than DDT, by a factor of about 100 (Sanders &
Cope,  1968).  However,  for other  freshwater organisms  TDE may  have
similar,  lower, or  greater toxicity  according to  the  organism  and
duration of test (Table 3).  For most marine invertebrates, DDT is most
toxic, followed by DDE and TDE (data from Mayer, 1987).

5.1.2  Physiological effects on aquatic invertebrates

    Butler (1964) demonstrated a 50% reduction in shell growth in young
eastern  oysters exposed  for 96-h  to DDT  at  14 g/litre.    Roberts
(1975)  showed  that  DDT at  50 g/litre   reduced  the  amplitude  of
ventricular  contractions in  the isolated  heart of  the bivalve  Mya 
 arenaria  within 4 minutes.  At higher concentrations, DDT stopped heart
contractions  altogether.  Recovery, even  of the arrested  heart,  was
rapid  after the immediate replacement  of the DDT solution  with clean
sea water.

    Kouyoumjian  &  Uglow  (1974) found  that  for  the planarian  worm
 Polycelis felina , TDE was most  toxic and DDT  least toxic, with  DDE
showing intermediate toxicity.  Sublethal effects of DDT and  TDE  were
demonstrated.  DDT reduced the rate of asexual fission.  Both  DDT  and
TDE were shown to reduce the righting time of animals turned onto their
backs.   This was presumed to be a nervous system effect.

    Maki & Johnson (1975) report 50% reduction in three  parameters  of
reproduction  in  the  water flea  Daphnia magna  at  0.5 g/litre,  for
total  young produced, at 0.61 g/litre  for average brood size, and at
0.75 g/litre for percentage of days reproducing.

     In vitro  effects on gill ATPases of two species of crab have been
reported  (Jowett et al., 1978; Neufeld & Pritchard, 1979).  There is a
transitory  effect in vivo on  gill ATPases and, thereby,  an effect on
plasma osmolarity.  However, this osmoregulatory effect soon disappears
(Pritchard & Neufeld, 1979).  Leffler (1975)  reported  metabolic  rate
elevation,  decreased  muscular  coordination, inhibition  of  autotomy
reflex,  and reduced carapace  thickness/width ratio in  juvenile crabs
exposed to DDT.  Osmoregulation was not affected.  The DDT was given in
the  food of the crabs  at a concentration of  0.8 mg/kg. DDT has  been
found to accelerate limb regeneration and the onset of the  next  moult
in fiddler crabs (Weis & Mantel, 1976).  The authors suggest  that  the
effect  is on the central  nervous system, with DDT  causing changes in
neurosecretory activity.


Table 3.  Toxicity of DDT and its derivatives to invertebrates
---------------------------------------------------------------------------------------------------------
Organismf                 Flow   Temp  Salinity   Compound   Parameter    Water          Reference
                          stata  ( C) o/oo                               concentration
                                                                          (g/litre)
---------------------------------------------------------------------------------------------------------
Estuarine and marine invertebrates

Eastern oyster (juv.)     flow   30    23         DDTd       96-h EC50j   9              Mayer (1987)
 (Crassostrea virginica)   flow   12    25         DDEd       96-h EC50j   14             Mayer (1987)
                          flow   20    30         TDEd       96-h EC50j   25             Mayer (1987)

Shrimp                    stat   20    sea water  DDTd       96-h LC50    0.4            McLeese & 
 (Crangon septemspinosa)   stat   10    sea water  DDTd       96-h LC50    31             Metcalfe (1980)
                                       + sediment

Mysid shrimp (adult)      stat   25    23         DDTd       96-h LC50    0.45           Mayer (1987)
 (Mysidopsis bahia)                                                        (0.39-0.52)

Pink shrimp (juv.)        flow   24    28         DDTd       48-h LC50    0.6            Mayer (1987)
 (Penaeus duorarum)        flow   16    31         TDEd       48-h LC50    2.4            Mayer (1987)

White shrimp (juv.)       flow   27    28         DDTd       24-h LC50    0.7            Mayer (1987)
 (Penaeus setiferus)                                                                        

Grass shrimp (juv.)       flow   27    28         DDTd       24-h LC50    0.8            Mayer (1987)
 (Palaemonetes pugio) 

Brown shrimp (juv.)       flow   28    17-27      DDEd       24-h LC50    52             Butler (1964)
 (Penaeus aztecus)         flow   28    17-27      DDEd       48-h LC50    28             Butler (1964)

Table 3.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism                 Flow  Temp  Alkali- Hard-  pH      Comp- Parameter  Water             Reference
                         Stata ( C) nityc   nessc          ound             concentration
                                                                             (g/litre)
---------------------------------------------------------------------------------------------------------
Freshwater invertebrates
Water flea               stat  20    192     138    8.2-    DDTd  48-h LC50  1.1 (1.0-1.3)     Randall et 
                                                    8.5                                        al. (1979)
 (Daphnia magna)          stat  15            44     7.1     DDTd  48-h LC50  4.7 (2.8-5.6)     Mayer &
                                                                                               Ellersieck 
                                                                                               (1986)
                         stat  20    192     138    8.2-    DDTe  48-h LC50  1.7 (1.5-1.8)     Randall et 
                                                    8.5                                        al. (1979)
                         statb 24            320-   7.6     DDT   14-day     0.67 (0.65-0.69)  Maki & 
                                             340            (99%) LC50                         Johnson
                         statb 24            320-   7.6     DDT   14-day     0.5 (0.48-0.52)   (1975)
                                             340            (99%) EC50g
                         statb 24            320-   7.6     DDT   14-day     0.61 (0.58-0.64)  Maki & 
                                             340            (99%) EC50h                        Johnson
                         statb 24            320-   7.6     DDT   14-day     0.75 (0.71-0.79)  (1975)
                                             340            (99%) EC50i
                         stat  10            44     7.1     TDEd  48-h LC50  9.1               Mayer &
                         stat  21            44     7.1     TDEd  48-h LC50  8.9               Ellersieck 
                                                                                               (1986)
  reared in              stat  20.5          250    7.8-8.2 DDT   24-h LC50  510 (230-1120)    Berglind & 
  soft water             stat  20.5          250    7.8-8.2 DDT   48-h LC50  1.1 (0.89-1.7)    Dave (1984)
  (CaCO3:                stat  20.5          250    8.4-8.5 DDT   24-h LC50  98 (75-127)       Berglind & 
  50 mg/litre)           stat  20.5          250    8.4-8.5 DDT   48-h LC50  1.3 (1.1-1.5)     Dave (1984)

  reared in              stat  20.5          250    7.8-8.2 DDT   24-h LC50  71 (41-130)       Berglind & 
  hard water             stat  20.5          250    7.8-8.2 DDT   48-h LC50  0.68 (0.46-1.0)   Dave (1984)
  (CaCO3:                stat  20.5          250    8.4-8.5 DDT   24-h LC50  42 (32-56)        Berglind &
  300 mg/litre)          stat  20.5          250    8.4-8.5 DDT   48-h LC50  0.5 (0.41-0.61)   Dave
                         stat  20.5          50     7.8-8.2 DDT   24-h LC50  0.99 (0.66-1.49)  (1984)

Water flea               stat  15            44     7.1     DDTd  48-h LC50  0.36 (0.28-0.47)  Mayer &
 (Daphnia pulex)                                                                                Ellersieck 
                                                                                               (1986)
Water flea               stat  15            44     7.1     DDTd  48-h LC50  2.5 (1.9-3.3)     Mayer &
 (Simocephalus            stat  21            44     7.1     DDTd  48-h LC50  2.8 (2.3-3.5)     Ellersieck 
  serrulatus)             stat  15            44     7.1     TDEd  48-h LC50  3.2 (2.3-4.4)     (1986)
                         stat  21            44     7.1     TDEd  48-h LC50  4.5 (3.1-6.6)     

Table 3.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism                 Flow  Temp  Alkali- Hard-  pH      Comp- Parameter  Water             Reference
                         Stata (C)  nityc   nessc          ound             concentration
                                                                             (g/litre)
---------------------------------------------------------------------------------------------------------

Scud                     stat  21    35      44     7.1     TDEd  24-h LC50  4.6 (3.6-5.8)     Sanders 
 (Gammarus fasciatus)     stat  21    35      44     7.1     TDEd  96-h LC50  0.6 (0.05-1.2)    (1972)
                         stat  21    35      44     7.1     DDTd  24-h LC50  15 (9.0-20)       Sanders
                         stat  21    35      44     7.1     DDTd  96-h LC50  3.2 (1.8-5.6)     (1972)
                         stat  21    260     272    7.4     TDEd  24-h LC50  3.2 (2.1-4.3)     Sanders
                         stat  21    260     272    7.4     TDEd  96-h LC50  0.86 (0.42-1.3)   (1972)
                         stat  21    260     272    7.4     DDTd  24-h LC50  4.2 (1.8-5.6)     Sanders
                         stat  21    260     272    7.4     DDTd  48-h LC50  3.1               (1972) 
                         stat  21    260     272    7.4     DDTd  96-h LC50  1.8 (1.0-3.1)     Sanders
                                                                                               (1972) 
                         stat  21    260     272    7.4     DDTd  120-h LC50 0.32              Sanders 
                         flow  18-21 260     272    7.4     DDTd  24-h LC50  1.1               (1972)
                         flow  18-21 260     272    7.4     DDTd  48-h LC50  1.0               Sanders 
                         flow  18-21 260     272    7.4     DDTd  96-h LC50  0.8               (1972)
                         flow  18-21 260     272    7.4     DDTd  120-h LC50 0.6               Sanders 
                                                                                               (1972)
Scud                     stat  21            44     7.1     DDTd  24-h LC50  4.7 (3.2-7.0)     Mayer &
 (Gammarus lacustris)     stat  21            44     7.1     DDTd  96-h LC50  1.0 (0.68-1.5)    Ellersieck 
                                                                                               (1986)
                         stat  15                           DDTe  96-h LC50  9.0               Gaufin et 
                                                                                               al. (1965)

Glass shrimp             stat  21    260     272    7.4     DDTd  24-h LC50  6.8 (6.2-7.5)     Sanders
 (Palaemonetes            stat  21    260     272    7.4     DDTd  48-h LC50  4.7               (1972)
  kadiakensis)            stat  21    260     272    7.4     DDTd  96-h LC50  2.3 (1.3-4.9)     Sanders
                         stat  21    260     272    7.4     DDTd  120-h LC50 1.0               (1972)
                         stat  21    260     272    7.4     TDEd  24-h LC50  11 (8.4-16)       Sanders
                         stat  21    260     272    7.4     TDEd  96-h LC50  0.68 (0.47-1.1)   (1972)
                         flow  18-21 260     272    7.4     DDTd  24-h LC50  9.4               Sanders
                         flow  18-21 260     272    7.4     DDTd  48-h LC50  7.7               (1972)
                         flow  18-21 260     272    7.4     DDTd  96-h LC50  3.5               Sanders
                         flow  18-21 260     272    7.4     DDTd  120-h LC50 1.3               (1972)


Table 3.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism                 Flow  Temp  Alkali- Hard-  pH      Comp- Parameter  Water             Reference
                         Stata (C)  nityc   nessc          ound             concentration
                                                                             (g/litre)
---------------------------------------------------------------------------------------------------------
Crayfish  (Orconectes nais) 
  mature                 stat  21    260            7.4     DDTd  24-h LC50  1100 (1000-1400)  Sanders
                         stat  21    260            7.4     DDTd  96-h LC50  100 (80-120)      (1972)
  1 day old - 15g        stat  21    260            7.4     DDTd  24-h LC50  1.4 (1.1-4.2)     Sanders
                         stat  21    260            7.4     DDTd  96-h LC50  0.3 (0.18-0.5)    (1972)
  1 week old - 20g       stat  21    260            7.4     DDTd  24-h LC50  1.0 (0.6-5.0)     Sanders
                         stat  21    260            7.4     DDTd  96-h LC50  0.18 (0.12-0.3)   (1972)
  2 weeks old - 23g      stat  21    260            7.4     DDTd  24-h LC50  1.2 (0.9-5.5)     Sanders
                         stat  21    260            7.4     DDTd  96-h LC50  0.2 (0.16-1.1)    (1972)
  3 weeks old - 30g      stat  21    260            7.4     DDTd  24-h LC50  1.0 (0.6-5.0)     Sanders
                         stat  21    260            7.4     DDTd  96-h LC50  0.24 (0.1-0.6)    (1972)
  5 weeks old - 50g      stat  21    260            7.4     DDTd  24-h LC50  3.2 (1.8-8.0)     Sanders
                         stat  21    260            7.4     DDTd  96-h LC50  0.9 (0.7-1.4)     (1972)
  8 weeks old - 500g     stat  21    260            7.4     DDTd  24-h LC50  45 (40-52)        Sanders
                         stat  21    260            7.4     DDTd  96-h LC50  28 (24-36)        (1972)
  10 weeks old - 1200g   stat  21    260            7.4     DDTd  24-h LC50  50 (48-56)        Sanders
                         stat  21    260            7.4     DDTd  96-h LC50  30 (26-42)        (1972)
                                                                  
Sowbug (isopod)          stat  21    35             7.1     DDTd  24-h LC50  8.7 (4.9-13.0)    Sanders
 (Asellus brevicaudus)    stat  21    35             7.1     DDTd  96-h LC50  4.0 (1.2-6.5)     (1972)
                         stat  21    35             7.1     TDEd  24-h LC50  18 (14-25)        Sanders
                         stat  21    35             7.1     TDEd  96-h LC50  10 (7.0-14)       (1972)

Caddis fly (nymph)       stat  10.5-                        DDTe  96-h LC50  48                Gaufin et 
 (Hydropsyche californica)      12                                                              al. (1965)

Caddis fly (nymph)       stat  10.5-                        DDTe  96-h LC50  175               Gaufin et 
 (Arctopsyche grandis)          12                                                              al. (1965)

May fly (nymph)          stat  8.8-                         DDTe  96-h LC50  25                Gaufin et 
 (Ephemerella grandis)          10                                                              al. (1965)

Stonefly (naiad)         stat  11-                          DDTe  96-h LC50  320               Gaufin et 
 (Acroneuria pacifica)          12                                                              al. (1965)

Table 3.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism                 Flow  Temp  Alkali- Hard-  pH      Comp- Parameter  Water             Reference
                         Stata (C)  nityc   nessc          ound             concentration
                                                                             (g/litre)
---------------------------------------------------------------------------------------------------------

Stonefly (naiad)         stat  11-                          DDTe  96-h LC50  1800              Gaufin et 
 (Pteronarcys                   12                                                              al. (1965)
  californica)            stat  15.5  35                     DDT   24-h LC50  41 (27-62)        Sanders &
                         stat  15.5  35                     DDT   48-h LC50  19 (14-27)        Cope (1968)
                         stat  15.5  35                     DDT   96-h LC50  7 (4.9-9.9)       Sanders &
                         stat  15.5  35                     TDE   24-h LC50  3000 (2100-4300)  Cope (1968)
                         stat  15.5  35                     TDE   48-h LC50  1100 (800-1500)   Sanders &
                         stat  15.5  35                     TDE   96-h LC50  380 (280-520)     Cope (1968)
                               
Stonefly (naiad)         stat  15.5  35                     DDT   24-h LC50  12 (8.8-16)       Sanders &
 (Pteronarcella badia)    stat  15.5  35                     DDT   48-h LC50  9 (7-11)          Cope
                         stat  15.5  35                     DDT   96-h LC50  1.9 (1.3-2.7)     (1968)

Stonefly (naiad)         stat  15.5  35                     DDT   24-h LC50  16 (12-20)        Sanders &
 (Claasenia sabulosa)     stat  15.5  35                     DDT   48-h LC50  6.4 (4.9-8.3)     Cope
                         stat  15.5  35                     DDT   96-h LC50  3.5 (2.9-4.2)     (1968)

---------------------------------------------------------------------------------------------------------
a  Stat = static conditions (water unchanged for duration of test); Flow = flow-through conditions (DDT 
   concentration in water continuously maintained).
b  Static conditions but test solution renewed every 24 h.
c  Alkalinity and hardness expressed as mg CaCO3/litre.
d  Technical grade (99%).
e  Emulsifiable concentrate (25% active ingredient).
f  Juv. = juvenile.
g  Value based on total number of young produced.
h  Value based on average brood size.
i  Value based on % days reproducing.
j  Effect on shell growth.
    Eggs  of the Chironomid midge, contaminated with DDE by exposure of
the female during ovarian development, failed to hatch as  many  adults
as  uncontaminated  eggs.   DDE in the water had less of an effect than
DDE  contamination  within  the eggs  obtained  from  the female.   The
females  had been maintained in water containing 30 g  DDE/litre; eggs
were kept in water containing 20 g DDE/litre (Derr & Zabik, 1972).

    Crayfish populations  exposed over long periods to DDT develop some
tolerance  to the insecticide (Albaugh,  1972).  In 48-h tests,    LC50
values for the crayfish  Procambarus clarkii  were 3.0 (2.5-3.6)  g/litre
for  the unexposed  population, and  7.2 (5.8-8.8)  g/litre   for  the
exposed  population (95% confidence  limits in parentheses).    Naqvi &
Ferguson  (1968) demonstrated the development of tolerance to DDT after
exposure   to  the   insecticide,  in   a  wide   variety  of   aquatic
invertebrates,  including cyclopoid copepods,  tubifex worms, and  pond
snails.  These tolerant populations occurred in the  Mississippi  delta
in areas of cotton cultivation.

5.2  Fish

Appraisal 

     DDT  is  highly toxic  to fish; the  96-h LC50s   reported  (static
 tests) range from 1.5 to 56 g/litre  (for largemouth bass  and  guppy,
 respectively).  Smaller fish are more susceptible than larger  ones  of
 the same species.  An increase in temperature decreases the toxicity of
 DDT to fish.

     The  behaviour of  fish is influenced by DDT.  Goldfish  exposed to
 1 g/litre   exhibit hyperactivity.  Changes  in the feeding  of  young
 fish  are caused by DDT levels commonly found in nature, and effects on
 temperature preference have been reported.

     Residue levels of > 2.4 mg/kg in eggs of the winter flounder result
 in  abnormal embryos in the  laboratory, and comparable residue  levels
 have been found to relate to the death of lake trout fry in the wild.

     Cellular  respiration  may be  the main toxic  target of DDT  since
 there are reports of effects on ATPase.

     The toxicity of TDE and DDE has been less studied than that of DDT.
 However, the data available show that TDE and DDE are both  less  toxic
 than DDT.

    The  exact mode of  action of DDT  in fish remains  unclear.  There
have  been  many  different suggestions  to  explain  both  lethal  and
sublethal effects.  Most of these are primarily the result  of  effects
on membranes.  DDT is very soluble in lipid and,  therefore,  dissolves
in  the  lipid  component of  membranes.   It  may interfere  both with
membrane  function  and with  many enzyme systems  that are located  on
membranes.   It has  been shown  experimentally to  interfere with  the
normal  function  of so  many systems that  a primary action  of DDT is
difficult to determine.

5.2.1  Short-term and long-term direct toxicity to fish

    The short-term toxicity of DDT to fish is summarized in Table 4.

    The  relatively few studies on TDE (Gardner, 1973;  Korn & Earnest,
1974; Mayer & Ellersieck, 1986; Mayer, 1987) show it to be  less  toxic
than DDT, in the same test system, by factors of 5-10.  The still fewer
studies  on DDE indicate a  similarly lowered toxicity relative  to the
parent  compound (Mayer & Ellersieck, 1986; Mayer, 1987).  Whilst there
is some variation between species, DDT has proved highly toxic  to  all
fish  tested; static 24-h LC50 values  range from 2.1 g/litre  for the
largemouth  bass (Mayer &  Ellersieck, 1986) to  180 g/litre  for  the
goldfish  (Henderson et al., 1959).  For 96-h tests, LC50 values  range
from  1.5 g/litre  for largemouth bass (Mayer & Ellersieck,  1986)  to
56 g/litre  for the guppy (Henderson et al., 1959).   Several  authors
have  stated that  DDT toxicity  varies somewhat  with temperature  and
water hardness.

    Buhler et al. (1969) studied the long-term effects, over  95  days,
of  feeding DDT-contaminated diets to juvenile chinook and coho salmon.
The  DDT was dissolved in  corn-oil and then incorporated  into a semi-
synthetic diet.  Fish were fed until they stopped actively  taking  the
slowly  sinking  food.   Pure  p,p' -DDT   was  slightly  more  toxic  to
juvenile   salmon than  the technical  product, and chinook salmon were
2  to  3  times more sensitive to the same dose of DDT in the diet than
coho  salmon.   Size was  an important factor  in the toxicity  of DDT,
smaller  fish being  more susceptible  than larger  ones.  The  authors
estimated, by  extrapolation, a 90-day LD50 value  of  27.5 g/kg   per
day for chinook and 64 g/kg  per day for coho salmon  juveniles.    In
fish  exposed to higher doses of DDT, pre-death symptoms were marginal.
Some increased agitation and slight photophobia were   reported.   Fish
exposed to low doses of DDT took longer to die, and other symptoms were
noted.   Many individuals developed ulceration of the nasal area.  This
spread  over the head and  in some cases eyes  were lost.  Pathological
examination  showed  a  specific and  severe  kidney  lesion; this  was
limited  to one short  section of the  distal convoluted tubule,  which
eventually  degenerated almost completely.  The  authors suggested this
as the main lethal lesion in the fish.

    In a later study (Buhler & Shanks, 1970), the same  authors  showed
that median survival time was directly proportional to body  weight  in
young  coho  salmon  fed technical  DDT.   Fish  were all  given a diet
containing  200 mg DDT/kg and  food consumption was monitored  for each
group  of fish.  The  main effect of  body size on  DDT  lethality  was
related  to the intake of  the chemical by the  fish; smaller fish  ate
more  of the contaminated diet  and consequently received the  greatest
dose  in mg/kg bodyweight  terms.  However, even  after correcting  for
dosage  received, the smaller  fish were more  susceptible than  larger
ones.   The authors suggested that  the lower lipid content  of smaller
fish  might have accounted for the remaining difference.  Twelve groups
of  100 fish ranged in weight (average for each group)  from 3 to 15 g.
Total  DDT intake ranged from 0.4 to 3 mg/fish; daily intake was higher
in  the  smaller  fish at 3 mg/kg per day, falling to 1.3 mg/kg per day
for  the  largest.  The  estimated LC50 ranged  from  95 mg/kg for  the
smallest  to 135 mg/kg for  the largest fish, and  median survival time
increased  from  30  days for  the smallest  fish to  106 days  for the
largest.

    Crawford & Guarino (1976) exposed killifish ( Fundulus heteroclitus )
to   a  twice-repeated schedule  of 24 h  in water containing  DDT at a

concentration  of  0.1  mg/litre and  24  h  in clean  water.   At this
exposure  level, there was a delay in the rate of development of ferti-
lized eggs but no apparent effect on the hatched fry.  Fertilization of
killifish  eggs was diminished when insemination was carried out in sea
water  containing DDT at  0.1 mg/litre.  Mortality  at a late  stage of
embryo  development has been  reported for a  variety of salmonids  and
related  to egg residues  of DDT (Allison  et al., 1964,  for cutthroat
trout;  Burdick et al.,  1964, for lake  trout; Macek, 1968,  for brook
trout; and Johnson & Pecor, 1969, for coho salmon).

    Smith  & Cole (1973)  reported effects on  embryos developing  from
eggs  laid  by  adult winter  flounder ( Pseudopleuronectes  americanus )
that  were exposed to 2 g  DDT/litre for various times and, therefore,
accumulated different residue levels in the eggs.  These residue levels
varied  from 1.15 to  3.70 mg DDT/kg  and from 0.07  to 0.4 mg  DDE/kg.
Embryos  showed abnormal gastrulation and  a high incidence (mean  39%)
of  vertebral  deformities.   Bone  erosion  and  haemorrhaging  at the
vertebral  junctures were often  associated with the  vertebral deform-
ities.

    Halter  &  Johnson (1974)   report that DDT  is toxic to  the early
life-stages  of  coho salmon.   Mean  survival times  were considerably
reduced by water concentrations of DDT greater than 0.5 g/litre.

5.2.2  Sublethal behavioural effects on fish

    Hansen (1969) and Hansen et al. (1972) investigated  the  avoidance
of DDT by sheepshead minnows and mosquitofish in a 'Y'-shaped avoidance
maze.   Although there was some  statistically significant avoidance of
DDT when fish were given the choice between DDT and clean  water,  this
only  occurred at  concentrations of  the insecticide  above  the  24-h
LC50.    Fish of both species, when given the choice between DDT at 0.1
and  0.01 mg/litre, chose  the higher concentration  of the   chemical.
This  suggests  that  the perception of DDT is poor and that fish could
not reliably avoid DDT in water at toxic concentrations.

    Olofsson  & Lindahl (1979) administered either 0.5 or 1.0 mg DDT/kg
body weight to cod by oral intubation.  There was a significant effect,
at the higher dose but not the lower one, on the ability of the fish to
compensate  its posture to cope  with a rotating tube  in which it  was
swimming.

    Hansen  (1972) allowed mosquitofish to select a desired salinity in
a  fluvarium with a salinity gradient.  Fish selected a higher salinity
than controls  when exposed to DDT, but only at exposure  levels  which
caused some mortality.  The author suggested that DDT might have affec-
ted  the osmoregulatory ability  of the mosquitofish.   Other  possible
explanations  include a change in sensitivity of nerves to stimuli or a
preference for the pre-exposure salinity, which was 15 g/litre.


Table 4.  Toxicity of DDT and its derivatives to fish
---------------------------------------------------------------------------------------------------------
Organism                  Size      Flow/   Tem-     Salinity  Compound  Parameter   Water      Reference
                          (g)/      stata   perat-   o/oo                            concen-       
                          agef              ure                                      tration   
                                            (C)                                     (ug/litre)
---------------------------------------------------------------------------------------------------------
Estuarine and marine fish

Dwarf perch               1.2-11.0  Stat    13       28        DDTc      96-h LC50   4.6        Earnest &
 (Micrometrus minimus)     1.2-11.0  flowb   14-18    26-28     DDTc      96-h LC50   0.26       Benville 
                                                                                  (0.13-0.52)   (1972)
Shiner perch              1.2-11.0  stat    13       26        DDTc      96-h LC50   7.6        Earnest &
 (Cymatogaster aggregata)  1.2-11.0  flowb   14-18    13-23     DDTc      96-h LC50   0.45       Benville 
                                                                                  (0.21-0.94)   (1972)
Striped bass              2.7       flowb   17       28        DDT(77%)  96-h LC50   0.53       Korn & 
 (Morone saxatilis)                                                                (0.38-0.84)   Earnest
                          0.6       flowb   17       30        TDEc      96-h LC50   2.5        (1974)
                                                                                  (1.6-4.0)
Sheepshead minnow         juv.      flow    15       30        DDTc      48-h LC50   2.0        Mayer 
 (Cyprinodon variegatus)                                                                         (1987)

Longnose killifish        juv.      flow    15       30        DDTc      48-h LC50   2.8        Mayer 
 (Fundulus similis)        juv.      flow    16       28        TDEc      48-h LC50   42.0       (1987)

Pinfish                   juv.      flow    22       29        DDTc      48-h LC50   0.3        Mayer 
 (Lagodon rhomboides)                                                                            (1987)

Striped mullet            juv.      flow    15       30        DDTc      48-h LC50   0.4        Mayer 
 (Mugil cephalus)                                                                                (1987)

Spot                      juv.      flow    12       26        DDEc      48-h LC50   > 100      Mayer
 (Leiostomus xanthurus)    juv.      flow    26       30        TDEc      48-h LC50   20.0       (1987)

Three-spined              0.4-0.8   stat    20       5         DDT       24-h LC50   22.0       Katz
stickleback               0.4-0.8   stat    20       5         DDT       48-h LC50   21.0       (1961)
 (Gasterosteus             0.4-0.8   stat    20       5         DDT       72-h LC50   18.5       Katz 
  aculeatus)               0.4-0.8   stat    20       5         DDT       96-h LC50   18.0       (1961)
                          0.4-0.8   stat    20       25        DDT       24-h LC50   18.0       Katz
                          0.4-0.8   stat    20       25        DDT       48-h LC50   15.0       (1961)
                          0.4-0.8   stat    20       25        DDT       72-h LC50   14.5       Katz 
                          0.4-0.8   stat    20       25        DDT       96-h LC50   11.5       (1961)

Table 4. (Contd).
---------------------------------------------------------------------------------------------------------
Organism               Size     Flow/  Tem-   Alkali- Hard-  pH     Com-  Parameter  Water     Reference
                       (g)      stata  perat- nityd   nessd         pound            concen-      
                                       ure                                           tration   
                                       (C)                                          (ug/litre)
---------------------------------------------------------------------------------------------------------
Freshwater fish

Black bullhead         1.2      stat   18             44     7.1    DDTc  24-h LC50  36.8      Mayer &
 (Ictalurus melas)                                                                  (20.3-67.0)
                       1.2      stat   18             44     7.1    DDTc  96-h LC50  4.8 
                                                                                   (3.4-6.8)   Ellersieckg
                       1.2      stat   18             272    7.4    DDTc  24-h LC50  26.2 
                                                                                   (22.0-31.3) Mayer &
                       1.2      stat   18             272    7.4    DDTc  96-h LC50  5.1 
                                                                                   (3.9-6.7)   Ellersieckg

Channel catfish        1.5      stat   18             44     7.1    DDTc  24-h LC50  22.0 
 (Ictalurus punctatus)                                                              (18.2-26.5) Mayer &
                       1.5      stat   18             44     7.1    DDTc  96-h LC50  21.5 
                                                                                   (17.7-26.1) Ellersieckg
                       1.5      stat   18             272    7.4    DDTc  24-h LC50  18.4 
                                                                                   (13.7-24.7) Mayer &
                       1.5      stat   18             272    7.4    DDTc  96-h LC50  17.3 
                                                                                   (13.0-23.1) Ellersieckg
                       0.7      stat   18             44     7.1    DDTc  24-h LC50  17.9 
                                                                                   (12.7-25.3) Mayer &
                       0.7      stat   18             44     7.1    DDTc  96-h LC50  6.9 
                                                                                   (5.7-8.5)   Ellersieckg
                       1.6      stat   18             44     7.1    DDTc  24-h LC50  44.0 
                                                                                   (37.0-52.0) Mayer &
                       1.6      stat   18             44     7.1    DDTc  96-h LC50  22.0 
                                                                                   (19.0-26.0) Ellersieckg
                       1.4      stat   18             44     7.1    DDTc  24-h LC50  30.0 
                                                                                   (22.0-41.0) Mayer &
                       1.4      stat   18             44     7.1    DDTc  96-h LC50  16.0 
                                                                                   (9.4-29.0)  Ellersieckg
                       1.4      stat   18             272    7.7    DDTc  24-h LC50  29.0 
                                                                                   (20.0-41.0) Mayer &
                       1.4      stat   18             272    7.7    DDTc  96-h LC50  7.0 
                                                                                   (4.3-11.0)  Ellersieckg

Table 4. (Contd).
---------------------------------------------------------------------------------------------------------
Organism               Size     Flow/  Tem-   Alkali- Hard-  pH     Com-  Parameter  Water     Reference
                       (g)      stata  perat- nityd   nessd         pound            concen-       
                                       ure                                           tration   
                                       (C)                                          (ug/litre)
---------------------------------------------------------------------------------------------------------

Atlantic salmon        0.45     stat   12             40     7.5    DDTc  24-h LC50  6.2 
 (Salmo salar)                                                                      (4.6-8.4)   Mayer &
                       
                       0.45     stat   12             40     7.5    DDTc  96-h LC50  1.8 
                                                                                   (1.3-2.6)   Ellersieckg
                       0.5      stat   12             44     7.5    DDEc  96-h LC50  96.0 
                                                                                   (52.1-177)  Mayer &
                                                                                               Ellersieckg

Coho salmon            2.7-4.1  stat   20     45-57        6.8-7.4  DDT   24-h LC50  66.0      Katz (1961)
 (Oncorhynchus kisutch) 
                       2.7-4.1  stat   20     45-57        6.8-7.4  DDT   48-h LC50  46.0      Katz (1961)
                       2.7-4.1  stat   20     45-57        6.8-7.4  DDT   72-h LC50  44.0      Katz (1961)
                       2.7-4.1  stat   20     45-57        6.8-7.4  DDT   96-h LC50  44.0      Katz (1961)
                       1.0      stat   13             44     7.1    DDTc  24-h LC50  10.0 
                                                                                   (7.0-12.0)  Mayer &
                       1.0      stat   13             44     7.1    DDTc  96-h LC50  4.0 
                                                                                   (3.0-6.0)   Ellersieckg
                       6.0      stat   13             40     7.1    DDTc  24-h LC50  26.9 
                                                                                   (18.1-40.0) Mayer &
                       6.0      stat   13             40     7.1    DDTc  96-h LC50  19.3 
                                                                                   (9.6-38.8)  Ellersieckg

Chinook salmon         1.5-5.0  stat   20     45-57        6.8-7.4  DDT   24-h LC50  38.0      Katz (1961)
 (Oncorhynchus          
  tshawytscha)          1.5-5.0  stat   20     45-57        6.8-7.4  DDT   48-h LC50  17.0      Katz (1961)
                       
                       1.5-5.0  stat   20     45-57        6.8-7.4  DDT   72-h LC50  14.0      Katz (1961)
                       
                       1.5-5.0  stat   20     45-57        6.8-7.4  DDT   96-h LC50  11.5      Katz (1961)

Table 4. (Contd).
---------------------------------------------------------------------------------------------------------
Organism               Size     Flow/  Tem-   Alkali- Hard-  pH     Com-  Parameter  Water     Reference
                       (g)      stata  perat- nityd   nessd         pound            concen-       
                                       ure                                           tration   
                                       (C)                                          (ug/litre)
---------------------------------------------------------------------------------------------------------

Rainbow trout          0.9      stat   7              44     7.1    DDTc  24-h LC50  7.5 
 (Salmo gairdneri)                                                                  (6.7-8.3)   Mayer &
                       0.9      stat   7              44     7.1    DDTc  96-h LC50  4.1 
                                                                                   (3.6-4.6)   Ellersieckg
                       0.9      stat   13             44     7.1    DDTc  24-h LC50  8.2 
                                                                                   (7.2-9.2)   Mayer &
                       0.9      stat   13             44     7.1    DDTc  96-h LC50  4.7 
                                                                                   (4.2-5.3)   Ellersieckg
                       0.9      stat   18             44     7.1    DDTc  24-h LC50  12.0 
                                                                                   (1.0-13.0)  Mayer &
                       0.9      stat   18             44     7.1    DDTc  96-h LC50  5.8 
                                                                                   (5.2-6.5)   Ellersieckg
                       3.2      stat   20     45-57        6.8-7.4  DDT   24-h LC50  42.0      Katz (1961)
                       3.2      stat   20     45-57        6.8-7.4  DDT   48-h LC50  42.0      Katz (1961)
                       3.2      stat   20     45-57        6.8-7.4  DDT   72-h LC50  42.0      Katz (1961)
                       3.2      stat   20     45-57        6.8-7.4  DDT   96-h LC50  42.0      Katz (1961)
                       1.8      flow   17             272    7.4    DDTc  96-h LC50  > 3.0    Mayer &
                       0.8      stat   12             44     7.1    DDEc  96-h LC50  32.0 
                                                                                   (26.0-40.0) Ellersieckg
                       1.0      stat   12             44     7.1    TDEc  96-h LC50  70.0 
                                                                                   (57.0-87.0) Mayer &
                       1.0      stat   12             272    7.4    TDEc  96-h LC50  70.0 
                                                                                   (58.0-85.0) Ellersieckg
                                                                          
Cutthroat trout        1.0      stat   13             44     7.1    DDTc  24-h LC50  8.4 
 (Salmo clarki)                                                                     (7.6-9.2)   Mayer &
                       1.0      stat   13             44     7.1    DDTc  96-h LC50  5.5 
                                                                                   (4.7-6.4)   Ellersieckg
                       1.8      stat   9              162    7.4    DDTc  24-h LC50  11.3 
                                                                                   (9.4-13.6)  Mayer &
                       1.8      stat   9              162    7.4    DDTc  96-h LC50  7.9 
                                                                                   (6.5-9.7)   Ellersieckg
                                                      
Brown trout            1.7      stat   13             44     7.1    DDTc  96-h LC50  1.8 
 (Salmo trutta)                                                                     (1.3-2.5)   Mayer &
                                                                                               Ellersieckg
Table 4. (Contd).
---------------------------------------------------------------------------------------------------------
Organism               Size     Flow/  Tem-   Alkali- Hard-  pH     Com-  Parameter  Water     Reference
                       (g)      stata  perat- nityd   nessd         pound            concen-       
                                       ure                                           tration   
                                       (C)                                          (ug/litre)
---------------------------------------------------------------------------------------------------------

Northern pike          0.7      stat   18             272    7.4    DDTc  24-h LC50  5.5       Mayer &
 (Esox lucius)          0.7      stat   18             272    7.4    DDTc  96-h LC50  2.7       Ellersieckg

Guppy                  0.1-0.2  stat   25     18      20     7.4    DDTc  24-h LC50  135       Henderson
 (Lebistes              0.1-0.2  stat   25     18      20     7.4    DDTc  48-h LC50  72.0      et al.
  reticulatus)          0.1-0.2  stat   25     18      20     7.4    DDTc  96-h LC50  56.0      (1959)

River shiner           0.3      stat   18             44     7.1    DDTc  24-h LC50  6.7 
 (Notropis blennius)                                                                (4.9-9.1)   Mayer &
                       0.3      stat   18             44     7.1    DDTc  96-h LC50  5.8 
                                                                                   (3.6-9.1)   Ellersieckg
Fathead minnow         1.2      stat   18             44     7.1    DDTc  24-h LC50  14.2 
 (Pimephales                                                                        (11.0-18.0) Mayer &
  promelas)             1.2      stat   18             44     7.1    DDTc  96-h LC50  12.4 
                                                                                   (10.0-15.4) Ellersieckg
                       1.2      stat   18             272    7.4    DDTc  24-h LC50  13.8 
                                                                                   (10.3-18.3) Mayer &
                       1.2      stat   18             272    7.4    DDTc  96-h LC50  13.2 
                                                                                   (10.1-17.3) Ellersieckg
                       0.9      flow   12             314    7.6    DDTc  96-h LC50  9.9 
                                                                                   (6.5-15.0)  Mayer &
                                                                                               Ellersieckg
                       1.0-2.0  stat   25     18      20     7.4    DDTc  24-h LC50  56.0      Henderson
                       1.0-2.0  stat   25     18      20     7.4    DDTc  48-h LC50  45.0      et al. (1959)
                       1.0-2.0  stat   25     18      20     7.4    DDTc  96-h LC50  42.0      Henderson
                       1.0-2.0  stat   25     360     400    8.2    DDTc  24-h LC50  78.0      et al. (1959)
                       1.0-2.0  stat   25     360     400    8.2    DDTc  48-h LC50  68.0      Henderson
                       1.0-2.0  stat   25     360     400    8.2    DDTc  96-h LC50  45.0      et al. (1959)
                       1.0-2.0  stat   25     18      20     7.4    DDT   24-h LC50  32.0      Henderson
                       1.0-2.0  stat   25     18      20     7.4    DDT   48-h LC50  26.0      et al. (1959)
                       1.0-2.0  stat   25     18      20     7.4    DDT   96-h LC50  26.0      Henderson
                       1.0-2.0  stat   25     360     400    8.2    DDT   24-h LC50  29.0      et al. (1959)
                       1.0-2.0  stat   25     360     400    8.2    DDT   48-h LC50  27.0      Henderson
                       1.0-2.0  stat   25     360     400    8.2    DDT   96-h LC50  26.0      et al. (1959)

Table 4.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism               Size     Flow/  Tem-   Alkali- Hard-  pH     Com-  Parameter  Water     Reference
                       (g)      stata  perat- nityd   nessd         pound            concen-       
                                       ure                                           tration   
                                       (C)                                          (ug/litre)
---------------------------------------------------------------------------------------------------------

Mosquitofish           0.2      stat   25                           DDTc  24-h LC50  22.7 
 (Gambusia affinis)                                                                 (16.6-31.1) El-Sebae (1987)
                       0.2      stat   25                           DDTc  96-h LC50  9.9 
                                                                                   (7.3-13.4)  El-Sebae (1987)
                       0.2      stat   25                           DDTe  24-h LC50  58.6 
                                                                                   (43.2-79.5) El-Sebae (1987)
                       0.2      stat   25                           DDTe  96-h LC50  27.7 
                                                                                   (21.3-36.0) El-Sebae (1987)

Bluegill sunfish       0.26     stat   19     138     192  8.2-8.5  DDTc  96-h LC50  3.4 
 (Lepomis macrochirus)                                                              (2.6-4.1)   Randall
                       0.26     stat   19     138     192  8.2-8.5  DDT   96-h LC50  9.0 
                                                                                   (7.4-10.6)  et al. (1979)
                                                                    (25%)
                       1.0-2.0  stat   25     18      20     7.4    DDTc  24-h LC50  26.0      Henderson
                       1.0-2.0  stat   25     18      20     7.4    DDTc  48-h LC50  21.0      et al.
                       1.0-2.0  stat   25     18      20     7.4    DDTc  96-h LC50  21.0      (1959)
                       1.5      stat   18             44     7.1    DDTc  24-h LC50  11.5 
                                                                                   (8.4-16.0)  Mayer &
                       1.5      stat   18             44     7.1    DDTc  96-h LC50  8.6 
                                                                                   (6.2-12.0)  Ellersieckg
                       1.5      stat   18             272    7.4    DDTc  24-h LC50  10.0 
                                                                                   (8.5-12.9)  Mayer &
                       1.5      stat   18             272    7.4    DDTc  96-h LC50  6.3 
                                                                                   (4.3-9.3)   Ellersieckg
                       0.9      stat   17             44     7.1    DDEc  96-h LC50  240 
                                                                                   (201-286)   Mayer &
                       0.9      stat   24             44     7.4    TDEc  24-h LC50  56.0 
                                                                                   (46.0-68.0) Ellersieckg
                       0.9      stat   24             44     7.4    TDEc  96-h LC50  42.0 
                                                                                   (36.0-49.0) Mayer &
                                                                                               Ellersieckg

Redear sunfish         3.2      stat   24             44     7.1    DDTc  24-h LC50  19.0      Mayer &
 (Lepomis microlophus)  3.2      stat   24             44     7.1    DDTc  96-h LC50  15.0      Ellersieckg

Table 4.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism               Size     Flow/  Tem-   Alkali- Hard-  pH     Com-  Parameter  Water     Reference
                       (g)      stata  perat- nityd   nessd         pound            concen-       
                                       ure                                           tration   
                                       (C)                                          (ug/litre)
---------------------------------------------------------------------------------------------------------

Green sunfish          1.1      stat   18             44     7.1    DDTc  24-h LC50  16.9 
 (Lepomis cyanellus)                                                                (12.7-22.3) Mayer &
                       1.1      stat   18             44     7.1    DDTc  96-h LC50  10.9 
                                                                                   (7.3-15.6)  Ellersieckg
                       0.8      stat   18             44     7.1    DDTc  24-h LC50  18.0 
                                                                                   (13.0-24.0) Mayer &
                       0.8      stat   18             44     7.1    DDTc  96-h LC50  6.5 
                                                                                   (4.1-10.4)  Ellersieckg
                       1.1      stat   18             272    7.7    DDTc  24-h LC50  19.8 
                                                                                   (15.0-25.6) Mayer &
                       1.1      stat   18             272    7.7    DDTc  96-h LC50  9.9 
                                                                                   (6.4-15.0)  Ellersieckg

Largemouth bass        0.8      stat   18             44     7.1    DDTc  24-h LC50  3.7 
 (Micropterus                                                                       (3.1-4.5)   Mayer &
  Salmoides)            0.8      stat   18             44     7.1    DDTc  96-h LC50  1.5 
                                                                                   (0.9-2.4)   Ellersieckg
                       0.8      stat   18             272    7.4    DDTc  24-h LC50  2.1 
                                                                                   (1.6-2.9)   Mayer &
                       0.8      stat   18             272    7.4    DDTc  96-h LC50  1.5 
                                                                                   (0.9-2.4)   Ellersieckg
                       0.7      stat   18             44     7.1    TDEc  24-h LC50  50.0 
                                                                                   (35.0-71.0) Mayer &
                       0.7      stat   18             44     7.1    TDEc  96-h LC50  42.0 
                                                                                   (34.0-51.0) Ellersieckg

Black crappie          1.0      stat   18             44     7.1    DDTc  24-h LC50  6.5 
 (Pomoxis                                                                           (5.4-7.8)   Mayer &
  nigromaculatus)       1.0      stat   18             44     7.1    DDTc  96-h LC50  5.6 
                                                                                   (4.6-6.7)   Ellersieckg
                 

Yellow perch           1.4      stat   18             44     7.1    DDTc  24-h LC50  10.0 
 (Perca flavescens)                                                                 (8.0-12.0)  Mayer &
                       1.4      stat   18             44     7.1    DDTc  96-h LC50  9.0 
                                                                                   (7.0-11.0)  Ellersieckg
Table 4.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism               Size     Flow/  Tem-   Alkali- Hard-  pH     Com-  Parameter  Water     Reference
                       (g)      stata  perat- nityd   nessd         pound            concen-       
                                       ure                                           tration   
                                       (C)                                          (ug/litre)
---------------------------------------------------------------------------------------------------------

Walleye                1.4      stat   18             44     7.1    DDTc  24-h LC50  4.2 
 (Stizostedion v.                                                                   (3.2-5.6)   Mayer &
  vitreum)              1.4      stat   18             44     7.1    DDTc  96-h LC50  2.9 
                                                                                   (2.4-3.5)   Ellersieckg
                       1.3      stat   18             272    7.4    DDTc  24-h LC50  4.6 
                                                                                   (3.9-5.4)   Mayer &
                       1.3      stat   18             272    7.4    DDTc  96-h LC50  4.6 
                                                                                   (3.9-5.4)   Ellersieckg
                       1.0      stat   18             44     7.1    TDEc  24-h LC50  20.0 
                                                                                   (16.0-24.0) Mayer &
                       1.0      stat   18             44     7.1    TDEc  96-h LC50  14.0 
                                                                                   (11.0-19.0) Ellersieckg

Tilapia                0.8      stat   24             44     7.1    DDTc  24-h LC50  19.0 
 (Tilapia mossambica)                                                               (16.0-23.0) Mayer &
                       0.8      stat   24             44     7.1    DDTc  96-h LC50  17.0 
                                                                                   (14.0-21.0) Ellersieckg
                       0.8      stat   24             272    7.4    DDTc  24-h LC50  15.0 
                                                                                   (13.0-17.0) Mayer &
                       0.8      stat   24             272    7.4    DDTc  96-h LC50  14.0 
                                                                                   (12.0-16.0) Ellersieckg
                       0.8      flow   18             272    7.4    DDTc  24-h LC50  24.0 
                                                                                   (17.0-32.0) Mayer &
                       0.8      flow   18             272    7.4    DDTc  96-h LC50  5.1 
                                                                                   (3.2-8.1)   Ellersieckg

Tilapia                0.8      stat   25                           DDTc  24-h LC50  21.8 
 (Tilapia zilli)                                                                    (17.0-28.0) El-Sebae (1987)
                       0.8      stat   25                           DDTc  96-h LC50  15.5 
                                                                                   (11.7-20.6) El-Sebae (1987)
                       0.8      stat   25                           DDTe  24-h LC50  12.8 
                                                                                   (9.6-17.1)  El-Sebae (1987)
                       0.8      stat   25                           DDTe  96-h LC50  9.5 
                                                                                   (7.4-12.3)  El-Sebae (1987)

Table 4.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism               Size     Flow/  Tem-   Alkali- Hard-  pH     Com-  Parameter  Water     Reference
                       (g)      stata  perat- nityd   nessd         pound            concen-       
                                       ure                                           tration   
                                       (C)                                          (ug/litre)
---------------------------------------------------------------------------------------------------------

Goldfish               1.0-2.0  stat   25     18      20     7.4    DDTc  24-h LC50  180       Henderson
 (Carassius auratus)    1.0-2.0  stat   25     18      20     7.4    DDTc  48-h LC50  47.0      et al.
                       1.0-2.0  stat   25     18      20     7.4    DDTc  96-h LC50  36.0      (1959)
                       0.9      stat   18             44     7.1    DDTc  24-h LC50  24.0 
                                                                                   (17.0-33.0) Mayer &
                       0.9      stat   18             44     7.1    DDTc  96-h LC50  15.5 
                                                                                   (9.1-26.0)  Ellersieckg
                       0.9      stat   18             272    7.4    DDTc  24-h LC50  22.2 
                                                                                   (16.0-31.1) Mayer &
                       0.9      stat   18             272    7.4    DDTc  96-h LC50  14.7 
                                                                                   (10.0-20.0) Ellersieckg

Common carp            0.6      stat   18             44     7.1    DDTc  24-h LC50  14.0 
 (Cyprinus carpio)                                                                  (10.0-19.0) Mayer &
                       0.6      stat   18             44     7.1    DDTc  96-h LC50  9.7 
                                                                                   (7.4-12.9)  Ellersieckg

---------------------------------------------------------------------------------------------------------
a  Stat = static conditions (water unchanged for duration of test); Flow = flow-through conditions 
   (DDT concentration in water continuously maintained).
b  Intermittent flow-through conditions.
c  Technical grade (99%).
d  Alkalinity and hardness expressed as mg CaCO3/litre.
e  25% emulsifiable concentrate.
f  Juv. = juvenile.
g  1986.
    Peterson   (1973)   monitored  the  selection  of  temperature   by
juvenile   Atlantic salmon ( Salmo salar ) previously  exposed to DDT  or
its   metabolites.   Low  concentrations  produced  no effect  on  tem-
perature  selection, but at higher  levels of exposure the  temperature
selected  by  the fish  increased.  Fish were  most sensitive, in  this
respect, to  p,p' -DDE     and   showed   decreasing   sensitivity   to
 o,p' -DDT,  p,p' -TDE, and  p,p' -DDT.    Increasing  the exposure to
 p,p' -DDE   from 0 to 1.0 mg/litre increased the  preferred  temperature
from about 16 C to 21 C.  There  was  no effect  of  p,p' -DDA   on
temperature  selection at concentrations as  high as 8 mg/litre.   In a
similar  experiment,  where  brook  trout (Salvelinus  fontinalis) were
exposed to a vertical rather than horizontal temperature gradient, fish
previously exposed to  p,p' -DDT and  p,p' -TDE  selected   higher
temperatures  than controls.  Conversely, Gardner (1973) found that DDT
and  its analogues induced  selection of lower temperatures by the same
species of fish over a dose range between 0 and 50 g/litre;   DDE  did
not  produce  any  temperature  preference.   Ogilvie  &  Miller (1976)
reported  that  Atlantic salmon  exposed to DDT  at a concentration  of
50 g/litre  selected higher temperatures, the effect persisting for at
least  4 weeks after exposure.  The authors suggested that the tempera-
ture  selection  response  to DDT  exposure  is  "biphasic".  At  low
exposure  levels,   similar  to those  used  by  Gardner (1973),  lower
temperatures  are selected, whilst higher temperatures are preferred at
higher exposure levels.

    Dill  &  Saunders (1974)  exposed  the  eggs  of   Atlantic  salmon
at   gastrulation to  DDT at   water  concentrations  of 5,  10, 50, or
100 g/litre,  and observed behavioural development in hatched fry over
30 days following hatch.  The two highest doses of DDT impaired balance
and retarded behavioural development of the fry (i.e.,  the  appearance
of normal behaviour patterns was delayed).  The authors considered that
the  effects observed  would affect  predation rates  and  feeding,  in
young fish, at "realistic" DDT exposure levels in the wild.

    Davy et al. (1973) reported that exposure to DDT,  at  10  g/litre
for  4 days,  affected the  exploratory behaviour  of goldfish  experi-
encing  a novel environment.  They  attributed the effect to  a central
nervous  system lesion caused  by DDT.  Weis  & Weis (1974)   showed an
increase  in individual  activity and  an increase  in  school-size  in
groups of goldfish exposed to DDT at 1 g/litre  for 7 days.   After  a
frightening  stimulus, schools scattered further and did not regroup as
readily as control fish.  The transfer of fish to clean water   led  to
a  return  to   normal behaviour  within  one  week.  An  effect on the
locomotor behaviour of goldfish after exposure to 10 g  DDT/litre per-
sisted  for  the remainder  of the observation  period of 130-139  days
(Davy et al., 1972).

5.2.3  Physiological effects on fish

    Hanke et al. (1983) investigated the effects of DDT on a  range  of
physiological  functions in carp ( Cyprinus carpio ).  At water  concen-
trations  of 100 or 500 g/litre,   the insecticide induced changes  in
plasma  cortisol and glucose levels,  liver glycogen level, and  plasma
and  brain acetylcholinesterase activity.  The response was biphasic in
all  cases.  Initially, after 6 hours, there was a stimulation of these
parameters   which,  within  24   hours,  changed  to   an  inhibition.

Ramalingam  & Ramalingam (1982) reported that the chronic effect of DDT
on  glycogen utilization in fish led to the use of protein as an energy
source.  The protein content of tissues declined after chronic exposure
to DDT.

    Janicki & Kinter (1971) found that DDT impaired fluid absorption in
the  intestinal sacs of eels  adapted to sea water  and exposed to  the
insecticide  at 50 g/litre.   DDT  also inhibited Na+-, K+-, and
Mg2+-dependent   ATPases in homogenates of the intestinal mucosa.  In a
later  study,  Kinter et al.  (1972) showed that plasma  osmolarity was
also  affected in sea-water-adapted  eels exposed to  DDT (1  mg/litre)
for  9  to  10 hours.  Haux & Larsson (1979) reported effects of DDT on
plasma   electrolytes in the flounder  Platichthys flesus  kept  in
hypotonic, brackish water.  The fish were force-fed with DDT in gelatin
capsules  to give a total  DDT dose of 1.5  or 15.0 mg/kg body  weight.
Plasma  sodium was reduced but  not significantly; plasma chloride  was
significantly  reduced in a dose-related  manner after 3 weeks  but not
after  6 weeks.  Waggoner &  Zeeman (1975) reported similar  effects on
plasma  electrolytes in the black  surfperch ( Embiotoca jacksoni ),  but
only  at  high  DDT exposure levels.  They injected DDT doses of 1, 10,
100, or 200 mg/kg; the only effect occurred with the dose of 200 mg/kg,
but  the fish did  not survive to  72 h.  The  authors  suggested  that
osmoregulatory effects are not the major cause of DDT-induced mortality
in marine fish.

    Desaiah   et  al.  (1975)  exposed  fathead  minnows ( Pimephales 
 promelas ) for long periods to  DDT at water concentrations  of 0.5 or
2.0 g/litre  and  also via  the food, and  monitored the activity  of
ATPases  in brain and  gill.  This study  followed up several  previous
studies  on  in vitro  effects  on these  enzymes.   After  266 days  of
exposure,   there   was  an   approximately  50%  reduction   in  brain
oligomycin-sensitive  (mitochondrial)  Mg2+-ATPase    activity.    In
contrast,  oligomycin-insensitive Mg2+-ATPase   activity  was increased
by  almost 40%.  Total  Mg2+-ATPase   activity was,  therefore,  almost
unaffected  by DDT.  There was a less obvious (about 18%) activation of
Na+-K+-ATPase  activity in the brain.  Gill tissue showed different
results;  all the ATPases studied  were inhibited by DDT.   The authors
suggested that a major factor in the toxicity of DDT to fish (and other
organisms)  could  be   the inhibition  of  oxidative  phosphorylation.
Moffett   &   Yarbrough   (1972)  investigated   the   enzyme  succinic
dehydrogenase   in  insecticide-resistant  and  insecticide-susceptible
mosquitofish ( Gambusia affinis )   in  an   attempt  to  discover   if
resistance  could be related  to membrane effects  of DDT.  They  found
that  the effect  on membrane-bound  enzymes was,  indeed,  reduced  in
resistant  fish.  This  may not  explain all  the factors  involved  in
resistance, since DDT uptake from water may also be reduced.

5.2.4  Development of tolerance

    The  development  of tolerance  to DDT in  fish has been  reported.
Vinson  et al. (1963) reported DDT tolerance in mosquitofish  ( Gambusia 
 affinis ) exposed  long-term  to DDT  in the wild,  and Boyd &  Ferguson
(1964) showed TDE tolerance in the same species.  However, fish exposed
long-term  to DDT do not always show tolerance.  Ferguson et al. (1964)
recorded tolerance to a variety of organochlorine insecticides in three

species  of freshwater fish from  the Mississippi delta area  of cotton
cultivation,  but  there  was no  tolerance  to  DDT.  El-Sebae  (1987)
determined  the LC50 values  for two populations of  Tilapia zilli  from
different  areas of Egypt.   Fish from the  Behera Governate which  had
been taken from agricultural drains showed exactly the  same  suscepti-
bility to DDT (25% EC) as fish taken from a less contaminated  area  in
the  Alexandria Governate.  Tolerance  had developed to  other insecti-
cides in these different strains.

5.3 Toxicity to Amphibians

Appraisal 

     The toxicity of DDT and its metabolites to amphibians  varies  from
 species to species; although only a few data are  available,  amphibian
 larvae seem to be more sensitive than adults to DDT.  TDE seems  to  be
 more  toxic than DDT to amphibians, but there are no data available for
 DDE.  All the studies reported have been static tests  and,  therefore,
 results should be treated with caution.

    The   toxicity  of DDT  and TDE  to   amphibians is summarized   in
Table  5.  Both compounds  are toxic to  amphibian larvae at  low water
concentrations.

    Two   studies  (Harri et  al., 1979;  Hudson  et al., 1984)  showed
that  DDT  is  moderately  toxic  to  adult  frogs when  given  orally.
Repeated   oral dosing of adult common frogs ( Rana temporaria ) with DDT
at  0.6 mg/kg body weight twice weekly for 8 weeks, led to no mortality
when  the animals were fed  (Harri et al., 1979).   Frogs dosed in  the
same  way, but not fed, showed 50% mortality by the end of dosing.  The
first animal died after the fifth dose and all others  showed  symptoms
of poisoning.

    A  study by Sanders  (1970) indicated that  the toxicity of  DDT to
tadpoles of Fowler's toad increased with age of the tadpole.   The  24-
and  96-h  LC50 values   of 5.3  and  0.75  mg/litre  for  one-week-old
tadpoles fell to 1.4 and 0.03 mg/litre, respectively, by the  time  the
tadpoles  were 7 weeks old.   TDE was only tested  on one age range  of
tadpoles  for a  maximum of  96 h, and was found  to be 3-8 times  more
toxic  than DDT.  The pattern of pesticide poisoning progressed through
irritability  and loss of equilibrium to death.  Tadpoles were affected
irreversibly  by concentrations well below  their calculated short-term
LC50 values  and, therefore, would succumb to DDT over time.   DDT  was
re-tested  several times  during over  the period  of the  study in  an
attempt  to identify any development  of resistance in the  population.
None  was found; the 24-h LC50 values  were stable throughout a 4-month
period.


Table 5.  Toxicity of DDT and its derivatives to amphibians
---------------------------------------------------------------------------------------------------------
Organism               Flow/   Tem-      Alkali-  pH   Compound Parameter  Water              Reference
                       Stata   perature  nityb                             concentration
                               (C)                                        (ug/litre)
---------------------------------------------------------------------------------------------------------
Fowler's toad (tadpole)
 (Bufo woodhousii) 

1 week old - 15 mg     stat    15.5      30       7.1  DDT      24-h LC50  5300 (2900-9900)   Sanders 
                       stat    15.5      30       7.1  DDT      48-h LC50  1800 (950-3300)    (1970)
                       stat    15.5      30       7.1  DDT      96-h LC50  750 (280-2000)     Sanders 
                                                                                              (1970)

2-3 weeks old - 56 mg  stat    15.5      30       7.1  DDT      24-h LC50  5400 (2900-10 000) Sanders 
                       stat    15.5      30       7.1  DDT      48-h LC50  1300 (320-5300)    (1970)

4-5 weeks old - 74 mg  stat    15.5      30       7.1  DDT      24-h LC50  2400 (730-8000)    Sanders
                       stat    15.5      30       7.1  DDT      48-h LC50  1000 (40-6500)     (1970)
                       stat    15.5      30       7.1  DDT      96-h LC50  1000 (20-3600)     Sanders
                       stat    15.5      30       7.1  TDE      24-h LC50  700 (250-2000)     (1970)
                       stat    15.5      30       7.1  TDE      48-h LC50  320 (210-450)      Sanders
                       stat    15.5      30       7.1  TDE      96-h LC50  140 (100-210)      (1970)

6 weeks old - 350 mg   stat    15.5      30       7.1  DDT      24-h LC50  2200 (550-15 000)  Sanders
                       stat    15.5      30       7.1  DDT      48-h LC50  410 (280-600)      (1970)
                       stat    15.5      30       7.1  DDT      96-h LC50  100 (20-600)       Sanders 
                                                                                              (1970)
                                                       
7 weeks old - 600 mg   stat    15.5      30       7.1  DDT      24-h LC50  1400 (900-2000)    Sanders
                       stat    15.5      30       7.1  DDT      48-h LC50  750 (610-1100)     (1970)
                       stat    15.5      30       7.1  DDT      96-h LC50  30 (6-400)         Sanders 
                                                                                              (1970)

Table 5.  (Contd).
---------------------------------------------------------------------------------------------------------
Organism               Flow/   Tem-      Alkali-  pH   Compound Parameter  Water              Reference
                       Stata   perature  nityb                             concentration
                               (C)                                        (ug/litre)

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

Western chorus frog    stat    15.5      30       7.1  DDT      24-h LC50  1400 (910-2800)    Sanders
 (Pseudacris            stat    15.5      30       7.1  DDT      48-h LC50  900 (400-1500)     (1970)
  triseriata)           stat    15.5      30       7.1  DDT      96-h LC50  800 (500-2300)     Sanders
(1-week-old tadpole)   stat    15.5      30       7.1  TDE      24-h LC50  610 (410-820)      (1970)
                       stat    15.5      30       7.1  TDE      48-h LC50  500 (210-750)      Sanders
                       stat    15.5      30       7.1  TDE      96-h LC50  400 (210-750)      (1970)

Bullfrog                                               DDT      acute LD50c > 2000 ug/kg     Hudson 
 (Rana catesbeiana)                                     (77.2%)                                et al. 
                                                                                              (1984)
Common frog                    15                      DDT      acute LD50c 7600 ug/kg        Harri 
 (Rana temporaria)                                                                             et al. 
                                                                                              (1979)
---------------------------------------------------------------------------------------------------------
a  Stat = static conditions (water unchanged for duration of test); flow = flow-through conditions 
   (DDT concentration in water continuously maintained).
b  alkalinity expressed as mg CaCO3/litre.
c  acute LD50 was calculated by administering a single oral dose.
    Cooke  (1970) exposed tadpoles of the common frog ( Rana temporaria )
to   0.1, 1.0, or  10 mg DDT/litre  for only one  hour and  reported  a
period  of  uncoordinated hyperactivity  beginning  less than  one hour
after  the end of  the exposure period.   Body weight decreased  during
this hyperactive period and development was restricted in some  of  the
tadpoles.   Smaller tadpoles were more vulnerable to the effects of DDT
than  larger ones.  In  a later study  (Cooke, 1979b), the  same author
reared  tadpoles of the  common frog at  two different densities.   The
densities differed 5-fold and resulted in a 2-fold  average  difference
in  body weight between the two groups.  The larger tadpoles, reared at
the  lower density, were completely  tolerant of concentrations of  DDT
that  caused  severe  sublethal  effects  in  smaller  tadpoles.  Field
populations of tadpoles included individuals with weights corresponding
to the two experimental groups, but these were at the two  extremes  of
the natural weight range.

    Cooke  (1972) exposed both  spawn and tadpoles  of the common  frog
( Rana temporaria ), the common toad ( Bufo bufo ), and the smooth  newt
( Triturus vulgaris ) for 24  and 48  hours to  concentrations  of  DDT
between 0.8 g/litre  and 0.5 mg/litre.  Results indicated that DDT did
not  penetrate well-developed spawn and was only detectable in tadpoles
hatched  from spawn that had been treated with DDT immediately after it
had  been laid.  Tadpoles hatching  from spawn treated when  newly laid
showed   hyperactivity,  symptomatic of  DDT  poisoning, only  later in
their  development at the point where external gills were lost.  In the
experiments  where tadpoles were exposed to DDT, they were most suscep-
tible  either  just before  or just after  the development of  hindlimb
buds.   At  these  two  stages,  the characteristic  hyperactivity  was
shown when DDT tissue concentrations reached between 2-3  mg/kg  before
the  tadpoles  developed limb  buds, and when  they reached 3-4  mg/kg,
immediately  after the tadpoles developed limb buds.  During resorption
of  the tail, small frogs, but not small toads, were susceptible to DDT
residues  that had  been acquired  during larval  development.  At  all
stages  of development,  toads were  more resistant  to DDT  than  were
frogs,  and some  toad tadpoles  survived despite  tissue  residues  in
excess of 300 mg/kg.  The metabolite DDE was often detectable  in  newt
tadpoles and in frog and toad tadpoles with hindlimbs.

    DDT  has an anatomical effect  on developing frog tadpoles  (Cooke,
1970; Osborn et al., 1981).  Exposure of tadpoles to 0.1  mg  DDT/litre
for  2  days  or to 0.1, 1.0, or 10 mg/litre for one hour produced some
individuals with abnormalities in the snout.  A  detailed  histological
and  behavioural study  suggested that  the effect  was caused  by  two
separate factors.  DDT had a direct effect on the development  of  skin
glands  in the  region above  the upper  mandible.   The  uncoordinated
hyperactivity  that followed DDT treatment caused the lower mandible to
strike  the upper, distorted mandible  and resulted in further  damage.
Some individuals recovered from this abnormality at various  stages  of
development.  However, froglets that were affected at the tadpole stage
frequently   have  blunt  snouts  and  deformed  brains.   The  authors
suggested that DDT caused the disruption by preventing the organisation
of  the epithelial cells into  gland units, possibly by  affecting cell
membranes  and disrupting cell-to-cell communication.  The mechanism of
recovery remained unclear and a full explanation of the  very  specific
nature of the abnormality was not possible.

    This toxicity of DDT to amphibians is of significance in its use as
an insecticide.  The use of DDT to control mosquito larvae has  been  a
major  source of  exposure of  tadpoles and  has led  to toxic  effects
(Mulla, 1963; Cooke, 1973a).

    The  widespread  use  of DDT  has  led  to the  development of some
resistance in two species of cricket frog ( Acris crepitans  and  Acris 
 gryllus ).  Boyd et al. (1963)  found that cricket frogs collected from
areas  of high DDT  usage for the  control of cotton  pests  were  more
tolerant to DDT than were frogs from other areas.


6.  TOXICITY TO TERRESTRIAL ORGANISMS

    There  is  evidence  that DDT  and  its  metabolites have  affected
wildlife in terrestrial ecosystems.  Laboratory studies covered in this
section  give  clear indication  of a variety  of lethal and  sublethal
effects.   The range  of organisms  studied is  not comprehensive.   No
review  has been made here of the effects of DDT on insects, the target
organisms.   The lethal effect of  DDT on insects is  thought to result
from changes in nerve transmission.

6.1  Terrestrial Invertebrates

Appraisal 

     There  have  been  few reports  on  the  effects  of  DDT  and  its
 metabolites on non-target terrestrial invertebrates.

     Earthworms  are insensitive to the  acutely toxic effects of  these
 compounds  at  levels  higher than  those  likely  to be  found  in the
 environment.  The uptake of DDT by earthworms is related to the concen-
 trations in soil and to the activity of the worms;  seasonally  greater
 activity increases uptake.  Thus, although earthworms are  unlikely  to
 be  seriously affected by  DDT, they pose  a major hazard  to predators
 because of the residues they can tolerate.

     Both  DDT and DDE are  classified as being relatively  non-toxic to
 honey bees, with a topical LD 50  at 27 g/bee.

    There  are no reports  on laboratory studies  using DDE or  TDE, in
spite of the fact that these are major contaminants of soil.

    The  toxicity of DDT  to insects, the  target organisms, is  exten-
sively  documented.   Uptake  of  DDT  and  its  metabolism  by   other
terrestrial  invertebrates  is also  well  covered in  the  literature.
However,  there  are  few reports  of  effects  of either  DDT  or  its
metabolites on non-target invertebrates.

    Johansen  (1962) classified DDT  as "moderately" toxic  to  honey
bees  in both laboratory and field tests.  Atkins et al. (1973)  quoted
a  topical LD50   for honey bees of 12.09 g/bee  and classified DDT as
"relatively non-toxic".

    DDT  has little or no effect on earthworms at dose levels likely to
be encountered in the field; worms were unaffected by 2000  mg/kg  soil
(Goffart,  1949).  The  early literature  has been  examined  by  Davey
(1963), whose review includes reports on a variety of earthworm species
that live in surface soil or deeper layers.  Thompson (1971) treated an
area of grassland with an emulsifiable concentrate of DDT at  the  rate
of  5.6 kg/ha.  Although there was a reduction in earthworm numbers and
biomass of about 30%, the author considered this to be of  little  sig-
nificance.  Results in tropical areas are similar to those of temperate
regions.   Cook et al. (1980)  examined the effects of  cultivation and
DDT   treatment  on  earthworm  activity  and  populations  in  Nigeria
following  the application of DDT (1 kg/ha) as a foliar spray on cowpea

plots.   The  number  of casts  on  the  surface  was  reduced  by  DDT
application,  but  there was  no effect on  the number of  worms in the
soil.

    Cooke   &  Pollard   (1973) treated   Roman  snails ( Helix pomatia )
with   p,p' -DDT    applied to  lettuce  leaves.  The snails were fed a
365  x 2.5 cm square  of leaf that had  been treated with 0.1  ml of an
acetone solution of DDT (either 0.025, 1.0, or 40 mg/ml).   The  dosing
started when the snails were 2 weeks old and continued for 17 weeks, at
which  point the dose was doubled and continued for a further 12 weeks.
The snails were then transferred outside to stimulate hibernation.  Low
doses  of  DDT reduced  the weight of  the shell and  operculum whereas
higher  doses  did  not.   After  re-emergence  from  hibernation,  the
incidence  of operculum eating  was significantly higher  among  snails
hibernating  late in the  season, and as  exposure to DDT  increased so
operculum  eating  became more  prevalent.   The authors  suggest  that
shell-thinning  is likely to have occurred in snails in heavily-treated
agricultural  areas if  the response  of all  snail species  to DDT  is
similar to that of  Helix pomatia .

    Critchley  et al. (1980)  investigated  the  effects of the  use of
DDT  for  4  years on  a  cultivated  forest  soil  in  Nigeria  on the
numbers of epigeal (surface-living) and subterranean species of invert-
ebrates.   DDT  was  applied as a foliar spray to crops of cowpeas at a
rate of 1 kg/ha annually.  After the first application of DDT there was
no  effect  on  ant or  millipede  numbers  but the  numbers of lycosid
spiders and crickets were reduced.  At the end of the study, after four
applications of DDT, ants and millipedes were also reduced in number.

    When  Shires (1985) treated cereals on clay loam soil in experimen-
tal  plots  with  DDT  (1  kg/ha),  the  numbers of  predatory  beetles
(Carabidae) were reduced by 50% one week after  application.   However,
the  numbers increased again after 4 to 6 weeks and remained at control
levels.   The  use of  other insecticides led  to a second  decrease in
Carabidae  numbers; this was attributed  by the authors to  a reduction
in  the food supply of aphids.  DDT failed to control the aphids, which
were tolerant to the compound.

6.2  Birds

Appraisal 

     DDT and its metabolites can lower the reproductive rate of birds by
 causing  eggshell thinning (which leads to egg breakage) and by causing
 embryo  deaths.  However,  different groups  of birds  vary greatly  in
 their  sensitivity to these  chemicals; predatory birds  are  extremely
 sensitive  and, in the wild,  often show marked shell  thinning, whilst
 gallinaceous   birds  are  relatively  insensitive.    Because  of  the
 difficulties  of  breeding  birds of  prey  in  captivity, most  of the
 experimental  work has been done  with insensitive species, which  have
 often  shown little  or no  shell thinning.   The few  studies on  more
 sensitive  species have shown shell thinning at levels similar to those
 found in the wild.  The lowest dietary concentration of DDT reported to
 cause shell thinning experimentally was 0.6 mg/kg for the  black  duck.
 The mechanism of shell thinning is not fully understood.

6.2.1  Short-term and long-term toxicity to birds

    DDT and its derivatives DDE and TDE have moderate to  low  toxicity
to  birds  when  given as an acute oral dose or in the diet.  The acute
oral  and  dietary  toxicities of  DDT,  DDE,  and  TDE  to  birds  are
summarized in Table 6.

    These compounds have been studied in a wide variety of  species  in
tests ranging from a single acute dose to 100 days of  dietary  dosing.
All three compounds, DDT, DDE, and TDE, have low to  moderate  toxicity
to  young  and adult  birds.  There is  no obvious pattern  of relative
toxicity between the three compounds.  In some species it is  DDT  that
is  the most toxic, while  in other species it  is TDE.  Most of  these
laboratory  tests  have  been conducted  on  species  that are  easy to
maintain  and breed in  captivity.  These species  are unusual in  many
respects;  they tend to be  gallinaceous birds with young  that are not
fed by the adults after hatching.  They also tend to have long breeding
seasons  untypical of most birds  in the wild.  In  the wild, the  most
severely  affected species  of birds  are raptors  at the  top of  food
chains.   There is little direct  laboratory data on toxicity  to these
birds.  Toxicity to small songbirds, which make up the majority of bird
species, has not been examined either in the laboratory or the field.

    Porter & Wiemeyer (1972) fed American kestrels on a diet containing
 p,p' -DDE    at a concentration of  2.8 mg/kg.  Two birds  died after 14
and  16  months  of treatment;  they  showed  residues of  DDE in brain
tissues  of 212 and 301 mg/kg, respectively.  This  compared with  mean
residues  of 14.9 (range: 4.47-26.6) mg/kg in 11 adult males sacrificed
after 12-16 months on the diet.  Van Velzen et al. (1972)  investigated
the   lethal   effect  of   stored  DDT  mobilization  by  brown-headed
cowbirds.  Cowbirds were fed for 13 days on a diet containing 100, 200,
or  300  mg   p,p' -DDT/kg, and were then  given reduced  rations  of
approximately  43% of normal  daily intake for  a 6-day period.   Of 30
birds  dosed,  21  died (6,  7,  and  8 from  the  three  dose  levels,
respectively).  After 4 months, the  remaining birds   were   subjected
to   a second  period  of  6 days   on  a reduced   diet.   Four   more
birds, out  of six, died.  In a  second experiment, cowbirds  were  fed
100 mg  p,p' -DDT/kg diet for 13 days and then subjected to 4 days  of
reduced food intake.  Seven out of 20 birds died.  There were no deaths
in  any  of  the control  groups  (i.e.,  birds dosed  but not starved,
undosed and starved, or undosed and unstarved).

6.2.2  Toxicity to birds' eggs

    Dunachie & Fletcher (1969) injected chicken eggs with DDT or TDE to
give  concentrations,  in the  egg, varying between  10 and 500  mg/kg.
Two different vehicles were used to dissolve the insecticides (corn oil
and  acetone), controls being injected with vehicle alone.  The authors
monitored  egg hatchability and  survival of chicks  to 4 days  of age.
Some  chicks were fed and  some were not.  No  dose of DDT, applied  in
either  vehicle, had any  significant effect on  egg hatchability  when
compared  to  controls.  However,  there was a  profound effect on  the
chick  survival rate.  All chicks hatched from eggs treated with DDT at
100  mg/kg,  and  which were  not fed,  were dead  within 4  days after
hatching.  Feeding the chicks eliminated this effect; the survival rate

of  fed  young was  similar to that  of controls.  Chicks  hatched from
eggs  treated with 50 mg  DDT/kg survived as well  as controls, whether
they were fed or not.  TDE was found to affect hatchability,  but  only
when applied in corn oil; the acetone-dissolved material did  not  have
any    significant  effect.   TDE   dissolved  in  corn   oil   reduced
hatchability  to  60%  of control levels at 100 and 200 mg/kg, to 7% at
300  and 400  mg/kg, and  to 0%  at 500  mg/kg.  The  effects on  chick
survivability  were similar to those  of DDT.  All chicks  hatched from
eggs treated with 100 mg TDE/kg were dead after 4 days if they were not
fed, whereas chicks from eggs treated with 50 mg/kg survived as well as
controls.  Chicks from either 100 or 200 mg/kg treatments  survived  as
well  as controls as long  as they were fed.   The significance of  the
different  vehicles  was discussed  by Cooke (1971)  and Gilman et  al.
(1978).   Acetone causes coagulation of  yolk protein whereas corn  oil
allows  the injected  organochlorine to  float through  the yolk  to  a
position directly under the blastodisc.


Table 6.  Toxicity of DDT and its derivatives to birds
---------------------------------------------------------------------------------------------------------
Species             Sexa  Age         Routeb  Comp-  Purityc Parameter    Concentration     Reference
                                              ound   (%)                  (mg/kg)
---------------------------------------------------------------------------------------------------------

Bobwhite quail            23 days     diet    DDE    99.9    5-day LC50   825 (697-976)     Hill 
 (Colinus virginianus)     23 days     diet    DDT    100     5-day LC50   611 (514-724)     et al.
                          23 days     diet    TDE    TG      5-day LC50   2178 (1835-2584)  (1975)
                          young       diet    DDT            5-day LC50   881 (796-975)     Stickel 
                                                                                            & Heath (1964)
        (wild)                        diet    DDT    TG      5-day LC50   1170 (830-1650)   Hill et al.
        (farm-reared)                 diet    DDT    TG      5-day LC50   1610 (1331-1948)  (1971)
                          young       diet    DDT            10-day LC50  1000              DeWitt et al.
                          young       diet    DDT            100-day LC50 400               (1963)
                          adult       diet    DDT            10-day LC50  2500              DeWitt et al.
                          adult       diet    DDT            100-day LC50 1000              (1963)

Japanese quail            7 days      diet    DDE    99.9    5-day LC50   1355 (1111-1648)  Hill 
 (Coturnix coturnix        7 days      diet    DDT    100     5-day LC50   568 (470-687)     et al.
  japonica)                7 days      diet    TDE    TG      5-day LC50   3165 (2534-3978)  (1975)
                    M     2 months    oral    DDT    77.2    acute LD50   841 (607-1170)    Hudson et al.  
                                                                                            (1984)
California quail    M     6 months    oral    DDT    TG      acute LD50   595 (430-825)     Hudson et al.
 (Callipepla         F     6 months    oral    TDE    > 95   acute LD50   > 760            (1984)
  californica) 

Mallard duck              17 days     diet    DDE    99.9    5-day LC50   3572 (2811-4669)  Hill 
 (Anas platyrhynchos)      17 days     diet    DDT    100     5-day LC50   1869 (1500-2372)  et al.
                          17 days     diet    TDE    TG      5-day LC50   4814 (3451-7054)  (1975)
                    F     3 months    oral    DDT    77.2    acute LD50   > 2240           Hudson et al.
                    F     3 months    oral    TDE    > 95   acute LD50    > 2000          (1984)
                          young       diet    DDT            5-day LC50   875 (650-1140)    Stickel & 
                                                                                            Heath (1964)
                          young       diet    DDT            10-day LC50  500               DeWitt 
                          young       diet    DDT            100-day LC50 > 200            et al.
                          adult       diet    DDT            100-day LC50 1000              (1963)

Pheasant                  10 days     diet    DDE    99.9    5-day LC50   829 (746-922)     Hill 
 (Phasianus colchicus)     21 days     diet    DDT    100     5-day LC50   311 (256-374)     et al.
                          10 days     diet    TDE    TG      5-day LC50   445 (402-494)     (1975)
                    F     3-4 months  oral    DDT    > 99   acute LD50    1334 (894-1990)  Hudson et al.
                    F     3-4 months  oral    TDE    > 95   acute LD50    386 (270-551)    (1984)
                          young       diet    DDT            5-day LC50   804 (686-942)     Stickel & 
                                                                                            Heath (1964)

Table 6. (Contd)
---------------------------------------------------------------------------------------------------------
Species             Sexa  Age         Routeb  Comp-  Purityc Parameter    Concentration     Reference
                                              ound   (%)                  (mg/kg)
---------------------------------------------------------------------------------------------------------
                          young       diet    DDT            10-day LC50  1000              DeWitt et al.
                          young       diet    DDT            100-day LC50 100               (1963)
                          adult       diet    DDT            10-day LC50  1000              DeWitt et al.
                          adult       diet    DDT            100-day LC50 > 100            (1963)

Red-winged blackbird                  diet    DDT            10-day LC50  1000              DeWitt et al.
 (Agelaius phoeniceus)                 diet    DDT            30-day LC50  500               (1963)

Cardinal                              diet    DDT    TG      5-day LC50   535 (420-700)     Hill et al.  
 (Richmondena cardinalis)                                                                    (1971)

House sparrow                         diet    DDT    TG      5-day LC50   415 (370-465)     Hill et al.  
 (Passer domesticus)                                                                         (1971)

Blue jay                              diet    DDT    TG      5-day LC50   415 (320-540)     Hill et al.  
 (Cyanocitta cristata)                                                                       (1971)

Rock dove           M,F               oral    DDT    77.2    acute LD50   > 4000           Hudson et al.  
 (Columba livia)                                                                             (1984)
                                                                         
Sandhill crane      M,F   adult       oral    DDT    > 99   acute LD50    > 1200          Hudson et al.  
 (Grus canadensis)                                                                           (1984)

Clapper rail        M                 diet    DDT            5-day LC50   1612              Van Velzen & 
(1975)                                                                                      Kreitzer
 (Rallus             F                 diet    DDT            5-day LC50   1896              (1975)
 longirostris) (1975)
---------------------------------------------------------------------------------------------------------
a  M = male; F = female.
b  oral = acute oral test (result expressed as mg/kg body weight); diet = dietary test (result expressed 
   as mg/kg diet).
c  TG   = Technical grade.
6.2.3  Reproductive effects on birds

    DDT,  or more specifically its metabolite DDE, causes the shells of
birds'  eggs to be thinner  than normal.  Results on  eggshell thinning
are  summarized in Table  7.  There is  considerable variation  between
species for this effect.  Galliform species are very resistant to shell
thinning whereas birds of prey are particularly susceptible.

    Lincer  (1975) dosed captive  American kestrels and  established  a
clear  relationship  between dietary  DDE  and thinning  of  eggshells.
There  was a similar close  correlation between the residues  of DDE in
individual  eggs and the degree  of shell thinning.  The  kestrels were
fed  with day-old cockerels  (which were injected  with 0.2 ml  of corn
oil,  containing the DDE, into  the breast muscle) and  received either
0.3, 3, 6, or 10 mg DDE/kg diet.  Residues of DDE in eggs laid  by  the
birds  correlated closely with  dietary DDE concentration;  residues of
1.9 mg/kg wet weight were associated with the lowest dose and 245 mg/kg
with  the highest dose given.   There was no shell  thinning associated
with the dose of 0.3 mg/kg.  The other doses showed 15.1%,  22.8%,  and
29.2%  thinning  (at 3,  6, and 10  mg/kg, respectively).  There  was a
straight-line  relationship between the   degree of shell  thinning and
the  logarithm  of  the DDE residue in the egg.  Data obtained from the
field showed exactly the same trend (Fig. 1).  This represents the best
evidence for the effect of DDE on shell thickness in a species actually
adversely affected in the field.


Table 7.  Thinning effects of DDT and its derivatives on bird egg shells
---------------------------------------------------------------------------------------------------------
Species               Route  Compoundc  Dose    Percentage  Significancee  Reference
                                        (mg/kg) change      (p)
---------------------------------------------------------------------------------------------------------

Ring dove             diet   DDE        10      - 9.2       0.01           Peakall et al. (1973)
 (Streptopelia         diet   DDE        40      - 6.8       0.01           Haegele & Hudson (1973)
  risoria) 

Mallard               diet   TDE        10      - 2.6       NS             Heath et al. (1969)
 (Anas platyrhynchos)  diet   TDE        10      - 5.4       NS             Heath et al. (1969)
                      diet   TDE        40      - 2.6       NS             Heath et al. (1969)
                      diet   TDE        40      - 5.4       NS             Heath et al. (1969)
                      diet   DDT        2.5     - 5.3       NS             Heath et al. (1969)
                      diet   DDT        10      - 7.9       NS             Heath et al. (1969)
                      diet   DDT        40/25   -13.2       0.01           Heath et al. (1969)
White pekin duck      diet   DDE        40      -20.3       0.001          Peakall et al. (1973)
     4 day            diet   DDE        40      - 3.3       0.01           Miller et al. (1976)
     1-3 months       diet   DDE        40      -18.2       0.01           Miller et al. (1976)

Black duck            diet   DDE        10      -17.6       0.01           Longcore et al. (1971)
 (Anas rubripes)       diet   DDE        30      -23.5       0.01           Longcore et al. (1971)

Screech owl           diet   DDE        2.8     -13.3       0.01           McLane & Hall (1972)
 (Otus asio) 

American kestrel      diet   DDE        3       -15.2       0.05           Peakall et al. (1973)
 (Falco sparverius)    diet   DDE        6       -21.0       0.01           Peakall et al. (1973)
                      diet   DDE        10      -26.3       0.001          Peakall et al. (1973)
                      diet   DDE        2.8     - 8.7       0.001          Wiemeyer & Porter (1970)
                      diet   DDE        0.3     + 2.1       NS             Lincer (1975)
                      diet   DDE        3       -15.1       0.05           Lincer (1975)
                      diet   DDE        6       -22.8       0.01           Lincer (1975)
                      diet   DDE        10      -29.2       0.001          Lincer (1975)


Table 7.  (Contd).
---------------------------------------------------------------------------------------------------------
Species               Route  Compoundc  Dose    Percentage  Significancee  Reference
                                        (mg/kg) change      (p)
---------------------------------------------------------------------------------------------------------

Japanese quail        diet   o,p'-DDT   100     - 4.0       0.001d         Bitman et al. (1969)
 (Coturnix coturnix    diet   DDT        100     - 5.6       0.001d         Bitman et al. (1969)
  japonica)            diet   DDT        100       0         NS             Cecil et al. (1971)
                      diet   DDE        100     - 2.5       NS             Cecil et al. (1971)
                      diet   DDE        2       + 1.9       NS             Davison et al. (1976)
                      diet   DDE        10      + 6.3       NS             Davison et al. (1976)
                      diet   DDE        40      + 5.0       NS             Davison et al. (1976)
                      diet   DDE        200     - 0.6       NS             Davison et al. (1976)
     strain 1a        diet   DDT        2.5     + 1.0       NS             Davison et al. (1976)
                      diet   DDT        10      - 1.5       NS             Davison et al. (1976)
                      diet   DDT        40      - 0.5       NS             Davison et al. (1976)
     strain 1b        diet   DDT        2.5     - 2.7       NS             Davison et al. (1976)
                      diet   DDT        10      - 1.6       NS             Davison et al. (1976)
                      diet   DDT        40      - 7.1       NS             Davison et al. (1976)
     strain 2a        diet   DDT        2.5     + 0.5       NS             Davison et al. (1976)
                      diet   DDT        10      + 1.6       NS             Davison et al. (1976)
                      diet   DDT        40      + 1.0       NS             Davison et al. (1976)
     strain 2b        diet   DDT        2.5     - 3.7       NS             Davison et al. (1976)
                      diet   DDT        10      - 2.6       NS             Davison et al. (1976)
                      diet   DDT        40      - 5.7       NS             Davison et al. (1976)

---------------------------------------------------------------------------------------------------------
a  Individually caged.
b  Caged in pairs.
c  DDT in the  p,p' - form unless stated otherwise.
d  Low calcium diet (0.56%).
e  S = not significant.
FIGURE 1

    Haegele  & Tucker  (1974) dosed  egg-laying Japanese  quail with  a
single  oral dose of  p,p' -DDE,  o,p' -DDT,  p,p' -DDT, or technical
DDT,  all at  125 mg/kg  body weight.   None of  the treatments  caused
appreciable eggshell thinning.  When Smith et al. (1969)  fed  Japanese
quail  with DDT at 100, 200, or 400 mg/kg diet, the two lower doses had
no  effect on hatchability  or fertility of  eggs laid.  At  400 mg/kg,
there was 50% mortality amongst dosed birds; survivors showed a decline
in  hatchability  and fertility  after 30 days.   Bitman et al.  (1969)
dosed Japanese quail with  o,p' -DDT or  p,p' -DDT at a  dietary  level
of  100 mg/kg.  The quail  were given a low  calcium diet (0.56%)   and
were,  therefore, under calcium stress during egg laying.  Both isomers
of  DDT  caused  significant thinning  of  eggshells  (P<0.001)  and  a
significant (P<0.01) reduction in shell calcium content.  Eggs produced
by birds dosed with the p,p    isomer were significantly  lighter  than
those laid by birds dosed with the  o,p'  isomer.

    Cecil  et al.  (1971) investigated  the effects  of  p,p' -DDT and
 p,p' -DDE on  the  egg  production  and  eggshell  characteristics of
Japanese quail receiving an adequate calcium diet, and  compared  their
results  with  previous studies  of the effects  of these compounds  on
quail  receiving low calcium diets.  They found a delay in the onset of
egg  production in quail fed a concentration of 100 mg/kg of either DDT
or DDE for about 3 weeks.  This result was similar to that  of  studies
with  low calcium diets.  In contrast to the earlier studies, there was
no  effect  of  either DDT or DDE on shell thickness or egg weight when
dietary  calcium was higher.  There  was an increased incidence  of egg
breakage  in  birds  fed DDT and DDE, but this was less pronounced than
with the low calcium diets.

    Robson  et  al. (1976)  studied the effects  of DDE and  DDT fed to
Japanese  quail  in  two different  diets  containing  adequate or  low
calcium.  DDT was fed at 100 mg/kg diet, whereas DDE was given  at   0,
199,  or  300  mg/kg diet, and the two calcium levels were 0.5% and 3%.

DDE at 300 mg/kg was detrimental to adult body weight,  fertility,  and
survivability.   There  was  no effect of either DDT or of DDE at up to
100  mg/kg diet on adult body weight, food consumption, egg production,
egg  weight,  fertility, hatchability,  cracking  of eggs,  or eggshell
thickness.   Low  dietary  calcium  had  the  effect  of  reducing  the
thickness  of eggshells, increasing the incidence of cracked shells and
decreasing egg production and hatchability.

    Davison  et al. (1976) fed  DDE (0, 2, 10,  40, or 200 mg/kg  diet)
to female Japanese quail that were individually caged and had 14  g  of
food  available each  day.  There  was no  effect on  body weight,  egg
laying,  egg weight, eggshell thickness,  or on shell calcium  content.
Quail were then fed a diet containing DDT at 0, 2.5, 10, or  40  mg/kg.
There  was  no  effect on  eggshell  thickness,  number of  eggs  laid,
fertility, or hatchability.  Quail fed 40 mg DDT/kg diet and  caged  in
pairs,  broke more eggs than  birds fed lower concentrations  of DDT or
any concentration when the birds were caged individually.  Paired quail
laid  fewer eggs than single quail and in one experiment they laid eggs
with thinner shells.

    When  Davison & Sell (1972)  dosed  white leghorn hens  with 100 or
200 mg DDT/kg diet for 12 weeks, the average egg production  per  bird,
egg weight, dry shell weight, shell thickness, and shell  calcium  were
all found to be unaffected by DDT at either dose level.

    Egg-laying  mallard ducks treated by Haegele & Tucker (1974) with a
single  oral  p,p' -DDE dose  of 500, 1000, or 2000 mg/kg  body weight
showed  a  clear  effect on  eggshell  thickness  at all  dose  levels.
Unfortunately, whilst the results are clear, no statistical analysis of
the results was presented.  The effect on eggshells was  dose  related,
quick  acting, and persistent.  Heath  et al. (1969) dosed  mallard for
two seasons with DDE or TDE at 10 or 40 mg/kg diet and with DDT at 2.5,
10,  or 40 mg/kg diet.  The highest dose of DDT was reduced to 25 mg/kg
in  the second season.   DDE at both  concentrations severely  impaired
reproductive  success, a more rapid initiation of the effect being seen
with the higher dose.  DDE significantly affected  eggshell  thickness;
eggs  from birds dosed with 40 mg/kg laid, in their second season, eggs
with  shells  13%  thinner than  controls.   There  was  a  significant
increase in egg cracking and decrease in egg hatchability at  both  DDE
dose levels.  TDE did not have a significant effect on shell thickness.
It  impaired reproductive success, but not as severely as did DDE.  DDT
induced  eggshell thinning  at a  dose of  25 mg/kg,  shells being  18%
thinner  than controls, and reduced  duckling survival  during 14  days
post-hatch by 35%.  DDT at 2.5 and 10 mg/kg had no effect.

    Vangilder   & Peterle (1980)  fed mallard a  diet containing 10  mg
DDE/kg,  and  brought  the birds  into  breeding  condition using  long
daylength.   Relative  to controls,  egg  laying was  delayed, eggshell
thickness was decreased, and hatchability was reduced in treated birds.
Ducklings, hatched from eggs laid by treated females, showed a signifi-
cantly  reduced survival time,  and a greater  proportion of  ducklings
were unable to initiate normal body temperature regulation.

    When   Longcore  et  al. (1971)  dosed black ducks with 10 or 30 mg
DDE/kg diet, there was significant eggshell thinning and an increase in
shell  cracking,  compared  to controls,  at  both  dose  levels.   The

survival of ducklings to 21 days was also significantly reduced at both
dose  levels.  Longcore &  Stendell (1977) fed  DDE (10 mg/kg  diet) to
black  ducks over two  breeding seasons and  then untreated food  for a
further 2 years.  The eggshells of treated birds during dosing were 20%
thinner  than  controls.   When  dosing  stopped,  eggshell   thickness
gradually increased but shells were still 10% thinner than  controls  2
years  after dosing had finished.  Similarly, there was still a reduced
survival of ducklings, to 3 weeks of age, 2 years after dosing with DDE
had ceased.

    Peakall  et  al.  (1973) studied  the  effects  of dietary  DDE  on
eggshell  thinning in three species of bird (white pekin duck, American
kestrel, and ringdove).  In addition to shell thinning, they reported a
reduced  rate of water  loss from eggs  laid by DDE-treated  birds; the
permeability  constants  of  the  eggs  were  significantly  decreased.
Scanning  electron micrographs  revealed a  decrease in  the number  of
pores  per unit shell area  and an increase in  the number of  globular
inclusions  in eggshells from treated  birds.  Greenburg et al.  (1979)
showed, also using scanning electron microscopy, that DDE affected both
organic and inorganic constituents of the eggshells of mallard dosed in
their diet.  The literature concerning the effects of DDE  on  eggshell
structure has been reviewed in detail by Cooke (1973b).

    In  studies by Miller et  al. (1976), laying white  pekin ducks and
white leghorn hens were dosed with 40 mg DDE/kg diet.  The ducks showed
significant  eggshell thinning within 4 days, and again between 1 and 3
months  of  the  start of dosing, but the hens did not show significant
eggshell effects within 2 weeks.

    Peakall et al. (1975a) dosed white pekin ducks at a  dietary  level
of  250 mg  DDE/kg for  10 days,  and, approximately   2 months  later,
started  to collect eggs and measure shell thickness for a period of 27
weeks.   At the beginning of the collection period, shells from treated
birds  were found to be  20% thinner than controls.   Recovery was slow
and shells were still 10% thinner at the end of the  study.   Haseltine
et al. (1974) dosed mallard and pheasant (10 mg DDE/kg diet)  and  ring
doves (40 mg DDE/kg diet) and found significant eggshell  thinning  and
depression  of serum  calcium levels  in both  mallard and  ring  dove.
However,  neither  parameter  was significantly  changed  in  pheasant.
Peakall  et  al.  (1975b)  maintained  paired  ring  doves  on  a  diet
containing  100  mg  DDE/kg for 3 weeks and white pekin ducks on 250 mg
DDE/kg  diet for  10 days.   Although both  species showed  significant
eggshell  thinning,  there was  no  significant difference  between the
levels of serum calcium of treated and control birds.

    Miller  et  al. (1976)  removed the shell  glands from white  pekin
ducks  and white leghorn chickens, dosed with 40 mg DDE/kg diet, when a
calcifying  egg was present  within the gland,  and assessed  enzymatic
activity.   There  was  a  significant  decrease  in  Ca2+-ATPase   and
carbonic  anhydrase activities in the  shell glands removed from  dosed
ducks, but no difference from controls in chicken shell glands.  Kolaja
(1977) maintained mallard ducks on a diet containing either  DDT,  DDE,
DDT  sulphonate, or DDE sulphonate  at dose levels of  10 or 50  mg/kg.
Eggs were collected for 30 days and were weighed and  measured.   There
was no significant difference between egg weights at the different dose
levels.   The thickness of eggshells of birds fed DDE was significantly

reduced.   Ducks fed DDT  laid  eggs with significantly thinner  shells
only  after  day  14.   The  two  sulphonate-treated  groups  were  not
significantly  different from each  other and were  only  significantly
different  from controls on day 18; eggshell weights followed a similar
pattern.

    Mendenhall  et al. (1983) dosed breeding barn owls with 3 mg DDE/kg
diet  during two breeding  seasons, and found  that treated birds  laid
thin-shelled  eggs and laid  significantly more eggs  per pair in  both
seasons.   In both years the  percentage of eggs broken  was increased,
relative  to controls, and  the mean number  of eggs hatched  and young
fledged  per  pair was  reduced.  There was  a significant increase  in
embryo deaths in one of the two years.

    Eggshell   thickness  has  been  monitored  in  different  ways  by
different   authors.   Some  direct  measurement  has  been  made  with
membranes  intact and some  without.  Other methods  have been used  to
compare recent eggs with museum specimens, which could not be broken to
measure thickness directly.  The various methods were reviewed by Cooke
(1973b),  who suggested standards.  Generally a log-linear relationship
between  DDE load and shell thinning is claimed.  In a recent consider-
ation of the theoretical treatment of such data, Moriarty et al. (1986)
suggested  that the main  methods of assessing  shell thickness do  not
adequately take into consideration the effects of shell size and shape.
This does not detract from the conclusion that shell  thinning  occurs,
but  suggests that the relationship  may be more properly  described as
curvilinear.

6.2.4  Reproductive hormones and behaviour

    After feeding mallard a diet contaminated with 3  mg  p,p' -DDE/kg
and  artificially incubating  eggs laid  by the  females, Heinz  (1976)
found  that the average  egg residue of  DDE was 5.8  mg/kg.  Ducklings
from  treated  eggs were  hyperresponsive  to a  tape-recorded maternal
call;  treated ducklings were significantly more likely to approach the
recorder.   In contrast, treated ducklings moved shorter distances away
from  a  frightening stimulus,  compared  to controls.   Japanese quail
chicks  fed a diet containing  50 mg DDE/kg for  8 days, starting at  7
days  of age, and  then a clean  diet for a  further 6 days  showed  no
significant effect on avoidance response to a moving silhouette.

    Haegele  & Hudson (1977) paired  ring doves for 12.5  min each day,
for  5 days, prior to dosing their diet with 10 or 50 mg  p,p' -DDE/kg.
The birds were also paired between days 31 and 35 and between  days  59
and  63  after  the start  of  dosing.   Two measures  of the courtship
behaviour  of males were made:  total courtship activity time  and mean
bow-coo  frequency.   Bow-cooing  behaviour is  the  initial  behaviour
displayed  by males to  attract females.  In  control birds, the  total
courtship  activity time  was 25%  (days 31-35)  and 23%  (days  59-63)
longer than it was in the predose period.  In birds dosed with   10  mg
DDE/kg, the courtship activity between days 31 and 35 was not different
from that in the predose period, whereas the final pairing  produced  a
decrease  of 55% in activity.   In birds dosed with  50 mg DDE/kg,  the
courtship activity decreased by 30% and 67% for the two  later  pairing
periods  compared  to the  predose period.  After  dosing at 10  mg/kg,
there  was  no  change in  bow-cooing between  days 31  and 35,   but a

reduction  of 53% between  days 59 and  63.  Birds dosed  at  50  mg/kg
showed  decreases in bow-cooing  behaviour of 43%  and 84%, in  the two
subsequent pairings respectively, when compared to the predose period.

    When  Richie & Peterle (1979)  paired ring doves and  fed them with
either 10 or 40 mg  p,p' -DDE/kg diet, there was a significant delay in
the  period  between  pairing  and  egg  laying  at both  dose  levels.
Leutinizing  harmone  levels in  blood  plasma, sampled  throughout the
experiment,  were  not significantly  altered  by the  DDE.  Similarly,
Jefferies   (1967)   reported   an   increase   in   the   time between
pairing  and  egg  laying in  Bengalese  finches  fed a  range of doses
of  p,p' -DDT between 75 and 1200  mg/kg diet.  Treated birds  were fed
for  2 h/day,  immediately following  a period  of 1  h of  starvation.
There was a  significant correlation between DDT intake by  the  female
and  the delay  in egg  laying.  Dobson  (1981)   measured  circulating
hormone levels and nest-building behaviour in pigeons dosed orally with
DDE  and found a delay in egg laying.  Hormone measurements showed that
ovulation was not delayed.  Nest building was reduced in treated birds.
The  delay in  egg laying  resulted from  a lengthening  of the  period
between  ovulation  and  oviposition.   Since  the  laying  of eggs  is
dependent on the stimulus of adequate nest material,  this  lengthening
of  the  period  between  pairing and egg  laying was considered  to be
primarily  an indirect effect  on reproduction, triggered  by a  direct
effect on behaviour; the egg was retained longer in the oviduct.

    Peakall  (1970)  maintained  ring  doves  on  a   diet   containing
10  mg  p,p' -DDT/kg for 3 weeks.  They  were kept in  isolation (with
short  daylengths) and  then paired  (with long  daylengths) to  induce
breeding.   The   females were  killed either 8  days after pairing  or
after   completion of their clutch of two eggs.  In those killed 8 days
after    pairing,  circulating  oestradiol  levels  were  significantly
reduced  and   hepatic  enzyme activity  was  significantly  increased.
There  was a significant  delay in the  laying of the  first egg and  a
decrease  in  egg  weight.  In  the  same  study, the  birds were given
oral 45Ca (7.4 x 104 Bq;    2 Ci)   on the day before pairing.   There
was  a  significant decrease  in the radioactivity  of eggs and  in the
bones   of  females  killed  8  days  after  pairing.   In  a  separate
experiment,   p,p' -DDT was injected  intraperitoneally at a   dose of
150  mg/kg  body  weight, into female ring doves within  1 day of their
first  egg being laid.   The birds were  killed after completing  their
clutch  of  two  eggs.   The  shell  weight  of  the  second  egg   was
significantly  reduced  when  compared to  the  first  and there  was a
significant  decrease in carbonic  anhydrase activity in  the  oviduct.
This enzyme is associated  with deposition of calcium into the shell.

6.2.5  Reproductive effects on the male

    Burlington  &  Lindeman  (1950) administered  a  daily subcutaneous
injection  of DDT to male   white leghorn chicks, gradually  increasing
the  dose from 15 to 300 mg/kg body weight.  The birds were treated for
60-89  days, and the  cockerels were killed  and their testes  removed,
weighed,  and sectioned.   Treated birds  were found  to  have  smaller
testes,  more  intertubular  tissue, and  retarded tubular development.
These  effects  were  accompanied  by  an  inhibition  of testosterone-
dependent secondary sexual characters; combs and wattles  were  reduced
in  both size and  colour development in  treated birds.  Locke  et al.

(1966)  dosed male bald eagles at dietary levels of 10 mg DDT/kg for 60
or  120 days, and  found no effects  on spermatogenic activity.   There
were some degenerative effects on the testis, but only at  doses  which
had severe neurological effects and ultimately led to death.

6.2.6  Effects on the thyroid and adrenal glands in birds

    When  Jefferies & French  (1972) fed pigeons  on a diet  containing
either 18, 36, or 72 mg  p,p' -DDE/kg for a period of 56  days, paired
thyroid  weights were  found to  be greater  in treated  birds than  in
controls.   There was no apparent dose relationship to this effect, but
bird  numbers were small.   Taking the dosed  birds as a  single group,
the results were significantly different from those of  control  birds.
Liver  weights were similarly increased,  and, at the two  highest dose
levels, there was an increase in paired adrenal weights.

    Biessman   &  von  Faber  (1981) dosed Japanese  quail for 9  weeks
with  technical  DDT  (either 50 or 250 mg/kg diet) or for 5 weeks with
 p,p' -DDT  or  p,p' -DDE (250  and 300 mg/kg,  respectively).  Adrenal
weights increased with all treatments but the increase in size was only
significant  for the 300  mg DDE/kg dose.   The percentage of  cortical
tissue,  measured from areas of sections of the gland, showed a similar
trend, but results were not statistically significant.  No changes were
detectable  in nuclear  size of  either cortical  or  medullary  cells.
Lehman et al. (1974) studied the effect of technical grade DDT  on  the
adrenal  glands of  bobwhite quail,  which were  maintained on  a  diet
containing 10, 50, or 150 mg DDT/kg for 242 days and then  killed.   No
effect  was found on adrenal  weight expressed as a  percentage of body
weight,  but there was a significant dose-related increase in the ratio
between areas of cortex and medulla.

6.2.7  Special studies in birds

   Dieter   (1974) fed Japanese quail  on a diet containing  5, 25, or
100 mg DDE/kg and, after 12 weeks of dosing, assessed the  activity  of
five  plasma  enzymes  (creatine  kinase,  aspartate  aminotransferase,
lactate   dehydrogenase,   cholinesterase,   and   fructose-diphosphate
aldolase).  There was an increase in the activity of all these enzymes,
which,  in each  case, was  proportional to  the logarithm  of the  DDE
dose.

    Bend  et al. (1977) dosed  immature puffins, orally by  intubation,
with DDE at 6 mg/day (equivalent to 50 mg/kg diet) for 16 to  21  days,
and, after killing the birds, determined the effect of DDE  on  hepatic
mixed-function  oxidases.   Both aniline  hydroxylase and benzphetamine
demethylase  activities were increased in  treated birds; the yield  of
microsomal protein remained unchanged.  In contrast, Sell et al. (1972)
demonstrated  a  depression  in aniline  hydroxylase  and N-demethylase
activities  after feeding Japanese  quail with DDT  at 200 mg/kg  diet.
Both  DDT and DDE inhibited aniline hydroxylase in vitro activity, when
present at concentrations of 10-7 mol/litre or more.

    Bunyan   et  al.  (1970)  measured  the  activities  of  glucose-6-
phosphate  dehydrogenase  (G-6-P) and  6-phosphogluconate dehydrogenase
(6-P-G)  in the liver of Japanese quail fed diets containing low levels
of   p,p' -DDT or a  number of saturated  and unsaturated analogues  of

 p,p' -DDT.   Generally, saturated compounds  lowered G-6-P levels  and
increased  6-P-G levels.   p,p' -DDMU   was anomalous in elevating G-6-P.
The authors suggested that these effects might be due  to  interference
with  protein  metabolism primarily  by  the unsaturated  analogues and
metabolites  of  DDT.  Bunyan  et al. (1972)  fed either DDT  or DDE to
Japanese   quail  and monitored hepatic  microsomal protein, cytochrome
P450,  aniline  hydroxylase,  aromatic  nitroreductase,  phenylbenzoate
esterase,  and  total vitamin  C.  Changes in  these factors were  more
readily  explained  in terms  of residues of  DDE in the  liver than in
terms  of  dietary  dose.  DDE was found to be a more potent inducer of
microsomal protein, cytochrome P450, and aniline hydroxylase  than  was
DDT.   The effects of DDT could be explained in terms of the effects of
the  DDE  produced  by  DDT  metabolism.   Aromatic  nitroreductase was
unaffected  by either compound.   Vitamin C levels  were raised by  DDT
more  than by  DDE.  Phenylbenzoate esterase showed a biphasic response
following  the  feeding of  DDE.  Bunyan &  Page (1973) extended  these
studies  by examining the effects of DDE and DDMU on hepatic microsomal
enzyme  systems.  Most of  the changes observed  in quail were  greater
with  DDMU than with any  other DDT metabolite.  The  authors suggested
that DDT metabolism in birds may be different to metabolism in mammals.
Metabolism  probably  gives  rise, via  the  production  of DDMU,  to a
highly active liver inducer.

    Heinz et al. (1980) fed ring doves on a diet containing 2,  20,  or
200 mg DDE/kg for 8 weeks, and found at the end of the dosing period, a
significant  decrease in dopamine  concentration in brain  tissue  from
birds  fed on the two  higher doses.  Brain noradrenalin  concentration
was also affected but only at the highest dose.  There was  a  signifi-
cant, negative correlation between concentration of both  dopamine  and
noradrenalin and the residue of DDE in the brain tissue.

    Friend   et  al.  (1973)   fed  a  dietary   dose  of  10,  100, or
1000  mg DDE/kg. to male mallard that had been previously maintained on
either fresh water or 1% salt water.  Birds were given  a  concentrated
salt  solution either 1,  3, 6, or  9 days after  the beginning of  DDE
treatment, the salt being administered both intraperitoneally (12 ml of
a  10% solution) and intravenously (3ml of a 5% solution).  The rate of
sodium  chloride excretion was  not reduced, relative  to controls,  in
DDE-treated  birds maintained previously on salt water, but was reduced
significantly in DDE-treated birds not previously given salt.

    When  Mahoney (1975) fed caged white-throated sparrows on technical
DDT  (either 5 or  25 mg/kg), the  onset of spring  nocturnal migratory
restlessness (Zugunruhe) and  weight increase was delayed by at least 1
week.   Although Zugunruhe onset was delayed, when  migratory nocturnal
activity  did commence it  was more pronounced  than in control  birds.
The increase in Zugunruhe was related to body residues of DDT.

    Haynes (1972) dosed male bobwhite quail with DDT (100  mg/kg  diet)
for  10  weeks  and, 1 week before the study was terminated, some birds
were transferred to clean food while others were starved for 4 days and
then  given clean food for  3 days before being  killed.  There was  no
significant  effect on liver glycogen,  either from dosing with  DDT or
from starvation, but liver lipid levels were significantly increased by
both  DDT and  starvation.  Body  lipid levels  were not  significantly
affected by DDT but were reduced after starvation.

6.2.8  Synergism with other compounds in birds

    Kreitzer  &  Spann  (1973),  in  a  study  on combined  effects  of
pesticides,   found  that  mixtures of  DDT and  dieldrin  in  Japanese
quail,  and DDE and Ceresan  M (organomercury fungicide) in  pheasants,
were  additive rather  than synergistic  in their  action.   The  study
compared known LD50 values with expected ones.  Mallard, maintained
on a diet containing a mixture of DDE (40 mg/kg) and Aroclor  1254  (40
mg/kg)  for  at least  30 days, laid  eggs with significantly   thinner
shells  than did controls.  This result was not significantly different
from  that produced by DDE  alone (Risebrough & Anderson,  1975).  In a
similar  study on American kestrels, Lincer (1972) dosed the birds with
Aroclor  1254 (10 mg/kg) and DDE (3 mg/kg) in the diet, both separately
and   in combination.   There was  no eggshell  thinning  with  Aroclor
alone,   but  Aroclor  and DDE  together had  a  significantly  greater
effect  on  shell  thickness  than  DDE  alone,  indicating  synergism.
Japanese  quail exposed to dietary  doses of 5 or  50 mg DDE/kg for  12
weeks,  and subsequently dosed orally with either parathion or paraoxon
at  2 l/g  body weight,  showed synergism between  the compounds  with
respect  to mortality and to  inhibition of brain cholinesterase.   The
synergistic action of DDE on cholinesterase inhibition was  apparent  3
days after exposure to 50 mg/kg and one week after exposure to 5 mg/kg.
Mortality due to DDE was increased from 10% to 90% in the  presence  of
the   organophosphorus  compounds.   Anticholinesterase   effects  were
increased by 50% in the presence of DDE (Ludke, 1977).

6.3 Non-laboratory Mammals

Appraisal 

     Experimental  work suggests that  some species, notably  bats,  may
 have  been  affected by  DDT and its  metabolites.  Species which  show
 marked  seasonal  cycles in  fat content are  most vulnerable, but  few
 experimental  studies on such species  have been made.  In  contrast to
 the  situation in birds,  where the main  effect of DDT  is  on  repro-
 duction,  the main known effect in mammals is to increase the mortality
 of  migrating adults.  The lowest  acute dose which kills  American big
 brown  bats is 20 mg/kg.  Bats collected from the wild  (and containing
 residues  of  DDE  in fat)  die  after  experimental  starvation  which
 simulates loss of fat during migration.

    In  studies into the effect  of DDE on bats,  Geluso et al.  (1976)
captured young Mexican free-tailed bats ( Tadarida brasiliensis ) before
their  first migratory flight and  transferred them to the  laboratory.
This  species  migrates  north from  Mexico  to  the USA  in spring and
returns  to winter in the  south.  Three groups of  bats were used.   A
reference  set was killed on  capture and, when the  bats were analysed
for  residues of organochlorines derived from environmental source, DDE
was  the only chemical found in significant amounts.  Brain residues of
DDE  were low; the median being 3.7 (range: 1.5 to 17.0) mg/kg in eight
younger  animals and 1.3  (range 1.1 to  11.0) mg/kg in  older animals.
Two  further groups were  maintained in the  laboratory where the  bats
were given water but not fed.  One group was regularly exercised, while
the  other  was given  no exercise.  All  exercised bats died  within 9
days;  4 bats in the unexercised group died and the other 4 were killed
after  9 days.   Analysis of  brain DDE  residues  showed  considerably
elevated levels compared to the reference group.  For  the  unexercised

bats,  the median residue  values were 47  (range 18 to  76)  mg/kg  in
younger  animals and 70 (range  10 to 95) mg/kg  in older animals.   In
exercised bats, the values were 160 (range 66 to 330) mg/kg for younger
animals   and  160 (range  37 to 260)  mg/kg for older  animals.  Those
animals that died before the end of the study showed  symptoms  charac-
teristic  of pesticide poisoning, including hyperactivity, intermittent
audiogenic  seizures, and violent  contractions of chest  muscles.  The
high  brain residues of DDE were considered to be the cause of death of
the animals.  It should be noted that these animals had not been  arti-
ficially  dosed with DDE.  The effects resulted from residues of DDT in
body fat, taken up in the maternity roost.  The authors considered that
their studies confirmed the suggestion that bats were being  killed  by
accumulated  residues of DDE during the period of migration, when their
fat reserves were used up.

    Clark & Kroll (1977) experimentally fed adult females of  the  same
species  of  bat ( Tadarida  brasiliensis ) for 40  days  with  mealworms
containing  107 mg DDE/kg and then killed four of the bats.  They had a
whole  body burden of 2.345-2.929  mg DDE (and 78-90  mg DDE/kg in  the
brain).   Twelve  of the  dosed bats were  then starved, and  they died
within   8  days.  The total  body burden of DDE  ranged from 1.952  to
3.711  mg DDE and brain  residues from 379 to  564 mg/kg.  These  brain
residues  were considered to be diagnostic of death from DDE poisoning.
Tremors  characteristic of poisoning were seen in the bats before death
occurred.

    The   toxicity  of  single oral  doses  of  DDT to  bats  has  been
estimated  in  two studies.   Jefferies  (1972) derived  an approximate
LD50 of 63 mg/kg body weight for the pipistrelle  bat ( Pipistrellus 
 pipistrellus ), a  small  British species.   There  was no  mortality at
doses  below  45  mg/kg and  100%  mortality  at doses  above 95 mg/kg.
Luckens & Davis (1964) found that the lowest dose which killed American
big  brown bats ( Eptesicus fuscus ) was 20 mg/kg and that 40  mg/kg was
invariably  lethal.  The LD50 for this species lies somewhere between
25 and 40 mg/kg for a single oral dose.

    Blus  (1978) determined dietary LC50  values of DDT, given in food
either  as  a  powder or  dissolved  in  oil, for  short-tailed  shrews
( Blarina brevicauda ) of different ages and sex.  In 2-week tests, the
range of LC50s   for DDT dissolved in oil was 651 to 1160  mg/kg  diet,
and for DDT added as powder it was 839 to >2552 mg/kg.   The  influence
of age and sex was sometimes more important in determining DDT toxicity
than  was body weight, though heavier shrews tended to be more tolerant
of  the chemical.  Among older animals, males were more tolerant of DDT
than  females.  Braham &  Neal (1974) found  an effect of  DDT  on  the
metabolic  rate of  the same  species of  shrew after  feeding it  with
earthworms contaminated with the insecticide.  After one week  of  this
diet,  the metabolic rate was significantly higher than that of undosed
shrews,  but  after 2-3  weeks of dosing  there was a  return to oxygen
consumption  rates not different from controls.  Two shrews were fasted
for  18  h,  after being fed earthworms containing DDT for 3 weeks, and
compared to untreated shrews similarly fasted.  The DDT-treated animals
showed  12.6% and  12.1% increases  in metabolic  rate  after  fasting,
whereas  controls showed decreases of 8.7% and 8.0%.  The DDT  exposure
was  environmentally realistic because earthworms used for feeding were
not artificially dosed with DDT but were collected from an  area  where
DDT had been used.

7.  ECOLOGICAL EFFECTS FROM FIELD APPLICATION

    There  have been  kills of  fish (Hunt  & Linn,  1970) and  aquatic
invertebrates  (Ide, 1957)  reported after  normal usage  of DDT  as  a
terrestrial insecticide and after its application to water for mosquito
control.   Reproductive failure in  commercial fisheries has  also been
attributed  to DDT (Hunt & Linn, 1970).  In addition, it has been shown
to  be toxic to  amphibia after water  application (section 5.3).   The
setting  of safe water levels  of DDT and its  metabolites is difficult
because its high bioaccumulation and high lipid solubility mean that it
can  have effects remote in time from its application.  The toxicity of
DDT  to  aquatic  microorganisms  and  invertebrates  is  very variable
between  species.  Exposure  to DDT  or its  stable metabolites  would,
therefore,  be expected to  kill certain species  selectively.   Short-
term,  there is  close correspondence  between the  96-h LC50 for  a
moderately sensitive fish (16 g/litre)  and the expected water concen-
tration after application of DDT at the normal rate.

    DDT and its metabolites, principally DDE, have been  implicated  in
reproductive  effects on birds in the field.  Large population declines
in  some bird species, mainly birds of prey, have been blamed on DDT or
on  combinations  of DDT  with  other persistent  organochlorines.  The
evidence  for this rests  on correlations.  There  is a correlation  in
time between the onset of effects on eggshells and the onset  of  major
DDT  use in  agriculture.  There  is also  a correlation  between  geo-
graphical  areas of high  DDT use and  effects on local  populations of
birds (compared to populations living in areas of low use).  There is a
clear  correlation  between  DDE residues  in  eggs  and the  degree of
thinning of the shells of those eggs, collected from the wild.  Storage
of DDT in body fat means that the effects of the compound can be remote
in  time from the application  of the chemical to  an area.  Only  some
species  of birds are  affected by DDT  or its metabolites.   There are
considerable data on the variability between species in their suscepti-
bility  to  these  compounds.  Widespread  monitoring  programmes  have
related the recovery of bird populations to reduced levels of  DDE  and
the  residual material of aldrin/dieldrin  use in the tissues  of birds
sampled  from  the  wild, following attempts to limit or ban the use of
the  parent pesticide in agriculture.   Because DDT is seldom  the only
chemical  residue found in  bird tissues from  the wild, there  is some
disagreement  on whether  DDT alone  can cause  population declines  in
birds.

    Ratcliffe  (1967,  1969,  1970),  Hickey  &  Anderson  (1968),  and
Anderson  & Hickey (1972,  1974) were the  first, in Britain  and North
America,  respectively, to compare  the thickness of  eggshells sampled
from  the wild with that of specimens measured from museums and private
collections  which predated the use  of DDT.  These authors  examined a
wide range of bird species but mainly those high in food chains.  Later
studies,  along the same lines, include those of Dilworth et al. (1972)
on  the  woodcock,  Wiemeyer et al. (1975) on the osprey, Fox (1976) on
the common tern, Cooke et al. (1976) on the grey heron, and  Koeman  et
al.  (1972)  and Newton  & Haas (1984)  on the sparrowhawk.   Ratcliffe
(1970)  collected eggshell data  on 17 species  of British birds,  9 of
which  showed significant decreases  in shell thickness  when comparing
the  period before 1947 with the period after 1947.  The birds affected

were  predominantly raptors, exceptions  being the carrion  crow, rook,
and shag.  Anderson & Hickey made eggshell comparisons between pre- and
post-DDT use on 25 different species of birds.  The same  species  from
different geographical areas of North America were investigated, making
166 comparisons in all. Of these, 62% showed significant decreases, 37%
showed  non-significant decreases or no  change, and only 1%  showed an
increase in shell thickness.

    King et al. (1978) found significant decreases in  eggshell  thick-
ness  in 15 out  of 22 aquatic  species of birds,  in Texas, USA,  when
comparing shells from 1970 with museum specimens from before 1943.  All
of  these studies, and many  more, demonstrated that, in  those species
that showed effects on eggshell thinning, the effect began suddenly and
markedly at the same time as the onset of DDT use.  In Britain, the use
of DDT in large quantities began in 1947.  Fig. 2 reproduces  the  data
(from  Newton  & Haas,  1984) on sparrowhawks  from 1870 to  1980.  The
persistence  of DDT in  bird tissues means  that recovery is  still not
complete, despite controls on the use of DDT.  In  Alaska,  populations
of peregrine falcons did not show the effects of DDT until  much  later
than  other  regions of  North America.  These  birds breed in  Alaska,
where  use  of DDT  was low, but  winter in Central  and South America.
Residues of DDT and its metabolites in Alaskan peregrines began to rise
in  1967,  along with  the use of  DDT in its  wintering grounds.  Con-
comitant reductions in breeding success and populations  of  peregrines
occurred  (White & Cade,  1977).  These data  are indicative of  a bird
breeding  and survival effect of DDT use, correlated both with time and
geographical area.  The index of eggshell thickness has  reflected  the
pattern  of use  of the  insecticide (Ratcliffe,  1970).  Before  1947,
there was no significant geographical variation in the  mean  thickness
of peregrine falcon eggshells in Britain.  Since 1947,  eggshells  from
non-agricultural  areas,  notably  the  central  and  eastern  Scottish
highlands, have shown a smaller decrease in shell thickness than shells
from highly agricultural regions.

    Anderson  & Hickey (1974)  showed that shells  of the  white-tailed
eagle  in  Greenland  were thicker  than  shells  of the  same  species
collected  in the  Baltic.  Compared  to early  reference  shells  from
museums,  the Greenland shells showed a slight increase in thickness of
3%, whereas Swedish shells showed a decrease of 16%.

    Lincer (1975) established a dose relationship between  dietary  DDE
and  eggshell  thinning  in captive  American  kestrels  and,  also,  a
relationship  between  DDE residues  in the eggs  and the thickness  of
their shells.  He then compared shell thickness with egg DDE residue in
kestrels  sampled from the wild.  The relationship was identical.  Many
other  authors have shown a  good correlation between egg  DDE residues
and  the  degree  of  eggshell  thinning.   These  studies  cover   the
following  species: double-crested cormorant  (Anderson et al.,  1969);
great blue heron (Vermeer & Reynolds, 1970); prairie falcon (Enderson &
Berger,  1970); peregrine falcon  (Peakall et al.,  1975c); grey  heron
(Cooke et al., 1976); sparrowhawk (Newton & Bogan, 1978);  and  gannet,
shag,  and great black-backed  gull (Cooke, 1979a).   In many of  these
studies, there is not only a correlation between eggshell thickness and
DDE but there are also correlations between DDE residues  and  residues

of other organochlorines.  Therefore, it is often difficult  to  deter-
mine  solely from the field data, exactly which chemical is responsible
for  the  effect.  This  problem has been  addressed by Newton  & Bogan
(1978).   They conducted  a statistical  analysis of  their  data  that
showed a correlation between DDE and shell thickness, egg breakage, egg
addling,  and hatching failure,  in addition to  a correlation  between
DDT,  PCB,  and dieldrin  residues.   After multivariate  analysis, DDE
appeared only to be responsible for eggshell thinning and egg breakage.
Relating  laboratory studies to field observations suggests that DDE is
the only organochlorine that causes eggshell thinning.

FIGURE 2

    Population declines in birds of prey differed between much of North
America  and  eastern  North America  and  western  Europe.   In  North
America,  apart  from in  the East, declines  were gradual, whereas  in
Europe and eastern North America declines were sudden and catastrophic.
The sudden declines in Europe have usually been attributed to  the  use
of  the chlorinated cyclodienes, which kill adult birds, rather than to
DDT.  A study of the recoveries of European birds of  prey  populations
provides evidence for this attribution.  Populations began to rise at a
time  when  residues  of DDE in tissues were stable but when use of the
cyclodienes and, therefore, residues of HEOD (dieldrin) were declining.
Some  populations in North America did not show high contamination with
cyclodienes and may have declined due to DDT use alone.   Henny  (1972)
showed  that in American populations  of osprey, American kestrel,  and
red-shouldered hawk there was a decrease in breeding  performance,  but
no increase in adult mortality, in response to DDT.   The  reproductive
effects  of DDT  may have  prevented population  recoveries  after  the
cessation  of dieldrin use and the return of mortality rates to normal.
The  question has  been reviewed  by Newton  (1979) and  Newton &  Haas
(1984).

    The  populations of many  species of birds  of prey were  monitored
throughout  a  period of  high DDT use.   This was done  by large scale
surveys  and studies of  population dynamics (Ratcliffe,  1972;  Henny,
1977; Lindberg, 1977; White & Cade, 1977), migration counts  at  obser-
vation  points (Rosen,  1966; Hackman  & Henny,  1971; Edelstam,  1972;
Ulfstrand et al., 1974; Nagy, 1977), and by sample counts  (Ash,  1965;
Bezzel, 1969).  Some species showed marked declines (in some areas this
led to local extinction), whilst others showed only  temporary  effects
or  no  effects  at all.   Declines  were  most marked  in  bird-eating
species,  such as the sparrowhawk and peregrine falcon, and fish-eating
species, such as the white-tailed and bald eagles, and were less marked
in  mammal-eating  species,  such as  the  kestrel,  golden eagle,  and
buzzard.   These variations  in decline  correspond to  the DDE  levels
found in these particular species (Newton, 1979).

    Perfect  (1980)  reported  the results  of  a  4-year study  on the
overall effects of the use of DDT as an insecticide on cowpeas crops in
a Nigerian forest soil.  In addition to effects on  soil  invertebrates
(section  6.1),  there  were effects  on  the  decomposition  of  plant
material.   The remains of  the plants after  harvesting were  ploughed
into the soil and this resulted in an increase in the residues  of  DDT
and  its metabolites in lower levels of the soil.  To confirm an effect
on  decomposition, these plant remains were buried in mesh bags and the
loss  of weight due to decomposition was recorded over time.  There was
a  significant reduction in the rate of decomposition of plant material
treated  with  DDT  and also  of  untreated  plant material  buried  in
contaminated soil.  Shires (1985) reported no significant effect on the
decomposition of sweet chestnut leaf litter in a temperate  area  after
the application of DDT at 1 kg/ha.

    Perfect  et al.  (1979) investigated  the effects  of repeated  DDT
applications   on  cowpea  crop   yield  in  Nigeria.    Yields  varied
considerably from season to season and from year to year  in  untreated
plots  because of  differences in  pest damage  and climate.   DDT  was
applied to the treated plots weekly between planting and harvest  at  a
rate of 1 kg/ha, and the site was studied for 4 years.  Over the 4-year
period  there was a considerable benefit in yield from DDT application;
the yield was 1.45 tonnes/ha in the untreated and 3.42 tonnes/ha in the
treated plots.  However, the benefit was most noticeable in  the  first
year of cultivation and declined over the four years to the point where
DDT use did not significantly increase yield.  The  authors  attributed
the effect to the deleterious action of the insecticide on soil biota.

8. EVALUATION

    In evaluating the environmental hazard of DDT and  its  metabolites
the following general points have to be kept in mind.

(a)     The  environmental distribution and effects of DDT are spread wider
        than   the  area  of  use,  because  the  parent  compound  or  its
        metabolites  are carried worldwide by air and ocean currents and in
        biota.

(b)     Some  of the breakdown products of DDT, principally DDE, are highly
        persistent  in  soil, sediment,  and  biota.  Thus,  problems  with
        residues of these materials last long after the cessation of use.

(c)     The  bioaccumulation of DDT, or more usually of its metabolites, is
        well   established   and   occurs  from   very   low  environmental
        concentrations  of  DDT.   The use  of "bioconcentration factors"
        (the ratio of concentration in the organism with  concentration  in
        the  medium) to estimate the  capacity of organisms to  take up DDT
        can be misleading if the exposure is high, since these  values  are
        ratios.

(d)     Residues  and effects are  often highly seasonal,  corresponding to
        changes  in body fat, since DDT metabolites are very lipid-soluble.
        Measurements  of these metabolites in the tissues of organisms must
        be  conducted  over  a  period  of time  if  they are  to  give any
        indication of the degree of contamination of the environment.

(e)     There  are  insufficient  data  on  the  effects  of  DDT  and  its
        metabolites  on communities of organisms and ecosystem functioning.
        Hazard assessment is, therefore, often made by  extrapolation  from
        single species studies.

(f)     Research and monitoring have concentrated on a few effects  of  DDT
        observed in the wild.  This could give the mistaken impression that
        the  effects of these  compounds are restricted  to a few  species.
        Other  effects could be  predicted but have  received little or  no
        attention from the scientific community.

(g)     The  major remaining use of  DDT is for malaria  control operations
        that  are normally carried out in tropical countries.  However, the
        majority of environmental studies on DDT have been carried  out  in
        conditions relevant to temperate regions.  Care must  be  exercised
        in extrapolating these results to tropical conditions.

8.1  Aquatic Organisms

    The  widespread  use  of DDT  as  an  insecticide has  resulted  in
worldwide contamination of the environment.  Due to the physicochemical
characteristics  of DDT and  its metabolites, concentrations  have been
recorded  in  different  environmental  compartments,  including  soil,
sediments, and terrestrial and aquatic organisms.  The bioconcentration
of  DDT and its metabolites  is a real hazard  to non-target organisms.
DDT  and its metabolites cause adverse effects at all trophic levels of
aquatic  ecosystems, particularly on  primary producers, which  are the

most  sensitive.  Although no data are available for the effects of DDT
on ecosystem function, it should be regarded as a  major  environmental
hazard  in this respect.  DDT  and its metabolites are  highly toxic to
fish  and,  besides  their  lethal  effect,  they  affect  development,
behaviour,  and biochemical processes.  DDT and its metabolites, should
be  regarded as  hazardous to  fish productivity and distribution  and,
hence, to human food supplies.  Accumulated DDT and its metabolites are
further  transferred  from  aquatic organisms  to  consumers, including
birds, mammals, and, ultimately, human beings.

8.2  Terrestrial Organisms

    DDT-type  compounds  are resistant  to  breakdown and  are  readily
adsorbed  onto soils and sediments,  from whence they can  act as long-
term  sources  of exposure  and  contribute to  terrestrial  organisms.
Accumulation in terrestrial organisms is via the food chain.

    These  chemicals  are  hazardous to  microorganisms,  but  repeated
application can lead to the development of tolerance in  some  species.
DDT causes fluctuations in some populations of microorganisms, and this
could  eventually lead to changes in species composition, disruption of
nutrient cycles, and changes in soil fertility.

    Earthworms  are  insensitive  to the  acute  toxic  effects of  DDT
residues in soil.  However, they are known to take up DDT from soil and
this uptake presents a major hazard to predators.

    DDT  is  a  non-selective insecticide  and  leads  to mortality  in
natural  enemies of the insect pest.  This results in impairment of the
balance  between predators and prey and leads to outbreaks of secondary
pests and occurrence of the primary pest in larger numbers.

    Laboratory  studies confirm field findings that bat populations are
adversely  affected by DDE, especially during migration.  These studies
are indicative of the potential hazard to other mammals, exposed to DDT
in  the environment,  when fat  containing DDT  residues is  mobilized,
e.g., during migration or temporary starvation.

    One  of the most widely studied effects of DDT is eggshell thinning
in birds, particularly in predatory species.  The metabolite  DDE,  not
DDT, has been shown to be responsible for this effect.   Other  effects
on  reproduction and survival of  birds have been demonstrated.   Large
population  declines  in  birds of  prey  can  be, at  least partially,
attributed  to  DDT.   It has been shown that DDE residues in birds and
their   eggs   reduced  the   rate  of  recovery   of  affected  raptor
populations.   A  factor  that  has  received  less  attention  is  the
secondary  effect of the increasing  numbers of pest rodents  that were
controlled principally by birds of prey in some countries.

                           *             *              *

    Because  of their lack  of degradation, their  resulting widespread
persistence  in the environment, their high acute toxicity to organisms
at   the   base  of   food  chains,  and   their  high  potential   for
bioaccumulation,  DDT and its metabolites should be regarded as a major
hazard  to the environment.  DDT should not be used when an alternative
insecticide is available.

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    See Also:
       Toxicological Abbreviations