DDT and its derivatives: environmental aspects (EHC 83, 1989)

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

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

ISBN 92 4 154283 7

The World Health Organization welcomes requests for permission
to reproduce or translate its publications, in part or in full.
Applications and enquiries should be addressed to the Office of
Publications, World Health Organization, Geneva, Switzerland, which
will be glad to provide the latest information on any changes made
to the text, plans for new editions, and reprints and translations
already available.

^(c) World Health Organization 1989

Publications of the World Health Organization enjoy copyright
protection in accordance with the provisions of Protocol 2 of the
Universal Copyright Convention. All rights reserved.

The designations employed and the presentation of the material
in this publication do not imply the expression of any opinion
whatsoever on the part of the Secretariat of the World Health
Organization concerning the legal status of any country, territory,
city or area or of its authorities, or concerning the delimitation
of its frontiers or boundaries.

The mention of specific companies or of certain manufacturers'
products does not imply that they are endorsed or recommended by the
World Health Organization in preference to others of a similar
nature that are not mentioned. Errors and omissions excepted, the
names of proprietary products are distinguished by initial capital
letters.

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 Baños, 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 µg/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 µg/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 µg/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 µg/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 µg/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 µg/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 µg/litre) but
very soluble in animal fats. The octanol-water partition coefficient
(log k_ow) 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:

------------------------------------------------------------------------------------
Name Chemical name R R' R"
DDT and its major
metabolites
------------------------------------------------------------------------------------
DDT 1,1'-(2,2,2-trichloroethylidene)- -Cl -H -CCl₃
bis[4-chlorobenzene]
DDE_a 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]
DDMU^a 1,1'-(2-chloroethenyldene)- -Cl None =CHCl
bis[4-chlorobenzene]-
DDMS^a 1,1'-(2-chloroethylidene)- -Cl -H -CH₂Cl
bis[4-chlorobenzene]
DDNU^a 1,1'-bis(4-chlorophenyl)ethlyene -Cl None =CH₂
DDOH^a 2,2-bis(4-chlorophenyl)ethanol -Cl -H -CH₂OH
DDA^a 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
chlorobenzilate^c ethyl 4-chloro-a-(4-chlorophenyl)- -Cl -OH -C(O)OC₂H₅
a-hydroxybenzeneacetate
chloropropopylate^c 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
------------------------------------------------------------------------------------

methoxychlor^c 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).

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 DDT^a
---------------------------------------------------------------------------------------------------------
Organism Biomass Flow Organ Tem- Duration Exposure Bioconcen- Reference
(µg/ml) stat^b perature (µg/litre) tration
( °C) factor^c
---------------------------------------------------------------------------------------------------------
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 3990^d Bedford & Zabik
(Anodonta grandis) (1973)

Table 2. (Contd).
---------------------------------------------------------------------------------------------------------
Organism Biomass Flow Organ Tem- Duration Exposure Bioconcen- Reference
(µg/ml) stat^b perature (µg/litre) tration
( °C) factor^c
---------------------------------------------------------------------------------------------------------

Earthworm 10 4 weeks 17 000 0.47^d 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)

Mosquito larva stat 30 3 days 2.0 110^d Metcalf et al.
(Culex quinquifasciatus) stat 30 3 days 0.9 74^d (1973)

Mosquito fish stat 30 3 days 2.0 344^d Metcalf et al.
(Gambusia affinis) stat 30 3 days 0.9 217^d (1973)

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

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

Fathead minnow flow 24-25.5 14 days 45.6 mg/kg 1.17^d Jarvinen et al.
(Pimephales promelas) flow 24-25.5 14 days 0.5 85 400^d (1977)
flow 24-25.5 14 days 2.0 69 100^d Jarvinen et al.
flow 24-25.5 112 days 45.6 mg/kg 1.33^d (1977)
flow 24-25.5 112 days 0.5 93 200^d Jarvinen et al.
flow 24-25.5 112 days 2.0 154 100^d (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 17 500^d Sanborn et al.
(1975)

Broiler hen fat 6 weeks 1.0 10.3^d Kan et al.
(1978)

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

Double-crested cormorant WB 9 weeks 0.95 236.3^d 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 /kg^d (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 µg/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 0.15^o/oo to 10^o/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 15^o/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 µg/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 µg/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 µg/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 µg/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 µg/litre in the culture medium, DDT
stimulated the growth of the bacterium Escherichia coli (Keil et al.,
1972). Yields of cultures exposed to 100 µg/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 µg/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 µg/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 µg/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 µg/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 µg/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 µg 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 µg/litre or
less (Wurster, 1968). Four different species showed increasing
inhibition up to DDT concentrations of 100 µg/litre, but no greater
effect at higher concentrations. A green alga, Pyramimonas , was
affected by DDT only at concentrations higher than 10 µg/litre. The
other three species, a diatom, a coccolithophore, and a dinoflagellate
were affected at DDT concentrations between 1 and 10 µg/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 µg DDT/litre and reached a maximum
at 100 µg/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 µg/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 µg/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

DDT is highly toxic, in acute exposure, to aquatic invertebrate, at
concentrations as low as 0.3 µg/litre. Toxic effects include
impairment of reproduction and development, cardiovascular
modifications, and neurological changes. Daphnia reproduction is
adversely affected by DDT at 0.5 µg 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 µg/ 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 µg/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 µg DDT/litre for 9
months, grew and moulted normally; there were no apparent sublethal
effects. However, exposure to 5 µg 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 µg/litre. Roberts
(1975) showed that DDT at 50 µg/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 µg/litre, for
total young produced, at 0.61 µg/litre for average brood size, and at
0.75 µg/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
---------------------------------------------------------------------------------------------------------
Organism^f Flow Temp Salinity Compound Parameter Water Reference
stat^a ( °C) ^o/oo concentration
(µg/litre)
---------------------------------------------------------------------------------------------------------
Estuarine and marine invertebrates

Eastern oyster (juv.) flow 30 23 DDT^d 96-h EC₅₀^j 9 Mayer (1987)
(Crassostrea virginica) flow 12 25 DDE^d 96-h EC₅₀^j 14 Mayer (1987)
flow 20 30 TDE^d 96-h EC₅₀^j 25 Mayer (1987)

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

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

Pink shrimp (juv.) flow 24 28 DDT^d 48-h LC₅₀ 0.6 Mayer (1987)
(Penaeus duorarum) flow 16 31 TDE^d 48-h LC₅₀ 2.4 Mayer (1987)

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

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

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

Table 3. (Contd).
---------------------------------------------------------------------------------------------------------
Organism Flow Temp Alkali- Hard- pH Comp- Parameter Water Reference
Stat^a ( °C) nity^c ness^c ound concentration
(µg/litre)
---------------------------------------------------------------------------------------------------------
Freshwater invertebrates
Water flea stat 20 192 138 8.2- DDT^d 48-h LC₅₀ 1.1 (1.0-1.3) Randall et
8.5 al. (1979)
(Daphnia magna) stat 15 44 7.1 DDT^d 48-h LC₅₀ 4.7 (2.8-5.6) Mayer &
Ellersieck
(1986)
stat 20 192 138 8.2- DDT^e 48-h LC₅₀ 1.7 (1.5-1.8) Randall et
8.5 al. (1979)
stat^b 24 320- 7.6 DDT 14-day 0.67 (0.65-0.69) Maki &
340 (99%) LC₅₀ Johnson
stat^b 24 320- 7.6 DDT 14-day 0.5 (0.48-0.52) (1975)
340 (99%) EC₅₀^g
stat^b 24 320- 7.6 DDT 14-day 0.61 (0.58-0.64) Maki &
340 (99%) EC₅₀^h Johnson
stat^b 24 320- 7.6 DDT 14-day 0.75 (0.71-0.79) (1975)
340 (99%) EC₅₀ⁱ
stat 10 44 7.1 TDE^d 48-h LC₅₀ 9.1 Mayer &
stat 21 44 7.1 TDE^d 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 DDT^d 48-h LC₅₀ 0.36 (0.28-0.47) Mayer &
(Daphnia pulex) Ellersieck
(1986)
Water flea stat 15 44 7.1 DDT^d 48-h LC₅₀ 2.5 (1.9-3.3) Mayer &
(Simocephalus stat 21 44 7.1 DDT^d 48-h LC₅₀ 2.8 (2.3-3.5) Ellersieck
serrulatus) stat 15 44 7.1 TDE^d 48-h LC₅₀ 3.2 (2.3-4.4) (1986)
stat 21 44 7.1 TDE^d 48-h LC₅₀ 4.5 (3.1-6.6)

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

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

Table 3. (Contd).
---------------------------------------------------------------------------------------------------------
Organism Flow Temp Alkali- Hard- pH Comp- Parameter Water Reference
Stat^a (°C) nity^c ness^c ound concentration
(µg/litre)
---------------------------------------------------------------------------------------------------------
Crayfish (Orconectes nais)
mature stat 21 260 7.4 DDT^d 24-h LC₅₀ 1100 (1000-1400) Sanders
stat 21 260 7.4 DDT^d 96-h LC₅₀ 100 (80-120) (1972)
1 day old - 15g stat 21 260 7.4 DDT^d 24-h LC₅₀ 1.4 (1.1-4.2) Sanders
stat 21 260 7.4 DDT^d 96-h LC₅₀ 0.3 (0.18-0.5) (1972)
1 week old - 20g stat 21 260 7.4 DDT^d 24-h LC₅₀ 1.0 (0.6-5.0) Sanders
stat 21 260 7.4 DDT^d 96-h LC₅₀ 0.18 (0.12-0.3) (1972)
2 weeks old - 23g stat 21 260 7.4 DDT^d 24-h LC₅₀ 1.2 (0.9-5.5) Sanders
stat 21 260 7.4 DDT^d 96-h LC₅₀ 0.2 (0.16-1.1) (1972)
3 weeks old - 30g stat 21 260 7.4 DDT^d 24-h LC₅₀ 1.0 (0.6-5.0) Sanders
stat 21 260 7.4 DDT^d 96-h LC₅₀ 0.24 (0.1-0.6) (1972)
5 weeks old - 50g stat 21 260 7.4 DDT^d 24-h LC₅₀ 3.2 (1.8-8.0) Sanders
stat 21 260 7.4 DDT^d 96-h LC₅₀ 0.9 (0.7-1.4) (1972)
8 weeks old - 500g stat 21 260 7.4 DDT^d 24-h LC₅₀ 45 (40-52) Sanders
stat 21 260 7.4 DDT^d 96-h LC₅₀ 28 (24-36) (1972)
10 weeks old - 1200g stat 21 260 7.4 DDT^d 24-h LC₅₀ 50 (48-56) Sanders
stat 21 260 7.4 DDT^d 96-h LC₅₀ 30 (26-42) (1972)

Sowbug (isopod) stat 21 35 7.1 DDT^d 24-h LC₅₀ 8.7 (4.9-13.0) Sanders
(Asellus brevicaudus) stat 21 35 7.1 DDT^d 96-h LC₅₀ 4.0 (1.2-6.5) (1972)
stat 21 35 7.1 TDE^d 24-h LC₅₀ 18 (14-25) Sanders
stat 21 35 7.1 TDE^d 96-h LC₅₀ 10 (7.0-14) (1972)

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

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

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

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

Stonefly (naiad) stat 11- DDT^e 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 µg DDE/litre; eggs
were kept in water containing 20 µg 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) µg/litre
for the unexposed population, and 7.2 (5.8-8.8) µg/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 µg/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.

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 µg/litre for the
largemouth bass (Mayer & Ellersieck, 1986) to 180 µg/litre for the
goldfish (Henderson et al., 1959). For 96-h tests, LC₅₀ values range
from 1.5 µg/litre for largemouth bass (Mayer & Ellersieck, 1986) to
56 µg/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 µg/kg per
day for chinook and 64 µg/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 µg 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 µg/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)/ stat^a perat- ^o/oo concen-
age^f ure tration
(°C) (ug/litre)
---------------------------------------------------------------------------------------------------------
Estuarine and marine fish

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

Longnose killifish juv. flow 15 30 DDT^c 48-h LC₅₀ 2.8 Mayer
(Fundulus similis) juv. flow 16 28 TDE^c 48-h LC₅₀ 42.0 (1987)

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

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

Spot juv. flow 12 26 DDE^c 48-h LC₅₀ > 100 Mayer
(Leiostomus xanthurus) juv. flow 26 30 TDE^c 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) stat^a perat- nity^d ness^d pound concen-
ure tration
(°C) (ug/litre)
---------------------------------------------------------------------------------------------------------
Freshwater fish

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

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

Atlantic salmon 0.45 stat 12 40 7.5 DDT^c 24-h LC₅₀ 6.2
(Salmo salar) (4.6-8.4) Mayer &

0.45 stat 12 40 7.5 DDT^c 96-h LC₅₀ 1.8
(1.3-2.6) Ellersieck^g
0.5 stat 12 44 7.5 DDE^c 96-h LC₅₀ 96.0
(52.1-177) Mayer &
Ellersieck^g

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 DDT^c 24-h LC₅₀ 10.0
(7.0-12.0) Mayer &
1.0 stat 13 44 7.1 DDT^c 96-h LC₅₀ 4.0
(3.0-6.0) Ellersieck^g
6.0 stat 13 40 7.1 DDT^c 24-h LC₅₀ 26.9
(18.1-40.0) Mayer &
6.0 stat 13 40 7.1 DDT^c 96-h LC₅₀ 19.3
(9.6-38.8) Ellersieck^g

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)

Rainbow trout 0.9 stat 7 44 7.1 DDT^c 24-h LC₅₀ 7.5
(Salmo gairdneri) (6.7-8.3) Mayer &
0.9 stat 7 44 7.1 DDT^c 96-h LC₅₀ 4.1
(3.6-4.6) Ellersieck^g
0.9 stat 13 44 7.1 DDT^c 24-h LC₅₀ 8.2
(7.2-9.2) Mayer &
0.9 stat 13 44 7.1 DDT^c 96-h LC₅₀ 4.7
(4.2-5.3) Ellersieck^g
0.9 stat 18 44 7.1 DDT^c 24-h LC₅₀ 12.0
(1.0-13.0) Mayer &
0.9 stat 18 44 7.1 DDT^c 96-h LC₅₀ 5.8
(5.2-6.5) Ellersieck^g
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 DDT^c 96-h LC₅₀ > 3.0 Mayer &
0.8 stat 12 44 7.1 DDE^c 96-h LC₅₀ 32.0
(26.0-40.0) Ellersieck^g
1.0 stat 12 44 7.1 TDE^c 96-h LC₅₀ 70.0
(57.0-87.0) Mayer &
1.0 stat 12 272 7.4 TDE^c 96-h LC₅₀ 70.0
(58.0-85.0) Ellersieck^g

Cutthroat trout 1.0 stat 13 44 7.1 DDT^c 24-h LC₅₀ 8.4
(Salmo clarki) (7.6-9.2) Mayer &
1.0 stat 13 44 7.1 DDT^c 96-h LC₅₀ 5.5
(4.7-6.4) Ellersieck^g
1.8 stat 9 162 7.4 DDT^c 24-h LC₅₀ 11.3
(9.4-13.6) Mayer &
1.8 stat 9 162 7.4 DDT^c 96-h LC₅₀ 7.9
(6.5-9.7) Ellersieck^g

Brown trout 1.7 stat 13 44 7.1 DDT^c 96-h LC₅₀ 1.8
(Salmo trutta) (1.3-2.5) Mayer &
Ellersieck^g
Table 4. (Contd).
---------------------------------------------------------------------------------------------------------
Organism Size Flow/ Tem- Alkali- Hard- pH Com- Parameter Water Reference
(g) stat^a perat- nity^d ness^d pound concen-
ure tration
(°C) (ug/litre)
---------------------------------------------------------------------------------------------------------

Northern pike 0.7 stat 18 272 7.4 DDT^c 24-h LC₅₀ 5.5 Mayer &
(Esox lucius) 0.7 stat 18 272 7.4 DDT^c 96-h LC₅₀ 2.7 Ellersieck^g

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

River shiner 0.3 stat 18 44 7.1 DDT^c 24-h LC₅₀ 6.7
(Notropis blennius) (4.9-9.1) Mayer &
0.3 stat 18 44 7.1 DDT^c 96-h LC₅₀ 5.8
(3.6-9.1) Ellersieck^g
Fathead minnow 1.2 stat 18 44 7.1 DDT^c 24-h LC₅₀ 14.2
(Pimephales (11.0-18.0) Mayer &
promelas) 1.2 stat 18 44 7.1 DDT^c 96-h LC₅₀ 12.4
(10.0-15.4) Ellersieck^g
1.2 stat 18 272 7.4 DDT^c 24-h LC₅₀ 13.8
(10.3-18.3) Mayer &
1.2 stat 18 272 7.4 DDT^c 96-h LC₅₀ 13.2
(10.1-17.3) Ellersieck^g
0