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on 89

Author

Braun, Daniel C.

Corporate Author
Report/Article TitlB Establishing Environmental Criteria

JOIirnal/BOOk Title

Archives of Environmental Health

Year

™™

Month/Day

September

Color

n

Number of Images

3

DOSCriptOll NOtOS

^'v'n *-• Young filed this Item under the category
"DDT/Human Toxicology and Environmental Fate"
Heading: Pollution Medical Research Conference.

Wednesday, April 11, 2001

Page 1189 of 1242

�lution Medical Research Conferefee

Establishing
j/
Environmental Qrtteria
1

Medical Perspectives
, MD;

reasonable
Nosuggestisthatperson todayofwould
pollution
the
environment not a serious problem,
one which demands the application of
all the intelligent, scientific, and
technical effort we can muster—and
can afford. Physicians are aware of
this. Industrialists, for the most part,
are aware of it. Scientists from a
number of disciplines are working
diligently to define the problems and
to find solutions. Unfortunately, the
greatest deterrent to sound progress
at present comes from those who engage in unscientific exaggerations
while demanding instant results. All
sorts of dire predictions are being
made by all sorts of people, but those
most frightening with respect to
health are being made by persons
who are not physicians.
In their importance to humanity,
the possible effects of pollution on
health far outweigh aspects of aesthetics or comfort. Health is the
Submitted for publication Dec 6, 197% accepted M««h 19,1978.

From the Industrial Health Foundation, Inc.,
PJUfburgh. Mr. tJurgiel it now with Byckman
Edgerley Tomiinfon * Awociatew, 8t Loufe.
Road before t)te Air Pollution Medical Research Conference of the American Medical A&gt;
•ocietion, Chicago, Oct a, 1972,
•
. |^|^ntr»a«eit« to Induitriil Health Paunda.
Won, Inc., 58$1 Centre Av», ntt*b,ur0h, PA
if. 0raun)i '-—-,.:
iron HMlth/Vol 27, Sept 1973

realm of physicians, and so it is important for physicians to know what
substances in the environment are
hazardous to health, or potentially so.
A major problem is that zealots are
calling some situations health hazards when they are in fact merely
nuisances, because this makes the
sequences dire. Sometimes this is
done out of ignorance of the significance of dose-response relationships.
Beyond all others, physicians are
aware of such relationships; they
know that for every substance a certain dosage level is needed to produce
an expected response.
Because health is the most important concern in community contamination, and because the doctor it best
able to understand the physiological
response to various levels of contaminanta, the physician should play a
more important role in public information about and community rosponse to pollution control.
Contaminant* emitted into the
atniosphere arise from maty ********
Sorn^ result from communiiy operations, such at garbage diapoaal and
incineration. Agricultural burninf,
fertilising, and insect-control account
tor tome, and still other* have their
origin in industrial proceaM* &lt;* &amp;•
jjjwration of automobile!, trucks,

Establishing Environment* CrtttftyBraun «t at t||

�buses, boats, and airplanes.
We call attention to the fact that
we said "contaminants" and not "pollutants," The introduction of harmful, impure, or otherwise undesirable
substances into something previously
untainted constitutes contamination,
The result may, for practical purposes, be negligible. It is only when
these substances render the atmosphere or water foul or noxious to
health or life that the word "pollution" is properly applicable.
This may seem to be only an exercise in semantics, but the point of
emphasis is that many people have
fallen into the sad practice of loose
speech and fuzzy definitions in the
whole area of environmental control.
They cry havoc when what is really
needed is merely nuisance abatement.
The fact is that the far-out claims
about air pollution are, at best,
frightening citizens, especially parents, and, at worst, are in a fair way
to leading to panic, simply because of
the lack of precise understanding of
the actual health effects of contaminants in the air we breathe. In a few
well-publicized acute episodes of
near-disastrous magnitude, serious
illness and death have resulted from
polluted air. Therefore, pollution in
high enough concentrations can be
serious. On the other hand, it is perfectly apparent that even in the urban areas of our country the life-span
and general state of health continue
to improve, and so the concentrations
commonly found in urban areas must
be less than disastrous. Again we
return to dose-response relationships.
High enough concentrations can be
harmful to health. Lower concentrations, even though they may offend us
in terms of aesthetics or comfort, can
be completely harmless to health.
Physicians know that the respiratory system is equipped with very
efficient self-cleansing mechanisms,
and can defend against and dispose of
even abnormal amounts of foreign
substances which are inhaled. One
seldom hears or sees this fact referred
to, however, in the talks or feature
articles on air pollution. Physicians
know that the body also has marvelous d«to«ifying mechanisms that can
III Arch Environ Health/Vol 27, Sept 1973

handle low doses of a wide variety of /"Spots and gases. Sulfur dioxide has
substances with no harmful effects, a
in the public press as
fact the public press almost unive%^ ttfe" 'jiq|St 'damaging, corrosive, and
sally ignores.
irritating to humans. Actually, in
f/
It is well, too, to keep in mind that
concentrations it can
"pollution" of the air is an inherent
bronchoconstriction. We
part of the phenomena of nature. Volioians would not be likely to
canic ash has been an important pol- lerm Such effect on airway resistance
lutant, as has smoke from forest fires.
as "corrosive." Careful research on
humans has shown that more than
Ozone in high concentrations is tem13,000/ig of SO, per cubic meter of air
porarily present in the air following
is needed to produce any measurable
lightning storms. Many others could
bronchoconstriction. This can be
be listed.
compared with the governmental
Man, blamed and maligned as the
community air quality standard of
worst polluter, produces only about
80/ng of SO, per cubic meter of air.
0.5% of the total air contamination
The physiological response to SO,
through his inventions and activities.
may be enhanced in the presence of
It is true that this relatively small
particulatefa, moisture, and oxidation,
amount can cause serious problems
because, in contrast to that from natand is also influenced by individual
ural sources, those for which man is
susceptibility. But it is apparent that
responsible are localized and may be
SO, levels in community air must
concentrated.
reach relatively high concentrations
Thus, a power-generating plant
to be deleterious to health.
may emit several hundred tons of sulfur dioxide (SO,) per day, and air
movement across an urban area can
increase the participate loading by
tenfold compared to the air of a nearby rural area.
The articles which follow will deal
in greater depth with specific contaminants and their effects. We wish
merely to touch on a few examples
that, in our judgment, indicate the
areas in which physicians have much
to offer and in which the medical
perspective is essential.
Of the millions of tons of material
thrown into the atmosphere each
year, carbon monoxide (CO), largely
from transportation sources, is the
major pollutant, constituting about
50% of the total loading by man. Its
most serious effects, of course, are to
be expected in persons with chronic
heart and lung disease, but at low
concentrations the effects may be
manifested by visual impairment and
slowed reaction time. To date, most
studies of the effects of CO have employed short-term, high-concentration exposure. Future CO toxicology
must be directed to physiological
changes produced by low levels ov«r
long periods of time.

Other major contaminants are the
oxides of nitrogen and sulfur, hydrocarbons, particulate matter, and* va-~

Hydrocarbons constitute approximately 15% of the total contamination in the ambient atmosphere. The
most important, from the standpoint
of being potential photochemical pollutants, ar j the double-bond olefins,
substituted aromatic hydrocarbons,
and aldehydes and ketones.
Polycyclic aromatic hydrocarbons
are universally present in the atmosphere, and much attention has been
directed to some of them because of
their carcinogenic potential. Thus
far, experimental production of lung
tumors in small animals has not been
accomplished by inhalation, and the
literature presents no clear-cut correlation between the effects of polynuclear aromatic hydrocarbon pollution and lung tumor production in
man. Neitiier does present information indicate any direct health effects
due to the gaseous hydrocarbons in
ambient a&lt;r, but "present information" is still inadequate to state unequivocally ihat there can be none, for
instance, under extremely adverse
meteorological conditions.

Of the teven oxides of nitrogen
known to exist, only two of toxicological importance are present in ambient air-nitric oxide (NO) and nitrogen dioxide (NO,). No data from
either aninal or human studies suggest thai NO is a health hazard at

Establishing Environmental Criteria/Braun et at

�concentrations found in ambient air,
but since it readily oxidizes to NO,, it
possesses potential toxicity. The toxicology &gt;f NO, is difficult to discuss
because of the inadequacy of relevant
data from human studies. An article
that follows will describe the effects of
NO, on schoolchildren in an urban
area. The effects of oxides of nitrogen
at levels of community air pollution
at this time must be considered as
potentially irritating Jlnd possibly
related to chronic pulmonary fibrosis,
but there is insufficient evidence of its
qualitative relationship to them.
With regard to water pollution, the
problems are vastly different today
from those of a few decades ago when
the major concern wns waterborne
bacteria responsible for cholera and
typhoid fever. Development of effective filtration and chlorination techniques has virtually eliminated such
epidem cs. At present, the volume of
industrial and metropolitan wastes is
tremendous and includes an ever-increasing number of synthetic chemical contaminants which did not even
exist a dozen years ago.
Most available data on the effects of
chemicals in water svpplies have
come from experiences in industry.
However, some information has been
obtained from episodes of acute illnesses v^iich result from the presence
of some uncommon natural constituents in crinking water, or accidental
contamination from spillage or jeepage of sc me chemical.
More than 500 new chemicals are
developed each year, and many of
these fir.d their way into our waterways. Sxtch chemicals as nitrates and
nitrites, arsenic and selenium, mercury, organic .carcinogens, and tracemetal antagonists present real challenges to w ater pollution central.
Scientific data on thii relative
importance of heavy metil toxicity
are scarce. The Food and Drug Administration admits to little knowledge regarding levels of toxicity for
metals in foods. Many chemical processes, for instance, use mercury,
which ultimately escapes into waste
water and tends to settle in the sediment of lakes and rivers. Small or-

ganisms not only ingest the metal,
they transform it into a more toxic *
form. Bottom-feeding fish eat the
small organisms and are in turn eaten by larger game fish. Mercury becomes increasingly concentrated with
each successive step. Although mercury probably has been present in
high concentrations in fish for many
years, and possibly has no effect on
persons eating the fish, it is nevertheless a cumulative poison. It exists in
food fishes as methyl mercury, which
is a highly toxic substance that
causes neurological damage, produces chromosomal aberrations, and
has teratogenic effects. Stopping the
discharge of mercury into our waterways is only one aspect of the problem; of greater concern is what to do
with the mercury already lying on
the river bottoms.
Recent studies raise the question as
to whether drinking water which contains minute amounts of carcinogenic
pollutants may, over many years,
contribute directly or indirectly to
cancer in man. Efforts to link organics in drinking water to cancer prevalence have so far been unsuccessful.
Of major consequence with regard
to soil pollution are the pebiicides.
The dilemma of pesticides lies in the
fact that while they do much good,
they threaten a great deal of harm.
They aid in increasing food and fiber
production through protection from
insects, rodents, and weeds, but by
their poisonous nature they may also
endanger human life by long-term,
low-level effects.
Because of recent adverse publicity, the public seems to believe that
pesticides have been spread with
reckless abandon all over the landscape, contaminating all food and
fiber crops and polluting the whole
environment beyond reclamation. As
a matter of fact, it is impossible to
find anything in current popular literature that puta pesticides in a favorable light. If it can be shown that a
pesticide has accumulated in animal
tissue, there is no end to the allegations made against it

For the last decade the dangers of
DDT, its buildup in the environment

as well as in human tissues, have
been a public health issue in this
country. It WM almost completely
banned from use in the United State*
by the Environmental Protection
Agency (EPA) this year. However,
after seven months of hearings by the
EPA during which a stream of scientific witnesses testified, the hearing
examiner found that there was no
conclusive evidence against DDT. In
fact, some of the evidence was clearly
questionable. The World Health Organization has recently sought to
persuade governments to recognize
the fact that although DDT may have
certain hazards, they should not be
allowed to obscure its immense advantages. The World Health Organization feels that, in spite of the adverse publicity, there is no present
justification for abandoning this valuable weapon in the fight against disease.
Physicians, especially those concerned with public health, are becoming more aware of the relationship of
man's well-being to his environment
It is imperative that they maintain a
scientific and professional approach,
and calmly appraise all the facts relating to health, disease, and ecology,
Scientific research is a slow, methodical process, and no amount of hyste
ria, government funding, or legisla
tion will hasten resolution of the
problems of physiological reactions.
This article has merely referred U
some of the aspects of the various
kinds of pollution, meanwhile urging
physicians to become involved, albeit
on a sound and professional basis
While we are all familiar with th&lt;
acute episodes of serious pollution
such as occurred in Donora, Pa, am
the Meuse Valley-and the disastei
at Minamata Bay, Japan, in whid
more than 100 died of mercury poi
soning- we, as physicians must lean
how to evaluate realistically the long
term effects of these pollutants at \o\
levels. With this background, th
medical profession can meet what w
consider to be its obligation to help I
development of proper criteria ft
environmental controls, and in mail
taining the medical perspective,

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                  <text>&lt;p style="margin-top: -1em; line-height: 1.2em;"&gt;The Alvin L. Young Collection on Agent Orange comprises 120 linear feet and spans the late 1800s to 2005; however, the bulk of the coverage is from the 1960s to the 1980s and there are many undated items. The collection was donated to Special Collections of the National Agricultural Library in 1985 by Dr. Alvin L. Young (1942- ). Dr. Young developed the collection as he conducted extensive research on the military defoliant Agent Orange. The collection is in good condition and includes letters, memoranda, books, reports, press releases, journal and newspaper clippings, field logs and notebooks, newsletters, maps, booklets and pamphlets, photographs, memorabilia, and audiotapes of an interview with Dr. Young.&lt;/p&gt;&#13;
&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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01190

Author
Corporate Author

U. s - ArlT|y Medlcal Bioengmeenng Research and Devel

RBDOrt/ArtidO Tltto Report: Problem Definition Studies on Potential
Environmental Pollutants, VII. Physical, Chemical,
lexicological, and Biological Properties of DDT and Its
Derivatives
'

Journal/Book Title
Year

1979

Month/Day
Color

rj

Number of Images

^

DQSCrlptQn NDtQ8

Alvin Li

Young filed this item under the category
"DDT/Human Toxicology and Environmental Fate"
Technical Report 7906

Wednesday, April 11, 2001

.

Page 1190 of 1242

�Technical Report 7906 .
/

•o* CO

PROBLEM DEFINIT70N STUDIES ON POTENTIAL ENVIRONMENTAL POLLUTANTS
VII. PHYSICAL, CHEMICAL, TOXICOLOGICAL, AND BIOLOGICAL
PROPERTIES OF DDT AND ITS DERIVATIVES

JUNE 1979

O

Prepared for the OFFICE of the PROJECT MANAGER
for CHEMICAL DEMILITARIZATION and INSTALLATION RESTORATION
by

US ARSSY MEDICAL BIOENGINEERING RESEARCH and DEVELOPMENT LABORATORY
ForlDfitrlck
Frederick, BSD 21701
Edited by
_W.. .JQickinson Burrows , _Ph . D .
David R ,-Gogley , -Ph . D .
Ph.D.

Jack C. Dacre, Ph.D.
jGeoffrey Woo4ard, Ph^

APPROVED FOR PUBLIC RELEASE;
DISTRIBUTION UNLIMITED

US ARMY MEDICAL RESEARCH and DEVELOPMENT COMMAND
FortDetr&amp;k
Frottertok, RSD217C1

81 1

28 00*

�NOTICE
Disclaimer
The findings in this report are not to be construed as an official
Department of the Army position unless so designated by other authorized
documents.
*»

Disposition
Destroy this report when it is no longer needed.
to the originator.

Do not return it

�Unclassified
SECURITY CLASSIFICATION Of THIS I*ACE
READ INSTRUCTIONS
BEFORE COMPLETING FORM

REPORT DOCUMENTATION PAGE
1. REPORT NUMBER

(fc

2. COVT ACCESSION NO.

3. R E S I E N T ' S CATALOG NUMBER

Technical Report 7906 •, V
J^ROBLEM DEFINITION STUDIES ONJPOTENTIAL

j

JNVIRONME^TAL POLLUTANTS, vii/PHYSICAL, ^CJBEMICAL,:
^JXiqOLOGICAL.AKD JIOLOGICAL PROPERTIES OF DDJ
'ID ITS DERIVATIVES^ ;
~~".

-

«. PERFORMING ORG. REPORT t^MBER
8. CONTRACT OR GRANT NUMBERf»;

Dickinson/Burrows
/T fw. Dick:
I /OS David R./Cogley
R
r
^~f William G./Light r~"

Jack C/ Dacre
Geoffrey/Woodard 1
NAME AND ADDRESS

O. PROGRAM ELEMENT. PROJECJ^T ASK
AREA « WORK UNIT N U M B S ^ ^

U.S. Army Medical Bioengineering Research and
Development Laboratory, ATTN: 'SGRD-UBG,
Fort Detrick, Frederick, MD 21701
H. CONTROLLING OFFICE NAME AND ADDRESS

U.S. Army Medical Research and Development Comtnan^
ATTN: SGRD-RMS
Fort Detrick, Frederick, MD 21701
*i"*"tv- »

L L

^^^- L j-^IP. ,

IIU

J.J. / VJX

14. MONITORING AGENCY NAME 6 AOORESSfl/ dlltettnt trom Controlling Olllce)

IS. SECURITY CLASS, fof Hit* rcporQ

UNCLASSIFIED
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16. DISTRIBUTION STATEMENT (at thlt Rtpott)

Approved for public release; distribution unlimited

17. DISTRIBUTION STATEMENT (ol th* mbtli-tst nnterfd In Block 30, It dlllorent from Rupert)

18. SUPPLEMENTARY NOTES

19. KEY WORDS (Contlnu* on rmvtrl* ila* It ne«»*»«iy and Identity by block number)

Amphibians
Analytical Methods
Bioconcentration
Biotransformation

Birds
Carcinogenesis
DDD
DDE

DDT •
Fish
Invertebrates
Mammals

Man
Metabolism
Microorganisms

iV\A BSTH ACT fCoaUaa* *a »»v»r»» •£&lt;*. H n&lt;KnH*JU]r nod Idmlllr fcr Wocfc numfcwj

This report is a data base of physical, chemical, toxicological, and
biological properties of DDT. Sufficient data are presented to allow a
preliminary assessment of the human health impacts and ecological impacts
of DDT at sites within the United States where DDT is found. Thia report
is intended to be used with chemical analysis data of DDT concentrations
in water, sediments, soils, and biota at particular sites of interest to
develop a qualitative assessment of potential hazard.
DD , KK. W3

EO moHo F , M o V «,so OSO L E T E

unclassifed
SeCOmTY CLASS! FICATtOH Of THIS PAGE (Mrm D*if £nf»»»d)

�ACKNOWLEDGMENT
The contributions of David R. Cogley and William G. Light to this report
were per f ormedyndfir U.~^~7trmjtsMedical Research and Development Command
Contract No. 4SAMD17~77-C-705o't^ Walden Division of Abcor, Inc., Wilmington,
MA. The human TWltrorrog JTlection of the manuscrilpt was reviewed by Dr.
Marcus Mason (Walden consultant) of Shrewsbury, MA. Guidance for the
.::
ecological impacts section was provided by Professor Charles F. Wurster
(Walden" consultant.) of the State University of New York at Stony Brook.
Geoffrey Woodard ^s consultant to the Environmental Protection Research
Division, U.S. Army Medical Bioengineering Research and Development
Laboratory.
.
Editorial assistance was provided by Franklin Research Center under
Contract No. DAMD17-79-C-9129, Marsha Hall, principal editor.

-1-

�TABLE OP CONTENTS
.

.

• •

-..:-...-•

-

Page

ACKNOWLEDGMENT . .. . . ., . . . . . . . . .... . .. . . . , , . . . 1
..
...
LIST OF FIGURES . .."...
3
LIST OF TABLES .. . . . ... . . .:v."V". . ... . . . i . "4
I.

INTRODUCTION . . •

5

Requirement for Report.
Format ..........'.........
.
Scope
..
Objective ................. . . . . . . . .
"
II. ALTERNATIVE NAMES
III.

..

7

PHYSICAL AND CHEMICAL PROPERTIES . . .

8

Composition of Technical DDT
Analysis

10
10

^
. MAMMALIAN TOXICOLOGY

10

Human Exposure
Laboratory Animals
V.

»•

VI.

STANDARDS AND CRITERIA FOR DDT

Air .......
Drinking Water and Food
Water for Aquatic Life
VII.

EFFECTS OF DDT ON A MODEL ECOSYSTEM

Manufacturing Practices . . .
Composite Hypothetical Site
Observed DDT Concentrations
Predicted Effects
Decontamination Objectives
VIII.

10
13

ENVIRONMENTAL CONSIDERATIONS

Behavior in Soil, Water, and Air ...'
Degradation
Bioaccumulation and the Food Chain
Effects on Terrestrial Animals.
Effects on Aquatic Organisms
Effects on Microorganisms

REFERENCES .

5
5
6
7

15

....

15
18
19
21
25
41
41

..... 41
41
42
42

...... 42
43
43
47
52
53

�LIST OF FIGURES

IV-1

Biodegradation of DDT. ...

IV-2

Further Degradation Products of DDT and DDE

V-l

Examples of DDT Bioaccumulation. .

V-2

Models of Bioaccumulation Pathways ..........

23

V-3

Effects of DDT on Frog Tadpoles

35

VII-1

Map of Model DDT Plant Site. ........... . . 44

VII-2

Biological Effects of Dietary DDT for Typical
Receptors
.......................

-3-

.....

......

.....

. . 16

......

17

.....

22

............

50

�LIST OF TABLES

1-1

Pollutants at Pine Bluff Arsenal

1II-1

Selected Physicochemical Properties of
Components of Technical DDT
.........

11

IV-1

Toxicity of DDT to Man

12

IV-2

Acute Oral Toxicity of DDT for Animals ;

V-l

Acute Toxicity of DDT to Birds

V-2

.

13

..

24

Concentrations of DDE in Bird Eggs Resulting
in 10% Reduction in Normal Shell Thickness ......

26

Acute Toxicity of p,p'-DDT to Fishes by
Static Bioassay

27

V-4

Sac-Fry Mortality for Various Fish Species

31

V-5

Acute Toxicity of p,p'-TDE to Fishes

33

V-6

Toxicity of DDT to Tadpoles. . .

34

V-7

Behavior and Morphological Abnormalities
of Tadpoles Exposed to DDT

36

V-8

Toxicicy of p.p'-DDT to Arthropods

37

V-9

Toxicity of DDT Isomers to Mosquito Larvae

39

V-10

Toxicity of p,p'-TDE to Arthropods

40

VII-1

Area and Wildlife Contamination Levels for
Various Sites

45

Environmental Concentrations of DDT at the
Model Site

48

lexicological Effects of DDT on Typical Wildlife as a Function of Concentrations of DDT in
Water, the Diet, and Tissues

49

Predicted Effects on Wildlife. .

51

V-3

VII-2
VII-3

VII-4

-4-

�I. INTRODUCTION
Requirement for Report
The U.S. Army Toxic and Hazardous Materials Agency (USATHAMA), formerly
the Office of the Project Manager for Chemical Demilitarization and
Installation Restoration, has identified an initial list of substances
requiring assessment because of their actual or potential presence in the
environment outside the boundaries of Pine Bluff Arsenal (PBA), Arkansas
(Table I-l).1 The U.S. Army Medical Bioengineering Research and
Development Laboratory (USAMBRDL) has divided the list into logical units
for problem definition studies. Substances used in pyrotechnic devices are
treated in two reports.*»' Thiodiglycol and elemental phosphorus have
been assessed previously in reports by Rosenblatt e_t_ al_.*»* and Dacre
and Rosenblatt;* a separate report on these substances specific to PBA has
been deferred indefinitely. DDT is considered separately here because (a)
it is neither military-unique nor installation-unique; (b) there is an
overwhelming amount of information available in the published literature;
and (c) most pertinent data have been suiwnarized in review articles. The
present report deals exclusively with DDT, its isomers and metabolites.

The format of this report departs from that of previous reports in this
series2"*'7»' because it incorporates both the data base and site-specific
TABLE I-l. POLLUTANTS AT PINE BLUFF APSENAL8
*"

DDT

Thiodiglycol
Phosphorus (white)
Auramine
Benzanthrone
1,4-Di-p-toluidinoanthraquinone
1,4-Diamino-2,3-dihydroanthraquinone
1-Methylaminoanthraquinone
a. As provided in Reference 1.

-5-

�considerations for a hypothetical installation. There are two reasons, for
this approach. First, Redstone Arsenal (RSA) also has major DDT contamination, and USATHAMA personnel have indicated that RSA data are as important
to their mission as PBA data. Second, contamination surveys and corrective
measures were initiated at both PBA and RSA while this report was in preparation. Thus, in view of the continuous output of new data, it appeared
neither practical nor useful to analyze site data for either installation.
Instead, a hypothetical site has been created (Section VII) to
illustrate the qualitative relationships of DDT levels in water, sediment,
and biota to effects of DDT on health and the environment. Quantitative
considerations for this site are derived from fragmentary data available for
PBA and RSA at the time this study was initiated. This section may be used
to estimate the potential ecological effects of DDT waste disposal relative
to past known or postulated declines in wildlife populations as well as to
the lower DDT concentrations in soil and water resulting from cleanup
operations. An important caveat must be given here. Concentrations of DDT
in soil, sediment, water, and biota, and the toxic effects predicted
therefrom, have been derived using concentration factors, i.e., the ratio of
DDT in sediment to DDT in water, DDT in biota to DDT in water, etc. To do
so is strictly valid only if these concentration factors represent true
equilibrium or steady state values. In very few cases are data sufficient
to make such a distinction, and for this reason, soil, sediment, water, or
food chain concentrations predicted to lead to a particular toxic effect may
be in error by an order of magnitude.

This report is ecologically oriented. Mammalian toxicology and human
health effects of DDT have been exhaustively reviewed in a 1979 document of
the World Health Organization (WHO).' Some representative data are
included in the present report, but investigators concerned with human
health aspects of DDT (and the tradeoff between health benefits and hazards)
should refer to the WHO text.
The volume of data on environmental effects of DDT has obliged USAMBRDL
to exercise considerable and arbitrary selectivity in choice of material to
review. For the most part, data relevant to the environments of south
central Arkansas and northern Alabama have been collected. The ecological
literature has been surveyed systematically through mid-1976 and selectively
thereafter. Because of the availability of many definitive reviews, efforts
concentrated on surveying the literature of the last ten years, and few
references published prior to 1970 were retrieved. In the case of aquatic
organisms, a search was conducted not only for DDT, but also for the seven
isomers and metabolites detected in the soil of PBA—p»p'-, o,p'-, and
m,p'-DDT; p,p'- and o,p'-TDE (ODD); and p,p'- and o,p'-DDE—and for
in,p'-TDE, m,p'-DDE, DDMU, and DDMS, metabolites not detected at PBA but
judged likely to be present (see Fig. IV-1 for structures). Throughout this
report, DDT (unprefixed) refers to the technical product, sometimes
designated DDTR in the literature.

-6-

�Objective
The objective of this report is to provide, to those charged with
assessment and amelioration of DDT contamination at Army installations,
guidance on the health and environmental hazards of DDT and the ecological
consequences of various actions.
II. ALTERNATIVE NAMES
DDT is the name approved by the International St&amp;iviards Organization for
the technical product of which p,p'-DDT is the predominant component. As
used in the present report, DDT refers to the technical product or any of
ten isomers or degradation products listed below.
DDT trade names: Anofex, Arkotine, Chlorophenothane, Dicophane, Estonate,
Gesarol, Guesarol, Neocid, Zerdane.
p,p'-DDT: 1 , l'-(2,2,2-trichloroe&lt;.-.hylidene)bis[4-chloro]benzene; o,o-bis(pchlorophenyl)-B,8,0-trichlorethane; 2,2-bis(p-chlorophenyl)-!,!,1trichloroethane; 4,4'-dichlorodiphenyltrichloroethane; l,l,l-trichloro-2,2bis(p-chlorophenyl)ethane.
o,p'-DDT: l-chloro-2[2,2,2-trichloro-l-(4-chlorophenyl)ethyl]benzene;
1,1,1-trichloro~2-(o-chlorophenyl)-2-(p-chlorophenyl.)ethane.
m,p'-DDT: l-chloro-3[2,2,2-trichloro-l-(4~chlorQphenyl)ethyl]benzene;
1,1,1-trichloro-2-(m-chlorophenyl)-2-(p-chlorophenyl)ethane.
p,p'-DDD: l,l'-(2,2-dichloroethylidene)bis[4-chloro]benzene;
l,l-dichloro-2,2-bis(p-chlorophenyl)ethane; p,p'-TDE.
o,p'-DDD: l-chloro-2l2,2-dichloro-l-(4-chlorophenyl)ethyl]benzene;
l,l-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane; mitotane;
o,p'-TDE.
m,p'-DDD: l-chloro-3[2,2-dichloro-l-(4-chlorophenyl)ethyl]benzene;
l,l-dichlorq-2-(m-chlorophenyl)-2-(p-chlorophenyl)ethane; n,p'-TDE.
p,p'-DDE: l,l'-(2,2-dichloroethenylidene)bis[4-chloro]benzene;
l,l-dichloro-2,2-bis(p-chlorophenyl)ethylene.
o,p'-DDE: l-chloro-2[2,2-dichloro-l-l(4-chlorophenyl)ethenyl]benzene;
1,l-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethylene.
DDMU: l,l'-(2-chloroethenylidene)bisl4-chloro}benzene; l-chloro-2,2-bi8(p-chlorophenyl)ethylene.
DDMS: l,l'-(2-chloroethylidene)bis[4-chloro]benzene; 2-chloro-l,l-bis(pchlorophenyDethane,

-7-

�PHYSICAL AND CHEMICAL PROPERTIES1*

III.
p,p'-DDT:

Chemical Abstracts Service Registry Number: 50-29-3
Toxic Substances List: KJ33250
Wiswesser Line Notation: GXGG YR DG&amp;R DG
Molecular Weight:

354.48

Molecular Formula:
Structural Formula:
CC1.

o.p'-DDT:
Chemical Abstracts Service Registry Number:
Toxic Substances List:

KH7910000

*" Wiswesser Line Notation: GXGG YR BG&amp;RDG
Molecular Weight: 354.48
Empirical Formula:
Structural Formula:

-K

789-02-6

�p,p'-TDE (DDD):

.

Chemical Abstracts Service Registry Number:

72-54-8

Toxic Substances List: KI0700000
Wiswessor Line Notation:
Molecular Weignt:

GYGYR DG&amp;R DG

320.0

Empirical Formula:
Structural Formula:
.CHC1.

p,p'-DDE
Chemical Abstracts Service Registry Number:
Toxic Substances Lint: KV9450000
Wiswesser Line Notation: GYGUYR DG&amp;R DG
Molecular Weight: 318.0
Empirical Formula:
Structural Formula:
CCL

/"*~~~\

ci—(\

/V-c-

-9-

72-55-9

�Composition of Technical DDT
DDT is the name approved by the International Standards Organization for
the technical product of which p,p'-DDT is the predominant component.
Pure p,p'-DDT is a colorless crystalline solid, whereas the technical
material takes the form of a white or cream-colored waxy solid or amorphous
powder.
Technical DDT is a mixture of isomers containing 65 to 80% p,p'-DDT and
up to 14 other components. The major impurities are o,p'~DDT (15 to 21%);
p,p'-TDE (&gt;4%; l-(p-chlorophenyl)-2,2,2-trichloroethanol (&gt;1.5%); traces
of o,o'-DDT and m,p'-DDT; and traces of bis(p-chlorophenyl)sulfone. On
exposure to sunlight or alkaline conditions, p,p'-DDT is converted to stable
p,p'-DDE, which may constitute a significant fraction of any environmental
sample.
Physicochemical properties of the pure substances comprising technical
DDT are summarized in Table III-l.
Analysis
No attempt has been made to review analytical methods for DDT. Approved
methods for detection and estimation of DDT and its derivatives in
environmental samples (soil, sediment, water, and tissues) have been
compiled by the U.S. Environmental Protection Agency, and are subject to
frequent revision. l ; »l *
IV. MAMMALIAN TOXICOLOGY
Human Exposure
was introduced in 1945 for t^e control of malaria mosquitoes. It is
a highly potent contact poison of the nervous system in insects. It is very
stable, so it persists, offering continuous protection for many months after
a single application. During World War II, DDT was widely used to prevent
insect vector-borne disease among troops, prisoners, and refugees. DDT vas
.applied directly to the skin and clothing in concentrations as high as 25%
in powder form. Despite these massive exposures, very few, if any,
authentic cases of human poisoning have been observed as a result.1* DDT
is moderately toxic to man by oral administration; Table IV-1 gives dosages
and expected or observed effects in man.
Laws £t £l. "» ls conducted extensive tests on 35 individuals
employed in the manufacture of DDT who had been exposed from 16 to 25 years
(21 years median) to amounts up to 18 mg per person per day. Phyi ical
examinations, medical histories, and liver function tests failed to reveal
any evidence of an untoward effect on human health. Experimental work on
human volunteers has not produced convincing evidence that DDT is harmful to
man at exposure levels 100 times those likely to be encountered in the
workplace or environment.1""1*
Despite extensive studies over the past 30 years, the exact mechanism of
DDT1 s toxic action in man is still uncertain. Based upon studies primarily
-10-

�TABLE tlt-l.

SELECTED PtnrSICOCHEHICAL PROPERTIES OF COMPONENTS OF TECHNICAL DDT

Pure Substance! Comprising Technical DDT
Property
Description
Melting point
Boilidg point
Solubility

Molecular .sight
Molecular formula
Volatility
Chenical
. reactivity
and atability

p,p'-DDT

o,p'-DDT

White, crystalline solid
Colorless crystal*
74.2*C
108.5*C
185*
Practically insoluble in water
Water, 0.085 ng/1 at
(1 vg/1), moderately soluble in
25'C; soluble in fat
hydroxylie and polar solvent!, readily and most organic solvents
soluble in most aromatic and
chlorinated solvents
354.5
354.5
Vapor pressure • 1.9 x 10"' Torr
at 20*C
Dehydrochlorinated at temperatures
Stable in concentrated
above its melting point into
sulfuric acid
ethylene derivative (DDE), a
reaction catalyzed by ferric and
aluminum chloride and by UV light.
In solution, it is readily
dehydtochlorinated by alkalis or
organic bases; otherwise it is stable
being unattccked by acid and alkaline
permanganate and by aqueous acids and
alkalis. With technical DDT.-dehydrochlorination may proceed at temperatures »« low as 50*C

p,p'-TDE (ODD)

p.p'-DDE

Colorless crystals
109'-110*C

White, crystalline solid
88.4*0

Similar to p,p'-DDT

Hater, 0.12 mg/1 at 25*C;
soluble in fat snd most
organic solvents

320.0

318.0

Similar to p.p'-DDT,
but it is more slowly
hydrolyzed by alkalis

Stable in concentrated
sulEuric acid. It may be
oxidized to p.p'-di'-Morobenzophenone•, a r« ction
catalyzed by UV radiation

�in laboratory animals, using relatively massive doses, it has been
speculated that DDT affects the metabolism of some of the biogenic
substances in the central nervous system and some of the carbohydratemetabolizing enzymes in the uterus, kidney cortex, and liver. The microsomal enzyme systems in the liver and possibly other tissues are increased
when exposure levels become sufficiently high.17 The occurrence of enzyme
induction in man at current environmental exposure levels has not been
established.
Human exposure to DDT has resulted in no reported cases of cancer or
other neoplasms, although carcinogenesis has been demonstrated in some
laboratory animal species. Feeding DDT to men for nearly 2 years did not
result in tumors,18 and no tumors were found in men whose occupation w&amp;s
the manufacturej formulation, or application of DDT." (However, the
latency period for appearance of cancer in humans may exceed the 35 years
since DDT was introduced.) The U.S. Environmental Protection Agency*' has
estimated an upper-limit lifetime cancer risk of 1 in 10^ for males
consuming 7.3 x 1CT* tng/day (10 ng/kg/day) of DDT. This estimate is
derived from the observation that Jewish males in Israel have higher fat
levels of DDT than males in New York State (16.S3 versus 9.04 ppra) and that
the lifetime incidence of nervous system cancer is correspondingly higher
(1.1 versus 0.5%). It is based on the assumption that cancer resulting from
DDT it^estion will be expressed in humans solely in the nervous system and
on tie admittedly unsupported corollary that the excess incidence of .nervous
system cancer results solely from excess DDT consumption.
TABLE IV-1.

TOXICITY OF DDT TO MANa

Dosage
(mg/kg/day)

mg
70-kg person

Remarks

Unknown''

—

Fatal

16-286b

1,100-20,000

Vomiting at higher doses, convulsions
in some

6-10b

400-700

Moderate poisoning in some

0.5

35

Tolerated. Periods lasted 21 months
with volunteers, 6.5 years with
workers

0.25 (inhalation ?) 18

Tolerated by workers for 19 years

a. Adapted from Jukes.1*
b. Precise dosage unknown.

-12-

�Laboratory Animals
Acute Toxicity.' Data on the acute toxicity of DDT to mammals are
summarized in Table IV-2.*1 These data indicate that the short-term
toxicity to mammals is moderate to high, depending on the mode of ingestion,
and that DDT i • generally more efficiently absorbed from the gastrointestinal
tract when dissolved in an oil vehicle.
TABLE IV-2.

ACUTE ORAL TOXICITY OF DDT FOR ANIMALS8

» tug/kg
Species

Water Suspension
or Powder

Oil Solution

Rat

500-2,500

113-450

Mouse

300-1,600

100-800

Guinea pig
Rabbit

2,000
275

250-560
300-1,770

Cat

100-410

Dog

&gt;300

From Hayes.*1

Careinogenicity. Carcinogenesis experiments have been performed in
which rodents were fed DDT at concentrations ranging from 2 to 1,650 pptn.**"'1
There appear to be wide ranges in susceptibility to DDT-induced carcinogenesis for different mammalian species and strains. Other studies have
found that no increase in tumors was induced by feeding DDT to golden
hamsters,11 and no tumors vere induced in a small number of dogs and
monkeys.1* DDT, TOE, and DDE were tested in the National Cancer Institute
Bioassay Program. The summary of their results follows.11

-13-

�"Bioajsays of technical-grade DDT, TDE, and p,p'-DDE for possible
carcinogenicity were conducted using Osborne-Mendel rats and B6C3F1
mice. Each compound was administered in the feed, at either of two
concentrations, to groups of 50 male and 50 female animals of each
species. Twenty animals of each species and sex were placed on test as
controls for the bioassay of each compound. The time-weighted average
high and low dietary concentrations of DDT were, respectively, 642 and
321 ppm for male rats, 420 and 210 ppm for female rats, 44 and 22 ppm
for male mice, and 175 and 87 ppm for female mice. The time-weighted
average high and low dietary concentrations of TDE were, respectively,
3294 and 1647 ppm for male rats, 1700 and 850 ppm for female rats, and
822 and 411 ppm for male and female mice. The time-weighted average
high and low dietary concentrations of DDE were, respectively, 839 and
437 ppm for male rats, 462 and 242 ppm for female rats, and 261 and 148
ppm for male and female mice. After the 78-week dosing period there was
an additional observation period of up to 35 weeks for rats and 15 weeks
for mice.
"There were significant positive associations between increased
chemical concentration and accelerated mortality in female mice closed
with DDT and in both sexes of rats and in female mice dosed with DDE.
This association was not demonstrated in other groups. There wr.s,
however, poor survival among control and dosed male mice used in th.5
bioassays of DDT and DDE. In all car.es adequate numbers of animals in
all groups survived sufficiently long to be at risk from late-developf • •}
tumors.
"When those male rats receiving TDE and their controls were combined
within each group so that the numerators of the tumor incidences
represented those animals with either a follicular-cell carcinoma or a
follicular-cell adenoma of the thyroid, the incidence in the low dose
group was significantly higher than that in the control. There was a
significant positive association between the concentration of DDE
administered and the incidences of hepatocellular carcinomas in male and
female mice.. Among dosed rats and mice no other neoplasms occurred in
statistically significant incidences when compared to their respective
control groups.
"Under the conditions of these bioassays there was no evidence for
the carcinogenicity of DDT in Osborne-Mendel rats or B6C3F1 mice, of TDE
in female Osborne-Mendel rats or B6C3F1 mice of either sex, or of
p,p'-DDE in Osborne-Mendel rats, although p,p'-DDE was hepatotoxic in
Osborne-Mendel rats. The findings suggest a possible carcinogenic
effect of TDE in male Osborne-Mendel rats, based on the induction of
combined follicular-cell carcinomas and follicular-cell adenomas or the
thyroid. Because of the variation of these tumors in control male rats
in this study, the evidence does not permit a more conclusive
interpretation of these lesions. p,p'-DDE was carcinogenic in B6C3F1
mice, causing hepatocellullar carcinomas in both sexes."

-14-

�Mutagenicity. The fact that DDE is tnutagenic in mammalian cells" and
DDT is not suggests that the proximate carcinogen is DDE, a metabolite of
DDT. It has been shown that chlorinated hydrocarbon carcinogens, such as
carbon tetrachloride and dieldrin, are negative in the standard Ames test.
These materials presumably require metabolic activation, possibly dehalogenation, for mutagenic activity. Because the Ames test includes only metabolic
activation mediated by the liver microsomal system and dehalogenation is not
so mediated, it is reasonable that pure DDT is negative in the Ames test.
Metabolism. The principal pathways for DDT metabolism are depicted in
Fig. IV-1, with lesser pathways presented in Fig. IV-2. It is important to
note that DDD and DDE arise by independent mechanisms and that DDE is
relatively inert. Hence, environmental DDT samples will show increasing
percentages of DDE with time where use of DDT has been discontinued.
Equivalent metabolites arising from the o,p'-DDT isomer in technical DDT
also appear in residues. The biological transformation of DDT is further
discussed in the following section of this report.
V. ENVIRONMENTAL CONSIDERATIONS
The literature on the toxicology, ecology, environmental fate, and
bioaccumulation of DDT is extensive and has been comprehensively reviewed
elsewhere, notably by Brown,'* Edwards,** Matsumura," Tahori,*7
White-Stevens," and Wurster and coworkers."'112 Information on the
environmental fate of DDT and the bioaccumulation of DDT in the food chain
is summarized in the following subsections.
Behavior in Soil, Water, and Air
To summarize, factors affecting the behavior of DDT in soil, water, and
air include low water solubility, ease of adsorption on soil, chemical
reactivity (p,p'-DDT conversion to p,p'-DDE), low vapor pressure, and ease
of uptake by plants and animals. When present in soil, DDT tends to remain
for years, acting as a long-lived reservoir for gradual release to surface
waters and biota. When present in surface waters, DDT is assimilated
rapidly by aquatic organisms and i,;. accumulated in the food chain.
Evaporation into the atmosphere also occurs. Atmospheric transport leads to
low (background) concentrations over wide geographic areas. Worldwide,
rainwater DDT levels fall in the range from 0.018 to 0.066 ppb.'
Although practically insoluble in water, DDT readily adsorbs to
particulate material in aquatic systems. In addition to accumulation
through the food chain, DDT may be incorporated into aquatic organisms by
direct contact with DDT-containing water or through ingestion of particulate
matter containing DDT.
DDT may enter an aquatic ecosystem by physical, chemical, or biological
transport. Atmospheric transport and erosion of contaminated solids appear
to be the most frequent routes. Eventually, the DDT tends to reach the

-15-

�DDE
R-C-R
(1

cc.i

t

R— CH

p __* R-CH-R —-»-R—C— R
.

1

1

CCI,

CHCIj

DDT

DDD

-

»^ R— CH — R

a R—C— R
»~

II
CHCI

1
CH2C!

II
CH,

DDMU

DDMS

DDNU

R-CH-R —-*- R— CH— R —-^- R^CHj— R —-»- R— CH— R CH2OH

COZH

DDOH

DDA

OH

DPM

DBH

Fig. IV-1. Biodegradation of DDT (R=C,H4CI)

-*•"-§-'
O
DBP

�R—CH—R
I
CC1,
DDT

OH
t
-R-C-R
I
CGI,

and

Kelthane

R-CH—R
I
CN
DDCN

CCb

OCli

DDE

Fig. tV-2. Further Degradation Products of DDT and DDE (R-C.H«CI)

CCI,

�water surface where it can co-distill with water and reenter the atmospheric
cycle. As noted earlier, DDT is converted to DDE by sunlight. Various
organisms also convert p,p'-DDT to p,p'-TDE and p,p'-DDE, the latter being
the most abundant DDT compound in the environment. For the purpose of this
review, the three compounds are considered collectively, unless specified
otherwise.
The amount of DDT that runs off into water bodies depends on the degree
of slope of the ground, the fineness of the ao'j.. ind th«» degree of vegetation cover.*8 Water transport of DDT depe: v. on .•rision runoff because DDT
is strongly adsorbed to soil particles. Dv. SVfo.uiMjs so tightly bound to
soil particles that it does not rea-'ily le.;ci LM'JV groundwater.** Nonpolar
compounds such as DDT either reach Che aqt-.-r,/r sink adsorbed onto soil
particles in the runoff or, when directly .ip\&gt;!Leil '&lt;.c water, become adsorbed
onto the suspended matter.
When a pond was treated with DDT at 0.02 '. vi, an Tfective concentration
for mosquito control, the DDT disappeared from the water after 3 weeks and
was found in the mud for 8 weeks after the treatment.** Greater amounts
of DDT reach the bottom of a water body when the sedimenting material is
composed of fine particles.*5
The stability of DDT in soil has been studied by Guenzi and Beard, who
have also reviewed the subject.**'** The rates and products of degradation
are dependent on temperature, oxidation-reduction potential, and moisture
content of the soil. In aerobic soils, DDT is converted to DDE by a
predominantly chemical process.** In anaerobic soils, the products are
TDE and its transformation products.***** In dry aerobic soils, DDT
is stable; loss is very slow by either degradation or volatilization.*'**7
Degradation
Reviews by.Fries** and Rhead51 summarize much of our knowledge
concerning the natural degradation of p,p'-DDT. A proposed scheme for
partial biodegradation of DDT is presented in Fig. IV-1. Although the
metabolites have all been identified, the pathway depicted must be considered only representative because no single organism has been found to
produce all the metabolites (with the possible exception of Aerobacter
aerogenes'*), and it is likely that different organisms emphasize
different pathways. TDE is by far the most prevalent metabolite of bacteria
and fungi, whereas phytoplankton species produce small amounts of DDE only.
Only TDE has been isolated from the intestinal microflora of the northern
anchovy (Engraulis mordax).* * Two other minor products of microbiai
degradation of DDT are Kelthane and DDCN (Fig. IV-2), although the latter
may result in part from chemical degradation. It should be emphasized
that complete biodegradation of DDT proceeding via a series of hydrodechlorination steps, as in Fig. IV-1, requires both anaerobic and aerobic
conditions.

-Itt-

�Fish that have received DDT by intravenous injection,** feeding,**
cr uptake from water produce TDE and DDE in various proportions in addition
to some DDMU. Brook trout receiving intramuscular DDT are reported to
produce only DDE.*' -DDT administered to lobsters (Homerus americanus) by
intravascular or oral routes is converted to TDE, DDE, and DDA.*7
Sheridan has shown that DDT concentrated from the water is converted to TDE
and DDE in the hepatopancreas of the blue crab, Callinectes sapidus.**
Lower aquatic invertebrates convert DDT to TDE, DDE, and other metabolites,
but daphnids are reported to produce only DDE.** Zinck and Addition have
noted that p,p*-DDE is probably a metabolic dead end.*' However, ringhydroxylated metabolites of DDE, shown in Fig. IV-2, have been isolated from
the fat of the guillemot (Uria algae) and grey seal (Halichoerus grypus).* *
Fries has reviewed data indicating that o,p'-DDT is degraded to o,p'-TDE
by mechanisms and rates similar to those for p,p'-DDT.*° It is likely
that the degradation pathways presented in Fig. 1V-1 are followed.
DDT may also undergo chemical degradation. Photolysis is reported to
convert DDT to TDE, DDE, DBF, and p,p'-dichlorobiphenyl, and heat also
converts DDT to TDE and DDE. DDT is unchanged after 8 weeks in river
water.'1
Bioaccumulation and the Food Chain
%
The direct accumulation of DDT from water may, in certain cases, make
the additional uptake from food insignificant. The algae and bacteria in
water are very efficient concentrators of DDT; their small size, and
consequently high surface-to-mass ratio, results in rapid and thorough
adsorption.** For example, bacteria concentrated DDT from 1 ppb in water
to 1,140 to 3,400 times that within 30 minutes,'* and freshwater algae
concentrated DDT from 1 ppm in water to 130 to 270 ppm in their cells within
1 week.'8 When exposed to DDT in water at concentrations between 50 and
100 ppt for 3 days, aquatic arthropods achieved increases in concentration
ranging from 3,000 to 114,000 times.'* When exposed to DDT in salt water
for 2 weeks, the Atlantic croaker concentrated 0.1 ppb by 40,000 times.'*
Brown trout exposed to 2.3 ppb and given DDT-free food for 3 weeks
concentrated the DDT in their tissues by 3,000 times."
DDT, applied onca at the rate of 1 Ib/acre (1.12 kg/ha), persisted in
the soil of Maine forests with little change throughout a 9-year period.'*
Robins li"v .- in the forest had higher DDT levels than those in surrounding
areas, indicating a period of continuous availability of residues through
the food chain, as shown in the following table:

-19-

�Robin Body DDT
Concentration (ppm)

Time of Analysis

13.53
4.50
3.55
0.47

1 year after treatment
3 years after treatment
9 yearn after treatment
Untreated areas

DDT applied to a forested area in Montana at the rate of 0.5 Ib/acre
(0.56 kg/ha) resulted in the following concentrations in the blue grouse.**

Concentration
in Fat (ppm)

Time of Analysis

80
22
18

Within 1 week of spraying
1 year after spraying
2 years after spraying

Predatory or fish-eating birds usually have higher DDT residues than
seed-eaters. Alaskan peregrine falcons, which feed primarily on birds,
contained far higher residues than the small birds in their area.i?«**
Scaup, which feed more heavily upon animal material than mallards,
accumulated residues that were 2 to 4 times as great when both were placed
on a DDT-treated marsh for the same periods of time.'*
Various small mammals were collected in Maine forests after a single
application of DDT at the rate of 1 Ib/acre (1.12 kg/ha).'* In the year
of treatment, shrews, mice, and voles contained an average of 15.6, 1.1, and
1.1 ppm, respectively. The relative differences between shrews and the mice
and voles prevailed throughout the years after treatment. In the same
areas, mink, which are carnivorous feeders like the shrews, accumulated
higher totcl DDT residues (8.5 ppm) in the first year of treatment than
hares (0.08 ppm). For areas treated seasonally with DDT, residues in small
mammals increased and decreased seasonally in relation to the treatment
times.
Food Chain. The bioaccumulation of DDT in the food chain is primarily a
consequence of its stability and high fat solubility. In the food chain,
energy is transferred from one trophic level to another. In general terms,

-20-

�only about IOZ of the energy in one troph.lc level will be transferred to the
next level, and the rest will be respired or released as wastes.•'
Chemicals that are preferentially taken up by living organisms and stored
for extended periods, svh as DDT and its derivatives, tend to be
concentrated in the foou chain. Examples of DDT bioaccunulation in the food
chain**"71 are displayed graphically in Fig. V-l.
A review of the extensive literature on aquatic and terrestrial food
chains is given by Brown.** These studies are based on measurements of
the DDT content in the environment (e.g., soil and water) as well as
measurements of the DDT content in tissues of various wildlife species. It
would be advantageous and would simplify an environmental assessment if it
were possible to relate the concentrations of DDT in the environment (viz.,
in soil and water) to the toxicological impact on wildlife by using
established factors for DDT bioaccumulation and translocation through the
food chain. Once the bioaccumulation factors were determined, it vould be
possible to relate toxicological effects at dietary concentrations to soil
and water concentrations. This relation could be represented by bioaccumulation pathway models, such as those shown in Fig. V-2, The bioaccumulation
factors given in Fig. V-2 were estimated from limited actual data for the
purpose of demonstration and should be considered hypothetical.
Although attempts have been made to predict mathematically the behavior
of DDT introduced into the environment,7* the predictive capacity and
utility of these models suffer from the enormous complexity of the
environment. Due to the many concomitant variables (e.g., environmental
site differences, species and strain differences, wide ranges in DDT base
concentrations, and different lipid/water partition coefficients and
equilibrium factors), it is not possible to establish categorically DDT
bioaccumulation factors that have a reasonable level of significance for all
ecosystems of the world. It is important to consider each environmental
setting individually.
Effects on Terrestrial Animals
Mammals. No information was retrieved concerning the effects of DDT on
mammalian wildlife. As noted in Section IV, acute toxicity for mammals is
low in terms of likely environmental concentrations. Data from laboratory
studies of mice indicate that teratogenesis and carcinogenesis could result
in mammalian wildlife exposed to DDT, but this has not been confirmed by
field studies. Likewise, there is no field evidence to indicate DDTassociated reproductive failure in mammals.
The high fat solubility of DDT may pose a threat to hibernating
insectivores and other mammals that are exposed to high levels of dietary
DDT and that release large amounts of DDT to the bloodstream from body fat
during periods of high activity and scant food supply. Such DDT releases
have been observed for bats containing certain chlorinated hydrocarbon
insecticides in their tissues and might also occur for mammalian carnivores.

-21-

�sea water
(0.1 ppb)

sea water
(0.1 ppb) '
sea water
(1 ppb)

40 days

oyster
(7ppm)

"7555

hooked mussel
(0.126 ppm)

1.260X

hard shell clam
(0 6ppm)

600X

'

sea water
ppb)

11 fish species
"(12-20 ppm)
phytoplankton

estuarlne waters
dppb)

2QOX

tidal marsh
surface water
(0.3 ppm)

lake sediments
(0.014 ppm)
pond
(0.02 ppm)
water
(1 ppm)

... .
»_ d'tcn

30X

3.4 ppm

drywt.

«^.. Insects
^..Insects
(0.41 ppm)
(0.41 ppm)

22QX

fish
(is ppm)

&lt;AV
&lt;ftY
10X

22X

75 ppm

drywt.

-

porpoise
(100 ppm)

^. 4 species of algae
(220 ppm)

Fig. V-1. Examples of DDT Bioaccumulation

-22-

4-89 ppm

wetwt

j^. risn
_»^__»""»
g^flsh
j^.8""8
(3.8-5.8 ppm) ?xx (90 ppm, muscl
(3.8-5.8 ppm) 2OTV (9°. ppm. muscle
^' 2,411 ppm, fat)

^ rainbow trout (4.15 ppm)
black bullhead (3.11 ppm)
crayfish (1.47 ppm)

150X
ay

1Q-100X

...
»». sediment __^ vegetation _^. J«J •

v

(4ppm)

13X

birds

�Amphibians (tadpoles)

w»t«r

?l

"S.

200X

'\

A—

~_k»&gt; tarlnolrti

fla

if

7"

sediments

—'

Fish and Birds

yf plants

-*«-

birds

»*.

fish

water
sediments
soil

300X

10X

—£^ birds {predatory)

20X

worms

Land-Dwelling Mammals (herblvoi es and ctrnlvores)

soil ,

20X

*~ plants

25X

mammals (herbivore)
j mammals Carnivore)

Insects
worms

SOX

birds

/^"

Fig. V-2. Models of Bloaccumulatlon Pathways

-23-

�Birds. DDT and its metabolites are universally distributed so that
exposure is essentially continuous, and few, if any, birds are free from
these compounds. Although the acute toxicity of DDT to birds is low, direct
toxic effects occur due to bioaccumulation of DDT in birds and in their
food. The most serious hazard of DDT to birds is that of decreasing their
reproductive capacity through eggshell thinning. It is estimated that as
little as 67 ppb of DDE (the proximate agent) in the diet can cause a
substantial increase in embryo mortality due to eggshell failure. The many
instances of bird kills in woodlands sprayed with DDT are believed to be due
to secondary poisoning by the oral route and not to contact poisoning.**-••
However, the direct lethal toxicities of DDT to birds are low, as indicated
in Table V-l.
TABLE V-l.

ACUTE TOXICITY OF DDT TO BIRDS7 »

Speoies

Dosage Route

Toxic Effects

Mallard
Pheasants
Coturnix
Sandhill cranes

Oral , capsule
Oral , capsule
Oral , capsule
Oral, capsule

LD5Q &gt; 2,240 mg/kg
LD5Q a 1,296 mg/kg
LDso s 841 mg/kg
LD50 &gt; 1,200 mg/kg

Mallard
Pheasants
Bobwhites
Coturnix

Oral, 5
Oral , 5
Oral , 5
Oral , 5

LC50
LCso
LCso
LCso

Pheasants

p,p'-DDT, oral
Technical DDT, oral

days
days
days
days

» 850-1,200 ppm
* 300-700 ppm
» 600-1,000 ppm
• 400-600 ppm

LC5Q - 550 ppm
LCso * 935 PPm

The direct toxic effects of DDT to birds accompany bioaccumulation in
the birds' food. Although bioaccumulation is most pronounced for precatory
birds, it also can be significant for birds lower on the food chain. i?or
example, soil contaminated with 5 to 10 ppm DDT is sufficient for earthworms
to pick up 50 to 200 ppm, which could result in a lethal dose for a robin
(ca. 3 rag)."* High residues of DDT in bird fat and other tissues can be
mobilised to become lethal if the birds are starved or hyperactive."*
These processes reduce the adipose fat and release DDT into the body
circulation to concentrate in the nervous system. House sparrows with DDT
residues of 800 ppm in body fat displayed no adverse physiological signs if
well fed, but died if not well fed; the DDT mobilization engendered tremors
that further reduced fat and sent lethal concentrations into nerve and
brain.•*&gt;•* The minimum content of DDT in the brain at which death
occurs is 50 ppm for American robins and 60 ppm for house sparrows,'1
while it is 14 ppm for female ring-necked pheasants."

-24-

�Concerning reproductive e f f e c t s , a 30% decline in breeding pairs'of the
fish-eating osprey on the coast jf Connecticut in 1963 was found to be
associated with a high body content of DDT residues, especially DDE, 111 ***
The reproductive failure was later related to a reduction of the eggshell'
thickness due to contamination of the eggs by DDT and its metabolites.
Feeding experiments with mallards showed that 40 ppm of DDE in the diet
resulted in frequent shell cracking, leading to 40% embryo mortality and 75%
reduction in duckling production.* 5 A concentration of 20 ppm of DDT in
the diet of mallards resulted in 20% reduction in eggshell thickness.** A
concentration of 10 ppm of DDE in the diet caused 25% shell thinning in the
American sparrow hawk, 8 7 13% in the screech owl,'* and 18 to 29% in the
black duck." DDT in the diet of pheasants had little or no effect on egg
production or fertility, but hatchability and chick survival were reduced at
concentrations of 100 ppm or more." In bobwhite quail on a diet containing 100 ppm, egg production was normal, but fertility and hatchability were
reduced, and chick survival was eventually zero.*' In addition, high
dietary doses of DDT have reduced sperm production in cockerels'* and the
bald eagle. 9 *
It is generally accepted that DDE is the major shell-thinning factor,
because a linear inverse relationship between shell thickness and DDE content
of the egg has been demonstrated for the prairie falcon, herring gull,
doublt crested cormorant, brown pelican, and peregrine falcon.'**** In
general, whenever the residues induced eggshell thinning more than 10% below
the normal thickness, that bird population would decline.'* Concentrations of DDE that elicit this effect in various species of birds are
listed in Table V-2. The bird prey for one population of peregrine falcons
have whole body residues of 0.3 to 6*0 ppm DDE, whereas the f.it and eggs of
the falcons contain 560 and 15 ppm DDE, respectively.* 7 This concentration
factor of 2.5 to 50 for eggs, combined with an observed concentration of 8
ppm in peregrine falcon eggs for onset of reproductive failure (Table V-2).
corresponds to a dietary limit of 0.16 to 3.2 ppm. If the same concentration
factor is arbitrarily assumed for other birds, then the dietary threshold
for reproductive failure would fall in the range of 1.6 to 32 ppm for the
great blue heron, 0.05 to 1.0 for the osprey, and 0,02 to 0.4 for the brown
pelican. Based on the latter two birds being fish-eaters, it appears that
substantially lower levels of DDE (and hence DDT) in fish may be required to
assure the survival of these birds than to protect human health.
Effects on Aquatic Organisms
Because the proportions of the various isomers and metabolites of DDT in
different environmental samples are quite distinct, and because the
toxicological data base for aquatic organisms is large, every effort has
been made to identify the toxic effects associated with each specific isomer
or metabolite throughout this section.

-25-

�TABLE V-2.

CONCENTRATIONS OF DDE TN BIRD EGGS RESULTING IN 10%
' REDUCTION IN NORMAL SHELL Tl'.iCKNESS

Bird Species

DDE Concentration in Eggs
(ppm wet weight)

Double-crested cormorant

Reference

20

95

Prairie falcon

7

96

Brown pelican

1

97

t r e a t b l u e heron

80

71

Herring gull

70

71

A t l a n t i c gannet

25

71

White pel lean

10

71

Fish-eating osprey

2.4

99

Alaskan peregrine f a l c o n

8

68

Fish. The acute toxicity of p,p'-DDT to fishes has bee.i reviewed by
Pimentel71 and others. 18C ~ I •* Some representative data are presented
in Table V-3, which shows that the 96-hr LC50 for most fishes falls between
1 and 20 wg/1. Fish and Wildlife Service investigators at the Fish-Pesticide
Research Laboratory in Columbia, Missouri, report 96-hr LCs^'s in this
range for 18 common freshwater fishes.110 They also report that p,p'-DDT
is roughly three times as toxic to bluegills (Lepotnis macrochirus) at 7°C as
at 24°C. Macek notes that for most common formulations containing DDT and
other pesticides, acute toxicities to bluegills are additive.11* The low
LC5Q valiies may be due to the rapid uptake and concentration of DDT in
fish. For example, brown trout exposed to 2 ppb DDT can concentrate it
about 500 times in the gill tissues and about 3,000 times in the
muscle.*' The gills of 2-lb brown trout pass about 700 liters of water
per day. 11 * In addition, certain fish, such as catfish, appear to be
fairly tolerant to DDT under laboratory conditions, whereas in a natural
setting they may succumb through bottom-feeding at the sediment level.
Sublethal concentrations of DDT to adult fish may lower their
reproductive success because DDT accumulates in egg yolk and kills the fry
shortly after they hatch from contaminated eggs.'*»102 The DDT is passed
into the egg yolk, the embryo develops and hatches, and at the stage of

-26-

�TABLE V-3. ACUTE TCXICITY OF p,p'-DDT TO FISHES BY STATIC BIOASSAY

Temp.
Species
Rainbow trout
Salmo gairdneri

Exposure
Time
(hr) LCso (ug/O

7 (5-10)a
3.8 (3.4-4.3)
1.72 (1.42--2.09)
28
0.26

Reference

104
105
106
107
108

13
16
12.9

96
96
96
96
360

Brown trout
Salmo trutta

13

96

2 U-3)

104

Brook trout
Salvelinus fontinalis

13

96

7.4-11.9

106

Cutthroat trout
Salmo clarki

13

96

0.85-1.37

106

13
9-11
13

96
96
96

13

96

0.68

110

18
24
23

96
96
96

8 (6-10)
2.2 ( . - . )
1826
7

104
105
111

Redear sun fish
Lepomis nticrplophus

18 .

96

5 (3.9)

104

Largemouth bass
Micropterus salmoides

18

96

2 (1-3)

104

18
24

96
96
96

Coho salmon
Oncorhynchus kisutch

Chinook salmon
Oncorhynchus tshawytschak &gt; c
Bliiegill
Lepomis macrochirus

Goldfish
Carassius auratus
Carassius carassius

-27-

11.3-18.5
13
4 (3-6)

21 (14-30)
9.8 (7.3-13.2)
25

106
109
104

104
105
107

�TABLE V-3. (Cont.)
Exposure
Time
(hr) LC50 (ug/D

Species

Temp,
CO

Carp
Cyprinufl carpio

18

96

10 (7-13)

104

Fathead minnow
Pimephales promelas

18

96

19 (13-27)

104

18
24
26

96
96
24

16 (9-28)
13.5 (9-20)

104
105
111

Black bullhead
Ictalurus me las

18

96

5 (3-7)

,
104

Yellow perch
Perca flavescens

18

96

9 (7-11)

104

Channel catfish
Ictalurus punctatus

Mosquitofish
Gambusia af finis

34

Reference

96
96

20
27

112
111

Guppy
Poecilia reticulata

96

3

112

Mozambique mouthbreeder
Tilapia mossambica

96

7

112

Aholehole
Kuhlia sandvicensis^

96

3.9

112

Nehu
Stolephorus purpureus^

12

1.0

112

96

0.53 ( . 8 0 8 )
03-.4
0.9

1.13
110

Striped bass
Roccus (Morone) saxatilis^

Roccus (Morone) saxatilis^

17

96

-28-

�TABLE V-3. (Cont.)

Temp.
Species
Shiner perch
Cymatogaster aggregate

Exposure
Time
(hr)
LC5Q (wg/O

Re f erence

13
17

96
96

7.6
0.45

114
110

Dwarf perch
Micrometrus minimus^
Micrometrus minimus'' » c

13
18

96
96

4.6
0.26

114
110

White seaperch
Phanerodon furcatus^« c

19

96

0.74

110

English sole
Parophrys vetulus^* 0

16

96

0.91

110

Pacific staghorn sculpin
Leptocottus armatus"*0

19

96

0.98

110

Rubberlip seaperch
Rhacochilus toxotes^« c

19

96

1.01

110

Goby
Acinthrogobius flavimanusb» c

19

96

2.40

110

19
19
19
19
19

24
48
96
120
144

Speckled sanddab
C i th ar i ch t h y s 8tigmaeus^» c

a.
b.
c.
d.

•

10.0
7.2
3.7
1.7
0.9

Numbers in parentheses are 95% confidence interval.
Seawater.
Dynamic bioassay.
Brackish water.

-29-

110
110
110
110
110

�final yolk sac adsorption after hatching, the fry will die if the DDT concentration in the yolk is sufficiently high. 11T » l l i This phenomenon
was first observed in the lake trout of Lake George, New York; 1 1 ' and
later at Ja-jper, Alberta; 1 4 * Lake Taupo, New Zealand; 121 Lake
Michigan; 1 * 2 Sebago Lake, Maine; 111 and other locations.'* Data for
studies in these areas are listed in Table V-4 and indicate that DDT
concentrations in water a» low as 0.004 ppb can cause a significant increase
in sac-fry mortality.
No reports were recovered describing systematic studies of the chronic
effects of DDT on life stages of fishes. A DDT concentration of 5 mg/1 has
been shown to result in 4(!% mortality of carp embryos reared j.n vitro.' 2 *
Exposure of Atlantic salmon (Salmp sf.lar) eggs to 50 pg/1 of DDT at
gastrulation retards behavioral development in the newly hatched
alevins. 1 2 * The coughing frequency in juvenile coho salmon was found to
be enhanced significantly after 4 days' exposure at a sublethal concentration
of 5 ug/1. 1 ** High sublethal (0.3 to 3 ug/1) levels of DDT have been
found to result in loss of glycogen and other pathological changes in the
liver of 7 zebrafish (Br^chydanio rgrio) and, to a much lesser extent, of
guppy. 1 2 Interrupted exposure of salmon;d fishes to high sublethal
concentrations of DDT is reported to raise the lower lethal temperatures,
alter the temperature selectivity,12diminish learning ability, and affect the
central nervous system in general. ** 1 ** Continuous exposure to 110
Mg/^? for 4 days is said to alter the exploratory1'1 and locomotor *2
behavior of goldfish (Carassius auratus).
Desaiah e_t al. have presented evidence for 50? or greater inhibition of
activity of mitochondrial Mg2+ ATPase, an important energy-linked enzyme,
in brain homogenates of fathead 1
minnows chronically exposed to DDT at a
level of 0.5 ug/1 for 266 days. " There is also a substantial, although
lesser, drop in gill Na-K-ATPase activity. The latter enzyme functions in
osmoregulation in marine fishes, and in this regard, Leadem e£ ajU have
found that seawater-acclimated rainbow trout receiving 2.75 tng/kg DDT/48 hr
in their diet exhibit 1 impaired osmoregulation as well as inhibition of gill
Na-K-ATPase activity. '* Kinter £t al. have reported similar disruption
of osmoregulation in two marine species, mummichog (Fundulus heteroclitus)
and American eel (Angui11a rostrata), at lethal DDT concentrations. 111
Weisbart and Feiner report that goldfish (C. auratus) exposed to DDT at a
level of 17.5 to 35 wg/1 exhibited no clear" evidence for impaired
osmoregulation. 1 " This agrees with the observation of Leadem e£^l_. that
osmoregulation is unimpaired by DDT in the diet of the freshwater rainbow
trout.
•

The 90-dose (30-day) oral LD5Q for juvenile coho and chinook
(Oncorhynchus tshawytscha) 7 salmon have been reported as 64 and 27.5
ing/kg/day, respectively. 1 ^ Sublethal 1oral doses may result in loss of
light discrimination in rainbow trout. '*

-30-

�TABLE V-4. SAC-FRY MORTALITY FOR VARIOUS FISH SPECIES

Fish
Species

DDT Cone.
in Eggs
(ppm)

Effect

Estimated
DDT Cone.
in Water*
(ppb)

Reference

Lake trout

3-355

Fry containing more
than 3 ppm died at
the time of final
adsorption of the
yolk sac

0.03

119

Brook, rainbow,
and cutthroat
trout

&gt;0.4

30 to 90% sac-fry
mortality

&gt;0.004

120

Rainbow trout

5

45% sac-fry mortality

0.05

121

Coho salmon

1.1-2.8

15 to 75% sac-fry
0.011-0.028
mortality, respectively

122

The DDT concentrations in water were estimated using a concentration factor
of 100,000. The factor was based on data from a study with fathead minnows
reared in 2 ppb DDT for a 9-month period. DDT concentrated in their eggs
to more than 100,000 times the water concentration.1** This is the only
long-term study giving both egg and water concentrations that could be
found in the literature.

Fragmentary evidence indicates that o,p'-DDT is less toxic to fish than
p,p'-DDT. The 96-hr LC5Q for goldfish (C. auratus) t as measured by
Ginsburg, 1 ** is 1.0 mg/1 for o,p'-ODT, compared with about 0.06 mg/1 for
the p,p'-isomer. Gardner reports that brook trout fingerlings are unharmed
by 24-hr exposure to o,p'-DDT at a concentration of 0.05 mg/1, although
there is a noticeable effect on temperature selection at 0*02 mg/1, i.e.,
cooler water is preferred by exposed fish. 1 ** According to Alabaster, the
24-hr LC5Q for harlequin fish (Rasbora heteromo_rj)ha) ie 30 ug/1 for
o,p'-DDT, compared with 13 jig/1 for the~p,p"'-"Isomer.l* * No information
was retrieved for m,p'-DDT.

-31-

�Toxicity data for p,p'-TDE (ODD) have been reviewed by McKee and
Wolfe. 1 " Fragmentary evidence, presented in Table V-5, indicates that TDK
is highly toxic to fishes, although perhaps a half ovder of magnitude less
toxic than p,p'-DDT. Gardner has demonstrated that high sublethal levels of
TDE affect temperature selection by fingerling brook trout. 12 ' He further
reports that brook trout are unharmed by 24-hr exposure to o,p'-TDE at a
concentration of 50 yg/1, although there is some effect on temperature
selection at 10 pg/1. 1 ** No information was retrieved for m,p'~TDE.
Gardner has found that brook tr&lt; u; •".•..-• 'mharmed by exposure to 50 -;g/l
of p,p'-DDE for 24 hours and that there la almost no effect on temperature
selection. 1 ** Applegate et_ al_. re &gt;orc' Chat v^inbow trout, bluegills, and
the larvae of sea lampreys -(Pt£: y .;&gt;I • *},"',.*•'.&gt;• "£ arc ""affected by 24-hr
;
exposure to DDE at 5 mg/1 and 5:
' " o t h t j . s " report 96-hr LC^Q'B of 10
to 100 ng/1 for bluegills and rai'•);-w trout at 24° and 13°C, respectively. 11 *
No information was retrieved for m,p'-DDE.
Reptiles. No quantitative toxicity data were recovered, but Stickel has
stated that the box turtle population of a Maryland forest was not noticeably
affected by DDT applied at a dosage of 2 Ib/acre (2.2 kg/ha). 1 **
Evidence both for and against loss of reptiles through land application of DDT
is summarized by McKee and Wolfe. 1 ** Direct treatment of ponds at DDT
concentrations of 2 ppm or more has killed water snakes and turtles. 1 ** In
the Brazos River floodplain of Texas, where cottonfields had been heavily
treated with DDT, the average residues in the fat bodies of aquatic snakes
were DDE, 510 ppm; TDE, 1.5 ppm; and DDT, 16.0 ppm. 1 * Tine DDT residues in
the brain did not exceed 1.5 ppm, and fat-body residues in terrestrial snakes
were much lower than in aquatic snakes.1**
In vitro treatment of cellular fractions from various tissues of six
species of terrestrial turtles resulted in negligible to substantial
inhibition of Mg2*-, (Na + , K*)-, and (Na+, K + , Mg2+)-dependent ATPase
at DDT levels of 2 to 76 mg/l. 1 *** 1 ** Similarly, in vitro treatment of
cellular fractions from various tissues of the red-eared turtle, Chrysemys
scripta elegans, resulted in negligible to substantial inhibition of ATPase
at TDE or DDE levels of 2 to 76 mg/1. 1 **
Amphibians. For tadpoles of Fowler's toad (Bufo woodhousii fowleri) and
the chorus frog (Pseudacris triseriata), Sanders reports 24-hr LC5Q
habitat water values of 2.4 and 1.4 mg/1, respectively, 1 * 7 whereas a 96-hr
LC5Q of 0.27 mg/1 for bullfrog tadpoles is reported by Carter and
Graves. 1 1 1 Another reference gives a 96-hr LC$Q of 0.8 mg/1 for
5-week-old tadpoles of P. triseriata and 0.74, 1.0, 0.1, and 0.03811
mg/1 for
B. woodhoasii tadpoles of 1, 4 to 5, 6, and 7 weeks, respectively. *
These data are summarized in Table V-6. A lethal concentration of 0.15 mg/1
is given for Bufo bufo tadpoles. 1 ** Some relative and highly ambiguous
toxicity assessments based on DDT application data have been provided by
Pimentel 71 and Cooke. 1 **

-32-

�TABLE V-5.

Species

ACUTE TOXICITY OF p,p'-TDE (DDD) TO FISHES

Temp.
CO

Exposure
Time
(hr&gt; LC50 (pg/1)

Goldfish3

Reference

1,000

100

&lt;2,600
15,000

100
110

Channel catfish8

20
18

96
96

Bluegill*

24

96

Striped bassc
Morone saxatilis

17

96

Brook trout
Salvelinus fontinalis

10

24

45

128

Rainbow trout 3

13

96

43-93

110

Fathead minnow3

18

96

1,000-10,000

110

largetnouth bassa

18

96

39

110

Walleye 3

18

96

10-100

110

a.
b.
c.
d.

30b
&gt;10

2.5 &lt;1.6-4)d

100
110

113

Species not given.
Toxicity threshold.
Bioassay in saline water.
Numbers in parentheses are 95Z confidence interval.

Field studies showed that 0.1 kg DDT/ha applied as an emulsion did not
kill tadpoles, but 1.0 kg DDT/ha achieved 80% mortality in two days.1**
The toxic effects on frog and toad tadpoles o_ DDT sprayed in the field at
0.4 to 0.5 kg/ha is given by Cooke.1*' The DDT was sprayed on the water
surface,.as would be appropriate to kill mosquito larvae. Five water sites
were monitored. DDT concentrations in surface water and in water at a depth
of 20 cm decreased as the size of the water body increased, to the extent
that DDT was not detected (&lt;0.02 ppb) in water from the two larger sites.
The DDT residue concentrations and the behavioral and morphological
abnormalities of the tadpoles for the three smaller sites are summarized in
Table V-7. The residues were measured one day after spraying. It is
important to note that virtually all of the DDT sprayed was taken ui&gt; by
algae or incorporated elsewhere within only 3 days. Hence, the increases in

-33-

�the DDT levels in the tadpoles after the third day may be due to direct
ingeoiion of DDT-contaminated algae. A schematic diagram of behavioral
abnormalities versus time after spraying DDT is given in Fig. V-3. Average
DDT concentrations are derived from data of Table V-7 assuming that there is
a linear gradient of concentration with depth.
TABLE V-6.

:
Species

TOXICITY OF DDT TO TADPOLES

Exposure Time
(hr)

LC5Q (tng/1)

Reference

Bullfrog

96

0.27

111

Chorus frog

24
96

1.4
0.8

147
110

Fowler's toad

24

2.4

147

(1 week)
(4-5 weeks)
(6 weeks)
(7 weeks)

96
96
96
96

0.74
1.0
0.1
0.038

110
110
110
110

For tadpoles of Pseudacris triseriata and Bufo exposed to p,p'-TDE, 96-hr
LC50's of 100 to 1,000 and 18 jig/1, respectively, have been reported. 11 '
No other information concerning isomers or metabolites was retrieved.
Invertebrates. For the most part, only references dealing with nontarget
species were retrieved. Toxicity data for arthropods, taken from Pimentel's
review, 71 Malina's review, 1 " and some recent papers, are summarized in
Table V-8, which shows that marine and freshwater species demonstrate about
the same order of acute sensitivity to DDT as fishes, although ostracods
appear to be more resistant. There is also evidence for impaired reproductive
capability in ostracods, 15 ' brine shrimp, 1 ** and Daphnia at sublethal
levels. 1 ** Ingested DDT has been shown to be harmful to crayfish
(Procambarus clarkii), blue crabs (Callinec tes sapiduii), *» T »*"
and fiddler crabs (Uca pugnax),'* * but the reported data are not readily
quantified. Larvae of two caddisflies (Hydropsyche pellucidula and H.
instabilis) have been found to construct irregular webs when exposed to DDT at
sublethal levels (2.5 jig/1). 1 '* In field studies, it was found that when
an unprotected stream was sprayed directly with 1 Ib/acre (1.1 kg/ha), nymphs
of all species of mayflies were exterminated and larvae of every species o
caddisfly were affected to some extent. 1 *
.

-34-

�Normal

k /"
Estimated Average DDT Concentrations
In the Water
17.5 ppb

£

2.26 ppb
——• 0.57 ppb

Reslgnet

Dead

4

6
8
1 0
Days After Spraying DDT

Fig. V-3. Effects of DDT on Frog Tadpoles

-35-

12

14

�TABLE V-7.
Total Water Residues
One Day After
Spraying3
(ng/1)
20 cm below
Surface

BEHAVIOR AND MORPHOLOGICAL ABNORMALITIES OF TADPOLES EXPOSED TO DDT

DDT Levels in Tadpoles
(vg/g)

Behavioral and Morphological Abnormalities
Day 1

Small
Ditch

36.2

Day 14°

7.90

6.52

None left

Franticc

None

3.27

None left

Frantic

None

0.70

0.77

0.24

Some normal,
Some frantic

None

0.64

0.38

Frantic

None

1.16
0.83

0.52
1.23

1.07
1.97

Frantic
Frantic

None
None

Behavior

Day 14

Day 3

Day 2

0.99

Surface

Day 1

1.21

Site

Abnormalities

Behavioral

Abnormalities

Behavior

Abnormalities
__

Larger 10.5

17.5

4.9

Bitch

Fool

2.7

1.9

Resigned

All survivors-abnormal No survivors
snouts, 4/8 dead tadpoles had tails
laterally curled to
left
Some frantic, All survivors-abnormal No survivors
some resigned snouts
4 normal,
Few normal, None
1 moribund
most frantic,
few resigned
13 normal.
Most frantic, 2 dead tadpoles with
3 moribund
upturned tails
few resigned
Frantic
Frantic

None
None

Normal
Mormal

a. Other than the 0.19 wg/1 from below-surface sample of small ditch taken on Day 3, no residues were detected in water samples on
Days 3 and 14, ...cone. &lt;0.02 wg/1; spraying was uneven; two large sites had no detectable (&lt;0.02 vg/1) DDT in water.
b. Increases probably due to eating DDT-contaminated algae.
c. ?raittic • hyperactivity, greatly excited, frencied
Resigned » passive, submissive
Progressive stages of abnormal behavior.
Moribund - dying.
/
(All showed slow rite of metamorphosis.)

—
1 downcurved in
body and tail

1 with abnomial
snout ,
2 dovncurved
None
None

�TABLE V-8. TOXICITY OF p,p'-DDT TO ARTHROPODS

Species

Exposure
Time
(hr)

EC50 or LC50
(wg/l)

Reference

Sand shrimp

24

3

71

Seed shrimp
Cypridopsis vidua

48

54

151

Glass shrimp
Palaemonetes kadiakensis
Grase shrimp
Stonefly
Pteronarcella badia
Classenia sabulosa
Pteronarcys californica

,
Acroneuria pacifica
Waterflea
Daphnia pule*
Daphnia magr. a
Simocephalus serrulatus

4.2
2.3

48
96

12

24

151
110
71
•/

12
1.9
16
10
3.5
41
19
100
7.0
180

24
96
24
96
96
24
48
96
96
96

0.36-3.6
4
1
0.67
0.4

48
48
96
366
48

71
110
71
150
110
71
71
150
110
150
71
151
150
152
71

Os traced
Cyprinotus incongruena
Cypridopsia vidua

48
48

l,300a
230a

153
153

Brine shrimp
Artemia selina

48

46a

154

-37-

�TABLE V-8 (Cont.)
Exposure
Time
(hr)

Species
Crayfish
Procambarus acutas
Orconectes nais
(10-week)

Reference

48
96
96

•**
Gammarus fasciatus

22.5
1.0

151
110

4.7
4.0

151
110

24
48
96
48
96

Am phi pod
Gammarus lacustris

155
108
110

48
96

Sowbug
Asellus brevicaudus

3(7. 2)c
0.24
30

48
96

Damseifly
Ishnui-a verticalis

Hermit crab3

EC50 or LCjo
(pg/D

4.7
2.1
1.0
3.6
3.2

71
71
110
151
110
71

7
1.85

110

96

Purple shore crab
Hemigrapsus nudus
*-•
Market crab
Cancer magister'""

24
96

'

4.6

110

48

3.3-10

156

»
*
•

Brown shrimp
Crangon crangon

a. Species not given.
b. Extrapolated from author's data.
c. Value in parentheses for crayfish acclimated to natural, DDT-contarainated
water of an unspecified concentration.

-38-

�Although mollusks are not so readily killed by DDT, the growth of
eastern oysters is reported to be reduced significantly (and reversibly) at
a level of 0.1 wg/1, 7 1 and survival of the larvae of the American oyster
(Cr88803trea virginica) is diminished by 202 at a level of 25 yg/1. 1 ' 1
Annelids are so insensitive to DDT intoxication as to present a dietary
hazard to predator organisms. The 96-hr 1050 for the buffalo leach
(Hirudinari manillgnsis) exceeds 100 mg/l, 1 '* and tubeficid worms
(Branchiura sowerbv_i"&gt; are said to exhibit no mortality after 72 hours at a
level of 4 mg/l and 21°C, although they are completely destroyed when
exposed to the same concentration at 4.4° and 32.2°C. l f l The extrapolated
96-hr LC5o for a planarian (Polycel.is felina) is 1.26 mg/l at-6.5°C."*
Earlier data for invertebrates have been reviewed by McKee and Wolfe, 1 1 *
and some additional toxicity data are contained in Reference 108.
Fragmentary evidence, presented in Table V-9, indicates that o,p'- and
m,p'-DDT may be less acutely toxic to mosquito larvae than the p.p'-isomer.
No information concerning nontarget species was retrieved.
TABLE V-9. TOXICITY OF DDT ISOMERS TO MOSQUITO LARVAE

Anopheles quadrimaculatus* » • » » » • •

Isomer
p,p'-DDT

24-hr LC50
(Mg/D

48-hr LC50
(Wg/l)

Aedes aegypti'**

96-hr LCso
(wg/1)

&lt; 2.5

2.5

11

350

o,p'-DDT

15

10

ra,p'-DDT

15

&lt;10

a. 4th instar.
Data relating the acute toxicity of p,p'-TDE to arthropods are
summarized in Table V-10. Comparison of Tables V-8 and V-10 reveals that
for many arthropods TDE is equal to or greater in tox;city than DDT. McKee
and Wolfe have reviewed pesticide application data and note that the larvae
of Chaoborus (phantom midge) and gnats are "controlled" at 13 tc 14 vg/l
and chironomid (midge) larvae are temporarily eliminated.1** With a 96-hr
LCso of 740 vg/1, TDE is slightly more toxic to the freshwater planarian
Polycelis felina than DDT.1**

-39-

�The 96-hr LC50 of p,p'-DDE to the freshwater planarian Polycelis
felina is 1.23 mg/1, only slightly more than the corresponding value for
DDT."* No further information was retrieved concerning isomers or
metabolites.
TABLE V-10. ACUTE TOXICITY OF p.p'-TDE (ODD) TO ARTHROPODS

Species

Exposure
Time
(hr)

EC50 or LC50
(ug/D

Reference

Amphipod
Gammarus lacustris
Gammarus fasciatus

96
96

Sowbug
Asellus brevicaudus

96

Water flea
Paphnia magna
Daphnia pulex
Simocephalus nerrulatus

72
48
AS

0.1«
3.2
4.5

167
108
108

96
72

0.68
O.la

108
167

Mosquito (4th instar)
Anopheles quadrimaculatus

24

2

168

Stonefly
Pteronarcys californica

96

380

1C8

Glass shrimp
Palaemonetes kadiakensis

0.64
0.86
10

a. Sublethal effects.

-40-

108
108
108

�Effects on Microorganisms
Luard has reviewed, in part, the literature on DDT toxicity to
freshwater and marine phytoplankton, and notes evidence for a wide range of
sensitivities. 1 *' Other data are contained in Reference 108. A few
marine species exhibit inhibition of photosynthesis at 1 to 10 yg/1, but
in general there is no e f f e c t on growth at levels below 100 ug/1 (see also
Pimentel 7 1 ). A recent study shows an even higher level of resisti.--** in
Euglena.' 7 *
Bacteria also appear to be resistant to DDT. The growth of Bacillus
megaterium in nutrient medis is unaffected by 100 mg/1 of DDT, although the
death rate of resting cells is measurably enhanced at 1 mg/1. 1 ** Growth
of Azotobacter^ chrooc occum is said to be unchanged in the presence of 400
mg/1. l7z The growth rated of Pseudomonas fluorcscens and Staphylococcug
aureus, but not Escherichia coli, are noticeably inhibited at 50 mg/1. 1 ''
It is probably safe to assume that microorganisms will be unaffected by
p,p'-DDT at levels selected to protect fish and invertebrates.
The chernolithotrophic nitrofier, Nitrobactor agilis, is completely v
inhibited by TDE at a concentration of 10 tng/l and measurably inhibited at
0.1 mg/1. 17 *
% DDE (as well as DDT) at a concentration of 10~6 to 10~5 M (0.35 to
3.5 mg/1) is said to inhibit photosynthetic electron transport in the green
algae Codium fragile and Chaetomorpha area^ and in isolated chloroplasts. 1 **
DDE is reported to be more toxic than DDT to the marine dinoflagellate
Exuviella baltica, causing significant growth inhibition at levels as low as
0.1 u g / 1 . 1 7 3 N o other information concerning isomers or metabolites was
retrieved.
*"

VI.

STANDARDS AND CRITERIA FOB DDT

Air

Threshold limit values for the workroom environment: 17 *
Time-weighted average: 1
Short-term exposure limit:

3

ink in g Water and Food
Allowable daily intake:* 0.005 mg/kg/day
Maxiuium concentration in fish and agricultural products for interstate
commerce: 177 5 ppra

�Water f or Aquat ic Lif e

-

EPA recommended criterion:20 0.00023 l»g/l (24-hr average) and
0.00041 (not to be exceeded at any time)
VII.

EFFECTS OF DDT ON A MODEL ECOSYSTEM

A model ecosystem is used here to illustrate the effects of DDT waste
product disposal at U.S. manufacturing sites operated from the mid-1940's to
the late 1960's. Data that would accurately and completely define the
extent of the hazards resulting from DDT contamination at particular sites
are not available. Thus, a hypothetical site was created to demonstrate an
approach for relating toxicological and ecological data to levels of
contamination and to demonstrate the types of data required for establishing
such a relation. The model site was developed from limited data available
from actual contaminated sites*7*""1*11 and from hypothetical circumstances
(such as geology and hydrology) offered for the purpose of demonstration.
The following topics are considered: manufacturing practices, composite
hypothetical site, observed DDT concentrations, predicted effects, and
decontamination objectives.
Manufacturing Practices
The contaminated areas of primary concern are those in the vicinity of
sites previously used for the manufacture of DDT, typically following World
War II until the late 1960's. As a result of manufacturing, handling, and
disposal practices prevalent then, large quantities of DDT and its isomers
and analogs were conveyed by surface water runoff through drainage ways into
traversing E-treams that empty into lakes and major rivers. Depending on the
manufacturing site, the methods of DDT handling and storage, and the time
manufacturing ceased, theie are wide ranges of possible levels of site
contamination. During the manufacturing period, it is possible that tons of
DDT in th« form of blocks were present on the ground surface, readily
accessible to leaching. After the plants were closed, massive quantities of
DDT were either disposed of in burial sites and landfills, destroyed by
incineration, or simply left on the ground surface.
The DDT residues in areas surrounding manufacturing sites built up over
the years as process water containing DDT was discharged to settling ponds
or ditches. Analyses of soil, sediment, water, and biological samples
showed that undegraded DDT at some sites was being leached to surrounding
areas. For example, fish caught in a major river about one mile from a
contaminated site contained as much as 500 ppm DDT, two orders of magnitude
greater than the maximum concentration allowable for interstate commerce.
Biological surveys of the streams in contaminated areas indicated that
species diversity is adversely affected in these areas."*

-42-

�Due to DDT's low solubility in water, the most highly contaminated areas
other than DDT storage or burial sites are streambed sludges. This is
because the waterways leading from a plant act primarily as carriers for
suspended DDT, which settles out in the streambeds. In addition, areas that
are not vegetated pose a particular problem since erosion by wind and rain
can carry land contaminants into surface waters. Similarly, open du.nps of
waste DDT can be constantly errded by surface runoff.
Composite Hypothetical Site
A map of a composite hypothetical site is given in Fig. VII-1. In later
sections of this report, the effects (approximate) of the site configuration
on the environmental impacts of various DDT concentrations are considered.
The features of the composite hypothetical site are:
1. the DDT manufacturing site discharging to a large drainage ditch
2. a train of shallow lakes and wetlands containing food fish and
surrounded by natural areas
3.

ipring flooding, periodically causing redistribution of sediments

4. ultimate drainage of DDT-containing waters into the river, which
is open to boating and fishing
5.

the possibility of free movement of fish and other wildlife from
lakes to and from the river.

Thus, there are wetland areas where DDT in sediments can persist over
many years. There are also physical and biological mechanisms for the
periodic redistribution of DDT in the environment. Finally, DDT can
enter wildlife and human food chains in many ways.
Observed DDT Concentrations
Concentrations of DDT in soil, sediment, and various water bodies as
well as in various wildlife species are listed in Table VII-1 as a
function of the downstream distance from the DDT plant. For simplification, it is assumed that the waste DDT that is buried or landfilled is
located at distance zero and, because the principal carrier of DDT is
water, that concentrations of DDT in water and underlying sediment are
indicative of the level of contamination at each downstream distance.
(The referenced data are those for actual areas surrounding DDT plants.
Some of these data, however, correspond to samples collected and analyzed
more than; 15 years ago and, thus, may not be representative of present
conditions in the areas. These data, possibly out of date, are included

-43-

�1 1

^(^••••ftTijr^WJtWR*.**-*^"'* "' "*-'^'^

/'nv.f~'"in''

Drainage
Ditch

Direction of
Spring Floods

^ X

\
\

Flp. VIM. Map of Model DDT Plant Site

-44-

�TABU! VII-1. AREA AHD WILDLIFE COOTAHTHAT1OH LEVELS FOR VARIOUS SITES

Approximate
Distance
from Plant
Site (*ilea)
0

Approximate
Location
Ground surface of
abandoned production
' area

Median
Sampled
in Area

Reference

Concentration
of DOT in
Area*

Open dumps of
vaste TOT, 100 Ib

Reference

Concentration of OOT°
&lt;PP»)
Huscle
Fat

1001

1002

0

Baseoent of abandoned
buildings

Blocks of DDT
covered vith
clay, 3 tont

0
*
;

Wildlife
Species
Stapled

Domsatic »ever in
plant

Water

181

6.0 ppb

0

Drainage ditch

Water

181

2.7 ppb

005
-.

Drainage ditch

Sediscnt

181

7 , 0 ppa
000

O.I

Clo«*d drainage ditch

Topsoil

181

110 p!»

1

Cloaed drainage ditch

Top*oil

181

0.1 pp*

1

Strea* A

Water
Sedinent

181

2.3 ppb
1 0 0 pp»
.0

2

Lake

Water
Sedinent

1 ppb
100 pp»

Crow
Rabbit
Oposaim
Fox
Fish
Fish
Birds
Fish
Deer
Birds Oterbivores)
Birds (carnivores)
Fish

179
179
179
179
183
184
184
182
183

40
1
23
27
314
20-200
10
300
0.2

2
20
200

750
17
240
SO

800-2.817

50
500
100
,0

�TABLE VTt-1.

Approximate
Distance
from Plant
Sice (niles)

Approximate
Location

Kediim
Sampled
in Area

Reference

(Coot.)

Concentration
of DDT in
Area*

Wildlife
Species
Sampled

Reference

Mannals
3

JS-

3

Lake
Bayou

Water
Sediaent

180
180

Creek6

Water
Sediwent

3

River

Water
Sediment

0.1 ppb
5 PP"
181

0.03 ppb
1 ppo

Shad
Carp
Bass
Catfish
Ban

SunfUh
Bluettill
Fish
Birds (herbivores)
Birds (carnivores)
Mamuls
a. Wf solubility in water • 1.2 F

50

0.5 ppb
IS ppa

4

b. FDA tolerance for fish • 5 p»»«
. e. Hypothetical data.

5

0.5 ppb
6 ppra

Water
Sediscnt

Concentration of DDTb
&lt;PP»&gt;
Muscle
Fat

182
182
182
184
ISA
184
184
178

71
29
6
112
112
7

35
412

O.OJ
1.0
0.5

1
10
S

�here to demonstrate an approach for relating toxicological and ecological
effects to levels of DDT contamination.)
The concentrations of DDT in wildlife at various distances downstream from the hypothetical site are listed in Table VI1-2, along with the
concentrations of DDT in water bodies and sediments at these distances. It
can be seen that the high concentrations in water and sediment at the
shorter distances are reflected in high concentrations in the tissues of the
species sampled. Conversely, the concentrations at a distance o£' 5 miles
approach the average levels in t.he United States. For these data, the
differences between concentrations found in muscle and fat were estimated
from actual measurements.
Predicted Effects
The ultimate objective of this analysis is to predict potential
site-specific environmental impacts of DDT contamination. The predictions,
in their simplest form, relate environmental impacts to concentrations of
DDT in soil and water. With such information and analyses of DDT in soil
(sediment) and water samples, one can estimate impacts of environmental
contamination and the benefits of cleaning up the soil and water to known
levels. Preceding sections of this report provide evidence that currently
available literature data are sufficient to relate environmental impacts to
four types of exposure information: DDT concentrations in an affected
organism, dietary DDT levels, acute or chronic; doses of DDT, and the DDT
concentration in water (for aquatic species). If these four types of
information can be related to soil and water concentration data, the
objective will be met.
USAMBRDL has devised a procedure for estimating safe exposure levels,
called preliminary pollutant limit values (PPLVs), from laboratory or field
dat/» to protect the health of humans and other animals." &gt;"7 This
procedure assumes an equilibrium (or steady state) relationship for a
pollutant distributed among soil or sediment, water, and biota. However, as
is evident in Tables VII-1 and VII-2, sediment:water and fish:water ratios
vary with distance from the model site. Apparently, the PPLV algebra fails
.for DDT concentrations that approach the water solubility limit. Thus, an
alternative procedufe is required to relate health effects to environmental
contaminant levels. For the model site, field data on concentrations of DDT
in soil, water, and biota are adequate to predict health and environmental
effects in qualitative terms.
Data presented earlier on the toxicological effects of DDT on wildlife
are summarized in Fig. VII-2 and Table VI1-3. Predicted impacts of DDT
contamination at the model site are summarized in Table VII-4, which was
derived from data presented in Tables VII-2 and VII-3. Acute toxicity is
predicted to be a problem for predatory and fish-eating birds, sensitive
fish species, and sensitive amphibian species at distances up to 2 miles
from the DDT plant. Very sensitive fish species might be affected over the
next few miles. No animal species are predicted to suffer acute toxicity
symptoms at greater distances.

-47-

�TABIS VII-2.

EWIROWBEOTA1. COHCENTRATIONS OF DDT AT THE HODEt SITE (pp»)

Distance fro* Plant Site (ailes)
Suple
Water

Reference
181

1

2

5

0.001

0.00003

i, 090(440 )«

100(100)

1(33)

2(2)

Sediasnt

0.0023

Average
U.S.
Levels
0.000008-0.000144

Reference
16

0.05(1.7)

0.17

Kuicle Ti*s«e
Birdt
Predatory end
fish-eating
Son- predatory
OB

179,184

Pith

182-184,186

KaBMU

179,184

179.184

750(330)

25(11)
20(20)

1(33)

300(130)

200(200)

100(3,300)

13(5.7)

5(5)

0.5(17)

50(50)

1(33)

500(500)

10(330)

F«t

Birds
Predatory «nd
fish eating
Non-predator*
Fi»h

182-184,186

1,800(780)

1,000(1,000)

500(16.000)

Maaoals

179,184

130(57)

50(50)

5(170)

a. Values in parentheses are non-steady state concentration factors tines 10~3.

2.3

It

�TABLE VII-3. TOXICOLOGICAL EFFECTS OF DDT ON TYPICAL WILDLIFE AS A
. FUNCTION OF CONCENTRATIONS OF DDT IN WATER, THE DIET, AND TISSUES

Medium
Water

Diet

Tissues

Approximate
Concentration

Species

0.01 ppb
1-20 ppb
5 ppb

Fish
Fish
Amphibians

Lethal to sac-fry
Lethal
Lethal

Birds
Mammals
Birds
Mammals

Eggshell thinning
Possible carcinogenic effects
Lethal
Lethal

Fish
Birds

Lethal to sac-fry
Eggshell thinning

0.15 ppm
2 ppm
600 ppm
200 mg/kg
1-5 ppm (eggs)
1 ,&gt;pm (egga)

Effect

Reproductive failure is expected for predatory and fish-eating birds
and for fish at distances up to 5 miles and more from the DDT plant
site. Repopulation of the model site with these species is to be
expected only for those species with some accessible breeding populations
at distances sufficient to avoid DDT-associated reproductive failure. In
other words, fish and predatory birds may be found at the model site, but
it is unlikely that sensitive species hatched within 5 miles of the DDT
plant.
Mammals are generally much more resistant to DDT than birds or
fishes. Even so, it is not improbable that fish-eating mammals, e.g.,
otters, could ingest toxic quantities of DDT, considering the high
dietary levels (Table VII-1). Their intake might, for example, exceed
the 20 ppm DDT reported to cause teratogenic or embryotoxic effects in
mice. Lower levels could conceivably induce cancer, but this would not
be ecologically significant because cancer from a weak carcinogen, such
as DDT, would be expected to afflict only senescent individuals. Fish
taken for human food within 5 miles of the site are virtually certain to
exceed the 5 mg/kg limit established by the Food and Drug Administration.
For average daily consumption of 18.7 g of such fish, tVie associated
lifetime cancer risk, by the EPA's method,2' exceeds 1 in 1,000. For
consumption of fish containing 50 mg DDT/kg, the associated risk would
exceed 1 in 100. (Note, however., that EPA considers the cancer risk from
DDT ingestion derived from epidemiological data to represent an upper
bound. The actual risk may be substantially lower.)

-49-

�LC» (short-term)

s

LCw (long-term) _

*c

Not lethal

-

Chromosome
abnormalities
&lt;D
«

?

Teratogenic
;
or embryotoxlc effects

c
£

Eggshell thinning,
increased embryo mortality

i

O
©
A
D

5
Possible
carcinogenic
effects

_L
0.1

0.4

1.0

4.0

Amphibians
Fish
Birds
Land-dwelling
mammals

I
10

40

100

I
400

1,000

Concentration of DDT in Diet (ppm)

Fig. VII-2. Biological Effects of Dietary DDT Typical Receptors

4,000

�TAiLE VII-4. PREDICTED EFFECTS ON WILDLIFE
Distance from DDT plant Site (miles)
i,
t-«
i

Effect
.

0-2

2-5
;

Acute toxicity for

Predatory and fish-eating
birds, sensitive fish,
sensitive amphibians

Very sensitive fish

Reproductive failure
due to

Eggshell thinning in
predatory and fish-eating
birds, dc»th of fish sac-fry

Eggshell thinning in
predatory &amp;id fisheatv.tg birds, death
of fish sac-fry

Eggshell thinning in
predatory and fisheating birds, death
of fish sac-fry

�\

Decontamina t ion Ob j ect i ves
In lieu of PPLV's, maximum environmental DDT levels for protection of
wildlife have been calculated directly from model site data (Table
VII-1). These are 0.1 ppb in water and 4 ppb in sediment for predatory
and fish-eating birds and 0.05 ppb in water and 2 ppb in sediment for
fish.
The critical effect for birds is eggshell thinning leading to
reproductive failure. Available data suggest that for sensitive birds,
such as the brown pelican, DDT concentrations greater than 1 ppm in the
egg can cause a significant decline in reproductive success. Other
studies suggest that DDT levels in bird fat are approximately 40 time«
the levels in bird eggs. Table VII-2 shows that the ratio of DDT in fat
of predatory birds to DDT in water is approximately constant and falls in
the ranjje of 300,000 to 500,000. Assuming a ratio of 400,000, it is
calculated that a DDT level in water not to exceed 0.1 j t&gt; will provide a
safe litnit of 40 ppm in fat and 1 ppm in eggs. This corv spends to a
sediment concentration of about 4 ppb. For less sensitive species, safe
concentration limits will be higher. (It should be emphasized th«t these
calculations assume that measured DDT concentrations are equilibrium or
7* steady-state levels. If not, derived values could be in error by an
order of magnitude or greater.)
For fish, the critical effect is mortality of sac-fry, which c*n
occur at DDT concentt-i.tions of about 1 ppm in fish eggs (Table V-4) and
estimated corresponding 'concentrations of 0.01 ppb in water and 0.4 ppb
in sediment (assuming a sediment-to-water ratio of 4 ) Data of Table
0.
VII-1 indicate that reproductive success could be expected at di»t«nct«
^greater than 5 miles from the model marufacturing site.
To establish engineering goals for cleanup efforts, benefitt to
wildlife and humans are predicted to occur for any degree of cleanup from
present levels uown to 2 ppb in sediments (0.05 ppb in water). These
concentrations are so low, and the area of dispersal so great, that it
may be better to focus on cleanup efforts giving the greatest reduction
of total mass of DDT, accepting the fact that decreases to ppb levels in
sediment will have to come through biodegradation. Regular monitoring of
DDT levels in fish and waterfowl will provide a measure of restoration.

-52-

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89. Longcore, J.R., F.B. Samson, and T.W. Whittendale, "DDE Thins
Eggshells and Lowers Reproductive Success of Captive Black Ducks,"
Bui 1. Environ. Contam. Toxicol. 6:485-490 (1971).
90. Azevedo, J.A., E.G. Hunt, and L.A. Woods, "Physiological Effects of
DDT on Pheasants," Calif. Fish Game 51:276-293 (1965).
91. DeWitt, J.B., "Chronic Toxicity to Quail and Pheasants of Some
Chlorinated Insecticides," J. Agr ic. Food Chem. 4:863-866 (1956).
92. Albert, T.F., "The Effects of DDT on the Sperm Production of the
Domestic Fowl," Auk 79:104-107 (1962).
93. Locke, L.N., N.J. Chura, and P.A. Stewart, "Spcrmatogenesis in Bald
Eagles Experimentally Fed a Diet Containing DDT," Condor 68:497-502
(1966).
94. Hickey, J.J. and D.W. Anderson, "Chlorinated Hydrocarbons and
Eggshell Changes in Raptorial and Fish-eating Birds," Science
162:271-273 (1968).
95. Anderson, D.W., J.J. Hickey, R.W. Risebrough, D.F. Hughes, and R.E.
Christensen, "Significance of Chlorinated Hydrocarbon Residues to
Breeding Pelicans and Cormorants," Can. Field Nat. 83:91-112 ( 9 9 .
16)
96. Fyfe, R.W., J. Campbell, B. Hayson, and K. Hodson, "Regional
Population Declines and Organochlorine Insecticides in Canadian
Prairie Falcons," Can. Field Na^. 83:191-200 (1969).
97. Bins, L.J., A.A. Belisle, and R.M. Prouty, "Relations of the Brown
Pelicans to Certain Environmental Pollutants," PCStic. Monit. J.
7:181-194 (1974).
98. Keith, J.A. and I.M. Gruchy, "Residue Levels of Chemical Pollutants
in North American Birdlife," Proc. 15th Int. Ornithol. Congr.t The
Hague, The Netherlands, pp. 437-454""(1972)'.

-60-

�99. Wiemeyer, S.N., P.R. Spitzer, W.C. Krantz, T.G. Lament, and E.
Cromartie, "Effects of Environmental Pollutants on Connecticut and
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McKee, J.E. and H.W. Wolfe, Water Quality^Criteria, 2nd edition,
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101. Katz, M., R.S. LaGore, D. Weitkamp, J.M. Cuunings, D. Anderson, and
D.R. May, "Effects on Freshwater Fish," J. Water Pollut. Control
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Johnson, D.W., "Pesticides and Fishes - A Review of Selected
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103.

McKim, J.M., G.M. Chriotensen, J.H. Tucker, D.A. Benoit, and M.J.
Lewis, "Effects of Pollution on Freshwater Fish," J. j/ater Pollut.
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104.

Macek, K.J. and W.A. McAllister, "Insecticide Susceptibility of
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105.
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Ingham, B. and M.A. Gallo, "Effect of Asulam in Wildlife Species:
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108. Committee on Water Quality Criteria, HAS-NAE, Water Quality
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111. Carter, F.L. and J.B. Graves, "Measuring Effects of Insecticides on
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�112.

Nunogawa, J.N., N.C. Burbank, and R.H.F. Young, "The Relative
Toxicities of Selected Chemicals to Several Speciej of Tropical
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(1970).

113. Korn, S. and R. Earnest, "Acute Toxicity of Twenty Insecticides to
Striped Bass, Morone saxatilis," Calif. Fish Game 60:128-131 (1974).
114. Earnest, R«D« and P.E. Benville, Jr., "Acute Toxicity of Four
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117. Macek, K.J., "Reproduction in Brook Trout (_S_a.ly_elinuft font inalis)
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Johnson, H.E. and C. Pecor, "Coho Salmon Mortality and DDT in Lake
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-62-

�126. Dill P. A. and R.C. Saunders, "Retarded Behavioral Development and
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Wei*, P., "Ultrastructural Changes Induced by Low Concentrations in
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128. Gardner, D.R. , "The Effect of Some DDT and Methoxychlor Analogs on
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," Proc. Roy. Soc. Londcn Ser. B. 111:307-320 (1971).

130. AsyJereon, J. M. and M.R. Peterson, "DL/T: Sublethal Effects on
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De'/y, F.B., H. Kleerekoper, and J.H. Matis, "Effects of Exposure to
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D«vy, F.B., H. Kleerekoper, and P. Gensler, "Effects of Exposure to
£ijj&gt; lethal DDT on the Locomotor Behavior of the Goldfish (Carassius
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E&gt;e*«iah, D. , L.K. Cutkomp, R.B. Koch, and A. Jarvinen, "DDT:
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134. iitedem, T.P., R.I&gt;. Cambell, and D.W. Johnson, "Osmoregulatory
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Kmter, W.B., L.S. Merkens, R.H. Janicki, and A.M. Guarino,
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136. Wfisbart, M. and D. Feiner, "Subl?thal Effect of DDT on Osmotic and
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-63-

�138. McNicholl, G. and W.C. Mackay, "Effect of DDT on Discriminating
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14%

Fleet, R.R., D.R. Clark, and F.W, Plapp, "Residues of DDT and
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Phillips, J.B. and M.R. Wells, "Adenosine 'Triphosphataae Activity
in Liver, Intestinal Mucosa, Cloacal Bladder, and Kidney Tissue of
Five Turtle Species Following In Vitro Treatment with
l,l,l-Ti-ichloro-2,2-bis(p-chlorophenyl)ethane (DDT)," J. Agr. Food
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»" "
146. Witherspoon, F.G., Jr. and M.R. Wells, "Adenosine Triphosphatase
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Sanders, H.O., "Pesticide Toxicities to Tadpoles of the Western
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148.

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149.

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-64-

�150.

Malina, J.F., Jr., "Toxicity of Petrochemicals in the Aquatic
Environmenty" Water Sewage Works 10:456-460 ( 9 4 .
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151. Macek, K.J. and H.O. Sanders, "Biological Variation in the
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152.

Maki, A.W. and H.E. Johnson, "Effects of PCB (Aroclor 1254) and
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153.

Khudairi, S.Y.A-D. and E. Ruber, "Survival and Reproduction of
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154.

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Performai.ce of Artetnia," Science 151:592-593 (1967).

155.

Albaugh, D.W., "Insecticide Tolerances of Two Crayfish Populations
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Contam. Toxi~col. 8:334-338 (1972).
'

156. Hann, R.W., Jr. and P.A. Jansen, "Water Quality Characteristics of
Hazardous Materials," Environmental Engineering Division, Texas A&amp;M
University, College Station, TX (no date).
157. Leffler, C.W., "Effects of Ingested Mirex and DDT on Juvenile
Callinectes sapidu^ Rathburn," Environ. Iollut. 8:283-300 (1975).
158.

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Interaction of Temperature and DDT Residues," Arch. Environ. Contam.
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159.

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from Organic Detritus by Fiddler Crabs," Science 16« 576-577 (1969).

160.

Decamps, H., K.W. Besch, and H. Vobis, "Effect of Toxic products on
the Construction of Webs by Hydropsyche (Insecta, Trichoptera),"
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161.

Davis, B.C. and H. Hidu, "Effects of Pesticides on Embryonic
Development of Clams and Oysters and on Survival and Growth of the
Larvae," U.S. Fish. yildl.Serv. Fish. Bull. 67(2)-.393-404 (1969).

162.

Kimura, T., H.L. Keegan, and T. Haberkorn, "Dehydrochlorination of
DDT by Asian Blood-sucking Leeches," Am. J. Trop. Med. Hyg.
16:688-690 (1967).

163. Naqvi, S.M.Z., "Toxicity of Twenty-three Insecticides to a
Tubeficid Worm Branchiura sowerbyi from the Mississippi Delta," ,r._
Econ. Entomol. 66:70-74 (1973).

-65-

�164.

Kouyoumjian, H.H. and R.F. Uglow, "Some Aspects of the Toxicity of
p,p'-DDT, p,p'-DDE and p,p'-DDD to the Freshwater Planarian
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165. Haller, H.L., "Wartime Development of Insecticides," Ind. Eng. Chem.
39:467-473 (1947).
166. Cristol, S.J., H.L. Haller, and A.W. Lindquist, "Toxicity of DDT
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167. Kemp, H.T., R.L. Little, V.L. Holoman, and R.L. Darby, Water
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Life, U.S. Government Printing Office, Washington, DC, 13050-HLA
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(1946).,

169.

Luard, E.J., "Sensitivity of Dunaliella an*' Pcenedesmus (Chlorophyceae) to Chlorinated Hydrocarbons," Phycologia 12:29-33 (1973).

170.

Poorman, A.E., "Effects of Pesticides on Eiiglena gracilis. I.
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171.

Hicks, G.F., Jr. and T.R, Corner, "Location and Consequences of
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172. Gil, I., J. Morales, A. Martin, C. Ruano, and F. Argones, "Effects
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�177.

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for Soil and Water," presented at the 1979 National Conference on
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Beach, FL (April 25-27, 1979).

-67-

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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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                  <text>&lt;p style="margin-top: -1em; line-height: 1.2em;"&gt;The Alvin L. Young Collection on Agent Orange comprises 120 linear feet and spans the late 1800s to 2005; however, the bulk of the coverage is from the 1960s to the 1980s and there are many undated items. The collection was donated to Special Collections of the National Agricultural Library in 1985 by Dr. Alvin L. Young (1942- ). Dr. Young developed the collection as he conducted extensive research on the military defoliant Agent Orange. The collection is in good condition and includes letters, memoranda, books, reports, press releases, journal and newspaper clippings, field logs and notebooks, newsletters, maps, booklets and pamphlets, photographs, memorabilia, and audiotapes of an interview with Dr. Young.&lt;/p&gt;&#13;
&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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