REPORT OF THE DDT ADVISORY.COMMITTEE*
TO
WILLIAM D. RUCKELSHAUS, ADMINISTRATOR
ENVIRONMENTAL PROTECTION AGENCY

September 9, 1971

♦Established Under Provisions of Section 4.c. of the Federal
Insecticide, Fungicide, and Rodenticide Act.
DSW 334222

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THE UNIVERSITY OF TEXAS MEDICAL BRANCH
GALVESTON. TEXAS 77550

DEPARTMENT Of- PHARMACOLOGY AND TOXICOLOGY

September 9, 1971

Mr. William D. Ruckelshaus
Administrator
Environmental Protection Agency
Washington, D. C. 20460
Dear Mr. Ruckelshaus:
On behalf of the DDT Advisory Committee, I am pleased to submit
the following report of our considerations of the scientific issues raised
by DDT.
The Committtee hopes that the information in this report will be
useful to you and your staff in evaluating the effects of this substance
upon man and his environment.
If there is any additional information that either the committee or
I may furnish you concerning the report or our considerations we will be
pleased to supply them.
Sincerely yours

James G. Hilton, Ph.D.
Chairman
DDT Advisory Committee
JGH:dwa
Enc

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CONTENTS
Page
Membership of the Advisory Committee

1

Introduction

2

Use and Residue Estimates

5

Analytical Interference with the Determination of
DDT by Polychlorinated Biphenyls in theEnvironment

19

Toxicology

24

Needs

35

Conclusions

39

Recommendations

41

Imminency of Hazard

42

Appendices
A.

References Cited

44

B.

Persons Appearing Before theCommittee

49

C.

Exhibits Furnished to theCommittee

51

D.

Abstract of Systems Model Report

52

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1

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MEMBERSHIP OF DDT ADVISORY COMMITTEE
James G. Hilton, Ph.D., Chairman
Professor of Pharmacology
University of Texas Medical Branch
Galvestoh, Texas
L. Eugene Cronin, Ph.D.
Director and Research Professor
Natural Resources Institute
University of Maryland
College Park, Maryland
Kenneth P. DuBois, Ph.D.
Director, Toxicity Laboratory
University of Chicago
930 East 58th Street
Chicago, Illinois
Orie L. Loucks, Ph.D. .
Professor, Institute of Environmental Studies
University of Wisconsin
Madison, Wisconsin
Ralph B. March, Ph.D.
Professor of Entomology
University of California
Riverside, California
David P. Rail, M.D., Ph.D.
Director, National Institute of Environmental
Health Services
National Institute of Health
Research Triangle Park, North Carolina
C. H. Van Middelem, Ph. D.
Professor of Pesticide Research Laboratory
Department of Food Science
University of Florida
Gainesville, Florida
'
*********'***

.

Secretariat to Committee, David L. Bowen
Environmental Protection Agency

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2-

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INTRODUCTION
DDT (Dichloro-dipKenyl-trichloroethane) was the subject of a
decision announced by the United States Court of Appeals for the
District of Columbia Circuit on January 7, 1971.

This decision

required the Environmental Protection Agency to take two steps:
(1) to commence the administrative process for cancelling the
registration of all products containing DDT; and (2) to consider
whether the present information available to the Agency warranted
the immediate suspension of the registration of all products con.

•

taining this chemical.

_

The Environmental Protection Agency

responded to the first by issuing a cancellation notice, PR 71-1,
for all products containing DDT on January 15, 1971.

It responded

to the second step requested by the court by issuing a position
paper dated March 18, 1971, titled "REASONS UNDERLYING THE
REGISTRATION DECISIONS CONCERNING PRODUCTS CONTAINING DDT, 2,4,5-T,.
ALDRIN AND DIELDRIN."

In it, the Agency outlined its responsibilities

under the Federal Insecticide, Fungicide, and Rodenticide Act and
explained why suspension of DDT registrations was not considered
necessary.
The administrative process for cancelling the remaining regis­
trations for DDT began with the issuing of the cancellation notice
of January 15, 1971.

Objections to this notice were filed by a

number of firms, most of which chose the option of requesting a
public hearing.

Montrose Chemical Corporation of California and

the Crop King Company of Yakima, Washington, however, requested
that the issues raised in the cancellation notice be referred .to
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"/ r- -

«'* **.*-•<* a&.j

-3-

an advisory committee named from a list of nominees provided by the
National Academy of Sciences in accordance with the Act.' The
DDT Advisory Committee was appointed by Mr. William D. Ruckelshaus,
Administrator of the Agency, in a letter dated April 30, 1971.
Due to the nature of the factors invotved in the issuance of
the cancellation notice, the charge to the Committee was very
broad.

This charge stated in part:

“The Committee is charged to

consider all relevant scientific evidence concerning DDT, and to
prepare a repbrt and recommendations as to the scientific issues
raised by the use of DDT."

Based upon the breadth of the charge

and the pressures of a fixed time deadline for its report, the
Committee has elected to depend upon the.two most comprehensive
.recent reports on DDT (Jensen Committee Report on Persistent Pesti­
cides to Administrator, Agricultural Research Service, U.S. Depart­
ment of Agriculture, May 27, 1969; and Mrak Commission Report of the
Secretary's Commission on Pesticides and Their Relationship to
Environmental Health, December, 1969) for the evaluation of much
of the prior scientific information concerning this compound.
This has allowed the Committee to concentrate its efforts upon
obtaining and evaluating whatever new information has become

For the sake of convenience this report is divided into four
t

major sections followed by the conclusions and recommendations of
the Committee.

In general, "DOT" is used to mean the combination

of DDT and its. metabolites.

DSW 334227

available since these reports.

\

The first section deals with the current

estimates of the quantities*of DDT being used, and the residues'present
in the various sections of the environment according to the most recent
STLCOPCB4080805

-4monitoring data available.

The second section presents briefly a

summary of the possible-interferences with the analytical determination
of DDT in environmental samples caused by the simultaneous presence of
the polychlorinated biphenyl compounds.

The third section presents the

toxicity of DDT .upon nontarget species with particular emphasis upon
•,
■
.
. the toxicity to the mammalian species. . The final section considers the
present need for DDT.

DS\N 334228

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USE AND RESIDUE ESTIMATES
U.S. Production History
The history of rapid expansion in the production of DDT and
closely related compounds from 1944 to about 1960 and general
decline since that date is well documented elsewhere and there is
no need for detailed summary here.

.

•

Figure 1 presents the available data on production in the
United States and usage in this country as estimated from the
difference between total production and the stored and exported
'

-

-

*

.

■

stocks reported for each year.
The rise was caused by growing recognition that DDT is an
-inexpensive, persistent, wide-spectrum insecticide.

The declines

have been attributed to developing resistance to DDT by many insect
species, the introduction of effective replacement insecticide, and
increasing concern about pesticides which are persistent and have a
wide spectrum of effects on species.
U.S. use apparently declined from about 70,000,000 annually for
1956-1962 to about 30,000,000 pounds in 1968 and 1969.

The Committee

has received estimates for 1970 and 1971 which indicate continuing
decline, but confirmed data are not yet available.

°SW 334229

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j

POUNDS I)DT X 1000

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STLCOPCB4080808

-/-

Environmental and Biological Load
In the following sections, we have summarized the most recent
data available on DDT in the environment, so as to provide the
means of determining whether the continuing decline in use has
produced a decline in the concentration of DDT in the environment­
'.
.
.
•*
•
soil, air, water, natural biota, human food, and man himself.
The levels in soil.

Data on the buildup of DDT and other

persistent pesticides in the environment were sketchy and frequently
misleading during the first fifteen years of widespread use (1946­
1960.)

.

•

•

.

The President's Science Advisory Committee Report of 1965 des­
cribed what was known up to that time of the buildup of residues
of DDT in soils with high pesticide use history as might have been
expected, and they attributed this result to the beginning of a
trend toward the use of less persistent pesticides.

A subcommittee

on soil contamination concluded, however, that the level of contamination
was increasing, and that the problem of soil pollution by chemicals had
grown to the point where it was a matter of immediate national concern.
That Committee recommended strongly that there should be a program of
monitoring by which the buildup of persistent materials in the environ­
ment could be documented as a basis for future steps toward improvement
in environmental quality.

'

More recent discussions of DDT levels in soils have considered the
diverse mechanisms by which this chemical leaves the soil to which it
is applied, and returns to the soil at another location through preci­
pitation, dust fall, and runoff (Edward 1966, Nash and Woolsen 1967,
Risebrough et al_. 1968, and Goldberg 1971).

Because of the difficulty
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in measuring losses to the atmosphere, and the effect of agricultural
treatment and weather on these exhanges, the early estimates of decom­
position rates.in soils and the concept of a "half-life" for DDT in
the environment are in doubt.
The present evidence available to the Advisory Committee was a
.
. .
summary of 1969-1970 results of monitoring by the Environmental Quality
Branch! Pesticides Regulation Division, EPA.

While these results were

for one and two years ago, they nevertheless represented the levels in
soils a full 10.years after the peak levels in use of DDT.

The 1969

f

results show that average levels for croplands are highest in the South­
western, Southern and Eastern Seaboard States.

All of these states

average above 0.10 ppm, but ranged as high as 0.56 ppm.

Urban and

orchard soil samples were highest, with average values between one
and two ppm, and individual samples as high as 52 ppm of DDT and its
metabolites.

Of six states sampled randomly in both 1968 and 1969,

four showed an increase in DDT residue and two decreased in 1969.
Because sampling sites were changed from year to year, the Committee
does not consider that these results demonstrate a trend.
The levels in air.

Recent research in the release of pesticides

into the air, movement in aerial transpprt systems, and persistence
in air was reviewed by the Mrak Commission in 1969, and no significant
additional information has come to the attention of the Committee.
Air transport is an important component in creating the worldwide
patterns of distribution, but it is abundantly evident that much
more evidence should be sought on the distribution, movements and
significance of pesticides in air.

Aerial application involves

opportunities for introduction of pesticides into the air mass
DSW 334232

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-y-

and for export from the sites of application.

Codistination and

evaporation may also introduce significant quantities and affect
global distribution.

The persistence of DDT and other materials

in air masses is also highly pertinent and insufficiently understood.
•

-

v.,

These and other fields of research require^continued attention for
optimal management of DDT. and many other chemical materials.

The

relatively large quantities of DDT present in the biosphere offer

- /

unique opportunities for understanding these movements and the
underlying mechanisms involved.
The levels in water.

The solubility of DDT in water is reported

to be 0.0012 ppm (Bowman et^ al_. 1960).

This means that observations

of DDT in water at greater than 1.2 ppb should be viewed as attributable
to contamination or other mechanisms.

Residues of DDT much higher than

this have been reported frequently in water, and in almost every case
the contamination has been traced to a local application.

Usually it

is associated with heavy rainfall that washes a portion, of the DDT
applied into adjacent streams or lakes.

Because of the low solubility

the high levels of DDT do not persist in water, instead the DDT
moves into the atmosphere or vs taken up by sediments, living organisms
and other particulate matter (Harrison et al_. 1970).
Other studies are giving clearer understanding of the fluctations
of DDT in water systems.
'

Because of low solubility, the DDT tends to

.

•

i

•

•

reach the surface of the water from which it enters the atmosphere.
Very little information has been available as to the levels of DDT in
the atmosphere during the period of hi.gh use in the 1950's but in the

^

mid-1960's in England rainwater samples averaged 0\08 ppb, and during

.

■

.

•

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1968-69 -jn Florida precipitation averaged 1 ppb (Tarrant and Tatton
1968, Yates et al_. 1970).

These results appear to vary widely

depending on season, dust levels in the atmosphere and other factors.
The most recent data available to the Advisory Committee were the
results'of the U. S. Geological Survey water quality monitoring program.
The results of these surveys indicate that DDT or its metabolites are
frequently found in rivers monitored by the USGS at levels approaching
the solubility of DDT (1.2 ppb), apparently because of the association
between DDT and the fine particles carried by streams.

These materials

are deposited on stream and lake bottoms during periods of low flow,
but undergo considerable re-suspension during storms or periods of peak
flow.

Storms such as hurricanes appear to be particularly important in

the re-suspension of DDT-contaminated sediments in the coastal water of
the United States.
These processes results in great variability in the levels of DDT
observed in unfiltered water samples.

Much of the time there is no

detectable contamination by DDT or its metabolites, but at other times
significant contamination is observed.

Because the contamination originates

from treated agricultural lands and from stream and marine bottom sediments,
it appears that no decrease in water contamination can be expected until
the levels in soils and sediments decrease.
The levels in natural food chains.

'

The level of DDT in the food

chains of native species, both on land and in the water resource systems,
has been documented by detailed analyses of selected native species over
the past 25 years.

Both State and Federal agencies have been involved,

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with a greatly increased program over the past five years.

There

are now a number of examples of important fish and game resources
that have reached a level of contamination that prevents distribution
in interstate commerce under Food and Drug Administration regulations.
The high level of"contamination in these species has been shown
•

,

-4

•

to result primarily from the process of biological concentration in
natural ecosystems.

Woodwell (1970) and Harrison etaK (1970) have

described the role of the trophic structure and mechanisms of'an
ecosystem in transporting and concentrating DDT.

Storage of DDT in

each trophic level, transport from one trophic level to another, and
the transformation of DDT into DDE or DDD by metabolism are all
involved.

In contrast to its near insolubility in water, DDT is

highly soluble in the lipids of organic materials.
■

The combination of high solubility in lipids and high chemical
stability allows "magnification" of DDT concentrations from organisms
•at the base of a food web to a higher trophic level fed on those in
the levels below, and a substance like DDT, which is stored in the
lipids and breaks down slowly, can accumulate to a high concentra­
tion in the higher trophic levels.

.

The review by Goldberg et al_. (1971) indicates that in the open
ocean, phytoplankton form the base of the food chain and may act as pri­
mary concentrators of the chlorinated hydrocarbons in the water.

There

is some evidence demonstrating inhibition of photosynthesis in single­
cell marine plants by DDT (Wurster 1968) but the important fact here may
not be the direct effect on plankton, but rather that plants serve as one
of the vehicles for transferring DDT from the water to higher trophic
DSW 334235

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levels.

Another major pathway .is through'-the utilization of DDT-con-

taminated dead organic matter in the sediments of water systems by
benthic organisms.
•

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■*

The Goldberg committee concluded from an analysis of chlorinated

hydrocarbons that marine fish are almost,universally contaminated with
chlorinated hydrocarbon .residues.

They note the effect of this con­

tamination on the marine populations themselves, citing the speckled
sea.trout on the south Texas coast, in which DDT residues in the ripe
eggs were af^out 8 ppm.
. •

Residues of 5 ppm in freshwater-trout cause
*

-

•

100 percent failure in the development of sac fry or young fish, and
they conclude that it is significant that extraordinarily few juvenile
fish have been observed in certain coastal areas in recent years.
The situation of freshwater ecosystems is probably- best illustrated
by the results of studies published by the Wisconsin Conservation.
Department (Kleinert £t al_. 1967, Poff and Degourse 1970).

Surveys

were initiated in 1965, and results are available through 1969.

These

authors conclude that the 1965 and 1966 surveys demonstrate a widespread
and .significant level of contamination in inland fisheries with DDT,
and that residues in fishes from certain Wisconsin waters had already
reached levels harmful to fish.

The 1970 report by Poff and Degourse

has more data for larger and older, fish, which show more severe contamin­
ation.

It is difficult to say that the higher levels reported by them

are entirely due to a continuing buildup in DDT level, but it appears
that concentrations in Lake Michigan Fish were about the same in 1969
as in 1965.

0SV^36

\
STLCOPCB4080814

-13-

The economic effects by 1970 were worse because the Food and Drug
Administration had set a tolerance of 5 ppm of DDT in fish products
marketed for interstate shipment.

A paper by Lues chow and Winter

(1970) concludes that "The Food and Drug Administration limitation
of 5 parts per million of DDT in fish whicji may be sold in inter­
state commerce has virtually eliminated the commercial market for
Lake Michigan fish."

They note that, based on the 1966 catch estimates

for the entire Great Lakes, approximately 42 percent of the commer­
cial catch would be unacceptable for interstate commerce.
The environmental load of DDT in.terrestrial ecosystems is most
.evident in certain species of birds.

Insects, other soil invertebrates,

and aquatic life serve as the food of these terrestrial bird species.
The effects have been recorded through studies of museum eggshells,
showing that thinning has occurred since the nrid-1940's in a wide range
of species.

Where shell thinning has occurred, the populations have

usually declined (Ratcliffe 1967, Hickey and Anderson 1968).

The decline

in populations of the peregrine falcon and bald eagle have both been
linked with substantial evidence to .the buildup in DDT or its metabolites
in their tissues.

In addition to many such observations of coincidence

between these pesticides and reduced bird populations, there are now
reports of well-designed experiments-which show that DDT and related
compounds can cause the observed physiological and behavioral effects
(Porter and Wiemeyer 1959, Heath e£ £l_. 1969).
.

The levels in market-basket foods. The Food and Drug Administration

has maintained strict control of pesticide residues in food throughout
the period of increasing pesticide use.. Monitoring of DDT in foods was

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initiated much earlier than the monitoring of DDT in other sectors of
the environment, and as'a resul t the change in levels of contamination
of foods is well documented,

.

The most up-to-date data provided to the Committee were those from
•

•

• *

v ,

.

a forthcoming publication titled, "Pesticide Residue Levels in Foods in
the United States from July 1, 1963, to June 30, 1969," by R. E. Duggan,
6. Q. Lipscomb, E. L. Cox, R. E. Heatwole, and R. C. Kling.

Their

report shows that the level of DDT and its metabolites in total-diet
samples'reached a peak in 1966, Table 1.

The higher level of contamina-

#

•

•

tion at that time is believed due to the use of DDT in proximity to
forage crops intended for beef and-dairy product production.

Table 1. DDT Levels in Market-Basket Diet (in mill igrams/day)
FDA Dat a
.

DDT + DDE
DDE

.

*

1965

1966

1967

1968

:

1969

1970

0.031

0.041

0.026

0.019 •

0.016

0.015

0.028

0.017

0.015

0.011

0.010

Pesticide regulations were modified in 1966 and a drop in DDT com­
pounds in the FDA total-diet samples was observed by 1967.

Continued

decline in contamination by DDT was apparent each year from 1967 to 1970,
i

but in smaller steps each year.

•

These data suggest that the levels in

food are now more closely in equilibrium with the levels of DDT in the
environment and thus cannot be expected to.change quickly as the result
of new restrictions in the use of DDT.
•

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The results of the FDA survey over the same period have also shown
a continuing rise in the percentage of diet samples showing a detect­
able level of DDT.

During the period when the concentration of DDT

in food was declining, 1967-1970, the percent of samples showing detect•

■

able levels of DDT increased from 38% to 56%.

‘A

Over the same period the

average daily intake of DDT compounds declined from 20 percent of the
FA0-WH0 acceptable daily intake (0.05 mg/kg of body weight per day) to
10 percent.
‘

.

The levels in man.

■

"

.

The concentration of DDT in man is highly vari­

able from one region to another of the country, and from one economic
class to another within regions.

As a result, it has been extremely

difficult to generalize as to the mean level of chlorinated hydrocarbons
‘ in man without a concerted large-scale sampling program.

Beginning in

1967, a sampling program large enough to overcome these difficulties and
provide meaningful data was initiated.
The Committee was provided with the results of this Human Monitoring
Survey (HMS) by the Environmental Protection Agency covering the period
from 1967 to 1970.

The results xire summarized in Table 2.

A change in

technique during 1968 poses some difficulty for direct comparisons, but
a pattern of peak contamination in 1968 is suggested.

Other data from

the HMS show that the ratio of DDE to DDE + DDT has increased from 0.60
to 0.80 in the past 15 years.

Probably because DDE is more persistent,

the levels of DDE from the HMS do not show a decline in the 1970 results.
Thus, the apparent sequence for DDT compounds appears to be made up of
a significant decline in DDT (possibly related to the decline of DDT in
food), and a continuing slow increase in the levels of DDE, the primary
breakdown: product of DDT.

'
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Table 2.

Mean Levels of Selected Chlorinated Hydrocarbon Pesticide
■Residues in Adipose of the General Population (ppm)
Dr. Ann Yobs

-

Human Monitoring Survey
Year

1967

‘ 1968

1968

1969

19701/

•I Samples

722

3300

3237 .

3264

2626

Method

(non­
cleanup)

(non- .
cleanup)

(Mod.l/
MOG)

(Mod.
MOG)

(Mod.
. MOG)

pp DDT

1.28

1.52

1.53

1.20

1.15

pp DDE

4.22

5.28

4.08

4.02

4.12

Total DDT
equivalent 6.22

7.60

6.26

5.81

5.9.7

■^Incomplete data 6/6/71
n/
.
—' MOG=Hodified Mills, Onley, Gaither cleanup procedure used

The Committee also reviewed the results of studies on DDT-derived
material in human milk summarized by the HMS.
data were available for the United States.

Unfortunately, no recent

Data from ten years ago

indicated levels in human milk that would lead to a daily intake by a
nursing infant at, or in excess of, the acceptable intake recommended
by FAO-WHO.

In view of the reduced intake of DDT by adults in the

United States, it is unfortunate that no more recent data are available
on the quantities of DDT and metabolites in human milk.

OS>NW«40

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Projections of the expected environmontal load.

Any survey of

recent trends in the levels of a contaminant such as DDT and its break­
down products must give attention to the expected levels over the next
5, 10, or 20 years.

Several methods are possible.

One can utilize a

direct plot of the data available of the levels in air, water, soil,

.

' •

•*

'

food and human tissue and consider the possibility of a continuation from
the trends evident in the plotted data points.

Due to the great vari­

ability in data on DDT levels in the environment and the short period
of observations, it is difficult to observe any significant trend at this
time.

.

’

A second procedure would be to consider the recent monitoring data
in the light of everything that is known about the processes of DDT re­
distribution, the concentration in the environment, and the rate of breakuGWi to nontoxic compounds.

Relatively little information is available

as to the rate of turnover of the DDT pool in sediments and in soils, or
the rate of breakdown of DDT in aquatic environments.

In spite of these

deficiencies, our understanding of movement of DDT in the environment
allows us to view the variability in reported levels as not due to any
decline in environmental load but as due to random movement of the DDT
stemming from major upsets in weather, erosion, and riverflow.

The

quantity of DDT involved in this movement may be traced to the relatively
heavy use of .DDT in the past 20 years.

Although the proportion of the

contamination made up by DDT itself probably will show an appreciable
decline in the next few years, the combined contamination by DDT and the
more stable DDE seems likely to show only a modest decline.

STLCOPCB4080819

-18-

A third approach to making projections of the DDT contamination
is to use a systems analysis to provide simulation of DDT levels over
the recent period of monitoring and continuing for up to 50 years in
the future.

Such an analysis has been done for the Committee by

Drs. O'Neill and Burke of the Oak Ridge National Laboratory and their
results are included as Appendix D.

The advantage of a systems model

is that each pool of DDT in the environment* and the rate at which it
feeds or is fed by other pools, is considered simultaneously in making
projections qf the anticipated DDT load.

The rates of exchange in the

environment have had to be estimated from the changes in concentration
apparent in the monitoring program.
.

Of the three approaches to estimating the expected rate of decon­

tamination, the systems study offers the most potential, but it also
identifies most clearly the deficiencies in our monitoring program and
in our understanding of DDT in the environment.

We believe that a re­

examination of the projections obtained by O'Neill and Burke should be
undertaken regularly as new data become available.

Within the limits

of the data available at this time, however, the systems study demon­
strates that only a slight reduction in environmental contamination can
be expected within the next decade.

It also shows quantitatively the

impact of different levels of use of DDT in the next-few years.

Although

the continued use of relatively small'quantities of DDT will not serious­
ly affect the slow decline in environmental load during the next 10
years, it will seriously affect the expected reduction of DDT in the
environment over the longer period of two generations.

DS*I

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ANALYTICAL INTERFERENCE WITH THE DETERMINATION OF
DDT BY POLYCHLORINATED BIPHENYLS IN THE ENVIRONMENT

■

A number of polychlorinated biphenyls (PCBs) have been commercially
available in the U.$. since 1930.
•

'

Currently PCBs are being marketed by
- .

*

.

-

Monsanto Chemical Company under the trade name of Aroclor with the per­
centage chlorine designated by the last two digits of their four digit
identification number.

The first two digits indicate the type; for

example, the 1200 series for the biphenyls which are the most common,
l
’
In the environment, PCBs behave like DDT and many other organochlorine
pesticides.

PCBs are very stable, resist degradation, are insoluble .

in water and highly soluble in lipids.

It is inevitable, therefore,

that PCBs would be concentrated in biological systems since they possess
all the characteristics associated with DDT and its metabolites.

PCBs

•are extracted and detected by the same techniques employed for the organochlorine pesticides and consequently residue chemists have had to develop
adequate analytical procedures to separate them from, associated chlorinated
pesticides, prior to quantification.
Prior to 1967, PCBs were either misidentified as specific pesticides
such as DDT or viewed as unidentified compounds, possibly unknown pesticidal metabolites.

PCBs were previously evident as extraneous, unidenti­

fied peaks in GLC chromatograms of extracts of marine fish and birds *
until identified in 1966 by Jensen and by Widmark in 1967 and
Holmes et al_. (1967).

It was not until a year or two later that

federal monitoring and surveillance sample analysis began to include
any routine screening for PCBs, in addition to the usual screening for
chlorinated pesticides.

The timelag between use and the detection of
DSW 334243

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-

PCBs in the environment can be attributed to accumulative concentration
over the years and/or recent sophistication in analytical techniques
and instrumentation.
The presence of PCBs, DDT and DDT-like moieties in environmental
samples presents the residue chemist with J>oth a qualitative and quanti­
tive analytical problem.

Because of the similiarity of retention

times of gas chromatographic peaks, concentration of certain PCBs can
interfere with the accurate determination of p,p'-DDT, p,p'-DDD and
p,p'-DDE depending on the type of GLC column employed.

One of the

most common PCBs found in the U.S. environment, Arcolor.1254, inter­
feres with the GLC peaks associated with p,p'DDT and p,p'DDD and
p,p'DDE.

Another common PCB, Aroclor 1260, interferes the least

with peaks associated with p,p'DDE.

The seriousness of the PCB

interference or bias in DDT, DDD, and DDE quantifications per se by
gas chromatography is dependent on several interrelated factors such
as the polarity of the gas chromatographic column packing, the
percentage of chlorine in the particular Aroclor being chromatographed,
and the concentration and ratio of PCB and DDT and metabolites in the
extract. .

J

■

-

" -- -...~

. ..

'

Considering the most common Aroclors found in the envirpnment,
such as 1254 and 1260, unless the ratio for PCB:DDT concentration in
the sample is greater than 2:1, the PCB bias to accurate quantifii

cations of DDT and its metabolities by electron capture gas
chromatography will be relatively negligible.

The PCB bias will .

interfere and can become serious if the ratio of PRC:DDT concentration
in the environmental sample approaches .5:1 or higher.
'

t

'

One reason for
. ‘

DSW 334244

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-

this is that electron capture detector usually employed in the gas
chromatography is considerably less sensitive to the PCB mixture
than to individual DDT compounds on a comparative weight basis.
The analytical problems associated with separating PCBs from
DDT, DDD and DDE have largely been overcome in the past few years.
It cannot be said that the extraction and isolation recovery of
PCBs is absolutely quantitative but it can approach 80-90% if
adequate preliminary procedures are carefully followed.

Separation

of PCBs by column chromatography using Florisil has been reported
for several pesticides by Reynolds (1969), but p,p‘-DDE is eluted
along with the PCBs.

Armour and Burke (1970) have developed a

separation of the DDT analogs and PCBs by employing a silicic acid
column.

Identification of these interfering PCBs by combined, gas

chromatography - mass spectrometry has been reported by Widmark
(1967) and more recently by Bagley et_al_. (1970) using a thin-layer
chromatography preliminary separation followed by GLC-mass spectrom­
etry.

Separation and identification of DDT analogs in the presence

of PCBs by two dimensional TLC has recently been proposed by Westfall
and Fehringer (1970).

.

Based on current data, results obtained from environmental
monitoring and market surveillance sampling of various foods and

contamination is in fish and fish-eating birds.

Apparently

i^s are

widely distributed among marine birds which are the terminal carnivors
of a complex mesh of food chains in the sea.
'

DSW 334245

other published data, it appears that the most serious chronic PCB

Concentrations of DDT and

•

PCB in marine birds tend to be an order of magnitude higher than in
marine fish according to Risebrough et. al_. (1968).

Occasional acute PCB

contamination occurs in various areas of our environment leaving the 7
STLCOPCB4080823

'

-■

' 'V

•..

.

• -f ? aa.i

22-

-

mis taken impression that serious PCR contamination is a universal
problem.

Most of the acute residues of PCBs found to date can be

attributed usually to inadvertent or accidental industrial causes.
A recent example of acute PCB contamination in poultry was traced

f

to contaminated fish meal resulting from unnoticed leakage of PCBs
in the sterlizing vats.

The PCB contamination found currently in

fruits, vegetables, and in most samples of milk, cheese and eggs
appear to be relatively insignificant, at least as to posing a
serious analytical bias to DDT or DDE determinations of these
samples.
..

"

.

Undoubtedly, prior to recent cognizance by the chemists of

possible PCB interference, some of the peaks or portions of them
could have been erroneously attributed to DDT, ODD or DDE presence
in the sample, particularly if adequate conformation procedures were
not followed.

In many environmental samples, the seriousness of the.

PCB bias on the DDT quantification is dependent on the significance
of the DDT concentrations in the sample.

According to Risebrough

et al.. (1969), although p,p! DDE is the most abundant of the DDT com­
pounds in the environment, there appears to be no significant PCB
interference in DDE quantifications.

Consequently, he concludes

that total DDT residues, in the past, before the extent of PCB inter­
ference was known, would not be greatly changed after correction
for this interference.
In summary and based on the rather limited knowledge currently

}

available, it would apnear that generally the PCB bias to the analytical
determination of DDT, DDD or DDE has been and continues to be insignificant
in most foods, feeds and environmental samples.

An exception, where it
..

DSW 334246

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-23-

appears there may sometimes be serious analytical bias due to the
presence of high ratios'of PCB:DDT, would be fish and fish-eating
birds and any associated byproducts.

.

Recent reports of PCB content in human adipose tissues indicated
•

-•

V.

.

-

that the PCB problem is not of widespread poncern.

Undoubtedly iso­

lated cases of abnormally high PCB levels will continue to be reported
but these are considered to be the exception rather than the rule.
The degree of carcinogenicity of the various common environmental
PCBs remains to be elucidated as well as a more complete evaluation
of their relative toxicity to mammals.

There is limited information

that toxicity is associated with the percentage of chlorine but
generally the Aroclors are less toxic to mammals than DDT and its
metabolites.

DSW 334247

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-24-

TOXICOLOGY
Over a period exceeding 25 years numerous careful studies have
been conducted on the toxicity of DDT in experimental animals, in
domestic animals, and In man. The Information available on the
•
*
v.
mammalian toxicity of DDT exceeds that available for most other .
pesticides and for many of the most widely used drugs.
Acute Toxicity.

The acute toxicity of DDT to mammals is low.

Animal experimentation conducted over 20 years ago established that
the median lethal dose of DDT by the oral route in mg/kg is 150-250
«

.

for mice and rats, 150-300 for cats and dogs, 300-500 for guinea
pigs and rabbits, over 200 for monkeys, over 300 for cows and horses
and 1000 for sheep and goats (O.Amer. Med. Assoc., 1951).

All

subsequent experimentation and use experience has confirmed the
early finding of low mammalian toxicity of DDT.

A remarkably small

number of cases of acute DDT poisoning have occurred in man and
there is no we11-documented case of fatal uncomplicated DDT poisoning.
This situation is in marked contrast to the high acute toxicity of
potential substitutes for DDT including organophosphorus insecticides.
The pharmacological effects of oral doses of DDT in man have
been studied.

There are some differences in the dpses reported to

produce various effects but the types of changes and their duration
were the same in all studies.

The lowest oral doses of DDT reported

to produce effects in man were those used by Velbinger (1947).

In

DSW 334248

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-25-

that study, oral doses of 250 or 500 mg per. man' in suspension or
oil solution produced no.effect except a variable, slight dis­
turbance of the sensitivity of the mouth.

Doses of 750 or 1000 mg

.

in oil solution led to disturbances of the sensitivity of the lower
part of the face, uncertainty of gait, malaise, hypersensitivity to
•
•.
.
*
'
contact, cool moist skin but no changes fn reflexes. Discomfort
reached a peak in about 6 hours.

A dose of 1500 mg in oil solution

produced prickling of the tongue beginning about 2.5 hours after
ingestion.

Disturbance of equilibrium, dizziness, confusion and

tremors of the extremities gradually increased.

A peak reaction

characterized by malaise, headache, fatigue, and delayed vomiting
was reached about 10 hours after ingestion and recovery was almost
complete in 24 hours.

.

Chronic toxicity.

Various studies on the chronic toxicity of

DDT have been conducted.

It should be noted that the parameters

measured in toxicity studies done 20 years ago were fewer than those
that are considered today.
Long-term exposure to low levels of DDT produces histological
changes predominantly in the liver.

All investigators who have

studied the chronic toxicity of DDT to rats have observed the same
■

.

»

•

-

changes although the doses required to elicit the effects were not
exactly the same in all studies.

In 1950 Laug et al_., reported
i

that rats fed 5 ppm of DDT for 6 months showed detectable liver
changes.

Ortega et al_., (1956) fed levels of DDT from 5 ppm to 400

ppm to rats for 6 months and followed recovery in some animals for
12 months.

The lowest dietary level that produced liver changes
o5^J 3-34249

STLCOPCB4080827

-26-

(hypertrophy, inclusion bodies, and cytoplasmic granulation) was
15 ppm in males but higher doses were required in females.

The

liver changes were reversible after withdrawal of the diet.

Mon­

keys fed dietary 1 eve!s of 5, 50, 200 and 5000 ppm of DDT for. a
prolonged period showed no liver pathology up to 200 ppm.
The most informative chronic studies on man were those done
by Hayes and associates (1956, 1971) in which known doses of DDT
were fed for prolonged periods.

In these studies some subjects

received doses as high as 35 mg per day for 21.5 months and some
of them v/ere observed for 5 years after completion of the feeding
.period.

The.level fed to these men was 535 times the average

normal intake and no clinical or laboratory evidence of an adverse
effect was observed.

Other studies have been conducted on man

with prolonged and intensive exposure to DDT in manufacturing
plants (Laws et al_., 1967).

In the most recent study of this

type 35 men with 11 to 19 years of exposure in a DDT manufacturing
plant showed no clinical or laboratory effects attributable to
exposure to DDT even though the average daily intake was estimated
from storage and excretion data to be 17.5 to 18 mg per man per
day as compared with an average of 0.04 mg per man for the general
population.

The chronic toxicity studies on DDT have provided no

indication that the insecticide is unsafe for humans when used in
accordance with commonly recognized practice.

The chronic toxi­

city tests on man have not been extensive enough with respect to
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ds\N

334250

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-27-

Carcinogenicity of DDT.

The question-of the potential car­

cinogenicity of DDT has been studied in a number of laboratories.
Fitzhugh and Nelson reported in 1947 that DDT fed in high doses to
rats causes a slight increase in hepatic cell tumors.

A statisti­

cally significant increase in hepatomas was noted in the Bionetics
Study (Innes et al_. 1969) in two strains of mice in both sexes.
#

•

Weisburger et al^. (1965) reported that the frequency of hepatomas
after N-2-fluorenylacetamine was increased as the latent period
decreased after DDT feeding.

Tarjan and Kemeny (1969) reported

mul ti generation studies in mice fed 3 ppm DDT.

-

A generalized increase

in the frequency of.tumors in the F2 and following generations was
noticed.

Multigeneration studies in mice, in progress, sponsored

through the International Agency for Research on Cancer both at
■Lyun and Milan, show a statiscally significant increased incidence
•of hepatomas - although the studies have not been completed and
final conclusions cannot be drawn.
Studies by Halver (1967) have shown that DDT does cause hepatic
cell tumor in trout at relatively low doses.

Some studies, generally

of a duration too short to detect any but strong carcinogens, have
not shown a carcinogenic effect of DDT.

(Ortega, 1956, Ottoboni,

1969).
It seems clear, therefore, that DDT is capable of causing
hepatomas in rodents and further that there is some evidence of
carcinogenicity with respect to other sites.
The significance of hepatoma induction is unclear.

In the

IARC Lyon Study, two of the hepatomas showed matastases to the
lungs, both in animals given. DDT.

With other hepatomas after
DSW 334251

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r i ftkJ

-28-

transplantations to other mice tumor growth did not occur.

Many

experts in carcinogenesis feel that hepatoma induction is
essentially equivalent to carcinogenesis, while others feel that
hepatomas are reversible lesions.

The demonstrated ability of

DDT to stimulate the hepatic endoplasmic reticulum and microsomal
.

*

-

mixed function oxidase activity and to cause an increase in liver
weighfmay.be involved.

Carbon tetrachloride, chloroform, and

brombenzine show increased liver toxicity after stimulation of
microsomal oxidase activity.
•
be hepatoma, production.

One expression of this toxicity might
...
•
,

The evidence to date clearly shows that DDT induces hepatomas
and suggests it may be carcinogenic. '
The implications of this finding for man must be drawn with
care.

Considerable uncertainty exists with respect to the ability

to extrapolate effects seen in small numbers of laboratory animals
at high doses to large numbers of humans exposed to low doses.

If

one accepts that an eventual human health hazard is a possibility,
it must be recognized that very little can be done at this time.
The world burden of DDT is so high compared to the current annual
use in the U.S., that instant as opposed to a rapidly phased
cessation of DDT usage would probably make no significant difference
in human exposure levels.

Expanded use of DDT is contraindicated.
i

-

■

There is no evidence from human epidemiological studies to
shed light on the possible human carcinogenicity of DDT.

Occupa­

tional exposure studies (Laws, 1967) have been too limited in
sample size and duration to follow-up to detect a moderate or
oS'N

STLCOPCB4080830

-29-

weakly carcinogenic action of DDT.

Long-term studies of occupa­

tional exposure of DDT are urgently needed.
Mutagenicity of DDT.

Few data exist in the literature con­

cerning the potential mutagenicity of DDT and its derivatives.

At

high doses, it can cause C. mitosis (colchicine-like effects) in
' .
.
4
.
"
•
dividing plant cells. A recent report suggests DDE may be asso­

’

ciated with chromosome rearrangements in wild Drosophila, but the
association was quite indirect
bodies of local frogs.

being related to DDE levels in fat

Unpublished data appear to be contradictory.

In general, acute high doses were used.

There exists an urgent

need for extended dose experiments with a proper dose range.

It

is impossible to state whether DDT is or is not mutagenic in
mammalian systems.

'

Effects, of DDT on reproduction in mammals.

The conventional

three-generation reproduction study on rats that is used to
evaluate drugs and pesticides teratogenicity has recently been done
with DDT fed at levels of 0, 20, and 200 ppm (Ottoboni, 1969).
There are no teratogenic effects and fertility and viability of the
young were not affected.

Another aspect of this study relates to

the influence of DDT consumed in the milk during the suckling period.
There were clearly no effects from feeding 20 ppm of DDT to the
mothers on the survival of young to the weaning age.

In another

study DDT fed to mice at 7 ppm produced a slight significant
reduction in the number of liters per pair in one strain of mice but not
in another strain (Ware and Good, 1967).

In one recent study doses

of DDT of 1 mg/kg and higher doses were given to rats daily by the

STLCOPCB4080831

•••

-30-

intraperitoneal route for 21 days beginning at 24 hours after birth
(Fahim et al^» 1970).

These high doses caused mortality and a

decreased growth rate.
. Toxicity of DDT to birds.

Evaluation of the toxicity of DDT

to various bird species has not kept pace over the last 25 years
* .

.

•

.

•

with mammalian toxicity studies on DDT.and other pesticides.

It

is only recently that standard toxicological procedures for
mammalian toxicity measurements have begun to be applied to selected
species of birds.

The needs in this area were summarized in 1968

by L. Stickel who indicated that interpretations concerning poten­
tially dangerous effects of organochlorine pesticides require
experimental studies designed for that purpose and aimed at finding

.

diagnostic methods for identification of lethal and sublethal toxic
limits.

The same author recommended that species differences should

be determined in the absence of extraneous physiological and environ­
mental stresses.

Thus it is being recognized that the important

concept of dose-response relationships and species differences have
an important bearing on DDT poisoning, in birds.

It has long been

recognized in mammalian toxicology that analysis of tissues for
toxic substances has limited value in established cause and effect
relationships for intoxication by chemical agents.

It is only the

presence of abnormally high levels of toxicants consistent with
levels known to be associated with lethality and the absence of
other toxic substance that can justify a conclusion that a certain
chemical agent is responsible for mortality.

Tissue levels that

have been found'justify a suspicion that bird populations have been
affected by DDT but the quantitative toxicological data needed to
DSW 334254

STLCOPCB4080832

-31-

support a definite conclusion are still meager.

The apparent

relationships between increased mortality of wildlife and DDT
spraying programs has been discussed by Dustman and Stickel (1969).
One example of the type of study that is extremely valuable
in Understanding the effects of DDT on survival and reproduction
is the one recently reported by Heath ert a^., (1969) in which "
mallard ducks were fed various levels of DDT, DDE, and DDD.

The

results of this study showed that DDE at levels of 10 ppm and 40
ppm severely impared reproduction success, caused eggshell thinning, : '
and increased embryo mortality.
affected.

Survival of hatchlings was not

DDD did not impair reproductive success.

DDT induced

thinning of shells and reduced duckling survival only when a level
of 25 ppm was fed.
ISM Vr^ll I I ll'jb ■

None of the treatments induced crippling among

This type of information is valuable because it shows

the higher sensitivity of this species to DDT and DDE than, is
observed in marranals and, on the other hand, it shows that dietary
levels far in excess of those in food of species that are pro­
tected by established tolerances are required to produce injury in
this bird species.

Many additional studies are needed not only

with individual pesticides but also with combinations of environ­
mental chemicals and DDT.

*

Toxicity of DDT to fish.' The available data on fish demon­
,
i
strate clearly that many species are highly susceptible to DDT.
The high susceptibility of fish and the hazards from injury to
their food chain by DDT have been known at least since 1944
*

(Ginsburg, 1945).

-

Thus the high toxicity of DDT to goldfish was
DSW 334255

STLCOPCB4080833

-32-

described in 1944 (Ellis et al_.) and deaths of young fish in waters
sprayed with .DDT were reported in 1946 (Pierlou).

Work of a

quantitative nature on the effects of DDT on fish has been in progress
for many years and it was perhaps greatly stimulated by the early
use of fish as a species for the bioassay ^of DDT.

Controlled'

studies of the effects of many pesticides on fish and shellfish
have been conducted by the U.S. Department of the Interior, Bureau
of Common cal Fisheries.
EPA).

(Now:

Gulf Breeze Marine Laboratory,

The development of• a monitoring system using oysters which

accumulate residues above 0.01 ppb of DDT from test solutions and
store it at magnifications ranging from 15 to 70 thousand times :
was an important advance in determining the contamination of water
sources.

The.work that has been accomplished in this area leaves

no doubt that the levels of DDT of importance for survival of
aquatic species are far
species.

below those of concern to mammalian

There is sufficient toxicological information on DDT

in aquatic species to indicate that reduction and prevention of
contamination of water sources is a problem of major concern.
Biochemical Effects on DDT.

DDT is capable of .modifying

the activity of hepatic microsomal enzymes that catalyze the
biotransformation of many drugs and other chemicals usually to
less active compounds.

DDT produces this effect by inducing

synthesis of these enzymes.

The consequent increase in

endoplasmic

reticulum explains the hypertrophy of the liver that has long been
an established effect of sufficiently high doses of DDT.

.

Very few

0S^6

STLCOPCB4080834

-33-

quantitative studies have been done on dietary levels of DDT .
required to produce enzyme induction.

In the male rat the minimum

dietary level that causes significant enzyme induction by DDT is .
1 ppm.

Female rats are less sensitive to enzyme induction by DDf

which correlates with failure to observe'morphological changes at.
the same dose in female rats as in males.
A study of 18 workers with an average of 14.4 years of
exposure to DDT in a manufacturing plant showed evidence of enzyme
induction.

However, even at this relatively high intake, the values,

although significantly different, mostly fall within the normal
range (Poland crt al_., 1970).
Recent evidence suggests that DDT can inhibit MG++ ATPase in
rabbit brain (Koch, 1969) and Na K ATPase in teleost 61 tract (Janicki
and Kinter, 1971) and

can form charge transfer complexes with nerve compo­

nents (Narahashi and Haas, 1967).

DDT also causes a decrease or abolition

of the potential difference and short circuits current across the isolated
toad bladder wall (Sides, 1971).

These observations may provide a begin­

ning insight into the acute and subacute CMS toxicity of DDT and since
Na K ATPase is important in maintaining salt and water balance in telesots
they may similarly provide the basis for an explanation of the very high
toxicity of DDT for teleosts.
Other recent reports describe an effect of DDT on the thyroid
function of birds (Jeffries and French, 1969).

Whether this effect, or

the effect of DDT on the hepatic mixed function oxidases plays a role
in the eggshell thinning action of DDT is uncertain.
Interactions involving mechanisms other than enzyme induction
DSW 334257

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-34-

are not known for DDT except for the antagonistic action of
barbiturates against the central nervous system action of DDT.
This antagonism constitutes the basis for the antidotal action of
phenobarbital in acute poisoning by DDT.

It should be noted,.how­

ever, that systematic studies on possible additive or synergistic
effects have not been conducted on DDT with other environmental
ichemicals such as PCB's.

DS\I\J 334258

STLCOPCB4080836

-35-

NEEDS
There is little question from man's viewpoint relative to the
protection of his health and welfare and to the production of food
and fiber that his’ broad-ranging competition with insects requires
.

t

4

measures for the control of their depredation.

-

Although there are

many types o.f useful insect control practices, it v/as essentially
concluded in the most recent scientific analyses (Reports of the
Jensen Committee and Mrak Commission, 1969), that, for the immediate
»
and perhaps even foreseeable future, insect control will depend to
a major extent on chemical insecticides, particularly as directed
toward integrated and supervised programs of insect pest management.
Encouraging progress is continuing on the development of non-insecticidal control techniques, but actual achievement of their broad-scale
applications to insect control problems remains for the future.
The specific question of whether DDT should or should not be
available for use as a component of the. presently available chemical
control resources is difficult.

The cumulative scientific evidence

concerning the persistant nature and toxicological actions of DDT
have been summarized and analyzed above.

It is obvious that there

are still a number of questions in which conclusive evidence is not
complete, even though DDT has been characterized as the most broadly
studied organic chemical ever produced.

Present scientific evidence

permits useful conclusion on many, but not all, important questions.
The production and use of DDT in the'United States has been
steadily decreasing for a variety of reasons since the peak period of
DSW 334259

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-36-

1960 and 1963.

The various types of registered uses have been

drastically reduced with recent cancellations of registrations for

__

use on tobacco and shade trees, in and around the home, and in
aquatic environments (except those essential to the control of
disease vectors as determined by Public Health-Officials) in 1969
and for other uses on a wide variety of crops, animals, and products
in 1970.

Of the comparatively small number of remaining uses,

approximately 70% is used for cotton insect control.

Other exten-

\

sive uses are for control of insects on soybeans and peanuts.
There is little difficulty on humanitarian grounds in appraising
the justification for the continued usefulness and cost-benefit,
ratio of DDT in such programs as the World Health Organization (WHO)
malaria control program,

Fven the most dedicated proponents of

banning DDT appear at this time to exclude this program from their
recommendations.

This apparently results from the acceptance of the

results of the program in terms of conservation of human lives and
alleviation of misery, the many factors justifying the choice of
DDT as the agent of use, and the apparent low potential of this use
to nontarget environmental contamination.

There is considerably

more difficulty in evaluating the necessity for other uses.
The Committee received information on essential uses of DDT
for continued registration presented by the various States and
evaluated by a Special Review Group on DDT Registration, advisory to
the Secretary of Agriculture.

It has not been possible in the time

available for the Committee to address itself to the specifics of justi­
fication for each registration recommended for continued use, and the
OS\N 334260
STLCOPCB4080838

-37-

range or variables for each is such that it is virtually impossible
to formulate responsible general criteria.

The impression of the

Committee is that the recommendations of the States as presented show
considerable variatioh^in the extent of scientific evidence on which
they were based.

The primary justification offered for the recommended

continuations appears to be that no effective substitutes for DDT are
available, but this actually derives from a broad variety of reasons.
Alternative insecticides may present a more acutely toxic hazard to.
both man and 'other nontarget organisms.
•

They are likely to he less
.

residual, requiring more frequent applications.

Because of the relatively

low cost of DDT formulations, alternative insecticides are almost certain
to be more expensive.

The substitution of less fully evaluated materials

than DDT may supplant the known problems of DDT with other unknown pro­
blems of more serious consequences.

Perhaps the most discouraging and

least permittable reason is that potential alternatives' are not registered
for such uses.

The development of satisfactory alternatives presents a

complex problem which may be further complicated by the continued use of
DDT tending to act as a deterrent to their development.

One obvious solu­

tion is to retain the cancellation of all DDT registrations, thus forcing
the further development and registration of alternatives.
the interim, when no alternatives are available?

But what then of

The Committee recognized

the significant reductions in domestic use which have already occurred and
,

t.

their potential implications.

The Committee was particularly interested

in assessing evidence for indications of decreases in environmental con­
tamination during the period of decreasing use.

.

'

Although the evidence

DSW 334261

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-38-

and projections from it are not indisputably clear, they strongly
suggest that residues of DDT have begun to decrease and that residues
of derived materials as represented by DDE appear to have peaked.
’

These suggest that registrations and use of DDT should continue to be
redueed with the ultimate goal of virtual^ elimination of any signfir
cant additions to the environment.

Thus, the registration of DDT

cancelled in PR 71-1, and the essential uses as receommended by the
various States should be reevaluated, and any continued uses of DDT
should be based on detailed scientific review, evaluations, and just­
ifications by appropriate panels of qualified entomologists and then
by independent panels of scientist knowledgeable in toxicological and
environmental sciences.

Additionally, provisions should be made for

continuing review so that new scientific research and evidence may be
taken into account in evaluating and justifying the continuing
essentiality of uses relative to assuring the further elimination of
nonessential uses as rapidly as possible.

The Committee is cognizant

that changes in existing laws concerned-with such matters are
currently in discussion stages and might be expected to facilitate
the courses of action discussed above.

DSW 334262

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CONCLUSIONS
From the data available to the Committee on the use of DDT
and its impact upon the environment* upon man, and upon other non­
target species the Committee has reached -the .following conclusions
•

’

.

on pertinent scientific issues.
1.

*

4

.

-

The quantities, uses, and acreage receiving DDT in the

United States have declined rapidly and continuously within the
past ten years, but the quantities of DDT (and its metabolites)
detectable in water and soil have not markedly decreased.
2.

DDT and its metabolites have spread from their sites of.

application throughout the global biosphere.

The routes and

mechanisms of movement are only partially understood, but include
atmospheric transport, surface runoff, re-suspension from sediments,
and the biological food chain.

Large quantities of DDT are accumu-

'lating in the estuaries and oceans.
3.

DDT and its metabolites persist for years, concentrate in

some nontarget organisms, display a variety of adverse biochemical
and physiological effects, threaten to reduce or eliminate some
nontarget species, and lower the marketability of valuable fish and
shellfish.

Evidence from a limited number of adequate studies and

a large number of less critical and interpretable observations convinces
us of present or probable damage to some molluscs, crustaceans,
fish, and birds.
4.

While forecasts of the prospective decline in DDT contamina­

tion of the environment are difficult and necessarily tentative the
evidence available indicates that present contamination of food
DSW 334263

STLCOPCB4080841

-40-

and native biota is principally attributable to a large existing
environmental, pool that is recycling at low concentrations and
which seems likely to decrease relatively slow over a number of
decades. .
5.

There has been slight but significant reduction in the

amount of DDT present in the foods ingested by man although the
frequency of low-level contamination has increased.

There has been

no significant reduction in the body burden of DDT and its meta­
bolites carried by man.
6.

■

.

DDT has a very low acute toxicity to man and his domestic

animals, and exposure to high doses for short periods of time does
not appear to cause any irreversible damage.
7.

•

Prolonged exposure to relatively high doses of DDT has been

demonstrated to be tumoragenic and possibly carcinogenic in rodents.
With our present knowledge and information, these data cannot be
directly extrapolated to man and his domestic animals.

Based upon

the current intake and storage levels of DDT and its metabolites in
these species, the probability of tumoragenesis and carcinogenesis
is low.
8.

The evidence that DDT may exert a mutagenic effect in

certain situations is incomplete and conflicting at the present time.
There is no evidence that DDT exerts a teratogenic effect.
9.

The polychlorinated biphenyl compounds, because of their

analytical similarily to DDT, have in the past been confused with
DDT and some of its metabolites.

These substances are also wide­

spread environmental pollutants and could have been responsible
for some of tbe reports of the wide distribution of DDT in the
environment.

DSW334264
STLCOPCB4080842

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RECOMMENDATIONS
1.

Reduce the use of DDT in the U. S. at the accelerated rate of
the past few years with the goal of virtual elimination of any
significant additions to the environment.

2.

Encourage effective development and registration of alternative
insecticides or insect control methods capable of replacing DDT
so as to accelerate the reduction of DDT recommended above.

3. ' Provide for review of any continued uses of DDT for scientific
basis and justifications by qualified entomologists and then by
independent scientists knowledgeable in the toxicological and
environmental areas.
4.

•

Create, by 1973, an appropriate panel of experts to review
and analyze new evidence on the remaining scientific questions
posed by the presence of DDT and its metabolites in the environ­
ment, and provide a mechanism for the review of the new information
about DDT at regular intervals.

5.

Review throughly the PCB compounds and their environmental distri­
bution, hazards, and interrelation with DDT.*

6.

.

Provide for continued availability of DDT for specific uses
essential to the Public Health control of disease-bearing insect
vectors until satisfactory alternatives are developed.

*

As this report was being completedv information was received that
a task force will be coordinated through the Office of Science and
Technology and the Council on Environmental Quality to investigate
polychlorinated biphenyls in food and other components.
_
■

0s\N

STLCOPCB4080843

«3B,I

-n2-

THE IMMINENCY OF HAZARDS
The Federal Insecticide, Fungicide, and Rodenticide Act
empowers the Administrator of the Environmental Protection Agency
to suspend immediately the registration of an economic poison
(pesticide) whenever he determines that "such action is necessary
’

t

4

to prevent an imminent hazard to the public."

The Committee has

been specifically requested to provide its expert, independent
judgement on the issue of whether products containing DDT con­
stitute "an imminent hazard to the public." We recognize the •
•
•
signal importance of a decision on this question, but consider it
to be outside of our primary charge "to deal with scientific
issues."

Therefore, we provide a separate statement of our

opinion of hazard.
The definition of "imminent hazard" is important in reaching
such a judgement.

The Committee has used the concept stated as

follows in the position statement of 18 March 1971 by the Environ­
mental Protection Agency titled "Reasons Underlying the Registra­
tion Decisions Concerning Products Containing DDT, 2,4,G~T, Aldrin
and Dieldrin."

•

.
"....This Agency will find that an imminent hazard
to’ the public exists when the evidence is sufficient to
show that continued registration of an economic poison
poses a significant threat of danger to health, or other­
wise creates a hazardous situation to the public, that
should be corrected immediately to prevent serious injury
and which cannot be permitted to continue during the
pendency of administrative proceedings. An "imminent
hazard" may be declared at any point in a chain of events
which may ultimately result in harm to the public. It is
not necessary that the final anticipated injury actually
have occurred prior to a determination that an "imminent
hazard" exists. In this connection, significant injury
dsniy 334266

STLCOPCB4080844

-43-

or potential injury to plants or animals alone-could
justify a finding of imminent hazard to the public from
the use of an economic poison...."
Using this concept of "imminent hazard", the Committee
agreed'that:
A.

‘

The present reported annual usage.level of DDT does not

present an imminent hazard to human health in terms of individual
bodily functions and safety.
B.

'

DDT and its derivatives are serious environmental pollu­

tants and present a substantial threat to the quality of the human
environment through v/idespread damage to some nontarget organisms.
There is, therefore, an imminent hazard to human welfare in terms
of maintaining healthy desirable flora and fauna in man's environ­
ment.

:
Although the Committee has agreed that DDT represents an

imminent hazard to human welfare because of the quantities of this
substance currently present in the environment, it believes that
either immediate suspension or rapid and continuous decrease in the
use of DDT will achieve essentially the same results.

Respectfully submitted

Jcimes 6. Hilton, Ph.D

DSW 334267

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-44-

APPENDIX A
REFERENCES
Armour, J. A. and Burke, J. A.: Method for separating polychlorinated
biphenyls from DDT and its analogs. 0. Assoc. Offic. Anal. Chemists
53: 761,1970.
. ~
^
Bagley, G. E., Reichel, W. L., and Croniartie, E.: Identification of
polychlorinated biphenyls in two bald eagles by combined gas-liquid
chromatography-mass spectrometry. 0. Assoc. Offic. Anal. Chemists
53:251, 1970.
Bowman, M. C., Acree, F., and Corbette, M. K.:
in water. J. Aqr. Food Chem. 8:906, 1960.

Solubility of DDT -C^

Butler, P.A.: Commercial fishing investigations in effects of
pesticides on fish and wildlife. Fish and Wildlife. Serv. Circ.
226:65-77, 1964.
“
:
Butler, P. A.: Monitorinq pesticide pollution.
19: 889:891,1969.

Bioscience

Butler, P. A.: Pesticide residues in estuarine mollusks.
National Symposium on Estuarine Pollution, Stanford
University, sponsored by American Society of Civil
Engineers, Sanftary Engineering Division, San Francisco
Section; and Stanford University Dept, of Civil Engineering,
107-121, August 1967.
Butler, P. A.: The sublethal effects of pesticide pollution.
Proc. of Symposium on the Biological Impact of Pesticides
in the Environment. Environmental Health Science Series
No. 1: 87-88, 1970. ~
Duke, T. W., Lowe, 0. I., and Wilson, A. S., Jr.: A polychlorinated
biphenyl (Arcohlor 1254) in the water, sediment and biota of
Escambia Bay, Florida. Bull. Environ. Contam. Toxicol. 5: 171-180,
1970.
.
.
Dustman, E. H. and Stickel, L..F.: The occurrence and significance
of pesticide residues in wild animals. Ann. N, V. Acad. Sci.
160: 162-172, 1969.
.
Edwards, C. A.: Insecticide residues in soils.
Reviews 13: 83-132,1966.

Residue

Ellis, M. M., Westfall, B. A., and Ellis, M. D.: Toxicity of Dichloro• diphenyl-trichioroethane (DDT) to goldfish and frogs. Science 100:
477, 1944.
'
DSW 334268

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-45-

Fahim, M. S., Bennett, R., and Hall, D. G.: Effect of DDT on the.
nursing neonate. Nature 228: 1222-1223, 1970.
. .
Fitzhugh, 0.' G. and Nelson, A. A.: The Chronic Oral Toxicity of
DDT (2,2-bis (p-chlorophenyl-1,1,1-trichlorothane). J. Pharm..
Exper. Thcrap. 89: 18-30, 1947.
•
Ginsburg, 0. M.: Toxicity of DDT to fish. J. Econ. Entomol.
38: 274-276, 1945.
■ .
.
.

4

.

-

Goldberg, E. D.: Chlorinated hydrocarbons in the marine environ­
ment. Report of the Panel on Monitoring Persistent Pesticides
in the Marine Environment of the Committee on Oceanography.
National Academy of Sciences, 1971.
Halver, J. E.: Crystalline aflatoxin and other vectors for trout
hepatoma. Bur. Sport Fish. .Wild!, Res. Rent. 70:78-102, 1967.
Harrison, H. L., Loucks, 0. L., Mitchell, J. W., Parkhurst, D. F.,
Tracy, C. R., Watts, F. G., and Yannacone, V. J., Or.: Systems
studies of DDT transport. Science 170: 503-408, 1970.
Hart, L. G. and Fouts, J. R.: Effects of acute and chronic
DDT administration on hepatic microsomal drug metabolism
in the rat. Proc. Soc. Exptl. Biol. Med. 114: 388-392, 1963.
Hayes, W. 0., Jr.:
against malaria.
71: 783, 1971.

The degree of hazard to man on OUT as used
World Health.Organization Report WHO/Mal/

Hayes, W. 0.,'0r., Dale, W. E., and Pirkle, C. I.: Evidence of
safety of long-term high, oral doses of DDT for man. Arch.
Environ. Health 22: 119-135, 1971.
■
Hayes, W. J., Or., Durham, W. F., and Cueto, C.: The effect of
known repeated oral doses of chlorophenothane (DDT) in Man.
J. Amer. Med. Assoc. 162: 890-897, 1956.
Heath, R. G. Spann, 0. W., and Kreitzer, J. F.: Marked DDE impair­
ment mallard reproduction in controlled studies. Nature 224:
27-28,-1969.
Hickey, J. J. and Anderson, D. W.: Chlorinated hydrocarbons and
eggshell changes in raptorial and fish eating birds.
Science 162: 271-273, 1968.
Hickey, J. 0., Keith, 0. A., and Coon, F. B.: An exploration of
pesticides in a lake Michigan ecosystem. In Pesticide in the
Environment and Their Effects on Wildlife. J. Appl. Ecol.
(Supplement): 141-154, 1966.
.
Holmes, D. C, Simmions, 0. H., and Tatton, 0. 0'G.: Chlorina-ted
Hydrocarbons in British wildlife. Nature 216: 227, 1967.
DSW 334269

STLCOPCB4080847

-46Innes, J. R. M., inland, B. M., Valerio-, M. G., Petrucelli, L.,
Fishbein, L., Hart, E. R., Pallotta, A. J., Bates, R. R.,
Falk, H. L., Gart, J. J., Klein, M., Mitchell, I., and Peters, J.:
Bioassay of pesticides and industrial chemicals for tumorigenicity
in mice. A. preliminary note. J. Nat. Ganc. Inst. 42: 1101-1114
• 1969.
'
'
:
Janick, R. and Kinter'j-W. B.: DDT: Effect on ATPase and water
absorption in fish. Federation Proceedings 30(2): 673
Jeffries, D. 0. and French, M. C.: Avian thyroid: Effect of
p,p-DDT on size and activity. Science 166 (1278-1280),
1969. ’•
Jensen, J. H.: Report of Committee on Persistent Pesticides,
Division of Biology and Agriculture, National Research Council
U. S. Department of Agriculture, 1969.
'
i

.
*

.

Jensen, S.: Report of a New Chemical Hazard.
32: 612,- 1966.

New Scientist
.

Kinoshita, F. K., Frawley, J. P., and DuBois, K. P.: Quantitative
measurement of induction of microsomal enzymes by various
dietary levels of DDT and toxaphene in rats. Toxicol. Appl. Pharm.
9: 505-513, 1966.
:
Kleinert, S. J., Degurse, P. E., Wirth, T. L., and Hall, L. C.:
DDT and dieldrin residues found in Wisconsin fishes from the
survey of 1966. Preliminary report. Wisconsin Conservation
Department, Research and Planning Division. 1967.
Koch, R.: Chlorinated hydrocarbon insecticides - inhibition of
rabbit brain ATPase activities. J. Neurochem. 16: 269-71, 1969.
Laug, E. P., Nelson, A. A., Fitzhugh, 0. G., and Kunz, F= M.:
Liver cell alteration and DDT storage in the fat of the rat
induced^by dietary level of 1 ppm to 50 ppm of DDT.
.
J. Pharm. Exper. Therap. 98: 268-273, 1950.
Laws, E. R., Curley, A., and Biros, F. J.: Men with intensive
occupational exposure to DDT. A. M. A. Arch, of Indust. Health
15: 766-775,1967.
Mrak, E. M.: Report of the Secretary's Commission on Pesticides
and Their Relationship to Environmental Health. H. E. W.
Parts I and-II, 1969.
Narahashi, T. and Haas, H. G.: Interaction of DDT with the
m
^ k ^ ?- ~ v
niciu.^ «i
COHuuC tuiiCc • u*1 • ucii«
components \J~ .cI Tiuu
^lci
Physiol. 51 (2): 177-198, 1968
i

DSW 334270

STLCOPCB4080848

-47Nash, R. G. and Woolso'n, E. A.: Persistence of chlorinated hydro­
carbon insecticides in soils.. Science 157: 924-927, 1967.
Ortega, P., Hayes, W. J., Jr., Durham, W. F., and Mattson, A.:
DDT in the diet of the rat. Public Health Monoqraph
No. 43. PHS 484, 1956.
;
~
Ortelee, M. F.: Study of men with prolonged intensive occupational
exposure to DDT. A. M. A. Arch, of Indust. Health 18:
433-440, 1958.
;
Ottonboni, A.:
Appl. Pharm.

Effect of DDT on reproduction in the rat.
14: 74-81, 1969.
'

Pierlou, D. P.: Lethal effects of DDT on young fish.
158: 4011, 1946.

Toxicol.

Nature

Poff, R. J. and Degurse, P. E.: Survey of pesticide residues
in Great Lakes fish. Wisconsin Conservation Department,
Bureau of Fish Management. Management Report 34, 1970.
Poland, A., Smith, D., Kuntzman, R., Jacobson, M., and Conncy, A. H.:
Effect of intensive occupational exposure to DDT on phenylbutazone'
and cortisol metabolism in human subjects. Clinical Pharm.
and Therap. 11: 724-732, 1970.
Porter, D. R. and Wiemeyer, S. N.: Dieldrin and DDT: Effects on
sparrow hawk eggshell and reproduction. Science 165: 199-200,
1969.
*
'
President's Science Advisory Committee: Restoring the Quality of
Our Environment. Report of the Environmental Pollution
Panel, 1965.
■ .
Ratcliffe, D. A.: Decrease in eggshell weight in certain birds of
prey. Nature 215: 208-210, 1967.
.
Report of the Committee on Pesticides: Pharmacologic and toxicologic
aspects of DDT {Chiorophenothane). J. Amer. Med. Assoc. 145:
728-733, 1951.
~
Reyonlds L. M.: Polychlorobiphenyls (PCBs) and their interference
with pesticide residue analysis. Bull. Environ. Contain, & Toxic.
4: 128. 1969.
•
'
‘ ■
’
Risebrough, R. W., Haggett, R. J. .Griffin, J. J., and Goldberg, E. D.:
Pesticides: Transatlantic movement in the northeast trades •
Science 159: 1233-1236,1968.
DSW 334271

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48Risebrough, R. W., Peakall, D. B., Herman, S. G., Kirven, M. N.,
and Reiche, P.: Polychlorinated biphenyls in the global
ecosystem. Nature 220: 1098-1102, 1968,
Risebrough, R. W., Reich, P., and Olcott. H. S.: Current progress
in the determination of the polychlorinated biphenyls.
Bull. Environ. Contain. & Toxic. 4: 192, 1969.
Sides, P. J.:- Effects of 2,2,-Bis (P-chlorophenyl)-l, 1, 1-Trichlorethane (DDT) on toad bladder. Federation Proceedings 30(2)
294 (565),'March-April 1971.
'
. Stickel, L. F.: . Organochlorine pesticides in the environment.
Fish and Wildl. Serv. Special Scientific Report. Wildlife No. 119,
T9'68.
.
Tarjan, R. and Kemeny, T.: Multi generation studies on DDT in mice-.
Fd. Costn. Toxicol. 7: 215-222, 1969.
«

•

Tarrant, K. B. and Tatton, J.: Organo-pesticides in rainwater in
the British Isles, Nature 219: 725-727, 1968.
-

Velbinger, H. H.: Zur Frage der 'DDT'-Toxizitat fur Meschen.
Deutsch. Gesundh. 2: 355-358, 1947.
‘
Velbinger, H. H.: Beitrag zur Toxikologie des 'DDT;-Wirkstoffes
Dichlorodip'nenyltrichloromethylmethan. Pharmazie, 2: 268-274, 1947.

•Ware, G. W. and Good, E. C.: Effects of insecticides on reproduction
in the laboratory mouse. Toxicol. Appl. Pharm. 10: 54-61, 1967.
Widmark, G.: Possible interference by chlorinated biphenyls.
IUPAC Commission on Methods of Pesticide Residue Analysis.
J. Assoc. Offic. Anal. Chemists 50: 1069, 1967.
Westfall, J. E. and Fe’nringer, N. V.: Separation and identification
of DDT analogs in the presence of polychlorinated biphenyls
compounds by two dimensional thin layer chromatography. FDA LIB
#1157, June 17, 1970.
Weisburge , J. H., Hadidian, Z., Fredrickson, T. N., and Weisburger,
E. K.: Carcinogenesis by.Simultaneous Action of Several Agents.
Toxicol. Appl. Pharm. 7: 502, 1965.
Woodwell, G.: Effects of pollution on the structure and physiology
of ecosystems. Science 158: 429-433, 1970.
Wurster, C. F.: DDT reduces photosynthesis by marine phytoplankton
Science 159: 1474-1475, 1968.
Yates, M. L., Holswade, W., and Higer, A. L. : Pesticide residues
hydrobiological environments. 159th ASC National Meeting, Houston,
Texas. -V/ater, Air and Waste Chemistry Section of the American
Society." ATI's tract". WWR-O'iTTT^TQ..
'
'
~
DSW 334272

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-49-

APPENDIX B
PERSONS APPEARING BEFORE THE COMMITTEE
First Meeting
June 7 & 8, 1971
Mr. Harold G. Alford, Pesticides Regulation Division, Environmental
Protection Agency
Dr. R. R. Bates, National Cancer Institute, National Institutes of
Health

1

Mr. C. B. Fielding, Office of General Counsel, Environmental Protection
Agency
Dr. 0. Garth Fitzhugh, Office of Pesticides Programs, Environmental
Protection Agency
Dr. Wayland J. Hayes, Jr., Vanderbilt University
Dr. William «_ * iiciz.0 I Uiit} Uu Itc ouUiiv-V y L.q i tTOi Hid,* i «G Q«i • c v> mu'Ci v.C«iiv.n u
District
0

Dr. Clarence Hoffman, Agricultural Research Service, United States
Department of Agriculture
Dr. C. R. Jordan, University of Georgia
Dr. Thomas H. Jukes, University of California, Berkeley
Dr. Edward R. Laws, Jr., Johns Hopkins University
Dr. Griffith E. Quinby, Wenatchee, Washington (spok’e'at the request of
Crop King)
Mr. Samuel Rotrosen, Montrose Chemical Corporation
Mr. Max Sobelman, Montrose Chemical Corporation
Dr. Fred H. Tschirley, Office of Secretary, United States Department
of Agriculture
'
Mr. P. W. Whiteaker, Pesticides Regulation Division, Environmental
rru tck uuti nytrnuj

Dr. Charles F. Wurster, Jr., University of New York at Stoneybrook,
representing Environmental Defense Fund
1 ■
Dr. David Young, Mississippi State University

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Second Meeting
June 24 & 25, 1971
Mr. Harold G. Alford, Pesticides Regulation Division, Environmental
Protection Agency
' •
•
.
*
'
Dr. Phillip A. Butler, Gulf Breeze Marine Laboratory, Environmental
Protection Agency
•
■ •
Dr. Fred DeSerres, Biology Division, Oak Ridge National Laboratory
Mr. Reo E. Duggan, Office of Compliance, Food and Drug Administration
Mr. Herman Feltz, Water Resources Division, U.S. Geological Survey
Dr. William M. Up'nolt, Office of Pesticides Programs, Environmental
Protection Agency
'
Dr. G. B. Wiersma, Office of Pesticides Programs, Environmental
Protection Agency
.
n.

i>

■

Environmental Protection.

Ann Yobs,
Agency

Third Meeting
Ouly 21, 22, & 23, 1971
Mr. Harold G.! Alford, Pesticides Regulation Division, Environmental
Protection Agency
Mr. Lowell E. Miller, Office of Pesticides Programs, Environmental
Protection Agency
Mr. Charles L. Smith, Pesticides Regulation Division, Environmental
. Protection Agency

33^

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-51-

APPENDIX C
EXHIBITS FURNISHED THE COMMITTEE
1.

Charge to DDT Advisory Committee

2.

PR Notice 70-19, Cancellation of Registration of Certain
DDT Products, August 18, 1970 ■
*

.

3.

PR Notice 71-1, Cancellation of Registration Under the Federal
Insecticide, Fungicide, and Rodenticide Act of Products
Containing DDT, January 15, 1971.
■

4.

PR Notice 71-5, Cancellation of Registration of Dichloro
Diphenyl Dichloroethane (TDE), March 18, 1971.

5.

Petition from I. T. Fisk, Counsel for Crop King Company, to
U.S. Department of Agriculture, Sentember 28, 1970.

6.

Petition from R. L. Ackerley, Counsel to Montrose Chemical Corp.,
to William D. Ruckelshaus, February 18, 1971.
.

7. Petition from I. T. Fisk, Counsel for Crop King Company, to
' Environmental Protection Agency, February 16, 1971.
8.

Reasons underlying the registration decisions concerning products
containing DDT, 2,4,5-T, Aldrin and Dieldrin, Environmental
Protection Agency, March 18, 1971.

9.

Environmental Defense Fund, Incorporated, et al. Petitioners
T. WTTham D. Ruckelshaus, Administrator, Environmental Pro­
tection Agency, Respondent. Petition for Review of an Order
of the Secretary of Agriculture, Docket 23,813, January 7, 1971.

'

10. List of References on DDT
A.

Mammalian Toxicity and Human Exposure

B.

Mammalian and Avian

C.

Aquatic and Marine

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.

APPENDIX D

A SIMPLE SYSTEMS MODEL FOR DDT AND DDE MOVEMENT
IN THE HUMAN FOOD-CHAIN
R.V. O'Neill 1and
O.W. Burke*1
Abstract of a Report submitted to the Advisory Committee on DDT^
At the request of the DDT‘Advisory Committee, a brief study
•

.

*

■•

has been carried out to develop a simple model of DDT and DDE
movement in the food chain supporting man.

The objective is to

examine the potential of a systems model, for estimating anticipated
DDT load in humans and in the environment under various options of
DDT usage and application.

The model was developed from the data

in Table 1 supplied by the Committee, but also includes' the ecoloical understanding of environmental transports and biological
flux processes developed from recent ecosystem modeling research.
However, the model is designed for a specific purpose and readers
are cautioned against drawing implications from it that are not
warranted by the data or the model at this time.

•

'

The limited data period constituted the first basic con­
straint on the model.

The second important constraint was the

^ Ecological Sciences Division GRNL
p
3

Instrumentation and Control Division, ORNL
Carried out and supported .in part through the Deciduous Forest
Bionic Study of the U.S. International Biological Program.
DSW 334276

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brief period of time available to design the model; derive values
for parameters, and utilize the model to examine prospective
future concentrations of DDT in the environment.
It appears that an adequate model of DDT movement should
consider DDT and DDE separately for'the environment, for food, and
for man, resulting in a total of six state variables and six
differential equations.

Ideally, the DDT in food supply should

be divided into a portion which has residual pesticide by direct
application, with subsequent losses at a rapid rate, and a portion
which receives a continuing low level contamination from an environ­
mental pool.

This division is dictated by an analysis of the data

which shows that after cessation of DDT applications near forage
in IS6G, the system has become dominated by an environiiiental pool
with a slow turnover rate.
' Because of the limited data on DDE, the model actually
developed was necessarily simple.

The model could not be solved,

with an explicit environmental pool, because data on this pool
were completely lacking.

Also, to reduce the number of parameters

to be fitted from the data, it was necessary to. consider DDT
plus DDE together in food and man.

Th-is allows a model with only

five unknowns, but incurs the disadvantage of not being able to
distinguish the dynamics of the two forms.
Concern about the statistical reproducibility of the data
has resulted in further limitations in the model.

Questions arise

with regard to the 1968, 1969, and 1970 data on human adipose
tissue.

The authors have had to assume that these data fluctuaOS'N 334217
STLCOPCB4080855

-54-

tlons in DDT and DDE levels were due to sampling errors, and that
the true response curve is a slow reduction in DDT and DDE from a
peak in 1968.

This assumption is partly based on the fact that to

postulate a recent upturn in the level of pesticides in man we
would require mechanisms that we do not know and cannot support
on biological grounds.

If'our assumption, that an initial down­

turn is evident from the 1967-1970 data, is not supported, then
our model is in serious error, and our forecasts underestimate .
prospective concentrations in‘man.

The authors view the decision

«

.

to assume that the data are variable, and to make conservative
estimates of concentrations in man, as the most important single
assumption of our model.

'

The model adopted was expressed as a system of three
differential equations where one expressed the fraction of the
food contaminated by direct spraying, another the portion of the
food which receives DDT from the environmental pool (both in
response to a forcing function of DDT usage), and the third
described concentration in human adipose tissue.

The parameters

in each equation are a^, expressing the rate of uptake in rela­
tion to the magnitude of the source, and b-j, elimination constants.
Intake by man, therefore, is proportional to the sum of the first
two elements, since the food concentration is the result of both
sources of contamination.

The model was first implemented on an

analog computer, programmed so that the values of the parameters
could be changed through a wide range of values, and the model
behavior compared to the data points.

Values of the parameters

were changed until the model successfully mimicked the data for
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-55-

1965-1970.

The function representing DDT input to the system

was taken from the data on DDT usage, and was assumed to be linear.
- The final model generated values for food concentrations and
human load that matched the data available very faithfully.
A series of simulations then was performed*on the digital

.

computer to examine changes in DDT and DDE concentrations in man
under various assumptions about DDT application.

A series of

six runs was made for a period of fifty years, four of which are
summarized in Table 2.
•

j

In the first case (column 1), the model

.

was used to extrapolate concentrations in human adipose tissue with
DDT usage continuing to decrease at the present rate of about seven
million pounds a year.

The assumption of linear decrease implied

an anticipated application of 5,000,000 pounds in 1972 dropping to
zero in 1973.

The model predicts that the level in man will con­

tinue to decline, reaching 1 ppm by 2002, but that fifty years
after .ceasing DDT usage, there would still be measurable quanti­
ties of DDT plus DDE in man.

The second column shows the result

of ceasing DDT usage in 1972 (i.e., a zero application).

The

differences between columns 1 and 2 are detectable only in the second
decimal place.

The third example shows the results when DDT usage

is maintained at five million pounds per year after 1972.

In this

instance, the levels in man would continue to decline, but would
be maintained at a significantly higher level in the long run,
remaining above 1 ppm after fifty years.

The fourth column describes

the reponse to continue DDT usage at the level of 1966.

After the

initial decline, apparently due to improved application practices,
'

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and the slowness of buildup in the environmental pool, the concen­
trations in man begin to rise by 1978, eventually reaching some
asymptotic value above 6.7 ppm.

.

In evaluating these results, the limitations of the model
structure, the data, period, and the data* reliability must all
be considered.

The predicted long-term concentrations should not

be viewed with as much confidence as the general response patterns
over time and the relative concentrations under the various
treatments.

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Table 1.

DATA UTILIZED FOR MODELING DDT AMD DDE MOVEMENT THROUGH
THE HUMAN FOOD CHAIN; THE DATA WERE SUPPLIED BY THE
ADVISORY COMMITTEE FROM THE RESULTS OF CURRENT
.

*

-

MONITORING PROGRAMS IN U. S. GOVERNMENT AGENCIES.

DDT
Usage

•

DDT + DDE
in marketplace diet
(mg./day)

DDT + DDE
in human
adipose tissue (ppm)

Year

(106 lbs.)

1965

53

1966

46

.040

40

.026

4.65

33

.019

5.61

1969

.016

5.22

1970

.015

5.27

1967
1968

'

■ •

.

.

.031

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Table. 2.

DDT + CONCENTRATIONS IN HUMAN ADIPOSE TISSUE PREDICTED
BY THE MODEL FOR VARIOUS ASSUMPTIONS ABOUT DDT USAGE.

'

-

■

.. Year

Continued
reduction
of DDT usage
at present
rate.

Zero future
usage of
DDT

DDT usage
maintained
at 5 x 106
lbs./year

DDT usage
maintained
at 1966
levels

1970
1974
1978
1982
1986
1990
1994
1998
2002
2006
2010
2014
2018
2022

5.14
4.18
3.41
2.78
2.27
1.86
1.52
1.24
1.01
0.82
0.67
0.55
0.45
0.37

5.14
4.13
3.35
2.73
2.23
1.82
1.49
1.21
0.99
0.81
0.66
0.54
0.44
0.36

5.14
4.20
3.53
3.02
2,60
2.25
1.98
1.75
1.56
1.41.
1.29
1.18
1.10
1.03

5.30
5.08
5.32
5.60
5.84
6.03
6.20
6.32
6.43
6.52
6.59
6.65
6.70
6.73

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