.OP1S-TECHNICAL INFORMATION CENTER
                                 REPORT






                                  of   the






                                    DDT






                               ADVISORY






                               COMMITTEE
                               September 9, 1971

-------
            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.

-------
                                  &>.iJwwilsi yJ
           THE UNIVERSITY DF TEXAS  MEDICAL BRANCH
                       BALVESTDN, TEXAS 7755D
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 ,

                                            <~7
                                        X/James G.  Hilton, Ph.D.
                                       {/  Chairman
                                            DDT Advisory Committee
  JGHrdwa

  Enc.

-------
                           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 the Environment      19
Toxicology                                                 24
Needs                                                      35
Conclusions                                                39
Recommendations                                            41
Imminency of Hazard                                        42
Appendices
     A.  References Cited                                  44
     B.  Persons Appearing Before the Committee            49
     C.  Exhibits Furnished to the Committee               51
     D.  Abstract of Systems Model Report                  52

-------
                 -1-
MEMBERSHIP OF DDT ADVISORY COMMITTEE
James G. Hilton, Ph.D.,  Chairman
Professor of Pharmacology
University of Texas Medical  Branch
Galveston, 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

-------
                              -2-
                            INTRODUCTION

      DDT  (Dichloro-diphenyl-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 ttie  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

-------
                              -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 involved 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 report 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
available since these reports.
     For the sake of convenience this report is divided into four
major sections followed by the conclusions and recommendations of
the Committee.  In general, "DDT" is used to mean the combination
of DDT and its metabolites.  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

-------
                                  -4-

monitoring data'avail able.  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.

-------
                               -5-
                   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.

-------
o
o
o
H
Q
Q


to
O
PU
   180 I
   160
   140
   120
   100
    80
    60
    20
         /     -*
*       *                              '*
          U.S.  Estimated  Domestic Use     \

«c m vo rx
-3- <• -icovrmvoi^-eo ON
^r-^mmininininininmirivovOvOvovovovovovo vo
CN ON ON ON ON ON ON ON ON OS OS OS ON ON ON OS OS ON ON ON ON Os
                                                       YEARS
                        Figure 1.   United States production and estimated usage of  DDT.   Data from

                                   Pesticides Review 1970; Stickel  1965;  Goldberg,  et  al_.  1971.

-------
                              -7-
 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.
f
     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  a]_.  1968, and Goldberg 1971).  Because of the  difficulty

-------
                                -8-
 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
 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 transport 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

-------
                               -9-
and for export from the sites of application.   Codistillation  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.
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 e_t 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 is 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
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 high use in the 1950's but in the
mid-1960's in England rainwater samples averaged (K08 ppb, and during

-------
                                -10-
 1968-69  in  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,

-------
                             -11-
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
to result primarily from the process of biological concentration in
natural ecosystems.  Woodwell (1970) and Harrison ejt al_. (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 ODD 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 ejt 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

-------
                               -12-
 levels.  Another major pathway is through the utilization of DDT-
 contaminated dead organic matter in the sediments of water systems
 by  benthic organisms.
     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 about 8 ppm.  Residues of 5 ppra 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 situtation of freshwater ecosystems is probably best illustrated
 by the results of studies published by the Wisconsin Conservation
 Department (Kleinert e_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.

-------
                              -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 Lueschow and Winter
(1970) concludes that "The Food and Drug Administration limitation
of 5 parts per million of DDT in fish which 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  mid-1940's in a wide  range
of species.  Where shell thinning has occurred, the populations  have
usually declined (Ratcliffe 1967, Mickey 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 1969, Heath et al_. 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

-------
                                -14-
 initiated much earlier  than the monitoring of DDT in other sectors of
 the  environment,  and as a result the change in levels of contamination
 of foods is well  documented.
      The most up-to-date data provided to the Committee were those from
 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,
 G. 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 1

DDT + DDE
DDE
.evels in Market-Basket Diet (in milligrams/day)
FDA Data
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,
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.

-------
                              -15-
     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%.   Over  the  same  period  the
average daily intake of DDT compounds declined  from  20 percent of  the
FAO-WHO 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 are 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.

-------
                                -16-
Table 2.  Mean Levels of Selected Chlorinated Hydrocarbon Pesticide
          Residues in Adipose of the General  Population (ppm)
                            Dr. Ann Yobs
                      Human Monitoring Survey
Year
# Samples
Method
pp DDT
pp DDE
Total DDT
equivalent
1967
722
(non-
cleanup)
1.28
4.22
6.22
1968
3300
(non-
cleanup)
1.52
5.28
7.60
1968
3237
(Mod.i/
MOG)
1.53
4.08
6.26
1969
3264
(Mod.
MOG)
1.20
4.02
5.81
1 970i/ 1 971
2626
(Mod.
MOG)
1.15
4.12
5.97
—'  Incomplete data 6/6/71
—  MOG=Modified 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.  Unfortunately, no recent
data were available for the United States.  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.

-------
                                -17-
     Projections of the expected  environmental  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
ti me.
     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 break-
down 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.

-------
                               -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 of 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.

-------
                             -19-
        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.S.  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.
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 organo-
chlorine 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 pesti-
cidal 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

-------
                              -20-
 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 both 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,  ODD, 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.
    Considering the most common Aroclors found in the environment,
 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 quantifi-
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 PBC:DDT concentration
in the environmental  sample approaches 5:1  or  higher.   One reason for

-------
                                -21-
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, ODD 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 e_t 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
other published data, it appears that the most serious chronic PCB
contamination is in fish and fish-eating  birds.  Apparently   PBCs are
widely distributed among marine birds which are  the terminal  carnivors
of a complex mesh of food chains in the  sea.   Concentrations  of DDT and
PCB in marine birds tend to be an  order  of magnitude  higher than  in
marine fish according to Risebrough e_t al_.  (1968).  Occasional acute PCB
contamination occurs in various areas of our  environment leaving  the

-------
                                -22-
 mistaken  impression  that  serious PCB contamination is a universal
 problem.   Most  of  the  acute  residues of PCRs found to date can be
 attributed usually to  inadvertent or accidental industrial causes.
 A  recent  example of  acute PCB contamination in poultry was traced
 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, DDD 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
 eŁ 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  appear that generally the PCR 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

-------
                             -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
that the PCB problem is not of widespread concern.  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.

-------
                                -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
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 (J.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 well-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 doses 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

-------
                               -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 in 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 chronrc 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 ejt al_., reported
that rats fed 5 ppm of DDT for 6 months  showed detectable liver
changes.  Ortega ejt 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

-------
                               -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 levels  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 were 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 eŁ  ^1_., 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
both  the numbers of individuals  and  duration of  follow-up to con-
tribute information concerning possible carcinogenic effects.

-------
                              -27-
     Carcinogenicity of DDT.  The question of the potential  car-
cinogem'city 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 ejt 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
multigeneration studies in mice fed 3 ppm DDT.  A generalized increase
in the frequency of tumors in the $2 ar}<* following generations was
noticed.  Multigeneration studies in mice, in progress, sponsored
through the International Agency for Research on Cancer both at
Lyon 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, b.oth in animals given DDT.  With other hepatomas  after

-------
                               -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
weight may be involved.  Carbon tetrachloride, chloroform, and
brombenzine show increased liver toxicity after stimulation of
microsomal oxidase activity.  One expression of this toxicity might
be hepatoma production.
     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.
     There is no evidence from human epidemiological studies to
shed light on the possible human carcinogen!city 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

-------
                               -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
dividing plant cells.  A recent report suggests DDE may be asso-
ciated with chromosome rearrangements in wild Drosophila, but the
association was quite indirect  being related to DDE levels in fat
bodies of local frogs.  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

-------
                               -30-
 intraperitoneal  route  for  21 days beginning at 24 hours after birth
 (Fahim e_t  aj_.,  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

-------
                               -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 e_t al_., (1969) in which
mallard ducks were fed various levels of DDT, DDE, and ODD.   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.  Survival of hatchlings was  not
affected.  ODD did not impair reproductive success.  DDT induced
thinning of shells and reduced duckling  survival only when a level
of 25 ppm was fed.  None of the treatments induced crippling among
hatchlings.  This type of information is valuable because it shows
the higher sensitivity of this species to DDT and DDE than is
observed in mammals 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-
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

-------
                               -32-
described in 1944  (Ellis ^t aK) 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 Commerical Fisheries.  (Now:  Gulf Breeze Marine Laboratory,
EPA).  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  below those of concern to mammalian
species.  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

-------
                             -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  DDT
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 ejt al_., 1970).
     Recent evidence suggests that DDT can inhibit  MG++ ATPase in
rabbit brain (Koch, 1969) and Na K ATPase  in  teleost  GI 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 telcosts.
     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

-------
                              -34-
are not known for ODT 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
chemicals such as PCB's.

-------
                              -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
measures for the control of their depredation.   Although there are
many types of useful insect control  practices, it was  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-insecti-
cidal 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

-------
                               -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.  Even 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

-------
                              -37-
range of 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 variation 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 DPT 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 be 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.  But what then of
the interim, when no alternatives are  available?  The Committee recognized
the significant reductions in domestic  use which have already  occurred and
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

-------
                               -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 signfi-
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.

-------
                              -39-
                          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.  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 biologi-cal 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

-------
                               -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 hody 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 the reports of the wide distribution of DDT in the
environment.

-------
                                -41-
                      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 completed, 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.

-------
                              -42-

                       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
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, 2,4,5-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 correcte'd 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

-------
                               -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 widespread 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,
                                                                /t^S'.
                                        JSmes G.  Hilton, Ph.D.

-------
                                -44-



                           APPENDIX A

                           REFERENCES


Armour, J. A. and Burke, J. A.:  Method for separating polychlorinated
  biphenyls from DDT and its analogs. J. Assoc. Offic. Anal.  Chemists
  53:  761, 1970.                     	

Bagley, G. E., Reichel, W. L., and Cromartie, E.:  Identification of
  polychlorinated biphenyls in two bald eagles by combined gas-liquid
  chromatography-mass spectrometry.  J. Assoc. Offic.  Anal.  Chemists
  53:251, 1970.

Bowman, M. C., Acree, F., and Corbette, M. K.:  Solubility of DDT -C14
  in water.  J. Agr. Food Chem.  8:906, 1960.

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.:  Monitoring pesticide pollution.  Bioscience
  19:  889:891, 1969.

Butler, P. A.:  Pesticide residues in estuarine mollusks.
  National Symposium on Estuarine Pollution, Stanford
  University, sponsored by American Society of Civil "
  Engineers, Sanitary 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, J. 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. Y. Acad. Sci.
  160:  162-172, 1969. -

Edwards, C. A.:  Insecticide residues in soils.  Residue
  Reviews 13:  83-132, 1966.

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

-------
                             -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. Therap.  89:  18-30,  1947.

Ginsburg, J. M.:  Toxicity of  DDT to  fish.  J. Econ. Entomol.
  38:  274-276, 1945.

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.  Wildl.  Res. Rept. 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. 0., Jr.:  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. J., Jr.:  The degree of hazard to man on DDT as used
  against malaria.  World Health  Organization Report WHO/Mal/
  71: • 783, 1971.

Hayes, W. J., Jr., 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., Jr., 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, J. 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. J., Keith, J. 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, J. H., and Tatton, J. O'G.:  Chlorinated
  Hydrocarbons in British wildlife.  Nature   216:   227, 1967.

-------
                               -46-
 Innes, J. R. M., inland, B. M., Valeric, 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. Cane.  Inst.  42:   1101-1114
  1969.

 Janick, R. and  Kinter, W. B.:  DDT:  Effect on ATPase and water
  absorption in fish.  Federation Proceedings 30(2):   673

 Jeffries, D. J. 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.

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

 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 arid 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
  components of lobster nerve membrane conductance.  J.  Gen.
  Physiol. 51 (2):  177-198, 1968

-------
                            -47-
Nash, R. G. and Woolson, 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  Monograph
  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.:  Effect of DDT on reproduction  in the  rat.  Toxicol.
  Appl. Pharm.  14:  74-81, 1969.

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

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  Conney, 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.  Contam.  & 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.

-------
                          -48-
 Risebrough, 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. Contam. & Toxic.  4:   192, 1969.

 Sides, P. J.:  Effects of 2,2,-Bis (P-chlorophenyl)-l, .1,  1-Tri-
   chlorethane (DDT) on toad bladder.   Federation Proceedings  30(2)
   294 (565), March-April 1971.

 Stickel, L. F.:  Organochlorine pesticides in the  environment.
   Fish and Wild!. Serv. Special Scientific Report.   Wildlife  No.  119.
   1968.

 Tarjan, R. and Kemeny, T.:  Multigeneration studies on  DDT in mice.
   Fd. Cosm. 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
   Dichlorodiphenyltrichloromethylmethan.   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 Fehringer, 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. Pharnu 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.  Water, Air and Waste Chemistry Section of the  American
  Society.~"Abstract. WATR-032,

-------
                              -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
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 E. Hazel tine,  Butte County (California)  Mosquito Abatement
  District
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 (spoke 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
  Protection Agency
Dr. Charles F. Wurster, Jr., University of New York at Stoneybrook,
  representing Environmental Defense Fund
Dr. David Young, Mississippi State University

-------
                              -50-
                       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. Upholt, Office of Pesticides Programs, Environmental
  Protection Agency

Dr. G. B. Wiersma, Office of Pesticides Programs, Environmental
  Protection Agency

Dr. Ann Yobs, Division of Community Studies, Environmental  Protection
  Agency
                         Third Meeting

                    July 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

-------
                               -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, September 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 alI. Petitioners
     Vi!  William 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

-------
                             -52-
                         APPENDIX D
       A SIMPLE SYSTEMS MODEL FOR DDT AND DDE MOVEMENT
                  IN THE HUMAN FOOD-CHAIN

                       R.V. O'Neill1
                           and
                       O.W. Burke2
Abstract of a Report submitted to the Advisory Committee on DDT3

   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 ecolo-
ical 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

1  Ecological Sciences Division ORNL
2 Instrumentation and Control Division, ORNL
3 Carried out and supported in part through the Deciduous Forest
  Biome Study of the U.S.  International Biological Program.

-------
                            -53-
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 1966, the system has become dominated by an environmental  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.  This 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  fluctua-

-------
                                -54-
 tions 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 ^, expressing the rate of uptake in rela-
 tion  to the  magnitude of the source, and b-,-, 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

-------
                           -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.  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,

-------
                             -56-
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.

-------
                              -57-
Table 1.  DATA UTILIZED FOR MODELING DDT AND 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.
Year
1965
1966
1967
1968
1969
1970
DDT
Usage
(106 Ibs.)
53
46
40
33


DDT + DDE
in market-
place diet
(mg./day)
.031
.040
.026
.019
.016
.015
DDT + DDE
in human
adipose tis-
sue (ppm)


4.65
5.61
5.22
5.27

-------
                           -58-
Table. 2.  DDT + CONCENTRATIONS IN HUMAN ADIPOSE TISSUE PREDICTED



           BY THE MODEL FOR VARIOUS ASSUMPTIONS ABOUT DDT USAGE.


Year


1970
1974
1978
1982
1986
1990
1994
1998
2002
2006
2010
2014
2018
2022
Continued
reduction
of DDT usage
at present
rate.
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
Zero future
usage of
DDT


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
DDT usage
maintained
at 5 x 106
Ibs./year

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
DDT usage
maintained
at 1966
levels

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

-------