;A£ h.
REPORT OF THE ALDRIN/DIELDRIN ADVISORY COMMITTEE*
TO
WILLIAM D. RUCKELSHAUS, ADMINISTRATOR
ENVIRONMENTAL PROTECTION AGENCY
March 28, 1972
*Established Under Provisions of Section 4.c of the Federal
Insecticide, Fungicide, and Rodenticide Act.
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CONTENTS
Page
Letter of Transmittal v
Membership of the Advisory Committee vii
Report
Human intakes and their significance 1
Effects on wildlife and plants 3
Aldrin and dieldrin in sediments 5
Economic considerations 6
Other committee reviews 9
Conclusions 11
Recommendati ons 12
Appendi xes
I. Uses of Aldrin and Dieldrin 15
II. Toxicology, Metabolism and Biochemical Effects
on Non-Human Species 27
III. Carcinogenic and Mutagenic Effects 41
IV. Residues in the Environment and Man 47
V. Environmental Movement and Change 52
VI. Soil Insect Control 62
Supplements: Occurrence of Aldrin and Dieldrin
in Biological Environments
A. Dieldrin Contents of Bottom Feeding Fish 72
B. Marine Environments 73
VII. Impact of Withdrawal of Soil Uses of Aldrin
and Dieldrin 74
Li terature References 77
Persons Appearing Before the Committee 99
iii
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COLLEGE OF ARTS * SCIENCES
Qf j ufE SCIENCES
A Statutory College of the State University
CORNELL UNIVERSITY
DIVISION OF BIOLOGICAL SCIENCES
ITHACA, N. Y. 14850
Office of the Director
200 Stimson Hall
607-256-5042
March 24, 1972
Dear Mr. Ruckelshaus:
The report of your advisory committee on aldrin and dieldrin is
enclosed. The report consists of first, a brief review of our analysis of
the situation, in which we have responded to the charge to the committee;
second, a series of six recommendations; third, a set of six technical
appendices, each of which reviews the pertinent scientific literature in
a given area, and upon which most of our analysis is based.
The committee had 4 day-long meetings in Washington. All of the
individuals or groups who wished to appear before us did so, and in addition
we received verbal and written testimony from several authorities whose
advice we solicited, on subjects as diverse as chemical carcinogenesis and
agricultural economics. In addition, each committee member performed, at
his own institution, extensive research and review in the area of his own
expertise, and had the benefit of the knowledge and views of appropriate
colleagues at that institution.
I am happy to tell you that the committee was unanimous in the views
and recommendations we bring to you, and that although our technical
backgrounds are so diverse, we readily found agreement both upon the
general approach we recommend to you, and upon the specifics.
Yours sincerely,
Enclosure
RDO'B: o
R. D. O'Brien, Chairman
Advisory Committee on
Aldrin and Dieldrin
Mr. William D. Ruckelshaus
Administrator
Environmental Protection Agency
Washington, D.C. 20460
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MEMBERSHIP OF ALDRIN/DIELDRIN ADVISORY COMMITTEE
Richard D. O'Brien, Ph.D., Chairman
Director, Division of Biological
Sciences
200 Stimson Hall
Cornell University
Ithaca, New York
Richard L. Doutt, Ph.D.
San Joaquin Valley Agricultural
Research & Extension Center
9240 S. Riverbend Avenue
Parlier, California
Mahlon L. Fairchild, Ph.D.
College of Agriculture
University of Missouri
Columbia, Missouri
Samuel D. Faust, Ph.D.
Department of Environmental
Sciences
Rutgers University
New Brunswick, New Jersey
Florence K. Kinoshita, Ph.D.
Toxicity Laboratory
Department of Pharmacology
University of Chicago
Chicago, Illinois
Richard A. Parker, Ph.D.
Department of Zoology
Washington State University
Pullman, Washington
Stephen S. Sternberg, M.D.
Sloan-Kettering Institute for
Cancer Research
410 East 68th Street
New York, New York
vii
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REPORT OF THE ADVISORY COMMITTEE ON
ALDRIN AND DIELDRIN 3/23/72
Aldrin and dieldrin are compounds used widely today for a
variety of insecticidal purposes. Their major use is for control
of soil insects in corn. Aldrin is readily converted to dieldrin
in soil and many biological systems, and thereafter is only slowly
deqraded to biologically inactive products; as a result dieldrin
has contaminated the American diet in a widespread way, although
the contaminating amounts are very small. Several reoorts claim
that the world's environment is generally contaminated with one
or both compounds, but these claims must be regarded with caution
because few studies have used analytical methods which respond
only to these compounds. For example, sulfur and PCB's (polychlor-
inated biphenyls) may be mistaken for aldrin. A compelling demon-
stration of the need for unusually careful analysis is the report
that standard assays for aldrin upon soil held in sealed storage
since 1909 (long before aldrin or dieldrin were in use) showed ap-
parent aldrin and dieldrin residues in 20 of the 34 samples assayed.
Human intakes and their significance.
There is clear evidence that Americans consume significant
amounts of aldrin and dieldrin daily; for 1968-9, for instance,
the average intake for a 70 kg adult was 5 ug/day. Levels in
dairy products were highest (0.05 pom of food), in meat products
a little less (0.03 ppm) and in cereals and vegetables quite small
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(below 0.01 ppm). It should be noted that these intakes do not
accumulate in the body indefinitely; instead the levels in the
body achieve a fixed concentration characteristic of the intake
level. In the United States the levels in the body fat of the
general population average 0.15 ppm. This raises the questions:
are these fat levels a cause for alarm, and can steps be taken to
reduce or eliminate them without disproportionate damage to the
national welfare?
We consider that the available evidence suggests that the
small human intakes and consequent body burdens are harmless. Not
only are they far below the amounts shown to be toxic to labora-
tory animals, but human beings, either volunteers or those exposed
industrially, have taken in much larger amounts than the general
population with no untoward results. For example, occupationally
exposed men received 50x the average intakes of dieldrin for peri-
ods of from 4 to 13 years, and not only showed no sign of toxi-
city, but failed to show the minor effects upon liver function
which are early signs of bodily changes produced by such compounds.
Supporting evidence is that we have a series of depositions from
University Extension Agents, pest control applicators and retailers
testifying that no untoward effects have been reported from the
use of aldrin or dieldrin.'
But there is no doubt that dieldrin can cause malignant
tumors of the liver in one strain of mice. In one other strain,
hyperplastic nodules of the liver were produced, but no carcinomas.
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Consequently one cannot dismiss the possibility that sufficient
doses of dieldrin could be carcinogenic in man, but the degree
of certainty is inadequate to reouire prompt elimination from the
diet. One must also note that in rats, dieldrin at 20 ppm or more
in the diet decreased malignant mammary and lymphatic tumors; for
instance, in males 14% of controls had such tumors, but only 6%
of treated animals had them.
It seems clear that the species selected for test is impor-
tant. Furthermore, there is reason to believe that fetal organisms,
because of their high mitotic rate, might be unusually sensitive,
and it is clear that placenta! transfer occurs in humans(271). Con-
sequently we would like to see studies on effects upon fetal
animals whose mothers are treated and which are also postnatally
exposed. We shall propose, below, tests to improve our ability
to estimate human hazard, as well as measures which we believe will
reduce human dietary intakes.
Effects on wildlife and plants.
Data upon the toxicity of aldrin and dieldrin to fish and
crustaceans lead us to accept such terrible accounts as that de-
scribing the effects of 1 Ib/acre of dieldrin on 2000 acres of
Florida salt marsh used for sandfly control: "--fish kill was
substantially complete. The minimum Immediate overall kill —
was 20-30 tons of fishes -—. Crustaceans were virtually exter-
minated throughout the area"(105). For such reasons, we believe
that applications to aquatic habitats must be forbidden; one
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should recall (see appendix) that even 3 ppb in water can cause
measurable toxic effects in some fish.
As for effects upon terrestrial vertebrates, the hazards are
less extreme. Thus rather high levels of dieldrin (ca. 1 ppm in
the diet) are needed for production of thin-shelled eggs in ducks,
in one of the few carefully controlled experiments(162). In sparrow
hawks, the high dose of 3 ppm of dieldrin plus 15 ppm of DDT pro-
duced a maximum eggshell thinning of 16%(202). Furthermore the re-
ported effects of dieldrin upon carbonic anhydrase (thought to be
causal in eggshell thinning) have recently been shown to be arte-
factual, being caused by coprecipitation of the soluble form of the
enzyme used in laboratory studies(201). Much of the data on effects
upon wild birds is impossible to evaluate because dead birds were
collected without establishing the cause of death, and they con-
tained a variety of pesticide residues. Data upon bald eagle deaths
is particularly suspect in this regard(191).
Nevertheless we accept that in at least some avian species,
quite low levels of aldrin or dieldrin may have adverse effects;
thus 1 ppm of aldrin in the diet reduced egg production of pheas-
ants by 17%, in quail by 23% and 1 ppm of aldrin or dieldrin was
lethal to 100% of quail chicks(56). To avoid adverse effects on
wildlife, aldrin and dieldfin must be used in ways which cannot
lead to intake levels of several ppm for birds. The use of aldrin
applied directly to soil at 1 Ib/acre over 16 years leads to levels
of about 1 ppm (aldrin plus dieldrin) in a variety of insects, and
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less than 0.02 ppm in a variety of seeds of plants grown in that
soil(155). Such usage is unlikely to lead to substantial effects
on wildlife.
There appear to be no reports that aldrin or dieldrin have
adverse effects upon plant life.
Aldrin and dieldrin in sediments.
Because use of aldrin in soils is so extensive, special atten-
tion needs to be given to the question of loss by means of sediment
run-off from the soils to which aldrin is applied and firmly bound.
The 1971 study of Rykman et al_, for EPA points to this as the dom-
inant route for contamination. It points to the millions of tons
of sediment carried in the country's major rivers, and provides
one estimate that, as an example, "about 10 tons of dieldrin are
annually carried in the Mississippi at St. Louis"(p.l5). If
these data were reliable, we would have to agree that their source
of pollution was exceptionally important and would perhaps suggest
that soil application of these agents should be banned. But this
estimate assumed that the residues in farm soils and in river
sediments are the same. On p.14 this same report states that for
Iowa (the only state for which both funds of data are given) the
dieldrin in farm soils averages 107 ppb, but in river sediments
„* ;
averages 11 ppb, and they compute that "if this amount of dieldrin
was in the sediment load passing St. Louis, the total annual diel-
drin pesticide load would be 260 IDS"; thus the alarming 10-ton
to
figure is utterly misleading.
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In addition, it is not at all clear what is the toxic signifi-
cance of these sediments. We do not know if the dieldrin or aldrin
which is bound to these sediments is biologically available. If
sufficiently firmly bound, it might be able to pass through the
tracts of bottom-feeding fish without being absorbed and in fact
the data of Appendix VI-A suggest that bottom-feeding fish do not
acquire especially large residues. By contrast we may assume the
water levels of dieldrin to be fully available biologically; diel-
drin (but not aldrin) is indeed widespread in river water, but the
highest recorded level (in 1968, in the Tombigbee River, Columbus,
Miss.) was 0.4 ppb; typical Mississippi River levels are about
0.015 ppb. The EPA suggests 10 ppb as acceptable water qualtiy
criteria (although data in Appendix II show that even 3 ppb can
have undesirable effects in some fish). The amounts in river water
do not seem to be alarming.
Economic considerations.
One of the problems we have encountered is the grave inade-
quacy of the estimates of the economic implications of insecticide
use. Let us illustrate this with the major economic usage; aldrin
for treatment of soil insects in corn. Some problems are:
(a) There is little experimental data to show the effects
upon yield of withdrawing aldrin or substituting it with non-
persistent compounds.
(b) The available estimates deal with average effects on
national yields. But in fact these will involve very drastic re-
ductions in limited areas of severe infestations, with lesser
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effects elsewhere. How much consideration should we give to the
impact upon individual farmers in such cases?
(c) The importance of insecticide withdrawal is likely to
vary from year to year, as pest infestation varies.
(d) Withdrawal effects may seem small at first, but become
progressively worse as the residues of aldrin or dieldrin dwindle
over the years.
(e) The implications of a given dollar loss, either in reduced
yield or increased treatment cost, depends on the margin of profit
the farmer operates on, and is hard to assess. Furthermore, the
profit depends largely upon such artificial factors as the support
prices in any year, and the status of the export market.
In spite of these grave difficulties, rough estimates have
been made by Dr. J. H. Berry of USDA, suggesting that the dis-
continuance of aldrin and dieldrln would lead to losses (at 1969
prices) of $14 million for crops where no replacement is possible,
plus $34 million for crops where alternative insecticides are
available (this includes aldrin use on corn), for a total of $48
million (these estimates assume no price increases for the crop;
clearly the losses could go to zero for the producer, if all extra
costs were passed along to the consumer). It should be emphasized
that although we have no quarrel with the procedures used by the
economists in assembling these estimates, the data which they used
were necessarily meager and some of them were 10 to 15 years old.
There has been no direct attempt to design field experiments to
find the economic costs of aldrin-dieldrin replacement. In the case
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of crops other than corn, there was an even graver deficiency of data
upon the economics of insecticide use.
These rough economic analyses provide an incomplete picture.
The reduction in corn yield by aldrin replacement could be as little
as 1% nationally. Should one neglect this in view of the current
national corn surplus? Should one be concerned if aldrin-dieldrin
withdrawal prohibited the continuance of certain crops in particular
farm areas? Or if it severly affected (or even eliminated) crops
such as mangoes, pineapples or sweet potatoes, whose national eco-
nomic impact is relatively slight, but whose local importance may
be major? Our response to such questions was to exercise caution
in recommending withdrawal.
Another factor is the steady growth of insect resistance for
aldrin-dieldrin, especially in soil insects. We believe that this
factor will lead to a progressive decrease, especially in aldrin
use, and that this will cause an important reduction in dietary
intakes; corn is the major usage of these compounds, and most di-
etary intake is from meat and dairy products (which derive much of
their nutrition from corn) so that human intakes are likely to be
geared to usage on corn.
An unexpected problem is that farmers may not know what pests
they are controlling! Thus we received 16 petitions from very
many rice farmers telling us how important was their use of diel-
drin for seed treatment to control rice water weevil. But our USDA
experts told us that this use of dieldrin was now ineffective for
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rice water weevil, but important for the grape colaspis. Even for
soil use on corn, there was disagreement about just what pests are
controlled. All that the farmers can know is that his regular use
of such compounds gives protection from undue insect damage. He
is not likely to omit treatment in order to find out what pests are
truly damaging that year.
The problem is compounded by the fact that corn farming (for
instance) has been improved to give very much larger yields, up to
two-fold increases in the last 15 years. This intensive farming
uses heavy investments in equipment, fertilizer and herbicides as
well as insecticides, leading to a high investment enterprise re-
quiring very efficient growth conditions. The economics are
correspondingly more fragile.
Other committee reviews.
We are keenly aware of the fact that we are a part-time com-
mittee whose recommendations are based upon a reading of the
literature but only a few meetings together. But our conclusions,
independently arrived at, are consonant with those of the other
expert committees who have examined the evidence in recent years.
In 1965, the Popper Committee (advisory to FDA) bearing in mind
principally the possible dangers to humans (but not to wildlife)
recommended continued use of aldrin and dieldrin for certain nes-
ticidal purposes. Also in 1965 the Jensen Committee (of NAS-
NRC) pointed to the importance of use of pesticides, including
persistent ones. In 1967 the Gunther Committee (advisory to FDA)
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reviewed aldrin and dieldrin use, and concluded that current toler-
ances were acceptable, but pointed to the need for additional
research e.g. on careinogenicity in more species, and epidemio-
logical studies. In 1969 a committee reporting to the Aa. Res.
Service, USDA, proposed that persistent pesticides as currently
used were necessary, but called for "steps to be taken to reduce
the needless or inadvertent release" of them. It also called for
further research e.g. on additional means of control and on long
term effects on man and wildlife. In 1969 the Wilson Committee
(advisory to the British Dept. of Education and Science) found
that there was no evidence that dieldrin was harmful to man, and
so "no high priority can be presently assigned to the removal ---
of dieldrin"; but that it is "undesirable that the human environ-
ment should contain substances capable of producing toxic effects".
In 1969 the Mrak Commission (advisory to the Secretary of HEW)
recommended that aldrin and dieldrin be restricted "to specific
essential uses which create no known hazards to human health or to
the quality of the environment and which are unanimously approved
by the Secretaries of Health, Education and Welfare, Agriculture
and Interior". The commission noted that it was "impractical to
attempt to eliminate the residues of such pesticides from foods by
the application of zero tolerance techniques" because analytical
techniques are so extraordinarily sensitive. In 1970 the Joint
FAO/WHO expert committee recommended a series of tolerances of
aldrin or dieldrin in foods such that the daily intake in man should
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not exceed 0.1 ug/kg/day (roughly twice the typical U.S. intake).
Conclusions.
We find no evidence of human injury from present or past use
of aldrin or dieldrin. Nevertheless the facts that fairly low
levels of dieldrin can cause cancer in mice and interfere with re-
production in some birds are matters for concern, and point to the
need for more careful evaluation of the hazard to man. There is
clear evidence that past usages have been deleterious to wildlife.
Several such past usages have been voluntarily abandoned by Shell
Co. Nevertheless, we feel that we must strive to find alternate
methods of pest control, including nonchemical methods, for all com-
pounds which lead to persistent residues in humans or wildlife,
even when such residues are not demonstrably harmful. How can we
move towards this objective?
When aldrin or dieTdrin can be safely and economically re-
placed by nonpersistent pesticides they should be so replaced.
Several practices which can readily lead to damaging effects upon
non-target organisms should be abandoned now in spite of the dif-
ficulty of economic replacement, including all applications which
lead to contamination of aqueous environments such as rice fields
and waterways.
The direct application of aldrin or dieldrin to soils leads
to negligible leaching or other transfer from those soils, and
environmental contamination-is.thus very small except where sub-
stantial erosion takes place. One of the few studies to estimate
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the amount which volatilized indicates that 3% escapes this way,
and thus contaminates the environment directly (we would like to
see more extensive data upon this point).
Recommendations.
The following recommendations are designed to build a basis
of facts on which permanent recommendations can be formulated, and
to eliminate now those uses of aldrin or dieldrin which result in
significant environmental contamination (especially to waterways).
We believe that applications directly to soil or to materials
buried in soil (e.g. termite control in foundations, and seed
treatments when properly applied) lead to little subsequent move-
ment of these insecticides, and should be permitted.
In the following recommendations, we use the term "experts"
and "acknowledged authorities" advisedly. The EPA must seek
contractual or other arrangements with individuals and institutions
accepted as authorities by their peers in the country at large.
1. A committee of experts in chemical carcinogenesis should
be formed to propose specific experiments and to agree upon suit-
able protocols to provide a firm indication of the extent of
carcinogenic hazard. These experiments should include studies (in
at least two vertebrate species) on the effects on the progeny of
mothers fed dieldrin during pregnancy and nursing, the progeny
also being fed dieldrin thereafter.
2. The economic consequences of total withdrawal of aldrin
and dieldrin should be explored in depth: On all major crops,
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actual experimental studies must be performed to obtain new, re-
liable data provided by acknowledged authorities, and should in-
clude studies with and without alternative nonpersistent pesticides,
over a series of years, and in appropriately distributed geograph-
ical areas.
3. The fraction of aldrin and dieldrin which escapes by
volatilization following application to a variety of soils, under
conditions of application and treatment levels commonly used in
pest control, should be measured by acknowledged authorities.
4. Monitoring stations should be established in the U.S. and
abroad, at which air and water samples can be taken at fixed places
over a series of years, and analyzed by unambiguous procedures for
aldrin and dieldrin. The intent is to study whether the restric-
tions we propose do indeed lead to a progressive removal of these
compounds from the environment. Agreement should also be sought
amongst a group of experts for unambiguous procedures for deter-
mination of aldrin and dieldrin in extracts of air, soil, water,
food and human and nonhuman tissues. Such procedures should be
standardized in the U.S. and preferably internationally as well.
5. The following uses of aldrin or dieldrin should be dis-
allowed.
(a) All applications by aircraft.
(b) All foliar spraying or dusting.
(c) Moth proofing by the hot acid dye bath method or re-
lated methods in which residues are discharged into waterways or
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14 .
settling ponds.
(d) All uses, whether by homeowners or pest-control
operators, in homes, barns, poultry operations or other structures
occupied by humans or livestock.
(e) Use upon turf (including lawns and non-grazing grassed
areas) except as supervised or controlled by trained or licensed
pest-control operators, greenskeepers and nurserymen.
(f) Any use which involves application to streams, ponds,
lakes, flooded areas or any other aquatic environments.
6. Specific uses of aldrin and dieldrin which we believe to
be valuable and not harmful include:
(a) Direct applications to soils.
(b) Seed treatments, when the treated seed is labelled
"not for food use".
(c) Dipping of plant roots or tops during transplantation.
(d) Treatment of foundations, by current procedures, for
termite control.
(e) Use of treated hot-caps.
7. Because our recommendations are based upon evidence which,
although the best available, is still not complete; we recommend
that the environmental and economic effects of the proposed re-
strictions be reviewed 5 vears after their imposition. Rv that
time, the completed results of recommendations 1,2,3 and 4 should
be available.
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APPENDIX I
USES OF ALDRIN AND DIELDRIN
Mahlon L. Fair-child and R. L. Doutt
The amounts of aldrin and dieldrin used in the United States
substantially decreased from 1966 to 1970 (from ca. 19 million
pounds aldrin, one million pounds dieldrin in 1966 to ca. nine
million pounds aldrin, 0.6 million pounds dieldrin in 1970)(232).
Among the reasons for this reduction are (a) an increased resistance
to aldrin/dieldrin by some target pests, (b) the development and
availability of substitute materials, and (c) the desire to restrict
the use of persistent organochlorine insecticides to essential needs.
A few examples of increased resistance to aldrin/dieldrin are
as follows:
(a) The rice water weevil, Lissorhoptrus oryzophilus, now
resistant to aldrin treated rice seed(159).
(b) The tobacco wireworm, Conoderus vespertinus, and the
southern potato wireworm, £. fal1i, in North Carolina(186).
(c) The seed-corn maggot, Hylemya platura, in Illinois(107)
and New York(141).
(d) The pear psylla, Psylla pyricola, in Washington(177).
(e) The European chafer, Amphitnallon ma jail's, in New York(247).
There are potential substitutes for aldrin/dieldrin in many
situations. Carbofuran is promising in the control of two major
pests of berry crops and ornamentals in the Pacific Northwest,
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namely the strawberry root weevil, Brachyrhinus ovatus, and the
black vine weevil, EL sulcatus(230). Carbofuran is also effective
against the nut curculio, Conotrachelus hicoriae(36). Although
dieldrin reduced cat facing in peaches caused by tarnished plant bugs,
Lygus 1ineolaris.and stink bugs, Euschistus, so did Gardona and
endosulfan(20). Where resistance had not developed, dosage rates for
dieldrin used against scarabeid grubs in turf were sucessfully re-
duced from 3 Ibs./acre to less than 1 lb./acre(244) and it is suggest-
ed that where applications are carefully timed such products as
diazinon, Dursban and Carbaryl are available substitutes(247). It
is established that the same amount of aldrin is less effective
against arthropods in soils of high organic content than in sandy
loam whereas possible alternative products are either not affected
by such organic matter (phorate) or only slightly affected (parathion,
Dyfonate^)(38). The screening of materials for control of maize bill
bug, Sphenophorus maidi's, showed that there are insecticides other
than aldrin which can be used as a preplant, broadcast, disked-in
treatment(59).
Wireworm control studies on potatoes in Idaho with side-dressed
and broadcast insecticide applications showed Bay-38156 and disul-
foton side-dressed'at rates of 8 and 18 ozs. A.I./1000 ft. row,
Agrito>®and Dasanil® side-dressed at .8 and 1.8 oz. A.I./1000 ft.
of row and propoxur was side-dressed at .9 and 1.7 oz. A.I./1000 ft.
of row resulted in significant reductions in wireworm injury.
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Dyfonate and Agritox controlled wireworms as well as chlor-
inated hydrocarbonous materials, represented by chlordane(221).
American Cyanamid 18133 at 1.2 Ibs. A.I./acre, Heptachlor at
1.5 Ibs. A.I./acre and Hercules 5727 at 1.13 Ibs. A.I./acre, seemed
to give significant reduction in sand wireworm injury to corn in
Missouri(143).
Bayer 25141, diazinon, GS-13005, Kepone, N-290, Niagara 9203
and parathion gave good results for wireworm control on cigar-
wrapper tobacco(241).
Investigations of controls on wireworms on potatoes in eastern
Washington found that Telone®, DD® mixture, ethylene dibromide,
diazinon, parathion, and phorate, gave economic control of the
Pacific Coast wireworm on potatoes in sandy loam soil(198).
Harris (1965) reported diazinon baits, Kepone baits, parathion
a
granules and diazinon granules to be somewhat effective against
wireworms in sweet corn. Brett et_al_. (1966) reported that diazinon
gave poor control of wireworms in sweet potatoes when it was incorp-
orated into the soil prior to planting, but a foliage-surface
application during August gave good control. Diazinon gave good
control when applied on th« surface late in July at the rate of
3 Ibs. active ingredient per acre in a granular formulation.
N-2790 and Zenophos at 5 Ibs./acre-broadcast and worked into the
soil shortly before planting, gave more than 90% wireworm-damage-
free potatoes compared with 26 to 55% damage-free potatoes in un-
treated soils. Diazinon at 7 Ibs./acre and Bay 25141, and-Bay
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37289 and UC 10854 at 10 Ibs./acre also gave more than 90% damage-
free potatoes(31).
Fumigation of the soil in autumn with ethylene dibromide, Telone®
or dichloropropane-dichloropropene mixture has given excellent con-
trol of Pacific Coast wireworms. Dyfonate at 2 Ibs./acre, 3/4
Ib./acre of diazinon or parathion, and 4 Ibs./acre of carbofuran
or Bay 37289 also gave excellent control when broadcast(196). On-
sager and Foiles(197) reported when granular carbofuran, Dyfonate,
and parathion were applied in mid-March for control of the Great
Basin wireworm, and the Pacific Coast wireworms on summer potatoes
that side-dress treatments at a rate of about 2.3 Ibs. of toxicant
per acre gave better average control with less variation than broad-
cast treatments with 4-8 Ibs. of the same toxicant per acre.
Flooding infested fields for 6 to 7 days with an inch or two
of water during extremely hot weather has been reported to kill
nearly all wireworms. Soil temperature must remaim above 68°F for
the entire period for best results. In contrast, when the upper 15
inches of infested soil is allowed to become very dry for several
weeks in summer, mast of the wireworms, especially the younger ones,
are killed. Drying has been recommended to keep wireworms below
economic levels on irrigated lands.
Plowing fields in the summer during the pupal stage has been
reported to reduce wireworm numbers. Mechanical injury to the wprms
and exposure to summer heat and low humidities account for most of
the mortality at this stage. :
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Crop rotation in certain areas has been reported to reduce
wireworms. The growing of truck crops in the same area continu-
ously will usually cause a build-up of wireworms. The growing of
potatoes in a short rotation with clover or grain is undesirable
because of wireworm build-up.
In Georgia in peanut fields Abate , monocrotophos, Dursban ,
Dyfonate, trichlorfon, methomyl, and Monitor"'^gave higher than 90%
•
control of granulated cutworm larvae within 24 hours after appli-
cation(188).
DDT, Bay 37289, Dursban, and. trichlorfon have been evaluated
for control of the dark-sided cutworms in rye grown in rotation
with tabacco. In plots using artificial infestations DDT and Dursban
gave 100% control while Bay 37289 provided 90% control, trichlorfon
at 1 Ib. per acre was not sufficiently effective. It was noted that
DDT, Dursban and Bay 37289 provided 88-90% control of heavy natural
infestations. It was noted, however, that the rapid dissipation of
the residues of Dursban and Bay 37289 would require a split applica-
tion to give adequate control(116).
Studies indicated that Dursban, Bayer 37289, and parathion warrant
further investigation as possible alternatives for the cyclodiene
insecticides as soil treatments for control of the black cutworm. It
was noted, however, these materials should be applied when the larvae
are in the early instars to be effective. Soil type, moisture, method
of application, and formulation must be taken into consideration for
effective control(113).
Further studies showed three compounds having potential as
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- 20 -
possible replacement for cyclodiene compounds as control agents for
dark-sided cutworms. These compounds were N-2596, phoxim and chlor-
phoxim. Chlorphoxim seemed to be somewhat less effective than the
other two compounds(115).
Unpublished studies (227) indicated that Niagara 10242 (Furadan^,
a combination of thimet and A.C. 47470, Dursban, Sevin®, and G.S.-10133
as well as Baygon® showed promise as effective insecticides against
black cutworms.
Diazinon, Dyfonate, dylox, Sevin, Bay 37289, GC-6506, EI-52160,
and Thimet + EI-4740 have been shown to be effective against cutworms
(224).
Begg e£ al_. in 1963(15) reported that soil treatments in gen-
eral did not reduce the infestations of the black cutworm to non-
economic levels during the first seven days after treatment. It
f
apparently took some time for the larvae to contact a lethal amount
of an insecticide in the soil. The results of field test conducted
with eight insecticides indicated their relative effectiveness in
test could be rated endrin>aldrin = dieldrin = heptachlor
> DDT = Dylox>Guthion = Sevin.
According to work done by Harris and Mazurek in 1961(110),
the regression line slopes would indicate that a small increase in
the rate of application of dieldrin should result in more effective
control of cutworms. Conversely, large increases in rate of appli-
cations of Dylox, Guthion and Sevin would result in little or no
increase in insecticide efficiency.
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- 21 -
Laboratory studies(109) conducted to determine the toxicity of
3 insecticides, DDT, Dursban, and Galecron®, to the various stages
in the life cycle of the darksided cutworm indicate that DDT was
effective against the early larval stages, but ineffective against
the later larval stages, eggs, pupae, and adults. Dursban was ef-
fective against eggs, early larval stages, and adults, but ineffec-
i
tive against the later larval stages and pupae. Galecron was highly
selective and was effective against eggs.
Laboratory tests(114) indicated that 5 of 7 insecticides tested
as direct-contact poisons against 3rd- and 4th-instar variegated
cutworms were more effective than aldrin. The most toxic was Lannate^>
DDT> parathion > Dursban> Ciba 8874. Birlane® and Bayer 37289 were
slightly less toxic than aldrin. As soil surface applications,
Dursban and aldrin were highly effective, DDT, parathion and Bayer
37289 were only slightly less so, and Lannate was ineffective. Soil-
surface applications of Dursban were 2-4 times as effective as soil
incorporations. Dursban, DDT, and Lannate were all highly effective
as stomach poisons. Lannate was 32 times more effective as a stomach
poison than as a soil insecticide.
Greenhouse studies have indicated several baits to be effec-
tive against black cutworm populations. The baits were: Trichlor-
fon Bait C, CL-47470 - 2% apple pomace, Abate - 2% apple pomace,
ethyl parathion - 2% apple pomace, mirex - 1.25% bran, TDE - 5% bran,
and carbaryl - 5% bran(225).
Studies by Harris in 1962 indicated that there was very little
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- 22 -
resistance building in black cutworms in certain areas of Canada
to soil insecticides. These studies also indicated that in general
organophosphates were less effective against black cutworms than
cyclodiene insecticides.
Several methods have been suggested for controlling white
grubs. Hot water has been suggested to control the Japanese
beetle in the soil, on the roots of nursery plants(73). Researchers
have reported on the success of using traps baited with geraniol
and eugenol for control of white grubs, particularly the Japanese
beetle(79,182).
The effectiveness of lead arsenate to control white grubs has
been explored by researchers(74,78). Napthalene and Derris have
been reported to be helpful repellents of the Japanese beetle.
Many studies have been conducted using cyclodienes to control
grubs. Cyclodiene compounds such as TDE, chlordane, methoxychlor
as well as ethylene oxide, methyl bromide, lead arsenate and several
imported parasites have been reported to control the larvae of the
Japanese beetle (Fleming, 1937), (101). Paris green and its homo-
logues have been effective insecticides against Japanese beetle
larvae(77).
Burrage and Gyrisco(29,30) studied the control of the Euro-
pean chafer in pasture sod. The test conducted by Burrage and
Gyrisco included six materials - parathion, dieldrin, aldrin, chlor-
dane, BHC, and DDT. Parathion and BHC did not perform as well as
the other materials. Grambel1(91,92,93,94,95,96,97,98) did
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- 23 -
extensive work on controlling the European chafer. Most of these
works included the use of cyclodiene insecticides for control.
Tashiro(243) reported that methyl bromide fumigation gave satis-
factory control of the European chafer in nursery stock.
Carbon-disulphide emulsion as well as lead arsenate could be
used to control Asiatic beetle larvae in lawns(102). Several
parasites have been reported to attack Scarabaeidae larvae(Fleming
1936);(32,60*83,86,148). Milky diseases in beetles have to be re-
ported to give rather effective control of several white grubs(119)
(Fleming, 1933).
There is very little information about the hazards to man and
the environment involved in the use of such substitute materials.
There is no evidence that aldrin/dieldrin are generally more harmful
to beneficial insects than some of the possible substitute materials.
It is known that aldrin/dieldrin are highly toxic to bees(3), but so
are carbamates and organophosphates. It appears that aldrin/dieldrin
are no worse than substitute materials in tests against certain pred-
ators and oarasitoids and dieldrin was reported to be somewhat less
toxic to syrphids than certain other insecticides including carbaryl,
endosulfan and parathion(220).
The bluegrass bill bug, Sphenophorus parvulus, became a pest
on lawns previously treated with dieldrin(246) (and other cyclodiene
insecticides), but there are in general very few reports of outbreaks
of other pests following the use of aldrin/dieldrin. Although in-
creases in mites and aphids have been mentioned, really adequate
documentation is lacking(13).
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- 24 -
The use of aldrin/dieldrin for control of the subterranean
termites Reticulitermes spp., poses minimal and insignificant hazards
to man or his environment and offers the most effective and durable
control of these structural pests at this point in time. The ap-
plications are generally made as water emulsions to the soil under
foundations and footings of buildings. Here there is a minimum
of weathering, erosion, or other disturbance and the persistent
characteristic is a tremendous asset giving control for 20 years
(188). Furthermore, tests have shown that dieldrin can be used in
the mix water for concrete to prevent tubing over by Reticulitermes
(14). Aldrin and dieldrin are somewhat less effective against the
Formosan termite, Coptotermes formosanus.
Similarly, there are minimal environmental hazards involved in
the use of aldrin/dieldrin against other structural, wood-boring
pests, or with dieldrin in stump treatments to control pales weevil,
Hylobius pales, or northern pine weevil, Pissodes approximatus(19).
In this latter case, however, endosulfan is an effective substitute.
The use of dieldrin as a seed protectant with its application
restricted solely to planting seed of certain specified crops is also
without demonstrable hazard to man or the environment. The use of
such treated seed eliminates the need for soil applications in some
situations(117). There is no documentation of any appreciable
hazard in the present use of dieldrin as a primary seed protectant on
cotton, corn (sweet, field, pop), b'eians (green, snap, lima and
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- 25 -
black-eyed-peas), peas, cowpeas, cucumbers, summer squash, onions,
small grains (oats, rye, barley, wheat, grain sorghum), and soy-
beans. The only hazard involved is that such planting seed might
be used inadvertently for food or feed.
The use of dieldrin for turf insects and for insects on commer-
cially grown ornamentals and in nurseries needs to be restricted to
the supervision and control of trained or licensed pest control
operators, greens keepers and nurserymen. This is proposed by one
registrant, Shell Chemical Co. Labels should restrict the sale to
commercial users, and dosages should be minimal and may need to be
revised downward in view of the control of Scarabaeid grubs with one-
third the ordinary dosage(244). These uses of dieldrin need constant
surveillance and revision in view of the developing resistance in
the pests and the increasing availability of suitable substitutes.
There are no scientific data on actual losses caused by Fuller's
rose beetle to citrus. It does not rank as a major pest in California
citrus, but apparently is considered damaging in Florida(232). A
substantial amount of aldrin has been applied against this insect
(estimated 143,300 pounds in 1970). The magnitude of this appli-
cation strongly suggests that the damage actually caused by Fuller's
rose beetle needs a thorough scientific appraisal. Until such in-
formation is obtained, there is no scientific basis for advisory com-
ment. This lack of information on pest population tolerance levels
(sometimes called economic threshold) is not limited to the Fuller's
rose beetle, but applies to most agricultural pest problems.
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- 26 -
Conclusions
1. Although pesticides such as aldrin/dieldrin should be ap-
plied solely on the basis of established need, there is almost a
complete lack of reliable scientific data to establish this basis
for treatment of most agricultural pests. Tolerance levels for such
pests need to be investigated, and better information on the pre-
cise time, place and manner of application needs to be obtained.
2. The use of aldrin/dieldrin for control of subterranean
termites gives effective protection to wooden structures and does
not pose any demonstrable hazard to the environment.
3. The hazards in the use of dieldrin a's a seed protectant
are minimal when it is restricted solely to the planting seeds of
the following crops: cotton, corn, beans (green, snap, lima and
black-eyed peas), peas, cowpeas, cucumbers, summer squash, onions,
small grains (oats, rye, barley, wheat, grain sorghum), and soy-
beans.
4. Certain turf insects are becoming tolerant of aldrin/
dieldrin and substitute materials are available. Where Scarabaeid
grubs are not resistant, the dosage rates can be reduced.
5. The application of aldrin/dieldrin for turf insects and
for insects on commercially grown ornamentals and in nurseries
should be restricted to trained or licensed pest control operators.
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- 27 -
APPENDIX II
.TOXICOLOGY, METABOLISM AND BIOCHEMICAL EFFECTS
ON NON-HUMAN SPECIES
Florence K. Kinoshita
Toxicology
A. Mammals: The acute oral toxicity of aldrin or dieldrin has
been summarized by Hodge et a]_. (129) as being between 20 and 70 mg/kg
for 12 different mammalian species. Of these species the cat was
the most sensitive; the cow, rat, guinea pig, mouse and monkey were
intermediate in susceptibility: the dog, pig and sheep were the most
resistant. The young of a species may be more susceptible to the
toxic effects of dieldrin than the adults(129). A sex difference
in toxicity has been noted in the rat. Female rats are less resis-
tant to dieldrin toxicity [LD^Q females = 51 mg/kg; males = 64
mg/kg](120). Male rats, however, have been reported to be more sus-
ceptible to the toxic effects of aldrin orally [LD5Q males = 39
mg/kg;. females = 60 mg/kg](82).
The symptoms of poisoning after an acute oral dose appear within
30 to 60 minutes after administration(120). Death occurs within 1
week. After the intravenous administration of a toxic dose [LD5Q to
female rats =8.9 mg/kg] the symptoms appear within 2 to 5 minutes
and death occurs within 40 minutes. The symptoms that occur are re-
lated to effects on-the central nervous system. These include hyper-
excitability, hyperactivity, incoordination, exaggerated body move-
ments which later lead to convulsions and depression of the central
nervous system and finally to death(9).
The mechanism of toxic action of aldrin and dieldrin is not
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28 -
known, although it is known that the nervous system is involved.
Aldrin has been shown to cause stimulation of the parasympathetic
nervous system peripherally leading to salivation and slowing of the
heart(89,90). Dieldrin has no peripheral action on the parasympathetic
system. Both aldrin and dieldrin have central effects which lead
to parasympathetic stimulation(88,89). There has been a report of the
effects of aldrin and dieldrin on brain betaines(131). The most recent
proposal for the mechanism of action of aldrin and dieldrin has been
that of Shankland(229) who reports evidence of dieldrin affecting the
cholinergic system of insects by its effect on presynaptic acetyl-
choline release. This mechanism has as yet not been verified in verte-
brates.
The effects of a single oral dose of dieldrin are long lasting;
the effects may persist for 3 weeks. If an animal is given a second
dose of dieldrin during this time, there is greater toxicity in terms
of mortality than would be expected(9,120).
With short-term administration of repeated doses there is no
mortality with doses of less than 25ppm in the diet(129). In chronic
studies monkeys fed 5 ppm dieldrin died after 1 year(129). In other
mammalian species mortalities are caused by levels of 10 to 20 ppm.
It has been noted by several investigators that starved rats or rats
on restricted protein diets are more susceptible to the toxic effects
of dieldrin administered as part of the diet(50, 136, 238).
Histopathology after the administration of aldrin or dieldrin
for long periods of time indicates changes in the liver, kidneys, lungs,
brain and vasculature(104,144).
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- 29 -
An increase in the liver weight to body weight ratios is seen
in rats fed 2 ppm aldrin or 0.5 ppm dieldrin and in dogs fed 3 ppm
aldrin or dieldrin(129). The increase in liver weight is accompanied
by a hypertrophy of the smooth endoplasmic reticulum of the liver(134).
A fatty metamorphosis in the central zone with increased amounts of
basophilic material and hepatic cell necrosis predominantly near the
central zone, but also scattered throughout the parenchyma occurs in
the mouse fed 3 ppm of aldrin or dieldrin(144). Higher levels of
dieldrin (25 to 50 ppm) cause enlargement of liver cells around the
central vein and margination(147).
With levels of 3 ppm aldrin given to mice moderate congestion
of the blood vessels of the lungs, mild alveolar emphysema and minute
hemorrhages in the alveoli have been reported(144). These authors also
report the presence of bronchiolar carcinoma and benign pulmonary
adenomas in mice fed 5 ppm aldrin.
The kidneys of mice fed 3 ppm aldrin or dieldrin and higher
levels have been reported to have vascular congestion, focal glomer-
ulonephritis, swelling of Bowman's capsules and dilation of the con-
vulated tubules and cloudy swell ing(144).
One group of investigators(104) report that rats being fed 2.5
to 10 ppm dieldrin had occasional neural spasms. The nervous tissue
of these animals demonstrated vascular congestion in the meninges,
edema in the parenchyma and swollen upper motor neurons. Also there
was focal degeneration and necrobiosis in the cortical laminae.
Cerebellar lesions included cloudy swelling, Purkinje's cell degener-
ation and degeneration foci in the granular layer. Brainstem
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- 30 -
lesions included neuron and myelin degeneration, glial swelling
and adventitial proliferation. The craniums of these rats contained
increased amounts of clear cerebrospinal fluid. With the feeding
of 0.31 to 10 ppm dieldrin edema of the leptomeninges was seen.
The brain concentrations of dieldrin in those rats showing convulsions
was between 9 and 11 ppm. The vascular effects of dieldrin in rats
fed 0.31 to 1.25 ppm were reported to be of a degenerative nature,
while those in rats fed 2.5 to 40 ppm were inflammatory in the males
and necrotic in the females(104). These observations have not been
confirmed by other reports.
The effects of dieldrin on reproduction have been studied in
rats, mice and dogs. At levels of 0.31, 1.25, 2.5 and 10 ppm
dieldrin, there is a decrease in the weaned litter size of rats
(87,103). At the higher levels of dieldrin intake by the dam, the
pups died in convulsions. Death often occurred within the first
5 days in pups due to the lack of nursing. In mice 3 and 5 ppm
aldrin lead to decreased viability in the 2nd generation and lower
fertility in the 3rd generation. 10 ppm dieldrin decreases fertility
in mice, while 3 ppm dieldrin decreases lactation in the 2nd and
3rd generations (144). The summary by Hodge £t al_. (129) indicates
that the lowest level of aldrin having an effect on reproduction in
rats is 12.5 ppm and the lowest level of dieldrin having an effect
is 2.5 ppm. The later study(103) indicates, however, that repro-
ductive effects are seen with 0.31 ppm dieldrin; these data are not
confirmed. In dogs the lowest level of aldrin and dieldrin having
an effect on reproduction are 8 and 25 ppm respectively(129).
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- 31 -
B. Birds: The acute oral toxicity of aldrin has been re-
ported for four species(252). The LDso's for these species are 6.6
mg/kg in the female bobwhite quail, 16.8 mg/kg in the female
pheasant, 29.2 mg/kg in the male fulvous tree duck and 520 mg/kg
in the female mallard duck. The lowest daily dose that can be
tolerated for 30 days by the mallard is 5 mg/kg.
The symptoms of poisoning by aldrin in birds include ataxia,
circling, low carriage, closure of the nictitating membrane, tremors,
phonation, wing-beat convulsions, seizures and opisthotonos. Death
occurs from 1/2 hour to 10 days after treatment.
Feeding studies in birds with aldrin indicate a no-effect
level of about 1 ppm(56). One day old quail fed feed containing 1
ppm aldrin survived for 47 days, one day old pheasants started on a
diet containing 5 ppm aldrin exhibited 100% mortality by the 46th day.
Symptoms of poisoning at these levels occur 48 to 72 hours after the
initiation of treatment; the symptoms are those that are seen in adult
birds with acute poisoning. Five ppm aldrin will cause 100% mortality
in adult quail and pheasants.
The effects of aldrin on reproduction in birds indicate a de-
crease in egg production with a level of 1 ppm, with a cessation of
egg production by the 6th week(56). The hatchability of the eggs laid
by birds fed 10 ppm decreased as did the fertility. There was no
effect on chick viability at this level.
The acute oral toxicity of dieldrin has been determined in
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32 -
various domestic and wild species of birds. In the chicken the oral
LD50 for adults has been reported to be between 20 and 30 mg/kg
while other studies indicate that 44 mg/kg causes no mortality(l29).
In wild species the LD50 is reported as being 381, 79, 23, 70, 27,
48, and 9 mg/kg for the mallard, pheasant, chukar, coturnix, pigeon,
sparrow and gray partridge respectively. The acute dose for the
Canada goose is between 50 and 150 mg/kg. The daily dose that can be
tolerated for 30 days is 2.5, 1.25 and 5.0 mg/kg for the fulvous
tree duck, gray partridge and mallard respectively(252,253). The symp-
toms of acute poisoning are hyperexcitability, jerky gait, ataxia,
dyspnea, myasthenia, fluffed feathers, immobility, opisthotonos and
terminal wing-beat convulsions. Death occurs within 1 to 9 days after
poisoning.
In feeding studies the administration of 5 ppm dieldrin to day
old quail causes 100% mortality, while 0.5 ppm has no effect on sur-
vival. One ppm causes 100% mortality after 76 days. A level of 5 ppm
will cause 100% mortality in pheasants by the 68th day(55). The sus-
ceptibility of adult birds to repeated feeding of dieldrin is not as
great. Adult pheasants fed 100 ppm dieldrin exhibit 100% mortality
between 10 days in the males and 39 days in the females. In quail
10 ppm dieldrin has no effect while a level of 20 ppm causes 50%
mortality between 13 and 63 days.
There have been reports that 10 ppm dieldrin fed to quail causes
a decrease in the hatchability of eggs and the survival of chicks(55,56),
while other reports indicate that levels of 20 and 30 ppm are needed
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- 33 -
to cause a decrease in egg laying(257). At the 20 and 30 ppm levels
there is increased chick mortality by the 3rd day after hatching(257).
In pheasants there is a slight decrease in egg laying by birds fed
25 ppm, while 50 ppm significantly decreases egg laying(84). The
survival of the chicks from the eggs of female pheasants fed 50 ppm
is decreased by 35%. In the gray partridge 3 ppm dieldrin given as
a pellet did not affect fertility or egg hatchability, however,
there was a slight increase in mortality in the shell(193). The growth
rate and chick survival after hatching were not affected by this
level. Dieldrin at levels of 1.6, 4 and 10 ppm given to penned
mallards caused a decrease in eggshell thickness(162).
The population of wild birds in areas treated with dieldrin did
not change after dieldrin application. The clutch size and hatch-
ability of gallinules are not affected when eggs contain as much as
13 ppm dieldrin(40). The use of rice bran contaminated with residue
levels of dieldrin to feed leghorn hens had no effect on egg produc-
tion, hatchability or chick survival(80,100). There is a correlation
between the amount of dieldrin found in the eggs and the amount of
dieldrin fed to the birds.t A dietary level of 20 ppm fed to quail
can cause over 45 ppm to be found in the eggs after 7 weeks(257).
C. Fish: There are few actual experimental data available on
the toxicity of aldrin or dieldrin to fish. The median tolerance
limits (TLrn) which is equivalent to the LD50 for a specified exposure
period has been reported to be 0.0155, 0.012, 0.0075 and 0.067 ppm for
periods of 24, 48, 72 and 96 hours respectively for the pumpkinseed
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- 34 -
sunfish(35). In a 96 hour exposure period levels of 0.32, 0.0155,
0.0087, and 0.0075 ppm were highly toxic while 0.0056 ppm caused no
mortality. However, the level of 0.0056 ppm caused 100% mortality by
the end of 1 week. The 96 hour TLm for minnows, blue gills, goldfish
and guppies is between 0.015 and 0.037 pom(129). Exposure of steel-
head trout to 1.2 ppb for 45 days leads to 100% mortality(41).
The levels of 0.0056 and 0.0032 ppm dieldrin caused toxic ef-
fects in the pumokinseed sunfish by decreasing cruising speed and
increasing the consumption of dissolved oxygen. Difficulty in
orientating to the current and an increased sensitivity to sunlight
were also noted at these levels(35). A concentration of 0.00168 ppm
dieldrin while causing no mortality causes an increase in oxygen con-
sumption and a decrease in cruising speed in sunfish.
Exposure of guppies to a level of 0.01 pom dieldrin leads to
the production of no fry after the 32nd week of exposure(34). These
authors noted an initial increase in population which they attributed
to a change in the behavior of the adults resulting in less predation
of the young by the adults. Exposure of steel head trout to a level
of 0.39 ppb dieldrin results in only a 3% survival rate of fry to
age 130 days(41). The growth of trout is not affected by levels of
0.12 ppb and below.
D. Invertebrates: Experimental data on invertebrates are in
shorter supply than that for fish. The 5 day median tolerance limits
*
for aldrin for the Louisiana red crawfish weighing 0.5 grams is 56
ppb(124). These authors report that up to 200 times this amount in
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- 35 -
the soil has no effect on the survival or growth of the crawfish.
Oysters exposed for 10 hours to water containing 1 ppm dieldrin
exhibit physiological irritation which is seen as a continual opening
and closing of the valvesC33). This continual opening and closing of
the valves indicates an abnormal feeding process. After 2 weeks of
exposure to 0.1 ppm dieldrin the oysters are only half as active as
the controls. There is interference with shell deposition by the
oyster in the presence of dieldrin. The oyster will also store chlori-
nated hydrocarbons when they are present in concentrations of 0.1
ppb or more.
Pharmacodynami cs-Metaboli sm
After the oral administration of dieldrin it is absorbed from
the upper gastrointestinal tract and is found in the liver, kidneys,
mesenteric and retroperitoneal fat after 1 hour. Redistribution
occurs and there are increasing amounts found in the fat and genital
organs while the concentration remains constant in the liver and
i
kidneys. At the end of 2 days after a single dose the highest con-
centrations are in the mesenteric and retroperitoneal fat(120).
Biliary excretion occurs(136,151). After a single dose about 90%
is excreted in the feces while the urine contains about 10%(45,120).
If the animal is starved or on a restricted diet, excretion is accel-
erated (120).
With continuous administration in the food or daily by the oral
route dieldrin is stored in the fat(10). The concentration in the
tissues is a function of the daily intake level(26). An upper limit of
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- 36 -
tissue concentration is reached which is characteristic of the in-
take level. A balance is reached between intake and elimination and
storage. The length of time required to reach a plateau storage
level is also a reflection of the daily intake level(53, 142). The con-
centration of dieldrin in blood is a reflection of the concentration
in various tissues for man, rats, dogs and birds(211). The storage
ratios in the tissues of mammals is blood:!iver:fat(53) and in birds it
is fat:l iver:muscle:brain(210). In birds (chickens) the amount of diel-
drin in blood is also a reflection of the amount that is in eggs(210).
In the rat a sex difference in storage is seen. Female rats store
more dieldrin than do males(151) and the excretion of labeled material
is greater by the male rats than by the females(45). Once intake is
terminated the amount of dieldrin in the tissues decreases(210). The
biologic half-life of dieldrin in the fat of rats is approximately
4.5 days(10).
In pregnant mammals dieldrin can cross the placental barrier and
concentrate in the tissues of the fetus(6,103). There is also excretion
of dieldrin in the milk of the lactating animals so that a nursing
pup has the same distribution in tissues as the adult by the end of
2 days. Dieldrin is also excreted in the milk of lactating dairy
cattle(22).
The administration of aldrin to animals and insects leads to
the formation of the epoxide, dieldrin(26,156,234). In the rat this
metabolic conversion occurs in the liver microsomes and is inducible
(26,239). The conversion of aldrin to dieldrin is also faster in the
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- 37 -
male rat than in the female rat(268). The epoxide is further meta-
bolized to hydrophilic compounds which are excreted in the urine
and feces(234). At least 6 metabolites have been isolated. One of
the metabolites found in both urine and feces and possibly existing
as a glucuronide conjugate(68,120,156,157) has been found in rabbits,
rats and sheep. This is the compound aldrin trans-diol.
The trans-diol is less toxic than either aldrin or dieldrin
by the intravenous and oral routes. The oral 1059 is reported to
be 1250 mg/kg to the mouse compared with 75 mg/kg for dieldrin and
45 mg/kg for aldrin(156).
Photoisomer: Upon exposure to sunlight a photoisomer of
dieldrin is formed. This compound is found as a residue on some
agricultural commodities(260). Acutely this photoisomer is more toxic
than dieldrin to rats, mice, guinea pigs and pigeons. The acute
oral LD50 for these species is 9.6, 6.8, 2.3 and 90 mg/kg respec-
tively compared to 47, 77, 18 and 250 mg/kg for dieldrin in a study
done by a single group(27). To hens dieldrin is more toxic than the
photoisomer, while in the beagle there is no difference.
It is reported that both photoaldrin and photodieldrin are
more toxic to freshwater animals than either aldrin or dieldrin(229).
The 24 hour 1059 to the bluegill for aldrin, photoaldrin, dieldrin
and photodieldrin are 0.26, 0.09, 0.17 and 0.03 ppm respectively.
The 24 hour LDso to the minnow for dieldrin and photodieldrin are
0.024 and 0.010 ppm respectively. The LT$Q (time to kill 50% of
the population at a given dose) is shorter for photodieldrin than
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- 38 -
for dieldrin for crayfish, planaria, tadpoles, guppies, bluegills
and minnows.
Subacutely, 3 to 10 ppm of the photoisomer is lethal to the
mouse, while 30 ppm of dieldrin is required for mortality(260).
Biochemical Effects
One of the effects of aldrin and dieldrin on the biochemical
mechanisms of the body have been the effects on hepatic microsomal
enzymes. These changes occur in mammalian and avian species. The
biochemical changes can usually be correlated with the histologic
changes in the liver such as the proliferation of the smooth endo-
plasmic reticulum. These inducible enzymes while affecting the
metabolism of a great many chemicals also metabolize steroids. Levels
of aldrin and dieldrin as low as 1 ppm(150) cause changes in the
metabolism of aminopyrine demethylase in the rat. The daily adminis-
tration of 2 mg/kg dieldrin to female rats enhances the activity
of aniline hydroxylase and £-nitroredutase(135). The administration
of 3 mg/kg dieldrin enhances the hepatic metabolism of estradiol and
estrone(264). Aldrin at a level of 20 ppm can affect the normal
estrous cycle of rats without affecting the growth of the rat(8).
The administration of 20 ppm dieldrin to hens increases aminopyrine
demethylase activity and cytochrome P450 content(228). In the pigeon
the feeding of 2 ppm ciieldrin for 1 week increases the in vitro
metabolism of testosterone and progesterone by liver microsomes(199).
In combination with 10 ppm DDT there is an additive effect on the
enhancement of testosterone and progesterone metabolism.
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- 39 -
Liver mitochondria! activity is inhibited by the administration
of 4 or 20 mg/kg dieldrin for 60 days. A depression NADH oxidase
activity is seen(17). It is postulated that electron transport in
the mitochondria is inhibited at the level of cytochrome b.
Xanthine oxidase and alkaline phosphatase of the livers of
rats fed 50 or 100 ppm aldrin is decreased in activity(4).
The in vitro addition of aldrin and dieldrin causes a slight
inhibition of the ATPases associated with oxidative phosphorylation
and plasma membrane transport of cations(153). Mg+2 activated ATPase
and the Na+-K+ activated ATPase of membranes are inhibited by
aldrin and dieldrin.
Long-term feeding of dieldrin to ducks affects behavior
through a depression of amine levels in the brain(231). The adminis-
tration of 30 ppm dieldrin to adult mallards and then immediately
feeding the same level to their young for 70 to 76 days causes a
depression of norepinephrine, dopamine and serotonin levels.
In rats fed a diet deficient in essential fatty acids, the
addition of 20 or 30 ppm dieldrin to the diet will enhance the
suppression of growth associated with essential fatty acid de-
ficiency(250).
A ten day treatment of rats with 5 mg/kg dieldrin results in
an increase in fasting blood glucose(126). A dose of 25 mg/kg given
for 4 days will also increase the fasting blood glucose level by
60%. In these same animals the plasma corticesterone levels were
i
45 to 98% higher than controls. These authors conclude that dieldrin
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- 40 -
has an effect on the normal utilization of endogenous glucose and
also has an effect on the adrenal cortex.
It is reported that dieldrin given in a gelatin capsule at
a dose of 20 mg/kg/day for 3 days to chickens causes a decrease in
the uptake of labeled methionine by the heart sarcosomes and liver
mitochondria in vitro(49).
The administration of dieldrin together with DDT leads to a
decrease in the amount of DDT stored in the fat depots in rats and
guinea pigs(256).
Using very low levels of dieldrin in dogs there is an indica-
tion that the prostatic fluid volume, the acid phosphatase activity
of the prostatic fluid and the zinc content of the prostatic fluid
is reduced. In these studies 15 ug/kg of dieldrin was given to
dogs. The administration of 6-chloro-6-dehydro-17-acetoxy pro-
gesterone alone reduces these indices of prostatic fluid to a
great extent. With the addition of dieldrin to the hormone there
is less reduction of these indices, leading to the conclusion that
there is a hormone-pesticide interaction(85).
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- 41 -
APPENDIX III
CARCINOGENIC AND MUTAGENIC EFFECTS
Stephen S. Sternberg, M.D.
MAN
The largest single study of the effects of aldrin and dieldrin
in man was by Jager (136). This was based on the occupational ex-
posure of more than 800 workers at an insecticide plant over a period
of about 15 years. From these workers, a group of 233 was selected
for long-term exposure studies and consisted of personnel who had
been exposed at least 4 years and up to 13-1/4 years, not only to
aldrin and dieldrin, but to endrin, telodrin as well. The average
blood level of dieldrin in this group was 0.035 ug/ml. This is equi-
valent to an average oral intake of 407 ug/man/day and represents over
50 times the daily intake of the general population of the U.S.A.
Medical examinations of this group of workers revealed no adverse
effects from this type of exposure. There were 23 instances of
intoxication among aldrin/dieldrin workers during the 15 year study,
none of which were fatal. Apparently, toxic manifestations were
confined to the central nervous system, and they were reversible.
In the long-term exposure group, there was no evidence of hepatic
disease, nor was the liver enlarged on physical examination. In
workers with high levels of dieldrin in the blood (at least 175
times the general population) no effect of pp'DDE metabolism was
found; in those with 85 times that of the general population, no
effect on steroid metabolism was seen, as measured by the ratio of
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- 42 -
6-B-hydroxy-cortisol/17-hydroxy-corticosteroid excretion in the urine.
The results of these determinations suggest a lack of enzyme in-
duction in man.
Another noteworthy study was one in which volunteers ingested
dieldrin (HEOD) on a daily basis, at a maximum dosage of 0.21 mg/
man/day (132, 133). All medical tests performed at intervals and at
the conclusion of the exposure at 24 months indicated a lack of effect.
In particular, no liver abnormalities were found, nor were there any
effects on the nervous system. Further, these same studies have shown
that the levels of HEOD in the blood and adipose tissue are proportional
to the daily dosage, and that there is a finite upper limit to storage
which is also related to the daily intake and after equilibrum is
reached. Thus, a steady-state occurs and there is no buildup; within
the body, and one can reasonably expect that in the absence of increased
exposure, storage levels will not rise.
Long-term oral-feeding studies in animals
Primates
In a long-term feeding experiment with 31 Rhesus monkeys, animals
were followed up to 6 years (270). Six were controls, and the remainder
received various dosage levels of dieldrin in the diet. At levels below
1.75 ppm, no adverse effects were seen. Animals that received 1.75 ppm
or more had ultrastructural hepatic changes and alterations in the
intracellular hepatic enzymes, presumably related to hyperplasia of
smooth endoplasmic reticulum, but no details are noted. In any event,
the livers of all animals were otherwise normal, and no tumors were
seen.
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- 43 -
Dogs
In a 2-year feeding experiment with dogs (258) at dose levels of
O.OOS^and 0.05 mg/kg/day, no tumors were seen. There were no histo-
pathologic alterations in the liver, although the alkaline phosnhatase
was elevated and the serum proteins slightly decreased in dogs that
received the high dose.
In an earlier study (69) dogs were given doses at levels (2 to
10 mg/kg/day) which caused convulsions, fatty liver and bone marrow
depression. The lowest dose used (0.2 mg/kg/day) was, in their study,
a no-effect level, and dogs survived for as long as 25 months, the
duration of the experiment. No tumors were seen.
Rats
A recent study with rats (Osborne-Wendel strain) fed up to 50
ppm of aldrin and dieldrin revealed no tumorigenic activity, but
rather a lower overall tumor incidence in treated animals as compared
to controls (54). A 2-year study (258) in CFE rats was made
using dietary concentrations as high as 10 ppm. There was no in-
creased incidence of tumors. However, 3 rats receiving the highest
dose had microscope nodules in the liver; nodules were also present
in one control rat. These are not further described.
Other studies have been performed in the rat which are difficult
to interpret because of lack of pertinent information. In any event,
there is no evidence that aldrin or dieldrin are carcinogenic in the
rat.
Mouse
A number of long-term studies have been performed using mice of
different strains. The most recent of these (259) indicated that
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- 44 -
HEOD enhances the incidence of naturally occurring hepatic nodules
in the CF1 strain. From the microscopic description of the 2 types
of nodules, it appears that the so-called type (a) is benign and that
the type (b) probably is a hepatocellular carcinoma. Both tyoes are
present in control animals of both sexes, but in general the type (a)
is more frequent than the type (b). However, in the treated groups,
the incidence of both types increases; to over 50% for type (b) mice
treated with 20 ppm for 2 years, and as much ^s 77% for tyoe (a) in
mice at 5.0 ppm level. It is worth noting, however, that metasteses
in mice with type (b) tumors were rare and in males were about the
same as in control animals. Female mice in one experiment had a 4%
incidence of lung metasteses of liver tumors, while no metasteses
were seen in female controls. In another study, however, (52) in
which Swiss mice were used, hyperplastic nodules were present in the
treated animals, but no hepatic carcinomas. The control mice were
free of nodules, quite unlike the CF1 mice used by Walker et al.
(259)
Thus, the finding of an increased incidence of liver tumors in
one strain of mice represents the closest approximation to what might
be considered a carcinogenic effect of dieldrin.
The significance of an enhancement in the incidence of a naturally
occurring tumor, as the only evidence of carcinogenicity, is difficult
to interpret. Mice, in particular, have an unusual lability in re-
sponse to various factors in long-term studies, and because of this
are perhaps an unfortunate mammal to work with for carcinogenicity
studies. It has been shown for instance that a "germ-free" status
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- 45 -
in C3H mice in effect protected against the early development of
liver tumors by a known carcinogen 7,12-dimethyl-benz(a) anthracene
(213). Earlier Heston e£ al_. (125) pointed-up the marked difference
2 standard diets had on the incidence of liver tumors in C3H mice,
and Tannenbaum and Silverstone in 1949 (240), the variations produced
by different levels of casein.
These and other considerations have led Roe and Grant (213) to
suggest that some chemical agents which increase the incidence of
certain tumors may act as co-carcinogens rather than carcinogens,
and that in the absence of other evidence, a carcinogenic action
should not be attributed to such agents.
In summary, no carcinogenic action has been demonstrated for
dieldrin in rats, dogs or primates. In one strain of mice the CF1,
an enhancement in the incidence of what are probably hepatocellular
carcinomas was observed. The incidence of metasteses in male mice
was the same in control and treated animals, while in treated fe-
male mice a relatively small percentage had metasteses. In another
strain (Swiss) in which there were no malignant hepatic tumors
in the controls, none were seen in the treated mice. If there is
a carcinogenic action in dieldrin, it likely is a weak one at a
level much like DDT.
Addendum
A major problem in evaluating long-term studies in animals
concerns the description and classification of hepatic lesions.
Not the least of these is use of the term "hepatoma." The word
is used either for benign tumors or for malignant ones, but probably
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- 46 -
most often as non-committal word when it is not known if the
lesions are benign or malignant. In the latter instance, if no
definition of the use of the word is given, and there is no satis-
factory microscopic description and no photomicrographs, then the
reader as well as the authors remain ignorant.
If there are difficulties in the pathological evaluation, these
should be stated. Microscopic descriptions and representative photo-
micrographs often permit the reader to make his t /n judgement, and
the value of the scienific work is greatly enhanced.
Non-mutagenicity of Aldrin/Dieldrin
In the literature review in "The Mutagenicity of Pesticides"
by Epstein and Legator (66) there is a solitary reference to
dieldrin (Markarian, 1966) wherein a 10% (sic) solution caused a
"C-mitosis effect and no chromosome breaks" in sprouts of Crepis
capillaris.
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- 47 -
APPENDIX IV
RESIDUES IN THE ENVIRONMENT AND MAN
Richard A. Parker
A preliminary analysis of aldrin and dieldrin residues in the
United States was conducted using a simulation model to develop a
better understanding of the potential long-term levels in man. It
must be emphasized that the specific results are of general utility
only; formal optimization measured by goodness-of-fit to widely
varying data in the literature was not attempted. Six components
were incorporated: domestic aldrin and dieldrin used (1950-70
data from Shell Chemical Company), aldrin and dieldrin residuals
in the environment, total intake by man from market basket food,
and dieldrin content of human adipose tissue.
Persistence of these pesticides depends a great deal on soil
type and climatic conditions. Estimates of half-life for dieldrin
under field conditions range from two to seven years, considerably
less for aldrin. Since an earlier simulation study (Parker unpub-
lished) suggested that assumed half-lives of 1.4 to 3.5 years for
aldrin and dieldrin combined had little immediate effect on the
accumulation in man, figures given by Edwards (61) were accepted:
2.4 years for dieldrin and 0.51 years for aldrin. Equations adopted
to approximate the quantities of aldrin (RA) and dieldrin (RD) pre-
sent in the environment immediately after a particular annual appli-
cation (A and D) were:
RAt = At + RAt_i exp (-1.36)
RDt = Dt + RDt_-, exp (-0.29) + 1.27 RAt.-| [exp (-0.29) - exp (-1.36)]
-------
- 48 -
Aside from A^ and Dt, these equations form a solution to the following
general pair of differential equations describing changes during one
year:
dA ,
-~- = -1.
g = 1.36A - 0.29D
Note that all of the aldrin was assumed to be converted to dieldrin.
It is well known that dieldrin is commonly found in meat, fish,
poultry and dairy products (see, for example, Corneliussen 1970 (46)
who gives values ranging from .004 to .052 mg/kg); residue levels may
be assumed due largely to food intake rather than direct contact.
Residuals in plant foods included in the diet of man are generally
proportional to levels found in the soil on which the plants are
grown; however, the proportionality constants are usually higher in
oil containing crops like soybeans than in grain or root vegetables
(39,111,152,170,200,267,269). Human dietary intake of aldrin and
dieldrin has been studied extensively and summarized for five years
by Duggan ejt aK (58):
Year
1964-65 1965-66 1966-67 1967-68 1968-69
ug/kg/day
Aldrin .01 .04 .01 .01 .001
Dieldrin .08 .09 .05 .05 .07
The equation utilized to relate combined intake F with environmental
residual was
Ft = 0.00088 (RAt + RDt).
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- 49 -
Since little data on human adipose levels is available before 1967,
the constant was calculated to approximate the observed values for
1967-69. In addition, major modifications in analytical techniques
make comparisons among many successive years questionable.
Dieldrin is usually present in human adipose tissue and, as
expected, the concentration seems to be a function of geographical
location (see the review by Jager 1970)(136). A continuing large
scale sampling program is carried out in the United States by the
Human Monitoring Survey, State Services Branch, Division of
Pesticides, Community Studies, Environmental Protection Agency. The
following survey results have been provided by EPA through Homer Wolfe,
Chief of the Wenatchee Research Section:
Year No. Samples No. States Method Mean Cone (mg/kg)
1967 722 11 Non-cleanup 0.14
1968 3,300 21 Non-cleanup 0.12
1968 3,237 23 Modified Mills 0.13
(better cleanup)
1969 3,264 33 + Modified Mills 0.13
Wash. D.C.
1970 (inc) 2,626 27 + Modified Mills 0.15
Wash. D.C.
Jager (136) points out that De Jonge has estimated the half-life of
dieldrin in man to be 0.73 years based on a study of 15 aldrin-dieldrin
workers. Aldrin levels were apparently too low for detection, and no
effort was made to distinguish aldrin and dieldrin in the simulation
model. Change in human adipose tissue content T was described by the
differential equation
^L= 2.20F , - 0.95T
dt t-1
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- 50 -
Since much of the aldrin-dieldrin entering plant foods occurs during
a relatively short growing season following pesticide application,
the intake by humans was treated as constant (2.20Ft_i) during a parti-
cular year (0.95 corresponds to a half-life of 0.73 years).
The system of equations was solved for two cases: one in which
aldrin and dieldrin were applied in 1971 and thereafter at constant
annual rates of 8 x 10 pounds and 0.6 x 10 pounds, respectively,
and another in which none was applied after 1971. The simulation
output for both cases is presented in Figure 1. The first assumption
yields predicted market basket intake of approximately 0.036 ug/kg/day
in 1982 and concurrent adipose tissue content of 0.084 mg/kg. The
second suggests 1982 levels of 0.002 ug/kg/day and 0.009 mg/kg.
-------
60
50
co
o
o 40
o
OL
U_
0 30
CO
z
o
J 20
_J .
10
.16
.12
.08
.04
- 51 -
-RD
— T
(mg/kg)
.00
1950 '' 54
58
62
70
66
YEAR
Figure 3.. Simulation Results
74
82
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- 52 -
APPENDIX V
ENVIRONMENTAL MOVEMENT AND CHANGE
Samuel D. Faust
Section I. "Occurrence, Distribution, and Persistence of Dieldrin
and Aldrin in Air and Water"
In view of the papers on the distribution, occurrence and persis-
\
tence of dieldrin and aldrin in the atmosphere and various bodies of
water, careful attention was given to the analytical techniques. It
is extremely important that confirmation was made of the presence of
these two pesticides. Most of the analysts used one form or another
of gas-liquid chromatography with an electron capture detector. This
detector is non-specific for organic pesticides, i.e., any organic com-
pound that captures an electron and gives a response will be recorded.
Therefore, there must be employed some such ancillary analytical tech-
nique as thin-layer chromatography or infrared spectroscopy that can
identify at the molecular level. There does not appear to be any
appreciable (see page 56) PCB interference with dieldrin and aldrin
(as is the situation with DDT), but there are organic interferences
in natural water, waste waters, bottom muds, stream sediments, etc.
Synoptic surveys of the major rivers of the U.S. have been con-
ducted since 1958 by various agencies in the Federal Government (23,24,
25,139,163,219,261). Dieldrin appeared more frequently than, for example,
endrin, DDT, DDE, ODD, BHC, etc., when placed on a basis of percent
occurrence. Also, dieldrin appeared in almost all of the major U.S.
-6 -9
rivers. Concentrations, however, were in the order of 10 to 10
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- 53 -
grams per liter (.001-1 ug/1). The highest concentration of dieldrin
may have been .407 ug/1 that was observed in the Tombigbee River at
Columbus, Mississippi, in 1968. Aldrin was infrequently, if ever,
reported. These surveys appear to be analytically sound and that it
is certain that dieldrin was confirmed. These observed concentrations
of dieldrin may be compared with the water quality criteria suggested
by the EPA which are 10 ug/1 for dieldrin, 10 ug/1 for aldrin, and
10 ug/1 for aldrin + dieldrin. These concentrations are being proposed
now by the National Academy of Sciences to the EPA for adoption as
water quality criteria and, as such, may undergo some revision before
final acceptance. The concentrations of dieldrin and aldrin reported
in the years 1958-1968 appear to be well below the proposed water
quality criteria.
In order to determine a trend with time, dieldrin concentrations
were plotted versus year in summary Figure 1 for two sampling sites.
There does not appear to be any upward or downward trend in dieldrin
concentration with time although the Ohio River Basin data may suggest
a decreasing content. It should be remembered that these synoptic
surveys grab samples at random. Therefore, these data may not be
representative of the whole.
Some stream and river surveys were conducted in England for chlori-
nated hydrocarbons (47,130,176). In "clean" Scottish waters, dieldrin
up to 0.01 ug/1 was found. In "contaminated" streams, dieldrin concen-
trations >1 ug/1 were found. In one survey (47), dieldrin was found
in more than 50% of samples from various surface and ground waters in
England and Wales. The highest concentrations of dieldrin were 2.48
-------
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- 55 -
and .56 ug/1 due to an industrial waste water discharge.
Some attempt has been made in the U.S. (43,237,263) and in England
(1,2,242,266) to determine the extent of atmospheric transport of or-
ganic pesticides. Dieldrin, .003 ppm, was found in dust fallout
collected in Cincinnati, Ohio (43,263). In an analysis of the atmos-
phere, air was sampled at nine locations in the U.S. (urban, rural, etc.).
Dieldrin was found in only one location, Orlando, Florida, and in 50 of 99
samples. The maximum concentration was 29.7 ng/m . Aldrin was found
3
in only one sample in only one location - Iowa City (8.0 ng/m ). In
both of these surveys no confirmation of the GLC peaks was attempted.
Identification was made by relative retention time on two or three
GLC columns. The English analysts were more careful than the U.S.
analysts. They examined rainwater samples by thin-layer chromatography
followed by gas-liquid chromatography and still called the results
"apparent organo-chlorine insecticides" because not enough pesticide
was available for infrared confirmation (265). Dieldrin concentrations
in this survey ranged 9-28 ng/1. In another English rainwater survey
-12
(242), dieldrin contents of 1-40 pg/1 (10 g/1) were observed in 7
sites throughout the British Isles. These concentrations represent
a decrease from previous surveys due to "abandonment of large scale
uses of aldrin and dieldrin" in Britain.
Some attempts have been made to evaluate the role of sedi-
ments in the transport of dieldrin and aldrin in surface waters
(12,44). In a survey of the sediments of the lower Mississippi
River, dieldrin concentrations ranged 0.15 to 931 ppm (dry weight)
whereas aldrin concentrations ranged 1.09 to 567 ppm (12). These
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- 56 -
sediments were collected from Wolf River and Cypress Creek, Memphis,
Tennessee, near the manufacturer of endrin and heptachlor. Apparently,
very little desorption of dieldrin and aldrin occurred because water
samples showed .04-.37 ug/1 dieldrin and 0.15-0.29 ug/1 aldrin at
the same sites.
In a persistence study (174), dieldrin, 1 mg/1, was added to a
lake water and to a soil water obtained from percolation. After 7
months, .02 mg/1 remained in the lake water and 0.16 mg/1 remained
in the soil water. After 12 months, 0.002 mg/1 remained in the
lake water whereas 0.07 mg/1 remained in the soil water. This is
very empirical and it is not clear on how the dieldrin disappeared.
Three papers were reviewed in order to answer the question of
PCB interference with the gas-liquid chromatography of aldrin and
dieldrin (205,206,208). It should be kept in mind that the most com-
monly used GLC columns for aldrin and dieldrin are the stationary
phases of QF-1 and DC-200. Most of the interference data, however,
were gathered from a 4% SE30 - 6% QF-1 column (205,206) where it was
demonstrated that Aroclor 1254 with its 14 major peaks does, indeed,
interfere with aldrin and dieldrin (i.e., the same relative retention
times). However, I was able to find only one reference (208) where
the DC-200 and QF-1 columns were used. In this one instance, diel-
drin appeared as a trailing peak to one of the PCB peaks on QF-1 and
came out ahead of the first major PCB peak on DC-200. No mention was
made of aldrin.
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- 57 -
Section II. "Dieldrin and Aldrin-Leaching from Soils - Sorption
and Desorption"
There have been surprisingly few studies, field, or laboratory,
that dealt specifically with the retention and release of aldrin and
dieldrin in and from soils. From the meager information, aldrin and
dieldrin appear to be retained in the soil with some downward and
lateral movement (21,39,63,67,106,164,248). In a rice paddy study (164),
no aldrin or dieldrin was found 5" from the drill row in which aldrin
was applied. Very low concentrations of aldrin and dieldrin were
found in the rice paddy water (<.008 ug/1 aldrin and .17 ug/1
dieldrin). In fact, these concentrations were about the same as
for an untreated area. In an adsorption on soil study (67) there
was somewhat of direct relation between the amount of dieldrin adsorp-
tion and organic matter content of soil. As the percent organic
content was increased, the amount if dieldrin, ng/g, was increased.
There was some evidence presented also (236) that more dieldrin may
be lost (as measured by vapor density) from "wet" soils than from
"dry" soils. Apparently, water molecules may replace previously
adsorbed dieldrin and when the soil becomes saturated with water,
the vapor density of dieldrin becomes constant and independent of
soil water content. In a translocation study (63,248), dieldrin
was applied to soils adjacent to four small ponds under three con-
ditions: no incorporation in the soil, light incorporation, and
thorough incorporation. In each case, no dieldrin (below analytical
sensitivity) was found in the pond water, and very little in pond
mud (<.02 ppm to .13 ppm, for example). Most of the dieldrin was
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- 58 -
found in the soil where it was originally applied.
Section III. "Aldrin and Dieldrin Residues in Soils, Persistence,
Degradation, Etc."
Many field and laboratory studies have been performed on the
occurrence, persistence, etc., of aldrin and dieldrin in the soil
environment. In the case of persistence (51,166,167,168,169,170,171,
172,173,192), aldrin and dieldrin disappeared slowly from soils, for
example, aldrin, 15.6 ppm, "decayed" to .860 ppm dieldrin over a 5-year
period (169,170). In a field study (266), aldrin and dieldrin were
observed to disappear in accord with first order kinetics (aldrin—>
dieldrin, then decay of the dieldrin), whereupon a "half-life" of
2-4 years for dieldrin was calculated. In another field study (192)
aldrin was found to have a half-life value of 5 years and dieldrin
of 7 years. In still another field study (173), it was found that
the presence of a cover crop permitted a greater persistence of
aldrin and dieldrin than when these pesticides were incorporated into
soils or applied on the soil surface. This study (173) speculated
that the greatest loss of aldrin and dieldrin from soils is through
volatilization. Four months after application of aldrin to the soil's
surface (173), most all of the aldrin and dieldrin were found in the
upper 2" and 75% in the upper 1". Twelve months after application, 90%
was found in the upper 3". Three years after application, 72-82% was
found in the upper 3", 11-16'% was found in 3-4", and "very little"
was found in the 4-9" depth. It should be stated here that many of
these studies used application rates of aldrin and dieldrin (5-25 Ibs/
acre) that are far in excess of actual agricultural application rates
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- 59 -
(1,3,4, Ibs/acre). There have been some analytical surveys of fields
treated with aldrin and dieldrin (57,108,265) where these pesticides
were found several years after initial treatment. One significant study
(81), however, should be mentioned. Soil samples, stored since 1909,
were analyzed for chlorinated hydrocarbons under conditions commonly
employed in soil surveys. 32 of 34 samples showed "apparent" insecticide
residues! In fact, "aldrin" was frequently observed. Epoxidation of
aldrin to dieldrin was observed (168) which, by now, should be common
knowledge. Some vegetable crops were grown on aldrin treated soils
(25 Ibs/acre). Translocation was observed with carrots taking up the
greatest amounts of aldrin (up to 1.5 DDITI). However, when the carrots
were grown on normal dosages of aldrin (1 Ib/acre), .05 -.09 ppm were
observed in this crop. Potatoes, beets, radishes, cucumbers, lettuce,
and turnips took up considerably lesser quantities of aldrin and dieldrin
Soil type is an apparent factor also in the persistence of aldrin
and dieldrin (12,172). Under laboratory studies, aldrin (applied 200
lbs/6" acre, 26°C), disappeared faster from Plainfield sand (0.8% or-
ganics) than from Miami silt loam (3.8% organics) than from muck soil
(40% organics) observed over 56 days. Apparently, the organic matter
retards whatever mechanism is responsible for the aldrin disapoearance
(note that the word degradation is not used). Similar results were
observed under laboratory conditions. Temperature was observed also
to be a factor as aldrin (20 lbs/6" acre) disappeared faster from a
silt loam soil faster at 46°C than at 26°C than at 6°C (laboratory
study over 56 days). In some early soil persistence studies (166,171),
aldrin would disappear to become undetected chemically but a "toxicant"
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to flys would remain behind. This "toxicant" proved to be dieldrin.
Section IV. "Microbiological Degradation of Aldrin and Dieldrin"
Very little research has been reported on the microbiological
degradation of aldrin and dieldrin. The most probable reason may be
that these pesticides are not degradable, at least, in accord with
this reviewer's definition (a change in the oxidation number of
carbon to +IV, i.e. C02). What information available shows that
(a) dieldrin may be converted to water soluble and solvent soluble
metabolites by soil organisms (179,180), (b) dieldrin may be converted
to photodieldrin by microbial isolates from various environments (181)5
(c) conversion of aldrin to dieldrin by a soil fungus'(251), (d) partial
hydrolysis of dieldrin by aerobacter aerogenes (262), and (e) partial
degradation of dieldrin to C02 by a soil fungus (18). It appears that
a wide variety of soil organisms can muster their courage to attack
aldrin and dieldrin, but that most give up since metabolites are formed
which have the basic ring structure in tact. There was one hardy
soil fungus Trichoderma Kom'ngi that thinks he can break the ring
14 14
structure as CC^ was produced from C dieldrin.
Section V. "Photodecomposition of Aldrin and Dieldrin"
It appears that aldrin and dieldrin in solid states or in solu-
tion may be converted by ultraviolet light to other products which are
usually more toxic to flies, mosquitoes, mice, etc., than the parent
compounds. The central question is, however, can sunlight catalyze
the decomposition of aldrin and dieldrin? The photoconversion of
dieldrin is wavelength dependent, i.e., it requires short-wavelength,
high energy irradiation of 2600A0 and lower. The earth's atmosphere
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absorbs all light of wavelengths less than 2863A0. Experiments were
conducted (122) in an effort to answer the photoconversion of dieldrin
under natural solar conditions. The leaves of corn plants were sprayed
with acetone solutions of dieldrin, dried, and placed in the beautiful
California sun for 64 days. Also some dieldrin sprayed corn leaves
were irradiated in the laboratory. Here the results as presented in
the paper become confusing. These statements were made without the
supporting evidence: "Gas chromatographic analysis of the residue
remaining on corn plants which had been treated with dieldrin showed
that none of the pentachloro compound (IV) was formed. Instead an-
other substance appeared which was identified as the photoisomerization
product (III) by comparison with an authentic specimen. However, when
the dieldrin-treated leaves were exposed to 2537A0 ultraviolet light
in the laboratory, considerable amounts of IV were found after only 15
minutes of irradiation." Based upon experiments, the authors stated
"this particular reaction (dieldrin to compound IV when a H replaces
one of the vinyl chlorines) would not be expected to occur in the
field during exposure to natural sunlight." Furthermore, compound
III could not be detected, in the laboratory, after irradiation of
dieldrin solutions at wavelengths between 25^0 and 3000A0. The signi-
ficance of compound III is that it is "approximately two times more
toxic than dieldrin to the house fly and mosquito," (216).
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APPENDIX VI
SOIL INSECT CONTROL
Mahlon L. Fairchild and R. L. Doutt
Wireworms
Scott and Carpenter (221) studied wireworm control on potatoes
in Idaho with side-dressed and broadcast insecticide applications.
In one experiment Bay-38156 and disulfoton were side-dressed at rates
of 8 and 18 ozs. A.I./1000 ft. row. Agritox and Dasanit were side-
dressed at .8 and 1.8 oz. A.I./1000 ft. of row. Propoxur was side-
dressed at .9 and 1.7 oz. A.I./1000 ft. of row. All treatments
resulted in significant reductions in wireworm injury. In a second
test, chlordane was broadcast at the rate of 10 Ibs. A.I./acre;
diazinon and parathion at 6 Ib. A.I./acre; phoxim at 3 Ibs. A.I./
acre, and Dyfonate and Agritox^at 4 Ibs. A.I./acre. Phorate was
side-dressed at 2.3 oz. A.I./1000 ft. of row and dichlorous at 3.8
oz. A.I./1000 ft. of row. The results indicated that 2 oraanophos-
phates compounds control wireworms as well as chlorinated hydrocarbon-
ous materials, represented by chlordane. These 2 materials were:
Dyfonate and Agritox^; Diazinon, phorate, and parathion gave poor
control in these tests. Dichlorous and phoxim were intermediate
in the control. Results of this experiment were not very promising.
Even if 80% control could be achieved in a population which could
cause 20% damage, the remaining wireworms could cause 6% damage.
This level of control would not be feasible economically under the
present grading system, since the potatoes would not meet U.S. No. 1
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grade requirements. Further 80% control would still allow many
wireworms to mature, mate, and lay eggs.
Keaster and Fairchild (143) studied control of sand wireworms
in Missouri. American Cyanamid 18133 at 1.2 Ibs. A.I./acre, Hepta-
chlor at 1.5 Ibs. A.I./acre and Hercules 5727 at 1.13 Ibs. A.I./
acre, seemed to give significant reduction in wireworm injury to
corn.
Tappan (241) tested 17 insecticidal compounds in various formu-
lations for wireworm control on cigar-wrapper tobacco. Compounds which
gave good results were: Bayer 25141, diazinon, GS-13005, Kepone, N-290,
Niagara 9203 and parathion.
Onsager e_t ah (198) investigated control of wireworms on potatoes
in eastern Washington by soil fumigants and organophosphorous insecti-
® .©
cides. These investigators found that Telone , DPT Mixture, and ethylene
dibromide applied at 20 gal., 25 gal., and 36 Ib./acre, respectively,
and broadcast applications of granulated diazinon, parathion, and pho-
rate, applied at 2, 4, and 3 Ibs./acre, respectively, gave economic
control of the Pacific Coast wireworm on potatoes in sandy loam soil.
Cullage was reduced 93.6-100%. Granulated disulfoton, broadcast at
3 Ib./acre was reported to give significantly less control. Post-planting
side-dressings of granulated parathion, phorate, Stauffer N-2790, and
Bayer 25141, applied at 3 Ib./acre reduced cullage 74.4-85.2%. Granu-
lated disulfoton and Bayer 37289 and naphalene crystals were signifi-
cantly inferior. Phorate and disulfoton granules gave as good control
when metered onto the soil surface in bands 6 in. wide in the furrow left
by the press-wheel potato planter as when side-dressed in the soil at
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the same rate. Of all diazinon, disulfoton, parathion, and phorate
treatments only phorate applied in the press-wheel furrow left a
detectable residue above the tolerance in tubes collected 3 weeks
before harvest.
Harris (1965) reported diazinon baits, Kepone baits, parathion
granules and diazinon granules to be somewhat effective against wire-
worms in sweet corn. These studies were conducted in organic soils
in Florida.
Brett et^ al_. (1966) reported that diazinon gave poor control of
wireworms in sweet potatoes when it was incorporated into the soil
prior to planting, but a foliage-surface application during August
gave good control. Diazinon gave good control when applied on the
surface late in July at the rate of 3 Ib. active ingredient per acre
in a granular formulation. Application in August were less effective.
Insecticides incorporated in the soil were less effective in organic
soils than in sandy soils. Soil tyoe show little effect on control
by surface-applied materials.
Burrage et^al_. (31) reported that granules of N-2790 and
Zenophos at 5 Ib./acre broadcast and worked into the soil shortly
before planting, gave more than 90% wireworm-damage-free potatoes
compared with 26 to 55% damage-free potatoes in untreated soils.
Diazinon at 7-lbs./acre and Bay 25151, and Bay 37289 and UC 10854
at 10 Ibs./acres also gave more than 90% damage-free potatoes.
Lower rates tested gave less than the 90% damage-free level re-
quired for Canada No. 1 potatoes. Granules of Bay 37289 and N-
2790 broadcast at 10 Ibs./acre caused an objectionable flavor.
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In 1969, Onsager (196) reported that fumigation of the soil
CR)
in autumn with ethylene dibromide, Telone^or dichloropropane-
dichlorapropene mixture gave excellent control of Pacific Coast
wireworms. Dyfonate at 2 Ibs./acre, 3/4 Ib./acre of diazinon
or parathion, and 4 Ibs./acre of carbofuran or Bay 37289 also
gave excellent control when broadcast. Broadcast treatments
tended to be more effective and less variable than band or side-
dress treatments with the same chemicals. Band treatments of 4
Ibs./acre of granular disulfoton and broadcast treatments with
up to 6 Ib./acre of granular Shell SD 8530 were inferior to
other treatments. However, Onsager and Foiles (197) reported
when granular carbofuran, Dyfonate"", and parathion were applied
in mid-March for control of the Great Basin wireworm, and the
Pacific Coast wireworms on summer potatoes that side-dressed
treatments at a rate of about 2.3 Ib. of toxicant per acre gave
better average control with less variation than broadcast treat-
ments with 4-8 Ib. of the same toxicant per acre.
Flooding infested fields for 6 to 7 days with an inch or
two of water during extremely hot weather has been reported to
kill nearly all wireworms. Soil temperature must remain above
68°F. for the entire period for best results. In contrast, when
the upper 15 inches of infested soil is allowed to become very
dry for several weeks in summer, most of the wireworms, especially
the younger ones, are killed. Drying has been recommended to keep
wireworms below economic levels on irrigated lands.
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Plowing fields in the summer during the pupal stage has been
reported to reduce wireworm numbers. Mechanical injury to the
worms and exposure to summer heat and low humidities account for
most of the mortality at this stage.
Crop rotation in certain areas have been reported to reduce
wireworms. The growing of truck croos in the same area continu-
ously will usually cause a build-up of wireworms. The growing of
potatoes in a short rotation with clover or grain is undesirable
because of wireworm build-up (160).
Cutworms
Morgan and French (188) evaluated fifteen compounds for control
of granulate cutworms on peanuts in Georgia. The materials were used
as baits, sprays, and one dust mixture in experiments during a 4-year
period 1966-69. Abate , monocrotoohos, Dursban , Dyfonate , trichlor-
fon, methomyl, and Monitor gave higher than 90% control of cutworm
larvae within 24 hours after application. In general the mixtures
containing wheat bran gave the highest percent control.
Harris et_ a]_. (1969) evaluated four insecticides for control of
the dark-sided cutworm in rye grown in rotation with tobacco. The
four materials tested were DDT, Bay 37289, Dursban, and trichlorfon.
In plots using artificial infestations DDT and Dursban gave 100% con-
trol while Bay 37289 provided 90% control, trichlorfon at 1 Ib. per
acre was not sufficiently effective. It was noted that DDT, Dursban
and Bay 37289 provided 88-90% control of heavy natural infestations.
It was noted, however, that the rapid dissipation of the residues of
Dursban and Bay 37289 would require a snlit application to give
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adequate control.
Harris and Svec (113) studied the effects of several insecti-
cides on black cutworm in the laboratory. These studies indicated
that Dursban, Bayer 37289, and parathion warrant further investigation
as possible alternatives for the cyclodiene insecticides as soil
treatments for control of the black cutworm. It was noted, however,
these materials should be applied when the larvae are in the early
instars to be effective. Soil type, moisture, method of application,
and formulation must be taken into consideration for effective control.
Further studies by Harris and Svec (115) showed three other com-
pounds having potential as possible replacement for cyclodiene compounds
as control agents for dark-sided cutworms. These compounds were:
N-2596, phoxim and chlorphoxim. Chlorphoxim seemed to be somewhat
less effective than the other two compounds.
Unpublished studies by Sechriest and York in 1966 (227) indicated
that Niagara 10242 (Furadari), and a combination of thimet and A.C.
47470 gave effective control against black cutworms. These studies
were conducted using artifical infestations. In a further unpublished
screening test conducted by Sechriest in 1966, Dursban , Sevin ,
® (§)
A.C. 47470 + Thimet and G.S. - 10133 as well as Baygorr showed
promise as effective insecticides against black cutworms.
Sechriest (224) reported that BaygorPaid not perform well as
® (E)
a cutworm insecticide. However, diazinon, Dyfonate , dylox, Sevin ,
Bay 37289, GC-6506, EI-52160, and Thimet + EI-4740 were shown to be
effective against cutworms.
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68 -
Begg et^ aj_. in 1963 (15) reported that soil treatments in general
did not reduce the infestations of the black cutworm to non-economic
levels during the first seven days after treatment. It apparently
took some time for the larvae to contact a lethal amount of an insecti-
cide in the soil. The results of field test conducted with eight
insecticides indicated their relative effectiveness in test could be
rated endrin>aldrin = dieldrin = heotachlor>DDT = Dylox>Guthion = Sevin
According to work done by Harris and Mazurek in 1961 (110), the
regression line slopes would indicate that a small increase in the
rate of application of dieldrin should result in more effective con-
trol of cutworms. Conversely, large increases in rate of applications
of Dylox, Guthion, and Sevin would result in little or no increase
in insecticide efficiency.
Laboratory studies by Harris and Gore in 1971 (109) were con-
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The most toxic was Lannate >DDT>parathion>Dursban >Ciba 8874.
Birlane and Bayer 37289 were slightly less toxic than aldrin.
As soil surface applications, Dursban and aldrin were highly ef-
fective, DDT, parathion and Bayer 37289 were only slightly less so,
and Lannate was ineffective. Soil-surface applications of Dursban
were 2-4 times as effective as soil incorporations. Dursban, DDT,
and Lannate were all highly effective as stomach poisons. Lannate
was 32 times more effective as a stomach poison than as a soil in-
secticide.
Greenhouse studies conducted by Sechriest (225) indicated
several baits to be effective against black cutworm populations.
The baits were: Trichlorfon Bait C, CL-47470 - 2% apple pomace,
Abate - 2% apple pomace, ethyl parathion - 2% apple pomace, mi rex
1.25% bran, TDE - 5% bran, and carbaryl - 5% bran. Apple pomace and
wheat bran were effective baits and the placement within 6 in. of the
row resulted in satisfactory kill of larvae.
Studies by Harris et^ al_. in 1962 indicated that there was very
little resistance building in black cutworms in certain areas of
Canada to soil insecticides. These studies also indicated that in
general organophosphates were less effective against black cutworms
than cyclodiene insecticides.
White Grubs
Several methods have been suggested for controlling white grubs.
Fleming and Baker (73) suggested using hot water to control the
Japanese beetle in the soil, on the roots of nursery plants.
Metzger and Maines in 1935 (182) as well as Fleming et al_. (79)
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reported on the success of using traps baited with geraniol and eugenol
for control of white grubs, particularly the Japanese beetle.
The effectiveness of lead arsenate to control white grubs has
been explored by researchers such as Fleming and Baker (74),
Fleming ert aj_. (78) and Fleming (70). Napthalene and Derris have
been reported to be helpful repellents of the Japanese beetle by Fleming
and Baker (75, 76).
Many studies have been conducted using cyclodienes to control grubs.
Fleming in 1947 reported that DDT was very effective against the grub of
the Japanese beetle. Hadley and Fleming (101) reported on the use of
other cyclodiene compounds such as TDE, chlordane, methoxychlor as well
as ethylene oxide, methyl bromide, lead arsenate and several imported
parasites for control of the larvae of the Japanese beetle. Fleming
and Baker (77) also reported that oaris green and its homologues were
effective insecticides against Japanese beetle larvae.
Burrage and Gyrisco (29,30) studied the control of the European
chafer in pasture sod. The test conducted by Burrage and Gyrisco
included six materials - parathion, dieldrin, aldrin, chlordane, BHC,
and DDT; parathion and BHC did not perform as well as the other
materials. Grambell (91, 92, 93, 94, 95, 96, 97, 98) did extensive
work on controlling the European chafer. Most of these works included
the use of cycl-odiene insecticides for control. Tashiro (243) reported
that methyl bromide fumigation gave satisfactory control of the European
chafer in nursery stock.
Hal lock (102) reported that carbon-disulphide emulsion as well as
lead arsenate could be used to control Asiatic beetle larvae in lawns.
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Several parasites have been reported to attack Scarabaeidae larvae.
Gardner and Parker (83), Glaser (86), Fleming (77), Burrel (32),
King and Holloway (148) and Dutky and Gooden (60) are among the re-
searchers who have studied parasites of the white grubs. Milky
diseases in beetles have to be reported to give rather effective
control of several white grubs. Hawley (119) and Fleming (1933)
among others conducted studies which show the effectiveness of milky
diseases.
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APPENDIX VI - A
OCCURRENCE OF ALDRIN AND DIELDRIN IN BIOLOGICAL ENVIRONMENTS
Samuel D. Faust
Dieldrin Contents of Bottom Feeding Fish
Four papers were reviewed in connection with the dieldrin con-
tents of bottom feeding fish. Dieldrin was found in carp, suckers,
channel catfish, and bigmouth buffaloes. In general, the contents
were less than 1 ppm (usually, whole fish). Also, the dieldrin
contents were less than DDT contents (see Table in ref. 121). The
analytical methodology consisted of the usual solvent extraction,
cleanup on Florisil and gas-liquid chromatographic separation on
DC-200 or some other non-polar phase with an electron capture
detector. Very, very seldom was any confirmatory technique applied.
An occasional thin-layer chromatogram was tossed in. Only one paper
(121) found (or at least reported) aldrin in these fish. Another
general observation may be made: the bottom feeders did not appear
to have dieldrin contents any higher than the non-bottom feeders.
For example, two small mouth bass (a bottom feeder) caught in the
Potomac River showed dieldrin contents of .05 and .01 ppm whereas
two large mouth bass showed dieldrin contents of .03 and .06 ppm
(121).
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APPENDIX VI - B
OCCURRENCE OF ALDRIN AND DIELDRIN IN BIOLOGICAL ENVIRONMENTS
Samuel D. Faust
Marine Environments
A few papers were reviewed in order to gain some insight into
the occurrence of aldrin and dieldrin in marine environments, espe-
cially the estuary. There is some evidence that oysters, mussels,
crabs, etc., contain residues of aldrin and dieldrin (28, 154, 187,
218). However, the frequency of occurrence and the concentrations were
not as great as suspected. For example, "dieldrin was not routinely
found" in oysters where typical concentrations were 10, 27, 20, 11, 18
ppb (ug/kg) (187). By routinely found may be interpreted as the
occurrence-of dieldrin in less than one-half of all samples. An
interesting observation came from the California study (187):
"expected high levels of pesticides were not found in San Francisco
Bay, the terminating point for the Sacramento and San Joaauin Rivers
which drain over 6 million acres of agricultural land in the Sacra-
mento and San Joaquin Valleys." Aldrin was reported in 17 of 133
samples of oysters taken from South Atlantic and Gulf of Mexico
waters at concentrations of 0.01 to 0.03 ppm with 0.01 ppm as the
median.
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APPENDIX VII
IMPACT OF WITHDRAWAL OF SOIL USES OF ALDRIN AND DIELDRIN
Mahlon L. Fairchild
Very little valid information is available indicating the
economic impact resulting from the withdrawal of aldrin and dieldrin.
Various individuals have attempted to use the meager information on
soil insect losses to predict a dollar value that might be lost if
soil insecticides were not used or substitutes were used in place of
the cyclodiene insecticides. Estimates of possible losses range from
$50,000,000 to $150,000,000 for corn alone. Of course additional
insect losses would be suffered on the many other commodities where
cyclodiene compounds are used for control of soil inhabiting arthro-
pods. Although these losses at first appear staggering this may not
place an immediate limitation on meeting the needs of corn production
for our nation. However, the withdrawal of these materials may result
in a complete loss of an individual farmer's crop.
Unfortunately soil insecticides are used as a preventive to soil
insect damage. If an individual farmer lost one crop every three years
it would result in economic disaster to the individual farmer but may
not have a tremendous impact on the corn production in the nation.
It is embarrassing to entomologists to admit how little they know
about the soil inhabiting arthropods. Before a preventive method of
insect control can be eliminated one must have the ability to predict
insect outbreaks. Unfortunately at the present time farmers do not
even know the number of various soil inhabitating pests they are
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- 75 -
controlling but are positive of return of their investment whenever a
pesticide is used. Furthermore if the pest is known and can be
identified in the field very little is known about the life history,
habits or host ranges of the many soil pests. The soil insect complex
is made up of white grubs, wireworms, cutworms, seed beetles, maggots,
and other incidental problems and little is known about individual
species within each group.
Another point that should be mentioned is the drastic changes
that have taken place in agricultural oroduction in the last 20
years that are coincidental with the use of soil insecticides. It
has been suggested that pesticides were not necessary 20 years ago
and, therefore, should not be necessary today. One must remember
that changes in fertility, irriaation procedures, plant stands all
relate to the economics of crop production and are also interrelated
with the use of pesticides. To illustrate the importance of these
changes the average per acre corn yields in 1950, 1960, 1970, and
1971 were 38.2, 54.7, 71.6, and 86.8 bushels, respectively. This
represents over a 2-fold increase and undoubtedly makes the insect
control more essential. Before one can back up 20 years in pesti-
cide usage, consideration should be given to the impact this would
have in interrelationships with all of the other factors that have
changed. Intensified agriculture has actually moved some pests
from the relatively unimportant to economic problems when the
above-mentioned changes took olace.
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- 76 -
RESEARCH NEEDS
Additional research should be initiated to establish economic
thresholds for the various soil inhabiting arthropods. Additional
work should also be undertaken to study the distribution, abundance,
biology and ecology of soil inhabiting arthropods. All of the above
information is basic to an integrated pest management approach to
insect control. This method of control includes non-chemical (bio-
logical, cultural, host plant resistance, etc.) and limited chemical
usaae.
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- 77 -
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PERSONS APPEARING BEFORE THE COMMITTEE
First Meeting
December 16, 1971
Mr. Harold 6. Alford, Pesticides Regulation Division, Environmental
Protection Agency
Mr. Thomas H. Kemp, Office of General Counsel, Environmental
Protection Agency
Second Meeting
January 25 & 26, 1972
Mr. Walter Appleby, Shell Chemical Company
Mr. William Bernholz, Drew Chemical Company
Dr. John Berry, Economic Research Service, United States Department
of Agriculture
Mr, P1et Bodenhorst, Lees Carpets, Div. of Burlington Industries
Dr. Frederick Coulston, Albany Medical College of Union University
Mr. Walter W. Goeppinger, National Corn Growers Association
Dr. Ralph Heal, National Pest Control Association
Dr. John McPhee, International Wool Secretariat
Mr. Lou Mitchell, Shell Chemical Company
Dr. Paul Porter, Shell Chemical Company
Mr. John Redston, Drew Chemical Company
Mr. G. Gregory Rohwer, Animal and Plant Health Service, United
States Department of Agriculture
Dr. Joseph Sloan, Shell Chemical Company
Dr. M. B. Slomka, Shell Chemical Company
Mr. Robert Thatcher, Forest Service, United States Department of
Agriculture
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Dr. Fred Tschirley, Office of Secretary, United States Department
of Agriculture
Dr. H. G. S. Van Raalte, Shell Chemical Company
Dr. Charles F- Wurster, Environmental Defense Fund
Third Meeting
February 23, 1972
Dr. F. F. Becker, College of Medicine, New York University
Dr. J. H. Berry, Economic Research Service, United States
Department of Agriculture
Dr. D. L. Coudriet, Agricultural Research Service, United
States Department of Agriculture
Dr. P. J. Luginbill, Agriculture Research Service, United
States Department of Agriculture
Dr. P. H. Schwartz, Agricultural Research Service, United
States Department of Agriculture
OU.S. GOVERNMENT PRINTING OFFICE: 19 Tt 4 84-4 86/241 1-3
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