‘»¡At'

other face

OF2,4D

A Citizens’ Report
SOUTH OKANAGAN
ENVIRONMENTALCOAUT ^

■£).//vri

(c)

South Okanagan Environmental Coalition, 1978

All rights reserved. No part of this book
may be reproduced (except by reviewers for the
public press) without written permission from
the South Okanagan Environmental Coalition.

First Printing - January, 1978
Second Printing - July, 1978

FRONT COVER: Children swimming in the restricted
area of Skaha Lake Beach, Penticton, B.C., on
June 27th, 1977. Four days earlier this area had
beentreated with 20 lbs. to 40 lbs. of 2,4-D
active ingredient per acre.

TITLE PAGE: Water Investigations Branch team
applies herbicide in shallow water on Skaha Lake
Beach on June 23rd, 1977. Eight days later,
thousands of vacationers used this beach during
the July 1st holidays weekend.

Penticton Commercial Printing Ltd.

V'n 1

THE OTHER FACE OF 2,4 D
a citizens’ report

JOHN W. WARNOCK
JAY LEWIS

SOUTH OKANAGAN ENVIRONMENTAL COALITION
PENTICTON, BRITISH COLUMBIA

S)

«

£

TABLE OF CONTENTS

Preface
I

Introduction

II

Teratogenic Effects of 2,4-D

III

Cancer and the Phenoxy Herbicides

IV

Is 2,4-D a Mutagen?

V

Dioxins in Phenoxy Herbicides

VI

Acute and Subacute Illness Caused by
Phenoxy Herbicides

VII

Environmental Effects of 2,4-D

VIII

The Persistence of 2,4-D in the Environment

IX

Conclusion

X

Addendum

XI

Tables
Bibliography
Bibliography II

4404
V - H S do

PREFACE
Genesis
One year ago the South Okanagan Coalition did not ex­
ist. Very few people in the Valley knew anything about the
phenoxy herbicide 2,4-D. It all began in May of 1976 with
the arrival of the B.C. Government's Advisory Committee on
the Ccfntrol of Eurasian Water Milfoil. Public hearings were
held, questions asked, and the answers on the safety of 2,4-D
were not reassuring enough for many people. The S.O.E.C. was
formed and the research began. This report is the result of
a seven month literature search and a large amount of primary
research. While we believe it to be the first effort of this
type on 2,4-D ever published, we realize that we have only
scratched the surface. Additional information arriver daily
and the picture becomes clearer bit by bit.
ning.

It is a begin­

How To Read It
Because of the length and the complexity of this report,
some instructions may be helpful. For a quick overview of
the situation, read the introduction, the chapter summaries
and the conclusion. A more in-depth understanding can be
obtained in any particular area by reading that chapter in its
entirety. All sources are completely listed in the biblio­
graphy and most are available in our files. Please do not
attempt to read this report in one sitting - brain damage
may result.
Bias, Fairness and Research
We have often been asked whether this report would be
"unbiased." We went into this project because we were worried
about the conflicting reports which we had read about the
health aspects of 2,4-D.

4405
61

2
We were suspicious of the phenoxy herbicides because of the
widespread reports of the ill effects on humans that emerged
during the latter part of the war in Vietnam.
When the Provincial Government appointed the Advisory
Committee, they selected three professors from the University
of British Columbia who had previously served as the B.C.
Royal Commission Inquiry into the Use of Pesticides and Herb­
icides. In the Final Report of the Royal Commission, and
elsewhere, these three individuals clearly established that
they believed that there was no damage to public health or the
environment from the traditional use of phenoxy herbicides.
Could a report by such a group be "unbiased"?
The Ministry of the Environment specifically instructed
the three man Advisory Committee to examine "all available
data" on the public health problems associated with the aquatic
use of 2,4-D. The three Interim Reports total only 44 pages,
have only 28 pages devoted to the use of the chemical, and
have no footnotes or bibliography. Even at first glance, the
end result appears deficient.
As the title suggests, "The Other Face of 2,4-D" is an
attempt to look beyond the findings of the Advisory Committee.
In fact, we feel that the B.C. Royal Commission did not ad­
equately deal with the evidence it had on the possible
dangers to public health from the widespread use of phenoxy
herbicides. In addition, much new data has become available
since May 1975.
We are publishing only that research which we feel will
stand up to rigorous scientific scrutiny. In that sense we
feel the report is fair. For the public, it fills in the gap
left by the B.C. Royal Commission and the three Interim
Reports of the Advisory Committee.

4406

3
Acknowledgements
So many people helped make this report possible it is
difficult to know where to start.

Tina Kramer, Clive & Melissa

Johnson, Ruel Smith, Don Rees, Peggy and Walt Taylor, Marge
Murton, Jim Cluett, Katy Madsen and Margaret Ingram of the
Coalition's Research and Information Committees helped with
the massive job of collecting and organizing the massive
amount of material.
Draft copies of the report were circulated to six out­
side readers with expertise in various fields, for their
comments. Because five of them are employed by the B.C.
Government or the B.C. University system, we will not mention
them by name. Their suggestions were an immense help to us
in producing the final draft. Of course, we take full re­
sponsibility for all the material in this report.
A large number of environmental groups from across the
U.S. and Canada forwarded material to us for use in this
study.

First and foremost on our list of contributors are

Sid Horton, Bill Boyd and John Hillian of the Kelowna Society
for Pollution and Environmental Control (SPEC).

They pro­

duced the first brief in the Okanagan Valley which pointed
to the health hazards associated with 2,4-D.

Much of our

research data were collected by this group.

Other organ­

izations and individuals supplying information were:

Linda

Pim, Pollution Probe, Toronto; Michael Singleton, Federation
of Ontario Naturalists, Toronto; Maureen Hinkle and Norma
Watson, U.S. Environmental Defense Fund, Washington, D.C.
and New York; Lynn Pederson, Citizens Against Toxic Sprays
(CATS), Eugene; Donna Waters, Minnesota Herbicide Coalition,
Chaska, Minn.; Michael Mann, Federation of American Scien­
tists, Washington, D.C.; David Fry, Center for Science in the
Public Interest, Washington, D.C.; Richard Semiklose,

4407
£>•4563

4
American Association for the Advancement of Science, Wash­
ington, D.C.; Committee For Environmental Information, St.
Louis; Mark Luppino, Citizens For a Better Environment,
Chicago; Peter Messina, Sierra Club, San Francisco; Robert
Nixon, Sierra Club, Victoria; and The National Audubon
Society, New York.
Several other organizations were helpful in supplying
information: Environmental Canada; Cancer Control Agency
of B.C.; Canadian Cancer Society; The U.S. Environmental
Protection Agency and most importantly, the South Okanagan
Health Unit.
Publication Support
The South Okanagan Environmental Coalition would like
to thank the British Columbia Government Employees Union,
Area Council #07 - Okanagan, for a substantial grant which
helped make reproduction of this report possible.

Production
We would also like to thank Loretta Scott for typing our
final draft.

Jack Davis designed and produced the Coalition

logo and was responsible for the cover artwork. Penticton
Commercial Printing got it all through the press. Melody
Ilessing proof read the final copy and corrected our errors.
All the staff at Apex Office Supplies helped with the detail
work.
Dedication
It is appropriate that this report should be dedicated
to Merriam Doucet of Port Moody, B.C.

Without her detailed

knowledge of the field, extensive files and delightful sense
of humour, this document would not have been possible.

D ' H S ùH

5
Her speaking tour through the Okanagan in the spring of 1977
provided local residents with the basic information on the
hazards associated with 2,4-D and provided the encouragement
for the formation of the South Okanagan Environmental Coal­
ition. As long as Merriara is around, people cannot be care­
less with pesticides and expect to escape unscathed.
Jay Lewis
John W. Varnock
Penticton, B.C.
January 18, 1978

Q-Hsog

One of the weed eradication machines, designed and built by the
Water Investigations Branch, here used in Skaha Lake Beach. While
this mechanism was very slow, new designs will soon be available
which should speed work.

4411
How Eurasian Water Milfoil spreads. This boat and trailer were on
their way to Calgary via Shuswap Lake. The owner was not interes­
ted in removing the weed.

£M5t/T

2,4-D monitoring programme by the B.C. Water Investigations Branch.
Note the brown tinted sample bottles sitting in the bright Okanagan
sunshine. 2,4-D degrades more rapidly in warm water.

One of the dead carp which showed up on Skaha Lake Beach five days
after 2,4-D application. A total of eight were seen. Carp and
Suckers taken in the area had high concentrations of the herbicide
in the stomach and flesh.

I
INTRODUCTION
Eurasian water milfoil (Myriophyllum spicatum L.) is
spreading through the Okanagan Basin lake system. This is a
perennial water plant that has spread throughout Europe and
the United States, and is now moving into Western Canada. It
has colonized all the lakes in the southern part of Ontario,
Quebec as well as upper New York state. (Holm et al, 1969)
During the summer months there is rapid growth from
the Milfoil root crown area which reaches up to the surface.
It requires sunlight for growth, and in the Okanagan lakes
is rarely seen in depths of over 15 feet. If the weed
spreads throughout the entire Okanagan lake system, it could
conceivably cover 8,000 acres or 10% of the lake surface.
(B.C. Department of Environment, 1976)
The weed reproduces from its seeds, which are known to
be spread by waterbirds, particularly coots. But the primary
method of reproduction is by fragmentation. Parts of the
plant break off, float for a period of time, lose their bouyancy, and sink to the bottom. At this point they root and
form a new colony. Authorities from the Tennessee Valley
Authority report that ”a single 2-inch fragment may take root
and grow 4 feet or more in length during a single growing
season. Calculations indicate that a single fragment the­
oretically could propagate almost 250 million new fragments
in one year.”

(T.V.A., 1972)

It is known to quickly es­

tablish where there are high levels of nutrients, as in silt
beds and downstream from sewage effluent outfalls. (Holm
et al, 1969)
Eradication programmes have been attempted in many areas
of the world, but because of the manner in which the milfoil
spreads, none have succeeded.

4413

1-2
In eastern Canada, government officials looked at the record
of past attempts and concluded that it was not worth the cost
to try to eradicate the weed.
Alternate Uses of the Milfoil Veed
Eurasian milfoil weed has become a serious problem in
the Kawartha lakes in Southern Ontario. Herbicide treat­
ments were tried by some individuals, but the rotting weeds
caused equally serious problems, and many felt the game pop­
ulation was threatened. The provincial government turned
instead to harvesting the weeds.
The main research project has been carried out by a
team of scientists from Ontario Agricultural College at
Guelph. Harvesting of the weeds was chosen for it gets the
plant out of the water, eliminates the depletion of the oxygen
level of the lake areas, and cuts back dangerous algae pro­
duction. They do not remove all the weeds, leaving beds to
protect the local game fish.
At first, the harvested weeds were distributed on farm­
ers fields with manure spreaders. While the weeds contain
nutrients and are an excellent soil conditioner, many farmers
believed the process took too much time. To easily manage
the weeds, it was necessary to remove much of the water.
The second experiment was to press out a "water weed"
pellet. This was a success, and the end-product was pal­
atable to both poultry and sheep. However, the costs of pro­
duction were too high to make it competetive with existing
feeds.
The third approach was to utilize the weed as a roughage
in cattle feed.

1-3
Experiments produced a silage that when top dressed with
corn and soy meal was quite successful for finishing cattle.
In test animals, the growth record and the beef were very
good.
The fourth experiment was conducted by the Horticulture
Department at Guelph. The weeds \irere used as an ingredient
in compost, using modern manufacturing equipment to remove
the water. The end result was a very good compost; there is
a good Ontario market for packaged material for potting and
commercial use. ("Nutrition” , 1977)
The Herbicide Alternative:

The Experience of the TVA

There have been several areas in North America where
there has been an attempt to control Eurasian water milfoil
weed by chemical means, but the most thorough experiment has
been in the Tennessee Valley Authority, a man-made lake system
running through six states from Virginia to Kentucky.
Milfoil was first identified in the T.V.A. system in
1960; by the end of 1968, there were more than 25,000 acres
of the weed in seven reservoirs. In 1962, the officials of
the T.V.A. began large scale applications of 2,4-D in two
forms: the butoxyethanol ester (BEE) in granular form and
the dimethylamine salt (DMA) in liquid form. Between 1962
and 1969 over 1.4 million pounds of 2,4-D were applied to
35,000 acres of weeds in the reservoir system.
How successful has the programme been? The history of
the programme in one lake, as reported in the Tennessee Valley
Perspective (Summer 1976), gives us a good indication of what
we can expect if a similar programme is introduced into the
Okanagan lakes.

4415

1-4
In 1969 Guntersville Lake in northeastern Alabama con­
tained around 14,000 acres of milfoil weed.

By applying

2,4-D at rates of between 20 and 40 lbs. of active ingredient
per acre, the infested acreage was reduced to 3,000 by 1973.
Even though the herbicide was continued every year, often
over the same beds, by 1976 the milfoil acreage had increased
to around 12,000 acres. Control at these levels required
herbicide applications every year.
In the overall valley, applications of 2,4-D reduced
the infested acreage to around 5,000 by 1973. But in 1976,
T.V.A. authorities reported that the total acreage had grown
to 16,000 acres in spite of annual applications. (TVA Per­
spective , Summer 1976)
Officials in the TVA have never believed that eradication
was possible. In their Environmental Statement, they state
that "the objective of the watermilfoil control program will
be to maintain at least the present level of control." (T.
V.A., 1972)
There are obvious reasons why eradication is impossible.
First, the weed spreads too easily through fragmentation and
movement of seeds. Secondly, the herbicides have not been
completely successful in killing all of the roots of the plant.
Under the best conditions in spring, the T.V.A. reports that
their kill rate was only 95%. During the remainder of the
year, kills averaged between 55% and 70%. (T.V.A., 1972)
The Drawbacks to the T.V.A. Programme
The experience of the T.V.A. should indicate some of the
problems we might experience if a similar programme were to
be introduced into the Okanagan.

4416

1-5
First, when the weeds are killed by herbicides but not re­
moved from the lake, the rotting weeds not only become a
nusiance, but the increase in nutrient release makes further
infestation easier.

(Moody, 1973; Sculthorpe, 1967)

Secondly, there is the problem of the increase in the
slimy dark green weed, filamentous algae. This more danger­
ous weed is taking over embayments where the herbicide has
been applied. This was also a major problem where the herb­
icide was used in Ontario. In the late 1960's, the outbreak
of blue-green algae in the beach area of Skaha Lake at Pen­
ticton became a serious health problem, causing illness to
residents and tourists. The South Okanagan Health Unit
believes that the heavy growth of Milfoil weeds in Skaha
Lake near Penticton, virtually eliminated the algae blooms
in this area. (B.C. Board of Health, 1976; Brooker and Ed­
ward, 1975)
The third problem has been the rising costs of herb­
icide applications and monitoring. The costs of application
in the T.V.A. alone rose from S37 an acre in 1973 to over
S100 in 1976. In that year, they abandoned the use of
Aqua-Kleen 20, as it costs more than the liquid form.
This is spread on the weed beds through the use of a hel­
iocopter. (TVA Perspective, 1976; Bates, 1977)
Finally, there is the concern over the buildup of the
herbicide in the lake system. While there is no irrigation
in the TVA system, there are many centers which depend on
the lakes for their domestic water. During application
periods, levels of 2,4-D in the water have exceeded the .1
ppm level (maximum concentration set by the U.S. Government)
in a number of the major water purification plants. (See
Section VIII) Regular ingestion of low levels of the herb­
icide may well produce chronic illnesses.

These are yet to be

recorded, but we do not know of any programme to detect such
problems in the T.V.A.

4417

V '^ S l 3

1-6
Experiments in the Okanagan Lakes
Research on the control of Eurasian water milfoil in the
Okanagan Lake system began in 1972. Tests of the effective­
ness of paraquat, diquat and 2,4-D were conducted in ex­
perimental plots in 1974, 1975 & 1976. In 1976, the provincial
government agreed to a 50-50 cost sharing agreement with
the Okanagan Basin Water Board. This was superceded by the
agreement of May 5, 1977 whereby the provincial government
agreed to finance, design and implement a weed control pro­
gramme in co-operation with local officials. (Newroth, 1976)
The year 1977 was chosen for major tests of the use of
2,4-D and mechanical harvesting methods in four Okanagan
lakes: Kalamalka, Okanagan, Skaha and Osoyoos. The Canadian
Wildlife Service excluded Vaseux Lake from the treatments as
it is a major waterfowl range.

Dr. Peter Newroth, a bio­

logist with the Environmental Studies Division, B.C. Min­
istry of the Environment, was placed in charge of the pro­
gramme. In his memorandum on the 1977 programme, Dr. Newroth
argued that "it will be impossible to remove the nuisance in
one or two years." He supported the five-year programme
advanced by the Advisory Committee. Nevertheless, he argued
that in 1977 "eradication of Myriophyllum spicatum would be
attempted in Kalamalka and Osoyoos lakes."

(Newroth, 1977)

In a previous memorandum on application, Dr. Newroth
suggested that it would be "inappropriate" to use 2,4-D in
three areas:
(b)

(a)

shallow areas frequented by waterfowl;

areas immediately adjacent to domestic, industrial or

irrigation water intakes;

and (c)

spawning areas for game fish.

areas which would be

(Newroth, 1976)

4418

1-7
The Reports of the Advisory Committee
On October 18, 1976, the Government of British Columbia
appointed a three-man Advisory Committee on the Control of
Eurasian Water Milfoil in the Okanagan Lake system. All three
members were professors at the University of British Columbia;
they were the same three who had served as the members of the
Royal Commission of Inquiry into the Use of Pesticides and
Herbicides between 1973 and 1975. The Chairman, Dr. C.J.G.
Mackenzie of the U.B.C. College of Medicine, also serves as
Chairman of the Pollution Control Board, as well as an ad­
visor to the federal government on the question of arsenic
poisoning at Yellowknife, N.W.T.
Dr. W.K. Oldham, a civil engineer, was also known as an
outside consultant. Between 1971 and 1974 he served on the
Joint Federal-Provincial Okanagan Study, and between 1972-1975
on the Kalamalka-Wood Lake Study.
The Third member, Dr. W.D. Powrie, Head of the Depart­
ment of Food Science, had also been involved as a consultant
in the establishment of the government-financed Swan Valley
Foods.
The Minister of the Environment instructed the Advisory
Committee "to review all available data including information
collected by the Royal Commission hearings and to advise him
on the programme and any public health problems associated
with the use of 2,4-D for the control of aquatic weeds in the
Okanagan Lakes."
The first Interim Report of this committee, issued three
months later, called for control methods to be utilized in
1977 "with the possible exception of the use of herbicides."

4419
P-HsiS

1-8
They recommended a "carefully conceived programme" for test­
ing 2,4-D hopefully to fill in for the insufficient data" on
the "overall scale of use, application, concentration and ex­
clusion areas."

(B.C. Advisory Committee, January 1977)

However, by the time the Second Interim Report was issued
in March 1977 the Advisory Committee was arguing that "an allout attack on the weeds should be launched in the 1977 season."
A five-year integrated programme of mechanical, hydraulic,
biological and chemical control was outlined. (B.C. Advisory
Committee, March 1977)
Around this time widespread concern was being expressed
throughout the Okanagan over the use of 2,4-D in the lakes.
By the middle of the summer, opposition had been expressed
by over 20 groups, ranging from boards of irrigation districts,
many trade unions, to the B.C. Medical Association and the
Penticton and Kelowna Registered Nurses Association. Only
three organizations, all connected with the tourist industry,
had passed resolutions supporting its use. This widespread
concern was reflected in the public meetings held by the
Advisory Committee in the Okanagan in the spring of 1977.
The Advisory Committee made no attempt to alleviate this
concern in its Third Interim Report, issued on May 20, 1977.
The final report of the Advisory Committee was only four pages
long, and contained no new material on 2,4-D. Residents of
the Okanagan were simply assured that "water entering intakes
in the Okanagan Valley will assuredly contain no detectable
2,4-D three days after the 2,4-D application, if the programme
is carried out according to recommendations." They admitted
that "the people of the Okanagan are entitled to assurances
that there will be no danger to humans or crops from any
herbicides used in the lake (sic)." They were sure that this
can be given "if zero tolerance is achieved in all cases."
(B.C. Advisory Committee, May 1977)

'X)-H5Kc

I

4420

1-9
The 1977 Programme
In order to approach the "zero tolerance level", the
Advisory Committee recommended that no applications of herb­
icides should be used in swimming areas, and that no herb­
icides should be applied within 500 metres of any potable
water intake systems or any irrigation intakes. (B.C. Ad­
visory Committee, March 1977) Both of these recommendations
were ignored by the provincial government.
The commitment of key officials in the B.C. Department of
the Environment to the use of 2,4-D was reflected in the
policy set down for the 1977 year of control. All communities
which wished provincial government financial support for con­
trol of the weed were required to accept a total package
which included chemical as well as mechanical control. When
the City of Kelowna requested funds for mechanical control,
but said that they did not want herbicides used, they were re­
fused provincial assistance.

Kelowna officials and others

accused the provincial government of engaging in a form of
blackmail to force use of 2,4-D where it was not wanted.
During the summer of 1977, test applications of 2,4-D
were applied in four areas:
one in the North Arm of Okanagan
Lake, one at Nasuhito Creek on Okanagan Lake, one at Westside Cays in the Okanagan Lake, and at the Skaha Lake beach
at Penticton. Application at the Penticton beach created
large public protests. An additional application was sche­
duled for an area near Kaleden on Skaha Lake, but strong
opposition from local residents, plus preparations for civil
disobedience, caused the provincial government to abandon
this test.

While it was at first planned to use the herb­

icide in Kalaraalka Lake and Osoyoos Lake, mechanical methods
were used instead.
with herbicides.

In total, less than 23.5 acres were treated

4421

1-10
The cost of mechanical control of herbicides was est­
imated at $800 an acre by Karl Marsden, public relations
director for the Okanagan programme in 1977. He claimed that
the application of herbicides cost only $100 an acre. However,
monitoring costs were much higher. Close to 5,000 samples
were taken in the 1977 monitoring programme. In July, Mr.
Marsden estimated that this aspect of the programme would cost
between $200,000 and $500,000. (Penticton Herald, July 21,
1977). If the minimum monitoring programme is continued,
this would bring the cost of herbicide use at least up to the
level of mechanical harvesting. Gordon Jennens, who is build­
ing a mechanical harvester, claims he will be able to harvest
the weeds for between $200 and$300 an acre, which would be far
less than the cost of applying herbicides.
The 1978 »All Out Attack"
The Advisory Committee and the B.C. Ministry of the En­
vironment have both announced that there will be an "all-out
attack" on the Eurasian water milfoil weed in 1978, including
widespread use of 2,4-D. It has been estimated that there
are now between 1,500 and 2,000 acres of the weed in the
Okanagan Basin lake system. This means that we could conceiveably expect between 30,000 and 80,000 lbs. of 2,4-D
active ingredient in the Okanagan lakes in 1978.
The first problem for the provincial government is how
to come up with the finances for such a programme. They will
either have to hire more employees or contract out the app­
lication. What Okanagan residents fear is that the monitor­
ing programme will be abandoned. That is how the costs were
lowered in the Tennessee Valley Authority area. We are cer­
tain that no one will want the monitoring programme abandonned.

£>-451 ?

1-11
The second problem concerns the monitoring programme
itself. There is only one laboratory in British Columbia
capable of doing the laboratory testing. And even here,
the gas chromatography, mass spectrometry, computer analysis
system used in 1977 is inadequate to test for organic pol­
lutants in water supplies. It can only test down to .001
parts per million. In 1977, by August 10 only 500 of 3000
samples had been processed.
samples had been tested.

In December, not all of the

If public health officials insist that the monitoring
in 1978 be at least as complete as it was in 1977, this means
that most of the lake areas that are treated will probably
be closed for the entire summer. The laboratory will simply
not be able to handle the testing, and public health officials
will not dare open recreation areas without first knowing the
level of 2,4-D residues in the water and silt. Otherwise, the
provincial government will have to abandon the "zero tolerance
level" promised by the Advisory Committee.
THE PHENOXY HERBICIDES
The herbicide 2,4-D is one of the chlorinated phenoxy
compounds developed at the U.S. Center for Chemical and Bio­
logical Warfare at Fort Dietrich, Maryland, during World War
II. The three most commonly used members of this herbicide
group are 2,4-D, 2,4,5-T and 2,4,5-TP (often called Silvex
in the United States and Fenoprop in British Columbia).
All of this family of herbicides are derived from ben­
zene and synthesized from the chlorophenols. All share the
benzene ring molecular structure, the main difference being
the number and placement of the chlorine atoms. The only
difference in the molecular structure between 2,4-D and 2,4,5-T
is one additional chlorine atom in the latter.

(See figure I)

4423

1-12
The only difference between 2,4,5-T and 2,4,5-TP is that the
former is manufactured with acetic acid, the latter with
picolinic acid.

(Ashton and Crafts, 1973)

There are various practical formulations of 2,4—D.
Sometimes they are converted to water-soluble amines; at
other times, they are in the form of oil-soluble esters. The
acid formulation is used to kill weeds like bindweed, Canada
thistle and Russian knapweed.
The 2,4-D esters are identified by the name of the al­
cohol used in the manufacturing process. In 1977, the pro­
vincial government used Aqua-Kleen 20, manufactured by the
American chemical company, Amchem. This is the butoxyethyl
ester formulation of 2,4-D. The esters are generally insoluable in water, but they are considered the most toxic to
plants. (Klingman, 1975)

The Mode of Action
All of the phenoxy herbicides initiate the same response
when applied to plants: they act like an auxin, a plant
hormone. Normal growth ceases within hours. Epinastic bend­
ing of the plant occurs within minutes. Over days there is
the formation of tumours, secondary roots, and fasciated
structure is pronounced.
Meristematic cells cease to divide.

Elongated cells stop

length growth, but continue radial expansion. In mature plants,
parenchyma cells swell and begin to divide. Young leaves
stop expanding and develop excessive vascular tissue. The
roots lose their ability to absorb water, photosynthesis is
inhibited, and the phloem becomes plugged.

4424

1-13
It is now recognized that the primary action takes
place in the plant cells themselves. 2,4-D is accumulated
and retained in the cells. Here, the phenoxy herbicides all
disrupt the normal function of the cell nucleus. They in­
crease the RNA, DNA, and protein. RNA and protein synthesis
are controlled by DNA, and the phenoxy herbicides disrupt
the normal role of DNA. It is also known that the phenoxy
herbicides act on the cell membrane, with cell wall loosening.
(Ashton and Crafts, 1973)
All of the phenoxy herbicides, including 2,4-D, promote
uncontrolled expansion and division of cells. This form of
action prompted Professor J. Van Overbeek to state that the
phenoxy herbicides "kill like cancer." (Van Overbeek, 1964)
Since the late 1940's, the phenoxy herbicides have been
widely used in North America for control of broad leaf plants,
brush and trees. 2.4-D is widely used in many agricultural
areas. Fenoprop (2,4,5-TP) is used as a growth promoter in
some agricultural areas. 2,4,5-T has been banned from gen­
eral use and use on agriculture since 1971, the result of
research by the U.S. government and the experience of its use
as a defoliant in Vietnam. But it is widely used in British
Columbia in forest management, range and pasture management,
spraying along power lines and along rights-of-way for roads
and railroads. Since 1971, two formulations of 2,4-D have
been registered for use in the United States for control of
aquatic weeds; in Canada, Acqua-Kleen 20 is registered for
such use under certain conditions and restrictions.
While 2,4-D is quite effective when used on plants, it
has a rather low lethal toxicity rating for humans and other
animals.

The lethal dose of 2,4-D for a human is around 6

grams, or slightly more than a teaspoon of the pure chemical.
For this reason, it has been widely used on food crops, as it
was believed that the herbicide was relatively harmless to
humans.

4425

1-14
While there has been considerable research done on 2,4-D,
it is only in recent years (since around 1971) that the ev­
idence of its acute and chronic effects on humans has been
demonstrated and, more significantly, received widespread
publicity.
The Legal Implications of the use of 2,4-D in Okanagan Lakes
It is widely known that herbicides are not supposed to
be used in water, or even sprayed near bodies of water or
streams. The B.C. Royal Commission of Inquiry into the Use of
Pesticides and Herbicides (1975) recommended that 2,4-D not
be used any closer than 300 feet to any water source. There
are good reasons for these restrictions: fear of possible
harmful effects to fish, animals (including humans) and the
environment in general.
Therefore, there is an obvious contradiction between
the traditional restrictions against the use of phenoxy herb­
icides in any water environment, and the registration of one
or two formulations of 2,4-D for actual use in water. To date,
the Control Products Section, Federal Production and Marketing
Branch, Department of Agriculture have not responded to our
letter requesting them to explain this situation.
In the United States, Aqua-Kleen 20, manufactured by
Amchem, has been registered by the U.S. Environmental Pro­
tection Agency for use in the control of Eurasian water mil­
foil, at dosages up to 100 lbs. per acre (40 lbs. active in­
gredient of 2,4-D). Applicators are warned not to apply the
herbicide "within 1/2 mile of potable water intakes."

The

only other warning is that "fish and other aquatic organisms
may be killed at application rates recommended on this label."
(EPA Reg. No. 264-109, June 12, 1976)

$

1-15
Aqua-Kleen is also registered for use in Canada, but the
restrictions are more significant.

The Control Products

Section of the federal Department of Agriculture (which reg­
isters pesticides in Canada) limits Aqua-Kleen and 15 other
aquatic herbicides as follows: "do not apply to waters used
for irrigation, agricultural sprays, watering dairy animals,
or domestic water supplies." (B.C. South Okanagan Health
Unit, 1976)
These restrictions became a public issue in the summer
of 1977 when the South Okanagan Environmental Coalition, in
co-operation with the West Coast Environmental Law Association
of Vancouver, began exploring legal actions to block the use
of 2,4-D in the Okanagan lakes system. It was later learned
that following consultation with the Control Products Section
of Agriculture Canada, the B.C. Ministry of the Environment
conducted its chemical program under a clause in the Pest
Control Products Act which allows experimental applications.
The size of the program was hardly of an experimental nature.
Survey by the B.C. Royal Commission
The legal implications of the use of herbicides was sub­
ject to a study done by James M. Mackenzie for the B.C. Royal
Commission of Inquiry into the Use of Pesticides and Herbicides
(1975).

The Final Report mentions some of the federal and pro­

vincial laws and regulations which may apply to the use of
2,4-D in the Okanagan lakes.
The most important federal legislation is the Pest Con­
trol Products Act.

Section 44 prohibits use of any control

product (like 2,4-D) in a manner inconsistent with the di­
rections shown on the label. Obviously, the provincial
government is violating the restrictions on the use of AquaKleen as imposed by the agency of control, the Control Pro­
ducts Section of the Department of Agriculture.
Under Section
5 of the Act, exemptions to normal regulations can be grant­
ed by the Governor General in Council.

4427

1-16
In reality, this is an action by the federal Cabinet.
Other federal legislation that is involved is the Fish­
eries Act of 1970.

Under section 33 (2) there is a pro­

hibition of depositing any "deleterious substances" in water
frequented by fish. This is a "strict liability" section;
no criminal intent needs to be established, and there are
fines to be layed up to $5000.
Under this act, a "deliterious substance" is defined as
"any substance that, if added to any water, would degrade or
alter or form part of a process of degradation or alteration
of the quality of that water so that it is rendered deleterious
to fish or to the use by man or fish that frequent that water."
In the past, the courts have held that most pesticides fall
into this category.
The third federal law which would seem to apply in this
case is the Migratory Birds Act of 1970. Regulations issued
in support of this act prohibit anyone from "depositing sub­
stances harmful to migratory birds into waters or any area
frequented by migratory birds" (sec. 35). As previously
stated, the Canadian Wildlife Service has denied permission
for the application of 2,4-D in Vaseux Lake, a migratory
waterfowl sanctuary.
There is also provincial legislation which directly
applies to the use of herbicides in the Okanagan lake system.
The Health Act (1960) in section 43 prohibits "the pollution
of water courses from which water or ice is taken for domes­
tic purposes." Section 66 of this act prohibits the deposit
of waste matter in any stream or lake so as to pollute its
waters. It specifically mentions "any poisonous, noxious,
or polluting liquid." The Act (Sec. 114) and the imple­
menting regulations (Sec. 71) provide penalties for vio­
lations .

1-17
It should be noted that there are over 400 domestic
water licenses issued for Okanagan Lake alone, plus another
200 unlicensed intakes.
takes.

Skaha Lake has over 80 licensed in­

(B.C. South Okanagan Health Unit, 1976)

The report by James M. MacKenzie argues that other
provincial legislation is applicable to large scale use of
pesticides, including the Pharmacy Act, the Litter Act, the
Pollution Act, the Water Act and the Wildlife Act. It would
seem that the provincial Ministry of the Environment is vio­
lating several federal and provincial acts when it adds
herbicides to the Okanagan basin lake system.
The Possibility of Suits for Damages
Across North America there is a growing movement bypeople to initiate legal suits for damages against companies
and governments responsible for pollution and direct damage
to individuals and their property.

In 1969, the Government of

Nova Scotia accidentally sprayed Robin Warren's farm with
phenoxy herbicides, resulting in destruction of his crops and
deaths to his farm animals.

After investigating, the Govern­

ment of Nova Scotia paid the Warren family $10,000 in damages.
(Ogden, 1971)
The people in Globe Arizona who were sprayed by phenoxy
herbicides during a range management programme have a $4
million damage suit waiting for court action. Dow Chemical
Company and the U.S. Forest Service have tried to postpone
this case, fearing it will set a precedent.

(Doucet, 1977)

In New Brunswick, Abram Friesen now has a case before
the courts claiming damages for illness to his family caused
by the provincial government's spraying of fenitrothian as
part of the spruce budworm control programme.

The spraying

of fenitrothian has been linked to Reye Syndrome, which has
resulted in the deaths of several children. (Globe and Mail.
November 24, 1977)

„ 4429

I 1F
-

Another important case involves workers in Ontario who
have contracted lung cancer while working in uranium mines
and refineries. The United Steelworkers of America, who are
pushing the case, have documented over 90 deaths from lung
cancer at Elliot Lake and Bancroft. Once the Ontario Work­
men's Compensation Board establishes that the industry
caused the lung cancer, then the companies involved become
subject to legal action for damages.
(Globe and Mail, Nov­
ember 24, 1977)
A landmark case is involved in the widely reported case
of poisoning by polybrominated biphenyl (PBBs) in Michigan
in 1973. This chemical, used as a fire retardant, was
accidentally mixed with cattle feed, causing widespread
pollution and illnesses among people very similar to those
caused by phenoxy herbicides. Like many of the chlorinated
phenols, PBBs persist in the environment for a long time.
There are 84 damage cases now in court, and if a few of them
are successful, they will bankrupt the Michigan Chemical
Corporation.

(Stadfeld, 1976)

Establishing Safe Levels for Pesticides
Those who are following the 2 ,4-D/0kanagan Lakes con­
troversy in British Columbia are aware that government of­
ficials repeatedly claim that if the water we drink contains
less than .1 ppm of 2,4-D, then this is safe and acceptable.
How are these levels reached?
First, most of these are at best guestimates, based on
established levels for acute toxicity in laboratory animals
and sometimes in humans themselves.

It is impossible to

determine threshold levels for chronic toxicity, as indi­
vidual resistance levels vary so widely.

1-19
For example, prior to 1975 the Plant Products Division
of Agriculture Canada required thcit all commercial form­
ulations of 2,4,5-T contain less than .5 ppm of tetra-dioxin
(TCDD). In 1975, they changed this to require a maximum
level of .1 ppm TCDD. To a large extent, this could be seen
as simply conforming to standards set in the United States.
But there was no scientific basis for making the determin­
ation. It was .just a bureaucratic adjustment, most likely
due to the increased publicity of the toxic and chronic
effects of TCDD.

(Agriculture Canada, 1974)

IIow such a decision is made is revealed in the case of
PBB pollution in Michigan in 1973. At the time, little was
known of the toxic levels of PBBs. The first maximum level
for PBBs in milk was established at 2.5 ppm; this was the
ievel previously established for polychlorinated biphenols
(PCBs). But some tests indicated that PBBs are five times as
toxic as PCBs. The U.S. Food and Drug Administration then
concluded that they should allow only one-tenth as much as
PBBs in milk as PCBs. Thus, they reduced the acceptable level
to .3 ppm. The other rationale for setting this level was
that .3 ppm could be tested with reasonable accuracy with
the average gas chromatograph.
Curtis K. Stadfeld, who investigated the PBB poisoning
case, concluded that "the miserable truth about the action
levels is that they are purely arbitrary. They are supported
only by sophisticated guessing." (Stadfeld, 1976)
The same can be said for the .1 ppm "safe level" set
for 2,4-D in drinking water. It is at best a guestimate.
It is not based on scientific knowledge of chronic illness,
established by testing, experimentation and epidimological
surveys. Just because this guestimate has been accepted for
the sake of expediency by the World Health Organization/Food
and Agriculture Organization Committee on Pesticides is no
guarantee of safety from chronic illness.

4431

0-4537

1—20
Summary
Eurasian milfoil weed is spreading throughout the Okan­
agan lake system and all across North America. Because of
the manner by which it spreads, it is impossible to eradicate
the weed through the use of herbicides.
Any use of 2,4-D is just "chemical mowing." If the
provincial government decides to use the herbicide for this
purpose, then it will have to be used far into the future.
Otherwise, there is no justification for its use in the first
place.
The B.C. Advisory Committee has recommended a five year
"all out attack" on milfoil weed including the use of 2,4-D.
They recommend that a "zero tolerance level" be maintained
with regard to water intakes for irrigation and domestic use.
This is simply impossible. There is also the fear that with
the rising costs of the herbicide, its application, and mon­
itoring, that the minimum monitoring programme that was used
in 1977 will be abandonned.
The phenoxy herbicides, including 2,4-D, kill plants
by disrupting the normal pattern of cell growth. There is
very little difference between the chemical basis, molecular
structure and mode of action of the different phenoxy herb­
icides .
The use of Aqua-Kleen in the Okanagan basin lakes is in
clear violation of the labelling restrictions on use of the
herbicide as set by the Control Products Sections, Agricul­
ture Canada. It also violates the federal Fisheries Act and
the Migratory Birds Act, as well as the provincial Health Act.
If the provincial government continues to use 2,4-D in
the Okanagan basin lake system, it runs the risk of legal
actions for damages from injured parties. Such cases are
multiplying across North America.

11-14
"If this is happening, our data collecting system may
not be sensitive enough to detect their presence in
the ponulation. British Columbia has one of the most
advanced registry systems for defects of this type in
North America. It is possible, nevertheless, that a very
small number of malformed children in the Province have
been damaged by herbicides, but their number is so small
that they are not distinguishable from the number of
damaged children born each year where the cause of
their infirmity is not explainable (Royal Commission,
1975).
What we are left with in most cases then, are raw field
reports of health damage in certain areas. These are often
the best we have as early warning systems after laboratory
testing. To wait for proper epidemiology studies may result
in delays which would allow toxic chemicals to go unchecked
for far too long.
Admittedly, it is very difficult to produce an air tight
causal relationship between a chemical and health damage in
normal living situations, much less during periods of turmoil
such as war or an industrial accident such as in Seveso, Italy.
Control groups are difficult to establish and there are an
almost unlimited number of possible causal factors. However,
to disregard field reports would result in a substantial amount
of unnecessary damage to the environment and thus human
health.
Thalidomide was identified as a powerful teratogen
through field reports rather than lab tests. The drug would
probably have been removed from the market sooner had scien­
tists been more willing to heed the warnings being observed
by doctors in the field.

The Vietnam Case

Vietnam was the first country to experience the use of
herbicides as a weapon of war

11-13
During this period, 2,4-D became widely used as a substitute
for 2,4,5-T.
Determining the effects on humans from field use of
2,4-D is often complicated by the fact that "T" and "D" are
often used together for defoliation and brush removal. When
health problems result, the damage is always blamed on 2,4,5-T
and TCDD. The Swedish studies mentioned earlier indicate
that both chemicals are teratogenic and may synergize to be­
come even more potent (Bage, et al., 1972).
To date, 2,4,5-T has received a lions share of the
attention, while 2,4-D was largely ignored. Laboratory
testing shows quite clearly that both chemicals pose serious
health problems. 2,4-D has traditionally been the most widely
used herbicide and there are consequently tremendous economic
forces at work to keep it on the market. This situation
may well be responsible for the lack of interest by regulatory
agencies under pressure from users and producers in placing
restrictions on 2,4-D similar to its sister compound, 2,4,5-T.

Field Reports - Epidemiology
Scientists are loath to give much credence to field
reports of damage to health through environmental contamination.
Until these reports are accumulated and statistically anal­
yzed into epidemiological data, they do not seem to have much
scientific appeal to many. In most countries epidemiological
(relating to the incidence, distribution and control of disease)
data are simply not collected. Even in the "advanced" nations
the science is still a very crude tool.
For instance the B.C. Royal Commission on Pesticides and
Herbicides speculates that herbicide induced defects may be
occurring now.

4434

11-12
Why then is it still being used today with virtually no re­
strictions outside of a few cursory label warnings?
As with all research that suggests that a product in
current use may be a health hazard, many users and producers
immediately attacked the testing procedures. One common
approach is to say that research on mice and rats has no
relationship to human beings. To this, Dr. Theodor Sterling
at Simon Fraser University replies that "the mouse is one
species that heralds teriitogenic effects in man" (Sterling,
1976). Not only will the effects of a chemical often be
similar in man, but they may be many times more potent. In
the case of thalidomide, Dr. Samuel Epstein reminds us that
"humans are 60 times more sensitive to thalidomide than mice,
100 times more sensitive than rats, 200 times more sensitive
than dogs and 700 times more sensitive than hamsters." (Ep­
stein, 1970) It is now well established by the authorities
in the field that testing with laboratory animals is approp­
riate to the human experience. Criticism of high dosage
levels is treated in the chapter on carcinogenicity.
Perhaps the main reason that 2,4-D is still unrestricted
in use is the existance of 2,4,5-T and its contaminant TCDD.
When Dow Chemical first produced their study showing the
extreme teratogenic potential of TCDD, all attention turned
toward 2,4,5-T (Sparschu, et al., 1970). This shift of focus
was not warranted as the test results show 2,4-D to be just as
damaging as 2,4,5-T. As a result of the studies done on TCDD
an effort was made by the U.S. Environmental Protection Agency
to have 2,4,5-T removed from use on crops. This further direct­
ed attention toward this chemical during the three years of
political and administrative manoeuvering which ultimately
resulted in restrictions (Epstein, 1972).

4435

11-11
Finally, the NCTR division of the U.S. Department of
Health, Education and Welfare checked the purified samples
of 2,4,5-T and found them to be teratogenic.

This latest

finding finally puts to rest the notion that the dioxin
contaminents are responsible for the teratogenic effects of
the phenoxy herbicides. The study also points toward a number
of testing deficiencies which should be corrected in the
future. These involve: inadequate numbers of test animals;
inadequate or nonexistent replications of tests; inadequate
testing at doses below 100 mg/kg; and the need for testing
in different strains and stocks of mice. (HEW, NCTR, 1975).

The Testing Game
We have found that scientific world is riddled with
accusations and back-biting over testing procedures and the
interpretation of results. A research programme can be set
up which will most likely show a desired result simply through
the manipulation of various parameters of the test. There is
probably no research effort which is free from bias and fault
and cannot be criticized. In fact, criticism by those inside
and outside a profession is the chief method of maintaining
high quality work. All studies will be picked apart by those
on one side or the other of a discussion. That research which
stands up the best to such analysis and is continually support
ed by additional data will probably become generally accepted.
Whether any use is made of the material is another matter.
As early as 1968 it was obvious to everyone paying close
attention to the research being done that there was reason
for concern about the safety of 2,4-D.

r

4436

11-10
Recent Studies
In 1972, the Laboratory of Teratology of the Karolinska
Institute in Stockholm, Sweden produced the results of their
study on 2,4-D and 2,4,5-T. Unfortunately, in this research,
2,4-D was not tested separately, but in combination with 2,4,
5-T at a ratio of 2:1 (Hormoslyr 64).
However, the Swedish government had concluded that Hor­
moslyr 64 had caused cancer in applicators working for the
national railway. At the high doses (110 mg/kg), fetal mor­
tality was significantly increased and fetal weight consider­
able reduced. Also noted were: increased rates of cleft
palate; rib and vertebral malformations; subcutaneous and
renal hemorrhages; and various spontaneous malformations such
as exencephaly (brain outside skull); hydrocephaly (abnormal
skull enlargement); open eye; small eyes; and ectrodactyly
(absence or fusion of toes or fingers).
Of particular interest was the observation that "the
teratogenic effects of the two substances (2,4-D & 2,4,5-T)
in combination at 110 mg/kg it seems, however, as if the 2,4-D
contributes more than would be expected from a purely add­
itive effect.”

They go on to urge that further studies be

undertaken to look into this possible synergistic effect
(Bage, et al., 1972).
Most recently, the U.S. Environmental Protection Agency
(EPA) has been retesting 2,4-D and 2,4,5-T. These results
reaffirmed that the phenoxy herbicides produced cleft palate,
depressed fetal weight and increased fetal mortality.

Of

particular concern for humans who may receive low doses
through contamination of water or air, was the finding that
"the greatest effects of 2,4-D were produced at the low doses
administered over long time periods" (Courtney, 1975).

4437
"IMS 33

II-9
They then go on to define teratogenesis as "that degree of
embryotoxicity which seriously interferes with normal develop­
ment or survival of the offspring” (Schwetz, et al., 1971).
Based on this system, those effects which all other researchers
and authorities in the field call teratogenic are now embryotoxic (Epstein, 1970; Royal Commission, 1975).
The study can also be criticized on other grounds. Be­
cause the dosages used were low as compared with other studies,
particularly the 12.5 mg/kg level, larger test animal .pop­
ulations should have been used for effective statistical
analysis. It is also said that rats are more resistant to
chemicals than mice and do not present as good a reading as
the latter (Sterling, 1974).
Finally, the Dow researchers suggest that the Bionetics
studies may have been faulty as the DMSO vehicle used was
thought to be a teratogen itself. This criticism doesn't seenr
to stand up as the DMSO treated control animals in those
tests did not show a statistically significant higher rate of
abnormalities than the untreated controls. (Royal Commission,
1975). It can also be noted that the doses administered orally
in honey also produced defects. The U.S. National Institute
of Environmental Health Sciences research looked into this
aspect as well and concluded that ”the administration of DMSO
or honey to mice or rats did not adversely affect the develop­
ment of the fetuses.” (Courtney, et al., 1970)
It is clear from the results of the Dow study, that
2,4-D caused significant defects similar to the other major
research efforts. In this case, however, the observed ab­
normalities have been defined as embryotoxic rather than
teratogenic.

II-8
Dow Study
The most extensive testing programmes by industry have
been conducted by the Chemical Biology Research division of
the Dow Chemical Company in Midland, Michigan.

In 1971, they

produced the results of their study of the effects of various
formulations of 2,4-D on Sprague-Dawley rats. 2,4-D acid and
its propylene glycol butyl ester (PGBE) and isooctyl (10) esters
were administered orally to the test animals in a corn oil
suspension on day 6 to 15 of pregnancy. The dosage levels
ranged from 12.5 mg/kg to 87.5 mg/kg. The relatively low
upper dose level was selected after it was found that 100 mg/
kg was lethal or produced acute toxicity symptoms in their
test animals. It is difficult to understand why Dow's test
animals are so sensitive to the chemical when other lab's
rats apparently tolerate more than twice this dosage without
apparent toxic effects.
At the higher dosages, subcutaneous oedema (abnormal
accumulation of fluid beneath the skin), delayed ossification
of the sternebrae (incomplete breastbone formation), wavy
ribs, lumbar ribs (misplaced), delayed ossification of skull
bones, and missing sternebrae were statistically significant
with some formulations. Hydrocephalus (abnormal swelling
of the skull) and dilated urinary bladder were produced ex­
tensively in a random litter (Schwetz, et al., 1971)
The report concludes that "no treatment-related tera­
togenic responses were observed in this study." Now, how
could this be, given the list of statistically significant,
observed terata (birth defects) mentioned above?
First, they indicate that "embryotoxicity is the toxic
effect on an embryo caused by treating pregnant females
during that period in which actual tissue differentiation and
organogenesis (formation of organs) occur."

4439

II-7
The former is used in granular form in the Okanagan weed
control programme and the latter is utilized extensively
in liquid form for Milfoil control by the Tennessee Valley
Authority.
The chemical was administered to the test animals in
aqueous oelatin or corn oil on a daily basis from day 6 to
15 of gestation. In the prenatal studies the dams were
sacrificed on the 22 day of pregnancy while some post natal
studies allowed the females to litter. The research indicated
that the dosages ranging from 25 mg/kg to 300 mg/kg of the
various formulations of both 2,4-D and 2,4,5-T produced tera­
togenic effects.
"The 4 prenatal parameters (No. of viable fetuses; No. of
dead fetuses; Fetal weight; and % of malformed fetuses) all
showed a statistically significant dose-related effect, except
for numbers of viable fetuses in the case of 2,4,5-T. The
malformative effect was particularly striking: the average
incidence of affected fetuses rising from less than 10# in
treated controls to usually more than 50% at the 150 mg/kg
dose level” (Khera & McKinley, 1972).
The report continues that "at the highest dose (usually
150 mg/kg), all derivities of 2,4-D (including butoxyethynol
ester) were associated with a significantly increased tera­
tologic incidence; the butyl and isooctyl esters tended to de­
press fetal weight." The most common defects observed were:
unilateral and bilateral wavy ribs; additional ribs (14);
retarded ossification (bone formation) of the frontal and
parietal (in skull) bones; sternal (breastbone) defects. In
the postnatal studies, a nondose-dependent low incidence of
delayed opening of eyelids, hydrocephalus, corneal opacity,
and chronic inflamation of the tear glands were seen. It is
also interesting to note that "at 25 mg/kg, 2,4,5-T gave neg­
ative results while 2,4-D gave significant results regarding
litter size and incidence of malformations."
1972) .

(Khera & McKinley,

II-6
The animals were fed three formulations of the chemical at
dosages ranging from 20 to 100 mg/kg on the 6th through 10th
days of pregnancy.

Fetal viability was decreased significant­

ly at the 100 and 60 mg/kg levels in one sample and at the 60
mg/kg dosage in another. Fetal abnormalities rose to 22% at
the 100 mg/kg level in one sample while the rate was 3.5% in
the control group. Hemorrhages per total live born were con­
sistently increased at the low dose levels. The abnormal­
ities most often seen were fused ribs.
The tests with 2,4,5-T used samples with varying TCDD
contents. Abnormalities which occured were clearly dose and
dioxin content related. However, samples with no detectable
dioxin levels produced a significant increase in abnormalities
and a decrease in fetal viability. The most common defects
observed were eye abnormalities and delayed skull ossification
(bone formation) while exencephaly (brain outside cranium),
hind limb deformities, cleft palate, ectopic heart (misplaced)
and fused ribs were also seen (Collins & Williams, 1971).
During this same period, German experiments also showed
’'purified" 2,4,5-T to be teratogenic (Roll, 1971)

Canadian Research
Canada's Food and Drug Directorate of the Departmemt of
National Health and Welfare produced their research findings
in early 1971. The testing, under the direction of K.S. Kera
and W.P. McKinley used several formulations of 2,4-D and 2,4,
5-T on Wistar rats. Of particular interest in this study
was the fact that the butoxyethynol (BEE) ester and dimethylamine (DMA) formulations of 2,4-D were examined.

.4441
£>-HS3 7

II-5
The problems of extrapolation preclude definition of the
hazard on the basis of these studies, but its existence seems
clear" (Epstein, 1972).

Further Testing
Shortly after the Bionetics studies were begun, research­
ers at the U.S. National Institute of Environmental Health
Sciences (NIEIIS) also began laboratory testing of the phenoxy
herbicides. Both 2,4-D and 2,4,5-T were found to produce
significant teratogenic effects. (Courtney, et al., 1970)
At this time, however, it was learned that the formulations
of 2,4,5-T which had previously been used for testing were
contaminated with high concentrations (30 ppm) of 2,3,7,8tetrachlorodibenze-p-dioxin (tetradioxin or TCDD), a substance
believed to be extremely teratogenic.
This discovery, set into motion a new testing programme
with "purified" phenoxy herbicides. The Dow Chemical Company,
NIEHS and the U.S. Food and Drug Administration produced re­
ports of testing 2,4-D and 2,4,5-T (containing less than 1 ppm
of TCDD) on mice, rats and hamsters. These all confirmed that
the phenoxy herbicides produced teratogenic effects even with
very low levels of TCDD. The Dow studies of 2,4,5-T were
conducted with very low dosages, the maximum being 24 mg/kg.
This research indicated that there was defective sternebral
ossification (incomplete bone formation of the breastbone)
which is a not uncommon reaction to teratogenic substances
(Emerson, et al., 1971).
The NIEHS study tested "purified" 2,4,5-T and TCDD on
mice at 100 mg/kg dosage levels. Both compounds produced
cleft palate and kidney malformations (Moore & Courtney, 1971).
FDA tests on golden Syrian hamsters with 2,4-D produced
generally inconclusive results.

II-4
NOTES
1.
2.

Trypan Blue - Known Teratogen
Significance Levels * (.10) ** (.05)

3.

Table modified from Royal Commission, 1975

*** (.01)

Some of the abnormalities which were observed in the
various strains of test mice were cleft palate (fissure in
roof of mouth); anophthalmia (no eyes); incomplete fusion of
face; agnathia (no lower jaw); microphthalmia (small eyes);
single medial naris (one nasal entry); exencephaly (brain
outside cranium); cystic kidney; clubfoot; ectopic intest­
ines (abnormally located); encephalocoele (protrusion of the
brain through a cranial fissure) extended legs (produced by
breakdown product-2,4-dichlorophenol); and hydrocephaly (ab­
normal enlargement of the cranium caused by blockage of cer­
ebral fluid) (HEW, 1969). After studying the Bionetics data,
the Commission's Panel on Teratogenicity recommended that the
butyl, isopropyl and isooctyl esters of 2,4-D be "immediately
restricted to prevent risk of human exposure" (Epstein, 1970).
Eight years after that statement was made, 2,4-D is the world's
most widely used, generally registered herbicide.
2,4-D's sister compound, 2,4,5-T was also among 48 pest­
icides and industrial chemicals tested by the Bionetics Lab­
oratories.

It was in fact tested to a greater extent than

any of the others. 2,4,5-T was administered to three strains
of mice and one strain of rat both subcutaneously and orally
during the 1965 to 1968 period. The dosage levels ranged from
4.6 mg/kg to 113 mg/kg. Both the mice and the rats showed a
statistically significant increase in fetal abnormalities as
compared with the control groups, even at the low dosage
levels.

The major abnormalities which were observed where

cleft palates and cystic kidneys in the mice and cystic kid­
neys, gastro-intestinal haemmorrhages and incread fetal mor­
tality in the rats.

The Bionetics researchers concluded that

"these results imply a hazard of teratogenesis in the use of
this compound.

D-4581

4443

II-3
The data from their report, while it has never been made
public, was included in Part III of the Mrak Report which was
produced after the main work of the Commission had been con­
cluded. The research findings had grave implications for the
phenoxy herbicdes. 2,4-D and its sister compound, 2,4,5-T,
were both found to be teratogenic in testing on mice.
The acid and a number of the ester formulations of 2,4-D
were administered to laboratory mice subcutaneously (beneath
the skin) with Dimethyl sulfoxide (DMSO) as a carrier. The
dosage levels ranged from 24 milligrams of 2,4-D per kil­
ogram of body weight (mg/kg) to 215 mg/kg with the treatment
running from the 6th to the 14th day of pregnancy. On the 18th
day the fetuses were sacrificed and examined. The fetal mor­
tality rate ran as high as 74%, while the abnormality rate
rose to 100% for the 215 mg/kg dosage of 2,4-D acid. The
following table lists the formulations which produced a
statistically significant number of birth defects when com­
pared with the control groups. (Similar test animals who
were not administered 2,4-D).
Bionetics Test Results-Teratogenic Effects of 2,4-D
Table I

Compound

Dose

% of
abnormal
litters

Negative controls
Untreated controls Controls - DMSO
Positive controls
Trypan Blue (1)
5
Experimental - esters
2.4- D isooctyl
48 mg/kg
2.4- D "
130 mg/kg
2.4- D butyl
100
2.4- D isopropyl
94
2.4- D methyl
106
2.4- D acid
98
v\0

% of
abn. fet./
all litters

% of
abn. fet./
abn. litters

40
46

10
13

25
29

60

32

54

100*(2)
67
75**
70**
83
36*

24
28**
25* **
26***
30*

24
41*
34
37*
36

8

23

II-2
For many, the test results may have come too late.
The lead arsenic and chlorinated hydrocarbon (DDT,
Aldrin, Dieldrin, etc.) insecticides have been largely re­
moved from use in North America now that their threat to
health has been established.

It took years of legal man­

euvering and political pressure to get the job done, however,
When a company spends time and money to get a new pesticide
on the market and begins to receive a return on their in­
vestment, they are often reluctant to believe that the pro­
duct might be a health hazard. It is all too easy for them
to assert that the testing is faulty or that other environ­
mental factors are to blame. Proving that a chemical is
harmful and getting it removed from the market is extremely
difficult, as we have seen with cyclamates, saccharin and the
chlorinated hydrocarbons. The concept that a pesticide must
be proven safe in all respects before it is allowed on the
market has not met with very wide acceptance by regulatory
agencies.

The Bionetics Study - First Warning
In the early 1960s, the U.S. Department of Health, Ed­
ucation and Welfare (HEW) appointed a Commission on Pesticides
and Their Relationship To Environmental Health. The final
product of this seven year, 3Vi million dollar study has come
to be known as the Mrak Report after Commission chairman. Emil
M. Mrak of the University of California at Davis. In 1969
as the final report was being prepared, the Bionetics re­
search was made available to the Commission Panel on Tera­
togenicity. The Bionetics Research Laboratories, under con­
tract to the U.S. National Cancer Institute, had been screen­
ing pesticides by laboratory testing from 1965 to 1968.

4445
V-HSHl

TERATOGENIC EFFECTS OF 2,4-D
BIRTH DEFECTS
There can be no doubt that the most spectacular example
of the teratogenic effects of a chemical on human beings was
the Thalidomide tragedy of the early 1960s. Teratogenesis
can occur when " a mother mammal is subjected to any condition
that can alter her methabolic balance, at a time when the
foetus within her is at a stage of developing organs" (Royal
Commission Inquiry Into The Use of Pesticides and Herbicides,
1975). The birth defects which resulted from the use of
Thalidomide by pregnant women are too easily remembered by
everyone. In a macabre sense, the gross foreshortening of
the limbs was a blessing in disguise. Had the effects been
less noticeable (such as reduced learning capacity or greater
susceptibility to disease), the situation could have gone
undetected for years. As it turned out, North Americans
largely escaped the disaster because, despite intense pres­
sure from the companies involved, a few key health officials
here refused to approve the drug until further testing was
done (Shea, 1973).
Detecting a teratogen can be a long and expensive
process. The standard procedure to date for the registration
of a pesticide has involved the submission of a producing
company's test results to the regulating agency (Agriculture
Canada and the U.S. Environmental Protection Agency). The
testing usually centered around acute toxicity factors in
laboratory animals. Long term research into the possible
teratogenic, carcinogenic, and mutagenic nature of the
chemical has not been part of the preregistration procedure.
Only after the product has been introduced and health pro­
blems identified, have the regulating agencies moved to
commission the necessary studies.

D-4SH3

FIGURE 1
The Most Widely Used Phenoxy Herbicides

2 ,4,5-trichlorophenoxypropionic acid (2,4,5-TP)

11-15
The U.S. Defense Department felt that infiltration and ambush
activities of the enemy could be reduced if major problem
areas were defoliated for better aerial visibility. Between
1961 and 1970, at least 10% of all forested areas or 6.5%
of all South Vietnam received at least one herbicide app­
lication (Galston, 1974). The main chemicals used in these
operations were production grade formulations of 50% 2,4-D
and 50% 2,4,5-T (Agent Orange). Also used was a mixture of
80% 2,4-D and 20% Picloram (Agent White) (Orians & Pfeiffer,
1970).
In the late 1960’s, reports began to filter out of Viet­
nam about a dramatic rise in miscarriages and birth defects.
(Grant, Moss and Unger, 1971) It was only after the Bionetics
test results were released that the medical profession began
to question the role of the phenoxy herbicides in the tera­
togenic effects which were reported. On April 21, 1970, the
U.S. Department of Defense, under great pressure from the
scientific community, announced that it was discontinuing its
spray programme.
Trying to assemble a clear picture of the health im­
pacts following the herbicide applications was extremely
difficult. In 1969, the American Association for the Advance­
ment of Science (AAAS) appointed a study team led by Dr.
Matthew Meselson of Harvard University to examine the effects.
The report which this group produced was instrumental in
eliminating the defoliation programme. (AAAS - HAC, 1972)
Another prestigious organization, the U.S. National
Academy of Sciences, also launched an investigation which was
funded by the U.S. Department of Defense. Both of these efforts
were severely hampered by the existing war situation in Viet­
nam which made on-the-ground inspection of the sprayed areas
impossible. The research was carried out largely through the
evaluation of those medical records which were available and
aerial reconnaisance flights over the defoliated regions.

P - tl5WS'

4449

11-16
Because many Vietnamese births do not take place in hospitals,
and inspection for birth defects is often not very thorough
outside of the major urban centres, both reports recommended
additional studies (NAS, 1974).
Some preliminary health problems were noted, which were
similar to those produced by 2,4-D in laboratory animals.
The Tay Ninh City provincial hospital, in an area where ex­
tensive spraying was carried out, reported a stillbirth rate
of 58 per 1,000 in 1970. The Saigon hospitals, where a few
people came into contact with herbicides, reported a rate of
29 per 1,000 during the same period (Aaronson, 1971). The
Saigon Children's Hospital was known to receive patients from
the entire country. Spina bifida, a congenital split of the
vertebral column which can result in paralysis and other
physical problems, increased from one case in 1966 to 13 and
12 cases respectively in 1967 and 1968. The incidence of pure
cleft palate went from two cases in 1964 and 1965 to twelve
in 1966, twenty-three in 1967 and twelve again in 1968 (Aaron­
son, 1971; Boffey, 1971).
In 1970, Dr. Ton That Tung and his colleagues at Hospital
"A" in Hanoi produced a report on their study of spray effects
on refugees from South Vietnam. Of the 73 pregnant women in­
terviewed, 22 had had miscarriages following spray applications.
There were also many reports of farm animals aborting and hens
failing to lay eggs after defoliation (Ton That Tung, 1970;
1973).
Unfortunately, the Vietnam war presented an opportunity
for an examination of the effects of major herbicide app­
lications on human health. All the studies which were completed
stressed the need for additional research. For various re­
asons, it appears that the work may not be done.

4450

11-17
We continue to have only a sketchy idea of the damage which
resulted.

Field Reports - Arizona
While Agent Orange was being used in Vietnam, the very
same formulations were being used regularly in North America.
As in Southeast Asia, the applications here have been mon­
itored haphazardly if at all. During the years 1965 to 1969,
five herbicide spray applications were made in the Tonto
National Forest near Globe, Arizona. The purpose of the pro­
gramme was to replace the chaparral groundcover with grass
for grazing (Shoecraft, 1971). Spray drift resulted in many
damaging effects at near-by residences. The Forest Service
was quick to deny that there had been any damage. They main­
tained that only 2,4,5-TP (Silvex, Fenoprop) was used, but it
was later learned that 2,4-D and 2,4,5-T had also been applied.
In July, 1970, the Arizona Commissioner of Health wrote
in a letter to the Gila County Board of Health (Globe) saying
that "... your county is leading the state in deaths caused
by diseases of early infancy and fetal deaths....there are
excessive deaths from congenital malformations" (Shoecraft,
1971).

The Canadian Experience
In July of 1969, the herbicides 2,4-D, 2,4,5-T and Dicamba
were sprayed on the Belleisle Marsh in Nova Scotia near the
farm of Robin Warren. During the aerial applications of the
herbicides, a wind was blowing which caused spray drift onto
the Warren pastures.

4451

11-18
One half of the dairy herd was grazing in the treated area
and the other half was upwind and did not come into contact
with the chemicals.

Of those in the sprayed pasture, 22

aborted their calves. The others in the "clean" area pro­
duced only one abortion. An analysis of hay samples 15 months
after the spraying operations showed 10 parts per billion
(ppb) of 2,4-D and a "trace" of 2,4,5-T. Mr. Warren was
later compensated by the government for damage done to his
farm. Fortunately no children were born in the area at the
time (Ogden, 1971).
A powerline right-of-way on Galiano Island, B.C. was
sprayed with 2,4-D in 1972. The line ran near the water
supply of Dan and Francine Renaud.

Their daughters, Sarah

and Tamie were born in 1973 and 1975, both with the spina
bifida malformations of the spine. There are other reports
of a high incidence of spina bifida and cleft palate in the
area at the time, as well as one child born with hydro­
cephalus (abnormal enlargement of the cranium) which died at
the age of two (Vancouver Sun, October 3, 1973; The Daily
Colonist, May 27, 1977).
Of the malformations reported by delivering physicians
in British Columbia, fifty percent are of the type reported
in laboratory testing of 2,4-D. These are spina bifida, cleft
palate, club foot, hydrocephalus and other skeletal mal­
formations. In the case of cleft palate, British Columbia
leads Alberta, Manitoba and New Brunswick by a substantial
margin (Elwood and Rogers, 1975)
As Dr. Samuel Epstein states clearly, the "continued use
of these herbicides (2,4-D and 2,4,5-T) in the environment
constitutes a large-scale human experiment in teratogenicity..
Such an experiment is unwarranted by any conceivable criteria
in the face of the unambiguous warning sounded by available
scientific data" (Epstein, 1970).

4452

11-19
Other Reports
In Guamo, Columbia it was reported that one million in­
habitants of the province of Tolima were exposed to 2,4-D and
2,4,5-T spraying. There followed an apparent epidemic of
human abortions, stillbirths and malformations. The incident
occurred in October of 1974 and the government promised an
investigation. As of this writing, we have not been able to
track down further research on this incident. (Environment,
January, 1975)
From 1971 to 1974, 2,4-D and 2,4,5-T were sprayed from
helicopters to control roadside weeds near Pittsville, Wiscon­
sin. Following the applications many abortions, deformities
and deaths were noted in wildlife and domestic animals. Six
pregnant women in the area aborted (Stevens Point, Wisconsin
Daily Journal, March 10, 1975).
During her testimony at the trial of Citizens Against
Toxic Sprays versus Earl Butz, Secretary of U.S. Department
of Agriculture, Dr. Eloise Kailan described patients which she
had examined after exposure to the phenoxy herbicides. All
exposure took place in the Siuslaw National Forest in Oregon.
Dr. Kailan testified that four of her nine female patients
experiencing miscarriages since living in the area, two of
them on two occasions and one 16 times (Kailan, 1976).

Summary
The public began to become aware of the potential of 2,4-D
to cause birth defects in early 1969. At lhat time the U.S.
Department of Health Education and Welfare released the Mrak
Report. This study included the test results of the Bionetics
Laboratories' research into the effects of 2,4-D on mice.

4453

11-20
The tests indicated clearly that the herbicide was terato­
genic in the laboratory animals. The Commission's Panel on
Teratogenicity r

amended strongly that the butyl, isoprop­

yl and isooctyl esters be "immediately restricted to pre­
vent risk of human exposure." 2,4,5-T was also found to
cause malformations during the tests.
In quick succession, the U.S. National Institute of
Environmental Health Sciences, the U.S. Food and Drug Ad­
ministration, the Canadian Food and Drug Directorate and
the Dow Chemical Company produced test results on 2,4-D.
All published findings which showed that 2,4-D, its various
formulations, and one breakdown product produced teratogenic
effects in mice, rats and hamsters. Some of the common ab­
normalities observed were cleft palate; clubfoot; no eyes;
no lower ,jaw; distorted, missing or extra ribs; unformed
breastbone; brain mislocation; enlargement of the skull and
various hemorrhages.
Testing procedures have been criticized as not being
appropriate for human comparison. However, it is asserted
that mice are good indicators of teratogenic potential in
humans and, as in the case of thalidomide, are often less
sensitive. Unfortunately, 2,4,5-T has distracted public
concern from 2,4-D because of its highly toxic contaminant,
TCDD. There are also powerful economic pressures keeping
any restrictions from being placed on this teratogen (2,4-D).
While field reports are a crude tool compared with so­
phisticated epidemiological investigation, in many cases, they
are our only early warning system beyond laboratory testing.
With 10% of the forests defoliated, Vietnam stands as the
most intensively herbicide contaminated country in history.

4454

11-21
Unfortunately, due to the war situation and the lack of ad­
equate birth defect information, we do not have the moutain
of data which we should. We do know, however, that the in­
cidence of stillbirths, spina bifida and cleft palate in­
creased significantly among those who had contact with the
herbicides.
In North America, birth defects have followed 2,4-D
applications in Arizona, Wisconsin, Nova Scotia and British
Columbia. There was also a major incident reported in Co­
lumbia. Statistics indicate that 50% of the malformations
seen by delivering doctors in British Columbia were present
in the test animals during herbicide testing. There is clearly
reason for concern that 2,4-D may have the potential to pro­
duce a significant number of birth defects in humans.

4 ,«■r*'y*
"P -M S fl

III-l
CANCER AND THE PHENOXY HERBICIDES

Cancer (neoplastic disease) is now a major killing and
disabling disease in Canada and the United States. It has
clearly reached epidemic proportions.

Today, one in every

four persons in North America is developing some form of
cancer, and 20% of all deaths are attributed directly to the
disease. (Epstein, 1976) The death rate since 1900 in North
America has risen 240% in terms of deaths per 100,000 people.
There is hardly a family today in our country which has es­
caped this dreaded disease.
Furthermore, there is growing evidence that most car­
cinogens (agents which produce neoplasms in animals including
man) are toxic substances in the environment.

It is often

said that cancer is "a disease of civilization."
In 1976 the Director of the U.S. National Cancer In­
stitute estimated that 90% of all cancers are caused by en­
vironmental carcinogens. (Epstein, 1976) The World Health
Organization took a similar stance that same year. (Webster,
1976) This means that not only is man responsible for most
cancers, ultimately we can reverse this disastrous course and
remove most of the carcinogens from the environment.
What is Cancer?
In the normal body, cell-reproduction is disciplined
and orderly. Cell growth occurs during reproduction following
fertilization, to repair damaged tissue and to replace "worn
out" cells.

A turnerous cell has a defect in the genetic

apparatus that results in the loss of repression of the DNA
synthesis and thus the loss of regulation of cellular re­
production.

A cancerous cell reproduces without regard for

its original function.

It is bizarre in shape, size and in

the form of cell groupings.

III-2
The nucleus of the cancerous cell is also deformed.
A neoplasm is an abnormal mass of tissue that grows
rapidly and continues to grow after the original stimulus
ceases.

It is referred to as a me tastasizing tumour when

it reproduces similar tumours in parts of the body remote
from the original site of the disease.
In recent years research has discovered that more and more
pesticides are carcinogenic to laboratory animals. There is
increasing public pressure to ban these potentially harmful
chemicals. In response to this pressure, the manufacturers
of pesticides and the primary users have argued that there is
a basic difference between malignant tumours (those which ex­
hibit uncontrollable growth) and benign tumours (those that
appear to have normal cell structure, and are often character­
ized by encapsulation). From this they have concluded that
pesticides which only cause benign tumours in test animals
should not be banned. (C.A.S.T., 1975; Ferg, 1977)
However, this position is challenged by medical author­
ities. Dr. Harold Stewart, former chief of pathology at the
U.S. National Cancer Institute, states that "you can't really
separate the two terms. We know that if tumours are untreated
they will very often metastasize." Dr. Sidney Weinhouse,
Director of the Fels Research Institute in Philadelphia,
which does extensive cancer research, holds that "there are
no strict, quantitative criteria that differentiate benign
from malignant tumours. So-called "benign" tumours simply
grow more slowly than malignant tumours." (Webster, 1976)
The World Health Organization takes the same stance. The
term "chemical carcinogen" is used to indicate a substance that
is known to induce or enhance neoplasia.
"Induction of tumours
and enhancement of tumour induction are not distinguished
for present practical purposes", the WHO stated in 1972.
They hold that "the terms 'tumorigen',

'oncogen' and 'blast-

omogen' have all been used synonymously with carcinogen".

*

4458

III-3
(Health Hazards, 1972)
In the United States, the Environmental Protection
Agency, which now licenses all pesticides, has been strongly
criticized for their decision to ban many of the chlorinated
hydrocarbons (the DDT family). In June 1976 the E.P.A. took
the position that a carcinogen is an agent which causes the
increase of "malignant or benign cancers in humans or animals."
(E.P.A., 1976)
The E.P.A.'s stance was supported by Dr. Russell W.
Peterson, Chairman of the President's Council on Environmental
Quality. At the annual meeting of the Society of Toxicology
in Atlanta in 1976, Dr. Peterson argued that "because certain
induced tumours transform into malignancies, and because we
can seldom predict which tumours will become malignant and
which will not, we should regard all tumorigens (tumour
causing agents) as possible carcinogens." (Webster, 1976)
Are All Chemicafc Carcinogens?
Many public officials, as well as spokesmen for the
chemical companies and their major users, claim that all
chemicals will cause cancer if given in large dosages.
There is absolutely no basis for this statement.
For example, the Bionetics Research Labratories tested
around 140 pesticides in the late 1960's for the U.S. National
Cancer Institute to determine whether or not they could cause cancer
when fed to two strains of laboratory mice. Less than 10% of
these pesticides were found to be carcinogenic.

(Epstein, 1975)

In 1977, the U.S. National Cancer Institute estimated
that only around 5% of the chemical compounds tested to that
time on labratory animals had proven to cause cancer. The
dosage levels of the chemicals when fed to experimental
animals made no difference.

(Miller, 1977)

4459

III-4
Is There a Tolerance Level for Carcinogens?
One often hears public officials claim that there is
nothing wrong with consuming toxic substances if it is in
very low doses. But this applies only to the acute toxicity
of a chemical: its immediate effect as a poison. It does not
apply to chronic toxicity.
For example, the B.C. Royal Commission of Inquiry into the
Use of Pesticides and Herbicides (1975) ooints out that
"tolerance of pesticides for drinking water have not been
established by the Provincial and Federal Governments." The
same is true in the United States.
In 1974 the U.S. Congress passed the Safe Drinking Water
Act. The U.S. Government asked the National Research Council,
an arm of the National Academy of Science, to undertake a
study of the major water system contaminants. This was com­
pleted in 1977. They were asked to set "acceptable daily in­
take levels "for 45 major organic chemicals found in water
supplies. They refused. The NRC held that "methods do not
now exist to establish a threshold for long-term effects of
toxic agents." (New York Times, July 21, 1977)
It is widely recognized that there is no tolerance level,
or threshold level, for carcinogens. This was the position
taken by the International Union Against Cancer in 1954, and
it has not been reversed. The Union argues that a sharp dis­
tinction must be made between reversible and irreversible
adverse effects from chemicals. For chemicals which induced
irreversible and possibly cumulative effects, particularly
carcinogens, there is no way to define a tolerable limit.
(Epstein, 1975)
The World Health Organization has traditionally taken
a similar position.

They hold that a "no effect" level cannot

be determined for carcinogenic substances. As they state in
1972, "this concept is based on experimental animal studies
showing that, unlike other forms of intoxication, carcinogenesis
is the result of an accumulation of irreversible cellular damage
rather than an accumulation of a toxic substance."

III-5
(W.H.O., 1972)
The Delaney Amendment to the U.S. Food and Drug Act,
adopted in 1958, reflected this thinking.

It holds that

"no additive shall be deemed safe if it is found to induce
cancer when ingested by man or animal, or if it is found,
after tests which are appropriate for the evaluation of the
safety of food additives, to induce cancer in man or animal.."
The U.S. Department of Health Education and Welfare has
supported this law. (Epstein, 1976) There is no comparable
law or regulation in Canada.
Paul N. Craig and Gene Miller of the Franklin Institute
in Philadelphia have conducted research on this question.
After reviewing 151 experiments with different chemicals
which produced cancer in labratory animals, they concluded
that there is no evidence that there is a threshold dose
below which a carcinogen will not cause cancer. (Miller, 1977)
One of the foremost authorities on cancer and teratogens
in North America is Samuel Epstein of the Case-Western Reserve
College of Medicine. Dr. Epstein argues that the "no threshold
level" position "reflects the overwhelming consensus of the
qualified scientific community." (Epstein, 1976) In 1976
the U.S. Environmental Protection Agency restated their
position in the issue:
"The only safe exposure level for a
carcinogen is zero." (E.P.A., 1976)
There is a wide variation in susceptibility of humans to
cancer depending on many factors, including heredity, race,
age, sex, diet and nutrition, and immunologic competence. It
is for these practical reasons that it is impossible to set
universal tolerance figures. (Meissner and Warren, 1971)
The Danger of Low Doses over Long Periods of Time
It is widely recognized that exposures to carcinogens
are irreversible as well as cumulative.

4461
"P-M5 $ 7

It is true that a single exposure may cause a cancer after
a latent period. But most cancers are a result of exposure
at low doses over a longer period of time. (B.C. Royal
Commission, 1975)
When humans are exposed to a variety of carcinogens, the
possibility of contracting the disease increases. For example
it is well known that those who smoke tobacco have a higher
rate of cancer than those who do not, and not merely lung
cancer. Certain industrial workers (like chemical workers
and uranium miners) have very high cancer rates. Those who
simply live near to heavy industrialized areas and who are
exposed to air pollution have a much higher rate of cancer.
(Epstein, 1976)
In some cases carcinogens can be synergistic, increasing
the effects through interaction with other carcinogens. There
is also the case of "cocarcinogenicity", where a known carcin­
ogen can be enchanced by combination with another agent which
itself carries no carcinogenic potency. Croton oil has this
effect on the carcinogenic hydrocarbons.
In addition, some known carcinogens are radiomimetic:
producing effects similar to that caused by radiation.
Chemicals that have an "estrogenic-hormonal-likc-activity"
fall into this category. For these, low doses over a long
period of time have proven to be more dangerous than large
doses over the same period of time. The small doses evoke
"tissue response", while the large doses do not. The tissue
response takes the form of proliferate cellular growth.
(Doucet, 1976)
The Time Lag in Exposure to Carcinogens
In many cases, environmental cancer is not detected until
many years after the original exposure.

This has even been

true in the case of industrial workers who have been exposed
to high levels of carcinogens on a regular basis.

III-7
Very often, cancer caused by environmental factors appears
around 15 years after exposure, and often even longer.
For example, in 1975 and 1976 cases of angiosarcoma, a
rare form of liver cancer, began to appear in older Wisconsin
farmers. Scientists from the U.S. Center for Disease Control
in Atlanta and Mt. Sinai Hospital in New York investigated the
cases.
Previously, this cancer had been linked to workers in
arsenic factories. In this case, the cancer was linked to
the use of lead-arsenic pesticides, at one time widely used
in Wisconsin, but also all over North America including the
Okanagan. The latency for angiosarcoma had been ranging from
20 to 30 years after the original exposure. (Western Producer,
April 1, 1976) The B.C. Royal Commission concludes that "the
greater frequency of cancers with increasing age suggests a
low level of long span exposure to a carcinogen." (B.C.
Royal Commission, 1975)
Is Animal Testing Adequate?
In recent years some public figures in North America have
criticized the dependence on labratory animals for determining
whether a chemical substance is a carcinogen, a teratogen or
a mutagen, but those dealing with cancer research remain con­
vinced of the relevance of tests on labratory animals.
For example, in 1977 the U.S. National Research Council
released a report on drinking water and health. They were
particularly concerned about organic chemicals which could
produce chronic toxicity in humans. They argued that effects
in animals, properly qualified, are applicable to man:

III-8
This premise underlies all experimental
biology and medicine. But because it is
continually questioned with regard to
human cancer, it is desire able to point
out that cancer in men and animals is
strikingly similar. Virtually every
form of human cancer has an experimental
counterpart; and every form of mult­
icellular organism is subject to cancer,
including insects, fish and plants.
(Miller, 1977)
Dr. John H. Weisburger, Head of the Carcinogen Screen­
ing Section of the U.S. National Cancer Institute, adds
that "every one of the agents with demonstrated carcinogenic
potency in man has also caused cancer in one or more species
of animals under specified conditions." We should expect
this to be so, for "in the main, biologic systems in animals
are not different from those in man." (Weisburger, 1973)
The necessity to use laboratory animals for testing is
obvious; it would be out of the question to use human beings.
Because it is "unacceptable to wait from 15 to 40 years to
find our whether a suspect chemical will produce cancer in
man", Dr. Russell Peterson argues that "every chemical that
induces cancer in animals must be regarded as a potential
carcinogen in humans."

(Webster, 1976)

Are High Dosage Tests Relevant to Human Beings?
The other popular attack on the scientific studies deals
with the dosage levels of the agent administered to the
labratory animals. Since these are usually higher than the
dosages that humans would actually consume, it is argued
that the tests are not relevant to the human experience.
The use of high doses is a practical necessity to
compensate for the small number of lahratory animals used in
a research project.

P

4464

III-9
Dr. Samuel S. Epstein points out that if a particular agent
were to cause cancer in 1/10,000 humans exposed, it would be
mere good luck for the cancer to show up in a test conducted
on only 50 laboratory rats or mice.

In theory, such a test

would need to use 10,000 rats or mice to yield one cancer.
Thus, the higher dosage is used to try to compensate for the
size of sample. (Epstein, 1976)
Here it might be well to recall that a carcinogen causes
cancer at low levels of exposure as well as at high levels.
But exposure to high doses makes the cancer appear more
quickly.
In addition, the high doses compensate for the faster
metabolism of the test animals relative to humans. Cell
turnover is much faster in small animals than it is in
humans. Furthermore, we know that lahratory animals, par­
ticularly rats and mice, detoxify and excrete chemicals
more rapidly than do humans.
The history of the method of testing for carcinogens is
outlined by Dr. John H. Weisburger. It was long suspected
that 2-naphthylamine was causing bladder cancer in industrial
workers. But lahratory tests on animals, using dosage levels
similar to human exposure, produced only negative results.
Then in 1937 Heuper proved in lahratory tests on dogs that it
did cause bladder cancer. He achieved this result by admin­
istering high dosages. Dr. Weisburger concludes that "this
was a vital finding, and is occasionally forgotten in con­
temporary discussions. The observations focused major
attention on the critical problem of dose and duration of
carcinogen administration to reproduce in animals lesions
seen in man." (Weisburger, 1973)
The Shortcomings of Lahratory Tests
Research studies on cancer reveal that there are sig—
nificant differences in laferatories between test species,
strain and sex.
(oI

I I I -1 0
And these factors vary with different chemicals.

For example,

the important human carcinogen, 2-naphthylamine, has proven
to be carcinogenic in dogs after a long latent period, in
hamsters after high dosage, and in the mouse where it pro­
duces liver cancer.

But it has not caused cancer in lab-

ratory rats.
There are other factors which are related to the en­
vironment. Lahratory animals are always in apparent good
health; those which are ill are discarded, or abandoned
half-way through the experiment. Normally, they are fed a
well-balanced diet. They may not be under as much stress as
many human beings. They live in regulated climates. They
are only exposed to the agent suspected of being a carcinogen
and used in the test; human beings are constantly exposed to
a wide variety of environmental carcinogens. (Epstein, 1970)
(Shea, 1973)
Dogs and monkeys appear to be better test animals than
rats, mice and hamsters. Their survival levels for acute
toxicity are much closer to that of human beings. Furthermore,
they have usually been exposed to the human environment and
are generally not bred through generations of labratory
conditions. (Seabury, 1963) However, experiments with these
animals take longer and are more costly.
Finally, most tests are done on only one generation.

In

the case of diethylstilbestrol (DES), cancer of the reproductive
organs appeared in the daughters of women who had taken DES
during pregnancy. In the case of saccharin, cancer appeared
in the second generation of labratory rats.

Most people

believe that we need three generations of testing to provide
more reliable results. But again, this is a costly and
time-consuming approach.

&

4466

III-ll

Is 2, 4-D a Carcinogen?
There have always been good reasons for suspecting that
all the phenoxy herbicides might be carcinogens.

First, they

act as an auxin hormone in plants, killing them through a
massive reproduction of cells. In plants, then, it has been
known that they attack the cell nucleus and upset the normal
controls on cell growth. Might they not act the same way in
animals?
Secondly, all phenoxy herbicides are manufactured from
benzene, a carbonization of coal. The polynuclear aromatic
hydrocarbons have been identified as causing cancer in
humans. Benzene has for over 60 years been suspected of
causing leukemia, although labratory test results have
varied. In 1977, the three year study by New York University's
Institute of Environmental Medicine established that benzene
fumes caused leukemia in labratory mice and rats. (Globe &
Mail, August 8, 1977)
All the phenoxy herbicides share the common "benzene
ring" structure of the molecule onto which other atoms are
attached. Many of the known carcinogens have as their core the
benzene ring. Some of these are the polynuclear aromatic
hydrocarbons, aromatic amines and aze dyes and some of the
nitrosamides and hydrazines.
Fourthly, a significant number of chlorine-based
chemical compounds have proven to be carcinogens. The most
widely known are the chlorinated hydrocarbon insecticides
(the DDT family). Another is chloroform. All the phenoxy
herbicides have chlorine atoms attached to the benzene ring.
(B.C. Royal Commission, 1975)

M G

7

III-12

Finally, there is the fact that the phenoxy herbicides
are synthesized from chlorophenols. It has been known at
least since the release of the Mrak Commission Report in 1969
that a number of the chlorophenols were carcinogenic to labor­
atory animals.

(Mrak, 1969)

It was not until the release of the Bionetic Research
Laboratories' studies in 1969 that interested people became
aware of the dancers of the phenoxy herbicides. In laboratory
tests on small animals, 2,4-D,

2,4,5-T and 2,4,5-TP (Silvex

or Fenoprop) all produced the same types of neoplasia.
The tests using 2,4-D were done by Dr. Berge M. Ulland
and were completed on October 18, 1967.

Tests performed on

two strains of mice produced leukemia (cancer of the bone
marrow), reticulum cell sarcoma type A (cancer of the lympth
glands and connective tissue), Pulmonary Adenoma (lung cancer),
Pulmonary carcinoma (Bronchogenic) and Hepatoma (liver cancer).
Benign tumours were also reported in the liver, spleen and
stomach of three of the test animals.
Ulland, 1967)

(Innes, et. al., 1969;

U.S. Food and Drug Administration Tests
In 1963 the U.S. Food and Drug Administration completed
a study of the effects of 2,4-D on dogs, and in 1964 they
did a study on rats.
appear until 1971.

Summaries of these results did not
(Hansen, et. al., 1971)

In the meantime, 2,4-D was widely being used on food
crops and residues were beginning to be noticed.

For example,

in 1974 there was no tolerance level established for 2,4-D
resudues in milk.

4468

III-13
However, one test done at GHT Laboratories in California
found .0007 ppm residue of 2, 4-D in milk. It also reported
1.02 ppm residues in apples.

(U.S. EPA, November 13, 1974).

Pressure was mounting to revise the residue limits.
On April 8, 1976 the EPA mailed reregistration guidance
packages to manufacturers and distributors of 670 food
products containing 2, 4-D residues. The agency cited the
1963 and 1964 lahratory tests as "sufficient" to satisfy the
"chronic" safety testing requirements for reregistration.
This action prompted an inquiry by the U.S. Senate Sub­
committee on Administrative Practice and Procedure headed by
Senator Edward M. Kennedy of Massachusetts.
The Subcommittee sent the data on 2, 4-D that was in the
E.P.A. files to Dr. Melvin D. Reuber for his evaluation. Dr.
Reuber served as a pathologist at the National Cancer In­
stitute between 1963 and 1971, and is considered a top expert
in the field.
Dr. Reuber's report was published in December 1976. The
FDA's study revealed that 2, 4-D caused malignant tumours in
male and female rats tested: he concluded that "2, 4- Dichlorophenoxyacetic acid is carcinogenic in rats."
The study on beagle dogs was less conclusive. The F.D.A.
experiment produced "scattered lesions such as atrophy of the
tests and prostrate, interstitial nephritis, hemangioma of
the adrenal, atrophic or cystic pituitary, atrophy of the
throid, and hypoplasia of the bone marrow. Most of the
lesions were seen in the endocrine organs."
However, even though the lesions occured predominately
in treated dogs, the FDA researchers concluded that "none of
these lesions in the dogs was believed to be due to the in­
gestion of 2, 4-D."

0-

III-14
Dr. Reuber noted that "previous experience at FDA has shown
that long-term chronic dog studies should be carried out for
six years or longer in order for tumours to develop."
(Reuber, December, 1976)

Studies of Organic Carcinogens in Water Supplies
In recent years there has been more research being done
on the question of organic and other contaminants in North
American drinking water. In 1970 the U.S. Geological Survey
found a wide variety of heavy metals in all water supplies.
Some of these are toxic at high levels. The main pollutants
were arsenic, chromium, cobalt, lead, mercury and zinc.
(Durum et al, 1971)
In 1970 the U.S. Environmental Protection Agency con­
ducted a survey of 66 organic chemicals found in drinking
water; 43 of these were tested for carcinogenicity, and 15
were found to definitely cause cancer in laboratory animals.
Another 87 organic chemicals were identified as "suspected
water contaminants," and of these 17 were known to cause
cancer in labratory animals. The phenoxy herbicides were
included as suspected carcinogens.

(U.S. EPA, 1970)

The most widely cited water contamination study was
that done by the EPA on drinking water in the lower
Mississippi River. They found 88 organic chemicals in the
Louisiana water supply.

In the treated water coming out

of the Carrollton Water Plant in New Orleans, they found 36
organic contaminants. The EPA concluded by pointing out the
strange situation where the U.S. Food and Drug Administration
had banned certain chemicals from foods because they were
known carcinogens but that they were in most municipal drink­
ing waters.

.4470

III-15
There were no standards of water quality in North America
covering carcinogens, teratogens and mutagens.
1972)

(U.S. EPA,

In a report issued in June 1975, Dr. Robert G. Tardiff,
research toxicologist with the EPA's Water Supply Laboratory
in Cincinnati,rated 128 organic chemicals commonly found
in North American drinking waters. Seven were found to be
"extremely toxic", one "super toxic" and 35 were identified
as "suspect carcinogens."

He cited eight organics as

"positive carcinogens", and among them was 2, 4-D.
1976; Tardiff, 1976)

(Haber,

These studies on water contaminants reveal the necessity
of testing down to the level of parts per trillion. Un­
fortunately, the testing done in the Okanagan Lakes was only
down to .001 parts per million.

This is simply inadequate.

For example, one pesticide commonly found in water
supplies, Dieldrin, has proven to be carcinogenic to labo
ratory animals at the lowest tested level, 100 ppb (part per
billion). Some carcinogens have produced tumours in test
animals at concentrations below 400 parts per trillion,
according to the testimony of the Environmental Defense Fund
before the U.S. House of Representatives Subcommittee on the
Environment and
the Atmosphere. (Haber, 1976)

Field Reports
It is very difficult to get field tests on carcinogens.
Most chemical carcinogens have been identified through
epidemiological surveys of industrial workers.

It is difficult,

to say the least, to clearly identify a chemical carcinogen
in the environment in a direct casual relationship.

III-16
We have some evidence of the carcinogenic nature of
pesticides through surveys done of agricultural workers.
However, most of these workers (and farmers) are exposed to
a variety of pesticides, and individual identification is
nearly impossible - except where the workers are only per­
forming a specific spraying task.
For example, in 1972 such as case was revealed by
The Expresser, the magazine of the Swedish Government Em­
ployees Union. It reported that 30 workers had been em­
ployed by the Swedish Government to clear brush along the
Swedish national railway. They were using a herbicide called
Hormoslyr, a mixture of 2, 4-D and 2, 4, 5-T.
By February 1972, five of the thirty workers had died
of cancer; a sixth died later in the year. The surviving
workers reported that they regularly suffered from headaches,
loss of taste, impairment of sight, bladder contraction and
impotency, all recognized as symptoms of phenoxy herbicide
pois oning. As a result of this case, the Swedish state
railway stopped all chemical spraying of weeds. Following
the reports from Vietnam in 1971, the Swedish Government had
also banned all aerial spraying of phenoxy herbicides.
(Province, February 22, 1973; Reuters Dispatch, February 26,
1972)
From this it was not possible to conclude that 2, 4-D
alone was the carcinogen. But the Swedish Government con­
cluded that the phenoxy herbicides were the cause.
The other source of epidemiological data comes from
Vietnam, from surveys of the people who lived in areas
sprayed with phenoxy herbicides during the American de­
foliation programme.

2

III-17
Normally, there is a relatively long period of latency
between exposure to a carcinogen and the development and
identification of cancer. However, evidence coming out of
Vietnam suggests that Hepatoma (liver cancer) is already
appearing in spray victims.
In a paper presented in 1973, Ton That Tung and his
associates at the faculty of medicine at Viet Due Huu Nghi
Hospital in Hanoi reported that primary carcinoma of the
liver had increased abnormally in Vietnam in the period since
the herbicide spraying. (Ton That Tung, 1973)
Similar conclusions were reported in a paper that the
group presented in 1976. They found that between 1956 and
1961 hepatic cancers accounted for 2.89% of all cancers in
Vietnam. Between 1962 and 1968, the period when the herb­
icide spraying actually took place, hepatic cancers rose to
9.07% of the total.

The Vietnam doctors attribute the rise

to the phenoxy herbicides, suggesting that it may possibly be
due to the various dioxins in them, particularly TCDD. (Laporte,
1977; Ton That Tung, 1976)
The Position of the Advisory Committee
The Advisory Committee on the Control of Eurasian Water
Milfoil covers the question of whether or not 2, 4-D is a
carcinogen in one short paragraph in the Second Interim
Report. When Senator Kennedy's report on the U.S. En­
vironmental Protection Agency was made public, one member of
the provincial Legislature requested the provincial government
to suspend the use of 2, 4-D in the Okanagan Lakes until it
was absolutely certain that the herbicide did not cause cancer.
The MLA in question stated the medical experts had stated
that one molecule of a carcinogen can cause cancer in a receptive
cell.

4473

III-18
In response, Dr. Courtland J. Mackenzie, Chairman of the Ad­
visory Committee agreed that the herbicide 2, 4-D "may be
linked to cancer - at least in theory." However, he then
added that there would be no risk if the programme of ad­
ministering the herbicide was "done properly": the idea is
that "nobody will get a molecule." (Penticton Herald, April
20, 1977)
Summary
Not all chemicals are carcinogens, but those that are
produce neoplasia at all dosage levels. Because of differences
among individual humans, it is impossible to set tolerance
levels for carcinogens.
Exposure to carcinogens is irreversible as well as cum­
ulative. Many carcinogens have proven to be more dangerous when
exposure is at a low dosage over a long period of time.
Research in both Canada and the United States reveals
that our potable water supplies are becoming increasingly
contaminated with organic chemicals. A number of these are
known carcinogens.
Research by the Bionetic Research Labratory (1967) and
the U.S. Food and Drug Administration (1963) demonstrate that
2, 4-D causes malignant tumours in labratory rats and mice.
Evidence from Sweden and Vietnam suggests that the phenoxy
herbicides cause cancer in humans as well.

4474

IV
IS 2,4-D A MUTAGEN?
A mutation is defined as any inherited alteration in the
genetic material. If they occur in germ cells (egg or sperm)
of an organism, they may be passed on to future generations.
Mutations can produce a wide diversity of deleterious
effects. Some mutant genes are dominant and will show up as
foetal deaths, achondroplasiz (dwarfism), polydactyly (having
more than normal fingers and toes), retinoblastoma (malignant
tumour of the retina) and sterility. There are also recessive
mutations which may not be expressed for several generations,
among which are albinism, Franconi anemia, amaurotic idiocy,
(childhood disease leading to loss of vision, paralysis and
death) and phenylketonuria (mental deficiency). The most
common genetic abnormalities are enhanced susceptibility to
various diseases (such as diabetes and inborn errors of met­
abolism), increased infertility, premature aging and alter­
ations in sex ratios. (U.S. IIEW, 1969; Crow, 1968)
One of the few comprehensive studies of genetic and
other diseases was done at Johns Hopkins Hospital, Pediatric
Service, between 1965 and 1969. Of the diseases recorded
among the patients, 7% were attributed directly to the in­
heritance of gene or chromosomal abnormalities. When the
diseases were added that were possibly genetically influenced,
the incidence rose to 39%. (13.C. Royal Commission, 1975)
It should also be noted that most genetic defects re­
sult in very early abortions and as a result are not added
to these data. It has been estimated that around 25% of
spontaneous abortions are due to chromosome abnormalities.
(Wellford, 1972)

IV-2
It has been known for some time that exposure to
certain types of radiation can be mutagenic. However, it
is less well known that a wide variety of chemicals can also
cause chromosome aberrations in plants and animals (including
man). The recognition that pesticides can cause mutations
dates from around 1931, when it was discovered that nicotine
sulphate induced chromosome abnormalities in tobacco, with
reduced seed set. In spite of this discovery, there has
been relatively little research done in this area. This is
perhaps due to the fact that environmentally caused mutations
are not different from others, so it has been quite difficult
to show a direct causal link. (Kimmins, 1975)
The Phenoxy Herbicides as Hormones
The phenoxy herbicides are "growth regulators" which
have hormone-like activity. At relatively low doses, they
will bring growth responses in plants that are distant from
the point of application.
Hanson and Slife (1969) have pointed out that auxins
(plant hormones) can alter nucleic acid metabolism in plants.
Holm and Abeles (1968) found that 2,4-D in soybean seedlings
increases the RNA and DNA in plant cells. Crispeels and Hanson
(1962) conclude that since RNA and protein synthesis are
controlled by DNA, the primary side of 2,4-D action is probably
the nucleus of the cell. Ashton and Crafts, in their widely
used textbook on herbicides, conclude that the evidence available
is that 2,4-D attacks the nucleus of the cell.

(Ashton and

Crafts, 1973)
This is what must be expected. After the application of
2,4-D cell division takes place. If the herbicide acts to
unhook the controls over cell division and development, it must
attack the nucleus of the cell.

4476

IV-3
Mutagenesis in Plants
There have been a number of studies of the triazine
herbicides for mutagenic properties.

Most of these pro­

duced mutations. The study by Plewa and Gentile (1976) of
the effects of Atrazine on maize plants found that the herb­
icide was degraded by the plant into environmental mutagenic
agents.
It appears that there are not as many tests done on 2,4-D,
which is somewhat surprising. However, Sawamura (1961) found
that 2,4-D caused chromosomal aberrations such as stickiness,
bridges and fragmentation in plants.
K.D. Wuu and W.F. Grant have done considerable research
on the mutagenic potential of 2,4-D in plants. In 1966 they
reported that barley seeds soaked in 2,4-D produced malformed
seedlings. They have concluded that far more rigorous analysis
of the health and environmental toxicology of herbicides is
required before they can be declared ,,safe."

(Kimmins, 1975)

In 1969 the report on pesticides by the U.S. Department
of Health, Education and Welfare ( Mrak Commission) listed
several studies that showed chromosomal changes in plants
treated with a 10 ppm concentration of 2,4-D. They con­
cluded that 2,4-D and 2,4,5-T have "mutagenic potential" as
demonstrated with plant systems.

(Mrak Commission, 1969)

Reviews of the effects of 2,4-D as a potential mutagen
were done by the U.S. Forest Service in 1973 and by J. P.
Kimmins for Environment Canada in 1975. They cite studies
by Unrau (1953, 1954) and Unrau and Larter (1952) which found
"highly significant" abnormalities of chromosome behaviour
in rapidly dividing cells of wheat and barley sprayed with
2,4-D. Huhling et al (1960) found chromosomal effects in
peas treated with 2,4-D.

t?-4573

IV-4
Thus, studies show that applications of phenoxy herb­
icides result in rapid cell division and cell elongation,
increased synthesis of ONA and UNA, and chromosomal ab­
normalities.

These aberrations can be inherited.

Wuu and

Grant (1967) have concluded that the chromosomal aberrations
induced by herbicide chemicals are essentially similar to
those caused hy x-rays.
This was the conclusion of Barbara H. Croker in her
study in 1953 on the effects of 2,4-L) on onions. Both 2,4-L)
and 2,4,5-T produced "physiological effects such as stickiness,
condensation of chromosomes, and delay in spindle formation."
The phenoxy herbicides produced chromatid breaks at all con­
centrations.
"Both 2,4-D and 2,4,5-T affect the nucleic acid
cycle, and it is suggested that the effect on the actual
chromosome structure is analogous with the action of radiation."
In this case study, reversibility or recovery was not demon­
strated. (Croker, 1953)
Phenoxy Mutant Effects on Laboratory Test Animals
Plant chromosomes are structurally like mammalian
chromosomes,so chromosome aberrations detected in plants are
relevant to mammals. (B.C. Royal Commission, 1975) However,
tests need to be done on animal species, and it is surprising
how little has been done in the field of pesticides in general,
and phenoxy herbicides in particular.
In 1971 Darving and Surner fed low doses of 2,4,5-T to
fruit flies. The result was a drastic reduction in fertility,
very high egg mortality, and total mortality of the first few
larvae that were produced. Ovaries of the flies were diminished
and rendered abnormally fragile, oogenesis was interferred
with, and chromosome aberrations were induced.
Another study involved the feeding of Mongolian gerbils
various doses of "pure" 2,4,5-T (i.e., "containing no measur­
able amount of TCDD") for five days.

4478

IV-5
Those receiving the higher doses showed substantial chromosome
damage, especially chromotid gaps and breaks.
Hall, 1972; B. C. Royal Commission, 1975)

(Majundar and

In a third study, male rats were fed 2,4,5-T at the very
low rate of 1 mg/kg. The results in the treated rats were
chromatid aberrations. (Novy and Ma.jundar, 1972) The only
reported study of 2,4-0 on mice concluded that 2,4-D was not
mutagenic at a rate of 125 mg/kg, the same dosage which
produced birth defects in hamsters.
1975)

(B.C. Royal Commission,

Three professors at the University of Heidelberg studied
the effect of 2,4-D on the growth of cultured chicken muscle
cells in 1974. Under the influence of 2,4-D, " a marked
increase of DNA-synthesizing cells was observed after 22 hours."
They concluded that "the morphologic and quantitative re­
sults of this study support the assumption that 2,4-D takes
effect on the level of chromosomes. Further investigations
based on biochemical parameters should be undertaken because
of the possible risks of exposure to man." (Haag et al, 1975)
After surveying the research on plants and animals,
•J.P. Kimmins, Associate Professor of the Faculty of Forestry,
University of British Columbia, concludes that it appears
that "the mutagenic and chromosomal aberration effects in­
duced by herbicides in plants may also occur in animals."
We should be concerned about this because "new and synthetic
substances are more likely to be mutagenic than old or
natural ones since organisms are less likely to be bio­
chemically prepared to deal with the former than the latter."
(Kimmins, 1975)
The Vietnam Experience
The best information of the effect of phenoxy herbicides
on human beings comes from the Vietnam experience.

4479

IV-6
Most areas of Vietnam were sprayed with Agent Orange, a 50-50
mixture of 2,4,5-T and 2,4-D. This same formulation is widely
used in British Columbia, although not on argicultural crops.
(See Table II)
The first medical report was presented by Dr. Ton That
Tung and four colleagues from Viet-Duc University Hospital of
Hanoi at the proceedings of the Reunion internationale de
scientifiques sur la guerre chimique au Vietnam, Paris,
December 12, 1970. As the war was still in progress at this
time, this report was the result of tests done on 179 human
beings who were refugees from areas sprayed in the Southern
part of Vietnam. (Ton That Tung et al, 1970; 1973)
As background, Ton That Tung reports that following
spraying there was an abnormal amount of human miscarriages.
For example, in the district of Long-Dien and An-trach (Fifth
Zone), out of 73 pregnant women, 22 had miscarriages. In
the district of An-nghia (Fifth Zone), after the spraying in
March 1966 there were many miscarriages in farm animals. Most
disturbing was the increase in molar miscarriages. The
Vietnamese doctors attribute this to herbicide exposure
during the beginning of pregnancy.
In a later report, Dr. Ton That Tung and colleagues
report that in the Hue district in the period 1969-1970,
following repeated spraying of Agent Orange by U.S. military
forces, the rate of stillbirths recorded at hospitals rose to
48.5%, and congenital malformations were observed in 7.4%
of children born in the same period. Laporte notes that
these figures may be understated, for the Vietnamese word
used to substitute for malformation is actually "monstrosity",
and therefore tends to exclude lesser malformations. (Ton
That Tung et al, 1976; Laporte, 1977)

4480

IV—7

News stories also reported a significant increase in
Downs Syndrome or Trisomy 21 (formerly called Mongolism) in
the areas sprayed by the phenoxy herbicides. In their first
study, the Vietnamese doctors report that Downs Syndrome was
appearing in very young women from the areas sprayed. Of
those cases in Hanoi at the time, the physicans conducted the
usual chromosome tests on mothers and children. They con­
cluded that Trisomy 21 was due to chromosomal breaks,
"present in a proportion of 3,3/100 of cells from the
children." This was roughly "six times as much as was
observed in the survivors of Hiroshima as reported by Bloom
et al."
Effects on Argricultural Workers
A second important source of information is the study
by Yoder et al, which was part of a project sponsored by the
U.S. Environmental Protection Agency. Three groups of in­
dividuals were tested for chromosome abnormalities over a
period of one year: a control group, a group of farm
workers who sprayed insecticides, and a group of farm workers
who sprayed herbicides. Most of the farm workers in the
insecticide group used organophosphates which are widely
used in British Columbia, although it did include a few
insecticides not used here. There were a number of herb­
icides applied, but 2,4-D was the most widely used. Tests
were made during the spraying season when exposure was high,
as well as in the off-season when no spraying was being done.
Blood samples were used.

The authors note that an

"analysis of chromosomal aberrations. . . is one of the major
methods for evaluating chemical mutagenesis."

D -*/577

IV-8
In the control group the mean number of gaps and breaks
in chromatids did not appreciably change at either sampling
period. In the groups exposed to insecticides, "the mean
number of breaks increased 5-folds" in the samples. Mean
breaks per person for those in the herbicide spraying group
"increased by a factor of 25 during this period." The
authors also found that "the subjects having the most gaps
and breaks, respectively, during the high exposure period
were members of the herbicide-exposed group." (Yoder et al,
1973)
Exposure to herbicides during the spraying season may
pose a danger to applicators. Chromatid abnormalities could
cause mutations, although in this case no tests were made on
sperm cells. Since mutations are very often carcinogens,
there is a likelihood that herbicide applicators will get
cancer more often than people not exposed to herbicides.
Furthermore, there is also the possibility that they Will
produce more children with birth defects than those not
exposed to herbicides. In reviewing this study, Prof. George
Streisinger of the Institute of Molecular Biology at the
University of Oregon states that "in view of the proportionality
between mutations and exposure, people exposed to any levels
of herbicides may be expected to experience some incidence of
mutation." (Streisinger, 1976) Dr. R.G. Camfield, in his
study on "Mutagenicity of Pesticides" done for the British
Columbia Royal Commission, points out that "compounds that
produce any type of cytogenetic abnormality have usually
been shown to induce point mutations, and it is usually con­
sidered that the induction of chromosome abnormalities is
an excellent indication of genetic damage."
Commission, 1975)

(B.C. Royal

4482

IV-9
Increase of Congenital Abnormalities in Canada
J. Mark Elwood and Janice R. Rogers have conducted a
survey of congenital abnormalities in Canada.

In British

Columbia, the incidence of Downs Syndrome was .86 per 1,000
births. This was higher than the Canadian average of .78
per 1,000 births.

(Elwood and Rogers, 1975)

A more specific study of Downs Syndrome was done by Jane
Evans, Alastjair Hunter and John Hamerton for the province of
Manitoba. Between 1965 and 1973 they found a marked increase
in Downs Syndrome among women in the 35-39 age group, rising
from 2.5 per 1,000 births in 1965 to 7.6 in 1973. Neither
study offers any reason for the present rates or changes.
(Evans et al, 1976)
The B. C. Royal Commission notes that around 25% of all
disease can be attributed to a genetic origin. This is in­
creasing because of the progressive decline of natural selection
in man.

(B.C. Royal Commission, 1975)

The Ames Test
The cost and time involved in conducting laboratory tests
limits the number that can be done given the present dis­
tribution of government budgets. In view of the potential
hazard to health, it is somewhat surprising how little test­
ing has been done on the mutagenic potential of chemicals,
and in particular pesticides. In recent years, simpler tests
have been devised using bacteria, yeast and human tissue
(bone marrow and blood cells).
Among these new tests, the Ames Test (named after Dr.
Bruce Ames of the University of California, Berkley) is the
best known.

In a series of tests of 174 chemicals known to

produce cancer in laboratory animals, 156 of them proved to
be mutagenic as well, using the bacteria test.
1973; McCann et al, 1975)

(Ames et al,

IV-10

Another test was devised by Toronto doctors Robert Bruce
and John Heddle.

They inject mice with the test substance, and

five days later they scan the bone marrow for chromosome
breaks. Then in four weeks they count the ratios of misshapen
sperm heads to normal sperm to try to determine the extent
of genetic damage. This takes longer than the Ames test but
has the advantage of using intact animals rather than just
cells.
However, they have discovered that some known carcinogens
and mutagens do not show up in these tests, indicating that
a system of cross-checks is needed. Heddle and Bruce argue
that "it is vital to monitor all environmental agents to avoid
breeding future populations riddled with genetic disease."
(Engel, 1975)
In September 1977 Dr. Bruce Ames described his new im­
proved test in an address to the American Chemical Society.
The new test was administered to 300 substances known to
produce cancer in animals, and it showed that they were all
mutagens. Dr. Ames concluded that "mutagens are also car­
cinogens, with few exceptions." He also suggested that the
"flood of chemicals" to which human beings have been exposed
since the 1950's "may be the main cause of death and disability
in advanced societies."

(Globe & Mail, September 1, 1977)

A similar position is argued by Professor J. P. Kimmins:

ft
ft

o

The increased rate of mutation imposed on the human
population by mutagenic agents such as radiation,
pesticides, and certain other synthetic chemicals
poses a great threat to the future of mankind. In
a natural population the process of natural selection
constantly removes non-adaptive mutants from the
population. In our sheltered, well-fed and doctored
society, this process has been eliminated, increasing
the so-called "genetic load": the percentage of the
population carrying deleterious but sublethal genetic
mutations. This load will ultimately cost society far
more in terms of both human suffering and health-care
dollars than the short-term benefits that the mutagenic
agents provide. We may indeed be "living on borrowed
time." (Kimmins, 1975)

4484

IV-11

Summary
2,4-D has produced genetic abnormtilities in a variety of
plants in laboratory tests. Very few tests have been done on
the mutagenic potential of the phenoxy herbicides on laboratory
animals, but two tests using 2,4,5-T produced chromosome
abnormalities in Mongolian gerbials and rats.
The Epidemiologic research done in Vietnam, in areas
sprayed with the phenoxy herbicides, reveals widespread and
extensive chromosome damage leading to a high rate of mis­
carriages, still births, congenital abnormalities and Downs
Syndrome. Medical authorities in that country compare the
effects to those on the survivors of Hiroshima and Nagasaki.
A study sponsored by the U.S. Environmental Protection
Agency found that applicators exposed to insecticides and
herbicides both experienced a significant increase in chrom­
atid breaks during the season of exposure. The rise in
congenital abnormalities in Canada may be attributed to the
elimination of much of the process of natural selection in
the human species.
There is obviously a need for greatly increased testing
in this area. However, there is enough evidence available
now to make us very suspicious of 2,4-D and the other phenoxy
herbicides.

448g

VII-8
In northern Sweden, 250 reindeer died and 40 aborted in
a herd of 600 after grazing in an area which had been treated
8 months previously with 2,4-D and 2,4,5-T. An analysis of
liver and kidneys of the dead animals showed that they con­
tained .45 - .50 ppm of 2,4-D and .05 - .10 ppm of 2,4,5-T
(Erne & Nordkvist, 1971)
In Vietnam, concern focused on the human populations
and agricultural crops following the massive spray programme
there. With upwards of 10% of the forest area defoliated
and mostly killed, the impact on wildlife must have been
substantial. Yale University biologist, Arthur Galston,
comments that he could obtain "no reliable data on effects
(herbicide) on animals, but with a destroyed or at least
drastically altered habitat, there is probably a concomitant
change of catastrophic proportions in animal populations.
The impact would be particularly obvious with respect to
insects and birds, but no less important for mammals, rep­
tiles, and other groups. I suspect that the only satisfied
animals, at least for the time, would be the termites"
(Galston, 1971). Observers did note that they did not see
any insectivorous or frugivorous birds in the defoliated
mangrove areas except barn swallows which were migrants
from the north. They also indicated that while fish eating
birds had not been as severely affected, their numbers were
also reduced (Orians & Pfeiffer, 1970).
Spray applications of 2,4-D, 2,4,5-T and 2,4,5-TP
(Silvex) made near Globe, Arizona during the period from
1966 through 1969 also resulted in reports of damage to
wildlife.

Charmion McKusik, an ornithologist specializing

in osteology (study of skeletons) was living in the spray
drift area at the time and made detailed observations.

Brown

Towhees were unable to fly, had eyes which were discharging
or swollen shut, and showed stiffness of the joints. They
were unable tb eat, drink or walk.

4487

VII-7

Of the 1066 treated eggs, 702 embryos (66%) were dead before
the 19th day of incubation. Of those embryos which reached the
latter stages of development, the majority had malformations
which prevented hatching. Of those which survived, more than
half were sterile and the fertility of the others was greatly
reduced. Other defects observed were spinal abnormalities,
fused neck vertebrae, muscular atrophy (decrease in size) of
the feet, shriveled and clenched toes, and feathers which were
missing or lacking pigment (Lutz-Ostertag & Lutz, 1970).
The effect of 2,4-D applications were clearly significant in
this experiment. This is of particular concern to the Okanagan,
as pheasants are just starting to reappear following the ban
on DDT and other chlorinated hydrocarbon insecticides.
Wildlife And 2,4-D
Following spray applications (2,4-D, 2,4,5-T and Dicamba)
at Belleisle Marsh, Nova Scotia, major effects were observed
in wildlife of the area. Sparrows feeding on wheat seed
flew poorly and spent a lot of time walking on the ground.
A cat which fed on the sparrows died shortly thereafter. A
fox found meandering in the area was taken to a veterinarian
where it died. During the four years prior to the application
of herbicides, the marsh had supported a 300 muskrat pelt per
season industry. In 1970, the harvest dropped to 100 pelts
and the following year the traps were not set due to the lack
of animals. Mr. Warren reported that the muskrats seemed tame
and "confused” and could be closely approached. Hay samples
from nearby were tested and were found to contain 10 ppb of
2,4-D and a trace of 2,4,5-T, fifteen months after the spray
applications (Ogden, 1971).

VII-6
Ducks and geese feeding on the plants and probing the bottom
sediments in these areas could consume a rather large dose
of the chemical in a short time. For the herbicide to be
most effective, applications are made in the spring. The
treatment could result in the exposure of the large migrating
waterfowl populations to substantial amounts of 2,4-D.
The Canadian Department of Agriculture reported that 10
Canada Geese were fed a diet of 100 ppm of 2,4-D over a period
of time, while another equal size control group was maintained.
As the experimental birds died or were killed, they were ex­
amined internally and compared with the control group. The
geese which had been fed the herbicide showed the following:
enlargement of the kidney, jaundiced appearance of other
organs; reduced weight gain; organs with general, progressive
"disorganization" of cellular structure; hepatic (liver)
cell destruction, round cell invasion and fatty degeneration
of liver tissue; kidney damage including capillary degeneration
and thrombosis, invasion of connective tissue and arteriole
wall enlargement (Royal Commission, 1975)
It would seem unlikely that a bird in the wild would
receive a daily 100 ppm dose of 2,4-D. It is possible, how­
ever, that geese feeding in a treated area could receive a
substantial amount of the chemical leading to some of the
internal organ deterioration which was observed in the test
birds. This information would certainly give wildlife
managers cause for concern as large numbers of Canada Geese
pause to rest and feed in the Okanagan Valley on their way
north to nest.
A major study was conducted in France in an effort to
explain a spectacular disappearance of major game birds in
Europe. The eggs of pheasant, red partridge and the common
gray partridge were sprayed with 2,4-D at a rate of 5.1 lbs
per acre (Slightly higher than the normal agricultural
application rate).

4489

A control group was sprayed with water.

VTI-5
Label restrictions on herbicides generally carry a warn­
ing to avoid contamination of water bodies. Forestry and
right-of-way applicators are instructed to leave buffer zones
near creeks, rivers and lakes. Water can obviously become
a means of moving the chemical away from the application site.
It is also the source of food and drink for wildlife and
human communities. Our understanding of the effects of 2,4-D
on the fishery of this province is obviously limited, though
some of the data available should give us cause for concern.
J.P. Kimmins, a Forestry professor at the University of
British Columbia, feels that "our very incomplete knowledge
of the sub-lethal effects of herbicide traces on aquatic
organisms requires that until we have more information we
should consider all herbicide contamination of forest waters
undesirable and work to eliminate or minimize it". (Kimmins,
1975)
Effect On Birds
One would expect waterfowl to be the most affected by
aquatic applications of 2,4-D. From the limited data available,
it would appear that the acute toxicity level for waterfowl
to this herbicide is relatively high. One report indicated
that the rate for mallard ducks was 1,000 to 2,000 mg/kg
(Tucker & Crabtree, 1970). Flocks of "dabbling" ducks have
often been observed in or near the Milfoil beds of the
Okanagan Lakes system. Apparently they feed on the Milfoil
as well as the other aquatic plant species which make up
the bulk of their diet.
A study by Lim and Lozoway, following 2,4-D applications
in the North Arm of Okanagan Lake in 1976, indicated that
Milfoil tissues could contain up to 80 ppm of the herbicide
following treatment (Morley, 1977)

VII-4
It should also be noted that acute toxicity can be in­
creased through a synergistic effect when 2,4-D is combined
with other pesticides. This factor is particularly important
in the Okanagan Valley where these chemicals are used ex­
tensively on crops. In one test, rainbow trout when exposed
to a combination of 2,4-D and Carcaryl (Sevin) showed an
increased mortality rate of up to 85%.(Stratham & Lech, 1975)
It may well be difficult to predict with any degree of
accuracy what the toxicity of 2,4-D will be for fish pop­
ulations given the general contamination of the water basin
with other pesticides.
The acute toxicity is not the main concern of wildlife
managers. Morley's study indicates that:
"Low concentrations of 2,4-D maintained over a period
of time could cause sublethal damage that is not
readily recognizable. Such effects can lead to gradual
decreases in fish populations through increased pre­
dation, reduced reproduction, increased susceptibility
to parasites, disease and stravation. Morphological
and histochemical changes in tissues and organs have
been demonstrated for sublethal doses of several herb­
icides."
Loss of habitat, as weeds and their indigenous organisms
are removed, is an additional problem. It is well established
that "the absence of aquatic plants could reduce the availability
of food and increase predation on these fish since shelter
would be depleted" (Morley, 1977)
The chemical is also directly toxic to bottom, fish-food
organisms. A study indicated that when exposed to a con­
centration of 1 to 4ppm of 2,4-D for a period of one week,
the various nymphs, larvae, midges, beetles and worms
suffered a population decline of 43%. At the end of one year
of exposure, the rate had climbed to 90% (Walker, 1962)
While this test was conducted in aquaria, it does indicate
that damage to aquatic food chains can result from relative­
ly low concentrations of this herbicide.

A ■»O *

V ; xJ 1

D -1S17

VTI-3
It appears that longer exposure times resulted in generally
higher mortality (Pimentel, 1971). The fact that the Salmonid family of fish seems to be particularly susceptible to
2,4-D should be of particular concern in British Columbia
now that the Milfoil is known to have spread beyond the
Okanagan Water Basin. A substantial concentration of the
herbicide in water used as a route to the salmon spawning
areas could result in an environmental and financial dis­
aster.
As is emphasized by Provincial Biologist R.L. Morley
in his excellent study entitled "2,4-D: A Summary Of In­
formation Relative To Its Possible Effects On Fish & Wildlife
When Used In Aquatic Weed Control Programs" - the "toxicity
of the ester formulations of 2,4-D to salmonids, and spe­
cifically rainbow trout, is very close to the concentration
(l-3ppm) required in water to assure control of the target
plants (Milfoil). This lack of adequate safety margin,
especially when liquid formulations are being used, can re­
sult in fish kills" (Morley, 1977) Thus, 2,4-D also poses
a threat to Okanagan game fish.
Five days after the application of 2,4-D in the weed
control effort on Skaha Lake Beach near Penticton, dead
carp and suckers appeared at the shoreline in varying states
of decomposition. A total of eight, all weighing over one
pound were observed. During and following this same period,
a fisheries biologist speared some carp and suckers which
were swimming lethargically in the treated area. A pesticide
analysis report by the B.C. Department of Agriculture in­
dicated that the carp flesh contained .44 ppm of 2,4-D while
the sucker contained .47 ppm. The gullet contents of the
carp showed a very high reading of 16.66 ppm. No salmonid
species were collected for examination in the application area.
(B.C. Fish and Wildlife, 1977)

$

9

.l\9

VII-2
It is reasonable to conclude then that pesticides in
general and the phenoxy herbicides specifically, could pose
a threat to any ecosystem. We watched in the past few years
as Peregrine Falcons and Ospreys nearly became extinct due
to the contamination of their food chains by the chlorinated
hydrocarbon insecticides. Species of life are now going
extinct at the rate of one per year. This compares with the
other period of rapid die-off at the end of the age of din­
osaurs when species went extinct at the rate of one per
thousand years (Myers, 1977). The long term effect of any
pesticide on an ecosystem is still largely unknown at this
point.
2,4-D*s Impact on Fisheries
Of particular concern to the Fish & Wildlife Branch
in British Columbia is the effect of 2,4-D on fish populations
of the Okanagan lakes system. In 1977 the granular Butoxyethanol
ester formulation of the herbicide (Aqua-Kleen) was placed
directly into the weed beds which also serve as fish habitat.
The Branch has good reason for concern as previous testing
resulted in health authorities advising fishermen not to eat
any catch in excess of three pounds. The reason for this
warning is that fish which have been sampled were found over
recent years to be contaminated with residues of mercury,
chlorinated hydrocarbon insecticides and polychlorinated
biphenyls (PCB).
The first concern of any researcher when testing a
chemical on an organism is the acute toxicity. How much
of the substance will it take to kill the test species?
The acute toxicity of 2,4-D on fish depends on the
species of fish and the formulation of herbicide used. Pi­
mentel compiled tests results which showed that death occurred
in 50% of the species treated (LC 50) at concentrations from
.8 ppm to 620 ppm, after 24 to 48 hours exposure.

4493

VII
ENVIRONMENTAL EFFECTS OF 2,4-D
2,4-D is a biocide, which is to say that it has been
formulated to kill a certain sector of an ecosystem. The
phenoxy herbicides are used to eliminate broad-leaved herb­
aceous plants. 2,4-D is therefore not very species specific,
as the group which it effects is rather large. This chemical
also can have an impact or other nontarget species which it
may come into contact with, depending on the rate of app­
lication and the environmental conditions. Several studies
indicate that wildlife can be deunaged when their habitats
become contaminated with the herbicide. This may happen in­
advertently when 2,4-D is transported from the application
site by air or water. In some cases, such as the Eurasian
Water Milfoil control programme, the chemical is intentionally
applied to a wildlife habitat in order to kill the weed.
Because the herbicide is used extensively in agriculture (2,4,
5-T has been banned from agricultural use in many countries
including Canada and the U.S. due to the health hazards in­
volved with it and the presence of the contaminent Tetradioxin)
increased interest in its effects on crops is resulting in
an accumulating body of research data.
It is necessary to examine some basic characteristics
of ecological systems before going further. While there is
some difference of opinion, a healthy ecosystem generally
exhibits a diversity of species with many complex inter­
relationships. Because of this incredible complexity, it is
unlikely that the effect of any manipulation of the system can
be predicted with long term accuracy. A major alteration in
one sector will often set off wide ranging reactions. The
impact of an intrusion in one area may be negligible, while
the same act in an overburdened, heavily stressed ecosystem
may have catastrophic effects. In essence, when we tamper
with the natural systems of our planet, we are stumbling in
the dark.

4494

VI-12
For example, in a 12 month survey covering 1972 and 1973
the Illinois Environmental Protection Agency, received notice
of or directly participated in 521 pollution accidents in­
volving the evacuation of 8 towns, injury to over 300 persons,
and damage to more than 1,100 homes and 350 businesses.
Most of these were storage and transportation accidents.
(Graham, 1977)
In many of these cases, large damage suits are being
filed. The victims of phenoxy herbicide spraying in Globe,
Arizona have a large suit against the Dow Chemical Co. and
the U.S. Forest Service. In the widely reported case of
poisoning of polybrominated biphenyl (PBB) in Michigan, there
are now 84 suits against the Michigan Chemical Company. In
April 1974, a leak in a storage tank produced a thick fog of
hydrogen chloride which soon engulfed 11,000 residents in
the Altgeld-Murray housing project in Chicago. Over 300 were
hospitalized and one died. The victims have a S100 million
law suit now in the courts. (Graham , 1977)
Summary
All the phenoxy herbicides, including 2,4-D cause acute
and subacute illnesses and psychological disorders in human
beings.

Those who report these illnesses include applicators,

those engaged in manufacturing the products, and those
accidentally sprayed. In relatively high exposure cases,
chloracne is produced in the victims.
Many of the chlorophenol-based chemicals have produced
serious toxic effects in humans.

There are many reported cases.

The phenoxy herbicides have also been responsible for a wide
variety of illnesses among workers in chemical plants engaged
in the production process. Furthermore, environmental accidents
are becoming much more frequent in North America as the use
of chemicals increases.

VI-11
(Chlorophenols are known to produce dioxins when heated.)
Tree planters have also reported phenoxy herbicide poisioning while working in areas sprayed with the herbicides.
There seems to be a pattern of attributing chloracne and
other phenoxy herbicide poisonings to tetra-dioxin in 2,4,5TP. Some have claimed that this can be solved by removing
the TCDD in manufacturing. More will be said about that in
the following section.
However, there is evidence that all the phenoxy herb­
icides produce chloracne, even 2,4-D and "purified” 2,4,5-T.
It could be the phenoxy herbicides themselves, or it could
be the presence of the other higher isomer dioxins known to
be in the phenoxy herbicides. TCDD is a potent stimuli for
chloracne.
Poland and his colleagues found chloracne among workers
in plants manufacturing 2,4-D and 2,4,5-T« as well as hypomania (mild mental disorder)personality problems. (Poland
et al, 1971)
Two doctors have reported treating more than 40 cases of
chloracne contracted by workers in plants engaged in the
synthesis of 2,4-dichlorophenol and 2,4,5-trichlorophenol.
There was some question as to whether TCDD exposure (from
the making of 2,4,5-T) was responsible for the chloracne in
all cases.
This question was resolved by Dr. Marcus Key of the Indistrial Disease Division of the U.S. Public Health Service.
He performed open patch tests on himself with the commercial
preparations of 2,4-D and 2,4,5-T. They both induced chloracne
on his arm. (Bleiberg and Brodkin, 1964)
Industrial accidents, exposure of workers, and accidents
outside the factory are much more widespread than is recognized.

4496

VI-10
Fifteen years later the exposed workers still reported the
common symptoms of phenoxy herbicide poisoning.
One of the most widely reported cases followed an ex­
plosion in an N.V. Philips plant in Amsterdam in 1963. Fifty
workers came down with chloracne, and many had damage to in­
ternal organs. The plant was closed for ten years, but con­
tamination remained so high that it was completely dismantled,
embedded in concrete, and dumped at sea off the Azores.
The Dow Chemical company closed one of its plants at
Midland, Michigan when more than seventy workers came down
with severe cases of chloracne. This occurred in 1964, when
they were manufacturing Agent Orange for use in Vietnam. Yet
Dow's representative at Senator Hart's hearings described
chloracne as a minor disease.

In reality, chloracne is an out­

ward sign that severe poisoning has occurred.
Between 1965 and 1969 a manufacturing plant in Czechslovakia had extensive leaks in the area where 2,4,5-Trichlorophenol was processed.

Workers experienced chloracne and other

less acute illnesses; eight years later they still reported
the illnesses.
An explosion took place in a Coalite and Chemical Product's
plant in Bolsover, England in 1968 during the manufacture to
2,4,5-T and hexachlorophene.

Seventy-nine workers developed

chloracne, as did members of their families having contact
with them. Several workers died. The equipment in the fac­
tory was removed and buried in an abandonned coal mine.
(Whiteside, 1977)
Chloracne has also been reported among people who have
been fighting brush and forest fires in areas treated with
phenoxy herbicides in Oregon and California.

4497

VI-9
Polychlorinated biphenals (PCB's) have also produced
severe chloracne in humans in proven cases. They are also
extremely toxic and build up in the environment and the food
chain. The most widely cited case of PCB poisoning occurred
in Japan in 1967 when PCBs accidentally contaminated rice oil.
Those exposed suffered from chloracne, and still births were
widely reported. (B.C. Royal Commission, 1975)
Another product which has been highly toxic is hexachlorobenzene (HCB). In 1960 seed grain which had been
treated with HCB was accidently consumed by over 3,000 people
in Turkey. Many of these people died from the contamination,
and chloracne was widely reported. (B.C. Royal Commission,
1975) (In 1967 six cases of poisoning were reported in
Czechoslovakia)
Industrial Accidents Manufacturing Phenoxy Herbicides
The dangers to humans from the phenoxy herbicides has
been known for quite some time due to the fact that there have
been a number of well-reported industrial accidents. Several
of these were cited by the B.C. Royal Commission of Inquiry
into the Use of Pesticides and Herbicides, but the best over­
all account easily available is that of Thomas Whiteside in
The New Yorker. July 25, 1977.
In 1949 two hundred and twenty-eight workers at the
Monsanto Company herbicide plant at Nitro, West Virginia came
down with chloracne as the result of an explosion while man­
ufacturing 2,4,5-T. A similar explosion happened in 1953
in a B.A.S.F. in West Germany. All the male workers and many
of their wives, children and pets broke out with chloracne.
A number of workers suffered damage to their internal organs.

VI-8
We can sum up this part by quoting from a letter from a
woman who lives in the Siuslaw National Forest Area of Oregon:
Down here the "flu season" starts when the herbicide use
begins. It depresses or destroys the thymus gland which
controls resistance to disease. We get colds, flu like
symptoms, uterine bleeding, nose bleeds, headaches,
double vision, asthma, dizziness, bronchitis and pheumonia.
It can cause your hair to fall out, gives you a gut pain,
nausea, and chloracne, which is similar to teenage acne
but may be anywhere on the body. Brown pigmentation
spots appear on the skin exposed to the sun, which once
there, stays. It affects memory, the liver, the heart
and causes bladder stones. It is vicious. (Pavel, 1976)
Chlorophenol Poisionings
It has been known for some time that many chlorophenolbased chemicals are dangerous to humans. Hexachlorophene,
which is synthesized from 2,4,5-Trichlorophenol, is neurotoxic
(poisonous to nerve tissue) and causes skin irritations. It
was widely used as a disinfectant until 1972, when three dozen
French infants died after being treated with a talc powder
which had been mixed with hexachlorophene.
Commission, 1975; Whiteside, 1977)

(B.C. Royal

Pentachlorophenol (PCP) has also proven to be quite toxic.
It is used in the processing of oils, leathers, paints, glues,
textiles, and as a wood preservative. Commercial preparations
have been found to be highly contaminated with tetra-dioxin
and dibenzofuran. In 1948, workers in a Germany factory pro­
ducing PCP broke out in chloracne and experienced nerve pains
in the lower extremeities. The B.C. Royal Commission (1975)
lists a number of PCP accidents, all of which brought some
deaths.
Sodium-PCP has appeared as a pollution problem in
effluent from pulp and paper factories which use PCP compounds
as slime-controlling agents.

It is extremely toxic to fish;

human exposure should clearly be avoided.
Shea, 1973)

(Crossland and

VI-7
Testimony Before Senator Hart's Committee, 1970
Following the reports of the accidental spraying at
Globe, Arizona and the reports out of Vietnam, Senator Philip
Hart's Committee on Commerce of the U.S. Senate held hearings
on the effects of the phenoxy herbicides on human beings.
Those medical specialists who testified reported similar
effects for both 2,4-D and 2,4,5-T poisoning.
Medical authorities reported that exposure to phenoxy
herbicides produced "pronounced hypochondria" and a decrease
in mental capacity. There are often general psychoneuropathic
complaints in the region of the extremities. Individuals
exposed have a sense of insecurity, inner restlessness, and
a feeling of illness. There is a change in normal behaviour,
with increased dissatisfaction, sullenness and irritation.
Fear and moodiness are common, what some doctors referred to
as "psycho-pathological intoxication".
Shoecraft, 1971)

(U.S. Senate, 1970;

A Case of the Flu
Dr. Granville F. Knight of Santa Monica, California has
had considerable experience with pesticides and their effects
on humans through his work with California farm workers. He
points out that the symptoms produced by exposure to the
chlorine-based herbicides (the phenoxy herbicides) and the
chlorinated hydrocarbon insecticides (the DDT family) "are
similar to, and perhaps identical with, the symptoms of many
virus infections which have now become common in the past
twenty years." He feels that many people have had pesticide
poisoning and have not sought medical help, concluding that
they just had a bad case of the flu. (Knight, 1973)

4500

VI-6
In early 1971 two British professors visited North Viet­
nam and interviewed a sample of 98 evacuees from sprayed
areas. The Vietnamese reported acute illnesses similar to
those cited in the previous American studies. However, a
greater incidence of skin burning and chloracne was reported.
The illnesses had lasted longer among the elderly and children.
(Rose and Rose, 1972)
The Committee of the U.S. National Academy of Science
reported symptoms of acute illness following spraying of
phenoxy herbicides in three separate studies. Children of the
Montagnard tribespeople reported coughing, vomiting, skin
sores, dizziness, and sometimes death. Similar effects were
reported in a survey of two provinces, and in a community in
the Rung Sat delta area. (Shapley, 1974)
The most thorough Epidimological work has been done by
the group of doctors operating out of Viet-Duc Hospital in
Hanoi, where a special monitoring programme was established.
They divided the effects of phenoxy herbicide spraying into
two categories;
(1) clinical symptoms during the first
hours, and (2) secondary effects.
The immediate effects on the Vietnamese were similar to
those widely reported in North America: tears and watery
discharge from the nose, intense weakness, giddiness, vomiting,
diarrhea, headaches, sensation of burning on the skin, and
fast heart beat. Asthenia (weakness) lasted for several
months in those exposed.
The secondary effects reported are prolonged asthenia,
chloracne and ocular syndrome (eye problems). The other
category of prolonged secondary effects is in the genetic
area;

chromosomal alterations and congenital malformations,

reported before.

(Ton That Tung et al, 1970; 1973)

4501
V - ^ i

VI-5
Four of her patients had frequent diarrhea following con­
sumption of water from areas sprayed with the herbicides.
Five experience peripheral neuritis (inflammation of the
terminal nerves) three had chloracne, and two of the nine
women reported unusual uterine bleeding.
Dr. Kailan also stated that she believed that exposure
to the phenoxy herbicides reduced resistance to infection,
based on the fact that these patients had a very high record
of pheumonia, colds, boils and bronchitis. On March 7, 1977,
the Judge of the District Court ordered a halt to herbicide
spraying in the Siuslaw National Forest.

(Kailan, 1976;

Skopill, 1977)
In 1976, Harmon Seaver's organic farm in northeastern
Minnesota was sprayed with 2,4-D and 2,4,5-TP (Fenoprop)
by the U.S. Forest Service. He tried to keep the heliocopters
away from his farm by shooting towards them with a deer rifle,
but when he was captured by the police, the U.S. Forest Service
returned and sprayed his farm. All his family experienced
headaches, nausea, dizziness and diarrhea. He was indicted
for assault. However, the jury acquitted him, agreeing that
he had a right to protect his family from poisoning.
1976; 1977)

(Seaver,

The Experience of Vietnam
Early reports out of Vietnam, including those by the
U.S. National Academy of Science and the American Association
for the Advancement of Science, were of limited use because
of the existence of the war. The commissions were unable to
conduct direct interviews and to gather on-the-spot data from
local medical records. The first firm reports were interviews
with refugees from the Central Highlands where there had been
considerable herbicide spraying.

“W

4502

VI-4
Three doctors at the Department of Medicine, University
of Kuopio (Finland) report similar symptoms in a farmer ex­
posed to MCPA, one of the phenoxy herbicides. They attribute
the illnesses to chemical substances which contain the halogenated benzene ring.

(Palva et al, 1975)

Accidental Sprayings
Similar illnesses have been noted in a number of cases
of accidental spraying
examples.

of human beings.

We will cite three

In June 1969 the U.S. Forest Service accidentally sprayed
a number of people while applying phenoxy herbicides in the
Tonto National Forest, near Globe, Arizona. One of these was
Mrs. Billie Shoecraft. She experienced swollen arms with
open sores, her hair fell out, and she reported the usual
"Flu symptoms." Others sprayed in the area reported similar
illnesses. (Shoecraft, 1971)
One of the best documented cases involved the spraying
of 2,4-D and 2,4,5-T in the Siuslaw National Forest. There
are a number of small farms in the National Forest.

In 1976,

the Citizens Against Toxic Sprays, the Oregon Environment
Council and Hoedad Inc. went to court to stop the spraying.
Hoedad, Inc. represented people who did contract forest work.
Included in the plaintiff's case was testimony by Dr.
Eloise W. Kailan. Dr. Kailan reported on the effects of
herbicide spraying on 11 of her patients, nine of whom were
female. Seven of the eleven reported severe headaches from
breathing the "red smoke" from burning areas which had been
treated with herbicides. Eight patients reported irritation
of eyes, nose and chest following spraying and exposure to
smoke from burn areas treated with phenoxy herbicides.

4503

VI-3
Electromyographic study showed denervation in several per­
ipheral muscles. Three years later she still had trouble
walking.
(3)

The third case cited was that of a 65 year old

farmer who had wetted his trouser legs while spraying a corn­
field with 2,4-D. He suffered from pain in the legs and
twitching of muscles for five months. He also reported head­
aches, nausea, vomiting, and eventual twitching in all
skeletal muscles. One year later he reported that he still
had constant pain in the upper and lower extremities.
stein, Jones and Brown, 1959)

(Gold­

In 1962 a group of doctors at Budapest, Hungary conducted
experiments to test the effect of 2,4-D on the central nervous
system. The test were performed on rats, dogs and cats; the
treated animals all experienced damage to the higher nervous
system. The researchers concluded that "according to con­
ditioned reflex experiments, the higher nervous activity
suffered severe damage." Caution and protection in the use
of 2,4-D, plus special neruological examinations of all work­
men applying the herbicide, was recommended. (Dest et al,
1962)
The Mrak Commission in 1969 reported a similar case
involving children playing in a yard which had been sprayed
with 2,4-D. During the first few days their eyes, mouths and
lips became swollen. Several days later the children experienced
incontinence
(inability to control discharge of urine) and
renal (kidney) damage. They also experienced "fatigue, nausea,
vomiting, anorexia (loss of appetite), diarrhea, swelling and
aching of the extremities." These symptoms progressed until
pain, paresthesias (general feeling of illness) and limb
paralysis were severe. Disability was protracted and re­
covery incomplete even after several years."

(Shoecraft, 1971)

VI-2
Billie Shoecraft, who spent 10 years digging into all
the studies done on phenoxy herbicides, reported that as
early as 1948 n2,4-D was known to produce liver and kidney
damage, heart attacks, severe destruction of the central
nervous system, genetic changes, reduction in potency,
hemmorages, paralysis, personality changes and extreme mental
disturbances."

(Shoecraft, 1971)

In 1953 Drill and Hiratzka reported that 2,4-D caused
leukopenia (decreased production of new blood cells). In
1957 Sellman reported ataxia (an inability to co-ordinate
voluntary muscle movements) and coma ( a state of profound
unconsciousness caused by disease, injury or poison).
The most widely cited study of acute and subacute effects
on humans is that done by a group of doctors at the Mayo
Clinic. They reported on three cases of 2,4-D poisoning:
(1) A 52 year old farmer spilled 60 cc. of 10# 2,4-D
on his forearms. He experienced fatigue, nausea and vomiting.
Two months later he accidentally wetted his legs with 2,4-D
while spraying, and experienced the same effects along with
diarrhea. This was followed by pain and numbness in the ex­
tremities, and six weeks later, inability to walk. Two years
later he still complained of numbness in feet and fingers
and the inability to move his toes and aching feet.
(2)

A 50 year old housewife wet her hands and legs with

a household 2,4-D preparation while spraying dandelions on
her lawn. At the first exposure she experienced swelling and
aching of feet and legs which lasted for around three weeks.
One year later, while again spraying dandelions, she was
similarly exposed. She became agitated and depressed, ex­
perienced weakness, rashes, numbness in the extremities, and
the inability to walk.

VI

acute and subacute

illness caused

by p h e n o x y h e r b i c i d e s

So far, we have only looked at severe chronic problems
caused by the widespread use of the phenoxy herbicides:
the
extent to which they are teratogens, carcinogens and mutagens.
But there are also dangers in ordinary use of these herbicides
which are known to produce illnesses that varys according to
exposure and physical health.
Since the phenoxy herbicides are not extremely toxic in
the acute sense of immediate poisoning, for a long period of
time they were assumed to be safe for general use. The
lethal dose for a human is said to be around 80 mg/kg, or for
the average-sized person, around six grams. This is slightly
more than a teaspoon of pure 2,4-D.
There is no question but that human beings are far more
sensitive to 2,4-D than are laboratory mice and rats. Dogs
and monkeys have sensitivity rates that are closer to humans.
In one study done in 1963, tests of 2,4-D on monkeys revealed
the same symptoms of acute illness that have been widely re­
ported in humans.
(Seaburv, 1963)

Early Evidence of Illnesses from 2,4-D

It has been known for quite some time that 2,4-D pro­
duces ill effects in animals and human beings. It 1946
Bucher reported myotonia (muscle spasms), motor disorders,
paralysis in the arms and legs, and gastrointestinal symp­
toms such as vomiting and diarrhea in experimental animals.
Hill and Carlisle reported similar findings in 1947.

4506
0^

4507
^p.^G>o3

V-15
TCDD is one of the most toxic chemicals known to man.
It persists in the environment for long period of time and
has entered the food chain. There is some evidence that it
biocumulates.
When heated (as in burning or cooking) all of the polychlorophenols, including 2,4-D, produce increased amounts of
the various dioxins. This has proven to be a hazard to
people fighting brush and forest fires in treated areas, and
if there are residues could cause a problem when cooking
foods containing any residues of 2,4,5-TP.
Hexa-dioxin, which has been identified in 2,4-D by the
U.S. Department of Agriculture, is very toxic. It was the
cause of the "chick edema factor" in the United States that
killed millions of chickens. It is also a teratogen and
produces chloracne in tests on laboratory animals.
The highly toxic nature of TCDD and HCDD at minute
amounts (the microgram level) reveal the necessity of testing
and monitoring for them in the environment at the parts per
trillion level.

.I

4508

V-14
In rejecting the bid by Dow Chemical Company to re-register
2,4,5-T, the U.S. Environmental Protection Agency cited as
one reason the fact that the herbicide was known to contain
hexa- and hepta-dioxin isomers "which are known to be tera­
togenic."

(U.S. EPA, 1974)

Chickens were also tested for the "chick edema factor".
The pericardial fluid was "markedly increased" when HCDD
was administered in the range of .01 to .1 mg/kg per day.
The general conclusion of the Dow researchers was that
"hexachlorodibenzo-p-dioxin is highly toxic but less toxic
than tetra-dioxin." (Schwetz et al, 1973)
These tests for HCCD, and the others cited for TCDD,
reveal the major shortcoming of the study of dioxins done by
the researchers for the U.S. Department of Agriculture
(Woolson et al, 1972). In the USDA test, levels below .5
ppm were considered "non-detectable", and therefore of no
significance. We know that both TCDD and HCDD are very toxic
at ranges far below that level. For this reason monitoring
for pesticides must be done at the parts per trillion level
to be of any real significance.
Summary
The various dioxins have been found in all chlorophenols,
including the phenoxy herbicides.

The most common dioxin

found in 2,4-D is 2,7-Dichlorodibenzo-p-dioxin, which is con­
sidered to be only slightly toxic.

However, the other higher

isomer dioxins, hexa-jhepta-, and octa-have also been isolated
in commercial samples of 2,4-D.
The most toxic dioxin, tetra-dioxin (TCDD), is an in­
evitable contaminant of 2,4,5-T and 2,4,5-TP (Fenoprop).
TCDD should not appear in carefully controlled commercial
2,4-©..

4509

V-13
During the search for the cause of the "chick edema
factor", new information emerged on the dioxins other than
TCDD.

Firestone found that hexa- and hepta-dioxins are de­

posited as residues in the tissues and organs of rats and
chickens, mainly in the liver.

(Firestone, 1970)

Cross land and Shea report that during this period IICDD
was tested on a variety of laboratory animals and "adverse
effects were found in monkeys, guineau pigs, rats and pigs."
Because of the buildup of HCDD in the tissue of chickens,
in 1961 the U.S. Food and Drug Administration ruled that
commercial fats had to be screened for HCDD before being
placed on the market.

(Crossland & Shea, 1973)

The highly toxic nature of HCDD was demonstrated in
the tests carried out by the research team from Dow Chemical
Corporation. The tests were done on Sprague-Dawley rats, the
strain which has shown the most resistance to the toxicity
of phenoxy herbicides, and chickens. Four rats were used
in the test for acute lethality, and one of two died when
given an oral dose of 100 mg/kg per day. The two which re­
ceived a dose of 10 mg/kg per day did not die, but all four
tested lost body weight.
HCDD was also tested by applying small amounts to the
eye and ear of a rabbit. After 27 days, the eyelid of the
rabbit became encrusted. HCDD also caused chloracne in the
rabbit ear.
The rats were fed HCDD at a rate of between .01 and .1
mg/kg per day; all dosages were "highly lethal to fetuses
during late gestation." At the highest dosage, 79% died.
The weight and length of the surviving fetuses were sig­
nificantly decreased.
At the dosage of .1 mg/kg, the surviving fetuses showed
fetal soft tissue and skeletal anomalies. "The incidence of
cleft palate, subcutaneous edema, vertebrae with split or
unfused centra, and split sternbral was significantly greater
than among control litters or the control fetal population."
(Schwetz et a l , 1973)

4510

V-12
No traces were found in the liver.

(Zitko and Choi, 1972)

The most widely cited study of octa- and hexa-dioxins
is that done by a group of researchers employed by Dow
Chemical Company. Octa-dioxin was fed to Sprague-Dawley rats
and Swiss Webster mice. At the level of 500 mg/kg per day,
"the incidence of subcutaneous edema was significantly in­
creased among the fetal population." Among the litters, 50%
of the treated experienced the same effect compared to 21%
for the control group. OCDD also caused "embryotoxicity"
at the level of 500 mg/kg per day. Hepatic lesions were also
observed. (Schwetz et al, 1973)
The highly toxic nature of hexa-dioxin (HCDD) was dis­
covered in the research that followed the deaths of millions
of commercially raised chickens in the United States in 1957.
The chickens affected had droopy and ruffled feathers and had
difficulty breathing. Autopsies showed fluid accumulation
surrounding the heart, beneath the skin, and in the abdominal
cavity. There was also liver and kidney deunage. Until the
source of the epidemic was found (it lasted into the 1960's),
it was referred to as the "chick edema factor." (Crossland
and Shea, 1973)
The toxic substance that caused the deaths of the chickens
was finally isolated in fats added to commercial poultry
feed. Chlorine was found and was at first suspected. Later
it was discovered that the cause was hexachlordibenzo-p-dioxin
(HCDD). It was believed that the dioxin came from 2,4-D
used on corn from which vegetable oil was processed. Others
theorized that HCDD could have been formed as condensation
from other chlorophenols when the oilseeds were heated. In
either cause, the source was the chlorophenols.
and Shea, 1973)

(Crossland

4511
£>.4kt>7

V-ll
After two years, the amount of dioxin was significantly in­
creased. (Shoecraft, 1971; Doucet, 1977)
Thomas Whiteside recounts how the U.S. government dis­
posed of the twenty-five thousand steel drums full of Agent
Orange left over at the end of the Vietnam war. Because they
had been sitting around in the sun for a long time, the level
of TCDD in the material was very high. As these drums began
to rust and leak, state officials in Mississippi demanded
that they be removed because of the hazard to the environ­
ment and human health. Both California and Oregon refused
to permit the burial of the herbicide in their states at dis­
posal sites.
Eventually, the U.S. Air Force contracted to have the
herbicide destroyed at sea. The Vulcanus, a German-built
ship owned by a company based in Singapore, took the barrels
to Johnston Island. In April 1976, the Vulcanus took the
material out to the middle of the Pacific Ocean, where it
was burned at temperature over 700 degrees centigrade. TCDD
is chemically stable up to that temperature. The drums were
to be crushed and smelted at steel mills, where temperatures
were said to be high enough to destroy the tetra-dioxin.
(Whiteside, 1977)
Hexa- and Octa-Dioxin
Octa-dioxin, which is found in the phenoxy herbicides
and other chlorophenal products, appears to be far less toxic
than TCDD.

In one study done for National Health and Welfare,

rats were fed extracts of octa-dioxin. Residues were detect­
ed in the faeces, liver and adipose tissue. Between 1% and
3% of the total intake was found in the gastrointestinal
tracts of the treated animals.

.4512

V-10
Independent studies had demonstrated that five different
chlorophenols, including 2 ,4-Dichlorophenol, the precursur
and major breakdown product of 2,4-D, formed dioxins, in­
cluding TCDD, when decomposed by heat.

(U.S. EPA, 1974)

Other data by Prof ess orS Baughman and O'Keefe of Harvard
University was presented in the case of C.A.T.S. v. U.S.
Department of Agriculture in Oregon in 1976-7. In an ex­
periment Prof. Baughman produced .1% TCDD by exposing sodium
salts of 2,4,5-T to temperatures of 300-400 degrees cent­
igrade at normal atmospheric pressure. The level of dioxin
generated in burning was greater than that allowed in co­
mmercial 2,4,5-T. The conclusion was that large amounts of
dioxins would be formed by fires in 2,4,5-T treated areas,
with the distinct possibility that the dioxin would be dis­
tributed by smoke particles.
Professor O'Keefe of Harvard University, who along with
Professors Meselson and Baughman had done pioneer work in the
detection of TCDD, reported that TCDD could be generated from
2,4,5-Trichlorophenol when it took the form of a breakdown
product of 2,4,5-T in soil and plants. TCDD could also be
generated from pentachlorophenoxyphenol, an intermediate
breakdown product of 2,4,5-T, when heated by fire.
S., 1977)

(C.A.T.

C.A.T.S. also cited the work by Buu-Hoi and his collea­
gues. These French scientists demonstrated that TCDD was
produced by heating the "purified" commercial preparations
of 2,4,5-T and 2,4,5-TP (Fenoprop).

(Buu-Hoi et al, 1971)

There are other reports that heating increases the amount
of TCDD in commercial formulas of the phenoxy herbicides.
At Phoenix, Arizona the U.S. Forest Service stored a number
of barrels of 2,4,5-TP on a tarmac for two years.

The

4Si

level of tetra-dioxin was measured at the beginning and
after two years. Sitting out in the hot summer sun in
Arizona greatly increased the temperature of the Fenoprop in
the barrels.

^p-J/é,C>9

3

V-9
Unfortunately, they tested only down to .5 ppm.

Most dioxins

are present at more minute levels, and several are highly
toxic at levels far below .5 ppm.
Nevertheless, the study found that one commercial sample
of 2,4-D contained 10 ppm of hexa-dioxin, an extremely high
level. Their sampling also found hexa, hepta and octa-dioxins
in formulations of tri-, tetra-and penta-chlorophenol.
(Woolston et al, 1972)
Heating the Phenoxy Herbicides
A number of studies done in the 1970's reveal that when
the phenoxy herbicides are burned, the heat created by the
fire intensifies the creation of the various dioxins. There
are news reports from California that people fighting brush
and forest fires in areas treated by the phenoxy herbicides
have come down with chloracne. This was also reported by
those who work in the Siuslaw National Forest. (C.A.T.S.,
1977)
Much of what we know about the various dioxins was dis­
covered during the search for the cause of the "chick edema"
problem of the late 1950's and the 1960's. The Agricultural
Research Service of the U.S. Department of Agriculture con­
cluded from all the studies done that "when any chlorophenol
is heated to elevated temperatures it can be converted to a
dibenzodioxin."

(Cowan, 1970)

In May 1974, the U.S. Environmental Protection Agency
presented their pretrial brief on the question of re-regis­
tration of 2,4,5-T for general use. In rejecting the re­
registration, they argued, among other things, that "there is
evidence that the polychlorophenols in 2,4,5-T may decompose
into dioxin (TCDD) when exposed to high temperatures, such
as might occur with incineration or even in the cooking of
food."

V-8

The buildup of TCDD in humans was also reported in a
separate test contracted by the U.S. EPA.

In 1976, they re­

ported that breast milk samples were taken from 1400 women
in 46 American states. The EPA tests showed continued pre­
sence of some of the chlorinated hydrocarbon insecticides.
But it also showed TCDD residues that "exceed the acceptable
daily intake levels established by the World Health Organ­
ization." A separate study done by the New York Department
of Health found pesticide levels in women's milk 5 to 10
times higher than average if they had been regularly eating
fish from Lake Ontario (Globe 8c Mail, September 29, 1977)
The Dioxins in 2,4-D
Dr. Samuel S. Epstein, who has served on the Mrak Co­
mmission and other advisory committees to the U.S. Depart­
ment of Health Education and Welfare, pointed out in his test­
imony before Senator Philip Hart's Subcommittee in 1970 that
2,4-D and its precursor, 2 ,4-Dichlorophenol, have been shown
to contain dioxins. Hexa, hepta and octa-dioxins have been
identified in 2 ,4-Dichlorophenol.

(Epstein, 1970)

Professor Gordon W. Gribble of Dartmouth College suggests
that the most likely dioxins in 2,4-D would be 3,8-DCDD or
1,3,6,8-TCDD. Both of these would be less toxic than 2,3,7,
8-TCDD. Further chlorination of 2,4-D can produce the
higher isomer dioxins. (Gribble, 1977)
The most widely cited study of dioxins is that done by
the Plant Science Research Division of the U.S. Department of
Agriculture in 1971.

They examined 129 samples of 17 diff­

erent pesticides derived from the chlorophenols.

IMfc"
4515

V-7
Where Agent Orange was used in Vietnam, measureable amounts
of TCDD have persisted in the Environment several years
after the final spraying. (Sterling, 1974)
Professors Meselson and Baughman of Harvard University
tested fish and crustaceans caught in Vietnam for human con­
sumption. In 1972, three years after the final herbicide
spraying, residues of TCDD were found. This study demon­
strated that TCDD was entering the food chain. (Baughman and
Meselson, 1973; Galston, 1974)
In 1973 the U.S. Environmental Protection Agency reported
a test involving beef cattle. They were fed diets contain­
ing 100 to 1800 ppm of 2,4,5-T containing .6 ppm of TCDD for
28 days. Their fat and liver retained substantial amounts
of the TCDD. (U.S. EPA, 1974)
There is evidence to suggest that at least 25# of the
dietary intake of tetra-dioxin may be stored in the body
tissue. The Pretrial Brief of the U.S. Environmental Pro­
tection Agency on the re-registration of 2,4,5-T reports one
study where rats were fed 20 ppb TCDD; 75% of the total re­
tained residue was stored in the liver. In another study
cited, 2,4,5-T containing only .04 ppm of TCDD was sprayed
on rangeland and then cattle and goats fed on this area.
Their fat revealed between 6 and 41 ppt of TCDD. (U.S. EPA,
1974; U.S. EPA, 1975)
Research done by Harvard Professors Meselson, Baughman
and O ’Keefe in 1976 found TCDD residues in samples of mother’s
milk taken in San Angelo, Texas and Siuslaw Forest, Oregon
where there had been aerial spraying of phenoxy herbicides.
They also found TCDD sample in bovine milk and fat samples.
(Meselson et al, 1976)

<y

0'

4516

V-6
Earlier, researchers with the U.S. Department of Agriculture
warned that "the presence of such highly chlorinated com­
pounds in the food chain is of concern because these com­
pounds are generally fat soluble and nonbiodegradable, tend­
ing to concentrate in the food chain, and many of them are
acutely toxic and even carcinogenic." (Pohland and Yang,
1972)
Early research indicate«/that TCDD could accumulate on
bare surface soil and water. (Crosby et al, 1971) A later
study revealed that when 1 ppm of tetra-dioxin was applied
to two types of soils, after 350 days 54% of the original
TCDD remained. At a higher dosage (100 ppm) 71% was recover­
ed after 350 days. (Kearney et al, 1973) Professor Streisinger comments that "the fate of the 50% that 'disappears'
is not known and the possibility of transformation into other
toxic substances needs to be investigated."

(Streisinger, 1976)

In one laboratory study, rats were administered TCDD
five times a week over a period of 13 weeks; the amounts that
were measured in the liver and fat appeared to increase
steadily up to 7 weeks, when measurements were stopped.
et al, 1976)

(Rose

The U.S. Airforce carried out some tests of its own on
various species of rodents and birds in a testing area which
had been sprayed with the phenoxy herbicides. These species
contained residues of TCDD which were higher than the levels
present in the environment.

(Streisinger, 1976)

Dr. Theodore Sterling of Simon Fraser University des­
cribed the dangers of TCDD in the environment in his brief
presented to the B.C. Royal Commission Inquiry into the Use of
Pesticides and Herbicides (1975). He reported that studies
show that TCDD "clearly is persistent and biocumulative. In
general, it resists microbiological deterioration."

4517

V-5

At the same trial, Professor George Streisinger argued
that the U.S. Forest Service was "negligent in failing to
emphasize the possible danger from mutagenic effects of the
herbicides, especially in light of the evidence from the tests
that have been performed in this area." They also failed "to
indicate that herbicides that are mutagenic are likely to be
carcinogenic as well: it has been shown that a large majority
of the chemicals tested that are mutagenic are also carcin­
ogenic." Similar warning came from Dr. C.D. Dewse in an
article in the British medical .journal, The Laucet. (Dewse,
1976)
Professor Arthur H. Westing, a member of the AAAS
Commission that studied the effects of phenoxy herbicides in
Vietnam states: "until new developments alter the current
situation the use of TCDD dioxin-contaminated herbicides pre­
sents an unacceptable risk to man and his environment."
(Skopill, 1977)
Persistence of TCDD in the Environment
Evidence to date

indicates that the phenoxy herbicides

and their dioxin contaminants may pose a threat to the en­
vironment as great as the chlorinated hydrocarbon insecticides.
There is evidence that the dioxins persist for a long time and
that they biocumulate.
The U.S. Environmental Protection Agency took samples of
animal tissues in the Siuslaw National Forest in 1973 and 1974
and they found TCDD residues, presumably from spraying of 2,4,
5-T and/or 2,4,5-TP (Fenoprop). This was confirmed by sub­
sequent tests conducted by Dr. P. O'Keefe of Harvard University.

4518

V-4
Allen and Norback reported in 1973 that TCDD fed to rhesus
monkeys resulted in changes in the kinds and growth patterns
of cells in the stomach, and changes in the kinds of cells
and secretion of the oils in the skin which formed chloracne.
(Skopill, 1977)
In more recent tests, eight female monkeys were fed a
daily dose of 500 npt of TCDD. All developed anemia and five
of the eight died. They had an almost complete lack of red
and white blood cells.
In another experiment, Allen fed rats 5 ppt of TCDD daily
for 18 months. Of the 60 treated animals, 23 developed can­
cerous tumours. Dr. Allen and his colleagues concluded that
"the possibility that dioxin (TCDD) is a potent promoter of
cancer rather than an inducer cannot be overlooked." (Whiteside, 1977; Cox, 1977)
Virgil C. Boekelheide, Professor of Organic Chemicstry at
the University of Oregon, has stated that
TCDD is fantastically toxic and is commonly quoted as
being the most toxic simple organic molecule known to
man . . .
At sublethal dose levels it still has highly
toxic effects on thymus, liver and other organs, as well
as being extremely teratogenic. Thus, minute quantities
of TCDD well below the acute lethal dose level have
adverse toxic effects and a threshold limit, below which
no toxic effects occur, has never been demonstrated for
TCDD. (Skopill, 1977)
The Chairman of the Laboratory of Pathology at the
Oregon Regional Primate Research Center, Dr. Wilbur P. McNulty,
Jr., has done research on the effects of TCDD on rhesus
monkeys. He suspended his experiments after he discovered
how extremely toxic TCDD was to primates. In the C.A.T.S.
case against 2,4,5-T in Oregon, he testified that "it is my
opinion that the deliberate environmental distribution of
TCDD or products known to contain TCDD at any level causes a
serious threat to human and animal health."

K

V-3
However, those most often identified in the phenoxy herb­
icides are tetra-dioxin (four chlorine atoms), hexa-dioxin
(six chlorine atoms) hepta-dioxin (7 chlorine atoms) and
octa-dioxin (eight chlorine atoms). (Epstein, 1970)

The Extreme Toxicity of Tetra-Dioxin
Arthur W. Galston, Professor of Botany at Yale Un­
iversity, describes TCDD as "one of the most poisonous
chemicals ever synthesized by man." The Science Policy
Division of the U.S. Library of Congress reports that 6
milligrams (or one drop) of TCDD is enough to kill 1200 human
beings.
(U.S. Library of Congress, 1974)
The acute oral dose (LD^q ) for male guinea pigs has been
established in a laboratory tests at .005 mg/kg, and in male
and female rats at .0225 mg/kg and .045 mg/kg respectively.
(Epstein, 1972) Pregnant hamsters were fed .009 mg/kg
tetra-dioxin in one laboratory study; 82# of the fetuses were
killed, and of those born, 82# were deformed. For rabbits,
a dose of .01 mg/kg killed all the animals; a lower dose of
.001 mg/kg resulted in chloracne and liver damage. In a study
by Dow Chemical Company, an application of .0003 mg on the
ear of a rabbit produced chloracne. Dow researcher L.C.
Silverstein reports that less than .01 mg on a surface wipe
sample creates an acute hazard to man. (Crossland and Shea,
1973)
The most widely publicized studies in recent years are
those done by Dr. James R. Allen and his colleagues of the
University of Wisconsin Medical School.

In 1967 Allen and

Carstens reported that repeated feedings of low levels of TCDD
to monkeys resulted in their deaths over periods of more than
445 days.

The lowest amounts of TCDD tested were lethal.

Iio

4520

V-2
This process yields 2,4,5-Trichlorophenol and tetra-dioxin.
The latter is considered an unwanted pollutant but occurrs
inevitably in the process. As the temperature rises, more
tetra-dioxin is formed. 2,4,5-Trichlorophenol is then
treated with sodium chloroacetate and an acid to yield 2,4,
5-T.

(Gribble, 1974)
In theory, TCDD should not be present in 2,4-D.

The

chemical phenol is chlorinated at temperature between 80 and
100 degrees contigrade. At these relatively low temperatures,
it is argued, TCDD should not be formed. The Plant Products
Division of Agriculture Canada wrote in February 1977 that
they had analyzed the Aqua-Kleen formulation of 2,4-D for
TCDD down to a level of 5 ppb and found no dioxins. However,
they also noted that "the laboratories are just now developing
the capability to analyse for the other dioxins ..."
(Agriculture Canada, 1977) (Advisory Committee, March 25, 1977)
In a pamphlet released by the B.C. Department of the En­
vironment in July 1977, it was claimed that "TCDD is not pro­
duced during the manufacture of 2,4-D." No mention was made
of any other dioxins.
1977)

(B.C. Department of the Environment,

Dow Chemical Corporation , while admitting that

commercial preparations of 2,4,5-T and 2,4,5-TP (Fenoprop)
contain TCDD, states that "there are no dioxin contaminants
in the 2,4-D materials which we sell." (Dow Chemical, 1973)
However, the chlorophenols also produced a number of
other dioxins. They differ according to the number of chlo­
rine atoms that are attached to the two benzene rings (see
Figure 2). There are eight positions where chlorine atoms
can be attached to the basic dibenzo-dioxin structure; thus,
depending on the orientation of the molecule, there is a
possibility of 60 different dioxins.

'V -H ti’i

4521

V

DIOXINS IN PMENOXY HERBICIDES
On July 10, 1977 an industrial accident at the Sevesco,
Italy plant of Hoffmann-LaRoche released a deadly cloud of
tetra-dioxin (TCDD) over the local valley. The news of the
horrible disaster spread around the world, even warranting an
article in Maclean’s Magazine, July 25, 1977. The regional
health officer in Italy called it "our own little Hiroshima",
and once again the world began to worry about the phenoxy
herbicides.
The Sevesco plant produced trichlorophenol, the chemical
substance from which 2,4,5-T is synthesized. Since the Viet­
nam war, there has been increasing concern over the toxic
nature of the various dioxins, and in particular tetra-dioxin
(TCDD). While the dangers of the dioxins had disappeared from
the headlines following the end of the war in Vietnam, they
have come to public attention following recent encironmental
accidents involving polychlorinated biphenyl (PCB), pentachlorophenal (PCP) and now, once again, 2,4,5-T.
1977)

(Whiteside,

What are the Dioxins?
The Council for Agricultural Science and Technology
(CAST), one of the main public relations organizations for the
use of pesticides, has pointed out that "a highly poisonous
kind of dioxin called TCDD is an unavoidable contaminant in
commercial supplies of 2,4,5-T and Silvex (2,4,5-TP)".
(C.A.S.T., 1975)
In the manufacture of 2,4,5-T, the chemicals 1,2,4,5-Tet/
rachlorobenzene and sodium hydroxide in methanol are heated "at
around 160 degrees centigade.

•

4522

VII-9
Populations of Cardinals, Jays, Tanagers and Bewick's Wrens
were eliminated entirely. Ducks, geese and chickens being
raised in the area failed to hatch any young. The one gosling
which did hatch, developed pneumonia, was paralyzed and
spastic and finally died. Major infestations of gall insects,
brown beetles and other species followed the applications
(Shoecraft, 1971). Other residents in the area reported un­
usual sightings such as quail, a fox, rabbits and dogs all
milling around in the same area without paying any attention
to each other. Normal instincts it appears were suppressed.
Much dead wildlife was reported in and around the spray area.
These included several species of birds, skunks, fox and
bobcats (Shoecraft, 1971).
2,4-D And Agriculture
2,4-D is being used extensively in agriculture in both
Canada and the U.S.
With labour and energy costs rising
rapidly, it is not unusual to find that farmers are sub­
stituting the extensive use of herbicides for these two
factors of production. With 2,4,5-T restricted from ag­
ricultural use, 2,4-D becomes the least cost acceptable
alternative in much of Canada.
We still know very little about the long term effects
of the continued use of herbicides on food crops. With sub­
stantial amounts of 2,4-D being applied in the lake systems,
it is likely that some of the chemical will find its way into
orrigation systems.

It is well known that grapes are par­

ticularly susceptible to herbicide damage. (Pimentai, 1971)
The B.C. Government's Advisory Committee on weed control was
concerned about this problem and recommended that tests be
Horducted on grape seedlings during the 1977 programme
Advisory Committee, March 25, 1977).

4523

VII-10
It was reported that the damage to vinyards in eastern
Washington became severe during the period from 1970 to
1974 due to the herbicide concentrations in the atmosphere.
Experimentation has shown that "a dosage of lppb 2,4-D in
air during a 6 hour period each week for a total of ten
applications can cause a yield reduction in grapes of 50%.
Furthermore, Concord grapes can be severely malformed from
the application of 0.1 ng of 2,4-D to the leaves" (Farwell,
et. al., 1976). In an effort to reduce the damage to the
grape crops, even the low volatile 2,4-D esters (such as
Butoxyethanol) have been restricted from use for the period
from May 16 to October 31 each year in eastern Washington
and Oregon.
The effect of various dosages of herbicides on most
crops is still not well understood even though some test re­
sults may be available. Fruit tree flowering and fruit
production abnormalities have been reported following spray
drift in both Arizona and Vietnam. In the latter case, trees
produced no flowers or fruit for at least three years after
contamination. Following an examination of damage done to
jack fruit, manioc and guava trees as well as field vegetables,
it was reported that the Vietnamese Ministry of Agriculture
found the destruction so great "that adequate financial com­
pensation to the owners of damaged trees would probably be
impossible" (Shoecraft, 1971; Orians & Pfeiffer, 1970).
On the Robbin Warren farm near Granville Island, Nova
Scotia, market garden crops showed highly abnormal growth
patterns following herbicide spray drift contact. Corn yields
dropped drastically and celery and cauliflower bolted to four
and six feet high. The government later compensated Mr.
Warren for this damage (Ogden,

1971).

’ 4524

VII-11
Kimmins discusses the effects of herbicides on flowering
crops. He points out that "there can be a reduction or al­
ternation in the number, size and shape of flower parts, and
there may be a differential effect on organs of different sex.
There can be a multiplication or reduction in flower number
and earlier flowering can be stimulated. The resulting fruit
may be larger due to increase in cell volume, but the shape
of the fruit may be aberrant if the concentration of herbicide
within the fruit is uneven" (Kimmins, 1975).
Quite obviously, a substantial amount of damage could be
done to fruit and vegetable crops should the chemical get into
the irrigation systems of the valley during regular applications
or through human error. There appears to be no information
available on the effect of small amounts of herbicide on the
growth patterns of dward fruit trees. It would be unfortunate
if the dwarf orchards which have been planted extensively in
the Okanagan Valley grew to standard size.
Research is just beginning into the genetic effects of
repeated 2,4-D applications near grain crops. Herbicide use
on the prairies is skyrocketing with the institution of the
"zero tillage" concept. This method involved the elimination
of plowing through an early spring herbicide treatment of new
vegetation. The seed is then drilled directly into the sod.
This method is thought to conserve soil moisture and topsoil
while resulting in reduced costs by the elimination of plow­
ing (McCalla, et. al., 1962).
Genetic alterations have been observed, however, which
may have serious implications for crop yields and quality in
areas of continuous hebicide use. As early as 1951, it was
discovered that barley and wheat plants showed abnormal cell
division after being sprayed with 2,4-D at various stages of
growth.

4525

VIÏ-L2
This effect persisted for a considerable length of time after
the applications (Unrau, 1953, 1954; Unrau & Larter, 1951).
Chromosomal defects in herbicide treated peas were reported
following testing (Hyhling, et. al., 1960). As genetic
defects are carried from one generation to the next, damage
done to crops through successive herbicide applications could
last indefinitely.
The zero tillage approach to cultivation could also
have an effect on seed germination rates as herbicide res­
idues build up in the soil and atmosphere. During the test­
ing of the effects of the vapors of various 2,4-D formulations
by Dow Chemical's Biochemical Research Laboratory, it was dis­
covered that the seed germination rate was decreased signif­
icantly by the highly volitile esters. The methyl, ethyl and
isopropyl esters caused a complete germination failure of
turnip, squash, radish and muskmellon seeds. The methyl and
ethyl esters produced success rates of 22% and 41% for wheat
while the control group rate was 92%. For rye, 40% of the
controls sprouted while none germinated after exposure to
these same two esters. The following effects of 2,4-D were
observed during the experiments:
"a) the embryonic plants failed to break
through the seed coats; b) the seedlings
emerged but failed to grow; this was usually
accompanied by abnormal swellings on the
seedlings, and in this case the roots often
did not develop properly; c) leaf modifica­
tion of the young leaves after emergence;
leaves showed typical malformations such as
are caused by 2,4-D when applied as a spray;
d) stunting of seedlings and a slower germ­
ination of the seeds; this might or might not
be accompanied by leaf modification" (Mullison
& Hummer, 1949).
Swelling of the stem sections (callus growth) was also
reported in a study done on 2,4-D treated bean plants (Bach &
Fellig, 1961).

4526

VII-13
There is certainly some evidence to indicate that seed germ­
ination rates and early seedling development may be affected
when seeds come into contact with this herbicide.
Dr. A.B. Carvers of the University of Ontario reports
that some weed species are becoming resistant to herbicides
(Doucet, 1973). This is a classic pesticide response. Often,
while the target species develops an immunity to a chemical,
other nontarget species which may be predators or competitors
are sharply reduced in numbers. The result is an explosion
of the pest population which cannot be stopped by the use of
chemicals.
Poisoning of cattle and other grazing animals has been
associated with herbicide applications in British Columbia,
Nova Scotia, Arizona, New Mexico and Vietnam. These incidents
have resulted from either the acute toxicity of the chemical
or from the high nitrate levels in plants after herbicide
treatment.
Until recently, it was assumed that the lethal dose of
2,4-D for cattle was between 500 and 2,000 mg/kg of body
weight.

Following an accident in Australia,

this level

should be revised downward to 150-188 mg/kg for a fatal
dose and 105-132 mg/kg for a toxic dose. Of the two cows
poisoned, one died within 12 hours while the other exhibited
signs of depression, loss of appetite and muscle weakness
which resulted in an inability to stand (McLennan, 1974).
It is difficult to determine if it is possible for
grazing animal poisoning to take place as a result of normal
applications. Studies have shown that forage in areas just
treated would contain about 100 to 150 ppm for each pound
of herbicide applied per acre. It would seem, however, that
while fatal poisoning is not likely, except in cases of
accident, other problems may develop.

In tests conducted

on sheep and cattle which had been fed 2,4-D in concentrations
ranging from 300 to 2,000 ppm residues were found in their
internal organs as well as fat and muscle.
£>~Yfca3

4527

VII-14
The most substantial amounts were located in the kidneys
(Clark, et. al., 1975)

Beside the possibility of outright

poisoning, grazing animals could contain enough herbicide
residues so as to complicate marketing.
An increased nitrate level in treated forage can combine
with a generally increased palatability to present a problem
for livestock and wildlife. Exactly why some plants become
preferred by animals after spraying is still somewhat of a
mystery although increased protein and mineral content may
play a part (Kimmins, 1975; Maxwell & Harwood, 1960). Herb­
icide applications are known to raise the hydrocyanic acid
levels of sudan grass and cherry leaves (Kimmins, 1975). It
is not surprising then to find that on Robin Warren’s Nova
Scotia farm, where herbicide spray drift occurred, the
cyanide levels were relatively high. An analysis of damaged
brussel sprouts showed 52 ppm of cyanide, while butchered cow
meat had 52-56 ppm and an aborted calf's liver showed 5 ppm
of the poison (Ogden, 1971). Again, marketing problems would
develop for this produce. There are varying theories as to
how long livestock should be kept off treated range. They
range from one week to two years, depending on the herbicide
used and the climate.
As mentioned earlier, herbicide applications have re­
sulted in insect population explosions and consequent damage
to trees and plants. It is also thought that the chemicals
damage the defense mechanism which have been established by
plants against insect attack. In tests conducted on corn
which had been sprayed with 2,4-D, the treated group showed
1,679 aphids per unit of plant mass, while the untreated
cornstalks had 618 aphids.

The sprayed group had a 28% in­

festation rate of corn borers versus 16% for the unspraved.
Borers in the herbicide treated corn were larger and pro­
duced larger eggs (Oka & Pimentel, 1976).

4528

VII-15
In another experiment, pea aphids were placed in a
cage with broad bean plants. Population increases between
the treated (with 2,4-D, dimethyl amine) and untreated
plants ran as high as 450# and averaged 81.9# (Maxwell &
Harwood, 1960).
Other reports indicate that aphid populations in New
Brunswick exploded after 2,4-D applications. It was thought
there that the predator ladybird larvae were killed and de­
formed, and pupation was delayed (Rudd, 1964).
Beside insect deunage to crops, some plant pathogens are
known to increase after 2,4-D applications. Oka and Pimentel
noticed an increase in the incidence of southern corn leaf
blight during their tests (1976). Another major study on
interactions between herbicides and plant pathogens indicated
that fungi on tomatoes and wheat, viruses on beans, tobacco,
cucumber and cotton and nematodes on oats are all increased
by applications of 2,4-D (Katan & Eshel, 1973).

It is quite

clear that the use of herbicides on or near crops can have
a definite effect on overall plant health and therefore, on
yield and quality.
Summary
As a biocide, 2,4-D acts to kill members of the broadleafed plant community. However, because of the complexity
of the ecosystem in which it operates, the effects of this
chemical can be wide ranging involving many nontarget species.
Fish populations can be reduced both directly through poison­
ing and indirectly by the reduction of habitat and increasing
susceptibility to disease and predation. Birds as well risk
damage to their health and reduced breeding viability. Other
forms of wildlife have been damaged when herbicide applications
destroyed homes and contaminated their food supplies.

4529

VII-16
2,4-D has been used on or near food crops for many years.
Grapes are known to be particularly susceptible to the herbicde damage and fruit trees can experience flowering problems.
Genetic damage has been noted after exposure to this chemical
of several plant species. Germination rates can be seriously
suppressed and resistance is developed by some weed species.
Both herbicide and associated nitrate poisoning of grazing
animals has been documented. Insect pests have been shown to
increase in 2,4-D treated crops and some plant diseases may
be more prevalent. In general, 2,4-D reduces the overall
health of the environment to which it is applied.

4530

VIII
THE PERSISTENCE OF 2,4-D IN THE ENVIRONMENT
Considerable concern has been expressed over what
happens to 2,4-D when it is put into a lake system. We
know that the provincial government has announced plans for
a five year programme for an "all-out attack" on Eurasian
water milfoil weed. If we look at the experience of the TVA,
then there is a good possibility that once the provincial
government becomes dependent on the use of herbicides for
control of milfoil, it will continue the programme in­
definitely.
The other major concern is the fact that the phenoxy
herbicides are based on benzene and chlorine, and other pest­
icides and chemical products with these two substances as
their base persist in the environment for a long time.
are biocumulative.

Many

The Position of the Provincial Government
In 1977 spokesmen for the government of British Columbia
and the City of Penticton repeatedly stated that 2,4-D breaks
down into harmless products in a matter of four or five days.
Skaha Lake beach was closed on June 23, 1977 following the
application of 2,4-D in the swimming area; but it was re­
opened the July 1st weekend in order to accomodate the influx
of tourists. At that time the public was told that tests
showed that there were "no detectable levels" of the herb­
icide in the beach water.
The three Interim Reports of the Advisory Committee on
the Control of Eurasian Water Milfoil say very little about
what happens to 2,4-D when it is put into the lake system.
The Second Interim Report (p. 9) states that 2,4-D will be
broken down by micro-organisms in lake bottom mud between
35 and 65 days, the rapidity of the breakdown depending on
whether or not the area has been previously treated with 2,4-D.

4531

VIII-2
The report also concludes that the milfoil tissue will
absorb and "metabolize" 2,4-0.
March 25, 1977)

(Second Interim Report,

The Third Interim Report of the Advisory Committee was
issued after public meetings were held in the larger pop­
ulation centres of the Okanagan Valley. At these meetings,
widespread opposition to the use of 2,4-D was expressed by
local residents.
The final report of the Advisory Committee claimed that
"the level of 2,4-D in potable water would be around zero,
but no higher than 0.0002 ppm when water is drawn from
Okanagan Lake for the first few days after herbicide
application." (Third Interim Report, May 25, 1977)
At the public meetings, the members of the Advisory
Committee reiterated the recommendations of their reports:
(1) no herbicides should be used within 500 metres of any
water intakes, and (2) mechanical methods of control should
be used in public recreation areas. The public was assured
that these two precautions would preclude the possibility of
human exposure to the herbicide.

Persistence in Water
Under ideal conditions, 2,4-D is broken down by chemical
and biological action. Exposure to sunlight increases the
degradation process. However, where actual field tests have
been monitored, it appears that all the phenoxy herbicides
can persist in the environment for quite some time.

4532

VIII-3
In the Tennesse Valley Authority water system, 2,4-D has
been used to control Eurasian water milfoil weed since 1961.
In their Environmental Statement, they record average levels
for Guntersville Reservoir during 1969. Three months after
application of the herbicide, residues were still found to
average in surface water at .042 ppm. Plankton had levels
at 1.1 ppm, and in the sediment it was .35 ppm.
Between April 1 and June 26, 1969 they monitored 2,4-D
residues in raw water at eleven water treatment plants on
Guntersville Reservoir. Five of the eleven water treatment
plants recorded 2,4-D levels in the raw water at above the
.1 ppm level set by the U.S. Environment Protection Agency
as a maximum permissible concentration. At the North Marshall
water treatment plant, 2,4-D residues in water reached the
very high level of 5.9 ppm. Even after water treatment
by coagulation, sedimentation, filtering and carbon treat­
ment, 2,4-D residues were at a 5.8 ppm level. This report
suggests that traditional water treatment systems do not
remove 2,4-D.
The TVA concludes that 2,4-D "persists in sediments
less than 1 year." However, they note that "significant
concentrations of 2,4-D" were found in some sediment samples
up to 10 months after treatment.

(TVA, 1972)

In the most widely cited study on 2,4-D residues in
the TVA system, Smith and Isom (1967) report that 2,4-D was
present in sediment samples 10 months after treatment. In
one test, the sediment reading was 58.8 ppm. In addition,
they report that 2,4-D residues were found in milfoil weed
24 months after application, at a rate of 8 mg/1.
also Wojatalik, 1971)

(See

4533

VTII-4
J.H. Patterson of the Canadian Wildlife Service found
that application of 2,4-D to marshy areas can result in
long persistence of the herbicide in outlet streams. The
Alberta Conservation Authority has also suggested that wet­
lands could act as a herbicide sink.

(Patterson, 1974)

Another researcher has pointed out that repeated applications
of a non-persistent pesticide makes that pesticide last in
the environment as long as a single dose of a pesticide
like DDT. (tfolling, 1971)
Higher Risks in Water
There seems to be general agreement that there are
greater dangers to using herbicides in water than on terres­
trial plants or soil. The herbicides move with the water
currents, carrying it far from the target area. (Mitchell,
1974) The U.S. Government, in its manual on disposal of
pesticides, warns of the "intimate interconnection between
ground and surface water." They report on tests conduced by
the U.S. Government which found pesticide residues in 60%
of the samples taken from wells. (U.S. Working Group on
Pesticides, 1970)
We have found a number of cases which illustrate that
the phenoxy herbicides persist far longer in the environment
than many people are willing to admit. In the ground water
in Colorado, phenoxy herbicides were found seven years after
the last spraying.

(Walker, 1961; Ogden, 1971)

In 1965

the U.S. Department of Agriculture conducted a herbicide
residue survey in 6 different areas in the United States,
and they found 2,4-D residues in all areas. (Shoecraft, 1971)

4534

VIII-5
In Globe, Arizona tests showed residues in soil as
long as six years after spraying. Samples of water taken
several weeks after spraying were tested by the Arizona
Department of Health; they all revealed phenoxy herbicide
residues. One sample, tested over one year later, still
showed almost 100 ppm of 2,4,5-T. (Shoecraft, 1971)
In another well-known incident, the U.S. Forest Service
sprayed the Cleveland National Forest in California with
2.4- D as part of a tree management programme. The herb­
icide worked its way through the soil and into the San
Gabriel River. It ended up in the reservoir system at Mont­
ebello, which supplies water to Los Angeles. Five years
later, 2,4-D residues were still detectable. In June 1973
it was still being found in the Morena Reservoir at a level
of .27 ppb. (Shoecraft, 1971; U.S. EPA, May-June, 1973)
Recently it was discovered that an industrial plant
in the Edmonton area was leaking 2,4-D into the North Sask­
atchewan River. Tests done by Environment Canada found
2.4- D in the river as far away as Deer Creek, Saskatchewan.
In addition, K.W. Reid, Chief of Fisheries and En­
vironment Canada's Water Quality Branch's Western and
Northern Region's office, reported that tests show "low
concentrations of 2,4-D in water almost everywhere we have
water even if the water is far from any agricultural areas."
He concluded that if the source of this 2,4-D is water trans­
port, "it would indicate that the herbicide is relatively
resistent to total degradation."
22, 1977)

(Letter to S.O.E.C., Sept.

It is well known that 2,4-D in the ester formulation
is very volatile and enters the atmosphere as a pollutant.

V-4t>3l

VIII-6
It has been reported that in Alberta it has caused
damage to crops and shelter belts. (B.C. Royal Commission,
1975) In Washington State, grapes have experienced damage
from 2,4-D spray drift miles from the application. (Otta,
1974) a recent study in Saskatchewan found significant con­
centrations of herbicides in the air in spring when grain
farmers are spraying to kill weeds. (Sask., 1977)
In 1969, the U.S. Environment Protection Agency tested
for 2,4-D residues in wheat and soils in 16 different states.
Where herbicides had been used, 20% of all soil samples showed
2.4- D residues. In wheat samples, 8% had residues between
.001 and .004 ppm. (Gowen et al, 1976)
2.4- D Residues in Humans
There is growing evidence that 2,4-D and the other
phenoxy herbicides are not entirely eliminated from the
human body, as claimed by some officials. Dr. E. Stanton
Maxey, Diplomat of the American Board of Surgery, reports
that tests done on farm workers in Florida who had de­
veloped cancer revealed residues of 2,4-D, 2,4,5-T and
2,4,5-TP in tissues. (Maxey, 1974)
Following the spraying of Globe, Arizona by the U.S.
Forest Service, Mrs. Billie Shoecraft had tests done on her
own tissue. They revealed residues of 2,4-D and 2,4,5-TP.
Ten years after the spraying ended Mrs. Shoecraft died of
cancer. A biopsy of her tissues revealed residues of both
phenoxy herbicides. (Shoecraft, 1971; Doucet , 1977)
Several people living in the Siuslaw National Forest
in Oregon had their blood tested in 1972 at GHT Laboratories
in Brawley, California, after their area was sprayed with
phenoxy herbicides. Their blood samples revealed between
.078 ppm and .11 ppm of 2,4-D and between .006 ppm and .03
ppm of 2,4,5-T.

.(GHT Laboratories, 1972)

4536

VIII-7
The Breakdown of 2,4-D
There have been a fair number of laboratory and field
tests done on the behaviour of 2,4-D in a water environment.
The consensus is that (1) "water as a carrier seems to in­
crease the volatility of 2,4-D" (Paris and Lewis, 1973) and
(2) that "aquatic environments are less favourable for
2.4- D degradation."

(Hirst and Bank, 1971; Patterson, 1973)

Degradation of 2,4-D takes place through several pro­
cesses. Partial metabolism occurs in the plant through
hydrolysis and decarboxylation, with the main breakdown
product being
2,4-Dichlorophenol. However, as the plant
dies the process ceases, leaving some 2,4-D and the break­
down products. The TVA notes that "a small amount of the
2.4- D absorbed or adsorbed by the watermilfoil may be re­
leased as it decays, but the levels in the water resulting
from such releases would be much lower than the levels when
the herbicide was applied."

(TVA, 1972)

It is also reported that 2,4-D degrades through
photolysis (decomposition by sunlight).

The main products

here are also the chlorophenols. (Plimmer and Klingebiel,
1971) Two other laboratory studies also reported that
2.4- D broke down when exposed to ultraviolet light; in both
cases the primary degradation product was 2,4-Dichlorophenol.
(Aly and Faust, 1964; Mitchell, 1961)
The other form of breakdown is by micro-organisms.

The

spokesmen for the B. C. Department of the Environment re­
peatedly claim that 2,4-D is quickly degraded through this
process.
claim.

However, existing studies cast some doubt on this

'P-^633

4537

VIII-8

In 1964, Aly and Faust demonstrated that the butyl ester
of 2,4-D was biologically degraded to 2,4-D and butyl alcohol,
but only the alcohol was oxidized further, not the 2,4-D.
The most widely cited study is that done by Schwartz in
1967. He found that under normal water supply conditions,
2,4-D was strongly resistant to chemical attack, and very
little of the herbicide was absorbed onto suspended mineral
solids. The microbial breakdown of 2,4-D was slow; over a
period of between 3 and 6 months, no more than 37% disappeared.
He concluded that in a natural water supply, 2,4-D would not
degrade materially. (Schwartz, 1967)
A second widely cited study was done by Demarco and
associates in 1967; it seems to be most relevant to the
Okanagan situation. They found that the biological break­
down of 2,4-D was greatly reduced by a drop in the oxygen
level of the water and the water temperature. (Demarco et
al, 1967) This is consistent with the early study by
Steenson and Walker (1957) on 2,4-D breakdown in soils.
The latter concluded that aerobic conditions were essential
for bacterial decomposition.
Hemmett and Faust (1968) also report that 2,4-D lasts
for long periods of time in cold lake water in which oxygen
has been depleted. They claimed that 2,4-D lasted for more
than six months under such circumstances.
Furthermore, there are indications that 2,4-D may not
break down at all under certain conditions. In May 1974
Robert Wicklund, a marine biologist from Hydrolab Research
Habitat in the Bahamas, and Jim English, a Memorial University
diving engineer, found eleven depressions in Resolute Bay in
the Canadian Arctic.

4538

VTII-9
These depressions were between 30 and 45 feet deep;
the oxygen levels were very low and marine life was non­
existent.

These holes in the floor of the Artie Ocean

had a high concentration of oil and 2,4-D.

Wicklund and

English described their existence as a "microcatastrophe,"
which trapped and killed fish and other slow moving organisms.
(Dotto, 1974)
The Breakdown Products
One of the major shortcomings of the 2,4-D monitoring
programme in the Okanagan lakes in 1977 was the failure of
the B.C. Ministry of the Environment to adequately test for
breakdown products of 2,4-D. The B.C. Royal Commission of
Inquiry into the Use of Pesticides and Herbicides (1975)
noted that for most classes of chemicals, the "degradation
products may be more toxic or more persistent than the
original product." This may be the case with the chlorophenoxy
herbicides, including 2,4-D.
It is widely recognized that the major breakdown
product of 2,4-D is 2,4-Dichlorophenol.

Unfortunately,

there appears to be very little research on the toxic
nature of 2,4-Dichlorophenol and the other breakdown products
of 2,4-D.
As noted before, the chlorophenols which are the
breakdown products of the phenoxy herbicides have a greater
incidence of the higher isomer dioxins, including HCDD
which is known to be quite toxic.

(Woolson, et. al., 1972)

The clearest information on the toxicity of 2,4-Di­
chlorophenol was provided in the Mrak Commission.

VIII-10
Unfortunately, this material appears in Volume III,
which to this date has not been published; therefore, it is
available only as pirated, unpublished zerox copies. The
report by the Bionetics Laboratory lists the teratogenic
nature of 2,4-Dichlorophenol; their tests on mice produced
"significant increase in the number of abnormal fetuses;
half of the anomolies consisted of extended legs." They
also found that "the fetal weights were significantly less
than those of the controls." The Bionetics Research Lab­
oratories report concluded that eight compounds studied were
"hazardous", enough to be classified as "potentially danger­
ous, but needing further study." Among these was 2,4-Dichlorophenol. (Shoecraft, 1971 reproduces the unpublished
report)
FIGURE III

Butyl ester of 2,4-D

(1)

2,4-D

hydroxy
"]
malonic
] — ► alanine
semialdehyae J

[

(10)

(4 ,9 . 1 0 )

► «-chlororauconic acid

3,5-dichlorocatechol 2,4-dichlorophenol

3,5-dichlorocatechol *
/

cis,c£s-2,4-dichloromuconic acid
a-

/

2-chloro-4-carboxymethylene but-2-enolide
(<»-chloro-T-carboxyinethylene-A*-butenolide)
cbloromaleylacetic acid
(7) /
2-chloro-4-ketoadipic
acid
chlorosuccinic acid

&

4-chlorocatechol
\

(5 ,8 )

cM,eM-3-chloromucoinc acid
\
4-carboxymethylene but-2-enolide
(y-carboxymethylene-A“-butenolide)

\
maleylacetic
acid

\
(7)
3-ketoadipic
acid

V .d

succinic acid

succinic acid

Fig. 1. Pathways of microbial degradation of butyl ester of 2,4-D. Numbers are references: (1)_A ly and F aust 1964,
(2) T iedje and Alexander 1969, (3) Steenson and W alker 195/, (4) Bell 195/, (o) Bollac et al. 1968,
(6) Loos et al. 1967, (7) Duxbury et al. 1970, (8) T iedje et al. 1969, (9) Audus 1960, (10) F ernley and
E vans 1959, and (11) E vans and Smith 1954.
SOURCE:

„

454C

Doris F. Paris and David L. Lewis, "Chemical and
Microbial Degradation of Ten Selected Pesticides in
Aquatic Systems, "Residue Reviews, Volume 45, 1973, p.107

VIII-11
The Dangers of Succinic Acid
The final breakdown of 2,4-D as identified by Paris and
Lewis (1973) is succinic Acid. (See Fig.Ill ) . Succinic acid
(2,2-dimethylhydrazide) is widely used as a growth regulator
on fruits and vegetables in North America, including the
Okanagan, where it is known by its brand name, Alar.
The Mrak Commission reported in 1969 that hydrazine
derivatives produced hepatomas in tests with laboratory mice.
The free enzyme liberation of hydrazine causes tumours. (Mrak,
1969; B.C. Royal Commission, 1975)
Another study revealed that maleic hydrazide was also
a mutagen. At the level of 2 mg/ml fed to laboratory mice,
there were chromosome aberrations and inhibition of cell
division. (Nooden, 1970; B.C. Royal Commission, 1975).
New evidence of the carcinogenic nature of the hydrazines
was revealed in March 1977. Dela Toth and Anna Tompa of the
Epply Institute for Research in Cancer, University of Nebraska,
reported to the American Association of Pathologists on the
10-year research into the "Alar group" of chemicals.
Of the hydrazines tested, thirty-six have been shown to
cause tumours of the intestines, blood vessels, lungs, liver,
kidneys breast and the central and peripheral nerve tissues
of laboratory animals. Some of the hydrazines are natural,
found in tobacco and some edible mushrooms, but most of them
are man-made.
The Omaha scientists reported that analysis of residue
levels in fruit from trees that received 1,500 ppm annually
for five years averaged 3.9 ppm.

They concluded that "this

means the population which consumes these fruits and vegetables
is exposed to this hazardous agent."

(Hollobon, 1977)

4541

VIII-12
The Effects of Synergism
Most studies on the toxic nature of chemicals deal with
the single chemical in an isolated situation.

Few are tested

to determine how they actually behave in the real environment.
Furthermore, toxicology tests are usually conducted in re­
lation to a certain non-target species; rarely are they tested
for their effects on a complex ecosystem.
A growing concern in North America is the buildup of
organic pollutants in our waters. How do these chemicals in­
teract? In some cases, different chemicals combine to form
new, toxic substances. In other instances two or more chemicals
co-operate to increase the total effect of the chemical.
This is commonly referred to as synergism.
All the recent surveys done in Canada and the United
States show a buildup of chemical pesticides in our waters.
Professor C.D. Sculthorpe reminds us that few herbicides are
chemically inert; most are constantly intereacting with other
compounds in the water environment.

lie warns that "accumula­

tion may occur in mud deposits, decaying organic matter, or
living tissues."
As an example, Professor Sculthorpe cites the use of
sodium arsenite to control certain water weeds in New Zealand.
Where used, mud, and the weeds themselves, contained high
levels of arsenic residues.

In addition, the treated weed

appeared to develop a resistance to the arsenic-based herb­
icides. He concluded that if accumulation occurs, this
"renders any concept of a safe dosage utterly meaningless."
(Sculthorpe, 1967)

4542

VIII-13
The Formation of New Chemical Compounds
We now have evidence that in water supplies chemicals
can combine to form new and often dangerous compounds. For
example, we know that chlorine interacts with other chemicals
to fora new substances, and in particular chlorinated hydro­
carbons.

The U.S. Environmental Protection Agency studies

of the lower Mississippi River reveal the persistence of
biphenyl, chlorine and a number of benzene compounds. Tests
have shown that in the presence of ultraviolet light, chlorine
and benzene produce Gammoxane and Lindane, both chlorinated
hydrocarbon insecticides.
(U.S. E.P.A., April 1972)
Subsequent research done by the U.S. Environmental
Protection Agency on treated water in 79 American cities
conclusively established that chlorine interacts with
pollutants to form new organic compounds. At Brownsville,
Texas chlorine was found to form dibromochloromethane.
Similar results were found in Miami's drinking water, which
in this case came from underground sources. The amount of
chloroform in all 79 cities increased significantly after
chlorine treatment.
(Haber, 1976)

Chloroform is a known carcinogen.

In July 1977 the U.S. National Research Council com­
pleted their 1,000-page study of water pollutants in the
United States.

Over an 18 month period they identified 161

water-system contaminants; of these, a number were proven
or suspected carcinogens and teratogens, including several
widely used pesticides, 2,4-D and 2,4,5-T. (New York Times,
July 21, 1977)
A similar study was released by the Ontario Ministry
of the Environment in November 1977. Chlorine treatment
of drinking water and sewage was cited as the cause of the
increase in chloroform and several haloforms including
bromodichloromethane, chlorodibromethane, carbon tetrachloride
and ethylene chloride.

4543

VIII-14
All of these are considered dangerous to the health of
humans.
Herbicides and pesticides were found in the water at
treatment plants in Amherstburg, Brantford, Cayuga, Dresden,
Goderich, Guelph, Niagara-on-the-Lake, Pembroke and Toronto.
Aromatic hydrocarbons containing the benzene ring were not
found in the raw matter, yet turned up in the water treated
by chlorine. (Malarek, 1977)
Another ma/jor problem is the buildup of nitrates in
North American water supplies. Since World War II there has
been a fourteenfold increase in the production of chemical
nitrogen^fertilizers, and a 70% increase in sewage nitrogen.
Fertilizer runoff is widely recognized as one of the main
causes of nitrate pollution. (Environment, 1969; Washington
University of St. Louis, 1970)
Within the human body, nitrates combine with certain
bacteria to form nitrites. One effect of nitrites in the
body is the reduction of the ability of the red blood cells
to carry oxygen.

In children this is known as infant meth­

emoglobinemia, a serious disease which can cause death.
(Crossland and Brodine, 1973)
In 1975 Dr. N. Lee Wolfe and Dr. Richard Zepp of the
U.S. Environmental Protection Agency research laboratory in
Athens, Georgia reported on the results of the interaction of
the herbicide Atrazine (a triazine compound) with nitrates
which are common in water supplies near agricultural areas.
Studies of drinking water in Iowa and Louisiana found that
Atrazine interacts with the nitrates from fertilizer runoffs
to produce N-nitrosoatrazine, a known carcinogen.

This is

the same problem caused when sodium nitrite, used as a meat
preservative, is heated.

(Prevention, November 1975)

4544

VIII-15
Atrazine, as well as other triazine herbicides, are
used in British Columbia, particularly along road and rail­
way rights-of-way.

(See Table II).

Intensifying Pesticide Toxicity
While there has been a rather general lack of research
done on the subject of synergism, that which has been done
seems rather conclusive. There are a number of studies which
show that polychlorinated biphenyl compounds (PCBs) increase
the toxicity of the chlorinated hydrocarbon insecticides
(the DDT family) as well as the organophosphorous insect­
icides now widely used in the Okanagan.

(Lichtenstein et al,

1973)
PCBs have been found in many water sources in North
America. They are considered a major threat in the Great
Lakes and the St. Lawrence River system. In one test, a
PCB formulation (Arochlor 1254) was combined with the insect­
icide carbaryl (Sevin) and administered to DDT-resistant house
flies. The toxicity of the pesticide was increased by more than
80 fold.

(Frawley, 1965)

In another study, three professors of entomology at the
University of Wisconsin tested the effects of four herbicides
when combined with 12 common insecticides on fruit flies,
houseflies and mosquito larvae. They found that "in most
cases all four herbicides increase the toxicity of the in­
secticides." The phenoxy herbicide 2,4-D increased the toxic
nature of parathion and DDT, both of which »ere extensively used
in the Okanagan in the past. The Wisconsin entomologists
concluded from their own research, and a survey of that done
by others, that "the phenomenon of synergism of insecticides
by selected herbicides is rather general."

(Lichtenstein, et

al, 1973)

' P h î H i

4545

VIII-16
Of perhaps more interest to us is the research done by
Dr. Charles N. Statham and Dr. John J. Lech of the Medical
College of Wisconsin. They tested the toxic levels of four
pesticides when combined with carbaryl (Sevin), the insect­
icide proposed for use on the Spruce Budworm in the Fraser
Valley. It is also widely used in orchards in the Okanagan.
The test species in this case was rainbow trout. One of
the pesticides included in this study was 2,4-D and it
greatly increased the toxicity of Sevin to rainbow trout.
(Statham and Lech, 1975)

Effects on Humans

If the toxicity of pesticides is increased by synergism,
then it is a matter of considerable concern to us in the
Okanagan.

Our lakes are deep and cold, with decreasing

oxygen levels towards the bottom.

These are ideal conditions

for the persistence of organic pollutants.
We know that there is a relatively high level of arsenic
and lead in our environment due to the widespread use of
lead arsenic pesticides. We also know that our environment
is polluted with DDT and the other chlorinated hydrocarbons,
the result of many years of usage by Okanagan farmers.

The

B.C. Royal Commission on Pesticides (1975) reports that
residues of these insecticides have been found in the tissues
of fish and game birds in the Okanagan.
The nitrate level in some water is increasing due to
fertilizer runoff and sewage outfalls. Our municipalities
are adding chlorine to sewage and the drinking water every day.
Heavy metals are also known to be in our water supply.

4546

VIII-17

That is why the Canadian government recommends that we
eat no fish larger than three pounds that has been caught in
the Okanagan lake system.
We have to be concerned about the effect of all this on
our health.

The 1977 study by thp U.S. National Research

Council on water pollution concludes th^t much, of the
"intestinal flu" that Americans get each year is probably
due to ailments caused by our present drinking water.
In an agricultural area like the Okanagan, where pest­
icides are widely used and run off into our major source of
potable water, there is particular concern. For example,
Dr. E. Stanton Maxey argues that "current animal work in­
dicates that herbicides in combination with organic pest­
icides are up to four times as toxic as either agent alone."
He is convinced that the interaction of herbicides and in­
secticides is a major cause of increased cancer among farm
workers in Florida.

(Maxey, 1974)

Summary
Under ideal conditions 2,4-D degrades by chemical and
biological action in a relatively short period of time.

How­

ever, it is well known that it persists for a long time in
deep, cold water with a low level of oxygen, precisely the
kind of conditions we have in the Okanagan lake system.

It

is also known that 2,4-D persists in bottom sediments for
many months.

Traces have been found in water sources years

after spraying, indicating that it does not all degrade.
2,4-D degrades to 2 ,4-Dichlorophenol, a toxic chemical.
The final breakdown product is reported to be succinic acid,
a hydrazine product proven to be a carcinogen in tests on
laboratory animals.

To date, the B.C. government has not

tested for the breakdown products of 2,4-D in areas treated
for Eurasian milfoil weed.

VIII-18

Across North America there is growing concern over the
increase of organic and other pollutants in our drinking water
supplies. New hazardous chemicals are being formed in many
waters. There is also good evidence that herbicides, in­
cluding 2,4-D increase the toxic nature of other pesticides
in a water environment.

CONCLUSION

There is a considerable body of evidence which indicates
that the phenoxy herbicides in general and 2,4-D specifically,
pose a substantial threat to environmental and thus human
health.

Laboratory research results show that test animals

develop chronic problems after administration of these chem­
icals. It has been noted that damage results from exposure
of people, livestock, wildlife, fish and crops to 2,4-D.
Extensive research on the effects of 2,4-D on test an­
imals indicates that the herbicide is teratogenic (causes
birth defects), carcinogenic and very likely mutagenic
(causes genetically transmitted defects). These findings
have resulted in authorities such as the Mrak Commission (1969)
recommending the immediate restriction of three esters of
2,4-D and all formulations of 2,4,5-T. Only the latter has
been removed from general use, but it is still applied selec­
tively in British Columbia.
ed.

2,4-D remains largely unrestrict­

All the phenoxy herbicides are from the same family with
the same chemical base.

There is very little difference

between them as to molecular structure, mode of action, and
the acute and chronic damage which they cause in humans, an­
imals and plants. In certain cases they persist in the en­
vironment for far longer than previously thought. It is
known that even the so-called "pure" 2,4,5-T and 2,4,5-TP
inevitable contain some of the dreaded TCDD, one of the most
toxic chemicals known to man. It has also been discovered,
however, that 2,4-D can contain the potent HCDD and other
higher isomer dioxins (whose effects are largely unknown).
There is evidence to indicate that crop yields and
quality can be effected by exposure to 2,4-D. What the effect
will be on fruit trees and grape vines of low levels of the
herbicide applied through irrigation water over a long period
of time, no one really knows.

4549

2
The fisheries resource is also known to be particularly
vulnerable to herbicide use. The concentrations of 2,4-D
required to control the weeds is close to the acute tox­
icity level of the salmonid family. The chronic effects,
habitat reduction and disturbance of the food chain which
are caused by applications of this herbicide are of some
concern to the managers of this resource.
In preparation for the 1977 programme, the B.C. Minister
of the Environment instructed the Advisory Committee on the
Control of Eurasian Water Milfoil to examine "all available
data" on the public health aspects of the aquatic use of
2.4- D. An examination of their three Interim Reports in­
dicates that this was not done. Even the concerns expressed
by this same group in the earlier B.C. Royal Commission In­
quiry into the Use of Pesticides and Herbicides were not
brought forward again with any force.
We have not been able to locate any area in the world
where Eurasian Water Milfoil has been eradicated using
chemical methods. The application of 2,4-D in the present
programme can only be defined as "chemical mowing". Those
in charge of the weed control effort have repeatedly pledged
that the chemical approach would be discontinued after five
years. Yet it is obvious that 2,4-D applications must go on
forever if any sort of control is to be maintained by this
method. It is also obvious that the cost of this programme
will skyrocket along with the price of the petroleum based
2.4- D.
As our research indicates that there are very real pro­
blems associated with the use of 2,4-D in the Eurasian Water
Milfoil Weed control programme, the South Okanagan Environ­
mental Coalition would like to make the following recommend­
ations.

4550

O

1)

That the use of 2,4-D be discontinued for aquatic
weed control.

That all phenoxy herbicide use be

re-examined in light of the information which is
available on their detrimental effects.
2)

That mechanical methods be used to control weeds
which interfere with recreational activities. This
approach would help provide employment as it is
labour intensive and could result in the establish­
ment of a weed removal equipment manufacturing in­
dustry in this province with considerable export
potential. Markets may be found for the harvested
weed which will help reduce the overall cost of the
operation.

3)

That in the long run, a species specific, safe
biological control should be sought. These controls
exist in other regions where Eurasian Water Milfoil
is not a problem. We must discover the controlling
agent (pathogen, parasite, etc.) and test it to
determine whether it can be safely introduced here.
This project will take time and money and would seem
to be a logical job for the Federal government as
the Eurasian Milfoil problem is national with in­
ternational implications.

4)

That nutrient levels in the lakes and rivers of the
province should be reduced to levels which will slow
weed proliferation. This involves curtailing man­
made sources such as sewage outfalls, storm drain­
age, septic tank leakage, fertilizer runoff, and
induced erosion. The Department of the Environment
has taken an important step in this direction in the
Okanagan Valley by requiring the city of Penticton
to begin land disposal of its effluent.

4551

A

4
This is part of a new policy designed to remove
all sewage outfalls from the lake system.
5)

That there is a pressing need to institute a more
elaborate and effective health monitoring programme
in British Columbia. A regular sampling analysis
of food, drinking water and human blood, hair and
milk should be established on a province wide basis
in order to detect contaminents in the system. This
would lead to identifying problems before they are
manifested as disease. Further, epidemiological
investigation should be improved particularly in
the areas of cancer, teratogenesis, mutagenesis and
acute illness so that more causes can be identified.
Regional local and occupational data must be made
available for purposes of early identification.

6)

That a particularly close monitoring system be
established for those who regularly come into con­
tact with pesticides, such as government applicators,
farmers and farm workers, forestry workers and
forest fire fighters. Research in other countries
indicates that these groups need to be watched
very closely for acute and chronic poisoning.

Many people today feel that there are not likely to be
any long term chemical solutions to biological situations.
The lake system of the Okanagan Basin is the life blood for
all species residing here.

Any project which causes the con­

tamination of those waters should be questioned, particularly
if the chemical is known to have detrimental effects on the
environment.
It has been claimed that health problems will be avoid­
ed by the implementation of a "zero tolerance" nrogramme.
In other words, the 2,4-D would not be allowed to come into
contact with human beings.

4552

5
One need only look at the cover photograph on this report to
see the effectiveness of this approach.

The picture was

taken on Skaha Lake Beach in Penticton, B.C. four days after
the application of 2,4-D at a rate of 20 to 40 pounds of
active ingredient per acre.
We should reject emphatically any programme which calls
for the contamination of a major water system with a chemical
which is a proven hazard to the health of our environment.
We cannot accept the claim that the programme will exclude
all risk, for that situation is clearly impossible.

4553

ADDENDUM

The response to the first printing of The Other Face of
2,4-D has been amazing, all the more so because it has been re­
viewed in only one publication to date, Acres Inc.

Yet we have

received orders for the book from all over North America, and as
far away as Australia, New Zealand and Belgium.

The environmen­

tal word-of-mouth network is quite impressive.
In January we printed 500 copies, and by May we were sold
out.

We must apologise to those who have placed orders months

ago and have yet to receive the book.

We were totally occupied

with fighting the provincial government's programme to put 2,4-D
in our lakes and simply had no time to update the book and do
another printing.
We have also greatly appreciated receiving the many letters .
from individuals and groups telling of their personal experiences
with the phenoxy herbicides. Those that have related personal
illness from exposure confirm our position and re-inforce the re­
search data we have collected.
We are also greatly encouraged by the fact that there is such
a groundswell around the world against the use of these herbicides
In British Columbia this year, there have been many local citizens
groups fighting spraying in their areas. The United Fishermen and
Allied Workers Union, and various native groups, are taking up the
struggle, now that they realize the threat that these herbicides
pose to the fishing industry.
Just recently the Dene Nation in the North has succeeded in
blocking the proposed spraying with Agent Orange of 284 launching
sites in the Mackenzie River Delta.

The federal government backed

this incredible plan, but the government of the Territories was
sensitive enough to recognize local concerns.

In Saskatchewan,

the National Farmers Union has prepared a very good brief to the
provincial government questioning the increasing use of these
herbicides.

Their research and tests results by Environment

lD-4i5\

4555

2

Canada revealed the buildup of the phenoxy herbicides, including
of course 2,4-D, in the local domestic water supplies.
In the United States, a number of local groups in Arkansas,
Idaho, Washington, Oregon and elsewhere have fought the use of
phenoxy herbicides in forest management programmes.

They have

put so much pressure on the federal government that the U.S. En­
vironmental Protection Agency has now put the herbicides manu­
factured from 2,4,5-Trichlorophenol on the Rebuttable Presump­
tion Against Registration list.
However, the most important development in 1978 is the
"discovery" that thousands of American veterans of the Vietnam
war have experienced long term chronic illnesses from exposure
to phenoxy herbicides while stationed in southeast Asia. Most
recently, over 800 have filed a class action suit for damages
against the U.S. government (see Uhl and Ensign, 1978).
Herbicide spraying in Vietnam by the U.S. military began in
the early 1960's and was abandoned in 1970.

Yet it has somehow

taken eight years for authorities to recognize (or admit) that
damage to veterans had actually happened.
It makes us wonder
if it would ever be possible to prove damage from the introduc­
tion of 2,4-D into the Okanagan Lake system.
Why is there such a growing concern and so many popular move­
ments against phenoxy herbicides springing up all over the world?
It is not an accident but stems directly from damage experienced
at the local level.

It is particularly true of areas where

there is herbicide spraying in forest management programmes.
In the 1940's and 1950's insecticides and fungicides were
predominant in the sales of pesticides, but this changed in the
1960's.

Since then, the sales of herbicides have grown and by

1967 exceeded other pesticide sales. By 1975, sales of herbi­
cides were more than double that of other pesticides (Seiler,
1978, Table I) .

D - *i£3
4 5 5 7

'R-'ttSH

'4558

3
In the 1960's, herbicide residues were being found in
foods, but it was not considered to be a serious problem
(Duggan, 1966).

However, this again had changed by the 1970's,

recognizing the growing use of phenoxy herbicides.
of 2,4-D now appear regularly in foods.

Residues

Tests have shown

residues as high as .13 ppm in leafy vegetables and some sugar
products (Manske and Comeluissen, 1974).

Residues of 2,4-D

are being widely found in water and air tests.
(Manigold and
Sehulze, 1969; Gowen, Wiersma and Tai, 1976). One study made
at Tallahasee, Florida found 2,4,5-T residues in 24% to 36% of
individuals of various groups tested; 60% of people tested had
residues of 2,4,5-Trichlorophenol, and absolutely everyone
tested had residues of Pentachlorophenol (PCP). Penta residues
were also found in local foods sampled; milk, soft drinks,
sugar, bread, candy bars, cereals, noodles, rice, and wheat.
It was also found in the city water supply.
(Dougherty and
Piotrowska, 1976). Clearly, the phenoxy compounds persist much
longer in the environment than their promoters are willing to
admit.
The Okanagan Situation
Readers might be interested in a brief update on the situ­
ation in the Okanagan, as this controversy led to the research
that produced this book.

In the spring of 1978 the Water In­

vestigations Branch of the so-called B.C. Ministry of Environ­
ment announced that they had applied for permits to apply
2,4-D at a rate of between 20 and 40 lbs. a.i. to 1,500 acres
in five Okanagan lakes. Due to our pressure, and the fact
that over 40 organizations in British Columbia had passed res­
olutions opposing this programme, the civil servants in the
provincial government who had to approve the permits were put
on the spot.

We understand from our inside sources that they

did not really want to approve the programme.

However,

4

tremendous pressure was applied by the political forces at the
top.

They finally approved all the applications, but with

major reductions and some time limitations.
In 1977, the Social Credit Government passed new pesti­
cide control legislation, and while it was deemed very inade­
quate by those outside the industry and users, it did contain
appeal procedures. The South Okanagan Environmental Coalition
appealed all 28 of the permits, and our action prompted other
individuals and groups to also appeal.
We had no illusions on the matter.

The W.I.B., of the

Ministry of the Environment, was asking for the permits. The
administrator approving (or possibly rejecting ) the permits
was also under the Ministry of the Environment. The Pesticide
Control Appeal Board was also nominated by the Ministry of the
Environment.

If it sounds like Catch-22, it is.

But that wasn't all.

Everytime we turned around we faced

professors from the University of British Columbia.

First,

there were the three who made up the Advisory Committee (see
Introduction).

Then four of the seven members of the Appeal

Board were U.B.C. professors. Outside consultation pays well
in this province. Furthermore, a majority of the members of
the Appeal Board represented institutions or disciplines which
are major manufacturers or users of herbicides.
The SOEC decided to go through this seemingly hopeless
exercise for several reasons.

First, for our own public credi­

bility, we had to exhaust all the proper channels.

Secondly,

we hoped that we could get some possible court action out of
the appeal procedure. Thirdly, this was the very first test
of the Appeal Board, and we wanted to demonstrate to the pub­
lic the realities of these government institutions. Fourthly,
we knew that we would have a chance to present our evidence,
get some publicity, and strengthen our case with the public.

4560

5

This certainly happened.

Finally, we decided it was cheaper to

make a long fight at this level than in the courts.
The hearings were held in Penticton in June.

For the

first two days, the Appeal Board heard opposition from various
groups and individuals in the Okanagan, plus the Consumers
Association of Canada (B.C.).
The following week, the SOEC in conjunction with Kelowna
SPEC and Vernon SPEC presented our case.

We took six and one-

half days to present our documentation. We called nine special
witnesses: Dr. Melvin Reuber, of the Frederick Cancer Research
Center in Maryland; Dr. Charles Huver, of the University of
Minnesota; Gil Zemansky, an environmental engineer from Seattle,
Washington; Dr. Theodor

Sterling, of Simon Fraser University;

Merriam Doucet, Chairman of the Pesticide Committee of SPEC
and one of the most knowledgeable people on herbicides in North
America; Dr. David Clarke, the South Okanagan Health Officer;
Drs. Barry Jones and Fred Van Seters of the Kelowna and Pentic­
ton Medical Associations; and Gary Taylar of the B.C. Grape
Growers Association. We were assisted throughout the hearings
by two very competent young legal people from the West Coast
Environmental Law Association, Gregg McDade and Kim Roberts.
In contrast, the Water Investigations Branch presented
their "case" in just three hours. They made no effort to re­
fute any of our medical testimony. They presented no evidence
on the safety of 2,4-D.

They called no witnesses, not even

the three U.B.C. professors who made up the Advisory Committee.
We suspect that the "Three Wise Men" did not want to undergo
cross-examination by SOEC.

The W.I.B. was extremely confident

that the Appeal Board would decide for them.

And they did.

While the hearings were going on, the WIB was preparing a
major application site at Kelowna. The Board announced it
would make its decision on Tuesday, June 20.

That morning the

' 4561

6

WIB was prepared to apply the herbicide.

The pressure was on

the SOEC, for we had to get the Board's decision, prepare a
court appeal, and try to get an injunction. This would take
time. The WIB knew we were going to make a court appeal.
They also knew that with their new machines they could cover
the 52 acre plot in 2 hours.
In the morning, bad weather held up application, as SOEC
lawyers struggled to put together a case.

Local Kelowna

citizens, under the direction of The Kelowna Chapter of Green­
peace had prepared a canoe demonstration, hoping to hold up
application until the courts had had a chance to intervene.
The WIB knew this as well. While forecasts were for rain,
and a wind or thunderstorm could destroy the effectiveness of
the application, the WIB decided to proceed.

They wanted to

set the precedent of applying 2,4-D.
At noon, despite the forecasts, the WIB decided to pro­
ceed.

Their application boats were met with a steady stream

of canoes manned by Kelowna residents.

The RCMP in their

launch and one WIB boat began arresting protesters.
went into the test area.

Others

While the WIB first announced to

the press that no 2,4-D would be applied while the canoeists
were in the test site, by 3 p.m. they changed their minds.
They wanted to make the application before the SOEC could get
its injunction.
Therefore, the hopper boats began the application.

Pro­

testers in the area were sprayed. One of the two WIB hopper
boats ran over a canoeist and dumped him in the water. They
succeeded in covering around 30% of the test site before the
SOEC obtained a temporary court injunction and stopped the
application.
However, the court appeal approach has very limited uses
in Canada.

In this case, the SOEC tried to show in the sub­

sequent appeal hearing in the B. C. Supreme Court in Vancouver

4562

7
that we were denied natural justice during the Board hearings.
This was made difficult by the fact that we had no transcript
of the hearings, and only two days to prepare our case. We
lost on this question, due to inadequate evidence; but we won
a major victory (in the Canadian context) in holding up all
major application in recreation areas.
As it now stands (July, 1978), the WIB will be applying
2.4- D to around 130 acres in the Okanagan lakes this summer.
We have succeeded in knocking out 90% of the 1978 programme.
But we know that we will face another round next year.

We

plan to take further political action in the elections this
fall. We are also going to prepare a paper on alternative con­
trol methods for milfoil weed. Venice Lake virus has elimin­
ated the plant in the Chesapeake Bay area, and it is now show­
ing up in other areas of North America.
solution.

It is the perfect

But for the WIB, it is no solution.

2.4- D programme continued.

They want the

They know it is an ongoing pro­

gramme, guaranteeing their jobs, as 2,4-D has not been success­
ful against Eurasian milfoil in any area of the world.

As the

top people in the WIB are biologists, they have similarly ex­
hibited little interest in the mechanical programmes used in
other areas.
New General Surveys
Since the first printing of The Other Face of 2,4-D we have
received or dug up a number of other papers and bibliographies
on 2,4-D and the other phenoxy herbicides.

We might mention

them here, so others fighting herbicide spraying have other
basic sources from which to start.
Gil Zemansky of Friends of the Earth, 4512 University
Avenue, N.E., Seattle, Washington, has produced two excellent
papers on Eurasian milfoil weed, the use of 2,4-D, and the

4563

8

politics involved.

His paper, "Risks, Benefits, Causal Factors

and Cosmetic Solutions," contains a good bibliography on 2,4-D.
The Consumers' Association of Canada (B.C. Branch), at
103 - 163 West Hastings Street, Vancouver, B.C., presented an
excellent brief to the Pesticide Control Appeal Board, well
documented, and containing a number of references on damages
to health and the environment which we did not have.
The Northwest Coalition for Alternatives to Pesticides,
P.O. Box 375, Eugene, Oregon, has produced an excellent Herbi­
cide Information Packet which it sells for $3.50. It has good
basic material, a good bibliography, and instructions on how
to take legal and other action in the United States. There
are also instructions on what to do if you get sprayed and how
to document damage.
Another good source on 2,4-D is the monograph by the
International Agency for Research in Cancer, Volume 15, 1977.
It is available in most good university libraries.

The mono­

graph is a summary of some of the studies on 2,4-D and its
effect on human health, but it is by no means complete, and
leaves out some major important studies.
Another basic source is the publication by the World
Health Organization in Geneva, "WHO Pesticide Residues Series,
No. 1, 1972."

This is an interesting source because of the

material that is not covered, and their interpretation of some
of the basic studies we have reviewed.

Their bibliography

reveals close contacts with Dow Chemical Co.
At our Appeal Board hearings, the B.C. Water Investiga­
tions Branch submitted as supporting evidence Part II, Chap­
ters 6 and 7 from The U.S. National Research Council, Advisory
Center on Toxicology, Drinking Water and Health.

This was

part of the widely publicized study which was released in
August, 1977.

This American agency produced only a six-page

9
summary of some studies on 2,4-D, a few of which we had not
seen.

What is striking is the number of widely publicized

major studies which they do not review.

They conclude, in

classic fashion, that because there are "substantial disagree­
ments in the results of subchronic and chronic toxicity with
2,4-D," we should have more studies done.
But the WIB also produced a paper on "Chlorophenoxy
Herbicides," which forms the background of the Canadian Drink­
ing Water Standards.

This four-page paper is totally inadequate.

Any first year university student could have prepared a much
better survey.

The paper concludes that "the approval limits

for these herbicides are meant to serve in the event that these
chemicals inadvertently occur in the water. Deliberate addi­
tion of these compounds to drinking water sources is neither
implied nor sanctioned."

And the WIB actually submitted this

as evidence supporting their case!
Cancer and 2,4-D
The above general surveys list other cases of general
effects on humans; there are some good studies on exposure of
plant workers.

But special mention should be made of the issue

of 2,4-D and cancer.

On February 28, 1978, Richard L. Reising,

Special Projects Branch, U.S. Environmental Protection Agency,
wrote Gil Zemansky explaining that 2,4-D had been put on the
Pre-RPAR list because the Agency's Cancer Assessment Group
(CAG), through a review of three studies, "found positive
evidence that 2,4-D is carcinogenic."

This letter, passed on

to the SOEC, was then made public in British Columbia and
caused a national news incident.
As a result of "The Canadian Incident," Edwin L. Johnson,
Deputy Assistant Administrator for the EPA in Washington, wrote
to Jim Nielsen, B.C. Minister of the Environment who is respon-

4565

10

sible for the 2,4-D programme in the Okanagan.

Johnson said

that because of "conflicting opinions" the EPA had no intention
of banning 2,4-D until there was further information.
However, through sources in the United States the SOEC had
received copies of an internal EPA memorandum dated April 27,
1975 from Janet Lambert of the Special Pesticide Review Divi­
sion to Ed Johnson. In this memo, Lambert explained how,
through administrative bungling, 2,4-D had been placed on the
Pre-RPAR list. Furthermore, she stated that their office "is
not conducting new studies to investigate potential carcino­
genicity - nor is there any intent to do so in the future."
In addition, the only tests reviewed were the 1963 and 1964
tests by the U.S. Food and Drug Administration; the other pub­
lished studies (listed below) were not included.
When he was in Penticton, Dr. Melvin Rueber, who had been
a member of the EPA Cancer Assessment Group and who had advised
Senator Edward Kennedy's Subcommittee on 2,4-D, made several
interesting comments on this situation.

As a top cancer re­

searcher, who had done a great deal of work with chlorinated
hydrocarbons, he found it interesting that there had been so
few tests done on 2,4-D considering the results of the Bionetics and FDA studies.

Most chlorinated hydrocarbons had

been subjected to more than a dozen studies.

He then recounted

the political and user pressures on the National Cancer Insti­
tute and the EPA not to ban 2,4-D, and not to do any further
testing. If 2,4-D were found to be carcinogenic, it would have
to be banned for use on food crops because of the Delaney
Amendment to the U.S. Food and Drug Act.

The refusal of the

EPA's Cancer Assessment Group to recommend further testing, in
the face of what was known, caused him to resign from it.
We now know that the same forces are at work in Canada.
Our fight against the phenoxy herbicides, and the publicity
resulting from it, has caused a minor panic among government

4566

11

agencies involved.

Dr. W. T. McKinley, now head of the Health

Protection Branch, pointed out at a conference in Saskatchewan
last winter that no testing was being done in Canada, and none
could be expected.

No one was doing this testing, as funds

were not being allocated.
The Position of the B. C. Government
Our major concern is that the application of 2,4-D in our
lakes over a long period of time will cause a chronic health
problem. As noted above (Chapter III), we accept the majority
position that carcinogens cause irreversible, cumulative dam­
age, even at low dosages.

This was the stand taken by the IARC

in the Lyon meeting in 1977 (McGinty, 1977).

As they noted,

because there is enormous individual variation in human reac­
tion to carcinogens, a threshold dose level is a practical im­
possibility. The SOEC stands behind the position taken by
Jens Steensberg, Chief Medical Officer, Danish Environment
Protection Agency:

"We cannot expect, or wait for, univer-

versally accepted proof of carcinogenic risks."

We must act

now to prevent humans from being test subjects.
In contrast, Dr. Peter Newroth, one of the biologists res­
ponsible for the 2,4-D programme in the Okanagan, told the
Kelowna Rotary Club on April 26, 1978 that "we have always
known that 2,4-D was carcinogenic in tests on small animals
but one has to take into account the amounts used.

In these

tests the lowest dosage level is 600 parts per million.

That's

the lowest; they go much higher." In contrast, he noted, they
had "set the amount to be used in the lake at .6 ppm and that's
minute comparatively."
In the public meeting in Penticton on May 2, 1978, Dr.
Courtland Mackenzie, a member of the Advisory Committee and
the University of British Columbia and the only independent

V'^C>C,3

12

medical adviser to the B.C. government, stated that "there is
a threshold level for many carcinogens.”

In response to ques­

tions from the SOEC, he admitted that on this point he "dis­
agreed with the general medical opinion."
A similar position was taken by Dr. W. D. Prowrie at the
public meeting in Kelowna on May 3, 1978. Dr. Prowrie, a mem­
ber of the Advisory Committee and a professor at the University
of British Columbia, stated that "high doses of chemicals are
what causes cancer."
New Evidence on Cancer and 2,4-D
A number of other published studies on 2,4-D and cancer
should be noted, as we did not have them at the time of the
first publication. The U.S. National Academy of Sciences sur­
vey reported that "studies on the in vitro and in vivo effect
of 2,4-D on the growth of Ehrlich ascites tumor in BALB/c mice
showed that the-herbicide was inhibitary at 45 mg/kg or more
(Walker et al, 1972)."
The IARC reports a Russian study where, of 165 rats fed
2,4-D at a level equal to 1/10 the LD5 0 level in their food,
3 (or 1.8%) developed malignant tumors (Arkhipov & Koslova,
1974).

J.P. Seiler reports a Polish study done in 1974 in

which an elevated number of tumors were observed in test ani­
mals (Jurek, 1974).

The U.S. N.A. S. survey also lists another

study which did not report any tumors when 2,4-D was adminis­
tered to mice, but found that it "had a cocarcinogenic effect
in mice when it was applied to the skin with 3-methylcholan*
trene.
(Haag et al, 1975).
Several studies we had not heard of are reported in the
paper by J. P. Seiler.

First he notes the case of the Swedish

railroad workers (cited above, Chapter III) ; the reports cited
for this "showed only slightly higher than expected tumor fre-

$)■

13

quencies" (Axelson, Rehn and Sundell, 1974; Axelson and Sundell,
1974). However, this data has been sorted out and reviewed,
and Seiler now notes that the recent study indicates that "a
significant trend showing a clear relationship with increasing
exposure to phenoxy acids was observed" (Axelson and Sundell,
1977) .
Seiler also cites a German study of pesticide-exposed agri­
cultural workers, which revealed lung cancer that was twenty
times as high as would normally be expected.

However, these

workers were exposed to pesticides other than just 2,4-D.
(Barthol, 1976). Finally, a survey of 87 men in Emea, Sweden
who were exposed to phenoxy herbicides in forest management
programmes revealed that males had twice as many mesenchymal
tumors as women, which was exactly the reverse of the national
average (Hardell, 1977).
Birth Defects and 2,4-D
There is very little doubt about the teratogenic nature of
2,4-D, as there are so many studies which have found positive
results.

No one in the B.C. government disputes this.

But

Dr. Charles Hu|ier gave us a copy of a paper that Dr. Jacqueline
Verrett of the U.S. Food and Drug Administration presented to
the Minnesota legislature in 1976.
test of 2,4-D,

This is a chicken embryo

2,4-5-T and several dioxins.

Two tests were

made of 2,4-D samples, one with all impurities removed.

Both

were teratogenic, but interestingly enough, the purified sample
proved to be more strongly teratogenic.

She also found the

same to be true of the purified sample of 2,4,5-T, which sup­
ports the research of the National Center for Toxological Re­
search (cited above).

Therefore, those groups which are con­

centrating on the dioxin contaminants in phenoxy herbicides,
believing them to be the only danger, are certainly on the
wrong track.

D-^fc4S'

4569

14

The internal memo of the EPA from Lambert to Johnson re­
veals that Dr. Diane Courtney has just completed another teratological study with 2,4-D, which again is reported to show
positive results.
Dioxins
The history of the edema factor problem (see Chapter V)
is also detailed in the paper by Dr. Jacqueline Verrett.

The

1969 outbreak in North Carolina was traced to the hexa-, heptaand Octa-chlorodibenzo-p-dioxins, most likely from 2,4-D resi­
dues in fats in chicken feed.
Dr. Verrett carried out her own tests on several dioxins.
Tetra-dioxin (TCDD) was highly toxic to chick embryos.

TCDD

and Hexa-Dioxin (HCDD) also proved to be teratogens.

(Verrett,

19 76) .
Mutagenicity
Our original publication was rather weak on the question
of 2,4-D and possible mutagenic effects.

This was primarily

due to the fact that we had not had time to do adequate re­
search. We have now discovered that in the 1970's there has
been considerable research done on the mutagenic potential of
2,4-D and the other phenoxy herbicides.
We have been fortunate to obtain a copy of a review ar­
ticle by J. P. Seiler of the Swiss Federal Research Station,
CH-8820, Waedenswil, Switzerland. Our copy of the paper was
obtained from Dr. George Streisinger of the Institute of
Molecular Biology, University of Oregon, but it is scheduled
for publication in the near future in Mutation Research.

A

similar review article by Dr. W. T. Grant on 2,4,5-T is also
scheduled for publication in Mutation Research, and both these

15

articles will be important contributions to the discussion on
the phenoxy herbicides.

In addition, the other general surveys

cited above also list a number of individual studies.

I will

not try to duplicate Seiler's review of 133 studies, but I will
try to summarize his own conclusions.
The three professors from the University of British Colum­
bia who comprise the Advisory Committee to the B.C. government
have repeatedly stated in public that there is no evidence
that 2,4-D is a mutagen.

While at public meetings they may

appear to be propagandists for the government, we have to as­
sume that their position is due to a lack of knowledge on the
issue.
J. P. Seiler concludes that there is no question but that
"phenoxy acids interact with nucleic acid metabolism."
do "influence nucleic acids and their synthesis."

They

Tests on

microrganisms have mostly been negative; however, "a weak muta­
genic effect of phenoxy acids cannot be completely excluded on
the basis of these bacterial results."
Quite different test results have been obtained using
yeasts.

Not only 2,4-D but the other phenoxy acids "have mostly

given positive results in yeast test systems."
In plants tests (see also Chapter IV), there are many
studies which show positive results.

At higher dosages, they

have produced radiomimetic effects.

Seiler concludes that "in

general plant systems have shown that phenoxy acids do in­
fluence the genetic material or the mitotic cycle or both."
Of more significance to humans are the tests on Drosophila
(fruit fly). Seiler concludes that "it can be assumed that in
general phenoxy acids possess weak, but significant genetic
activity in Drosophila."
The tests on mammals suggest that the primary influence
of 2,4-D is on the spindle protein.

Several cases cited found
XX

4571

16
that 2,4-D caused chromosome aberrations in human tissue cul­
tures. "In vivo tests have been performed on mice, and most of
the investigations report positive findings with respect to
chromosome breakage under the influence of 2,4-D."
Seiler concludes that "until we know more about the pene­
tration of phenoxy acids into different cell types, an evalua­
tion of the mutagenic potency must remain tentative, although
they can clearly be considered as potentially mutagenic agents."
Agriculture
We have no new studies on the dangers of 2,4-D to crops to
report, simply because we have not had the time to do this re­
search as we have been concentrating on damage to human beings.
But during the summer of 1978 the question of damage to grapes
became a major news event in the Okanagan Valley.
First, 2,4-D damage to grape vineyards and crops in Wash­
ington state had been regularly reported in the Goodfruit Grower,
and these news reports were made public at the Pesticide Appeal
Board hearings.

Both the B.C. Grape Growers Association and

the B.C. Fruit Growers Association passed resolutions at their
annual meetings opposing the use of 2,4-D in the Okanagan lakes.
Right at this time, a number of vineyards in Osoyoos and
Oliver reported 2,4-D damage.

The Grape Growers Association

made strong public statements and took their appeal to the
Board.

It is widely known that at the parts per trillion level

2,4-D is damaging to grape vines, and it may be for these
reasons that the Board turned down all 2,4-D applications for
Vaseaux and Osoyoos lakes, where most of the B.C. vineyards
are located.

However, the Board never presented any reasons

for the decision that they took, and thus they appear to be
arbitrary.

4572

Fish and Wildlife
In British Columbia

,there is growing concern about damage

to commercial fisheries from phenoxy herbicides.

In fact,

there is fear that our fishing industry may be destroyed by
pollution in general.

A very alarming article by Lawrence

Wright documents the decline of the commercial fishing industry
in the United States due to the pollution of fresh water bodies
with chemical pollutants (Wright, 1977).

'ÿ-Hblb

TABLE I
HERBICIDE USE IN BRITISH COLUMBIA
1973

Lbs. of Active
Ingredient

User
The Forest Industry
(a)
(b)

27,150
12,478

Private use
Government use
sub total

2.

B.C. Hydro
(a)
(b)
c
(d)

30,070
377
675
13,283

Transmission Rights of Way
Gas Division
Railway Section
Soil Sterilants
sub total

3.

B.C. Department of Highways

4.

Railways
(a)
(b)
(c)

6,820
18,555
144,013

Canadian National Railroad
Canadian Pacific Railroad
B.C. Railroad

169,388

Agriculture and Home and Garden
(a)
(b)
(c)
d
(e)
(f)

(g)
(h)
(i)
(j)

9,318
45,943
1,435
96
2,094
4,428
8,662
839
44,240
26,276

Phenoxy herbicides
Phenols
Benzoic Acids
Toludines
Chloroal phatic acids
Ami des
Carbamates
Ureas
Nitrogen Heterocuclics
Inorganic compounds
sub total

6.

44,405
37,266

sub total
5.

39,628

TOTAL - all herbicides

SOURCE:

143

4575

1.

434,018

British Columbia. Royal Commission of Inquiry into the Use
of Pesticides and Herbicides, Final Report of the Commissioners,
May 30, 1975, Vol. II, Part II, Table MM - 1.

TABLE II
HERBICIDES USED IN BRITISH COLUMBIA
Government and Industrial Use
1973

Herbicides

Trade Name

Lbs. of Active
Ingredient

Trichloroacetic Acid

Sodium T.C.A.

99,104
65,836

2,4-D
2,4-D/2,4,5-T

Agent Orange

22,009

Triazine Herbicides

Simmaprim,
Primatoi

21,266

Picloram

Tordon 10K

19,585

Picloram/2,4-D

Agent White
Tordon 101

13,718
13,215

2,4,5-T
2,4-D/2,4-DP

Weedone 170

9,718

Fenitrothion

Sumithion

7,250

M.S.M.A.

Glowon

7,240

Mi sc.

11,595

T O T A L

290,536

SOURCE:

British Columbia. Royal Commission of Inquiry into the Use
of Pesticides and Herbicides. Final Report of the Commis­
sioners , May 30, 1975. Volume II, Part II, Table MM - 1.

4576

TABLE III
2,4-D APPLICATION RATES

Target Plant

Environment

Active Ingredient
per Acre

Lambs Quarters, Wild
Mustard, Ragweed

Cereal Crop Land

6 oz.

Russian Thistle

Cereal Crop Land

12 oz.

Broad leaf annual
weeds

Field Corn

8 oz.

Broad leaf
weeds

Pasture and forage
grasses

8 oz.

Trees and bushes

Prairie rangeland

32 oz.

Broad leaf weeds

Lawns

1/2 lb.

Woody Plants

Forests

2 - 4 lbs.

Water hyacinth

Aquatic

1 - 2 lbs.

Floating weeds

Aquatic

4 lbs.

Bulrushes, cattails,
water lilies

Shoreline areas

4-6

Forests and rubber
plantations

Cambodia - 1969

1/2 - 3 lbs.
(Agent Orange)

Jungle vegetation

Vietnam - 1961-1969

5 - 12 lbs.
(Agent White)

Eurasian Milfoil weed

Aquatic-Okanagan
Lake System - 1977

20 - 40 lbs.

NOTE:

lbs.

It has been claimed that the U.S. military used Agent Orange at
as high a rate as 27 lbs. per acre in Vietnam. Normal usage,
however, appears to have been far lower, as the Cambodia report
and field manuals demonstrate. The UC-123 Aircraft which ap­
plied the spray were calibrated to spray at a rate of 3 gallons
total fluid per acre.

T>

According to the B.C. Royal Commission of Inquiry into the use
of Pesticides and Herbicides, one gallon of 2,4-D, 2,4,5-T or
Agent Orange contains 4 lbs. of active ingredient. Regular com­
mercial preparations used in Vietnam are reported to have the
same ratio.

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4578

TABLE IV
2,4-D AND 2 ,4,5-T USE IN BRITISH COLUMBIA
ESTIMATES 1976

Acres
Home and Garden

5,000

Agriculture

250,000

Forestry and Industry

17,000

2 ,4,5-T
Agriculture
Forestry and Industry

SOURCE:

200
6,900

Bai ne Vance
Pesticide Control
B.C. Department of Agriculture
Verbal Information

D - Vé ViT

4579

4580

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