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Pesticides and Polio:
A Critique of Scientific Literature
By Jim West
The following statement appeared in the Handbook of Pesticide
Toxicology, 1991, edited by Wayland J. Hayes and Edward R. Laws:
"It has been alleged that DDT causes or contributes to a wide variety
of diseases of humans and animals not previously recognized as associated
with any chemical. Such diseases included. . . poliomyelitis, . . .
such irresponsible claims could produce great harm and, if taken seriously,
even interfere with scientific search for true causes. . ."1
Hayes and Laws were informing their readers about the heretic, Dr.
Morton S. Biskind. In 1953, when Biskind's writings were published,
the United States had just endured its greatest polio epidemic. The
entire public was steeped in dramatic images--a predatory poliovirus,
nearly a million dead and paralyzed children, iron lungs, struggling
doctors and dedicated nurses. The late president Franklin D. Roosevelt
had been memorialized as a polio victim who was infected with the deadly
poliovirus near the beautiful and remote island of Campobello. The media
was saturated with positive images of scientific progress and the marvels
of DDT to kill disease-carrying mosquitos. Jonas Salk was in the wings,
preparing to be moved center stage.
Through this intellectually paralyzing atmosphere, Dr. Biskind had
the composure to argue what he thought was the most obvious explanation
for the polio epidemic: Central nervous system diseases (CNS)
such as polio are actually the physiological and symptomatic manifestations
of the ongoing government- and industry-sponsored inundation of the
world's populace with central nervous system poisons.
Today, few remember this poignant writer who struggled with the issues
of pesticides, issues that Rachel Carson would be allowed to politely
bring to public awareness nine years later, as the lead story in The
New Yorker magazine and then as a national best seller, by limiting
her focus to the environment and wildlife. Biskind had the audacity
to write about human damage.
I found "M.S. Biskind" in the endnotes to Hayes' and Laws' diatribe.
What could possibly have motivated Hayes' and Laws' biased genuflection
towards germ theory? Such offerings, commonly written into the final
paragraphs of scientific articles, are usually done with an appearance
of impartiality. With great anticipation, I went to a medical library
and found Biskind's 10-page 1953 article in the American Journal
of Digestive Diseases.2 Presented below are excerpts
regarding polio from the article.
Biskind's Warnings
"In 1945, against the advice of investigators who had studied the pharmacology
of the compound and found it dangerous for all forms of life, DDT (chlorophenoethane,
dichloro-diphenyl-trichloroethane) was released in the United States
and other countries for general use by the public as an insecticide.
. . .
"Since the last war there have been a number of curious changes in
the incidence of certain ailments and the development of new syndromes
never before observed. A most significant feature of this situation
is that both man and all his domestic animals have simultaneously been
affected. In man, the incidence of poliomyelitis has risen sharply.
. . .
"It was even known by 1945 that DDT is stored in the body fat of mammals
and appears in the milk. With this foreknowledge the series of catastrophic
events that followed the most intensive campaign of mass poisoning in
known human history, should not have surprised the experts. Yet, far
from admitting a causal relationship so obvious that in any other field
of biology it would be instantly accepted, virtually the entire apparatus
of communication, lay and scientific alike, has been devoted to denying,
concealing, suppressing, distorting and attempts to convert into its
opposite, the overwhelming evidence. Libel, slander and economic boycott
have not been overlooked in this campaign. . . .
"Early in 1949, as a result of studies during the previous year, the
author published reports implicating DDT preparations in the syndrome
widely attributed to a 'virus-X' in man, in 'X-disease' in cattle and
in often fatal syndromes in dogs and cats. The relationship was promptly
denied by government officials, who provided no evidence to contest
the author's observations but relied solely on the prestige of government
authority and sheer numbers of experts to bolster their position. .
. .
"['X-disease'] . . . studied by the author following known exposure
to DDT and related compounds and over and over again in the same patients,
each time following known exposure. We have described the syndrome as
follows: . . . . In acute exacerbations, mild clonic convulsions involving
mainly the legs, have been observed. Several young children exposed
to DDT developed a limp lasting from 2 or 3 days to a week or more.
. . .
"Simultaneously with the occurrence of this disorder [X-disease], a
number of related changes occurred in the incidence of known diseases.
The most striking of these is poliomyelitis. In the United States the
incidence of polio had been increasing prior to 1945 at a fairly constant
rate, but its epidemiologic characteristics remained unchanged. Beginning
in 1946, the rate of increase more than doubled. Since then remarkable
changes in the character of the disease have been noted. Contrary to
all past experience, the disease has remained epidemic year after year."
DDT vs Polio
In the graph below, I provide confirmation of Biskind's observations
for 1945-1953, in terms of polio incidence and pesticide production.
I have utilized pesticide data from Hayes and Laws which they had obtained
from the US Transportation Board. Polio incidence data was gathered
from US Vital Statistics.3 Although I argue herein
against Hayes' characterization of Biskind's work, credit goes to Hayes
for publishing arcane pesticide data.
Physiological Evidence
Biskind also describes physiological evidence of DDT poisoning that
resembles polio physiology: "Particularly relevant to recent aspects
of this problem are neglected studies by Lillie and his collaborators
of the National Institutes of Health, published in 1944 and 1947 respectively,
which showed that DDT may produce degeneration of the anterior horn
cells of the spinal cord in animals. These changes do not occur regularly
in exposed animals any more than they do in human beings, but they do
appear often enough to be significant."
He continues, bearing his exasperation in trying to make the obvious
plain. "When the population is exposed to a chemical agent known to
produce in animals lesions in the spinal cord resembling those in human
polio, and thereafter the latter disease increases sharply in incidence
and maintains its epidemic character year after year, is it unreasonable
to suspect an etiologic relationship?"
Before finding Biskind's work, I had spent months engaged in a nearly
futile search for the physiology of acute DDT poisoning. I began to
sense that American DDT literature as a whole intends to convey that
DDT is not dangerous except with regard to its general environmental
effects due to persistent bioaccumulation, and that the physiology of
acute DDT poisoning is therefore trivial. DDT literature uniformly jumps
from descriptions of symptoms, over physiology, to the biochemistry
of DDT-caused dysfunction in nerve tissue. It was as though detectives
had come upon a mass-murder scene and immediately became obsessed with
the biochemistry of dying cells around bullet holes, while ignoring
the bullet holes.
Eventually, I did find one study, in a German publication, of the physiology
of acute DDT poisoning.4 The study confirmed that DDT poisoning
often causes polio-like physiology. "Conspicuous histological degeneration
was, however, often found in the central nervous system. The most striking
ones were found in the cerebellum, mainly in the nucleus dentatus and
the cortex cells. Among other things an increase of the neuroglia and
a necrotic degeneration and resorption of ganglionic cells was found.
The Purkinje cells were less seriously affected than the other neurons.
Also in the spinal cord abnormalities of a degenerative nature were
found. . . . such changes were not found invariably. . . there is neither
an obvious relation between the size and spreading of the lesion and
the quantity of DDT applied. . . . information of adequate precision
about the nature of the anomalies is lacking."
Thus we find that the cerebellum and the spinal cord are especially
affected by DDT.
And more recently, in the works of Ralph Scobey, MD,5 I
found that from ancient times to the early 20th century, the symptoms
and physiology of paralytic poliomyelitis were often described as the
results of poisoning. It wasn't until the mid-19th century that the
word "poliomyelitis" became the designation for the paralytic effects
of both severe poisoning and polio-like diseases assumed to be germ-caused.
Today, various other forms of the word "polio" are still used to describe
the effects of neurotoxins, although usually with regard to paralysis
in animals. (See below.)
In contemporary Britain, a farmer turned scientist, Mark Purdey, has
found substantial evidence that mad cow disease, a form of polio-like
encephalitis, was caused by a government mandated cattle treatment consisting
of organophosphate pesticide and a compound similar to thalidomide.6
Unlike most scientists, Mark Purdey became legally embroiled with the
government during his research, and " . . . was shot at, blockaded in
his home to prevent him giving a lecture, and saw a new farmhouse go
up in flames the day he was due to move in."7
Morton S. Biskind had the courage to write about humans. His views
fell into disfavor after the introduction of the polio vaccines, which
was a grand act that proved in most people's minds that polio was caused
by a virus. By October, 1955, Biskind, whose works had been published
in established medical journals and who testified before the Senate
on the dangers of pesticides, was forced to self-publish his writings,
one of which I found while browsing through an old card catalog. A scan
of MEDLINE finds no other works by him except for a very tame article
in 1972, warning that diseases incurred during a patient's stay in a
hospital are not necessarily due to microbes. He died not long thereafter,
in his late 60s.
A Contemporary Study
I have compiled information that confirms Biskind's observations,
utilizing data that extend far beyond his observations. These data are
presented in the next three graphs.
Due to the paucity of data regarding pesticide exposure and locale,
production data are given as an indication of exposure, keeping in mind
the great changes in public awareness and legislation beginning in 1950.
Again, this pesticide data comes from Hayes and Laws.
In the graph below, I did not include DDT data for the period of 1954
onward because, even though the US production of DDT skyrocketed, its
distribution was then being shifted out of the US and into developing
nations.
Governmental hearings, including those with Biskind, Scobey and others,
brought about greater awareness of DDT dangers, as well as better labeling
and handling methods.8 Due to public governmental debate
in 1950-51 and numerous policy and legislative changes afterward,8,9,10,11
DDT production figures after these dates do not correlate with US usage
or exposure to DDT.
After 1950, DDT was continually incriminated until its registration
cancellation in 1968 and ban in 1972. So 1950 marked a point of increased
public awareness, changes in legislation and policy, voluntary phaseout,
labeling requirements and discouragement from use in dairy farms. Much
of the usage in the US may have moved over to forestry applications,
placing less DDT directly into the food chain.
Therefore, DDT production, as an indicator of human exposure in the
US, is estimated in the graph above by reviewing levels of DDT in adipose
tissue (National Adipose Tissue Survey, and other studies)12
and considering the context of DDT in imported food. Levels of DDT in
adipose tissue before 1955 were estimated by drawing a straight line
from the low to the high levels of DDT in adipose tissue for that period.
The estimate of DDT exposure is fairly accurate because DDT has a half-life
of about one year. To achieve any downward trend in the DDT/adipose
line, DDT exposure had to have decreased sharply. It is, however, not
an assumption, but a fact, that the lowering of DDT levels in adipose
tissue parallels the hyped advent of the Salk vaccination programs.
BHC vs Polio
BHC (benzene hexachloride), a persistent, organochlorine pesticide,
is several times more lethal than DDT, in terms of LD50 (lethal dosage
required to kill 50 percent of a test population).
As shown in the graph below, BHC was produced in 1945-1954 at quantities
similar to DDT. In spite of BHC's lethal quality, it has received much
less publicity than DDT. While DDT was banned for such things as an
association with the thinning of eagles' eggs, BHC was phased out of
production because it was found, after 15 years, to impart a bad taste
to food. It is still used in developing nations. One is tempted to ask
whether the more controversial DDT, known to be dangerous, was "fronting"
for the more dangerous BHC? BHC's correlation with polio incidence is
astonishing.
Lead-Arsenic vs Polio
Note that the period 1940-46 is unaccounted for in terms of polio-pesticide
correlation in the DDT and BHC graphs. The missing piece of the puzzle
for this six-year period is supplied by the lead and arsenic compounds,
shown in the graph below. These central nervous system (CNS) poisons
were the major pesticides during the several centuries previous to the
advent of the organochlorines in the early 1940s. For those who think
that "organic" food was the norm before the release of DDT to the civilian
sector in 1945, the immense production of lead-arsenic compounds seen
in this graph proves otherwise. This data requires a reconsideration
of statements regarding the "natural" quantities of arsenic found in
apple seeds, apricots, or almonds or "natural" chemotherapies derived
from seeds where pesticides can accumulate in the ground.
Pesticide Composite: Summary
Just over three billion pounds of persistent pesticides are represented
in the graph below. Virtually all peaks and valleys correlate with a
direct one-to-one relationship with each pesticide as it enters and
leaves the US market. Generally, pesticide production precedes polio
incidence by 1 to 2 years. I assume that this variation is due to variations
in reporting methods and the time it takes to move pesticides from factory
to warehouse, through distribution channels, onto the food crops and
to the dinner table. A composite of the three previous graphs, of the
persistent pesticides--lead, arsenic, and the dominant organochlorines
(DDT and BHC)--is represented.
These four chemicals were not selected arbitrarily. These are representative
of the major pesticides in use during the last major polio epidemic.
They persist in the environment as neurotoxins that cause polio-like
symptoms, polio-like physiology, and were dumped onto and into human
food at dosage levels far above that approved by the FDA. They directly
correlate with the incidence of various neurological diseases called
"polio" before 1965. They were utilized, according to Biskind, in the
"most intensive campaign of mass poisoning in known human history."
Virus Causation
A clear, direct, one-to-one relationship between pesticides and polio
over a period of 30 years, with pesticides preceding polio incidence
in the context of the CNS-related physiology just described, leaves
little room for complicated virus arguments, even as a cofactor, unless
there exists a rigorous proof for virus causation. Polio shows no movement
independent from pesticide movement, as one would expect if it were
caused by a virus. Both the medical and popular imaginations are haunted
by the image of a virus that invades (or infects) and begins replicating
to the point of producing disease.
In the laboratory, however, poliovirus does not easily behave in such
a predatory manner. Laboratory attempts to demonstrate causation are
performed under conditions which are extremely artificial and aberrant.
Poliovirus causation was first established in the mainstream mind by
publications of an experiment by Landsteiner and Popper in Germany,
1908-1909.13 Their method was to inject a pulverized purée
of diseased brain tissue into the brains of two monkeys. One monkey
died and the other was sickened. Proof of poliovirus causation was headlined
by orthodoxy. This, however, was an assumption--not a proof--of
virus causation. The weakness of this method is obvious to everyone
except certain viropathologists and has recently been criticized by
the molecular biologist Peter Duesberg regarding a modern-day attempt
to establish virus causation for kuru, another CNS disease.14
Since 1908, the basic test has been repeated successfully many times
using monkeys, dogs and genetically altered mice. The injected material
has even been improved--scientists now use a saline solution containing
purified poliovirus. However, a crucial weakness exists--polio
epidemics do not occur via injections of poliovirus isolate into the
brains of the victims through a hole drilled in their skull--except,
of course, in laboratories and hospitals.
If injection into the brain is really a valid test for causation then
it should serve especially well as a proof for pesticide causation.
I propose that pesticides be injected directly into the brains of test
animals. If paralysis and nerve degeneration subsequently occur, we
then would have proved that pesticides cause polio.
Going further, towards much higher standards of proof than those used
to prove virus causation, pesticides could be fed to animals and found
to cause CNS disease. This has already been done with DDT and the histology
of the spine and brain was poliomyelitis. Virus proofs require injection,
often intracranial, to get any reaction from the experimental animal.
It is axiomatic that a theory is only as good as its ability to predict
future events. I predict that such a test would prove pesticides to
be the most reliable causative factor.
The injection of purée of diseased brain tissue into the brains
of dogs was the method preferred by Louis Pasteur to establish virus
causation with rabies, another CNS disease. A recent, definitive biography
of Pasteur finds him to be a most important publicist for germ theory,
a crucial promoter for the notion that rabies is caused by a virus.
Unfortunately, his rabies experiments were biased and unsupported by
independent studies.15
Therefore, in my opinion, even a cofactor theory, where pesticides
catalyze predatory poliovirus activity, or where pesticides weaken the
immune system to allow opportunistic predatory poliovirus activity,
cannot stand up to simple, common sense explanations that include the
concept of a symbiotic virus. Neurotoxins are enough of a cause for
neurological disease.
The most obvious theory--pesticide causation--should be the
dominant theory. But the opposite exists, a pervasive silence regarding
pesticide causation juxtaposed against a steady stream of drama regarding
virus causation. In light of the evidence presented herein, the silence
could ultimately discredit mainstream medical science, institutions
of the environmental movement, and the World Health Organization.
LEFT:
Before 1950, DDT was hailed as a miracle of progress that was virtually
nontoxic to humans, in spite of the FDA's attempts to keep it off the
market. The photo above is one of several similar photos from DDT: Killer
of Killers, 1946, by O. T. Zimmerman, PhD, and Irvin Lavine, PhD.
BELOW RIGHT: Zimmerman and his colleagues advised that DDT be sprayed
directly on dairy cows, their feed, bedding and water, in a 5 percent
solution. Dairy products are ideal pesticide carriers because they are
emulsions of fats and water. DDT is a waxy organochlorine with an affinity
for fats, and is efficiently carried by dairy products through the digestive
tract into the organs. In the mid-1940s the FDA advised against the
use of DDT, especially on dairy farms. However, the pressure of the
industry to promote DDT was overwhelming and the FDA's advice went unheeded.
Years
later, the compelling nature of the evidence ensured the passage of
stronger labeling laws and restrictions from use on dairy farms. In
the early 1950s, scientists at the US Department of Agriculture found
that although fodder treated with DDT caused no damage to the cows eating
it, the health of their calves was severely impaired, sometimes with
fatal results. The DDT was passed along from cow to calf via the milk
(Van Nostrand's Encyclopedia of Science and Engineering, Van Nostrand
Reinhold 1995, v 5, p1775). DDT is a neurotoxin and the calves developed
something very much like infantile poliomyelitis. Calves weren't the
only infants drinking cow milk during the early 1950s.
Virus Presence
When the symptoms of polio are recognized, there is often a claim of
virus presence in the body of the polio victim. Sometimes a virus is
found. Sometimes that virus is an enterovirus (a virus of the digestive
tract). Sometimes that enterovirus is a poliovirus. During polio epidemics,
orthodoxy blames the poliovirus, and therefore, in my argument for the
innocence of the poliovirus, it is necessary to explain the claims of
virus presence and the actual presence of the poliovirus.
First we must consider the economic motivation. During the great epidemic
of 1942-1962 polio victims were diagnosed with poliovirus-caused polio,
regardless of whether or not the poliovirus was found, because the NFIP
(March of Dimes) funds paid only for this kind of polio. Therefore,
if patients were going to spend time hospitalized, in iron lungs and
undergoing therapy, it would have been economically imperative for the
hospital to diagnose them in this way.16 Thus, presence of
poliovirus in poliomyelitis was rarely determined in order to arrive
at a diagnosis of polio.
Even if one believes in virus culpability, other viruses are also claimed
by orthodoxy to be the cause of polio-like CNS diseases that are "clinically
indistinguishable" from polio. During the 1940-50s, relatively few polio
victims were confirmed technically for presence of the poliovirus. In
1958, a laboratory analysis of 222 diagnosed polio victims of the Detroit
epidemic found poliovirus in only 51 percent of the cases.17
In other studies, lab tests for multiple pathogens reveal that a mix
of pathogens, multiple viruses, fungi, and bacteria can be associated
with a single diagnosed case of polio.18
Coxsackievirus and echoviruses can cause paralytic syndromes that
are clinically indistinguishable from paralytic poliomyelitis.19
These "polio" cases are usually categorized as encephalitis or meningitis
during a proclaimed polio epidemic.
Benign Virus?
The poliovirus is considered to have been endemic throughout the world
going back to ancient times, yet this is not the case with paralytic
polio. According to Arno Karlen, author of Man and Microbes,
the "polio virus lives only in people; it probably adapted to the human
small intestine countless millennia ago." He continues, ". . . some
historians have claimed that [paralytic] polio goes back to ancient
Egypt; it may, but the evidence is thin."20
Karlen makes a lot of sense here in view of the pesticide graphs, Biskind's
arguments and ancient statements regarding paralysis from inhalation
of vaporized chemicals during blacksmithing operations. However, Karlen
goes on to write that "the first undisputed case dates from the late
eighteenth century." This statement, however, must be invalid (in its
attempt to establish polio images that have a basis in early history)
because of Menkes' statement (above) that other viruses can also be
causative for polio symptoms and because common industrial poisons such
as arsenic and lead compounds can cause polio-like symptoms. Poisoning,
as a method of assassination has also been frequently employed. It is
not unreasonable to assume that unsuccessful poisonings may have left
their victims paralyzed. Thus, Karlen's offer of an undisputed case
as early as the late 18th century can be no more than a guess.
Orthodox medical literature can offer no evidence that the poliovirus
was anything else than benign until the first polio epidemic, which
occurred in Sweden in 1887. This small epidemic occurred 13 years after
the invention of DDT in Germany, in 1874, and 14 years after the invention
of the first mechanical pesticide crop sprayer, which was used to spray
formulations of water, kerosene, soap and arsenic. The epidemic also
occurred immediately following an unprecedented flurry of pesticide
innovations. This is not to say that DDT was the actual cause of the
first polio epidemic, as arsenic was then in widespread use and DDT
is said to have been merely an academic exercise. However, DDT or any
of several neurotoxic organochlorines already discovered could have
caused the first polio epidemic if they had been used experimentally
as a pesticide. DDT's absence from early literature is little assurance
that it was not used.
We need to remember that the poliovirus is an enterovirus. There are
at least 72 known enteroviruses discovered to date. According to Duesberg,
many enteroviruses are harmless "passenger viruses."21 In
view of the material presented here, probably unknown to Duesberg, it
is reasonable that we also view poliovirus as harmless outside of extreme
laboratory conditions.
The Symbiotic Poliovirus
Having now established the possibility of an innocent poliovirus, its
presence in polio can be explained as follows: accelerated genetic recombination.
Genetic recombination is accelerated whenever a biological system is
threatened22 and pesticides can be that threat. The proliferation
of viruses can be part of the process of accelerated genetic recombination.
When a cell is critically threatened, accelerated genetic recombination
(which may include virus proliferation) is just one of a set of events
that may occur. This set of events is called the "SOS response," which
is known to be triggered by exposure to toxic chemicals or radiation.23
Arnold Levine, writing in Field's Virology, provides an example:
"When lysogenic bacteria were lysed [split open] from without, no virus
was detected. But from time to time a bacterium spontaneously lysed
and produced many viruses. The influence of ultraviolet light in inducing
the release of these viruses was a key observation that began to outline
this curious relation between a virus and its host."24
It is ironic that common medical procedures such as chemotherapy, radiation
therapy, and the use of toxic pharmaceuticals accelerate genetic recombination
and thus the potential for a necessary virus proliferation.
The SOS response is utilized in the Ames Assay Test, a standard test
whereby chemical toxicity is determined. According to the procedure,
bacteria are exposed to a chemical solution in question, and if a genetic
recombination accelerates via the spontaneous proliferation of viruses
from these bacteria, then the chemical is determined to be a poison.
The phenomenon is analogous to a poker player with a bad hand who must
request an exchange of cards and a reshuffled deck to improve the possibilities
for survival. In the Ames Assay Test, bacteria are concerned with their
genetic "hand" in order to improve their abilities to metabolize poisons,
create utilizations for poisons, and shield against poisons. Thus they
engage in this well-known phenomena of "gene shuffling," facilitated
by virus proliferation.
Thus, I propose that the poliovirus is a symbiotic (and possibly a
dormant) virus that behaves in a manner suggested by the phenomenon
found in the Ames Assay Test, a test used to determine toxicity.
Conclusion
The word "virus" is ancient Latin, meaning "slime" or "poison." Mainstream
science admits that most viruses are harmless, yet the word "virus"
adds to a biased and highly promoted language of fear regarding nature.
Definitions of viruses range from "pathogenic" to "not usually pathogenic."
The more popular the media source, the more frightening the definition.
Less fearful definitions would change the relationship between the medical
industry and its "patients."
Paradoxically, early virus studies considered virus filtrates to be
a poison, not a microbe, thus the name virus. Today, we know that viruses
are information.
Now, nearly a half-century later, the validity of Dr. Biskind's work
appears even more certain. Biskind's warning bears repeating:
"It was even known by 1945 that DDT is stored in the body fat of
mammals and appears in the milk. With this foreknowledge the series
of catastrophic events that followed the most intensive campaign of
mass poisoning in known human history, should not have surprised the
experts. Yet, far from admitting a causal relationship so obvious
that in any other field of biology it would be instantly accepted,
virtually the entire apparatus of communication, lay and scientific
alike, has been devoted to denying, concealing, suppressing, distorting
and attempts to convert into its opposite, the overwhelming evidence.
Libel, slander and economic boycott have not been overlooked in this
campaign."
The unique correlations between CNS disease and CNS poisons present
a variety of research opportunities not only in medical science, but
political science, philosophy, media studies, psychology, and sociology.
About the Author
Jim West has a background in engineering science and music composition.
Since 1999, he has served as Chairman of the Science Committee for the
NoSpray Coalition in New York City. The NoSpray Coalition has organized
environmentalists against the city's pesticide spray campaigns against
"West Nile virus." NoSpray, with the help of an environmental legal
team from Pace University and the New York Environmental Law and Justice
Project, sued the City of New York in federal court. That suit is ongoing.
NoSpray educates the public, engages its democratic and medical leadership
and holds press conferences. For details, see www.nospray.org.
©HARPUB 1985, 1998, 1999. All Rights Reserved.
Website: www.geocities.com/harpub
Email: harpub@hotmail.com
REFERENCES
- Handbook of Pesticide Toxicology, edited by Wayland J.
Hayes, Jr. and Edward R. Laws, Academic Press Inc., Harcourt Brace
Jovanovich, Publishers, San Diego, 1991, p769
- Morton S. Biskind, MD. Public Health Aspects of the New Insecticides.
American Journal of Digestive Diseases, New York, 1953, v
20, p331.
- US Vital Statistics, US Government Printing Office, Washington,
D.C.
- Daniel Dresden, Physiological Investigations Into The Action
Of DDT, G.W. Van Der Wiel & Co., Arnhem, 1949.
- Ralph R.Scobey, MD. The Poison Cause of Poliomyelitis and Obstructions
to Its Investigation. Archive of Pediatrics, April 1952.
- Mark Purdey's work can be found on the NIH website (PUBMED ID's
9572563, 8735882, 8735881) and in Wise Traditions, Spring
2000 and Spring
2002.
- www.whaleto.freeserve.co.uk.
- Thomas R. Dunlap, DDT: Scientists, Citizens and Public Policy,
Princeton University Press, 1981.
- Public Law 518, Federal Statutes, Volume 68, 1954, p 511.
- Public Law 905, Federal Statutes, 1956.
- The Federal Insecticide, Fungicide and Rodenticide Act, Federal
Statues, Volume 61, 1947, p 163.
- The National Adipose Tissue Survey, reported in Handbook of
Pesticide Toxicology, edited by Wayland J. Hayes, Jr. and Edward
R. Laws, Academic Press Inc., Harcourt Brace Jovanovich, Publishers,
San Diego, 1991, p 303.
- The Landsteiner and Popper study, first published in Germany, was
reported in Robert W Lovett, MD. The Occurrence of Infantile Paralysis
in Massachusetts in 1908. Boston Medical and Surgical Journal,
July 22, 1909, page 112.
- Peter Duesberg and Brian J. Ellison, Inventing the AIDS Virus,
Regnery Pub., 1996.
- Gerald L. Geison, The Private Science Of Louis Pasteur,
Princeton University Press, 1995.
- Julie Silver. Three Signs of Post Polio Problems. Accent on
Living, Winter 1995, v 40.
- Polio Packet, Centers for Disease Control, 1959.
- Richard T. Johnson, at the Department of Neurology, Johns Hopkins
University School of Medicine, published in Annals of the New
York Academy of Sciences, 1995 and excerpted in Jane Colby, ME:
The New Plague, First and Best in Education, Ltd, 1996.
- John H. Menkes, Textbook Of Child Neurology, 5th ed.,
Williams & Wilkins, 1995, p 420.
- Arno Karlen, Man and Microbes, G.P. Putnum's Sons, 1995.
- Peter Duesberg and Brian J. Ellison, Inventing The AIDS Virus,
Regnery Press, 1996, pp14, 74, 80.
- Molecular Approaches to Environmental Biology, edited
by Pickup, R.W and J.R. Saunders, Ellis Horwood publishers, 1996.
- Mark Ptashne, A Genetic Switch, Cell Press and Blackwell
Scientific Publications, 50 Church St., Cambridge, MA 02138, 1992.
- Fields Virology, edited by B.N. Fields and others, Lippincott-Raven
Publishers, Philadelphia, 1996, p 6.
SIDEBAR
Polio and Poison
A search of MEDLINE ("polio" and "poison") finds about 45 contemporary
articles where polio-like disease is attributed to poison. This recognition
of the relationship between polio and poison is restricted to the agriculture
industry--animals cannot hold industry liable. The terminology found
includes the following:
polioencephalomalacia
poliomyelomalacia
polyradiculoneuritis
polioencephalomyelomalacia
lumbal poliomyelomalacia
multifocal-poliomyelomalacia
spinal poliomalacia
polio and high-sulfate diets
bovine polioencephalomalacia
neurological picture similar to that of poliomyelitis
cerebrocortical necrosis (polioencephalomalacia)
lead poisoning in grey-headed fruit bats (Pteropus poliocephalus)
atypical porcine enterovirus encephalomyelitis: possible interaction
between enteroviruses and arsenicals
Polioencephalomalacia and photosensitization associated with
Kochia scoparia consumption in range cattle
SIDEBAR
Food for Thought
Polio outbreaks occurred most often during the summer and were blamed
on viruses picked up in swimming pools. But summer was the time when
DDT spraying was at its peak and exposure would have been greatest,
either directly or through foods from animals eating sprayed crops.
Summer foods like ice cream from DDT-sprayed dairy cows would have been
a likely source.
In developing countries, polio is blamed on poor sanitation. But in
the United States, polio was blamed on lack of immunity due to good
sanitation!
Until the advent of AIDS, polio was the only disease whose cause was
enshrined in legislation. US public health law stated that poliomyelitis
was an "infectious contagious disease," yet proof of poliovirus causation
is astoundingly weak, and the obvious toxicology was entirely avoided.
The man most responsible for the view that poliomyelitis was contagious
was Dr. Simon Flexner, author of the famous (or infamous) Flexner Report,
which led the way to the closing of the naturopathic and homeopathic
colleges in the United States. Said Flexner: "It was not easy to establish
in an individual case precisely how the disease was acquired; it was
difficult to bring evidence that was not at all convincing that this
disease was contagious." In discussing Flexner's report, L. Emmett Holt
stated: "Even five years ago, if anyone had suggested that the disease
under discussion was an infectious or contagious one, it would have
been looked upon as a joke (Scobey, Archives of Pediatrics,
May 1951).
In 1953, Dr. Kumm was appointed Director of Research of the National
Foundation for Infantile Paralysis (NFIP). The NFIP was funded by its
"March of Dimes" program, and it sponsored the hasty development of
the Salk vaccine in the early 1950s, at the height of the DDT/polio
controversy. Dr. Kumm also "served as a civilian consultant to the Surgeon
General . . . directing field studies of the use of DDT. . ." (American
Journal of Digestive Diseases, 1953 20:330).
The World Health Organization directs both DDT application (for mosquito
control) and polio vaccination worldwide.
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