POLIO & DDTIn 1953, when Biskinds writings were published, the United States had just endured its greatest polio epidemic. The entire public was steeped in dramatic imagesa 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 mosquitoes. 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 epi-demic: Central nervous system diseases such as polio are actually the physiological and symptomatic mani-festations of the ongoing government and industry sponsored inundation of the worlds populace with central nervous system poisons.

Today, few remember this poignant writer who strug-gled 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 sell-er, by limiting her focus to the environment and wild-life. 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 fi-nal paragraphs of scientific articles, are usually done with an appearance of impartiality. With great antici-pation, I went to a medical library and found Biskinds 10-page 1953 article in the American Journal of Diges-tive Diseases. Presented below are excerpts regarding polio from the article.

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, dichlorodiphenyl-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 devel-opment 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 commu-nication, 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 over-looked 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 fa-

tal syndromes in dogs and cats. The relationship was promptly denied by government officials, who provid-ed no evidence to contest the authors 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 fol-lowing known exposure. We have described the syn-drome as follows:

...In acute exacerbations, mild clonic convulsions involving mainly the legs, have been observed. Several young children exposed to DDT developed a limp last-ing 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 in-cidence of polio had been increasing prior to 1945 at a fairly constant rate, but its epidemiologic character-istics remained unchanged. Beginning in 1946 the rate of increase more than doubled. Since then remark-able 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 (1945-1953)

In the graph above, I provide confirmation of Biskinds observations for 1945-1953, in terms of polio incidence and pesticide production. I have utilized pesticide data from Hayes and Laws which they had derived from US Tariff Commission data. Polio incidence data was gathered from US Vital Statistics. Although I argue herein against Hayes characterization of Biskinds work, credit goes to Hayes for publishing arcane pesticide data. All graphs refer to paralytic polio.

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 de-generation 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 main-tains its epidemic character year after year, is it unrea-sonable to suspect an etiologic relationship?

Before finding Biskinds work, I had spent months en-gaged 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 en-vironmental 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 bio-chemistry 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 Germany) of the physiology of acute DDT poisoning by Daniel Dres-den (Physiological Investigations Into The Action Of DDT, G.W. Van Der Wiel & Co., Arnhem (1949)). This study confirms that DDT poisoning often causes polio-like physiology:

Conspicuous histological degeneration was, however, often found in the central nervous system. The most strik-ing 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.

So we find that especially the cerebellum and the spinal cord are histologically affected by DDT.

And more recently, in the works of Ralph Scobey, MD, 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 wasnt 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 usu-ally with regard to paralysis in animals. A search of Medline (polio and poison) finds numerous contemporary articles where poison causation is attributed to polio. The terminology found: polioencephalomalacia, poliomy-

elomalacia, neurological picture similar to that of po-liomyelitis, polioencephalomyelomalacia, lumbal poliomyelomalacia, cerebrocortical necrosis (polio-encephalomalacia), multifocal-poliomyelomalacia, spinal poliomalacia, Polio and high-sulfate diets, Atypical porcine enterovirus encephalomyelitis: pos-sible interaction between enteroviruses and arseni-cals, Polioencephalomalacia and photosensitization associated with Kochia scoparia consumption in range cattle, bovine polioencephalomalacia.

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. 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.(http://www.whaleto.freeserve.co.uk)

Morton S. Biskind had the courage to write about hu-mans. His views fell into disfavor after the introduc-tion of the polio vaccines, which was a grand act that proved in most peoples 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 pesti-cides, 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 patients stay in a hospital are not necessarily due to microbes. He died not long thereafter, in his late 60s. I dont have the precise date of death, though his birth was in 1906.

A Contemporary Study

Below are three graphs that confirm Biskind, utilizing data that spans far beyond his observations. Due to the paucity of data regarding pesticide exposure and locale, these findings of production data are presented as an in-

dication of exposure, keeping in mind the great changes in public awareness and legislation beginning circa 1950, which also served to reduce DDT exposure. Pesticide production data comes from Hayes and Laws.

DDT vs Polio (1940-1970)

In this graph (next page) I did not include DDT data for the period of 1954 onward because DDT distribution was then being shifted out of the U.S. and into developing nations, while its U.S. production skyrocketed.

Governmental hearings, including those with Biskind, Scobey and others, brought about greater awareness of DDT dangers, as well as better labeling and handling methods. Due to public governmental debate in 1949-51 and numerous policy and legislative changes afterward, DDT production figures after these dates do not correlate with US usage or exposure to DDT.

DDT Before 1950

Before 1950, DDT was hailed as a miracle of progress that was virtually non-toxic to humans, in spite of FDAs warnings and attempts to keep it off the market. This photo on the left is one of several similar photos from Zim-merman, et al, DDT: Killer of Killers (1946). The advertisement on the right is from an unknown source, though it appears to be circa 1954.

DDT after 1950

Governmental hearings, including Biskind and Scobey, et al, brought about greater awareness of the dangers, bet-ter labeling and handling methods.

DDT after 1954

This period is given special consideration for DDT.

After 1954, DDT production increased tremendously, but mainly as an export product. Due to public governmen-tal debate in 1950-51 and numerous policy and legislative changes afterward, its production figures thereon do not at all correlate with U.S. usage or exposure to DDT.

As many studies demonstrate, DDT exposure after 1954 declined sharply, and this decline is represented in the following graph, along with supporting data. DDT production is not shown, post-1954.

Historical context: DDT was incriminated from 1950 until its registration cancellation in 1968 and ban in 1972. Thus, 1950-1951 represent a point of increased public awareness, changes in legislation and policy, voluntary phase-out, and labeling requirements. It is significant for this comparison of DDT against infantile paralysis, that before the period of increased awareness, DDT was mandated on dairies, yet afterward, ruled out of dairies. Much of the domestic usage was shifted to forestry applications, placing less DDT directly into the food chain.

The visual impact of all the persistent pesticide graphs rests upon the assumption that production correlated with human exposure. Given the lack of regulation and the extreme media hype surrounding DDT before 1953, this is not an unrealistic assumption.

It is clear that post-1954 DDT production did not correlate with human exposure. Yet, it is possible to estimate relative values for exposure post-1954. This can be accomplished by reviewing DDT levels in adipose tissue (Na-tional Adipose Tissue Survey, and other studies), considering DDT in imported food, and considering the daily amounts of ingested DDT.

The early trend of National Adipose Tissue Surveys can be interpolated back to 1944, six years from 1950, the first Survey year, because it is safe to assume that DDT tissue levels were zero in 1944, since DDT was intro-duced for domestic usage in 1945. The estimate of DDT exposure is a reasonable 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.

Note that no scale or factor is provided for relative DDT exposure. The Sur-vey values are presented without distortion, linearly, with the starting point at 1954, and values for DDT exposure are estimates based on the the Survey and DDT ingestion data.

Error is limited by two boundaries, for the estimated values of DDT exposure. 1) Exposures downward slope must be much greater than the Survey lines downard slope, because of DDTs half-life. 2) Exposure values must continue at least through 1968.

Hayes and Laws also used a secondary evaluation, DDT intake per day, to ex-plain that from 1954 to 1964-67, DDT ingestion decreased by an approximate factor of five. Significantly, the Salk vaccine program began in 1954.

The observed decrease in the concentration of DDT in food (Walker et al., 1954; Durham et al., 1965a; Duggan, 1968) offers an adequate reason for the decrease in storage in people. The average intake of p,p-DDT and of total DDT-derived material was 0.178 and 0.280 mg/human/day, respectively, in 1954, but only 0.028 and 0.063 mg/human/day, respectively, during the period 1964-1967. - Hayes and Laws, page 303.

BHC vs Polio (1940-1970)

BHC (benzene hexachloride), a persistent, organochlorine pesticide, is several times more lethal than DDT, in terms of LD50, i.e., the lethal dosage required to kill 50 percent of a test population.

Unlike the situation with DDT, in which there have been few recorded fatalities, there have been a number of fatalities following poisoning by the cyclodiene and hexachlorocyclohexane-type insecticides. The chlorinated cy-clodiene insecticides are among the most toxic and environmentally persistent pesticides known. - Hayes & Laws

As shown in the graph below, BHC was produced in 1945-1954 at quantities similar to DDT. In spite of BHCs 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. It is tempt-ing to ask whether highly public DDT was fronting for the more dangerous BHC. BHCs correlation with polio incidence is astonishing.

From The DDT Patent Issued June 17th, 1952:

DT presents a definite toxicity hazard to warm-blooded animals

From The DDT Patent Issued June 17th, 1952:

An insecticidal composition having prolonged residual effectiveness

Lead-Arsenic vs. Polio (1940-1970)

After viewing the DDT and BHC graphs above, note that the period of 1940-46 is unaccounted for in terms of polio-pesticide correlation. The missing piece of the puzzle for this six-year period is supplied by the lead and arsenic compounds. These types of central nervous system (CNS) poisons have been the central component of pesticides since their widespread use beginning approximately 1868 until the advent of the organochlorine pesti-cides in the early 1940s. For those who have thought that organic food was the norm before the release of DDT to the civilian sector in 1945, the immense production of lead-arsenic compounds presented in this graph is disap-pointing. This data requires a reconsideration of any perception regarding natural quantities of arsenic found in apple seeds, apricots, or almonds, where pesticides can accumulate systemically from contaminated earth.

the most intensive campaign of mass poisoning in known human history

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 ware-house, 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 organo-chlorines (DDT and BHC) is represented in the following:

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 relation between pesticides and paralytic 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 com-plicated virus arguments, even as a co-factor, unless there exists a rigorous proof for virus causation. Polio shows no movement independent from pesticide movement as one would expect for the virus model.

Medical propagandists promote images of a predatory, infectious virus, invading the body and quickly replicating to a level that causes disease, however, in the laboratory, poliovirus does not easily behave in such a predatory manner. Attempts to demonstrate virus causation are performed under extremely artificial and aberrant condi-tions.

Poliovirus causation was first established in the mainstream mind by publications of an experiment by Landsteiner and Popper in Germany, 1908-1909. Their method was to inject a pulverized pure of diseased tissue intraperito-neally into two monkeys. One monkey died after six days 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 re-cently been criticized by the molecular biologist Peter Duesberg regarding a modern-day attempt to establish vi-rus causation for kuru, another CNS disease. 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 pes-ticide 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 pure 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.

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 per-vasive silence regarding pesticide causation juxtaposed against a steady stream of drama regarding virus causa-tion. 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 (which directs both DDT appli-cation for mosquito campaigns and polio vaccination, world-wide).

Virus Presence

When the symptoms of polio are recognized, there is often a claim of virus presence in the body of the polio vic-tim. 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, my argu-ment for the innocence of the poliovirus requires an explanation of these claims of virus presence and the presence of an agent called the poliovirus. Here are three points:

a) Economic Impetus: 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. Thus, presence of poliovirus in poliomyelitis was rarely determined in order to arrive at a diagnosis of polio.

b) Other Pathogens: Even if one believes in virus culpability, other viruses are also claimed by orthodoxy to be the cause of polio-like CNS diseases which are clinically indistinguishable from polio. In the 1940-50s, rela-tively few polio victims were confirmed technically for presence of the poliovirus. In 1958, a laboratory analyses of 222 diagnosed polio victims (Detroit epidemic) found poliovirus in only 51% of the cases. When multiple pathogens are hunted, a mix of pathogens, multiple viruses, fungi, and bacteria, can be associated with a single diagnosed case of polio.

Coxsackievirus and echoviruses can cause paralytic syndromes that are clinically indistinguishable from paralytic poliomyelitis. (John H. Menkes, Textbook Of Child Neurology, 5th ed., (1995 p420)

During a polio epidemic, such cases, would have likely been diagnosed as polio. After the 1970s, with the supposed approaching extinction of the poliovirus, such cases would have been diagnosed as encephalitis or meningitis.

c) 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.

Karlen makes a lot of sense here in view of the pesticide graphs, Biskinds arguments and ancient historians de-scribing paralysis from the 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 assassina-tion has also been frequently employed. It is not unreasonable to assume that unsuccessful poisonings may have left their victims paralyzed. Thus, Karlens 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. DDTs 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 virus-es. In view of the material presented here, probably unknown to Duesberg, it is reasonable that we also view poliovirus as harm-less 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, with five more points:

a) Accelerated Genetic Recombination: Genetic recombination is accelerated whenever a biological system is threatened. Pesti-cides can be that threat. The proliferation of viruses are known to be part of the process of accelerated genetic recombination.

b) The SOS Response: When a cell is critically threatened, ac-celerated genetic recombination (which may include virus prolif-eration) 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 trig-gered by exposure to toxic chemicals or radiation.

Arnold Levine, writing in Fields Virology, provides an example:

When lysogenic bacteria were lysed [split open] from without, no virus was detected. But from time to time a bacterium spon-taneously lysed and produced many viruses. The influence of ul-traviolet 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.

Is this mere irony? Common medical procedures such as chemo-therapy, radiation therapy, and the use of toxic pharmaceuticals accelerate genetic recombination and thus the potential for a necessary virus proliferation.

c) The Ames Assay Test: 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.

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 worlds

populace with central nervous system poisons

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.

One could object to this analogy on the grounds that because the Ames Test utilizes prokaryote cells (bacteria-like cells) rather than eukary-ote cells (nucleus-containing cells that comprise multicellular tissue) and because it is asserted that poliovirus invokes damage by infecting eukaryote cells, the explanation is invalid. However, the evolution of eukaryotes includes structures and functions inherited from symbiot-ic unions of prokaryotes. Eukaryotes continue to possess to this day prokaryote functionality such as found in the genetic independence of the organelles within the eukaryote cells, such as mitochondria (Lynn Margulis and Dorion Sagan, What Is Life? (1995), and, Lynn Margulis, Dorion Sagan, Slanted Truths: Essays on Gaia, Symbiosis, and Evolu-tion (1997)). Thus, generalizations derived from the Ames Test can contribute well to a valid hypothesis for the presence of poliovirus in polio.

d) Dormant Virus: When a cell is critically threatened by toxic chem-icals (or radiation) it can invoke survival mechanisms (the SOS Re-sponse) such as the suspension of metabolism, or the activation of dor-mant viruses, triggering their proliferation from the cell such viruses are said to be dormant or latent. These words are not my preference because the way that they are popularly used implies that viruses are only externally generated and are found in the cell in a condition of tem-porary rest (dormancy). In cyclical phenomena, such as the life cycle of the virus, the starting point is a political-philosophical decision. The orthodox virus image (possibly a projection of the orthodox mind) is of an external, selfish, non-living parasite that tricks cells into infect-ing themselves with the virus and then to replicate said virus with cell machinery. Dormant viruses are publicized as external life forms that spend most of their time (as much as several decades) waiting inside cells, awaiting activation to perform parasitic activities.

Recently it has become known that a tremendous amount of human DNA is devoted to virus proliferation. The virologist, Eleni Papadopu-los-Eleopulos, stated in Continuum, Autumn 1997:

...its accepted that endogenous retroviral DNA forms about 1% of hu-man DNA... thats about 3,000 times larger than what the experts claim is the size of the HIV genome. And whats more, new retroviral ge-nomes can arise by rearrangements and recombination of existing ret-roviral genomes.

Like the retroviruses, the poliovirus is an RNA virus and has a genome of similar weight and length. There is suspicion of dormant character-istics because enteroviruses have been found by several independent investigators, in post-polio (PMID: 8818905, UI: 96415998 (Lyon, France, Aug., 1996) and others).

e) Gene Sharing: Viruses represent shared capability, shared data, and data in transit. They are genetic couriers. Shared data decreases the burden on each cell to carry all capabilities. Capability, in the form of genetic informa-tion, can be stored in the environment as virus gene packets, and different capabilities can be stored in different cells, just as humans each have, to some degree, uncommon capabilities which are shared with the community as needed. In the microbiotic world, when a specific capability is needed, cells share genetic information from the dynamically changing universal library of free floating genetic material, such as exists in viruses, free organelles, symbiotic parasites, and free nucleic acid, in addition to straight sexual intercourse where nucleic acid is trans-ferred directly form cell to cell. It could be said that cells can carry unused (dormant) genetic information in the form of nucleic acid and when that information is required, share it through the proliferation of viruses.

For example, in terms of disease, a symbiotic virus presence could be explained as a provider of cathartic capabilities or mechanisms, appropriate for various toxic or stressed environments. These cathartic mechanisms are manifested as disease symp-toms, in the form of masses of sacrificed leucocytes, obviously found in boils, pim-ples, and pocks. Orthodoxy gives the label transduction to the processes of virus infection. Transduction is one of several modes of intercellular transport of genetic material, which allows for direct, laterally passed genetic data. Such data is routinely used to alter cell structure and metabolism modes dynamically, without engaging in the slower, more formal, sexual reproduction cycles. The concept of the symbiotic virus is explained in Encyclopedia Britannica, Macropaedia (1990) p507:

Although viruses were originally discovered and characterized because of the diseases they cause, most viruses that infect bacteria, plants, and animals (including humans) do not cause disease. In fact, bacteriophages [bacteria viruses] may be helpful in that they rapidly transfer genetic information from one bacterium to another, and viruses of plants and animals may convey genetic information among similar species, aiding the survival of their hosts in hostile environments.

Britannica continues with a praise of industrial biotechnology, and abruptly converts the probable-present into a future-made-possible by dependent consumers:

This could in the future be true for humans as well. Recombinant DNA biotechnology may allow genetic defects to be repaired by injecting afflicted persons with harmless viruses that carry and integrate functional genes to supplant defective ones.

The implication is that humans are not part of nature, however, in the next sentence Britannica states that we humans may already utilize symbiotic viruses:

Such events may actually occur in nature in the transmission of good viruses from one person to another.

The nature-friendly view, that viruses are effective genetic symbionts, dilutes the market impact of genetic-based treatments alluded to by Britannica, and threatens biotech profits. Perhaps this explains certain aspects of the cur-rent worldwide war against virus-carrying mosquitoes?

Virus Contradictions

The concept of a predatory poliovirus becomes less certain in the context of these little known virus facts:

1. Poliovirus [I]nfectosomes have yet to be experimentally demonstrated, writes Roland R. Rueckert,

under the subtitle, Infection: A Rare Event in Fields Virology.

2. Eukaryote cells have a wide arsenal of activities to control the half-lives of mRNAs, and these nucleases have made it difficult to isolate intact RNA viral genomes from cells. (Virus Evolution, Ellen G. Strauss, et al, Fields Virology, Lippincott - Raven Publishers, Philadelphia (1996), v1p163) In view of item 1, this appears to be another careful way of saying never.

3. The poliovirus does not always infect in accordance to its notoriety, For every 200 or so virus particles that encounter a cell, only one will successfully enter and replicate, so research in this area is often confounded by

the rarity of successful entry. (http://cumicro2.cpmc.columbia.edu/PICO/Chapters/Cellular.html)

4. Only herpesvirus has been traced enroute to site of disease from site of in-fection. Viruses during retrograde transport on their way up to the cell bodies have so far been localized ultrastructurally only in the case of herpes simplex and herpes virus suis. (Martin E. Schwab and Hans Thoenen, Encyclopedia of Neuroscience, edited by George Adelman, pub, Birkhaser Bros. Inc., Boston (1987), Chapter 39, p102-3)

5. A poliovirus has been electrophotographed in cell tissue. Due the lack of any photos of the virus as an infectosome, these photos should be interpreted as evidence of the cells SOS response rather than of poliovirus causation. Electro-photography has existed for several decades and has yet to photograph a poliovirus infectosome. An infectosome is a membrane-associated particle... which transfers genomic viral RNA through the membrane. (Fields Virology (1996), p635)6. It seems likely that all viruses trace their origins to cellular genes and can be considered as pieces of rogue nucleic acids. (Encyclopedia Britannica, Micro-paedia (1997), Virus) This demonstrates the great potential for a symbiotic relation between viruses and hosts.

7. The point in history when known viruses began their evolution has been calculated by molecular biochemists who have interpolated backwards through time the speed and direction of virus evolution. They found that most viruses we know today have probably evolved since the last ice age. (Virus Evolution, Ellen G. Strauss, et al, Fields Virology (1996), p164)

8. Viruses are involved in a process called transduction, one of the three modes of ge-netic transfer between cells, a process that can accelerate genetic recombination when

cells are critically threatened by poisons.

9. Virus infection is used by clone technology to transfer genetic material into cells.

10. Genetic information moves between viruses and their hosts to the point where definitions and classifica-tions begin to blur. (Fields Virology (1996) p6)

11. In terms of genetic similarity, [T]here was a remarkable continuum... from virus to host. (Fields Virol-ogy (1996) p6)

12. Carrel (1926) was able to produce tumors resembling Rous sarcoma and transmissible by cell-free fil-trates with indol, arsenic, or tar in chicken embryo. Carrels observations have been confirmed by other workers.

Delousing at Dachau with DDT

Fischer (1926), by treating cultures of normal cells with arsenic obtained on one occasion a filtrable virus capable of causing tumors. (Ralph R. Scobey, M.D., Poliomyelitis Caused by Exogenous Virus?, Science, v71 (1954))

Redefinition

Any of the items listed above can be used to direct work towards a refreshing view of viropathology. For instance, Alexis Carrel and Albert Fischers experiments, in 1925-1926, preceded the discovery of the cellular SOS Response by decades. Their work is important in its impact on the basic tenants of viropathology, the contemporary proofs of virus causation, and definitions of immunity. Carrel, who happens to be one of the most recognized of all the Nobel Laureates, has stated without equivocation that the Rous sarcoma tumour is not infective, is caused by an agent within the cells themselves, yet is transmissible by cell-free Berkfeld fil-trate of tumour extract. He states that the agent could not be a virus because of his assumption that a virus is an external, disease-causing, infectious entity. In retro-spect such statements reveal the first (unrecognized) discovery of the dormant ret-rovirus. Carrel also clearly demonstrates poison causality for cancer. These land-mark experiments are very simple, very clear, and totally ignored by orthodoxy.

If one views Carrel and Fischer as a reinforcement of the symbiotic virus para-digm, then two strong alternative views can be defined regarding work that has been based on injections.

Virus Disease

In the case of classical induction of disease by injection of extremely high quanti-ties of virus, the alternative view would be that the presence of such quantities of virus serve as an informational context, a context that indicates imminent toxic death to nave tissue, with an expected tissue reaction (disease). Or in other words, disease induction (via injection) is no more than an over-reaction (like jumping out of a window when someone yells fire) in terms of inflammation and cathar-sis (disease manifestations).

Immunity: In the case of the classical demonstration of immunity whereby surviv-ing subjects are found immune to attempts to induce disease by subsequent injec-tions of virus, the alternative view is you cant fool them twice.Thus, a) inducement of disease by the injection of high-quantities of virus, and b) acquired immunity in survivors of these injections, can both be viewed as parlour tricks, though claimed to be demonstrations of virus causation for disease.

Conclusion

The word virus is ancient Latin, meaning slime or poison. Mainstream sci-ence 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. Biskinds work appears even more certain. Again, according to Biskind:

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 relation-ship 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 boy-cott 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, phi-losophy, media studies, psychology, and sociology.

Peregrine Falcons and DDTUnderstanding Bio-accumulation Of Toxins In The Environment

Scanning EM comparing eggshell thickness between 1896 and 1969Even the youngest students that we talk to in the third and fourth grade seem to understand what it means to be listed as endangered and that the peregrine falcon and bald eagle were added to the endangered species list largely because of the impact of dichloro-diphenyl-trichloroethane (DDT).

DDT was considered to be a safe and effective insecticide in the 1940s and 1950s. It was used worldwide as an agricultural insecticide, and to combat lice and mos-quitos responsible for the spread of human diseases such as typhus, and malaria. At the time, there were no known significant adverse effects to either animal or human health. Scientists later discovered the harmful effects of this pesticide and its derivatives in the environment. Select image at right to enlarge view.

Crushed Wild EggWhen DDT was in wide and common use, daily doses of the chemical accumulated in the fatty tissue of the peregrine. The use of DDT was diminished and for some uses banned in 1972, however residual DDT in the en-vironment today continues to contaminate peregrine falcons. Through a biologi-cal coincidence, the stored chemicals acted to block the movement of calcium during eggshell formation causing the shells to be thin. Peregrine falcon eggs broke and embryos died at an alarming rate around the world, alerting biologists long-term to search for a cause.

Chemical Structure of DDT (C14 H9 Cl5)DDT is an organochlorine, and is highly persistent in the environment. In soil DDT is reported to have a half life between 2-15 years. Its metabolic products (DDE, DDD) accumulate through the food chain, with top level predators such as raptors having a higher systemic concen-tration of the chemicals than other animals sharing the same environment. DDE

(dichloro-diphenyl-ethylene) is the most stable and toxic of the DDT metabolites.

Original Documents: Long history of DDT trouble, from U.S. Fish and Wildlife Service

Archives of the U.S. Fish and Wildlife Service (FWS) reveal a long history of trouble with DDT, almost from the first uses of the chemical as an insecticide during World War II. Youll find ex-tensive links to historic press releases from FWS below the fold. Critics of the various restrictions on DDT use often claim that DDT is a God-sent chemical that nearly eradicated malaria from the world (absolutely untrue) and which was banned only because of hysteria caused by Rachel Car-sons 1962 book, Silent Spring (untrue at both ends, hysteria and the power of Carsons book). This is history revisionism at its worst, it is bogus history.

A careful study of the history of the use of DDT shows that scientists were concerned about its dangers from the first uses as a pesticide. The U.S. Fish and Wildlife Service reported dangers in a press release on August 22, 1945, just a week after the surrender of Japan ended World War II (VJ Day was August 15 in Tokyo, August 14 in Washington). In that release FWS noted the ben-eficial uses of DDT to fight insect and lice infes-tations that threatened troops and civilians with typhus and other diseases, but cautioned that such use should not become common, that more study

was needed:

Praising DDT as an outstanding scientific achievement and a very valuable tool, Dr. Clarence Cottam, Direc-tor of Wildlife Research of the Fish and Wildlife Service, said that caution in its use is essential because of our incomplete knowledge of its action on many living things, both harmful and beneficial.

Its use by the armed forces in Europe and the Pacific in killing disease-carrying insects was so effective and the need so urgent that its effects on other organisms had to be overlooked. Present information is based largely on single applications of DDT spray. The effects of repeated applications are little known.

FWS had good reason for concern. Their tests had already shown DDT could kill waterfowl, which started the agency on a long quest for alternatives to DDT spraying of estuaries and swamps, in order to protect migratory waterfowl and the ecosystems that maintain their habitat.

Repeatedly through the next 50 years FWS noted serious problems with DDT and its effects on wildlife. FWS created an on-line archives of their press notices on DDT which traces this history clearly and convincingly.

Teachers can use these documents for document-based questions (DBQ) and exercises. Students can track the history of the ban of DDT through this one series of press releases, or supplement projects they may propose on DDT and its effects.

Because raptors and especially peregrine falcons exist at the top of food chains, regular surveys of their popu-lation status can reveal threats to environmental health before they become hazards to human beings. The Pred-atory Bird Research Group continues to study the per-egrine falcon and monitor its breeding status because we believe it is an important indicator of ecosystem health. Our longterm studies of the peregrine falcon population in California could be very important to future assess-ments of the natural environment and have value for pre-dicting future threats to human health.

Organic Versus Man Made

A panel of experts, put together by the president and known as the cancer panel, released a report yesterday that brings to light the potential danger of all sorts of chemicals found in everyday products that Americans use. The report also shines a spotlight on the negative effects of under-regulation and points out that out of 80,000 or so products, only several hundred have even been tested for safety. The final report included a slew of suggestions for consumers, including the use of or-ganic foods and products (I can just see how the right will characterize this as Obamas organic arugula re-port?). The fact that people are seeing this report as be-ing a departure from the norm should tell us a lot about our priorities as a society.

The struggle against companies out to make a profit, no matter what the risk to our health, has been around for ages. Remember DDT? Then theres the entire tobacco industry. Oh, and dont forget our more recent struggle with the plastic additive BPA. Though federal legislation has been proposed to ban its use, the bill is none too pop-ular, especially considering the lobbying powers of the food industry. Corporations have never really had our best interests at heart, it seems. Just the other day I listened to Maureen Storey - Senior Vice President, Science Policy, American Beverage Association try to argue on NPR that soda is comprised mostly of water, and therefore its good for you. Uh, yeah. Sort of like Bill Cosbys conclusion that its ok to eat chocolate cake for breakfast because it contains eggs and milk (except that hes a comedian, and shes scientist). The panel also pointed out that when evidence of the effect of a substance is unclear, we err on the side of the chemical, rather than our health. Though the government may urge us to steer clear of endocrine disruptors(which sound like something from a sci-fi thriller), they wont go so far as to ban them from the products we use in our everyday lives. I cant help assuming that these decisions are being motivated by some companys bottom line.

Is it silly to think that this new report could be the beginning of a shift in values? Might we begin to place more emphasis on protecting Americans from chemicals that cause cancer and other health issues and less emphasis on protecting a corporations right to make a profit at any cost? I suppose theres always hope. And until then, you should very carefully check out the safety of all of the products you use and avoid known poisons.

Policy makers and concerned citizens will notice that in these releases are direct refutations of claims made by pseudo-science groups such as JunkScience.com, that the 1927 EPA ban on most uses of DDT was not fully con-sidered, not based on long-term research, or not based on research at all. These releases directly refute claims that DDT was not found harmful to birds and other wildlife. A collection of these Press Releases appears below:

MERE TRACE OF PESTICIDE KILLS AQUATIC LIFE, INTERIOR DEPARTMENT STUDY REVEALShttp://www.fws.gov/news/historic/1965/19650907a.pdf

DEAD AND DYING BIRDS ARE FOUNDhttp://www.fws.gov/news/historic/1945/19450822.pdf

INTERIOR ENDORSES RESEARCH PROGRAM ON EFFECTS OF PESTICIDES ON WILDLIFE http://www.fws.gov/news/historic/1959/19590621.pdf

SECRETARY UDALL TESTIFIES ON PESTICIDE PROBLEMS, WARNING OF HAZARDShttp://www.fws.gov/news/historic/1963/19630522a.pdf

HIGH PERCENTAGE OF NORTH AMERICAN BALD EAGLES CARRY DDT, http://www.fws.gov/news/historic/1964/19641115.pdf

PESTICIDE RESIDUES FOUND IN ANIMALS THROUGHOUT WORLDhttp://www.fws.gov/news/historic/1966/19660203.pdf

SECRETARY HICKEL BANS USE OF 16 PESTICIDES ON ANY INTERIOR LANDS OR PROGRAMShttp://www.fws.gov/news/historic/1970/19700618.pdf

TEN YEARS LATER: BIRD POPULATIONS RISE AS DDT DECLINES IN THE ENVIRONMENThttp://www.fws.gov/news/historic/1982/19820308a.pdf

Mutant Polio Virus Spreads in Nigeria124 Children Afflicted This Year

By A Paralyzing DiseaseBelieved To Be Caused By The Same Vaccine Used To Fight It

Aug. 14, 2009

(AP) Polio, the dreaded paralyzing disease stamped out in the industrialized world, is spreading in Nigeria. And health officials say in some cases, its caused by the vaccine used to fight it.

In July, the World Health Organization issued a warn-ing that this vaccine-spread virus might extend beyond Africa. So far, 124 Nigerian children have been para-lyzed this year - about twice those afflicted in 2008.

The polio problem is just the latest challenge to glob-al health authorities trying to convince wary citizens that vaccines can save them from dreaded disease. For years, myths have abounded about vaccines - that they were the Western worlds plan to sterilize Africans or give them AIDS. The sad polio reality fuels misguided fears and underscores the challenges authorities face using a flawed vaccine. Nigeria and most other poor nations use an oral polio vaccine because its cheaper, easier, and protects entire communities. But it is made from a live polio virus - albeit weakened - which car-ries a small risk of causing polio for every million or so doses given. In even rarer instances, the virus in the vaccine can mutate into a deadlier version that ignites new outbreaks.

The vaccine used in the United States and other West-ern nations is given in shots, which use a killed virus that cannot cause polio. So when WHO officials discov-ered a polio outbreak in Nigeria was sparked by the polio vaccine itself, they assumed it would be easier to stop than a natural wild virus. They were wrong. In 2007, health experts reported that amid Nigerias ongoing out-break of wild polio viruses, 69 children had also been paralyzed in a new outbreak caused by the mutation of a vaccines virus. Back then, WHO said the vaccine-linked outbreak would be swiftly overcome - yet two years later, cases continue to mount. They have since identified polio cases linked to the vaccine dating back as far as 2005. It is a worrying development for officials who hope to end polio epidemics in India and Africa by the end of this year, after missing several earlier deadlines. Its very disturbing, said Dr. Bruce Aylward, who heads the polio department at the World Health Organization.

This year, the number of polio cases caused by the vaccine has doubled: 124 children have so far been paralyzed, compared to 62 in 2008, out of about 42 million children vaccinated. For every case of paralysis, there are hun-dreds of other children who dont develop symptoms, but pass on the disease.

When Nigerian leaders suspended polio vaccination in 2003, believing the vaccine would sterilize their children and infect them with HIV, Nigeria exported polio to nearly two dozen countries worldwide, making it as far away as Indonesia. Nigeria resumed vaccinations in 2004 after tests showed the vaccine was not contaminated with estrogen, anti-fertility agents or HIV. Experts have long believed epidemics unleashed by a vaccines mutated virus wouldnt last since the vaccine only contains a weakened virus strain - but that assumption is coming under pressure. Some experts now say that once viruses from vaccines start circulating they can become just as danger-ous as wild viruses.

The only difference is that this virus was originally in a vaccine vial, said Olen Kew, a virologist at the U.S. Centers for Disease Control and Prevention. The oral polio vaccine used in Nigeria and elsewhere contains a

mild version of the live virus. Children who have been vaccinated pass the virus into the water supply through urine or feces. Other children who then play in or drink that water pick up the vaccines virus, which gives them some protection against polio. But in rare instances, as the virus passes through unimmunized children, it can mutate into a strain dangerous enough to ignite new outbreaks, particularly if immunization rates in the rest of the population are low. Kew said genetic analysis proves mutated viruses from the vac-cine have caused at least seven separate outbreaks in Nigeria. Though Nigerias coverage rates have im-proved, up to 15 percent of children in the north still havent been vaccinated against polio. To eradicate the disease, officials need to reach about 95 percent of the population. Nigerias vaccine-linked outbreak under-lines the need to stop using the oral polio vaccine as soon as possible, since it can create the very epidemics it was designed to stop, experts say. WHO is research-ing other vaccines that might work better, but none is on the horizon. Until a better vaccine is ready, WHO and U.S. CDC officials say the oral vaccine is the best available tool to eradicate polio and that when inocula-tion rates are nearly 100 percent it works fine.

Nigeria is almost a case study in what happens when you dont follow the recommendations, Kew said.

Since WHO and partners began their attempt to rid the world of polio in 1988, officials have slashed the diseases incidence by more than 99 percent. But numerous deadlines have been missed and the number of cases has been at a virtual standstill since 2000. Critics have also wondered whether it is time to give up, and donors may be sick of continuing to fund a program with no clear endgame.

Eradication is a gamble, said Scott Barrett, an economist at Columbia University who has studied polio policies. Its all or nothing ... and there is a very real risk this whole thing may fall apart.

Aside from Nigeria, polio persists in a handful of other countries, including Afghanistan, Pakistan, India, Chad, Angola and Sudan. Aylward agreed the Nigeria situation was another unwelcome hurdle, but was confident eradi-cation was possible. We still have a shot, he said. Were throwing everything at it including the kitchen sink.

Whooping Cough and Pesticide ProgramsCalifornia Counties 2010 by Jim West

This is in response to unsupported mainstream media claims that vaccine exemptions caused the recent Whooping Cough (pertussis) epidemic. Those claims were made by omitting the obvious toxicology of pertussis epidem-ics. I have created a table (see below) with toxicological data included with pertussis data for California. The table demonstrates that pest quarantines (implicit pesticide spray programs) correlate well with the recent 2010 pertussis epidemic. June, 2010, pertussis spiked in California. June-Aug is the season for pertussis epidemics, which is also the season for pesticide spray programs, quarantines, and peak outdoor air pollution.

Legend for Table

Quarantine programs These implicity require pesticide applications. Produce cannot be moved unless it is certified pest-free. [lbam]= light brown apple moth; [egm]= euro grapevine moth; [mff]= medfly; [kb]= karnal bunt; [acp]= asian citrus psyllid; [off]= oriental fruit fly

Spray programs These explicitly require pesticide application. [chp2 = chp2_Prog Desc.pdf map]

Light Blue= Counties with zero pertussis incidence and no quarantine programs. Yellow= Counties with quarantine programs. Light Blue-Green= Counties with no quarantine programs listed.

Disease incidence is cases per 100,000 population. Other environmental factors are included.

All zero-incidence counties are not quarantined. All pertussis counties are quarantined or have explicit spray programs.

What About Claims Of Bacterial Causation?

Diagnostics can include tests for B. Parapertussis bacteria, however, Because the symptoms during the catarrhal stage are nonspecific, pertussis is usually not diagnosed until the appearance of the characteristic cough of the paroxysmal stage. [wiki pertussis] The diagnosis for pertussis is usually based on symptoms, not germ diag-nostics.

The bacteria is said to be infectious. The bacterial paradigm deserves critical investigation due to the problems often found with other germ paradigms, because for example, poliovirus and HIV isolations have not actually been demonstrated. Apparently the pertussis paradigm originated as a Petri-dish disease, and such bacterial cul-tures obviously cannot exhibit the symptoms of asthma-like coughing, in order to fulfill Koch Postulate 3, that requires symptoms to establish a germ paradigm. Aside: Wiki claims 2 (isolation) can be dispensed with if the germ cannot be isolated, but that is false. xxx With Octave Gengou, he [Bordet] isolated Bordetella pertussis in pure culture in 1906 and posited it as the cause of whooping cough. [wiki gengou] Vaccines were devised and immunization programs soon followed. Pertussis bacterial paradigm was declared by laboratory researcher Bordet around 1906, and then vaccine programs followed.xxx

Three Postulates

On the basis of the table and a distrust of the bacterial paradigm, we can postulate three revisions: 1) Pertussis is a seasonal pesticide disease, although it possibly can occur any time due to indoor air pollution, such as stove exhaust, indoor pesticide application, etc., or other sources. Pertussis could also occur due to outdoor air pollu-tion, mining, refineries, vehicular, etc. Pertussis is a respiratory disease and its symptoms are the bodys attempts to avoid breathing polluted air. The symptoms are a call for help and community alert. 2) Pertussis is not germ caused. 3) The bacterial paradigm is misinfo to confuse pesticide and other pollution diagnostics and to exploit the resulting confusion and disorders.

This Research

This article is a response to recent mainstream propaganda from The New York Times, The Bay Citizen, and Cali-fornia Watch, which promotes the idea that vaccine exemptions cause pertussis, utilizing manipulative titles such as, Are 10,000 kindergartners driving whooping cough epidemic? and Vaccination Rate Lags As an Epidemic Spreads. Journalist Cristina Jewett, or California Watch, wrote on 7/20/2010:

Last month, I reported on the high rate of cases in Marin County, where the countys health officer pointed to personal-belief vaccine exemptions as a possible culprit. The Bay Citizen expanded on my piece in an article in the New York Times, talking to Marin parents who declined to immunize their kids. The controversy over kids and vaccines tends to pit public health officials, who favor vaccines, against jittery parents uncertain about the role that shots play in unexplained increases in autism and similar disorders.

Researchers took a global look at how personal-belief waivers drive whooping cough in a 2006 article in the Journal of the American Medical Association. They found that states like California that have easy-to-obtain-vaccine waivers saw a 90 percent higher incidence of whooping cough than other states.

I wrote Jewett on 7/21/2010, twice, to inform her of the association of pesticides and pertussis, and have received no reply to date. Jewetts researchers omitted the obvious toxicology of pertussis. Jesse McKinley, of The New York Times, wrote on 6/23/2010:

After the deaths of five infants, California health authorities declared an epidemic of whooping cough in the state on Wednesday, urging residents particularly those of Latino background to get vaccinated against the disease.

With regard to NY Times, particularly those of Latino background, obviously, Latinos in California are often agricultural workers, i.e., those who are maximally exposed to pesticide spray programs. Such literature, that advocates germ-theory and omits toxicology, is, at best, moot, since the character of the germ cannot be known in the absence of toxicology. Obviously, the treatments, prescribing poisons (antibiotics) would be disastrous if pertussis is a toxicological disease. That is, most pertussis deaths could be the result of antibiotics exacerbating a toxicological disease. Wikipedia, an example of mainstream medical norms, avoids toxicology and advocates antibiotics (poisons) while claiming that bacteria are causative. See http://en.wikipedia.org/wiki/Pertussis

Map: California Counties

Exploring The Polio VaccineA critical assessment of its arcane history, efficacy, and long-term health-related consequences

Polio (poliomyelitis) is a potentially dangerous viral ail-ment. To combat this disease, researchers developed two polio vaccines (inactivated and live) grown in cultures made from monkey kidneys. Beginning in the 1950s, these vaccines were administered to millions of people in the United States and throughout the world. Official-ly, the polio vaccine is considered safe and effective, and has been credited with singularly reducing the inci-dence of this disease. These tenets are not supported by the data.

A cancer-causing monkey virus SV-40 was discov-ered in polio vaccines administered to millions of peo-ple. SV-40 has been found in brain tumors, bone can-cers, lung cancers and leukemia. SV-40 is transmitted through sexual intercourse, and from mother to child in the womb. Monkeys that were used to make polio vaccines were infected with simian immunodeficiency virus (SIV), a virus closely related to human immuno-deficiency virus (HIV), the infectious agent associated with AIDS. Some researchers question whether HIVs may simply be SIVs residing in and adapting to a human host. Polio vaccines also contain calf serum, glycerol and other parts of the cow that may have been infected with bovine spongiform encephalopathy (BSE), or mad cow disease, a fatal brain-wasting ailment that some re-searchers link to Cruetzfeldt-Jakob disease (CJD), its human equivalent.

Current disease reduction techniques that emphasize short-term gains over long-term health consequences need to be reevaluated and discontinued while new and safer health paradigms are researched and implemented.

What Is Polio? Polio is a contagious disease caused by an intestinal virus that may attack nerve cells of the brain and spinal cord. Symptoms include fever, headache, sore throat, and vomiting. Some victims develop neurological complications, including stiffness of the neck and back, weak muscles, pain in the joints, and paralysis of one or more limbs or respiratory muscles. In severe cases it may be fatal, due to respiratory paralysis.

How Is Polio Contracted? Polio can be spread through contact with contaminated feces (for example, by changing an infected babys dia-pers) or through airborne droplets, in food, or in water. The virus enters the body by nose or mouth, then travels to the intestines where it incubates. Next, it enters the bloodstream where anti-polio antibodies are produced. In most cases, this stops the progression of the virus and the individual gains permanent immunity against the disease.

Many people mistakenly believe that anyone who con-tracts polio will become paralyzed or die. However, in most infections caused by polio there are few distinctive symptoms. In fact, 95 percent of everyone who is ex-posed to the natural polio virus wont exhibit any symp-toms, even under epidemic conditions. About 5 percent of infected people will experience mild symptoms, such as a sore throat, stiff neck, headache, and fever often diagnosed as a cold or flu. Muscular paralysis has been estimated to occur in about one of every 1,000 people who contract the disease. This has lead some scientific researchers to conclude that the small percentage of people who do develop paralytic polio may be anatomi-cally susceptible to the disease. The vast remainder of the population may be naturally immune to the polio virus.

Injections

Several studies have shown that injections (for antibi-otics or other vaccines) increase susceptibility to polio. In fact, researchers have known since the early 1900s that paralytic poliomyelitis often started at the site of an injection. When diphtheria and pertussis vaccines were introduced in the 1940s, cases of paralytic poliomyelitis skyrocketed (Figure 1). This was documented in Lancet and other medical journals. In 1949, the Medical Research Council in Great Britain set up a committee to inves-tigate the matter and ultimately concluded that individuals are at increased risk of paralysis for 30 days following injections; injections alter the distribution of paralysis; and it did not matter whether the injections were subcutaneous or intra-muscular. Figure 1. Polio cases skyrocketed after diphtheria and pertussis vaccines were introduced. Several studies show that in-jections increase susceptibility to polio. When diphtheria and pertussis vaccines were introduced in the 1940s, cases of paralytic poliomyelitis skyrocketed. This chart shows the average number of polio cases per 100,000 people during five year periods before and after the vaccines were introduced. Source: National Morbidity Reports taken from U.S. Public Health surveillance reports; Lancet (April 18, 1950), pp. 659-663.

Polio

A 1992 study, published in the Journal of Infectious Diseases, validated earlier findings. Children who received DPT (diphtheria, tetanus, and pertussis) injections were significantly more likely than controls to suffer paralytic poliomyelitis within the next 30 days. According to the authors, this study confirms that injections are an impor-tant cause of provocative poliomyelitis.

In 1995, the New England Journal of Medicine published a study showing that children who received a single injection within one month after receiving a polio vaccine were 8 times more likely to contract polio than children who received no injections. The risk jumped 27-fold when children received up to nine injections within one month after receiving the polio vaccine. And with ten or more injections, the likelihood of de-veloping polio was 182 times greater than expected. Why injections increase the risk of polio is unclear. Nevertheless, these studies and others indicate that injections must be avoided in countries with endemic poliomyelitis. Health authorities believe that all unnecessary injections should be avoided as well.

Nutritional Deficiencies

A poor diet has also been shown to increase susceptibility to polio. In 1948, during the height of the polio epidem-ics, Dr. Benjamin Sandler, a nutritional expert at the Oteen Veterans Hospital, documented a relationship between polio and an excessive use of sugars and starches. He compiled records showing that countries with the highest per capita consumption of sugar, such as the United States, Britain, Australia, Canada, and Sweden (with over 100 pounds per person per year) had the greatest incidence of polio. In contrast, polio was practically unheard of in China (with its sugar use of only 3 pounds per person per year).

Dr. Sandler claimed that sugars and starches lower blood sugar levels causing hypoglycemia, and that phosphoric acid in soft drinks strips the nerves of proper nourishment. Such foods dehydrate the cells and leech calcium from the body. A serious calcium deficiency precedes polio. Weakened nerve trunks are then more likely to malfunction and the victim loses the use of one or more limbs.

Researchers have always known that polio strikes with its greatest intensity during the hot summer months. Dr. Sandler observed that children consume greater amounts of ice cream, soft drinks, and artificially sweetened prod-ucts in hot weather. In 1949, before the polio season began, he warned the residents of North Carolina, through the newspapers and radio, to decrease their consumption of these products. That summer, North Carolinians reduced their intake of sugar by 90 percent and polio decreased by the same amount! The North Carolina State Health Department reported 2,498 cases of polio in 1948, and 229 cases in 1949 (data taken from North Carolina State Health Department figures).

One manufacturer shipped one million less gallons of ice cream during the first week alone following the publica-tion of Dr. Sandlers anti-polio diet. Soft drink sales were down as well. But the powerful Rockefeller Milk Trust, which sold frozen products to North Carolinians, combined forces with soft drink business leaders and convinced the people that Sandlers findings were a myth and the polio figures a fluke. By the summer of 1950 sales were back to previous levels and polio cases returned to normal.

Can Polio Be Treated? Paralytic polio is rarely permanent. Usually there is a full recovery. Muscle power begins to return after several days and continues to improve during the next 12-24 months. A small percentage of cases will experience residual paralysis. In rare cases, paralysis of the muscles used to breathe can lead to death. Treatment mainly consists of putting the patient to bed and allowing the affected limbs to be completely relaxed. If breathing is affected, a res-pirator or iron lung can be used. Physical therapy may be required.

Does A Polio Vaccine Exist? In 1947, Jonas Salk, an American physician and microbiologist, became head of the Virus Research Laboratory at the University of Pittsburgh. He was interested in developing a polio vaccine. In 1952, Salk combined three types of polio virus grown in cultures made from monkey kidneys. Using formaldehyde, he was able to kill or inactivate the viral matter so that it would trigger an antibody response without causing the disease. That year he began his initial experiments on human subjects. In 1953, his findings were published in the Journal of the Ameri-

can Medical Association. And in April of 1954 the nations first polio immunization campaign, directed at school children, was launched. However, shortly thereafter hundreds of people con-tracted polio from Salks vaccine; many died. Apparently, his killed-virus vaccine was not completely inactivated. The vac-cine was redeveloped, and by August 1955 over 4 million doses

were administered in the United States. By 1959, nearly 100 other countries were using Salks vaccine. In 1957, Albert Sabin, another American physician and microbiologist, developed a live-virus (oral) vaccine against polio. He didnt think Salks killed-virus vaccine would be effective in preventing epidemics. He wanted his vaccine to simulate a real-life infection. This meant using an attenuated or weakened form of the live virus. He experimented with thousands of monkeys and chimpanzees before isolating a rare type of polio virus that would reproduce in the intestinal tract without penetrating the central nervous system. The initial human trials were conducted in for-eign countries. In 1958, it was tested in the United States. And in 1963 Sabins oral sugar-cube vaccine became available for general use.

Which Vaccine Is In Use Today? In 1963, Sabins oral vaccine quickly replaced Salks injectable shot. It is cheaper to make, easier to take, and appears to provide greater protection, including herd immunity in unvaccinated people. However, it cannot be given to people with compromised immune systems. Plus, it is capable of causing polio in some recipients of the vaccine, and in individuals with compromised immune systems who come into close contact with recently vac-cinated children. As a result, in January 2000, the CDC updated its polio vaccine recommendations, reverting back to policies first implemented during the 1950s: Children should only be given the killed-virus shot. The oral polio vaccine should only be used in special circumstances.

Are Polio Vaccines Safe? When national immunization campaigns were initiated in the 1950s, the number of reported cases of polio following mass inoculations with the killed-virus vaccine was significantly great-er than before mass inoculations, and may have more than doubled in the U.S. as a whole (chart at right). For example, Vermont reported 15 cases of polio during the one-year report period end-ing August 30, 1954 (before mass inoculations), compared to 55 cases of polio during the one-year period ending August 30, 1955 (after mass inocu-lations) a 266% increase. Rhode Island reported 22 cases during the before inoculations period as compared to 122 cases during the after inocula-tions period, a 454% increase. In New Hampshire the figures increased from 38 to 129; in Connecticut they rose from 144 to 276; and in Massachusetts they swelled from 273 to 2027, a whopping 642% increase.

A cancer-causing monkey virus SV-40 was discovered in polio vaccines administered to millions of people

When national immunization campaigns were initiated in the 1950s, the number of reported cases of polio fol-lowing mass inoculations with the killed-virus vaccine was significantly greater than before mass inoculations, and may have more than doubled in the U.S. as a whole. Doctors and scientists on the staff of the National Institutes of Health during the 1950s were well aware that the Salk vaccine was causing polio. Some frankly stated that it was worthless as a preventive and dangerous to take. They refused to vaccinate their own children. Health departments banned the inoculations. The Idaho State Health Director angrily declared: I hold the Salk vaccine and its manufacturers responsible for a polio outbreak that killed several Idahoans and hospitalized dozens more. Even Salk himself was quoted as saying: When you inoculate children with a polio vaccine you dont sleep well for two or three weeks. But the National Foundation for Infantile Paralysis, and drug companies with large investments in the vaccine coerced the U.S. Public Health Service into falsely proclaiming the vaccine was safe and effective.

In 1976, Dr. Jonas Salk, creator of the killed-virus vaccine used in the 1950s, testified that the live-virus vaccine (used almost exclusively in the U.S. from the early 1960s to 2000) was the principal if not sole cause of all re-ported polio cases in the U.S. since 1961. (The virus remains in the throat for one to two weeks and in the feces for up to two months. Thus, vaccine recipients are at risk, and can potentially spread the disease, as long as fecal excretion of the virus contin-ues.) In 1992, the Federal Centers for Disease Control and Prevention (CDC) published an admission that the live-virus vaccine had be-come the dominant cause of polio in the United States. In fact, according to CDC figures, every case of polio in the U.S. since 1979 was caused by the oral polio vaccine. Authorities claim the vaccine was responsible for about eight cases of polio every year. However, an independent study that analyzed the governments own vac-cine database during a recent period of less than five years uncovered 13,641 reports of adverse events following use of the oral polio vaccine. These reports included 6,364 emergency room visits and 540 deaths (chart above). Public outrage at these tragedies became the impetus for removing the oral polio vaccine from im-munization schedules.

The following story is typical of the damage associated with oral polio vaccines: Four months ago my son was taken to a local clinic for his polio vaccine. I wasnt aware that he was going to have one, and would have pre-vented it if I had known. Unfortunately, he changed from that day high-pitched screaming, smelly stools, non-stop crying, difficulty in breathing, high temperature, and lethargy. He also lost weight. Weeks of sleepless nights for all of us followed. His development ceased. He had been able to stand and move around, but he went back to remaining in basically whatever position we left him in.

My wife was six months pregnant at the time, and about a week after our sons polio vaccine, she began to have headaches, loss of balance, muscular weakness, and frequent tiredness. I panicked because everything seemed to be pointing to polio infection. Then, a week after her continuous headaches began, she had to go to the hospital because there was something wrong with the pregnancy; she lost our daughter. I tried to get a polio test, and to find the cause of this tragic series of events, but the medical profession was extremely unhelpful. They laughed

In the mid-1990s, during a period of less than five years, there were 13,641 documented adverse reactions to the oral polio vaccine. 6,364 of these were serious enough to require hospital emergency room visits. 540 people

died. Source: Vaccine Adverse Event Reporting System (VAERS); OPV Vaccine Report: Doc. #14.

at me. I will never know why our son suddenly stopped growing or why his development regressed. I will never know why we lost our daughter. The only thing I am sure about is that the precursor to these events was the polio vaccine. [From an unsolicited e-mail received by the Thinktwice Global Vaccine Institutewww.thinktwice.com] Today, fact sheets on polio published by the U.S. Department of Health and Human Services, warn parents that the inactivated polio vaccine (IPV) can cause serious problems or even death... The company that manufactures the current inactivated polio vaccine warns that Guillain-Barre Syndrome, a debilitating ailment characterized by muscular incapacitation and nervous system damage, has been temporally related to administration of another inactivated poliovirus vaccine. And although this company makes the claim that no causal relationship has been established, it also admits that deaths have occurred after vaccination of infants with IPV. Yet, like the days of old, despite these danger alerts, medical authorities continue to assure parents that the currently available inactivated polio vaccine is both safe and effective.

How Effective Are Polio Vaccines?

Polio is virtually nonexistent in the United States today. However, according to Dr. Robert Mendelsohn, medical investigator and pediatrician, there is no credible scien-tific evidence that the vaccine caused polio to disappear. From 1923 to 1953, before the Salk killed-virus vaccine was introduced, the polio death rate in the United States and Eng-land had already declined on its own by 47 percent and 55 percent, respectively (chart at left). Statistics show a similar decline in other European countries as well. And when the vaccine did become available, many Eu-ropean countries questioned its effectiveness and refused to systematically inoculate their citizens. Yet, polio epidemics also ended in these countries.

The chart at left show that from 1923 to 1953, before the Salk killed-virus vaccine was in-troduced, the polio death rate in the United States and England had already declined on

its own by 47 percent and 55 percent, respectively. Source: International Mortality Statistics (1981) by Michael Alderson. Source: Congressional Hearings, May 1962; and National Morbidity Reports taken from U.S. Public Health surveillance reports.

The standards for defining polio were changed when the polio vaccine was introduced. The new definition of a polio epidemic required more cases to be reported. Paralytic polio was redefined as well, making it more difficult to confirm, and therefore tally, cases. Prior to the introduction of the vaccine the patient only had to exhibit para-lytic symptoms for 24 hours. Laboratory confirmation and tests to determine residual paralysis were not required. The new definition required the patient to exhibit paralytic symptoms for at least 60 days, and residual paralysis had to be confirmed twice during the course of the disease. Also, after the vaccine was introduced cases of aseptic meningitis (an infectious disease often difficult to distinguish from polio) and coxsackie virus infections were more often reported as separate diseases from polio. But such cases were counted as polio before the vaccine

was introduced. The vaccines reported ef-fectiveness was therefore skewed (chart at right). Source: Congressional Hearings, May 1962; and National Morbidity Reports taken from U.S. Public Health surveillance reports. The fact that dubious tactics were used to fabricate efficacy rates was corroborated by Dr. Bernard Greenberg, chairman of the Committee on Evaluation and Standards of the American Public Health Associa-tion during the 1950s. His expert testimony was used as evidence during Congressio-nal hearings in 1962. He credited the de-cline of polio cases not to the vaccine, but rather to a change in the way doctors were required to report cases: Prior to 1954 any physician who reported paralytic poliomy-elitis was doing his patient a service by way of subsidizing the cost of hospitalization... two examinations at least 24 hours apart was all that was required... In 1955 the criteria were changed... residual paralysis was determined 10 to 20 days after onset of illness and again 50 to 70 days after on-set... This change in definition meant that in 1955 we started reporting a new disease... Furthermore, diagnostic procedures have continued to be refined. Coxsackie virus infections and aseptic meningitis have been distinguished from poliomyelitis. Thus, simply by changes in diagnostic criteria, the number of paralytic cases was predeter-mined to decrease.

Polio Vaccines And Cancer In 1959, Bernice Eddy, a brilliant government scientist working in Biologics at the National Institutes of Health, discovered that polio vaccines being administered throughout the world contained an infectious agent capable of causing cancer. When Eddy attempted to report her findings and halt production of these contaminated polio vac-cines, her government superiors barred her from publicly revealing the problem. Instead, her lab and equipment were taken away and she was demoted.

In 1960, Drs. Ben Sweet and M.R. Hilleman, pharmaceutical researchers for the Merck Institute for Therapeutic Research, were credited with discovering this infectious agentCSV-40, a monkey virus that infected nearly all rhesus monkeys, whose kidneys were used to produce polio vaccines. Hilleman and Sweet found SV-40 in all three types of Albert Sabins live oral polio vaccine, and noted the possibility that it might cause cancer, espe-cially when administered to human babies. According to Sweet, It was a frightening discovery because, back then, it was not possible to detect the virus with the testing procedures we had... We had no idea of what this virus

would do... Sweet elaborated: First, we knew that SV-40 had oncogenic (cancer-causing) properties in ham-sters, which was bad news. Secondly, we found out that it hybridized with certain DNA viruses... such that [they] would then have SV-40 genes attached [to them]... When we started growing the vaccines, we just couldnt get rid of the SV-40 contaminated virus. We tried to neutralize it, but couldnt... Now, with the theoretical links to HIV and cancer, it just blows my mind.

Further research into SV-40 uncovered even more disturbing information. This cancer-causing virus was not only ingested via Sabins contaminated oral sugarcube vaccine, but was directly injected into peoples blood streams as well. Apparently, SV-40 survived the formaldehyde Salk used to kill microbes that defiled his