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.
“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.
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.”