Reevaluating the Etiology of Poliomyelitis
Toxicology vs Virology
In 1952, Dr. Ralph R. Scobey MD, professor of clinical pediatrics and president of the Poliomyelitis Research Institute, Syracuse, N.Y. prepared a statement for the US Congress, entitled The Poison Cause of Poliomyelitis and Obstructions To Its Investigation.
He states that the disease that we now know as poliomyelitis was not designated as such until about the middle of the 1800s. Prior to that, it was designated by many different names at various times and in different localities. The simple designations, paralysis, palsy and apoplexy, were some of the earliest names applied to what is now called poliomyelitis.
“Paralysis, resulting from poisoning, has probably been known since the time of Hippocrates.”
Throughout the medical literature, one can find that certain substances have caused paralysis, documented and collected in Dr. Scobey’s statement.
In 1765 for example, a physician named Dr. Herman Boerhaave, wrote:
“We frequently find persons rendered paralytic by exposing themselves imprudently to quicksilver [mercury], dispersed into vapors by the fire, as gilders, chemists, miners, etc., and perhaps there are other poisons, which may produce the same disease, even externally applied.”
In 1824, the English physician John Cooke made similar observations:
“Among the exciting causes of the partial palsies we may reckon the poison of certain mineral substances, particularly of quicksilver [mercury], arsenic, and lead. The fumes of these metals or the receptance of them in solution into the stomach, have often caused paralysis.”
Scobey reviewed the literature and found many instances of poliomyelitis resulting from poisoning:
“The foregoing reports indicate that poisons can cause poliomyelitis. It would appear that not any one poison in particular would be responsible for all cases of poliomyelitis but the effect of any one of several could produce the same ultimate result.”
He also noted a relationship of harvest to polio:
“The material presented above appears clearly to indicate that there is a correlation between the harvesting of fruits and vegetables and epidemics of poliomyelitis.”
Why did outbreaks of paralysis begin to rage in the late 1800s?
Sporadic cases of polio-like illnesses have been reported since the end of the 1700s. Late in the 1800s, larger and more frequent outbreaks of paralysis began to occur in industrialized nations.
This could be attributed to the fact that arsenic-based pesticides were becoming increasingly popular in the late 1800s.
According to The Agency for Toxic Substances and Disease Registry, the adverse effects of arsenic exposure may be that of:
“…ascending weakness and paralysis may be evident in more severe poisoning.”
It therefore makes particular sense to take poisoning by industrial and agricultural pollution into consideration, to explain why this nervous disease began to appear in the late 1800s, in the course of industrialization.
Paris green (copper acetoarsenite), also known as Schweinfurt green, is an arsenic based organic pigment that was invented in the early 1800s, and was mainly used in manufacturing and household products. Paris green became a popular pesticide as well.
In 1867, an American farmer sprayed his potato bushes with the green compound in an attempt to protect them from the devastating Colorado potato beetle. News of Paris green’s resounding success in controlling the beetle quickly traveled far and wide, and American farmers began applying it to other crops as well.
The connection between pesticides and poliomyelitis was already noted in 1882, by a prominent neurologist, E. C. Seguin. He presented his research entitled Myelitis Following Acute Arsenical Poisoning (by Paris or Schweinfurth green) at the New York Academy of Medicine.
Seguin describes the work of Popow, of St. Petersburg, who in 1881 published an essay upon the pathological anatomy of arsenical paralysis as produced artificially in animals. Popow concludes that arsenic, even in a few hours after its ingestion, may cause acute central myelitis or acute poliomyelitis.
“Arsenic, even in a few hours after its ingestion, may cause distinct lesions of the spinal cord, of the type known as acute central myelitis, or acute poliomyelitis.”
Seguin gives condensed accounts of a few of the cases reported in the literature of the subject, and also reports three cases of his own, all poisoning with the arsenical insecticide Paris green.
His conclusions are practically the same as those of Popow:
“If we compare the symptoms present in the various human cases related and quoted, and the pathological appearances found by Popow in his animals, it is, it seems to me, legitimate to reach the following conclusions:
Arsenical paralysis is the expression of a myelitis.
This myelitis approximates the type known as poliomyelitis in so far as the symptoms are chiefly motor; that the paralyzed muscles undergo some atrophy, and exhibit the degeneration reactions to electrical currents; that the bladder is never palsied; and that in animals the ganglion cells of the anterior horns are extensively diseased.”
Some other noteworthy examples can be found in a 1908 issue of the Boston Medical and Surgical Journal:
“Vulpian produced, experimentally, paralysis of the extensors and lesions resembling those of poliomyelitis in a dog by lead poisoning, and in a case of lead poisoning found pronounced poliomyelitis with colloid degeneration and cell atrophy. Phillippe and Gauthard report a case of anterior poliomyelitis from lead poisoning, and Obrastoff one from arsenical poisoning. Onuf reported the case of a painter with flaccid paralysis of both legs, in whom autopsy showed lesions characteristic of the disease.”
Paris green maintained its lead in the pesticide market until the 1890s, when it was dethroned by lead arsenate, a compound made from lead and arsenic, as the name implies. Lead arsenate was a new-and-improved insecticide invented to fight infestations of moths.
Lead arsenate became the most important pesticide in the industrialized world, since the main pesticide that had been used, Paris green, wouldn’t stick to fruits and vegetables very well. Lead arsenate on the other hand was much more adhesive, contributing to its efficacy, popularity and danger.
In a paper entitled The History of Lead Arsenate Use in Apple Production the following information can be found:
In the late 1800s inorganic pesticides were used extensively to control pests in agriculture. These natural chemicals, including arsenic (As), copper (Cu), lead (Pb), and sulfur (S), were mixed in varying formulations and were quite effective in controlling pests. Newly emerging pests and growing labor costs led to increased pesticide use by growers.
Lead arsenate (PbHASO4) was first used as an insecticidal spray in 1892 against the gypsy moth, Lymantria dispar (Linnaeus), in Massachusetts.
The introduction of lead arsenate was accompanied by an increase in the incidence of poliomyelitis. As seen on the chart below, shortly after the introduction of the insecticide lead arsenate in Massachusetts, there was a large increase of polio cases, around the time of harvest, in Massachusetts.
The use of synthetic pesticides became widespread after the end of World War II, following the discovery of the effectiveness of organochlorine chemicals, such as DDT and lindane .
Thus, the metal-based pesticides were by and large replaced by other synthetic pesticides, mainly DDT.
The incidence of polio increased as a result, as noted by several eminent invividuals.
Ralph Scobey, 1954:
“The increase in poliomyelitis during recent years runs parallel with the increasing use of insecticides which may be more than a coincidence.”
The Council on Pharmacy and Chemistry of the American Medical Association on the toxicologic effects of DDT:
“DDT is a “cerebrospinal” poison which acts primarily on the central nervous system in man and higher animals … The principal systemic effects in higher animals are disturbances of the central nervous system characterized by…spastic or flaccid paralysis.”
After the introduction of the Salk vaccine in 1955, there were drastic changes in diagnostic methods and procedures. Because of these changes, the number of polio cases were therefore destined to fall.
Redefinition of an epidemic: More cases were required to refer to polio as epidemic after the introduction of the Salk vaccine (from 20 per 100,000 to 35 per 100,000 per year).
Redefinition of the disease: In order to qualify for classification as paralytic poliomyelitis, the patient had to exhibit paralytic symptoms for at least 60 days after the onset of the disease. Prior to 1955 the patient had to exhibit paralytic symptoms for only 24 hours. Laboratory confirmation and the presence of residual paralysis was not required.
Polio-like diseases were branched off: Polio-related diseases that had been diagnosed as paralytic polio were excluded from the definition of the disease.
A graph was provided which shows what the incidence of paralytic polio would have been from 1951 through 1959 if the figures were corrected for the radical changes in diagnostic practices since the introduction of the Salk vaccine:
Restrictive diagnosing: Doctors were more restrictive in diagnosing their patients with poliomyelitis.
The symptoms of polio are non-specific, and can therefore be reclassified into other labels. Thus, case numbers can be manipulated by lumping pre-existing syndromes into different diagnoses.
DDT phase out
In 1950 Congress set up a special committee to “investigate the use of chemicals in food and cosmetics.” The committee, chaired by Congressman James Delaney, summoned over 200 witnesses and devoted much time to examining the toxicity of pesticides. Its final report, published in 1952, contained a recommendation to Congress to “pass legislation to control the flow of chemical substances into the nation’s food supply.”
Congress complied with the committee’s recommendation, and relevant laws were indeed enacted; the Pesticide Residues Amendments of 1954 and the Food Additives Amendments of 1958.
The PCA of 1954 was the first time Congress passed guidance regarding the establishment of safety limits for pesticide residues on food.
According to the Environmental Protection Agency, The Department of Agriculture began regulating DDT in the late 1950s, ending with the cancellation of the use of the pesticide in the US in 1972.
In the late 1950s, DDT usage began to decline greatly, as seen on the graph below:
DDT storage in body fat declined accordingly. From 1954 to 1964-67, DDT ingestion decreased by an approximate factor of five.
Some caution must be exercised in interpreting the results from 1955 to 1962:
DDT was largely phased out of the food chain. Before its cancellation in the early 1970s, 80% of it was applied on cotton, with the remainder being used predominantly on peanut and soybean crops.
Rachel’s Carlson’s book Silent Spring published in 1962 stimulated widespread public awareness over the use of the pesticide.
The foregoing information has made it clear that there is a distinct connection between the use of certain substances known to be neurotoxic, and the incidence of poliomyelitis; this connection should have made it worth pursuing a toxicological investigation.
The change in polio incidence from a few cases a year to outbreaks of hundreds or more that began in the 1890s is consistent with the transition from the use of Paris green (copper acetoarsenite) to lead arsenate, a more adhesive pesticide, contributing to its efficacy and danger.
The sudden onset of polio epidemics in industrialized countries after World War II clearly coincides with the sudden explosion in DDT use. The phase out of DDT in the late 1950s corresponds with the reduction of polio morbidity.
Unfortunately, the medical establishment has ignored this connection between neurotoxins and paralysis and has only pursued the hypothesis that a ‘virus’ is the causal agent of polio. Astoundingly, instead of following up the obvious evidence, medical authorities viewed the pesticides as weapons in the ‘battle’ against polio.