This is a summary of literature on the truth of Polio. This summary has a lot of “cut and paste” of original sources. It’s my belief that you should read the original sources to learn the truth. A quick summary:
The polio virus never caused the symptoms associated with "polio." In the early 20th century "polio" was caused by lead and arsenic spraying of fruit trees. Doctors as early as 1907 and throughout the 1920s, 1930s, and 1940s noted that poliomyelitis was caused by spraying of fruit trees.
In the 1940s, DDT was added to the mix of toxic elements causing neurological damage. Dr. Morton Biskund published his research in 1949 that DDT also caused the symptoms associated with polio, but he was restricted to reporting that "Disease X" was not cause by a "hypothetical Virus X." Later in 1951 he testified in front of Congress. He was ignored and censored like doctors today are on Ivermectin. I found one old grainy photo of this brilliant and brave man.
DDT also caused "Polio," or neurological damage. DDT was marketed to the public as a preventative measure for Polio. Sound familiar? The public believed they should kill mosquitos that carried the "virus" which did not cause Polio.
After Jonas Salk made a vaccine in 1955, the AMA required doctors to no longer use the term Polio in 1956 to make it appear as if the "virus" had disappeared. In reality, the vaccines were also causing the same paralysis. The “virus” never spread at all and everyone knew it. It was one big lie.
Before Christ, Ancient Greece, undated. Gross toxic effects of lead on the nervous system were reported by ancient Greek physicians. A brief summary of such reports, and those of Roman physicians and 18-19th century toxicologists described a syndrome was known as "painter's colic", which included abdominal pain, constipation and paralysis, symptoms now covered by the term "lead encephalopathy.” PubChem Compound Summary: Lead Arsenate
Egypt, 1580-1350 BC. The following image is from History of Polio from the Polio Global Eradication Initiative. Text: “An Egyptian stele portrays a priest with a withered leg, suggesting that polio has existed for thousands of years.” According to the timeline of Polio Global Eradication Initiative, their alleged polio virus must have went dormant for over 3,000 years before reappearing in 1789 AD. Both lead and arsenic were used in Ancient Egypt.
1712. The division of industrial hygiene of the New York State Industrial Commission has recently completed an investigation into the manufacture of paris green. The inquiry was made by Chemical Engineer John H. Vogt and Acting Medical Inspector Lester L. Roos, M. D., and their report, as it appears in the Bulletin of the Industrial Commission for June, 1917 (pp. 181 to 183), is here reproduced: …. According to Desamle and tierron, paris green was first discovered in the year 1712 by Russ and Sattler in Schweinfurt, Bavaria, Germany, from basic-verdigris and arsenic. According to others, Voumitis, of Vienna, Austria, was the first manufacturer. Liebig published the manufacturing process in 1822, and in 1872 its manufacture was undertaken in Brooklyn, N. Y. The striking bright shade and popularity of this material led to its manufacture bynearly all color makers at that time, which circumstance is the cause of the various names under which it is known besides that of paris green; such names as " Empero rGreen," "NewGreen," "MineralGreen," "OriginalGreen,"and "Patent Green,"were given to it by the various makers. The object of this, no doubt, was to lead the public to believe that th eso-called colors were not of a poisonous nature. "These colors, or tints, were produced by mixing paris green with barytes, chromáte of lead, china clay,and other white mixtures, thus lowering the cost of manufacture." Scheele's Green" is the name givento the commercial product used as an insecticide, which is manufactured in one establishment in the State. The original method of its manufacture was kept a strict secret. In an attempt to manufacture paris green it was discovered by C. W. Scheele in 1742, a native German chemist who resided in Sweden, that a substance could be produced which greatly resembled paris green and manufactured at less cost. To this substance the name "Scheele's Green" was applied, by which it is still known. Paris green and Scheele's green are manufactured by 10 firms in the United States, of which 7 firms are located in the State of NewYork, only 6 of which were actually making thematerials when the investigation was conducted. DANGERS IN THE MANUFACTURE OF PARIS GREEN AND SCHEELE'S GREEN
1767, West Indies. Lead poisoning was well recognized as an occupational hazard. However, it was also associated with consumption of lead-contaminated water, wine, cider, rum from the West Indies, and food prepared or stored in lead or lead-glazed utensils. ... Cases of lead poisoning in girls resulting from consumption of drinking-water kept in lead-lined cisterns, and ... the Devonshire colic attributed by Sir George Baker in 1767 to the consumption of cider prepared in presses made of lead or lead alloys were described. PubChem Compound Summary: Lead Arsenate. Reference: An essay, concerning the cause of the endemial colic of Devonshire, By George Baker, 1767
1789. The first documented cases of what is now believed to be poliomyelitis was recorded in 1789 by British physician Michael Underwood.12Underwood described polio as “…the debility of the lower extremities which gradually become more infirm, and after a few weeks are unable to support the body”3 and noted that it was not a common disorder. What is the history of Polio in America and other countries?
1809. The following interesting case was published, in 1809, by Dr. G. Thilenius.6 A young lady having observed a hard lump in her left breast, neglected it until the ensuing spring, when it became very painful. A miserably ignorant barber who was consulted, applied a preparation of arsenic. This was followed by ulceration and increased pain, and, according to the father’s statement, three days later her arms and legs became insensible, and so much paralyzed that she could neither walk nor feed herself. The limbs were also cold. In the course of two months the arms recovered, and the legs improved steadily. Electricity was used ; the tumor removed by the knife. At various times there occurred prickling and jerking in the legs. Anaesthesia and atrophy not mentioned. In about a year after the attack the patient was able to walk without a cane ; her limbs were warm, and the wound in the breast well healed. MYELITIS FOLLOWING ACUTE ARSENICAL POISONING (BY PARIS OR SCHWEINFURTH GREEN; E. C. SEGUIN, M.D.; Journal of Nervous and Mental Disease, VoI. ix, No. 4, October 1882.
1824. In 1824, Cooke,4 England, stated: "Among the exciting causes of the partial palsies we may reckon the poison of certain mineral substances, particularly of quick silver, arsenic, and lead. The fumes of these metals or the receptance of them in solution into the stomach, have often causes paralysis." Ralph Scobey testimony to Congress (1953). Reference: Cooke, John: Treatise of Nervous Diseases, 1824
1834. In 1834, the first outbreak of paralysis was reported on the South Atlantic island of St. Helena and one year later, John Badham described the onset of acute paralysis affecting four English children.45 Five years later, Jacob von Heine published an analysis of unique form of paralysis and referred to it as infantile paralysis. What is the history of Polio in America and other countries?
1835, Worksop, England. In the center of England in a small town called Worksop, a physician named Charles Badham felt compelled to write about a disturbing illness he had witnessed during the summer of 1835. Four children, all under the age of three, had come down with paralysis, mainly in their legs, or “lower extremities.” All of them appeared healthy with the exception of “an unusual appearance of the eyes, which… appeared to be turned inwards.” Badham documented the particular symptoms of these children because it was something he had never heard of. Apparently his father, also a physician, wasn’t familiar with it either. Paralysis was not out of the ordinary at the time, but the fact it had struck four different people—all of them under the age of three—felt to him, remarkable. That their health was otherwise unimpaired was also odd. The Moth in the Iron Lung. Referenced Source: Charles Badham, “Paralysis in Childhood: Four remarkable cases of suddenly induced paralysis in the extremities occurring in children without any apparent cerebral or cerebrospinal lesion,” London Medical Gazette 17 (1834-35):
1841, Louisiana. The first outbreak of polio in the U.S. occurred in 1841 in Feliciana, Louisiana and caused paralysis in 10 children. 7 This outbreak was referred to as ‘teething paralysis’ as it had affected children under the age of 2, all of whom eventually improved or recovered.8. What is the history of Polio in America and other countries?
1841. Even an obscure article regarding paralysis amongst a group of children in Louisiana in 1841—thought of as possibly the first reference to polio in the United States—was called ”Paralysis in Teething Children.” The association with dentition was so common that many parents, having never heard the term infantile paralysis, referred to what had happened to their children as teething paralysis. This period in a child’s life was thought of as so dangerous, some considered calling dentition itself a disease. … It is difficult for a modern human to understand the ubiquity of mercury, the earth’s most toxic substance (besides plutonium), in the every day life of someone living two hundred years ago. Examine any medical literature of the 1800s and early 1900s and one will not have to look far before seeing mercury-based treatments and medicines: Mercury cyanide, mercuric iodide, mercury benzoate, and mercuric chloride. These were not concoctions sold on the back pages of newspapers by traveling salesmen who would clear town as soon as they had your money—these were commercial products produced in laboratories by large companies like Sharpe & Domme and Eli Lilly. … In the early 1800s, a popular medicine stormed onto the market: Steedman’s Teething Powders. Each package contained eight folded up pieces of paper on which the following was written: “Dose. From one to three months, the third of a powder; from three to six months, half a powder; and above that age, one powder only, and no more; for further particulars read the large bill of directions.” Each paper contained around 47 milligrams of mercury chloride powder to be placed on the back of the infant’s tongue and washed down with milk or water. While they knew the mercury could have toxic effects, the drive to clear the infant’s bowels was believed so essential to their health it was thought worth the risk. As such, mercurial medicines were dispensed to infants for nearly any complaint, including the privation of teething. Paralysis is now a known side effect of mercury poisoning, but, at the time, they would not have believed the powder to have this effect. The Moth in the Iron Lung.
1855. In 1855, French physician Duchenne reported that polio impacted the anterior horn cells of the spinal column. His findings were also supported by Charcot and Joffroy, who discovered atrophy of the anterior horns in the grey matter of the spinal cord.910. What is the history of Polio in America and other countries?
1862. The Arsenic Waltz (1862), by Punch cartoonist John Leech, depicts the high price of wearing arsenic-dyed fashion: literally, dancing with death. Wellcome Library, London. Arsenic and Old Tastes Made Victorian Wallpaper Deadly
1862. In 1862, physician Thomas Orton was called in by a couple by the name of Turner to investigate the mysterious illness that had killed three of their children, and threatened the life of their remaining daughter. Earlier doctors concluded that the children had suffered from diphtheria, and their symptoms were consistent with those of the condition. However, Orton noted that none of the family’s neighbors had caught the disease, leading him to suspect another cause: the green wallpaper that covered the walls of their home. It had long been a rumor in the medical community that the arsenic in the paints might be released into the air under certain conditions, creating a poisonous atmosphere in the rooms that used them. Orton believed this to be the case. Though he was unable to save the Turner child’s life, he immediately asked to conduct an autopsy on her body. A certain “Dr. Letheby” ended up being the one to test samples of her tissue, and he determined that the cause of death was, indeed, arsenic poisoning. At the inquest, however, the presiding judge found his findings “objectionable,” leading the jury to rule the child’s death as a result of natural causes. In the years that followed, the use of Paris green and other arsenic-based greens reached their peak, although with a rising undercurrent of fear. While the colors remained fashionable, more and more stories of arsenic-related deaths came to light. Even the Queen herself was not immune to the panic. Paris Green: The Trendy Color That Killed Many in Victorian Society
1867, Philadelphia. It was 1867 in Philadelphia, and a surgeon named Charles Taylor published a short 119-page work illuminating a phenomenon that he and his colleagues had begun to notice more of: infantile paralysis. He was concerned not only about the age of the victims, but the rise in the number of cases. “There seems to be no doubt that this disease is much more frequent now, and in this country, than formerly, and is rapidly increasing.”4 A puzzling cause was mentioned several times throughout the book— something that had been noted elsewhere. Both parents and doctors alike attributed the onset of paralysis to the same thing: ”Case 6.—T. T., aged two years and a half, was paralyzed while teething.” Taylor made it clear at the beginning of the book that the “majority of those cases, however, have about this history: the child is getting its first molar teeth.” Within the book, a father gave a personal testimony of what had happened to his daughter: “My daughter Josie, who was placed under your care in May and November, 1865, and has at home followed your directions in wearing more or less apparatus adjusted to her partially paralyzed leg, first manifested to us that her leg was debilitated when about eighteen months of age. She walked when about a year old, then gave up walking. We attributed the fact to debility from teething. When she resumed walking, at about eighteen months of age, the weakness in one leg was discovered.”5. The Moth in the Iron Lung
1868. The first epidemics appeared in the form of outbreaks of at least 14 cases near Oslo, Norway, in 1868 and of 13 cases in northern Sweden in 1881. About the same time, the idea began to be suggested that the hitherto sporadic cases of infantile paralysis might be contagious. Albert Bruce Sabin Britannica
1869, Boston.. Just north of the National Peace Jubilee, across Boston’s Charles and Mystic Rivers, a man was fumbling through the grass and bushes that lined the side of his small two-story house. Neighbors walked by and remarked at his frantic search as he clawed through blades of grass on his hands and knees. It was a pleasant spring day, but the wind had picked up, frustrating his efforts. Clearly distraught, he went back to the window from where his search had begun. Just a few minutes earlier, he had placed a mass of moth eggs on the kitchen sill when a gust of wind lifted them up in the air and out into the yard. He burst through the front door and leapt off the porch in an attempt to collect them before the mass broke apart, littering the yard with hundreds of tiny eggs. It was too late. He groped through foliage looking for signs of the furry brown sac, but it was gone. The eggs contained inside had probably separated and been carried up into the wind. They could have landed anywhere in his yard—or his neighbors. He had lost other eggs, caterpillars, and moths before, but they were native species—perfectly suited for the local environment due to thousands of years of natural selection. These were not. He knew enough about moths and their voracious appetite to be severely distressed. The fact that these were an invasive species of moth— brought to the United States from Europe—made it all the more troubling. The Moth in the Iron Lung.
1873. Cotton leafworm (Alabama argillacea H.) was the primary pest of cotton (Gossypium hirsutum L.) in the USA during the 1800s. It was controlled by non-chemical means, such as hand-crushing the caterpillars, keeping large poultry yards, and using fires and lamps to attract and kill the adult moths. In 1873, USDA scientists recommended Paris green, a copper acetoarsenite compound, for control of cotton worm. Historical Use of Arsenical Insecticides and Desiccants on Cotton in the USA
1873. In 1873, a graduate student at the University of Strasbourg named Othmar Zeidler published work describing the synthesis of a white powder from the condensation between trichloroacetaldehyde and chlorobenzene [2] [3]. The chemical, dichlorodiphenyltrichloroethane (Figure 1), contributed to Zeidler’s dissertation, but otherwise brought him little recognition during his lifetime. However, by the 1930s, scientists had determined that compounds with similar structure as Zeidler’s were effective pesticides. The Swiss Chemist Paul Müller was aware of that fact, and in 1939, he determined that dichlorodiphenyltrichloroethane—later called DDT—was particularly powerful for killing a range of insects [2]. DDT: The rise and fall of a "miracle" chemicalby Alister R. Olson, Michael P. Clough, and Benjamin C. Herman
1874. By 1874, the potato beetle had reached the Atlantic Coast. Apparently, Paris green had followed with it because a few years later an ominous bit of research was presented at the New York Academy of Medicine by a prominent neurologist, E. C. Seguin. Although the topic had been studied before, he felt compelled to address a growing problem: paralysis following arsenic poisoning. Seguin spent considerable time providing obscure references within the medical literature about the phenomenon, noting a familiar theme: “In lead paralysis the forearms are usually affected (sometimes only one) arsenical paralysis tends to involve all the limbs ; the lower limbs are more affected…”11. The Moth in the Iron Lung.
1876. 1876 — Congress fund US Entomological Commission to investigate insect damage on crops, especially the Rocky Mountain locust. Various forms of pesticides are tested, including arsenic, lead and pyrethrum flower based compounds. Late industrial 1850-90
1881. In 1881, Seeligmuller placed on record four cases; two after acute poisoning, and two after chronic intoxication. In his acute cases he noted paralysis, numbness, and anaesthesia (in toes), contractures, wasting of the extensors especially. The paretic and wasted muscles showed fibrillary contractions ; the nails were gradually lost. Electro-muscular contractility was diminished or even lost. He gives the following points for differential diagnosis from lead palsy : the acute origin of the paralysis, disorder of sensation as well as of motion, rapid muscular wasting, absence of blue line on the gums, and of cachexia. In the same year appeared the essay of Popow, of St.
1882. In fact, one of the early pesticides used at the time was an arsenic based product frequently referred to as Paris Green or Schwein-Furth Green. By 1882, it was already known that exposure to arsenic, including the arsenic contained in these pesticides, could cause paralysis and lesions of the spinal cord in both humans and animals. What is the history of Polio in America and other countries?
1882. Petersburg, upon the pathological anatomy of arsenical paralysis as produced artificially in animals. Popow carried on his experiments under the guidance of Prof. Mierzejewski ; giving arsenious acid to dogs in doses ranging from fa to 2 grains at a dose, producing acute and chronic intoxication. In cases where death ensued in four to five hours after ingestion of the poison, the spinal cord showed both macroscopic and microscopic lesions. The gray matter appeared swollen, intensely red, more especially in its two enlargements. Microscopic examination revealed enlargement and congestion of the small blood-vessels, and accumulations of lymph corpuscles in the lymph-spaces. There were also abundant extravasations of blood-corpuscles and plasma around the vessels, especially in the central portions of the gray matter, The walls of the bloodvessels were in a state of fatty degeneration. The ganglion cells exhibited three degrees of change. A first degree of alteration showed cells well stained by carmine, and containing vacuoles of variable sizes, some of which could be traced into the cell-processes. A second form of cells had no processes, were feebly colored by carmine and exhibited a punctate granular infiltration. Lastly, here and there were cells in a third state of change, consisting only of a nucleus surrounded by dark brick-red pigment. The white substance only showed pigment masses here and there, more especially about the blood-vessels. In cases of acute intoxication in which a fatal result ensued in the course of three, five, or six days, the spinal cord presented very much the same appearances. The distinction between the white and gray substances was less defined. The vascular injection and the exudation of plasma were less marked, but on the other hand the changes in the ganglion cells were more distinct, the vacuoles larger, and the granular state more pronounced. There were more cells, or properly remains of cells, of the third category above described. The white substance was normal, except some enlargement of blood-vessels, and considerable accumulations of pigment. In the chronic cases, those in which death occurred in the course of three months (one animal had paresis of the hind legs not long before death), the spinal cord appeared less firm, and the microscopic appearances differed noticeably from those observed in the acute cases. The walls of the blood-vessels were much thickened, and showed a distinct fibrillary structure, with diminution of the calibre of the vessels, and exudation of blood in the perivascular spaces. In the meshes of the perivascular spaces were extensive hyaloid masses. The number of ganglion cells was much diminished ; those remaining showed large vacuoles, and belonged to the first group described. In these cases the white substance was much more affected, especially in the postero-lateral columns. The cylinder-axes exhibited points of swelling here and there; they were granular; in many preparations they were merely represented by groups of fine granulations. The septa of the white substance likewise exhibited a granular change ; and the periphery of the white and gray substances was thickly strewn with small masses of black pigment. The spinal nerves, carefully examined at their origin, and at various points of their course and distribution, presented no pathological alterations. From these post-mortem observations Dr. Popow concludes that :
I. 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.
2. In the more chronic cases the pathological changes are found in the white as well as in the gray substance, constituting a diffused myelitis.
3. The peripheral nerves remain normal, even three months after intoxication.
1888. It wasn’t just scientists that had noticed. Articles and letters from concerned farmers began to appear in agricultural journals like Insect Life and The Country Gentlemen. Thanks for Nos. 1 and 2 of “Insect Life.” Your publications are great public educators and special aids to farmers… A more thorough knowledge of our friends and foes among insects and birds would increase our farm products. We hope you may find out insecticides which are less dangerous to humanity than arsenic. Two cases of serious illness, but not fatal, have occurred in our neighborhood—one from eating strawberries planted alternately with potatoes which had been dusted with Paris green, and the other from eating raspberries adjoining the potato patch, from which the poison had blown. We hope that Congress will make all necessary appropriations for the carrying on of the good work.—[R. Bingham, Camden, N. J., September 22, 1888. REPLY.—* * * I am glad to get the account of the two cases of poisoning from the treatment of potatoes by Paris green, and agree with you that a less dangerous remedy would be good. With proper care, however, there is very little danger, and in both the instances which you mention the application was evidently very carelessly made.—[September 25, 1888.]13. The Moth in the Iron Lung
1889. Surprisingly, it wasn’t evidence from doctors or scientists that initially turned many wallpaper manufacturers away from the preferred green color. Instead, it was peer pressure from the public. By the 1870s, the popularity of the deadly green wallpaper was starting to wane, even before factories eventually discontinued its production altogether due to rising medical evidence. This particular advertisement (above) from the late 1880s let the customers know that their product was safe for any home by showcasing that arsenic free dyes were used. Toxic Walls: Why Was Victorian Green Wallpaper So Deadly?
1889. During the Second Industrial Revolution (late 19th to early 20th centuries), countries such as the United States, the United Kingdom, and France began investing large amounts of resources in agricultural research. Poor health of fruit crops in Europe and the United States during the second half of the 19th century prompted much of this effort. Phylloxera infestations of grape and numerous disease and insect problems with apples, peaches, and other fruit crops plagued agriculture on both continents. As a result, new chemical products, application technology, and methods introduced in Europe found their way to the United States. Nowhere was this more evident than in the 1889 Paris Exposition (Riley, 1891). The works of American and European pioneers in pest management were exhibited at the event. New spray machines, nozzles, and application methods were demonstrated and eventually adopted by farmers anxious to combat the pest and disease problems of the day. The U.S. Department of Agriculture (USDA) expanded its efforts in this area, creating new departments and hiring some of the first pest management specialists. The History of Lead Arsenate Use in Apple Production: Comparison of its Impact in Virginia with Other State
May, 1889. One morning in May of 1889, Medford residents awoke to a nightmare. Brighter-than-usual sun poured in through their bedroom windows, casting them from sleep an hour earlier than was typical. Shielding their eyes from the light, they drew their curtains to reveal a disturbing scene: the leaves were gone on the grand trees outside their homes—completely stripped bare, as if fire had consumed every leaf in sight. The shade the trees had once provided was no more, and now they could clearly see every house on either side of their street. A block away, a horde of caterpillars were ascending the last remaining oak on their street, searching for food. Within a day, it would be completely destroyed. Homeowners raced down the stairs and into their backyards, confirming their fears—their gardens, their fruit and vegetables, all had been consumed by swarms of the hairy creatures. Once outside, they scraped them with dustpans from the sides of their houses and swept them from their front porches with brooms. As the sources of food disappeared, millions of hungry caterpillars began crossing Myrtle Street in an attempt to satisfy their voracious appetite. A black, pulsating carpet rippled across the road as passing carriages could do nothing to avoid them. Homeowners tried in vain to destroy them, scraping them into giant barrels of kerosene and burning them by the gallon. It seemed like nothing could stop the onslaught. Walking down Myrtle Street became impossible, as slipping on the throng of creatures was a constant hazard. The houses themselves were under attack as caterpillars crawled through every gap and crack looking for food. They could be found inside closets and pantries, coat pockets and shoes, under pillows and between the sheets. It wasn’t just Myrtle Street—other pockets of attack emerged across the area. As night fell, the constant sound of a million tiny scissors clipping through the leaves kept anyone from sleeping. The trees would be gone by the morning, and many of the caterpillars would probably be inside the houses before then. The attack would continue until summer, when the millions of caterpillars would spin their cocoons throughout the town to emerge as moths a week or two later. Although the flying insect’s range was limited, they would mate and lay between 500 to 1,000 eggs for each pairing. As authorities toured the destruction on Myrtle Street and the surrounding areas, the devastation was surreal. The thermometer read seventy-five degrees, but the landscape was by all appearances the dead of winter, the carcasses of trees all that remained. Even parts of the houses themselves— steps, porch rails, and siding—had been destroyed as they were cast aside in a frantic search to destroy the insects. The number of caterpillars which attacked Medford that summer defied belief. As its citizens scoured every square inch of their property, trying to strip the hundreds of spongy brown egg masses coating nearly every vertical surface they could see, they realized their efforts would not be enough. There would not be another Blizzard of 1888 for almost one hundred years, and although the authorities began spraying Paris green aggressively, even that would not be sufficient to stop the gypsy moth’s advance. The Moth in the Iron Lung
1892. Lead arsenate is an insecticide that was commonly used in apple orchards from its introduction in 1892 until the early 1940s. Its use declined, but was banned from use in the US in 1988. PubChem Compound Summary: Lead Arsenate.
1892. It is only in more recent years that lead arsenate has been used as an insecticide for spraying purposes. Its use was first suggested by Mr. F. C. Moulton in 1892, while acting as chemist for the gypsy moth commission of Massachusetts, after having made a study of numerous materials to be used as insecticides for the extermination of the gypsy moth. It was found that Paris green could not be used successfully for this purpose, principally because it could not be applied in sufficient quantity to kill the caterpillars without seriously injuring the foliage. While lead arsenate was not found entirely satisfactory in destroying this pest, it possessed several advantages over Paris green, and this has resulted in its replacing the latter material for spraying purposes to -a very large extent, in fact, almost entirely in some of the Rocky Mountain and Pacific Coast States. Lead arsenate. I. Composition of lead arsenates found on the market. II. "Home-made" lead arsenate and the chemicals entering into its manufacture. III. Action of lead arsenate on foliage, US Department of Agriculture, 1910
1892. By 1892, the moths covered an area over 200 square miles. A “Gypsy Moth Commission” had been formed, and men were hired to work full-time in attempts to control the insect’s advance. Police inspected vehicles leaving the area for hitchhiking pests, and the spraying of Paris green increased, despite its apparent futility. A chemist, employed by the commission to develop an insecticide more formidable than Paris green, stumbled onto a new formulation: the arsenic remained, but a new component was added— lead. The new mixture—dubbed lead arsenate—appeared promising. It was toxic to the caterpillars—that was paramount. Where repeated coatings of Paris green seemed to have little effect on them, lead arsenate killed more readily. … Throughout 1892, word spread quickly about the promise of a miraculous new pesticide. Many who’d ignored the earlier warnings of the gypsy moth had already lost everything, but those who lived nearby clearly saw the destruction they could impose. No amount of Paris green or manual disposal appeared to have any effect on the insect’s proliferation. The mood was dire, but lead arsenate appeared to offer them a weapon with which they might win. The Moth in the Iron Lung.
1893. The ingredients were readily available at any local druggist, and, with the spring of 1893 fast approaching, employees of the commission, farmers, woodsmen, even homeowners, began to fan out from Medford and beyond in a furious attempt to stop the moth’s spread. Makeshift sprayers were made by connecting hoses and nozzles to hand-operated water pumps mounted on top of garden barrels. The wheels of carriages were coupled with chains and sprockets to power automatic devices that could propel lead arsenate high into the treetops. … Boston, 1893 By this time, poliomyelitis was beginning to appear less often as isolated cases but instead within what they called epidemics. Rather than an infant here or a young boy two towns away, they might discover seven or eight cases of poliomyelitis that either went to the same school or had contacts who did. …. In the previous year—1892—the combined hospitals of Boston had seen six cases of poliomyelitis from August to November. The bustling Massachusetts General Hospital saw none. In November 1893, neurologist James Putnam asked in the Boston Medical and Surgical Journal if acute poliomyelitis had been unusually prevalent that year. There had been twenty-six cases. Although he seemed relatively non-plussed, it was the largest recorded outbreak of polio in America at the time. In fact, nothing came close to it besides the early reference to the 11 or 12 children suffering from teething paralysis in Louisiana in 1841—assumed by modern historians to be polio. The Moth in the Iron Lung.
November 1893. As winter approached and manual laborers continued scouring tree trunks, fence posts and clapboard siding for gypsy moth eggs, a foreboding article appeared in a November 1893 issue of the widely circulated Boston Medical and Surgical Journal. It was called “Is Acute Poliomyelitis Unusually Prevalent This Season?” The Moth in the Iron Lung.
1894. Thankfully, whatever the illness was, it was completely rare. Rare—at least—until the summer of 1894, when just north of Boston in a small New England town in Vermont, polio would strike with a vengeance that no one had ever seen before. The Moth in the Iron Lung.
1894, Vermont. In the late 1800s, the Vermont Tree Fruit Growers Association reports, for-profit orcharding began in earnest: “By 1894, northern Vermont had become one of the most important apple-growing regions of the continent, supplying markets in the United States, Canada, South America, and even Europe.” According to the Report of the State [Vermont] Board of Agriculture in 1894-95, apple growers were meeting with specialists in fertilization, cultivation, and spraying, and knew the importance of handling fruit carefully for market. The stage was set for the commercial orchard era, which began in 1890, became extensive around 1910, and continues today. Apples: A fall staple that wasn’t always in Vermont
1894. The next significant epidemic, 10 times larger than previous outbreaks, with 132 recognized cases, erupted in the U.S. state of Vermont in 1894. Albert Bruce Sabin Britannica
1894, Vermont. While the gypsy moth was making steady gains, it would be a few years before it reached Vermont. Regardless, many in the state were ecstatic about news of a more effective pesticide because they had their own pest to deal with—the codling moth. While not as voracious as their gypsy moth brethren, the codling moth’s cuisine was decidedly more personal to many in New England. They didn’t prefer leaves as much as they did the fruit itself—particularly pears and apples—a diet which gave the moth its nickname, the “appleworm.” Shortly after winter, local farmers would begin to ready themselves for a long spring of tilling, planting and protecting their crops from the many invaders that could threaten their livelihood. The frequent—and often times unsuccessful—applications of Paris green left much to be desired. The Rutland druggist may have suggested they purchase materials to make lead arsenate, the miracle pesticide being used to wide acclaim in Massachusetts. Although it had been employed for the past two summers in the areas around Boston, commercial production had not ramped up to fill the demand. Because of this, the correct blend for making the pesticide and its application procedures were still being determined. The amount of water to apply it with—some suggested two pounds of lead arsenate for 50 gallons of water, while others would suggest double, triple, or even quadruple that amount—was another variable that was being established on the fly. Whatever the recipe called for, its toxicity to humans was not a remote concern. Lead arsenate was remarkably gentle on foliage and could be liberally applied without fear of burning the leaves. Its adhesive property prevented it from easily washing off with rain or dew. These traits had worked to great effect in Boston where the tenacious gypsy moth was destroying every tree in its path. In Vermont, however, it wasn’t trees that needed protection so much as food—fruits and vegetables that were planted in spring and harvested throughout the summer. Lead arsenate appeared to be much more toxic than Paris green and would inevitably be sprayed directly onto produce meant for human consumption. The poliomyelitis that physicians had seen in Boston the previous summer was but a prelude. Within months, Charles Caverly, a physician and President of the Vermont State Board of Health began hearing accounts from his colleagues of unexplainable “acute nervous disease” in the children of Rutland. More concerning—it was accompanied by paralysis. Throughout the summer and into fall, more reports of illness trickled into his office. By the time he had compiled them all and published his findings in the Yale Medical Journal, 123 people would be stricken by this new illness and eighteen of them would die—many of them children. The Moth in the Iron Lung.
The following "Notes" are the result of an investigation undertaken by me in an official capacity at the time of the outbreak, and since continued through private and professional intercourse. The epidemic was one of an acute nervous disease whose chief distinguishing characteristic was motor paralysis, more or less complete, of one or more members or groups of muscles, and which prevailed in the State of Vermont, chiefly in a single valley, during the summer of 1894. The results of my investigations, as far as completed at the time, were published in the Yale Medical Journal for Nov., 1894, and in the New York Medical Record for Dec. 1, 1894. At the time of making these reports, it did not seem possible to speak of the epidemic more definitely than as one of "acute nervous disease of unusual type." A further careful study of the complex features of the epidemic, however, and of the subsequent history of many of the cases, together with the cor roborative opinions of many able medical men, seems to clear up any doubt that at the time existed, as to the correct diagnosis of the essential disease that prevailed. The epidemic, as I have indicated, invaded our valley in the early summer of 1894. It prevailed with increasing severity during July, apparently reached its climax about the first of August, and steadily declined until about the first of October, the last case occurring early in that month. …. The outbreak of which I speak consisted of upward of 130 cases of disease in which the commonest clinical manifestation was some degree of motor paralysis of widely varying extent. It will not surprise anyone that so large a number of cases presenting a bewildering variety of initiatory constitutional symptoms, as well as local paralyses, should have proved a very knotty problem for the diagnostician. It was long a question whether this was an epidemic of one, two, or more diseases, and along the established lines of symptomatology and pathology there was no solution of the problem. I have been able to collect histories more or less complete of 132 cases directly affected in this epidemic, and this number probably represents at least 90 per cent of the whole number.
1897. Arsenic trioxide (white arsenic) was an ingredient listed in a recipe for an insecticidal spray printed in a local Denver newspaper in 1897, so it was in use prior to when pesticide registration was required. Arsenic trioxide was used as an herbicide, insecticide, miticide, antifoulant, and rodenticide (NPIRS, 2002). Environmental Protection Division Denver Department of Environmental Health 2004
1900. Onuff 10 (1900) reported a case of a painter with flaccid paralysis of both legs, in whom the autopsy showed lesions characteristic of poliomyelitis. Ralph Scobey testimony to Congress (1953)
September 18, 1900, Louisiana. Some nightmare material for you, on this day 119 years ago: Dr. Moffett's Teethina, a teething remedy advertised in the Colfax Chronicle of Grant Parish, Louisiana in September of 1900. Note the baby's head on a pig's body, which was used to entice mothers to buy this powder to help her baby gain weight, cure ailments, make it sleep better, etc. However, the powder's main ingredient was mercury, disguised as the more innocent-sounding "calomel." Just a few applications of this quack medicine led to mercury poisoning, which caused babies to lose weight, cry incessantly, and scratch away their own skin. The Colfax Chronicle is a newspaper chock-full of ads; it's almost like today's Penny Saver. Ads like these bolstered pushes for regulations in medicine, pharmacology, and advertising. (Science Friday: Murderous malpractice of the 19th century; Library of Congress). Facebook- Red River Historian
1905. The polio outbreaks gradually became more severe, more frequent and widespread throughout Europe and the United States at the beginning of the 20th century. The epidemiology of PV was gradually understood. The model of polio spread was irregular and many patients had no direct contact with a known source. In 1905, Wickman first recognized that poliomyelitis was an infectious disease. Baicus A. History of polio vaccination. World J Virol 2012; 1(4): 108-114 [PMID: 24175215 DOI: 10.5501/wjv.v1.i4.108]
1907. In 1907, Dr. H. C. Emerson54, Massachusetts State Inspector of Health, District 14, investigating an epidemic of poliomyelitis in that state, made a careful inquiry regarding the diet. No infant who was fed exclusively on the breast developed poliomyelitis. He found in six cases that fruit and berries had been a large item of the diet. In the cases of two infants, bananas and berries had been given in the diet in addition to breast milk. In three cases of poliomyelitis, the illness was attributed to the eating of large amounts of blackberries and blueberries. In one case the illness was credited to eating heartily of English mulberries. In 39 instances it was stated that food supplied were bought from fruit and vegetable peddlers in their localities. Ralph Scobey testimony to Congress (1953). BACKGROUND ON HISTORY OF PESTICIDE USE AND REGULATION IN THE UNITED STATES
1907. Chemical industry begins production of lead arsenate; home manufacture no longer recommended; Usage reaches 40 mil. lbs. by 1934
1907. As early as 1907, lead was recognized for its cumulative properties. Agricultural workers preferred using arsenic because lead was an accumulative poison. It was believed that arsenicals, except lead arsenate, should be permitted in agriculture. In 1907, a controversy erupted in Europe when the German Imperial Health Commission opposed the use of lead arsenate on grapes because arsenic and lead were found in the wines (Moore, 1935). Nonetheless, lead arsenate became the most popular and widely used insecticide of the period. The History of Lead Arsenate Use in Apple Production: Comparison of its Impact in Virginia with Other States
1909. It had been recognized for some years prior to 1909 that acute poliomyelitis must be due to some specific infection; and quite a number of observers had isolated from the nervous system of patients suffering from the disease bacteria which they believed to be the specific causative agent. Some observers claimed to have reproduced the disease in lower animals by injections of pure cultures of such bacteria. However, the bacteria found by different observers belonged to different species; many competent bacteriologists constantly failed to find any bacteria whatsoever, and the lesions occasionally produced in lower animals did not correspond to the lesions of human poliomyelitis. Consequently, none of the above claims were generally accepted. In the spring of 1909, Landsteiner and Popper * succeeded in transmitting the disease to two monkeys by inoculation with the spinal cord of a child which had died of acute poliomyelitis. The lesions found in the cords of these monkeys were typical, but Landsteiner and Popper failed in their attempts to transmit the disease from these to other monkeys. Later in the year Flexner and Lewis? succeeded in confirming the work of Landsteiner and Popper, and further succeeded in transmitting the infection from monkey to monkey through an indefinite number of passages. Testimony to Congress by Wade Frost, 1912
1910. Passage of the Food and Drug Act of 1906 occurred as public concerns for the wholesomeness of food supplies took a major turn when Upton Sinclair’s book, “The Jungle”, was published the previous year. It highlighted problems with the safety of the food supply, particularly that produced by the meat packing industry and wholesomeness as related to sanitation, product quality and handling practices. Pesticide residues were not an apparent major concern at the time. Nevertheless, the Insecticide Act of 1910 provided for establishment of tolerances for specific insecticides, which was done later by regulation, primarily for arsenic and lead on apples and pears. BACKGROUND ON HISTORY OF PESTICIDE USE AND REGULATION IN THE UNITED STATES
1910, Vermont. In 1910, another polio outbreak occurred again in Vermont. And while most cases were still being reported in children, persons of all ages were being affected. In this outbreak, Dr. Charles Caverly reported that outbreaks of polio had also occurred again in animals, but this time in pigs and calves.18 Humans are the only known carriers of the poliovirus,19 and therefore it is reasonable to believe that these early epidemics of paralysis were not necessarily caused by the poliovirus. What is the history of Polio in America and other countries?
1921. Rosenau 102 (1921) stated: "Monkeys have so far never been known to contract the disease "spontaneously" even though they are kept in intimate association with infected monkeys." Twenty years later (1941), Dr. John A. Toomey103, a poliomyelitis authority, stated: "No animal gets the disease from another no matter how intimately exposed." Ralph Scobey testimony to Congress (1953)
August 10, 1921.
On August 10, 1921, FDR spent a strenuous day sailing and swimming near his family's summer home on Campobello Island. Tired and feverish, he went to bed early, not realizing he was suffering the first symptoms of a polio attack. FDR Library and Museum. And Roosevelt’s presence in the world’s commercial blueberry capital at harvest time when his illness struck seems remarkable in light of the lead arsenate theory, which already had been proposed more than once in the decade before his illness. Eleanor herself did the family’s grocery marketing in Eastport, and Roosevelt’s love of blueberries and other fresh fruit is well documented. His chef in the White House, Henrietta Nesbitt, wrote that he was “fond of blueberry and other pies.”[xxxiii] In the cafeteria at FDR’s presidential library in Hyde Park, the Henrietta Nesbitt Café, the most prominent picture is of the broadly grinning president being served a big piece of pie. The Age of Polio. Blueberry Pudding – A Favorite of President Franklin Roosevelt’s. Arsenical pesticides and herbicides were extensively used on apple, blueberry, and potato crops in New England during the first half of the twentieth century. Lead arsenate was the most heavily used arsenical pesticide until it was officially banned. CONTAINING ARSENIC-ENRICHED GROUNDWATER TRACING LEAD ISOTOPIC COMPOSITIONS OF COMMON ARSENICAL PESTICIDES IN A COASTAL MAINE WATERSHED CONTAINING ARSENICENRICHED GROUND WATER
1920s. Lead Artesenate Spraying of Apple Trees in Virginia
Prototype “iron lung” negative-pressure ventilators were developed in the late 1920s and early 1930s by industrial hygienist Philip A Drinker (1894-1972), physiology instructor Louis Agassiz Shaw Jr. (1886-1940), and inventor/medical-equipment manufacturer John Haven (“Jack”) Emerson (1908-1997). From around 1926 to 1928, Drinker and Shaw, both at Harvard Medical School in Boston, designed an electrically powered tank respirator. On October 13, 1928, Drinker and pediatrician Charles F McKhann demonstrated the potential of this device in an 8-year-old girl with poliomyelitis, respiratory failure, and coma who was treated at Boston Children’s Hospital and briefly survived before succumbing to pneumonia. A second trial on Friday, September 13, 1929, at Peter Bent Brigham Hospital in Boston, on a 21-year-old Harvard student, was unquestionably successful: Hoyt was weaned from the respirator in 4 weeks and was discharged from the hospital before Christmas. Emerson built a mechanically superior device in the summer of 1931; Emerson’s device was first used clinically to save the life of a priest with polio at the Providence City Hospital in Providence, Rhode Island.
1928. 'The Autumn Ghost' tells of innovation that saved lives during polio epidemic “The iron lung, which came in in 1928, was really revolutionary,” says critical care physician Dr. Hannah Wunsch. “In fact, it was the first time you had a machine that could support people's breathing.” Though revolutionary, it still had a host of setbacks. Patients often felt trapped in a huge metal casket, a major downside to the iron lung. Plus, doctors and nurses had trouble treating patients because they had to stay encapsulated in the machine to create negative pressure that would suck air into the lungs. Additionally, for patients with bulbar polio, the mortality rate still hovered around 90% even when using the iron lung. To address these shortcomings, Dr. Bjørn Aage Ibsen started working to create a positive pressure ventilator in 1953. The technology would effectively push air into the lungs. And, the technology was much smaller and less invasive than the iron lung. The mortality rate of the disease reduced from 90% to 20%.
1929. In the year 1929, almost 30 million pounds of lead arsenate and calcium arsenate were spread across this country's fields and orchards. A is for Arsenic (pesticides, if you please)
1930. In the spring of 1930, there occurred in Ohio, Kentucky, Alabama, Mississippi and other states an epidemic of paralysis.16,17 The patients gave a history of drinking commercial extract of ginger. Ralph Scobey testimony to Congress (1953)
1932-1933. Toomey and August59 (1932) pointed out that some authors thought that poliomyelitis is a disease of gastrointestinal origin which might follow the ingestion of foodstuffs. In 193360, they noted that the epidemic peak of poliomyelitis corresponds with the harvest peak of perishable fruits and vegetables. They called attention to the fact that the disease occurs only in those countries which raise the same type of agricultural products. Ralph Scobey testimony to Congress (1953)
1933. On February 21, 1933, the federal government passed a law limiting lead residues on fruit to 0.025 grains of lead per pound of fruit. It was believed that arsenic residues were acceptable on fruit, but lead was hazardous. Although nothing could beat its efficacy, lead arsenate as a compound was unacceptable (Moore, 1935) The History of Lead Arsenate Use in Apple Production: Comparison of its Impact in Virginia with Other State
1935. "in 1935, on a weekly radio program sponsored by the U.S. Food and Drug Administration, the host suggested that the old-time school rhyme "A is for Apple" be changed as follows: A is for Arsenate/Lead if you please/Protector of Apples/Against Archenemies." A is for Arsenic (pesticides, if you please)
1936. In 1936, during a campaign to eliminate yaws in Western Samoa by the injection of arsenicals, an epidemic of poliomyelitis appeared simultaneously.23 In one community all of the patients developed paralysis in the same lower limbs and buttocks in which they had received the injections and this pattern was repeated in 37 other villages, whereas there was no paralysis in uninoculated districts. The natives accused the injections as the cause of the epidemic of poliomyelitis. Most of the cases of paralysis occurred one to two weeks after the injection of the arsenic.Ralph Scobey testimony to Congress (1953)
1938. The next major development was passage of the Federal Food, Drug and Cosmetic Act (FFDCA) in 1938, which provided for tolerances to be established for chemicals including pesticides, primarily arsenicals such as lead arsenate and Paris green. The Act required that color be added to the formulations to prevent their misuse and set tolerances for residues in food where these materials were necessary for production of the food supply. (Grodner, p. 3). BACKGROUND ON HISTORY OF PESTICIDE USE AND REGULATION IN THE UNITED STATES
1939. Barber 64 (1939) reported four cases of poliomyelitis that developed simultaneously on the same day from the eating of strawberries in a single house of a boarding school. He says that the simultaneous onset of these cases resembled food poisoning. The seasonal and climatic incidence of poliomyelitis, he points out, agree closely with the seasonal increase in the consumption of fresh garden production. He says that the epidemiological distribution of poliomyelitis resembles food poisoning. Ralph Scobey testimony to Congress (1953)
1939. Dichlorodiphenyltrichloroethane (DDT) is an organochlorine insecticide that had a broad range of agricultural and nonagricultural applications in the United States and worldwide beginning in 1939. Toxicological Profile for DDT, DDE, and DDD
1941. Chenault65 (1941) noted that the history of poliomyelitis points to a "suggested parallelism between a number of epidemics and the appearance of fresh fruits and vegetables." [With regard to these numerous statements regarding fruit and milk, note the high production of pesticides in the form of lead and arsenic compounds during this pre-DDT period, graphed] Ralph Scobey testimony to Congress (1953)
1943. In 1943, researchers at the FDA identified three potential hazards related to DDT that demanded further research: (1) DDT in solution was readily absorbed through the skin causing tremors, paralysis, and even death in rabbits; (2) chronic exposure to DDT produced a wide range of organ damage in test animals; and (3) while inhalation of DDT had little effect on some animals (e.g., dogs), it killed others, such as mice [5]. DDT: The rise and fall of a "miracle" chemical by Alister R. Olson, Michael P. Clough, and Benjamin C. Herman
September 1943. While researchers were again scrambling to find a suitable insecticide in 1942, J. R. Geigy A. G.—the Swiss company that employed Paul Müller—gave the United States a sample of DDT [6]. DDT testing, which again was dramatically accelerated due to the urgency of the war, revealed that the chemical was incredibly potent, long-lived, killed a range of pests, and could be relatively easily produced. DDT was adopted by the American armed forces in September of 1943, less than a year after the first samples were received, and production was dramatically increased [5]. That winter, DDT was utilized in a groundbreaking effort to defeat a typhus epidemic in Naples [7] [5]. DDT: The rise and fall of a "miracle" chemical by Alister R. Olson, Michael P. Clough, and Benjamin C. Herman
1944-1945. n 1944-1945 alone, reports included: (1) widespread death of fish, crabs, and insects due to DDT use in the Pacific; (2) recognition that DDT resembled known carcinogens in appearance and effect; (3) fish mortality from low dose DDT application, and significant declines in bird populations with higher doses; and (4) harm to some crops, beneficial insects, and animals [5]. Some scientists during this period even warned that heavy use of DDT could result in “biological deserts” that would be “devoid of life” [5]. DDT: The rise and fall of a "miracle" chemical by Alister R. Olson, Michael P. Clough, and Benjamin C. Herman
1945.DDT spraying to control mosquitoes at Jones Beach State Park on Long Island in 1945.You and Me and DDT.
April 1945: The emerging reports and research led the army and United States Public Health Service to enact regulations in April 1945 that severely limited domestic aerial spraying of DDT [5]. Such restrictions may seem incongruent with the wide use of the spray at this time by the U.S. armed forces to protect soldiers overseas, but the press release announcing the 1945 regulations addressed the apparent inconsistency:… DDT distributed over the countryside not only wipes out malaria carrying mosquitoes but also may kill other insects, many of which are beneficial. Much still must be learned about the effect of DDT on the balance of nature important to agriculture and wild life before general outdoor application of DDT can be safely employed in this country. It may be necessary to ignore these considerations in war areas where the health of our fighting men is at stake, but in the United States such considerations cannot be neglected. U.S. Army, & U.S. Public Health Service, p. 284 [15]. DDT: The rise and fall of a "miracle" chemical by Alister R. Olson, Michael P. Clough, and Benjamin C. Herman
August 1945: However, the U.S. Army and U.S. Public Health Service only controlled DDT use in the United States as long as military need exceeded the amount of pesticide being produced. When manufacturers managed to exceed wartime need in the latter half of 1945, the prospect of selling DDT to civilians for domestic use loomed large. Despite the concerns of prominent scientists such as Clarence Cottam of the USFWS, who asked for further testing of the environmental impacts of DDT before allowing the public to buy it, the War Production Board allowed the public to begin purchasing surplus stock of the pesticide in August 1945 [5]. The U.S. Army and U.S. Public Health Service regulations did not apply to the public, and beyond some limited labeling requirements, the sale and use of DDT therefore became virtually unchecked by the United States government. DDT: The rise and fall of a "miracle" chemical by Alister R. Olson, Michael P. Clough, and Benjamin C. Herman
1946. Gebhardt and McKay68 (1946) found during an epidemic of poliomyelitis in Utah that of a total of 206 persons surveyed, 192 persons, or 93.2 per cent, had one to two weeks prior to the onset of the disease eaten fresh fruits. The authors found in Utah, New York and California, during 1943, that the cases of poliomyelitis paralleled the harvest peaksRalph Scobey testimony to Congress (1953)
“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.”
1947. The 1910 and 1938 Acts did relatively little but set the stage for passage of the Federal Fungicide, Insecticide and Rodenticide Act (FIFRA) in 1947, as the synthetic organic pesticide industry was in its take off stages. Dramatic increases in production and usage of such chemicals as DDT, BHC, dithiocarbamic fungicides and 2,4-D were occurring and it was apparent there was a need to update pesticide regulation. FIFRA replaced the Federal Insecticide Act of 1910. Among other things it expanded coverage to all pesticides (not just insecticides) and required that all pesticides be registered with the U.S. Department of Agriculture (which had responsibility for pesticide regulation, going back to the 1910 Act). FIFRA maintained the function of protecting against ineffective or dangerous products from a farmer or other user’s standpoint and labels were to be approved by USDA before products were sold. Products were to be safe when used as directed by the label. The 1947 Act was primarily a labeling act, providing no sanctions for misuse, no authority for immediate stop-sale orders against dangerous pesticides and limited penalties for companies selling such products. (Briggs, p. 279) Also, a company could obtain a “protest registration” and sell the product even if USDA would not register it, which was done for a number of products. (Briggs, p. 279) These were major defects in FIFRA and were changed by amendments in later years (Miller, p. 435) FIFRA was later amended to add federal registration number as part of registration of pesticides (1959), include warnings on labels (1961) and remove safety claims from labels (1964). BACKGROUND ON HISTORY OF PESTICIDE USE AND REGULATION IN THE UNITED STATES
1947. Advertisement in Time Magazine.
1948. Abbott71 (1948), of Auckland, New Zealand, stated: "The public has always been fully convinced that they caught poliomyelitis from one another by direct infection. The 'germ' idea is indeed deeply ingrained in both the profession and the public. It will be many years before our prolific writers of medical textbooks attain the degree of sophistication that would enable them to understand how and why poliomyelitis would be more likely to be contacted from the flour-bag, or some homely article of food, rather than from their neighbors." Ralph Scobey testimony to Congress (1953)
Barondes72 (1949) points out that a study of the epidemiology of poliomyelitis shows a definite correlation with the harvesting of fruit and vegetable crops and to changes in climate, weather and humidity. The harvesting of such fruits as cherries, grapes, berries, apricots, etc. and the edible vegetables, as lettuce, radish, cucumbers, etc. usually from June to September, corresponds with the period of poliomyelitis epidemics, Barondes points out.Toomey et al74 (1949) made some important experimental observations that appear to show a correlation of the poison and virus theories of poliomyelitis. They considered it possible that a food (fruit) which enters the gastrointestinal tract could in some way act as a precursor of catalytic enzyme on a normal constituent of the tract and accelerate the production of poliomyelitis. Various materials, together with fruit extracts, were tested. Ralph Scobey testimony to Congress (1953)
1949. Dr. Morton Biskund and Irving Beiber publish their researh that "X disease" that had been attributed to a "hypothetical virus X" was actually caused by DDT.
1951. Rodney Dodson writes "In 1951, American researcher Albert Sabin noticed that the US Military in the Philippines had an astonishingly high rate of Polio. Approximately 1 in 79 recruits. The native Philippine people considered Polio the white man's disease, as it didn’t seem to affect anyone else. Sabin also noticed similar coincidences in China and Japan. Every US Military recruits had to undergo a delousing with DDT. This required complete body fumigation. Villagers near the military bases however were not fumigated, nor were they affected by Polio. Although they were often intermixing with the soldiers, they never contracted the “killer virus.”
April 1952. Testimony of Ralph Scobey to Congress. "Paralysis, resulting from poisoning, has probably been known since the time of Hippocrates (460-437 B.C.), Boerhaave,3 Germany, (1765) stated: "We frequently find persons rendered paralytic by exposing themselves imprudently to quicksilver, 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, Cooke,4 England, stated: "Among the exciting causes of the partial palsies we may reckon the poison of certain mineral substances, particularly of quick silver, arsenic, and lead. The fumes of these metals or the receptance of them in solution into the stomach, have often causes paralysis."
1953. 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.Pesticides and Polio: A Critique of Scientific Literature
1954. Even as sales of DDT were skyrocketing, concerns about the chemical persisted. Publications highlighting problematic issues related to pesticides continued to cross the desk of Carson, who in 1949 had become editor in chief of USFWS publications. Additionally, many popular news media articles being published about DDT highlighted concerns about its use and safety. In reaction to the increasing concerns about DDT, Paul Mayfield, then president of the National Agricultural Chemicals Association, complained in 1954 about propaganda, misinformation, exaggeration, and “pseudoscientific double talk” that was harming the pesticide industry. He wrote: Only 10 years ago DDT was being hailed as a wonder chemical to rank with the drugs which are eliminating such diseases as malaria and typhus. The aerosol bomb was a symbol of the American Army to many of the people of North Africa and Italy. … But today we find the other side of public opinion being aroused while the favorable aspects are neglected. The Sunday supplements are being loaded with allegations that DDT and other “poisonous chemicals” cause all manner of human ills. Mayfield, p. 176 [16]. News coverage was actually predominantly positive in the early 1950s, although the frequency of negative articles significantly increased as the decade wore on [17]. DDT: The rise and fall of a "miracle" chemical by Alister R. Olson, Michael P. Clough, and Benjamin C. Herman
In 1955, the World Health Organization (WHO) launched the Global Malaria Eradication Program (GMEP). The program centered on distributing the drug chloroquine for malaria prevention and treatment and spraying insecticides—namely, dichlorodiphenyltrichloroethane (DDT)—to reduce mosquito populations. Reported cases fell worldwide, but by the early 1960s, strains of insecticide-resistant parasites emerged, along with growing concerns about the environmental and public-health risks of DDT. Research efforts, as well as political and financial support for GMEP, waned, and WHO suspended the program in 1969.
April 12, 1955. An announcement is made that Jonas Salk's polio vaccine is safe and effective.
1956. In 1956 the AMA (The American Medical Association) instructed each licensed medical doctor that they could no longer classify polio as polio, or their license to practice would be terminated. Any paralysis was now to be diagnosed as AFP (acute flaccid paralysis) MS, MD, Bell’s Palsy, cerebral palsy, ALS (Lou Gehrig’s Disease), Guillian-Barre (GBS), meningitis, provocation poliomyelitis, transverse myelitis, viral or “aseptic” meningitis, Chinese Paralytic syndrome, Chronic Fatigue Syndrome, etc Included under the umbrella term “Acute Flaccid Paralysis” are Poliomyelitis, Transverse Myelitis, GBS, enteroviral encephalopathy, traumatic neuritis and Reye’s syndrome. http://bit.ly/1Ml3rpX This was orchestrated purposely to make the public believe polio was eradicated by the polio vaccine campaign but because the polio vaccine contained toxic ingredients directly linked to paralysis, polio cases (not identified as polio) were skyrocketing…but only in vaccinated areas. http://bit.ly/1WEHYzR Today most vaccine inserts declare paralysis as a potential side effect but “reframe it” as Guillian Barre or simply “paralysis”. This is purposely designed to obfuscate the public’s understanding of what causes paralysis, which is heavy metal poisoning plus vaccine induced autoimmunity……that ends with the body attacking and destroying its’ own nervous system pathways, in an rabid attempt to clean itself of the injected toxins. Guillian Barre and paralysis, as listed vaccine side effects, are also a way to get the public running east looking for a sunset, keeping them as far away as possible from connecting the dots around this medical polio obfuscation. Aluminum and mercury are ingredients in most (if not all) vaccines today and both are proven to cause paralysis and motor neuron destruction………..known as many different names, depending on just how much the science/medical authority figure in the room wants to lead you astray that day. Polio Planned To Be Used To Coverup Vaccine Caused Guillain-Barré Syndrome (odysee.com).20 Things You Didn't Know About Polio
1959. Production of DDT rapidly grew over the subsequent years, and the military technology that had been rushed through safety testing due to extraordinary wartime needs soon became the top pesticide for civilian use in the United States. In 1959 alone, Americans used 79 million pounds of DDT [8]. Government officials and agencies at various levels were also responsible for a considerable amount of DDT use, as they engaged in large-scale efforts to eradicate pests such as the gypsy moth, beetles carrying Dutch elm disease, and tent caterpillars [14]. For many, DDT was seen as nothing short of a miracle. DDT: The rise and fall of a "miracle" chemical by Alister R. Olson, Michael P. Clough, and Benjamin C. Herman
1962. CBS documentary on Rachel Carson’s book, Silent Spring. At a press conference on August 29, 1962, President John F. Kennedy said that he had instructed government agencies to investigate the toxic effects of DDT due to the concerns raised in Rachel Carson’s book.
1962-1963. Pesticides were an issue at the forefront of the environmental movement leading to the establishment of EPA. The publication of Rachel Carson’s book “Silent Spring” in 1962 dramatized the risks of DDT (and other pesticides) and helped crystallize the publics’ concerns in general about chemicals contaminating the air, water, wildlife and food supplies (and as found as residues in human tissues). In 1963, the President’s Science Advisory Committee issued a report entitled “The Use of Pesticides” which called for reduced use of pesticides, especially the persistent ones. BACKGROUND ON HISTORY OF PESTICIDE USE AND REGULATION IN THE UNITED STATES
2005. In November 2005, under authority of the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA), EPA released its biannual list of hazardous substances. The top two substances on the list were arsenic and lead; they’ve held that ranking for the preceding ten years. These two substances are most commonly found at sites on the National Priorities List (NPL). The History of Lead Arsenate Use in Apple Production: Comparison of its Impact in Virginia with Other State
2006. In 2006, the World Health Organization (WHO) brought DDT back for indoor spraying as part of a rotation of insecticides to help combat malaria [27]. In deciding to do so, the WHO acknowledged the many benefits of DDT, and argued that the health concerns related to the pesticide would not outweigh the benefits in malaria prone areas as long as the chemical was carefully utilized in the manner they described [27]. However, the organization also stressed its support for the Stockholm Convention, a United Nations’ treaty that seeks to curtail the use of organic pollutants that persist in the environment long after they are first applied. The first twelve chemicals addressed by the treaty—dubbed the “dirty dozen”—included DDT, which the treaty emphasized should be replaced with an acceptable alternative as soon as possible. The WHO’s position statement therefore reflects the complexity of carefully weighing the pros and cons of the pesticide in certain situations. DDT: The rise and fall of a "miracle" chemicalby Alister R. Olson, Michael P. Clough, and Benjamin C. Herman
2007. /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Following repeated doses, convulsions and paralysis were observed in dogs. American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. CD-ROM 2007. PubChem Compound Summary: Lead Arsenate
2007. BILL GATES et al., POLIO VACCINES, DDT, PARALYSIS, MONKEY VIRUSES & CANCER In 2007, the US Centre for Disease Control and Prevention (CDC) alarmingly admitted that between 1955–1963 over 98 million American children and pregnant women received one or more doses of a polio vaccine which was found to be contaminated with a cancer-causing monkey virus called Simian Vacuolating 40 (SV40)! [1
Skeletal muscle injury makes sufferers exposed to complications of concurrent poliovirus infection. The phenomenon, labelled as “provocation poliomyelitis” (PPM), continues to haunt polio programme in the province as detection of polio cases in the past few months have baffled the people associated with the programme.
This phenomenon continues to cause numerous cases of paralysis in the province due to unnecessary administration of injections to children. …
The rate of injection prescription is estimated to be from 6.5 to 15 injections per person per year, with children under five years receiving as many as 21 injections annually, according to experts.
A recent national survey indicated that a high proportion of these injections were unnecessary and they were administered in unsafe manner. Traumatic injection neuritis can occur because of unsafe intramuscular injection practice as it involves the sciatic and radial nerves and presents as acute peripheral neuropathy with flaccid paralysis of the injected limb within 24 hours after injection. …
During the study, 193 AFP patients were observed. Of them, 72 per cent children aged one to seven years, 28 per cent eight to 15 years and 57 per cent were male and 43 per cent were female. Of them, 17 children had TIN, of whom 13 belonged to rural areas.
Health department found 26 TIN cases in 2019, six in 2020 and 69 in 2022. All of the affected children were given injections by unqualified medical practitioners.
Senior paediatricians, however, say that TIN occurs usually due to accidental trauma to sciatic nerve by giving injection in buttocks. “Muscles are prone to weakness due to many causes including polio patients, who are infected but yet not paralysed. They may be precipitated with intra-muscular injection,” they said.
Paediatricians say that it is a coincidence and injection is not the cause. They say that real cause of polio infection is non-vaccination in the country. “Intra-muscular injection can precipitate paralysis in a polio infected child,” they said.
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It's a popular money making scam. SARS-CoV-2 vaxs lower immunity which increases viral load from STD spread monkeypox. You take the smallpox vax, it reactivates latent HIV, HIV cases follow it around. Next you have a HIV vax and so on, rinse and repeat.
It's a popular money making scam. SARS-CoV-2 vaxs lower immunity which increases viral load from STD spread monkeypox. You take the smallpox vax, it reactivates latent HIV, HIV cases follow it around. Next you have a HIV vax and so on, rinse and repeat.
Of course.
Can’t sue a “ virus”.
Rockefeller knew all too well what a money maker viruses and vaccines are.
Create an illness, create a shot. Money.