Polio: Rethinking the Origins of Paralysis

Exploring Environmental Toxins and Their Role in Historical Outbreaks

“The Idaho data simply confirm the fact that poliomyelitis is a low-incidence disease and there is a high degree of acquired immunity and many natural factors preventing the occurrence of the disease (as contrasted to an “infection”) in the Nation at large.”[1]

— Herbert Ratner, MD, Health Commissioner, Oak Park, Illinois

“How is it that today you hear from members of this panel that the Salk vaccine situation is confused; yet what everybody knows from reading the newspapers, and has known since the vaccine was introduced, is that the situation as far as the Salk vaccine is concerned was and is marvelous? The reason for this discrepancy lies, I think, in a new attitude of many public health and publicity men. It is hard to convince the public that something is good. Consequently, the best way to push forward a new program is to decide on what you think the best decision is and not question it thereafter, and further, not to raise questions before the public or expose the public to open discussion of the issues.”[2]

— Paul Meier, PhD, 1962

"It is conceivable that a future age may disdainfully look at our preoccupation with vaccination. Indeed, the entire concept may be replaced with another approach. In such an eventuality, it would record as statesmen or tyrants the lawmakers who protected or trampled the rights of those who opposed the concept for one reason or another in this age."[3]

— Clinton Miller, assistant to the president of the National Health Federation, 1962

Driven almost frantic by the spread of infantile paralysis in New York, parents are hustling their little ones out of the infected zones. Every day there is an exodus of children and their parents to mountain and seaside homes to escape the dreaded disease in the congested city. — “New Yorkers Fleeing City To Escape the Dreaded Infantile Paralysis,” The Courier-Journal, July 11, 1916.

Polio—a word that conjures haunting images of children in metal braces and iron lungs, a disease we were told had one cause—a virus—and one solution—a vaccine. But does history support this narrative? But is this really the case? Does the history match this narrative of a single cause? Is there more to the story?

Polio–A summer disease that is historically rarely, if ever, transmitted

A 1911 investigation by Frederick Batten, M.D. noted that the diseases primarily occurred during summer.

Seasonal Relationship.—In the Northern Hemisphere the disease always has the greatest prevalence during the months of July, August, September and October, the month of August being nearly always that in which the greatest number of cases occur.[4]

Hospital observations and family case studies from the early 1900s challenge the idea that polio is highly contagious. In hospitals, infected children were placed in wards without isolation, yet no secondary cases occurred among the 70 children exposed. Similarly, within households, close family members—including siblings who shared beds—remained unaffected, even when living with an infected person. Additionally, cases appeared in individuals with no known exposure to others with the disease, suggesting that direct person-to-person transmission was not a key factor in polio’s spread.

Against the infectivity of the disease may be urged, first, the absence of spread of infection in hospital. The cases of poliomyelitis admitted to hospital freely mixed with other cases in the ward without any isolation or disinfection, some 70 children came in contact, but no infection took place. On these grounds it is probable that the paralytic stage of the disease is not contagious.

Secondly, there is a striking absence of infection when contact is most close. In November, 1909, H. E. was taken ill with poliomyelitis; all five brothers and sisters, although in closest contact, remained unaffected. In October, 1909, M. K., aged 2 1/2, was taken ill; two sisters, aged 6 and 11 respectively, slept with and were in close contact with the child and remained unaffected. Twin sisters, aged 21, one was affected, the other unaffected.

Thirdly, that contact is not the only possible method of dissemination of poliomyelitis is proved by the fact that the disease may arise in persons in whom all contact with affected persons can be excluded.[5]

In 1912, John J. Moren noted in the Kentucky Medical Journal that polio was not very infectious.

It is known that it [polio] is not a very infectious disease, for monkeys suffering from polio in the same cage with healthy monkeys, do not infect others. Also, in the majority of cases occurring in an epidemic only one member of a family is affected. In proportion to the number exposed, very few suffer.[6]

In 1924, Charles S. Caverly, MD, reported on infantile paralysis in Vermont from 1894 to 1922. He noted the seasonal nature of the disease.

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…[7]

In his report, he found polio primarily affects children and occasionally youth and adults up to age 25, typically in sparsely populated river valley communities during hot, dry summer months. Investigations suggest the disease is only mildly contagious, as a large number of children in close contact with infected individuals showed only a small minority developing the illness.

With regard to the contagiousness of the disease, the investigation of this group of cases suggests that the disease is but mildly contagious to say the most. A large number of children were in intimate contact with those that were sick, and of these children an insignificant minority developed the disease.[8]

In a 1926 article in the Journal of the American Medical Association, a number of doctors emphasized their findings that cases were widespread and transmission between people was quite rare or non-existent.[9]

Dr. W. L. Holt, Little Rock, Ark.:

I investigated an epidemic of poliomyelitis in a suburb of Newark, N.J., in the summer of 1916, when there was a big epidemic in New York state. It started in Brooklyn. We had twenty cases in our town during the summer. I investigated the best I could and was much surprised that I could trace hardly any cases to personal contact with others, there rarely being successive cases.

Dr. I. D. Rawlings, Springfield, Ill.:

Anyone who has had much experience with poliomyelitis is struck by the infrequency, relatively, of the secondary cases among direct contacts.

In 1916, in Chicago, we became very much excited over the horrible situation in New York, with so many persons dying of the disease, and we took very stringent precautions through cooperation of the public health service and the local authorities in New York... Every patient was taken out of the home and hospitalized, but the contacts under 16 were kept in the home for sixteen days. So there were approximately 1,500 direct contacts, and yet but one possible case occurred among them. Also, among the large number of people that came from New York and other infected areas, not a single case occurred. One is constantly struck with the fact that there are relatively few contact cases.

Dr. A. C. Nickel, Rochester, Minn.:

I should like to emphasize the fact brought out by Dr. Aycock concerning the occurrence of sporadic cases of poliomyelitis. Last summer, Dr. E. C. Rosenow and I saw about fifty-five cases of poliomyelitis within a radius of 75 miles of Rochester, and frequently we would see a case in a very secluded spot where contact infection was quite unlikely.

A 1938 article in The British Medical Journal examines an outbreak of acute anterior poliomyelitis in a boys' boarding school, where four cases out of the entire school were presented on July 15.[10] Initially admitted with varying symptoms, the boys were later confirmed to have polio, with three developing paralysis. All four were well scattered in different classes in the school. The boys had minimal shared activities, though they had separate dining and staff arrangements in the same house with 50 boys. The author investigated potential sources of infection and found no prior cases in the school, making a persistent carrier unlikely.

A particularly intriguing hypothesis explored in the article is the resemblance of poliomyelitis epidemiology to food poisoning. Barber notes several key points, including:

1. The seasonal and climatic patterns of polio align with the increased consumption and peak production of fresh garden produce. The chart illustrates the progression of the yearly epidemics in New York between 1916 and 1931, revealing that the vast majority of cases emerged in the summer, declined in the fall, and disappeared entirely by winter.

2. The disease’s epidemiological distribution does not follow that of respiratory infections but instead resembles food poisoning and typhoid.

3. Polio is not highly infectious. Historically, patients were nursed in general hospital wards without spreading the disease, and there were no well-authenticated cases of transmission to close contacts, even within crowded households.

Curves showing the course of the epidemics of 1916 and 1931 in New York The similarity of the two is remarkable: note that the highest count in each year occurred on the same day, August 1.— “Poliomyelitis,” The Journal of Pediatrics, July 1941.

In a 1941 article in The Journal of Pediatrics, the epidemiology of poliomyelitis is explored with a focus on its seasonal patterns.[11] The article highlights a strong seasonal correlation, with outbreaks typically occurring from mid-July to early November, aligning with the ripening of perishable fruits and vegetables. This summertime trend is observed in both the Northern and Southern Hemispheres. Many patients recall dietary indiscretions, such as consuming unripe or possibly contaminated produce, suggesting that foodborne transmission may play a role in the spread of the disease. The article proposes that contaminated fruits, vegetables, milk, and water—potentially spread by infected handlers, cattle, or flies—could explain the seasonal outbreaks. While fruits themselves do not cause the disease, they may serve as vehicles for infection, underscoring the significance of contaminated food and milk as key sources of transmission. Also noted was that in experiments with animals:

The natural disease never acts like an upper respiratory infection in the experimental animal for no animal gets the disease from another, no matter how intimately exposed.

In a 1951 article, Archibald L. Hoyne, MD too, noted that polio was a hot-weather summer disease.

There is nothing about poliomyelitis which seems more strange than its epidemiologic character. It has long been crowned as a hot weather disease. In 1916 New York City had its warmest summer in more than 40 years and recorded approximately 13,000 cases of poliomyelitis…[12]

At the Cook County Contagious Disease Hospital, where isolation procedures were not implemented, no doctor, nurse, or hospital staff member contracted polio over a 35-year span. Furthermore, no patient developed polio after being admitted, further challenging the idea of widespread person-to-person transmission.

…in the Cook County Contagious Disease Hospital where the latter procedure has not been used there has never been a doctor, intern, nurse or any other member of the personnel who contracted poliomyelitis within a period of at least thirty-five years, nor has any patient ever developed poliomyelitis after admission to the hospital.[13]

Early Pesticides: The Rise and Fall of Lead Arsenate

Inorganic compounds were among the early pesticides used to control pests. Paris Green, an arsenical compound, was first used against the potato beetle in the Rocky Mountain region in 1865. In 1886, lime sulfur washes and hydrogen cyanide fumigation were introduced in California to combat scale insects. Lead arsenate was introduced in 1892 as an insecticide to target the gypsy moth in Massachusetts, while sodium arsenite found use as both an insecticide and a weed killer.[14]

Spraying apple trees with lead arsenate at Blandy Experimental Farms (Boyce, VA). (1920s) — The History of Lead Arsenate Use in Apple Production: Comparison of its Impact in Virginia with Other States.

In the early 1900s, successful commercial apple production relied on specific farming techniques, including a carefully managed spray schedule for fungicides and insecticides. Lead arsenate quickly became a preferred insecticide due to its persistence and effectiveness in controlling major pests like the codling moth, which could damage 20% to 95% of apples without treatment. The larvae of the moth would tunnel into the fruit, reducing its market value and storage quality. Farmers initially mixed lead arsenate onsite but was also available in powder and paste forms.[15]

Lead arsenate displayed in two different types of formulations, powder (left) and paste (right). — The History of Lead Arsenate Use in Apple Production: Comparison of its Impact in Virginia with Other States.

By the early 1900s, it was widely used in apple orchards, with almost all commercial orchards treating their crops with arsenic. However, concerns arose in 1919 when researchers discovered that standard washing practices couldn’t remove arsenic residues from the fruit. A 1931 study from the Virginia Agricultural Experiment Station found that while three sprays of lead arsenate in early summer didn’t require residue removal, additional sprays later in the season, combined with dry weather, left excessive arsenic on the apples, with cleaning methods only removing about a third of the residues.

In 1947, the introduction of DDT and other synthetic insecticides marked a breakthrough in pest management, leading to a decline in the use of inorganic insecticides like lead arsenate. Additionally, the codling moth had developed resistance to arsenical compounds, further diminishing their effectiveness.

Health Hazards of Lead Arsenate

Lead arsenate is a white, heavy powder. Inhalation or ingestion causes dizziness, headache, paralysis, cramps, constipation, collapse, and coma. Subacute doses cause irritability, loss of weight, anemia, and constipation. Following repeated doses, convulsions and paralysis were observed in dogs.[16]

Acute inorganic arsenical poisoning affects multiple organ systems, with initial symptoms including throat constriction, difficulty swallowing, abdominal pain, vomiting, and profuse diarrhea. As the poisoning progresses, systemic symptoms such as muscular cramping, headache, and, in severe cases, convulsions, coma, and death may occur. Between 1951 and 1963 in California, 42 fatal arsenic poisoning cases involving children were reported, primarily caused by sodium arsenite-containing herbicides. The removal of this hazardous product from the market in 1961 led to a decrease in fatal childhood arsenical poisoning cases.[17]

Chronic arsenical poisoning may be divided into three phases.

In the first, phase, the victim complains of weakness and loss of appetite. There may also be nausea and vomiting.

The second phase of intoxication is characterized by symptoms of coryza, hoarseness and mild bronchitis. Perforation of the nasal septum is a common finding. Skin manifestations are common at this stage of poisoning.

The third phase of chronic arsenical intoxication is marked by peripheral neuritis, which is often mild, at first, but which may progress to motor in more severe cases paralysis.[18]

Polio Symptoms

Polio can present in three main forms:[19]

· Abortive Polio: This mild form includes symptoms such as fever, fatigue, headache, sore throat, nausea, and diarrhea.

· Non-paralytic Polio: In addition to the symptoms of abortive polio, this form also features neurological symptoms like sensitivity to light and neck stiffness.

· Paralytic Polio: After an initial period of viral-like symptoms, this form leads to loss of superficial reflexes, muscle pain, spasms, and eventually asymmetric paralysis. Paralysis occurs in fewer than 1%-2% of cases, and most individuals recover completely.

Animals and Paralysis

In 1911, veterinary Dr. C. S. Shore observed a disease in one- and two-year-old colts exhibiting symptoms closely resembling anterior poliomyelitis in children.

In my veterinary practice during the past five or six years, I have found a disease appearing among one- and two-year-old colts that shows a line of symptoms corresponding very closely to anterior poliomyelitis of children. I have had from five to ten cases a year during this time, the cases always occurring during the summer months, and the majority of them during the month of August.[20]

Dr. W. H. Frost’s 1911 report notes that during several polio epidemics, domestic animals such as chickens, dogs, horses, hogs, cattle, and sheep in the same communities exhibited paralytic diseases similar to those affecting humans, suggesting a potential link between animal and human paralytic conditions.

As regards the relation of paralytic diseases of animals to epidemic poliomyelitis, it has been noted in connection with a number of epidemics that domestic animals, especially chickens, dogs, horses, hogs, cattle and sheep, were found in the same community to be suffering from paralytic diseases clinically similar to the disease prevailing among human beings.[21]

In May 1912, Dr. Jacolyn Van Vliet Manning published an article in The Medical Times highlighting a significant correlation between paralytic cases in humans and animals during polio epidemics. The article provided a table of affected animals.

A close relationship between paralytic cases in man and animal during epidemics of poliomyelitis has been observed in nine States of the United States, and in Sweden, Westphalia, and England...

The State of California had an epidemic of 100 known cases of poliomyelitis in 1910. The majority of these cases occurred in San Joaquin County, and according to the September, 1910. Bulletin of the California State Board of Health, “veterinarians report a considerable number of puzzling paralyses of colts in San Joaquin County, where the largest number of cases have occurred so far.”[22]

Acute Paralytic Disease and Death Among Domestic Animals Occurring Coincidentally with Epidemic Poliomyelitis in Man. — “The Correlation of Epidemic Paralysis in Animal and Man,” The Medical Times, May 1912.

In his 1924 report on paralysis in Vermont, Charles S. Caverly, MD, in the 1894 epidemic, that in the same area, animals were affected with the same symptoms.

During this epidemic and in the same geographical area, an acute nervous disease, paralytic in its nature, affected domestic animals. Horses, dogs and fowls died with these symptoms... That domestic animals suffered with human beings in our epidemic is a noteworthy fact and one, so far as I can learn, hitherto unobserved. That such was the case cannot be doubted. It has long been known that animals were often attacked by meningitis during an outbreak of that disease in epidemic form.[23]

Conclusion

The seasonal nature of polio outbreaks, particularly in the early 1900s, raises questions about the virus’s sole role in the disease. Polio cases typically peaked during the summer, tapered off in the fall, and disappeared by winter, aligning with the seasonal use of lead arsenate in agriculture. Lead arsenate was widely used as a pesticide, especially in apple orchards, coinciding with the peak of polio outbreaks. Studies from the 1930s and 1940s indicated that patients often recalled consuming fruits and vegetables that may have been contaminated with lead arsenate during their illness. The difficulty in removing arsenic residues meant that contaminated produce could have served as a vector for poisoning, mimicking the viral presentation of polio. A greater incidence of polio in the drier part of the summer occurred when pesticide residues accumulated on crops, particularly apples.

Moreover, reports from the era highlighted domestic animals, such as chickens, dogs, horses, and cattle, often exhibited paralytic diseases resembling polio, suggesting a potential environmental link between animal and human paralytic conditions.

Additionally, studies from the era indicated that secondary transmission among household contacts was negligible or non-existent, and in animal experiments, no animal transmitted the disease to another, regardless of the level of exposure.

Lead arsenate poisoning presents symptoms such as nausea, vomiting, diarrhea, muscle cramps, headache, and paralysis—symptoms that bear a striking resemblance to those attributed to polio. These similarities make it critical to consider that environmental neurotoxins may have contributed to, or even been mistaken for, cases of paralysis historically labeled as polio.

In light of these factors, it is plausible that lead arsenate and other environmental influences played a significant role in paralysis cases attributed to polio. The seasonal patterns, lack of substantial person-to-person transmission, symptom overlap in both humans and animals and widespread use of lead arsenate suggest that a broader view of polio’s historical etiology is necessary—one that considers environmental toxins as a potential primary cause or a significant compounding factor.

As noted by Lumsden MD in 1938:

On epidemiological grounds alone, it appears conceivable that poliomyelitis is not caused by a living micro-organism or a virus but by a toxin somewhat comparable to that of a tick paralysis.[24]

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[1] Journal of the American Medical Association, January 21, 1956, https://jamanetwork.com/journals/jama/article-abstract/303826

[2] “Intensive Immunization Programs,” Hearings Before the House of Representatives Committee on Interstate and Foreign Commerce on The Vaccination Assistance Act of 1962, H.R. 10541, May 15, 1962, p. 100.

[3] “Intensive Immunization Programs,” Hearings Before the House of Representatives Committee on Interstate and Foreign Commerce on The Vaccination Assistance Act of 1962, H.R. 10541, May 15, 1962, p. 86.

[4] Frederick E. Batten, M.D., “The Epidemiology of Poliomyelitis,” May 1911, Sect Epidemiol State Med, p. 204, https://journals.sagepub.com/doi/10.1177/003591571100401308

[5] Frederick E. Batten, M.D., “The Epidemiology of Poliomyelitis,” May 1911, Sect Epidemiol State Med, pp. 208-209, https://journals.sagepub.com/doi/10.1177/003591571100401308

[6] John J. Moren, “Acute Spinal Paralysis; Diagnosis and Treatment,” Kentucky Medical Journal, vol. X, no. 1, March 1, 1912, pp. 195-198.

[7] Charles S. Caverly, MD, Infantile Paralysis in Vermont 1894-1922, 1924, Burlington, Vermont, State Department of Public Health, p. 22.

[8] Charles S. Caverly, MD, Infantile Paralysis in Vermont 1894-1922, 1924, Burlington, Vermont, State Department of Public Health.

[9] W. LLoyd Aycock, MD, “The Epidemiology of Poliomyelitis,” The Journal of the American Medical Association, July 10, 1926, https://jamanetwork.com/journals/jama/article-abstract/241678

[10] G. O. Barber, M.A., M.B., B.Ch., “Acute Anterior Poliomyelitis,” The British Medical Journal, December 3, 1938, pp. 1137-1139, https://www.jstor.org/stable/20301564

[11] John A. Toomey, MD, “Poliomyelitis,” The Journal of Pediatrics, Vol. 19, Issue 1, July 1941, pp. 103-130, https://www.sciencedirect.com/science/article/abs/pii/S002234764180033X

[12] Archibald L. Hoyne, MD, FACP, “Poliomyelitis Problems,” Medical Clinics of North America, vol. 1, issue 1, January 1951, pp. 175-188.

[13] Archibald L. Hoyne, MD, FACP, “Poliomyelitis Problems,” Medical Clinics of North America, vol. 1, issue 1, January 1951, pp. 175-188.

[14] Report of the Secretary's Commission on Pesticides and Their Relationship to Environmental Health, 1969, United States Department of Health, Education, and Welfare. Secretary's Commission on Pesticides and Their Relationship to Environmental Health, p. 45, https://www.google.com/books/edition/Report_of_the_Secretary_s_Commission_on/TWBApv27ZpcC

[15] Therese Schooley, Michael Weaver, Donald Mullins, and Matthew J Eick, The History of Lead Arsenate Use in Apple Production: Comparison of its Impact in Virginia with Other States, Journal of Pesticide Safety Education, 2009, pp. 22-53.

[16] Lead Arsenate, National Library of Medicine, https://pubchem.ncbi.nlm.nih.gov/compound/24572

[17] Report of the Secretary's Commission on Pesticides and Their Relationship to Environmental Health, 1969, United States Department of Health, Education, and Welfare. Secretary's Commission on Pesticides and Their Relationship to Environmental Health, p. 362, https://www.google.com/books/edition/Report_of_the_Secretary_s_Commission_on/TWBApv27ZpcC

[18] Report of the Secretary's Commission on Pesticides and Their Relationship to Environmental Health, 1969, United States Department of Health, Education, and Welfare. Secretary's Commission on Pesticides and Their Relationship to Environmental Health, pp. 362-363, https://www.google.com/books/edition/Report_of_the_Secretary_s_Commission_on/TWBApv27ZpcC

[19] Polio, History of Vaccines, https://historyofvaccines.org/history/polio/overview

[20] Frederick E. Batten, M.D., “The Epidemiology of Poliomyelitis,” May 1911, Sect Epidemiol State Med, pp. 206-207, https://journals.sagepub.com/doi/10.1177/003591571100401308

[21] Dr. W. H Frost, “Epidemic Anterior Poliomyelitis, Conference of Sanitary Officers,” New York Department of Health Annual Report, 1911, p. 944.

[22] Jacolyn Van Vliet Manning, MD, “The Correlation of Epidemic Paralysis in Animal and Man,” The Medical Times, May 1912, pp. 134-136.

[23] Charles S. Caverly, MD, Infantile Paralysis in Vermont 1894-1922, 1924, Burlington, Vermont, State Department of Public Health, pp. 33, 38.

[24] L. L. Lumsden, MD, “Poliomyelitis: Facts and Fallacies,” Southern Medical Journal, May 1, 1938, https://archive.org/details/sim_southern-medical-journal_1938-05_31_5