The Age of Polio: How an Old Virus and New Toxins Triggered a Man-made Epidemic -- Part 2, A Gypsy Moth Flaps Its Wings
By Dan Olmsted and Mark Blaxill
Etienne Leopold Trouvelot arrived in the United States from France in the late 1850s and settled into his brand new house at 27 Myrtle Street in Medford, a suburb of Boston. A self-taught scientist and later an astronomer affiliated with Harvard, his interest alighted first on insects, and he turned the land adjoining his home into a virtual boarding house for bugs.
“To contain his hordes of larvae he constructed a stupendous barricade to encircle his grounds – a wooden fence eight feet high that encompassed his full five acres of shrubs and small trees,” writes author Robert J. Spear. “Netting was stretched from the perimeter of the fences across the trees and was supported in the middle on posts, making it possible for Trouvelot to walk upright through his specialized insectary.”[i]
A decade later, he acquired a handful of gypsy moths, probably on a trip back to France – there were none in the United States. What happened next can be deduced from the title of Spear’s book, The Great Gypsy Moth War. Inevitably, insects escaped, not least because birds continually pecked their way into what they viewed as a very large diner.
The gypsy moths did not make their presence known outside the “stupendous barricade” for about a decade, but when they did, the results were apocalyptic. Lacking natural predators, they denuded trees – especially fruit trees – in what seemed like a single collective gulp. Then they crawled onward and upward. “Citizens could only stare in disbelief as the dirt streets became carpeted with millions of larvae across Myrtle Street,” writes Spear, “turning its surface black with the bodies of fast-moving caterpillars.”
Horrified residents combed gypsy moth larvae out of their hair, shoveled them off the steps, stomped them underfoot and burned huge clusters in noxious kerosene fires. But humans were simply outmatched. The Hellstrom Chronicles, the 1970s movie that suggested insects would inherit the earth, was coming alive in suburban Boston.
Even professional bug-killers were defenseless against the new arrival – Paris Green and London Purple, two state-of-the–art arsenic compounds that were potent against most pests, didn’t work at all. To some, it appeared that the food supply of the United States was at imminent risk. The state put together a Gypsy Moth Commission with an urgent mandate: Kill the bugs dead.
Fortunately – or so it seemed – a scientist working for the commission quickly found a solution. Adding lead to arsenic proved lethal to the larvae, and the new compound was sprayed on trees in and around Boston starting in 1893. It quickly proved its value against not just gypsy moths but all manner of agricultural pests. In fact, it worked better against codling moths, the source of the proverbial “worm in the apple.”
“In the case of insects which do not readily yield to Paris Green, a different substance, used with great success by the Gypsy Moth Commission, with which it originated, may be applied,” wrote George H. Perkins, state entomologist of Vermont in his annual report for 1893, published in early 1894. “This is arsenate of lead; sodic arsenate 29.93%, lead acetate 70.07%, are mixed in water, from which arsenate of lead is soon formed.”[ii]
Something else of note happened in 1893 in the Boston area. Two doctors used to seeing sporadic cases of paralysis in infants became concerned when the small caseload suddenly increased, to 23. There had only been six in the same September-November time span the year before.
“Is Acute Poliomyelitis Unusually Prevalent This Season?” asked Drs. James J. Putnam and Edward Wyllys Taylor in the Boston Medical and Surgical Journal for November 23, 1893.[iii] “It would not have seemed worthwhile to report these few observations had it not been that the number of cases observed at the Massachusetts General Hospital in September and October of this year is decidedly larger than usual,” they wrote. (The comment shows that isolated cases of paralysis were not unusual in Boston, where the Gypsy Moth War had been raging since 1890. It was the number and timing that drew their attention.)
While the doctors noted the time of year, they did not notice that September and October were apple-harvesting season. They did ask “other physicians who have seen these interesting cases, or may see them in future, to send brief records.”
The future came quickly. Within seven months, Vermont – where George H. Perkins had given the formula for lead arsenate in his annual report – was hit hard. “The first major polio outbreak to be recognized in the United States did not occur until 1894,” writes well-known vaccine developer Samuel Katz. “It came in Rutland, Vermont, for reasons I need an epidemiologist to explain to me. There had been scattered individual cases prior to that date, but this was the first recorded outbreak resulting in 18 deaths and 32 individuals with residual paralysis among a total of 132 cases.”[iv]
The outbreak was described in a classic report by Dr. C.S. Caverly, a Rutland physician and president of the Vermont Board of Health.[v] “During the month of June, 1894, there appeared in a portion of the valley of the Otter Creek, in the State of Vermont, an epidemic of nervous disease, in which the distinctive and most common symptom was paralysis.” Caverly didn’t know what to make of it, but he noted that the cases tended to cluster along Otter Creek and its tributaries.
In 1896, in a follow-up report in the Journal of the American Medical Association, Caverly noted something strange: “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.”
A horse “died paralyzed in the hind legs,” a fowl was paralyzed in its legs and wings. In the horse, the spinal cord showed “atrophy of the anterior nerve root”; in the fowl, “an acute poliomyelitis of the lumbar portion of the cord ...”[vi]
After the Boston and Rutland outbreaks, poliomyelitis clusters were reported in the United States almost every year. Earlier, we mentioned the 33 U.S. outbreaks recorded before 1910. Returning to that list, there appears to be an overlooked association with intensive commercial fruit and vegetable growing. After its introduction in 1893, lead arsenate was soon used on apples, apricots, asparagus, avocados, blackberries, blueberries (huckleberries), boysenberries, celery, cherries, citrus (in Florida), cranberries, currants, dewberries, eggplant, gooseberries, grapes, loganberries, mangoes, nectarines, peaches, pears, peppers, plums, quinces, raspberries, strawberries, tomatoes and youngberries.[vii]
With that in mind, consider these pre-1910 outbreaks:
--Boston, 1893. The year lead arsenate was first used there or anywhere.
--Rutland, Vermont, 1894. The year the state entomologist gave the formula for making it.
-- Cherryfield, Maine, 1896. Commercial blueberry-producing center.
-- San Francisco and the Napa Valley, 1896. Home to vineyards and many other crops.
-- Dutchess County and Poughkeepsie, N.Y., 1899. Agriculture and especially orchards – the county’s Web site features a stylized apple.
-- San Joaquin Valley, California, 1899. The nation’s Salad Bowl.
-- San Francisco and vicinity, 1901. A reprise of 1896.
-- Galesville, Wisconsin, 1907. Apples again. The Chamber of Commerce logo features an apple, and the annual Apple Affair is held the first Saturday in October. “Orchards from the area set up stands on the square where visitors can purchase apples and apple treats served up by local growers. Apple pie, apple slices, caramel apples, Apple Normandy, Queen's Apple, apple cider, apple juice -- if it's apple, you'll find it here.”
-- Oceana County, Michigan, 1907. Self-proclaimed Asparagus Capital of the World, the largest asparagus producer in Michigan and one of the largest in the nation. Home to the National Asparagus Festival held the second week of June. (One of us, born in Chicago in June 1952, spent summers in Pentwater, in Oceana County. His parents wanted to get their children away from the risk of polio in the big city.)
These links, we suggest, are far from random, pointing instead to locations where circulating poliovirus strains might combine with the growing use of the new lead arsenate insecticide to disastrous effect. Other locations point more generally to agriculture – Central Illinois in 1905, the states of Iowa and Wisconsin in 1908, rural locations in Pennsylvania in 1907 and 1908 – or to population centers where produce would be shipped – particularly New York City in 1907, a veritable fresh fruit and vegetable market to this day.
So the convergence of time and place in the early natural history of poliomyelitis outbreaks raises intriguing questions. But what can we say about the toxin itself and its relation to features of poliomyelitis? We can say:
Lead and arsenic can kill and paralyze humans.
Whether ingested or inhaled, several metals have long been recognized as hazards in the workplace and for miners; in Roman times, work in mercury mines was so lethal that only slaves and prisoners were sent into them. More recently, lead was removed from gasoline and paint because both inhalation and ingestion can stunt the mental development of children; arsenic has been banned from medicine and agricultural use in the United States; small amounts in apple juice, made from apples grown in China, triggered a national controversy this month.
“That arsenic can produce paralysis was already known in the 14th century,” begins the monograph On Arsenical Paralysis, written in 1893 by S.E. Henschen in Sweden. “Since then many similar cases have been observed; and at present there are more than 150 cases of arsenical paralysis mentioned in the literature.”[viii]
The cases, he said, were comparatively few, and most recovered. He described the case of Maja Lisa Blomster, age 49, who in 1883 took “a white tasteless powder” on the advice of a traveler who said it would help her epilepsy. “After that the patient experienced a prickly sensation or slight pains in the inside of the hands and soles of the feet, and when she walked she thought she felt something like needles between her feet and the floor.
“The following morning she noticed on waking that the feet refused to do service. She tried in vain to bend and stretch out the foot joints and on trying to stand and walk the feet turned on the sides.”
Lead is even more toxic to humans. “The ancients were unquestionably aware of the dangerous character of lead and knew that it was poisonous when taken internally,” wrote H.A. Waldron in “Lead Poisoning in the Ancient World.”[ix] The most toxic sources appeared to be lead drinking goblets. “And yet” – shades of mistakes and misjudgments to come – “the Romans and Greeks continued to expose themselves to the effects of a metal they knew to be harmful through their food and drink.”
In the seventh century, Paul of Aegina gave the first account of an epidemic of lead colic he described as “having taken its rise in the country of Italy, but raging also in many other regions of the Roman empire, like a pestilential contagion, which in many cases terminates in epilepsy, but in others in paralysis of the extremities. … of the paralytics the most recovered, as their complaint proved a critical metastasis of the cause of the disorder.”
In Lead and Lead Poisoning in Antiquity, Jerome R. Nriagu of Environment Canada writes “literary classics sparkle with passages on lead poisoning, reflecting, no doubt, the attempts by men of letters to deal with problems of their time."[x] In The Uncommercial Traveler, Charles Dickens describes a woman who worked in the lead mills because she had no alternative but desperate poverty. “What could she do? Better be ulcerated and paralyzed for eighteen pence a day, while it lasted, than see the children starve.”
In the Book of Minerals, Albertus Magnus wrote in 1262 that “care must also be taken lest it [lead] cause paralysis of the lower limbs, and unconsciousness. This, then, is the nature of lead in its constitution and effects.”
And these, then, were the compounds chemists were mixing beginning in 1893 in Boston. Is it any wonder that Dr. Putnam raised the question the same year whether infantile paralysis was “unusually common this season?”
In fact, just two years before, a speech Putnam gave to the Massachusetts Medical Society was described in a British Medical Journal article titled, “The Injuriousness of Arsenic as a Domestic Poison.”[xi] Putnam “points out that paralysis is only the final and gross symptom of a neuritis which may have been going on for a long time.” Arsenic was hard to avoid, he added, because it was still widely used in medicine (a book about the ubiquity of arsenic during the era is titled The Arsenic Century).
Lead arsenate can paralyze and kill animals that ingest it. In January 1920, Veterinary Times published an article by J.W. Kalkus, head of Veterinary Science at the State College of Washington Agricultural Experiment Station, titled “Orchard Horse Disease.” This revealing piece begins: “The writer recently had an opportunity of making an investigation of a disease which has been causing considerable loss among horses in certain sections of Washington.”[xii]
It went by several names, Kalkus reported, among them orchard horse disease; orchard poisoning; alfalfad horses; arsenate of lead poisoning; mold poisoning.
Regardless of the name, the circumstances were the same: “The condition occurs in enzootic form in the irrigated apple orchard districts. … The disease was little known prior to the last three years. … It is now claimed by many that it is practically impossible to keep a horse for any great length of time on an irrigated orchard tract, where orchard-grown hay is fed, without the animal attracting the disease. … Present knowledge indicates this disease is confined to the irrigated apple orchard districts where fruit is grown on a commercial basis, and where it is common practice to use arsenate of lead in spraying fruit trees.”
Alfalfa was grown as a cover crop between orchard trees. Lead arsenate spray was often applied so thickly that it dropped onto the alfalfa, giving it a gray color. While some veterinarians did not believe lead arsenate caused the problems – because it did not exactly mimic what was known of lead and arsenic poisoning – Kalkus seemed in little doubt. One reason is that such problems had already been reported.
Experiments with lead arsenate conducted on pigs, calves, and sheep produced symptoms similar to horse orchard disease, Kalkus wrote. Another researcher fed different amounts of lead arsenate to five cows, “all of which died following symptoms of violent purgation, in some cases followed by paralysis.”
The horses Kalkus describes all became ill with fever, apparent abdominal pain and a cough. Some started to recover, but were then affected by paralysis of the vocal cords. Kalter quotes a veterinarian who was convinced lead arsenate was the cause: “As lead and arsenic are contained in the spray material it is highly possible that an idiosyncrasy exists, some individuals being susceptible to lead and acquiring the chronic form and others showing an acute form due to arsenic.”
In early polio epidemics, both animals and people suffered from paralysis. In May 1912, The Medical Times published an article by Jacolyn Van Vliet Manning titled, “The Correlation of Epidemic Paralysis in Animal and Man.”[xiii]
“A close relationship between paralytic cases in man and animal during epidemics of poliomyelitis has been observed in nine Western states of the United States” as well as in England and Sweden, he wrote, affecting dogs, cats, sheep, hogs and fowl. One case: On May 27, 1911, a boy contracted poliomyelitis. “One week before the boy’s illness a horse belonging to this lad’s father had an attack of what is locally known as ‘poke-neck;’ it is said to have been paralyzed in the neck and forequarters; it fell down in the stable and was unable to rise.”
In Minnesota in 1909, during an epidemic of 1,000 cases in humans, a state epidemiologist reported that a disease “strongly analogous in clinical history and symptoms to the disease in the human” had simultaneously afflicted three colts. Wrote Dr. C.S. Shore: “In my veterinary practice of the past five or six years I have found a disease appearing among one or two year old colts that shows a line of symptoms corresponding closely to anterior poliomyelitis in children. I have had from five to six cases a year during this time, always occurring during the Summer months, and the majority of them during the month of August.”[xiv]
In fact, as Manning notes, C.S. Caverly made the same observation about the first U.S. epidemic in Vermont in 1894. Something was causing polio-like symptoms in both humans and animals at the same time, in the same place.
The poliovirus may have been a key co-factor in the human cases of poliomyelitis, but the local presence of lead arsenate is also demonstrated by the paralytic cases of animals. These could not have been caused by the virus, which only produces illness in primates. The simultaneous illness of humans and animals is thus a crucial but overlooked clue to causation.
There were concerns lead arsenate caused polio outbreaks. Astonishingly, lead arsenate was proposed as a cause of polio outbreaks early on. In Massachusetts, where the compound was first used, the State Forester reported in 1912, under a section headed Infantile Paralysis: “In view of the fact that a feeling has been entertained by some people in the State that infantile paralysis has been caused in some instances by arsenate of lead used in spraying for the gypsy and brown-tail moths, the State Forester has caused a rigid investigation to be made in order to determine if there is any foundation upon which to base such fears.”[xv]
On the other side of the globe, a New Zealand newspaper reported in 1914: “The oft-expressed opinion that the arsenate of lead spray on fruit is the cause of the prevalence of infantile paralysis will be discussed at the next meeting of the Upper Clutha Fruit-growers’ Association at Bannockburn. The association is taking steps to obtain the result of Government experiments regarding this matter.”[xvi] (We have not found a follow-up report.)
Toxins as a possible factor in outbreaks of paralysis were dismissed by biased investigators. Given these connections and concerns, what happened? Or rather, what didn’t happen? Why did such strong clues about the nature of a disease that followed the planting season like clockwork year after year fail to crystallize in the minds of researchers?
The simple answer is that right from the start, the wrong people were in charge of connecting the dots. Regarding the fears of Massachusetts residents, the State Forester – whose job is to look after trees, not people – wrote that “as a result of his research he is firmly convinced that the use of arsenate of lead has in no way been responsible for the existence of the disease [infantile paralysis], and apprehends no danger in the future from its use. Any anxiety concerning the danger from the use of arsenate of lead is entirely unwarranted.”[xvii]
As for animals, in 1897 A.H. Kirkland, a researcher for the Gypsy Moth Commission in Massachusetts, home to lead arsenate, conducted an experiment with a single horse fed the pesticide. The animal not only remained “well and hearty” but in “better condition” [italics in original] than before.[xviii] That contradicted not only the Washington state report that described horse orchard disease, but several other veterinary studies.
A 1917 article in the journal Economic Entomology – by and for specialists who make their living controlling pests that threaten profits – also examined the risk to livestock and, by extension, people. “So far as our experiments with guinea pigs may be relied on, the results indicated that five or even ten times the average maximum per apple found in our analyses could not be expected to constitute a dangerous single dose for a human being.”[xix]
In the 1962 classic Silent Spring, Rachel Carson addressed this kind of convenient blindness and bias when she wrote about the inability of parties with an economic interest to acknowledge the damage pesticides caused to wildlife.
"The credibility of the witness is of first importance,” she wrote. Compared to a wildlife biologist, “the entomologist, whose specialty is insects, is not so qualified by training, and is not psychologically disposed to look for undesirable side effects of his control program.
“Yet it is the control men in state and federal governments – and of course the chemical manufacturers – who steadfastly deny the facts reported by the biologists and declare they see little evidence of harm to wildlife. Like the priest and the Levite in the biblical story, they choose to pass by on the other side and to see nothing. Even if we charitably explain their denials as due to the shortsightedness of the specialist and the man with an interest this does not mean we must accept them as qualified witnesses."[xx]
And so poliomyelitis spread unchecked through the first two decades of the 20th century before snaring, in 1921, its most famous victim.
(Next: Making sense of Campobello.)
[i] Robert J. Spear, The Great Gypsy Moth War (Amherst, University of Massachusetts Press, 2005), p. 14.
[ii] G.H. Perkins, “Report of the Entomologist,” in Seventh Annual Report of the Vermont Agricultural Experiment Station, 1893. St. Alban’s, Vermont: St. Alban’s Messenger Co., 1894. 124-124.
[iii] James J. Putnam, M.D., and Edward Wyllys Taylor, M.D. “Is Acute Poliomyelitis Unusually Prevalent This Season?” Boston Medical and Surgical Journal, Vol. CXXIX, No. 21, November 23, 1893.
[iv] Samuel L. Katz, M.D. “The Albert B. Sabin Gold Medal Address,” May 6, 2003, Arlington, Va. http://sabin.org/files/attachment/Katz_medal_speech.pdf
[v] C.S. Caverly. “History of an Acute Nervous Disease of Unusual Type.” Medical Record, Volume 46, No. 22, Dec. 1, 1894.
[vi] C.S. Caverly. “Notes of an Epidemic of Severe Anterior Poliomyelitis.” The Journal of the American Medical Association, Vol. XXVI, No. 1, January 4, 1896.
[vii] “EPA proposing to revoke tolerances for calcium arsenate and lead arsenate.” Cornell University Cooperative Extension, Pesticide Management Education Program, 1986. http://pmep.cce.cornell.edu/profiles/insect-mite/fenitrothion-methylpara/lead-arsenate/prof-calcium-ars-revoke.html
[viii] S.E. Henschen. “On Arsenical Paralysis,” Presented to the Royal Society of Sciences of Upsala, Sweden, September 30, 1893.
[ix] H.A. Waldron, “Lead Poisoning in the Ancient World,” Med Hist. 1973 October; 17(4): 391–399.
[x] Jerome O. Nriagu, Lead and Lead Poisoning in Antiquity, New York: John Wiley & Sons, 1983.
[xi] James J. Putnam. “The Injuriousness of Arsenic as a Domestic Poison,” J Am Med Assoc. 1891;XVI(22):778-781.
[xii] J.W. Kalkus, “Orchard Horse Disease.” American Journal of Veterinary Medicine. Volume XV, No. 4, April 1920.
[xiii] “Jacolyn Van Vliet Manning, The Correlation of Epidemic Paralysis in Animal and Man,” The Medical Times, May 1912.
[xiv] Henry W. Frauenthal, A Manual of Infantile Paralysis, With Modern Methods of Treatment. Philadelphia: Davis, 1914.
[xv] Frank W. Rane, Annual Report, State Forester of Massachusetts, 1911. Boston: Wright & Potter Printing Company, State Printers, 1911.
[xvi] Feilding Star, Feilding, New Zealand, November 25, 1914, page 2.
[xvii] Op. cit
[xviii] James V. Paige, D.V.S , “Cattle poisoning from arsenate of lead,” Bulletin: Issues 120-131, Massachusetts Agricultural Experiment Station, 1909, p 184
[xix] “Results of Feeding Lead Arsenate and White Arsenic to Guinea Pigs,” New Hampshire Agricultural Experiment Station, Bulletin 183, in Economic Entomology, Pamphlets: Volume 116, June 1917.
[xx] Rachel Carson, Silent Spring. New York: Houghton Mifflin Company, 1962.