Note: Here is the "The Age of Polio: Explosion" series to date, revised and combined. Each new installment published on AOA will be added to it.
By Dan Olmsted
"Everything should be made as simple as possible, but not simpler." -- Albert Einstein
On May 1, 1916, thirteen-month-old Lettie Caruso* moved with her family to a tenement at 1295 Gates Avenue, Brooklyn. A fifty-six-year-old woman named Mrs. G.H. Franklin lived and worked on the first floor, where she ran a small ice cream parlor that “the children naturally frequented,” according to a subsequent report by the New York Health Department. Lettie and her family lived in the apartment adjacent to the ice cream shop. On May 9, Lettie became ill. “A private physician was called the first day and came several days,” the Department reported. “She was examined with the stethoscope and at the first visit the doctor thought it was only a cold. As she grew worse a physician from New York was called in consultation. Mrs. Caruso thought the diagnosis was pulmonary bronchitis. So far as she knew the child was not paralyzed, but she cannot remember any special examination for that. There has been no Infantile Paralysis in this house, nor in the adjoining properties.”
That was about to change.
Looking back with perfect hindsight, Brooklyn in May 1916 was ground zero for an explosion that no one saw or heard for a month and more -- and, to this day, no one has satisfactorily explained. Before it ended late that summer, 25,000 people in the Northeast developed paralytic poliomyelitis, most of them young children, and an extraordinary 5,000 died -- nearly half of them in the City of New York, a toll approaching the September 11 tragedy. It was by far the largest and most lethal polio epidemic to date, and it remains one of the biggest ever (see chart).
As spring turned to summer, polio gripped every family with fear, not just in the Northeast but nationwide. It was a fear that never entirely lifted until the outbreaks ended in the United States and most other countries after the Salk vaccine was introduced a half-century later, an occasion so momentous that church bells rang out across the country. But 100 years ago, and especially Brooklyn, there was barely suppressed panic that the authorities and the media did their best to tamp down.
"While there is no need of undue alarm," the Brooklyn Daily Eagle reported in a careful front-page (but one column) article on June 17 announcing the epidemic, "the officials of the board of health are somewhat worried and are taking measures to stamp out the disease."
Since 1894, clusters had occurred with increasing frequency and virulence in the U.S.. The first, in Vermont, affected 132 and killed 18. The worst, in 1907, killed 125 in New York City. It almost seemed like a rehearsal, or a warning. But 1916 marked the moment the Age of Polio arrived in America.
No one could explain why the epidemics began appearing around the turn of the century. As Albert Sabin, inventor of the live virus polio vaccines, mused in 1947: “No circumstance in the history of polio is so baffling as its change during the past fifty or sixty years from a sporadic to an epidemic disease.” It certainly wasn’t a matter of better diagnosis or greater awareness – this of all diseases, with its sudden onset and often permanent disability or death, was as impossible to miss as a child in an iron lung.
“There was no idea in the eighteenth and early nineteenth centuries that poliomyelitis was contagious,” wrote John R. Paul, a professor of preventive medicine and epidemiology at Yale who conducted important polio research himself. “Had there been larger outbreaks in the early or mid-19th century it seems highly unlikely that they would have gone unnoticed.”
In 1917, the year after the Great Northeast Epidemic, John Ruhrah and Erwin E. Mayer wrote, “It seems to be a disease of comparatively recent origin. In the history of most diseases there is a gradual shading off into the older writers until the disease is lost in confusion of inaccurate descriptions. Not so with polio.” They continued: “The disease is so striking in its symptomatology, so devastating in its results, and produces such a deep impression on the popular mind that it does not seem possible that any very considerable epidemics could have happened in the countries in which there were physicians making records of what occurred.”
Perhaps because the outbreak rose and fell so suddenly, bracketed by much that came to define the turbulent 20th century -- war in Europe in 1914, the sinking of the Lusitania, which departed from New York Harbor, the next year; shark attacks along the crowded Jersey shore that sweltering summer of 1916 that caused sensational press coverage and became fodder for Jaws 60 years later; U.S. entry into WW I in 1917; and the Influenza Pandemic that killed 2,157 New York City residents in the week of November 1, 1918, alone -- the epidemic has faded from collective memory.
But the question remains, and it remains important in an age of new diseases like EV-68 and Zika, and disorders like autism, that seem to come out of nowhere and spread like wildfire: What caused the Explosion of 1916? If I'm right, an environmental bomb dropped on Brooklyn set it off, spreading with a smooth but terrible precision like a pebble dropped in a still volcanic lake. That kind of bomb could go off again at any time, anywhere. We need to understand it.
I've foreshadowed some of this saga in ways not yet apparent. It takes twists and turns I never imagined when I began. I only ask that you withhold judgment till the keystone has locked the blocks into place.
(*Sources and notes: Information about the sugar industry in 1916 comes from multiple sources including articles on newspapers.com and in specialized sugar journals. Case histories of Lettie Caruso, Mrs. Franklin and others are from the New York City Health Department archives of the 1916 epidemic at the American Philosophical Association library in Philadelphia. All names have been changed, which the library required as a condition for access. The chart showing the spike in the polio rate is by my colleague Mark Blaxill. Our series in 2011 proposing a new explanation for the roots and rise of polio epidemics paved the way for this series.)
On May 23, Lettie Caruso died. She was an only child.
The cause of death was listed as “fatal pneumonia.” Soon there was more sickness and death in the building. At some point in May, “there was a woman living on the top floor of the house over her [Mrs. Franklin's ice cream] store whose baby was taken ill and died suddenly. … The doctor was an Italian and never told the mother the cause of the baby’s death.” Based on another report in the file, this second infant was probably a male named Peter: “After an illness of 4 days, Peter Pinchero of 1295 Gates Ave. died on May 24th. Eight days before he was taken ill, his cousin, living at the same address, had also died following a similar illness of about two weeks.” (This is probably an imprecise reference to Lettie.)
Contact tracing, as it's called, was not an easy task, as the jumble of interviews and observations in Lettie's file attest a century later. Between the language barrier in this Italian neighborhood, the poverty, and especially the fear that health officials might take children away, the truth comes out in dribs and drabs and even then remains incomplete. Children get sick and die, their heartbroken and terrified families move away, someone remembers and someone else misremembers what happened and when. Nor did the health workers exhibit much empathy, calling their clients "suspicious and ignorant." “These people neither understand not speak Eng. So I could get very little accurate information,” a nurse wrote August 24 as she tried to complete a questionnaire on “possible source of infection” at the tenement in May. (Apparently there were no Italian speakers in the employ of the City of New York to call on in the midst of the worst polio epidemic ever.)
Another typed note from a nurse suggests two more Pinchero cousins and an aunt who lived in the tenement became ill during May, but recovered. Summing up: Three or four related Italian families lived at 1295 Gates Avenue in Brooklyn in May 1916. Two children died, two of their cousins and an aunt got sick but recovered. Exactly what they suffered from was unclear. If Lettie Caruso and her cousin did have polio, they were among the handful of very early cases with onset that fateful May.
A near-simultaneous polio outbreak in an Italian neighborhood around the Gowanus Canal, about four miles west of Gates Avenue, became known as the epicenter of the epidemic. The neighborhood has been studied ever since: Was the virus in the canal? Did it get into the drinking water? Did the Italians bring a new strain with them from Italy? One recent medical paper proposed the virus got loose from the Rockefeller Institute, which was studying it in Manhattan, and traveled a few subway stops to Brooklyn. In any event, half of the 24 cases of polio in Brooklyn that month clustered around the canal.
Today the area is hip, hot and happening, anchored by a Whole Foods nestled in the fork of the canal. A Superfund project aims to clean the whole area up, and former warehouses have been recast as pricey lofts. Hillary Clinton’s campaign headquarters is less than two miles away. Back in 1916, there was nothing organic about this neighborhood. It was hard by an area called Pig Town, named for the animals that were raised there by the immigrants, with a soupçon of general squalor implied. It was known for the filthy conditions brought on by poverty, poor municipal services and its general location near heavy industry that casually flung its garbage over its shoulder. Sewers overflowed, vacant neighborhood lots where kids played were overrun by garbage. The whole thing was barely above sea level -- most of the time.
According to a description from the Brooklyn Daily Eagle of May 9, 1885:
“The overflow from the pig wallows at the bottom of the other lots comes down through drains beneath the filled in streets. At high tide the water backs up through these drains as far as Huntington street. The furthest inland of the chain of ponds thus formed is only a block away from Public School No. 27, on Nelson street, near the corner of Columbia, at which 1,500 children attend. Within 100 yards of the public school is a vast public dumping ground, running westward for a long block, from Delevan street, between Dwight and Richards. A great deal of putrid and offensive matter lies on this dumping ground, mingled with the ashes which the contractors' men bring there. Among the worst of this decaying animal and vegetable matter may be classed refuse from the sugar refineries in the neighborhood.” (The “pig wallows” described above are to the left of the canal, and sustained many cases of polio.)
That polio would break out in such an area might seem inevitable, because polio is a microbe that thrives in filth and is transmitted by feces. But it’s counter to the now-orthodox belief that polio epidemics arose because sanitation had finally improved. This is the crux of the “hygiene hypothesis.” Under this widely accepted theory, children in less sanitary times used to be exposed to illnesses earlier, when they were still protected by temporary immunity passed on from their mother. The later you got a disease, the more that immunity had waned, and the worse it was, under this theory. In other words,” an authoritative account puts it, “epidemic poliomyelitis can be considered an unfortunate consequence of the invention of the flush toilet.” If the hygiene hypothesis is true (I don't buy it), this was the last place on earth from which you’d expect the worst polio epidemic in history to emerge.
Lettie Caruso was just 13 months old and lived in a tenement, for God's sake.
Mrs. Franklin soldiered on in her storefront ice cream shop on Gates Avenue, though it’s easy to imagine that after two deaths and several illnesses among her clients an oppressive cloud hung over a place "all the children" frequented. “During this time she had kept the store open and had herself waited on the customers who came into the store,” the health department reported later. By the beginning of June she was beginning to feel ill, with pains in her neck, arms and legs. But like some sort of Calvinist Typhoid Mary, she just kept at it. On June 19, Mrs. Franklin was working at the store as usual when she suddenly fell unconscious to the floor. When she came to, she was paralyzed. She was taken to the hospital and began a long journey we will return to later.
What was going on here? Two children in the building had already died -- of what is uncertain -- and two more along with an aunt were sick but recovered. Now a 56-year-old woman -- way past the usual age -- had succumbed to something that looked a lot like polio. When all the statistics were recorded for the New York City epidemic, Mrs. Franklin's remained the oldest case on record.
The cases in Brooklyn that May did not immediately catch the attention of the health department. It’s not that polio was unknown or unexpected: Since the turn of the century, epidemics hit the city with deadly regularity, though usually later in the summer. The Brooklyn Daily Eagle story that reported “no need of undue alarm” on June 17 also said "the officials of the board of health are somewhat worried and are taking measures to stamp out the disease," mostly centered on travel restrictions, quarantine, removal of sick children to hospitals, and sanitation efforts. In retrospect, Health Commissioner Dr. Haven Emerson wrote the next year: “To judge by the reports of physicians up to June 1, there was nothing to excite suspicion that we were already at the outset of an epidemic. Within the first eight days of June, 6 cases were reported from Brooklyn, from which borough no cases had been reported up to this time in 1916 and none in June from the other boroughs. The six cases were reported as follows”:
But even in these critical early days of June, it took another 10 days to raise the battle flag. Emerson claimed he had moved as fast as possible – given obstacles decidedly not of his creation. “Only a thoroughly alert public and a forewarned profession could have prevented the delay in official knowledge of the threatening epidemic,” he wrote in the department’s exhaustive and self-serving 391-page history, "A Monograph on the Epidemic of Poliomyelitis (Infantile Paralysis) in New York City in 1916: Based on the Official Reports of the Bureaus of the Department of Health,” published the next year.
“That energetic measures were taken as soon as six verified cases of the disease were reported on June 6th and 8th, is a sufficient reply to any lingering suspicions that the Department of Health awaited the actual presence of a calamity before taking measures of protection.” That sounds like a guilty conscience that needed no accuser, but might have encountered a few. Just whose responsibility was it to alert the public and forewarn the doctors about an annual epidemic that visited New York with increasing virulence?
Now help, too late and perhaps too much, was on the way.
“On July 6,” Emerson writes, “the Secretary of the Treasury in person offered to the Mayor the assistance and cooperation of the United States Public Health Service. … The offer was gratefully accepted.” (I’ll bet it was.) That, said John R. Paul, whose 1971 “A History of Poliomyelitis” is considered the authoritative text, “posed a certain amount of competition for Dr. Emerson’s own working force.” (I’ll bet it did.)
Nonetheless, Paul wrote, Emerson displayed “earnest zeal” and “gave to this cause the very best that was in him – according to his lights.” But he and the Public Health Service zeroed in on quarantines and travel restrictions and studies of horse stables and side issues like documenting secondary exposures, which Paul called “a thankless task indeed.” (Those are the files at the American Philosophical Society in Philadelphia on which my account is based.) A better focus would have been to collect information that “had to do with poliovirus – its distribution within the body and its distribution within nature,” Paul wrote. The fact that polio infection was caused by a "filterable virus" had only been established in 1908, after the last big epidemic, so a focus on it now would have been a significant contribution.
As for Emerson the man (below), “In appearance Haven Emerson’s tall, almost ascetic figure has epitomized the title which had been bestowed on him, 'the last of the great Puritans.'" He was related to Ralph Waldo Emerson. But earnest zeal and rectitude did not always win the day. “After the lapse of fifty or more years it is easy to say what should have been done,” Paul wrote. “In retrospect, the tragedy was that, in view of the galaxy of talent which had been assembled on advisory committees and working forces alike and the administrational and laboratory facilities that were at their disposal, a golden opportunity to advance knowledge of the clinical virology of poliomyelitis had been allowed to slip by.” As regards Emerson’s own claim that the department’s response proved “the efficacy of co-operation,” Paul writes ruefully, “It cannot be said that these words have stood the test of time, though they may have been appropriate in 1916-17.”
Earlier notice from the health department might have stopped Mrs. Franklin working at her ice cream store on Gates Avenue sooner. Nor did officials notice or follow up on any number of anomalies -- deviations from the norm that often contain the best clues to causation, especially when they occur early on.
Mrs. Franklin herself was among them. How, working with children every day, had she remained immune from the poliovirus for 56 years? To the world of polio orthodoxy, this will seem like a joke, but it's hard not to notice that her business was selling ice cream, and that ice cream and polio epidemics have an infamous connection. If you want to look like a fool, mention them in the same sentence, as I just did. The two are icons of false correlation – you might as well write "Stupid" on your forehead, backwards. Yes, it’s possible to show an amazing association between the two – ice cream sales rose in the summer, and so did poliomyelitis cases, but only because the virus made its appearance in peak season for ice cream. Just for fun, here’s one of those charts.
Similar "pairings" connect ice cream sales with shark attacks, shark attacks with polio outbreaks -- you get the idea. Pick two seasonal events and plot whatever nonsense you want. (I myself have been ice-creamed: An article I wrote on another topic was once accused of this exact fallacy.) But to persist in folly just a bit longer, where did the ridiculous idea of polio and ice cream come from? The ice cream hypothesis, as it has reached us today, appears to date from a 1948 effort to get the nation to cut out sweets, based on a doctor’s hypothesis that ice cream sales and polio cases were correlated because blood-sugar levels were supposedly related to polio risk. The doctor’s suggestions included: “1. Eliminate from the diet sugar and foods containing sugar, such as soft drinks, fruit juices (except tomato juice), ice cream, cakes, pastries, pies, candies, canned and preserved fruits. Saccharin may be substituted for sugar. Cut down the consumption of starchy foods, such as bread, rolls, pancakes, potatoes, rice, corn, cereals, grits.”
The diet drive was centered in North Carolina but became national news, and the polio rate did seem to dip a bit that year both there and nationwide, if you counted in a very particular way (see chart). You can read about it here. The chart essentially shows that while polio deaths were projected to reach 2,200 in 1948, they only hit 1,800, about the same as 1946, and slowed just as the diet plan was introduced. This kind of speculative correlation was not likely to excite the mainstream medical world.
The experts laughed, and they've kept laughing. Less well-known is that by 1916 there was already concern about exactly those foods -- sugar and foods containing sugar, such as soft drinks, fruit juices, ice cream, cakes, pastries, pies, candies, canned and preserved fruits. A lot of people in New York City that awful summer thought ice cream, cake, soda, candy and other sweets were involved. "In previous epidemics, the theory has been repeatedly advanced that food or drink may act as vehicles of infection in poliomyelitis," Dr. Emerson wrote. "The regular water supply and various foods and drink, particularly ice cream cones and soda water, have been under suspicion and investigation."
Just a few pages later he derided such speculation with a Puritan’s version of LMFAO!
Dr. Emerson: “It may not add to the sum of scientific data to quote the suggestions received by the Department of Health as to the cause and means of curing or preventing poliomyelitis; but as a record of human interest the letters sent from all over this country and from many foreign lands present a picture which it is well for health officers to bear in mind. One hardly knows whether to laugh at the fantasies or weep over the ignorance and superstition exhibited.
“Two hundred and thirty suggestions as the cause of the disease were received, the largest number of authors (80) attributing the existing calamity to foods. Ice cream, soft drinks, candy and summer fruits were generally accused, cereals and canned foods coming second in favor.”
Well, hold that thought, because a few pages later Emerson says this about the 1916 epidemic: “There seems to be a well-marked tendency for cases in Manhattan to appear in the immediate vicinity of stables, groceries, meat or poultry markets, lunch rooms, delicatessen shops and bakeries or macaroni factories. … It is surprising with what regularity one or the other is found in the building next door to a house in which poliomyelitis has occurred. Others who have also examined the same districts with an unbiased mind, seem always to believe that cases range themselves with a definite relation to shops of this type. It has been repeatedly pointed out in earlier epidemics that stables are often associated with cases of poliomyelitis. This has been undoubtedly true in New York during the present summer, but the other association with provision shops has also forced itself upon our attention.”
In 1916 “unbiased observers," and not just loony-toon letter writers, noticed "with regularity" and in fact "always" (just quoting the man here) a "definite relation" between cases of polio and places that served and sold food, especially certain kinds of food (along with that hoary old suspect, stables). Even more amazing: On the facing page, the book includes a chart of associations between food and infection in “one of the somewhat better districts where there has been a group of scattered cases in the Bronx,” as well as a group from Manhattan.
Here's what I take away:
Doesn't that match the list Dr. Emerson had just dismissed: “Ice cream, soft drinks, candy and summer fruits"? Aren't they all foods you'd get at a deli, a grocery, a lunchroom? And isn’t that just about the same list as the 1948 diet plan suggested cutting out -- "sugar and foods containing sugar, such as soft drinks, fruit juices (except tomato juice), ice cream, cakes, pastries, pies, candies, canned and preserved fruits"? I vote yes. Yet Emerson's commentary puts stables first, the generic "grocery" second and meat markets third, and doesn't mention ice cream or candy at all, despite their equal or greater preponderance on the full-page list. Digging through a couple dozen folders in the health department archive of case reports, I found more references. From my notes:
another case of child died, on july 26, father works in bakery rear apartment, a kitchen and bedroom which adjoin an ice cream shop in a filthy condition – also shop condition poor – selling ice cream and lemonade.
died age 4.5
used dipped milk from grocery. Unwrapped bread, apples that were peeled before given to child. Child would go to corner of street for horton’s ice cream in cones.
20 months old was taken sick august 1. … the grandfather bought ice cream for her on west end ave. near 66th st about two days before she was sick. They afterwards found there was a child in the family ill with poliomyelitis.
These, let’s remind ourselves before others do, are random anecdotes, the kind that led to snickering about ice cream and polio correlations in the first place. So let's be cautious. Nonetheless, these references in the first few files I examined, our of several thousand, make me think there must be many more such reports.
Let's look at another possible "tell" for certain foods: The high prevalence of poliomyelitis in both Coney Island and Rockaway Beach, two resort havens full of cheap amusements, fun food that appeals to kids, and whatever the 1916 version of Whack-a-Mole was. “In proportion to its resident population, Coney Island, which forms the southern end of Brooklyn, has suffered quite heavily,” according to the health department report. “Here there have been two more or less clearly defined foci with a few more scattered cases. The greater part of these has been in old houses under bad sanitary conditions, and neither rodents, flies or insects would be excluded.” You can almost sense the foreclosing of fresh thinking here as the focus returns to the old favorites -- rodents, flies or insects. There's no evidence; they just should not "be excluded."
“One other locality in the Borough of Queens which suffered rather heavily was the extensive summer colony which extends along Rockaway Beach. Many cases appeared here in three or four poorly defined groups. Here the conditions are similar to Coney Island except that the houses are of better construction and in somewhat better conditions. They are, however, old and not of the small type with open-air space below mentioned in connection with Staten Island.” So rodents, flies and insects don't seem to be as likely here, just as they didn't in the "better districts" of the Bronx where food emporiums were implicated by "unbiased observers." What does seem just as likely: fun food like ice cream, sodas and candy. Correlation completely missed.
Several folders I examined mentioned families going to Coney Island over the Fourth of July 1916 holiday (the peak day for the epidemic was July 30); one said their child got sick “possibly the day they visited Coney Island.” Brooklyn's extensive streetcar system made it easy to get to the beaches; trains brought kids from as far as Pennsylvania for a Disney-style day trip. Suddenly that summer, they stopped.
Still, one can’t help thinking of ice cream, soft drinks, candy, fruit, and baked goods like hamburger and hot dogs buns -- because the are all represented on the Nathan's sign (and notice the child at left-middle). Here is an obituary from the Brooklyn Daily Eagle; I’ve read this many times. The treasured kindergarten Eagle Honor Roll medal he was the only one “ever to receive” – an award likely to have been forgotten in the onrush of a full life -- seems an especially poignant memento of a foreshortened one:
Of course, these could just be places where children with active polio infections congregated and ate and shared food and drink and infected each other with the virus. End of story. (Measles at Disneyland, the prelude.) But then, why isn’t there more evidence of school-based infections in May and June? The presence of polio by early May 1916, sans vaccination, should have spelled more trouble and left more markers of person-to-person contagion on the city’s schools, churches, playgrounds.
Emerson wrote: “On June 24th, in order to give immediate reply to many anxious inquiries and suggestions as to the part played by schools in the spread of the disease, a press bulletin was issued, pointing out the facts that 90 per cent of the cases were in children under school age, that the cases were not limited to any one school district or to children of the same classroom.
“The school term ended on June 30th. At the same time there was issued a special bulletin for parents, emphasizing the known facts which would be of service in preventing the spread of the disease in homes. The presence of the virus in the discharges from nose and throat, and bowels of infected individuals, the probability that atypical and non-paralytic cases were as dangerous and as numerous as the paralytic cases, and that little value or protection could be expected from the use of so-called antiseptic gargles and nose-sprays, were explained.” So Frederick Chapin still had 10 more days of school when he went to Coney Island on June 20, but it was that visit that stood out to his family.
Some children may already have been immune, and many developed inapparent or mild cases, but that doesn't quite explain the strange pattern of poliomyelitis. Was there some X factor, or co-factor, hidden in these patterns, in the black dots strewn along beach towns, in Mrs. Franklin’s ice cream shop, in the letters flooding the health department, in the realization that “provision shops” looked like loci of contagion to unbiased observers? Humor me, and let's reread this passage by Dr. Emerson. Its circumlocutious significance got past me many times.
“There seems to be a well-marked tendency for cases in Manhattan to appear in the immediate vicinity of stables, groceries, meat or poultry markets, lunch rooms, delicatessen shops and bakeries or macaroni factories. … It is surprising with what regularity one or the other is found in the building next door to a house in which poliomyelitis has occurred. Others who have also examined the same districts with an unbiased mind, seem always to believe that cases range themselves with a definite relation to shops of this type. It has been repeatedly pointed out in earlier epidemics that stables are often associated with cases of poliomyelitis. This has been undoubtedly true in New York during the present summer, but the other association with provision shops has also forced itself upon our attention.” (italics added.)
Of the millions of words put together about polio, these may be among the most important and at the same time the easiest to read right over: They point to a signal picked up by the health department for the first time in 1916 ("during the present summer") -- a correlation with "ice cream and soda water" not just by John Q. Public but by "unbiased observers." Let's repeat for emphasis. This observation was "surprising." It was "definite." It occurred "with regularity ... repeatedly ... always." It "forced itself" upon the attention of investigators who were looking the other way, back toward their comfortable hypotheses of stables and rats and filth and flies.
In its specificity, in its clarity, in its credibility, it was new. Rhymes with clue. It's as if Emerson had gotten so used to considering a connection to food such nonsense that when it came up in a much more convincing context, he was effectively blinded to its consequence. We've seen the same connection ourselves: the cluster at 1295 Gates Avenue. Lettie Caruso. Peter Pinchero. Mrs. Franklin dishing out ice cream until she collapsed on the floor, paralyzed. All of it, apparently, nothing but a bad joke.
Public health officials had enough to do in the summer of 1916 without having to listen to nonsense put forth provincials in Baltimore, for God's sake. “Germ of Paralysis Carried by Food – Theory of Baltimore Health Official – Seat of Disease is Large Intestine,” The New York Times reported October 15, after the epidemic had subsided but while sensitivities to the failure to contain or comprehend it were evidently still raw. The New York experts must have been so not thrilled to see this theory resurface.
The short article cited a Dr. H.T. Burrows of Johns Hopkins and Dr. J.F. Hempel of the Baltimore Health Department. “Dr. Hempel has a theory that candy, ice cream, fruit, and other uncooked foods that children eat, are primarily responsible for bringing the germ into the system. That theory will be fully tested when the physicians have completed their transmissions experiments.” Nope. That was not gonna happen. The very next day, Dr. William H. Welch, head of the Hopkins medical faculty, caved to what must have been intense pressure from the health establishment: “Denies Hopkins Rumors: Stories of Startling Discoveries in Paralysis Untrue, Dr. Welch Says." The Times quoted Welch saying “the work which the Hopkins pathologists were doing in association with the physicians of the city health department on infantile paralysis had not developed anything that would change any views of the disease previously held.” Furthermore:
Writes Samira Kawash, who calls himself the Candy Professor: “The official reply to Burrow’s and Hempel’s claims was swift and brutal. The very next day Johns Hopkins Professor of Pathology Dr. William Henry Welch, perhaps the most powerful medical authority of the day, contacted The Times to defend the reigning medical orthodoxy. Welch’s refutation of Burrows and Hempel singled out the particular claim connecting infantile paralysis and candy: 'The statement that the disease may be transmitted through candy is entirely gratuitous.' Welch could have more diplomatically called Hempel’s theory 'unfounded,' or 'incorrect' or even 'wrong.' Instead, Welch seemed to make a point of expressing scorn for the poor medical man who dared challenge the orthodox establishment. It was, according to Dr. Welch, preposterous even to wonder whether candy had some relation to polio.”
How many times now have we read about candy, ice cream, baked goods, fruit and so on being suspected in poliovirus contagion? I count five -- the letters to the New York Health Department that mentioned ice cream, candy, summer fruits and soda water, followed by cereals and canned foods; the observation recorded by the health department itself that stores selling "provisions" like ice cream, candy, and baked goods seemed to be new epicenters around which contagion clustered (along with stables, meat shops and so on); Sandler's no-polio diet in 1948 that forbad "sugar and foods containing sugar, such as soft drinks, fruit juices (except tomato juice), ice cream, cakes, pastries, pies, candies, canned and preserved fruits"; the concerns of parents and others recorded in the contact-tracing files preserved in Philadelphia, and now some crackpots at Johns Hopkins and the Baltimore Health Department who were about to put their ideas about "candy, ice cream, fruit and other uncooked foods" to the test when they got swatted down. Each of them seems to have had a slightly different rationale for citing food as a factor in polio -- blood sugar fluctuations, observations about how cases clustered, concerns about raw and uncooked food, reports about individual children's experience. So they varied, yet they converged on the same vectors.
That makes them more credible and compelling, not less.
At 6:45 p.m. on Saturday, July 1, 1916, a 25-year-old Philadelphia man named Charles Epting Vansant lay on the manager’s desk at the Engleside Hotel in Beach Haven and bled to death. A few minutes earlier, taking a dip before dinner, he was happily playing in shallow water with a Chesapeake Bay Retriever. When the shark struck, bystanders at first thought he was still splashing with the dog. That briefly delayed coming to his aid, but it probably didn’t matter. The shark tore the flesh off his thigh in one bite.
Already, fishermen had reported an especially active “shark summer,” with hundreds swimming in the mid-Atlantic. But the idea that one would attack humans on a populated beach so near to shore.? Not bloody likely. Even after it happened, the powers that be, concerned about summer tourism, played down the threat. The sharks weren't listening: Several more attacks occurred, immortalized in Steven Spielberg’s Jaws.
Sharks were not the only plague at the water's edge that summer before America entered world war. It's where the polio epidemic surfaced -- in the hardscrabble world of Pigtown, not far from the East River, where first one child and then another was pulled under by the circling virus. The monster-from-the-deep analogy is not stretching things. After 1916, children were told "to regard [polio] as a fierce monster that lurked in the damp hollows of their experience," wrote Jane B. Smith. In a 1934 article titled Death Walks In Summer, B. Davies called the disease "a grim terror... more menacing, more sinister than death itself."
When health department workers went door to door later that summer, they counted up 29 polio cases from the month of May -- mainly clustered around the Gowanus Canal, as we've noted. Plotting them on the map, they identified “a thickly populated Italian section, bounded by Fourth Avenue, Nevins, Carroll and Union streets.”
Because these were close to the waterfront, and because the department suspected the rats than ran freely on the docks, they took a look at the cases closest to the water. Of the 1,403 cases in Brooklyn by July 15, they identified 119. That led to a remarkable observation: “91 occurred on six streets, namely 3rd and 4th and 5th avenues, 17th and 20th and 21st streets.” The total ranged from 9 to 34 cases on each street, with the most on Third Avenue. I took that list, added back in all the streets with at least four cases to catch patterns but not isolated cases, and, armed with the amateur historical epidemiologist’s best friend, a red felt-tip pen, made a dot for each.
Well now. These dots connected, at least in my mind, in a new and interesting way. They were proximate not just to the water, but to two well-defined marine terminals -- the Bush Terminal in the lower part of the map and the Red Hook Marine Terminal towards the top (where On the Waterfront with Marlon Brando was set though for logistical reasons it was filmed in Hoboken). Those that were not on the waterfront were all on main arteries, like Third and Fourth avenues, that led to those terminals. On the map above, they cut diagonally in tandem from lower left to upper right.
The father of a girl who lived at 345 Third Street, in the Gowanus Canal cluster, was listed as “dockman.” To go to work, he probably walked to the corner of Fourth and Union, got on the Fourth Avenue subway and hopped off at the Bush Terminal, where so many other dots form a grid. In the photo below, "dockman’s" home is marked by a circle. It’s just three blocks away from the epicenter of the epidemic.
So why the docks? To answer that question, we need to back away from our closeup and adopt a much wider view. Fasten you're seatbelts, we're heading on a 4,884 mile excursion.
“The summer wind came blowin’ in from across the sea …" (Summer Wind by Henry Mayer and Johnny Mercer, 1965)
The Big Island of Hawaii rises out of the Pacific like a ridge-backed dinosaur, its volcanic spine splitting the island between the arid leeward side and the green, rain-drenched windward half. The westerly breeze, rolling unimpeded across the vast expanse of ocean, finally brushes up against the spine and pauses, pulling up water and pouring it back down. An average year brings up to 200 inches of rain to the eastern side, making it one of the wettest places on Earth – three times the annual rainfall of, say, Brooklyn.
Sugarcane has been called the thirsty plant, craving constant water for its roots and leaves and stalks, reaching twice the height of humans in densely packed rows that obscure the sun. A warm and saturated climate, like much of Hawaii, is a perfect place for cane. Unfortunately, it’s not a convenient place – nor is Cuba or Brazil or the West Indies or Puerto Rico. Cane is grown in places that can’t afford it, then shipped to places that can, a Third-to-First-World transaction that fed a sordid history. Slavery arose in significant measure because someone needed chop down and haul the stalks to the nearby mill, a job no one wanted.
Raw sugar, the end result of all this planting, tending, harvesting and milling, was not even the end result. This is not the kind of "raw sugar" you tear open and dump in your coffee at Starbucks; it is unsafe to eat, full of dirt and organic matter and sugar in a coating of molasses. Stray buttons and coins turned up inthe mix.
This raw product was loaded onto freighters bound for the continental U.S.. Most went to the great East Coast refineries in New York Harbor, Philadelphia and Boston. These refineries -- half a dozen ringed New York Harbor, centered in Brooklyn -- put the raw sugar through the wringer all over again – a brochure from the 1933 World’s Fair lists 71 steps from arrival to packaged product at a refinery in Long Island City, Queens. A good deal of the “refining” was simply designed to turn the sugar white, an ironic accomplishment given the black lives laid waste along the way. (I had to quit reading the book Sugar because the description of how slaves were treated on the sugar plantations was so horrifying.)
After the Domino Sugar Factory stopped operating a few years ago in Brooklyn (its huge sign an icon on the waterfront), an art installation in its cavernous ruins called the Sugar Sphinx, by Kara Walker, spoke to that history. The New Yorker called it “triumphant, rising from a kind of half-world—the shadowy half-world of slavery and degradation.” (Full title: “A Subtlety, or the Marvelous Sugar Baby – An Homage to the Unpaid and Overworked Artisans Who Have Refined Our Sweet Tastes, From the Cane Fields to the Kitchens of the New World on the Occasion of the Demolition of the Domino Sugar Refinery Plant.” That pretty much tells the story, except for the fact that sugar as a food is now recognized as worse than worthless. The world would have been far better off if chewing on a sugar cane stalk from time to time but otherwise leaving it as it lay.)
Even after slavery ended, the paternalistic and colonial impulse remained. That 1933 Jack Frost brochure shows jaunty dark people gathering up the cane and refers to them as “natives” who “cut down row after row of the cane with a machete” and load it onto horse-drawn wagons (in 1933!). It sounded almost pleasant, “the picturesque acres of green-leafed ‘bamboo’ reeds stretching as far as the eye can see.”
Things were somewhat better in Hawaii. The plantations relied on coaxing laborers to immigrate. most often from Japan or the Philippines. The American owners – many of them former missionaries – became power players with mercenary interests of their own, leading to the overthrow of the indigenous monarchy and the slow incorporation of Hawaii into the United States. By 1900 trade relations were so advantageous that it made sense to cultivate more marginal acreage.
Chief among them was the Olaa plantation, which, while on the rainy side of the Big Island's backbone, was iffy real estate. The volcanic soil was porous and uneven, the ground on the lower mountainside where the cane was planted sloped inconveniently, and the immense rainfall meant that everything, not just the cane, grew like Jack's beanstalk. Weeds ran wild, more than could profitably be pulled over the longll, two-year growing season.
By 1913, barely a decade into the Olaa enterprise, the bottom line looked bleak. The owners got rid of the current manager and went all-in on an unlikely savior – C.F. Eckart, head of the experiment station of the Hawaii Sugar Planters Association. His new salary was rumored to be an astronomical $12,000 a year -- $290,000 in today’s dollars. His mission was to cut costs by making the crop less labor-intensive and, while he was at it, increase the yield.
Desperate times called for desperate measures. Eckart set to work doing what he had been paid so handsomely for. He experimented.
Along with his generous salary, Charles Eckart reaped other benefits that went with being a Hawaiian plantation manager in 1913. In vivid contrast to his former life as an experiment station official, he lived in a mansion two miles from the Olaa plantation office. A book about a subsequent Hawaiian sugar strike by Masayo Umezawa Duus captures the world that awaited him as he approached for the first time his new home with its immense veranda, stables for riding horses, and distant view of the Pacific.
"The mansion still stands,” Duus wrote in 1987, “its landmark a huge banyan tree that is said to date from the era when native chieftans held power. Along the private road leading to the mansion dozens of tall coconut trees pierced the sky. The three-story white structure sits on the crest of a rise surrounded by an expansive lawn.” Although decrepit now, the place is imposing enough to “hint at the status and power of the plantation manager, who the Japanese laborers likened to a daimyo, a feudal lord, and whom they likened to the ‘owner’ of the plantation.”
Eckart barely had time to settle in. He quickly set about addressing Olaa’s weed woes. The manpower required to keep ahead of such indiscriminate fecundity over the two-year growing season threatened whatever profit the plantation might eke out. At the experiment station, Eckart and a fellow researcher, H.P. Agee, had been working on a solution -- literally.
A solution of arsenic.
“New method of weed control,” the journal Sugar reported in June 1915, after the solution had been widely implemented on Olaa’s sugarcane fields. “The system which would appear to be the most satisfactory is that of Agee and Eckart, in which the weeds are sprayed with arsenite of soda. Two special spraying apparatus have been invented, the spread sprayer and the knapsack sprayer.”
Early concerns about the method had been alleviated, the article said. One was whether the arsenic would kill the golden goose – the sugarcane – and not just the weeds. It didn’t: “Experiments carried out in Olaa, in which arsenic was applied to the soil between the rows at the rate of 5 lbs. per acre each week for six months, showed that the arsenic had no injurious effect on the growth of the cane plant.”
If you think the second issue was whether arsenic might kill you, you would be mistaken. “The second problem, as to whether the poison employed in the process damages the cane itself, has also been answered in the negative. It is true that, even with the best apparatus, small quantities of the spray cannot be prevented from coming into contact with the leaves of the young cane occasionally. But this is not a matter of importance, because it is at most occasions a slight check to the cane, from which it recovers entirely within a few weeks.”
What a relief – to the owners, at any rate. You could spray thousands of gallons of an arsenic solution for two years and still harvest a healthy crop. Sure, a lot of arsenic got into the sloping, rain-soaked soil, and who could help sloshing a little onto the sugarcane plant from time to time? Meanwhile, the dead weeds were left where they lay to decompose. The point was, the plant recovered. It was not a matter of importance.
Here we are, then, in June 1915, with arsenic being sprayed for the first time – ever, anywhere, as far as I can tell – on a sugarcane crop. “It may be said that this method of weed control already has passed the experimental stage,” the article stated, “as it has been adopted as a part of the normal field work in the extensive plantation at Olaa.” Well, yes, it was part of the "normal" field work, but it was still "experimental" in its effect on humans.
The article gives the formula – 5 pounds of arsenite [an arsenic-based compound] to 100 gallons of water. Eckart, the article said, was ordering as much sled-spraying as possible, with a “light hand-spraying to touch up the spots that may have been missed by the sleds.” According to an unnamed authority, “by observing the proper rules and ordinary intelligence, spraying can save a plantation in labor from $15 to $30 per year per acre. This seems to have gotten under way not long after Eckart’s arrival in 1913. Given the two-year growing season, followed by harvesting, hauling, and milling at a nearby factory, the first crop that got the full arsenic treatment was doubtless the one that arrived on the East Coast of the United States -- New York, Boston, Philadelphia -- early in 1916.
My antenna go up whenever I hear about the first time something is tried, because, almost by definition, no one knows what the hell he or she is doing. It’s one thing to try arsenic out at the experiment station, another to experiment on thousands of gallons on thousands of acres that will yield thousands of tons of sugarcane, without giving a thought to its effect on those who would consume it.
Spraying arsenic around food doesn’t seem like a very good idea to me, but if you read the scientific literature of the time, you start to think it's like sprinkling a little parmesan on your spaghetti. I was about ready to try a spoonful myself (you could do that too for many years – it was called Fowler’s Solution!). So I reached out on AOA to find someone familiar with toxicology to give me a more modern understanding. A reader with an advanced degree in environmental toxicology got in touch and proved to be terrific. I gave her all the information I had about the use of arsenic on the plantation and she gave me her feedback over several exchanges.
She displayed the straightforward approach that I associate with good science, and I’m going to share what she said pretty much verbatim – saving some for later when it’s more appropriate. As I explained to her upfront, my interest was whether enough arsenic could have made it from Olaa’s cane fields through the harvesting and milling and refining processes to become a potential factor in the 1916 epidemic. I sensed she would tell me if this seemed dubious, so I waited with interest for her e-mail to pop up in my inbox. It read:
Hi Dan – I would not discount the presence of arsenic (used as a pesticide) in the sugar. Here are some thoughts on what you sent me:
-- Just as background, arsenic is sometimes a metal and at other times a metalloid. This property makes it very versatile in the forms it can take – arsenic can form a number of different compounds.
-- Arsenic is an immune suppressant as are heavy metals in general. Arsenic binds to sulfur compounds and impairs enzymes; it also competes with phosphate, which is needed to synthesize ATP to produce energy.
-- Arsenic does act quickly, and a child would get a disproportionately large dose from a “regular” serving of whatever sugary food was eaten, so arsenic could act relatively quickly to suppress a child's immune system.
-- Regarding the formulation of the arsenic spray in Hawaii: What they were doing with the caustic soda (NaOH) and heat is making white arsenic more water-soluble, so that it would remain in solution – i.e. spray easily and not settle out. That would increase its utility as a pesticide by improving its “flow” and its “shelf life.”
I don’t have any idea what spraying equipment looked like in 1916 but even today it’s difficult to hit only the weeds and not the crop with pesticide spray. (I shudder to think of the occupational exposure.) Moreover since the arsenic pesticide was highly water soluble it would have been carried into the soil and been available for uptake by the roots of any plant that was nearby. So yes the sugar cane could have been contaminated by inorganic arsenic. I need to do a little reading on arsenic uptake in plants to understand this better. It’s kind of the opposite of using plants to clean a Super Fund site: in that case the plants are destroyed after binding heavy metals in the soil, while here the plants were refined into food.
How helpful was that! I replied:
Thanks so much.
-- I've found various and quite different discussions of whether sugarcane takes up arsenic. There was a study around 1933 in Hawaii that said a field on which arsenic was used had no more arsenic in the plant than a field that was arsenic-free. But I've also read about how rice -- which has a major arsenic-uptake problem -- and sugarcane are two of the major plants that take up silicon in large amounts. In the case of rice, the silicon transporters mistake arsenic for silicon and take it up. I have no idea if that could happen to sugarcane.
Hi Dan – I have done a little more reading on arsenic and here are further thoughts (four journal articles attached).
- The form in which arsenic was sprayed onto weeds is highly bioavailable to plants, which is why it kills weeds so fast (in 1-2 days). It’s also highly bioavailable to humans. I would have to believe that at least a small amount of arsenite sprayed onto weeds would have made contact with the proximate sugar cane. In addition, the “splashing” effect of rain would have carried some arsenite from surface soil onto surrounding plants including the nearby sugar cane. That arsenite could have been taken up by the cane.
- The paper from the USDA assumes that the arsenite was washed out of the soil, and that may very well be correct given the hilly terrain and porosity of the soil. But that takes a little bit of time, so the arsenite is available to the cane roots for some brief period of time (a week? a month? three months? I don’t know). Also the plants down the hill would be exposed to arsenic migrating from uphill so there’s a “gradient” effect.
- The killed weeds were left in place to decay, which would have caused the arsenic in their tissues to be recirculated back into the soil. That becomes a “secondary” source of arsenic exposure, which would have been available to the sugar cane roots. This variable was not included in the USDA paper on the fate of arsenic in Hawaii soil: it assumed the only source of arsenic was the original spray.
- The Brazilian researchers found that sugarcane does take up arsenic into its tissues and that more is found in the cane than in the leaves. So it is entirely reasonable to assume that arsenic was assimilated by the sugar cane and made it into the raw sugar.
Regarding the growing season: Hawaii is largely a year-round growing season, right? So the arsenic weed-killer would have been applied at regular intervals throughout the year. Cane is fast-growing so it would take up water and minerals in the soil at a rapid rate. The cane was taking up arsenic, but it also seemed to be growing normally (no mention of it being stunted or having small leaves, etc.) so the amount present wasn’t enough to interfere with growth. However the refining process would concentrate that type of small contaminant.
Well, this is quite educational, wouldn’t you agree?
I had read before that if a contaminant did get into sugarcane there could be hell to pay because the refining process would concentrate it. I must say that I still didn’t quite get that – I imagined a centrifuge spinning all the flotsam and jetsam and buttons and coins to the side and leaving pure sugar crystals at the center, ready to fall neatly into one pound bags, pure as the driven snow. After all it was "refined"! So I asked:
“One more -- why would refining concentrate the impurity rather than remove it? I was assuming it was pulled out of the sugar itself ... ” Her answer:
The arsenic that was spread throughout multiple plants has now been concentrated into a small amount of sugar. Very roughly, it takes 80 tons of cane to extract one ton of sugar. So the arsenic in 80 tons of cane was released with the sugars. More of the impurities remained in the syrup than the crystals, but there would have been some in the crystals too.
To quote Leader of the Pack – yes, we see. I had a new appreciation for the uniqueness and complexity of sugar as a food – unlike a strawberry, which you “process” by planting, growing, and harvesting, sugarcane went through an amazing manufacturing process, and not just once but twice. You could wash off a strawberry before you ate it (or try to!), but you were pretty much stuck with whatever was in that bag of "pure cane sugar." Sugar, it seems to me, is the most manufactured food in the world.
This is insidious, for sure, if it’s true -- arsenic in the sugar in the food. Nobody would blame the sugar. They would ”blame” ice cream and candy and baked goods and soda water and cereal with sugar sprinkled on it. They would blame summer fruit (much of which was treated with lead arsenate pesticide, a topic to which we will return.) They would observe that cases clustered around provision shops that served and sold those foods. They'd wonder why the docks looked like a node of infection.
People did notice those things and blame those things and wonder about them. But nobody on high was listening for the common truth. Ice cream causes polio? Please!
It wasn’t the ice cream, per se, in this theory; the ice cream was just a vector. It was the arsenic in the sugar in the ice cream, and that was still only half the equation. The virus itself was the other half. Simple math would explain why, in a group of four children playing on swings in the park, one might develop poliomyelitis while the other three did not. One had the virus and one didn't; one had the arsenic exposure and one didn't; one had neither; one had both. The one with both was the one at risk.
My toxiciological correspondent concluded: “This would have constituted a “light’ exposure (‘background’ is the wrong word because it implies the arsenic was found naturally in the soil, which it wasn’t, and ‘trace’ and ‘light’ aren’t good words either because they're not quantitative). But a ‘light’ exposure to arsenic could affect a human. Plus children are smaller than adults and thus more vulnerable to a given dose of toxicant than an adult, just because of body weight.”
Oh, in case you’re wondering how much arsenic really got applied at Olaa, here’s a current map, decades after they stopped. They’re still trying to get rid of it. (Keeau is the modern name for Olaa.)
Author's personal copy Bioaccessible arsenic in soils of former sugar cane plantations, Island of Hawaii William G. Cutler a , b , ⁎ , Roger C. Brewer c , Aly El-Kadi b , d , Nguyen V. Hue e , Patrick G. Niemeyer f , 1 , John Peard g , Chittaranjan Ray d
By 1915, things were finally looking up for the Olaa Plantation. Eckart was reaping the rewards of his bold experiment. The newspapers were full of plaudits.
“Olaa shows remarkable improvement,” the trade journal Louisana Planter and Sugar Manufacturer reported in September 1915. “The two years administration of the affairs of the Olaa Sugar Company on the island of Hawaii by Mr. C.F. Eckart, the former director of the Hawaiian Sugar Planters’ Experiment Station, have been marked by increases in yields and lowering of costs beyond the most sanguine hope of stockholders. The improvements have been general and while particularly noticeable in the data on crops, are, nevertheless, in evidence in the handling of labor and other activities of the company.” Although not mentioned, the arsenic treatment must have been a big part of boosting the crop and cutting costs.
On February 9, 1916, Eckart was quoted in the Hawaiian Gazette as saying that “the harvesting of this crop commenced on December 7, 1914, and completed on November 25, 1915. An unusually early start to the grinding season [at the mill] was considered advisable owing to the increased output of sugar expected. … Altogther 283,116 tons were harvested, yielding 32,308.22 tons of sugar.” So this 1915 crop, for early 1916 delivery, did so well they had to start harvesting it early. Finally, the gods were cooperating. He told the press:
On February 25, the Honolulu Star-Bulletin was effusive: “Cost of Producing Ton of Olaa Cane Cut Almost 50 Percent.” Again, that had to be due in significant measure to the cost savings from the arsenic spraying, although it wasn't specifically mentioned. On May 19, the Hawaiian Gazette reported, “Olaa Sugar Company to Pay First Dividend. This Year’s Crop [for 1917 delivery] Probably Last One To Run Under 30,000 Tons; Yield Per Acre Grows.” Eckart outlined expansive plans to increase the size of the mill, add more railroad equipment, even buy 20 more mules – a total cost of $150,000. Once more, no mention of arsenic's role.
“War prices for sugar, good management, a constructive policy on the part of agents and directors, and a dogged determination to win have brought this great property through to this successful issue,” the paper said. Eckart was the toast of the planter’s world. Thus endeth the homilies to the sugar crop harvested at Olaa Plantation on the Big Island of Hawaii, a crop delivered in early 1916 to Brooklyn and other East Coast points.
In October 1916 -- just five months later -- the Louisiana Planter said that year’s Olaa's next crop [for 1917 delivery] was a disappointment. “Olaa Plantation, whose varying fortunes have been often the subject of comment by sugar statisticians and publicists, has further reduced its 1916 crop estimates [for 1917 delivery] … The new estimate is now 21,500 tons … The disappointment of the investors and of the stock market players is keen over Olaa’s showing this year.” You can see the figure below, fifth from the end.
So feast had turned to famine. Anyone familiar with farming knows that fortunes can turn quickly, and for any number of reasons -- drought, pests, prices. The newspaper story seemed to suggest a deeper discontent with Olaa than mere vagaries of weather, though. One thing is for sure: Eckart was experimenting again. Olaa began grinding up sugar cane refuse – called bagasse – and mulching it into paper. The paper was laid over the sugar fields to deprive the weeds of sun and water. Voila, dead weeds! It’s hard to see exactly how arsenic fit this model.
"A succession of experiments molded the history of Olaa Sugar Company," according to the sugar planters' archive at the University of Hawaii. "An experiment in paper mulching was started in 1916. The object of the paper mulch was to suppress the weed growth and keep the soil warm. But it also reduced labor costs for hoeing by 50 percent and provided an extra application of fertilizer.
“In 1919, Olaa Sugar Company had the distinction of operating the first bagasse paper mill in the Territory and the only one of its kind in the United States at that time. The mill was erected alongside the sugar factory where bagasse was converted into mulching paper. C.F. Eckart, manager, originated the idea. The mill produced enough paper daily to cover 9 to 11 acres, with about 1,600 lbs. of paper per acre. The paper was used over the young ratoons, which pierced their was through to the light, while the weeds died. This asphalt-saturated paper used at Olaa became a forerunner of mulch paper developed for use in Hawaii's pineapple industry. Eventually the paper mill was dismantled, but mulching was still used for weed control.”
So what happened to the arsenic treatment, since it was also for weeds? I can’t find any reference at all to Olaa and arsenic after 1916. It’s probably there somewhere, but the difference between the fanfare leading up to the harvest, and the silence afterwards, is striking. By 1922 Eckart himself had disappeared from the press coverage, no longer manager at Olaa.
In 2003 the Honolulu Star-Bulletin reported," State health officials have found high levels of arsenic in the soil at two community gardens in Keaau [Olaa] on the Big Island, and are offering free medical tests to residents to see if they have absorbed the potentially toxic element."
The article said "the probable source was herbicides sprayed on the local sugar plantation from 1915 to 1950." So the use of arsenic at Olaa apparently continued. But the variables that may have triggered the 1916 Brooklyn outbreak did not remain static. With American participation in World War I in April 1917, everything about sugar distribution changed. The American-Hawaiian Steamship freighters stopped their runs to the East Coast and were leased, profitably, to the Navy to carry troops and cargo. The few freighters that remained delivered the raw sugar from Hawaii to San Francisco for overland transport by train; eventually more Hawaiian sugar stayed on the West Coast instead of the inconvenient East.
If arsenic from Olaa sugarcane did in fact lead to a poliomyelitis outbreak in the Northeast, this would help explain why it was a one-year phenomenon (see chart in Part 1): a toxin (arsenic) found a vector (sugar) that delivered it to a place (Brooklyn) where a virus (polio) was circulating, triggering an outbreak of paralysis and death (poliomyelitis). The effect, in scientific terms, was amplification -- the toxin made the virus far more dangerous than either would have been alone. In lay terms, you could call it an Explosion. Brooklyn in 1916 may offer a uniquely clear vantage point to witness cause and effect.
The Star-Bulletin interviewed a 94-year-old man who sprayed arsenic on those Hawaiian fields in the 1920s and '30s. "As a young man, Henry Texeira's fingernails and hair fell out, and his skin broke out in blisters when he sprayed an arsenic-based herbicide in sugar cane fields south of Hilo. ... The chemical he used was Penite, a brand name for sodium arsenite. 'People used to suffer like hell with Penite,' Texeira said." It's a form of sodium arsenite, an inorganic arsenic compound also known as arseneous acid, sodium salt and sodium meta-arsenite.
"Another brand name for the stuff," Texeira recalled, "was Kill-All."
Next: To the refineries.
Dan Olmsted is Editor of Age of Autism.