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By Dan Olmsted
The first articles in this series told the story of the 1916 polio epidemic in New York City and the North Atlantic States. I put forward a theory that arsenic, used for the first time as a pesticide on a Hawaiian sugarcane plantation, got into the sugar supply in the refineries in New York as well as Boston and Philadelphia. The arsenic interacted with the poliovirus -- "amplified" its ability to cause paralysis and death by gaining it access to the nervous system and the anterior horn cells at the top of the spine. That led to the largest polio outbreak up to then, with nearly 2,500 dead in New York City alone.
This is a novel idea, to say the least, and the evidence I presented for it was indirect – above all, the widespread observation by ordinary people that certain foods like ice cream, candy, soft drinks and baked goods, and the places that sold them, were vectors and epicenters of the epidemic. Along with other evidence, these observations pointed, in my mind, to sugar as the common ingredient. I tracked cases from the docks in Brooklyn where raw sugar from Hawaii was unloaded to the refineries in Queens and Yonkers and Boston and Philadelphia where it was processed, to the wider North Atlantic distribution area that mirrored the spread of the epidemic. Public health officials of the day disregarded and even mocked the observations; when more than half of all letter-writers mentioned food, and the list began with ice cream, soft drinks, candy and summer fruit, the New York Health Commissioner said he didn't know "whether to laugh at the fantasies or weep over the ignorance and superstition exhibited." Germ theory was in ascendancy and environmental illness was not even on the radar, which did not exist, either. Two factors as the root of polio epidemics would have seemed fiendishly implausible. Wasn't one more than enough to try to wrap your mind around?
If the arsenic co-factor theory is true, and I certainly believe it is, we ought to be able to apply it to other polio epidemics, whatever the delivery and exposure mechanism. That would be a reasonable and fundamental test. But how do we logically proceed? I can think of four ways. We could look for direct evidence of arsenic in other polio epidemics. We could look for other toxins beside arsenic that could have been co-factors separately or in combination. We could look at sugar and see whether, in subsequent years and places, it emerges once again. Or we could look for signs of an association with food more broadly.
In fact, I'm going to do all that. But for starters, let’s pick food, which is the big clue from the New York epidemic. This week, I happened to come across an account of an outbreak in 1926 while doing other research this at the National Library of Medicine in Bethesda, Maryland. It just popped up, as facts tend to do around a good hypothesis. The article, no more than a page long, concerned a 1926 outbreak in the Broadstairs area of Kent, England.
The article ran in the January 15, 1927, edition of the British Medical Journal.
The epidemic began in October and primarily affected children at certain schools in the area. Under “interesting features” of the outbreak were four facts:
- “The disease was limited mainly to the children attending private schools in the district, particularly boarding schools … the private schools had very little communication with each other.”
- “The disease started almost simultaneously in all the schools affected, and ceased almost entirely at the end of a fortnight.”
- “The disease did not spread to the adjoining districts.”
- “The disease did not spread in the elementary schools.”
Out of 67 cases, in fact, “there were 12 … that were not connected with the schools or institutions, except indirectly – for example, one whose brother attended a school where a case occurred.” (That was the only such example given, alas. Having a brother who attended the school seems barely "indirect.") One mistress and two members of domestic staffs at the private schools were also affected. In one convalescent home there were two children and three staff members affected.
“Then,” the report continues, “there was the case of a waiter, aged 22, employed in a hotel in Broadstairs during the season, who left the town on October 6, developed the disease on the 16th, and died in a London hospital on October 21; and that of a young woman, age 29, who stayed in Broadstairs from October 2 to October 9, and died on the 22nd.”