4. But the medical profession is in two minds

The 8th edition (2024) of the book, “Plotkin’s Vaccines”, seems to promote an entirely different theory – that it is poor sanitation which leads to polio: “Lower socioeconomic status is a risk for paralytic poliomyelitis in developing countries, probably because children belonging to the lower socioeconomic group experience more intense exposure to poliovirus. …

In addition, these children are at higher risk for primary vaccine failure after OPV because of more frequent concurrent enterovirus infections, diarrheal disease and/or malnutrition”. And CDC’s 2006 Pink Book noted that lameness studies in developing countries challenge the predictions of the “excess sanitation” theory.

5. The “excess sanitation” theory fails

The first prediction of the “excess sanitation” theory is itself questionable. In the early epidemics, polio was lethal in very young children, contrary to the idea that older children get the more severe disease. Ivar Wickman’s 1913 book show that in 8 out 10 global epidemics till 1909, children below the age of 3 experienced most paralytic polio. In New York’s 1916 epidemic, 83% of the 2,407 who died were children under the age of five.

Consider also predictions based on the maternal antibody angle. Chlorination of water kills the polio virus, so polio should have disappeared by 1916 from New York’s water that was consumed both by the rich and poor (New York’s water supply was almost entirely chlorinated since 1911). At that stage, the only way for polio to spread was via poor hygiene, which would implicate the poor more than the rich (in reality, the rich got more polio). Most importantly, all mothers would still have polio antibodies from infections before 1911, so their infants born in 1914 and 1915 would have received antibodies, but infants still died in the greatest number. And why 1916 for the epidemic, why not 1915 or 1917?
If the excess sanitation theory is correct, places with poor sanitation should have mild, early-life polio infections with rare paralytic disease and almost no deaths. But studies in the 1960s in India showed that although the median age of polio disease was low (between 12 and 18 months) – consistent with the theory – “[t]he incidence of paralytic polio in India was among the highest reported anywhere … more than 2 children among 1000 under-fives developed polio paralysis annually” (T. Jacob John et al., 2013). Not only that, many of them died, as reported by H. V. Wyatt in 1998 – “about 2% of children with polio die in the acute illness”. India’s case doesn’t fit the theory’s prediction.

The proponents of the theory have an answer through a new word, “hyperendemic polio”. Apparently, when the virus is excessively prevalent, the child’s body can’t defend itself despite maternal antibodies and early re-infection. But a similar “hyperendemic” situation prevailed in 18th and early 19th century London without high prevalence of paralytic polio. One can’t argue both sides of a case and still have a credible theory.

But there are many other problems. If the sanitation theory is true, then the UK, with excellent water supply by 1860, should have been the first to have polio epidemics, but that’s not where they started. Instead, as the report on the 1916 New York epidemic noted, the overwhelming proportion of early epidemics both in Sweden and USA were in rural areas. In New York, as well, in 1916, “the Boroughs of Richmond and Queens, the only boroughs which are to any extent rural, have suffered more severely than their heavily populated neighbors”4. Rural areas typically did not get modern sanitation systems or clean water till after the cities. And, of course, this theory can’t explain the coterminous epidemics of polio in animals.

6. Theory 3: Arsenic pesticides

According to this theory, polio rose in lethality when lead arsenate became commonly used as a pesticide in the West. There are two types of arsenic theory: (a) direct and (b) indirect.

The direct theory argues that arsenic poisoning from lead arsenate pesticide (used in the USA from around 1892) led to polio-like paralysis. If so, then farmers should have died first but it was infants and little children who suffered in the early epidemics. It is argued that these children must have eaten arsenic-laden fruit. But that is speculative and even if it so, why only in the epidemic areas? More importantly, symptoms of arsenic poisoning are different to those of polio and any paralysis can only occur after extensive arsenic poisoning. Since arsenic is a well-known poison with a long history, investigative doctors would have suspected it immediately if the observed symptoms had matched. In favour of the arsenic poisoning theory, though, is the simultaneous emergence of paralysis in a wide range of animals. It is argued that these animals might have consumed the poison through their food. But once again, there is no detailed proof.

The indirect theory claims that ingested arsenic pesticide can lead to a dysfunction of the intestines (where the virus first reproduces), allowing the virus to gain entry into the blood stream and reach the spinal cord. This would also allow other polio-like viruses to get through. But data don’t stack up. While there exists a broad correlation between increasing arsenic pesticide use in the USA and the rise of polio, it can’t explain specific epidemics. The first known epidemics of polio occurred in Sweden and Norway ten years prior to the use of lead arsenate. Further, one of the places in 1905 where the polio epidemic occurred in Sweden was a remote village with no interaction with the rest of the world. The arsenic proponents would need to prove that all these people were using pesticides.

Finally, peak mortality rates from bulbar polio occurred in the USA mainly in first two decades of the 20th century when pesticide use was still relatively low; polio mortality rates declined after 1916 while lead arsenate use increased. There are too many gaps in the arsenic theory.

END OF ARTICLE