The lethality of polio has been a subject of debate since the 1880s, with various theories attempting to explain its rise. One prominent theory, the 'excess sanitation' hypothesis, suggests that improved sanitation leads to more severe cases of polio as children are less exposed to the virus early in life. However, historical evidence contradicts this notion, showing that early epidemics predominantly affected very young children, with high mortality rates, particularly in urban areas like New York during the 1916 epidemic. Additionally, studies conducted in India revealed that despite low median ages for polio infection, the incidence of paralysis was alarmingly high, challenging the sanitation theory’s assumptions about socioeconomic status and disease severity.

Another theory attributes the rise in polio to the use of arsenic pesticides, specifically lead arsenate. Proponents argue that arsenic poisoning could lead to polio-like symptoms, but this theory lacks strong evidence. Notably, early polio outbreaks occurred in regions before the widespread use of lead arsenate, and peak mortality rates from bulbar polio were recorded when pesticide use was still low. Both theories face significant gaps in evidence, making it clear that the complexities of polio's lethality require further investigation beyond simplistic explanations.