Saturday, May 16, 2020

Vaclav Smil Is A Party Pooper: "History and Risk"

Again, a bit dated (April 3, 2020) but it's Smil and he tends to get things right.
From Inference Review:
Too many people are occupied in modeling the duration and impact of COVID-19. I have no intention of adding to this runaway genre. It is now the first week of April 2020—too early to make any solid judgments even as far as the first pandemic wave is concerned. It may be dying down in China and sputtering in South Korea, but it is raging in Italy, Spain, and France, and it has only entered its early exponential phase in the United States.1 Once the first wave recedes, we will still not be sure when the next wave might arrive. That is why I will provide only some important historical perspectives and comparative risk assessments, and list a few lessons that are already absolutely clear.

Looking Back
For several reasons, the 1918–1919 flu pandemic is not the best point of reference. That we still do not know where it began would be irrelevant if we were certain about its global impact and if we could calculate reliable mortality rates for the most affected countries. We can do neither. The most commonly cited estimate of total global mortality is between 20 and 40 million. The World Health Organization put it “upwards of 40 million people,” and Niall Johnson and Juergen Mueller go as high as 50 million.2 Even the lower estimate surpasses all military and civilian deaths of World War I, while the total of 50 million would be almost certainly higher than the toll of the 1347–1351 plague and about equal to another uncertain aggregate, that of all those who perished in the USSR between 1929 and 1953, and in Maoist China between 1949 and 1976.3

We will never know how many people were infected, but with 20–40 million deaths within a global population of 1.8 billion, the 1918–1919 pandemic had an average mortality rate of 11 to 22 per 1,000. National mortalities are not highly accurate, but the most likely US count is 550,000.4 That number is higher than all the deaths sustained by the country’s servicemen in all of the twentieth century’s wars, and equal to a pandemic-specific mortality rate of 5.3 per 1,000. Both the North American and European data clearly show three successive waves. The British mortality had its smallest peak at just 5 per 1,000 in July 1918, the highest peak at five times that rate in October 1918, and an intermediate wave slightly above 10 per 1,000 during late February 1919.5 Good epidemiological data are available for several large cities, including New York, Toronto, and Montreal. Between February 1918 and April 1920, New York experienced four waves, together with a heat wave, with peak mortalities shifting from teenagers during the first wave to young adults, with excess mortalities peaking at 28 years of age.6
Exactly the same age peak was found in Toronto and Montreal in October 1918. Alain Gagnon et al. have argued that this heightened mortality could be explained by an early exposure to the Russian flu pandemic of 1889–1890.7 The development of early immunological memory may adversely affect the immune response to new strains encountered later in life, and thus increase risk of death.

We know the complete genome and virulence of the influenza virus responsible for the 1918–1919 pandemic;8 but we also know that most 1918–1919 pandemic deaths were due to bacterial pneumonia. Some 80% of cultures taken from preserved lung-tissue samples contained bacteria causing secondary lung infection. A generation before the development of antibiotics, no treatment was available.9 Andrew Noymer and Michel Garenne discovered that individuals with tuberculosis were more likely than others to die of influenza;10 this helps to explain the pandemic’s unusual middle-age mortality profile as well as its higher incidence among men, which matches the differential incidence of tuberculosis between the sexes.

Excess mortality in 1918–1919 appears less extreme if some deaths were, in effect, borrowed against future deaths due to tuberculosis. Because neither pre-existing tuberculosis nor bacterial pneumonia have been important factors in post-WWII pandemics, the Spanish flu is worth studying for its sequence of waves and their growth patterns; but its overall and age-specific mortality were clearly unique.

Comparing Risks
Pandemics are feared because of their relatively high mortalities, but it is impossible to pinpoint those rates while the infection is spreading, and it is difficult to do so even after it ends. The preferred epidemiological approach is to calculate the case-fatality risk, the ratio of deaths to cases. The numerator is not as clear as one might wish because comorbidities are often neglected even when they are noted on death certificates. Still, it is the choice of the denominator that can make a difference in risk assessment as large as two orders of magnitude.

Studies of the 2009 influenza A(H1N1)pdm09 pandemic used three different case definitions: laboratory-confirmed cases, estimated symptomatic cases, and estimated infections (based on serology or on assumptions regarding the extent of asymptomatic infections). As expected, laboratory-confirmed approaches yielded the highest risk of death—mostly between 100 and 5,000 per 100,000; symptomatic approaches were in the range of 5 to 50 per 100,000; and approaches based on estimated infections yielded risks of just 1 to 10 per 100,000. The first approach showed fatalities up to 500 times higher than the last.11....

Also at Inference Review and linked here February 1, 2020:
"The Great Transition: Climate, Disease and Society in the Late-Medieval World"