What is the average lifespan in a stationary population viewed at a single moment in time? Even though periods and cohorts are identical in a stationary population, we show that the answer is not life expectancy, but a length-biased version of life expectancy. That is, the distribution of lifespans of the people alive at a single moment is a self-weighted distribution of cohort lifespans, such that longer lifespans have proportionally greater representation. This result connects stationary population lifespan measures to a well-developed body of statistical results; provides new intuition for established demographic results; generates new insights into the relationship between periods, cohorts, and prevalent cohorts; and offers a framework for thinking about mortality selection more broadly than the concept of demographic frailty. Acknowledgements:

Over the early twentieth century, urban centers across the United States adopted full-time public health departments. Using an event-study design, we show that opening full-time administration had no impact on mortality (all-cause, infant, by-cause). Then, we use city financial records to explain why health departments were ineffective. First, cities with and without health departments had comparable spending on public health. Second, per capita expenditures (and per capita expenditures interacted with a health department) correlate with infant mortality reductions. While urban public health administration as a bureaucratic apparatus appears unnecessary, public health system funding may be more meaningful for local health. JEL codes: I15, I18, H51, N32.

The 1918 influenza pandemic stands out for its extreme virulence and unusual age pattern of mortality. Here, we aim to elevate a third unusual feature of its course through United States cities to the same level of scientific prominence: the pandemic produced strikingly small racial disparities in mortality, against a backdrop of extreme racial inequality in the era. We provide the most complete account of racial disparities in influenza and pneumonia mortality in U.S. cities in 1918, showing that they were almost uniformly small. We also advance and evaluate four hypotheses as to why racial disparities in the 1918-1919 pandemic were so small relative to those in proximate years. In particular, we assess hypotheses related to socio-demographic characteristics like segregation, city-level implementation of non-pharmaceutical interventions, racial differences in exposure to the 1918 herald wave, and racial differences in early-life exposures to other influenza strains that could have resulted in differences in immunological vulnerability to the 1918 flu. The results suggest the importance of considering in depth the interactions between the natural history of a particular microbial agent and the social history of the populations it infects.

BACKGROUND