Abstract
This study examines the roles of age, period, and cohort in influenza mortality trends over the years 1959–2016 in the United States. First, we use Lexis surfaces based on Serfling models to highlight influenza mortality patterns as well as to identify lingering effects of early-life exposure to specific influenza virus subtypes (e.g., H1N1, H3N2). Second, we use age-period-cohort (APC) methods to explore APC linear trends and identify changes in the slope of these trends (contrasts). Our analyses reveal a series of breakpoints where the magnitude and direction of birth cohort trends significantly change, mostly corresponding to years in which important antigenic drifts or shifts took place (i.e., 1947, 1957, 1968, and 1978). Whereas child, youth, and adult influenza mortality appear to be influenced by a combination of cohort- and period-specific factors, reflecting the interaction between the antigenic experience of the population and the evolution of the influenza virus itself, mortality patterns of the elderly appear to be molded by broader cohort factors. The latter would reflect the processes of physiological capital improvement in successive birth cohorts through secular changes in early-life conditions. Antigenic imprinting, cohort morbidity phenotype, and other mechanisms that can generate the observed cohort effects, including the baby boom, are discussed.
Highlights
At the beginning of the twentieth century, pneumonia and influenza (P&I) were the leading causes of death in the United States (Deaton 2015), and today, they remain the most important causes of death among infectious diseases (Armstrong et al 1999)
Had the 1967 U.S population shared the size and age structure of the 2015 U.S population, the number of deaths due to influenza during the whole epidemic season would have been more than three times higher (39,973 vs. 12,463), primarily because older age groups experiencing the highest risk of influenza mortality would have accounted for a larger share of the population
The other two significant contrasts identified for the ~1896–1901 and ~1928 cohorts could be interpreted as imprinted cohort effects, but we believe that they point to longer-term changes in mortality at older ages, in line with the cohort morbidity phenotype
Summary
At the beginning of the twentieth century, pneumonia and influenza (P&I) were the leading causes of death in the United States (Deaton 2015), and today, they remain the most important causes of death among infectious diseases (Armstrong et al 1999). The following three influenza pandemics (1957, 1968, and 2009) and the appearance of new subtypes, such as the highly pathogenic avian H5N1 and H7N9 influenza viruses (Haque et al 2007), demonstrate that influenza remains a significant threat to public health. Population aging makes it likely that casualties will increase (Simonsen et al 2011), given that about 90 % of all influenza deaths occur among people aged 65 and over (Thompson et al 2003). Only a few studies (see, e.g., Azambuja 2009, 2015; Cohen et al 2010) have undertaken an analysis of influenza mortality variation over time in an age-period-cohort (APC) framework
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