Background: The objective of this study is to document whether and to what extent there is an association between socioeconomic status (SES) and disease outcomes in the last five influenza pandemics.Methods/principle findings: The review included studies published in English, Danish, Norwegian and Swedish. Records were identified through systematic literature searches in six databases. We summarized results narratively and through meta-analytic strategies. Only studies for the 1918 and 2009 pandemics were identified. Of 14 studies on the 2009 pandemic including data on both medical and social risk factors, after controlling for medical risk factors 8 demonstrated independent impact of SES. In the random effect analysis of 46 estimates from 35 studies we found a pooled mean odds ratio of 1.4 (95% CI: 1.2–1.7, p < 0.001), comparing the lowest to the highest SES, but with substantial effect heterogeneity across studies,–reflecting differences in outcome measures and definitions of case and control samples. Analyses by pandemic period (1918 or 2009) and by level of SES measure (individual or ecological) indicated no differences along these dimensions. Studies using healthy controls tended to document that low SES was associated with worse influenza outcome, and studies using infected controls find low SES associated with more severe outcomes. A few studies compared severe outcomes (ICU or death) to hospital admissions but these did not find significant SES associations in any direction. Studies with more unusual comparisons (e.g., pandemic vs seasonal influenza, seasonal influenza vs other patient groups) reported no or negative non-significant associations.Conclusions/significance: We found that SES was significantly associated with pandemic influenza outcomes with people of lower SES having the highest disease burden in both 1918 and 2009. To prepare for future pandemics, we must consider social vulnerability. The protocol for this study has been registered in PROSPERO (ref. no 87922) and has been published Mamelund et al. (2019).

Seasonal influenza takes its most pronounced toll on children and the elderly, giving the crude age-specific mortality rates a U-shape. In contrast, A(H1N1) 1918-20 pandemic mortality was W-shaped. When adjusting for the seasonal baseline, young adults had higher but the elderly lower than expected mortality. The lower than expected mortality for the elderly is one reason why total mortality in urban societies were relatively low in 1918-20 (30 years was protected because they were exposed to H1-like viruses prior to 1889. This hypothesis assumes that people lived within the reach of the urban disease pools. Here I analyze mortality after age 30 in aboriginal populations assumed to be infrequently exposed to influenza due to their geographic isolation. Results show that Arctic and Pacific peoples also experienced a decline in relative mortality after age 30. However, the remotely living elderly did not have lower than expected mortality, suggesting that they had less prior exposure to influenza than their urban counterpart. Crude total mortality and mortality for all adults >30 years was nevertheless extremely high in the remote populations. Parish records quantitatively confirmed the anecdotes that children 5-14 years were the only survivors in some Arctic communities. Low exposure to H1-like viruses in adults could not alone explain the high total mortality in remote populations (up to 90%). A high concurrent disease load, crowding, low genetic variability, a lack of basic care, and infrequent exposure to other forms of influenza virus 1890-1917 may have played a role as well. This form of immunological cross-protection from previous exposure to A-type influenza viruses other than H1N1 can only be explained as a consequence of cellular immunity against internal proteins that show less inter-strain variation than the surface proteins.

This paper examines short-term birth sequelae of the influenza pandemic of 1918-1920 in the United States using monthly data on births and all-cause deaths for 19 US states in conjunction with data on maternal deaths, stillbirths, and premature births. The data on births and all-cause deaths are adjusted for seasonal and trend effects, and the residual components of the 2 time series coinciding with the timing of peak influenza mortality are examined for these sequelae. Notable findings include: 1) a drop in births in the 3 months following peak mortality; 2) a reversion in births to normal levels occurring 5-7 months after peak mortality; and 3) a steep drop in births occurring 9-10 months after peak mortality. Interpreted in the context of parallel data showing elevated premature births, stillbirths, and maternal mortality during times of peak influenza mortality, these findings suggest that the main impacts of the 1918-1920 influenza on reproduction occurred through: 1) impaired conceptions, possibly due to effects on fertility and behavioral changes; 2) an increase in the preterm delivery rate during the peak of the pandemic; and 3) elevated maternal and fetal mortality, resulting in late-term losses in pregnancy.

During epidemics, the poorest part of the population usually suffers the most. Alfred Crosby noted that the norm changed during the 1918 influenza pandemic in the US: The black population (which were expected to have higher influenza morbidity and mortality) had lower morbidity and mortality than the white population during the autumn of 1918. Crosby’s explanation for this was that black people were more exposed to a mild spring/summer wave of influenza earlier that same year. In this paper, we review the literature from the pandemic of 1918 to better understand the crossover in the role of race on mortality. The literature has used insurance, military, survey, and routine notification data. Results show that the black population had lower morbidity, and during September, October, and November, lower mortality but higher case fatality than the white population. The results also show that the black population had lower influenza morbidity prior to 1918. The reasons for lower morbidity among the black population both at baseline and during the herald and later waves in 1918 remain unclear. Results may imply that black people had a lower risk of developing the disease given exposure, but when they did get sick, they had a higher risk of dying.