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Against a backdrop of extreme racial health inequality, the 1918 influenza pandemic resulted in a striking reduction of non-White to White influenza and pneumonia mortality disparities in United States cities. We provide the most complete account to date of these reduced racial disparities, showing that they were unexpectedly uniform across cities. Linking data from multiple sources, we then examine potential explanations for this finding, including city-level sociodemographic factors such as segregation, implementation of nonpharmaceutical interventions, racial differences in exposure to the milder spring 1918 “herald wave,” and racial differences in early-life influenza exposures, resulting in differential immunological vulnerability to the 1918 flu. While we find little evidence for the first three explanations, we offer suggestive evidence that racial variation in childhood exposure to the 1889–1892 influenza pandemic may have shrunk racial disparities in 1918. We also highlight the possibility that differential behavioral responses to the herald wave may have protected non-White urban populations. By providing a comprehensive description and examination of racial inequality in mortality during the 1918 pandemic, we offer a framework for understanding disparities in infectious disease mortality that considers interactions between the natural histories of particular microbial agents and the social histories of those they infect. [ABSTRACT FROM AUTHOR]

Quantitative studies of racial health disparities often use static measures of self-reported race and conventional regression estimators, which critics argue is inconsistent with social-constructivist theories of race, racialization, and racism. We demonstrate an alternative counterfactual approach to explain how multiple racialized systems dynamically shape health over time, examining racial inequities in cardiometabolic risk in the National Longitudinal Study of Adolescent to Adult Health. This framework accounts for the dynamics of time-varying confounding and mediation that is required in operationalizing a "race" variable as part of a social process (racism) rather than a separable, individual characteristic. We decompose the observed disparity into three types of effects: a controlled direct effect ("unobserved racism"), proportions attributable to interaction ("racial discrimination"), and pure indirect effects ("emergent discrimination"). We discuss the limitations of counterfactual approaches while highlighting how they can be combined with critical theories to quantify how interlocking systems produce racial health inequities. [ABSTRACT FROM AUTHOR]

Though Hispanics live long lives, whether a "Hispanic paradox" extends to older-age health remains unclear, as do the social processes underlying racial-ethnic and immigrant-native health disparities. Using data from the Health and Retirement Study (2004-2012; N = 6,581), we assess the health of U.S.- and foreign-born Hispanics relative to U.S.-born whites and blacks and examine the socioeconomic, stress, and behavioral pathways contributing to health disparities. Findings indicate higher disability, depressive, metabolic, and inflammatory risk for Hispanics relative to whites and similar health profiles among Hispanics and blacks. We find limited evidence of a healthy immigrant pattern among foreign-born Hispanics. While socioeconomic factors account for Hispanic-white gaps in inflammation, disparities in other outcomes persist after adjustment for socioeconomic status, due in part to group differences in stress exposure. Hispanics may live long lives, but their lives are characterized by more socioeconomic hardship, stress, and health risk than whites and similar health risks as blacks. [ABSTRACT FROM AUTHOR]