The social environment, both in early life and adulthood, is one of the strongest predictors of morbidity and mortality risk in humans. Evidence from long-term studies of other social mammals indicates that this relationship is similar across many species. In addition, experimental studies show that social interactions can causally alter animal physiology, disease risk, and life span itself. These findings highlight the importance of the social environment to health and mortality as well as Darwinian fitness—outcomes of interest to social scientists and biologists alike. They thus emphasize the utility of cross-species analysis for understanding the predictors of, and mechanisms underlying, social gradients in health.

Coronavirus disease 2019 (COVID-19) is disproportionately burdening racial and ethnic minority groups in the US. Higher risks of infection and mortality among racialized minorities are a consequence of structural racism, reflected in specific policies that date back centuries and persist today. Yet, our surveillance activities do not reflect what we know about how racism structures risk. When measuring racial and ethnic disparities in deaths due to COVID-19, the CDC statistically accounts for the geographic distribution of deaths throughout the US to reflect the fact that deaths are concentrated in areas with different racial and ethnic distributions than that of the larger US. In this commentary, we argue that such an approach misses an important driver of disparities in COVID-19 mortality, namely the historical forces that determine where individuals live, work, and play, and consequently determine their risk of dying from COVID-19. We explain why controlling for geography downplays the disproportionate burden of COVID-19 on racialized minority groups in the US. Finally, we offer recommendations for the analysis of surveillance data to estimate racial disparities, including shifting from distribution-based to risk-based measures, to help inform a more effective and equitable public health response to the pandemic.

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Background: The incidence of TB in Michigan was 1.5 per 100,000 people in 2012, roughly half the U.S. incidence. Despite successes in TB control, disparities in TB still exist in Michigan, particularly by race, age, and nativity. A major challenge in understanding disparities in TB burden is distinguishing between TB cases resulting from recent transmission and those resulting from reactivation of latent TB infection, information critical to tailoring control strategies. We examined nine-year trends in tuberculosis (TB) incidence patterns for the entire population of Michigan, and within demographic subgroups. Methods: Using a cross-sectional study of TB surveillance data, we analyzed 1254 TB cases reported in Michigan during [2004][2005][2006][2007][2008][2009][2010][2011][2012]. Cases included were those for whom both spoligotyping and 12-locus-MIRU-VNTR results were available. Using a combination of the genotyping information and time of diagnosis, we then classified cases as resulting from either recent transmission or reactivation of latent TB infection. We used multivariable negative binomial regression models to study trends in the TB incidence rate for the entire population and by race, nativity, gender, and age. Results: Overall, the incidence rate of TB declined by an average of 8% per year-11% among recently transmitted cases, and 9% among reactivation cases. For recently transmitted disease, Blacks had an average incidence rate 25 times greater than Whites, after controlling for nativity, gender, and age. For disease resulting from latent TB infection Asians had an average incidence rate 24 times greater than Whites, after controlling for nativity, gender, and age. Conclusions: Disparities in incidence persist despite ongoing TB control efforts. Greater disparities were observed by race and nativity demonstrating some of the ways that TB incidence is socially patterned. Reducing these disparities will require a multi-faceted approach encompassing the social and environmental contexts of high-risk populations.

Purpose Using genotyping data of Mycobacterium tuberculosis isolates from new cases reported to the TB surveillance program, we evaluated risk factors for recent TB transmission at both the individual- and neighborhood-levels among U.S.-born and foreign-born populations. Methods TB cases (N=1,236) reported in Michigan during 2004–2012 were analyzed using multivariable Poisson regression models to examine risk factors for recent transmission cross-sectionally for U.S.-born and foreign-born populations separately. Recent transmission was defined based on spoligotype and 12-locus-MIRU-VNTR matches of bacteria from cases that were diagnosed within one year of each other. Four classes of predictor variables were examined: demographic factors, known TB risk factors, clinical characteristics, and neighborhood-level factors. Results Overall, 22% of the foreign-born cases resulted from recent transmission. Among the foreign-born, race and being a contact of an infectious TB case were significant predictors of recent transmission. More than half (52%) of U.S.-born cases resulted from recent transmission. Among the U.S.-born, recent transmission was predicted by both individual- and neighborhood-level socio-demographic characteristics. Conclusions Interventions aimed at reducing TB incidence among foreign-born should focus on reducing reactivation of latent infection. However, reducing TB incidence among the U.S.-born will require decreasing transmission among socially disadvantaged groups at the individual- and neighborhood-level. This report fills an important knowledge gap regarding the contemporary social context of TB in the U.S., thereby providing a foundation for future studies of public health policies that can lead to the development of more targeted effective TB control.

The disproportionate burden of prevalent, persistent pathogens among disadvantaged groups may contribute to socioeconomic and racial/ethnic disparities in long-term health. We assessed if the social patterning of pathogen burden changed over 16 years in a U.S.-representative sample. Data came from 17 660 National Health and Nutrition Examination Survey participants. Pathogen burden was quantified by summing the number of positive serologies for cytomegalovirus, herpes simplex virus-1, HSV-2, human papillomavirus and Toxoplasma gondii and dividing by the number of pathogens tested, giving a percent-seropositive for each participant. We examined sex- and age-adjusted mean pathogen burdens from 1999–2014, stratified by race/ethnicity and SES (poverty-to-income ratio (PIR); educational attainment). Those with a PIR < 1.3 had a mean pathogen burden 1.4–1.8 times those with a PIR > 3.5, with no change over time. Educational disparities were even greater and showed some evidence of increasing over time, with the mean pathogen burden among those with less than a high school education approximately twice that of those who completed more than high school. Non-Hispanic Black, Mexican American and other Hispanic participants had a mean pathogen burden 1.3–1.9 times non-Hispanic Whites. We demonstrate that socioeconomic and racial/ethnic disparities in pathogen burden have persisted across 16 years, with little evidence that the gap is closing.

Purpose of Review Socioeconomic status (SES) has long been understood to be a key determinant of the distribution of tuberculosis (TB), and the role of social factors has long been a truism of TB epidemiology. We review studies that have examined the social determinants of TB in the USA in the past 20 years. We pay particular attention to how the findings of these studies fit within the framework of fundamental cause theory and argue that a more explicit linkage with fundamental cause theory is critical for understanding the current state of TB health disparities in the USA and for charting a way towards TB elimination in the USA. Recent Findings and Summary Our review finds that while in the past 20 years there have been studies that have documented the ongoing association between social factors and TB disease in the USA, few studies explore the precise mechanisms through which social factors continue to influence TB patterns. We advocate for a move towards a system-based approach both in theory development and analyses, allowing for the incorporation of more complex social dynamics to address long-standing disparities in TB disease.

Background Prior studies in humans have suggested that telomere shortening may be accelerated by infection, but research on multiple pathogens and use of large population-based study samples has been limited. We estimated cross-sectional associations between seropositivity to five persistent pathogens (Herpes Simplex Virus Type-1 (HSV-1), Herpes Simplex Virus Type-2 (HSV-2), cytomegalovirus (CMV), Helicobacter pylori (H.pylori), and Hepatitis B) as well as total pathogen burden and leukocyte telomere length. Data were derived from the National Health and Nutrition Examination Survey (1999–2000) for individuals 20–49 years of age, N = 1708. We analyzed the influence of each pathogen separately, a pathogen count score and a latent class model of pathogen burden on log telomere length using linear regression models, adjusted for covariates. Results Individuals in a latent pathogen burden class characterized by high probabilities of infection with HSV-1, CMV, and H. pylori, had significantly decreased log telomere length (− 0.30 [95% CI: − 0.36, − 0.24]) compared to those in a latent class characterized by low probabilities of all five infections. There were limited significant associations using other pathogen measures. Conclusions These results suggest that infection with specific combinations of pathogens may be one mechanism contributing to accelerated cellular senescence with possible origins early in the life course.