Synergistic effects of social determinants of health and race-ethnicity on 30-day all-cause readmission disparities: a retrospective cohort study.

OBJECTIVE: The objective of this study is to assess the effects of social determinants of health (SDOH) and race-ethnicity on readmission and to investigate the potential for geospatial clustering of patients with a greater burden of SDOH that could lead to a higher risk of readmission. DESIGN: A retrospective study of inpatients at five hospitals within Henry Ford Health (HFH) in Detroit, Michigan from November 2015 to December 2018 was conducted. SETTING: This study used an adult inpatient registry created based on HFH electronic health record data as the data source. A subset of the data elements in the registry was collected for data analyses that included readmission index, race-ethnicity, six SDOH variables and demographics and clinical-related variables. PARTICIPANTS: The cohort was composed of 248 810 admission patient encounters with 156 353 unique adult patients between the study time period. Encounters were excluded if they did not qualify as an index admission for all payors based on the Centers for Medicare and Medicaid Service definition. MAIN OUTCOME MEASURE: The primary outcome was 30-day all-cause readmission. This binary index was identified based on HFH internal data supplemented by external validated readmission data from the Michigan Health Information Network. RESULTS: Race-ethnicity and all SDOH were significantly associated with readmission. The effect of depression on readmission was dependent on race-ethnicity, with Hispanic patients having the strongest effect in comparison to either African Americans or non-Hispanic whites. Spatial analysis identified ZIP codes in the City of Detroit, Michigan, as over-represented for individuals with multiple SDOH. CONCLUSIONS: There is a complex relationship between SDOH and race-ethnicity that must be taken into consideration when providing healthcare services. Insights from this study, which pinpoint the most vulnerable patients, could be leveraged to further improve existing models to predict risk of 30-day readmission for individuals in future work.

The Impact of Environmental Benzene, Toluene, Ethylbenzene, and Xylene Exposure on Blood-Based DNA Methylation Profiles in Pregnant African American Women from Detroit.

African American women in the United States have a high risk of adverse pregnancy outcomes. DNA methylation is a potential mechanism by which exposure to BTEX (benzene, toluene, ethylbenzene, and xylenes) may cause adverse pregnancy outcomes. Data are from the Maternal Stress Study, which recruited African American women in the second trimester of pregnancy from February 2009 to June 2010. DNA methylation was measured in archived DNA from venous blood collected in the second trimester. Trimester-specific exposure to airshed BTEX was estimated using maternal self-reported addresses and geospatial models of ambient air pollution developed as part of the Geospatial Determinants of Health Outcomes Consortium. Among the 64 women with exposure and outcome data available, 46 differentially methylated regions (DMRs) were associated with BTEX exposure (FDR adjusted p-value < 0.05) using a DMR-based epigenome-wide association study approach. Overall, 89% of DMRs consistently exhibited hypomethylation with increasing BTEX exposure. Biological pathway analysis identified 11 enriched pathways, with the top 3 involving gamma-aminobutyric acid receptor signaling, oxytocin in brain signaling, and the gustation pathway. These findings highlight the potential impact of BTEX on DNA methylation in pregnant women.

Precocious infant fecal microbiome promotes enterocyte barrier dysfuction, altered neuroendocrine signaling and associates with increased childhood obesity risk.

Early life gut microbiome composition has been correlated with childhood obesity, though microbial functional contributions to disease origins remain unclear. Here, using an infant birth cohort (n = 349) we identify a distinct fecal microbiota composition in 1-month-old infants with the lowest rate of exclusive breastfeeding, that relates with higher relative risk for obesity and overweight phenotypes at two years. Higher-risk infant fecal microbiomes exhibited accelerated taxonomic and functional maturation and broad-ranging metabolic reprogramming, including reduced concentrations of neuro-endocrine signals. In vitro, exposure of enterocytes to fecal extracts from higher-risk infants led to upregulation of genes associated with obesity and with expansion of nutrient sensing enteroendocrine progenitor cells. Fecal extracts from higher-risk infants also promoted enterocyte barrier dysfunction. These data implicate dysregulation of infant microbiome functional development, and more specifically promotion of enteroendocrine signaling and epithelial barrier impairment in the early-life developmental origins of childhood obesity.