Structural racism in primary schools and changes in epigenetic age acceleration among Black and White youth.

Structural racism generates racial inequities in U.S. primary education, including segregated schools, inequitable funding and resources, racial disparities in discipline and achievement, and hostile racial climates, which are risk factors for adverse youth health and development. Black youth are disproportionately exposed to adverse school contexts that may become biologically embedded via stress-mediated epigenetic pathways. This study examined whether childhood exposure to adverse school contexts is associated with changes in epigenetic aging during adolescent development. DNA methylation-based epigenetic clocks were calculated from saliva samples at ages 9 and 15 among Black (n = 774) and White (n = 287) youth in the Future of Families and Child Wellbeing Study (2009-2015). We performed latent class analyses to identify race-specific primary school contexts using administrative data on segregation, discipline, achievement, resources, economic disadvantage, and racial harassment. We then estimated change in epigenetic age acceleration from childhood to adolescence across school typologies using GrimAge, PhenoAge, and DunedinPACE epigenetic clocks. Three distinct school contexts were identified for Black youth: segregated and highly-disadvantaged (17.0%), segregated and moderately-disadvantaged (52.1%), and integrated and moderately-disadvantaged (30.8%). Two school contexts emerged for White youth: integrated and unequal (46.5%) and predominantly White & advantaged (53.5%). At age 15, Black youth who attended segregated and highly-disadvantaged primary schools experienced increases in their speed of epigenetic aging with GrimAge and DunedinPACE. Slowed epigenetic aging with GrimAge was observed for Black youth who attended integrated and moderately-disadvantaged schools. School contexts were not associated with changes in epigenetic age acceleration for White youth. Our findings suggest that manifestations of structural racism in primary school contexts are associated with early-life epigenetic age acceleration and may forecast future health inequities.

Sociodemographic profiles and organ damage accural in the Black Women's Experience Living with Lupus study.

OBJECTIVE: Black/African American women with systemic lupus erythematosus (SLE) experience greater organ damage and at younger ages than white women. The objective of this study was to advance research on SLE inequities by identifying sociodemographic risk profiles associated with organ damage accrual specifically among Black/African American women. METHODS: Latent profile analysis was conducted among 438 Black/African American women with SLE living in Atlanta, GA and enrolled in the Black Women's Experiences Living with Lupus (BeWELL) Study (May 2015 to April 2017). Proportional hazard and Poisson regression models examined prospective associations between sociodemographic profiles and the timing and degree of organ damage accrual over 2 years. RESULTS: Four profiles emerged: (1) "Younger/Lower SES with Uncontrolled SLE" (44.8%), (2) "Older/Lower SES with Uncontrolled SLE" (23.3%), (3) "Mid-SES with Controlled SLE" (19.6%), and (4) "Higher SES with Controlled SLE" (11.2%). Approximately 42% of participants experienced new organ damage during the follow-up period. Proportional hazard models indicated that "Older/Lower SES with Uncontrolled SLE" participants were at greatest risk of new organ damage (HR = 2.41; 95% CI = 1.39, 4.19), followed by "Younger/Lower SES with Uncontrolled SLE" participants (HR = 1.56; 95% CI = 0.92, 2.67), compared to those in the "Higher SES with Controlled SLE" profile. Poisson regression models revealed that these two groups also exhibited greater organ damage accrual (b = 0.98, SE = 0.24, 95% CI = 0.52, 1.44 and b = 0.72, SE = 0.23, 95% CI = 0.27, 1.17, respectively). CONCLUSIONS: Black/African American women with fewer socioeconomic resources and uncontrolled SLE are at greatest risk for increasing disease severity over time. Social inequities likely contribute to racial inequities in SLE progression.

Area racism and birth outcomes among Blacks in the United States.

There is increasing evidence that racism is a cause of poor health outcomes in the United States, including adverse birth outcomes among Blacks. However, research on the health consequences of racism has faced measurement challenges due to the more subtle nature of contemporary racism, which is not necessarily amenable to assessment through traditionally used survey methods. In this study, we circumvent some of these limitations by examining a previously developed Internet query-based proxy of area racism (Stephens-Davidowitz, 2014) in relation to preterm birth and low birthweight among Blacks. Area racism was measured in 196 designated market areas as the proportion of total Google searches conducted between 2004 and 2007 containing the "n-word." This measure was linked to county-level birth data among Blacks between 2005 and 2008, which were compiled by the National Center for Health Statistics; preterm birth and low birthweight were defined as <37 weeks gestation and <2500 g, respectively. After adjustment for maternal age, Census region, and county-level measures of urbanicity, percent of the Black population, education, and poverty, we found that each standard deviation increase in area racism was associated with relative increases of 5% in the prevalence of preterm birth and 5% in the prevalence of low birthweight among Blacks. Our study provides evidence for the utility of an Internet query-based measure as a proxy for racism at the area-level in epidemiologic studies, and is also suggestive of the role of racism in contributing to poor birth outcomes among Blacks.