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

Autor: Martz CD; Population Research Center, The University of Texas at Austin, United States. Electronic address: connor.martz@austin.utexas.edu., Benner AD; Population Research Center, The University of Texas at Austin, United States; Department of Human Development and Family Sciences, The University of Texas at Austin, United States., Goosby BJ; Population Research Center, The University of Texas at Austin, United States; Department of Sociology, The University of Texas at Austin, United States., Mitchell C; Institute for Social Research, University of Michigan, United States., Gaydosh L; Population Research Center, The University of Texas at Austin, United States; Department of Sociology, The University of Texas at Austin, United States.
Jazyk: angličtina
Zdroj: Social science & medicine (1982) [Soc Sci Med] 2024 Apr; Vol. 347, pp. 116724. Date of Electronic Publication: 2024 Mar 02.
DOI: 10.1016/j.socscimed.2024.116724
Abstrakt: 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.
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Databáze: MEDLINE
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