Population Research Center, The University of Texas at Austin, United States.
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.
Soc Sci Med. 2024 Apr;347:116724. doi: 10.1016/j.socscimed.2024.116724. Epub 2024 Mar 2.
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.
结构性种族主义在美国基础教育中造成了种族不平等,包括隔离的学校、不平等的资金和资源、纪律和成就方面的种族差异,以及敌对的种族氛围,这些都是青少年健康和发展不良的风险因素。黑人青年不成比例地面临不利的学校环境,这些环境可能通过压力介导的表观遗传途径在生物学上被嵌入。本研究探讨了童年时期暴露于不利的学校环境是否与青少年发育过程中表观遗传衰老的变化有关。在未来家庭和儿童福利研究(2009-2015 年)中,从黑人(n=774)和白人(n=287)青少年的唾液样本中计算了基于 DNA 甲基化的表观遗传时钟,在 9 岁和 15 岁时。我们使用关于隔离、纪律、成就、资源、经济劣势和种族骚扰的行政数据,使用潜在类别分析来识别特定种族的小学环境。然后,我们使用 GrimAge、PhenoAge 和 DunedinPACE 表观遗传时钟,根据学校类型学来估计从童年到青春期的表观遗传年龄加速变化。为黑人青少年确定了三种不同的学校环境:隔离且高度贫困(17.0%)、隔离且中度贫困(52.1%)和融合且中度贫困(30.8%)。为白人青少年确定了两种学校环境:融合且不平等(46.5%)和主要是白人且有利(53.5%)。在 15 岁时,就读于隔离且高度贫困小学的黑人青少年的 GrimAge 和 DunedinPACE 表观遗传衰老速度加快。在融合且中度贫困的学校就读的黑人青少年的 GrimAge 表现出表观遗传衰老速度减慢。对于白人青少年,学校环境与表观遗传年龄加速变化无关。我们的研究结果表明,小学环境中结构性种族主义的表现与早期生活中的表观遗传年龄加速有关,并可能预测未来的健康不平等。