Division of Epidemiology, School of Public Health, University of California, Berkeley, 2121 Berkeley Way #5302, Berkeley, CA, 94720, USA.
Department of Obstetrics, Gynecology, & Reproductive Sciences, University of California, San Francisco, USA.
Soc Sci Med. 2024 Nov;360:117229. doi: 10.1016/j.socscimed.2024.117229. Epub 2024 Aug 10.
We assessed the link between two manifestations of structural racism-historical redlining and contemporary racial residential segregation-and baseline and 10-year changes in leukocyte telomere length (LTL).
We used data on Black and Hispanic/Latinx participants from Exams I and V of the Multi-Ethnic Study of Atherosclerosis Stress Ancillary Study (N = 741, age range = 45-84 years). LTL was defined as the ratio of telomeric DNA to a single copy gene (T/S), and 10-year changes were adjusted for regression to the mean. We used 1930s Home Owners' Loan Corporation maps to assign three historical redlining grades (A&B: best/still desirable, C: declining, D: hazardous/redlined) to participants' neighborhoods (census-tracts) at baseline. The Getis-Ord G∗ statistic was used to evaluate census-tract level baseline residential segregation (low/moderate/high).
In mixed-effects regression models accounting for neighborhood clustering, individual characteristics, and current neighborhood environments, those living in highly segregated Black neighborhoods had 0.08 shorter baseline LTL (95% CI: -0.13, -0.04), than those residing in the least segregated neighborhoods. We did not find a relationship between residing in segregated neighborhoods and 10-year LTL changes, and associations between residing in historically redlined neighborhoods and both baseline LTL and 10-year changes in LTL were null. Across discriminatory disinvestment trajectories examined, individuals residing in highly segregated but non-redlined neighborhoods had 0.6 shorter baseline LTL than individuals residing in non-redlined neighborhoods with low/moderate segregation (95% CI: -0.12, -0.01).
Our results highlight the impact of racial segregation on cellular aging and underscore the need to ameliorate structural inequities within segregated neighborhoods.
我们评估了结构种族主义的两种表现形式——历史上的红线政策和当代的种族居住隔离——与白细胞端粒长度（LTL）的基线和 10 年变化之间的联系。
我们使用来自动脉粥样硬化多民族研究压力辅助研究（Multi-Ethnic Study of Atherosclerosis Stress Ancillary Study，MESA-SA）的 I 期和 V 期的黑人和西班牙裔/拉丁裔参与者的数据（N=741，年龄范围 45-84 岁）。LTL 的定义是端粒 DNA 与单拷贝基因的比值（T/S），10 年变化调整了回归均值。我们使用 20 世纪 30 年代的房主贷款公司（Home Owners' Loan Corporation）地图，根据参与者的社区（普查区）在基线时的历史红线政策等级（A&B：最好/仍然理想，C：下降，D：危险/红线）分配三个等级。Getis-Ord G∗ 统计量用于评估普查区层面的基线居住隔离（低/中/高）。
在混合效应回归模型中，考虑到邻里聚类、个体特征和当前邻里环境，居住在高度隔离的黑人社区的人，其基线 LTL 短 0.08（95%CI：-0.13，-0.04），而居住在隔离程度最低的社区的人。我们没有发现居住在隔离社区与 LTL 10 年变化之间的关系，也没有发现居住在历史上的红线社区与 LTL 的基线和 10 年变化之间的关系。在我们检查的所有具有歧视性的投资不足轨迹中，居住在高度隔离但非红线社区的个体的基线 LTL 比居住在低度/中度隔离的非红线社区的个体短 0.6（95%CI：-0.12，-0.01）。
我们的研究结果强调了种族隔离对细胞衰老的影响，并强调了需要在隔离社区内减轻结构性不平等。
