Xia Yingjing, Rebello Vida, Bodison Stefanie C, Jonker Deborah, Steigelmann Babette, Donald Kirsten A, Charles Weslin, Stein Dan J, Ipser Jonathan, Ahmadi Hedyeh, Kan Eric, Sowell Elizabeth R, Narr Katherine L, Joshi Shantanu H, Odendaal Hein J, Uban Kristina A
Public Health, University of California, Irvine, Irvine, CA, United States.
Department of Occupational Therapy, College of Public Health and Health Professions, University of Florida, Gainesville, FL, United States.
Front Integr Neurosci. 2023 Jul 18;17:1104788. doi: 10.3389/fnint.2023.1104788. eCollection 2023.
Alcohol and tobacco are known teratogens. Historically, more severe prenatal alcohol exposure (PAE) and prenatal tobacco exposure (PTE) have been examined as the principal predictor of neurodevelopmental alterations, with little incorporation of lower doses or ecological contextual factors that can also impact neurodevelopment, such as socioeconomic resources (SER) or adverse childhood experiences (ACEs). Here, a novel analytical approach informed by a socio-ecological perspective was used to examine the associations between SER, PAE and/or PTE, and ACEs, and their effects on neurodevelopment.
= 313 mother-child dyads were recruited from a prospective birth cohort with maternal report of PAE and PTE, and cross-sectional structural brain neuroimaging of child acquired via 3T scanner at ages 8-11 years. SER was measured by maternal education, household income, and home utility availability. The child's ACEs were measured by self-report assisted by the researcher. PAE was grouped into early exposure (<12 weeks), continued exposure (>=12 weeks), and no exposure controls. PTE was grouped into exposed and non-exposed controls.
Greater access to SER during pregnancy was associated with fewer ACEs (maternal education: β = -0.293, = 0.01; phone access: β = -0.968, = 0.05). PTE partially mediated the association between SER and ACEs, where greater SER reduced the likelihood of PTE, which was positively associated with ACEs (β = 1.110, = 0.01). SER was associated with alterations in superior frontal (β = -1336.036, = 0.046), lateral orbitofrontal (β = -513.865, = 0.046), caudal anterior cingulate volumes (β = -222.982, = 0.046), with access to phone negatively associated with all three brain volumes. Access to water was positively associated with superior frontal volume (β=1569.527, = 0.013). PTE was associated with smaller volumes of lateral orbitofrontal (β = -331.000, = 0.033) and nucleus accumbens regions (β = -34.800, = 0.033).
Research on neurodevelopment following community-levels of PAE and PTE should more regularly consider the ecological context to accelerate understanding of teratogenic outcomes. Further research is needed to replicate this novel conceptual approach with varying PAE and PTE patterns, to disentangle the interplay between dose, community-level and individual-level risk factors on neurodevelopment.
酒精和烟草是已知的致畸物。从历史上看，更严重的产前酒精暴露（PAE）和产前烟草暴露（PTE）一直被视为神经发育改变的主要预测因素，而很少纳入较低剂量或也会影响神经发育的生态背景因素，如社会经济资源（SER）或童年不良经历（ACEs）。在此，采用一种基于社会生态视角的新型分析方法来研究SER、PAE和/或PTE与ACEs之间的关联，以及它们对神经发育的影响。
从一个前瞻性出生队列中招募了313对母婴，母亲报告了PAE和PTE情况，并在孩子8至11岁时通过3T扫描仪对其进行了横断面结构性脑神经成像检查。SER通过母亲教育程度、家庭收入和家庭设施可用性来衡量。孩子的ACEs通过研究人员协助下的自我报告来测量。PAE被分为早期暴露（<12周）、持续暴露（>=12周）和无暴露对照组。PTE被分为暴露组和非暴露对照组。
孕期获得更多的SER与较少的ACEs相关（母亲教育程度：β = -0.293，p = 0.01；有电话：β = -0.968，p = 0.05）。PTE部分介导了SER与ACEs之间的关联，即更多的SER降低了PTE的可能性，而PTE与ACEs呈正相关（β = 1.110，p = 0.01）。SER与额上回（β = -1336.036，p = 0.046）、外侧眶额回（β = -513.865，p = 0.046）、尾侧前扣带回体积改变相关（β = -222.982，p = 0.046），有电话与这三个脑区体积均呈负相关。有水供应与额上回体积呈正相关（β = 1569.527，p = 0.013）。PTE与外侧眶额回（β = -331.000，p = 0.033）和伏隔核区域体积较小相关（β = -34.800，p = 0.033）。
关于社区层面PAE和PTE后的神经发育研究应更经常地考虑生态背景，以加速对致畸结果的理解。需要进一步研究以不同的PAE和PTE模式复制这种新型概念方法，以厘清剂量、社区层面和个体层面风险因素在神经发育上的相互作用。
