Contextualizing the impact of prenatal alcohol and tobacco exposure on neurodevelopment in a South African birth cohort: an analysis from the socioecological perspective.

Contextualizing the impact of prenatal alcohol and tobacco exposure on neurodevelopment in a South African birth cohort: an analysis from the socioecological perspective.
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DOI:
10.3389/fnint.2023.1104788
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发表时间:
2023
影响因子:
3.5
通讯作者:
Uban, Kristina A.
Uban, Kristina A.
中科院分区:
医学3区
文献类型:
--
作者:
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.

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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)已被视为神经发育改变的主要预测因素,很少纳入低剂量或生态环境因素,也可能影响神经发育,如社会经济资源(SER)或不良儿童经历(ACE)。在这里,一种新的分析方法通知社会生态学的角度被用来检查SER,PAE和/或PTE,ACE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N = 313对母子,母亲报告了PAE和PTE,儿童在8-11岁时通过3 T扫描仪获得了横断面结构脑神经成像。子宫内SER通过母亲的教育程度、家庭收入和家庭公用设施的可用性来衡量。在研究者的协助下,以自我报告的方式测量儿童的ACE。PAE分为早期暴露(<12周)、持续暴露(>=12周)和无暴露对照组。PTE分为暴露和非暴露对照组。怀孕期间获得SER的机会越多,ACE越少(母亲教育:β =-0.293,p = 0.01;电话访问:β =-0.968,p = 0.05)。PTE部分介导SER与ACE之间的关系,SER越高,PTE发生的可能性越低,与ACE呈正相关(β = 1.110,p = 0.01)。SER与上级额叶(β = −1336.036,q = 0.046)、外侧眶额(β = −513.865,q = 0.046)、尾侧前扣带回体积(β = −222.982,q = 0.046)的变化相关,而使用电话与所有三种脑体积均呈负相关。饮水量与上级额容量呈正相关(β=1569.527,q = 0.013)。PTE与外侧眶额区(β = −331.000,q = 0.033)和延髓核区(β = −34.800,q = 0.033)体积较小相关。在社区层面的PAE和PTE之后的神经发育研究应该更经常地考虑生态背景,以加速对致畸结果的理解。需要进一步的研究来复制这种具有不同PAE和PTE模式的新概念方法,以解开剂量,社区水平和个人水平风险因素对神经发育之间的相互作用。
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. N = 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. In utero 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,p = 0.01; phone access: β = −0.968,p = 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,p = 0.01). SER was associated with alterations in superior frontal (β = −1336.036, q = 0.046), lateral orbitofrontal (β = −513.865, q = 0.046), caudal anterior cingulate volumes (β = −222.982, q = 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, q = 0.013). PTE was associated with smaller volumes of lateral orbitofrontal (β = −331.000, q = 0.033) and nucleus accumbens regions (β = −34.800, q = 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.
DOI: 10.1016/j.socscimed.2012.11.027
发表时间: 2013-02
影响因子: 5.4
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