Association of adverse prenatal exposure burden with child psychopathology in the Adolescent Brain Cognitive Development (ABCD) Study.

Association of adverse prenatal exposure burden with child psychopathology in the Adolescent Brain Cognitive Development (ABCD) Study.
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DOI:
10.1371/journal.pone.0250235
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发表时间:
2021
期刊:
影响因子:
3.7
通讯作者:
Dunn EC
Dunn EC
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Roffman JL;Sipahi ED;Dowling KF;Hughes DE;Hopkinson CE;Lee H;Eryilmaz H;Cohen LS;Gilman J;Doyle AE;Dunn EC

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许多不利的产前暴露已个别与精神疾病的风险在后代。然而,这类接触经常同时发生,引起了对其累积影响的疑问。我们评估了累积不良产前暴露负担对学龄儿童精神病理学风险的影响。使用美国的基线调查-基于青少年大脑和认知发展(ABCD)研究(来自21个地点的7,898名9-10岁的非收养、无关儿童及其主要照顾者),我们回顾性地检查了8例产前不良暴露与所有人报告的儿童行为量表(CBCL)总分和子量表评分的关系。我们还评估了这些因素对CBCL总数的累积效应,作为一个连续的指标,以及对临床显著精神病理学(CBCL总数≥60)的几率的累积效应,在初始集和一个单独的ABCD样本中,包括额外的696对兄弟姐妹。在调整14个人口统计学和环境协变量之前和之后进行分析。在最低限度和完全调整的模型中,6种暴露(计划外妊娠;母亲在妊娠早期使用酒精、大麻和烟草;妊娠并发症;和出生并发症)与CBCL总分显著但小幅增加独立相关。在这6种药物中,没有一种药物本身增加了越过临床显著症状阈值的几率。然而,超过该阈值的几率在2次暴露时变得显著(OR = 1.86,95% CI 1.47-2.36),并随每个暴露水平线性增加(OR = 1.39,95% CI 1.31-1.47),≥4次暴露与无暴露相比高达3.53倍。在兄弟姐妹之间的验证性分析中观察到类似的效果。在兄弟姐妹对,更大的不一致性暴露负荷与更大的CBCL总差异,表明结果没有混淆未测量的家庭水平的影响。暴露于多种常见的不良产前事件的儿童在9-10岁时表现出广泛的、临床显著的精神病理学的剂量依赖性增加。需要进行充分的前瞻性研究来证实和阐述这种模式。
Numerous adverse prenatal exposures have been individually associated with risk for psychiatric illness in the offspring. However, such exposures frequently co-occur, raising questions about their cumulative impact. We evaluated effects of cumulative adverse prenatal exposure burden on psychopathology risk in school-aged children. Using baseline surveys from the U.S.-based Adolescent Brain and Cognitive Development (ABCD) Study (7,898 non-adopted, unrelated children from 21 sites, age 9–10, and their primary caregivers), we examined 8 retrospectively-reported adverse prenatal exposures in relation to caregiver-reported total and subscale Child Behavior Checklist (CBCL) scores. We also assessed cumulative effects of these factors on CBCL total as a continuous measure, as well as on odds of clinically significant psychopathology (CBCL total ≥60), in both the initial set and a separate ABCD sample comprising an additional 696 sibling pairs. Analyses were conducted before and after adjustment for 14 demographic and environmental covariates. In minimally and fully adjusted models, 6 exposures (unplanned pregnancy; maternal alcohol, marijuana, and tobacco use early in pregnancy; pregnancy complications; and birth complications) independently associated with significant but small increases in CBCL total score. Among these 6, none increased the odds of crossing the threshold for clinically significant symptoms by itself. However, odds of exceeding this threshold became significant with 2 exposures (OR = 1.86, 95% CI 1.47–2.36), and increased linearly with each level of exposure (OR = 1.39, 95% CI 1.31–1.47), up to 3.53-fold for ≥4 exposures versus none. Similar effects were observed in confirmatory analysis among siblings. Within sibling pairs, greater discordance for exposure load associated with greater CBCL total differences, suggesting that results were not confounded by unmeasured family-level effects. Children exposed to multiple common, adverse prenatal events showed dose-dependent increases in broad, clinically significant psychopathology at age 9–10. Fully prospective studies are needed to confirm and elaborate upon this pattern.
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