Developmental consequences of prenatal tobacco exposure
Developmental consequences of prenatal tobacco exposure
复制标题
DOI：
10.1097/wco.0b013e328326f6dc
复制
发表时间：
2009-04-01
影响因子：
4.8
通讯作者：
Day, Nancy L.
中科院分区：
文献类型：
--
作者：
Cornelius, Marie D.;Day, Nancy L.
回顾的目的本文回顾了2007年和2008年发表的，在新闻界，和会议记录的结果，连接在子宫内烟草暴露的后代的神经发育outcomes.Recent findingsPrenatal tobacco exposure（PTE）影响的语音处理，易怒和高张性水平，注意力水平，自我调节能力，需要处理，并在婴儿对新奇偏好的反应。在儿童早期，PTE效应主要表现为行为结果，包括活动和注意力不集中以及外化行为，包括行为障碍和反社会行为。在青少年中，PTE预示着注意力缺陷多动障碍、大脑皮层和白色物质结构的调节以及尼古丁成瘾的增加。几项研究发现PTE和遗传易感性（包括多巴胺转运蛋白、多巴胺能突触功能和单胺氧化酶途径）的调节作用。其他研究表明，环境和遗传因素可能是更重要的PTE.SummaryThe大多数研究回顾的直接致畸作用是前瞻性和烟草暴露量化生物。大多数证明了PTE和神经发育结果之间的直接关联。需要做更多的工作来研究多因素的影响。PTE对后代的影响似乎是由遗传变异，神经行为去抑制和性别缓和。
Purpose of reviewThis paper reviews results from published, in press, and conference proceedings from 2007 and 2008 that link in-utero tobacco exposure to neurodevelopmental outcomes in exposed offspring.Recent findingsPrenatal tobacco exposure (PTE) affected speech processing, levels of irritability and hypertonicity, attention levels, ability to self-regulate, need to be handled, and response to novelty preference in infants. In early childhood, PTE effects were mostly behavioral outcomes including activity and inattention and externalizing behaviors, including conduct disorder and antisocial behavior. In adolescents, PTE predicted increased attention deficit hyperactivity disorder, modulation of the cerebral cortex and white matter structure, and nicotine addiction. Several studies found moderating effects with PTE and genetic susceptibilities including dopamine transporter, serotonergic synaptic function, and monomine oxidase pathways. Other studies suggested that environmental and genetic factors might be more important than the direct teratological effects of PTE.SummaryThe majority of studies reviewed were prospective and tobacco exposure was quantified biologically. Most demonstrated a direct association between PTE and neurodevelopmental outcomes. More work is needed to examine multifactorial influences. Effects of PTE on the offspring appear to be moderated by genetic variability, neurobehavioral disinhibition, and sex.