Adgent Margaret A
ASPH Environmental Public Health Fellow, National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, Washington, DC 20460, USA.
Birth Defects Res B Dev Reprod Toxicol. 2006 Feb;77(1):69-85. doi: 10.1002/bdrb.20068.
Environmental tobacco smoke (ETS), containing the developmental neurotoxicant, nicotine, is a prevalent component of indoor air pollution. Despite a strong association with active maternal smoking and sudden infant death syndrome (SIDS), information on the risk of SIDS due to prenatal and postnatal ETS exposure is relatively inconsistent. This literature review begins with a discussion and critique of existing epidemiologic data pertaining to ETS and SIDS. It then explores the biologic plausibility of this association, with comparison of the known association between active maternal smoking and SIDS, by examining metabolic and placental transfer issues associated with nicotine, and the biologic responses and mechanisms that may follow exposure to nicotine. Evidence indicates that prenatal and postnatal exposures to nicotine do occur from ETS exposure, but that the level of exposure is often substantially less than levels induced by active maternal smoking. Nicotine also has the capacity to concentrate in the fetus, regardless of exposure source. Experimental animal studies show that various doses of nicotine are capable of affecting a neonate's response to hypoxic conditions, a process thought to be related to SIDS outcomes. Mechanisms contributing to deficient hypoxia response include the ability of nicotine to act as a cholinergic stimulant through nicotinic acetylcholine receptor (nAChR) binding. The need for future research to investigate nicotine exposure and effects from non-maternal tobacco smoke sources in mid to late gestation is emphasized, along with a need to discourage smoking around both pregnant women and infants.
环境烟草烟雾（ETS）含有发育神经毒物尼古丁，是室内空气污染的普遍成分。尽管与母亲主动吸烟和婴儿猝死综合征（SIDS）有很强的关联，但关于产前和产后接触ETS导致SIDS风险的信息相对不一致。这篇文献综述首先讨论和批判了与ETS和SIDS相关的现有流行病学数据。然后通过研究与尼古丁相关的代谢和胎盘转运问题，以及接触尼古丁后可能出现的生物学反应和机制，探讨这种关联的生物学合理性，并与母亲主动吸烟和SIDS之间已知的关联进行比较。证据表明，产前和产后确实会因接触ETS而接触尼古丁，但接触水平通常远低于母亲主动吸烟所导致的水平。无论接触来源如何，尼古丁都有在胎儿体内浓缩的能力。实验动物研究表明，不同剂量的尼古丁能够影响新生儿对缺氧状况的反应，这一过程被认为与SIDS结局有关。导致缺氧反应不足的机制包括尼古丁通过与烟碱型乙酰胆碱受体（nAChR）结合而作为胆碱能刺激剂发挥作用的能力。强调了未来研究调查妊娠中后期非母亲烟草烟雾来源的尼古丁接触及其影响的必要性，同时也需要劝阻在孕妇和婴儿周围吸烟。
