Amna Zar, Shahad A Al-Amri, Abdelrahman A Karen, Albara S Elkhalaf, Almaha M Almalki, Aysha M Abdulrahman, Mashael H Al-Framarzi, Giridhara Rathnaiah Babu, Angham Ibrahim Tartour
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We used Stata-18 for logistic regression to estimate the adjusted odds ratio (AOR) of the association between PTE and neurodevelopmental delay, adjusting for socioeconomic status, maternal age, and prenatal alcohol exposure. Additionally, we explored the mediation effects of birthweight.</p><p><strong>Results: </strong>Active maternal smoking during pregnancy was associated with 84% higher odds of cognitive delay (AOR=1.84; 95% CI 1.25-2.7), 2-fold higher odds of language delay (AOR=2.04; 95% CI 1.49-2.8), and 16% higher odds of motor delay (OR=1.16; 95% CI 0.76-1.78) compared to children whose mothers did not smoke during pregnancy. However, adjusted models showed that SHS exposure did not affect the three domains. Additionally, mediation analysis revealed that birthweight partially mediated the negative effect of maternal smoking on cognitive function, with a natural indirect effect of -0.08 (95% CI: -0.16 - -0.01; p=0.028) and a marginal total effect of -0.81 (95% CI: -1.20 - -0.43; p=0.0001), indicating both direct and indirect pathways of influence.</p><p><strong>Conclusions: </strong>Our study supports the growing evidence linking PTE to cognitive delay. 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引用次数: 0
摘要
前言：我们旨在探讨孕妇产前烟草暴露（PTE）与婴幼儿神经发育之间的关系。我们使用环境对儿童健康结果的影响（ECHO）进行了一项研究。方法：我们纳入了1970名母亲和孩子年龄在1-42个月的婴儿。PTE通过母亲主动吸烟和二手烟（SHS）暴露的自我报告来测量。使用Bayley-III评估神经发育，重点是认知、运动和语言领域。延迟定义为综合评分≤85分。我们使用Stata-18进行逻辑回归，以估计PTE与神经发育迟缓之间关联的调整优势比（AOR），调整了社会经济地位、母亲年龄和产前酒精暴露。此外，我们还探讨了出生体重的中介作用。结果：与母亲在怀孕期间不吸烟的孩子相比，母亲在怀孕期间积极吸烟与认知延迟的几率高84% (AOR=1.84; 95% CI 1.25-2.7)，语言延迟的几率高2倍（AOR=2.04; 95% CI 1.49-2.8），运动延迟的几率高16% （OR=1.16; 95% CI 0.76-1.78）相关。然而，调整后的模型显示，SHS暴露对这三个领域没有影响。此外，中介分析显示，出生体重部分介导了母亲吸烟对认知功能的负面影响，自然间接效应为-0.08 (95% CI: -0.16 - -0.01; p=0.028)，边际总效应为-0.81 (95% CI: -1.20 - -0.43; p=0.0001)，表明既有直接影响途径，也有间接影响途径。结论：我们的研究支持越来越多的证据表明PTE与认知延迟有关。此外，我们的研究结果强调了在怀孕期间优化产前戒烟干预措施以减轻儿童早期神经发育迟缓风险的重要性。
Association of prenatal tobacco exposure and child neurodevelopment: Analysis of the ECHO cohort study.
Introduction: We aimed to explore the association between exposure to prenatal tobacco exposure (PTE) in pregnant women and the neurodevelopment of infants and toddlers. We conducted a study using the Environmental Influences on Child Health Outcomes (ECHO)-wide cohort dataset.
Methods: We included 1970 mother-child dyads with children aged 1-42 months from the ECHO-wide cohorts. PTE was measured via self-reported active maternal smoking and secondhand smoke (SHS) exposure. Neurodevelopment was assessed using the Bayley-III, focusing on cognitive, motor, and language domains. Delay was defined as a composite score ≤85. We used Stata-18 for logistic regression to estimate the adjusted odds ratio (AOR) of the association between PTE and neurodevelopmental delay, adjusting for socioeconomic status, maternal age, and prenatal alcohol exposure. Additionally, we explored the mediation effects of birthweight.
Results: Active maternal smoking during pregnancy was associated with 84% higher odds of cognitive delay (AOR=1.84; 95% CI 1.25-2.7), 2-fold higher odds of language delay (AOR=2.04; 95% CI 1.49-2.8), and 16% higher odds of motor delay (OR=1.16; 95% CI 0.76-1.78) compared to children whose mothers did not smoke during pregnancy. However, adjusted models showed that SHS exposure did not affect the three domains. Additionally, mediation analysis revealed that birthweight partially mediated the negative effect of maternal smoking on cognitive function, with a natural indirect effect of -0.08 (95% CI: -0.16 - -0.01; p=0.028) and a marginal total effect of -0.81 (95% CI: -1.20 - -0.43; p=0.0001), indicating both direct and indirect pathways of influence.
Conclusions: Our study supports the growing evidence linking PTE to cognitive delay. Moreover, our findings underscore the importance of optimizing prenatal smoking cessation interventions during pregnancy to mitigate the risk of neurodevelopmental delay in early childhood.
期刊介绍：
Tobacco Induced Diseases encompasses all aspects of research related to the prevention and control of tobacco use at a global level. Preventing diseases attributable to tobacco is only one aspect of the journal, whose overall scope is to provide a forum for the publication of research articles that can contribute to reducing the burden of tobacco induced diseases globally. To address this epidemic we believe that there must be an avenue for the publication of research/policy activities on tobacco control initiatives that may be very important at a regional and national level. This approach provides a very important "hands on" service to the tobacco control community at a global scale - as common problems have common solutions. Hence, we see ourselves as "connectors" within this global community.
The journal hence encourages the submission of articles from all medical, biological and psychosocial disciplines, ranging from medical and dental clinicians, through health professionals to basic biomedical and clinical scientists.
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