Association of prenatal tobacco exposure and child neurodevelopment: Analysis of the ECHO cohort study.

Abstract

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. 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. 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. 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.