Abstract
BackgroundThe association between exposure to secondhand smoke (SHS) during pregnancy and a child’s neurodevelopment has not been established yet. We explored the association between prenatal exposure to SHS and neurodevelopment at 24 months of age considering genetic polymorphism and breastfeeding in 720 mothers and their offspring enrolled in the Korean multicenter birth cohort study (Mothers and Children Environmental Health, MOCEH).MethodsWe quantified urine cotinine concentrations in mothers once from 12th to 20th gestational weeks and excluded those whose urine cotinine levels exceeded 42.7 ng/ml to represent SHS exposure in early pregnancy. Mental developmental index (MDI) and psychomotor developmental index (PDI) values were measured using the Korean version of the Bayley Scales of Infant Development II (K-BSID-II) at 24 months of age. A general linear model was used to assess the relationship between maternal urinary cotinine level and neurodevelopment.ResultsMDI scores were inversely associated with cotinine [β = − 2.73; 95% confidence interval (CI): − 5.32 to − 0.15] in children whose mothers had early pregnancy urinary cotinine levels >1.90 ng/ml. No association was evident in children whose mothers had cotinine levels ≤1.90 ng/ml. This negative association was more pronounced in children whose mothers had both Glutathione S-transferases mu 1 (GSTM1) and theta 1 (GSTT1) null type [β = − 5.78; 95% CI: -10.69 to − 0.87], but not in children whose mothers had any present type of GSTM1/GSTT1 [β = − 1.64; 95% CI: -4.79 to 1.52]. The association was no longer significant when children received breast milk exclusively for up to 6 months [β = − 0.24; 95% CI: -4.69 to 4.20] compared to others [β = − 3.75; 95% CI: -7.51 to 0.00]. No significant association was found for PDI.ConclusionsMaternal exposure to SHS during pregnancy may result in delayed MDI in early childhood. This effect might be modified by genetic polymorphism and breastfeeding behavior.
Highlights
The association between exposure to secondhand smoke (SHS) during pregnancy and a child’s neurodevelopment has not been established yet
We further excluded 28 children whose mothers were considered as active smokers because their urine cotinine levels exceeded 42.7 ng/ml
The significance of this negative association disappeared in infants whose mothers had high cotinine levels when infants received breastmilk exclusively up to 6 months of age (β = − 0.24, 95% confidence interval (CI): -4.69 to 4.20)
Summary
The association between exposure to secondhand smoke (SHS) during pregnancy and a child’s neurodevelopment has not been established yet. World Health Organization (WHO) has recently reported that environmental risks including SHS take lives of 1.7 million children under 5 years of age every year [2]. Harmful exposure to these environmental risks could begin in the mother’s womb and affect fetal development. It is well known that SHS exposure brings about almost the same adverse health outcomes as active smoking [3]. Tobacco smoke contains over 7000 chemicals including nicotine, polycyclic aromatic hydrocarbons (PAHs), aromatic amines, and carbon monoxide Placental passage of these environmental toxicants might affect prenatal nervous system development. Measure of cotinine in hair, blood, and urine permits the assessment of SHS exposure or active smoking
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