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Exposure to prenatal secondhand smoke and early neurodevelopment: Mothers and Children's Environmental Health (MOCEH)
Myeongjee Lee1, Mina Ha2, Yun-Chul Hong3
1Department of Occupational and Environmental Medicine, School of Medicine, Ewha Womans University, Seoul, Republic of Korea.
Background:
The 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).
Methods:
We 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.
Results:
MDI 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.
Conclusions:
Maternal exposure to SHS during pregnancy may result in delayed MDI in early childhood. This effect might be modified by genetic polymorphism and breastfeeding behavior.