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Exposure to prenatal secondhand smoke and early neurodevelopment: Mothers and Childrens Environmental Health (MOCEH) study

Cited 13 time in Web of Science Cited 14 time in Scopus
Authors
Lee, Myeongjee; Ha, Mina; Hong, Yun-Chul; Park, Hyesook; Kim, Yangho; Kim, Eui-Jung; Kim, Yeni; Ha, Eunhee
Issue Date
2019-03-20
Publisher
BioMed Central
Citation
Environmental Health. 2019 Mar 20;18(1):22
Keywords
Secondhand smokeUrine cotinineInfant neurodevelopmentGenetic polymorphismBreastfeeding24 months
Abstract
Background
The association between exposure to secondhand smoke (SHS) during pregnancy and a childs 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.
ISSN
1476-069X
Language
English
URI
https://hdl.handle.net/10371/147215
DOI
https://doi.org/10.1186/s12940-019-0463-9
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Graduate School of Public Health (보건대학원)Dept. of Environmental Health (환경보건학과)Journal Papers (저널논문_환경보건학과)
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