Abstract

Background/ObjectiveNeurodevelopment of infants have been associated with exposure to secondhand smoke (SHS) and air pollution (AP), respectively. There has been very few previous studies of combined effect of AP and SHS on early neurodevelopment. We aim to investigate the combined effect of postnatal AP and SHS exposure on neurodevelopment of infants at 36 months of age.MethodsThis study is a part of the Mothers and Children Environmental Health (MOCEH) study, a Korean multi-center prospective birth cohort study initiated in 2006. We measured infants’ urinary cotinine at 24 months and 36 months of age to represent postnatal SHS exposure. PM2.5 (particulate matter<2.5 in diameter) level from conception was modelled using the Community Multiscale Air Quality Modeling. The exposure estimations of PM2.5 of each subject were assigned in district level. Infant’s mental developmental index (MDI) and psychomotor developmental index (PDI) were measured using the Bayley Scales of Infant Development at 36 months of age. General linear model was used to assess the relationship between combined exposure of PM2.5 and SHS and neurodevelopment.ResultsMDI score of 36 months aged infants was marginally associated with log-transformed urinary cotinine level at 24 months [β= -1.94, 95%confidence interval (CI): -3.92, 0.04] after adjusting for log-transformed urinary cotinine level at 36 months and PM2.5 level after birth. The association was statistically significant when the effect of PM2.5 level at early pregnancy was considered, β= -2.02 (95%CI: -4.01, -0.03). The effect was pronounced in the metropolitan city, β= -7.92 (95%CI: -13.15, -2.70). No association was found in PDI score.ConclusionsThese findings suggest that infants’ postnatal exposure to SHS combined with exposure to PM2.5 may result in delayed neurodevelopment in early childhood. Therefore, we should take care of both indoor and outdoor air pollution with regards to the neurodevelopment of infants.

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