Abstract

It is well documented that maternal exposure to second-hand smoke (SHS) during pregnancy causes low birth weight (LBW), but its mechanism remains unknown. This study explored the potential pathways. We enrolled 195 pregnant women who delivered full-term LBW newborns, and 195 who delivered full-term normal birth weight newborns as the controls. After controlling for maternal age, education level, family income, pre-pregnant body mass index, newborn gender and gestational age, logistic regression analysis revealed that LBW was significantly and positively associated with maternal exposure to SHS during pregnancy, lower placental weight, TNF-α and IL-1β, and that SHS exposure was significantly associated with lower placental weight, TNF-α and IL-1β. Structural equation modelling identified two plausible pathways by which maternal exposure to SHS during pregnancy might cause LBW. First, SHS exposure induced the elevation of TNF-α, which might directly increase the risk of LBW by transmission across the placenta. Second, SHS exposure first increased maternal secretion of IL-1β and TNF-α, which then triggered the secretion of VCAM-1; both TNF-α and VCAM-1 were significantly associated with lower placental weight, thus increasing the risk of LBW. In conclusion, maternal exposure to SHS during pregnancy may lead to LBW through the potential pathways of maternal inflammation and lower placental weight.

Highlights

  • The structure and functioning of the placenta[17]

  • After controlling for potential confounders, maternal SHS exposure was significantly and positively associated with lower placental weight, increased maternal TNF-α and IL-1β

  • This study tested the hypothesis that maternal SHS exposure during pregnancy leads to full-term LBW through maternal inflammation and lower placental weight

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Summary

Introduction

The structure and functioning of the placenta[17]. Placental weight partially mediates the effects of prenatal factors such as pre-pregnancy obesity, gestational diabetes mellitus and excessive gestational weight gain on foetal growth[18]. Abnormal inflammatory markers have been found in the placentas of LBW cases[19]. To the best of our knowledge, there is no research that links the above evidence together to explore the plausible mechanisms. This study aimed to explore the potential pathways that integrate maternal inflammation and the placenta, which might explain the mechanism by which maternal exposure to SHS during pregnancy leads to LBW

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