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Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight
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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850398/ https://www.ncbi.nlm.nih.gov/pubmed/27126191 http://dx.doi.org/10.1038/srep24987 |
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author | Niu, Zhongzheng Xie, Chuanbo Wen, Xiaozhong Tian, Fuying Yuan, Shixin Jia, Deqin Chen, Wei-Qing |
author_facet | Niu, Zhongzheng Xie, Chuanbo Wen, Xiaozhong Tian, Fuying Yuan, Shixin Jia, Deqin Chen, Wei-Qing |
author_sort | Niu, Zhongzheng |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4850398 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-48503982016-05-05 Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight Niu, Zhongzheng Xie, Chuanbo Wen, Xiaozhong Tian, Fuying Yuan, Shixin Jia, Deqin Chen, Wei-Qing Sci Rep Article 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. Nature Publishing Group 2016-04-29 /pmc/articles/PMC4850398/ /pubmed/27126191 http://dx.doi.org/10.1038/srep24987 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Niu, Zhongzheng Xie, Chuanbo Wen, Xiaozhong Tian, Fuying Yuan, Shixin Jia, Deqin Chen, Wei-Qing Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight |
title | Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight |
title_full | Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight |
title_fullStr | Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight |
title_full_unstemmed | Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight |
title_short | Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight |
title_sort | potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850398/ https://www.ncbi.nlm.nih.gov/pubmed/27126191 http://dx.doi.org/10.1038/srep24987 |
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