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Air pollution, maternal hypertensive disorders, and preterm birth
BACKGROUND: Air pollution has been associated with hypertension and preterm birth. We examined if prenatal exposure to air pollutants was associated with gestational hypertension and if its association with preterm birth was modified by maternal hypertension. METHODS: Data were from birth certificat...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer Health
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7015251/ https://www.ncbi.nlm.nih.gov/pubmed/32051927 http://dx.doi.org/10.1097/EE9.0000000000000062 |
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author | Weber, Kari A. Yang, Wei Lurmann, Frederick Hammond, S. Katharine Shaw, Gary M. Padula, Amy M. |
author_facet | Weber, Kari A. Yang, Wei Lurmann, Frederick Hammond, S. Katharine Shaw, Gary M. Padula, Amy M. |
author_sort | Weber, Kari A. |
collection | PubMed |
description | BACKGROUND: Air pollution has been associated with hypertension and preterm birth. We examined if prenatal exposure to air pollutants was associated with gestational hypertension and if its association with preterm birth was modified by maternal hypertension. METHODS: Data were from birth certificates and hospital discharge records of 252,205 women in San Joaquin Valley of California from 2000 to 2006. Air quality data were assigned from 24-hour averages of nitrogen dioxide (NO(2)), particulate matter <10µm (PM(10)) and <2.5µm (PM(2.5)), and carbon monoxide (CO) for different averaging periods over pregnancy. We estimated odds of preterm birth and multiplicative interaction between each pollutant and hypertensive disorder. RESULTS: Among normotensive women, odds of preterm birth were slightly higher for higher exposure to all pollutants over the entire pregnancy. Patterns were similar among women with a hypertensive disorder. Among 32–36 week births, there was effect modification for exposure to NO(2) and CO during the first trimester with higher odds among hypertensive women, and PM(2.5) and CO during the last 6 weeks with higher odds among normotensive women. For 28–31 week births, there was effect modification by hypertensive status for PM(10) exposure for the entire pregnancy, first, and second trimester with hypertensive women consistently having lower odds of preterm birth than normotensive. CONCLUSION: There was some evidence of effect modification in the direction counter to our hypothesis for exposure to PM(10) and early preterm birth, and CO and PM(2.5) at the end of pregnancy, but overall, hypertension did not modify the relationship between pollution and preterm birth. |
format | Online Article Text |
id | pubmed-7015251 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Wolters Kluwer Health |
record_format | MEDLINE/PubMed |
spelling | pubmed-70152512020-10-01 Air pollution, maternal hypertensive disorders, and preterm birth Weber, Kari A. Yang, Wei Lurmann, Frederick Hammond, S. Katharine Shaw, Gary M. Padula, Amy M. Environ Epidemiol Original Research BACKGROUND: Air pollution has been associated with hypertension and preterm birth. We examined if prenatal exposure to air pollutants was associated with gestational hypertension and if its association with preterm birth was modified by maternal hypertension. METHODS: Data were from birth certificates and hospital discharge records of 252,205 women in San Joaquin Valley of California from 2000 to 2006. Air quality data were assigned from 24-hour averages of nitrogen dioxide (NO(2)), particulate matter <10µm (PM(10)) and <2.5µm (PM(2.5)), and carbon monoxide (CO) for different averaging periods over pregnancy. We estimated odds of preterm birth and multiplicative interaction between each pollutant and hypertensive disorder. RESULTS: Among normotensive women, odds of preterm birth were slightly higher for higher exposure to all pollutants over the entire pregnancy. Patterns were similar among women with a hypertensive disorder. Among 32–36 week births, there was effect modification for exposure to NO(2) and CO during the first trimester with higher odds among hypertensive women, and PM(2.5) and CO during the last 6 weeks with higher odds among normotensive women. For 28–31 week births, there was effect modification by hypertensive status for PM(10) exposure for the entire pregnancy, first, and second trimester with hypertensive women consistently having lower odds of preterm birth than normotensive. CONCLUSION: There was some evidence of effect modification in the direction counter to our hypothesis for exposure to PM(10) and early preterm birth, and CO and PM(2.5) at the end of pregnancy, but overall, hypertension did not modify the relationship between pollution and preterm birth. Wolters Kluwer Health 2019-08-29 /pmc/articles/PMC7015251/ /pubmed/32051927 http://dx.doi.org/10.1097/EE9.0000000000000062 Text en Copyright © 2019 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of Environmental Epidemiology. All rights reserved. This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY) (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Weber, Kari A. Yang, Wei Lurmann, Frederick Hammond, S. Katharine Shaw, Gary M. Padula, Amy M. Air pollution, maternal hypertensive disorders, and preterm birth |
title | Air pollution, maternal hypertensive disorders, and preterm birth |
title_full | Air pollution, maternal hypertensive disorders, and preterm birth |
title_fullStr | Air pollution, maternal hypertensive disorders, and preterm birth |
title_full_unstemmed | Air pollution, maternal hypertensive disorders, and preterm birth |
title_short | Air pollution, maternal hypertensive disorders, and preterm birth |
title_sort | air pollution, maternal hypertensive disorders, and preterm birth |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7015251/ https://www.ncbi.nlm.nih.gov/pubmed/32051927 http://dx.doi.org/10.1097/EE9.0000000000000062 |
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