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Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data
BACKGROUND: Because only 25% of cases of premature ovarian insufficiency (POI) have a known etiology, the aim of this review was to summarize the associations and mechanisms of the impact of the environment on this pathology. MAIN BODY OF THE ABSTRACT: Eligible studies were selected from an electron...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384040/ https://www.ncbi.nlm.nih.gov/pubmed/28388912 http://dx.doi.org/10.1186/s12940-017-0242-4 |
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author | Vabre, Pauline Gatimel, Nicolas Moreau, Jessika Gayrard, Véronique Picard-Hagen, Nicole Parinaud, Jean Leandri, Roger D. |
author_facet | Vabre, Pauline Gatimel, Nicolas Moreau, Jessika Gayrard, Véronique Picard-Hagen, Nicole Parinaud, Jean Leandri, Roger D. |
author_sort | Vabre, Pauline |
collection | PubMed |
description | BACKGROUND: Because only 25% of cases of premature ovarian insufficiency (POI) have a known etiology, the aim of this review was to summarize the associations and mechanisms of the impact of the environment on this pathology. MAIN BODY OF THE ABSTRACT: Eligible studies were selected from an electronic literature search from the PUBMED database from January 2000 to February 2016 and associated references in published studies. Search terms included ovary, follicle, oocyte, endocrine disruptor, environmental exposure, occupational exposure, environmental contaminant, pesticide, polyaromatic hydrocarbon, polychlorinated biphenyl PCB, phenol, bisphenol, flame retardant, phthalate, dioxin, phytoestrogen, tobacco, smoke, cigarette, cosmetic, xenobiotic. The literature search was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We have included the human and animal studies corresponding to the terms and published in English. We have excluded articles that included results that did not concern ovarian pathology and those focused on ovarian cancer, polycystic ovary syndrome, endometriosis or precocious puberty. We have also excluded genetic, auto-immune or iatrogenic causes from our analysis. Finally, we have excluded animal data that does not concern mammals and studies based on results from in vitro culture. Data have been grouped according to the studied pollutants in order to synthetize their impact on follicular development and follicular atresia and the molecular pathways involved. Ninety-seven studies appeared to be eligible and were included in the present study, even though few directly address POI. Phthalates, bisphenol A, pesticides and tobacco were the most reported substances having a negative impact on ovarian function with an increased follicular depletion leading to an earlier age of menopause onset. These effects were found when exposure occured at different times throughout the lifetime from the prenatal to the adult period, possibly due to different mechanisms. The main mechanism seemed to be an increase in atresia of pre-antral follicles. CONCLUSION: Environmental pollutants are probably a cause of POI. Health officials and the general public must be aware of this environmental effect in order to implement individual and global preventive actions. |
format | Online Article Text |
id | pubmed-5384040 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-53840402017-04-12 Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data Vabre, Pauline Gatimel, Nicolas Moreau, Jessika Gayrard, Véronique Picard-Hagen, Nicole Parinaud, Jean Leandri, Roger D. Environ Health Review BACKGROUND: Because only 25% of cases of premature ovarian insufficiency (POI) have a known etiology, the aim of this review was to summarize the associations and mechanisms of the impact of the environment on this pathology. MAIN BODY OF THE ABSTRACT: Eligible studies were selected from an electronic literature search from the PUBMED database from January 2000 to February 2016 and associated references in published studies. Search terms included ovary, follicle, oocyte, endocrine disruptor, environmental exposure, occupational exposure, environmental contaminant, pesticide, polyaromatic hydrocarbon, polychlorinated biphenyl PCB, phenol, bisphenol, flame retardant, phthalate, dioxin, phytoestrogen, tobacco, smoke, cigarette, cosmetic, xenobiotic. The literature search was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We have included the human and animal studies corresponding to the terms and published in English. We have excluded articles that included results that did not concern ovarian pathology and those focused on ovarian cancer, polycystic ovary syndrome, endometriosis or precocious puberty. We have also excluded genetic, auto-immune or iatrogenic causes from our analysis. Finally, we have excluded animal data that does not concern mammals and studies based on results from in vitro culture. Data have been grouped according to the studied pollutants in order to synthetize their impact on follicular development and follicular atresia and the molecular pathways involved. Ninety-seven studies appeared to be eligible and were included in the present study, even though few directly address POI. Phthalates, bisphenol A, pesticides and tobacco were the most reported substances having a negative impact on ovarian function with an increased follicular depletion leading to an earlier age of menopause onset. These effects were found when exposure occured at different times throughout the lifetime from the prenatal to the adult period, possibly due to different mechanisms. The main mechanism seemed to be an increase in atresia of pre-antral follicles. CONCLUSION: Environmental pollutants are probably a cause of POI. Health officials and the general public must be aware of this environmental effect in order to implement individual and global preventive actions. BioMed Central 2017-04-07 /pmc/articles/PMC5384040/ /pubmed/28388912 http://dx.doi.org/10.1186/s12940-017-0242-4 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Review Vabre, Pauline Gatimel, Nicolas Moreau, Jessika Gayrard, Véronique Picard-Hagen, Nicole Parinaud, Jean Leandri, Roger D. Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data |
title | Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data |
title_full | Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data |
title_fullStr | Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data |
title_full_unstemmed | Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data |
title_short | Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data |
title_sort | environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384040/ https://www.ncbi.nlm.nih.gov/pubmed/28388912 http://dx.doi.org/10.1186/s12940-017-0242-4 |
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