Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data

Abstract 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 e...

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Main Authors: Pauline Vabre, Nicolas Gatimel, Jessika Moreau, Véronique Gayrard, Nicole Picard-Hagen, Jean Parinaud, Roger D. Leandri
Format: Article
Language:English
Published: BMC 2017-04-01
Series:Environmental Health
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12940-017-0242-4
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author Pauline Vabre
Nicolas Gatimel
Jessika Moreau
Véronique Gayrard
Nicole Picard-Hagen
Jean Parinaud
Roger D. Leandri
author_facet Pauline Vabre
Nicolas Gatimel
Jessika Moreau
Véronique Gayrard
Nicole Picard-Hagen
Jean Parinaud
Roger D. Leandri
author_sort Pauline Vabre
collection DOAJ
description Abstract 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.
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spelling doaj.art-4356bcb29ac944b0b7ce109d3674fae12022-12-22T00:43:45ZengBMCEnvironmental Health1476-069X2017-04-0116111810.1186/s12940-017-0242-4Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human dataPauline Vabre0Nicolas Gatimel1Jessika Moreau2Véronique Gayrard3Nicole Picard-Hagen4Jean Parinaud5Roger D. Leandri6Médecine de la Reproduction, CHU de Toulouse, Hôpital Paule de ViguierMédecine de la Reproduction, CHU de Toulouse, Hôpital Paule de ViguierMédecine de la Reproduction, CHU de Toulouse, Hôpital Paule de ViguierInstitut National de Recherche Agronomique, Unité Mixte de Recherche 1331, Toxalim, Research Center in Food ToxicologyInstitut National de Recherche Agronomique, Unité Mixte de Recherche 1331, Toxalim, Research Center in Food ToxicologyMédecine de la Reproduction, CHU de Toulouse, Hôpital Paule de ViguierMédecine de la Reproduction, CHU de Toulouse, Hôpital Paule de ViguierAbstract 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.http://link.springer.com/article/10.1186/s12940-017-0242-4Premature ovarian insufficiencyOvarian reserveEnvironmentPollutantsFertility
spellingShingle Pauline Vabre
Nicolas Gatimel
Jessika Moreau
Véronique Gayrard
Nicole Picard-Hagen
Jean Parinaud
Roger D. Leandri
Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data
Environmental Health
Premature ovarian insufficiency
Ovarian reserve
Environment
Pollutants
Fertility
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 Premature ovarian insufficiency
Ovarian reserve
Environment
Pollutants
Fertility
url http://link.springer.com/article/10.1186/s12940-017-0242-4
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