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Environ Health. 2017 Apr 7;16(1):37. doi: 10.1186/s12940-017-0242-4.

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

Author information

1
Médecine de la Reproduction, CHU de Toulouse, Hôpital Paule de Viguier, 330 avenue de Grande Bretagne, F-31059, Toulouse Cedex, France.
2
Université de Toulouse; UPS; Groupe de Recherche en Fertilité Humaine (EA 3694, Human Fertility Research Group), F-31059, Toulouse, France.
3
Institut National de Recherche Agronomique, Unité Mixte de Recherche 1331, Toxalim, Research Center in Food Toxicology, F-31027, Toulouse, France.
4
Université de Toulouse, Institut National Polytechnique de Toulouse, Ecole Nationale Vétérinaire de Toulouse, Ecole d'Ingénieurs de Purpan, Université Paul Sabatier, F-31076, Toulouse, France.
5
Médecine de la Reproduction, CHU de Toulouse, Hôpital Paule de Viguier, 330 avenue de Grande Bretagne, F-31059, Toulouse Cedex, France. parinaud.j@chu-toulouse.fr.
6
Université de Toulouse; UPS; Groupe de Recherche en Fertilité Humaine (EA 3694, Human Fertility Research Group), F-31059, Toulouse, France. parinaud.j@chu-toulouse.fr.

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. 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.

KEYWORDS:

Environment; Fertility; Ovarian reserve; Pollutants; Premature ovarian insufficiency

PMID:
28388912
PMCID:
PMC5384040
DOI:
10.1186/s12940-017-0242-4
[Indexed for MEDLINE]
Free PMC Article

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