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 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.

Transcriptional profiling of long noncoding RNAs and their target transcripts in ovarian cortical tissues from women with normal menstrual cycles and primary ovarian insufficiency

“…These processes are likely associated with our modern lifestyle, including the use of pesticides, cosmetics, additives in food, as well as the use of plastics. These results are consistent with the notion that the increased incidence of infertility observed in recent years is associated with the environment and our modern lifestyle (Vabre et al, ).…”

Novel inactivating mutations in the FSH receptor cause premature ovarian insufficiency with resistant ovary syndrome

“…Most POI cases are categorized into two forms: syndromic or non-syndromic POI (Lacombe et al, 2006). In addition to genetic causes, other aspects, such as autoimmunity, environmental factors and iatrogenic (chemotherapy and pelvic surgery) factors, contribute significantly to POI (Goswami and Conway, 2005;Vabre et al, 2017).…”

Endocrine Disruption by Mixtures in Topical Consumer Products

“…Similarly, some EDCs were linked to decreased fertility and diminished ovarian reserves in women [30][31][32][33][34]. Animal studies confirmed that EDC exposure can affect mammary gland and uterine development, both in terms of timing and in terms of morphological changes and in silico analyses contributed to predict the mechanics behind this [16,35,36].…”