Abstract
Primary ovarian insufficiency is a cause of infertility that affects about 1% of women under 40 years old, and is considered as idiopathic in 75% of cases. This review aims to carry out a critical synthesis of the knowledge of the chemical agents likely to affect follicular stock in humans and / or animals, by direct toxicity to follicles, or by increasing their recruitments. For the majority of toxic agents, only experimental data are currently available. We propose a strategy to encourage progress in identifying occupational factors responsible for premature ovarian failure.
Highlights
A definition of endocrine disruptors Women may be exposed to gonadal toxicity when they are in contact with endocrine disrupting chemicals present in food, water, air, or products they use at home or at work
This paper presents the current knowledge on the correlation between exposure to toxic agents and ovarian reserve involvement leading to primary ovarian insufficiency and discusses recommendations to prevent exposure to endocrine disruptors and safeguard gonadal function
Most significant studies selected A prospective study examined the associations between the levels of eight urinary phthalate metabolites in 599 couples submitted to in vitro fertilization (IVF)
Summary
A definition of endocrine disruptors Women may be exposed to gonadal toxicity when they are in contact with endocrine disrupting chemicals present in food, water, air, or products they use at home or at work. Some chemicals are known to affect hormones critical for female endocrine and reproductive development (Wang et al, 2016). Compounds known as endocrine disruptors can mimic or antagonize the activity and change the signaling of steroid hormones, contributing to adverse ovarian function outcomes (Wang et al, 2016). Adequate ovarian cycle function relies on multiple factors, including gonadal exposure to potentially toxic environmental products. This paper presents the current knowledge on the correlation between exposure to toxic agents and ovarian reserve involvement leading to primary ovarian insufficiency and discusses recommendations to prevent exposure to endocrine disruptors and safeguard gonadal function
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