Endocrine disruptors and the menstrual cycle
Endocrine disruptors have various effects on the menstrual cycle and fertility, with the effects depending on the type of disruptor.
For example, the pesticide DDT has been associated with reduced progesterone levels and a shorter luteal phase in women, of approximately 1.5 days for the highest DDT exposure [8]. No matter how well you take your best food supplement to get pregnant, acting on one's environment is the first lever.
One study showed that women with high serum DDT levels experienced an earlier onset of menopause, by 5.7 years [9].
Furthermore, one study also found that exposure to TCDD (the most toxic dioxin) was associated with a longer time to pregnancy and infertility [10].
Overall, they tend to promote a hormonal imbalance.
Endocrine disruptors and PCOS
Polycystic ovary syndrome (PCOS) is a disorder encompassing a broad spectrum of conditions affecting the hormonal, metabolic and reproductive spheres.
Endocrine disruption by environmental chemicals may indeed contribute to the pathogenesis of PCOS. It is plausible that in utero exposure of female human foetuses to androgenic endocrine-disrupting chemicals could lead to PCOS in adulthood.
Other pathways may be involved in the endocrine disruption of PCOS. Women with PCOS have higher levels of BPA (Bisphenol A, found in food packaging and which contaminates food) [11], and the increase in testosterone observed in these women is consistent with reduced BPA elimination [12]. Although exposures in adulthood do not necessarily imply earlier life exposures, there are data demonstrating BPA levels nearly 5 times higher in amniotic fluid compared to other bodily fluids, suggesting significant prenatal exposure [13].
Endocrine disruptors and ovarian insufficiency
Premature ovarian insufficiency (cessation of normal ovarian function before the age of 40) occurs in approximately 1% of women of reproductive age [14].
As the total pool of ovarian follicles is established before birth in humans, anything that interferes with this, leading to a reduction in ovarian reserve, may lead to premature ovarian insufficiency.
Exposure of mice to BPA, both in adulthood [15] and in utero [16], resulted in damage to oocytes.
Currently, there are no data on in utero or adult BPA exposure in humans, but the possibility that similarities exist is likely.
Exposure of rats to TCDD (the most toxic dioxin) in utero and throughout their reproductive life results in dose-dependent deterioration of reproductive cells, likely due to direct effects on ovarian function [17]. TCDD also disrupts the LH hormone and its stimulation by FSH [18].
Endocrine disruptors and fibroid risk
Uterine leiomyomas (fibroids) are benign smooth muscle tumours of the myometrium that can cause significant morbidity in women, including menorrhagia, abdominal pain, pelvic prolapse, infertility and miscarriage. The greatest risk factor in adult women is prolonged exposure to unblocked oestrogens.
For example, studies show that bisphenol A and phthalates increase the risk and severity of fibroids [19].
The link between endocrine disruptors and endometriosis
Theendometriosis is an oestrogen-dependent gynaecological disorder most commonly associated with pelvic pain and, in some cases, infertility.
One study found that exposure of adult monkeys to TCDD promotes the growth and survival of endometriosis lesions, indicating that this endocrine disruptor is involved in the progression, and possibly the pathogenesis, of this condition [20]. Studies in mice have also demonstrated this link [21].
There are also findings regarding phthalate levels in plasma and endometriosis. For example, researchers found elevated plasma phthalate concentrations in women with endometriosis [22].
An increased risk of breast cancer
A hypothesis has been put forward suggesting that the significant increase in breast cancer incidence observed in the industrialised world over the past 50 years may be due to exposure to hormonally active chemicals, particularly xenoestrogens [23].
Studies that measured exposure several years before cancer diagnosis found a positive association between breast cancer and chemical exposure to toxaphene [24] and DDT [25]. In particular, the study established a link between DDT and an increased risk of breast cancer when exposure was measured before the age of 14. This study used samples collected before the ban on DDT for agricultural purposes and therefore represents higher exposures than those measured today, as traces of DDT are still found in soils and water, and therefore in food.
In animals exposed to BPA perinatally, a significant increase in progesterone receptor-positive (PR+) cells is also observed at puberty (PR+ cancer is a form of breast cancer). In rats, foetal exposure to BPA multiplies the number of pre-cancerous lesions by three or four, an effect also observed at puberty and during adult life [26].
