**3. Female infertility**

EDCs are thought to affect women's menstrual cycle, estrogen deficiency, infertility, and are also associated with diseases such as polycystic ovary syndrome (PCOS) and endometriosis, spontaneous abortions, birth defects, endometriosis, breast cancer, premature ovarian failure [23, 25]. Female are at a greater risk than men, especially with the rise in environmental estrogens. However, since research on these exposures often tends to focus on male fertility, it is unlikely that EDCs will answer questions about female fertility [25, 81]. Because females are relatively sensitive to estrogens and are heavily exposed to environmental estrogens, women will also be most affected by EDCs. The origin of endocrine disruption hypothesis was related to exposure to estrogens. Literature data also show that long-term and combined exposure to environmental estrogens will have an impact on female fertility. Although it has long been known that female fertility is impaired by estrogen exposure, there are limited data on whether long-term low-dose exposure to environmental pollutants with weak estrogenic effect causes problems such as infertility in women [81].

There is little epidemiological information about trends in female infertility. Data on the effects of EDCs on the female reproductive system and fertility are insufficient. However, it has been suggested that there is a relationship between exposure to EDCs and their long-term effects [7, 81].

#### *Endocrine Disruptors and Infertility DOI: http://dx.doi.org/10.5772/intechopen.104403*

The most common direct or indirect causes of female infertility are endocrine problems. EDCs alter endocrine function through various mechanisms. One of these mechanisms is that these substances directly bind to estrogen receptors and increase aromatase activity, thereby increasing estrogen sensitivity. Another mechanism is that EDCs indirectly lead to an increase in endogenous estrogen production and exert their effects through both receptor-dependent and receptor-independent mechanisms through their effects on gonadotropin-releasing hormone. Both mechanisms result in altered ovarian function by altering endocrine signaling with several processes in ovary and the other reproductive organs [3, 33, 82].

EDCs act on female reproductive hormones and receptors through estrogenic, anti-estrogenic, androgenic, and anti-androgenic mechanisms [23, 25]. Estradiol (E2) plays a very important role in female fertility. The functions of estrogens are mediated primarily by two estrogen receptors: ESR1 (ERalfa) and ESR2 (ERbeta), both of which are widely expressed in cells throughout the female reproductive system [83]. Most EDCs interfere with female reproductive function by activating or inhibiting ESRs. EDCs have different binding affinities to ESRs and therefore exert different effects in ovary. In ovary, the main function of ESR1 is to regulate steroidogenesis in theca cells. On the other hand, the function of ESR2 is granulosa cell differentiation toward FSH, follicle maturation, and ovulation. Many EDCs interfere with female reproductive function by activating or inhibiting ESRs. Different EDCs exert different effects in the ovary depending on their binding affinity to different ESRs [82, 83].

The sensitivity of the developing female reproductive system to estrogens raises the question of whether exposure to EDCs with estrogenic activity (such as heavy metals, pesticides, and cosmetics) can affect the female fertility [81].
