**1. Introduction**

In the human, female germ cells develop during the first trimester of pregnancy, whereas primordial follicles develop between the second and third trimesters. Females are born with an entire lifetime supply of non‐proliferating oocytes (primordial follicles) that survive for ∼50 years [1]. Folliculogenesis is the process by which immature primordial follicles develop into preovulatory follicles (Graafian follicles). More than 99% of follicles never enter the preovulatory stage; instead, they undergo atresia through cell apoptosis. After ovulation, granulosa and theca cells undergo luteinisation and develop into the corpus luteum (CL). Folliculogenesis and oocyte health depend on ovarian and systemic hormones.

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The cycling ovary comprises follicles and the CL. During steroidogenesis, antral follicles produce oestrogens [principally 17β‐oestradiol (E<sup>2</sup> )] from androgens [androstenedione (A4) and testosterone (T)], whereas the CL produces progesterone (P<sup>4</sup> ). This balance can be disrupted by altering the concentrations of oestrogen, androgen and/or P<sup>4</sup> or by affect‐ ing the expression of steroid hormone receptors. The ovarian steroid hormone receptors include those for oestrogen (ER), androgen (AR) and P<sup>4</sup> (PR), as well as those for luteinis‐ ing hormone (LH) and follicle‐stimulating hormone (FSH). The endocrine system is dis‐ rupted when a hormone can no longer bind its receptor due to a disruption in hormone synthesis or receptor binding (**Figure 1**). Additionally, a disruption in folliculogenesis or CL formation can lead to reproductive disturbances, such as aneuploidy, anovulation, decreased fertility, polycystic ovary syndrome (PCOS) and premature ovarian failure (POF). The overall damage to the ovary and its effects on fertility depends on the type of follicles affected [2].

Hormonal disturbances also underlie ovarian carcinogenesis and oestrogens, androgens, P<sup>4</sup> , LH and FSH have been proposed to promote ovarian cancer development [3]. Depending on the cellular origin of the tumour, ovarian cancer can be classified as epithelial, stromal or germinal, with each tumour possessing different histopathological features and clinical outcomes (**Figure 2**). Epithelial cell tumours account for ∼80–90% of ovarian malignancies, whereas stromal tumours account for ∼8%. The most frequently diagnosed type of stromal tumour is the granulosa cell tumour (GCT).

Previous studies show correlations between women working in graphics and printing indus‐ tries and increased risk of ovarian cancer [4], as well as between women working in similar industries and ovarian cancer mortality [5]. The increased incidence of ovarian cancers cannot be explained by genetic factors. We believe that environmental factors, such as toxic chemi‐ cals, can cause ovarian cancer, but it is very difficult to prove cause and effect.

**Figure 1.** Ovarian steroidogenic enzymes and steroid hormone receptors are targets of endocrine disruption. Oestrogen receptor (ER), androgen receptor (AR) and progesterone receptor (PR), luteinising hormone receptor (LHR) and follicle‐ stimulating hormone receptor (FSHR) and dehydroepiandrosterone (DHEA).

**Figure 2.** Different types of ovarian cancer. Stars indicate the developmental origins of the tumour.
