Water and soil pollution as determinant of water and food quality/contamination and its impact on male fertility

Abstract

Over the past two decades, public health has focused on the identification of environmental chemical factors that are able to adversely affect hormonal function, known as endocrine disruptors (EDs). EDs mimic naturally occurring hormones like estrogens and androgens which can in turn interfere with the endocrine system. As a consequence, EDs affect human reproduction as well as post and pre-natal development. In fact, infants can be affected already at prenatal level due to maternal exposure to EDs. In particular, great attention has been given to those chemicals, or their metabolites, that have estrogenic properties or antagonistic effects on the activity of androgen or even inhibiting their production. These compounds have therefore the potential of interfering with important physiological processes, such as masculinization, morphological development of the urogenital system and secondary sexual traits. Animal and in vitro studies have supported the conclusion that endocrine-disrupting chemicals affect the hormone-dependent pathways responsible for male gonadal development, either through direct interaction with hormone receptors or via epigenetic and cell-cycle regulatory modes of action. In human populations, epidemiological studies have reported an overall decline of male fertility and an increased incidence of diseases or congenital malformations of the male reproductive system. The majority of studies point towards an association between exposure to EDs and male and/or female reproductive system disorders, such as infertility, endometriosis, breast cancer, testicular cancer, poor sperm quality and/or function. Despite promising discoveries, a causal relationship between the reproductive disorders and exposure to specific toxicants has yet to be established, due to the complexity of the clinical protocols used, the degree of occupational or environmental exposure, the determination of the variables measured and the sample size of the subjects examined. Despite the lack of consistency in the results of so many studies investigating endocrine-disrupting properties of many different classes of chemicals, the overall conclusion points toward a positive association between exposure to EDs and reproductive system. Future studies should focus on a uniform systems to examine human populations with regard to the exposure to specific EDs and the direct effect on the reproductive system.

Keywords: Endocrine disruptors; Infertility; Male health; Seminal parameters; Sexual development.

Fig. 1

Schematic representation of endocrine disruptors’ (EDs) effects on male fertility and the related mechanisms of toxicity. Results from both pre-clinical and clinical studies are summarized for each ED. If proposed effects are common to more EDs, they are reported together within black squares. Black arrows refer to stimulatory pathways. Red arrows with blunt ends represent inhibitory regulation. Hypotalamic-pituitary regulation of testicular function is impaired by most EDs (a). Within the testis, gonadotropins stimulates steroidogenesis in Leydig cells (b) and spermatogenesis in Sertoli cells (c). Overall, EDs disrupt endocrine function by reducing testosterone release or its activity on target tissues. In addition, EDs can reduce semen quality by directly impairing cell structure/viability or indirectly by interfering with hormonal patwhays. GnRH: Gonadotropin-releasing hormone; LH: Lutehinizing Hormone; FSH: Follicle-Stimulating Hormone; T: testosterone; AR: Androgen Receptor; FSHR: FSH Receptor; LHR: LH Receptor; E2: Estradiol; ROS: Reactive Oxygen Species; BTB: Blood-Testis Barrier; BPA: Bisphenol A; Ps: Phtalathes; Cd: Cadmium; Ops: Organophosphate pesticides; PFCs: Perfluoroalkyl Compounds