Ovarian cancer is the fifth most frequently occurring cancer among women and leading cause of gynecological cancer deaths in North America. Although the etiology of ovarian cancer is not clear, certain factors are implicated in the etiology of this disease, such as ovulation, gonadotropic and steroid hormones, germ cell depletion, oncogenes and tumor suppressor genes, growth factors, cytokines, and environmental agents. Family history of breast or ovarian cancer is a prominent risk factor for ovarian cancer, with 5–10% of ovarian cancers due to heritable risk. Reproductive factors such as age at menopause and infertility contribute to greater risk of ovarian cancer, whereas pregnancy, tubal ligation, and hysterectomy reduce risk. Oral contraceptive (OC) use has clearly been shown to be protective against ovarian cancer. In contrast, large epidemiologic studies found hormone replacement therapy (HRT) to be a greater risk factor for ovarian cancer. The marked influence of hormones and reproductive factors on ovarian cancer suggests that endocrine disrupters may impact risk; however, there is a notable lack of research in this area. Lifestyle factors such as cigarette smoking, obesity, and diet may affect ovarian cancer risk. Exposure to certain environmental agents such as talc, pesticides, and herbicides may increase risk of ovarian cancer; however, these studies are limited. Further research is needed to strengthen the database of information from which an assessment of environmental and toxicological risk factors for ovarian cancer can be made.

Reproductive pathology in the male represents about 20% of infertility cases. Male infertility may be attributed to a number of causes, including genetic and congenital abnormalities, infection, multisystemic diseases, varicocele, and others; however, a significant number of cases are idiopathic. Global declines in semen quality were suggested to be associated with enhanced exposure to environmental chemicals that act as endocrine disrupters as a result of our increased use of pesticides, plastics, and other anthropogenic materials. A significant body of toxicology data based upon laboratory and wildlife animals studies suggests that exposure to certain endocrine disrupters is associated with reproductive toxicity, including (1) abnormalities of the male reproductive tract (cryptorchidism, hypospadias), (2) reduced semen quality, and (3) impaired fertility in the adult. There is, however, a relative paucity of studies designed to measure exposure to endocrine disrupters on semen quality parameters (sperm concentration, motility, morphology). An overview of the human semen quality literature is presented that examines the role of endocrine disrupters including organochlorines (OC), dioxins, phthalates, phytoestrogens, and chemical mixtures (pesticides and tobacco smoke).

Background: Extreme heat caused by climate change is a major public health concern, disproportionately affecting poor and racialized communities. Gestational heat exposure is a well-established teratogen in animal studies, with a growing body of literature suggesting human pregnancies are similarly at risk. Characterization of extreme heat as a pregnancy risk is problematic due to nonstandard definitions of heat waves, and variable study designs. To better focus future research in this area, we conducted a scoping review to assess the effects of extreme heat on pregnancy outcomes. Methods: A scoping review of epidemiological studies investigating gestational heat-exposure and published 2010 and 2020, was conducted with an emphasis on study design, gestational windows of sensitivity, adverse pregnancy outcomes and characterization of environmental temperatures. Results: A sample of 84 studies was identified, predominantly set in high-income countries. Preterm birth, birthweight, congenital anomalies and stillbirth were the most common pregnancy outcome variables. Studies reported race/ethnicity and/or socioeconomic variables, however these were not always emphasized in the analysis. Conclusion: Use of precise temperature data by most studies avoided pitfalls of imprecise, regional definitions of heat waves, however inconsistent study design, and exposure windows are a significant challenge to systematic evaluation of this literature. Despite the high risk of extreme heat events and limited mitigation strategies in the global south, there is a significant gap in the epidemiological literature from these regions. Greater consistency in study design and exposure windows would enhance the rigor of this field.

We report here that intracellular pH (pH_i) in cleavage-stage human embryos (2–8-cell) is regulated by at least two mechanisms: the HCO₃^–/Cl^– exchanger (relieves alkalosis) and the Na⁺/H⁺ antiporter (relieves acidosis). The mean pH_i of cleavage-stage embryos was 7.12 ± 0.008 (n = 199) with little variation between different stages. Embryos demonstrated robust recovery from alkalosis that was appropriately Cl^–-dependent, indicating the presence of the HCO₃^–/Cl^– exchanger. This was further confirmed by measuring the rate of intracellular alkalinization upon Cl^– removal, which was markedly inhibited by the anion transport inhibitor, 4,4′-diisocyanatostilbene-2,2′-disulphonic acid, disodium salt. The set-point of the HCO₃^–/Cl^– exchanger was between pH_i 7.2 and 7.3. Embryos also exhibited Na⁺-dependent recovery from intracellular acidosis. Na⁺/H⁺ antiporter activity appeared to regulate recovery up to about pH_i 6.8; this recovery was HCO₃^–-independent and amiloride-sensitive, with a pH_i set-point of ~6.8–6.9. A second system that was both Na⁺- and HCO₃^–-dependent appeared to mediate further recovery from acidosis up to about pH_i 7.1. Thus, pH_i of early human preimplantation embryos appears to be regulated by opposing mechanisms (HCO₃^–/Cl^– exchanger, Na⁺/H⁺ antiporter, and possibly a third acid-alleviating transporter that was both Na⁺- and HCO₃^–-dependent) resulting in the maintenance of pH_i within a narrow range.