Women are unintentionally exposed to endocrine-disrupting chemicals (EDCs) daily, particularly organochlorine (OCPs) and organophosphate pesticides (OPPs), which target female sexual and reproductive health, causing complications such as abnormal sex steroid hormone levels and premature ovarian failure, ultimately leading to infertility. Most of the toxicological research data related to reproductive issues comes from short-duration and high-dose animal studies. Therefore, more research is needed on the long-term effects of chronic, low-level environmental and dietary exposure to these pesticides on women's reproductive and thyroid function. This is particularly relevant as these are the more common exposure scenarios for the general population. OCPs and OPPs interfere with and impair the reproductive system and its mechanisms, which are under neuronal and hormonal control, thereby damaging female fertility. Some common consequences of these pesticide exposures include disruption of endocrine function, irregular estrous cycle, amenorrhea, thyroid disorder, polycystic ovarian syndrome (PCOS), follicular atresia, altered physiology of ovulation, and recurrent miscarriages. Pesticides not only cause reproductive disorders but also affect subsequent generations, especially in women. OCP and OPP metabolites found in breast milk samples, placenta, maternal, and cord blood samples demonstrated that mothers have the highest load of pesticide exposure and continued partial transfer of such residues to their fetuses. Non-occupational exposure to pesticides has increased and poses risks to reproductive organs. Further research is needed to fully understand the long-term outcomes of these exposures on infertility, hypothyroidism, and hormonal disorders.
Amjad et al. (2026) studied this question.