Differential life cycle toxic effects and molecular mechanisms of Di(2-ethylhexyl) phthalate (DEHP) exposure on the female reproductive system.

Di(2-ethylhexyl) phthalate (DEHP), the most prevalent plasticizer worldwide, can enter the human body via various exposure pathways, including ingestion, inhalation, skin contact, and medical applications. It has been observed to exhibit characteristic patterns of accumulation in the female reproductive system. Research has demonstrated that DEHP poses a threat to reproductive health in females across various life stages. Exposure during childhood has been demonstrated to induce central precocious puberty (CPP). Exposure during reproductive age has been shown to be closely associated with reduced fertility, reproductive system tumors, polycystic ovary syndrome (PCOS), and increased risk of endometriosis. Furthermore, exposure during the perinatal period has been demonstrated to increase the risk of embryo implantation failure, placental dysfunction, and abnormal ovarian development in offspring. The toxic effects of DEHP exhibit transgenerational transmission characteristics, with its metabolic products' endocrine-disrupting activity and oxidative stress-inducing capacity being the core toxic factors. This study integrates toxicological evidence linking DEHP exposure to female reproductive damage, providing important references for environmental health risk assessment and the prevention and control of female reproductive diseases.