Environmental endocrine disruptors and breast cancer: The role of bisphenols, polychlorinated biphenyls, parabens, and dioxins

Breast cancer is the most common malignancy in women, and environmental factors such as endocrine-disrupting chemicals (EDCs) contribute to its development and progression. This review examines the roles of four major EDCs—bisphenols, polychlorinated biphenyls (PCBs), parabens, and dioxins—integrating mechanistic and epidemiological evidence. A key pathway is the cross-talk between estrogen receptor (ER) and aryl hydrocarbon receptor (AhR), which regulates proliferation, survival, and immune evasion. Bisphenol A (BPA) promotes proliferation, migration, epigenetic reprogramming, and immune escape. PCBs, particularly PCB-153, are linked to metabolic alterations, inflammation, and variable epidemiological associations. Parabens, common in cosmetics, display estrogenic activity and affect oxidative stress, tumor marker expression, and metastasis. Dioxins, especially TCDD, act via AhR to induce inflammation, immunosuppression, and metastasis, with epidemiological links to cancer risk near emission sources. Collectively, these EDCs disrupt hormonal pathways, alter gene expression, and modulate the tumor microenvironment, underscoring the need for further research, regulation, and public health interventions.