Bisphenol A (BPA) is a synthetic chemical widely used in polycarbonate plastics, epoxy resins, and consumer products, including food containers, thermal papers, and medical devices. Over the past decades, BPA has been identified as an endocrine-disrupting chemical (EDC) due to its structural similarity to 17β-estradiol, enabling it to interfere with hormonal signaling pathways. Accumulating evidence links BPA exposure—even at low, environmentally relevant doses—to adverse health outcomes, including reproductive disorders, metabolic diseases, and hormone-related cancers such as breast cancer. This review synthesizes current research on BPA’s carcinogenic potential, focusing on its molecular mechanisms, influence on breast cancer subtypes, and interactions with the tumor microenvironment. BPA exerts its effects through genomic pathways (e.g., estrogen receptor-mediated gene activation) and non-genomic signaling (e.g., GPER, MAPK/ERK, and PI3K/AKT pathways), promoting proliferation, survival, and metastasis. Notably, BPA impacts not only estrogen receptor-positive (ER+) breast cancers but also triple-negative breast cancer (TNBC) through estrogen-independent mechanisms. Furthermore, BPA reprograms cancer-associated fibroblasts (CAFs) and immune cells within the tumor microenvironment, fostering a pro-tumorigenic niche. Emerging evidence suggests that dietary factors can modulate BPA’s effects—either exacerbating its toxicity (e.g., high-fat diets, alcohol) or mitigating harm (e.g., phytoestrogens, polyphenols). Given the limitations of current regulatory thresholds, this review underscores the need for revised safety standards, increased public awareness, and interdisciplinary strategies to reduce exposure. Understanding BPA’s multifaceted role in breast carcinogenesis is critical for developing preventive and therapeutic interventions.
Ariba et al. (2024) studied this question.