Table 1.

Pathological effects of the exposure to ECDs.

EDCs	Pathological Effects of EDC Exposure	References
DES	in utero exposure dysregulates gene expression and transcriptional reprogramming in adult fibroblasts, ECM composition and collagen deposition in adult mammary gland, molecular alteration develops over time and contributes to increased BCR in adulthood, induces epigenetic alterations/epimutations with intergenerational/transgenerational effects	[157,182]
PAHs (BaP and DB(ah)A)	in mammary gland, affect cellular morphology, cell-cell junctions, division, growth, repair, and number of p53 mutations, increase EVs production, changes in exosome content and gene expression control	[99,165]
BPA and other bisphenols (AF, F, S) and TBBPA	affect mammary gland development, resulting in precancerous and cancerous lesions in adulthood, exert estrogenic effects, activate the expression of genes associated with cell proliferation and BC; associated with EMT and BC progression; activate VEGF associated with angiogenesis, MAPK signaling pathway, Wnt/β-catenin pathway, STAT3 signaling, and DNA repair; induce changes in genes associated with apoptosis and DNA methylation; inactivate p53; increase expression of BRCA1/2, BARD1, CtlP, RAD51, and BRCC3 involved in DNA repair; downregulate PDCD5 and BCL2L11 involved in apoptosis	[103,155,162,163,164,183,184]
Phtalates (DBP)	mimic estradiol, interact with ER and PR, promote BC, especially ER+ BC, interfere with DNA methylation and DNA damage	[170,185]
PCBs (PCB-153, PCB-180, PCB29-pQ)	BC cell proliferation by regulating ERK1/2 activation; induce cancer cell stemness and EMT via Wnt/β-catenin signaling	[166,184]
Organochlorine insecticides (DDT)	increase in utero BCR, BC progression by interfering with androgen signaling pathways, BC cells proliferation, negative effects on OS	[184,186]
Parabens (MeP, EtP, PrP, BuP) and their metabolites	promote protumorigenic effects in BC; modulate local estrogen-converting enzymes and increase local estrogen levels; cross-talk with HER2 pathway and affect ER signaling to increase pro-oncogenic c-Myc expression in ER+/HER2+ BC cells; alter ER target gene expression and cell viability	[172,173,181]