Endocrine disruption by emergent brominated flame retardant Decabromodiphenyl ethane (DBDPE) promotes cancer-associated characteristics in human breast cells and zebrafish xenografts.

Reports show that at least 1000 manufactured chemicals released into the environment are associated with endocrine disruption. Among these, halogenated flame retardants are a source of concern due to their ubiquity, toxic properties, and adverse health effects. Replacing polybrominated diphenyl ethers (PBDEs), a well-studied family of compounds whose use is currently restricted, with compounds of similar chemical structure and fire resistance, such as Decabromodiphenyl ethane (DBDPE), leads to the presumptions of comparable health effects. Because of the reported toxicity of PBDEs, the presence of DBDPE in breast milk raises concerns about its potential effects on breast cancer. We used cancerous and non-cancerous human breast cell lines, as well as a zebrafish xenograft model, to investigate the toxicity of this replacement compound. Exposure to DBDPE led to a non-significant increased expression of progesterone receptor B (PRB) at lower doses followed by a dose-dependent decreasing trend, while thyroid hormone receptor a1 (THRa1) was decreased in cancer cells (T47D). The β-catenin/Wnt pathway, associated with proliferation regulation and the mesenchymal epithelial transition, was also affected. Interestingly, while proliferation and migration were not affected in both cell lines exposed to DBDPE in classical cell culture, both capacities were increased when cells were xenografted in exposed zebrafish. These results suggest that, such as PBDEs, DBDPE can affect breast cells, and highlight the importance of testing the potential hazards of replacement molecules before their widespread use.