Decabromodiphenyl ether (BDE209) has been demonstrated to be associated with thyroid dysfunction and thyroid carcinoma risk as a widely used brominated flame retardants. Although dabrafenib has been confirmed to be a promising therapeutic agent for papillary thyroid carcinoma (PTC) harboring BRAFV600E mutation, the rapid acquired dabrafenib resistance has brought a great challenge to clinical improvement and the underpinning mechanisms remain poorly defined. By treating PTC-derived and normal follicular epithelial cell lines with BDE209, we assessed its impact on the MAPK pathway\'s activation and evaluated the resultant effects on cell viability and signaling pathways, utilizing methods such as Western blot, IF staining, and RNA-seq bioinformatic analysis. Our findings reveal that BDE209 exacerbates MAPK activation, undermining dabrafenib\'s inhibitory effects by triggering the EGFR pathway, thereby highlighting BDE209\'s potential to diminish the pharmacological efficacy of dabrafenib in treating BRAF-mutated PTC. This research underscores the importance of considering environmental factors like BDE209 exposure in the effective management of thyroid carcinoma treatment strategies.

In this work, the magnetic nanocomposite Fe@SiC was prepared by a hydrothermal method and determined by SEM, XRD, XPS, FTIR and VNA. Fe3O4 particles were loaded onto SiC with great success, and the synthesized composites had favorable microwave absorption properties. Fe@SiC was used to activate persulfate in a microwave field for the degradation of BDE209 in soil. Specifically, the synergistic interaction between microwaves and Fe@SiC showed excellent catalytic performance in activating PS to degrade BDE209 (90.1% BDE209 degradation in 15 min). The presence of •OH, O2•- and 1O2 was demonstrated based on quench trapping and EPR experiments. LC‒MS was applied to determine the intermediates and propose the possible degradation pathway for BDE209 in the MW/Fe@SiC/PS system, and it was found that BDE209 produced almost no lower brominated diphenyl ethers. Therefore, the toxicity of BDE209 was found to be reduced using toxicity assessment software. Overall, this work provides an effective approach for the degradation of BDE209 in environmental remediation.

Decabromodiphenyl ether (BDE209), an essential industrial flame retardant that is widely used, has recently been reported to be increasing in human serum. Due to the structural similarity between BDE209 and thyroid hormones, its toxic effects on the thyroid are of particular concern.
Original articles in the PubMed database were collected using the terms \"BDE209\", \"decabromodiphenyl ether\", \"endocrine disrupting\", \"thyroid\", \"carcinogenesis\", \"polybrominated diphenyl ethers\", \"PBDEs,\" and their synonyms from inception up to October of 2022.
Of the 748 studies initially identified, 45 were selected, which emphasized the adverse effects of BDE209 on endocrine system. BDE209 may have a toxic effect not only on thyroid function but also on thyroid cancer tumorigenesis at multiple levels, such as by directly interfering with the TR, hypothalamic-pituitary-thyroid (HPT) axis, enzyme activity, and methylation. However, it is impossible to draw a definitive conclusion on the exact pathway of thyroid toxicity from BDE209.
Although the toxic effects of BDE209 on the thyroid have been well investigated, its tumorigenic effects remain unclear and further research is necessary.

The current study aimed to assess the connection between the mixture of lead (Pb), cadmium (Cd), arsenic (As), methylmercury (MeHg) and decabrominated diphenyl ether (decaBDE) and thyroid function, by using in silico toxicogenomic data-mining approach. To obtain the linkage between investigated toxic mixture and thyroid diseases (TDs), the Comparative Toxicogenomics Database (CTD) was used, while gene ontology (GO) enrichment analysis was performed by ToppGeneSuite portal. The analysis has shown 10 genes connected to all chemicals present in the mixture and TDs (CAT, GSR, IFNG, IL1B, IL4, IL6, MAPK1, SOD2, TGFB1, TNF), most of which were in co-expression (45.68%), or belonged to the same pathway (30.47%). Top 5 biological processes and molecular functions affected by the investigated mixture emphasized the role of two common mechanisms - oxidative stress and inflammation. Cytokines and inflammatory response was listed as the main molecular pathway that may be triggered by simultaneous exposure to toxic metal(oid)s and decaBDE and connected to TDs. The direct relations between Pb/decaBDE and redox status impairment in thyroid tissue was confirmed by our chemical-phenotype interaction analysis, while the strongest linkage between Pb, As and decaBDE and thyroid disorders was found. The obtained results provide better understanding of molecular mechanisms involved in the thyrotoxicity of the investigated mixture, and can be used to direct further research.

Hydrophobic organic compounds (HOCs) in e-waste disposal sites are difficult to remove effectively. There is little reported about zero valent iron (ZVI) coupled with persulfate (PS) to achieve the removal of decabromodiphenyl ether (BDE209) from soil. In this work, we have prepared the flake submicron zero valent iron by ball milling with boric acid (B-mZVIbm) at a low cost. Sacrifice experiments results showed that 56.6% of BDE209 was removed in 72 h with PS/B-mZVIbm, which was 2.12 times than that of micron zero valent iron (mZVI). The morphology, crystal form, atomic valence, composition, and functional group of B-mZVIbm were determined by SEM, XRD, XPS, and FTIR, and the results indicated that the oxide layer on the surface of mZVI is replaced by borides. The results of EPR indicated that hydroxyl radical and sulfate radical played the dominant role in the degradation of BDE209. The degradation products of BDE209 were determined by gas chromatography-mass spectrometry (GC-MS), accordingly, the possible degradation pathway was further proposed. The research suggested that ball milling with mZVI and boric acid is a low-cost means of preparing highly active zero valent iron materials. And the mZVIbm has promising applications in improving the activation efficiency of PS and enhancing the removal of the contaminant.

Due to the characteristics of persistent organic pollutants (POPs), some legacy brominated flame retardants (LBFRs) were prohibited from use, and then gradually replaced by novel brominated flame retardants (NBFRs). However, till now little research focused on the effects of NBFRs on the benthos. In the present study, 0.5, 5, and 50 mg/kg dw of pentabromotoluene (PBT), hexabromobenzene (HBB), 1,2-bis(2,4,6-tribromophenoxy) ethane (BTBPE), decabromodiphenyl ethane (DBDPE) and decabromodiphenyl ether (BDE209) were added into sediments to test freshwater clams (Corbicula fluminea). In the 35-day exposure experiment, C. fluminea had different enrichment behaviors in three treatment groups. It was conjectured that in the lower dose group, the clams ingested contaminants and tended to be stable over time. While in higher dose groups, the clams were induced by the chemicals, leading to the changes in physiological activities so that the concentrations showed a downward trend first and then went up. The half-lives of contaminants in freshwater clams were between 0.911 and 11.6 days. DBDPE showed stronger bioaccumulation ability than BDE209 in this study. Parabolic relationships were observed between log BSAF and log Kow values in clam tissues. Debromination, hydroxylation, and methoxylated products were detected. Additionally, the gill samples of C. fluminea exposed to 50 mg/kg dw of single substance were observed by scanning electron microscope (SEM), indicating that the adhesions, tissue hyperplasia, and messy cilia occurred on the surface. Our research potentially contributes to further evaluations of the environmental risks posed in sediments contaminated by PBT, HBB, BTBPE, DBDPE, and BDE209, particularly the benthic organisms.

Polybrominated diphenyl ethers (PBDEs) have been reported to possess endocrine-disrupting and tumour-promoting activity. However, the effects of long-term exposure to decabromodiphenyl ether (BDE209) on thyroid tumourigenesis of papillary thyroid carcinoma (PTC) and the underlying mechanisms remain poorly defined. In this study, functional assays in vitro and mouse models in vivo were used to evaluate the toxic effects of long-term exposure to environmental concentrations of BDE209 on the pathogenesis and progression of PTC. MTS, EdU and colony-forming assays confirmed the chronic toxicity of BDE209 on the proliferation of human normal follicular epithelial cell line (Nthy-ori 3-1) and PTC-derived cell lines (TPC-1 and BCPAP). Wound and Transwell assays showed that BDE209 exacerbated the aggressiveness of PTC cells. BDE209 significantly promoted cell proliferation during the S and G2/M phases of the cell cycle. Mechanistically, BDE209 altered the thyroid system by acting as a competitive inhibitor of thyroid receptor beta (TRß) expression and function, which was further proven by public databases and RNA-seq bioinformation analysis. Taken together, these results demonstrated that BDE209 has chronic toxicity and potential tumourigenic effects on the thyroid by inhibiting TRß.

Effective removal of polybrominated diphenyl ethers (PBDEs) from the environment is essential for the ecosystem and human health. Reductive debromination of PBDEs by nanoscale zerovalent iron (nZVI) has become an important technology. However, the agglomeration and low persistence catalytic activity of nZVI particles have become urgent problems to be improved. Herein, we report the first application of a new organo-attapulgite (OA) supported Fe/Pd nanoparticles (OA-Fe/Pd) composite for decabromodiphenyl ether (BDE209) removal. BDE209 was efficiently removed using OA-Fe/Pd with a reaction rate that was 9.97 times greater than that of the nZVI due to the synergetic effect of support material OA and Pd loading. OA could prevent nZVI particles from agglomeration and adsorb BDE209 molecules to its surface. Pd could supply atomic hydrogen and also prevent the oxidation of nZVI particles. The degradation of BDE209 by OA-Fe/Pd was affected by many factors and followed pseudo first-order kinetics. The degradation of BDE209 by OA-Fe/Pd underwent a stepwise debromination manner with the H-transfer dominant mechanism. BDE209 (25 mg∙L-1) could be degraded to penta-BDEs to diphenyl ether (DE) by 3.0 g∙L-1 OA-Fe/Pd within 240 min under neutral condition. This study provides some inspiration for improving the removal efficiency of PBDEs with nZVI-based materials.

Although it has been suggested that plastic may act as a vector for pollutants into the tissue of seabirds, the bioaccumulation of harmful contaminants, such as polybrominated diphenyl ethers (PBDEs), released from ingested plastics is poorly understood. Plastic ingestion by the procellariiform species northern fulmar (Fulmarus glacialis) is well documented. In this study, we measured PBDEs levels in liver tissue of northern fulmars without and with (0.13-0.43 g per individual) stomach plastics. PBDE concentrations in the plastic sampled from the same birds were also quantified. Birds were either found dead on beaches in southern Norway or incidentally caught in longline fisheries in northern Norway. PBDEs were detected in all birds but high concentrations were only found in liver samples from beached birds, peaking at 2900 ng/g lipid weight. We found that body condition was a significant factor explaining the elevated concentration levels in livers of beached birds. BDE209 was found in ingested plastic particles and liver tissue of birds with ingested plastics but was absent in the livers of birds without ingested plastics. This strongly suggests a plastic-derived transfer and accumulation of BDE209 to the tissue of fulmars, levels of which might prove useful as a general indicator of plastic ingestion in seabirds.

Decabromodiphenyl ether (BDE209) is a widely used brominated flame retardant that has become a common soil contaminant of concern due to its persistence and toxicity. However, little is known about molecular-level effects of BDE209 on soil invertebrates. Here, we detected changes in gene transcription of the soil springtail, Folsomia candida, exposed to BDE209 (0.81 mg/kg) in soil for 2, 7 and 14 days. We identified 16 and 771 significantly differentially expressed genes after 2 and 7 days of exposure respectively, and no significantly regulated genes were shared among the two time points. No genes were affected after 14 days of exposure. According to the annotation of the significantly differently expressed genes at 2 and 7 day exposure, we found that BDE209 affected the transcription of genes involved in moulting, neural signal transmission and detoxification. Our results suggested that BDE209 could disrupt moulting of F. candida via the ecdysteroid pathway, and cause neurotoxicity through disrupting some neurotransmitter signalling pathways. This study provided insights into the toxic mechanism of BDE209 on F. candida.