Atmospheric concentrations of polychlorinated biphenyls, brominated flame retardants, and novel flame retardants in Lagos, Nigeria indicate substantial local sources.

Polychlorinated biphenyls (PCBs), brominated flame retardants (BFRs) like polybrominated diphenyl ethers (PBDEs), hexabromocyclododecane (HBCDD), and novel flame retardants (NFRs) like decabromodiphenyl ethane (DBDPE) are ubiquitous environmental pollutants. Despite this, little is known about their concentrations in outdoor air in the African continent. To address this knowledge gap, concentrations of BFRs, NFRs, and PCBs were measured in outdoor air at 8 sites located within the metropolitan area of Lagos, Nigeria. Concentrations of ∑8BDEs, ∑HBCDD, ∑7NFRs and ∑8PCBs were: 21-750 (median = 100) pg/m3, <12-180 (median = < 12) pg/m3, 34-900 (median = 300) pg/m3 and 85-460 (median = 300) pg/m3, respectively. Decabromodiphenyl ether (BDE-209, range: <16-620 pg/m3, median = 71 pg/m3) and DBDPE (range: <37-890 pg/m3, median = 280 pg/m3) were the dominant BFRs detected, while the non-Arochlor PCB 11 (range: 49-220 pg/m3, median = 100 pg/m3) was the dominant PCB. To the authors' knowledge, these are the first data on the non-Arochlor PCB 11 in outdoor air in Africa. In general, concentrations of all target contaminants in this study were within the range reported elsewhere in Africa and worldwide. Likely due to the tropical climate of Lagos, no seasonal variation in concentrations was discernible for any of the target contaminants. While concentrations of PBDEs and some NFRs were correlated with population density, concentrations of PCBs appear more impacted by leaks from electrical transformers and for PCB 11 to proximity to activities like textile factories that produce and use dyes.

Fat mass and obesity-associated gene (FTO) hypermethylation induced by decabromodiphenyl ethane causing cardiac dysfunction via glucolipid metabolism disorder.

Decabromodiphenyl ethane (DBDPE) is a major alternative to BDE-209 owing to its lower toxicity. However, the mass production and increased consumption of DBDPE in recent years have raised concerns related to its adverse health effects. However, the effect and mechanism of DBDPE on cardiotoxicity have rarely been studied. In the present study, we investigated the impacts of DBDPE on the cardiovascular system in male SD rats and then explored the underlying mechanisms to explain the cardiotoxicity of DBDPE using AC16 cells. Under in vivo conditions, male rats were administered with an oral dosage of DBDPE at 0, 5, 50, and 500 mg/kg/day for 28 days, respectively. Histopathological analysis demonstrated that DBDPE induced cardiomyocyte injury and fibrosis, and ultrastructural observation revealed that DBDPE could induce mitochondria damage and dissolution. DBDPE could thus decrease the level of MYH6 and increase the level of SERCA2, which are the two key proteins involved in the maintenance of homeostasis during myocardial contractile and diastolic processes. Furthermore, DBDPE could increase the serum levels of glucose and low-density lipoprotein but decrease the content of high-density lipoprotein. In addition, DBDPE could activate the PI3K/AKT/GLUT2 and PPARγ/RXRα signaling pathways in AC16 cells. In addition, DBDPE decreased the UCP2 level and ATP synthesis in mitochondria both under in vitro and in vivo conditions, consequently leading to apoptosis via the Cytochrome C/Caspase-9/Caspase-3 pathway. Bisulfite sequencing PCR (BSP) identified the hypermethylation status of fat mass and obesity-associated gene (FTO). 5-aza exerted the opposite effects on the PI3K/AKT/GLUT2, PPARγ/RXRα, and Cytochrome C/Caspase-9/Caspase-3 signaling pathways induced by DBDPE in AC16 cells. In addition, the DBDPE-treated altered levels of UCP2, ATP, and apoptosis were also found to be significantly reversed by 5-aza in AC16 cells. These results suggested that FTO hypermethylation played a regulative role in the pathological process of DBDPE-induced glycolipid metabolism disorder, thereby contributing to the dysfunction of myocardial contraction and relaxation through cardiomyocytes fibrosis and apoptosis via the mitochondrial-mediated apoptotic pathway resulting from mitochondrial dysfunction.

Decabromodiphenyl ethane induces male reproductive toxicity by glycolipid metabolism imbalance and meiotic failure.

Decabromodiphenyl ethane (DBDPE) is a typical flame retardant found in various electrical and textile items. DBDPE is abundantly available in the surrounding environment and wild animals based on its persistence and bioaccumulation. DBDPE has been shown to cause apoptosis in rat spermatogenic cells, resulting in reproductive toxicity. However, the toxicity of DBDPE on the male reproductive system and the potential mechanisms are still unclear. This study evaluated the effect of DBDPE on the reproductive system in male SD rats and demonstrated the potential mechanisms of reproductive toxicity. DBDPE (0, 5, 50, and 500 mg/kg/day) was administered via gavage to male SD rats for 28 days. DBDPE caused histopathological changes in the testis, reduced sperm quantity and motility, and raised the malformation rate in rats, according to the findings. Furthermore, it caused DNA damage to rat testicular cells. It inhibited the expressions of spermatogenesis-and oogenesis-specific helix-loop-helix transcription factor 1 (Sohlh1), piwi-like RNA-mediated gene silencing 2 (MILI), cyclin-dependent kinase 2 (CDK2), and CyclinA, resulting in meiotic failure, as well as the expressions of synaptonemal complex proteins 1 and 3 (SYCP1 and SYCP3), leading to chromosomal association disorder in meiosis and spermatocyte cycle arrest. Moreover, DBDPE induced glycolipid metabolism disorder and activated mitochondria-mediated apoptosis pathways in the testes of SD rats. The quantity and quality of sperm might be declining due to these factors. Our findings offer further evidence of the harmful impact of DBDPE on the male reproductive system.

Decabromodiphenyl Ether versus Decabromodiphenyl Ethane: Source, Fate, and Influencing Factors in a Coastal Sea Nearing Source Region.

Both decabromodiphenyl ether (BDE 209) and decabromodiphenyl ethane (DBDPE) are still produced in large quantities in China, especially in the Shandong Province closed to the Bohai Sea (BS). This study conducted a comprehensive investigation of the distribution and budget of brominated flame retardants (BFRs) in the BS. BDE 209 was the predominant BFR in most of the investigated rivers flowing into the BS, although DBDPE exceeded BDE 209 in certain rivers as a result of the replacement of BDE 209 with DBDPE in North China. The spatial distributions of BFRs in the rivers were controlled by the proximity of the BFR manufacturing base and the extent of urbanization. BFRs' spatial distribution in the BS was influenced by a combination of land-based pollution sources, environmental parameters (e.g., suspended particulate matter, particulate organic carbon, and particulate black carbon), and hydrodynamic conditions. The spatial variation trend of BDE 209/DBDPE ratios in various environmental media provided useful information. Vertically, the BDE 209/DBDPE ratio decreased from the seawater surface layer to the sediment, indicating their differential transport in the BS. A multi-box mass balance model and analysis of BDE 209 showed that degradation was the primary sink of BFRs in seawater (∼68%) and surface sediment (∼72%) in the BS.

Emerging and legacy brominated flame retardants in the breast milk of first time Irish mothers suggest positive response to restrictions on use of HBCDD and Penta- and Octa-BDE formulations.

The brominated flame retardants (BFRs) hexabromocyclododecane (HBCDD), eight polybrominated diphenyl ethers (PBDEs), and decabromodiphenyl ethane (DBDPE) were measured in 16 pools of human milk from Ireland. Concentrations of BDEs-47, -99, -100, -153, and HBCDD were significantly lower (p < 0.05) than those in Irish human milk collected in 2011. In contrast, concentrations of BDE-209 in our study exceeded those in 2011, and while decabromodiphenyl ethane (DBDPE) was not detected in 2011 it was detected in 3 of our samples. This suggests increased use of DBDPE and that while restrictions on the Penta- and Octa-BDE formulations are reducing human exposure, those on Deca-BDE use have yet to reduce body burdens. Estimated exposures for nursing infants to all target BFRs do not suggest a health concern. A one compartment pharmacokinetic model was used to predict body burdens arising from BFR intakes via air, dust and diet. While for most targeted BFRs, predicted and observed body burdens derived from our human milk data compared reasonably well; predicted BDE-209 and DBDPE values were substantially lower than observed. This suggests exposure pathways not included in the model like dermal uptake from fabrics may be important, and highlights knowledge gaps about the human half-lives and bioavailability of these contaminants.

Transcriptome-based approach to identify mechanisms underlying locomotor abnormality induced by decabromodiphenyl ethane in zebrafish larvae.

The brominated flame retardant decabromodiphenyl ethane (DBDPE) has been extensively used following restrictions on BDE-209 and thus, been frequently detected in aquatic environment. However, information on impact of DBDPE on fish development and the potential mechanisms remains scarce. In present study, developing zebrafish were employed as a study model. Embryos were exposed until 5 d to DBDPE at concentrations of 0, 3, 30, and 300 µg/L, following which the impact on larval development was investigated. DBDPE bioaccumulation and locomotor hyperactivity were observed in developing zebrafish exposed to DBDPE. Transcriptome and bioinformatics analyses indicated that pathways associated with cardiac muscle contraction and retinol metabolism were notably affected. The mechanisms of DBDPE to induce locomotor abnormality were further investigated by analyzing levels of retinol and retinol metabolites, eye and heart histology, heart rates, and ATPase activity. Our results indicate that locomotor hyperactivity observed in larvae exposed to DBDPE results from abnormal heartbeat, which in turn is attributable to inhibition of Na+/K+-ATPase activity. Furthermore, DBDPE did not change larval eye histology and contents of retinoid (retinol, retinal, and retinoic acid). This study provides insight into the mechanisms underlying DBDPE-induced developmental toxicity and highlights the need for addressing the environmental risks for aquatic organisms.

Toxicity of decabromodiphenyl ethane on lettuce: Evaluation through growth, oxidative defense, microstructure, and metabolism.

Decabromodiphenyl ethane (DBDPE) as the most widely used novel brominated flame retardants (NBFRs), has become a ubiquitous emerging pollutant in the environment. However, its toxic effects on vegetable growth during agricultural production have not been reported. In this study, we investigated the response mechanisms of hydroponic lettuce to DBDPE accumulation, antioxidant stress, cell structure damage, and metabolic pathways after exposure to DBDPE. The concentration of DBDPE in the root of lettuce was significantly higher than that in the aboveground part. DBDPE induced oxidative stress on lettuce, which stimulated the defense of the antioxidative system of lettuce cells, and the cell structure produced slight plasma-wall separation. In terms of metabolism, metabolic pathway disorders were caused, which are mainly manifested as inhibiting amino acid biosynthesis and metabolism-related pathways, interfering with the biosyntheses of amino acids, organic acids, fatty acids, carbohydrates, and other substances, and ultimately manifested as decreased total chlorophyll content and root activity. In turn, metabolic regulation alleviated antioxidant stress. The mechanisms of the antioxidative reaction of lettuce to DBDPE were elucidated by IBR, PLS-PM analysis, and molecular docking. Our results provide a theoretical basis and research necessity for the evaluation of emerging pollutants in agricultural production and the safety of vegetables.

Biochar supported nanoscale zero-valent iron for the kinetics removal and mechanism of decabromodiphenyl ethane in the sediment.

The extensive applications of decabromodiphenyl ethane (DBDPE), a novel brominated flame retardant, have induced its accumulation in sediment, which may have a great negative impact on the ecological environment. In this work, the biochar/nano-zero-valent iron materials (BC/nZVI) were synthesized to remove DBDPE in the sediment. Batch experiments were carried out to investigate the influencing factors of the removal efficiency, and kinetic model simulation and thermodynamic parameter calculation were performed. The degradation products and mechanisms were probed. The results indicated that the addition of 0.10 g·g-1 BC/nZVI to the sediment with an initial concentration of 10 mg·kg-1 DBDPE could remove 43.73% of DBDPE during 24 h. The water content of the sediment was a critical factor in the removal of DBDPE, which was optimal at 1:2 of sediment to water. The removal efficiency and reaction rate were enhanced by increasing dosage, water content, and reaction temperature or decreasing initial concentration of DBDPE based on the fitting results of the quasi-first-order kinetic model. Additionally, the calculated thermodynamic parameters suggested that the removal process was a spontaneously and reversibly endothermic reaction. The degradation products were further determined by GC-MS, and the mechanisms were presumed that DBDPE was debrominated to produce octabromodiphenyl ethane (octa-BDPE). This study provides a potential remediation method for highly DBDPE-contaminated sediment by using BC/nZVI.

Temporal trends in concentrations of brominated flame retardants in UK foodstuffs suggest active impacts of global phase-out of PBDEs and HBCDD.

Global restrictions on use of legacy brominated flame retardants (BFRs) such as polybrominated diphenyl ethers (PBDEs) and hexabromocyclododecane (HBCDD) have generated demand for novel BFRs (NBFRs) as substitutes. Our research group has previously reported decreased concentrations of PBDEs and HBCDD and increased concentrations of NBFRs in UK indoor environments, suggesting that restrictions on PBDEs and HBCDD are exerting an impact. In this study, we analysed UK foodstuffs collected in 2020-21 and compared the BFR concentrations found with those found in similar samples collected in 2015 to investigate whether similar trends in BFR concentrations would be observed. Concentrations of PBDEs and HBCDD isomers detected in our samples had declined by 78-92 % and 59-97 % since the 2015 study, respectively. Moreover, concentrations of NBFRs (dominated by 1,2-bis(2,4,6-tribromophenoxy) ethane (BTBPE or TBE), and bis(2-ethyl hexyl) tetrabromophthalate (BEH-TEBP or TBPH)) in UK foodstuffs increased significantly (28-1400 %) between 2015 and 2020-21. Combined, these findings suggest that restrictions on use of PBDEs and HBCDD have had a discernible impact on concentrations of these legacy BFRs and their NBFR replacements in UK foodstuffs. Interestingly, given recent reports of a significant increase in concentrations of decabromodiphenyl ethane (DBDPE) in UK house dust between 2014 and 2019, a significant decline (70-84 %) in concentrations of DBDPE was observed in UK foodstuffs.

New brominated flame retardant decabromodiphenyl ethane (DBDPE) in water sediments: A review of contamination characteristics, exposure pathways, ecotoxicological effects and health risks.

As an alternative to polybrominated diphenyl ethers (PBDEs), decabromodiphenyl ethane (DBDPE) has become one of the most important new brominated flame retardants (NBFRs). However, little is known about whether this emerging contaminant may has an environmental fate similar to PBDEs. Sediments are the main sink for DBDPE in the aqueous phase. Worldwide concentration data, since it was first found in sediments to date, have been collated, and the following conclusions have been drawn. (1) DBDPE concentrations in sediments have increased rapidly, often with a higher risk of contamination in source discharge areas. Compared with other countries, DBDPE contamination in China is more severe, especially in Guangdong Province, which is closely related to its being an e-waste dismantling area. (2) The amount of DBDPE in surface sediments has exceeded that of legacy brominated flame retardants (BFRs), and data recorded in sediment cores also corroborate that DBDPE is replacing decabromodiphenyl ether (BDE-209) as one of the most dominant NBFRs in the environment. (3) The exposure pathways of DBDPE include dietary intake, air or indoor dust intake, cutaneous absorption and endogenous exposure. For sediments, dietary exposure and endogenous exposure pathways need to be considered. Sediment DBDPE can enter the human body through bioenrichment such as contaminated seafood and the food chain. (4) DBDPE can exhibit neurotoxicity, thyrotoxicity, reproductive and developmental toxicity, hepatotoxicity and oxidative stress in organisms. Long-term DBDPE exposure may increase hyperthyroidism risk and inhibit normal cells activity. This review focuses on the distribution characteristics and exposure risks of DBDPE in global water sediments, providing a strong reference for environmental management and related legal policy formulation. The next steps are to focus on continuous source monitoring, process control and sediment clean-up of DBDPE. The development of sustainable water management options for waste microplastics (MPs) and e-waste spiked with DBDPE is a priority.

DBDPE and ZnO NPs synergistically induce neurotoxicity of SK-N-SH cells and activate mitochondrial apoptosis signaling pathway and Nrf2-mediated antioxidant pathway.

Decabromodiphenyl ethane (DBDPE), a new brominated flame retardant, could negatively affect neurobehavior and pose health risks to humans. Humans are also exposed to widely used nanomaterials. This study investigated the combined toxic effects and action types of DBDPE and Zinc oxide nanoparticles (ZnO NPs) on human neuroblastoma SK-N-SH cells and the toxicity mechanisms. DBDPE inhibited the viability of SK-N-SH cells by 21.87% at 25 mg/L. ZnO NPs synergistically exacerbated the toxic effects of DBDPE. DBDPE and ZnO NPs caused excessive ROS production and inhibition of antioxidant enzyme (SOD and GSH) activity in cells, thus causing oxidative cellular damage. Moreover, DBDPE and ZnO NPs caused apoptosis by disrupting mitochondrial kinetic homeostasis, reducing mitochondrial membrane potential (MMP), increasing cytochrome C release and regulating Bax/Bcl-2 and Caspase-3 mRNA and protein expression. DBDPE and ZnO NPs increased the mRNA expression of nuclear factor erythroid 2- related factor (Nrf2) and its downstream genes. The molecular mechanisms revealed that oxidative stress, apoptosis and mitochondrial dysfunction were the critical factors in combined cytotoxicity. The bioinformatics analysis further indicated that co-exposure affected Nrf2 activation, apoptotic factors expression and mitochondrial fusion. The findings enrich the risk perception of neurotoxicity caused by DBDPE and ZnO NPs.

Investigating the adverse outcome pathways (AOP) of neurotoxicity induced by DBDPE with a combination of in vitro and in silico approaches.

Current studies have shown an association between DBDPE and neurotoxicity. In this study, the adverse outcome pathway (AOP) and mechanistic analysis of DBDPE-induced neurotoxicity were explored by a combination of in vitro and in silico approaches in SK-N-SH cells. DBDPE-induced oxidative stress caused DNA strand breaks, resulting in the activation of poly (ADP-ribose) (PAR) polymerase-1 (PARP-1). Activation of PARP1 could cause toxic damage in various organ systems, especially in the nervous system. DBDPE-induced apoptosis via the caspase-dependent intrinsic mitochondrial pathway and the PARP1-dependent pathway. Activation of PARP1 by DBDPE was deemed the initiating event, thereby affecting the key downstream biochemical events (e.g., ROS production, DNA damage, membrane potential changes, and ATP reduction), which induced apoptosis. Furthermore, excessive activation of PARP1 was accompanied by the translocation of the apoptosis-inducing factor (AIF), which was associated with PARP1-dependent cell death. The inhibition of PARP1 by PJ34 reduced DBDPE-induced apoptosis and maintained cellular ATP levels. PJ34 also prevented the translocation of AIF from the mitochondria to the nucleus. These findings improve the understanding of the mechanism of DBDPE-induced neurotoxic effects and provide a theoretical basis for the ecological risk of DBDPE.

Historical record of legacy and alternative halogenated flame retardants in dated sediment from a highly industrialized saltwater lake in Korea.

Legacy and alternative halogenated flame retardants (HFRs), such as polybrominated diphenyl ethers (PBDEs), novel brominated flame retardants (NBFRs), and dechlorane plus (DP), were measured in dated sediments from a highly industrialized lake in Korea. All HFRs were detected in almost all of the sediment depth layers for more than 70 years, indicating a history of long-term contamination. Similar historical trends in PBDEs, 1,2-bis(2,4,6-tribromophenoxy)ethane (BTBPE), and DP were observed in dated sediments, whereas decabromodiphenylethane (DBDPE), and 2-ethylhexyl-2,3,4,5-octabromo-1,3,3-trimethyl-1-phenylindane (OBIND) concentrations sharply increased since the 1990s. Moreover, the concentration ratios of DBDPE/BDE 209 increased from the early 1990s to the present. Our findings suggest that DBDPE and OBIND have been used as HFR alternatives. The historical record of the concentrations and profiles of legacy and alternative HFRs corresponded with industrial activities, consumption of FRs, and coastal development activities. Inventories of legacy and alternative HFRs were similar to those reported for highly industrialized regions around the globe.

Toxicity evaluation of decabromodiphenyl ethane (DBDPE) to Pleurotus ostreatus: Oxidative stress, morphology and transcriptomics.

Decabromodiphenyl ethane (DBDPE), one widely used new brominated flame retardant, was of great concern due to its biotoxicity. The toxic evaluation of DBDPE (1-50 mg/L) to white-rot fungus (Pleurotus ostreatus), including oxidative stress, morphology and transcriptomics was conducted aiming at improving its biodegradation. Fungal growth and ATPase activity were obviously inhibited by DBDPE at ≥ 10 mg/L with the exposure from 48 h to 96 h. DBDPE could induce oxidative stress to P. ostreatus. The activity of SOD (superoxide dismutase), CAT (catalase) and GSH (glutathione) were all promoted by DBDPE at ≤ 5 mg/L and inhibited at > 5 mg/L with 96-h exposure. MDA (malondialdehyde) content rose obviously with DBDPE exposure (10-50 mg/L). The mycelium was wizened under 20 mg/L DBDPE exposure according to SEM observation. Transcriptomics analysis suggested that DBDPE could change many functional genes expression of P. ostreatus. GO analysis indicated DBDPE could affect biological process and cellular component by inhibiting electron transport, mitochondrial ATP synthesis, oxidoreductase activity as well as transporter activity. KEGG enrichment pathways analysis indicated DBDPE could inhibit oxidative phosphorylation, tricarboxylic acid (TCA) cycle and carbon metabolism by down-regulating the genes related to NADH reductase/dehydrogenase, succinate dehydrogenase, cytochrome-c reductase/oxidase, cytochrome C1 protein and ATP synthase.

Integration of transcriptomic and proteomic reveals the toxicological molecular mechanisms of decabromodiphenyl ethane (DBDPE) on Pleurotus ostreatus.

Decabromodiphenyl ethane (DBDPE), as one of the most widely used new brominated flame retardants (NBFRs), can pose a potential threat to human health and the environment. An integrated transcriptome and proteome was performed for investigating the toxicological molecular mechanisms of Pleurotus ostreatus (P. ostreatus) during the biodegradation of DBDPE at the concentrations of 5 and 20 mg/L. A total of 1193/1018 and 92/126 differentially expressed genes/proteins (DEGs/DEPs) were found, respectively, with DBDPE exposure at 5 and 20 mg/L. These DEGs and DEPs were mainly involved in the cellular process as well as metabolic process. DEPs for oxidation-reduction process and hydrolase activity were up-regulated, and those for membrane, lipid metabolic process and transmembrane transport were down-regulated. The DEGs and DEPs related to some key enzymes were down-regulated, such as NADH dehydrogenase/oxidoreductase, succinate dehydrogenase, cytochrome C1 protein, cytochrome-c oxidase/reductase and ATP synthase, which indicated that DBDPE affected the oxidative phosphorylation as well as tricarboxylic acid (TCA) cycle. Cytochrome P450 enzymes (CYPs) might be involved in DBDPE degradation through hydroxylation and oxidation. Some stress proteins were induced to resist DBDPE toxicity, including major facilitator superfamily (MFS) transporter, superoxide dismutase (SOD), molecular chaperones, heat shock proteins (HSP20, HSP26, HSP42), 60S ribosomal protein and histone H4. The findings help revealing the toxicological molecular mechanisms of DBDPE on P. ostreatus, aiming to improve the removal of DBDPE.

Severe contamination and time trends of legacy and novel halogenated flame retardants in multiple environmental media from Lake Shihwa, Korea: Effectiveness of regulatory action.

Novel halogenated flame retardants (HFRs) were introduced to industrial markets as alternatives to legacy brominated FRs (BFRs), such as polybrominated diphenyl ethers (PBDEs). In the present study, PBDEs and their brominated and chlorinated alternatives, novel BFRs (NBFRs) and dechlorane plus (DP), were measured in multiple environmental matrices in a highly industrialized lake in Korea. Legacy and novel HFRs were detected in multiple samples, indicating ubiquitous contamination. Concentrations of HFRs in water and sediment observed in creeks running through machine, textiles, and automobile industrial complexes were significantly higher than those observed in inside and outside of the lake. Higher bioaccumulation levels of HFRs were observed in inshore compared with offshore waters. Results suggest that multi-matrix distribution of legacy and novel HFRs was dependent on the geographical proximity to industrial sources. Compared with previous studies, the highest levels of PBDEs and NBFRs were recorded in water samples on a global scale, implying on-going emissions from industrial activities. Decabromodiphenyl ethane (DBDPE) was a dominant compound in water samples, whereas the concentrations of PBDEs, NBFRs, and DP in sediment were similar to each other. This suggests a shift in consumption from legacy to novel HFRs, preferentially in water environments. A significant declining trend in PBDEs was observed in water and sediment collected between 2008 and 2015, indicating the effectiveness of regulatory actions. Based on their environmental occurrence and bioaccumulation potential, pentabromoethylbenzene and bis(2-ethylhexyl) tetrabromophthalate may pose emerging concerns regarding contamination of aquatic environments.

Bioaccumulation, elimination and metabolism in earthworms and microbial indices responses after exposure to decabromodiphenyl ethane in a soil-earthworm-microbe system.

As a novel brominated flame retardant (NBFR), decabromodiphenyl ethane (DBDPE) has been poorly understood for the environmental fate and toxicity in terrestrial invertebrates. For the first time, the bioaccumulation, elimination, metabolism and detoxification of DBDPE in earthworms as well as its potential impacts on soil microbes were investigated. The results showed much higher DBDPE concentrations in casts than in earthworms. The bioaccumulation factor (BAF) and elimination rate constant (ke) values were 0.028-0.213 (gdw, worm/gdw, soil) and 0.323-0.452 (day-1), respectively. The detoxifying enzymes (CYP450 and GST) could be induced by DBDPE within the range of exposure dosage, and the activities were significantly increased at 21 d (p < 0.05). The results were identified by GC-ECNI-MS, and it showed that at least eleven unknown peaks were separately observed in the earthworms, which were the biotransformation products of DBDPE in earthworms. Additionally, the damages, including skin shrinkage, setae impairment, and intercellular vacuolization, were clearly observed by SEM/TEM. Based on these data, DBDPE could accumulate in earthworms, yet, with low bioaccumulation ability. Moreover, DBDPE exposure resulted in minimal harmful impacts on microbial activities including microbial biomass C (MBC), Microbial basal respiration (MBR), Urease (US) activity and fluorescein diacetate hydrolase (FDA) activity (p < 0.05). Our findings would provide some essential information for interpreting the ecological risks of DBDPE in soil.

Legacy and alternative halogenated flame retardants in Lake Geneva fish.

Legacy (i.e., polybrominated diphenyl ethers (PBDEs) and hexabromocyclododecane (HBCDD)) and alternative halogenated flame retardants (HFRs) were analyzed in 31 whole fish samples from Lake Geneva in 2018. Two fish species, namely, the burbot (Lota lota) and the roach (Rutilus rutilus), were selected, hypothetically representing different habitats, feeding behaviors, and different metabolic capacities. Roach (N = 20) and burbot (N = 11) displayed similar size and mass, but the latter species was overall leaner than the former. The sum of individual PBDE concentrations (0.54-9.86 ng g-1 wet weight (ww)) was similar in both species, but the respective molecular profiles suggested contrasted metabolic capacities. HBCDD sum of isomer concentrations ranged from non-detected to 3.477 ng g-1 (ww), also similar in both species. Both PBDEs and HBCDD levels were far below the threshold that indicates a risk to fish predators. Referring to previous surveys, which involved a wider range of species, PBDE concentrations have declined or are stable. HBCDD concentrations remained low, despite the PBDE ban, which could have fostered the consumption of other HFRs. The occurrence of alternative HFRs was also low for most compounds analyzed. Only dechloranes and decabromodiphenyl ethane (DBDPE) had detection rates above 50%. Dechloranes spanned a concentration range between 5 and 10 times the quantification limits (0.002 to 0.005 ng g-1 wet weight), lower than DBDPE (< 0.005 to 2.89 ng g-1 wet weight). Quality standards targeting biota are currently missing for these emerging chemicals.

Long-term trends of airborne halogenated flame retardants (HFRs) by means of tree leaf and shoot analyses.

The historical air pollution with halogenated flame retardants (HFRs) in Germany was assessed by investigating tree leaf and shoot samples which have been archived in the German environmental specimen bank. Samples covered the period from 1985 to 2016. 43 HFRs comprising polybrominated diphenyl ethers as well as emerging brominated and chlorinated compounds such as Dechlorane Plus, DBDPE, or DPTE, were analysed in 115 samples from ten sub sites originating from six areas characterised by different land uses, including urban as well as a background site. HFRs were observed in each sample showing the widespread distribution of HFRs in Germany in tree leaves and shoots as bioindicators of past and present atmospheric pollution. Analytes observed at elevated concentrations were BDE 209, DBDPE and DPTE. Observed HFR-levels differed between analytes as well as sampling locations, particularly prior to the year 2000. They were typically highest at conurbation areas. Concentrations at the background site often belonged to the lowest ones observed, however, lowest values were not exclusively found there. The quantification frequencies appeared to decrease from the past to most recent samples. With few exceptions, atmospheric pollution of both, legacy and emerging HFRs, decreased significantly.

Determination of brominated flame retardants including polybrominated diphenyl ethers, pentabromoethylbenzene, hexabromobiphenyl, and decabromodiphenyl ethane in sediment samples: Validation of a rapid and efficient clean-up method and application to a sediment core from Lake Biwa, Japan.

The development of rapid and efficient analytical method for the determination of legacy and current-use brominated flame retardants (BFRs) has been performed due to environmental concern related to these pollutants. In the present study, we used an automated clean-up device equipped with pre-packed micro-column sets (containing sulfuric acid impregnated silica gel and silver-modified alumina) to develop an effective purification method for polybrominated diphenyl ethers (PBDEs), pentabromoethylbenzene, hexabromobiphenyl, and decabromodiphenyl ethane (DBDPE) in sediment extracts. Matrix-spiked sediments (n = 6) and the Standard Reference Material® 1944 samples (n = 6) were tested. Our method showed acceptable accuracy, repeatability, and sensitivity for almost all the target compounds with reduced processing time, labor requirement, and solvent amounts as compared to conventional clean-up method (e.g., sulfuric acid treatment and self-packed chromatographic columns). The validated method was applied to sediment core samples (n = 16) collected in 2019 from Lake Biwa, the largest lake in Japan. PBDEs were detected in sediment samples of 0-13 cm depth (dated between 1990 and 2019) at relatively low concentrations (median 5.7; range 2.6-9.4 ng/g dry weight). PBDE profiles were dominated by BDE-209, which accounted for 91 ± 10% of total PBDEs. Among other BFRs, only DBDPE was found in sediment layers of 0-9 cm depth (deposited between 2005 and 2019). DBDPE concentrations ranged from 0.43 to 1.6 (median 0.71) ng/g and showed increasing trend toward shallower depths.