Decabrominated Diphenyl Ether Research Articles

Role of autonomic nervous system in BDE-209 maternal exposure induced immunotoxicity in female offspring.

Decabrominated diphenyl ether (BDE-209) is a typical persistent organic pollutant that can cross the placental barrier, increasing the exposure risk for offspring. Norepinephrine (NE) from nerve terminals and acetylcholine (Ach) can bind to specific receptors on immune cells, inhibit the immune function of the body then cause immunotoxicity. However, whether maternal exposure to BDE-209 could lead to immunotoxicity in the offspring by acting on the sympathetic and parasympathetic nervous systems remains unclear. In view of this, the pregnancy and lactation rat BDE-209 exposure model was established and the results demonstrated that pregnancy and lactation BDE-209 exposure could induce immunotoxicity to female offspring via affecting immunopathology (hematological and biochemical parameters, organ indices, and spleen histopathological), decreasing humoral immunity (serum hemolysin, immunoglobulins, and cytokine productions), damaging cellular immunity (splenic lymphocytes and spleen cytokine productions), and restraining nonspecific immunity. Moreover, a dramatically significant correlation was observed between spleen nerve indices and immunity indices. Additionally, the mechanism revealed that maternal BDE-209 exposure caused offspring immunotoxicity through (1) activating MHC/PKCθ/NF-κB pathway; (2) promoting sympathetic nervous pathway, by upregulating the expression of β2AR protein, which in turn elevating cAMP, following activate PKA and phosphorylate CREB, ultimately leading to immunotoxicity;(3) activating parasympathetic nerve pathway by reducing the binding with Ach and α7nAchR, upregulating the expression of JAK2 and phosphorylating STAT3, induced immunotoxicity of female offspring.

Dynamics of leaching of POPs and additives from plastic in a Procellariiform gastric model: Diet- and polymer-dependent effects and implications for long-term exposure.

Procellariiform seabirds are known to have high rates of plastic ingestion. We investigated the bioaccessibility of plastic-associated chemicals [plastic additives and sorbed persistent organic pollutants (POPs)] leached from plastic over time using an in vitro Procellariiform gastric model. High-density polyethylene (HDPE) and polyvinyl chloride (PVC), commonly ingested by Procellariiform seabirds, were manufactured with one additive [decabrominated diphenyl ether (PBDE-209) or bisphenol S (BPS)]. HDPE and PVC added with PBDE-209 were additionally incubated in salt water with 2,4,4'-trichloro-1,1'-biphenyl (PCB-28) and 2,2',3,4,4',5'-hexachlorobiphenyl (PCB-138) to simulate sorption of POPs on plastic in the marine environment. Our results indicate that the type of plastic (nature of polymer and additive), presence of food (i.e., lipids and proteins) and gastric secretions (i.e., pepsin) influence the leaching of chemicals in a seabird. In addition, 100% of the sorbed POPs were leached from the plastic within 100 hours, while only 2-5% of the additives were leached from the matrix within 100 hours, suggesting that the remaining 95% of the additives could continue to be leached. Overall, our study illustrates how plastic type, diet and plastic retention time can influence a Procellariform's exposure risk to plastic-associated chemicals.

Hepatotoxicity evaluation and possible mechanisms of decabrominated diphenyl ethers (BDE-209) in broilers: Oxidative stress, inflammatory, and transcriptomics

Decabrominated diphenyl ether (BDE-209), a persistent organic pollutant, is linked to a great number of health problems, the most severe of which impact the liver due to its role in the elimination and degradation of exogenous harmful substances. Though the hepatotoxicity of BDE-209 has been observed, its underlying mechanism is yet unknown. The purpose of this study is to thoroughly investigate the hepatotoxicity of BDE-209 and its molecular processes in broilers by subjecting 120 male broilers to varied concentrations of BDE-209 for 42 days. We observed that the bioaccumulation of BDE-209 in the liver in a dose-dependent manner, and that BDE-209 exposure can raise the concentrations of ALT, AST, and GGT, accompanied by hepatocyte fatty degeneration and inflammatory foci. In the hepatic homogenates, oxidative stress was evidenced by elevated levels of MDA and ROS and decreased activies of SOD and CAT. Additionally, pro-inflammatory cytokines including IL-1, IL-1β, TNF-α, IL-8 levels were increased, whereas anti-inflammatory cytokine IL-4 level was declined. Furthermore, RNA sequencing revealed that genes involved in inflammation were considerably dysregulated, and real-time PCR verified the expressed alterations of numerous genes related to the MAPK and WNT signaling pathways. The protein concentrations of NF-κB, β-catenin, and WNT5A, and the phosphorylation levels of JNK and ERK were all dramatically enhanced. The current study indicates that BDE-209 exposure can cause hepatotoxicity in broilers via bioaccumulation and oxidative stress, which then activates the MAPK and WNT signaling pathways, subsequently generating inflammation and hepatic injury.

Curcumin alleviates spleen immunotoxicity induced by decabrominated diphenyl ethers (BDE-209) by improving immune function and inhibiting inflammation and apoptosis in broilers

This study was conducted to assess the mitigating effects of curcumin (Cur) on immunotoxicity in the spleen of broilers induced by the polybrominated diphenyl ether BDE-209. Eighty one-day-old broilers were allocated to the following four groups: control group, BDE-209 (0.4 g/kg) group, BDE-209 (0.4 g/kg) + Cur (0.3 mg/kg) group, and Cur (0.3 mg/kg) group. Growth performance, immunological function, inflammation, and apoptosis were assessed after 42 days of treatment. The findings demonstrate that firstly, Cur restored spleen damage caused by BDE-209 by increasing body weight, decreasing feed-to-gain ratio, correcting the spleen index, and improving the histopathological structure of the spleen. Secondly, Cur relieved BDE-209-induced immunosuppression by increasing the levels of the immunoglobulins IgG, IgM, and IgA in the serum, as well as the levels of white blood cells and lymphocytes. The levels at which GATA binding protein 3, T-box expressed in T cells, interferon-γ, and interleukin (IL)− 4 are expressed were controlled. The ratio of T helper (Th) type 1 (Th1) to Th2 cells in the spleen of broilers was also controlled. Thirdly, Cur reduced the expression of Toll like receptor (TLR) 2, TLR4, nuclear factor (NF)-κB, IL-8, IL-6, and IL-1β, which alleviated BDE-209-induced inflammation in broilers. Cur reduced BDE-209-induced apoptosis by increasing the expression of the bcl-2 protein, decreasing the expression of cleaved caspase-3 and bax proteins, decreasing the bax/bcl-2 protein ratio, and decreasing the mean optical density of TUNEL. These results suggest that Cur protects broiler spleens from BDE-209-induced immunotoxicity via modulating humoral immunity, the equilibrium between Th1 and Th2 cells, the TLRs/NF-κB inflammatory pathway, and the apoptotic pathway.

In silico assessment of mixture toxicity mechanisms involved in the pathogenesis of thyroid diseases: The combination of toxic metal(oid)s and decabrominated diphenyl ether

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.

Legacy and novel brominated flame retardants in animal-derived foods from China Total Diet Study (CTDS): Temporal trends, evidence of substitution, and dietary exposure assessment.

Based on the 6th China Total Diet Study (CTDS) conducted in 2016-2019, the occurrence of both legacy and novel brominated flame retardants (BFRs) was measured in animal-derived foods collected across China. Most BFRs could be frequently detected in food samples, indicating their ubiquity in the environment. Decabromodiphenyl ethane (DBDPE), a typical novel BFR, presented the highest contamination level, whereas legacy BFRs, including decabrominated diphenyl ether (BDE-209), tetrabromobisphenol A (TBBPA), and hexabromocyclododecane (HBCDD), still presented high detection frequencies and relatively abundant proportions in total BFRs. Compared with previous CTDSs conducted from 2007 to 2011, the levels and estimated dietary intakes (EDIs) of most BFRs showed a significant downtrend, which suggested that flame retardant consumption in China has transferred from legacy BFRs to novel BFRs (mainly DBDPE) and from BFRs to other kinds of flame retardants. Based on probabilistic estimation, the median EDIs of mainly used BFRs for the Chinese population ranged from 41.0 to 1.67×103 pg/kg bw/day, and meat consumption was the primary source in dietary BFR intake. By conducting the margin of exposure (MOE) approach or comparing with the reference dose (RfD), it can be concluded that daily dietary intakes of BFRs were still unable to cause significant health risks to the general population in China.

The thermal degradation and soil recovery of thermal treatment of field-weathered decabrominated diphenyl ether-contaminated soil

A farm at Taoyuan in Taiwan was highly contaminated with decabrominated diphenyl ether (BDE-209), a widely used commercial brominated flame retardant and persistent in the environment, more than 10 years. Since crops are able to absorb and accumulate BDE-209 from soils in our previous research, posing a hazardous risk for humans, it is essential to develop a practical method of soil treatment. Thermal treatment was studied among different approaches. In our previous study (Ko et al., 2022), we found that heating to 450 °C for 30 min achieved a complete removal of BDE-209 in soil. However, the high temperature significantly decreased the original soil organic matter (SOM) from 2.47% to 0.27%, altering the soil texture, damaging microbial biomass, and thus affecting the revegetation after the thermal treatment. Sugarcane bagasse, a common agricultural residue, served as an amendment to restore soil fertility. Current results indicate that 2.5% bagasse can improve the SOM in soil by up to 2.73% and restore its bacterial composition, making the plant growth conditions similar to those of the untreated contaminated soil. In light of the high removal efficiency provided by the 450°C-thermal treatment and the high recovery efficiency of sugarcane bagasse, the strategy presented in this study serves to be a promising method for sustainable remediation.

Toxicokinetics and edible tissues-specific bioaccumulation of decabrominated diphenyl ethers (BDE-209) after exposure to the broilers

Decabromodiphenyl ether (BDE-209), the primary constituent of a widely used flame retardant formulation, is often present in high levels in avian derived products and could be transferred to humans through consumption. The purpose of this study was to investigate the toxicokinetics and bioaccumulation patterns of BDE-209 in different tissues of broilers, which would benefit the evaluation of chicken product safety. Male broilers received a single oral administration of BDE-209 at 25 mg/kg.BW and then BDE-209 concentrations in the plasma, liver, leg muscle, breast muscle, and other tissues were measured using gas chromatography-electron capture detection (GC-ECD). The changes of BDE-209 concentrations in the plasma were fitted to a non-compartmental model for kinetic analysis. Peak values were observed at 24 h (t1/2 =168.28 h), and trace levels remained for four weeks. Additionally, Cmax in the liver was much higher than that in leg and breast muscles, and Tmax from the liver and muscle were 12 and 24 h, respectively. Residual BDE-209 was detected in all broiler tissues after 2 weeks, and concentrations were ranked as follows: fat > liver > thymus gland > heart > testis > thigh muscle > skin > lung > kidney > breast muscles > spleen (wet weight (ww)). Our results suggested that BDE-209 was widely distributed in different tissues after intestinal absorption, and preferentially accumulated in adipose and liver tissues. Observations of bioaccumulation and slow elimination in the liver and muscles provide critical insight into the toxicity of BDE-209 and risk assessment of edible tissues from broilers.

Vitamin C supplementation rescued meiotic arrest of spermatocytes in Balb/c mice exposed to BDE-209

Deca-brominated diphenyl ether (BDE-209) is a ubiquitous industrial chemical as brominated flame retardant (BFRs). Exposure to BDE-209 has been clearly associated with male reproductive disorders. However, the meiotic arrest mechanism of spermatocytes exposed to BDE-209 is still unclear. The present work aimed to explore the protective effect of vitamin C on BDE-209-induced meiotic arrest of spermatocytes and its possible mechanism. Vitamin C (100 mg/kg BW) was administered to BDE-209-exposed (80 mg/kg BW) male Balb/c mice once daily by intraperitoneal injection for 2 weeks. Our results showed that vitamin C played male reproductive protection effects as showed by attenuated BDE-209-induced testicular damage, and reduced sperm abnormality rate. Vitamin C also attenuated BDE-209-induced increase in SOD and MDA in testes and GC-2 spd cells. Moreover, vitamin C promoted meiotic prophase in BDE-209-induced mice, with suppressed γ-H2AX, restored DMC1, RAD51, and crossover marker MLH1 levels, and prevented BDE-209-induced DNA impairment. In addition, vitamin C supplementation also interfered with BDE-209-induced upregulation of testicular H3K4me3 through inhibition of KDM5s capacity and decreasing ferrous ion concentration. Furthermore, ferrous sulfate pretreatment could partially restore the expression of H3K4me3 via maintaining the concentration of ferrous ions. Taken together, vitamin C exerts a potential therapeutic agent for preventing BDE-209-induced reproductive toxicity with meiotic arrest, which is attributed to its antioxidant and electron donor properties, as well as, modulation of ferrous ion levels and demethylation of H3K4me3.

A cleanup method of serum extracts with molecular sieves as SPE sorbents for the analysis of polybrominated diphenyl ethers.

Based on the size- and shape-selective sorption, 13X molecular sieves were developed as solid-phase extraction adsorbents to cleanup serum extract for the determination of polybrominated diphenyl ethers. The important parameters affecting the cleanup efficiency were investigated including the amount of sorbents, the type, and volume of solvents. Under the optimized conditions, the capacity for removing impurities was evaluated via gel permeation chromatography and gas chromatography with mass spectrometry. The results demonstrated that up to 99% of lipids in corn oil (13 mg) can be removed after cleanup, and endogenous compounds in serum can also be effectively eliminated. The cleanup efficiency is not only superior to hydrophile-lipophile balance column, but also close to acid silica gel and multifunction impurity sorbents. Generally, the developed cleanup method exhibited higher recovery for polybrominated diphenyl ethers with more than four bromines, especially for nona- and deca-brominated diphenyl ethers (99.1-117.8%). The cleanup method can be coupled with gas chromatography and tandem mass spectrometry for polybrominated diphenyl ethers analysis in human serum. The method detection limits were 0.01-0.27 ng/mL and average recovery was 50.9-113.3%, except 2,3',4',6-tetrabrominated, 2,3',4,4',6-pentabrominated, and 2,3,3',4,4',5',6-heptabrominated diphenyl ethers. 2,2',4,5'-Tetrabrominated diphenyl ethers had the highest detection frequency (95%) in human serum, whereas decabrominated diphenyl ethers had the maximum mean concentration (0.50 ng/mL).

Photodegradation of Decabrominated Diphenyl Ether in Soil Suspensions: Kinetics, Mechanisms and Intermediates

Pollution by polybrominated diphenyl ethers (PBDEs) is a major concern due to their bioaccumulation, persistence, and carcinogenicity. This study aimed to investigate the decabrominated diphenyl ether (BDE-209) photodegradation in soil suspensions. The results indicate BDE-209 can degrade in soil suspensions and its degradation follows pseudo-first-order kinetics. The light sources and intensity effects were studied and the photodegradation rates were 500 W Mercury Lamp > 300 W Mercury Lamp > 500 W Xenon Lamp > 300 W Xenon Lamp, which indicates UV light is the main reason for BDE-209 degradation. Soil particle inhibits BDE-209 photodegradation due to the light-shielding effect. BDE-209 photodegradation rates increased from 0.055 to 0.071 h−1 with pH value increasing from 3.5 to 9.5. This may be because the products are more easily produced in higher pH soil suspensions. The presence of humic acid (HA) may inhibit BDE-209 photodegradation by photo-shielding. Fe3+ and Cu2+ have an adverse effect on BDE-209 photodegradation due to the photo competition. The •OH and 1O2 were detected in soil solutions. Analysis of the photoproducts of BDE-209 by gas chromatography mass spectrometry (GC-MS) and liquid chromatography time of flight mass spectrometry (LC-TOF-MS) showed that BDE-209 was mainly debrominated to the lower-brominated BDEs and the reactive oxygen radicals may not lead to BDE-209 degradation.

Extracellular chemoreceptor of deca-brominated diphenyl ether and its engineering in the hydrophobic chassis cell for organics biosensing

• Global gene expression analysis reveals a novel biorecognition receptor of PBDEs. • Chemoreceptor of PBDEs is an extracellular Cache domain-containing sensor protein. • Sensor protein is displayed on the cell membrane of a hydrophobic chassis cell. • Hydrophobic whole-cell biosensor provides a specific and sensitive response to PBDEs. • It provides a new approach for quality monitoring and toxicity assessing of organics. Polybrominated diphenyl ethers (PBDEs) belong to a group of persistent organic pollutants and pose a risk of causing adverse effects to human health and the environment. Detection and monitoring of these compounds therefore is of great interest and need for remediation and health risk assessment. However, no specific receptor protein can be used as a biorecognition element for the development of PBDE-detecting whole-cell biosensor until now. The lack of knowledge of PBDEs metabolic pathways of bacteria and of bacterial regulatory networks is the main limitation in the successful biosensor design. In this study, the global gene expression analysis of promoter activation as a consequence of deca-BDE exposure led to the finding of a novel sensory element, extracellular Cache domain-containing sensor protein Chr1_2466, for specific biorecognition of PBDEs. A genetically engineered hydrophobic chassis cell, Sphingobium xenophagum C1, expressing firefly luciferase in place of Chr1_2466 on the cell membrane served as a whole-cell biosensor for PBDEs detecting. This biosensor was highly specific for PBDEs and had minimal interference from their structural analogues polychlorinated biphenyls, diphenyl ether, phenol, metals, and inorganic ions. The extracellular luminescence intensity of the hydrophobic whole-cell biosensor showed a linear relationship (R 2 = 0.98) from 0.05 to 6.0 µM of deca-BDE with a detection limit of 0.01 µM and a cytotoxicity threshold of 6.25 µM. Compared to the hydrophilic strain as chassis cell, such hydrophobic biosensor significantly increased the bioavailability and detection sensitivity of PBDEs. It provides a new approach for quality monitoring and toxicity assessing of hydrophobic organics.

Decabromodiphenyl ether induces ROS-mediated intestinal toxicity through the Keap1-Nrf2 pathway.

Polybrominated diphenyl ethers (PBDEs) arewidely used brominated flame retardants as commercial products. PBDEs have been demonstrated to induce hepatic, reproductive, neural, and thyroid toxicity effects. This study aimed to clarify the potential intestinal toxicity effects of decabrominated diphenyl ether (PBDE-209) in vivo and in vitro. First, we investigated the change of PBDE-209 on oxidative stress in the intestine of mice. Subsequently, the potential toxicity mechanism of PBDE-209 in vitro was investigated. Caco-2 cells were treated with different concentrations of PBDE-209 (1, 5, and 25 μmol/L) for 24 and 48 h. We determined the cell viability, reactive oxygen species (ROS) level, multiple cellular parameters, and relative mRNA expressions. The results showed that PBDE-209 significantly injured the colon of mice, increased the intestinal levels of malondialdehyde (MDA), and changed the antioxidant enzyme activities. PBDE-209 inhibited the proliferation and induced cytotoxicity of Caco-2 cells. The change in ROS production and mitochondrial membrane potential (MMP) revealed that PBDE-209 caused oxidative stress in Caco-2 cells. The real-time PCR assays revealed that PBDE-209 inhibited the mRNA expression level of antioxidative defense factor, nuclear factor erythroid 2-related factor 2 (Nrf2). Furthermore, the FAS and Cytochrome P450 1A1 (CYP1A1) mRNA expression levels were increased in Caco-2 cells. These results suggested that PBDE-209 exerts intestinal toxicity effects in vivo and in vitro and inhibits the antioxidative defense gene expression in Caco-2 cells. This study provides an opportunity to advance the understanding of toxicity by the persistent environmental pollutant PBDE-209 to the intestine.

The Removal Mechanism and Soil Recovery of Thermal Treatment of Highly Decabrominated Diphenyl Ether Contaminated Soil

The Removal Mechanism and Soil Recovery of Thermal Treatment of Highly Decabrominated Diphenyl Ether Contaminated Soil

BDE-209 induce spermatocytes arrest at early-pachytene stage during meiotic prophase I in mice

Deca-brominated diphenyl ether (BDE-209) is a common flame retardant utilized in electronic products, textiles, furniture, and upholstery materials. Environmental BDE-209 exposure results in spermatogenesis disorder, because of the characteristics of bioaccumulation, persistence, and probably toxicity. Meiotic prophase I is a crucial phase during spermatogenesis which is a key influential factor of normal sperm production. However, the effects of BDE-209 on meiotic prophase I during spermatogenesis are poorly understood. The present study aimed to evaluate whether BDE-209 exposure impairs meiotic prophase I during spermatogenesis of spermatocytes. We validated the effects of BDE-209 on alternations of meiotic prophase I in Balb/c male mice. Firstly, we analyzed sperm quality in cauda epididymis with decreasing sperm count, increasing abnormal sperm, and male reproductive dysfunction after exposure to BDE-209. Then, reactive oxygen species (ROS) and malondialdehyde (MDA) levels in testis and GC-2spd cells were significant increased after treated with BDE-209. Furthermore, we found that meiotic prophase I arrest at early-pachytene stage during spermatogenesis with increasing of DSBs damage and trimethylated histone H3 at lysine-4 (H3K4me3) in spermatocytes exposed to BDE-209. Finally, we conducted homologous recombination (HR) analyses to identify the progression of meiosis. The recombination markers, including DMC1 and RAD51, and crossover marker MLH1 were decreased during spermatogenesis after exposure to BDE-209. Collectively, our data indicated that BDE-209 has detrimental impacts on meiotic prophase I of spermatocytes in mice.

Microplastics habituated with biofilm change decabrominated diphenyl ether degradation products and thyroid endocrine toxicity

Microplastics (MPs) are rapidly colonized by microbial biofilms in a natural aquatic environment, and the nature of the microbial community and type of MP can result in different degradation products of organic pollutants. Here, we quantified the degradation products of a ubiquitously detected pollutant, decabrominated diphenyl ether (BDE-209), under both light-only and biota conditions and in the absence or presence of three kinds of MPs, styrofoam polystyrene, hard polyamide, and polypropylene film. The results showed that the BDE-209 concentration increased by 0.7–2.8 fold in the presence of MPs, probably due to the “sustained release” desorption effect. Under light-only conditions, the penta- and hexa-BDE concentrations in the presence of styrofoam or hard MPs were significantly reduced, which can be deemed a beneficial effect. However, when biota were present, the debromination products increased with the addition of MPs, particularly in the presence of styrofoam MPs. These products caused a 1.7-fold upregulation in triiodothyronine content and a 5.9-fold upregulation of thyroid stimulating hormone β expression in zebrafish larvae. The increase in debromination products could be attributed to the distinct high abundance of the bacteria Chloroflexi, Proteobacteria, and Basidiomycotina on styrofoam MPs that can participate in pollutant degradation. Collectively, our results indicate that MPs can alter the degradation pathways of BDE-209 and increase the toxicity to the endocrine system and the thyroid in aquatic organisms.

Reduced mitochondrial DNA copy number in occupational workers from brominated flame retardants manufacturing plants

Decabrominated diphenyl ether (BDE-209) and its substitute decabromodiphenyl ethane (DBDPE) are two flame retardants that have similar structure and are widely used in various industrial products. The accumulation and potential toxicity of them to human health have already aroused attention, and some research showed that they may affect mitochondrial function. Therefore, this study focused on the population with high exposure to brominated flame retardants (BFRs) and the related changes in mtDNA copy number (mtDNAcn) in whole blood. 334 blood samples were collected from three groups of people in Shandong Province, including 42 BDE-209 occupational exposure workers from the BDE-209 manufacturing plant, 131 DBDPE occupational exposure workers from the DBDPE manufacturing plant, and 161 non-BFRs occupational exposure residents from the BFRs contaminated area. We measured the levels of BDE-209, DBDPE in serum sample, and the mtDNAcn in whole blood sample and analyzed these data by multiple linear regression. The average concentrations of BDE-209, DBDPE and ∑(BDE-209 + DBDPE) in BDE-209 occupational workers were 3510, 639 and 4600 ng/g lw, respectively; the average concentrations of BDE-209, DBDPE and ∑(BDE-209 + DBDPE) in DBDPE occupational workers were 229, 4040 and 4470 ng/g lw, respectively; the average concentrations of BDE-209, DBDPE and ∑(BDE-209 + DBDPE) in non-BFRs occupational exposure residents were 66.3, 45.7 and 137 ng/g lw, respectively. The relative mtDNAcn was 0.823 in BDE-209 occupational workers, 0.845 in DBDPE occupational workers and 0.989 in non-BFRs occupational exposure residents. A 10-fold increase in BDE-209, DBDPE concentrations was separately associated with a 0.068 and 0.063 decrease in mtDNAcn. Therefore, our study implied that BFRs may affect mitochondrial function. As increasing BFRs exposure has emerged in recent years, the relationship between BFRs exposure and mitochondrial function needs further study.

Thermal treatment of decabrominated diphenyl ether in its highly contaminated soil in Taiwan

Polybrominated diphenyl ethers (PBDEs) were commonly used flame retardants in the world, while some of PBDEs have been listed as persistent organic pollutants (POPs). Decabrominated diphenyl ether (BDE-209) was the most commercially used PBDEs. A farm near the factory located in Northern Taiwan was highly contaminated with BDE-209. Since PBDEs in the contaminated soils can be uptake by crops shown in our previous studies and could be potentially consumed by humans, it is very important to establish a feasible treatment method for PBDE remediation in this contaminated farm. Thermal treatment of PBDEs in soil was studied. The initial concentration of BDE-209 in contaminated soil was 1.472 mg/kg. A series of thermal experiments under different operating conditions including various temperature (105, 150, 200, 250, 300, 350, 400 and 450 °C), holding time (10, 20 and 30 min), heating rate (5, 10, 20 and 40 °C/min), and soil amount (10, 100, 1000 and 2000 g) were investigated. The optimal heating conditions for thermal treatment of contaminated soil were heating at 450 °C for 30 min with a heating rate of 10 °C/min. Under this condition, the removal of BDE-209 in the different weights of contaminated soil was tested. The soils in the contaminated farm were tested to further evaluate the feasibility of remediating the on-site PBDE contaminated soil through thermal treatment, suggesting that the holding time was extended to 2 h for the field-scale contaminated soil. The results showed that BDE-209 had been removed to below the detection limit in on-site soil. This investigation is the first study using thermal treatment to remediate soils really contaminated with PBDEs.

Assessing the combinatorial cytotoxicity of the exogenous contamination with BDE-209, bisphenol A, and acrylamide via high-content analysis

Food is often exposed to multiple types of contaminants, and the coexistence of contaminants may have antagonistic, additive or synergistic effects. This study investigated the combinatorial toxicity of the three most widespread exogenous contaminants, decabrominated diphenyl ether (BDE-209), bisphenol A (BPA), and acrylamide (ACR) to HepG2 cells. A mathematical model (Chou-Talalay) and high-content analysis (HCA) were used to probe the nature of the contaminants’ interactions and their cytotoxicity mechanisms, respectively. The results highlighted that for the individual pollutants, the cytotoxicity order was BDE-209> BPA > ACR, and varying combinations of contaminants exhibited additive/synergistic effects. In general, combining multiple contaminants significantly increased intracellular reactive oxygen species (ROS), Ca2+ flux, DNA damage and Caspase-3, and decreased mitochondrial membrane potential (MMP) and nucleus roundness, indicating that the additive or synergistic mechanism of the combined contaminations was disturbance to multiple organelles. This study emphasizes the complexity of human exposure to food contaminants and provides a scientific basis for formulating strict regulatory standards.

Radiolytic degradation of BDE-209 in rice-vegetable rotation soils induced by electron beam irradiation

Deca-brominated diphenyl ether (BDE-209) is shown to be persistent in soil and it's urgent to find an effective method to remove BDE-209 from contaminated soil. In this study, the investigation of BDE-209 degradation in three different rice-vegetable rotation soils induced by electron beam (E-beam) irradiation under flooded and non-flooded conditions was conducted. The reductive efficiency of 14C-BDE209 reached the highest level at 50 kGy and the values in flooded soils of rice-eggplant rotation soil (RES), rice-peanut soil (RPS), and rice-chili pepper soil (RCS) were 93.5%, 87.2%, and 73.8%, respectively. The reductive efficiencies in non-flooded soils of RES, RPS, and RCS were 73.4%, 81.0%, and 78%, respectively. The D0.5 values (dose required for reducing 50% BDE-209) of BDE-209 in non-flooded soils were lower than those in flooded soils, suggesting greater degradation efficiency of BDE-209 in non-flooded soils than in flooded soils. The BDE-209 was degraded into higher-brominated PBDEs and lower-brominated PBDEs by E-beam irradiation. The results demonstrate that BDE-209 in the soil can be degraded by E-beam irradiation, non-flooded condition is better than flooded condition for the removal of BDE-209, and the main degradation mechanism of BDE-209 by E-beam irradiation is debromination. This study provides a rapid and effective method for degrading BDE-209 that is persistent in soils, and has important implications for the remediation of soil contaminated by PBDEs in and around E-waste dismantling areas.