The effect and underlying mechanism of tetrabromobisphenol A (TBBPA), a plastic additive, on biofilm formation of methicillin-resistant Staphylococcus aureus (MRSA USA300) remain unknown. This study first investigated the impact of different concentrations of TBBPA on the growth and biofilm formation of USA300. The results indicated that a low concentration (0.5 mg/L) of TBBPA promoted the growth and biofilm formation of USA300, whereas high concentrations (5 mg/L and 10 mg/L) of TBBPA had inhibitory effects. Further exploration revealed that the low concentration of TBBPA enhance biofilm formation by promoting the synthesis of extracellular proteins, release of extracellular DNA (eDNA), and production of staphyloxanthin. RTqPCR analysis demonstrated that the low concentration of TBBPA upregulated genes associated with extracellular protein synthesis (sarA, fnbA, fnbB, aur) and eDNA formation (atlA) and increased the expression of genes involved in staphyloxanthin biosynthesis (crtM), suggesting a potential mechanism for enhanced resistance of USA300 to adverse conditions. These findings shed light on how low concentrations of TBBPA facilitate biofilm formation in USA300 and highlight the indirect impact of plastic additives on pathogenic bacteria in terms of human health. In the future, in-depth studies about effects of plastic additives on pathogenicity of pathogenic bacteria should be conducted. CAPSULE: The protein and eDNA contents in biofilms of methicillin-resistant Staphylococcus aureus are increased by low concentrations of TBBPA.

Gestating mice were exposed to three chemicals, tetrabromo-bisphenol A (TBBPA; 2 mg/kg/day), amitrole (25 and 50 mg/kg/day) and pyraclostrobin (0.4 and 2 mg/kg/day) to assess their capacity to act as thyroid hormone disruptors and compromise neurodevelopment. Propyl-thio-uracyl, a known pharmacological inhibitor of thyroid gland secretion, was used at both high and low dose as a reference thyroid hormone system disruptor (1 ppm, 1500 ppm). A combination of plasma metabolomics and striatum transcriptomics revealed the induced change in pups at the postnatal stages. Although the underlying mechanism is unlikely to involve thyroid hormone disruption, these chemicals had a detectable effect on pups\' neurodevelopment.

The response sensitivity to toxic substances is the most concerned performance of animal model in chemical risk assessment. Casper (mitfaw2/w2;mpv17a9/a9), a transparent zebrafish mutant, is a useful in vivo model for toxicological assessment. However, the ability of casper to respond to the toxicity of exogenous chemicals is unknown. In this study, zebrafish embryos were exposed to five environmental chemicals, chlorpyrifos, lindane, α-endosulfan, bisphenol A, tetrabromobisphenol A (TBBPA), and an antiepileptic drug valproic acid. The half-lethal concentration (LC50) values of these chemicals in casper embryos were 62-87 % of that in the wild-type. After TBBPA exposure, the occurrence of developmental defects in the posterior blood island of casper embryos was increased by 67-77 % in relative to the wild-type, and the half-maximal effective concentration (EC50) in casper was 73 % of that in the wild-type. Moreover, the casper genetic background significantly increased the hyperlocomotion caused by chlorpyrifos and lindane exposure compared with the wild-type. These results demonstrated that casper had greater susceptibility to toxicity than wild-type zebrafish in acute toxicity, developmental toxicity and neurobehavioral toxicity assessments. Our data will inform future toxicological studies in casper and accelerate the development of efficient approaches and strategies for toxicity assessment via the use of casper.

As widely used alternative brominated flame retardants, tetrabromobisphenol S (TBBPS) and its derivatives have attracted increasing amounts of attention in the field of environmental science. Previous studies have shown that TBBPS and its derivatives easily accumulate in environmental media and may cause risks to environmental safety and human health. Therefore, to explore the environmental behaviours of TBBPS and its derivatives, in this paper, we summarized relevant research on the distribution of these compounds in water, the atmosphere, soil and food/biota, as well as their transformation mechanisms (biological and nonbiological) and toxic effects. The summary results show that TBBPS and its derivatives have been detected in water, the atmosphere, soil, and food/biota globally, making them a ubiquitous pollutant. These compounds may be subject to adsorption, photolysis or biological degradation after being released into the environment, which in turn increases their ecological risk. TBBPS and its derivatives can cause a series of toxic effects, such as neurotoxicity, hepatotoxicity, cytotoxicity, thyrotoxicity, genotoxicity and phytotoxicity, to cells or living organisms in in vitro and in vivo exposure. Toxicological studies suggest that TBBPS as an alternative to TBBPA is not entirely environmentally friendly. Finally, we propose future directions for research on TBBPS and its derivatives, including the application of new technologies in studies on the migration, transformation, toxicology and human exposure risk assessment of TBBPS and its derivatives in the environment. This review provides useful information for obtaining a better understanding of the behaviour and potential toxic effects of TBBPS and its derivatives in the environment.

BACKGROUND: Brominated Flame Retardants (BFRs) have attracted widespread concern due to their environmental persistence and potential toxicity. This study aims to examine the association between BFRs exposure and hypertension.
METHODS: We used data from the National Health and Nutrition Examination Survey (NHANES) spanning 2005 to 2016 for the cross-sectional analysis. To evaluate the individual and combined impacts of BFRs exposure on hypertension, we utilized multivariate models, including generalized additive models, weighted quantile sum (WQS) regression, and Bayesian kernel machine regression (BKMR) models.
RESULTS: 9882 individuals (48% male) aged ≥ 20 were included in the final analysis, of whom 4114 had hypertension. After controlling for potential covariates, higher serum concentrations of PBDE100 (OR: 1.26; 95% CI: 1.01, 1.57) and PBDE153 (OR: 1.50; 95% CI: 1.18, 1.88) were significantly associated with hypertension. A nonlinear relationship between PBDE28 and hypertension was observed (P = 0.03). Moreover, BFRs mixture were positively associated with the prevalence of hypertension in both the WQS (β:1.09; 95% CI: 1.02, 1.17; P = 0.02) and BKMR models.
CONCLUSIONS: Our study suggested that BFRs exposure is positively associated with hypertension in the general population. To confirm this association and elucidate the mechanisms, further research is required.

In this study, we investigated the degradation of the flame retardant tetrabromobisphenol A (TBBPA) using platinized tungsten oxide (Pt/WO3), synthesized via a simple photodeposition method, under visible light. The results of degradation experiments show a significant enhancement in TBBPA degradation upon surface platinization of WO3, with the degradation rate increasing by 13.4 times compared to bare WO3. The presence of Pt on the WO3 surface stores conduction band electrons, which facilitates the two-electron reduction of oxygen and enhances the production of valence band holes (hVB+) and hydroxyl radicals (●OH). Both hVB+ and ●OH are significantly involved in the degradation of TBBPA in the visible light-irradiated Pt/WO3 system. This was verified through fluorescence spectroscopy employing coumarin as a chemical probe and oxidizing species-quenching experiments. The analysis of degradation products and their toxicity assessment demonstrate that the toxicity of TBBPA-contaminated water is significantly reduced after Pt/WO3 photocatalysis. The degradation rate of TBBPA increased with increasing Pt/WO3 dosage, reached an optimum at a Pt content of 0.5 wt%, but decreased with increasing TBBPA concentration. The decrease in degradation efficiency of Pt/WO3 was minor, both in the presence of various anions and after repeated use. This study proposes that Pt/WO3 is a viable photocatalyst for the degradation of TBBPA in water under visible light.

Brominated flame retardants (BFRs) are a kind of brominated compounds widely used in electronic and electrical appliances, textiles, construction materials and other industrial products to improve the flame retardant property. Because of its strong chemical stability, environmental persistence, long-distance transmission, biological accumulation, the exposure of humans and organisms in the ecosystem is increasing, and its potential biological effects are of great concern. Now BFRs can be detected in breast milk, serum, placenta and cord blood. Studies have shown that exposure to BFRs during pregnancy can lead to adverse birth outcomes such as low birth weight, malformation, gestational age changes and impairment of neurobehavioral development. This article summarizes the pollution and population exposure of three traditional BFRs, polybrominated diphenyl ethers (PBDEs), hexabromocyclododecane (HBCD), and tetrabromobisphenol A (TBBPA), as well as the impact and mechanism of prenatal exposure on offspring birth outcomes and growth and development. It explores the harm of prenatal exposure to BFRs to offspring and proposes preventive measures for occupational populations for reference.
溴系阻燃剂（brominated flame retardants，BFRs）是一类广泛用于电子电器、纺织、建筑材料等工业产品以提升阻燃性能的含溴化合物。由于其化学稳定性强，具有环境持久性、远距离传播性和生物蓄积性，目前母乳、血清及胎盘、脐带血中均可检测到BFRs。研究表明孕期暴露BFRs与多种不良出生结局如低体重、畸形、胎龄改变、神经行为发育损害有关。本文总结了三大传统BFRs，多溴二苯醚、六溴环十二烷、四溴双酚A的污染与人群暴露情况、孕期暴露对子代出生结局、生长发育的影响及作用机制，对BFRs孕期暴露对子代的危害进行探讨，为职业人群的预防措施提供参考。.

Tetrabromobisphenol S (TBBPS) is a brominated flame retardants (BFRs). TBBPS is widely used as a new type of BFR to replace TBBPA. Here, we used gastric cells as a model for evaluating the effect of TBBPS on the toxicology of gastric cells. Biochemical assays such as indirect immunofluorescence, cell proliferation assay were performed to analyze the toxicological effects of TBBPS on gastric cells. Cell proliferation analysis showed that TBBPS caused inhibition of gastric cell proliferation, and TBBPS induced gastric cell death. Further analysis showed that TBBPS led to ferroptosis and senescence of gastric cells by detecting ferroptosis-related marker molecules. Further work showed that TBBPS treatment resulted in lowered ferritin expression alongside heightened transferrin levels, which may be a potential molecular mechanism for TBBPS-induced ferroptosis and senescence in gastric cells. Here, our team investigates the effects of TBBPS on gastric cells in an in vitro model, and found that TBBPS caused toxicological damage to gastric cells. This study indicates potential toxic effects of TBBPS on the gastric cells, thereby providing a basis for further research into the toxicology of TBBPS.

Tetrabromobisphenol-A-bis(2,3-dibromopropyl ether) (TBBPA-BDBPE), a novel additive brominated flame retardant, is being developed for use in polyolefin and copolymers. Despite its emerging application, the neurotoxicity and mechanisms of action of TBBPA-BDBPE remain unexplored. Caenorhabditis elegans was utilized as the model organism to study the neurotoxic effects of TBBPA-BDBPE across environmental concentrations ranging from 0 to 100 μg/L. This investigation focused on various toxicological endpoints such as locomotive behavior, neuronal injury, neurotransmitter transmission, and the regulation of nervous system-related gene expression. Acute exposure to TBBPA-BDBPE at concentrations of 10-100 μg/L significantly impaired nematode movement, indicating potential neurotoxicity. In transgenic nematodes, this exposure also caused damage to γ-aminobutyric acid (GABAergic) and serotonergic neurons, along with notable changes in the levels of GABAergic and serotonergic neurotransmitters. Further molecular studies indicated alterations in neurotransmission-related genes (cat-4, mod-1, unc-25, and unc-47). Molecular docking analysis confirmed the binding affinity of TBBPA-BDBPE to key neurotransmission proteins-CAT-4, MOD-1, UNC-25, and UNC-47. These findings demonstrate that TBBPA-BDBPE exerts neurotoxic effects by impacting GABAergic and serotonergic neurotransmission in nematodes. This study provides new insights into the potential environmental risks of TBBPA-BDBPE.

Wastewater containing tetrabromobisphenol A (TBBPA), a commonly used flame retardant found in wastewater, can present significant toxic effects on biota, yet its impact on tropical freshwater environments is not well understood. This study explores the effectiveness of two independent anaerobic treatment systems, the acidogenic reactor (AR) and the methanogenic reactor (MR), for the ecotoxicity reduction of TBBPA-rich wastewater in four tropical freshwater species. Despite presenting good physicochemical performance and reduced toxicity of the influent for most species, AR and MR treatments remain acute and chronic toxicity. Overall, MR exhibited greater efficacy in reducing influent toxicity compared with AR. TBBPA bioaccumulation was observed in Chironomus sancticaroli after short-term exposure to 100% MR effluent. Multigenerational exposures highlighted changes in the wing length of C. sancticaroli, showing decreases after influent and AR exposures and increases after MR exposures. These findings underscore the need for ecotoxicological tools in studies of new treatment technologies, combining the removal of emerging contaminants with safeguarding aquatic biota. PRACTITIONER POINTS: Acidogenic and methanogenic reactors reduced the acute and chronic toxicity of wastewater containing tetrabromobisphenol A. Both treatments still exhibit toxicity, inducing short- and long-term toxic effects on four native tropical species. The aquatic species Pristina longiseta was most sensitive to effluents from acidogenic and methanogenic reactors. TBBPA concentrations recovered from Chironomus sancticaroli bioaccumulation analysis ranged from 1.07 to 1.35 μg g-1. Evaluating new treatment technologies with multiple species bioassays is essential for a comprehensive effluent toxicity assessment and ensuring aquatic safety.