Mass transfer of PBDEs from plastic TV casing to indoor dust via three migration pathways - A test chamber investigation

Polybrominated diphenyl ethers (PBDEs) are widely detected in humans with substantial exposure thought to occur in indoor environments and particularly via contact with indoor dust. Despite this, knowledge of how PBDEs migrate to indoor dust from products within which they are incorporated is scarce. This study utilises an in-house designed and built test chamber to investigate the relative significance of different mechanisms via which PBDEs transfer from source materials to dust, using a plastic TV casing treated with the Deca-BDE formulation as a model source. Experiments at both room temperature and 60 degrees C revealed no detectable transfer of PBDEs from the TV casing to dust via volatilisation and subsequent partitioning. In contrast, substantial transfer of PBDEs to dust was detected when the TV casing was abraded using a magnetic stirrer bar. Rapid and substantial PBDE transfer to dust was also observed in experiments in which dust was placed in direct contact with the source. Based on these experiments, we suggest that for higher molecular weight PBDEs like BDE-209; direct dust: source contact is the principal pathway via which source-to-dust transfer occurs

Test chamber investigation of the volatilization from source materials of brominated flame retardants and their subsequent deposition to indoor dust

Numerous studies have reported elevated concentrations of brominated flame retardants (BFRs) in dust from indoor micro-environments. Limited information is available, however, on the pathways via which BFRs in source materials transfer to indoor dust. The most likely hypothesized pathways are (a) volatilization from the source with subsequent partitioning to dust, (b) abrasion of the treated product, transferring microscopic fibers or particles to the dust (c) direct uptake to dust via contact between source and dust. This study reports the development and application of an in-house test chamber for investigating BFR volatilization from source materials and subsequent partitioning to dust. The performance of the chamber was evaluated against that of a commercially available chamber, and inherent issues with such chambers were investigated, such as loss due to sorption of BFRs to chamber surfaces (so-called sink effects). The partitioning of polybrominated diphenyl ethers to dust, post-volatilization from an artificial source was demonstrated, while analysis in the test chamber of a fabric curtain treated with the hexabromocyclododecane formulation, resulted in dust concentrations exceeding substantially those detected in the dust pre-experiment. These results provide the first experimental evidence of BFR volatilization followed by deposition to dust

Characterization and quantification of oxidative stress induced particle debris from polypropylene surgical mesh

Explanted polypropylene (PP) surgical mesh has frequently been reported to show surface alterations, such as cracks and flaking. However, to date the consequence of PP mesh degradation is not clearly understood, particularly its potential to influence the biological host response of surrounding tissues. Of particular concern is a possible host reaction to polypropylene particles released through degradation of surgical mesh in vivo. This concern is driven by previous studies which have postulated that an oxidative stress environment has the potential to etch away particles from the surface of a PP fibers. The release of such particles is of considerable significance as particles in the nano- to micro range have been shown to have the capacity to irritate cells and stimulate the immune system. The authors are not aware of any previous studies that have attempted to characterize, quantify or identify any particles released from PP mesh after exposure to an oxidative stress environment. Characterization of the PP mesh, post oxidative stress exposure, including identification of particles was achieved through application of a range of techniques: low voltage-scanning electron microscopy (LV-SEM), pyrolysis gas chromatography mass spectrometry (Pyr-GCMS), nano-Fourier transform infrared spectroscopy (nano-FTIR), scattering-type, scanning near-field optical microscopy (s-SNOM), atomic force microscopy (AFM), attenuated total reflectance-Fourier transform infrared spectroscopy (ATR-FTIR) and uniaxial tensile testing. The findings of this study indicate that oxidative stress alone is a major factor in the production of PP particle debris. PP debris identified within solution, using Pyr-GCMS, was shown to be in order of the micron scale

<i>InSpectra</i> - A platform for identifying emerging chemical threats

Non-target analysis (NTA) employing high-resolution mass spectrometry (HRMS) coupled with liquid chromatography is increasingly being used to identify chemicals of biological relevance. HRMS datasets are large and complex making the identification of potentially relevant chemicals extremely challenging. As they are recorded in vendor-specific formats, interpreting them is often reliant on vendor-specific software that may not accommodate advancements in data processing. Here we present InSpectra, a vendor independent automated platform for the systematic detection of newly identified emerging chemical threats. InSpectra is web-based, open-source/access and modular providing highly flexible and extensible NTA and suspect screening workflows. As a cloud-based platform, InSpectra exploits parallel computing and big data archiving capabilities with a focus for sharing and community curation of HRMS data. InSpectra offers a reproducible and transparent approach for the identification, tracking and prioritisation of emerging chemical threats

Deep dive into the chronic toxicity of tyre particle mixtures and their leachates.

This is the final version. Available from Elsevier via the DOI in this record. Data Availability: Data will be made available on request.Particles from the tread of vehicle tyres are a global pollutant, which are emitted into the environment at an approximate rate of 1.4 kg.year-1 for an average passenger-car. In this study, popular tyre brands were used to generate a tyre tread microparticle mixture. The chronic toxicity of both particles and chemical leachates were compared on a planktonic test species (Daphnia magna). Over 21 days of exposure, pristine tyre tread microparticles were more toxic (LC50 60 mg.L-1) than chemical lechates alone (LC50 542 mg.L-1). Microparticles and leachates showed distinct effects on reproduction and morphological development at environmentally relevant concentrations, with dose-dependent uptake of particles visible in the digestive tract. Chemical characterization of leachates revealed a metal predominance of zinc, titanium, and strontium. Of the numerous organic chemicals present, at least 54 were shared across all 5 tyre brands, with many classified to be very toxic. Our results provide a critically needed information on the toxicity of tyre tread particles and the associated chemicals that leach from them to inform future mitigation measures. We conclude that tyre particles are hazardous pollutants of particular concern that are close to or possibly above chronic environmental safety limits in some locations.Natural Environment Research Council (NERC

TNFR1 and TNFR2 regulate the extrinsic apoptotic pathway in myeloma cells by multiple mechanisms

The huge majority of myeloma cell lines express TNFR2 while a substantial subset of them failed to show TNFR1 expression. Stimulation of TNFR1 in the TNFR1-expressing subset of MM cell lines had no or only a very mild effect on cellular viability. Surprisingly, however, TNF stimulation enhanced cell death induction by CD95L and attenuated the apoptotic effect of TRAIL. The contrasting regulation of TRAIL- and CD95L-induced cell death by TNF could be traced back to the concomitant NFκB-mediated upregulation of CD95 and the antiapoptotic FLIP protein. It appeared that CD95 induction, due to its strength, overcompensated a rather moderate upregulation of FLIP so that the net effect of TNF-induced NFκB activation in the context of CD95 signaling is pro-apoptotic. TRAIL-induced cell death, however, was antagonized in response to TNF because in this context only the induction of FLIP is relevant. Stimulation of TNFR2 in myeloma cells leads to TRAF2 depletion. In line with this, we observed cell death induction in TNFR1-TNFR2-costimulated JJN3 cells. Our studies revealed that the TNF-TNF receptor system adjusts the responsiveness of the extrinsic apoptotic pathway in myeloma cells by multiple mechanisms that generate a highly context-dependent net effect on myeloma cell survival