Engineered stones are novel construction materials associated with a recent upsurge in silicosis cases among workers in the stonemason industry. In order to understand the hazard for the short latency of lung disease among stonemasons, we simulated real-time dust exposure scenario by dry-machining engineered stones in controlled conditions, capturing and analysing the respirable dust generated for physical and chemical characteristics. Natural granite and marble were included for comparison. Cutting engineered stones generated high concentrations of very fine particles (< 1 µm) with > 80% respirable crystalline silica content, in the form of quartz and cristobalite. Engineered stones also contained 8–20% resin and 1–8% by weight metal elements. In comparison, natural stones had far lower respirable crystalline silica (4- 30%) and much higher metal content, 29–37%. Natural stone dust emissions also had a smaller surface area than engineered stone, as well as lower surface charge. This study highlighted the physical and chemical variability within engineered stone types as well as between engineered and natural stones. This information will ultimately help understand the unique hazard posed by engineered stone fabrication work and help guide the development of specific engineering control measures targeting lower exposure to respirable crystalline silica.
We demonstrate the use of injected gallium electrodes for capacitively coupled contactless conductivity detection (C(4)D) within a microchip electrophoresis device. Evaluation of the electrodes for quantitative detection of electrophoretically separated lithium, sodium and potassium ions showed the system offers competitive detection limits of 6.1 × 10(-6) M, 6.7 × 10(-6) M and 8.5 × 10(-6) M, respectively. The fabrication process is fast, highly reproducible, and eliminates difficulties with electrode alignment. Using this approach C(4)D can be readily achieved in any microchip by simply adding extra 'electrode' channels to the microchip design.
Background and objective: E-cigarettes are often marketed and thought of as emitting harmless vapour; however, verification of their safety for non-smokers is scarce. We have previously shown that E-cigarettes cause decreased phagocytosis of bacteria by macrophages via reductions in surface bacterial recognition receptors. This study assessed the effect of E-cigarette constituents, 3 E-liquid apple flavours, nicotine, vegetable glycerine and propylene glycol, on bronchial epithelial cell viability, apoptosis and cytokine secretion and macrophage phagocytosis of apoptotic airway cells and phagocytic recognition molecules. Methods: Cell necrosis and apoptosis were measured by Sytox Green stain and Annexin V. Efferocytosis was measured by internalization of pHrodo Green labelled apoptotic airway cells by macrophages. Expression of macrophage cell surface apoptotic cell receptors was measured by flow cytometry. Cytokine release by E-cigarette-exposed airway cells was measured by cytokine bead array.Results: E-cigarette vapour increased primary bronchial epithelial necrosis and apoptosis. E-cigarette vapour reduced efferocytosis (lowest flavour 12.1%) versus control (20.2%, P = 0.032). The efferocytosis receptor CD44 was reduced by one flavour (MFI 1863 vs 2332 control, P = 0.016) and all components reduced expression of CD36, including the glycol bases (MFI 1067-12 274 vs 1415 control). Reduced secretion of TNF-α, IL-6, IP-10, MIP-1α and MIP-1β was observed for all flavour variants. Conclusion: E-cigarettes can cause bronchial epithelial apoptosis and macrophage efferocytosis dysfunction via reduced expression of apoptotic cell recognition receptors. These data further show that E-cigarettes should not be considered harmless to non-smokers and their effects may go far beyond cytotoxicity to cells. SUMMARY AT A GLANCEE-cigarettes are increasing in popularity, especially amongst non-smokers. We assess not only the toxicity of E-cigarettes on healthy airway epithelial cells and effect on secreted cytokines, but also, for the first time, the effect on efferocytosis of apoptotic airway cells by macrophages. RESULTS E-cigarettes cause apoptosis and necrosisWe assessed toxicity of EVE on human bronchial epithelial cells, via release of LDH (Fig. 1A), and found Respirology (2020) 25, 620-628
Rationale: The growing interest in regulating flavoured E-liquids must incorporate understanding of the "flavouring profile" of each E-liquid - which flavourants (flavouring chemicals) are present and at what concentrations not just focussing on the flavour on the label. Methods: We investigated the flavouring profile of 10 different flavoured E-liquids. We assessed bronchial epithelial cell viability and apoptosis, phagocytosis of bacteria and apoptotic cells by macrophages after exposure to E-cigarette vapour extract (EVE). And validated in normal human bronchial epithelial cells (NHBE) and alveolar macrophages (AMs) from healthy donors. We also assessed cytokine release and validated in the saliva from E-cigarette users. Results: Increased necrosis/apoptosis (16.1-64.5% apoptosis) in 16HBE cells was flavour dependent, and NHBEs showed an increased susceptibility to flavours. In THP-1 differentiated macrophages phagocytosis was also flavour dependent, with alveolar macrophages (AM) also showing increased susceptibility to flavours. Furthermore, Banana and Chocolate were shown to reduce surface expression of phagocytic target recognition receptors on alveolar macrophages. Banana and Chocolate increased IL-8 secretion by NHBE, whilst all 4 flavours reduced AM IL-1β secretion which was also reduced in the saliva of E-cigarette users compared with healthy controls. Flavourant profiles of E-liquids varied from simple 2 compound mixtures to complex mixtures containing over a dozen flavourants. E-liquids with high benzene content, complex flavouring profiles, high chemical concentration had the greatest impacts. Conclusions: The flavourant profile of E-liquids is key to disruption of the airway status quo by increasing bronchial epithelial cell apoptosis, causing alveolar macrophage phagocytic dysfunction and altering airway cytokines.
We demonstrate the use of microchip electrophoresis with capacitively coupled contactless conductivity detection (C 4 D) for the direct detection of histamine in fish flesh samples. Optimization of the background electrolyte (BGE) conditions showed that a competitive detection limit of 0.43 mg L À1 was achievable using a mixed 2-[4-(2-hydroxyethyl)piperazin-1-yl]ethanesulfonic acid and histidine BGE at pH 6.03. The developed method was successfully applied to the determination of spiked histamine in yellowfin tuna flesh samples with recoveries ranging from 88.8 to 112.5% with relative standard deviations below 13%. Further versatility of the method was demonstrated with the analysis of histamine levels in four frozen fish samples, purchased from a local supermarket, showing all contained concentrations well below the Australian and New Zealand Food Standards Code maximum limit for decomposition (200 mg g À1 ). The reported method eliminates the need for analyte derivatization associated with common optical detection techniques and the use of C 4 D offers increased portability.Further, this approach could easily be adapted for the detection of histamine in other food and beverage samples.
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