The quartz hazard: effects of surface and matrix on inflammogenic activity.
The quartz hazard: effects of surface and matrix on inflammogenic activity.
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石英危害：表面和基质对致炎活性的影响。
DOI：
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发表时间：
2001
期刊：
影响因子：
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通讯作者：
Paul J. A. Borm
中科院分区：
文献类型：
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作者：
Ken Donaldson;Vicki Stone;R. Duffin;A. Clouter;R. Schins;Paul J. A. Borm
在颗粒的历史过程中对石英表面的修饰是理解石英灾害的变异性的一个强有力的想法。石英与其他矿物之间的相互作用可能发生在沉积物中，在工业加工过程中，或在基质结合的石英中。我们讨论了有关石英表面变化的基础的新证据，这些变化与其引起炎症的能力变化有关。对不同的石英样品进行了不同的生物检测。观察指标包括向气管支气管树内注入石英，测量支气管肺泡灌洗液(BAL)和肺组织中PMN的数量，BAL中趋化因子MIP-2的水平，以及BAL细胞中转录因子NF-kappaB的核转位。体外生物测定包括对上皮细胞的细胞毒性、溶血活性和电子自旋共振法测定颗粒表面的自由基活性。用乳酸铝处理石英可削弱其在BAL中引起PMN募集、趋化因子释放和核因子-kappaB核转位的能力。工作场所的石英石没有促炎活性，这与它们引起溶血的能力有关，但与它们的电子自旋共振(ESR)活性无关。在含有煤尘和飞灰的基质中，石英表现出不同的效果。在煤尘中，毒性被掩盖，但煤尘在体外对上皮细胞的毒性比纯石英更大；然而，滴注后的长期炎症与体外活性无关。石英表面活性的改善可以发生在工作场所的石英样品和表面受到保护的石英样品中，其程度是它们几乎没有致炎活性，并且无法激活导致炎症的关键亚细胞通路。表面受到影响的工作场所的石英，或煤矿粉尘或飞灰等基质中的石英，其毒性可能会受到调节。这些影响是由于矿物和有机化合物既可以降低(例如铝盐)生物活性，也可以增强(例如煤矿粉尘基质)生物活性，因此可能以一种难以预测的复杂方式造成毒性。铁就是一个很好的例子。有报道称，它可以增强石英的毒性，或者它在其毒性中起到的作用很小，就像这里对几乎纯的石英颗粒所显示的那样。在我们对石英的毒性机理有一个合理的了解之前，还需要一个广泛的进一步研究计划。
Modification of the quartz surface during the history of the particle is a powerful idea in understanding the variability of the quartz hazard. Interactions between quartz and other minerals are likely to occur in sediments, during industrial processing, or in matrix-bound quartz. We discuss new evidence regarding the basis of changes in the quartz surface that relate to changes in its ability to cause inflammation. Different samples of quartz were subjected to various biological assays. Endpoints included instillation of quartz into the tracheobronchial tree and measurement of PMN numbers in bronchoalveolar lavage (BAL) and in lung tissue, levels of the chemokine MIP-2 in BAL, and nuclear translocation of the transcription factor NF-kappaB in BAL cells. In vitro biological assays included cytotoxicity to epithelial cells, hemolytic activity, and radical activity of the particle surface as measured by electron spin resonance. Treatment of quartz with aluminium lactate impaired its ability to cause PMN recruitment, chemokine release, and NF-kappaB nuclear translocation in BAL. Workplace quartzes had no proinflammatory activity, which correlated with their ability to cause hemolysis but not their electron spin resonance (ESR) activity. Quartz in a matrix with coalmine dust or fly-ash showed different effects. In fly-ash, the toxicity was masked, but coalmine dusts were more toxic to epithelial cells than pure quartz in vitro; however, after instillation, the long-term inflammation was not related to the in vitro activity. Amelioration of quartz surface activity can occur in workplace samples of quartz and quartz samples whose surface is protected, to the extent that they have very little inflammogenic activity and display an inability to activate key subcellular pathways that lead to inflammation. Quartz from a workplace whose surface has been affected, or in a matrix such as coalmine dust or fly-ash, can have its toxicity modulated. These effects are due to minerals and organic compounds that can both decrease (e.g., aluminium salts) or enhance (e.g., coalmine dust matrix) biological activity and thus may contribute to toxicity in a complex way that is not easily predicted. Iron is a good example. There are reports that it can enhance quartz toxicity, or it may have little role to play in its toxicity, as shown here for almost pure quartz particles. A broad program of further research is needed before we have a sound understanding of the mechanisms of quartz toxicity.