Donaldson K, Stone V, Duffin R, Clouter A, Schins R, Borm P
Biomedicine Research Group, Napier University, Edinburgh, Scotland.
J Environ Pathol Toxicol Oncol. 2001;20 Suppl 1:109-18.
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.
在颗粒形成过程中石英表面的改性是理解石英危害性变化的一个重要观点。石英与其他矿物之间的相互作用可能发生在沉积物中、工业加工过程中或基质结合的石英中。我们讨论了关于石英表面变化基础的新证据，这些变化与其引发炎症的能力变化有关。对不同的石英样品进行了各种生物学检测。检测终点包括将石英滴入气管支气管树、测量支气管肺泡灌洗（BAL）和肺组织中的中性粒细胞数量、BAL中趋化因子MIP - 2的水平以及BAL细胞中转录因子NF - κB的核转位。体外生物学检测包括对上皮细胞的细胞毒性、溶血活性以及通过电子自旋共振测量的颗粒表面自由基活性。用乳酸铝处理石英会削弱其在BAL中引起中性粒细胞募集、趋化因子释放和NF - κB核转位的能力。工作场所的石英没有促炎活性，这与其溶血能力相关，但与它们的电子自旋共振（ESR）活性无关。与煤尘或飞灰混合的基质中的石英表现出不同的效应。在飞灰中，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，长期炎症与体外活性无关。工作场所的石英样品以及表面受到保护的石英样品，其表面活性会有所改善，以至于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途径。来自表面受到影响的工作场所的石英，或者处于煤尘或飞灰等基质中的石英，其毒性可能会受到调节。这些效应是由于矿物质和有机化合物既能降低（如铝盐）也能增强（如煤尘基质）生物活性，因此可能以一种不易预测的复杂方式导致毒性。铁就是一个很好的例子。有报道称它可以增强石英毒性，或者它在石英毒性中可能作用不大，如此处几乎纯石英颗粒所示。在我们对石英毒性机制有深入了解之前，需要开展广泛的进一步研究计划。
