Fibrous chrysotile has been the most commonly applied asbestos mineral in a range of technical applications. However, it is toxic and carcinogenic upon inhalation. The chemical reactivity of chrysotile fiber surfaces contributes to its adverse health effects by catalyzing the formation of highly reactive hydroxyl radicals (HO•) from H2O2. In this Haber-Weiss cycle, Fe on the fiber surface acts as a catalyst: Fe3+ decomposes H2O2 to reductants that reduce surface Fe3+ to Fe2+, which is back-oxidized by H2O2 (Fenton-oxidation) to yield HO•. Chrysotile contains three structural Fe species: ferrous and ferric octahedral Fe and ferric tetrahedral Fe (Fe3+tet). Also, external Fe may adsorb or precipitate onto fiber surfaces. The goal of this study was to identify the Fe species on chrysotile surfaces that catalyze H2O2 decomposition and HO• generation. We demonstrate that at the physiological pH 7.4 Fe3+tet on chrysotile surfaces substantially contributes to H2O2 decomposition and is the key structural Fe species catalyzing HO• generation. After depleting Fe from fiber surfaces, a remnant fiber-related H2O2 decomposition mode was identified, which may involve magnetite impurities, remnant Fe or substituted redox-active transition metals other than Fe. Fe (hydr)oxide precipitates on chrysotile surfaces also contributed to H2O2 decomposition, but were per mole Fe substantially less efficient than surface Fe3+tet. Fe added to chrysotile fibers increased HO• generation only when it became incorporated and tetrahedrally coordinated into vacancy sites in the Si layer. Our results suggest that at the physiological pH 7.4, oxidative stress caused by chrysotile fibers largely results from radicals produced in the Haber-Weiss cycle that is catalyzed by Fe3+tet. The catalytic role of Fe3+tet in radical generation may also apply to other pathogenic silicates in which Fe3+tet is substituted, e.g. quartz, amphiboles and zeolites. However, even if these pathogenic minerals do not contain Fe, our results suggest that the mere presence of vacancy sites may pose a risk, as incorporation of external Fe into a tetrahedral coordination environment can lead to HO• generation.

中文翻译：

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确定温石棉表面上过氧化氢分解和羟基自由基形成的反应部位。

在许多技术应用中，纤维温石棉是最常用的石棉矿物。但是，它吸入有毒并致癌。温石棉纤维表面的化学反应性通过催化由H2O2形成高反应性羟基（HO•）对其健康造成不利影响。在此Haber-Weiss循环中，纤维表面上的Fe充当催化剂：Fe3 +将H2O2分解为还原剂，还原剂将表面Fe3 +还原为Fe2 +，然后被H2O2逆氧化（芬顿氧化），生成HO•。温石棉包含三种结构性铁物种：亚铁和八面铁三价铁和四面铁三价铁（Fe3 + tet）。同样，外部铁可能吸附或沉淀到纤维表面上。这项研究的目的是确定在温石棉表面上能催化H2O2分解和HO•生成的Fe物种。我们证明，在生理pH 7.4时，在温石棉表面上的Fe3 + tet基本上有助于H2O2的分解，并且是催化HO•生成的关键结构Fe物种。从纤维表面消耗铁后，发现了与纤维有关的残余H2O2分解模式，该模式可能涉及磁铁矿杂质，残余Fe或除Fe以外的取代的氧化还原活性过渡金属。在温石表面上沉淀的Fe（氢）氧化物也有助于H2O2的分解，但每摩尔Fe的效率远低于表面Fe3 + tet。添加到温石棉纤维中的铁只有在被掺入并四面体配位到硅层的空位时才增加HO•的生成。我们的结果表明，在生理pH 7.4下，温石棉纤维引起的氧化应激很大程度上是由Fe3 + tet催化的Haber-Weiss循环中产生的自由基引起的。Fe3 + tet在自由基产生中的催化作用也可能适用于其他被Fe3 + tet取代的致病性硅酸盐，例如石英，闪石和沸石。但是，即使这些致病矿物不含铁，我们的结果也表明，仅存在空位可能会带来风险，因为将外部铁掺入四面体配位环境会导致HO•的生成。