Fubini Bice, Fenoglio Ivana, Ceschino Raffaella, Ghiazza Mara, Martra Gianmario, Tomatis Maura, Borm Paul, Schins Roel, Bruch Joachim
Dipartimento di Chimica I. F. M., Interdipartimental Center G. Scansetti for Studies on Asbestos and other Toxic Particulates, Università di Torino, Via P. Giuria 7, I-10125-Torino, Italy.
Int J Hyg Environ Health. 2004 Feb;207(2):89-104. doi: 10.1078/1438-4639-00277.
Four commercial quartz dusts (flours), two inflammogenic in vivo and activating macrophages in vitro (Qz 2/1-c and Qz 3/1-c) and two mostly inert (Qz 5/1-c and Qz 11/1-c), have been compared regarding their surface properties, in order to detect chemical differences which may account for their different biological behaviour. The following features have been examined: 1) extent of the amorphous fraction (heat associated alpha<-->beta transition of quartz) and its solubility in HF; 2) potential to cleave a carbon-hydrogen bond with consequent generation of carbon centred radicals (spin trapping technique, EPR); 3) evolution of surface functionalities upon heating (FTIR spectroscopy); 4) mechanisms of adsorption of water on dusts outgassed at 150 degrees and at 800 degrees C (adsorption calorimetry). HCl treated samples have also been examined. The two "less toxic" quartzes are more resistant to HF attack, coordinate irreversibly H2O molecules and exhibit strong adsorption sites, which are absent in the other two and in a very pure quartz dust. Conversely all samples show the same potential to release free radicals. The different behaviour of the two sets of dust is consistent with a different level of impurities, namely aluminium ex kaolin, carbon and alkaline ions. The less inflammogenic quartzes appear to be covered by aluminium ions (and possibly iron) which strongly holds molecular water or carbonates, thus reducing the silanol patches to a large extent and changing the surface properties of the particles. We hypothesize that cellular response, and particularly macrophage activation and death, is mediated by strong interactions between silanol patches and some cell membrane components, but inhibited when the surface of the particle is modified by the presence of aluminium ions, surface carbonates and other metal contaminants. This hypothesis suggests that grinding procedures with little appropriate additives, e.g. kaolin, alumina, can reduce the biological activity of quartz dusts.
对四种商用石英粉尘（粉末）进行了表面性质比较，其中两种在体内具有致炎作用且在体外可激活巨噬细胞（Qz 2/1-c和Qz 3/1-c），另外两种基本呈惰性（Qz 5/1-c和Qz 11/1-c），目的是检测可能导致其不同生物学行为的化学差异。研究了以下特性：1）无定形部分的程度（石英的热相关α⇄β转变）及其在氢氟酸中的溶解度；2）断裂碳氢键并随之产生碳中心自由基的潜力（自旋捕获技术，电子顺磁共振）；3）加热时表面官能团的演变（傅里叶变换红外光谱）；4）在150℃和800℃下脱气的粉尘对水的吸附机制（吸附量热法）。还对盐酸处理过的样品进行了研究。两种“毒性较小”的石英对氢氟酸侵蚀更具抗性，能不可逆地配位水分子并表现出强吸附位点，而另外两种以及一种非常纯的石英粉尘中则不存在这些位点。相反，所有样品释放自由基的潜力相同。两组粉尘的不同行为与杂质水平不同有关，即来自高岭土的铝、碳和碱性离子。炎症性较小的石英似乎被铝离子（可能还有铁）覆盖，这些离子强烈吸附分子水或碳酸盐，从而在很大程度上减少了硅醇斑块并改变了颗粒的表面性质。我们假设细胞反应，特别是巨噬细胞的激活和死亡，是由硅醇斑块与某些细胞膜成分之间的强相互作用介导的，但当颗粒表面因铝离子、表面碳酸盐和其他金属污染物的存在而发生改变时，这种反应会受到抑制。这一假设表明，使用少量合适的添加剂（如高岭土、氧化铝）进行研磨程序，可以降低石英粉尘的生物活性。
