Surface reactivity in the pathogenic response to particulates
Surface reactivity in the pathogenic response to particulates
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DOI：
10.2307/3433502
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发表时间：
1997-09-01
影响因子：
10.4
通讯作者：
Fubini, B
中科院分区：
文献类型：
--
作者：
Fubini, B
讨论了与颗粒-生物介质界面处的过程有关的粉尘毒性的独特特征。由于表面反应性，固体的毒性不仅可以像水溶性化合物那样通过化学成分和分子结构来预测。对于具有相同体积成分的颗粒，微形态（灰尘的热和机械历史以及环境中的吸附）决定了活性表面位点的种类和丰度，从而调节对细胞和组织的反应性。通过比较不同材料获得的剂量-反应关系，讨论了剂量的定量评估。与颗粒表面相关的响应在每单位表面上比在每单位重量基础上进行比较更好。参考二氧化硅和石棉毒性描述了微形态、亲水性和反应性表面阳离子在确定吸入颗粒致病性中的作用。加热结晶二氧化硅会降低亲水性，从而改变膜溶解电位、保留和运输。暴露在表面的过渡金属离子在水悬浮液中产生自由基，铁的连续氧化还原循环，以及随后释放自由基的表面位点的活化-再活化，可以解释吸入含铁纤维引起的长期致病性。在混合粉尘引起的各种致病性中，成分之间的接触会改变毒性。硬金属肺病是由接触金属和碳化物的混合物引起的，通常是钴 (Co) 和碳化钨 (WC)，但不是单一成分。毒性源于 Co 金属和 WC 相互接触的机制中活性氧的产生。提出了玻璃纤维的吸水程度和生物持久性之间的关系。描述了铁质体和温石棉纤维的逐渐粉碎在体内发生的表面改性。
The peculiar characteristics of dust toxicity are discussed in relation to the processes faking place at the particle-biological medium interface. Because of surface reactivity, toxicity of solids is not merely predictable from chemical composition and molecular structure, as with water soluble compounds. With particles having the same bulk composition, micromorphology (the thermal and mechanical history of dust and adsorption from the environment) determines the kind and abundance of active surface sites, thus modulating reactivity toward cells and tissues, The quantitative evaluation of doses is discussed in comparisons of dose-response relationships obtained with different materials. Responses related to the surface of the particle are better compared on a per-unit surface than per-unit weight basis, The role of micromorphology, hydrophilicity, and reactive surface cations in determining the pathogenicity of inhaled particles is described with reference to silica and asbestos toxicity. Heating crystalline silica decreases hydrophilicity, with consequent modifications in membranclytic potential, retention, and transport. Transition metal ions exposed at the surface generate free radicals in aqueous suspensions, Continuous redox cycling of iron, with consequent activation-reactivation of the surface sites releasing free radicals, could account for the long-term pathogenicity caused by the inhalation of iron-containing fibers. In various pathogenicities caused by mixed dusts, the contact between components modifies toxicity. Hard metal lung disease is caused by exposure to mixtures of metals and carbides, typically cobalt (Co) and tungsten carbide (WC), but not to single components. Toxicity stems from reactive oxygen species generation in a mechanism involving both Co metal and WC in mutual contact. A relationship between ti-ie extent of water adsorption and biopersistence is proposed for vitreous fibers. Modifications of the surface taking place in vivo are described for ferruginous bodies and for the progressive comminution of chrysotile asbestos fibers.