Fubini B
Università di Torino, Facoltà di Farmacia, Dipartimento di Chimica Inorganica, Italy.
Environ Health Perspect. 1997 Sep;105 Suppl 5(Suppl 5):1013-20. doi: 10.1289/ehp.97105s51013.
The peculiar characteristics of dust toxicity are discussed in relation to the processes taking 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 membranolytic 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 the 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.
结合在颗粒 - 生物介质界面发生的过程,讨论了粉尘毒性的特殊特征。由于表面反应性,固体的毒性不像水溶性化合物那样仅由化学成分和分子结构就能预测。对于具有相同总体组成的颗粒,微观形态(粉尘的热历史和机械历史以及来自环境的吸附)决定了活性表面位点的种类和数量,从而调节对细胞和组织的反应性。在比较不同材料获得的剂量 - 反应关系时,讨论了剂量的定量评估。与颗粒表面相关的反应在以单位表面积而非单位重量为基础进行比较时更好。参照二氧化硅和石棉的毒性,描述了微观形态、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,从而导致膜溶解潜能、滞留和运输的改变。表面暴露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之而来的表面位点的激活 - 再激活释放自由基,可能解释了吸入含铁纤维引起的长期致病性。在由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),而不是单一成分。毒性源于在涉及相互接触的Co金属和WC的机制中产生的活性氧。对于玻璃纤维,提出了水吸附程度与生物持久性之间的关系。描述了体内发生在铁蛋白体以及温石棉纤维逐渐粉碎过程中的表面变化。