Pott F, Roller M
Medizinisches Institut für Umwelthygiene an der Heinrich-Heine-Universität Düsseldorf.
Zentralbl Hyg Umweltmed. 1997 Aug;200(2-3):223-80.
During the last few years, the findings could be confirmed which led to the conclusion that very fine solid particles which are not known to have an intrinsic toxicity, can induce lung tumours in rats. The carcinogenic potency seems to increase parallel to increasing specific surface area and decreasing particle size. However, many questions remain open. Organic compounds which contain many carcinogenic polycyclic aromatic hydrocarbons (PAH) can explain only less than 1% of the carcinogenic effect of diesel exhaust in the rat lung. Therefore, the carcinogenicity of diesel exhaust cannot be reduced by an oxidizing catalyst. It burns a part of the organic substances adsorbed on the surface of the carbonaceous core of diesel particles and thus helps to follow the low standard for particles in diesel emissions, but without reduction of the carcinogenic potential because it does not reduce the emission of the insoluble carcinogenic part of the particles, the elementary carbonaceous core. The search for a hypothetical threshold for the carcinogenicity of particles in the rat lung aims at the determination of mechanisms which are preconditions for the development of a tumour. If certain doses do not induce such lesions they are considered safe. Chronic inflammation, proliferation of epithelial cells and fibrosis are discussed to be preconditions. However, the pathways which lead to inflammation and proliferation could proceed independent of the molecular carcinogenesis. Therefore, a cancer risk from diesel particles and other very fine particles may occur under environmental conditions. If the positive epidemiologic studies are relevant, a lung cancer risk for humans can be calculated which is higher than that calculated from inhalation studies with rats.
在过去几年中，一些研究结果得到了证实，这些结果得出的结论是，一些本身无毒的极细固体颗粒能够在大鼠体内诱发肺部肿瘤。致癌效力似乎随着比表面积的增加和颗粒尺寸的减小而增强。然而，许多问题仍然悬而未决。含有许多致癌多环芳烃（PAH）的有机化合物只能解释柴油废气对大鼠肺部致癌作用的不到1%。因此，氧化催化剂无法降低柴油废气的致癌性。它燃烧了吸附在柴油颗粒碳质核心表面的一部分有机物质，从而有助于使柴油排放中的颗粒符合低标准，但由于它没有减少颗粒中不溶性致癌部分——基本碳质核心的排放，所以并没有降低致癌潜力。在大鼠肺部寻找颗粒致癌性的假设阈值旨在确定肿瘤发生的前提机制。如果特定剂量不会诱发此类病变，那么它们就被认为是安全的。慢性炎症、上皮细胞增殖和纤维化被认为是前提条件。然而，导致炎症和增殖的途径可能独立于分子致癌作用而进行。因此，在环境条件下，柴油颗粒和其他极细颗粒可能会带来癌症风险。如果积极的流行病学研究具有相关性，那么就可以计算出对人类的肺癌风险，该风险高于根据对大鼠的吸入研究计算出的风险。
