矽尘暴露工人中的肺癌：探寻偶然与必然之间的真相。

Cocco P, Dosemeci M, Rice C

Dipartimento di Sanità Pubblica, Sezione di Medicina del Lavoro, Università di Cagliari, Italy.

Med Lav. 2007 Jan-Feb;98(1):3-17.

BACKGROUND

In 1997, IARC upgraded crystalline silica to a Group 1 human carcinogen. However, the IARC report itself acknowledged variations in risk depending on inherent characteristics of the crystalline silica or external factors affecting its biological activity or distribution of its polymorphs.

METHODS

We reviewed silica physical and physico-chemical properties and how such properties may affect its interaction with the target cells. Studies of silica, silicosis and lung cancer published from 1997 onwards are then reviewed in the search of any new advances in knowledge about silica carcinogenicity. Finally, other possible confounding factors contributing to inconsistent findings on silica, silicosis, and lung cancer are reviewed.

RESULTS

Host factors, physico-chemical characteristics of the surface of silica particles, exposure circumstances, and the mineral ore composition experimentally affect the ability of silica particles of inducing release of reactive oxygen species (ROS) and TNF-alpha by alveolar macrophages, possibly accounting for the great variation in lung cancer risk among dust exposed workers across the individual studies. Most recent epidemiological studies do not consider such complex pattern of modifying factors, and they keep replicating inconsistent findings. The hypothesis of a silicosis-mediated pathway, although more consistent from an epidemiological perspectives, and reassuring in terms of the effectiveness of current standards in preventing lung cancer risk among silica exposed workers, does not seem to explain elevated risks at low silica exposure levels.

CONCLUSION

Future studies of lung cancer risk among workers exposed to silica-containing dust should consider measurement of ROS and TNF-alpha release by workplace dust samples as intermediate end-points predicting lung cancer risk better than silica concentration, allowing to more effectively address preventive action.

背景

1997年，国际癌症研究机构（IARC）将结晶二氧化硅升级为1类人类致癌物。然而，IARC报告本身承认，风险存在差异，这取决于结晶二氧化硅的固有特性或影响其生物活性或多晶型物分布的外部因素。

方法

我们回顾了二氧化硅的物理和物理化学性质，以及这些性质如何影响其与靶细胞的相互作用。随后对1997年以来发表的关于二氧化硅、矽肺和肺癌的研究进行了综述，以寻找有关二氧化硅致癌性的任何新的知识进展。最后，对导致二氧化硅、矽肺和肺癌研究结果不一致的其他可能混杂因素进行了综述。

结果

宿主因素、二氧化硅颗粒表面的物理化学特征、接触情况和矿物矿石成分在实验上会影响二氧化硅颗粒诱导肺泡巨噬细胞产生活性氧（ROS）和肿瘤坏死因子-α（TNF-α）的能力，这可能是导致个体研究中接触粉尘工人肺癌风险差异巨大的原因。最近的流行病学研究没有考虑到这种复杂的调节因素模式，并且不断重复不一致的结果。矽肺介导途径的假说，尽管从流行病学角度来看更一致，并且就当前标准在预防接触二氧化硅工人肺癌风险方面的有效性而言令人放心，但似乎无法解释低水平二氧化硅接触时风险升高的情况。