Heppleston A G
Am J Ind Med. 1985;7(4):285-94. doi: 10.1002/ajim.4700070404.
The current argument about the carcinogenicity of inhaled silica is not clarified by reliance on morbidity and mortality experience divorced from or incompletely related to data on environmental exposure. Human evidence provides the ultimate basis for assessing such risks, and numerous studies of the effects of inhaling dusts rich or poor in silica content on the prevalence of pulmonary carcinoma have been performed on large series of cases from major mining areas of the world. When due allowance is made for substances inhaled concomitantly with exposure to silica and for personal pollution by cigarette smoking, the weight of evidence is against a carcinogenic role for uncombined silicon dioxide. Moreover, pneumoconiosis due to compact mineral particles does not appear to determine the onset of lung cancer. Cellular behaviour suggests reasons for the different responses to compact and fibrous particles acting alone.
目前关于吸入二氧化硅致癌性的争论,并未因依赖与环境暴露数据脱节或不完全相关的发病率和死亡率经验而得到澄清。人体证据为评估此类风险提供了最终依据,并且已经对来自世界主要矿区的大量病例进行了许多研究,以探讨吸入二氧化硅含量高低不同的粉尘对肺癌患病率的影响。当适当考虑与接触二氧化硅同时吸入的物质以及吸烟造成的个人污染时,证据的权重表明未结合的二氧化硅不具有致癌作用。此外,由致密矿物颗粒引起的尘肺病似乎并不能决定肺癌的发病。细胞行为为单独作用的致密颗粒和纤维颗粒产生不同反应提供了原因。