Checkoway H, Hughes J M, Weill H, Seixas N S, Demers P A
Department of Environmental Health, Tulane University, New Orleans, Louisiana, USA.
Thorax. 1999 Jan;54(1):56-9. doi: 10.1136/thx.54.1.56.
The role of silicosis as either a necessary or incidental condition in silica associated lung cancer remains unresolved. To address this issue a cohort analysis of dose-response relations for crystalline silica and lung cancer mortality was conducted among diatomaceous earth workers classified according to the presence or absence of radiological silicosis.
Radiological silicosis was determined by median 1980 International Labour Organisation system readings of a panel of three "B" readers for 1809 of 2342 white male workers in a diatomaceous earth facility in California. Standardised mortality ratios (SMR) for lung cancer, based on United States rates for 1942-94, were calculated separately for workers with and without radiological silicosis according to cumulative exposures to respirable crystalline silica (milligrams per cubic meter x years; mg/m3-years) lagged 15 years.
Eighty one cases of silicosis were identified, including 77 with small opacities of > or = 1/0 and four with large opacities. A slightly larger excess of lung cancer was found among the subjects with silicosis (SMR 1.57, 95% confidence interval (CI) 0.43 to 4.03) than in workers without silicosis (SMR 1.19, 95% CI 0.87 to 1.57). An association between silica exposure and lung cancer risk was detected among those without silicosis; a statistically significant (p = 0.02) increasing trend of lung cancer risk was seen with cumulative exposure, with SMR reaching 2.40 (95% CI 1.24 to 4.20) at the highest exposure level (> or = 5.0 mg/m3-years). A similar statistically significant (p = 0.02) dose-response gradient was observed among non-silicotic subjects when follow up was truncated at 15 years after the final negative radiograph (SMR 2.96, 95% CI 1.19 to 6.08 at > or = 5.0 mg/m3-years), indicating that the association among non-silicotic subjects was unlikely to be accounted for by undetected radiological silicosis.
The dose-response relation observed between cumulative exposure to respirable crystalline silica and lung cancer mortality among workers without radiological silicosis suggests that silicosis is not a necessary co-condition for silica related lung carcinogenesis. However, the relatively small number of silicosis cases in the cohort and the absence of radiographic data after employment limit interpretations.
矽肺在硅相关肺癌中是必要条件还是偶然条件仍未明确。为解决这一问题，我们对根据是否存在放射性矽肺分类的硅藻土工人中结晶硅与肺癌死亡率的剂量反应关系进行了队列分析。
通过1980年国际劳工组织系统的中位数，由三名“B”级阅片者对加利福尼亚一家硅藻土工厂2342名白人工人中的1809名进行读片，确定放射性矽肺。根据15年滞后的可吸入结晶硅累积暴露量（每立方米毫克数×年；mg/m³-年），分别计算有和无放射性矽肺工人基于1942 - 94年美国发病率的肺癌标准化死亡比（SMR）。
共确诊81例矽肺病例，其中77例有≥1/0的小阴影，4例有大阴影。矽肺患者中肺癌的超额数略高于无矽肺工人（SMR 1.57，95%置信区间（CI）0.43至4.03）（无矽肺工人SMR 1.19，95%CI 0.87至1.57）。在无矽肺工人中检测到硅暴露与肺癌风险之间的关联；随着累积暴露，肺癌风险呈统计学显著（p = 0.02）的上升趋势，在最高暴露水平（≥5.0 mg/m³-年）时SMR达到2.40（95%CI 1.24至4.20）。当在最后一次阴性胸片后15年截断随访时，在非矽肺受试者中观察到类似的统计学显著（p = 0.02）剂量反应梯度（≥5.0 mg/m³-年时SMR 2.96，95%CI 1.19至6.08），这表明非矽肺受试者之间的关联不太可能由未检测到的放射性矽肺解释。
在无放射性矽肺的工人中观察到的可吸入结晶硅累积暴露与肺癌死亡率之间的剂量反应关系表明，矽肺不是硅相关肺癌发生的必要伴随条件。然而，队列中矽肺病例数量相对较少以及就业后缺乏影像学数据限制了对结果的解读。
