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矽肺对肺癌及总死亡影响的回顾性队列研究
引用本文:余德新,谢立亚,梁子超,黄子惠,谭卓明,陈志权.矽肺对肺癌及总死亡影响的回顾性队列研究[J].中华劳动卫生职业病杂志,2008,26(1):29-33.
作者姓名:余德新  谢立亚  梁子超  黄子惠  谭卓明  陈志权
作者单位:1. 香港中文大学社区及家庭医学系
2. 香港卫生署肺尘埃沉着病诊所
摘    要:目的 利用香港矽肺患者队列的资料进行分析,探讨矽尘、矽肺与肺癌的关系.方法 选择1981年1月1日至1998年12月31日期间在香港尘肺诊所登记的2789例男性矽肺病例为研究对象,取用同时期一般男性人群作为对照.用人年的方法估计各死因的标化死亡比(SMR),用Axelson's法间接调整吸烟的混杂影响.矽尘与肺癌的剂量-效应关系采用多因素p-spline平滑法模型来拟合最佳风险模型.结果 该组研究队列人数为2789,共观察24 992.6人年,失访率仅为2.9%.该队列主要工种为建筑工人(5 1.09%)和地下沉箱操作工人(37.54%).队列总死亡人数为853人,平均死亡年龄为(63.8±10.27)岁,整个队列中86例死于肺癌.全死因及全癌的SMR均明显上升,首位死因是呼吸道疾病,肺癌的5MR明显增加(SMR:1.69,95%CI:1.35~2.09).去除年龄、时期和吸烟的混杂因素的影响,矽肺对肺癌的相对危险度下降到1.12(95%CI:0.89~1.38).间接调整吸烟的混杂影响后建筑工人及地下沉箱工人肺癌的相对危险度分别为1.09(95%CI:0.82~1.42)和1.56(0.98~2.36).多因素p-spline平滑法风险模型分析显示,肺癌与累积呼吸性矽尘总量或平均矽尘浓度的关系无剂量-效应关系.结论 队列研究未发现接触矽尘或矽肺能增加肺癌死亡的危险,平滑法模型拟合的风险模型并不支持矽尘与肺癌死亡之间存在剂量-效应关系.

关 键 词:矽肺  肺肿瘤  死亡率  队列研究

A retrospective cohort study on mortality among silicotic workers in Hong Kong with emphasis on lung cancer
Ignatius TS YU,Lap ah TSE,Chi Chiu-leung,Tze wai-wong,Cheuk ming-tam,Alan ck-chan.A retrospective cohort study on mortality among silicotic workers in Hong Kong with emphasis on lung cancer[J].Chinese Journal of Industrial Hygiene and Occupational Diseases,2008,26(1):29-33.
Authors:Ignatius TS YU  Lap ah TSE  Chi Chiu-leung  Tze wai-wong  Cheuk ming-tam  Alan ck-chan
Institution:Department of Community & Family Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.
Abstract:OBJECTIVE: To investigate the relationship between silica or silicosis and lung cancer in a large cohort of silicotic workers in Hong Kong. METHODS: All workers with silicosis in Hong Kong diagnosed between 1981 and 1998 were followed up till the end of 1999 to ascertain their vital status and causes of death, using the corresponding mortality rates of Hong Kong males of the same period as external comparison. Standardized mortality ratios (SMR) for lung cancer and other major causes of death were calculated. Person-year method was used. Axelson's indirect method was performed to adjust for the confounding effect of smoking. Penalized smoothing spline (p-spline) models were used to evaluate the exposure-response relationship between silica dust exposure and lung cancer mortality. RESULTS: A total of 2789 newly diagnosed cases of silicosis were included in the cohort, with an overall 24 992.6 person-years of observations. The loss-to-follow-up rate was only 2.9%. Surface construction workers (51%) and underground caisson workers (37%) constituted the major part of the cohort. There were 853 silicotics observed with an average age at death of 63.8 years. The SMR for all causes and all cancers increased significantly. The leading cause of death was non-malignant respiratory diseases. About 86 deaths were from lung cancer, giving a SMR of 1.69 (95% CI: 1.35 approximately 2.09). The risk of lung cancer death among workers in surface construction, underground caisson, and entire cohort was reduced to 1.12 (95% CI: 0.89 approximately 1.38), 1.09 (95% CI: 0.82 approximately 1.42) and 1.56 (95% CI: 0.98 approximately 2.36) respectively, after indirectly adjusting for smoking. RESULTS: from P-spline model did not show a clear exposure-response relationship between silica dust (CDE and MDC) and lung cancer mortality. CONCLUSION: This cohort study did not show an increased risk of lung cancer mortality among silicotic workers. P-spline model does not support an exposure-response relationship between silica dust exposure and lung cancer mortality.
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