矽肺对肺癌及总死亡影响的回顾性队列研究

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.     

某矿井下接尘,矽肺,吸烟与肺癌发病关系的研究

为了评价井下接尘、矽肺、吸烟与肺癌发病的关系,在大厂锡矿职工人群中进行了一次肺癌的病例-对照研究。结果发现,职工肺癌发病主要与井下接尘和吸烟有关。非条件Logistic回归模型的多因素分析表明,矽肺与增加肺癌发病的危险度无显著性意义,接尘与吸烟之间也无效应修饰作用。     

不同类型厂矿接尘工人肺癌病因学研究──矽尘或矽肺与肺癌的关系

为评价游离二氧化硅（简称矽尘或ＳｉＯ２）是否致肺癌？矽肺是否是肺癌前变基础？选择四类接尘厂矿进行队列和队列内病例对照研究。队列对象６８２８５人。有矽肺６４８７例，肺癌３３０例（男３１９，女１１），配对照１３５８例。根据厂矿历年工业卫生记录和近期对已知致癌物监测结果，定量评估了每个对象的接尘水平及每个病例对照的累积接触量。研究对象追访到１９８９年底，死亡６１９２人。与全国居民死亡平均数计算的期望值近似。全死因中癌症是第一死因，但全癌低于国家居民死亡率。分析结果说明：（１）矽尘单独存在时不是肺致癌剂。肺癌不超高，与接尘关系不明显；（２）在６４８７名矽肺队列中，肺癌相对危险度仅比非矽肺高０．２２倍，主要反应在铜铁矿工人中（Ｒ＝２．２），而矽肺患病率最严重的钨矿工人，其肺癌危险度反而随接尘水平上升而下降，再则肺癌死亡率与矽肺期别不呈正比；形态学上观察也不支持肺癌病变与矽肺纤维化病变相关。本研究结果难以支持矽尘或矽肺与肺癌病因学相关的假说。     

吸烟校正因素间接调整法在职业流行病学队列研究中的应用

目的介绍一种新的吸烟校正因素间接调整法在职业流行病学队列研究中的应用。方法以1981—1999年香港男性矽肺回顾性队列研究人群纯石英暴露组作为研究实例,用吸烟组[1/((1-PAR%)×RR)]与非吸烟组(1/(1-PAR%))各自的吸烟校正因素校正原始的标准化死亡比(SMR),用暴露超相对危险度和增效指数作为指标来判断吸烟与暴露对肺癌死亡的危险有无偏离乘法和相加模型。结果非吸烟和吸烟组矽肺队列人群的吸烟校正因素分别为1/0.33和1/1.62,校正吸烟后矽肺队列肺癌的SMR由原来的1.61(95%CI:1.22～2.10)显著地下降到1.08(95%CI:0.81～1.41),结果与Axelson方法完全一致。矽肺超相对危险度和增效指数分别为0.63(95%CI:0.08～0.79)和0.90(95%CI:0.42～1.94),提示吸烟与矽肺对肺癌死亡的危险呈明显的负相乘交互作用。结论吸烟校正因素间接调整法的优势是能定量分析和评估吸烟的混杂和交互作用的影响,但也有局限性。     

二氧化硅,矽肺与肺癌的关系

通过耐火材料等四个行业的接尘人员中肺癌死亡回顾性队列调查,发现接尘人员中肺癌危险性明显高于非尘毒暴露组,而且肺癌标化死亡率随含硅量及接触浓度变化呈现出平行的趋势。矽肺合并肺癌多为早期矽肺,肺癌病变多分布在肺上叶,病理形态鳞癌较多。肺癌发生晚于矽肺。吸烟和矽肺同时存在时,有必要注意协同作用。     

铁矿工肺癌流行病学研究

对武钢3个铁矿10753名男性职工作了肺癌死亡的回顾性队列研究,测定了目前生产环境的粉尘、镍、镉、砷、氡及多环芳烃等的浓度,并对铁矿历史上的工业卫生资料作了总结分析。结果提示:赤铁矿(大冶铁矿)井下开采工中矽肺患者的肺癌死亡率超高,SMR=3.13(6/1.92)以1988年全国中小城市男性肺癌死亡率作参比,P<0.01。死亡率超高与是否接尘以及接尘水平无关。也不能用井下存在其他低水平致肺癌因子作解释。吸烟工人肺癌相对危险度大为升高,竟达13.71,但吸烟与接尘这2个因素对肺癌的作用是独立的。     

吸烟与矽肺：某矿区的定群研究

通过对1077名井下矿工队列的28年回顾性定群研究,发现吸烟组矽肺发病率为13.02%,非吸烟组为6.85%。吸烟组矽肺的标化发病率比为171.43(95%CI=144.69～203.97)。以接尘工龄作时间变量,用Weibull回归模型分析累积接尘量和吸烟对矽肺的影响。结果表明在平衡了接尘工龄后,累积接尘量和吸烟对矽肺发病的影响有显著性意义,说明了有吸烟习惯的接尘工人发生矽肺的危险度比不吸烟者大。因此,在预防矽肺的措施上,应强调控制吸烟的重要性。     

铁矿工人肺癌回顾性队列研究

对１５个铁矿采矿工人的肺癌进行了回顾性队列研究。队列由１６９５１名１９７１年前入放的男职工组成,观察期从１９８０年至１９８９年,失访７６０人（４．５％）,队列内非接尘人群是接尘人群各群的对照人群。接尘人群及其井下、露天、赤铁矿、磁铁矿各舸矿各组中癌均无明显超量。但接尘人群分为非矽肺和矽肺两群时组,矽肺患者人群的肺癌显示超量。赤铁矿、磁铁矿、井下矿、吴矿各群组都再分为非矽肺和矽肺两群组时,除露天采矿     

金属矿尘接触与肺癌发病的危险度定量评价

本文对大厂矿长坡锡矿1960～1974年井下接尘的工人进行了一次回顾性定群研究。研究队列共1113人,贡献人年26780。观察期间死于肺癌45人,与全国、上海人口比较,SMR分别为2184和519。以累计接尘量作定量评价的结果表明,工人吸入的矿尘与肺癌发病呈明显的剂量—反应关系。用对数线性模型拟合接尘量与吸烟量对肺癌发病的作用,发现接尘量与吸烟量同时引入模型后拟合优度最佳。控制吸烟因素后,不同累计接尘量水平对肺癌发病的相对危险度逐次为4.18、5.20、13.01、16.07;控制接尘量后,不同吸烟量的相对危险度分别为1.74、4.19,接尘量与吸烟量及肺癌发病危险度都呈现剂量—反应关系,表明接尘和吸烟同时为肺癌发病的危险因子。     

不同类型厂矿接尘工人肺癌病因学研究

为评价游离二化硅是否致肺癌？矽肺是否是肺癌前变基础？选择四类接尘厂矿进行队列和队列内病例对照研究。队列对象６８２８５人。有矽肺６４８７例，肺癌３３０例，配对照１３５８例。根据厂矿历年工业卫生记录和近期对书籍致癌物监测结果，定量评估了每个对象的接尘水平及每个病例对照的积接触量。研究对象追访到１９８９年底，死亡６１９２人，与全国居民亡平均数计算的期望值近似。全死因中癌症是第一死因，但全癌低于国家居民死     

Lung cancer mortality among a cohort of men in a silicotic register

To examine any association between silicosis and lung cancer, the clinic records of a cohort of 1502 silicotic workers diagnosed after 1981 were reviewed. All of the essential data, including occupational exposure, smoking habits, radiographic extent of silicosis, and vital status of each subject, were noted. The standardized mortality ratio for various causes of death was calculated. Thirty-three patients died from lung cancer, giving a standardized mortality ratio of 1.94 (95% confidence interval, 1.35 to 2.70). However, smoking accounted for most of the excess of lung cancer deaths among the silicotic workers in the cohort, and no consistent relationship between lung cancer mortality risk and either duration of exposure to silica dust or severity of silicosis was observed. There is no conclusive evidence in our data to support the hypothesis that lung cancer may be associated with silicosis.     

肺癌病因研究中接尘量计算的真实性评价

为评价肺癌病例对照研究中接尘剂量估算方法的真实性,对广西锡矿病因研究对象进行了重新计算。广西锡矿队列发现男性肺癌死者１３０例,配对照６２７例。共７５７人。其中接法工人５７２名,发现各期矽肺共２４３例,根据在斩工业卫生监测资料估算所有接尘工人的累积总粉尘接触量,再计算不同接尘水平下矽肺的发病率。结果显示,随接尘水平上升,矽肺发病率升高,两者存在明显的接触剂量反应关系。完全符合矽肺发病特点。从而间接证     

Silica exposure, silicosis, and lung cancer: a necropsy study

Recent studies of the association between lung cancer and silicosis and silica dust have been inconclusive; some showing positive association and some showing none. The present study matched 231 cases of lung cancer with 318 controls by year of birth. Subjects were selected from the necropsy records of the National Centre for Occupational Health. Data on intensity and duration of exposure to silica dust were obtained from personnel records. Presence or absence of lung cancer and the presence and severity of silicosis of the parenchyma, pleura, and hilar glands were documented from necropsy reports. Smoking data were abstracted from records of routine examinations. No case-control differences were noted for any of the exposure indicators including cumulative dust exposure, total dusty shifts, weighted average intensity of exposure, total underground shifts, and shifts in high dust. Similarly, no association was found between lung cancer and the presence or severity of silicosis and any site. Stratified analyses showed neither significant nor suggestive trends when case-control comparisons for silicosis were examined by level of dust exposure or smoking. Reasons for disparity between these results and those of some other studies may include concomitant exposures to radon daughters, asbestos, diesel emissions, and cigarette smoking; idiosyncracies of the compensation process; and the possibility of a threshold in the relation(s).     

Silica exposure, silicosis, and lung cancer: a necropsy study.

Recent studies of the association between lung cancer and silicosis and silica dust have been inconclusive; some showing positive association and some showing none. The present study matched 231 cases of lung cancer with 318 controls by year of birth. Subjects were selected from the necropsy records of the National Centre for Occupational Health. Data on intensity and duration of exposure to silica dust were obtained from personnel records. Presence or absence of lung cancer and the presence and severity of silicosis of the parenchyma, pleura, and hilar glands were documented from necropsy reports. Smoking data were abstracted from records of routine examinations. No case-control differences were noted for any of the exposure indicators including cumulative dust exposure, total dusty shifts, weighted average intensity of exposure, total underground shifts, and shifts in high dust. Similarly, no association was found between lung cancer and the presence or severity of silicosis and any site. Stratified analyses showed neither significant nor suggestive trends when case-control comparisons for silicosis were examined by level of dust exposure or smoking. Reasons for disparity between these results and those of some other studies may include concomitant exposures to radon daughters, asbestos, diesel emissions, and cigarette smoking; idiosyncracies of the compensation process; and the possibility of a threshold in the relation(s).     

Case-control study of silicosis, silica exposure, and lung cancer in white South African gold miners

A case-control study was undertaken to assess the association between lung cancer and silicosis or silica dust exposure in white South African gold miners. Cases and controls were identified from deaths reported to the Gold Miners Provident Fund for the period January, 1979-October, 1983. Two controls were matched to each case by year of birth (+/- 2 years) and by smoking (+/- 5 cigarettes or equivalents per day) assessed 10 years (+/- 2 years) prior to death. One hundred thirty-three matched triplets were identified. The results showed no overall association between lung cancer and radiological silicosis (OR = 1.08, p = 0.92). Autopsy data indicated no overall associations between lung cancer and silicosis of the lung parenchyma (OR = 1.49, p = 0.11), the pleura (OR = 0.72, p = 0.30), or the hilar glands (OR = 0.85, p = 0.72). A trend toward increased severity of silicosis of the parenchyma was evident; however, this was not statistically significant (p = 0.08). Odds ratios for lung cancer and silicosis were higher at lower levels of cumulative silica dust exposure (ORs = 2.43, 1.72, 1.35 and 0.62 for lung cancer and autopsy silicosis of the parenchyma for the lowest, second, third, and highest quartiles of dust exposure, respectively; all p greater than 0.05). Cases did not differ from controls for total silica dust exposure, length of exposure, weighted average intensity of exposure, or number of shifts at high dust (all p greater than 0.20). The data do not support the hypothesis of a carcinogenic role for silica dust and no statistically significant associations were found between lung cancer and silicosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nested case-control study of lung cancer in four Chinese tin mines

Objectives: To evaluate the relation between occupational dust exposure and lung cancer in tin mines. This is an update of a previous study of miners with high exposure to dust at four tin mines in southern China.

Methods: A nested case-control study of 130 male lung cancer cases and 627 controls was initiated from a cohort study of 7855 subjects employed at least 1 year between 1972 and 1974 in four tin mines in China. Three of the tin mines were in Dachang and one was in Limu. Cumulative total exposure to dust and cumulative exposure to arsenic were calculated for each person based on industrial hygiene records. Measurements of arsenic, polycyclic aromatic hydrocarbons (PAHs), and radon in the work sites were also evaluated. Odds ratios (ORs), standard statistic analysis and logistic regression were used for analyses.

Results: Increased risk of lung cancer was related to cumulative exposure to dust, duration of exposure, cumulative exposure to arsenic, and tobacco smoking. The risk ratios for low, medium, and high cumulative exposure to dust were 2.1 (95% confidence interval (95% CI) 1.1 to 3.8), 1.7 (95% CI 0.9 to 3.1), and 2.8 (95% CI 1.6 to 5.0) respectively after adjustment for smoking. The risk for lung cancer among workers with short, medium, and long exposure to dust were 1.9 (95% CI 1.0 to 3.5), 2.3 (95% CI 1.3 to 4.1), and 2.3 (95% CI 1.2 to 4.2) respectively after adjusting for smoking. Several sets of risk factors for lung cancer were compared, and the best predictive model included tobacco smoking (OR=1.6, 95% CI 1.1 to 2.4) and cumulative exposure to arsenic (ORs for different groups from low to high exposure were 2.1 (95% CI 1.1 to 3.9); 2.1 (95% CI 1.1 to 3.9); 1.8 (95% CI 1.0 to 3.6); and 3.6 (95% CI 1.8 5 to 7.3)). No excess of lung cancer was found among silicotic subjects in the Limu tin mine although there was a high prevelance of silicosis. Exposures to radon were low in the four tin mines and no carcinogenic PAHs were detected.

Conclusions: These findings provide little support for the hypothesis that respirable crystalline silica induces lung cancer. Ore dust in work sites acts as a carrier, the exposure to arsenic and tobacco smoking play a more important part in carcinogenesis of lung cancer in tin miners. Silicosis seems not to be related to the increased risk of lung cancer.

     

Silica exposure, silicosis, and lung cancer: a mortality study of South African gold miners.

The effects of exposure to gold mining dust with a high concentration of free silica and tobacco smoking on mortality from lung cancer was assessed in a sample of 2209 white South African gold miners who started mining exposure during 1936-43, and were selected for a study of respiratory disorders in 1968-71 when they were aged 45-54. The mortality follow up was from 1968-71 to 30 December 1986. The relative risk for the effect of dust cumulated to the start of the follow up period was estimated as 1.023 (95% confidence interval (CI) 1.005-1.042) for a unit of 1000 particle-years. The combined effect of dust and tobacco smoking was better fitted by the multiplicative model than the additive model, suggesting that the two exposures act synergistically. No association between lung cancer and silicosis of the parenchyma or pleura was found, but a positive association existed between silicosis of the hilar glands and lung cancer.