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1.
职业医学     
04 2 12 4 广西锡矿矿尘致矽肺的危险度评价 /张华生…∥中华劳动卫生职业病杂志 2 0 0 2 ,2 0 ( 6 ) 4 30~4 32探索锡矿矿尘的致病强度和最低无害作用水平。选择广西锡矿 196 0~ 1974年期间接触矿尘至少 1年的男性矿工 4 471名建立回顾性接尘队列 ,并用以同一方法建立的瓷厂接尘队列与其进行比较 ;采用SAS中的生存检验分析软件进行非参数估算 ,评价锡矿矿尘致矽肺的危险度。结果 ,随访到 1994年底 ,锡矿队列工人矽肺发病 971例 ( 2 1 7% ) ,其中 81%的病例为19 58年前接尘对象 ,累积接触总粉尘量 (CTD)与矽肺危险度明显相关 :当C…  相似文献   

2.
目的 探讨钨矿接尘工矽肺危险度并对其防治措施进行评价。方法 采用职业流行病学队列研究方法 ,按接尘水平进行定量分析和定性分析 ,估算钨矿接尘工矽肺危险度。结果 ①接尘工累积接总粉尘不到 10mg/(m3 ·a) ,就有 45例矽肺发病 ,发病率为 0 7% ;②累积接总粉尘量与观察期矽肺发生差异有显著性 (P <0 .0 5 ) ;③钨矿矿尘空气中最高容许水平是 2mg/m3 ,相当累积呼吸性游离二氧化硅尘 0 0 41mg/(m3 ·a) ,此值在钨矿仍有病例发生。结论 我国当前采用的粉尘卫生标准在钨矿不是最低危害作用水平。同时也说明各类接尘厂矿的接触限值是有区别的。  相似文献   

3.
锡矿工人接尘与矽肺危险度评价   总被引:7,自引:1,他引:6  
目的探讨粉尘暴露与矽肺危险度之间的接触效应关系。方法选择广西4个锡矿1960~1965年间工作1年以上的3010名接尘工人进行队列研究。用生存分析法统计累积粉尘接触量和矽肺出现的关系。结果追访到1994年底,检出矽肺1015例(33.7%)。矽肺平均潜伏期21.3年。总粉尘浓度7.5mg/m3(TWA)。拟合生存分析模型表明:矽肺发病危险度与累积接尘量的关系适合Weibul分布。累积总粉尘接触量低于10mg·m-3·a-1时,矽肺危险小于1%;累积总粉尘接触量超过20mg·m-3·a-1时,矽肺累积危险度升高加快;累积总粉尘接触量达150mg·m-3·a-1时,矽肺危险超过68%。接尘时间与接尘量和矽肺危险度呈正相关。结论矽肺危险度与累积接尘量之间存在接触效应关系。  相似文献   

4.
滑石粉尘对陶瓷工人的健康效应   总被引:1,自引:0,他引:1  
目的:探讨滑石粉尘对陶瓷工人呼吸系统疾病发生发展的影响。方法:采用历史前瞻性队列研究,全体队列成员按是否接触矽尘和滑石尘分为不接尘组,矽尘组和滑石尘矽尘组,运用优势比(Odds Ratios,OR)方法作计算分析。结果:滑石尘矽尘组工人的非恶性呼吸道疾病(如尘肺)和肺心病的死亡危险度与矽尘组类似,但其癌症的死亡危险度,特别是肺癌死亡比不接尘组明显超高,OR=4.73,P<0.01)。结论:认为颗粒型滑石可能是瓷厂工人中致肺癌因子,滑石粉尘对矽肺发病也有明显的促进作用。  相似文献   

5.
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  相似文献   

6.
杨剑  傅华 《中国职业医学》1991,18(5):270-273
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。  相似文献   

7.
我国矽尘防治中对矽尘表面性质重视的必要性   总被引:2,自引:1,他引:2  
矽尘是我国煤炭、采矿、橡胶、陶瓷、耐火材料、玻璃、冶金、铸造、石雕等多种行业的主要职业病危害因素之一.已报道的与接触矽尘有关的疾病包括矽肺、肺癌、慢性肾病、肺部感染、慢性阻塞性肺病、自身免疫性疾病、肺泡蛋白沉积症和肝细胞癌等.矽尘中游离二氧化硅百分含量的致矽肺作用已为世人公认,但同济医学院近20年来对4类接尘工人的研究发现:(1)54 651名钨矿、锡矿和瓷厂接尘工人中的10 053名矽肺患者,在吸入的粉尘量及其游离二氧化硅百分含量大致相等的情况下,钨矿工人发病率分别为锡矿工人和瓷厂工人的1.87及3.66倍;(2)接触低于国家容许浓度的铁矿尘(游离二氧化硅百分含量未超过10%),工人的尘肺发病率居高不下,与锡矿工人发病差异不大.这些研究提示除游离二氧化硅百分含量外,势必存在其他对矽尘致病作用有重大影响的因素.近20年来国内外研究较多的是矽尘表面性质对矽尘致病的影响.大量实验室资料表明,矽尘的表面性质可影响其毒性机制中的多个关键环节如自由基的形成,肺泡巨噬细胞的活化及凋亡等.国外一些学者已建议政府应重视矽尘的表面性质对矽尘毒性的影响.这一部分的研究在我国起步较晚,研究资料较少,为了探索矽尘表面性质在我国防治矽尘危害工作中的应用,本文汇总了1996~2005年矽尘表面性质对其毒性的影响以及影响矽尘表面性质的因素,包括实验室资料和流行病学资料,并介绍了矽尘表面性质的检测技术.  相似文献   

8.
瓷厂陶工尘肺发病规律探讨及影响因素分析   总被引:1,自引:1,他引:0  
目的 分析景德镇瓷厂陶工尘肺的发病规律,探讨陶工尘肺发病的影响因素,以指导今后的陶工尘肺防治工作.方法 采用队列研究方法对景德镇3个瓷厂1960年1月1日至1974年12月31日在册且工作>1 a的所有职工建立队列进行随访调查至2003年12月31日,队列人员中陶工尘肺诊断由景德镇疾病预防控制中心诊断组确诊,同时收集瓷厂历年粉尘监测资料.结果 队列人群4968例,共有接尘工人2992例.累计诊断0 期陶工尘肺757例、陶工尘肺587例,接尘工人陶工尘肺发病率为0.5%.陶工尘肺患者开始接尘年份以1950~1960年最多,发病年龄集中在40~60岁,平均潜伏期为(31.7±7.7)a,平均晋级年限分别为0 期晋Ⅰ期为7.5 a,Ⅰ期晋Ⅱ期为4.4 a,Ⅱ期晋Ⅲ期为6.9 a.陶工尘肺累积危险度与累积粉尘接触量之间有明显的接触剂量-反应关系,除累积粉尘接触量外,影响陶工尘肺发病的因素包括是否合并结核(RR=20.9,P<0.01),吸烟量(RR=1.3,P<0.05),开始接尘年份(RR=1.5,P<0.01)和性别(RR=2.0,P<0.01).结论 累积总粉尘接触量与陶工尘肺之间存在明显的剂量反应关系,合并结核,吸烟量,开始接尘年份和性别是影响陶工尘肺发病的危险因素.与其他行业的粉尘危害比较,陶工尘肺呈现潜伏期长,0 期陶工尘肺比例大,晋级快的特点.  相似文献   

9.
生产性粉尘作业危害程度分级标准修订方法的探讨   总被引:4,自引:0,他引:4  
目的为修订<生产性粉尘作业危害程度分级>(GB5817-86)标准提供依据.方法采用相关和回归方法,分析回顾性调查资料和用呼吸同步采样法测尘获得的现场调查资料,探讨以呼吸接触总粉尘浓度(mg/m3)、接尘时间肺总通气量(m3·d-1·人-1)和粉尘中游离SiO2含量(%)三者乘积值为呼吸接触游离SiO2剂量(mg·d1·人-1),作为粉尘作业危害程度分级剂量标准值.结果利用接触游离SiO2剂量并结合矽肺的剂量-效应关系,可将粉尘作业危害程度划分为5级0、Ⅰ、Ⅱ、Ⅲ、Ⅳ级(接触游离SiO2剂量分别为0~8.0、8.1~12.0、12.1~16.0、16 1~24.0、>24.0 mg·d-1·人-1.结论接触游离SiO2剂量与矽肺发病关系密切,用接触游离SiO2剂量作为粉尘危害程度分级指标可靠且简捷易行.  相似文献   

10.
某宝石加工厂矽肺的调查分析   总被引:4,自引:4,他引:4  
目的 调查某宝石加工厂工人矽肺的发病特征。方法 对某宝石加工厂接尘工人进行矽肺横断面流行病学调查。结果 该厂作业场所矽尘浓度平均为 3 3mg/m3 ,游离SiO2 含量平均为 93 1%。该厂矽肺发病率为 3 94%( 10 /2 5 4) ,发病年龄 ( 2 3 8± 3 0 2 )岁 ,接尘工龄为 ( 3 3 3± 1 47)年。患者X线胸片表现以q影为主。矽肺肺结核并发率为2 0 % ;矽肺患者肺活量 (VC)、用力肺活量 (FVC)、1秒钟用力呼气量 (FEV1) ,最大通气量 (MVV)值明显低于接尘工人 (P <0 0 5或P <0 0 1) ;完全丧失劳动能力者占 70 %。结论 宝石加工工人矽肺符合急进型矽肺的诊断 ,其特点为发病年龄小 ,接尘工龄短 ,肺通气功能明显损伤 ,致病残程度较重 ,预后较差。  相似文献   

11.
BACKGROUND: Epidemiological evaluations of the risk of silicosis in relation to exposure to crystalline silica have raised the question of whether different types of silica dust exposures vary with respect to their ability to cause silicosis. The aim of this study is to compare the risk of silicosis among cohorts of silica dust-exposed Chinese tin miners, tungsten miners, and pottery workers and to assess whether gravimetric measurements of respirable silica dust sufficiently determine the risk of silicosis or whether other factors of exposure may play a significant role. METHODS: Cohorts were selected from 20 Chinese mines and potteries. Inclusion criteria were starting employment after January 1, 1950 and being employed for at least 1 year during 1960-1974 in one of the selected workplaces. Radiological follow-up for silicosis onset was from January 1, 1950 through December 31, 1994. Silicosis was assessed according to the Chinese radiological criteria for diagnosis of pneumoconiosis (as suspect, Stage I, II, or III). Exposure-response relationships were estimated for silicosis of Stage I or higher. Silica dust exposure was estimated in terms of cumulative total dust exposure, calculated from a workplace, job title, and calendar year exposure matrix, and individual occupational histories. Cumulative total dust exposure was converted in two steps into cumulative respirable dust exposure and cumulative respirable silica dust exposure using conversion factors estimated from side-by-side measurements conducted in 1988-89. RESULTS: The male cohorts included 4,028 tin miners, 14,427 tungsten miners, and 4,547 pottery workers who had similar onset of employment and duration of follow-up. For a given exposure level, the risk of silicosis was higher for the tin and tungsten than the pottery workers. CONCLUSION: The observed differences in the risk of silicosis among the three cohorts suggest that silica dust characteristics, in addition to cumulative respirable silica dust exposure, may affect the risk of silicosis.  相似文献   

12.
OBJECTIVES—To investigate the risk of silicosis among tin miners and to investigate the relation between silicosis and cumulative exposure to dust (Chinese total dust and respirable crystalline silica dust).
METHODS—A cohort study of 3010 miners exposed to silica dust and employed for at least 1 year during 1960-5 in any of four Chinese tin mines was conducted. Historical total dust data from China were used to create a job exposure matrix for facility, job title, and calendar year. The total dust exposure data from China were converted to estimates of exposure to respirable crystalline silica for comparison with findings from other epidemiological studies of silicosis. Each worker''s work history was abstracted from the complete employment records in mine files. Diagnoses of silicosis were based on 1986 Chinese pneumoconiosis Roentgen diagnostic criteria, which classified silicosis as stages I-III—similar to an International Labour Organisation (ILO) classification of 1/1 or greater.
RESULTS—There were 1015 (33.7%) miners identified with silicosis, who had a mean age of 48.3 years, with a mean of 21.3 years after first exposure (equivalent to 11.0 net years in a dusty job). Among those who had silicosis, 684 miners (67.4%) developed silicosis after exposure ended (a mean of 3.7 years after). The risk of silicosis was strongly related to cumulative exposure to silica dust and was well fitted by the Weibull distribution, with the risk of silicosis less than 0.1% when the Chinese measure of cumulative exposure to total dust (CTD) was under 10 mg/m3-years (or 0.36 mg/m3-years of respirable crystalline silica), increasing to 68.7% when CTD exposure was 150 mg/m3-years (or 5.4 mg/m3-years of respirable crystalline silica). Latency period was not correlated to the risk of silicosis or cumulative dose of exposure. This study predicts about a 36% cumulative risk of silicosis for a 45 year lifetime exposure to these tin mine dusts at the CTD exposure standard of 2 mg/m3, and a 55% risk at 45 years exposure to the current United States Occupational Safety and Health Administration and Mine Safety and Health Administration standards of 0.1 mg/m3 100% respirable crystalline silica dust.
CONCLUSIONS—A clear exposure-response relation was detected for silicosis in Chinese tin miners. The study results were similar to most, but not all, findings from other large scale exposure-response studies.


  相似文献   

13.
BACKGROUND: It is hypothesized that surface occlusion by alumino-silicate affects the toxic activity of silica particles in respirable dust. In conjunction with an epidemiological investigation of silicosis disease risk in Chinese tin and tungsten mine and pottery workplaces, we analyzed respirable silica dusts using a multiple-voltage scanning electron microscopy-energy dispersive X-ray spectroscopy (MVSEM-EDS). METHODS: Forty-seven samples of respirable sized dust were collected on filters from 13 worksites and were analyzed by MVSEM-EDS using high (20 keV) and low (5 keV) electron beam accelerating voltages. Changes in the silicon-to-aluminum X-ray line intensity ratio between the two voltages are compared particle-by-particle with the 90th percentile value of the same measurements for a ground glass homogeneous control sample. This provides an index that distinguishes a silica particle that is homogeneously aluminum-contaminated from a clay-coated silica particle. RESULTS: The average sample percentages of respirable-sized silica particles alumino-silicate occlusion were: 45% for potteries, 18% for tin mines, and 13% for tungsten mines. The difference between the pottery and the metal mine worksites accounted for one third of an overall chi-square statistic for differences in change in measured silicon fraction between the samples. CONCLUSION: The companion epidemiological study found lower silicosis risk per unit cumulative respirable silica dust exposure for pottery workers compared to metal miners. Using these surface analysis results resolves differences in risk when exposure is normalized to cumulative respirable surface-available silica dust.  相似文献   

14.
OBJECTIVES: To investigate the following questions. (1) Is silica dust on its own, without the presence of silicosis, associated with an increased risk of pulmonary tuberculosis (PTB) in workers exposed to silica dust? (2) In the absence of silicosis is the excess risk dose related? (3) What is the predominant chronological sequence between the development of PTB and the development of silicosis after the end of exposure to dust? METHODS: A cohort of 2255 white South African gold miners has been followed up from 1968 to 1971, when they were 45-55 years of age, to 31 December 1995 for the incidence of PTB. During the follow up 1592 (71%) men died. Of these, 1296 (81%) had a necropsy done at the National Centre for Occupational Health (NCOH) to determine the presence of silicosis and PTB. The incidence of PTB in the cohort was studied relative to cumulative exposure to dust and the onset of silicosis. For the miners with necropsy, the incidence for PTB was studied relative to the severity of silicosis found at necropsy. RESULTS: There were 115 subjects who developed PTB. The total person- years of follow up was 39,319. For the whole cohort, the factors associated with increased risk of PTB were cumulative exposure to dust (mg/m3.y) (the adjusted rate ratio (RR) 1.07; (95% confidence interval (95% CI) 1.04 to 1.10)), silicosis diagnosed radiologically (3.96 (2.59 to 6.06)), and tobacco pack-years (1.02 (1.01 to 1.03)). The RR (95% CI) for PTB increased with increasing quartiles of cumulative exposure to dust 1.0, 1.51 (0.78 to 2.91), 2.35 (1.28 to 4.32), and 3.22 (1.75 to 5.90). In miners who did not have radiologically diagnosed silicosis (n = 1934, PTB = 74), the adjusted RR (95% CI) for PTB and cumulative exposure to dust was 1.10 (1.06 to 1.13), and increased with quartiles of cumulative exposure to dust as 1.00, 1.46 (0.70 to 3.03), 2.67 (1.37 to 5.23), and 4.01 (2.04 to 7.88). For the subjects who had a necropsy (n = 1296, PTB = 70), the adjusted RR (95% CI) for PTB increased with the severity of silicosis found at necropsy; 1.0 for no silicosis, 1.88 (0.97 to 3.64) for negligible, 2.69 (1.35 to 5.37) for slight, and 2.30 (1.16 to 4.58) for moderate or marked silicosis. For subjects who had a necropsy and no silicosis (n = 577, PTB = 18), the adjusted RR (95% CI) increased slightly with quartiles of cumulative dust 1.0, 1.11 (0.31 to 4.00), 1.42 (0.43 to 4.72), and 1.38 (0.33 to 5.62). CONCLUSION: Exposure to silica dust is a risk factor for the development of PTB in the absence of silicosis, even after exposure to silica dust ends. The risk of PTB increases with the presence of silicosis, and in miners without radiological silicosis, with quartiles of exposure to dust. The severity of silicosis diagnosed at necropsy was associated with increasing risk of PTB and even < 5 nodules--that is, undetectable radiologically--was associated with an increased risk of PTB. The diagnosis of PTB was on average 7.6 years after the end of exposure to dust, at around 60 years of age. The onset of radiological silicosis preceded the diagnosis of PTB in 90.2% of the cases with PTB who had silicosis. The results have implications for medical surveillance of workers exposed to silica dust after the end of exposure.    相似文献   

15.
OBJECTIVES. This study sought to estimate the risk of silicosis by cumulative exposure-years in a cohort of miners exposed to silica, as well as the lifetime risk of silicosis under the current Occupational Safety and Health Administration (OSHA) standard (0.09 mg/m3). METHODS. In a cohort study of 3330 gold miners who worked at least 1 year underground from 1940 to 1965 (average 9 years) and were exposed to a median silica level of 0.05 mg/m3 (0.15 mg/m3 for those hired before 1930), 170 cases of silicosis were determined from either death certificates or two cross-sectional radiographic surveys. RESULTS. The risk of silicosis was less than 1% with a cumulative exposure under 0.5 mg/m3-years, increasing to 68% to 84% for the highest cumulative exposure category of more than 4 mg/m3-years. Cumulative exposure was the best predictor of disease, followed by duration of exposure and average exposure. After adjustment for competing risks of death, a 45-year exposure under the current OSHA standard would lead to a lifetime risk of silicosis of 35% to 47%. CONCLUSIONS. Almost 2 million US workers are currently exposed to silica. Our results add to a small but increasing body of literature that suggests that the current OSHA silica exposure level is unacceptably high.  相似文献   

16.
An analysis was conducted on a cohort of Chinese pottery workers to estimate the exposure-response relationship between respirable crystalline silica dust exposure and the incidence of radiographically diagnosed silicosis, and to estimate the long-term risk of developing silicosis until the age of 65. The cohort comprised 3,250 employees with a median follow-up duration of around 37 years. Incident cases of silicosis were identified via silicosis registries (Chinese X-ray stage I, similar to International Labor Organisation classification scheme profusion category 1/1). Individual exposure to respirable crystalline silica dust was estimated based on over 100,000 historical dust measurements. The association between dust exposure, incidence and long-time risk of silicosis was quantified by Poisson regression analysis adjusted for age and smoking. The risk of silicosis depended not only on the cumulative respirable crystalline silica dust exposures, but also on the time-dependent respirable crystalline silica dust exposure pattern (long-term average concentration, highest annual concentration ever experienced and time since first exposure). A long-term "excess" risk of silicosis of approximately 1.5/1,000 was estimated among workers with all annual respirable crystalline silica dust concentration estimates less than 0.1 mg/m(3), using the German measurement strategy. This study indicates the importance of proper consideration of exposure information in risk quantification in epidemiological studies.  相似文献   

17.
To estimate the quantitative relation between exposure to respirable silica dust and risk of an attack of silicosis, 1151 workers exposed to silica dust and employed from 1958 to 1987 in a tungsten mine in China were investigated. The results showed that the ratio of respirable silica dust concentration to total silica dust concentration was 0.529. Then, the total silica dust concentration in historical surveillance and monitoring data was converted to respirable silica dust concentration. The free silica content in respirable dust determined by x ray diffraction averaged 24.7%. Multiple logistic regression was used for the dichotomous dependent variables (presence or absence of silicosis). The independent variables in the multiple logistic regression with presence of silicosis as the dependent variable were age when first exposed, tuberculosis (presence or absence), and cumulative exposure to respirable silica dust. The partial regression coefficient of individual cumulative exposure was estimated as 0.079. It implied a positive association between exposure to respirable silica dust and risk of an attack of silicosis. The exposure limit for respirable silica dust was estimated as 0.24 mg/m3 under given conditions.  相似文献   

18.
Nested case-control study of lung cancer in four Chinese tin mines   总被引:2,自引:0,他引:2  
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.

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